Clinical Diagnosis and Management of OCULAR TRAUMA

System requirement: • Windows XP or above • Power DVD player (Software) • Windows media player 10.0 version or above Accompanying DVD ROM is playable only in Computer and not in DVD player. Kindly wait for few seconds for DVD to autorun. If it does not autorun then please do the following: • Click on my computer • Click the DVD drive labelled JAYPEE and after opening the drive, kindly double click the file Jaypee Clinical Diagnosis and Management of OCULAR TRAUMA

Editors

Ashok Garg MS PhD FIAO (Bel) FRSM FAIMS ADM FICA Jose M Ruiz-Moreno MD PhD International and National Gold Medalist Professor of Ophthalmology Chairman and Medical Director Albacete Medical School, University of Garg Eye Institute and Research Centre Castilla La Mancha 235-Model Town, Dabra Chowk Avendia de Almansa, 14 02006, ALBACETE Hisar-125005, India Spain

B Shukla MS PhD MAMS FICS T Mark Johnson MD FRCS Director of Research Consultant Vitreo Retinal Surgeon RJN Institute of Ophthalmology National Retina Institute Chandra Bhawan, 1, Jhansi Road Suite 101, 5530 Wisconsin Ave Gwalior-474002, India Chevy Chase 20815, USA

Jerome Jean Bovet MD Keiki R Mehta MS DO FRSH FIOS Consultant Ophthalmic Surgeon FMH Chairman and Medical Director Clinique de L’oeil Mehta International Eye Institute and 15, Avenue Du Bois-de-law-Chapelle Colaba Eye Hospital CH-1213, Onex, Switzerland Seaside, 147, Shahid Bhagat Singh Road, Mumbai-400005 Mahipal S Sachdev MD India Chairman and Medical Director Centre for Sight, B-5/24, Safdarjung Enclave Bojan Pajic MD New Delhi-110029, India Chief of the Cornea and Refractive Surgery Department CS Dhull MS PhD FIAO Klinik Pallas Louis Giroud- Professor and Head Str. 20 4600, Olten Regional Eye Institute of Ophthalmology Switzerland Pt. BD PGIMS, Rohtak-124001, India

Belquiz A Nassaralla MD PhD Consultant Ophthalmic Surgeon Department of Cornea and Refractive Surgery Goiania Eye Institute, Goiania GO, Brazil

Cyres K Mehta MS FSVH FAGE Director and Consultant Mehta International Eye Institute and Colaba Eye Hospital Seaside, 147, Sahid Bhagat Singh Road, Mumbai-400005, India Foreword Bruce Wallace

®

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi • Ahmedabad • Bengaluru • Chennai • Hyderabad • Kochi • Kolkata Lucknow • Mumbai • Nagpur • St Louis (USA) Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd Corporate Office 4838/24 Ansari Road, Daryaganj, New Delhi - 110002, India, +91-11-43574357 (20 lines) Registered Office B-3 EMCA House, 23/23B Ansari Road, Daryaganj, New Delhi 110 002, India Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672, Rel: +91-11-32558559, Fax: +91-11-23276490, +91-11-23245683 e-mail: [email protected], Website: www.jaypeebrothers.com Branches • 2/B, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380 015, Phones: +91-79-26926233, Rel: +91-79-32988717 Fax: +91-79-26927094, e-mail: [email protected] • 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East Bengaluru 560 001, Phones: +91-80-22285971, +91-80-22382956, +91-80-22372664 Rel: +91-80-32714073, Fax: +91-80-22281761, e-mail: [email protected] • 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road Chennai 600 008, Phones: +91-44-28193265, +91-44-28194897, Rel: +91-44-32972089, Fax: +91-44-28193231, e-mail: [email protected] • 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road Hyderabad 500 095, Phones: +91-40-66610020, +91-40-24758498, Rel:+91-40-32940929 Fax:+91-40-24758499, e-mail: [email protected] • No. 41/3098, B & B1, Kuruvi Building, St. Vincent Road Kochi 682 018, Kerala, Phones: +91-484-4036109, +91-484-2395739, +91-484-2395740 e-mail: [email protected] • 1-A Indian Mirror Street, Wellington Square Kolkata 700 013, Phones: +91-33-22651926, +91-33-22276404, +91-33-22276415 Rel: +91-33-32901926, Fax: +91-33-22656075, e-mail: [email protected] • Lekhraj Market III, B-2, Sector-4, Faizabad Road, Indira Nagar Lucknow 226 016, Phones: +91-522-3040553, +91-522-3040554 e-mail: [email protected] • 106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital, Parel Mumbai 400012, Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896 Fax: +91-22-24160828, e-mail: [email protected] • “KAMALPUSHPA” 38, Reshimbag, Opp. Mohota Science College, Umred Road Nagpur 440 009 (MS), Phone: Rel: +91-712-3245220 Fax: +91-712-2704275, e-mail: [email protected]

USA Office 1745, Pheasant Run Drive, Maryland Heights (Missouri), MO 63043, USA, Ph: 001-636-6279734 e-mail: [email protected], [email protected]

Clinical Diagnosis and Management of Ocular Trauma © 2009, Editors All rights reserved. No part of this publication and DVD ROM should be reproduced, stored in a retrieval system, or transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the editors and the publisher. This book has been published in good faith that the material provided by Contributors is original. Every effort is made to ensure accuracy of material, but the publisher, printer and editors will not be held responsible for any inadvertent error(s). In case of any dispute, all legal matters to be settled under Delhi jurisdiction only.

First Edition: 2009 ISBN 978-81-8448-470-0

Typeset at JPBMP typesetting unit Printed at Ajanta Offset Dedicated to

- My Respected Param Pujya Guru Sant Gurmeet Ram Rahim Singh Ji for his blessings and motivation. - My Respected Parents, teachers, my wife Dr Aruna Garg, son Abhishek and daughter Anshul for their constant support and patience during all these days of hard work. - My dear friend Dr Amar Agarwal, a renowned International Ophthalmologist for his constant support, guidance and expertise.

Ashok Garg

My family (Magali, my wife and Jorge, Guillermo and Magali my children) for the time, comprehension and patience that they have had with me during all these years of hard work.

Jose M Ruiz-Moreno

Sir Stewart Duke-Elder, my ideal and inspiration for ophthalmology.

B Shukla

My wife Joanne and my son Connor for providing me with their love, wisdom and support throughout the years.

T Mark Johnson

- Yveric, Luc and Fanny Laure. - Silvio Korol, who was not only a teacher but also an intellectual guide and a friend.

Jerome Jean Bovet Zena the light of my life. Keiki R Mehta

My family without whose help it would not have been possible to do book.

Mahipal S Sachdev

To my son Valentin Aleksandar.

Bojan Pajic

My dear wife Dr Indira Dhull and my children Tushar and Chirag.

CS Dhull

To my parents Lucia and Justino, for their blessings and motivation. To my husband Joao, a great partner at home and at work. To my children Arthur, Joao Neto and Anna Paula, who have been giving me constant support and love.

Belquiz A Nassaralla

- My parents for everything. - To Vini my Best friend.

Cyres K Mehta Contributors

Ajay Aurora MS Athiya Agarwal MD DO FRSH Chandresh Baid MS Divector Consultant Dr. Agarwal’s Eye Hospital Retina-Clinic Dr. Agarwal’s Eye Hospital 19, Cathedral Road Dr. Chaudhary Eye Centre and 19, Cathedral Road Chennai-600086, India Laser Vision, 4802 Bharat Ram Road Chennai-600086, India 24, Daryaganj, Chitra Ramamurthy MS New Delhi Belquiz A Nassaralla MD PhD Director India Consultant Ophthalmic Surgeon The Eye Foundation Department of Cornea and DB Road, Coimbatore-641002 Refractive Surgery Amar Agarwal MS FRCS FRC Ophth India Goiania Eye Institute, Goiania Consultant GO, Brazil Dr. Agarwal’s Eye Hospital Cristina Masini MD 19, Cathedral Road B Shukla MS PhD MAMS FICS Institute of Ophthalmology Chennai-600086, Director of Research University of Modena and Reggio Emilia India RJN Institute of Ophthalmology via del Pozzo 71-41100, Modena Chandra Bhawan, 1, Jhansi Road Italy Amol Mhatre MS Gwalior-474002, India Aditya Jyot Eye Hospital Pvt. Ltd Cyres K Mehta MS FSVH FAGE Binoo Nayer DOMS Plot No. 153, Road No.9 Director and Consultant Consultant Ophthalmologist Major Parmeshwaran Road Mehta International Eye Institute and Hindu Rao Hospital Opp. SIWS College, Gate No.3 Colaba Eye Hospital New Delhi, India Seaside, 147, Sahid Bhagat Singh Wadala, Mumbai-400031 Road, Mumbai-400005 India Bojan Pajic MD India Chief of the Cornea and Refractive Arturo Perez-Arteaga MD Surgery Department Klinik Pallas Louis Giroud- Daljit Singh MS DSC Medical Director Director Centro Oftalmologico Tlalnepantla Str.20 4600, Olten Switzerland Dr Daljit Singh’s Eye Hospital Dr Perez - Arteaga Vallarta No. 42 57-Joshi Colony Tlalnepantla, Centro, Boris Malyugin MD Phd Amritsar-143001, India Estado de Mexico Chief of Department of Cataract and 54000, Mexico Implant Surgery David F Chang MD Dy. Director General Clinical Professor of Ophthalmology Ashok Garg MS PhD FIAO (Bel) S. Fyodorov Eye Microsurgery University of California FRSM FAIMS ADM FICA Complex State Institution, 762, Altos Oaks Drive, Suite-1 International and National Gold Medalist 127486 Moscow Los Altos, CA 94024, Chairman and Medical Director Beskudnikovsky blvd 59A USA Garg Eye Institute and Research Centre Russia 235-Model Town, Dhivya A MS Brigitte Pajic-Eggspuhler MD Dabra Chowk AugenZentrumPajic (AZP) Dr. Agarwal’s Eye Hospital Hisar-125005 Research Institute 19, Cathedral Road India Titlisstrasse 44, 5734 Chennai-600086, Reinach, Switzerland India Ashok Sharma MS Director CS Dhull MS PhD FIAO Douglas W Morck MD Dr. Ashok Sharma’s Corneal Centre Professor and Head Department of Ophthalmology SCO 833-834 (2nd Floor) Regional Eye Institute of The Eye Care Centre Sector 22-A, Ophthalmology 2550, Willow St., Section G Chandigarh-160022 Pt. BD PGIMS, Rohtak-124001 Vancouver, BC V5Z3N9 India India Canada viii Clinical Diagnosis and Management of Ocular Trauma

D Ramamurthy MS GK Das MD Jerome Jean Bovet MD Medical Director Professor of Ophthalmology Consultant Ophthalmic Surgeon FMH The Eye Foundation UCMS and GTB Hospital Clinique de L’oeil D.B. Road Shahdara, New Delhi 15, Avenue Du Bois-de-law-Chapelle Coimbatore-641002 India CH-1213, Onex, Switzerland India Harmit Kaur MS João J Nassaralla Jr MD PhD D Shukla MS MAMS Daljit Singh Eye Hospital Rua L no 53 # 12o andar, Setro Oeste Consultant 57, Joshi Colony Goiania, Goias Vitreo Retina Unit Amritsar-143001 Brazil, ZC : 74.120-050 Aravind Eye Care System India Madurai (Tamil Nadu) John D Sheppard MD MMSc India Henry D Perry MD FACS Associate Professor of Ophthalmology Chief of Corneal Services Microbiology and Immunology Earl Crouch MD Nassau University Medical Center Clinical Director, Thomas R. Lee Eastern Virginia Medical School East Meadow, New York Centre for Ocular Pharmacology 880, Kemphsville Road 2000 North Village Ave Eastern Virginia Medical School Suite 2500, Norflock, Virginia-23502 Rockville Centre, NY 11570 Norfolk, Virginia 23501 USA USA USA

Eric D Crouch MD Hsi-Kung Kuo MD Jose M Ruiz-Moreno MD PhD Assistant Professor of Pediatric Department of Ophthamology Professor of Ophthalmology Ophthalmology Chang Gung Memorial Hospital Albacete Medical School, University of Eastern Virginia Medical School Castilla La Mancha 880, Kemphsville Road Kaohsiung Medical Center Avendia de Almansa, 14 02006, Suite 2500, Norflock, Virginia-23502 123, Ta-PEi Road, Niao-Sung ALBACETE USA Hsien, Kaohsiung, Hsien, 883 Spain Taiwan, ROC

Eric D Donnenfeld MD FACS Kanupriya Mhatre MS Ophthalmic Consultants of Long Island Ian Bell MD Aditya Jyot Eye Hospital Pvt. Ltd Suit 402 Consultant Ophthalmologist Plot No. 153, Road No.9 2000 North Village Ave. NY Eye Institute, New York Major Parmeshwaran Road Rockville Centre, NY 11570 USA Opp. SIWS College, Gate No.3 USA Wadala, Mumbai-400031 Indu R Singh MS India Essam El Toukhy MD FRCOPH Daljit Singh Eye Hospital Assistant Professor of Ophthalmology Karol Stasiak MS Cairo University 57, Joshi Colony Department of Pediatric Debuty Director, National Eye Center, Amritsar-143001 Ophthalmology, Hertza 9, 04-603 Egypt India Warsaw, Poland

Jaroslaw Kulinski MD Gaurav Luthra MS Keiki R Mehta MS DO FRSH FIOS Department of Pediatric Director, Drishti Eye Centre Chairman and Medical Director Dehradun, Uttrakhand Ophthalmology, Hertza 9, 04-603 Mehta International Eye Institute and India Warsaw Colaba Eye Hospital Poland Seaside, 147, Shahid Bhagat Singh Gian Maria Cavallini MD Road, Director Jasna Ljubic MD Mumbai-400005 Institute of Ophthalmology General Hospital India University of Modena and Reggio Emilia Department of Physical Medicine & via del Pozzo 71-41100, Modena Rehabilitation, 16000 Leskovac Kiranjit Singh MS Italy Serbia Daljit Singh Eye Hospital 57, Joshi Colony Gina Chavez MD Amritsar-143001 Javier A Montero MD Director India Pio del Rio Hortega University Department of Ophthalmology Hospital, Ophthalmology Unit The Eye Care Centre KK Bhalla MS 2550, Willow St., Section G C/Rondilla de Sta Teresa 9, Valladolid Daljit Singh Eye Hospital Vancouver, BC V5Z3N9 47010, 57, Joshi Colony Canada Spain Amritsar-143001, India Clinical Diagnosis and Management of Ocular Trauma ix

Leonardo Toledo Netto MD P Dutta MS Ritika Sachdev MS Medical Director Director Sr. Resident Olho.com Eye Clinic Dutta Eye Clinic, Gwalior Dr. RP Centre for Ophthalmic Sciences Department of Cornea and Cataract India AIIMS, Ansari Nagar Surgery, Aparecida de Goiania New Delhi-110029, India GO, Brazil Pei-Chang Wu MD Department of Ophthalmology Rupal H Trivedi MD MSCR Luca Campi MD Chang Gung Memorial Hospita- MUSC - Storm Eye Institute Institute of Ophthalmology Kaohsiung Medical Center 167 Ashley Ave University of Modena and Reggio Emilia 123, Ta-PEi Road, Niao-Sung Charleston, SC 29425, USA via del Pozzo 71-41100, Modena Hsien, Kaohsiung, Hsein, 883 Italy Taiwan, ROC Rupesh V Agrawal MD Consultant M Edward Wilson MD Quresh B Maskati MD Comprehensive Ophthalmology Professor of Ophthalmology Maskati Eye Clinic Uveitis and Ocular Trauma Department of Ophthalmology Mumbai, India LV Prasad Eye Institute Storm Eye Institute Kallam Anjil Reddy Campus Miles Center for Pediatric Rajni Sharma MD Banjara Hills, Hyderabad-500034 Ophthalmology Ex-Senior Resident India Medical University of South Carolina Department of Pediatrics Charleston, SC 29425 AIIMS, Ansari Nagar S Natarajan MS USA New Delhi-110029, India Chairman and Medical Director Aditya Jyot Eye Hospital Pvt. Ltd Mahipal S Sachdev MD Rajpal Vohra MD Plot No. 153, Road No.9 Chairman and Medical Director Professor of Ophthalmology Major Parmeshwaran Road Centre for Sight, B-5/24, Safdarjung Dr Rajendra Prasad for Ophthalmology Opp. SIWS College, Gate No.3 Enclave All India Institute of Medical Sciences Wadala, Mumbai-400031 New Delhi-110029, India New Delhi, India India

Marek E Prost MD Rania Abdel Salam MD Satish Desai MS Professor of Ophthalmology and Lecturer of Ophthalmology Consultant Ophthalmologist Cairo University, Director Center for Pediatric Shri Ganapati Netralaya National Eye Center, Egypt Ophthalmology Hertza 9, 04-603 Jalna (India) Warsaw, Poland Ranjit Singh MS Director Saumil Sheth MS Matteo Piovella MD Daljit Singh Eye Hospital Aditya Jyot Eye Hospital Pvt. Ltd Director 57, Joshi Colony Plot No. 153, Road No. 9 CMA Centro Microchirurgia Amritsar-143001, India Major Parmeshwaran Road Ambulatoriale Opp. SIWS College, Gate No. 3 Via Donizetti 24-20052 Ritesh Gupta MD Wadala, Mumbai-400031 Monza, Italy Senior Resident India Vitreo-Retina, Shui Lee MD FRCS Neeraj Sanduja MD Trauma and ROP Service Central Square Unit Director Dr. RP Centre for Ophthalmic Sciences 255-4231 Hazelbridge Delhi Retina Centre, AIIMS, New Delhi-110029, India Way Richmond 4802 Bharat Ram Road Rene Cano-Hidalgo MD BC, V6X-3L7 24, Daryaganj, New Delhi Chairman Canada India Institute of Ophthalmology Conde De Valenciana Simon P Holland MB FRCSC FRCOph NR Biswas MD DM Vitreous and Retina Department Clinical Professor Professor of Ocular Pharmacology Professor of Ophthamology Department of Ophthalmology Dr. RP Center for Ophthalmic Sciences National Institute of Mexico (UNAM) The Eye Care Centre AIIMS, Ansari Nagar Mexico 2550, Willow St., Section G New Delhi, India Vancouver, BC V5Z3N9 Richard Mathias MD Canada Department of Ophthalmology P Bhasin MS Simone Pelloni MD The Eye Care Centre Director Institute of Ophthalmology RJN Ophthalmic Institute 2550, Willow St, Section G University of Modena and Reggio Emilia Gwalior Vancouver, BC V5Z3N9 via del Pozzo 71-41100, Modena India Canada Italy x Clinical Diagnosis and Management of Ocular Trauma

Soosan Jacob MS Syed Asghar Hussain MS Viney Gupta MD Dr. Agarwal’s Eye Hospital Aditya Jyot Eye Hospital Pvt. Ltd Assistant Professor of Ophthamology 19, Cathedral Road Plot No. 153, Road No.9 Dr RP Center for Ophthalmic Sciences Chennai-600086, Major Parmeshwaran Road AIIMS, Ansari Nagar India Opp. SIWS College, Gate No.3 New Delhi-110029, India Wadala, Mumbai-400031 Sumit Sachdeva MS India Assistant Professor of Ophthalmology Yog Raj Sharma MD RIO, PGIMS Professor of Ophthalmology T Mark Johnson MD FRCS Rohtak, India Dr. R.P. Center for Ophthalmic Sciences Consultant Vitreo Retinal Surgeon AIIMS, Ansari Nagar National Retina Institute Sunil Vasani MS New Delhi -110029, India Suite 101, 5530 Wisconsin Ave “Eye-r-Us” Clinic Chevy Chase 20815, USA Gowalia tank, Mumbai-400036 Yumi G Ohashi B.Sc India Department of Ophthalmology Tracy L Lee MD The Eye Care Centre Department of Ophthalmology Sunita Agarwal MS DO PSVH The Eye Care Centre 2550, Willow St., Section G Dr. Agarwal’s Eye Hospital Vancouver, BC V5Z3N9, Canada 19, Cathedral Road 2550, Willow St., Section G Chennai-600086, India Vancouver, BC V5Z3N9, Canada Yuri Flores MD Consultant Supriya Dabir MS Vandana Jain MD Aditya Jyot Eye Hospital Pvt. Ltd Aditya Jyot Eye Hospital Pvt. Ltd Vitreoretina Surgeon Plot No. 153, Road No.9 Plot No. 153, Road No. 9 Centro Oftalmologico Tlalnepantla Major Parmeshwaran Road Major Parmeshwaran Road Dr. Perez - Arteaga Vallarta no.42 Opp. SIWS College, Gate No.3 Opp. SIWS College, Gate No. 3 Tlalnepantla, Centro, Wadala, Mumbai-400031 Wadala, Mumbai-400031 Estado de Mexico 54000, India India Mexico Foreword

I was called to examine a man in the hospital emergency room who had been injured in a motor vehicle accident. I was told the patient had an eye that was “red and swollen”. There was urgency in the voice of the consulting doctor, so I hurried to the hospital to examine this patient. After I arrived, I found the patient to have no evidence of a sight threatening problem. But, this man had definite signs of a skull fracture, open fracture of the right femur and probable rib fractures. And I was the first specialist called to see this patient. This experience reminded me of how serious ocular trauma can be to patients, their families and even our medical colleagues outside of Ophthalmology. The impact of an accident that could lead to loss of visual function is frightening. Fortunately, the evaluation and treatment of ocular injuries has improved significantly. Newer imaging systems and other diagnostic equipment provide better methods for detecting the extent of damage to the eye and adnexa. Advancements in microsurgical technology give us new equipment needed to repair a wide variety of ocular injuries. This important textbook, edited by Professor Garg, offers a step by step update to modern evaluation and treatment of ocular and adnexal trauma. Since all injury cases are unpredictable by nature, having a reliable reference to access information on the latest in diagnostic and surgical repair is valuable to all medical care professionals involved in the care of patients who are suddenly afflicted with traumatic eye disease. Congratulations to Professor Garg and his contributing editors who have provided us with a well organized, thorough and practical guide to handle traumatic ocular conditions.

Prof. Bruce Wallace MD Medical Director Wallace Eye Surgery 4110 Parliament Drive Alexandria, LA 71303 (USA) Tel.: 318-448-4488 www.wallaceeyesurgery.com

Preface

Ocular Trauma is an important and vast subject and has assumed greater significance in this present era of Modern Technology when greater industrial and vehicular revolution have taken place. As a result of this incidence, ocular trauma has increased sharply and now it is one of the leading causes of monocular blindness specially in children and in young generation. Early and effective treatment of ocular trauma is mandatory to achieve best possible outcome thus decreasing blindness. With latest technologies, equipment and techniques, it is possible to manage traumatized eyes in a better way. Very few International quality books are available on this important subject for the Ophthalmologists. Present book has been conceived and written to provide latest uptodate information on this vast subject. 56 chapters of this book have been written by International experts on this field covering both anterior and posterior segment ocular trauma. We have tried to cover all clinical aspects of ocular trauma in both segments. Accompanying video DVD ROM shows surgical skills by International Masters for Ocular Trauma Management. We are grateful to Shri Jitendar P Vij (CEO), Mr. Tarun Duneja (Director Publishing) and all staff members of M/s Jaypee Brothers Medical Publishers Pvt. Ltd. who took extraordinary efforts in the preparation of this book. We are sure that present book shall provide deep insight into state of art ocular trauma management in a simplified and comprehensive manner. This book shall be an integral part of shelf of every Ophthalmologist clinical chamber who have to encounter ocular trauma cases in their professional practice.

Editors

Contents

SECTION I PRELIMINARY AND BASIC CONSIDERATIONS IN OCULAR TRAUMA

1. Epidemiology and New Classification of Ocular Trauma ...... 3 João J Nassaralla Jr, Belquiz A Nassaralla (Brazil) 2. New Classification of Ocular Trauma...... 7 B Shukla, D Shukla (India) 3. Clinical Evaluation of Ocular Trauma...... 10 B Shukla (India) 4. Evaluation and Initial Management of a Patient with Ocular Trauma ...... 13 Rupesh V Agrawal (India)

SECTION II ANTERIOR SEGMENT OCULAR TRAUMA

5. Role of Ultrasound Biomicroscopy in Evaluation of the Anterior Segment in Closed Globe Injuries ...... 25 Ritika Sachdev, Mahipal S Sachdev, (India) 6. Management of Eyelid Inju0ries ...... 28 Rania Abdel Salam, Essam El Toukhy (Egypt) 7. Management of Lacrimal Injuries ...... 33 Rania Abdel Salam, Essam El Toukhy (Egypt) 8. Hyphema ...... 35 Earl Crouch, Eric Crouch (USA) 9. Management of Corneal Injuries ...... 41 Ashok Sharma (India) 10. Chemical Injuries of the Eye ...... 50 Quresh B Maskati (India) 11. Injuries of the Eye due to Physical Agents (Thermal, Ultrasonic and Electrical Injuries) ...... 55 Rupesh V Agrawal (India) 12. Radiational Injuries to the Eye ...... 59 Rupesh V Agrawal (India) 13. Traumatic Angle Recession GlaucomaL An Overview ...... 64 Cyres K Mehta, Keiki R Mehta (India) 14. Management of Blunt Trauma of Anterior Segment ...... 67 Ashok Sharma (India) 15. Management of Traumatic Cataract ...... 74 Rupesh V Agrawal, Satish Desai (India) 16. Management of Traumatic Luxation of the Crystalline Lens ...... 80 Arturo Pèrez-Arteaga, Yuri Flores (Mexico) xvi Clinical Diagnosis and Management of Ocular Trauma 17. Traumatic Cataract in Children ...... 86 Rupal H Trivedi, M Edward Wilson (USA) 18. Scleral Fixated IOL in Trauma ...... 94 Rupesh V Agrawal (India) 19. Iris Trauma ...... 100 Rupesh V Agrawal (India) 20. Post-traumatic Strabismus ...... 106 B Shukla, P Bhasin (India) 21. Management of Orbital Trauma and Fractures ...... 108 Rania Abdel Salam, Essam El Toukhy (Egypt) 22. Management of Anterior Segment Trauma: An Update ...... 125 CS Dhull, Sumit Sachdeva (India) 23. Glued IOL ...... 132 Amar Agarwal, Dhivya A, Soosan Jacob, Athiya Agarwal, Chandresh Baid, Ashok Garg (India)

SECTION III POSTERIOR SEGMENT OCULAR TRAUMA

24. Management of Traumatic Hemorrhages to the Posterior Segment ...... 139 Javier A Montero, Jose M Ruiz-Moreno (Spain) 25. Traumatic Retinal Detachments ...... 149 Neeraj Sanduja, Ajay Aurora, Gaurav Luthra (India) 26. Retained IOFB ...... 155 Neeraj Sanduja, Ajay Aurora, Gaurav Luthra (India) 27. Penetrating Posterior Segment Trauma ...... 160 T Mark Johnson (USA) 28. Traumatic Retinopathies ...... 167 Scott Pfahler, T Mark Johnson (USA) 29. Management of Endophthalmitis ...... 174 Pei-Chang Wu, Hsi-Kung Kuo (Taiwan) 30. Management of Pediatric Ocular Trauma ...... 181 Yog Raj Sharma, Ritesh Gupta, Rajni Sharma (India) 31. Management of Blunt Retinal Trauma ...... 189 Arturo Pérez-Arteaga, Yuri Flores (Mexico) 32. Applications of Stem Cell Therapy in Ophthalmology ...... 200 Rajpal Vohra (India) 33. Primary Globe Repair ...... 214 Rupesh V Agrawal (India)

SECTION IV IATROGENIC OCULAR TRAUMA AND ITS COMPLICATIONS MANAGEMENT

34. Management of Iatrogenic Inflammation of the Eye ...... 223 NR Biswas, GK Das, Viney Gupta (India) 35. Management of Postrefractive Keratitis ...... 229 Eric D Donnenfeld (USA) Clinical Diagnosis and Management of Ocular Trauma xvii 36. Optimized NSAIDs and Antibacterial Prophylaxis in Cataract Surgery ...... 232 Ashok Garg (India), Ian Bell (USA) 37. Optimizing Visual Outcomes with NSAIDs Therapy in Cataract and Refractive Surgery ...... 235 Eric D Donnenfeld, Henry D Perry (USA) 38. Management of Cystoid Macular Edema ...... 242 Arturo Pérez-Arteaga, René Cano-Hidalgo (Mexico) 39. Managing Intraoperative Floppy Iris Syndrome ...... 250 David F Chang (USA) 40. Toxic Anterior Segment Syndrome...... 254 Simon P Holland, Douglas W Morck, Richard Mathias, Tracy L Lee, Gina Chavez, Yumi G Ohashi (Canada) 41. Small Pupil Phaco: An Innovative Technique ...... 259 Boris Malyugin (USA)

SECTION V CURRENT CONCEPTS AND RECENT ADVANCES IN MANAGEMENT OF OCULAR TRAUMA

42. Trauma after Refractive Surgery ...... 269 D Ramamurthy, Chitra Ramamurthy (India) 43. Complication and Contusion after Phakic IOL ...... 273 Jerome Jean Bovet (Switzerland) 44. Management of Corneal Lacerations...... 279 Shui Lee (Canada) 45. Sports Injuries in Eye ...... 283 B Shukla, Binoo Nayar (India) 46. Management of Travel Eye Injuries ...... 286 Leonardo Toledo Netto, Belquiz A Nassaralla (Brazil) 47. Ocular Injuries after Vehicular Accident and Possible Prevention ...... 290 Bojan Pajic, Brigitte Pajic-Eggspuehler, Jasna Ljubic (Switzerland) 48. Bottle Cork Injury to the Eye...... 296 Gian Maria Cavallini, Matteo Forlini, Cristina Masini, Luca Campi, Simone Pelloni (Italy) 49. Ocular War Injuries...... 300 Jaroslaw Kulinski, Karol Stasiak, Marek E Prost (Poland) 50. Trauma of Anterior Eye Segment: An Update ...... 311 Boris Malyugin (Russia) 51. Management of Ocular Trauma with Plasma (Fugo) Knife ...... 319 Ranjit Singh, Indu R Singh, Kiranjit Singh, Harmit Kaur, KK Bhalla, Daljit Singh (India) 52. Chandelier Illumination and Bimanual Vitrectomy Used to Remove a Dislocated IOL ...... 328 Amar Agarwal, Soosan Jacob, Athiya Agarwal, Sunita Agarwal, Ashok Garg (India) 53. Principles and Management of Ocular Trauma...... 331 Syed Asghar Hussain, Amol Mhatre, Kanupriya Mhatre, Supriya Dabir, Saumil Sheth, Vandana Jain, S Natarajan (India) 54. Eyelid Injuries and Reconstruction: An Update ...... 345 Quresh Maskati, Sunil Vasani (India) 55. Prevention of Ocular Trauma ...... 349 B Shukla, P Dutta (India) 56. Endophthalmitis Preventiion Strategies ...... 352 John D Sheppard (USA) Index ...... 355 Preliminary and Basic Considerations in Ocular Trauma

CHAPTER Epidemiology and New Classification of Ocular Trauma 1 João J Nassaralla Jr, Belquiz A Nassaralla (Brazil)

Introduction WEIR; clinical trials in the field of ocular trauma cannot be planned; and the communication between An injury to the eye or its surrounding tissues is the ophthalmologists remains ambiguous.1,2 So, a most common cause for attendance at an eye hospital standardized terminology for eye injury has been emergency department. The extent of trauma may developed by the USEIR based on extensive range from simple superficial injuries to devastating experience and repeated reviews by international penetrating injuries of the eyelids, lacrimal system, and ophthalmic audiences. By always using the entire globe globe. The surgical management of such injuries is as the tissue of reference, classification is unambiguous, directed primarily at the restoration of normal ocular consistent, and simple. It provides definitions for the anatomy; the ultimate goal is to prevent secondary commonly used eye trauma terms within the complications and maximize the patient’s visual framework of a comprehensive system.1 prognosis. Dramatic improvements in the surgical management of ocular trauma have evolved over the past two decades. However, persistent inadequacy in Epidemiology the standardized documentation of eye injury morbi- dity and treatment outcome limits the development Eye injuries are a major and under recognized cause and widespread introduction of techniques for preven- of disabling ocular morbidity that especially affect the ting and improving the prognosis of serious eye young. The public health importance of such ocular trauma. trauma is undeniable. Injuries generate a significant Professional associations like the International and often unnecessary toll in terms of medical care, Society of Ocular Trauma (ISOT), and the United human suffering, long-term disability, productivity loss, States Eye Injury Registry (USEIR), have been formed rehabilitation services, and socioeconomic cost.1-3 to promote research, elaborate epidemiologic Globally, more than 500.000 blinding injuries investigations, highlighting preventable sources of occur every year. Approximately 1.6 million people injury, emerging patterns of trauma, treatment are blind owing to ocular trauma, 2.3 million are outcomes and disseminate its results. The USEIR is bilaterally visually impaired, and 19 million have presently working with the ISOT to establish the World unilateral visual loss.3,4 Every year, approximately 2 Eye Injury Registry (WEIR). International registries million eye injuries occur in the United States, of which, have been established or are in start-up phase in Brazil, more than 40 thousand results in permanent visual British Armed Forces, Bolivia, Canada, China, impairment.6,7 Prior studies in which the incidence of Colombia, Croatia, Finland, India, Italy, Germany, eye injury has been examined have produced varied Greece, Hungary, Israel, Kenya, Korea, Lithuania, results, in part because of study design differences.8- Mexico, New Zealand, Portugal, Romania, Saudi 13 When considering eye injuries requiring hospital Arabia, Singapore, Slovakia, Slovenia, South Africa, admission, rates have ranged from 8 to 57 per Spain, Switzerland, Turkey, Venezuela, West 100.000.8-13 Despite the heterogeneity of results, these Indies(Trinidad), Yugoslavia, Zimbabwe with assistance studies provide important information regarding the from the United States Eye Injury Registry.1 burden of eye injury. However, they have all been Unfortunately, the lack of an unambiguous limited to a single year or narrow time frame making common language remains a major limiting factor in it difficult to determine trends in injury rates over time. effectively sharing eye injury information. Without a In the United States, a population-based study standardized terminology of eye injury types, it is reported a prevalence rate of 19.8% and an average impossible to design projects like the USEIR or the annual incidence rate of 3.1 per 1000 population.14 4 Clinical Diagnosis and Management of Ocular Trauma In a more recent study from 1992 through 2002, the incidence of eye injury declined overall and the estimated rate of eye injury ranged from 8.2 to 13.0 per 1000 population.5 Worldwide, ocular trauma is a leading cause of no congenital monocular blindness among children.16-20 Children are disproportionately affected by ocular injuries. In the United States, a population-based study reported an annual incidence of ocular trauma in children of 15.2 per 100.000.18 In general, males are more frequently reported to have eye injuries than females.17-24 Results varied across studies regarding the age-specific frequency of eye injuries17-26 with some reporting a higher incidence in older children and others

in younger children. A study conducted among Fig. 1.2: Sources of eye injury1 Brazilian children found that the group aged 0 to 5 years was at greatest risk, regardless of sex, and that among those older than 5 years, eye injuries were in other industrialized countries, like Italy, where clinical more frequent in boys.26 research on ocular trauma is limited to the pediatric Although the overall financial cost derived from population and sportsmen.22,29,30 Available information ocular injuries can only be estimated, direct and indirect regarding the distribution and magnitude of ocular costs combined run into hundreds of millions of dollars trauma in developing countries is very scarce, and the per year. Developing countries carry the heaviest existing data are difficult to interpret because reporting burden, and they are the least able to afford the costs.8 is extremely poor and especially because of the Domestic accidents (40%), industrials (13%), and completely different settings of the occurrence of ocular street/highway accidents (13%) are the most common trauma.3 Among other factors, underreporting and lack circumstances in which ocular injury occurs, (Fig. 1.1). of standardized forms and national integrated databases Eye injuries incurred during athletic activity (13%) are make assessment of the current picture and compari- becoming more common with the increasing popularity sons within and across countries practically impossible.2 of indoor court games. A recent survey found In addition, developing countries often lack adequate racquetball to exceed other sports in generating ocular infrastructure for persons with eye injuries to reach a injuries, followed by tennis, baseball, basketball, and primary care center, when one exists, and the lack of soccer.1 awareness of preventive measures and/or immediate actions increases the risk for complications and consequent visual disability and blindness.8 From a public health and injury prevention perspective, current information on eye injuries rates is needed to develop effective plans for disseminating eye injury prevention materials to the public and to earmark adequate funding for these initiatives.1,2

New Classification The new classification of ocular trauma has been endorsed by the Board of Directors of the International Society of Ocular Trauma, the United States Eye Injury Fig. 1.1: Places of eye injury1 Registry, the Hungarian Eye Injury Registry, the Vitreous Society, the Retina Society, and the American Academy The most common sources of eye injuries are blunt of Ophthalmology. This classification system object (31%), sharp object (18%), and motor vehicle categorizes ocular injuries at the time of initial crash (9%), (Fig. 1.2). examination. It is designed to promote the use of While the incidence of ocular trauma has been standard terminology and assessment, with applications described in the United States,6,8,12,15 United Kingdom,10 to clinical management and research studies regarding Sweden,27 and Greece,28 it has not been well studied eye injuries (Fig. 1.3).1,2,32 Epidemiology and New Classification of Ocular Trauma 5 is present, each must have been caused by a different agent. 7. Intraocular foreign body injury (IOFB)—Retained foreign object(s) causing entrance laceration(s). An IOFB is technically a penetrating injury but is grouped separately because of different clinical implications (treatment modality, timing, endophthalmitis rate, etc.). 8. Perforating injury—Two full-thickness lacerations (entrance and exit) of the eyewall, usually caused by a sharp object or missile. The two wounds must have been caused by the same agent. Participation of individual treating ophthalmologists is critical to the development of comprehensive epidemiologic eye injury data. Documentation of each serious eye injury is important work, and, through this cooperative effort, will ultimately benefit all patients and physicians. It is expected that this system eventually will become the standardized international language Fig. 1.3: The proposed new ocular traumatology system.1 of ocular trauma terminology, improving accuracy in The green boxes show the diagnoses that are used in both clinical practice and research, irrespective of clinical practice geographic origin.

The new ocular trauma terminology system.1,2,31,32 provides definitions for the commonly used eye trauma terms as follows: References 1. Eyewall—For clinical and practical purposes, the 1. United States Eye Injury Registry. Eye trauma term eyewall must be restricted to the rigid epidemiology and prevention. Available at: http:// structures of the sclera and cornea. www.useironline.org/prevention.htm. Accessed July 6, 2008. 2. Closed-globe injury—The eyewall does not have 2. World Eye Injury Registry. Available at: http:// a full-thickness wound. Either there is no corneal www.weironline.org/prevention.htm. Accessed July 6, or scleral wound at all (contusion) or is it only partial 2008. thickness (lamellar laceration). 3. Serrano JC, Chalela P, Arias JD: Epidemiology of 3. Open-globe injury—The eyewall has a full-thickness Childhood Ocular Trauma in a Northeastern Colombian wound. The cornea and/or sclera sustained a Region. Arch Ophthalmol 2003;121:1439-1445. through-through injury; depending on the inciting 4. Pizzarello LD. Ocular trauma: time for action. Ophthalmic Epidemiol 1998;5:115-116. object’s characteristics and the injury’s circum- 5. Negrel AD, Thylefors B. The global impact of eye injuries. stances, ruptures and lacerations are distinguished; Ophthalmic Epidemiol 1998;5:143-169. the choroid and the retina may be intact, prolapsed 6. McGwin G, Xie A, Owsley C: The rate of eye injury in or damaged. the United States. Arch Ophthalmol 2005;123:970-976. 4. Rupture—Full-thickness wound of the eyewall, 7. Mieler W: Overview of ocular trauma. In Principles and caused by a blunt object; the impact results in Practice of Ophthalmology. 2nd edition. Edited by: Albert momentary increase of the intraocular pressure. D, Jakobiec F. Philadelphia, WB Saunders Co. 2001;5179. The eyewall gives way at its weakest point (at the 8. Tielsch JM, Parver L, Shankar B: Time trends in the impact site or elsewhere; example: an old cataract incidence of hospitalized ocular trauma. Arch wound dehisces even though the impact occurred Ophthalmol 1989; 107:519-523. elsewhere); the actual wound is produced by an 9. McCarty CA, Fu CL, Taylor HR: Epidemiology of ocular inside-out mechanism. trauma in Australia. Ophthalmology 1999; 106:1847- 5. Laceration—Full-thickness wound of the eyewall, 1852. usually caused by a sharp object; the wound occurs 10. Desai P, MacEwen CJ, Baines P, Minassian DC: Incidence of cases of ocular trauma admitted to hospital and at the impact site by an outside-in mechanism. incidence of blinding outcome. Br J Ophthalmol 1996; 6. Penetrating injury—Single laceration of the eyewall, 80:592-596. usually caused by a sharp object. No exit wound 11. Klopfer J, Tielsch JM, Vitale S, See LC, Canner JK: Ocular has occurred; if more than one entrance wound trauma in the United States: eye injuries resulting in 6 Clinical Diagnosis and Management of Ocular Trauma hospitalization, 1984 through 1987. Arch Ophthalmol 23. May DR, Kuhn FP, Morris RW, et al. The epidemiology 1992; 110:838-842. of serious eye injuries from the United States Eye Injury 12. Karlson TA, Klein BE: The incidence of acute hospital- Registry. Graefes Arch Clin Exp Ophthalmol treated eye injuries. Arch Ophthalmol 1986; 104:1473- 2000;238:153-157. 1476. 24. Nelson LB, Wilson TW, Jeffers JB. Eye injuries in 13. Wong TY, Tielsch JM: A population-based study on the childhood: demography, etiology, and prevention. incidence of severe ocular trauma in Singapore. Am J Pediatrics 1989;84:438-441. Ophthalmol 1999; 128:345-351. 25. Rapoport I, Romem M, Kinek M, et al. Eye injuries in 14. Wong TY, Klein BE, Klein R: The prevalence and 5-year children in Israel: a nationwide collaborative study. Arch incidence of ocular trauma. The Beaver Dam Eye Study. Ophthalmology 2000; 107:2196-2202. Ophthalmol 1990;108:376-379. 15. McGwin GJr, Hall TA, Xie A, Owsley C: Trends in Eye 26. Moreira CA Jr, Debert-Ribeiro M, Belfort R Jr. Injury in the United States, 1992–2001. Epidemiological study of eye injuries in Brazilian children. 16. MacEwen CJ, Baines PS, Desai P. Eye injuries in children: Arch Ophthalmol 1988;106:781-784. the current picture. Br J Ophthalmol 1999;83:933-936. 27. Blomdahl S, Norell S: Perforating eye injury in the 17. Jandeck C, Kellner U, Bornfeld N, Foerster MH. Open Stockholm population. Acta Ophthalmologica 1984; globe injuries in children. Graefes Arch Clin Exp 62:378-390. Ophthalmol 2000;238:420-426. 28. Mela EK, Dvorak GJ, Mantzouranis GA, Giakoumis AP, 18. Strahlman E, Elman M, Daub E, Baker S. Cause of Blatsios G, Andrikopoulos GK, Gartaganis SP: Ocular pediatric eye injuries: a population-based study. Arch trauma in a Greek population: review of 899 cases Ophthalmol 1990;108:603-606. resulting in hospitalization. Ophthalmic Epidemiol 2005; 19. Takvam JA, Midelfart A. Survey of eye injuries in 12:185-190. Norwegian children. Acta Ophthalmol (Copenh) 1993; 29. Capoferri C, Martorina M, Menga M, Sirianni P: Eye 71:500-505. injuries from traditional sports in Aosta Valley. 20. Cascairo MA, Mazow ML, Prager TC. Pediatric ocular Ophthalmologica 1994; 208:15-16. trauma: a retrospective survey. J Pediatr Ophthalmol 30. Bianco M, Vaiano AS, Colella F, Coccimiglio F, Moscetti Strabismus 1994;31:312-317. 21. MacEwen CJ. Ocular injuries. J R Coll Surg Edinb. M, Palmieri V, Focosi F, Zeppilli P, Vinger PF: Ocular 1999;44:317-323. Invest Ophthalmol Vis Sci 2006; complications of boxing. Br J Sports Med 2005; 39:70- 47:521-527. 74. 22. Cillino S, Casuccio A, Di Pace F, Pillitteri F, Cillino G: A 31. International Society of Ocular Trauma at: http:// five-year retrospective study of the epidemiological www.isotonline.org. Accessed July 6, 2008. characteristics and visual outcomes of patients 32. Kuhn F, Morris R, Witherspoon CD, Heimann K, Jeffers hospitalized for ocular trauma in a Mediterranean area. JB and Treister G. A standardized classification of ocular BMC Ophthalmology 2008; 8:6 trauma. Ophthalmology 1996;103(2):240-243. CHAPTER

New Classification of Ocular Trauma 2 B Shukla, D Shukla (India)

Introduction Classification is the basis of understanding a subject. Duke-Elder has broadly divided ocular trauma (Injuries) into mechanical and non-mechanical.1 He has also divided them into several types depending on the environment such as industrial, agricultural, travel, etc.2 Several other authors have also classified ocular trauma is different ways.3,4 However, one problem with all these classification has been the variability of terminology which has been used by different authors in different ways like laceration, penetration, perforation, blunt, sharp, etc. In absence of standardization of terminology the literature has become confusing and non-comparable. In a landmark paper Kuhn et al standardized the terminology in ocular trauma and gave a standardized Fig. 2.1: Classification of ocular trauma after Kuhn et al classification of ocular trauma which has been 5 universally accepted. Other authors have further above classification. For them better classification are elaborated this and gave more details which are useful available, e.g. Dua’s classification for ocular surface 6,7 for prognosis. burns.8 Secondly the ocular adnexa including the lids, Kuhn et al have basically divided eye injuries into lacrimal apparatus, conjunctiva and orbit are parts of closed globe and open globe types, the tissue of ocular trauma. The above classification has not taken reference being the cornea and sclera which they account of this category. termed as eyewall.5 Closed globe injuries include Lastly it may be mentioned that any subject can contusion in which there is no wound of cornea or be viewed from many angles and thus can have more sclera. In lamellar laceration there is a partial thickness than one classifications on the parameter chosen as wound in cornea or scleara. In either case there is the basis of classification and each of the classifications no full thickness wound. In open globe injury there has its validity. Thus uveitis can be divided is always a full thickness wound. This can occur from anatomically into anterior, intermediate, posterior, a blunt object with an inside out mechanism and is and pan uveitis. From pathological point of view it termed rupture. It can also occur by sharp objects could be granulomatous or non-granulomatous; clinically it could be acute, chronic or recurrent and by an outside in mechanism and is termed laceration. etiologically it could be infective, allergic, toxic or Laceration includes penetration (single laceration with traumatic.9 Similarly keratoplasty can be lamellar or one wound of entry), perforation (double laceration penetrating or mushroom from depth consideration. with one wound of entry and one wound of exit) It can be partial, sub-total or total from diameter and intra-ocular foreign bodies with single entrance consideration. From objective point of view it could laceration. Figure 2.1 explains this classification. be optical, therapeutic, cosmetic or preparatory.10 The above classification is ideal for mechanical Considering the above points it was thought to injuries. However, ocular trauma includes many non- develop a more comprehensive type of classification mechanical injuries like chemical, thermal, traditional, of ocular trauma which is being presented in and others. These injuries can not be classified by the Fig. 2.2. 8 Clinical Diagnosis and Management of Ocular Trauma

Fig. 2.2: General classification of ocular trauma

Ocular trauma is first divided into local, associational In this group the author has also included IMFB and environmental. In local the injury is limited to (intra-mural foreign bodies). If the tissues of reference eyeball and ocular adnexa; in associational it is is cornea and sclera (eyewall) what is within it will be associated with head injury (affecting visual pathway) intra-ocular and what is outside it will be extra-ocular. or face as in blast injuries or with many organs of the But whatever is within the coats of eyewall is neither body known as polytrauma. Here the life of the patient intra-ocular nor extra-ocular. The author has coined assumes primary importance. As the name suggests this word ‘EMFB’ quite some time back and it has the environmental injuries depend on the environment been used at other places. This group also includes and could be congenital, industrial, agricultural, travel dislocations which may be anterior, posterior, and (RTA*) criminal or casual (usually domestic). The local inferior (rarely they could be superior). In the injuries are further divided into mechanical and non- pathological group in addition to closed and open globe mechanical types. The latter includes the chemical, there can also be destructive globe injuries which thermal, radiational, electrical, ultrasonic and includes traumatic enucleation, evisceration and a full barometric. The mechanical injuries are divided into thickness laceration which covers one third of globe adnexal and global. The former include the lids, circumference or more. In these cases chances of lacrimal apparatus, orbit and conjunctiva. Globe functional recovery are absent. injuries are again divided into structural (anatomical) The subject of ocular trauma is very wide and and pathological. The former include the anterior variable and perhaps no classification can adequately segment and posterior segment injuries with the details encompass all the entities included in ocular trauma. of structures included in each group. The pathological Nevertheless in our present state of knowledge it group represents the current classification suggested address some of points lacking in the existing classi- by Kuhn et al.5 Though open globe injury includes fication and is fairly comprehensive. It may be stated IOFB (intra-ocular foreign bodies) but the closed globe that this classification is not totally exclusive and different group does not include EOFB (extra-ocular foreign combination of different categories are possible. bodies) in Kuhn’s classification. The author has Acknowledgement: I wish to express may gratitude to included them firstly because they are extremely the Ocular Trauma Society of India to encourage me common: they are extremely painful and lastly if they in formulating this classification and accepting it after are in center they can cause extreme loss of vision. giving useful suggestions.

* Road Traffic Accident. New Classification of Ocular Trauma 9 References 7. Raja SC, Pieramici DJ : Classification of Ocular Trauma, In : Kuhn F, Pieramici DJ, Editor. Ocular Trauma, 1. Duke-Elder S. System of Ophthalmology, Vol XIV, Principles & Practice, Thieme Publication, New York, Injuries, Part 1, Henry Kimpton, London, 1972, P. ix. 2002. P. 6-8. 2. Ibid. p.7-60. 8. Dua HS, King AJ, Joseph A: A new classification of 3. Lambah P : Trans Ophthal Soc, Adult eye injuries at surface burns, Br J Ophthalmol 2001;85:1379-83. Wolverhampton, 1968; 88:661–73. 4. Roper Hall M : Brit J Ophthal, 1954;38:65 9. Duke-Elder S, Perkins ES: System of Ophthalmology, Vol. 5. Kuhn F, Morris R, Witherspoon CD et al : Ophthalmology, IX Diseases of the uveal tract, Henry Kimpton, London, 1996;103:240-43. 1990;41-130. 6. Pieramici DJ, Sternberg P, Aaberg TM et al : Amer J 10. Dhanda RP, Kalevar V: Corneal Surgery, Chapter 9, Ophthal, 1997;123:820-31. Classification, RK Publications, Indore, 1994, P. 95-101. CHAPTER

Clinical Evaluation of Ocular Trauma 3 B Shukla (India)

Introduction pre-trauma vision in both eyes and the time when food/ drink was taken last. Medical and/or surgical A disease can be managed adequately only when it treatment received should be noted in details and is properly evaluated. Evaluation can either be clinical, tetanus immunization should be ascertained. In past done by the clinician himself or investigational done history diseases like diabetes mellitus, hypertension, by sophisticated machines usually by other specialists bleeding disorders, HIV/AIDS, and allergy to drugs like pathologists, radiologists, etc. Clinical evaluation should be noted. It is important to know alcohol includes a careful history and a thorough clinical consumption and use of other drugs. All previous eye examination of the patient. surgeries done should be recorded especially cataract, Before taking a detailed history two conditions keratoplasty, and radial keratotomy. have to be ruled out. If with ocular trauma there is After a careful history, examination of the eye is a life threatening situation; respiratory, cardiovascular very important for clinical evaluaiton. This includes or neurological, the patient should be immediately general, structural and functional examination. referred to appropriate physician or surgeon after a Structural examination would include adnexal, 1 quick preliminary examination. Secondly if there is anterior segment and posterior segment examination. an acute ocular emergency like chemical burn, severe bleeding or central retinal artery occlusion treatment has to be started before or during evaluation. General Examination Injuries are very common in children.2-6 In clinical In all serious injuries pulse, respiration, temperature, evaluation the approach to child has to be a little and blood pressure should be recorded first to decide different from that in adults. Pain may cause severe whether the case should be first seen by an ophthalmo- blepharospasm, watering and in an unfamiliar situation logist or to be referred to a physician or surgeon. The the child is bound to be most unwilling to be examined general behavior of the patient and level of concious- or even questioned. The approach has to be very ness should also be noted. Any evidence of injury in gentle and indirect. It is better not to touch the patient the neighboring area or organs should also be observed. initially and let him remain comfortable in mother’s lap. After some time it may be possible to examine the eye with fine retractors along with assurance and Structural Examination coaxing. Should these tricks fail the child has to be examined under sedation or general anesthesia. In OCULAR ADNEXA some cases it may be feasible to treat also once he is under anesthesia. Orbit In older patients one should begin with a careful The position of globe in orbit should be noted. There detailed history. History may be taken from the may be exophthalmoso, enophthalmos, downwards patient, a relative or a witness. In rural areas there dislocation (hypophthalmos) or upward dislocation is more risk of infection. The exact circumstances of (hyperophthalmos) which is rate. Orbital rim should the injury has to be ascertained first. This includes the be palpated for any local irregularity or tenderness location, object of injury along with its shape, size, indicating fracture. Emphysema in the surrounding and velocity. Its chemical nature and whether its is area would be additional proof. Compressibility of solid, fluid, or gaseous has also to noted. Exact time globe into orbit should be noted. More resistance of injury and the various symptoms along with their indicates orbital hemorrhage or hematoma besides severity should be recorded. It is important to know tumor mass. Clinical Evaluation of Ocular Trauma 11 Conjunctiva IOP Conjunctiva should be examined for congestion, sub- Intra-ocular pressure is important and may be conjunctival hemorrhage and foreign bodies attempted by non-contact tonometer. By no means particularly in the lower fornix and sulcus subtarsalis pressure should be exerted on the globe in an open small areas of chemosis, hemorrhage or pigmentation globe injury as intra-ocular content may prolapse. A may some times be indicative of globe laceration.8 low IOP is indicative of open globe injury, a ciliary Conjuctival abrasions can be stained by rose bengal. shock or retinal detachment. Raised IOP is suggestive of severe hyphema, angle recession or severe uveitis. Lids However, it does not rule out an occult laceration of globe.13,14 Lids are meant to protect the globe, hence, they bear the brunt of trauma quite often. In injuries the lids may show edema, contusion, partial and rarely Ocular Motility complete laceration. In blast injuries they may be Ocular motility like IOP it is important but has to studded with multiple foreign bodies. It is desirable avoided in an open globe injury for the risk of extrusion to evert the upper lid only after ensuring that there of intra-ocular contents.15 It is important in cranial nerve is no open globe injury. Singeing of cilia is a typical injuries (III,IV,VI). However, pseudo-squint due sign of flame burn.9 In late cases entropion, ectropion, mechanical reasons must be ruled out. For this a forced or ptosis may be seen. duction test can be done after some time if there is no full thickness laceration of globe.16 Lacrimal Apparatus Lower lid injuries with sharp objects is commonly Field Testing associated with division of the lower canaliculus. It must Central field by Amsler’s chart and peripheral fields be looked for at the earliest under microscope and by confrontation test can be done at initial examination. confirmed by syringing with any colored fluid. Later Visual field loss usually indicate visual pathway lesion. treatment becomes very difficult. Rarely there may be More sophisticated tests can be done later if indicated. dislocation of the lacrimal gland.10 Malingering FUNCTIONAL EXAMINATION This is not very uncommon in some trauma patients Visual Acuity particularly those who want to avoid their duties or It is by far the most important part of eye examination who can get some advantage by compensation. These which is usually done first. In trauma cases it may be tests are not very easy and there is a battle of wits slightly delayed till the patient settles down. Ideally between the patient and doctor. However a few tests vision should be recorded in each eye with a standard done carefully can prove malingering. chart (Snellen/ ETDRS). In many serious injuries the By following a definite routine in clinical evaluation vision is often too low and may be recorded by finger much information is gained and future strategy for counting, hand movements or perception of light (PL). treatment can be chalked out with confidence. The The last one has to be done very carefully and following assessments can be made after a proper repeatedly by a strong light (indirect ophthalmoscope). clinical evaluation: Projection of rays (PR) should also be tested with a a. Open globe or closed globe injury pen torch. Visual acuity has great importance in work b. Immediate treatment or reference related injuries, medico-legal cases and in assessing the c. Prognosis. effect of treatment. In some conditions the vision tends It may be added that a properly drawn diagram to fluctuate.11 If correcting glasses are not available pin is much more useful than written words, hence a few hole vision may be taken. Knowledge of pre-trauma labeled diagram of injury must be drawn. vision is important in assessing the loss. References RAPD 1. Harlan JB, Ng EWM, Pieramici DJ. In Kuhn F Pieramici DJ (Eds): Ocular Trauma, chapter 9, p. 52. Thieme It is important to assess afferent pupillary defect by Publication: NY, 2002. swinging light test. It is affected by optic nerve lesion, 2. Shukla B: Epidemiology of Ocular Trauma, Chapter 3, gross retinal lesion but rarely by anterior segment Observation and analysis. Jaypee Brothers Medical lesions.12 Publishers: New Delhi, 2002;32-36. 12 Clinical Diagnosis and Management of Ocular Trauma 3. Canavan YM, O’Flaherty MJ et al. A 10 year survey of 10. Ibid. Part 1, p. 307. eye injuries in Northern Ireland. Brit J Ophthal 1980; 11. Anderson RL, Panje WR, Gross EE: Optic Nerve 64:618–25. blindness following blunt forehead trauma. Ophthal- 4. Rapoport I, Romem M, Kinek M et al. Eye injuries in mology 1982;89:445–55. children in Israel. Arch Ophthal 1990;108:376-79. 12. Sharma YR, Singh, DV. Clinical Evaluation in ocular 5. Gothwal K, Adolph S, Jalali S et al. Demography and trauma. In Shukla B, Natarajan S (Eds): Management of prognostic factors of ocular injuries in Southern India, Ocular Trauma, Section 1, Chapter 4, p. 16, CBS Publishers, New Delhi, 2005. Aus NZ J Ophthalmol 1999;27:318-25. 13. Cherry PMH. Rupture of globe. Arch Ophthalmol 1972; 6. Niiranen M, Raivio I. Eye injuries in children. Brit J 88:498–507. Ophthalmol 1981;65:436–38. 14. Rusell SR, Olsen KR, Folk JC. Predictors of scleral rupture 7. Boldt HC, Pulido JS, Blodi CF et al. Rural Endo- and the role of vitrectomy in severe blunt ocular trauma, phthalmitis. Ophthalmology 1989;96:1722–26. Amer J Ophthal 1988;105:253-57. 8. Hamil, MB. Clinical Evaluation. In Shingleton BJ, Hersh 15. Fackler ML. Wound Ballistics, a review of common PS, Kenyon KR (Eds): Eye Trauma, Chapt. 1, p. 9, Mosby misconceptions. JAMA 1988;259:2730-36. Year Book: St. Louis, 1991. 16. Long JA, Mann TM. Orbital Trauma. In Ocular Trauma, 9. Duke – Elder S. System of Ophthalmology, Vol XIV Edit. Kuhn F Pieramici DJ, Chapter 36, p. 385. Thieme Injuries, Part 2, p. 758, Henry KImpton, London, 1972. Publication: NY 2002. CHAPTER

Evaluation and Initial Management of a Patient with Ocular Trauma 4 Rupesh Vijay Agrawal (India)

Introduction have the basic understanding about the initial evaluation, diagnosis and primary management before Fact is much different from fiction, fact is reality of referring to a qualified ophthalmologist for further life while fiction is hope of life and today the fact is management. that the rate of incidence of ocular trauma has A standardized terminology of eye injury is increased tremendously in this world of modernization important to fulfill a very basic requirement in due to road traffic accident and many other day-to- medicine to prevent unambiguous communication. day mishaps. An ideal ocular trauma terminology system was No one starts a day believing that he will sustain introduced by Birmingham Eye. Trauma Terminology trauma to his organ of vision, yet thousands of people (BETT) and satisfies all elements requested by an ideal are injured each day. The sudden realization that what system. had been taken for granted is lost and life may be When confronted with the ocular trauma patient, the initial evaluation always begins with the assessment changed forever leads to extreme anxiety for the of the patient. As ophthalmologist in evaluating the patient as well for the patient’s family. eye trauma patient, one should always assess the whole The human eye is a delicate, vital organ — and patient, keeping in mind that the person may have repairing damage to it can often challenge the limits sustained non-ocular injuries which may be life of medical science. Ophthalmologists — those threatening and must be addressed first. In such surgeons who specialize in treatment of eye injuries situations, the ophthalmologist should not hesitate to — must constantly stay abreast of new developments refer the injured patient to trauma center for initial and techniques to keep their skills finely honed. triage. Once it has been determined that the patient The significance of eye injuries is obvious to is stable, and other serious nonocular injuries have everyone even though the eyes represent only 0.1% of been addressed, a thorough medical/surgical history the total body surface, it is through this organ that is taken followed by a more focused ocular history. most of the information reaches the human animal, Key elements include prior surgery, vision prior to whether living in a big city or in the wind. A person the trauma and detailed history of the traumatic with ocular trauma has to go through severe initial incident. anxiety, changes in career and lifestyle, impaired A full examination is carried out in a methodical quality of life, economical setbacks and occasionally and rational fashion, beginning with gross external inspection. Visual acuity is measured in each eye permanent physical disfigurement. Ocular trauma has separately. Optic nerve function is assessed by testing therefore had a significant socioeconomic impact on for relative afferent pupillary defect. Ocular exami- both the involved family and on society in general. nation is done with help of torch light and followed In the present era of specialization and super- by detailed slit lamp evaluation without much specialization where many of us deal with only a certain manipulation of the injured globe. Obvious open group of disease; most patients who present with globe injury can often be appreciated with a simple complaints of other segment of the eye are not treated pen light examination. Fundus examination should but, referred to a colleague. A patient with ocular be carried out at the initial setting if the view of the trauma however need immediate attention and fundus is not precluded secondary to media opacity. referral is an option only after certain diagnostic or Presence or absence of any obvious infection is primary first aid therapeutic procedures have been documented. performed. Uncooperative and pediatric patients should be Ocular trauma cuts across specialities and for that examined under anesthesia in a controlled setting matter a medico either a physician or a surgeon should involving experienced critical care personnel. 14 Clinical Diagnosis and Management of Ocular Trauma Additional information in cases of suspected retained rounding the injury should be elicited from the patient, intraocular foreign bodies can be obtained by perfor- family members, and witnesses to know: ming radiological investigations. Photodocumentation • Activity at the time of injury is recommended whenever feasible. • Involved parties • Where the incident occurred • What happened, and Approach to a Patient with • How events progressed following injury Ocular Trauma • History of contact lenses, spectacles, or protective eyewear at the time of injury. THE GOALS OF THE INITIAL EVALUATION From this, one can assess potential severity of the I. Complete evaluation of the eye and ocular adnexa injury and the risk for occult ocular damage—retained foreign bodies, posterior globe rupture and orbital A. Recognition of emergent conditions fracture. 1. Life-threatening injuries a. Respiratory distress b. Cardiovascular compromise Pastocular and Medical History c. Massive bleeding and shock • Previous ophthalmic surgery, d. Major trauma to any organ system • Non penetrating procedures: radial keratotomy 2. Emergent ocular conditions (appropriate (↑ed vulnerability of traumatic damage) emergency treatment can be started) • Presence of periocular appliances (e.g. scleral buckle a. Chemical injuries or orbital implant) or b. Central retinal artery occlusion (CRAO) • Intraocular lenses (may become dislodged or B. Recognition of the complete extent of ocular dislocated and complicate injury) involvement • Prior ophthalmic medical conditions: e.g. glaucoma patient—↑ed risk for visual field compromise even II. Identification of confounding factors after short duration of elevation of intraocular A. Other associated non-life threatening pressure injuries: • Preinjury visual acuity 1. Bleeding • Amblyopia or other ophthalmic conditions asso- 2. CNS trauma ciated with ↑ed visual acuity important in cases of 3. Other injuries litigation B. Concurrent medical conditions 1. Diabetes mellitus 2. Atherosclerotic cardiovascular disease General Medical History Regarding 3. Sickle cell hemoglobinopathy • Hematological condition 4. Bleeding disorders • Bleeding disorder 5. Infectious diseases: • Anticoagulant medications a. Hepatitis • Sickle cell anemia (inpatients with hyphema) b. AIDS • Possibility of pregnancy in females of childbearing C. Foreign bodies age (may influence the choice or use of medications or other types of therapy) III. Need for further testing • Alcohol or drug abuse A. Radiologic • Neurologic disorders e.g. epilepsy B. Ultrasonographic • All medications currently being taken by the patient C. Electrophysiologic • Allergies D. Hematologic/serologic • Tetanus immunization status (patients with IV. Development of initial therapeutic plan lacerating or penetrating injuries ay require tetanus prophylaxis)

Approach in Emergency History of Prior Treatment HISTORY • Previous treatment for the injury • Any self-treatment (e.g. use of eye irrigants, History of the event compresses, and ocular medications) Once emergent life or sight threatening conditions are • Dosage and duration of therapy (may confound ruled out, complete description of the events sur- the results of microbiologic culture tests) Evaluation and Initial Management of a Patient with Ocular Trauma 15 • Name and location of physician from whom Electrical burns treatment is taken Amount of electrical energy involved (i.e., amperage • Amount and time of recent food intake (affect and voltage of the current) and location of entrance decisions about anesthesia, if surgery is required) and exit points is important Animal Bites History of Specific Injuries • Identify the type of animal and circumstances. Chemical injury: • Attack was spontaneous or provoked? • Can cause extremely rapid and serious tissue • Location of the animal to test for the presence of destruction transmissible disease • Treatment – (irrigation) should begin simul- taneously with the examination. EXAMINATION • Detailed history should be obtained following the Goal institution of emergency treatment. Complete evaluation of the injured eye and determi- • All chemical injuries should be presumed initially to be alkali injuries until proven otherwise. nation of the absolute and relative position, stability, and integrity of each ocular and intraocular structure History: and need for further testing and treatment. • Type of agent (can take help of local poison control center) Examination Technique • Characteristics of the exposure • Look for the presence of occult or unsuspected • Amount of material in contact with the eye injury • Duration of contact, and • To prevent further damage and avoid inappropriate • Physical character of the material (i.e. fluid, paste, examination techniques. gel, or particulate). • Any prior treatment, such as lavage or irrigation • Eye shield protection—in open globe injury • Examination of facial structures and airway • In children or uncooperative adults—examination • Evaluate for possible presence of a foreign body under sedation or general anesthesia is preferred. • No drops or ointments should be instilled, until Foreign-Body Injury rupture is ruled out. Foreign-Body Injury Checklist • If transportation of patient is not possible, 1. Source material emergency examination kit should be available. • Composition: determines ocular toxicity (eg. • Appropriate culture equipment and materials iron or copper versus glass or plastic) should be available for. • Associated activity at time of injury 2. Origin: External Examination • Size and shape • Energy Face and Lids (Fig. 4.1) • Temperature 3. Probable trajectory Points to be recorded: 4. Risk of microbiologic contamination • Any abnormal position of the globe relative to other bony structures Blunt trauma • Presence of subcutaneous emphysema (indicate # History to determine: of sinuses) 1. The amount of energy transferred to the globe and • Presence of any foreign bodies orbit: involves—vector and quantity of the force • Depth and extent of skin lacerations generated by the impact and size of the impact • Visualization of orbital fat area. • Associated injuries to the face, head, and neck . 2. Physical characteristics of the object: include density, • Small puncture wounds size, and presence of sharp or cutting edges. • Lacrimal drainage system or lid margin involvement 3. Location of the impact • Ptosis, levator function and lid fissure size Thermal burn • In canthal structures abnormality, Unusual type: • Medial canthal distances should be measured, and 1. The amount of thermal energy transferred depends • Sketch of the observed dimensions is made. on temperature of the agent, Bleeding should be controlled with tamponade and 2. Duration of contact, tissue cleaned gently with a gauze sponge and sterile 3. Character of the agent saline or hydrogen peroxide. 16 Clinical Diagnosis and Management of Ocular Trauma Pupil • Pupillary findings can indicate intracranial pathology and lesions responsible for diminished vision. • In an unconscious patient, the pupillary reflexes may be the only indicator of visual system function that can be evaluated. • Note – Shape – Location – Light reaction and – Eccentricity or irregularity. Dilated pupil in head injury: • May indicate increasing intracranial pressure with Fig. 4.1: Lid laceration associated neurologic problems. • Iris sphincter damage and Note: • Pharmacologic mydriasis, • Periorbital and lid ecchymosis or hemorrhage Preexisting pupillary abnormalities unrelated to the (Location and character) injury should be looked. (In #of orbital roof—upper lid hemorrhage and Eccentric or peaked pupils: s/o intraocular damage lateral bulbar SCH is + or scleral or corneal rupture In basal skull fractures—periocular ecchymosis may Always look for the consensual light reflex of the be present) fellow eye in case of distorted pupil in the injured eye • Inspect orbital and facial bones and palpate for (Fig. 4.2). areas of step-off, or discontinuity and note any RAPD is s/o: asymmetry. Injury in the afferent pathway: may be due to: • Injuries to the midface—occlusion of the teeth. • Optic nerve injuries such as: contusion, avulsion • Areas of skin anesthesia (s/o underlying #) and transection • In patients with a history of trauma and sudden • Retinal injuries: commotio retinae (Berlin’s edema) onset of a red eye, and retinal detachment - auscultate the closed lids and temporal area for the presence of a bruit • Profound vitreous hemorrhage. - may indicate a carotid-cavernous fistula. Extraocular Motility Conjunctiva Note: • First rule out the presence of a ruptured globe • Areas of subconjunctival hemorrhage • Post-traumatic orbital congestion may affect ocular • Abnormal pigmentation of the bulbar conjunctiva motility. (+ in globe rupture) Note: • Lacerations or breaks in the bulbar conjunctiva • All defects in ductions and versions and grade it • Presence of contact lenses, especially in the for later comparison unconscious patient. Cornea: Evaluate the epithelial surface and light reflex and any visible abnormalities of the anterior segment.

Visual Acuity • Establish a baseline visual acuity. • No light perception (NLP) should be carefully confirmed and documented with help of indirect ophthalmoloscopy light (have a profound impact on subsequent surgical decisions). • If visual acuity recording is not possible for some reasons, one should specify the reasons for inability to check the vision. Fig. 4.2: Consensual light reflex Evaluation and Initial Management of a Patient with Ocular Trauma 17 • Diplopia or • Edema and suppuration • Restriction of movement of the globe and identify Generalized – after some toxic or chemical insults any paretic or underacting muscles or severe concussive injury. Restriction of movement may be due to: Localized – common, • Orbital floor # (hyesthesia of the cheek and secondary to regional endothelial dysfunction enophthalmos may be +) seen following concussive injuries • Secondary to injury to motor innervation with lacerating injuries of the stroma • Direct muscle trauma or • Infection of the cornea—If a microbial keratitis – • Intraorbital injury from foreign bodies or scraping done penetrating wound • The endothelium—inspected for discontinuities, Forced duction test may be in intact globe guttata, enlarged endothelial cells, and pseudo- guttata. (overlying stromal edema may indicate a Visual Fields concussive endotheliopathy, resolves without Confrontation technique - appropriate in the sequelae) emergency setting. Anterior Chamber Slit Lamp Examination of Anterior Segment Step-by-step examination from the lid margins to the Note palpebral, bulbar, and tarsal conjunctiva, followed by 1. Depth and contour of anterior chamber across its the cornea, anterior chamber, iris, lens, and vitreous entire height and width. is performed. Irregular Eg. Gonioscopy may be performed if globe is intact • Choroidal detachment or hemorrhage, and if there is no hyphema. • Foreign bodies in or behind the iris, • Localized intumescence of the lens following Conjunctiva: 1. Subconjunctival hemorrhage – record the area and rupture of the lens capsule, extent • Iridocorneal adhesion with leakage of aqueous 2. Conjunctival chemosis – nonspecific or may have secondary to corneal perforation. underlying injury Shallow anterior chamber 3. Conjunctival abrasions – staining with fluorescein • In loss or misdirection of aqueous humor or rose bengal highlights abrasion • Posterior pressure from a suprachoroidal hemor- 4. Inspect embedded foreign material. rhage. 5. Conjunctival lacerations – isolated or multiple Deep anterior chamber—rupture of the posterior sclera and vitreous loss. Cornea 2. Contents of the anterior chamber: Examine all the layers using variety of slit-lamp lighting and inspection techniques (Fig. 4.3). • Cells and flare reaction – • Any foreign body – size, shape and location seen in traumatic iritis (sequelae of blunt • Corneal opacities. trauma). • Corneal discontinuity or laceration Note the degree of inflammatory response and • Depth of a laceration or perforating injury grade (important for future comparison) • Seidel’s test • Blood (hyphema) (Fig. 4.4). confirmed or ruled out in all cases of blunt or penetrating injury bleeding source identified if possible. • Others (Fig. 4.5): Hypopyon, lens fragments, vitreous, or foreign bodies Iris (Fig. 4.6) Note: • Contour and geometry – if abnormal- indicate local damage to the iris or to structures located behind it (e.g. rupture of the lens capsule, lenticular foreign bodies, or ciliary body hemorrhage or detachment). • Irregularities in the iris • Direct illumination, retroillumination of the iris – Fig. 4.3: Corneal laceration to detect small holes or perforations. 18 Clinical Diagnosis and Management of Ocular Trauma

Fig. 4.4: Hypahaema Fig. 4.7: Ruptured traumatic cataract with intraocular foreign body

Fig. 4.5: Hypopyon in anterior chamber Fig. 4.8: Subluxated lens

• Pupil shape: – irregular or elliptical pupil—an occult scleral perforation with peripheral iris, – peaked pupil—vitreous prolapse in anterior chamber, • Sphincter tears and bleeding sites. Lens (Figs 4.7 and 4.8) Note: Lens position, stability, clarity, and capsular integrity, (Examine both before and after dilatation) Sclera (Figs 4.9 and 4.10) Note: The presence or absence of scleral laceration with or without vitreous prolapse and presence of associated intraocular foreign body.

Intraocular Pressure • Have direct prognostic and diagnostic significance • Should not be checked in cases with open globe Fig. 4.6: Traumatic cataract with iridodialysis injury Evaluation and Initial Management of a Patient with Ocular Trauma 19

Fig. 4.9: Scleral laceration with vitreous prolapse Fig. 4.11: Berlins edema

Character of vitreous opacity or irregularity - localized or diffuse. A complete inspection of the retina and choroid should be performed in all trauma patients, from the ora to the posterior pole in all quadrants. Edema of the retina (Fig. 4.11) Commotio retinae, Berlin’s edema- response of the retina to concussive injury characterized by pale swelling and obscuration of choroidal detail. May be associated with a significant loss of vision. Retinal hemorrhage Note: • Location and character Fig. 4.10: Foreign body • Hemorrhage of the nerve fiber layer—flame shaped • Intraretinal hemorrhages - blotches with irreregular Vitreous Body and Retina border Inspect the vitreous body, posterior pole, and • Subinternal limiting membrane hemorrhages – may peripheral retina stream into vitreous cavity Document Tears or breaks in the retina • posterior scleral ruptures or discontinuities • Can follow concussive or penetrating injury • foreign bodies, • Most common in superonasal quadrant, followed • retinal tears or detachments, by inferotemporal quadrant • edema, Retinal holes should be noted • hemorrhage, and • vitreous opacities • Retinal detachments—10-15% of retinal detach- Scleral depression is attempted only when globe ments are secondary to trauma rupture is ruled out. • Retained intraocular foreign bodies—frequently Fundus examination is done in all trauma patients surrounded by halo of edema with central plume (except exempt for neurosurgical or other reasons) of blood. Use of a magnet to test for ferrous after bilateral pupillary dilation. composition of foreign body is contraindicated can Dilation should be performed cautiously in uncons- lead to further retinal damage or detachment. cious patients ,with significant head trauma or • Scleral ruptures contusion (after neurologist opinion). • Choroidal injuries: Document in the chart the time, dose, and identity – Rupture appears as a hemorrhagic linear zone of the dilating agents in confused or unconscious with overlying retinal edema may be obscured patients. by vitreous hemorrhage white in colour 20 Clinical Diagnosis and Management of Ocular Trauma 0ptic Nerve according to the strategic plan, he or she must make It is the third most frequently damaged cranial nerve adjustments as demanded by additional findings on by indirect injury. the operation table based on the scientific literature and personal experience. Note: Compared with only few years ago, we are in a • Edema, much better position to actually help people with ocular • Loss of margin clarity, trauma. Not only do we have a better understanding • Hemorrhages in nerve fiber layer. of the postinjury processes occurring inside the eye • Spontaneous venous pulsations of the central retinal but the expertise of the surgeon and the equipment vein-suggests normal IOP at our disposal to actually improve the outcome is • Cup disc ratio- if increased - possibility of previous constantly improving. There are organizations that glaucomatous have ocular trauma as one of their missions in terms The optic nerve trauma of its prevention, treatment and rehabilitation. Direct: It is the responsibility of physician, surgeon and • In penetrating injuries to the orbit the ophthalmologist to reduce the incidence of ocular – Severe trauma can lead to avulsion either trauma by taking into consideration the preventive partially or completely aspects of ocular trauma and to decrease the morbidity – Leads to hole in the posterior sclera at the site caused by same to the extent possible. of optic nerve through which retinal vessels pass Last but not the least, every effort should be made posteriorly. for a visually handicapped person to achieve a positive • Blunt trauma to the forehead or brow - contusion attitude about his or her capabilities to successfully use of the intracanalicular portion of the optic nerve. residual vision and live a full and enjoyable life as a visually impaired person. Special Studies: ERG and VEP in the Acute Setting • ERG—a valuable prognostic test in injuries complicated by opaque media. Pearls • Hirosee and coworkers found that: • Recordable ERG and VEP not always indicate good I. Trauma Patient in emergency prognosis. • But non-recordable ERG – indicate a poor visual Ophthalmologist must ‘take a step back’ outcome. Rule out life threatening injuries • Hutton found normal VEP as a single predictor for • Emergency good postoperative visual acuity in trauma patients • Brief history • ERG in the acute setting has little value in predicting • Clinical examination eventual visual outcome nonrecordable ERG may • Initial management indicate poor prognostic sign. • Patient counseling • Diagnostic tests • Surgical or conservative management Visual Evoked Potential (VEP) Main benefit is to support for clinical decision to proceed II. Predictors of scleral rupture: with enucleation in cases with nonrecordable VEP. Predictors of Scleral rupture • Bullous subconjunctival hemorrhage • Decreased digital tension Initial Management of Ocular • Abnormally deep/shallow AC Trauma Patient • Subconjunctival pigmentation The initial management of a traumatized patient III. Predictors of RIOFB: comprises of the steps to minimize further trauma, minimize infectious risks, minimize psychological trauma Clinical indicators of RIOFB and most importantly minimize legal problems. The • History and mode of ocular trauma designing of subsequent management plan is then • Entry wound in sclera/limbus/cornea/iris individualized for the particular patient and injury. The • Localised traumatic cataract surgeon must not act on a trial and error basis but • Direct visualisation Evaluation and Initial Management of a Patient with Ocular Trauma 21 IV.Factors indicating significant ocular injury: • Minimize risk of infection Factors indicating a significant ocular injury • Minimize psychological trauma • Markedly reduced visual acuity • Minimize legal problems • A relative afferent pupillary defect • Relative shallowing of the anterior chamber Bibliography • Irregularity of the pupil • Conjunctival chemosis 1. AK Gupta. Current topics in ophthalmology-VII, page No. • Hyphema and vitreous hemorrhage 435-86. • Markedly reduced intraocular pressure 2. Bradford J. Shingelton, Eye Trauma; Clinical evaluation: V. Four pronged initial management: 3-24. Initial management 3. Hung Cheng. Emergency ophthalmology, chapter 6- • To minimize possibility of further trauma Trauma 130-58. Anterior Segment Ocular Trauma

CHAPTER Role of Ultrasound Biomicroscopy in Evaluation of the Anterior Segment in Closed Globe Injuries 5 Ritika Sachdev, Mahipal S Sachdev (India)

Ultrasound Biomicroscopy structures in cross-section allows a new quantitative method of gonioscopy. The ability to define the The original ultrasound biomicroscope developed by relationship of the iris, posterior chamber, zonules, Pavlin, Sherar and Foster is based on 50 to 100 MHz ciliary body and lens is potentially helpful in transducers, incorporated into the B-mode clinical understanding the mechanisms of glaucoma. Anterior scanner. Higher frequency transducers permit segment tumors difficult to define with conventional increased resolution, but only at the expense of can be measured and the extent of invasion decreased tissue penetration depth. The commercially determined. Differentiation of the tissue on the basis available UBM is most often configured with a of internal acoustic characteristics is aided by very fine 50 megahertz transducer, which provides a tissue backscatter speckle patterns at these frequencies. resolution of approximately 50 microns and a Clinical ultrasound biomicroscopy has shown penetration depth of 4-5 mm. This permits significant potential as an aid in diagnosis of ocular visualization of the anterior segment. At 60 MHz the disease. However, the extent of associated injuries and zonular apparatus is slightly better visualized. the open nature of ocular injuries precludes the time Increasing the transducer frequency to 100 MHz increases the tissue resolution to approximately and manipulation necessary for such an examination. 20 microns, but the decreased penetration depth limits scanning to the cornea and has been used in refractive surgery. The increased penetration depth afforded with Ultrasound Biomicroscopy in a 42 MHz transducer permits visualization of the entire Ocular Trauma ciliary body and may be useful in studies of accommodation. Berinstein et al described ultrasound biomicroscopy The clinical use of this instrument is no more difficult as a safe and effective adjunctive tool for the clinical than the conventional immersion ultrasonography. assessment and management of ocular trauma, The technique is similar to the traditional immersion especially when visualization is limited and multiple 1,2 B-scan. traumatic injuries are involved. The ultrasound probe is suspended from an Ocular trauma may result in diverse anterior articulated arm to diminish motion artifacts. Lateral segment pathologies such as hyphema, cyclodialysis displacement is minimized by the linear scan format. and angle recession. Many of these anatomical Scanning is performed in the supine position. disturbances can be detected and differentiated with Following instillation of topical anesthetic, a 20 mm UBM. eye cup is inserted between the lids The purpose of In angle recession, blunt trauma to the anterior the cup is to hold the methylcellulose or other coupling segment forces the iris against the anterior lens capsule, medium. After insertion of the probe in the coupling trapping the aqueous within the anterior chamber and medium, the real time image is displayed on the video displacing it towards the angle recess (Figs 5.1A to monitor and can be stored for later analysis. C). The increased pressure within the angle recess The plane of the section, distance from the center may result in a tear in the face of the ciliary body, of the anterior chamber, and the orientation of the resulting in the gonioscopic appearance of an probe with respect to the perpendicular may affect abnormally wide ciliary body band or angle recession. the apparent structural configuration of the anterior On the other hand, if the ciliary body is avulsed segment. from its normal attachment from the scleral spur, a Pathology behind anterior segment opacities can cyclodialysis cleft, creating a direct communication from be imaged in detail and the ability to image angle the anterior chamber to the suprachoroidal space may 26 Clinical Diagnosis and Management of Ocular Trauma

Figs 5.2A and B: Zonular assessment- Role of UBM examination. Direct visualization of zonules- Detailed 360o scanning

important because visual recovery may occur with resolution of hypotony and is dependent on its extent and duration. Disinsertion of the iris root from its insertion into the ciliary body (iridodialysis), pupillary block, peripheral anterior synechiae in the presence of complete hyphema preventing visualization of the anterior chamber, and vitreous prolapse into the anterior segment can also be identified with UBM. Zonular damage after closed globe injury is not uncommon and its significance is well known to the anterior segment surgeon. The loss of zonular fibres, in association with a traumatic cataract, might result in an unstable lens and with an increased probability of vitreous presentation and in the worst case scenario, Figs 5.1A to C: UBM examination of the angle and the iris loss of lens into the vitreous cavity. Visualization of zonules requires a careful 360 degree be formed. Gonioscopy shows a dehiscence between scanning with the long axis of the transducer the ciliary muscle and the sclera, beginning at the scleral perpendicular to the zonules and has a significant spur and continuing to the ciliochoroidal space. learning curve. Zonular defects, when present, are seen Although cyclodialysis clefts may be visualized by as abrupt cessation of the bright reflective lines of direct visualization during gonioscopy, the attempt may zonular fibres associated with blunting of the ciliary be unrewarding in post-operative and traumatized eyes processes (Figs 5.2A and B). because of the presence of hazy media, disturbed UBM can also detect small foreign bodies of various anatomy and hypotony. When hazy media or compositions, including those missed by computed abnormal anterior segment architecture prevent or limit tomography (CT) or B-scan ultrasound. It is particularly adequate visualization during gonioscopy, UBM can valuable in the detection of small, non-metallic foreign be used to differentiate cyclodialysis, angle recession bodies. and ciliary body detachment. In addition, the presence Ozdal et al reviewed the indications for performing of supraciliary fluid and visualization of a connection ultrasound biomicsroscopic examination in 109 from the anterior chamber to the supraciliary space patients.3 UBM examinations were preformed for the confirms the diagnosis of cyclodialysis. Early diagnosis evaluation of zonules before cataract surgery (49.5%), and appropriate management of cyclodiaysis clefts are examination of the anterior segment in the presence Role of Ultrasound Biomicroscopy in Evaluation of the Anterior Segment in Closed Globe Injuries 27 of media opacity such as total hyphema or corneal bagacrylic intraocular lens, and descemet membrane scar (32.1%), detection of suspected ocular foreign dehiscence at the corneal tunnel through which the bodies (10.1%) and the evaluation of ocular hypotony iris had extruded.8 (8.3%).The time course of imaging after trauma was Ultrasound biomicroscopy has been described as variable and ranged from one day to 55 years. a safe, accurate and non-invasive diagnostic tool in In all 61.5% eyes had a closed globe injuries the diagnosis of cyclodialysis clefts and is of particular whereas 38.5% had open globe injuries. use when other conventional methods of diagnosis The most common UBM findings in closed globe are inconclusive.9 injuries were zonular deficiency (64.2%), angle recession The pathogenesis of transient high myopia after (43.3%), iridodialysis (17.9%), dislocated lens (16.4%), traumatic myopia was evaluated in two patients using hyphema in 13.4%, peripheral anterior synechiae ultrasound biomicroscopy by Ikeda et al.10 UBM (8.9%). showed annular ciliochoroidal effusion with the ciliary The most UBM common findings in open globe body edema, anterior rotation of the ciliary processes, injuries were zonular deficiency (54.8%), iridodialysis and disappearance of the ciliary sulcus and a myopia (26.2%), peripheral anterior synechiae (26.2%), angle of –9.75 dioptres was noted. The myopia and the UBM recession (14.3%) and ruptured anterior capsule findings normalized in eleven days. In the second (14.3%). patient UBM revealed a partial cyclodialysis, shallowing of the anterior chamber and thickening of the ASSESSMENT OF ZONULES crystalline lens. The resolution of these UBM findings and the normalization of the myopia was seen Pavlin and Foster were the first to describe the imaging seventeen days after trauma. of zonular fibres using UBM. UBM thus has a well-established yet only partly The role of ultrasound biomicroscopy in pre- explored role in evaluating cases of ocular trauma and operative assessment of zonular status after trauma was providing an insight to the pathology of the various evaluated by McWhae et al4. 59 cases with no clinically visible zonular damage were examined by ultrasound manifestations of concussional injuries. biomicroscopy with a 50 MHz probe. Occult zonular loss was identified in 42.9% of the patients. Referring References surgeons found the information helpful in surgical 1. Berinstein DM, Gentile RC, Sidoti PA, Stegman Z, Tello planning and anticipating complications in these cases. C et al. Ultrasound biomicroscopy in anterior segment This study concluded that UBM is an effective method trauma. Ophthalmic Surg Lasers, 1997; 28: 201-07. for identifying occult zonular damage in patients in 2. Genovesi F, Rizzo S, Chiellini S, Romani A, Gabbriellini patients with anterior segment trauma. There is however et al. Ultrasound Biomicroscopy in the assessment of a significant learning curve in the examination techni- penetrating or blunt anterior chamber trauma. que. A similar study by Liu Y Z et al also established Ophthalmologica. 1998; 212 Suppl 1:6-7. the the role of ultrasound biomicroscopy in delineating 3. Ozdal MP, Mansour M, Deschenes J. Ultrasound biomicroscopic evaluation of traumatized eye. Eye. 2003; the presence and extent of zonular loss in subluxated 17(4): 467-77. 5 lenses. 4. Mcwhae JA, Crichton AC, Rinke M. Ultrasound biomicroscopy for assessment of zonules after blunt FOREIGN BODIES trauma. Ophthalmology.2003 ;110(7): 1340-3. Foreign body detection rates were 36.5% by 5. Liu Y Z et al. Zhonqua Yanke Za Zhi. 2004; 40(3): ultrasound, 88.9% by CT scan and 99.4% with UBM. 186-88. 6. Guha S, Bhende M, Baskaran M, Sharma. Role of UBM The diagnosis of foreign body on UBM was based on in detection and localization of anterior segment high reflective echoes causing shadowing or foreign bodies. T Ann Acad Med Singapore. reverberations.6 2006;35(8):536-45. UBM was particularly valuable in picking up 7. Vincent A. Dermano et al. Ultrasound biomicroscopy as nonmetallic foreign body. In cases with intracorneal a tool for detecting and localizing occult foreign bodies and intrascleral foreign bodies, UBM was used to after ocular trauma. Ophthalmology.1999;106:301-05. 7 8. Doro D, Deliqianni V. Ultrasound biomicroscopy in determine the depth of the visible foreign body. traumatic aniridia 2 years after phacoemulsification. Journal of cataract and refractive surgery. 2006 ;32(10): IRIS AND CILIARY BODY STATUS 1753-55. Total traumatic aniridia after blunt trauma in a 9. Bhende et al. UBM in the diag UBM in diagnosis and management of cyclodialysis cleft. Indian Journal of psuedophakic patient was detected using UBM as the Ophthalmology. 1999;47(1):19-23. near total hyphema precluded a detailed slit lamp 10. Ikeda N, Ideka T, Nagata M, Mimura O. Pathogenisis of examination of the iris structures. UBM revealed iris transient high myopía alter blunt eye trauma. root remnants, a normal ciliary body, an in the Ophthalmology. 2002; 109(3): 501-07. CHAPTER

Management of Eyelid Injuries 6 Rania Abdel Salam, Essam El Toukhy (Egypt)

Introduction In case of animal bite, the rabies immunization of the animal and if the animal has been quarantined Eyelid and adnexal injuries can be a part of should be cleared. multisystem trauma. The basic ABCs of the trauma management should be considered and applied in EXAMINATION every trauma patient. This includes securing a patent This should include evaluation of the globe, adnexal airway and stabilization of the circulation. Ophthalmic tissue, orbit and face. If the patient is conscious and evaluation and management are deferred until more cooperative, visual acuity, pupillary responses, serious problems are addressed. Once the patient is stable, attention could be intraocular pressure measurement as well as dilated directed to the eyelid injuries. The patient should be fundus examination should be performed. Sometimes evaluated for any globe or optic nerve injuries. This examination under anesthesia can be done to avoid may be difficult especially in patients who are further globe injuries during manipulation of the unconscious or uncooperative. The eyelid may be eyelid. swollen and difficult to open, so care should be taken The eyelid is examined for the extent of the wound to avoid forceful opening of the eyelid as this may and if it involves the septum, the muscle, lid margin worsen the already traumatized globe. or canaliculus. Canalicular injury is suspected when the injury lies medial to the punctum which is usually laterally displaced compared to the other side or the Evaluation of Lid Injury opposite one. Medial or lateral canthal injuries as well as tissue loss should be ruled out HISTORY Evaluation of the orbit includes searching for ocular Circumstances of the injury can help determine the motility deficit, surgical emphysema, hyposthesia of type and extent of the trauma. The mechanism of the check, nose or upper lip in addition to palpable injury can give an idea about the depth of the wound orbital rim fractures. Orbital imaging with CT is as well as the possibility of foreign body presence. requested when orbital wall fracture or presence of Falling to the grounds or in contaminated places foreign body is suspected. especially of the patient is young to report should raise The lid injuries can be associated with face and a high index of suspicion for the presence of foreign neck injuries. A thorough examination of head and bodies especially of organic nature. neck should be carried out and other specialties may Some symptoms can also give a clue about the be involved in the repair process. All findings should extent of damage. Drop of vision suggests globe or be documented and photographed. optic nerve injuries. Presence of diplopia or hypothesia suggests orbital wall fracture. History of any ocular diseases or surgeries should be documented. Any medical problems, topical or systemic medications, Principles of Wound Repair drug allergy as well as problems from anesthesia The wound should be closed as soon as possible. Yet should be known. History of tetanus immunization the repair can be delayed if the patient is systemically is essential. If the patient had not tetanus immunization not stable or there are more life-threatening injuries. within 5 years, tetanus toxoid 0.5 ml should be Any globe injuries should be addressed first. Lid wound administered. If the patient had never been repair could still be delayed up to 48 hours following immunized, 250 units of tetanus immunoglobulins are trauma without jeopardizing the outcome. administered. Management of Eyelid Injuries 29 During the repair, the wound should be properly of the wound. Any wound extension or further incisions inspected for the presence of any retained foreign taken should be fashioned so as to be parallel to the bodies, deep orbital injuries or occult globe injuries. lid margin. For example, lacerations of V type shape The extent of the wound should be established. Foreign could be closed and transformed into Y shape. bodies should be removed as they may be missed and cause chronic infection, abscess or sinus formation, or Deep Lacerations Involving the Levator Complex granuloma. The lid tissue is highly vascular and minimal If the upper lid septum is involved in the injury, the debridement is required. Gentle handling of lid thin orbital pre-aponeurotic fat becomes exposed and the skin is necessary to minimize further trauma. levator muscle may be violated. So in such situation, It should be remembered to re-establish the the muscle should be identified while the wound is integrity of the basic lid parts; anterior lamella, posterior repaired. If it is found dehiscent, it should be primarily lamella, the lid retractors mainly the levator, the reattached to the tarsal plate at its normal attachment canaliculi and the canthal tendons. The wound level. Care should be taken to avoid incorporating or landmarks are identified and reattached first. These suturing the opened orbital septum. include the wound angles, apex of skin flaps and brow hair line. The orbital septum should not be incorpora- ted in the repair as it may lead to lid retraction and Marginal Wounds lagophthalmos. It is crucial to close the marginal lid wounds Most lid wounds could be repaired under local meticulously to achieve a proper anatomic repair thus anesthesia using lidocaine1% with epinephrine reducing postoperative complications. Bad wound 1:100.000. This can be done in the emergency room repair will lead to lid notching, lagophthalmos and if minor or in the operative theater in most injuries. corneal exposure. If there is no or minimal tissue loss, General anesthesia is reserved for extensive injuries, primary repair of the wound can be done. It should associated canalicular injuries or poorly cooperative be in two layers. The wound edges are approximated patients. The skin is usually closed by non-absorbable by 6/0 silk suture passing through the tarsal palate and sutures, e.g. 6-0 polyprolene, nylon or silk. Some exiting at the meibomian gland orifices 1.5-2 mm from surgeons use 6-0 polyglycolic acid (Vicryl) for repair the wound edge. It is approximated to make sure that in young children. Interrupted sutures are usually used, the wound edges are coapted and slightly everted. however, linear parts of the skin wounds could be closed Other two sutures are taken at the lash line and the by running sutures. Skin sutures are usually removed grey line. None of them is secured until the tarsal wound after 5-7 days. is closed with 6/0 Vicryl sutures that involve 90% of Major lid reconstructions should be delayed unless the tarsus thickness so as to avoid rubbing against the the cornea is seriously at risk. It is advisable to defer cornea (Fig. 6.1). The marginal sutures arms are left interference for 3-6 months before repairing a defect long and tied beneath a skin suture so as to keep them such as lid retraction, unsightly scars or ptosis unless away from the cornea. The skin wound is closed. The the patient develops signs of corneal exposure that margin sutures are removed after 10 days as earlier cannot be controlled conservatively by local lubricants.

WOUNDS WITH NO OR MINIMAL TISSUE LOSS Superficial Lacerations They involve the skin and underlying muscle. It should be emphasized that proper examination of the wound extent is very important as an innocent superficial wound may have a significant underlying injury. Simple wound closure is done with no tension. This could be facilitated by undermining the edges. Horizontal muscle lacerations will approximate themselves without suturing yet vertical muscle lacerations should be closed with 6-0 Vicryl sutures. In more complex wounds such as stellate injuries, care should be taken to follow the skin lines as much as possible and avoid shortening of the anterior lamella Fig. 6.1: Lower lid marginal wound with marginal that may lead to lid retraction. Closure of these wounds approximating sutures and a suture that involves 90% of is individualized and depends on the site and extent the tarsal thickness 30 Clinical Diagnosis and Management of Ocular Trauma removal may lead to wound separation and notching. be used (Figs 6.3A and B). Care should be taken In children the marginal sutures can be taken using to place the lateral canthal angle at a higher position 6/0 Vicryl and left to dissolve spontaneously (Figs 6.2A as it usually descends in few months. Posterior lamella and B). could be formed using periosteal flaps of free tarsoconjunctival grafts form the other eye (in case WOUNDS WITH SIGNIFICANT TISSUE LOSS of upper lid) or even from the same eye (in case of Tissue loss may be in anterior lamella or it can be full the lower lid injury). Mustarde flaps as well as lid sharing thickness involving the lid margin. In such conditions, procedures could be considered in defects > 50% of it should be remembered to avoid undue tension on the lid length. the wound margins. This situation can be dealt with in a manner similar to lid reconstruction after tumor excision. Lateral canthotomy and graded cantholysis WOUNDS ASSOCIATED WITH of the corresponding crus of the lateral canthal ligament CANALICULAR INJURIES can be helpful in a lot of conditions. If more anterior They can result from direct trauma to medial canthal lamellar tissue is needed a Tenzel flap techniques could area or indirectly by avulsive forces caused by trauma

Figs 6.2A and B: Lower lid full thickness wound involving Figs 6.3A and B: A 24 years old male with upper lid wound the margin in a 5 years child (A). Same eye 10 days after with tissue defect (A). Same eye 3 weeks after repair using the repair with remnants of the vicrly sutures (B) Tenzel flap (B) Management of Eyelid Injuries 31 to the orbit. They are common with dog bites and midface injuries. Early repair of the canalicular injury is much easier and more successful than late repair or conjunctivo-dacryocystorhinostomy with Jone’s tube. Canalicular lesions may be missed. They should be suspected in injuries medial to the punctum that may be and may be laterally displacement. The diagnosis is confirmed by direct visualization of the cut edge or passing a probe into the canaliculus. Repair of canalicular injuries is done under general anesthesia. A stent should be placed through the transected canaliculus. Bicanalicular silicone tube is commonly used, however, some surgeons use monocanalicular tubes. In case of bicanalicular tube use, the severed canaliculus is intubated first. Both are retrieved from the nose. The marginal wound is then repaired and canthal tendon wound is also repaired before tying the silastic tube (Fig. 6.4). After the wound is approximated, the tube is secured by three square knots and left in place for 6 months (Figs 6.5A and B). The medial cut end of the canaliculs could be identi- fied under the microscope with high magnification. It can also be identified using injection of a fluorescein dye or vescoelastic material into the sac through the intact canaliculus. Pooling saline in the medial canthal area with injecting air into the intact canaliculus will point at the site of cut canaliculus where the air bubbles. If the wound is ragged freshening of the edges may be helpful. Retrograde intubation using Pigtail probes is better avoided as it can cause a false passage. If the punctum is lacerated, the medial canaliculus Figs 6.5A and B: Lower lid marginal wound involving the could be marsupialized or opened to the conjunctival lower canaliculus (A). After inserting the tube and repair sac and the lid woundis repaired ignoring the injured of the wound (B) punctum and canaliculus. WOUNDS ASSOCIATED WITH CANTHAL TENDON INJURIES Medial Canthal Tendon Their injuries are usually associated with canalicular injuries that should be repaired before repairing the severed tendon. The injury may involve any part of tendon. Repair of the cut posterior limb of the tendon is crucial as if not repaired, the lid globe apposition is markedly affected and traumatic telecanthus usually results (Fig. 6.6). It should be put in mind that repair of medial canthal tendon should provide a posterior pull on the medial canthus thus keeping the lid globe apposition and gives a good cosmetic appearance. By the time of injury repair, either:

Fig. 6.4: Lower canalicular injury with a bicanalicular tube i. The two ends of the cut tendon could be identified: inserted first before the repair of the marginal wound In this condition, the tendon is repaired using non- 32 Clinical Diagnosis and Management of Ocular Trauma of the tendon could not be identified, the sutures are passed through the intact periorbital at the region of the posterior lacrimal crest. The tendon is totally avulsed from the bone: This may be associated with medial orbital wall fractures. If the bone is and the periorbita are intact, suturing into the periorbita at the posterior lacrimal crest using non- absorbable suture may be a solution (Fig. 6.7B). Y shaped microplate could also be used. In case of bone fracture, the bone should be stabilized then a microplate is placed. In case of unstable or absent bone fragment, Fig. 6.6: A 3-year-old child who had a dog bite with badly repaired medial canthal tendon injury showing medial transnasal wiring of the medial canthal tendons should ectropion and traumatic telecanthus be done.

Lateral Canthal Tendon i. The two cut ends of tendon could be identified: A horizontal mattress suture is used across the cut ends using non-absorbable material. If the lateral end could not be identified, the tendon is fixated to the periostium, if intact, at a higher position than its normal as wound contracture and the effect of gravity will pull the lateral canthus slightly inferior. ii. The tendon is avulsed from the bone: A small drill hole could be done in the lateral orbital rim just above the lateral orbital tubercle. A non-absorbable suture attached to the remnants of the lateral canthal tendon is passed through the hole and tied.

Lid Burns Burns of the eyelid are rare. They can be due to thermal, chemical or electric current injuries. They usually occur in patients who have suffered significant burns over a large surface area of the body. The first priority is to establish and maintain a patent airway. Once stable, the globe should be properly examined. If the globe is injured, topical antibiotics and cycloplegics are administered. Topical steroids should not be used as they can cause corneoscleral melting. An amniotic membrane scleral shell could be also applied. The lid skin should be covered with a broad spectrum antibiotic ointment Most of these patients are semiconscious or heavily sedated and need proper corneal protection using lubricants. The lids may be swollen and form a protection to the cornea. If this is not the case especially with marked exposure, a large Figs 6.7A and B: Repair of the medial canthal tendon injury temporary tarsorrhaphy could be performed. with reattachment to its remnants (A). Reattachment of the avulsed tendon to the intact periorbita (B) Once cicatricial changes start to develop usually associated with deterioration of the ocular surface absorbable or wire suture. A horizontal mattress suture condition, early intervention should occur. Early use is placed in the distal end of the tendon. The two of full thickness skin grafts or variable types of flaps needles are brought from posterior to anterior through had been suggested to reduce the ocular morbidity the proximal part (Fig. 6.7A). If the proximal part in selected cases. CHAPTER

Management of Lacrimal Injuries 7 Rania Abdel Salam, Essam El Toukhy (Egypt)

Introduction In case of late presentation of lacrimal drainage system injuries, systematic evaluation should be Lacrimal injuries are usually not isolated. They are adopted. This includes, evaluation of the conjunctiva almost always associated with lid injuries or orbital or for presence of adhesions as well as assessment of nasal fractures. Eyelid, orbital and adnexal injuries the punctual position, direction and patency. Positive can be a part of multisystem trauma. The basic ABCs regurge test is a sure sign of nasolacrimal duct of the trauma management should be considered and obstruction. Dye disappearance test show delay as once the patient is stable, it is possible to properly compared to the other side. Probing may show examine the eyelid with the upper lacrimal passages, strictures of the canaliculi or fibrosis of the lacrimal orbital injuries as well as the associated globe or optic sac that usually felt as a soft stop. Irrigation test can nerve affection. It should be remembered that upper show the extent of NLD obstruction. Nasal lacrimal drainage system can be involved in chemical examination is very important is such cases as a or thermal injuries. deviated septum resulting from the original trauma may be the reason of the lacrimal passage problems. Orbital CT whither conventional cuts or in three Evaluation of Lacrimal Injuries dimensions can show the fractures sites and their extent as well as associated nasal deformities.. Dacryocysto- HISTORY graphy can show nasolacrimal duct obstructions site The conditions of trauma can give an idea about the and extent. nature and the extent of injury. Being usually Proper lacrimal system evaluation is necessary for associated with lid or orbital injuries, high index of choosing the treatment protocol. suspicion should exist to be able to detect lacrimal passage injuries. Lacrimal gland injury is usually rare Wounds Associated with Canalicular Injuries and may be associated with orbital roof fractures or They can result from direct trauma to medial canthal deep upper lid wound. area or indirectly by avulsive forces caused by trauma Review of medical history is essential as well as to the orbit. They are common with dog bites and drug allergy history of tetanus immunization and midface injuries. Early repair of the canalicular injury problems encountered with anesthesia. is much easier and more successful than late repair or conjunctivo-dacryocystorhinostomy with Jone’s EXAMINATION tube. Routine systematic examination of the eyelid, globe Canalicular lesions may be missed. They should and orbit should be performed. Canalicular injury is be suspected in injuries medial to the punctum that suspected when the injury lies medial to the punctum may be and may be laterally displacement. The which is usually laterally displaced compared to the diagnosis is confirmed by direct visualization of the other side or the opposite one. Medial or lateral canthal cut edge or passing a probe into the canaliculus. injuries as well as tissue loss should be ruled out Repair of canalicular injuries is done under general Lacrimal passage injuries associated with orbital anesthesia. A stent should be placed through the or nasal fractures may be overlooked especially with transected canaliculus. Bicanalicular silicone tube is the edema or ecchymosis. However, associated nasal commonly used. However, some surgeons use bone fractures as well as traumatic telecanthus should monocanalicular tubes. In case of bicanalicular tube raise the index of suspicion. use, the severed canaliculus is intubated first. Both 34 Clinical Diagnosis and Management of Ocular Trauma

Fig. 7.1: Lower canalicular injury with a bicanalicular tube inserted first before the repair of the marginal wound

are retrieved from the nose. The marginal wound is then repaired and canthal tendon wound is also repaired before tying the silastic tube (Fig. 7.1). After the wound is approximated, the tube is secured by three square knots and left in place for 6 months (Figs 7.2A and B). The medial cut end of the canaliculs could be iden- Figs 7.2A and B: Lower lid marginal wound involving the tified under the microscope with high magnification. lower canaliculus (A) After inserting the tube and repair of It can also be identified using injection of a fluorescein the wound (B) dye or vescoelastic material into the sac through the intact canaliculus. Pooling saline in the medial canthal area with injecting air into the intact canaliculus will If the fracture is detected and repaired, irrigation of point at the site of cut canaliculus where the air bubbles. the lacrimal system by the end of the repair should be If the wound is ragged freshening of the edges may done. If there is a free system irrigation, nothing more be helpful. Retrograde intubation using Pigtail probes is needed to be done. If there is some minor resistance is better avoided as it can cause a false passage. exists, probing and bicanalicular silicone intubation If the punctum is lacerated, the medial canaliculus where the tube is left for 3-6 months may be of use. could be marsuplized opened to the conjunctival sac If these fractures are not detected and corrected, and the lid woundis repaired ignoring the injured chronic dacryocystitis can occur and needs dacryo- punctum and canaliculus. cystorhinostomy (DCR). It is sometimes associated with excess bone formation in the area of the nasal and Lacrimal Sac and Nasolacrimal Duct Injuries lacrimal bone that accentuates the possibly present These lesions may be missed as these parts are included traumatic telecanthus. This bone can be debulked in a protective bony structure. A high index of suspicion while performing the DCR. The surgery can be should be present to anticipate these problems. They associated with repair of the present telecanthus. are usually associated with nasoethmoidal fractures, sometimes with blow out fractures of the orbit and Old Traumatic Lacrimal Passage Injuries types II and III Le Fort fractures. Management of such injuries varies according to the A nasoethmoidal fracture usually results from a site and extent of obstruction and addressed in a similar force delivered across the nasal bridge and it’s very way as non-traumatic cases. For example, destruction common in automobile accidents in which the face of the upper lacrimal system especially with chemical strikes the dashboard. The nasal bones become injuries and obliteration of the canaliculi usually fractured and displaced. The lacrimal and sphenoidal necessitates conjunctivo-dacryocystorhinostomy bones are usually crushed. They are associated with (CDCR) with insertion of Lister Johns tube. Chronic surgical emphysema. Traumatic telecanthus is usually dacryocystitis or complete NLD obstruction are treated present in association with lacrimal passage injury. by conventional DCR. CHAPTER

Hyphema 8 Earl Crouch, Eric Crouch (USA)

Introduction Examination Blunt trauma to the eye may result in injury to the A hyphema may be graded by the following system: iris, angle structures, and other intraocular structures. grade 1—layered blood occupying less than 1/3 the Hemorrhage into the anterior chamber, or hyphema, anterior chamber, grade 2—blood filling 1/3 to 1/2 is common in children. Generally, a projectile that of the anterior chamber, grade 3—blood filling more strikes the eyeball produces the hyphema. A great than 1/2 but less than the total anterior chamber, and variety of projectile missiles and objects have been grade 4—total clotted hyphema filling the anterior commonly found to cause hyphema including balls, chamber, often referred to as an blackball or “eight rocks, projectile toys, air gun, paint balls, bungee ball” hyphema. Alternatively, hyphemas may be cords, and the human fist. With the increase of child graded by measuring the height of the hyphema in abuse, fists and belts have started to play a prominent millimeters from the inferior limbus. These grading role. Boys are involved in three-fourths of cases. systems enable the ophthalmologist to monitor the Rarely, spontaneous hyphemas occur and may be progress of the hyphema resolution. confused with traumatic hyphemas. Spontaneous Secondary hemorrhage associated with traumatic hyphemas are secondary to neovascularization, ocular hyphema results in a markedly worse prognosis. neoplasms (retinoblastoma), and vascular anomalies Eventual visual recovery to an acuity of 20/50 (juvenile xanthogranuloma). Vascular tufts that exist at (6/15) or better occurs in approximately 64% of the pupillary border have been implicated in patients with secondary hemorrhage compared with spontaneous hyphema. A traumatic hyphema may be 79.5% of those in whom no rebleeding occurred. True graded by measuring the height of the layered hyphema secondary bleeding into the anterior chamber is in the anterior chamber in millimeters. A hyphema is indicated by an obvious increase in the amount of an ocular emergency and should be referred imme- blood in the anterior chamber. Secondary diately. hemorrhage occurs in approximately 22% of all hyphema patients (range 7 to 38%). The rate of secondary hemorrhage is Caucasians is between 8- History 10%. The incidence of secondary hemorrhage is An exact history of the trauma should be obtained higher in hyphemas that occupy 50% or more of the to assess the velocity involved, which in turn may anterior chamber. indicate the extent of ocular damage that may have There are specific complications of traumatic occurred. Inquiry must be made to determine if visual hyphema. They are directly attributed to the retention acuity changes occurred immediately after the injury. of blood in the anterior chamber and include posterior Flashing lights are often seen at the instant of injury synechiae, peripheral anterior synechiae, corneal and indicate irritation of the retina, as any message blood staining, and optic atrophy. Optic atrophy may to the brain from the retina is perceived as light. result from either acute, transiently elevated intraocular Persistent blurred vision is indicative of a more serious pressure or chronically elevated intraocular pressure. injury. It may indicate blood in the anterior chamber Posterior synechiae may form in patients with traumatic that is suspended in the aqueous humor. Free-floating hyphema. They are secondary to iritis or iridocyclitis. blood in the anterior chamber can generally not be Posterior synechiae are uncommon in patients treated appreciated by direct ophthalmoscopy. A slit-lamp is medically but occur more frequently in patients who necessary to observe the suspended red blood cells have had surgical evacuation of the hyphema. in the anterior chamber. Peripheral anterior synechiae occur frequently in 36 Clinical Diagnosis and Management of Ocular Trauma medically treated patients in whom the hyphema has nation may reveal a contusion of the lids and periorbital remained in the anterior chamber for a prolonged tissues. A black eye may be serious or relatively minor. period (9 days or more). If accompanied by severe pain, bleeding, or constant Corneal blood staining occurs primarily in patients blurred vision, more serious eye trauma must be who have a total hyphema and associated elevation considered. An orbital CT scan and ophthalmologic of intraocular pressure. Factors that may increase the consultation should be considered to rule out a likelihood of corneal blood staining are: (1) initial state ruptured globe. Depending on the mechanism of of the corneal endothelium (decreased viability injury, corneal and scleral lacerations may also occur. resulting from trauma or advanced age, e.g. cornea Frequently, signs of corneal and scleral lacerations guttata); (2) surgical trauma to the endothelium; (3) include unequal pupils, decreased intraocular pressure, a large amount of formed clot in contact with the iris prolapse, or hyphema. Frequently, a corneal endothelium; and (4) prolonged elevation of laceration also involves the lens. Almost all ocular intraocular pressure. Each of these factors affects trauma cases include bleeding or dilation of blood endothelial integrity. Corneal blood staining may occur vessels on the surface of the eye resulting in the with low or normal intraocular pressures; it may also formation of subconjunctival hemorrhages. This sign occur in hyphemas that are less than total. Corneal may be observed with any degree of eye injury. For blood staining has a larger potential for occurrence instance, a subconjunctival hemorrhage may be in patients who have a total hyphema that remains spontaneous and often indicates minor injury. In the for at least 6 days with concomitant, continuous presence of a hyphema, a subconjunctival hemorrhage intraocular pressures above 25 mm Hg. Corneal blood suggests more serious injury and necessitates the staining may require several months or more to clear. evaluation for a possible occult ruptured globe. Non-glaucomatous optic atrophy in hyphema Hyphema may result in lacerations of the sphincter patients may be due either to the initial trauma or to muscle of the pupil. They are manifested by traumatic transient periods of markedly elevated intraocular mydriasis. Unlike the unequal pupils seen with pressure. Diffuse optic nerve pallor is the result of congenital anisocoria, traumatic mydriasis is transient periods of markedly elevated intraocular characterized by recent onset of unequal pupils and pressure; it occurs with constant pressure of 50 mm by the irregularity of the dilated pupil. Although Hg or higher for 5 days or 35 mm Hg or higher for traumatic mydriasis by itself is not harmful, it suggests 7 days. We have observed a number of patients with severe blunt trauma and is an indication for a careful sickle cell trait who developed a non-glaucomatous assessment of other ocular structures, including the optic atrophy with relatively small elevations of vitreous and retinal periphery. intraocular pressure (35 to 39 mm Hg) that lasted 2 to Ophthalmologists should consider posterior injuries 4 days. Despite maximum medical therapy, final visual to the globe may be present, including retinal acuity was less than 20/400 in all patients. We continue detachment, retinal tear, and vitreous hemorrhage. to observe optic atrophy in sickle cell trait patients An increase in previous floaters or the onset of new referred to our institution that have not had vigorous control of intraocular pressure and/or delay in floaters may occur with hyphema. In such cases, a paracentesis. Other studies indicate that patients with complete eye exam including either dilation should sickle cell hemoglobinopathies and anterior chamber be performed to evaluate for a retinal detachment. hyphemas have more sickled erythrocytes in their In cases of hyphemas that obscure direct visualization anterior chambers than in their circulating venous of the posterior segment B-scan ultrasonography blood. The sickled erythrocytes obstruct the trabecular should be completed. Additional evaluations may meshwork more effectively than normal cells, and there include orbital CT imaging to evaluate for associated is a concomitant elevation of intraocular pressure to orbital fracture. Traumatic detachment of the retina higher levels with lesser amounts of hyphema. can be observed after blunt eye injury, especially in Moderate elevation of intraocular pressure in patients older individuals. The patient may complain of reduced with sickle cell hemoglobinopathy may produce rapid overall brightness in the involved eye or may have deterioration of visual function due to profound continuous light flashes, indicating retinal traction. After reduction of central retinal artery and posterior ciliary eye trauma it is imperative to inspect not just the central artery perfusion. portions of the retina but the peripheral portions as well. Other serious post-traumatic injuries are traumatic tears of the iris, subluxation or dislocation of the lens Associated Exam Findings that occasionally displaces into the anterior chamber, There are a variety of complications associated with and blowout fracture of the orbit that present with hyphema and blunt globe trauma. External exami- impaired eye movement in the upward direction Hyphema 37 because of entrapment of the inferior rectus muscle. These serious injuries are generally readily identified. Patients presenting with hyphema should also have evaluations to rule out penetrating injuries of the globe, acute angle-closure glaucoma, pupillary block, corneal foreign body, and acute iritis. Blunt trauma may also result in vitreous hemorrhage, posterior vitreous detachments, and commotio retinae.

Prognosis and Treatment of Hyphema Fig. 8.1: Traumatic hyphema Cataract, choroidal rupture, vitreous hemorrhage, angle recession glaucoma, and retinal detachment are commonly associated with traumatic hyphema, compromising the final visual acuity. It is important to recognize that the prognosis for visual recovery from traumatic hyphema is directly related to three factors: 1. Amount of associated damage to other ocular structures (i.e. choroidal rupture or macular scarring) 2. Whether secondary hemorrhage occurs 3. Whether complications of glaucoma, corneal blood staining, or optic atrophy occur. Treatment modalities should be directed at reducing the incidence of secondary hemorrhage and Fig. 8.2: Traumatic hyphema—Grade II the risk of corneal blood staining and optic atrophy. The success of hyphema treatment, as judged by recovery of visual acuity, is good in approximately 75% of patients. Approximately 80% of hyphema patients with less than one-third filling of the anterior chamber regain visual acuity of 20/40 (6/12) or better. Approximately 60% of those with more than half but less than total hyphema regain 20/40 or better, whereas only approximately 35% of those with initially total hyphema have good visual results. Approximately 60% of hyphema patients below age 6 years have good visual results; older age groups have progressively higher percentages of good visual recovery. Fig. 8.3: Traumatic hyphema—Grade IV Hyphema should be carefully managed with bed rest, shielding the injured eye, and appropriate treat- ment either pharmacologically or surgically in order 7 days and topical dexamethasone 0.1% 4 times a to minimize potential complications. Patients with sickle day. Additionally, treatment includes a protective shield cell disease or sickle cell trait should be closely for the involved eye. monitored for possible elevated intraocular pressure In general, hyphemas are best managed with and rebleeding events. Some ophthalmologists use medical treatment followed by surgical treatment as aminocaproic acid or oral steroids in addition to topical indicated. Surgical management can be difficult and treatment with steroids and mydriatics. Some studies is associated with a series of potential complications. have demonstrated a lower incidence of secondary Surgery is best reserved for severe hyphemas or thus hemorrhage with aminocaproic acid treatment. Patients unresponsive to medical management. Surgery is often with hyphema and angle recession require life-long unnecessary when less than 50% of the anterior evaluation for possible glaucoma. Common treatment chamber is involved. In general, corneal staining with plans include atropine sulfate 1% 3 times a day for blood resolves, but may take several weeks. Even total 38 Clinical Diagnosis and Management of Ocular Trauma

Fig. 8.4: Optic atrophy secondary hyphema-induced glaucoma Fig. 8.7A: Angle resection

Fig. 8.5: Commotio retinae associated with hyphema Fig. 8.7B: BB ball relative size

Fig. 8.8: Choroidal rupture with macular scar and Fig. 8.6: Retinal detachment with subretinal hemorrhage retinal hemorrhage Hyphema 39 with the trabeculectomy. Two 10-0 nylon scleral flap sutures are used to close the trabeculectomy site. Because these surgical procedures have a variety of associated complications, the surgeon should approach each case with a patient-specific treatment plan.

Bibliography 1. Allingham RR, Crouch ER Jr, Williams PB, et al. Topical aminocaproic acid significantly reduces the incidence of secondary hemorrhage in traumatic hyphema in the rabbit model. Arch Ophthalmol 1988;106(10):1436-38. 2. Allingham RR, Williams PB, Crouch ER Jr, et al. Topically applied aminocaproic acid concentrates in the aqueous humor of the rabbit in therapeutic levels. Arch Ophthalmol 1987;105(10):1421-23. 3. Bakri SJ, Peters GB 3rd. Sympathetic ophthalmia after a hyphema due to nonpenetrating trauma. Ocul Immunol Inflamm 2005;13(1):85-86. 4. Blanton FM. Anterior chamber angle recession and Fig. 8.9: Choroidal rupture involving macula secondary glaucoma: A study of the after effects of traumatic hyphemas. Arch Ophthalmol 1964;72:39. 5. Campbell DG. Ghost cell glaucoma following trauma. hyphemas should be conservatively managed for Ophthalmology 1981;88(11):1151-58. 4 days before considering surgery. Spontaneous 6. Crawford JS, Lewandowski RL, Chan W. The effect of resolution often occurs rapidly during this period. After aspirin on rebleeding in traumatic hyphema. Am J Surgical intervention is usually indicated on or after Ophthalmol 1975;80(3 Pt 2):543-45. 7. Crouch ER Jr, Frenkel M. Aminocaproic acid in the the fourth day for total hyphemas. Surgical indications treatment of traumatic hyphema. Am J Ophthalmol 1976; also include: intraocular pressure of 50 mm Hg or 81(3):355-60. greater for 4 days, Grade III hyphemas lasting 6 days 8. Crouch ER Jr, Williams PB, Gray MK, et al. Topical or with pressures of 25 mm Hg, or Grade II hyphemas aminocaproic acid in the treatment of traumatic hyphema. lasting longer than 8 days. Also, special attention should Arch Ophthalmol 1997;115(9):1106-12. be given to sick cell trait and sickle cell disease patients. 9. Crouch ER Jr, Williams PB. Trauma: ruptures and In these patients, an intraocular pressure great than bleeding. In: Tasman W, Jaeger EM (Eds). Duane’s Clinical Ophthal-mology. Philadelphia: JB Lippincott Co; 35 mm Hg for more than 24 hours increases the need 1993:118. for surgical evacuation. 10. Crouch ER Jr. Traumatic hyphema. J Pediatr Ophthalmol Complications of hyphema surgery include damage Strabismus 1986;23(2):95-97. to the corneal endothelium, lens, or iris; prolapse of 11. Darr JL, Passmore JW. Management of traumatic the intraocular contents; rebleeding; and increased hyphema. Am J Ophthalmol 1967;63(1):134-36. synechiae formation. The preferred technique is eva- 12. Deans R, Noel LP, Clarke WN. Oral administration of cuation of the hyphema with vitrectomy instrumen- tranexamic acid in the management of traumatic tation. The initial clear corneal incision is fashioned hyphema in children. Can J Ophthalmol 1992 Jun; 27(4): 181-83. and a vitrectomy hand piece is gently placed into the 13. Diddie KR, Dinsmore S, Murphree AL. Total hyphema anterior chamber. Extreme care is required to avoid evacuation by vitrectomy instrumentation. Ophthalmo- any contact with the iris, the lens, or the corneal logy 1981;88(9):917-21. endothelium. Intraoperative secondary hemorrhage 14. Ehlers WH, Crouch ER Jr, Williams PB, Riggs PK. Factors may occur. Raising the infusion bottle to approximately affecting therapeutic concentration of topical 70 cm above the eye for several minutes provides amino-caproic acid in traumatic hyphema. Invest tamponade in most cases. At the end of the surgical Ophthalmol Vis Sci 1990;31(11):2389-94. procedure, filling the anterior chamber with an air 15. Farber MD, Fiscella R, Goldberg MF. Aminocaproic acid bubble is helpful. Standard closure is created with versus prednisone for the treatment of traumatic hyphema. A randomized clinical trial. Ophthalmology 10-0 nylon corneal sutures. 1991;98(3):279-86. In patients with total hyphema, some surgeons 16. Farber MD, Fiscella R, Goldberg MF. Aminocaproic acid advocate trabeculectomy with peripheral iridectomy. versus prednisone for the treatment of traumatic The trabeculectomy is performed through a partial thick- hyphema. A randomized clinical trial. Ophthalmology ness sclera incision. Peripheral iridectomy is performed 1991;98(3):279-86. 40 Clinical Diagnosis and Management of Ocular Trauma 17. Goldberg MF. The diagnosis and treatment of sickled hyphema. A randomized clinical trial. Ophthalmology erythrocytes in human hyphemas. Trans Am Ophthalmol 1999;106(2):375-79. Soc 1978;76:481-501. 32. Recchia FM, Saluja RK, Hammel K, Jeffers JB. Outpatient 18. Hoskins HD. Secondary glaucoma. In: Heilman K, management of traumatic microhyphema. Ophthalmo- Richardson KT (Eds). Glaucoma: Conceptions of a logy 2002;109(8):1465-70. Disease, Pathogenesis, Diagnosis Therapy. Philadelphia: 33. Rocha KM, Martins EN, Melo LA Jr, Moraes NS. WB Saunders Co; 1978:376. Outpatient management of traumatic hyphema in 19. Karkhaneh R, Naeeni M, Chams H, Abdollahi M, children: Prospective evaluation. J AAPOS 2004; 8(4): Mansouri MR. Topical aminocaproic acid to prevent 357-61. rebleeding in cases of traumatic hyphema. Eur J 34. Romano PE, Robinson JA. Traumatic hyphema: A Ophthalmol 2003;13(1):57-61. comprehensive review of the past half century yields 20. Kennedy RH, Brubaker RF. Traumatic hyphema in a 8076 cases for which specific medical treatment reduces defined population. Am J Ophthalmol 1988;15:106(2): rebleeding 62%, from 13% to 5% (P<.0001). Binocul 123-30. Vis Strabismus Q 2000;15(2):175-86. 21. Laatikainen L, Mattila J. The use of tissue plasminogen 35. Romano PE. Systemic prednisolone prevents rebleeding activator in post-traumatic total hyphaema. Graefes Arch in traumatic hyphema. Ophthalmology 2000; 107(5): Clin Exp Ophthalmol 1996;234(1):67-68. 812-14. 22. Listman DA. Paintball injuries in children: More than 36. Rynne MV, Romano PE. Systemic corticosteroids in the meets the eye. Pediatrics. 2004;113(1 Pt 1):15-18. treatment of traumatic hyphema. J Pediatr Ophthalmol 23. Loewy DM, Williams PB, Crouch ER Jr, et al. Systemic Strabismus 1980;17(3):141-43. aminocaproic acid reduces fibrinolysis in aqueous 37. Rynne MV, Romano PE. Systemic corticosteroids in the humor. Arch Ophthalmol 1987;105(2):272-76. treatment of traumatic hyphema. J Pediatr Ophthalmol 24. Mattox C, Williams PB, Crouch ER, et al. Aqueous Strabismus 1980;17(3):141-43. humor concentrations after use of reservoir systems for 38. Santander, SH, et al. A phase III, multicenter, randomized, topical delivery of aminocaproic acid. Invest Ophthalmol placebo-controlled clinical trial of topical aminocaproic Visual Sci 1991;32:1293. acid (Caprogel) in the management of traumatic 25. McCuen BW, Fung WE. The role of vitrectomy hyphema. Ophthalmology 2003;110(11):2106-12. instrumen-tation in the treatment of severe traumatic 39. Sheppard JD, Nozik RA. Practical diagnostic approach hyphema. Am J Ophthalmol 1979;88(5):930-34. to uveitis. In: Duane TA, Jaeger EW (Eds). Clinical 26. Milauskas AT, Fueger GF. Serious ocular complications Ophthalmology. Philadelphia: JB Lippincott; 1989;(4)33. associated with blowout fractures of the orbit. Am J 40. Spoor TC, Hammer M, Belloso H. Traumatic Ophthalmol 1966;62(4):670-72. hyphema. Failure of steroids to alter its course: A 27. Morris DS. Ocular blunt trauma. Loss of sight from an double-blind prospective study. Arch Ophthalmol 1980; ice hockey injury. Br J Sports Med 2006;40(3):45. 98(1):11619. 28. Palmer DJ, Goldberg MF, Frenkel M, et al. A comparison 41. Starck T, Hopp L, Held KS, et al. Low-dose intraocular of two dose regimens of epsilon aminocaproic acid in tissue plasminogen activator treatment for traumatic total the prevention and management of secondary traumatic hyphema, postcataract, and penetrating keratoplasty hyphemas. Ophthalmology 1986;93(1):102-08. fibrinous membranes. J Cataract Refract Surg 1995; 29. Parver LM, Dannenberg AL, Blacklow B, et al. 21(2):219-24. Characteristics and causes of penetrating eye injuries 42. Walton W, Von Hagen S, Grigorian R, Zarbin M. Manage- reported to the National Eye Trauma System Registry, ment of traumatic hyphema. Surv Ophthalmol 2002; 1985-91. Public Health Rep 1993;108(5):625-32. 47(4):297-334. 30. Radius RL, Finkelstein D. Central retinal artery occlusion 43. Weiss JS, Parrish RK, Anderson DR. Surgical therapy of (reversible in sickle trait with glaucoma. Br J Ophthalmol traumatic hyphema. Ophthalmic Surg 1983;14(4): 1976;60(6):428-30. 343-45. 31. Rahmani B, Jahadi HR. Comparison of tranexamic 44. Wilson FM. Traumatic hyphema. Pathogenesis and acid and prednisolone in the treatment of traumatic management. Ophthalmology 1980;87(9):910-19. CHAPTER

Management of Corneal Injuries 9 Ashok Sharma (India)

Introduction TABLE 9.1: Open-globe injury classification Incidence of eye injuries requiring hospitalization has Type been reported 15.2 per 100000 population/year. Rupture Open globe injuries occur four times more often than Penetrating Intraocular foreign body close globe injuries. Accidental injuries may occur while Perforating at work, during sports activities and in vehicular Mixed accidents. Children usually get accidental injuries while Grade playing or as a result of accidental fall. Rarely children > 20/40 may present with self inflicted injuries, which are 20/50 to 20/100 usually mild. A case of bilateral self infiltrated 19/100 to 5/200 4/200 to light perception penetrating needle injury been reported. Majority No light perception (95%) of occupational injuries occur in the workers Pupil who are negligent of using protective measures as per Positive: Relative afferent papillary defect present in norms. Injuries due to assaults mostly occur in males affected eye and are more severe in nature. The worst eye injury Negative: Relative afferent papillary defect absent in occurs during the war or terror attacks. affected eye Zone Isolated to cornea (including the corneoscleral limbus) Corneoscleral limbus to a point 5 mm posterior into Terminology in Ocular Trauma the sclera Posterior to the anterior 5 mm of sclera Penetrating eye injury, perforating eye injury, globe rupture and corneal laceration are commonly used terms to describe anterior segment trauma. In this chapter the discussion will be centered on Penetrating injury is defined as full thickness wound the management of corneal injuries and complications. of eye-ball coat caused by sharp object. Penetrating injury may have an associated retained intraocular foreign body. Perforating injury has both entry and Management of Acute exit wounds caused by the same object. Globe Corneal Injury rupture is the term used to describe open globe injury with a blunt object. Laceration wound of the Open globe injury (OGI) needs emergency eyeball coat caused by a sharp object. It can be management. Brief history including mode of injury, partial thickness (lamellar) or full thickness causative agent and prior treatment should be (penetrating). recorded. Infants and children may not allow eye examination to assess the severity of injury. One should not force examination as it may aggravate eye injury. Ophthalmic examination should aim at Classification ascertaining whether or not the patient requires The ocular trauma classification group has developed surgical intervention. In case the patient requires a classification system for mechanical injuries of the surgical intervention he should be prepared for general eye.1 Open globe injury classification has been anesthesia. Tetanus prophylaxis should be described as under (Table 9.1). administered. In case there is suspicion of retained 42 Clinical Diagnosis and Management of Ocular Trauma intraocular foreign body, an X-ray orbit (AP) and lateral or 10 days. In acute injury patient may be view should be done. Primary repair of the corneal apprehensive and may not be co-operative due to injury should be performed as early as possible. In pain. Anterior chamber examination should also rule case a preliminary examination reveals that no surgical out uveitis (flare, cells and keratic precipitates) and intervention is required and the patient is co-operative hyphema. then patient may be examined in detail. In case child is unco-operative for examination and it is not possible Lens to decide whether he needs surgical intervention the Crystalline lens may be clear or cataractous. In case child should be examined under general anesthesia. lens is clear look for phacodonesis, an indication of Children and apprehensive patients should be subluxation or irregular anterior chamber suggestive examined using simple pen light or flashlight. Slit-lamp of dislocation of the lens. Vitreous into the anterior biomicroscopy and indirect ophthalmoscopy are chamber defects may present. In case of cataractous preferred and ideal methods of examination and lens rupture of anterior capsule should be ruled out. should be performed on all the co-oprerative patients. The findings of the clinical examination should be recorded in detail. Clinical signs on slit-lamp biomicro- SLIT-LAMP BIOMICROSCOPY scopy may be recorded by drawing schematic color Conjunctiva coded diagrams. Photographic documentation of the Conjunctiva should be examined to rule out any foreign clinical findings should also be done (Figs 9.1 and body, and conjunctival tear. One should specifically 9.2). look for scleral laceration. Parent’s counseling is the most important, as they may be anxious and have lot of questions to ask. Parents and child should be explained the nature of injury. Cornea The prime importance of primary repair should be Detailed examination of cornea on slit lamp should be performed to detect, corneal abrasion, corneal foreign body, corneal opacity and corneal ulceration. Corneal perforation if detected should be confirmed on Seidel’s test. Schematic corneal drawing should be prepared to record width, depth of corneal laceration.

Sclera Sclera laceration may go undetected due to overlying intact conjunctiva. It is better to suspect scleral wound in case of conjunctival chemosis, discoloration of con- junctiva and extensive sub-conjunctival hemorrhage. Scleral perforation should also be suspected in case of unexplained hypotony. Corneal laceration extending to the limbus may be extending to the sclera. In all such situation it is better to expose the sclera Fig. 9.1: Full thickness corneal laceration after peritomy and rule out scleral wound.

Anterior Chamber Anterior chamber examination should include examination of pupil, iris, and angle of the anterior chamber. Deep anterior chamber may indicate angle recession and subluxated lens. The shallow anterior chamber suggests choroidal detachment, anterior dislocation of lens and leaking corneoscleral wound. Detailed examination of the iris to detect sphincter tears, iridodialysis and iridodonesis should be done. Gonioscopy should be performed to detect angle recession. In case of acute injury, if open globe injury Fig. 9.2: Corneal laceration repair followed by cataract is not there gonioscopy may be performed after a week extraction and PCIOL implantation Management of Corneal Injuries 43 emphasized. Visual prognosis may be explained after laceration. Even scleral or corneal laceration can be primary repair. In case patient is having lens damage further subdivided by putting sutures in between at or posterior segment injury necessity of future certain landmarks such as pigmentary lines on the surgeries may be explained. corneal epithelium. Corneal sutures should be deep upto 80-90% of corneal thickness. Corneal sutures Anesthesia with shallow bites cause posterior wound gap. Corneal Primary repair in cases with open globe injuries is always surgeons use adequate number of sutures in the performed under general anesthesia. Use of succinyl- peripheral cornea and less number of sutures near choline during anesthesia is avoided as it increases the the visual axis. Corneal sutures produce compression intraocular pressure.2 Inhalational agents including of the corneal wound on either side of the corneal 6 halothane, more recently isoflurane and sevoflurane suture. The length of the wound compression is equal do not raise the intraocular pressure and are safer for to half of the suture length. Corneal sutures should day care surgery. Patient should be kept at a deeper be placed in such a way so that the compression zone plane of anesthesia and recovery should be uneventful. around the corneal sutures just overlap each other. Under local anesthesia there is always danger of Corneal sutures with longer bites induce larger corneal worsening of injury due positive intraocular pressure. astigmatism. The depth of the corneal sutures on either In a recent study regional anesthesia with monitored side should be equal. The unequal depth of the corneal anesthesia care has been found a reasonable alternative sutures may produce corneal step. The bites of the to general anesthesia for selected patients with open sutures should be at right angle to the corneal wound. globe injuries.3 The patients treated with this option The oblique placement of the sutures may cause had corneal/limbal laceration, smaller length of horizontal displacement of the corneal wound edges. laceration (<6.5 mm), formed anterior chamber and To close clean incised wound without any tissue no afferent pupillary defect. The operating time in the incarceration continuous suture may be used. Any local anesthesia/sedation group is reported to be shorter corneal suture causes flattening of the overlying cornea mean than in the general anesthesia group. surface. Corneal sutures cause steepening of the 180° meridian and flattening of the meridian 90° to the PRINCIPLES OF REPAIR: PRINCIPLES OF suture. The tension across the sutures used in repairing SURGICAL REPAIR corneal laceration should be adequate. The tighter Extent of corneal injury should be measured and sutures cause more steepening. Intraoperative possible extension to the sclera should be ruled out. keratometer is useful to be adjust the tension across In case, the corneal laceration is extending up to the the sutures to reduce postoperative corneal limbus, peritomy should be performed and the end of astigmatism. At the end of the repair of the corneal the corneal laceration should be identified. The extent laceration anterior chamber should be reformed. A of scleral laceration from the limbus should be separate stab incision should be used to infect air into measured. Wound should be thoroughly cleaned off the anterior chamber. In the repair of corneal laceration the debris. Corneal lacerations should be carefully air has advantage over Ringer’s lactate. In case child examined for the present of eyelash. Eyelash presence has an associated lid laceration, corneal repair is in the corneal wound or intracorneal may lead to cyst performed first and lid repair later. Canalicular injuries formation. Cilia may also get implanted into the anterior should be meticulously repaired. Continuity of the chamber and even the traumatic cataractous lens. canaliculus should be ensured. Patient in whom multiple cilia impacted in the capsular bag and their removal before intraocular lens CORNEAL LACERATION WITH TISSUE LOSS implantation has been reported.4 Irrigation of the wound and removal of corneal foreign bodies is performed. Approximation of corneal laceration with tissue loss Recent iris prolapse presenting within few hours should is extremely difficult. Conventional sutures fail to be reposited. Old iris prolapse, torn iris and iris with achieve the water tight closure and in addition distort possible focus of infection should be abscised. In case cornea grossly. Special measures may be needed to of ciliary body prolapse, it should not be abscised. Ciliary close these lacerations. body can be reposited. Light cautry may be applied 1. Purse string suture: Radial linear limbs of the corneal to small portion if required. Anterior chamber fluid laceration should be closed with conventional should be sent for microbial cultures.5 interrupted sutures. The central defect may be It is good practice to divide the corneal scleral closed with the 360° continuous purse string suture. laceration into the smaller segments. One should put Purse string suture will generate centripetal a suture at limbus and divide it into corneal and scleral compression force and aid in achieving firm closure. 44 Clinical Diagnosis and Management of Ocular Trauma 2. Cyanoacrylate tissue adhesive: Another option to obtain water tight closure in corneal laceration with tissue loss is to apply cyanoacrylate tissue adhesive (CTA). CTA application in this situation may be combined with either interrupted sutures or with purse string suture. Any tissue iris or anterior capsule incarcerated in the corneal wound should be disengaged before CTA application. Area around the tissue loss should be de-epithelialized. A minimum quantity of CTA should be applied. This will provide a firmly adherent adhesive plug that will seal the perforation. Bandage contact lens should be placed to prevent irritation and dislodgment of the adhesive plug. 3. Penetrating keratoplasty: In extensive loss of corneal tissue even purse string suture may not work. These cases may not be amenable to either purse string suture or CTA application. Larger loss of the corneal tissue may be better managed with penetrating keratoplasty. Penetrating keratoplasty takes care of the tissue loss and provides better and secured anterior chamber. All corneal perforations should be considered infective unless proved otherwise and should be treated accordingly (Fig. 9.3). Infective corneal laceration may also be treated with application of cyanoacrylate tissue adhesive application in addition to topical antibiotics (Figs 9.4A to D). Lamellar corneal injuries with tissue loss may be treated with cyanoacrylate tissue adhesive application, deep lamellar keratoplasty and multi Figs 9.4A and B: Infective corneal perforation in patient layered amniotic membrane transplant (Figs 9.5 with prior RK and 9.6). In addition one can always use air in the anterior VISCOELASTIC MATERIALS chamber. Air gives clear view of the tissue incarcenated Viscoelastic substance should be used to deepen the in the corneal wound. Mobility of the air bubble and anterior chamber and protect corneal endothelium. extent of the air bubble give useful information that the anterior chamber is deep. Multiple small air bubbles indicate that there may be vitreous in the anterior chamber.

MANAGEMENT OF INJURY TO LENS In general lens extraction is avoided at the time of primary repair of corneal laceration. There is always a risk of aggravation of sub-clinical infection and developing endophthalmitis. However, if there is gross laceration of capsule and lose lens matter in the anterior chamber, one should aspirate the lens matter. In case there is lens matter mixed with vitreous one can perform anterior vitrectomy with lensectomy. In the exceptional case with clean incised corneal wound lens capsule laceration may be present. In since a patient one can perform aspiration of the lens matter and perform Fig. 9.3: Corneal perforation with infection with posterior chamber intraocular lens implantation. Small traumatic cataract corneal laceration (1-2 mm) self-sealing may be left Management of Corneal Injuries 45

Fig. 9.4C: Glue application in infective corneal Fig. 9.6: Deep anterior lamellar keratoplasty for corneal perforation scarring and multiple stromal foreign bodies

there is tissue incarcerations iris or capsule, corneal wound should repaired even if it is already sealed. The incarcerated tissue must be disengaged to avoid fibrous in growth and avoid fistula formation. Iris incarceration may also pre-dispose to sympathetic ophthalmia.

TYPE OF SUTURES Corneal laceration is repaired using 10 ‘0’ monofila- ment nylon (Alcon or Ethicon) suture. Scleral ruptures are repaired using polypropylene sutures. Iridoplasty and pupiloplasty is also performed using 10(0) polypropylene sutures. Conjunctival tear should be Fig. 9.4D: Healing of infective corneal perforation with sutured using polyglactin (vicryl 8 (0) sutures. Lid repair glue application and bandage contact lens is done using 6 (0) silk sutures.

POSTOPERATIVE TREATMENT Following corneal injury repair child is put on systemic antibiotic, systemic steroids and systemic anti- inflammatory drugs. In addition the child should be put on frequent topical antibiotic, topical steroids and cycloplegics. In the postoperative period one should monitor intraocular pressure and postoperative inflammation. Once postoperative inflammation has subsided one should perform posterior segment evaluation. In case adequate view of the retina is not obtained because of corneal edema, corneal scar or cataractous lens one should get B-scan ultrasonography, to make suture that there is no retinal detachment, endophthalmitis or vitreous hemorrhage. Fig. 9.5: Large corneal injury with tissue loss Delayed post traumatic propionibacterium acnes endophthalmitis has been reported. Children may unsutured if the wound is stable and there is no tissue recover good vision after surgery for traumatic cataract incarceration. Shelving wound is more stable than despite corneal scar. In some cases of adequate vertical edges of the wound. Bandage contact lens may posterior capsular support is not available they may be considered making the wound more stable. In case need scleral fixated PCIOL. 46 Clinical Diagnosis and Management of Ocular Trauma TRAUMATIC WOUND DEHISCENCE ruptures were associated with increased rates of retinal FOLLOWING PENETRATING KERATOPLASTY detachments, phthisis, and enucleation, contributing Penetrating keratoplasty requires long-term follow-up. to the poorer visual prognosis in these patients. Major potential complications include graft reaction, Although extremely rare systemic complication of suture related problems, infective keratitis, recurrence venous air embolism has been reported during repair of disease and cataract. Wound dehiscence is a rare of penetrating injury in a child. complication occurring in an otherwise normal graft. Traumatic wound dehiscence may occur any time after TRAUMATIC CATARACT penetrating keratoplasty. Cases of traumatic wound Significant open globe injury is frequently associated dehiscence have been reported many years after with development of cataract. Details of management successful keratoplasty. In various series incidence options will be discussed in a separate chapter. ranging from 1.3 to 2.5% has been reported. Young male patients are most often affected. CORNEAL INFECTION Keratoconus, pseudophakic corneal edema, graft failure, endothelial dystrophy and viral keratitis have During examination and surgery patient should be been reported as indications of keratoplasty in cases specifically looked for presence of any infiltrate. Patient of wound dehiscence. The indication of the original with history of injury with dental wires may get graft is not thought to influence the risk wound polymicrobial keratitis. Patient suffering corneal injury dehiscence. Grafts on avascular corneas heal without with wooden splinter or with retained intracorneal vascularization. The vascularization of the corneal wooden foreign bodies may develop fungal infection. wound strengthen the corneal scar. Larger grafts have Corneal foreign body should be removed on longer scars and are theoretically at higher risk of emergency basis. In case such a patient develops an dehiscence. Corneal wounds closer to the limbus heal infiltrate corneal scraping should be performed. The better. Post-penetratng keratoplasty corneal scars never material obtained on corneal scraping should be regain the normal corneal strength even after years. subjected to direct microscopy and cultures (bacteria Therefore corneal graft remains at risk of wound and fungus). Intensive topical antibacterial/antifungal dehiscence even after years. Bilateral wound dehiscence treatment should be initiated in these patients. In case has been reported. Bilateral poor visual acuity, alcohol of fungal keratitis systemic antifungal treatment should abuse and use of non-inflammatory sutures are be given in moderate and severe keratomycosis. predisposing factors. Immediate wound repair of the original graft is IRIS/CAPSULAR INCARCERATION needed. Even if the original graft is opaque or Any tissue iris or capsule tags incarceration in the corneal edematous immediate primary repair is warranted. wound should be prevented. In case incarceration of Delay in primary wound repair enhances the risk of the tissue is there it should be removed. In case it is infective karatitis, suprachoroidal hemorrhage and persisting after primary repair, it should be treated endophthalmitis. Advanced age is another risk factor during the second operation. Tissue incarceration may for development of suprachoroidal hemorrhage. lead to wound leak, corneal fistula, inadvertent blebs, endophthalmitis, fibrous ingrowth or epithelial Prognosis downgrowth. The corneal fistula should be detected Older patients record poor visual outcome after using Seidel’s test and should be treated immediately. treatment of traumatic wound dehiscence. Fibrous ingrowth or epithelial down growth should be avoided as it may later lead to intractable glaucoma. Traumatic iris cyst is a rare complication of full thickness Complications of Corneal Injury corneal laceration (Fig. 9.7). The objective of repair of anterior segment injury is SECONDARY GLAUCOMA to repair the damage, prevent the complications and Patients undergoing repair of eye injury should be provide effective visual rehabilitation to the patient. closely mentioned for development of secondary Following successful repair of the injury, the patient glaucoma. Intraocular pressure should be recorded should be monitored for development of following on every visit. In case of corneal scarring non-contact complication. Traumatic cataracts were the most tonometer may be used to record IOP. In case IOP is common vision-limiting factor in all categories of open- high it should be controlled medically. Surgical option globe injuries. Injuries in zones II and III. Blunt-force may be desirable once it is not controllable with medical Management of Corneal Injuries 47 POST-TRAUMATIC ENDOPHTHALMITIS Endophthalmitis following OGI is a serious complica- tion. Microbial contamination is an important risk factor for development of endophthalmitis. Despite high frequency of microbial contamination, it develops only in few cases. Systemic antibiotics, virulence of organisms and host factors play role in the development of endophthalmitis. Poor vision at presentation, isolation of virulent organism, longer length of corneoscleral laceration (>8.0 mm), delayed primary repair (>72 hours) and uveal tissue and vitreous prolapse have been identified as risk factors favoring development of endophthalmitis.7 The incidence of endophthalmitis can be reduced by early referral of Fig. 9.7: Iris cyst following repair of corneal laceration trauma cases.8 Prophylactic intravitreal broad spectrum antibiotic injection has been found to decrease the risk of post-traumatic endophthalmitis.9 In a recent series endophthalmitis due to Bacillus species has been reported. Bacillus isolates have been found to be sensitive vancomycin, gentamycin and fluoroquinolones.10 The organism was not found to be sensitive to penicllin or cefalosporins. Endophthalmitis caused by Bacillus cerus results in poor visual outcome.10

SYMPATHETIC OPHTHALMIA Sympathetic ophthalmia is defined as bilateral, granu- lomatous, pan-uveitis generally occuring following open globe injury or rarely following intraocular surgery. Incidence between 0.2% and 1% has been reported follwing open globe injury and 0.001% Fig. 9.8A: Clear graft in a patient with corneal traumatic following surgery has been reported.11 Risk is more corneal scar if the injury extends into the ciliary body region. Uveal tissue/iris incarceration into the corneal or scleral wound also enhances the risk of sympathetic ophthalmia. Patient should be educated that difficulty in reading may be the earliest sign of the disease. In the early stage the disease present as granulomatous uveitis. Once clinical diagnosis is established, the patient should be put on topical and systemic steroids.

POSTERIOR SEGMENT COMPLICATIONS Every patient suffering penetrating eye injury should be subjected to the detailed retina evaluation even if there is not obvious injury to the posterior segment. These patients should be kept under follow-up. The retina should be examined with scleral depression at Fig. 9.8B: Ahmed gluaucoma valve for post-PK least 2 times a year. Patients who need penetrating glaucoma grafts or secondary scleral fixated PCIOL should be critically examined for any retina problem before treatment. Glaucoma may occur after penetrating undertaking surgery. These patients may develop keratoplasty done for visual rehabilitation. These cases retinal detachment months to years after the primary may need glaucoma surgery, Ahmed valve to control repair. In case the media is not clear patient should intraocular pressure (Figs 9.8A and B). undergo ultrasonography to rule out posterior segment 48 Clinical Diagnosis and Management of Ocular Trauma problem before performing cataract surgery or penetrating keratoplasty.

ASTIGMATISM Patients with less than 3 mm corneal laceration usually have corneal astigmatism (<3.00D) where as 4 mm or longer incision has higher corneal astigmatism. Low or moderate astigmatism (<3.00 D) is common and can be easily managed with prescription of glasses. High astigmatism (>3.00D) requires different set of evaluation and management. High astigmatism may occur despite meticulous primary repair.12 High astigmatism with sutures still in place may decrease with selective suture removal. Once all the corneal sutures are out, accurate refraction should be done. Fig. 9.9: Secondary scleral fixated intraocular lens In case of a child it should done as cycloplegic refraction. implant in patient with corneal injury Best corrected visual acuity with spectacle correction should be noted. In case visual acuity with pin hole is better than spectacle correction, it means that there is significant irregular astigmatism. Corneal topography should be performed and surface regularity index may be high in these cases. Such a patient should under go rigid gas permeable contact lens trial. In addition to irregular astigmatism, problems such as ametropia following aphakia, high astigmatism or aniridia can be solved with good visual results, good tolerance and less complications.14 High astigmatism can be managed with astigmatic keratotomy. LASIK, epi-LASIK and photo-astigmaic keratotomy may be performed to treat corneal ametropia and corneal astigmatism.12 Fig. 9.10A: Traumatic corneal scar involving visual axis Visual Rehabilitation In case visual acuity with spectacle correction does not improve RGP contact lenses should be considered. Reverse geometry RGP contact lens, with large diameters, could be another alternative in irregular corneal surface with corneal scar.13 Fluorescein pattern analysis could be better fitting technique in these cases. This fitting could involve less time and fewer visits. Computer-aided fitting was of limited value in these cases.14 In case patient does not want rigid gas permeable contact lens, the patient may be considered for alternate surgical options. Patents intolerant to RGP may be considered for astigmatic keratotomy or laser vision correction. In case of child with poor compliance for contact lenses, Fig. 9.10B: Clear graft in patient with traumatic corneal scar secondary intraocular lens implantation may be useful in preventing amblyopia (Fig. 9.9).15 be performed at the same sitting. In case the iris has Patients who have corneal scar passing through the been damaged iridoplasty may be performed. If the visual axis may need deep anterior lamellar keratoplasty longer sector of the iris is missing the special intraocular or penetrating keratoplasty (Figs 9.10A and B). lenses with opaque periphery may be implanted to avoid Secondary intraocular lens implantation if required may glass and improve cosmetic appearance. Management of Corneal Injuries 49 WAR RELATED INJURIES it is possible to rehabilitate eyes with corneal injuries The most common cause of the eye injuries during to near normal. the war are explosions with fragmentation injury. Open globe injuries, are more common and usually bilateral. OGIs received during war are for more serious and References devastating. It is difficult to salvage the eye. A large 1. Pieramici DJ, Sternberg P Jr, Aaberg TM Sr, et al. A number of eyes (30 to 35%) may need to be removed system for classifying mechanical injuries of the eye (enucleation, evisceration, or exenteration). Some of (globe). The Ocular Trauma Classification Group. Am J the patients may even require bilateral enucleation. Ophthalmol 1997;123820-31. Injuries to other body systems are common. In 2. Chidiac EJ, Raiskin AO Succinylcholine and the open Operation Iraqi Freedom 797 severe eye injuries eye.Ophthalmol Clin North Am 2006;19:279-85. including 483 OGIs (49 bilateral) were treated by 3. Scott IU, Gayer S, Voo I, Flynn HW Jr, Diniz JR, United States Army ophthalmologists.These injuries Venkatraman A. Regional anesthesia with monitored anesthesia care for surgical repair of selected open globe were most commonly caused by explosion trauma.16 injuries. Ophthalmic Surg Lasers Imaging 2005;36:122-28. OGIs may also occur in survivors of terror attacks 4. Ram J, Sharma A. Traumatic implanation of cilia into the victims that involve the use of explosive materials. capsular bag. Afro Asian J Ophthalmol 1992;Vol These explosives are commonly of a high explosive XI(2):194-95. type (HE) and may be fashioned into improvised 5. Gupta A, Srinivasan R, Kaliaperumal S, Setia S. Microbial explosive devices (IED) that incorporate additional cultures in open globe injuries in southern India. Clin materials to maximize trauma and injuries. Serial IED Experiment Ophthalmol. 2007;35:432-38. explosions have occurred in commuter trains in several 6. Hamill MB. Corneal and Scleral trauma. Ophthamol Clin cities including London, Madrid and Mumbai. In a N Am 2002;15:185-94. 7. Gupta A, Srinivasan R, Gulnar D, Sankar K, Mahalakshmi report 16 of 28 patients (57.1%) had ocular injuries T. Risk factors for post-traumatic endophthalmitis in whereas 12 (42.8%) were found to be normal. Injuries patients with positive intraocular cultures Eur J were seen in 22 eyes, 10 unilateral and six bilateral. Ophthalmol 2007;17(4):642-47. The common injuries were periorbital hemorrhages 8. Narang S, Gupta V, Simalandhi P, Gupta A, Raj S, Dogra (09 eyes, 40%); first or second degree burns to the MR. Paediatric open globe injuries. Visual outcome and upper or lower lids (seen in 07 eyes, 31.8 %) and risk factors for endophthalmitis. Indian J Ophthalmol corneal injuries (seen in 08 eyes, 36.3%). Open globe 2004;52:29-34. injuries were seen in two eyes of two patients (09%). 9. Narang S, Gupta V, Gupta A, Dogra MR, Pandav SS, Das One patient (4.5%) had a traumatic optic neuropathy.17 S. Role of prophylactic intravitreal antibiotics in open globe injuries. Indian J Ophthalmol 2003;51:39-44. Ophthalmologists should be aware of this pattern 10. Miller JJ, Scott IU, FlynnHW Jr, et al. Endophthalmitis of ocular injuries. Protocols should include the caused by Bacillus species. Am J Ophthalmol screening of patients in a short time, diagnostic tests 2008;145:883-88. including B-scan, visual evoked potential (VEP), etc 11. Marak GE. Recent advances in sympathetic ophthalmia. and performing early surgery at the time of injury. Surv Ophthalmol 1979;24:141-56. Most of the severe eye injuries are missed and are not 12. Jain S, Azar DT, Pineda RP. Management of astigmatism treated at an initial assessment. after corneal trauma. Int Ophthalmol Clin 1986;47-55. 13. Martin R, de Juan V. Reverse geometry contact lens fitting in corneal scar caused by perforating corneal injuries. Prevention of Eye Injuries Cont Lens Anterior Eye 2007;30:67-70. 14. Grünauer-Kloevekorn C, Habermann A, Wilhelm F, Occupational open globe injuries are usually severe Duncker GI, Hammer T. Contact lens fitting as a possibility and are associated with a poor visual outcome. for visual rehabilitation in patients after open globe Mandatory use of protective eyewear and alcohol-free injuries Klin Monatsbl Augenheilkd 2004;221:652-7. environment at the work place is likely to reduce the 15. Sharma A, Basti S, Gupta S. Secondary IOL implantation incidence of severe occupational open globe injuries. in children. J Cataract Refract Surg 1997;23:675-680. Educating parents and children about the potential 16. Thach AB, Johnson AJ, Carroll RB, Severe eye injuries for eye injuries at home and during hazardous activities in the war in Iraq, 2003-2005 Ophthalmology should be an important public health goal.18 In 2008;115:377-82. 17. Mehta S, Agarwal V, Jiandani P. Ocular injuries in addition, promoting the use of appropriate protective survivors of improvised explosive devices (IED) in eyewear by children during activities with a high risk commuter Trains BMC-Emerg Med 2007;27;7:16. of ocular trauma will help prevent future eye injuries. 18. Brophy M, Sinclair SA, Hostetler SG, Xiang H. Pediatric Although the path is long and arduous but with eye injury-related hospitalizations in the United States. the current advancements in microsurgical techniques Pediatrics 2006;117:1263-71. CHAPTER

Chemical Injuries of the Eye 10 Quresh B Maskati (India)

Introduction severe disruption of stromal mucopolysaccharides. Thus they are able to progressively penetrate deeper Among the ocular hazards that modern day humans into the stroma. Alkali injuries are hence considered to face, the incidence of chemical injuries has been have a poorer prognosis as compared to acid injuries.3 forever on the rise. Causes range from industrial and agricultural accidents, domestic accidents, assaults and chemical warfare. Uncommon causes are self inflicted Classification injuries and improper use of drugs.1,2 The eye is exposed to a wide variety of chemicals Several classifications have been in vogue in the past. of diverse nature, either by accident or design. The a. Hughes’ classification: Mild, moderate and severe. injuries so caused vary considerably, from the most This depended on the visibility of anterior chamber trivial causing transient irritation to the most severe, details and the blanching of the surrounding causing complete loss of integrity of the visual apparatus. conjunctiva. However, it did not assess the area The protective mechanisms of the eye are generally of surface involvement. of not much help in these types of injuries. The bony b. Thoft’s classification: 4 grades of severity from orbit protects against large size objects, but offers no grade1 to grade 4 based on area of perilimbal barrier to liquids and gases. The eyelids may suffer conjunctival necrosis and amount of corneal extensive damage themselves in cases of chemical epithelial loss.4 injury. Liquids mix with tears and spread rapidly, However, in those days, the concept of limbal stem extending the area of contact. Reflex lid closure and cells and their role in regeneration of the conjunctival blepharospasm may trap solid particles, especially lime, and corneal epithelium was not well understood. beneath the lids, leading to prolonged contact.1,2 Modern classifications such as that proposed by Dr. Harminder Dua of Nottingham, UK (Table 10.1) fill in that lacuna and hence give the reviewer a better Pathogenesis idea of the prognosis of such cases.7 The commonest types of chemicals are acids and alkalis. Most chemical injuries have a striking similarity in their pathogenesis, following the pattern of acid Management or alkali burns. GENERAL PRINCIPLES ACIDS First Aid They cause their damage within the first few hours. They This consists of immediate and thorough removal of the produce a coagulation of the surface proteins into chemical to the extent possible. Ideally the antidote of insoluble acid albuminates, which form a barrier to the chemical can be used. Practically this is usually not further penetration. Therefore the damage is restricted feasible—the easiest way is a liberal washing of the eye and the lesions are sharply demarcated and non- with Ringers lactate or Normal saline or even tap water, progressive. if nothing else is available, for 30 to 60 minutes.

ALKALIS Examination These cause a saponification of cellular barriers, A thorough examination of the involved structures denaturation of mucoids, swelling of collagen and is then carried out with a good illumination (slit lamp, Chemical Injuries of the Eye 51

TABLE 10.1: Dua classification of chemical burns Grade Prognosis Clinical findings Conj.involvement Analogue scale I Very good 0 clock hours of limbal involvement 0% 0/0% II Good < 3 clock hours of limbal involvement <30% 0.1-3/1-29.9% III Good >3-6 hours of limbal involvement >30-50% 3.1-6/31-50% IV Good to guarded >6-9 hours of limbal involvement >50-75% 6.1-9/51-75% V Guarded to poor >9-<12 hours of limbal involvement >75-<100% 9.1-11.9/75.1-99.9% VI Very Poor Total limbus (12 hours) Involved Total conj (100%) 12/100% The analogue scale records accurately the limbal involvement in clock hours of affected limbus/percentage of conj. Involvement. While calculating percentage of conj. Involvement, only involvement of bulbar conjunctiva, up to and including the conjunctival fornices is considered. if possible) and the extent of damage assessed. Any Role of Vitamin C particles, especially in cases of lime are picked up with Topical ascorbic acid has been advocated to promote a forceps or a cotton bud. The fornices must be corneal regeneration as it has been found that the searched well, with double eversion of the lids, which aqueous in most cases of chemical injuries, especially will reveal trapped lime particles. If the patient is a alkali are markedly scorbutic (very low to unrecordable child this may require examination under general levels of vitamin C). Ascorbic acid is very necessary anesthesia as soon as the general condition of the patient for fibroblasts to lay down healthy collagen.4 This permits. The author has discovered lime particles deep reparative process starts soon after the injury occurs. in the fornix even months after the injury, which have This is a cheap and freely available drug. It is sold been missed by others because the child was not as ampoules of 500 mg in 5 cc or as 1000 mg in examined under general anesthesia with double 10 cc. This is the exact concentration that is required eversion. Special attention is paid to examination of of topical vitamin C, i.e. 10%. It does not need any the adnexa, as their involvement will considerably further dilution. All you have to do is break an ampoule worsen prognosis. Also, the lesions are graded of vitamin C injection, pour into a sterile glass bottle, according to Dua’s or any other classification. put an eyedropper on the mouth of the bottle and dispense. In case ampoules of vitamin C are not Medication available, tablets of Vitamin C, 500 mg can be dissolved Topical anesthetics should be sparingly used, as they in distilled water (5 cc) and dispensed. The drops tend to retard epithelial healing. Systemic analgesics should be used frequently – every few minutes for can be administered. A cycloplegic like atropine should the first 2 hours and then hourly for the first 48 hours. be instilled to reduce the pain and discomfort of They can be continued 4-6 times a day for the first Cyclitis. Topical antibiotics should be used to prevent couple of weeks. Studies have shown this significantly infection. Acetazolamide should be started in cases with reduces the risks of perforations and cornel melts. moderate to severe burns to prevent secondary glaucoma. This is a wise precaution, as intraocular Autohemotherapy pressure cannot be taken in the early stages of chemical injuries. Many researchers have tried the use of blood and blood products in the treatment of chemical injuries and some Surgical Maneuvers of the earliest results of this technique were reported Early paracentesis has been recommended, especially by Dubrovina (1951). In fact it is even mentioned in in cases of alkali burns, though its advantages have the early Duke-Elder (2) volumes on ophthalmology, not been proved. Mechanical removal of now sadly no longer looked at by most postgraduates! contaminated, necrotic tissue will promote faster In this technique, 0.5 to 1.5 ml of the patient’s own healing. According to a study done at L.V. Prasad Eye venous blood drawn from the ante-cubital vein is Institute, use of amniotic membrane grafts in the early injected under the conjunctiva in the perilimbal region stages significantly reduced overall morbidity of and in the fornices. This is repeated every other day chemical burns lesions.6 Sweeping of a glass rod around or as required. The aim of this therapy is manifold. the fornices is done daily, especially in the areas where Blood acts as a buffer, ensures more intimate contact symblepharon is threatening to develop. A conformer with the diffusing chemical, than that achieved by or moulded scleral contact lens can also be inserted surface irrigation. It thus causes a dilution of the to prevent symblepharon. chemical, besides ensuring separation of the tissues 52 Clinical Diagnosis and Management of Ocular Trauma and acting as a barrier against deeper penetration. This burns, there are several options. If there is an is of great advantage, especially in severe alkali burns. unaffected area, a small piece of limbal tissue can be Also, its fibrinolytic action tends to inhibit the formation cultured in vitro and the cultured stem cells can be of symblepharon and it acts as a cushion in between transplanted to one or both eyes. The other option the superficial and deeper tissues. Platelets fill the gaps is use of stem cells donated by living related donors. on the denuded surface. They also adhere to collagen If these are not possible, one can use cadaveric stem by changing their shape from the usual oval to an cells from eye bank eyes. In all these cases however, amoeboid shape. Antiproteases in the blood inhibit it is mandatory to give prolonged systemic collagenases, preventing the breakdown of newly immunosuppressive therapy for a period of at least formed collagen. 6 months. Several authors are in favor of much longer dosage regimens, over years. Stem cell transplant is Newer Drugs usually always done in association with amniotic membrane transplantation. There is increasing research on the use of citrates, progesterone, epidermal growth factors and some other medications to promote healing. It may be a Amniotic Membrane Transplant few years before they attain mainstream status for use As said earlier, in partial stem cell deficiency, it may in all cases. be sufficient to repeatedly scrape the diseased epithelium and place a large piece of amniotic RECENT ADVANCES IN THERAPY membrane tissue (AMT) over the cornea. Amniotic membrane is the innermost lining of the foetus and Stem Cells is obtained from healthy donors who are HIV free, It is now well established that stem cells for the cornea delivered by cesarean section. Ideally, the membrane as well as conjunctival epithelium are located in the is preserved in liquid nitrogen after mounting on limbal palisades of Vogt. In chemical injuries one or specially treated nitrocellulose paper for 6 months. The more clock hours of the limbus may be affected, mother is then retested for HIV to eliminate the window causing destruction of these cells. These stem cells, in period effect. If negative, the AMT can be used in the normal circumstances, divide into daughter cells, which manner described above. AMT has several properties, undergo transformation into ‘transient amplifying cells’ which make it an ideal tissue – it down regulates then into ‘terminally differentiated cells’ as they move inflammatory processes and up regulates healing into the cornea, finally forming healthy corneal processes. It also provides an ideal substrate for epithelial cells. If the stem cells are destroyed, healthy epithelial cells to grow over it and populate the areas corneal epithelium will not fill the surface defects. This of epithelial defects. AMT has 2 sides – a smooth side, causes persistent epithelial defects. These invite which is the epithelial side and a sticky side, which is vascularization and ‘conjunctivalization’ or growth of the stromal side. It has increasingly wider applications cells of conjunctival phenotype on the corneal surface. in anterior segment surgeries, such as in pterygium Penetrating keratoplasties in cases with stem cell repair, which are outside the scope of this chapter. It deficiency are doomed to failure for cast off corneal is occasionally used in acute chemical burns epithelium cannot be replaced from the depleted stem management for its antiinflammatory properties. The cell reservoir. Diagnosis of stem cell deficiency can be greater the inflammation, the faster the AMT gets made by direct observation of loss of the limbal absorbed, but not before down regulating the existing palisades and limbal ischemia and by indirect evidence inflammation. However, it is more commonly used in such as persistent epithelial defects, conjunctivalization ‘cold’ cases, in partial stem cell deficiency and in total and vascularization of the cornea in cases of chemical stem cell loss (in combination with stem cell transplants). burns. It handles fairly easily and can be sutured using either If there is a partial stem cell deficiency, it can be 8/0 polyglycolic acid sutures or 10/0 nylon. It can be treated by scraping of the conjunctivalised area of the sutured directly on the cornea. It can also be used cornea and amniotic membrane grafting. This gives for symblephara release and fornix reconstruction. a chance for the distal, unaffected stem cells to grow Here, after release of the symblephara, the AMT is down and populate the areas of stem cell loss. This pushed deep into the fornices. Sutures passed through process may have to be repeated several times.7 the AMT are brought out through the eyelid and If however, there is a total or near total stem cell sutured over small cut pieces of rubber tubing on the deficiency, the stem cells need to be transplanted to outside. Results are amazing – patients with moving the affected eye. The donor stem cells can be taken body vision can regain 6/6 vision with a combination from the other eye in unilateral burns (ideal). In bilateral of stem cells and AMT! Chemical Injuries of the Eye 53 Keratoprosthesis In cases where there is total stem cell loss and bilateral blindness with disfigured anterior segments and gross tear deficiency, the above 2 treatments will not help. These are the cases where Keratoprosthesis surgery (KP) has a role. This surgery is reserved for those who have good perception of light with accurate projection in the better eye and a B-scan showing attached retina. There are several types of KPs available in the world. The commonly used ones are the Dohlmann’s, the Pintucci and the OOKP (osteo-odonto-KP). The largest number of KPs implanted is the Singh-Worst KPs. The author has till date (2008) done 75 Pintucci KPs with a 11-year follow-up. 65% of operated patients regained useful vision i.e. they were able to carry out activities of daily living independently. This is the largest series of KPs in Asia outside Amritsar.

Fig. 10.3: Post-alkali burns pseduopterygium

Fig. 10.1: Acid burns with pseudopterygium

Fig. 10.4: Chemical burn treated with subconjunctival venous blood

Conclusion Chemical injuries are increasing in the modern world. Acids and alkalis are the main chemicals implicated. Emergency treatment if reported early may make all the difference between saving the eye and irreversible blindness. Early use of cheaply and freely available treatments such as topical vitamin C and auto- hemotherapy can reduce morbidity in these cases Modern methods of managing post-burns corneal Fig. 10.2: Acid burns problems such as AMT, stem cell transplant and finally 54 Clinical Diagnosis and Management of Ocular Trauma Keratoprosthesis have considerably improved overall 4. Sfalangakos L, Tranos, Mitsonis J, Kouroubetsis J. The prognosis in these unfortunate patients. management of chemical burns of the cornea. The cornea in health and disease. Abstracts of VI Congress of European Society of Ophthalmology 1980;245. References 5. Thoft RA, Friend J Kenyon KR. Ocular Surface response to trauma. International Ophthalmology Clinics. Summer 1979;19(2). 1. Duke Elder, Sir Stewart. Diseases of the Outer Eye. Henry 6. Sridhar MS, Sridhar MS, Bansal AK, Sangwan VS, Rao Kimpton Publishers 1965;8(2):604-31,995-1002. GN. Amniotic Membrane Transplantation in Acute 2. Duke Elder, Sir Stewart. Non-Mechanical Injuries. Henry Chemical and Thermal Injury. American Journal of Kimpton Publishers; 1972;Vol. XIV, Part 2:011-1088. Ophthalmology July 2000;130:134-36. 3. Henriquez AS. Scanning Electron Microscope in 7. Dua HS, King AJ, Joseph A. A New classification of Experimental Alkali Burnt Corneas. Abstracts of VI Congress Ocular Surface Burns. Br J Ophthalmol 2001;85: of European society of Ophthalmology 1980;240. 1379-83. CHAPTER Injuries of the Eye due to Physical Agents (Thermal, Ultrasonic and Electrical Injuries) 11 Rupesh V Agrawal (India)

Introduction however the tarsal plates remain intact, cornea shrivelled, ocular tissues damaged in varying degrees, The injuries to the eye due to physical agents can in worst cases whole eye and the orbital contents result from thermal, ultrasonic or electrical agents in incinerated, areas of black eschar may appear which addition to radiation injuries of the eye. In the present as they fall off leave raw islands, extensive loss of tissue chapter, we will highlight: on forehead, cheeks, eyelids leads to black and I. Thermal injuries to the eye. shapeless mask, infection can occur and can spread II. Ultrasonic injuries to the eye. inwards causing orbital cellulitis and infective III. Electrical injuries to the eye. dacryoadenitis. Healing is slow and can leads to inexorable contraction distorting the face. Non-mechanical Eye Injuries

• Radiational injuries Contact Burns • Thermal injuries It can occur secondary to contact of the eye and the • Ultrasonioc injuries adnexa with lighted ends of cigars or cigarettes, shreds • Electrical injuries of tobacco from pipes, head of lighted match or a firework, glowing coal or hot cinders from a fire, industry-flying pieces of glowing metal, slag, solder, lead or glass or with solid bodies such as slag, molten Thermal Injuries metal with high melting point such as iron, molten The injuries of the eye and the adnexa can be caused glass, very hot bodies above 1000°C. by both extremes of temperature and are hence Clinical lesions: In the conjuntiva, hyperemia, associated with thermal burns and freezing or exposure violent chemosis, greyish white coagulated plaque. In to cold. the cornea – superficial or deeper burns, superficial burns will be grey or yellowish clouding of the epithelium HYPERTHERMAL INJURIES which develops into erosion whereas in deeper burns Flame Burns cornea become grey and opaque like ground glass or white like procelain, a line of demarcation eventually It can occur secondary to explosion of stove/Gas forms and the slough is cast off, leaving an ulcer which heater, industrial cases – from high temperatures and if deep becomes infected and may perforate. Healing inflammable fluids, gases, Ovens, Furnaces, petrol is by formation of fibrous tissue, resultant leucoma stores, burning building wherein people are trapped, is permanent.The other complications of contact burns accidents in travel, in automobiles, trains, ships, can be bullous keratitis, ectasia, corneal staphyloma, airplanes, in war-the flame thrower, the napalm bomb, pseudopterygium, symblepharon and on the other explosive fire in the confiance of tank on land, burning hand deeply penetrating lesion involves the sclera which plane in the air, explosion of gun-turret of a ship, may be perforated resulting in prolapse of uvea and tragedy of swimming through boiling or burning oil vitreous, purulent uveitis, panophthalmitis. floating on the sea. Clinical lesions: Eyes themselves are rarely involved Scalds in a flame burn unless the heat is intense and It occurs secondary to burns by hot fluids affecting prolonged, lashes and brows may be scorched, skin the lids, can lead to conjunctival swelling and chemosis of the lids deeply burned, lids may be destroyed, and symblepharon in chronic cases. 56 Clinical Diagnosis and Management of Ocular Trauma Treatment Accidental Hypothermia Treatment of the lid burn: It occurs on exposures at high altitudes in snow-storm. • The best emergency measure is to cover the face Aviators in open aircraft, in a damaged cockpit or while with sterile dressing or handkerchief. bailing out from an aircraft in difficulties can also suffer • In early stage the affected area thoroughly cleansed from hypothermia. with saline and surrounding area with soap and Clinical lesions: Clinical cases are rare because of water the protection afforded by the richly vascular lids and • All the aseptic measures to be taken while treating the care usually taken of them even in conditions of this patients severe stress and even the temperature of cornea is • Blisters to be fully opened, loose epidermis cut away, 3 to 5 degrees less than the other tissues of the body. remnants of signed lashes removed There can be varying degrees of conjunctival • Antibiotic cream applied over the denuded area. hyperemia, corneal erosion or opacity which may • Sofratulle dressing applied disappear without any ill effects. Severe bilateral • For full thickness burns of the lids, the only effective ulceration of the cornea leading to permanent opacity treatment is graft of the cornea. • Full thickness skin graft should be carried out as an emergency measure. Cryosurgery Treatment of the burns of the eye: It is used as a therapeutic modality in different cases • Local analgesics avoided owing to their deleritious with varying indications. The effects of the freezing on effect on epithelialization. the various ocular tissues and intraocular fluids depends • Topical cycloplegics – Atropine eye drops on the temperature used, the area involved, the length • Systemic NSAIDs/Sedatives to achieve comfort of application and the type of cell principally concerned. • Antibiotics to prevent secondary infection • Ocular lubrication for corneal burns Clinical lesions: • Glass rod to be passed in the fornices to prevent • Conjunctiva: Congestion, edema. the risk of symblepharon or use of symblepharon • Muscles and tendons: Edema and hemorrhage ring • Sclera: Swelling and separation of scleral fibers seen • Conjunctival transposition flap microscopically, no clinically evident change • Corneal leucomatous opacity at later stage can be • Ciliary body: Freezing of ciliary body resulting in replaced by corneal graft-PK or LK reduce aqueous humor formation • Amniotic membrane graft or Limbal cell transplant • Lens: Freezing of the lens utilised in cryoextraction also has a role to play of the lens • Topical corticosteroids also can be used judiciously • Retina and choroid: Adhesive chorioretinal reaction in case to case basis. • Vitreous: Vitreous ice balls.

HYPOTHERMAL INJURIES Ultrasonic Injuries Surgical Hypothermia Sound waves (sonic or acoustic energy) which are It occurs in cardiovascular surgery and in neurosurgery audible to the human ear produce no recognizable or by immersing the patient in ice packs and cold baths, ocular injury. Ultrasonic vibrations above the limits of supplemented by injection of lytic cock-tail. hearing may produce characteristic biological reactions. Besides its diagnostic and therapeutic applications, Clinical lesions: At temperatures far under the ultrasonic energy can produce the following injuries therapeutic range opacities developed in the cornea to the eye. and lens associated with widespread cellular and hemorrhagic changes in the ocular tissues, particularly CLINICAL LESIONS in the ciliary body and retina. Retinal arteries and veins • Eyelids—epilation, ulceration of the skin edema. become indistinct and show a fine stippling of the blood • Cornea—slight and transient turbidity and swelling column and the retina becomes pale and optic disc in superficial corneal layers, earlier changes are white, however, within two seconds of restoration of reversible but the later are irreversible and lead to the circulation the fundus assumes its normal necrosis. High intensities of radiation cause necrosis appearance. and ulceration of the epithelium, a general Injuries of the Eye due to Physical Agents (Thermal, Ultrasonic and Electrical Injuries) 57 thickening of the stroma with the formation of dense • Corneal lesions—The commonest lesions are leucomatous opacities. interstitial opacities which can be punctate, striate • Lens—Two types of cataract—Cavitation and or diffuse. This type of generalised corneal Thermal. In cavitation cataract a zone of frothy, cloudiness usually clears up in few days. However, spume like turbidity of the deeper layers of the if destructive electrical burn is formed the epithelium cortex around the nucleus. In thermal cataract there may become necrotic and exfoliate and sensation is densely white permanent opacity and it develops may be impaired or lost so that serious ulceration after radiation of high frequency and greater intensity. may develop and become recurrent and • Vitreous—liquefied irreversibly by a few seconds permanent scar may form. In some cases there can exposure. be purulent infiltration of entire cornea, extensive • Retina and choroid—adhesive chorioretinal necrosis, perforation or phthisis of the globe. adhesion with less damage to the sclera than caused • Lesions of the iris and ciliary body—Iris and ciliary by diathermy or by ultrasonic energy of megahertz body show irritative changes in any type of electrical frequencies, retinal edema within 12-24 hours injury. There can be mild and transient iritis, followed by proliferative and pigmentary changes. sometimes widespread synechiae formation with heavy aqueous flare and occasionally hyphema. • Lesions of the pupil—Unilateral or bilateral extreme Electrical Injuries miosis with sluggish or absent reactions, spasm of Electrical injuries are due to passage of an electric accomodation. current through the body and the commonest cause • Electric cataract—Lenticular opacities form being direct double contact between two live electric sometime after the accident and is sometimes the conductors or a single contact either direct or by short only finding in cases with electrical injury. Main circuit, between a conductor and the earth so that the changes are localized in the capsule itself and in circuit is completed. The similar effect result on being the immediate cortex underneath the capsule. It stuck by lightning. There is a point of entry and often involves both anterior and posterior surface of lens. of exit of the elctric current causing an electrical burn, There is formation of vacuoles underneath the the passage of current usually produces violent tetanic capsule. The type of opacification varies from slight spasms of the muscles, low voltage currents cause indefinite haze to densely crowded punctate auricular fibrillation and high voltage currents affects opacities. There can be evident polychromatic the central nervous system and lead to loss of lusture seen on the lens. consciousness or death from respiratory failure or • Lesions of the retina and choroid—Retinal edema, cardiac arrest and shock. The high resistance offered papilledema, hemorrhages, traumatic chorioretinitis by the non-nervous tissue accounts for the thermal in the periphery, detachment of the retina, vitreous effects of electric injuries, which may result in immediate coagulation of the proteins of the cells. opacities. Most dramatic changes are at the posterior pole which can be combination of the electric current and radiation resulting in macular edema, CLINICAL LESIONS punctate pigmentary degeneration, cystoid changes. • Lesions of the lids—Typical electrical burn at the • Optic nerve—Optic neuritis. point of entry – imprint as a sharply defined necrotic • Functional disabilites—Photophobia, blepharo- mark without surrounding hyperemia. Lid burns spasm, transient blindness to permanent bilateral differs from heat burns in that the former are visual loss, concentric contraction of the field, ring painless, dry and aseptic and usually circumscribed, scotoma, absolute central scotoma, disturbance of mainly due to the very high temperatures and short binocular fusion. duration. Electrical gangrene may supervene in the subsequent days or weeks due to circulatory LIGHTNING INJURY impairment. • Lesions of the conjunctiva—There can be • Even in fatal cases the body may be unmarked, substantial damage to the eye in both electrical as • In some a deep necrotic burn is formed at the point well as lightning injuries. Minor degree of of entry, conjunctival hyperemia and ciliary injection will • In others an arborescent tracery of linear burns invariably occur in each and every case of electrical appears (lightning prints). burn. There can be subconjuctival effusion of blood • Mydriasis, partial internal ophthalmoplegia, which is transient and which disappears in few days blindness from optic atrophy, deafness, loss of time. memory, nervous damage. 58 Clinical Diagnosis and Management of Ocular Trauma • Injury to the retina caused by brilliance of flash • Treatment of ocular lesions is on the general plays an inconspicuous part in the total damage, principles: Rest, atropine, local heat. retinal damage in the macular area, rupture of the choroid. Bibliography 1. Ophthalmology Clinics of North America by Ferenc Kuhn TREATMENT et al. volume 15, Non mechanical injuries. 2. System of ophthalmology by Sir Stewart Duke Elder, Vol. • First and foremost is saving of life. XIV, Injuries, Part 2, Non Mechanical Injuries. • Local burns of the skin of the lids or in the vicinity 3. Work and the Eye, 2nd edition of Rachel V North, is treated as in case of thermal burns. Woburn MA, Butterworth – Heinemann, 2001;51-74. CHAPTER

Radiational Injuries to the Eye 12 Rupesh V Agrawal (India)

Introduction physicists who experimented with radiation, is a measure of actual radioactivity given off by a Radio and television signals, radar, heat, infrared, radioactive element, not a measure of its effect. The ultraviolet, sunlight, starlight, cosmic rays, gamma rays, average annual human exposure to natural and X-rays all belong to the electromagnetic spectrum background radiation is roughly 3 milliSieverts (mSv). and differ only in their relative energy, frequency, and It is reasonable to presume that any amount of wavelength. These waves all travel at the speed of ionizing radiation will produce some damage. light, and unlike sound they can all travel through However, there is radiation everywhere, from the sun empty space. The frequencies above visible light have (cosmic rays) and from traces of radioactive elements enough energy to penetrate and cause damage to in the air (radon) and the ground (uranium, radium, living tissue, damage that can be as minor as a sunburn carbon-14, potassium-40 and many others). Earth’s caused by ultraviolet light or as extreme as the atmosphere protects us from most of the sun’s incineration of Hiroshima, Japan, during World War radiation. Living at 5,000 feet altitude in Denver, II. Lower frequencies do not penetrate, but can cause Colorado, doubles exposure to radiation, and flight eye and skin damage, primarily due to the heat they in a commercial airliner increases it 150-fold by lifting transmit. The energy of electromagnetic radiation is us above 80% of that atmosphere. Because no a direct function of its frequency. The high-energy, amount of radiation is perfectly safe and because high-frequency waves, which can penetrate solids to radiation isever present, arbitrary limits have been various depths, cause damage by separating molecules established to provide some measure of safety for into electrically charged pieces, a process known as those exposed to unusual amounts. Less than 1% of them reach the current annual permissible maximum ionization. Atomic particles, cosmic rays, gamma rays, of 50 mSv. X-rays, and some ultraviolet are called ionizing It is therapeutic, accidental, and deliberate radiation radiation. The pieces they generate are called free that does the obvious damage. There has not been radicals. They act like acid, but they last only fractions much in the way of deliberate radiation damage since of a second before they revert to harmless forms. Nagasaki, but accidental radiation exposure happens Adjusting the energy of therapeutic radiation can select periodically. Between1945 and 1987, there were 285 a depth at which it will do the most damage. Ionizing nuclear reactor accidents, injuring over 1,550 people radiation also does damage to chromosomes by and killing 64. The most striking example, and the breaking strands of DNA. DNA is so good at repairing only one to endanger the public, was the meltdown itself that both strands of the double helix must be of the graphite core nuclear reactor at Chernobyl in broken to produce genetic damage. Because radiation 1986, which spread a cloud of radioactive particles is energy, it can be measured. There are a number across the entirecontinent of Europe. Information of units used to quantify radiation energy. Some refer about radiation effects is still being gathered from that to effects on air, others to effects on living tissue. The disaster. There have also been a few accidents with roentgen, named after Wilhelm Conrad Roentgen, medical and industrial radioactivity. who discovered X-rays in 1895, measures ionizing Nevertheless, it is believed that radiation is energy in air. A rad expresses the energy transferred responsible for less than 1% of all human disease and to tissue. The rem measures tissue response. A for about 3% of all cancers. This figure does not include roentgen generates about a rad of effect and produces lung cancer from environmental radon, because that about a rem of response. The gray and the sievert information is unknown. The figure could be are international units equivalent to 100 rads and significant, but it is greatly confounded by the similar rems, respectively. A curie, named after French effects of tobacco. 60 Clinical Diagnosis and Management of Ocular Trauma Radiation can damage every tissue in the body. within three months from vomiting, diarrhea, The particular manifestation will depend upon the starvation, and infection. Victims receiving 6-10 Sv all amount of radiation, the time over which it is at once usually escape anintestinal death, facing absorbed,and the susceptibility of the tissue. The fastest instead bone marrow failure and death within two growing tissues are the most vulnerable, because months from loss of blood coagulation factors and the radiation as much as triples its effects during the growth protection against infection provided by white blood phase. Bone marrow cells that make blood are the cells. Between 2-6 Sv gives a fighting chance for survival fastest growing cells in the body. A fetus in the womb if victims are supported with blood transfusions and is equally sensitive. The germinal cells in the testes and antibiotics. One or two Sv produces a brief, non-lethal sickness with vomiting, loss of appetite, and generalized ovaries are only slightly less sensitive. Both can be discomfort.It is clearly important to have some idea rendered useless with very small doses of radiation. of the dose received as early as possible, so that More resistant are the lining cells of the body—skin attention can be directed to those victims in the 2- and intestines. Most resistant are the brain cells, because 10 Sv range that might survive with treatment. Blood they grow the slowest. transfusions, protection from infection in damaged The relative sensitivity of various tissues gives a good organs, and possibly the use of newer stimulants to idea of the wide range that presents itself. The numbers blood formation can save many victims in this category. represent the minimum damaging doses; a gray and Local radiation exposures usually damage the skin and a sievert represent roughly the same amount of require careful wound care, removal of dead tissue, radiation: and skin grafting if the area is large. Again infection Fetus 2 grays (Gy). control is imperative. Bone marrow 2 Gy. Ovary 2-3 Gy Testes 5-15 Gy. Injuries of the Eye due to Lens of the eye 5 Gy. Child cartilage 10 Gy. Ionizing Radiation Adult cartilage 60 Gy. X-rays, beta rays, and other radiation sources in Child bone 20 Gy. adequate doses can cause ocular injury. Adult bone 60 Gy. Kidney 23 Gy. LIDS Child muscle 20-30 Gy. The eyelid is particularly vulnerable to X-ray damage Adult muscle 100+ Gy. because of the thinness of its skin. Loss of lashes and Intestines 45-55 Gy. scarring can lead to inversion or eversion (entropion Brain 50 Gy. or ectropion) of the lid margins and prevent adequate Notice that the least of these doses is a thousand closure. times greater than the background exposure and nearly 50 times greater than the maximum permissible annual CONJUNCTIVA dosage. The length of exposure makes a big difference in what happens. Over time the accumulating damage, Scarring of the conjunctiva can impair the production if not enough to kill cells outright, distorts their growth of mucus and the function of the lacrymal gland ducts, and causes scarring and/or cancers. In addition to thereby causing dryness of the eyes. leukemias, cancers of the thyroid, brain, bone, breast, skin, stomach, and lung all arise after radiation. Damage LENS depends, too, on the ability of the tissue to repair itself. X-ray radiation in a dose of 500-800 R. directed toward Some tissues and some types of damage produce the lens surface can cause cataract, sometimes with much greater consequences than others. a delay of several months to a year before the opacities Immediately after sudden irradiation, the fate of appear. the patient depends mostly on the total dose absorbed. This information comes mostly from survivors of the atomic bomb blasts over Japan in 1945. Massive doses Injuries due to Ultraviolet incinerate immediately and are not distinguishable from the heat of the source. A sudden whole body Radiation dose over 50 Sv produces such profound neurological, heart,and circulatory damage that patients die within CORNEA the first two days. Doses in the 10-20 Sv range affect Ultraviolet radiation of wave lengths shorter than 300 the intestines, stripping their lining and leading to death nm (actinic rays) can damage the corneal epithelium. Radiational Injuries to the Eye 61 This is most commonly the result of exposure to the welding arc can also damage the the retinal macula. sun at high altitude and in areas where shorter wave There may be permanent decrease in visual acuity. lengths are readily reflected from bright surfaces such The intensity of light, lenght of exposure, and age as snow, water, and sand. are all important factors. The older ones are more Exposure to radiation generated by a welding arc sensitive, also those who have had cataract surgery can cause welding flash burn, a form of keratitis. because filtration of light by the lens is impaired.

LENS Wavelengths of 300-400 nm. are transmitted through Injuries due to Infrared Radiation the cornea, and 80% are absorbed by the lens, where Potters may be exposed to this type of radiation. they can cause cataractous changes. Wavelengths greater than 750 nm. in the infrared Epidemiologic studies suggest that exposure to solar spectrum can produce lens changes. radiation in these wavelengths near the equator is La “cataracte des verriers”(glassblower’s cataract) correlated with a higher incidence of cataracts. is an example of a heat injury that damages the anterior They also indicate that workers exposed to bright lens capsule among unprotected artists. Denser sunlight in occupations such as farming, truck driving cataractous changes can occur in unprotected workers and construction work appear to have a higher who observe glowing masses of glass or iron for many incidence of cataract than those who work primarily hours a day. indoors. Another important factor is the distance between Experimental studies have shown that these wave- the worker and the source of radiation. In the case lengths cause changes in the lens protein, which lead of arc welding, infrared radiation decreases rapidly as to cataract formation in animals. a function of distance, so that farther than 3 feet away from where welding takes place, it does not pose an ocular hazard anymore but, ultraviolet radiation still Injuries due to Visible Radiation does. That is why welders wear tinted glasses and surrounding workers only have to wear clear ones. (Light) When we speak of type of exposure, potters look Visible light has a spectrum of 400-750 nm. If the at their cone packs for very short periods of time in wavelengths of this spectrum penetrate fully to the a repeated way, more often nearing the end of firing; retina, they can cause thermal, mechanical, or photic and also according to the use of other methods for injuries. measuring temperature, like the concomitant use of a thermocouple and a reading device. THERMAL INJURIES So, these “short-term” exposures are spaced by They are produced by light intense enough to increase quite longer “exposure-free” periods and the sum of the temperature in the retina by 10-20C. the former does not correlate with the concept of many Lasers used in therapy can cause this type of injury. hours a day. The light is absorbed by the retinal pigment epithelium, We have searched the literature pertaining to where its energy is converted to heat, and the heat Occupational Health and Safety and have not found causes photocoagulation of retinal tissue. a single case of presumed “ceramicist’s or potter’s cataract”, even if the trade of potter is quite older than the one of glassblower. MECHANICAL INJURIES Therefore, I do not think that any of the above They can be produced by exposure to laser energy types of radiation present a threat to potters. from a Q-switched or mode-locked laser, which It is a good thing, mainly at high temperature, to produces sonic shock waves that disrupt retinal tissue. wear lightly tinted industrial grade safety glasses to better visualize cones (ocular ergonomics) and also to PHOTIC INJURIES reassure those who are more worried. They are caused by prolonged exposure to intense These glasses also offer a better protection than light, which produces varying degrees of cellular typical sun-glasses in case of projection of hot dust damage in the retinal macula without a significant particles from a gas kiln when looking through the increase in the temperature of the tissue. peephole in a soft brick door. Sun gazing is the most common cause of this type By the way with ageing, most if not all of us, will of injury, but prolonged unprotected exposure to a suffer from cataracts of the senile type. 62 Clinical Diagnosis and Management of Ocular Trauma The progress or change and the related reduction in returning to work in less than two days and 95 percent vision is usually quite slow. in less than seven days, some eye injuries are Nuclear sclerosis-an increasing density in the central irreversible and permanent visual impairment occurs. mass of protein-causes a myopic change than can be This is especially true with infrared and visible spectrum corrected by changing glasses for some years-in many (bright light) radiation. Both can penetrate through instances restoring vision to near normal. to the retina and—although this is rare—can cause permanent retinal damage, including cataracts, diminished visual acuity, and higher sensitivity to light Welding Arc Injuries and glare. And welders are not the only workers at risk. While Eye injuries account for one-quarter of all welding the welding arc is the principal source of UVR, other injuries, making them by far the most common injury workers in the area can sustain eye damage from the for welders, according to research from the Liberty radiation as far as 50 feet away from UVR reflecting Mutual Research Institute for Safety. Those most at off shiny surfaces, concrete, or unpainted metals. To risk for welding-related eye injuries are workers in counteract this reflection, you should install shielding industries that produce industrial and commercial curtains where practical or require that all workers in machinery, computer equipment, and fabricated metal the area wear appropriate eye protection. products. Yet, despite the insidious damage radiation can The best way to control eye injuries is also the most cause, molten and cold metal particles striking the eye simple: proper selection and use of eye protection. are still the most common sources of eye injuries. Helmets alone do not offer enough protection. Welders should wear goggles or safety glasses with sideshields. Goggles provide better protection than safety glasses Eye Protection Goes Beyond from impact, dust, and radiation hazards. Unfortunately, workers don’t always wear goggles the Helmet or safety glasses because of low perception of risk, Helmets and protective clothing shield welders from poorly maintained lenses, discomfort, having to wear “sunburn” and “welder’s flash,” but with the majority prescription lenses underneath, and vanity. It is of their work performed with the helmet up, welders important to stress to workers that welding-related eye also need to wear goggles or safety glasses with injuries come from a number of sources, including: sideshields. These will protect them from particles sent mechanical damage from being struck by flying flying during pre-job grinding, hammering, and particles and chipped slag; radiation and power chipping that make it past the helmet’s photochemical burns from ultraviolet radiation protective front. (UVR), infrared radiation, and intense blue light; Some guidelines and safety warnings for welding and irritation and chemical burns from fumes suggest workers should not wear contact lenses, even and chemicals. though there does not appear to be any research that To help in reducing eye injuries, you should educate would support such a recommendation. In fact, the workers about all of the dangers they face and should National Safety Council, the American Welding Society, implement an eye protection plan that outlines proper and the FDA all acknowledge that wearing contact welding behavior. lenses while welding is safe and even can provide UV protection. The only caveat is that contact lenses should not be used as eye protection in place of safety glasses Cumulative Damage Risks or goggles. All of the most common types of welding (shielded Once the proper goggles/shields are in hand, you metal-arc or stick welding, gas metal-arc welding, and can turn your attention to the type of helmet best suited oxyacetylene welding) produce potentially harmful for the job. Published tables are available through the ultraviolet, infrared, and visible spectrum radiation. welding helmet vendor or the Internet, which can help Damage from ultraviolet light can occur very quickly. you determine the most appropriate lens shade based Normally absorbed in the cornea and lens of the eye, on the type of welding and the amperage of the ultraviolet radiation (UVR) often causes arc eye or arc welding unit. It is a common misconception that a flash, a very painful but seldom permanent injury that darker shade provides more protection against UV. is characterized by eye swelling, tearing, and pain. Properly maintained welding helmets, regardless of While most welding-related eye injuries are shade, provide 100 percent protection against UV, reversible, with more than half of injured workers according to the manufacturers. Radiational Injuries to the Eye 63 Arc welding helmets can be fixed shade or variable Now that your workers have the right eye protection shade. Typically, fixed shade helmets are best for daily for the job, it is time to implement an ongoing eye jobs that require the same type of welding at the same protection plan that ensures they use the equipment current levels, and variable helmets are best for workers properly. with variable welding tasks. Helmet shades come in Bibliography a range of darkness levels, rated from 9 to 14 with 1. Occupational and Environmental Medicine. Joseph 14 being darkest, which adjust manually or Ladoue and al, last edition. automatically, depending on the helmet. To determine 2. Occupational Medicine, Zenz C, 2003. the best helmet for the job, select a lens shade that 3. Oshline and Nioshtic database, 2004. provides comfortable and accurate viewing of the 4. Precis de Medecine du Travail, Desoille H, Scherrer J, “puddle” to ensure a quality weld. Truhaut R, last edition. CHAPTER

Traumatic Angle Recession Glaucoma: An Overview 13 Cyres K Mehta, Keiki Mehta (India)

This chapter deals with blunt trauma to the eyeball 6. Tearing of the lens zonules leading to leading to angle recession glaucoma. phacodonesis, iridodonesis, subluxation or total Synonyms: Angle-recession glaucoma, post- dislocation of the lens backwards. traumatic angle recession glaucoma, contusion angle 7. Retinal dialysis at the ora or a giant retinal tear. recession glaucoma, contusion angle deformity. After blunt trauma to the globe we can divide pressure fluctuation into EARLY (few days to few weeks) and LATE (few weeks and later). Intraocular History pressure (IOP) may be reduced because of 2 reasons. Treacher Collins described the micropathology of angle Firstly due to to trauma to the ciliary body the recession glaucoma as a “split into the ciliary muscles amount of aqueous secretion is reduced and secondly in its entire circumference so that angle of the chamber due to a total tear of the trabecular meshwork into was prolonged out”. In 1945 D’Ombrain postulated Schlemms canal the aqueous outflow is greatly that angle recession led to increased intraocular tension. exaggerated, or, due to a cylodialysis developing Angle recession may be associated with many other the aqueous is been drained out via uveoscleral conditions associated with the ocular trauma sustained ouflow. such as, such as dislocation or subluxation of the lens, Alternatively in the short-term the pressure can traumatic cataract, iridodialysis, cyclodialysis, hyphema rise up for several weeks.This is due to increased and retinal detachment, extraocular muscle resistance to the outflow of aqueous due to trabeculitis avulsion,orbital trauma and globe rupture in extreme (swelling of the meshwork) due to circulating cytokines cases. and prostaglandins.Treatment with corticosteroid is When Blunt (non-penetrating) injury is sustained advocated here. by the eye by an object moving parallel to the visual axis,the cornea and anterior sclera is displaced backwards. This leads to a compensatory equatorial Late Post-traumatic Glaucoma: expansion. Aqueous and vitreous are relatively incompressible and transmit the force so that the ocular Angle Recession Glaucoma tissues undergo sudden expansion and possibly tearing. INTERNATIONAL INCIDENCE The General features of non-penetrating trauma are (Campbells classification of the 7 tissue rings). In 60-94% of cases of patients with blunt ocular injury 1. Pupillary sphincter tears. in Africa angle recession was noted. 2. Iridodialysis. In Africa angle recession glaucoma was frequently 3. Anterior ciliary body tear—We can have a angle bilateral. recession or a tear in the face of the ciliary body. The presence of angle recession does not neces- The rupture of the ciliary body between its sarily mean the onset of raised IOP and nerve head longitudinal and circular fibers shows that this is pathology. the weakest portion of the ciliary body.This leads Other studies have indicated that 6-20% of all to deepening of the Anterior chamber also known individuals with angle recession went on to develop as angle recession. late onset glaucoma. 4. Cyclodialysis, or a separation of the ciliary body Again another study showed a 5-8% conversion from the sclera. to glaucoma after angle recession. 5. Trabecular dialysis or a tear through the trabecular A 3:1 to 4:1 male preponderance was noted by meshwork. some studies. Traumatic Angle Recession Glaucoma: An Overview 65 INDIAN INCIDENCE (ACCORDING TO Also a descemets like membrane is seen growing from SIHOTA AND SOOD) the cornea over the angle similar to the membrane Of all traumatic glaucoma patients, 71% were below seen in iridocorneal endothelial syndrome. 30 years of age. There was a 90% male preponderance Chandler claimed that glaucoma is due to Blunt trauma was the mode of injury in 85% of cases. impairment of the action of ciliary muscles,due to the The cricket ball, tennis ball, gilli-danda (a small flying tear in its body, which open the pore of the trabecular stick), hockey stick, bamboo stick and stone were meshwork responsible for 30% cases; fire cracker injury in 20% Cases with involvement of lesser area of angle cases and 50% were work-related, assaults or accidental showed no rise of intraocular pressure during the follow injury. In eyes having angle recession, two or more up period. This agrees with the findings of Alter who quadrants were involved in 87% cases. Other features observed glaucoma to be associated more commonly of trauma like sphincter tear, hyphema, iridodialysis, in cases having 240 degrees or more of angle subluxation, dislocation, vitreous hemorrhage, retinal detachment, and cataract could be seen in various involvement. combinations in about 95% cases. Fifty percent of It is usually agreed that more than 180 degrees traumatic glaucomas had an IOP of =30 mm Hg and of angle involvement are required for pressure 56% had a vision =20/200. elevation in most cases. Its interesting to note that that the other eye in SLITLAMP FINDINGS unilateral angle recession glaucoma are more likely to The chamber appears deeper than the other eye.Other have elevated IOP as well as be steroid responders. features of blunt trauma such as phacodonesis, Its safe to conclude that eyes with a tendency to iridodialysis and hyphema might be seen. develop higher IOP have a greater tendency to develop glaucoma after blunt trauma. GONIOSCOPIC FINDINGS Gonioscopically angle recession is characterized by widening of the ciliary body and prominence of the cilary spur. Sometimes trabecular meshwork tears are seen along with iridodialysis and cyclodialysis. After the injury scar tissue may fill the angle recession cleft confounding the diagnosis at later follow ups, so, as soon as blunt trauma is noted and the cornea is clear enough and the patient cooperative enough a gonioscopy should be carried out.

FURTHER INVESTIGATIONS Ultrasound Biomicroscopic Study and or Anterior Segment OCT • Ultrasound biomicroscopy produces high-resolution images of the anterior segment, providing cross- sectional views of the angle in vivo similar to those of a histologic section. • This noninvasive procedure is readily performed in a clinical setting in an intact globe. • High-resolution images of angle recession, irido- dialysis, and cyclodialysis have been described. • Anterior segment OCT is another modern diagnostic tool which can study the angle (Ziess Visante and others). Pathology After the initial injury to the ciliary body and or trabe- cular meshwork, scarring occurs, causing obstruction. Figs 13.1A and B: Traumatic glaucoma 66 Clinical Diagnosis and Management of Ocular Trauma Management of Angle Recession In Angle Recession Glaucoma beta blockers like Levobunolol, alpha agonists like Brimonidine, prostag- landin analogues like Latanoprost and carbonic anhydrase inhibitors like Dorzolamide all can help lower intraocular pressure. However, Pilocarpine and other miotics are contra- indicated as they decrease uveoscleral outflow.Once the meshwork is scarred uveoscoleral outflow is the predominant pathway for aqueous egress. Nd:Yag Laser trabeculopuncture as well as laser trabeculoplasty have proved to be ineffective in the long term and mildly effective in the short-term at best. Non-Penetrating Deep Sclerectomy has no role to play in these cases as trabecular meshwork is scarred in its entirety usually. Filtering surgery is less effective in angle recession glaucoma eyes than in eyes with chronic simple glaucoma.Mitomycin –C application increases the success rate in some studies to beyond 50% for 5 years. Valve implants such as the Molteno and Ahmed have proved to be successful with certain studies showing 57% survaival rate at 5 years. Continual follow-up with effective medical and surgical management is the key to long-term glaucoma management in these cases.

Figs 13.2A and B: Cyclodialysis Bibliography 1. Alper MG. Contusion angle deformity and glaucoma. Arch Ophthal (Chicago) 1963;69:455. 2. Campbell DG. Traumatic Glaucoma. In Shingleton BJ, Hersh PS, Kenyon KR (Eds): Eye Trauma, St Louis,1991,Mosby. 3. Chandler, P. A. Secondary glaucoma. Tr. Ophthal. Soc. Australia 1960;20:17. 4. d'Ombrain, A. Traumatic or 'Concussion' chronic glaucoma. Brit. J. Ophthal 1949;33:495. 5. Ellong A, Ebana MC, Nyouma ME, Bella HA, Ngosso A, Fig. 13.3: Angle recession (wide CBB) Njoh LC. Post-traumatic glaucoma with irido-corneal angle injuries in Cameroon. Bull Soc Belge Ophtalmol 2005;298:21-28. 6. Girkin CA, McGwin G Jr, Long C, Morris R, Kuhn F. Glaucoma after ocular contusion: A cohort study of the United States eye injury registry. J Glaucoma 2005;14: 470-73. 7. Pettit, T. H. and Keates, E. U. Traumatic cleavage of the chamber angle. Arch. Ophthal, (Chicago) 1963;69:438. 8. Sihota R, Sood NN, Agarwal HC. Traumatic glaucoma. Acta Ophthalmol Scand 1995;73:252-54. 9. Treacher-Collins, E. T. On Pathological examination of three eyes lost from Contusion. Tr. Ophthal. Soc. U.K. 1962;12:180 10. Wolff, S. M. and Zimmerman, L. E. Chronic Secondary Fig. 13.4: Iridodialysis glaucoma. Amer. J. Ophth 1962;54:547. CHAPTER

Management of Blunt Trauma of Anterior Segment 14 Ashok Sharma (India)

Introduction posterior segment involvement with 47% chance of achieving 20/20 or better visual acuity. Blunt ocular trauma usually causes closed globe injury resulting several vision threatening complications. Injuries to the posterior segment structures causes Closed-globe Injury: poorer visual outcome compared to the anterior segment lesions. In this chapter the injuries to the Classification1 anterior segment lesions will be discussed. Injuries to the crystalline lens also will be discussed in detail in TYPE a separate chapter. Ocular trauma classification group A. Contusion has developed a classification system for mechanical B. Lamellar laceration injuries of the eye. Closed globe injury classification C. Superficial foreign body is described in detail. Open globe injury classification D. Mixed. will be included in the chapter on open globe injury. Specific variable including vitreous hemorrhage, retinal detachment and hyphema have not been GRADE included in the classification of closed globe injuries. Visual acuity Study on identification of prognostic factors affecting 1. > 20/40 visual outcome in all types of closed globe injures in 2. 20/50 to 20/100 lacking. Patients suffering from closed globe injuries 3. 19/100 to 5/200 and presenting with hyphema have been studied in 4. 4/200 to light perception detail. In these patients visual acuity at presentation 5. No light perception. has been shown to predict final visual acuity. In a retrospective study on pediatric ocular trauma, patients with only anterior segment involvement had PUPIL 82% chance of getting final visual acuity of 20/30 or Positive: Relative afferent papillary defect present in better, in comparison to combined anterior and affected eye.

Flow chart 14.1: Classification of ocular trauma 68 Clinical Diagnosis and Management of Ocular Trauma Negative: Relative afferent papillary defect absent in affected eye.

ZONE I. External (limited to bulbar conjunctiva, sclera, cornea) II. Anterior segment (involving structures in anterior segment internal to the cornea and including the posterior lens capsule; also includes pars plicate but not pars plana) III. Posterior segment (all internal structures posterior to the posterior lens capsule).

Birth Trauma Fig. 14.1: Total corneal blood staining following blunt trauma It is rare and has been reported to occur during parturi- tion. Trauma usually results from faulty application of forceps during child birth. This may result in vertical Descemet’s membrane tear, resulting in severe corneal edema.2, 3 It may take 8-12 weeks for corneal edema to resolve. Once corneal edema subsides, the child has very high astigmatism (8-12 D). High astigmatism is due to flattening of meridian 90° to the Descemet’s membrane tear and corresponding steeping of meridian parallel to the Descemet’s membrane tear. At the time of presentation with corneal edema it should be differentiated from other causes of congenital corneal clouding. Congenital Hereditary Endothelial Dystrophy is bilateral and corneal edema in buphthalmos has associated high intraocular pressure. In the acute stage mild topical steroids, Fig. 14.2: Spontaneous resorption (Partial) of corneal hyperosmotic agent and anti-glaucoma drug to keep blood staining the intraocular pressure low should be given. In the later stage when edema has subsided astigmatism may Raised intraocular pressure (IOP) occurs in 24 to 32% be treated with either glasses or RGP contact lens. RGP of all traumatic hyphemas.4 Treatment options should filling may be difficult in neonates. Astigmatic aim at controlling the IOP, reducing the incidence of keratotomy and compression sutures may be tried. secondary hemorrhage, decreasing intraocular In case the astigmatism is higher the astigmatic inflammation and reducing the associated vision keratotomy and compression sutures may be threatening complications including corneal blood combined. One should aim for higher correction as staining and optic nerve damage (Figs 14.1 and regression is bound to occur. In case astigmatism is 14.2). not manageable astigmatic keratotomy and compres- sion sutures, deep anterior lamellar keratoplasty may be the ideal option. In non-resolving cases optical PKP OPHTHALMIC EXAMINATION may be considered. The patient with traumatic hyphema should undergo a complete ophthalmologic evaluation. The time of onset and type of injury should be recorded accurately Hyphema and in detail. The object producing the injury and the The occurrence of blood in the anterior chamber method by which it produced the injury give additional following blunt trauma signifies severe intraocular information to assess the extent intraocular damage. trauma associated damage to intraocular tissues. The ocular examination should be in detail. Hypersthesia Traumatic hyphema may cause significant visual or anesthesia on periorbital skin may indicate blowout reduction, particularly if secondary hemorrhage occurs. fracture. Examination of the ocular adenexa, the eyelids Management of Blunt Trauma of Anterior Segment 69 and the conjunctiva should be done for any laceration. sixth day. The initial raised IOP is probably the result Proptosis may indicate retrobulbar hemorrhage; of trabecular clogging by erythrocytes. This is followed enophthalmos and/or restrictions in extraocular muscle by a period of reduced pressure due to decreased rotations suggest a blowout fracture. Visual acuity with aqueous production. Subsequently with the recovery best optical correction should be recorded. In case the of the ciliary body function the intraocular pressure visual acuity is markedly reduced, perception and rises. Significant number of patients may present with projection of the light should be tested. Response to persistent raised intraocular pressure. consensual reaction of the pupil of the normal eye should be recorded. Extremely poor visual acuity Secondary Hemorrhage suggests optic nerve or macular damage. Secondary bleed into the anterior chamber results in The cornea should be examined for presence of a markedly increased incidence of complications and preexisting disease. The cornea with compromised worse prognosis. Secondary hemorrhage may occur endothelium is prone to develop blood staining. in nearly 20% of all patients with hyphema.4 The Record the amount and character of the hyphema. incidence of secondary hemorrhage is higher in Careful drawing of the shape of the clot or of the level hyphemas of grades 3 and 4. Secondary bleed usually of free cells aids in evaluation of secondary hemorrhage occurs on the third or fourth day, but may occur or resolution of the hyphema. One should note the anytime from the second to the seventh day .4 Several iris and the lens details that are visible beyond the studies documented that secondary hemorrhage occurs hyphema.The pupil should be dilated if one suspects more frequently in African American patients.5 In a intraocular foreign body, rupture or perforation of the study four (40%) of the 10 patients with secondary globe, or retinal tears or detachment. In most instances, hemorrhage had positive sickle cell trait or SA a detailed fundus examination may only be possible hemoglobin. Secondary bleed is attributed to lysis and later, following resolution of the hyphema. In such cases retraction of the clot that has occluded the injured B-scan ultrasonography should be performed. vessel.4 The secondary bleeding may result in raised Ultrasound biomicroscopy is provides accurate details IOP and corneal blood staining. Secondary bleed is of the angle structures including zonular status, angle associated with a poorer visual prognosis. recession, cyclodialysis, and the detection of small superficial and intraocular foreign bodies. IOP should be recorded by applanation tonometry. Avoid COMPLICATIONS OF HYPHEMA gonioscopy until a week or 10 days as it may be painful Complications from traumatic microhyphema treated and the patient may not be able to co-operate. with standard measures are few.6 Hyphema may cause posterior synechiae, peripheral anterior synechiae, SEVERITY GRADES OF HYPHEMA corneal blood staining, and optic atrophy. Optic Grade 1: Hyphema less than one-third of the anterior atrophy may result from acute rise of IOP or persistent chamber. Grade 2: Hyphema one-third to one-half high IOP. Posterior synechiae may secondary to iritis of the anterior chamber. Grade 3: Hyphema one-half or iridocyclitis. Peripheral anterior synechia occur more to less than total. Grade 4: Hyphema total clotted frequently in patients who had under gone surgical hyphemas. Total clotted hyphema is often referred to intervention. Closeness of follow-up may be as black-ball or eight-ball hyphema. determined by IOP on presentation. The source of blood into the anterior chamber is a tear at the iris or ciliary body, usually at the angle structures. A tear at the anterior aspect of the ciliary Medical Management body is the most common site of bleeding. The Standard protocol for traumatic microhyphema resolution of hyphema occurs through trabecular includes atropinization, bed rest, shield and restriction meshwork and Schlemm’s canal or the juxtacanalicular of antiplatelet medications. Bilateral patching, complete tissue. bed rest and sedation are not recommended. Patient remains ambulatory and mild sedation can be given Raised Intraocular Pressure to apprehensive patients. Patient should be advised

Raised IOPs (above 21 mm Hg) may accompany to keep the head elevated at 30-45° as it allows the hyphemas of any grade. Severe and persistent hyphema to settle inferiorly. Superior angle remains elevations of IOP are associated with near total or total free for the aqueous drainage. This also allows proper hyphemas. The initial period of elevated IOP within monitoring of the progress and also allows early 24 hours is often followed by a period of either normal recognition of rebleed. The antiplatelet effect of aspirin or below normal pressure during the second to the tends to increase the incidence of rebleeding in 70 Clinical Diagnosis and Management of Ocular Trauma traumatic hyphema and should be avoided. Surgical Intervention Nonsteroidal anti-inflammatory drugs such as mefenamic acid, also share this antiplatelet effect. Most hyphemas, including total hyphema, should be Various topical medications including cycloplegics for treated medically for the first 4 days. Spontaneous the traumatic iridocyclitis and miotics to increase the resolution of the hyphema occurs rapidly during this surface area of the iris to enhance resorption of the period. In general the patients with grade1 and 2 hyphema have been recomended. Topical atropine respond to the medical treatment favorably. Immediate sulfate 1% is indicated for iritis and to break the surgical intervention is indicated in case the IOP remains pupillary block. Topical use of steroids after the fourth elevated at 50 mm Hg or higher for 4 days. In case or fifth day of persistant hyphema may be the surgical intervention is delayed optic atrophy may advantageous to decrease iridocyclitis and to prevent occur in 50% and corneal blood staining in 43% of the formation of PAS or posterior synechiae. Secondary patients with total hyphemas.9 Surgery for hyphema hemorrhage seems to be unaffected by the use of should be carefully planned. Risks of surgery include topical corticosteroids. In one of the studies the systemic damage to corneal endothelium, lens, and/or iris, administration of ACA has been found effective in the prolapse of intraocular contents, rebleeding, and prevention of recurrent bleed.7 The antifibrinolytic increased synechia formation. activity of ACA given systemically has been demons- trated to decrease the incidence of secondary hemorrhage in other areas of the body. PARACENTESIS ACA retards clot lysis by preventing plasmin from Paracentesis causes little surgical trauma and reduces binding to lysine molecules in the fibrin clot. ACA, a the elevated IOP. Paracentesis is especially beneficial lysine analogue, competitively inactivates plasmin by in patients with sickle-cell trait or disease. However, occupying the lysine-binding site on plasmin that would the decrease in IOP may be transient, and there may normally bind to fibrin. In addition, ACA binds to be no appreciable reduction in the amount of the plasminogen, so that when activated to plasmin, it formed clot. cannot attach to fibrin. These effects stabilize the clot- vessel-wall interface, decreasing the potential for secondary hemorrhage. When ACA was administered IRRIGATION in a dosage of 100 mg/kg every 4 hours, orally, for Irrigation by a single- or double-needle technique has 5 full days, a statistically significant reduction in the the advantage of a small incision. We prefer entry at incidence of rebleeding of traumatic hyphemas was the 1 o’clock position in the right eye and at the 11

observed. Systemic ACA should be used in patients o’clock position in the left eye with a diamond blade. with hyphemas that occupy 75% or less of the anterior The entry should be through clear cornea. The chamber since the clot may persist in the anterior irrigating needle should then extend just through the chamber for an increased period during administration corneal endothelium and a slow push-pull maneuver of the drug. The continued retention of the clot in with the single-needle technique washes out the the anterior chamber would be a disadvantage with erythrocytes from the anterior chamber clot, often larger, grade 4 hyphemas. leaving the fibrin matrix. To reduce the likelihood of Topical ACA appears to be a safe, effective rebleeding during the operative procedure, care treatment to prevent secondary hemorrhage in should be undertaken not to produce violent traumatic hyphema. It is as effective as systemic ACA alterations in the anterior chamber pressure. If in reducing secondary hemorrhage. No systemic side rebleeding does occur, sodium hyaluronate can be effects were observed with topical use. Topical ACA effectively introduced for tamponade. After a 5-minute provides an effective outpatient treatment for traumatic wait, irrigation maneuvers can be resumed. hyphemas. In a study topical ACA group had a final visual acuity of 20/40 or better in 86% of patients, Using a one- or two-needle technique, the surgeon compared with 69% of patients in the systemic group. must be particularly careful to have direct visualization Some studies have investigated the application of of the anterior chamber, but this technique has some intracameral tissue plasminogen activator (t-PA) in the disadvantages. Maintaining the position of the needle management of traumatic hyphema.8 A potential risk tip in the anterior chamber may be difficult during the with t-PA is the associated risk of developing rebleeding procedure. A hazardous situation is created when the of the initial wound. The application has been collar-button type of formed clot occupies both the considered in resolving hyphemas that either fail to anterior and posterior chambers. This produces clear spontaneously or are associated with malignant pupillary block with anterior displacement of the iris- IOP. lens diaphragm. Management of Blunt Trauma of Anterior Segment 71 ANTERIOR CHAMBER MAINTAINER CORNEAL BLOOD STAINING Anterior chamber maintainer has been found useful Corneal blood staining usually occurs following trau- in the surgical management of traumatic hyphema.10 matic hyphema. Hyphema combined with secondary Two paracentesis are made as in standard technique glaucoma are most common risk factors for developing of evacuation of hyphema. The first one is made in corneal blood staining.11 Cornea blood staining may the lower temporal quadrant and accommodates a rarely occur following non-traumatic hyphema. Coneal 20-gauge anterior chamber maintainer (ACM) that is blood staining has been reported following hyphema 12 connected to a bottle of Balanced Salt Solution. The due proliferative diabetic retinopathy. Severe corneal second paracentesis is made in an upper quadrant and blood staining in the left eye secondary to a “sponta- serves to evacuate liquefied blood and blood clots. neous” total hyphema and raised intraocular pressure With an ACM in place, the fluctuations of intraoperative in an eye with iris neovascularization has been reported in a 54-year-old man with severe proliferative diabetic IOP are minimized and the AC depth is stabilized retinopathy. Despite anterior chamber washout, the throughout the operation. The risk of renewed cornea remained virtually opaque and thickened. The bleeding is reduced because of the continuous positive patient subsequently underwent pars plana vitrectomy intraoperative IOP. The ACM is an important tool in with endolaser using a temporary keratoprosthesis, the surgical management of traumatic hyphemas insertion of a Morcher iris-surround intraocular lens and because it facilitates AC washout and reduces iatrogenic penetrating keratoplasty. Histopathology of the excised damage to the iris and corneal endothelium. corneal button revealed fine eosinophilic granules composed of aggregations of hemoglobin and its REMOVAL OF HYPHEMA WITH VITRECTOMY breakdown products dispersed throughout the stroma, with occasional foci of weakly positive Perl staining for The evacuation of the hyphema can be performed intracellular hemosiderin. Fluorescence confocal with vitrectomy. The initial clear corneal incision is microscopy revealed a marked increase in fluorescence made with a diamond blade. To avoid the iris and throughout the corneal stroma and the basal epithelial lens, the blade is oriented and pushed into the anterior layer. chamber in such a manner that it is parallel to the A case of corneal blood staining due to a plane of the iris. With the vitrectomy cutting port half hemorrhagic descemet membrane detachment has open and the infusion line in place, it is possible to been reported. A 72-year-old man had an anterior- irrigate and aspirate free blood from the formed clot. chamber intraocular lens removed for presumed The aspiration mode is initially set at 200 mm Hg uveitis-glaucoma-hyphema syndrome, developed an vacuum and the cutting speed set at 200 cycles per intraoperative hemorrhagic detachment of the minute for the procedure. Aspiration mode is Descemet membrane attributed to peripheral corneal increased to 400 mm Hg as needed. Extreme care neovascularization. Corneal blood staining rapidly is required to avoid contact with any iris, lens, or developed, and a partial-thickness paracentesis was required to evacuate the lamellar hematoma and corneal endothelium. This operative procedure is used allow reattachment of the Descemet membrane: to remove the central portion of the clot. It is not Hemorrhage from posterior corneal vessels can result necessary to remove the entire clot in the periphery in a hemorrhagic detachment of the Descemet of the anterior chamber. membrane. Corneal blood staining can develop Bleeding during the surgical procedure can be rapidly in an intracorneal or retrocorneal hemorrhage. controlled by elevation of the infusion bottle to The blood can be removed without incising the approximately 70 cm above the eye for several Descemet membrane by making a partial-thickness minutes. In case the bleeding persists the anterior paracentesis13. chamber may be filled with sodium hyaluronate to Corneal blood staining mostly occurs in patients tamponade the bleeding site. At the completion of the who have a total hyphema and associated raised IOP. surgical procedure, an air bubble may be left in the Predisposing factors for development of corneal blood anterior chamber. This will help to control any staining include compromised endothelium, grade ¾ secondary bleeding during the post-operative period. hyphema, raised IOP and surgical trauma in removing Visual outcome in these cases depends upon the large clot. Rarely corneal blood staining may occur extent of posterior segment injuries. Poor visual with low or normal IOPs, this occurs in cases in whom outcome in patients with posterior segment injuries the endothelium is already compromised. However, has been observed. In contrast patients with occurrence these latter two instances can probably be anticipated of secondary hemorrhage may have better outcome only in eyes with a severely damaged or compromised in absence of posterior segment injury. endothelium. Risk of developing corneal blood staining 72 Clinical Diagnosis and Management of Ocular Trauma is more in patients with full chamber hypema and pressure 2 weeks to 3 months later. The erythrocytes persistently raised IOP of more than 25 mm Hg. after losing hemoglobin, become “ghost cells” in the Spontaneous clearing of corneal blood staining is vitreous cavity. The ghost cells may pass forward into known and may require 8 months to 2 years.14 the anterior chamber, with resultant elevation of IOP. The condition is described as Ghost Cell glaucoma. IRIS AND ANGLE CHANGES The treatment of secondary post-traumatic open angle glaucoma is disappointing. The patients are The classical sign suggestive of close globe injury is the young, the disease is advanced, and the compliance presence of ring of pigment clumps over the anterior to the treatment and follow-up are poor. The capsule. The ring is known as Vossius ring. The size prevention of post-traumatic glaucoma is based on of the ring is smaller than the size of the pupil. the control of ocular trauma and the periodic follow- Iridoschisis is lamellar separation of anterior and up of patients with and history of non-perforating injury posterior iris. The blunt force compresses the globe of the eye. In another study several independent in the anterior - posterior direction and thus stretches predictive factors including poor initial visual acuity, the equatorial diameter. Sudden increase in the advancing age, lens injury, angle recession, and pressure in the anterior chamber puts stress on the hyphema were found to be significantly associated with iris sphincter, root of the iris circular and longitudinal the development of posttraumatic glaucoma. cilliary muscle fibers, resulting angle recession. Iris is torn at thinnest portion and the thinnest portion of the iris is at root, iris insertion at anterior ciliary body. MISCELLANEOUS CHANGES Clinically the condition is described as iridodialysis. Changes in the refractive status of the eye have been Blunt trauma may cause separation of longitudinal reported following blunt trauma. Ultrasound biomicro- fibers from the scleral spur creating a cyclodialysis cleft. scopy (UBM) and ultrasonography of the anterior A technique for repair of traumatic iridodialysis that segment in the eye may be helpful to diagnose and avoids the need for iris sutures has been described.15 confirm these changes.17 Blunt trauma can dislocate Following a limbal peritomy, sclerostomy sites level with angle-supported pIOLs. Implantation of these IOLs the iris base are created at each clock hour of the irido- should be discouraged in patients who perform dialysis using a microvitreoretinal blade. Vitreoretinal activities that put them at risk for eye trauma.18 Tube forceps passed through these ports are used to extension using angiocatheter material is used in incarcerate the peripheral iris. No suture material is glaucoma flitering surgery. This surgery is a viable, cost- used to secure the iris. The conjunctiva is closed with effective option in difficult cases. Following blunt absorbable sutures. The technique has been reported trauma intrusion of the tube into the anterior chamber successful in simple iridodialysis repair and in has been reported.19 Placing a securing suture in patients conjunction with intraocular procedures. prone to eye trauma can be considered The c-fos and c-jun mRNAs have been observed to transiently express 20 SECONDARY GLAUCOMA in corneal and lens epithelial cells after blunt trauma. Ocular blunt trauma activates corneal and lens Glaucoma in hyphema may develop due to variety epithelial cells without apparent corneal ablation or of mechanisms. These mechanisms include trabecular direct injury in the lens epithelium. Such activation in blockage with erythrocytes, pupillary block due to full lens epithelium has been postulated to be involved chamber clotted blood, angle recession and peripheral in cataractogenesis.. anterior synechia. Clinically, the presence of increased Eyes with scleral rupture after blunt trauma may pigmentation at the angle, elevated baseline IOP, rarely get complicated by proliferative vitreo- hyphema, lens displacement, and angle recession of retinopathy. In certain cases, retinal detatchment or more than 180 degrees have been significantly proliferative vitreoretinopathy may not develop associated with the occurrence of chronic glaucoma following extensive scleral rupture. A 56-year-old man 16 after closed globe injury. On UBM findings such as sustained blunt trauma to his left eye. Visual acuity was a wider angle and the absence of cyclodialysis were light perception. The fundus was obscured by hyphema. significant predictors for the subsequent development Computed tomography imaging and the presence of of traumatic glaucoma. Less than 10% of patients extensive subconjunctival hemorrhage suggested scleral having angle recession develop glaucoma. The rupture. Prompt primary surgery to repair a 25-mm mechanism of glaucoma is outflow obstruction due scleral rupture was performed under general anesthesia. to scarring or a hyaline membrane covering the angle. No retinal detachment developed. Two years Patients presenting with hyphema and associated postoperatively, visual acuity increased to 12/20. This vitreous hemorrhage may have raised intraocular case shows that retinal detachment and proliferative Management of Blunt Trauma of Anterior Segment 73 vitreoretinopathy may not complicate extensive scleral 9. Weiss JS, Parrish RK, Anderson DR. Surgical therapy of ruptures in certain patients.21 Sympathetic ophthalmia traumatic hyphema. Ophthalmic Surg 1983;14:343-345. has been reported to occur following nonpenetrating 10. Yu T, Dahan E, Yin ZQ, Levitz LM. Use of an anterior ocular trauma.22 chamber maintainer in the surgical management of traumatic hyphaemas. Clin Experiment Ophthalmol Prevention of blunt ocular trauma is of paramount 2008;36:206-08. importance in decreasing the incidence of these injuries. 11. Kloek C, Brauner S, Chen TC. Corneal blood staining Use of preventive measures while at work or during after traumatic hyphema J Pediatr Ophthalmol Strabismus high risk sports should be strictly complied. Public 2007; 44: 256. education on the use of protective glasses and other 12. Patel H, Patel DV, Brookes NH, McGhee CN. Clinico- protective measures should be given at regular pathological features of severe corneal blood staining intervals. In case blunt trauma occurs prompt associated with proliferative diabetic retinopathy. Clin Experiment Ophthalmol 2006 ;34:272-74. examination and urgent treatment may limit the ocular 13. Sharma PS, Stone DU. Corneal blood staining secondary morbidity. to hemorrhagic descemet membrane detachment. Cornea 2007;26:1273-74. 14. Fraser C, Liew S, Fitzsimmons R, Arnold J. Spontaneous resolution of corneal blood staining. Clin Experiment References Ophthalmol 2006;34:279-80. 1. Pieramici DJ, Sternberg P Jr, Aaberg TM Sr, et al. A 15. Richards JC, Kennedy CJ. Sutureless technique for repair system for classifying mechanical injuries of the eye of traumatic iridodialysis. Ophthalmic Surg Lasers Imaging 2006;37:508-10. (globe). The Ocular Trauma Classification Group. Am J 16. Sihota R, Kumar S, Gupta V, Dada T, Kashyap S, Insan Ophthalmol 1997;123820-31. R, Srinivasan G. Early predictors of traumatic glaucoma 2. Al-Amry M, Khan AO. Descemet’s membrane breaks after closed globe injury: trabecular pigmentation, following forceps delivery. J Pediatr Ophthalmol widened angle recess, and higher baseline intraocular Strabismus 2007;44:192. pressure. Arch Ophthalmol 2008;126:921-26. 3. Regis A, Dureau P, Uteza Y, Roche O, Dufier JL. [Ocular 17. Kim SI, Cha YJ, Park SE. A case report on the change injuries and childbirth] J Fr Ophtalmol 2004;27:987-93. of the refractive power after a blunt trauma. Korean J 4. Crouch ER Jr, Williams PB. Trauma: Ruptures and Ophthalmol 2008;22:53-57. bleeding. In: Tasman W, Jaeger EM, eds. Duane’s Clinical 18. Leccisotti A Traumatic pupillary capture of the haptic of Ophthalmology. Philadelphia, Pa: JB Lippincott an angle-supported phakic intraocular lens. J Cataract 1993;4:1-18. Refract Surg 2006;32:2133-34. 5. Palmer DJ, Goldberg MF, Frenkel M, Fiscella R, 19. Sheets CW, Ramjattan TK, Smith MF, Doyle JW Migration Anderson, RJ. A comparison of the two dose regimens of glaucoma drainage device extender into anterior of epsilon aminocaproic acid in the prevention and chamber after trauma. J Glaucoma 2006;15:559-61. management of secondary traumatic hyphemas. 20. Shirai K, Saika S, Okada Y, Miyamoto T, Ueyama T, Ophthalmology 1986;93:102-108. Ohnishi Y. Transcriptional activation in lens epithelial cells 6. Recchia FM, Saluja RK, Hammel K, Jeffers JB. following an ocular blunt trauma. J Cataract Refract Surg Outpatient management of traumatic microhyphema. 2005 ;31:1226-30. Ophthalmology 2002;109:1465-70. 21. Takayama K, Yasukawa T, Okada M, Sumida A, Watanabe 7. Crouch ER Jr, Frenkel M. Aminocaproic acid in the N, Uchida S. Large blunt scleral rupture without retinal treatment of traumatic hyphema. Am J Ophthalmol detachment. Ophthalmic Surg Lasers Imaging 2008;39: 1976;81:355-60. 242-45. 8. Laatikainen L, Mattila J. The use of tissue plasminogen 22. Bakri SJ, Peters GB 3rd. Sympathetic ophthalmia after activator in post-traumatic total hyphaema. Graefe’s Arch a hyphema due to nonpenetrating trauma. Ocul Immunol Clin Exp Ophthalmol 1996:234:67-68. Inflamm 2005;13:85-86. CHAPTER

Management of Traumatic Cataract 15 Rupesh V Agrawal, Satish Desai (India)

Introduction SEX Male-to-female ratio in cases of ocular trauma is 4:1. Cataract is by far the commonest complication causing loss of vision following any type of ocular injury. The management of such cases is an important problem AGE in ophthalmology and prognosis is variable. Extent Work- and sports-related eye injuries most commonly of associated damage to anterior and posterior segment, occur in young adults and children. time of intervention, operative and postoperative complications go a long way in determining the ultimate HISTORY prognosis. The type of trauma, extent of lenticular • Mechanism of injury—Sharp versus blunt involvement and associated secondary rise of • Past-ocular history—Previous eye surgery, glau- intraocular pressure are factors of paramount coma, retinal detachment, diabetic eye disease importance which could dictate the exact time of • Past medical history—Diabetes, sickle cell, Marfan management of traumatic cataract. Cataracts caused syndrome, homocystinuria, hyperlysinemia, sulfate by blunt trauma classically form stellate or rosette oxidase deficiency shaped posterior axial opacities that may be stable • Visual complaints or progressive, whereas penetrating trauma with – Decreased vision—Cataract, lens subluxation, disruption of lens capsule forms cortical changes that lens dislocation, ruptured globe, traumatic optic may remain focal if small or may progress rapidly to neuropathy, vitreous hemorrhage, retinal total cortical opacification. Lens dislocation and detachment subluxation are found commonly in conjunction with – Monocular diplopia—Lens subluxation with traumatic cataract. partial phakic and aphakic vision – Binocular diplopia—Traumatic nerve palsy, Pathophysiology orbital fracture Blunt trauma is responsible for coup and contrecoup – Pain—Glaucoma secondary to hyphema, ocular injury. Coup is the mechanism of direct impact. pupillary block, or lens particles; retrobulbar It is responsible for Vossius ring (imprinted iris pigment) hemorrhage; iritis. sometimes found on the anterior lens capsule following blunt injury. Physical Examination When the anterior surface of the eye is struck bluntly, there is a rapid anterior-posterior shortening • Complete ophthalmic examination (tailored in accompanied by equatorial expansion. This equatorial cases of globe compromise) stretching can disrupt the lens capsule, zonules, or – Vision and pupils—Presence of afferent pupi- both. Combination of coup, contrecoup, and llary defect (APD) indicative of traumatic optic equatorial expansion is responsible for formation of neuropathy traumatic cataract following blunt ocular injury. – Extraocular motility—Orbital fractures or Penetrating trauma that directly compromises the traumatic nerve palsy lens capsule leads to cortical opacification at the site – Intraocular pressure—Secondary glaucoma, of injury. If the rent is sufficiently large, the entire lens retrobulbar hemorrhage rapidly opacifies, but when small, cortical cataract can – Anterior chamber—Hyphema, iritis, shallow seal itself off and remain localized. chamber, iridodonesis, angle recession Management of Traumatic Cataract 75 – Lens—Subluxation, dislocation, capsular inte- Causes of Postoperative grity (anterior and posterior), cataract (extent and type), swelling, phacodonesis Non-improvement of BCVA – Vitreous—Presence or absence of hemorrhage, in Traumatic Cataract posterior vitreous detachment – Fundus—Retinal detachment, choroidal • Amblyopia rupture, commotio retinae, preretinal hemorr- • Corneal scar involving visual axis hage, intraretinal hemorrhage, subretinal • Cortex in papillary area hemorrhage, optic nerve pallor, optic nerve • Subluxation of IOL avulsion. • IOL tilt • CME • Traumatic optic neuropathy Traumatic Cataract (Types) • Pupillary capture. • Penetrating • Concussion (Rosette cataract) Medical Care • Infrared irradiation (Glass Blower’s cataract) • If glaucoma is a problem, control intraocular pres- • Electrocution sure with standard medications; add corticosteroids • Ionizing radiation. if lens particles are the cause or if iritis is present. • Focal cataract: – Observation if cataract is outside the visual axis Causes – Miotic therapy may be of benefit if the cataract Traumatic cataracts occur secondary to blunt or is close to the visual axis. penetrating ocular trauma. • In some cases of lens subluxation, miotics may correct monocular diplopia; mydriatics may allow for vision around the lens with aphakic correction. Other Problems to be PRACTICAL POINTS IN MANAGEMENT OF Considered TRAUMATIC CATARACT • Globe rupture • Corneoscleral integrity • Orbital fractures • Meticulous restoration of normal relationships • Retinal detachment • Sufficient release of posterior synechiae • Secondary glaucoma • Capsular and zonular integrity • Traumatic optic neuropathy. • Vitreoretinal changes.

Factors to be Analyzed Surgery Depending on the clinical situation, the surgical • Corneal involvement management of a traumatic cataract is performed • Preoperative and postoperative BCVA either a standard anterior limbal or posterior pars plana • Visual axis involvement approach. An anterior approach is best for a traumatic • Breach in anterior capsule cataract unless there is complete lens dislocation or • Lens matter in anterior capsule capsular rupture with significant lens material • Pre-existing posterior capsular rent on ultrasound incarcerated in the vitreous. • Subluxation of the traumatic cataractous lens • Associated iridodialysis. PRACTICAL TIPS WHILE PERFORMING TRAUMATIC CATARACT SURGERY Imaging Studies • Planning surgical approach is of utmost importance • B-scan—If posterior pole cannot be visualized in cases of traumatic cataract. • A-scan—Prior to cataract extraction • Preoperative capsular integrity and zonular stability • CT scan orbits—Fractures and foreign bodies. should be surmised. 76 Clinical Diagnosis and Management of Ocular Trauma • In cases of posterior dislocation without glaucoma, – Sulcus fixation is safe if posterior capsule is inflammation, or visual obstruction, surgery may compromised but zonular support is maintained. be avoided. – Suture fixation is chosen if both capsular and • Indications for surgery include the following: zonular supports are insufficient and the angle – Unacceptable decreased vision is damaged minimally. – Obstructed view of posterior pathology – Anterior chamber placement is an option if no – Lens-induced inflammation or glaucoma posterior support remains and iris or ciliary body – Capsular rupture with lens swelling trauma prevents suture fixation. – Other trauma-induced ocular pathology – Aphakia may be a better choice in young necessitating surgery. children and patients with highly inflamed eyes; • Standard phacoemulsification or manual small they may experience better outcomes if lens incision cataract surgery may be performed if lens implantation is deferred. capsule is intact and sufficient zonular support remains. COMPLICATIONS • Intracapsular cataract extraction is required in cases of anterior dislocation or extreme zonular instability. Surgery for traumatic cataract is associated with high Anterior dislocation of the lens into the anterior incidence of complications and surgeon should chamber requires emergency surgery for its anticipate and be prepared for complications during removal, as it can cause pupillary block glaucoma. the surgery. The different complications during • Pars plana lensectomy and vitrectomy may be best traumatic cataract surgery can be: in cases of posterior capsular rupture, posterior • Posterior capsular rent dislocation, or extreme zonular instability. • Zonular dialysis • Automated irrigation/aspiration can be used in patients younger than 35 years. Look for the posterior capsular support preoperatively, should be careful while performing automated irrigation aspiration and while switching the anterior chamber maintainer on as the fluid flow inside the eye can enlarge the pre-existing posterior capsular dehiscence and can result in lens matter drop or nucleus drop. • Lens implantation: – Capsular fixation is the preferred placement if lens capsule and zonular support are intact. In the case of surgery to remove a traumatic cataract, the CTR may be implanted before or after phacoemulsification. Although early inser- tion provides support during phacoemulsifi- cation, it may create additional zonular trauma. Fig. 15.1: CTR in bag The use of iris or capsule retractors at the capsulorhexis’ edge or the use of a capsular tension segment (CTS; Morcher GmbH, Stuttgart, Germany (not currently approved by the FDA]) during phacoemulsification are other alternatives that do not induce significant capsular torque during insertion. The CTS is a partial PMMA ring segment containing an anteriorly offset eyelet through which an iris retractor or suture may be placed. – Capsular tension ring should never be implanted in cases with broken capsulorrhexis and in eyes with pre existing posterior capsular rent. – Polymethyl methacrylate (PMMA) capsular tension rings allow capsular fixation in cases of zonular dialysis less than 180 degrees. Fig. 15.2: Traumatic cataract with torn anterior capsule Management of Traumatic Cataract 77

Fig. 15.3: Deposits on IOL Fig. 15.6: Traumatic cataract with breached AC

Fig. 15.4: Partial lens abscess Fig. 15.7: Traumatic cataract with foreign body

Fig. 15.5: Postcataract surgery with partially Fig. 15.8: Traumatic cataract with haem repaired iris 78 Clinical Diagnosis and Management of Ocular Trauma

Fig. 15.9: Traumatic cataract with IOL in torn bag Fig. 15.11: Traumatic cataract with loose lens mattter in AC

Fig. 15.10: Traumatic cataract with iris hole Fig. 15.12: Traumatic cataract with subluxation of lens

Fig. 15.13: Early Rosete cataract

• Nucleus or lens matter drop Bibliography • Postoperative unusual inflammation • Posterior capsular opacification 1. Benezra D, Cohen E, Rose L. Traumatic cataract in • Pupillary capture of IOL children: correction of aphakia by contact lens or • Postoperative refractive surprise. intraocular lens. Am J Ophthalmol. 1997;123(6):773-82. Management of Traumatic Cataract 79

2. Eckstein M, Vijayalakshmi P, killedar M, Gilbert C, Foster 6. Krishnamachary M, Rathi V, Gupta S. Management of A. Use of intraocular lenses in children with traumatic traumatic cataract in children. J Cataract Refract Surg cataract in south India. Br J Ophthalmol 1998;82(8): 1997;23(Suppl 1):681-87. 7. Mian SI, Azar DT, Colby K. Management of traumatic 911-15. cataracts. Int Ophthalmol Clin Review 2002 Summer; 3. Gain P, Thuret G, Maugery J. Management of traumatic 42(3):23-31. cataracts. J Fr Ophtalmol. Review French 2003; 8. Moreno J, Sainz C, Maldonado MJ. Intraoperative and 26(5):512-20. postoperative complications of Cionni endocapsular ring 4. Jacob S, Agrawal A, Agrawal A, Agrawal S, Patel N, Lal implantation. J Cataract Refract Surg 2003;29(3):492-97. V. Efficacy of a capsular tension ring for phaco- 9. Panda A, Kumar S, Das H, Badhu BP. Striving for the emulsification in eyes with zonular dialysis. J Cataract perfect surgery in traumatic cataract following penetrating trauma in a tertiary care hospital at eastern Nepal.JNMA Refract Surg 2003;29(2):315-21. J Nepal Med Assoc 2007;46(167):119-25. 5. Kazem MA, Behbehbani JH, Uboweja AK, Parmasivam 10. Praveen MR, Vasavada AR, Singh R. Phacoemulsification MB. Traumatic cataract surgery assisted by trypan blue. in subluxated cataract. Indian J Ophthalmol 2003; Ophthalmic Surg Lasers Imaging 2007;38(2):160-63. 51(2):147-54. CHAPTER

Management of Traumatic Luxation of the Crystalline Lens 16 Arturo Pèrez-Arteaga, Yuri Flores (Mexico)

Introduction associated or not, to some other damage to the eye structures; if well not all the possibilities of damage This chapter will cover different criteria regarding the can be review (even in the whole textbook), a didactic management of the Traumatic Luxation of the Lens. classification has been done in this chapter, trying this Many authors have spoke about this topic worldwide way to cover as much alternative lesions as possible, and the clinical and surgical concepts are not uniform. in order to obtain a didactic scheme useful during These differences might be in some cases because the the clinical evaluation, the plan of a surgical approach, blunt eye trauma is different from one patient to the intraoperative management, the eventual another, and so the degree of zonular damage can postoperative complications and the clinical prognosis. be different, and also some associated lesions-, but furthermore, as new technologies are arising in the ophthalmic field (e.g. iris claw IOLs, iris fixation IOL techniques), some ophthalmic surgeons developed Luxation and Subluxation of the more experience in some particular technique or Crystalline Lens device, and so the management can be complete different from one surgeon to another. (Figs 16.1 and 16.2) We will try to review different approaches In many circumstances these conditions are not easy according the current literature and our personal even to distinguish between them, since the finding experience, but the reader must consider that science of a proper definition; for some authors when some is always working ahead in benefit of the patients, zonular attachments still exist the condition is defined so some criteria might be “out of site” after a short as subluxation, and the complete crystalline lens period of time. luxation is defined by the whole loose of zonular attachments. Even so, sometimes the clinical evaluation of these two forms of crystalline lens Blunt Eye Trauma dislocation can be difficult to perform; if well this might As the reader has noticed viewing this book, the be difficult in a non-traumatized eye (e.g. Marfan possibilities of damage (going from mild, to moderate syndrome), you can now imagine an evaluation of and severe) to the eye structures during a blunt trauma this condition in a traumatized eye, when sometimes are enormous; no one particular case is exactly the some other lesions can decrease the visualization of same than another, and distinctive considerations must the examinator (e.g. hyphema, suprachoroid be taken in count in each clinical evaluation and hemorrhage), not only at the clinical approach, but approach. It is also known that the clinical condition furthermore, at the paraclinical evaluation (e.g. eye of the eye can have variations according the time of ultrasound, eye scan). Because of this, sometimes the evolution of the lesion, clinical management, pre- final definitions are performed at the intraoperative existent eye diseases (e.g. high myopia, pseudo- period, and so the clinical evaluation and trans- exfoliation), and many other possibilities that can operative decisions are the rule. So, we think that for influence the clinical course and so the management the starting point of evaluation of these cases of of the case, and finally the outcome. dislocated crystalline lens because of a traumatic We will describe the condition in which the condition, the surgeon must think from the start, that crystalline lens has been moved from its anatomical all the zonular attachments have been lost, and only position because of a blunt eye trauma, either during the intraoperative period the real dimension Management of Traumatic Luxation of the Crystalline Lens 81 appraise, in order to establish an adequate medical criteria of management. Keep always in mind during the diagnostic period, the proper evaluation of damage to the rest of the structures of the eye and the evolution that the lesions might have, by their own, during a certain period of time.

Previous Medical Conditions The medical history of some previous conditions of the particular patient, have great importance. Systemic conditions like diabetes, connective tissues diseases, coagulation pathologies between others, enhance our multidisciplinary point of view of the case; systemic medication like aspirin or other anticoagulants are mandatory to know. Previous eye diseases and/or ocular surgeries and Fig. 16.1: Traumatic lens dislocation with trauma, are of course mandatory to ask to the patient; cataract formation but furthermore, and of particular importance for the evaluation of the crystalline lens feature, some particular eye conditions like diseases associated with progressive zonular weakening and capsular contraction (e.g. pseudoexfoliation syndrome, uveitis, myopia, Marfan syndrome); the possibility of a previous zonular weak, can change by complete our point of view, and so our surgical approach; with some previous condition of zonular weakening, even a minor ocular trauma, can dislocate by complete the crystalline lens. Also alternative treatments (prescribed or not) that the patient had has, in an attempt to solve the traumatic condition of the eye before our first contact with him, are very value to appraise; some of them are able to affect the initial lesion and even convert it into a worst scenario; keep in mind and ask for them. Sometimes because the anxiety experienced by the patient, relatives and medical personal, a complete clinical history is not properly taken; the surgeon must be aware of the previous medical conditions of the Fig. 16.2: Traumatic lens subluxation patient, because some factors of the medical history might be decisive in the decision taking process. of the zonular damage can be seen. Even so, sometimes Trauma Mechanism after and accurate evaluation and management of a The evaluation of the trauma mechanism is of critical subdislocated crystalline lens, with cataract surgery and importance in the possibility of a zonular weakening; “in-the-bag” IOL implantation, a late IOL dislocation because of the transmission of forces into the ocular can be seen; it means that a long term complication globe, sometimes the surgeon can see an eye almost is still changing our first clinical impression. free of damage during the first clinical evaluation (maybe some low degree of traumatic uveitis), but CLINICAL EVALUATION the eye might have severe zonular damage (even A complete preoperative evaluation of the condition without cataract formation); so the proper history and situation of the crystalline lens, is of crucial taking about the trauma mechanism is mandatory. As importance for the design of the management of these you might see in different parts of this book, there lesions. Situations like position, movement, degree of are currently types of trauma mechanism that cause opacity, integrity of the capsular bag and degree of a particular kind of damage in the eye; they are well hydration, are maybe the most important features to known. 82 Clinical Diagnosis and Management of Ocular Trauma Associated Lesions to the Lens Luxation ultrasonic evaluation of the globe (eye echography); It is difficult to find a traumatic lesion of the ocular I do believe, that echograhy must be performed in globe capable to cause only zonular weakening and all cases of eye trauma, not only because it helps a luxation or subluxation of the crystalline lens as an evaluate the integrity of the globe and some other unique lesion; if well it can happen, it is almost a rule associated features in presence of not-clear media, but that the crystalline damage is accompanied by injury also because it helps demonstrate the weakening of to some other ocular and extraocular (e.g. orbital) the zonula in cases of suspected lens subluxation, and structure, that must be complete addressed during a furthermore, in cases of complete luxation helps clinical and paraclinical approach. Also, the surgeon achieve the location of the crystalline lens within the must keep in mind that some conditions might change eye. with the running of time; sometimes the initial clinical So, thinking in performing echography in all cases features are not related to the crystalline lens lesion of ocular trauma (even in the presence of clear media), itself (e.g. increase in the intraocular bleeding, not only some subclinical conditions can be discovered presentation of retinal detachment, increase in the by this way, moreover the weak of the zonula is very intraocular pressure because an angular recession), but easy to evaluate with this method; remember to have within the evolution, a non-primary lens-related a good communication with your echographist, and situation, can become an indication of lens removal even think that you must be present during the study, (e.g. evolution from a subluxation to a complete because the dynamic ultrasonography (echography luxation, development of phacomorphic, phacolitic or under ocular movement) is very helpful to achieve narrow-angle glaucoma). So, the critical observation some subclinical zonular damage. Finally, in cases of of associated lesions in the first and ulterior evaluations, complete luxation, echography helps the surgeon are of critical importance. achieve integrity of the capsular bag and movement capacity of the crystalline lens inside the vitreous cavity Zonular evaluation (dynamic evaluation, (dynamic echography with changes in the patient clinical and with ultrasound) position), of particular importance for planning the surgical strategies. Is mandatory to consider the possibility of zonular Some other studies can be very helpful in the damage in all cases of ocular trauma; the condition evaluation of the traumatized (and maybe dislocated) of the crystalline lens attachments conforms an lens (e.g. Computed Tomography), but the dynamic important part of the design of further activities in the ultrasonic evaluation conforms a nice approach to management of these patients. obtain a mostly complete information regarding the The first clinical evaluation is the observation; crystalline lens conditions and associated features. despite the complete clinical view of the anterior and posterior segments of the eye, a particular focus must be pointed into the crystalline lens. Integrity of it, presence of opacities, integrity of the capsular bag and Surgical Approach possible clinical visualization of the zonules under Despite the whole evaluation of the complete damage maximum pupil dilation, are between others, to the intra- and extraocular structures caused by the mandatory points that must be seen during the trauma, the management of the dislocated crystalline ophthalmic exploration of a traumatized eye; a lens will be pointed here. The management includes dynamic clinical evaluation of the lens, is also a broad spectrums of actions, going from “doing obligatory; it means to ask the patient to move the nothing” in case of a moderate dislocation without eye in slow and rapid movements, in order to achieve phacodonesis. cataract formation, until a complete cataract extraction Sometimes the degree of subluxation is easy to from the vitreous cavity and an IOL implantation observe, but even so the dynamic evaluation is very without capsular support. useful to achieve a clinical approach to the degree of The surgical approach must take in count also as zonular weakening. If a complete luxation is present, a very important concept, “the correct time to act”; a complete clinical indication in the ocular fundus is it means that sometimes the surgeon has to wait and mandatory, with the objective to plan the surgical not to plan a surgical approach until some particular approach. features have been solved (e.g. bleeding resolution, In some cases, because of media opacities and decrease in inflammation), but in some other occasions inflammatory process, it is not easy to evaluate the the urgent surgery indication must be the rule to follow real condition of the zonular attachments; this (e.g. development of phacolitic or phacomorphic conforms for many surgeons the indication of an glaucoma, high intraocular pressure because of Management of Traumatic Luxation of the Crystalline Lens 83 hydrated cataract, incomplete dislocation with weak INTRACAPSULAR EXTRACTION zonulas and possibility to develop a drop nucleus into Intracapsular extraction means to take outside the the vitreous cavity). This is why the management of eye the entire crystalline lens contained in its capsular this type of conditions requires knowledge but also bag. It is a maneuver that even in our times should a good dose of common sense; sometimes to share be considered in some special cases, for example the case with some colleagues can be useful. complete lens luxation to the anterior chamber, or The concept of the touch of the crystalline as the furthermore into the subconjuntival space, as we saw first step in case of a surgical approach, is still alive; in some occasion, in which a simple conjunctival it is a very objective method to evaluate the integrity incision was enough to remove he entire dislocated and the weakness of the zonula and can corroborate lens. If well, the entire lens removal through a wide or change by complete the tentative surgical plan; it incision is not frequently seen in the ophthalmic surgery must be carefully performed in order to avoid cause in our days, it is something that must be keep inside more zonular damage; it is a useful maneuver that the surgeon’s mind for some particular cases of helps obtain more information about the case. complete lens luxation after severe eye trauma. Anyhow, during the entire time of a surgical approach, the surgeon must be aware to experience surprises PARSPLANA VITRECTOMY PLUS because it is a traumatized eye; these precautions must PHACOEMULSIFICATION IN be in the mind even in the postoperative period, THE VITREOUS CAVITY because unexpected complications are the rule. Now we will describe some different possibilities of It is indicated in cases of complete lens luxation into surgical approaches, depending upon the complete the vitreous cavity; should be performed after a diagnostic, trying to cover diagnostic and technique complete study that allows the surgeon to obtain of choice. information about the position of the crystalline lens and the additional damage caused by the eye trauma; the medical indication for this technique increases when PHACOEMULSIFICATION there is a suggestion of inflammatory process or some AND IOL PLACEMENT IN SUBLUXATED structural damage caused by the subluxated lens. CRYSTALLINE LENS A complete pars plana vitrectomy must be The indication should be subluxated cataractous lens, performed prior to remove the lens from inside the or subluxated non-cataractous lens that compromises vitreous cavity; it helps increase visualization inside the the vision. Remember that sometimes, is better “not globe (remove of vitreous opacities), but also helps to perform surgery”, and this possibility must be decrease the retinal traction during the lens removal. discussed with the patient according the particular case. After the vitrectomy, many techniques have been For the special purpose of lens extraction in described to remove the lens like phacoemulsification subluxation, helpful maneuvers and devices can be in the vitreous cavity, chopstick, FAVIT, phacoemulsi- used; some examples are wide capsulorhexis to avoid fication in the anterior segment and for soft lenses the pressure over the capsular bag, capsulectomy instead lensectomy during the vitrectomy by itself, between to capsulotomy to avoid pull the capsule, iris retractors others. The goal is to remove the complete lens inserted in the capsular bag to center it during phaco, material just after a complete vitrectomy has been capsular tension rings for subluxated lens, ultra-small performed; after that a complete review of the incision technology, phacoemulsification “out of the retina, periphery and optic nerve is done, and some bag” (phaco at the iris plane to avoid force applied other maneuvers if needed like endophotocoagulation, to the capsular bag), positive intraocular pressure subretinal fluid drainage or silicon oil insertion if during the entire procedure, bi-axial irrigation/ required; remember that always the surgeon aspiration, continuous viscoelastic injection inside the must be aware of surprises because of the traumatized capsular bag and transscleral bag fixation with sutures eye. (with or without capsular rings) between others. When performing these techniques, the objective is to maintain the integrity and the center position of the PERFORMING A COMPLETE PLACEMENT OF capsular bag with the main objective of an IOL CRYSTALLINE LENS INTO THE VITREOUS implantation, “in the bag” and, as much as possible, CAVITY in the center of the pupil. “Just like in the old times of cataract surgery”, the Remember wait for surprises any time during the complete luxation to the crystalline lens (with cataract surgery and at the postoperative period, because it or not), or the non-surgical approach in case of a is a traumatized eye. complete lens dislocation into the vitreous cavity, is 84 Clinical Diagnosis and Management of Ocular Trauma also an option that must be inside the mind of the emmetropia in eyes without capsular support; attending surgeon of these traumatized eyes. controversies still are in the field, because if well they It was demonstrated, since the early days of cataract have not angle complications, they still have the corneal surgery, that in presence of integrity of the capsular features, with the consequent need to long-term bag, the crystalline lens must remain inside the vitreous follow-up. Anterior chamber lenses, angle supported cavity for many years without consequences. So, or iris supported, are a good option for correction of depending upon the case, the surgeon has the option aphakia in traumatized eyes according the needs of of leave it for years inside the vitreous cavity, if it is the case. already there, and there is not inflammatory response Posterior chamber lenses are preferred because they or mechanical damage; sometimes the principle “better are far away from the corneal endothelium and it has not to damage” applies very well; if the case has an been demonstrated the less incidence of corneal almost complete luxation, sometimes the surgical edema. Many techniques have been described for the technique to follow can be to convert it to a complete implantation of a posterior chamber lens without the vitreous luxation, with particular careful of not to posterior capsule support; scleral fixation, iris suture damage the capsular bag; if this occurs, a complete and scleral glue between others; the technique of lens extraction is mandatory. choice will depend upon the particular features of the If the surgeon choose this option talking with the traumatized eyes and the preferences of the surgeon. patient, both must be aware that when a reaction It has been demonstrated the long-term safety of the occurs inside the eye any time during the life (e.g. posterior chamber IOLs, so it can be described as the inflammatory process), the lens extraction must be method of choice for correction of aphakia in performed; a good communication is mandatory; traumatized eyes, any time that it can be possible and anyhow, the IOL implantation can be performed even the surgeon has the experience enough to implant with the lens inside the vitreous cavity. this mode.

IOL PLACEMENT CONSIDERATIONS If well some particular patients because of the Prognosis and Long-term conditions of the eye should not be implanted and must be managed with contact lens, in most of the Considerations cases the rule to follow is to obtain the maximum of The luxation of the crystalline lens, after a traumatic visual rehabilitation by replacing the crystalline lens lesion of the eye is a severe medical condition that with a IOL; even so, sometimes because of the much of the times is not coming alone, if well particular lesions caused by the eye trauma, some accompanied by some other severe injuries if the eye individual considerations must be done. that can lead to potential bad visual recovery. A perfect We can divide this topic in two big fields: evaluation of the conditions associated to the luxation 1. With capsular support: If during the surgery the are mandatory in order to establish the priorities of capsular bag was conserved (with or without action to solve the injuries; sometimes other lesions, capsular tension ring), an “in the bag” IOL like retinal detachment or acute glaucoma, have implantation is feasible. Just think about the priority of action; sometimes during a single surgical possibilities between “one piece” or “three pieces” procedure, many features can be corrected, including IOL`s according your particular case and needs. the luxation or subluxation of the lens; in some other Never forget that a IOL placed in the capsular bag traumatic lesions is better not to do nothing; the criteria with a zonular lesion, can lead to long term will depend upon the severity of the lesions, a perfect complications; you are not safe forever… evaluation of all of them, the experience of the surgeon, 2. Without capsular support: We can divide this point the surgical findings and the possible postoperative between anterior chamber and posterior chamber complications. It is not an easy thing to do, and lens. sometimes long-life follow-up is needed. An anterior chamber lens is still an option for many A particular condition will be mentioned at the end surgeons; some others try not to use them because of this chapter as a remainder that a traumatic lesion of the endothelial cells consequences; some surgeons of the lens can lead to long term complications; it is feel more frightened to use them in traumatized eyes, the late in-the-bag IOL dislocation, condition that has because of some potential lesions in the anterior been studied for many authors and that if well it is chamber structures, like iris lesions, trabecular lesions, not exclusive of the traumatic lesions of the eye (e.g. and angle structure lesions, between others. Some pseudoexfoliation, high myopia, Marfan syndrome), surgeons are using iris claw IOLs (e.g. Artisan) to achieve it is a severe condition that allows us to keep in mind Management of Traumatic Luxation of the Crystalline Lens 85 that a good communication with our patients and capsular tension ring. Journal of Cataract and Refractive medical service according to ethic principles through Surgery. 2006;32(10):1756-8. the years is mandatory. 7. Khalid Hasanee, Iqbal Ike K. Ahmed. Capsular tension As a final point do not forget in these cases, to rings: update on endocapsular support devices. Ophthalmology Clinics of North America December perform an individualized informed consent, with the 2006;19(4):507-19. enumeration of each and every preoperative diagnosis 8. Manuel Monteiro, Antonio Marinho, Salgado Borges, and possible short and long term complications; never Lucas Ribeiro, Castro Correia. Scleral fixation in eyes with give a definitive prognosis to these patients. loss of capsule or zonule support. Journal of Cataract and Refractive Surgery April 2007;33(4):573-6. 9. Marije L Sminia, Monica Th.P. Odenthal, Nitza Gortzak- Bibliography Moorstein, Liesbeth JJM. Wenniger-Prick, Hennie J 1. Amar Agarwal, Athiya Agarwal, Soosan Jacob, Sugandha Völker-Dieben. Implantation of the Artisan® iris Sinha. Chopstick technique aids IOL implantation in reconstruction intraocular lens in 5 children with aphakia broken posterior capsule cases. Ocular Surgery News, and partial aniridia caused by perforating ocular trauma, US edn, December 1, 2007. 10 March 2008. Journal of AAPOS. 2008;12(3):268-72. 2. Amar Agarwal, Swati Agarwal. Technique helps remove 10. Sharon P Bord, Judith Linden. Trauma to the Globe and lens fragments that have fallen into the vitreous. Ocular Orbit. Emergency Medicine Clinics of North America Surgery News Eudope/Asia-Pacific Edition, December 2008(26)1:97-123. 2006. 11. Sunil K Rao, Paul B Greenberg, Theodoros 3. Amar Agarwal. Technique helps remove lens fragments Filippopoulos, Ingrid U. Scott, Nickolas P. Katsoulakis, that have fallen into the vitreous. Ocular Surgery News, Yoash R. Potential impact of seatbelt use on the spectrum US edn, May 1, 2006. of ocular injuries and visual acuity outcomes after motor 4. Gimbel HV, Condon GP, Kohnen T, Olson RJ. Late in- vehicle accidents with airbag deployment, 31 August the-bag intraocular lens dislocation: Incidence, prevention 2007. Enzer Ophthalmology 2008;115(3):573-6. and management. Journal of Cataract and Refractive 12. Süleyman Kaynak, Zeynep Ozbek, Eser Pasa, F Hakan Surgery. Nov. 2005;Vol 31; issue 11, 2193-2204. Oner, Güray Cingil. Transscleral fixation of foldable 5. Gundula Bading, Jost Hillenkamp, Helmut G. Sachs, intraocular lenses. Journal of Cataract and Refractive Veit-Peter Gabel, Carsten Framme. Long-term Safety and Surgery April 2004(30)4:854-57. Functional Outcome of Combined Pars Plana Vitrectomy 13. Wojciech Omulecki, Katarzyna Stolarska, Aleksandra and Scleral-Fixated Sutured Posterior Chamber Lens Synder. Phacofragmentation with perfluorocarbon liquid Implantation, 18 June 2007. American Journal of and anterior chamber or scleral-fixated intraocular lens Ophthalmology. September 2007;144(3);371-7. implantation for the management of luxated crystalline 6. F Hakan Oner, Nilufer Kocak, A. Osman Saatci. lenses. Journal of Cataract and Refractive Surgery 2005; Dislocation of capsular bag with intraocular lens and 31(11):2147-52. CHAPTER

Traumatic Cataract in Children 17 Rupal H Trivedi, M Edward Wilson (USA)

Introduction versus 32%3). The majority of traumatic cataract cases occur in children while playing or when they are invol- Children are highly vulnerable to ocular injury, ved in sport-related activities. Commonly implicated especially sports-related ocular injury. Traumatic objects include knives, BB guns, firecrackers, sticks, cataracts can be an immediate, early or late sequel thorns, rocks, pencils, arrows, airbags, paintballs, and of any ocular trauma. Management of traumatic toys. Prevention of eye injuries is of utmost importance cataract remains a challenge, in part because each and is the team responsibility of parents, teachers, case is unique. Surgical techniques need to be coaches, ophthalmologists, pediatricians, and customized case by case based on associated ocular optometrists.4 The American Academy of Pediatrics injuries. Pediatric cataract surgery is challenging and and the American Academy of Ophthalmology pub- a traumatic etiology simply adds more challenges. lished a statement recommending types of protective Such surgery in children should draw from both the lenses and frames for specific sports.4 In addition, soft- principles of pediatric non-traumatic cataract removal core baseballs have been recommended for youth techniques and the advancements in adult traumatic league games. However, a case report of 7-year old cataract removal techniques. Optimum timing of boy is published who was struck in his left eye by cataract surgery (duration between development of a soft core baseball, which was lobbed to him from cataract and removal of cataract) is debatable. The a short distance by his father, an ophthalmologist.5 timing of lens removal surgery is important in children – not only to achieve better anatomical outcome but also to achieve better visual outcome. Surgery too Pathophysiology early may result in excessive postoperative Blunt trauma is responsible for coup and countercoup inflammation and many cell deposits on the 6 intraocular lens (IOL). Surgery too late may result in ocular injury. Coup is the mechanism of direct impact. deprivational amblyopia. It is responsible for the Vossius ring (imprinted iris pigment) sometimes found on the anterior lens capsule following blunt injury. Countercoup refers to distant Epidemiology injury caused by shockwaves traveling along the line of concussion. When the anterior surface of the eye Cataract formation after traumatic injury is a common is struck bluntly, there is a rapid anterior posterior cause of ocular morbidity and visual loss. While no shortening accompanied by equatorial expansion. segment of society escapes the risk of eye injury, the This equatorial stretching can disrupt the lens capsule, victims primarily at risk are the young (median age zonules, or both. Combinations of coup, countercoup, 26 years).1 The majority of all eye injuries occur in and equatorial expansion are responsible for the persons under thirty years of age (57%).1 The toll of formation of traumatic cataract following blunt ocular injury in terms of human suffering, as well as long- injury. Penetrating trauma that directly compromises term disabilities, loss of productivity, and economic the lens capsule often leads to cortical opacification impact, can only be imagined.1 at the site of injury. If the rent is sufficiently large, the Trauma has been reported to be responsible for entire lens rapidly opacifies (Fig. 17.1). When the up to 29% of all childhood cataracts.2 At the Storm capsular rent is small, however, the capsule may seal Eye Institute, our database includes 103/866 eyes and the cortical cataract may remain localized. (11.9%) with traumatic cataract (unpublished data). Cataracts caused by blunt trauma classically form Boys are more frequently affected than girls (68% stellate—or rosette-shaped posterior axial opacities Traumatic Cataract in Children 87 The initial patient evaluation is one of the most important critical steps in the management of any traumatic cataract. Data gathered during this exami- nation, to a large extent, direct further investigations and establish immediate priorities. One of the most important aspects of this first examination is the description of the exact circumstances of the injury. This facilitates the development of risk estimates for occult injuries, such as intraocular foreign body (IOFB), chemical exposure, and posterior rupture of the globe. Examination BEFORE DILATION 1. Best-corrected visual acuity (BCVA). Fig. 17.1: Total cataract in an eye with ruptured 2. Fixation preference. anterior capsule 3. Pupillary reflex: Presence of afferent pupillary defect may be indicative of traumatic optic neuropathy. that may be stable or progressive, whereas penetrating 4. Intraocular pressure (if there is no evidence of ocular trauma with disruption of the lens capsule forms cortical rupture). changes that may remain focal if small or may progress 5. Iris: Multiple small ruptures of the pupillary rapidly to total cortical opacification. Anterior and/or sphincters are common and result in a permanent posterior capsule defect, intralenticular foreign body, traumatic mydriasis (Fig. 17.2). The clinical evalua- partial/total zonular loss, and dislocation and tion should also include a careful predilatation subluxation of the lens are often found in combination examination of the iris for trans-illumination defects. with traumatic cataract. Other less common associated If present, it should be documented and following complications include glaucoma (usually related to dilatation, the underlying lens surface should also hyphema and angle recession), retinal detachment, be inspected for anterior capsular defect that choroidal rupture, intraocular hemorrhage, retrobulbar indicate a penetrating injury or IOFB. hemorrhage, traumatic optic neuropathy, and globe 6. Zonule: Although detection of zonular loss is not rupture. Anterior capsule rupture (with flocculent lens always possible prior to pupil dilation, suggestive matter in the anterior chamber) may be associated findings include phacodonesis, an increase in with an increased intraocular pressure. However, myopic refractive error, abnormal peripheral lens flocculent lens material in the anterior chamber is much curvature in one or more quadrants, an abnormal better tolerated in children than in adults. This may light reflex on retinoscopy, a visible lens equator, allow the surgeon to delay surgery for 1-3 weeks until or vitreous in the anterior chamber. the inflammation from the original injury (or injury repair) subsides.

Preoperative Evaluation In the setting of traumatic cataract, the ophthalmologist must first “take a step back” and examine other ocular injuries in detail.7 The surgeon doing cataract surgery should be suspicious of injury to other ocular structures. Management depends on the degree and type of injury. Localized traumatic cataracts (especially if not in the visual axis) may be managed conservatively, while more significant lens opacities generally require cataract extraction. Similarly, capsular perforation may be managed with observation if small and not centrally located. Frequently, such injuries will develop only very Fig. 17.2: Postoperative follow-up of a child operated at localized opacification of the underlying cortex without 14 years of age for traumatic cataract showing traumatic progression to generalized cataract. mydriasis 88 Clinical Diagnosis and Management of Ocular Trauma AFTER DILATION repair even when anterior capsular rupture is present. 1 . Slitlamp examination (after pupillary dilation) is Cataract surgery can be deferred while the recommended if feasible. This helps identify and inflammatory response is treated with topical steroids. document the type of cataract, the position and Advantages of secondary cataract removal are better stability of the lens, integrity of the lens capsule and visibility, better IOL power calculation, anterior segment the overall status of the anterior segment. When reconstruction, and stabilization of a hemato-ocular slitlamp examination is not possible in the awake barrier. Ten of our patients (43.4%) had anterior state, it can be done using a portable instrument capsule rupture and crystalline lens involvement at the in the operating room in conjunction with the time of injury and had their cataract surgery deferred examination using the operating microscope. for times ranging between 2 days and 6 months 11 2. A posterior segment examination, including (average 20 days). Cataract surgery is usually not examination of the retinal periphery, should be performed concurrent with the primary repair of an carried out in detail if the view through the lens open globe. The exception to this rule would be a allows. Greven and colleagues8 found that only small eyewall laceration that can be closed securely 30% of eyes that suffered from contusion injuries prior to cataract surgery and that doesn’t significantly had normal preoperative posterior segments; interfere with visualization of the cataract. If cataract emphasizing need for B-scan if the posterior pole surgery is delayed for several weeks, it can be cannot be visualized. combined with the removal of the sutures used to close 3. Gonioscopy may be helpful to evaluate the angle the corneal laceration thereby minimizing the number structures and for recognizing vitreous at the lens of times the child has to be anesthetized. If it is unclear equator or areas of loss of zonular support. if the cataract is visually significant, cataract surgery 4. If planning for IOL implantation, keratometry and should be delayed until the cornea is fully healed and immersion A-scan ultrasound for globe axial length the child’s vision can be tested with an optical measurement should be attempted. Even when correction. If the cataract is visually significant, its corneal scarring is present, keratometry of the removal should not be delayed too long because of injured eye should be attempted. Changes in the potential for the child to develop amblyopia and corneal curvature as the result of an injury will lose binocularity. The median interval between the change the IOL power needed to achieve the injury and cataract was 8 weeks in a series by Gardin 3 refractive goal. At times the keratometry readings and Yorston. Authors noted that children older than of the fellow eye need to be used but this will 7 years at the time of surgery were more likely to have further compromise the accuracy of the a delay of 1 year or more (P=0.016). postoperative refraction in relation to the postoperative goal. Cohen9 reported a 4 D of IOL power surprise in a adult patient when the IOL Surgical Details power was calculated using the K and AL of the General principles of pediatric cataract surgery should fellow eye. be followed. Specific differences have been described A Guarded prognosis for anatomical and herein. functional outcome is to be thoroughly explained • Anesthesia: In anticipation of difficult surgery, to the patient and patient’s relatives. The full extent general anesthesia is preferable even in older of the eye injuries are not always known prior to children who might otherwise be cooperative for cataract surgery. It is also important to explain about local anesthesia. the possible need for additional surgeries • Anterior capsule management: Performing the depending on the type of injury (retinal capsulorhexis may be difficult in pediatric traumatic detachment, keratoplasty for dense corneal scar cataract. Besides higher elasticity of pediatric obstructing visual axis, etc). anterior capsule, traumatic cataracts are often associated with ruptured anterior lens capsule or fibrosis of the anterior capsule. In addition, Timing of Surgery performing the capsulorhexis may be difficult in The timing of traumatic cataract surgery in children a case of traumatic cataract due to a lack of the is important. Some authors have reported cataract usual zonular counter traction forces. To address surgery at the time of primary repair.10 While the this situation, initiate the capsular tear in the location development of amblyopia in children necessitates of the greatest zonular stability and complete it in prompt removal of a cataract when it develops, cataract the direction of the zonular dialysis. Very dense surgery is not necessarily required at the time of initial fibrous capsule can be removed with intraocular Traumatic Cataract in Children 89 scissors, radiofrequency diathermy or Fugo plasma • Intraocular lens implantation: Intraocular lens blade. Staining of the anterior lens capsule may implantation offers a constant optical correction be helpful to enhance visibility in these eyes with and, as such, helps in the prevention of amblyopia. a “torn anterior capsule” or “white cataract.” Children often have difficulty wearing contact lenses

Anterior capsule staining can be successfully done due to poor comfort, and poor motivation to wear using nontoxic capsular dyes such as indocyanine the lens. In addition, aphakic contact lenses are green 0.5% or trypan blue 0.1%. Typically, these not suitable for the developing world because of cataracts may be white in many instances, and their high cost and the need for meticulous hygiene. indocyanine green or trypan blue can be very The use of IOLs has been studied in children with helpful. An intact capsulorhexis is also mandatory traumatic cataract since Choyce first reported the for a capsular tension ring (CTR) placement. After the capsulorhexis is complete, in cases of zonular use of an anterior chamber lens in a child after 12 dialysis, capsular retractors can aid in visualization trauma in 1958. BenEzra and associates had of the lens and in its removal. reported a better visual acuity and less strabismus • Avoid doing hydrodissection if the integrity of the in children with traumatic cataract after implanting posterior capsule is in question. an IOL, when compared to those wearing contact • Posterior capsule and vitreous management: lenses. Continued advances in IOL design, Management of the posterior capsule depends on biomaterial and power calculations are making it the age of the patient and the status of the posterior the preferred option. capsule (intact v/s torn). In young patients with In young children, it is generally best to under- complex trauma, staged approach (leaving behind correct an eye in anticipation of a myopic shift as intact posterior capsule at the time of initial cataract the child becomes older. In-the-bag fixation is surgery and planning a secondary surgery to believed by most to be the best site for IOL remove the center of the posterior capsule after implantation as it sequesters the implant from uveal the IOL is properly fixed into the lens capsule) may structures, reduces the chance of lens decentration, help proper placement of the IOL. This staged and delays PCO formation.13 In-the-bag placement approach may not be necessary for the surgeon who operates on children frequently. However, it of the IOL haptics improves implant stability and 14 may be better for surgeons unaccustomed to minimizes uveitis and pupillary capture. Fifteen operating on children. Posterior capsule of our 21 eyes with primary implantation had the opacification occurs quickly in most cases of IOL placed in the capsular bag.11 Traumatic cataract complex traumatic cataract surgery. Therefore, cases often present unique challenges, as it is not prepare the family that the best vision will likely always possible to fixate the IOL haptics in the come after this planned second surgery. Repair of capsular bag due to anterior and/or posterior iris defects or other more elective surgical capsule tears from trauma or the difficult surgical maneuvers can also be done during this secondary procedure. If the IOL must be placed in the ciliary procedure, which is often done 4-8 weeks after sulcus, as with extensive traumatic posterior capsule the initial cataract removal. Kenalog can be used rupture, try to capture the IOL optic through the to identify residual vitreous (Fig. 17.3). anterior capsulotomy. Gardin and Yorston noted that they could implant an IOL in the capsular bag in 32% of eyes, in the sulcus in 28% and asymmetrical (bag/sulcus) in 5.6% of eyes (34% unknown).3 Care should be taken to position the haptics of the IOL on the most stable remnants of the lens capsule. Malplacement of the IOL is more common, however, in traumatic cataracts since damage to the capsular bag, zonules and iris may predispose to decentration and pupil capture. Using ciliary sulcus-fixated IOLs in children following traumatic cataract removal resulted in visual outcomes similar to those for capsular bag IOLs but with more complications, in particular uveitis and pupillary capture. The use of multifocal capsular Fig. 17.3: Use of kenalog in identifying residual bag IOLs following removal of a traumatic cataract vitreous in anterior chamber has also been explored. In comparison with 90 Clinical Diagnosis and Management of Ocular Trauma standard, monofocal, capsular bag IOLs, the haptics should be oriented toward the area of multifocal lenses resulted in improved uncorrected incompetence in order to expand and stabilize the near visual acuity and stereopsis, as well as capsular bag fully. With more significant zonular decreased spectacle dependency. However, disruption, IOL implantation should be combined multifocal IOLs reply on centration of the IOL and with CTR. They are not recommended when the the pupil. Neither are achievable in all cases of integrity of the posterior capsule has been breeched. trauma. Since traumatic cataracts are most often For zonular dialysis of up to 150 degrees, the use unilateral, the child will rely mostly on the natural of a conventional CTR followed by standard accommodation of the uninjured eye for near cataract removed and IOL implantation is often viewing. Multifocal IOLs are best when used successful. The CTR can be implanted before or bilaterally. For these reasons, the use of multifocal after the cataract is removed. Although early IOLs in pediatric trauma has remained low. insertion provides support during cataract removal, Several reports on groups of patients with angle- it may create additional zonular trauma. The use supported anterior chamber IOLs in traumatic of iris or capsule retractors at the capsulorhexis edge pediatric aphakia have been published. Due to the or the use of capsular tension segments (CTS) high incidence of secondary glaucoma, progressive during cataract removal are other alternative that pupil distortion, endothelial loss, and the limited do not induce significant capsular torque during experience with these IOLs in children, angle- insertion. For more significant or progressive zonular supported IOLs have not gained widespread dialysis the Cionni-modified CTR is useful alternative to the conventional CTR. It can be acceptance. Scleral-fixated IOLs are considered a sutured to the sclera without compromising the more acceptable alternative for the bag or ciliary capsular bag, thus allowing the CTR and capsule sulcus implantation of posterior chamber IOLs, in to be held in place even in the presence of significant the absence of capsular support in children. zonular incompetence. Otherwise one or two CTS However, concerns have been raised about the risk devices may be used and may also be placed in of conjunctival and scleral erosion of scleral sutures cases of an anterior capsular tear, incomplete leading to infection, IOL tilt, dislocation of the lens capsulorhexis, or posterior capsular rupture. in the vitreous cavity, vitreous or ciliary body • Iris damage: Occasionally the iris may require hemorrhage, and secondary glaucoma. Recently, suturing. Iridodialysis defects are usually repaired at 15 Sminia ML and colleagues described the long- the time of IOL implantation using a series of double- term follow-up of Artisan aphakia IOL implantation armed10.0 prolene sutures (Figs 17.4A to C) on in five aphakic eyes without capsular support, after a long straight STC-6 needle. A small paracentesis cataract extraction following penetrating ocular is made 180 degrees away from the iridodialysis. trauma. The authors noted that the Artisan aphakic Both needles of the double-armed prolene are IOL offers a useful alternative for correction of passed through the paracentesis (one at a time) traumatic childhood aphakia. Although results were and across the anterior chamber. The needle is from a small series, the authors feel that allowed to pick-up the peripheral detached edge implantation of the Artisan aphakic IOL can be of the iris base and then exits the sclera as close considered a treatment option in aphakic eyes of to where that iris segment should naturally attach children that lack capsular support due to trauma. as possible. Each double-armed prolene is passed • Zonular loss: Zonular dialysis may also exist in other in a mattress fashion and is tied external to the conditions that are not traumatic, such as pseudo- sclera. Rather than using a scleral flap, we simply exfoliation or Marfan’s syndrome. The difference leave the suture ends long and tuck then under is that these conditions involve diffuse, progressive the conjunctiva and Tenon fascia. This seems to zonular disease as opposed to a one-time focal prevent suture ends from gradually eroding disturbance that occurs upon trauma. Although the through the conjunctiva. Cuts and tears in the pupil surgical approach to cataract surgery may be similar margin are also often closed with the same type in both scenarios, long-term capsular stability is of suture material. This can be done at the initial better in traumatic cases. The degree of zonular surgery but is often easier when done as a dehiscence dictates the management approach. The secondary procedure in a well-healed pseudo- choice and positioning of the IOL depends on the phakic eye. The use of aniridia implant devices such degree and location of zonular disruption. In eyes as iris diaphragm rings and iris section shields may with no zonular disruption and an intact posterior be appropriate in cases of a significant loss of iris capsule, a standard capsular bag-fixated IOL may tissue. These devises are not yet FDA approved be used. With a small area of zonular incompetence, for use in the USA. Pupilloplasty and/or repair of a capsular bag IOL may also be used, but the iridodialysis may also be required. Traumatic Cataract in Children 91

Fig. 17.5: Corneal suture removal can be done at the time of cataract surgery if wound appears to be healed

be seen transiently after cataract surgery. Prophylactic oral Diamox is recommended during the early healing phase in such cases.

Postoperative Complications Gardin and Yorston noted that the most frequent early complications was severe anterior uveitis with fibrin formation in the anterior chamber, which occurred in 51.2%.3 Fibrinous uveitis was common in recently injured eyes, occurring in 60% of eyes injured 6 weeks or less before surgery and 44% if injured more than 6 weeks before cataract surgery (P=0.02). Eckstein and colleagues however did not find an association between postoperative fibrinous uveitis and recent trauma.16 Other sequel include posterior capsular opacification (PCO) and/or secondary membrane formation, pupillary capture, IOL precipitates (Fig. 17.6), and decentration/dislocation of the implant. Complications in our series included visually Figs 17.4A to C: Iris sutured for traumatic iris tear significant PCO in 5 cases (21.7%), pupillary capture in 2 cases (8.6%) and IOL dislocation in 1 case • Removal of corneal suture: If corneal suture from (4.34%).11 We continue to recommend planned original trauma is present and wound healing has primary posterior capsulectomy in children too young been completed, corneal suture can be removed to undergo an awake Nd: YAG laser capsulotomy. at the time of cataract surgery (Fig. 17.5). Occurrence of pupillary capture can be reduced after a precise fixation of the IOL within the capsular bag or the use of optic capture into the anterior or posterior Postoperative Medication capsulorhexis. Decentration/dislocation of an IOL can occur because of traumatic zonular loss and/or Depending on the case, we may sometimes increase inadequate capsular support. Posterior capture of the the frequency of steroid drops. Also, a short course of IOL optic may be useful, at times, to obtain better systemic steroids may be indicated. If IOP control had centration of the implanted IOL. Asymmetric IOL been a problem after the original trauma, perhaps during fixation, with one of the haptics in the capsular bag hyphema resolution, it is likely that elevated IOP will and the other in the ciliary sulcus can also lead to 92 Clinical Diagnosis and Management of Ocular Trauma series originally published by Mc Kimura in 1961. Twenty-six children with unilateral traumatic cataract had been treated at McGill University Hospital and the University of California Medical Center in San Francisco. Despite treatment, most of the patient’s had visual acuity in the range of counting fingers; only one child retained visual acuity better than 20/200. Binkhorst and Gobin22 recommended the use of IOLs in this situation and suggested this treatment would improve the visual outcomes in children with lenticular opacity. Our results (as well as the experience of several other authors) confirm that good visual outcome is frequently possible following IOL implantation in children. In our patients, 78% achieved a best- corrected visual acuity of 20/40 or better after a mean follow-up of 2.3 years. Koenig et al20 reported 20/40 Fig. 17.6: Deposits on IOL optic or better visual acuity in 87% (7 out of 8) of eyes undergoing IOL implantation for pediatric traumatic cataracts. The average follow-up in their series was 10 decentration and should, therefore, be avoided. months. Gupta et al19 reported that 9 (50%) of 18 Explantation or repositioning of the IOL may be children with unilateral traumatic cataract achieved 20/ necessary in some cases presenting with significant 40 (or greater) visual acuity after IOL implantation, decentration/dislocation. Fracture of an implanted with an average follow-up of 12 months. In many cases posterior chamber IOL after trivial trauma in a child corneal leucomata contributed to decreased operated originally for traumatic cataract has been postoperative visual acuity. Similarly, Anwar et al,10 reported. Such spontaneous fracture of IOL may be BenEzra et al,12 Eckstein et al16, Pandey et al,14 and Brar because of mechanical weakening, commonly et al,13 reported visual acuity of 20/40 or better in attributed to a defective lens production or repetitive 73.3%, 79.0%, 65.2%, 67.0%, 85% and 62% of cases, movements of the IOL during psuedoaccomodative respectively, after traumatic cataract surgery with IOL effort. Moreover, in children extensive fibrosis around implantation in children. Gardin and Yorston3 noted the IOL can induce torsion at the optic haptic junction. that amblyopia was found in 42 of 108 children Perhaps a sudden anterior movement of the vitreous (38.9%) 8 years or younger at the time of injury with due to a rapid head movement induced by trauma, a minimum follow-up of 1 month. The risk of in the setting of a relatively fixed pupillary captured amblyopia significantly increased when there was a IOL, may break the IOL at its already stressed optic- long interval between trauma and cataract surgery. haptic junction, resulting in optic lying in the anterior Fourteen of 23 eyes (60.9%) in children 8 years or chamber. The possibility of this complication can be younger at the time of injury who had surgery at least explained while explaining while discussing a guarded 1 year after the trauma were amblyopic. Of the 85 prognosis to the parents.17 who had surgery less than 1 year after their injury, 28 (32.8%) were amblyopic (P=0.015). The authors further noted that of the 21 eyes with unfavorable Visual Outcome visual outcome (worse than 20/200), amblyopia was the most common cause (9 eyes, 42.8%), followed The prognosis for retention of good vision in pediatric by retinal detachment (5 eyes, 23.8%). eyes suffering traumatic cataracts has greatly improved over the last few decades. Primary IOL implantation has a greatly improved visual outcome. Several Summary surgeons from countries with high traumatic cataract Cataract formation is a well-recognized consequence rates and conditions prohibitive of contact lens wear, of blunt and penetrating ocular trauma. It results from have recently reported successful IOL implantation in direct lens injury, contusive ocular damage, or lens injured children.10, 12-14, 18-21 Compliance with amblyopia dislocation and is often associated with traumatic injury therapy is necessary in younger children to get to the cornea, iris, and vitreous. Traumatic cataract maximum visual outcome, even following an excellent can present many challenges to the ophthalmologist. surgical result. Binkhorst and Gobin22, reviewed a case It adds the challenges presented by childhood cataract. Traumatic Cataract in Children 93 Comprehensive examinations, careful planning for 9. Cohen KL. Inaccuracy of intraocular lens power surgical management and a close follow-up are calculation after traumatic corneal laceration and cataract. necessary for a favorable outcome in these cases. J Cataract Refract Surg 2001;27:1519-22. 10. Anwar M, Bleik JH, von Noorden GK, el-Maghraby AA, Further prospective studies are probably needed to Attia F. Posterior chamber lens implantation for primary specifically address the optimum timing of cataract repair of corneal lacerations and traumatic cataracts in surgery in cases of pediatric traumatic cataract. children. J Pediatr Ophthalmol Strabismus 1994;31: However, based on our experience, we suggest primary 157-61. repair of the injury first, and cataract surgery after a 11. Wilson ME, Trived RH, Pandey SK. Traumatic cataracts 2-4 weeks of topical steroid and atropine treatment. in children. In: Wilson ME, Trivedi RH, Pandey SK This delay may be helpful in achieving the optimum (editors). Pediatric Cataract Surgery: Techniques, Complications, and Management Ahmedabad: Lippincott surgical outcome by reducing the postoperative Williams and Wilkins, 2005. inflammation in these eyes and allowing healing to 12. BenEzra D, Cohen E, Rose L. Traumatic cataract in occur. Long delays before cataract removal must be children: correction of aphakia by contact lens or avoided during the amblyopia prone years, which intraocular lens. Am J Ophthalmol 1997;123:773-82. extend to approximate the age of 8 years. Successful 13. Brar GS, Ram J, Pandav SS, Reddy GS, Singh U, Gupta surgery requires a wide variety of techniques to the A. Postoperative complications and visual results in uniocular pediatric traumatic cataract. Ophthalmic Surg particular occasion and case. These factors include the Lasers 2001;32:233-8. history and circumstances of the ocular trauma, 14. Pandey SK, Ram J, Werner L, et al. Visual results and hypotony or the elevation of IOP, inflammation, and postoperative complications of capsular bag and ciliary the extent of associated anterior segment trauma. We sulcus fixation of posterior chamber intraocular lenses support the continued use of IOLs in children in eyes in children with traumatic cataracts. J Cataract Refract Surg with traumatic cataract. 1999;25:1576-84. 15. Sminia ML, Odenthal MT, Wenniger-Prick LJ, Gortzak- Moorstein N, Volker-Dieben HJ. Traumatic pediatric References cataract: a decade of follow-up after Artisan aphakia intraocular lens implantation. J Aapos 2007;11:555-8. 1. http://www.useironline.org/Prevention.htm 2008. 16. Eckstein M, Vijayalakshmi P, Killedar M, Gilbert C, Foster 2. Eckstein M, Vijayalakshmi P, Killedar M, Gilbert C, Foster A. Use of intraocular lenses in children with traumatic A. Aetiology of childhood cataract in south India. Br J cataract in south India. Br J Ophthalmol 1998;82: Ophthalmol 1996;80:628-32. 911-5. 3. Gradin D, Yorston D. Intraocular lens implantation for 17. Sachdev N, Brar GS, Sukhija J, Ram J. Fracture of an traumatic cataract in children in East Africa. J Cataract implanted posterior chamber intraocular lens after trivial Refract Surg 2001;27:2017-25. trauma in a child. Indian J Ophthalmol 2007;55:161-2. 4. Protective eye wear for young athletes. A joint statement 18. Bienfait MF, Pameijer JH, Wildervanck de Blecourt- of the American Academy of Pediatrics and the American Devilee M. Intraocular lens implantation in children with Academy of Ophthalmology. Ophthalmology 1996; unilateral traumatic cataract. Int Ophthalmol 1990;14: 103:1325-8. 271-6. 5. Brasch PC, Tien DR, DeBlasio PF, Jr., Loporchio SJ. Traumatic 19. Gupta AK, Grover AK, Gurha N. Traumatic cataract cataract in a 7-year-old boy caused by low-velocity impact surgery with intraocular lens implantation in children. J with a soft-core baseball. J Aapos 2005;9:493-4. Pediatr Ophthalmol Strabismus 1992;29:73-8. 6. Datiles MB, Magno BV. Cataract: clinical types. Duane’s 20. Koenig SB, Ruttum MS, Lewandowski MF, Schultz RO. ophthalmology. Philadelphia: Lippincott Williams and Pseudophakia for traumatic cataracts in children. Wilkins, 2001. Ophthalmology 1993;100:1218-24. 7. Harlan JB Jr Pieramici DJ. Evaluation of patients with ocular 21. Cheema RA, Lukaris AD. Visual recovery in unilateral trauma. Ophthalmol Clin North Am 2002;15:153-61. traumatic pediatric cataracts treated with posterior 8. Greven CM, Collins AS, Slusher MM, Weaver RG. Visual chamber intraocular lens and anterior vitrectomy in results, prognostic indicators, and posterior segment Pakistan. Int Ophthalmol 1999;23:85-9. findings following surgery for cataract/lens subluxation- 22. Binkhorst CD, Gobin MH, Leonard PA. Post-traumatic dislocation secondary to ocular contusion injuries. Retina artificial lens implants (pseudophakoi) in children. Br J 2002;22:575-80. Ophthalmol 1969;53:518-29. CHAPTER

Scleral Fixated IOL in Trauma 18 Rupesh V Agrawal (India)

Introduction important in every trauma case. Also there can be posterior segment complications such as retinal Ocular trauma is one of the leading common problems detachment or a retained intraocular foreign body that ophthalmologists dealing with. The incidence of in the posterior chamber, vitreous hemorrhage and ocular trauma is going up day-by-day with increasing choroidal rupture and scar. This is important as the population and varied occupations. It is very common prognosis of the outcome depends on the associated occupational hazard with certain occupations such as damage as the cause of vision loss can be due to these building construction workers, carpenters, and also additional injuries than due to the anterior segment very commonly seen during road traffic accidents and injury. Patient counselling and prognostication, hence in children. With the advances in surgical techniques becomes a very important aspect of treating ocular and availability of facilities, the prognosis of traumatic trauma. cases is improving significantly and the management Aphakia is one of the common problems and the visual prognosis of ocular trauma has changed encountered in patients with trauma. It can be a result significantly over the past few days. of complete loss of the lens and capsular support Lens injury during ocular trauma is one of the during the trauma itself or it can be as a result of commonest associations and traumatic cataract is one zonular dialysis or lens subluxation beyond a few clock of the commonest finding in any ocular trauma. hours in which case capsular support for implantation of a posterior chamber lens can be inadequate. In some cases, doing an ICCE or performing pars plana Mode of Lens Injury in Ocular lensectomy is required for managing the cataract. In these circumstances the options that remain are an Trauma and its Presentation implantation of an anterior chamber IOL or a The lens can be injured by various ways during ocular secondary scleral fixated IOL in the sulcus. trauma. There can be direct trauma to the lens leading to its rupture and cataract. In other cases there can be an indirect trauma as during blunt trauma without Scleral Fixated IOL vs Anterior causing a direct injury but leading to a cataract due to altered lens metabolism more commonly known Chamber IOL as the rosette-shaped cataract. The exact mechanism With the advances in the techniques in the surgery is not known but postulated mechanism include and availability of vitrectomy machines in most of the microtrauma to the lens fibers and the capsule leading centers and availability of scleral fixated lenses more to influx of aqueous in the lens and hydration of the readily in the market, the trend is shifting towards lens fibers and cataract. inserting a scleral fixated IOL, whenever possible. Traumatic cataracts can be associated with A traumatised eye is very commonly associated subluxtaion or zonular dialysis and/or intralentiular with additional complications such as posterior foreign bodies. It is not uncommon to find posterior segment complications and corneal tears which need segment complications associated with the cataract. to be dealt with. In addition there can be damage Many times the lens is dislocated out of the wound to the anterior chamber angle structures. Hence, a and can be absent or can even lay subconjunctivaly. patient with traumatized eye need routine follow-up More often than not it can get dislocated into the and detailed evalution of the angle by gonioscopy, vitreous posteriorly. Hence careful evaluation is intraocular pressure and posterior segment. Also there Scleral Fixated IOL in Trauma 95 can be additional damage to the iris structures such 2. Detailed slitlamp examination of the anterior as iridodialysis or damage to the iris sphincter leading segment should be carried out. It involves checking to a dilated pupil. In other circumstances, the iris may for the status of the cornea including corneal scars, have been abscised during the primary wound repair, astigmatism, and endothelial status. Anterior leading to inadequate iris support. Hence, an ACIOL chamber depth and anterior chamber cells and flare implantation may not always be possible. should be checked for. Zonular dialysis, lens In some circumstances, an ACIOL is best avoided capsular rupture and intralenticular foreign bodies such as when the patient will need detailed posterior should be noted. A careful examination should be segment evaluation with fully dilated pupils which is made to look for vitreous prolapse into the anterior not possible with an ACIOL in situ. This is important chamber in which case cataract extraction needs as patients with ocular trauma are prone for retinal to be carried out more carefully to avoid further detachments and need detailed fundus evaluation with damage and inadvertent traction on the vitreous. indentation. It is also avoided in patients who may 3. Detailed fundus examination is a must in all cases otherwise have normal posterior segment in the eye of ocular trauma; to rule out traumatic endoph- in question but may have a history of retinal thalmitis, retinal dialysis and detachments and any detachment in the other eye or in the family, in which foreign body in the posterior segment. Choroidal case routine examination is necessary. ACIOLs are also rupture should be looked for. A choroidal rupture contraindicated in patients with glaucoma and in involving the macular area is associated with poor patients with narrow angles, in whom frequent gonioscopy is required which can be difficult with the visual outcomes. Careful examination of the haptics of an ACIOL in the angle. There can be macular are should be done to rule out Berlin’s associated angle recession in traumatized eyes and an edema and cystoid macular edema or a traumatic ACIOL can further aggravate the damage. ACIOLs macular hole which may need to be tackled during are also not advisable in patients with corneas with the surgery. Optic nerve should be also examined low endothelial counts as the ACIOL can lead to for traumatic optic neuritis or atrophy or in some corneal decompensation and bullous keratopathy. cases traumatic optic nerve avulsion. Moreover, the advantage of SFIOL over ACIOL 4. In cases where the fundus view is not there an is its placement in the anatomical location with a ultrasonography B-scan needs to be done to rule placement closest to the nodal point of the eye giving out any posterior segment complications. better optical properties. 5. Biometry and A-scan for axial length should be done. Indications of SFIOL 1. Monocular aphakia in patients with contact lens Technique of Insertion of SFIOL intolerance. Can be classified as: 2. Old and disabled persons with tremors, A. 2 point fixation Parkinsonism or other physical disabilities which B. 4 point fixation makes handling and using spectacles and contact lenses difficult. Can also be classified depending on the technique of 3. Children in whom maintaining contact lenses can passing the sutures as: be a problem and contact lens wear may be A. Ab-interno procedure where the suture is passed difficult. Also, non-compliance with the contact from inside out (i.e. from the anterior chamber to lenses can lead to amblyopia. the exterior) 4. Young patients who find the prospect of using a B. Ab-externo procedure where the suture is passed contact lens lifelong, unacceptable. from outside in (i.e. from the exterior into the 5. In patients undergoing penetrating keratoplasty for anterior chamber. corneal scars involving visual axis. Can also be classified as: 6. Contralateral pseudophakia. A. Anterior approach—more commonly followed by anterior segment surgeons and easy to perform. B. Posterior approach—more commonly performed Preoperative Workup by posterior segment surgeons. Requires greater 1. Detailed history with previous surgical notes, if surgical skill and more advanced vitrectomy available should be procured. setup. 96 Clinical Diagnosis and Management of Ocular Trauma 2 POINT FIXATION ANTERIOR APPROACH In this technique, the IOL is fixed to the sclera at 2 In the anterior approach, the SFIOL is inserted after points with 2 10-0 prolene sutures. This is a faster doing only anterior and core vitrectomy from the technique and less cumbersome. Hence, it is easier anterior approach with making the par plana to perform and good for beginners. However, the sclerotomies. The advantage of this approach is that stability of the IOL is lesser as compared to 4 point it is simpler and easier to perform. The technique is fixation and the chances of decentration or tilts are also faster. However, the chances of postoperative higher. complications are higher as the removal of vitreous is incomplete and this can be a constant source of 4 POINT FIXATION irritation resulting in chronic cystoid macular edema, In this technique, the IOL is fixed to the sclera at 4 secondary glaucoma or uveitis. points with 10-0 prolene sutures. However, it requires more skill and is more time consuming. The sutures POSTERIOR APPROACH can get entangled and a mix-up of sutures can cause In this approach, conventional 3 port pars plana improper fixation of the IOL. Hence this procedure vitrectomy is performed completely with an induction can become cumbersome and difficult to perform. of posterior vitreous detachment. Limited base excision is also performed in the area where the SFIOL will AB-INTERNO TECHNIQUE be placed. The SFIOL is then inserted either with the This is a blind technique wherein after making 3 mm ab-externo or the ab-interno technique by 2 point or × 3 mm scleral flaps at the limbus, the 10-0 prolene 4 point fixation. needle is passed through the eyelet of the haptic and We preferably perform ab-externo 4 point fixation then the needle is passed through the AC and brought of SFIOL by the posterior approach in traumatized out about 1 mm from the limbus under the scleral eyes and it will be described in detail. flaps. This technique requires lot of skill and experience • After doing routine surgical asepsis, the eye to be as while passing the needle underneath the iris, it can operated is painted and draped. damage the iris itself or the ciliary body or in some • 270 degree conjunctival peritomy is performed. cases if the needle goes more posteriorly it can cause • 2 partial thickness square shaped limbal based breaks in the retina and can cause a retinal detachment. scleral flaps of 3 × 3 mm are made at 3 and Also the most important factor which makes it a non- 9 O’ clock. preferred technique by many is that the placement • A self sealing trilaminar 7 mm scleral tunnel is made of IOL is more posterior with this technique rather at 12 O’ clock. than in the ciliary sulcus as has been found in many • 3 sclerotomies are made at 3 mm from the limbus. studies. Hence, this technique although fast may not • If a cataract is present, then lensectomy is done be suitable for beginners and who are inexperienced. with a vitrectomy cutter. In cases where the cataract AB-EXTERNO TECHNIQUE is dense, it is either delivered out through the tunnel or by phacoemulsification. This technique is easier to perform and requires little • Complete par plana vitrectomy is done. In cases experience and the learning curve is faster. Also, the where the posterior vitreous is not detached, PVD procedure is done under direct view and hence more is induced with either by suction or by an accurate as to the placement of the IOL perfectly in intraocular forceps. In traumatized eyes this step the sulcus. In this procedure after making scleral flaps is very important as the chances of a cystoid or grooves, a 27G needle is passed 1mm from the macular edema are very high. Also if the PVD gets limbus into the eye behind the iris and held in place in the pupillary axis. From the opposite side, a induced in the postoperative period it can lead to 10-0 prolene suture with a straight needle is passed retinal break formation in the already compromised into the eye and passed into the bore of the 27G needle eye and cause retinal detachment. under observation and the 27G needle is pulled out • Then limited base excision is done in the region bringing with it the needle. A superior 7 mm wound where the SFIOL haptics will be placed; in this case is then created and the loops brought out, cut and tied at 3 O’clock and 9 O’ clock position. This has to the eyelets of the haptics of an SFIOL and the IOL 2 advantages. It prevents the constant irritation of is then inserted in sulcus and the sutures pulled out and the vitreous by the haptics on movement of the fixed to the sclera in the bed. The flaps are then sutured eye and also prevents traction on the vitreous by back with 7-0 vicryl covering the prolene knot. the haptics preventing retinal breaks. Scleral Fixated IOL in Trauma 97 • A detailed fundus examination is then carried out This can induce fresh breaks in some instances and with indirect ophthalmoscope with scleral inden- can cause retinal detachment. Also, the trauma can tation. cause macular involvement by way of a traumatic • Any breaks in the retina or dialysis or suspicious chronic cystoid macular edema or an epiretinal areas are treated with cryopexy. membrane formation or, in some cases, full-thickness • A double armed 10-0 prolene suture with straight macular holes. These can also be managed during the needle is used for the procedure. The suture is cut IOL implantation itself by combining it with total in the center. vitrectomy with internal limiting membrane peeling. • A 27G or 28G needle is passed from the inferior end of one of the scleral grooves into the eye behind the iris and help in place in the pupillary area. The Complications of SFIOL needle of the 10-0 prolene suture is then passed from the opposite side and passed into the bore CYSTOID MACULAR EDEMA of the 27G needle and the needle is withdrawn It is the most common complication seen after ant IOL pulling the suture along with it. The procedure is implantation. The incidence increases whenever it is repeated on the superior end of the grooves. So, associated with complications. In the absence of the now there are 2 10-0 prolene sutures passing across posterior capsule this more common due to the antero- the anterior chamber behind the iris with the ends posterior vitreous traction on the macula. In of the sutures on the outside. traumatised eyes, the trauma itself may cause CME, • The loops of the sutures are then brought out from more often chronic and non-responding. This can be the scleral tunnel and cut in the center and the reduced with good vitrectomy releasing all traction on ends secured. the macula and preferably with an induction of PVD. • The sutures on the left side are then to the eyelet of the haptic of an SFIOL. The procedure is GLAUCOMA repeated on the other side. This is also fairly common with SFIOL. This can be • The IOL is then inserted in the sulcus and the due to incomplete vitrectomy or due to viscoelastic sutures are pulled out on either side taking care device induced. It can also be secondary to entangled that the IOL does not flip. vitreous in the vitreous which can cause uveitic • The left side sutures are then tied to each other glaucoma. Rarely, the SFIOL can cause a pupillary and the procedure is repeated on the other side. block and lead to rise in IOP. In same cases glaucoma • The ends of the knots are left long, about 1 mm, can be unrelated to the SFIOL itself and can be due and are covered by the scleral flaps and the flaps to damage to the trabecular meshwork during the are sutured back by 7-0 or 8-0 prolene sutures. primary trauma. • The sclerotomies are then closed by 7-0 vicryl and conjunctiva is closed. LENS DECENTRATION AND LENS TILT Advantages of Posterior Approach in There can occur some amount of lens decentration and Traumatized Eyes tilt during the placement of the SFIOL in the sulcus and while tying the sutures to the sclera. Sometimes, the More often than not, there is some amount of posterior sutures can be loose causing an inferior subluxation of segment involvement due to the primary trauma. There the IOL. This can cause significant glare or diplopia. The can be posterior dislocation of the lens or IOL into the lens can also get tilted during the tying of the sutures or vitreous which needs to be removed. In other cases, due to passage of sutures at different levels in the sclera there can be incarceration of the vitreous into the wound on the two sides. The incidence of this complication is which can be a source of traction on the retina and lesser in SFIOLs fixed to sclera by the 4 point fixation hence needs treatment. There may be associated technique and by the ab-externo technique. However, vitreous hemorrhage which needs vitrectomy if present some amount of lens tilt is very well tolerated by the since a long time. Also, retinal breaks and dialysis are patients with glasses and in clinical practice does not pose fairly common after closed globe injuries which may a big problem. However, lens subluxation needs not be always be possible to see during the preoperative treatment if the patient is symptomatic. period due to either vitreous hemorrhage or due to a non-dilating pupil due to posterior synechiae or due to a corneal scar. These can be better visualized and RETINAL DETACHMENT treated by the posterior approach. Posterior vitreous It is a rare complication than can occur in any detachment is almost universal in traumatised eyes. complicated cataract surgery including SFIOL. This can 98 Clinical Diagnosis and Management of Ocular Trauma be prevented by doing a good preoperative evaluation and a good intraoperative fundus examination to identify any breaks and treat them.

CHOROIDAL DETACHMENT It a very rare complication but can occur. There can be a leak from the site of entry of the 27G needle or from a leaking sclerotomy leading to hypotony. This can be managed by countering the hypotony by injecting intraocular air or saline and by a course of oral steroids.

UVEITIS Fig. 18.2: Site of scleral tunnel for insertion of SFIOL and It is more commonly seen in SFIOLs operated from partial thickness scleral grooves for 10–0 prolene sutures the anterior route in which vitrectomy is incomplete and this leads to constant irritation of the vitreous leading to uveitis. Trauma itself can lead to some amount of uveitis. This can be managed by adequate vitrectomy ensuring the lens is free of vitreous and by using topical steroids in the postoperative period.

ENDOPHTHALMITIS The 10-0 prolene suture forms a tract for the micro organisms to gain entry into the posterior segment leading to endophthalmitis. The knot of the suture also provides a nidus for the proliferation of organisms. There can occur delayed endophthalmitis or in some cases even acute endophthalmitis. This can be Fig. 18.3: Technique of passing 10–0 Prolene suture: 10– prevented by adequately rotating the knot in the scleral 0 prolene passed through one end of scleral groove, bed or by covering it with a scleral flap. In established engaged out through another scleral groove with help of cases, intravitreal antibiotics and topical antibiotics can 27 G, 1 inch needle bent at the tip be started.

SUTURE EROSION This is again a rare complication but possible. The knot can erode through the scleral bed and can be constant source of irritation leading to foreign body sensation, pain, watering, and discomfort. The knot can provide a nidus for micro-organisms and cause an endophthalmitis. If there complete erosion of

Fig. 18.4: Passing of suture through IOL islet in SFIOL haptics

suture, it can break and the lens can dislocate in which case the procedure may have be repeated. Suture erosion can be prevented by burying the knot in the Fig. 18.1: Applied anatomy for SFIOL sclera and/or covering it with scleral flap. This should Scleral Fixated IOL in Trauma 99 trauma will increase. Hence, the management will of ocular trauma and post-trauma rehabilitation will also need to change with changing times and increasing patient demands and expectations. Traumatic cataracts being complicated on most occasions, the need for a scleral fixated IOL will always be there. Hence the need to learn the technique and implement it is the need of the hour for ophthalmologists today. However, patient counseling and regarding the risks and benefits should be discussed in detail with the patients. Patients should be well informed about the intra-operative and post-operative complications and the availability of alternatives. Only highly motivated patients are ideal Fig. 18.5: Scleral tunnel candidates for an implantation of SFIOL. In such patients, SFIOL is a boon and will be a very good and viable option vis-à-vis contact lenses.

Bibliography 1. Ab externo scleral suture loop fixation for posterior chamber intraocular lens decentration: clinical results. J Cataract Refract Surg. Chan CC, Crandall AS, Ahmed II. 2006;32(1):121-28. 2. Anterior chamber and sutured posterior chamber intraocular lenses in eyes with poor capsular support. Cataract Refract Surg. Donaldson KE, Gorscak JJ, Budenz DL, Feuer WJ, Benz MS, Forster RK 2005;31(5):903-09. 3. Asadi R, Kheirkhah A. Long-term results of scleral fixation Fig. 18.6: SFIOL in situ of posterior chamber intraocular lenses in children. Ophthalmology. 2008 Jan;115(1):67-72. Epub 2007;3. 4. Comparison of outcomes of primary and secondary implantation of scleral fixated posterior chamber intraocular lens. Br J Ophthalmol Lee VY, Yuen HK, Kwok AK 2003;87(12):1459-62. 5. Comparison of Outcomes of Primary Scleral-Fixated versus Primary Anterior Chamber Intraocular Lens Implantation in Complicated Cataract Surgeries. Ophthalmology, Kwong, H. Yuen, R Lam, V Lee, S Rao, D Lam.Volume 114, Issue 1, Pages 80-85 Y. 6. Comparison of secondary implantation of flexible open- loop anterior chamber and scleral-fixated posterior chamber intraocular lenses. J Cataract Refract Surg. Evereklioglu C, Er H, Bekir NA, Borazan M, Zorlu F 2003;29(2):301-08. Fig. 18.7: Traumatic cataract with posterior 7. Long-term safety and functional outcome of combined pars capsular dehiscence plana vitrectomy and scleral-fixated sutured posterior chamber lens implantation. Am J Ophthalmol. Bading G, Hillenkamp J, Sachs HG, Gabel VP, Framme C be in turn covered by the conjunctiva. In case suture 2007;144(3):371-377. erosion still occurs, a scleral patch graft should be used 8. Scleral-fixated intraocular lens implantation in unilateral to cover the exposed suture aphakic children. Ophthalmology. Kumar M, Arora R, Sanga L, Sota LD 1999;106(11):2184-89. 9. Scleral-fixated posterior chamber intraocular lenses in non- Conclusion vitrectomized eyes. Eye. Yang YF, Bunce C, Dart JK, Johnston RL, Charteris DG. 2006;20(1):64-70. IOL implantation has come a long way in the recent 10. Secondary intraocular lens (IOL) implantation: anterior years. With the advances in techniques, the options chamber versus scleral fixation long-term comparative that will be available will increase. With the growth evaluation. Eur J Ophthalmol. Dadeya S, Kamlesh, Kumari of industries and population, the number of ocular Sodhi P. 2003;13(7):627-33. CHAPTER

Iris Trauma 19 Rupesh V Agrawal (India)

Iris Prolapse CLINICAL PROFILE OF A PATIENT WITH IRIS PROLAPSE

INTRODUCTION History • The iris is a sensitive tissue in the eye. At the time The iris is a thin, colored diaphragm that is situated of an iris prolapse, patients often experience pain. anterior to the lens. Although the root of the iris is Patients with a perforated corneal ulcer frequently attached to the ciliary body, the rest of the iris is provide a history of severe pain that has since unsupported. In the event of a corneal wound, the subsided. iris tends to prolapse out. Iris prolapse occurs when • The iris can prolapse after surgery (e.g. cataract, the iris tissue is observed outside of the wound; iris corneal transplant), following trauma (e.g. corneal incarceration occurs when the iris tissue reaches the laceration, scleral laceration), through a perforated wound without prolapsing outside the eye. Iris prolapse corneal ulcer, or through a corneal melt associated can occur secondary to cataract surgery also. with rheumatoid arthritis. • However, the commonest cause by and large of iris prolapse is the ocular trauma. PATHOPHYSIOLOGY Iris prolapse can occur when the cornea is perforated Signs due to any cause. In 1995, using flow mechanics and the Bernoulli principle, Allan provided a theoretical In peripheral iris prolapse, the iris appears as a knuckle explanation of iris prolapse. With a corneal perforation, of colored tissue, resulting in a partial peripheral the aqueous humor rapidly escapes, and a relative synechia. When the prolapse is central, the entire pupillary margin may prolapse, resulting in a total vacuum is created in front of the iris, thus leading to anterior synechia. In patients with a perforated cornea, iris prolapse. Prolapsed iris tissue can be healthy or the prolapsed iris is exposed. inflamed or infected or epithelialized with inflammatory Depending on the duration of prolapse, the membrane or with conjunctival tissue. Depending on appearance of the iris may vary. In cases of recent the status of the prolapsed iris tissue, the iris is either prolapse, the iris appears viable. With time, the iris reposited or abscessed or left untouched. appears dry and nonviable. In patients who have undergone corneal transplant surgery or cataract surgery with a clear corneal incision, the appearance MORTALITY/MORBIDITY of the iris is the same as in a perforated cornea. When Iris prolapse is a serious condition and, if left the iris prolapses through a scleral wound, it appears untreated, can result in infection and loss of the eye. as a colored mass beneath the overlying conjunctiva. It acts as nidus for infection and route of entry for In this case, the iris remains viable for a long time. microorganisms to enter into the eye. If the prolapsed The pupil appears peaked in the region of the iris iris is exposed (e.g. corneal laceration), immediate prolapse. The anterior chamber is formed as the surgical intervention is needed because infection can prolapsed iris seals the wound. Minimal or no wound spread through the iris and into the eye. If the prolapsed leakage occurs. Wound leak is verified using the Seidel iris is covered by the overlying conjunctiva (e.g. surgical test. A drop of 2% fluorescein sodium is instilled in wound), immediate surgical intervention is usually not the conjunctival sac. The wound is examined under needed. the slit lamp with cobalt blue light. The fluorescein Iris Trauma 101 appears greenish. Wound leak can be easily identified No eye drops or ointment should be applied in when the fluorescein is diluted by the aqueous humor. open eyes with prolapse iris. Intravenous antibiotics Gentle pressure on the eye may be needed to induce should be considered because infection from an iris leakage. prolapse can spread to the intraocular contents. Broad However, whenever the iris tissue is plugging the spectrum antibiotics are recommended. Tetanus toxoid internal lip of corneoscleral wound, the Siedel’s test is may be considered depending on the immunization of no significance, as it will be false negative mainly status and the wound type. because of the iris and inflammatory membrane pluging the internal lip of corneal or corneoscleral wound. Surgical Care Intraocular pressure is lower than normal, but Prompt surgical management is necessary when hypotony is uncommon after iris prolapse. conjunctival coverage is not present or in the presence In long-standing iris prolapse, chronic iridocyclitis, of complications. The primary goal of surgery is to cystoid macular edema, or glaucoma may be seen. restore the anatomical integrity of the eye. Visual The prolapsed iris may act as a scaffold for infection, restoration is only a secondary goal. epithelial downgrowth, or fibrous ingrowth. Rarely, General anesthesia should be used during surgery. sympathetic ophthalmia may occur. Carefully Retrobulbar anesthesia and peribulbar anesthesia are examining the fellow eye for flare and cells is important not recommended because they increase both to rule out sympathetic ophthalmia. intraorbital pressure and loss of additional intraocular tissue; however, they may be used if general anesthesia Lab Studies is contraindicated. Iris prolapse is a clinical diagnosis. Through a paracentesis incision, a viscoelastic agent is injected into the anterior chamber in the region of the iris prolapse. This mechanical force may be enough Imaging Studies to release the prolapse and to reposition the iris. • In long-standing iris prolapse, if cystoid macular If the viscoelastic method is unsuccessful, then a edema is suspected, fluorescein angiography may cyclodialysis spatula with the longer end is introduced be performed. Cystoid macula edema appears as through the paracentesis incision. The spatula is swept a flower petal in the late stages of the angiogram. from the center to the periphery of the prolapse to • CT scan of the orbits is indicated with traumatic avoid unnecessary tension on the iris root. The corneal iris prolapse to aid in diagnosing other ocular and wound may be sutured depending on its length and orbital trauma and especially if the history is integrity. suggestive of intraocular foreign bodies. If the prolapse occurred within the previous 24- • In traumatic iris prolapse, ocular ultrasound may 36 hours and if the iris is viable, the iris is reposited. be gently performed by experienced personnel. The sings of viable iris tissue are glistening iris tissue This imaging modality may help to locate with no inflammatory membranes on surface of iris intraocular foreign bodies and to assess the status tissue. The texture and glow of iris tissue are the of the posterior segment of the eye. Care should be taken while performing the ocular ultrasound important indicators for viability of iris tissue. because undue pressure can cause prolapse of the If the iris does not appear viable, then it is abscised. intraocular contents. The iris should be abscised if signs of epithelialization are present. The abscission involves pulling of the iris TREATMENT tissue and cutting some part of normal healthy iris tissue along with non-viable iris tissue which is prolapsed out. Conservative Treatment The excision involves just cutting the prolapsed iris tissue Iris prolapse is a serious condition that requires prompt flushing through the corneal surface. medical management. As soon as the diagnosis is made, If the iris prolapse occurs after surgery, the same an eye shield should be applied to prevent further principle is used. The wound must be revised, or damage. One should try and avoid pressure patch over additional sutures should be applied to make the wound the traumatized eye as the pressure patch by itself can watertight. act as nidus for infection and with the eye being closed, When the iris prolapse occurs after a corneal the organisms can flourish inside the closed eye. perforation, the iris can be reposited. Cyanoacrylate Medical treatment is only indicated when the glue and a bandage contact lens may be used to seal prolapse is small, is covered by the conjunctiva, and the perforation. If unsuccessful or if the perforation is without any other complications. In these cases, the is large, an emergency corneal patch graft or corneal eye may be observed. transplant is necessary. 102 Clinical Diagnosis and Management of Ocular Trauma Holistic Approach TREATMENT AND MANAGEMENT In patients with a corneal melt due to medical causes In our enlightened age of small incision, closed-system (e.g. rheumatoid arthritis), appropriate consultations anterior segment surgery, we have increased surgical must be obtained. control over the intraocular environment and have developed the skills for more sophisticated iris repair. Simultaneously, we are more attentive to glare and Iridodialysis photophobic complaints from our cataract and refractive surgery patients. The confluence of increased INTRODUCTION AND CAUSES awareness and surgical abilities set the stage for the Iridodialyses, sometimes known as a coredialysis, is a new epoch in iris surgery. localized separation or tearing away of the iris from Iridodialysis causing an associated hyphema has to its attachment to the ciliary body, are usually caused be carefully managed, and recurrent bleeds should

by blunt trauma to the eye, but may also be caused be prevented by strict avoidance of all sporting by penetrating eye injuries. An iridodialysis may be activities. Management typically involves observation an iatrogenic complication of any intraocular surgery and bed rest. Red blood cells may decrease the outflow and at one time they were created intentionally as part of aqueous humor, therefore the eye should be kept of intracapsular cataract extraction. Iridodialyses have soft by giving oral acetazolamide. Accidental trauma been reported to have occurred from boxing, airbag during sleep should be prevented by patching with

deployments, high-pressure water jets, elastic bungee an eye shield during night time. Avoid giving aspirin, cords, bottle caps opened under pressure, water heparin/warfarin and observe daily for resolution or balloons, fireworks, and various types of balls. progression. A large hyphema may require careful anterior chamber washout. Rebleeds may require SYMPTOMS AND SIGNS additional intervention and therapy. Abnormal pupils affect patients in several ways, Later, surgical repair may be considered for larger including photophobia and glare. These patients often avulsions causing significant double vision, cosmesis describe discomfort or difficulty in brightly lit areas, or glare symptoms. Surgical repair is usually done by such as supermarkets, or on sunny days. Typically, they 10-0 prolene suture taking the base of iris avulsion report that sunglasses do not alleviate their symptoms and suturing it to the scleral spur and ciliary body either outside or indoors. Edge glare from an exposed junction. intraocular lens optic margin can elicit similar complaints and may induce disturbing crescents, arcs of light, “tails” SURGICAL PLANNING on lights and other optical aberrations. Like most intraocular procedures, repairing a damaged Rarely, an irregular pupil may induce an undesired iris requires preoperative planning and meticulous refractive effect. Since the visual axis usually goes technique. With careful attention to detail and basic through the geometric center of the pupil, the visual principles, you can master the art of iris repair. axis-corneal intercept may be abnormally placed Preoperatively, you must determine whether there through an area of irregular corneal topography. is sufficient iris tissue remaining to achieve the desired Those with small iridodialyses may be asymptomatic goals. It is often difficult to assess how much tissue is and require no treatment, but those with larger dialyses present because the iris stroma may be contracted or may have corectopia or polycoria and experience rolled over. Careful examination and review of prior monocular diplopia, glare, or photophobia. Iridodia- operative notes are helpful in determining whether lyses often accompany angle recession and may cause tissue has been removed. Typically, there is more iris glaucoma or hyphema. Hypotony may also occur. present than you might think based on slit-lamp An abnormal pupil may also have deleterious examination. psychosocial effects. As a society, we place a psychic Furthermore, iris tissue is usually very stretchable premium on the appearance of the eyes. It is common and can cover larger areas than you might initially for people to make instant judgments about others anticipate. Usually, if the patient retains two-thirds or based on how their eyes look. A shifty gaze, for more of normal iris tissue, surgical repair can produce example, may be interpreted as dishonest. If people a good functional and anatomic result. For cases in are uncomfortable looking into the eyes of a person which large amounts of iris tissue is absent, artificial with an abnormal iris, that can play an important role iris diaphragms, overlapping rings or sectoral implants in that individual’s interpersonal interactions and, may be a more appropriate option to augment the perhaps, affect his self-esteem. remaining native iris tissue. Iris Trauma 103 PRINCIPLES OF IRIS REPAIR minimizes iris traction. This technique allows the knot The basic principles of iris repair are fairly straight- to slide into the anterior chamber without pulling iris forward. First, instillation of a miotic agent such as tissue to the wound margin and without cumbersome pilocarpine, puts the iris stroma on maximal stretch, intracameral knot-tying maneuvers. Once the suture increasing the surface area. Intracameral manipulations has been passed, place a Kuglen hook through the should be performed under viscoelastic agents to initial paracentesis tract, engage the suture just beyond prevent chamber volatility, iris stretching and corneal the distal iris pass and draw a loop of suture out through endothelial damage. When choosing your viscoelastic the paracentesis site. Maintaining proper orientation agent, remember that you may be removing it of the sutures is of utmost importance in creating a manually through a small incision. Highly retentive knot. The orientation should be: agents may be difficult to remove without automated 1. Trailing suture strand; irrigation and aspiration, while retained bits of overly 2. Part of loop from distal iris pass and; viscous materials can cause a significant postoperative 3. Part of loop exiting peripheral cornea. intraocular pressure rise. The very soft and friable If the loop folds over and changes the relative consistency of the iris demands an atraumatic position of 2 and 3, a twist occurs instead of the technique. Often, posterior or peripheral anterior intended knot. Pass the trailing suture around the synechiae prevent proper mobilization of the iris middle arm of the loop twice. Then gently draw leaflets. Therefore, gentle blunt or sharp synechiolysis together the trailing strand and the exited strand on may be the first step in repair. When the sphincter the opposite side of the eye, pulling the two iris leaflets is involved in the injury or damage, reapposing the together and creating the first throw of a knot. Retrieve severed pupil margin establishes a central pupil and the suture loop a second time for a single locking throw creates a more taut iris diaphragm, facilitating further and trim the knot. steps. Because patients may develop glare symptoms Repair of Iridodialysis when the optic margin of an implant lens is exposed, Iridodialysis and iris repair share similar principles and the repaired iris leaflets should cover all IOL edges. some similar techniques, with a few caveats. Use a When an implant placement or exchange is performed double-armed suture. In a similar closed-chamber coincident with iris repair, a larger optic implant may approach, I engage the peripheral iris margin with the facilitate this task. first needle tip and pass the suture through the scleral wall at the level of the iris root. I pass the second needle Suture Placement through the same paracentesis and engage the Suture and needle choices are up to the surgeon’s peripheral iris root about one to two clock hours away. preference. With a long track record in the anterior The second needle is similarly passed out the sclera segment, the prolene suture appears resistant to and the suture is tightened and tied externally, drawing hydrolysis in the anterior chamber and, therefore, may the peripheral iris to the scleral wall. The knot is be a better choice than nylon. trimmed and rotated internally. The needle enters the anterior chamber via a conveniently placed paracentesis site. The paracentesis Iris Implants should be large enough to allow easy ingress of a When significant amounts of iris tissue are damaged Kuglen hook. Take special care to avoid catching any or missing, iris repair may be impossible. In these eyes, corneal fibers as the needle passes through the artificial iris implants can augment the iris diaphragm, paracentesis tract. The sharp-tipped needle passes thereby reducing photophobia and glare. A variety through the iris with a minimum of countertraction of artificial implant designs are available in Europe and and minimal iris tearing. The long, curved shape elsewhere, though currently none are Food and Drug permits passage of the needle in a closed-chamber Administration approved for use in the United States. fashion through a paracentesis. The proximal iris leaflet The currently manufactured iris implants come in five is engaged by the needle tip, then the distal iris leaflet. categories: The needle is then passed out through the peripheral 1. Large diameter, rigid iris diaphragms with or cornea. without a central optic (Morcher GMBH, Germany and Ophtec, The Netherlands). Suture Tying 2. Overlapping, interdigitating iris rings (Morcher). Tying the suture with the sliding knot technique 3. Capsular tension rings with opaque iris segments (introduced to ophthalmology by Steven Seipser, MD) (Morcher). 104 Clinical Diagnosis and Management of Ocular Trauma

Fig. 19.1: Sphincter tear Fig. 19.4: Iris and ciliary body prolapse

Fig. 19.2: Iridiodialysis with macerated iris Fig. 19.5: Iris prolapse

Fig. 19.3: Iridodialysis with traumatic cataract Fig. 19.6: Postcataract surgery withh CTR Iris Trauma 105

4. Intracapsular Hermeking iris prosthetic system 4. Brown SM. “A technique for repair of iridodialysis in implants (Ophtec). children.” J AAPOS. 1998;2(6):380-2. PMID 10532731. 5. Cassin B, Solomon S. Dictionary of Eye Terminology. 5. Custom iris implants with enclavation fixation Gainsville, Florida: Triad Publishing Company 1990. (Ophtec). 6. Cline D, Hofstetter HW, Griffin JR. Dictionary of Visual Science. 4th ed. Butterworth-Heinemann, Boston COMPLICATIONS 1997;ISBN0-7506-9895-0. 7. Cornea and External Diseases: Trauma: Traumatic Those with traumatic iridodialyses particularly by blunt Iridodialysis.” Digital Reference of Ophthalmology. trauma are at high risk for angle recession, thereby Accessed 2006. causing increased intraocular pressure (IOP). This is 8. Kiel J, Chen S. “Contusion injuries and their ocular typically seen about 100 days or three months after effects.” Clin Exp Optom. 2001 Jan;84(1):19-25. PMID the injury, and is thereby called 100 day Glaucoma. 12366340. 9. Ogawa GS. The iris circlage suture for permanent Medical or surgical treatment to control the IOP may mydriasis: a running suture technique. Ophthalmic Surg be required if glaucoma is present. Soft opaque contact Lasers 1998;29(12):1001-09. lenses may be used to improve cosmesis and reduce 10. Osher RH. Peripupillary membranectomy. Video J the perception of double vision. Cataract Refract Surg. 1991;Volume VII, Issue 4. 11. Osher RH. Surgical repair of the fixed, dilated pupil. Consultation Section. J Cat Refract Surg 1994;20(6): 665-66. Bibliography 12. Sullivan BR. “Glaucoma, Angle Recession”. eMedicine.com. August 16, 2006. Accessed October 11, 1. Arya SK, Malhotra S, Dhir SP, Sood S. “Ocular fireworks 2006. injuries. Clinical features and visual outcome.” Indian J 13. Viestenz A, Kuchle M. Eye contusions caused by a bottle Ophthalmol 2001;49(3):189-90. PMID 15887729. cap. A retrospective study based on the Erlangen Ocular 2. Beetham WP. “Cataract Extraction with Iridodialysis.” Contusion Register (EOCR) Ophthalmologe Trans Am Ophthalmol Soc 1941;39:104-15. PMID 2002;99(2):105-08. German. PMID 11871070. 16693243. 14. Walker NJ, Foster A, Apel AJ. “Traumatic expulsive 3. Behndig A. “Results with a modified method for scleral iridodialysis after small-incision sutureless cataract suturing of intraocular lenses.” Acta Ophthalmologica surgery.” J Cataract Refract Surg 2004;30(10):2223-24. Scandinavica 2002;80(1),16-18. PMID 15474840. CHAPTER

Post-traumatic Strabismus 20 B Shukla, P Bhasin (India)

Introduction

After ocular trauma strabismus is not a common finding. Shukla1 in a study of 1600 cases found cranial nerve involvement in 57 cases. Of these there were 12 cases of VII N. Palsy. If these are excluded the involvement of III, IV, VI N palsy would be in 45 cases (2.8%) (Figs 20.1 to 20.3). Many studies have shown the ocular cranial nerve involvement in head injuries. Thus Rucker2 found it in 13.9% cases and Rush3 in 19.7% cases. It is quite possible that there might be involvement of both as orbits and eye balls cannot be strictly excluded from head injury. Prakash4 and Menon5 have also reported the invol- vement of head trauma as a cause of cranial nerve Fig. 20.2: Immobile on dextro-version with dilated and fixed pupil palsies (III, IV, VI N). They have not mentioned as to how many cases of cranial nerve palsies were due to ocular trauma or whether ocular trauma was also a part of head injury. After head trauma they found the VI N to be commonly affected. Distribution of ocular cranial nerve involvement after ocular trauma was as follows (Table 20.1).

Fig. 20.3: VI nerve palsy after jeep accident

TABLE 20.1: Distribution of ocular cranial nerve involvement after ocular trauma Cranial N. Number Percent IIIrd N 29 64.45 IVth N 05 11.11 VIth N 11 24.44 Fig. 20.1: III N palsy with ptosis LE Total 45 100.00 Post-traumatic Strabismus 107 Thus the III cranial nerve was found to be most some help and rest to the movement of eye ball should commonly involved. For obvious reasons all cases of be given. post-traumatic strabismus are of paralytic nature. In most cases the squint appeared shortly after injury. However in flew cases it appeared late after develop- Entrapment of Muscle ment of contracture in the muscles. Hence the management in most cases in conservative up to This is the result of fracture of the orbital walls. It is 6-8 months. Surgery may be planned for residual commonly seen in blow out fractures where the floor squint after this period. of the orbit gives way and inferior rectus muscle gets Traumatic squint can result from: entrapped at the fracture site. If there is diploma in 1. Disintegration of extra-ocular muscles. the primary and down ward position surgical 2. Intramuscular edema or hemorrhage. intervention is indicated with release of muscle and 3. Entrapment of muscles in bony fractures. repair of floor of orbit by silastic plates. 4. Direct injury to the extra-ocular muscles or their nerve supply. The management will also differ according to the Direct Trauma pathology involved. This is usually do to blunt objects causing traumatic inflammation to the muscles and their nerve supply. Anti-inflammatory and steroids would be useful in such Traumatic Disinsertion cases. These injuries usually recover soon. This may be due to intra-orbital penetration of sharp During the recovery period it may be useful to objects like a knife or after some surgical procedures occlude one eye to prevent intractable diploma or like excision of pterygium or limbal dermoid removal. prescribe prismatic glasses to minimize it. Alternate The muscles may be partially or totally disinserted from occlusion should be done to prevent amblyopia. On its attachment on the globe. This can be diagnosed the whole prognosis is good in these cases and surgery by forced duction test (FDT), ultrasound, EMG or CT is rarely required. scan. The disinserted muscle should be re-attached to its original insertion. References 1. Shukla B., Epidemiology of Ocular Trauma, Ist Ed., Jaypee Intramuscular Hemorrhage Brothers Medical Publishers, New Delhi 2002;82. This is usually caused by a blunt object to the orbit 2. Recker C.W., Amer J. Ophthal 1996;61:1293-98. 3. Rush JA, Young B.R., Arch. Ophthal 1981;99:76. or to the muscle. The muscle gets swollen due to blood 4. Prakash P, Reddy S.K. Ind. J. of Orthopt and Pleoptics and is unable to contract or relax properly. The 1979;15:1. treatment in conservative by anti-inflammatory and 5. Menon V., Singh J., Prakash P., Ind. J. Ophthal 1983;32: anti-hemorrhagic drugs. Cold compression may be of 447-53. CHAPTER

Management of Orbital Trauma and Fractures 21 Rania Abdel Salam, Essam El Toukhy (Egypt)

Orbital Injuries and the orbital plate of the frontal bone. Trauma to this wall is frequently associated with orbital hemor- Orbital injuries may be part of panfacial trauma that rhage, epistaxis and surgical emphysema. range from mild even nonsignificant to severe and debilitating, however, such injuries are of secondary importance to securing airway, stabilizing the circulation and protecting the cervical spine. Trauma to the orbit can involve the globe, eyelid, sinuses and the brain. The nature and severity of the injury depend on the mechanism of trauma. After securing the lifesaving measures, a team approach incorporating a plastic surgeon, otolaryngo- logist, a neurosurgeon in addition to the ophthalmolo- gist is needed for the facial trauma patient’s evaluation. A systematic ocular and orbital examination is necessary to delineate any subtle injuries as delay in the diagnosis of orbital and ocular problems may worsen the prognosis.

ANATOMIC CONSIDERATIONS The orbit is a four-sided conical structure with its base directed forwards and apex projecting medially towards Fig. 21.1: Bones forming the medial wall the optic foramen. The base or the orbital rim is outlined by thick strong bone: the supraorbital arch The roof is composed mainly of the orbital plate of the frontal bone above, the zygoma and maxilla of the frontal bone and posteriorly the lesser wing of inferiorly, the zygoma laterally and the frontal process sphenoid separating the orbit from the frontal lobes of the maxilla medially. The walls of the orbit consist of the brain. It is thinnest anteriorly where it is related of relatively thin bone. The orbital volume is about to the frontal sinus. 30 ml and the orbital depth is approximately 4.5 cm. The orbital floor is composed of the orbital plates Consequently, slight change in the bony anatomy will of the maxilla and zygomatic bones with a small be reflected on soft tissue and globe position. contribution from the palatine bone posteriorly. The The medial wall is formed of the frontal process posterior limit of the floor is defined by the inferior of the maxilla and the lacrimal bone forming the orbital fissure and a small vertical component of the lacrimal fossa behind which is the extremely thin, less palatine bone posteromedially. Near the apex the than 0.5 mm, lamina paparycea of the ethmoids and inferior orbital fissure transmits venous channels as well finally the lesser wing of the sphenoid and the optic as the infraorbital and zygomatic nerves. Contained foramen (Fig. 21.1). Being exceptionally thin and entirely in the maxilla, the infraorbital groove posteriorly fragile, medial wall fractures are usually subtle and becomes the infraorbital canal as it gains a roof accompany many orbital injuries. The medial wall (Fig. 21.2). It opens 4 mm below the orbital rim as transmits the anterior and posterior ethmoidal arteries the infraorbital foramen that transmits the infraorbital and nerves at the junction between the ethmoidal bone nerve and vessels. The floor is also thin, 0.5 to 1.0 mm Management of Orbital Trauma and Fractures 109 Pupil diameter and responses to light as well as swinging flash light test should be also documented. Presence of afferent papillary defect denotes optic nerve injury, however if both optic nerves are equally damaged, this sign may be absent. The lid, adnexa, conjunctiva, cornea, anterior chamber, iris and lens should be examined with magnification either by slit lamp or a magnifying loupe for lacerations, tissue loss, hemor- rhage, opened globe injuries, presence of foreign bodies or lens displacement. When ocular rupture is suspected, globe exploration should take place before any fracture repair. The retina and optic nerve should be examined on both sides using the ophthalmoscope looking for Fig. 21.2: Orbital floor retinal edema or hemorrhages as well as optic nerve pallor or edema. The caliber of the retinal vessels thus it easily fractures especially medial to the comparing arteries to veins is also evaluated. Engorged infraorbital canal. non-pulsatile veins may signify increased orbital The lateral wall is thick formed of the frontal process pressure, similarly central retinal artery pulsations of the zygomatic bone and the frontal bone anteriorly denotes increased ocular or orbital pressure. B scan and the greater wing of sphenoid posteriorly. It ultrasound can be performed if media opacity transmits the zygomatic nerve and artery which often precludes the visualization of the retina. splits into the zygomaticotemporal and zygomaticofacial The position of the globe on the affected side in branches before entering the bone. comparison to contralateral one should be noted and measured, if possible, by the exophalmometer. The eye positions should be evaluated from the vertex EVALUATION OF ACUTE ORBITAL AND prospective; however, significant lid edema may cause PERIORBITAL INJURIES bias. Vertical globe displacement can be estimated by Initial evaluation starts with complete history to putting a ruler across the medial canthi and noting determine the circumstances of the present injuries. the point at which it crosses the globe at each side. Low velocity impact such as a human punch usually A depressed orbital floor fracture leads to globe ptosis. produces injury limited to the region of impact. High Enophthalmos occurs with increased orbital volume velocity injury such as motor vehicle accidents is often such as in wall fractures. While proptosis occurs due associated with soft tissues and skeletal injuries that to increased soft tissue contents such as hemorrhage and/or reduction of orbital volume associated with are more extensive and may be remote from the inward displacement of one or more of its walls. If impact. With projectile injuries such as with shattered the condition is associated with reduced vision or glass or missiles, intraocular, subcutaneous and orbital afferent papillary defect, computed tomography (CT) foreign bodies should be ruled out. examination is immediately done and intervention It is better to remove blood and debris as well as should not be delayed. Presence of pulsatile proptosis any superficial foreign bodies to do a careful and precise suggests abnormal vascular communications or examination of the injured area as well as the sur- transmission of dural pulsations through a fractured rounding areas. Blunt low velocity trauma usually cause displaced orbital roof. edema and contusions and the extent of the facial In a conscious cooperative patient with minimal lid fractures is often more than in cases associated with edema eye movements all directions of gaze should extensive lacerations as the energy of the impacting be examined. The patient is asked to report any force in the former is dissipated by the skeleton rather diplopia at any direction of gaze. Gaze restriction can than soft tissue. Palpation of the orbital rims, malar be caused by nerve injury, soft tissue swelling, direct eminences, zygomatic arches and nose may show muscle injury or entrapped muscle within a skeletal fractures and surgical emphysema. fracture. Forced duction and diplopia fields are A complete ophthalmic examination is a must to performed when indicated. rule out globe injuries and present medicolegal Hyposthesia in areas around the orbit should be problems. If the patient is conscious, the visual acuity looked for especially in the cheek which is supplied and field by confrontation should be documented. by the commonly injured infraorbital nerve. Upper 110 Clinical Diagnosis and Management of Ocular Trauma lid position should be noted and documented as ptosis anterior to the orbital septum due to direct tissue injury. may occur as a result of nerve injury, levator aponeu- These tissues afford extensive hemorrhage that may rosis laceration or dehiscence or later from fibrosis. extend to the lid margin and even cross the nasal bridge Soft tissue landmarks of the orbit such as canthal to the uninvolved eyelid. angles may be displaced by fractures of the underlying Mild to moderate orbital hemorrhage commonly bone. For example, increased intercanthal distance accompany orbital trauma. Both conditions can cause suggests nasoethmoidal fractures involving the variable degrees of proptosis, globe displacement and reflected part of the medial canthal tendon while motility disturbance. If severe, they may cause inferiorly placed lateral canthus suggests inferior increased intraocular pressure, central retinal artery dislocation of the zygoma. If the medial wall is involved, occlusion, marked proptosis with corneal exposure as the lacrimal drainage system should be evaluated. well as compressive optic neuropathy leading to vision loss. Radiological Evaluation Blood may also accumulate in the subperiosteal space. The extent of the blood is limited by bone suture Radiological studies especially computed tomography lines where periorbita becomes firmly adherent. If the (CT) play an indispensable role in evaluating the orbital periotrbita is intact, the patient may present with mild trauma and detecting radio-opaque foreign bodies. proptosis and globe displacement. If the periorbita is Both axial and coronal CT sequences are required. disrupted the hemorrhage becomes extensive and Coronal images in 2 mm sections delineate the moves towards the orbital septum and bulbar orbital floor, roof, medial and lateral walls, the naso- conjunctiva. ethmoid region, the orbital rim and the face If there is mild proptosis with normal or minimally surrounding the orbit. It helps delineate the size, shape elevated intraocular pressure with no visual compro- and location of fractures and associated soft tissue mise, follow up can be safe and the hemorrhage will injuries. gradually resolve over 1 to 3 weeks usually without Axial scans permit evaluation of the lacrimal sequalae. drainage pathways, nasal and paranasal sinuses, medial In sudden and extreme orbital hemorrhage threa- and lateral walls of the orbit, superior and inferior tening vision, lateral canthotomy and cantholysis of orbital rims, zygomatic arch, pterygoid plates, the superior or inferior crura should be performed. tempromandibular joint, base of the skull, superior If this is not effective, the hematoma should be drained orbital fissures and optic canal. It allows to show globe either through lid crease incision if placed superiorly placement in comparison to the unaffected side. or though lower lid blepharoplasty incision if inferiorly The combination of axial and coronal scans can placed. In either condition, the orbital septum must give most of the needed information in trauma cases. be opened to allow the egress of the blood from the Three dimensional scans are helpful in obtaining a more socket. The stab incisions and canthal tissue could be accurate evaluation and understanding of the situation, repaired when swelling decreases. hence help in deciding the best line for treatment. They are generated from the reformatting 1.5 mm slices on Surgical Emphysema conventional CT scan using a special software computer program. They are very helpful in old trauma cases This means accumulation of air in the subcutaneous as they show the deformity, the site, size and tissue (Fig. 21.3). This is a common finding in medial appearance of bony defects as well as bone fractures. wall and floor fractures as they involve walls of the paranasal sinuses. The condition usually increases when Problems associated with orbital trauma: the patient blows his nose and there is a crepitus felt • Orbital hemorrhages and emphysema on palpation. Reassurance of the patient and • Traumatic optic neuropathy instruction not to forcibly blow his nose are usually • Orbital fractures enough till the symptoms are relieved provided there • Septic cavernous sinus thrombosis are no associated orbital or ocular problems detected. • Carotid cavernous fistula • Orbital foreign bodies Traumatic Optic Neuropathy Optic neuropathy may accompany orbital and head PROBLEMS ASSOCIATED WITH injuries.This is diagnosed by presence of decreased ORBITAL TRAUMA vision, afferent papillary defect with otherwise normal Orbital Hemorrhages eye in a patient with trauma history. The cause of this Bleeding is frequently associated with periorbital trauma problem is multifactorial including direct or indirect and fractures. Blood may be found in the eyelid mechanisms. Management of Orbital Trauma and Fractures 111 Indirect optic neuropathy is diagnosed when there are no radiologic findings of abnormalities damaging the nerve. It may be caused by abrupt brain deceleration with forwards movement causing compression of the intracranial optic nerve. It can also be due to contusion and edema resulting from deformation of the optic canal. The small arterioles in the intracanalicular optic nerve my rupture leading to infarction or hematoma of the optic nerve or sheath. Edema and vasospasm are thought to cause nerve ischemia. Patients may suffer from sudden complete loss of vision after trauma which is usually caused by actual tear or primary complete optic nerve necrosis. These patients have poor prognosis in spite of treatment. Other patients experience delayed visual loss (hours to days) or partial visual loss usually due to partial ischemic infarction or compression by edema or hemorrhage however, these patients have better prognosis. Treatment remains controversial. High-dose corticosteroids are used in treating indirect optic neuropathy. Extracranial transethmoidal optic canal decompression is an alternative treatment especially if the vision drops while on steroid treatment. Direct optic neuropathies attributable to mechanical nerve Fig. 21.3: Fracture in the medial wall associated with surgical emphysema and air could be seen within the orbital cavity compression usually require surgical treatment and removal of the offending factor such as repair of floor fracture, intracranial optic canal decompression, hema- Direct optic neuropathy results from compression along toma drainage and optic nerve sheath fenestration. the course of the optic nerve by bone fragments (Fig. 21.4), retrobulbar or subperiosteal hematoma, CAROTID CAVERNOUS FISTULA and foreign body or by fractures that narrow the optic It results from shearing of intracavernous carotid artery canal. Rarely, the optic nerve may be avulsed. When during deceleration injuries, or direct artery injury by clinically suspected, CT evaluation of the orbit, optic foreign body or bone shrapnel. They develop shortly canal and sinuses can identify the cause. after trauma but the onset of symptoms may be delayed. They present with progressive proptosis usually pulsatile with subjective and objective bruit. IOP is usually elevated with engorged retinal veins. Brain CT scans with contrast confirm the diagnosis. The fistula can be closed using endovascular occlusion with coils which is the preferred technique.

Septic Cavernous Sinus Thrombosis Fracture of the posterior ethmoidal or sphenoidal sinuses may allow concomitants with the paranasal sinuses to reach the cavernous sinuses. They usually have a rapid presentation and associated with low grade fever, headache, orbital pain or diplopia. This is followed by progressive proptosis, mydriasis, ophthalmolplegia due to nerve palsy and eventually Fig. 21.4: A case of a 7-year-old child with trauma to the visual loss due to compressive optic neuropathy. If not sinuses and fracture of the ethmoid and sphenoidal bones. treated, septic thrombosis may spread to the cerebral There is a bony fragment that is pressing the optic nerve veins leading to increased intracranial tension. 112 Clinical Diagnosis and Management of Ocular Trauma MRI may show a mass caused by thrombus in the disturbance to the eye and orbit. Copper is poorly sinus compressing the intracavernous part of the tolerated and can induce purulent inflammation. Glass, internal carotid. Cerebral arteiography and venography stone, plastic, and bullets are often well-tolerated and may be used however MRA presents a good need no intervention unless they migrate to the surface alternative. Early diagnosis is of extreme importance and become extruded or palpable so that they can as it improves the prognosis. Systemic antibiotics are be easily removed. Organic foreign bodies are poorly the main line of treatment. Anticoagulant treatment tolerated and are usually associated with chronic is used to prevent progressive thrombosis if not inflammatory reaction and abscess formation. controlled by antibiotics within 48-72 hours; however, CT is necessary to detect and localize the foreign they should not be used if a fungal etiology is suspected body (Fig. 21.5). It can estimate its size and the extent due to increased risk of mycotic aneurysm formation. of damage to the surrounding structures. The combination of axial and coronal scans can give three Orbital Foreign Bodies dimensional localization of the foreign body. CT resolution of metal foreign bodies is approximately A high index of suspicion may lead to discovery of 0.05 mm; of wood, 2.0 mm and of glass 0.75 to intraorbital foreign bodies. The patient usually reports 2.0 mm according to the lead content. One millimeter a history of trauma to the face with a foreign body sections in the scan are recommended to detect orbital entering the eye or the orbit. In case of loss of foreign bodies. Absence of foreign body in the scan consciousness, or psychiatric illness, the patient may does not totally exclude its presence especially with fail to give a helpful history. Foreign bodies may be the suggestive history and presence of symptoms. found without any antecedent history of trauma where Although MRI has no established role in foreign the initial injury is thought to be insignificant and usually body detection, it should be remembered to avoid forgotten. Such patients may remain asymptomatic its use in cases of suspected metallic foreign bodies for long periods of time until the foreign body provokes as they may be drawn out of their location with injury a reaction, forms an abscess or begins to extrude. to the globe or adjacent orbital structures. Some foreign bodies may inflict immediate, Most of inert foreign bodies do not require inter- sometimes irreversible, damage to the globe, extra- vention, and the surgical removal decision should be ocular muscles, orbital bone, optic nerve as well as consider the risk benefit. If the foreign body is to be cranial nerves. Infection and inflammation can result removed, the surgical approach is planned according secondary to contaminated foreign body entering the to the site of the foreign body. The entrance wound globe or penetrating an adjacent sinus. The latter can should be explored in a manner that won’t cause present with associated surgical subcutaneous damage to orbital tissue. In case that such wound is emphysema. The long term effects of the foreign body not present or healed, anterior, medial or lateral can be due to chronic inflammation, migration and orbitotomy can be used. If the foreign body is located scar tissue formation. Chronic inflammation causes foreign body granuloma that can be of significant size causing mechanical effects with globe displacement and limitation of its motility. The latter can also result form extraocular muscle fibrosis or soft tissue scarring. A fistula to the skin or conjunctiva may be formed with pus drainage or extrusion of the foreign body. The anatomic structure of the orbit allows large pieces of metal or organic material to be imbedded without significant signs or symptoms unless one of the orbital contents is involved. The location of the foreign body within the orbit influences the presenting picture as well as the management decision. Large objects usually tend to enter the inner canthus injuring the caruncle or the lacrimal drainage system and may become deeply buried within the orbit and in some cases tend to displace the globe. The nature of the foreign body contributes to the severity of the response and considerably affects the decision of foreign body removal. Most metals are inert Fig. 21.5: Axial CT scan showing an intra-orbital and in the absence of infection, they cause no metallic foreign body near the lateral orbital margin Management of Orbital Trauma and Fractures 113 at the orbital apex, a neurosurgical anterior craniotomy approach is required. If the foreign body is thought to be metallic, a surgical magnet can be used. Metal foreign body localizers can be used intraoperatively to confirm the radiographic information about the location of the foreign body. Organic foreign bodies foreign bodies must be removed with great care as they usually fragment. This is followed by irrigation to remove the pus and small fragments. Pus is sent for culture and sensitivity for bacteria and fungi and appropriate treatment is given. Complications associated with such procedure may be due to the surgery or the foreign body itself. The surgeon may fail to localize the foreign body, the foreign body may become fragmented or it may cause adjacent tissue damage, e.g. blood vessels, nerves and muscles leading to hemorrhage, diplopia or loss of vision.

Orbital Fracture Orbital fractures can be generally divided to blow out fractures and fractures that involve the orbital rim.

ORBITAL FLOOR AND BLOW OUT FRACTURES Figs 21.6A and B: A. Shows a blunt trauma to the anterior Blow out fractures are the most common periorbital orbit. B. Shows that the contents are compressed with increases intraorbital pressure so that the floor gives way fracture seen in ophthalmic plastic surgical practice. A blow out fracture by definition does not involve the inferior orbital rim. On the contrary, a floor fracture should involve the orbital rim. However, the findings separate at the groove, close spontaneously entrapping and treatments are similar. muscles and soft tissue and they are very common in children, hinged fracture along the inferior border PATHOGENESIS of the ethmoid entering the maxillary sinus, Two theories exist to explain the origin of orbital floor comminuted or combination of all of the above. Non- blow out fractures. The hydraulic theory by Smith and displaced and trap door type are more associated with Regan postulated that when a blunt object (usually diplopia while enophthalmos is more associated with spherical and larger than the orbital base) hits the orbit, hinged and comminuted types. the globe and soft tissues are retropulsed suddenly increasing the intraorbital pressure. To relieve this Clinical Presentation pressure, the orbital floor “blows out” into the maxillary Diagnosis of such fracture depends on suggestible sinus usually medial to the infraorbital canal where history, periorbital ecchymosis and emphysema. the bone is thinnest (Figs 21.6A and B). Sometime Palpation of the inferior orbital rim may reveal a step the medial wall gives way due to its fragility. This is considered a safety mechanism for the globe. off deformity, discontinuity or point tenderness. If the Fujino proposed a buckling force theory. When a infraorbital canal is involved in the fracture, anesthesia blow strikes the inferior orbital rim, the rim is displaced may involve the ipsilateral cheek, upper lip, gums and posteriorly and the force is transmitted to the thin nose. orbital floor that buckles and fractures into the maxillary Enophthalmos can be due to orbital expansion due sinus, then the inferior rim returns back to its normal to inferior displacement of the orbital floor. This could position intact. In general, variable degrees of both be accentuated by soft tissue herniation into the mechanisms are supposed to be present in a given maxillary sinus mainly the periorbita, fat and patient with a blow out fracture. connective tissue, damage to the Lockwood suspensory The fracture may be linear just parallel and medial ligament as well as collapse of the fine fibrous septa to the inferior orbital groove, trap door that transiently that support the orbital fat and muscles. Globe ptosis 114 Clinical Diagnosis and Management of Ocular Trauma is uncommon even with large floor fractures however, it can results from significant diminution of Lockwood’s ligament support. Immediately after injury, enophthalmos can be masked by orbital hemorrhage and edema posterior and inferior to the globe. If enophthalmos is severe, a prominent superior sulcus deformity can be present. Diplopia is a frequent finding in blow out fractures. This was attributed to inferior rectus or inferior oblique muscle entrapment in the fracture. Yet it was found that actual muscle entrapment is rare. Orbital fat entrapment is commoner and the fibrous septa that connect the fat and the periostium with the inferior rectus and oblique muscles tighten due to edema or intraorbital hemorrhage thus restricting ocular motility and felt as restriction on forced duction test. With time, these septa may stretch and relax improving the ocular motility and diplopia. The patient usually suffers from vertical diplopia. The patient may have limited supraduction, infraduc- tion or both. If the inferior rectus restriction is anterior to the equator, hypotropia results while if it is posterior to it, hypertropia results. Injuries to the extraocular muscle or the motor nerves are additional causes for diplopia. Direct contu- sion or laceration of the muscle can be worsened by muscle hematoma. While the motor nerves can be damaged by hemorrhage within their sheath, stretched by orbital edema or hemorrhage or suffer from concussion. Radiologic studies are helpful in establishing the diagnosis. Waters plain X-ray views provide an excellent view of the orbital floor, showing any bone disruption Figs 21.7A and B: A. Shows coronal CT scan with fracture floor and the tear drop appearance. There is a fluid level or herniation. Orbit CT especially the coronal cuts in the maxilla. B. Shows a fractured mid floor with tissue delineates the fracture and the bone soft tissue herniation relationship (Figs 21.7 and 21.8). However, the mere radiologic presence of a fracture is not an indication for surgical repair.

Management Repair of the orbital floor fractures is mainly indicated in restricted ocular motility showing no improvement, diplopia especially within the central 30º field, enoph- thalmos of ≥ 3 mm or progressive, defects of more than 50% of the orbital floor that are almost always likely to cause enophthalmos as well as incarcerated muscle causing oculocardiac reflex on ocular motility and rare cases of globe ptosis.

Timing No universally agreed guidelines exist for the repair of blow out fracture. If in doubt, the patient should be evaluated every 2-3 days during the first 2 weeks, diplopia fields and forced ductions are followed carefully Fig. 21.8: A combined floor and medial wall fracture Management of Orbital Trauma and Fractures 115 for any change. During this time, hemorrhage and It is better to be avoided in patients with chronic edema will resolve during the first week allowing more sinusitis due to the reported incidence of accurate assessment. As long as motility improves, the systemic toxicity and late infection. patient should be followed up. On the other hand, d. Microplates: They are used of there is no if surgery is to be done, the best time is not beyond enough bone to support the implant. They are 2 weeks. After this, adhesions between bone fragments, made of titanium alloy. There are less corrosive sinus mucosa and the orbital tissues render the repair than steel and produce less scatter on CT quite difficult. studies. They are not magnetic and can be safely imaged by MRI. They are used to reform the Procedure orbital rim, medial and lateral canthal angles as well as walls. The alloplastic implants are Surgical repair of blow out fractures comprises good placed over them to augment the orbital exposure through incision, periosteal dissection and volume. exposure of the fracture, release of the entrapped e. Porous polyethylene implants with embedded tissues as placement of an implant to prevent adhesions titanium provide a new alternative to alloplastic between the orbital tissues and nasal mucosa. The implant materials for orbital reconstruction with surgeon can proceed from an orbital (subciliary or a profile that combines several advantages of fornix) approach or an antral (Caldwell- Luc) porous polyethylene and titanium implants. approach. The orbital approach is preferred as it is f. Others like Supramid and Teflon safer and more effective. In selected cases with large g. Experimental work was done on bone floor defects or with tenaciously herniated orbital morphogenetic protein (BMP) implant with and contents, a combined orbital and antral approach can without platelet-rich plasma (PRP), which is be used. supposed to promote fracture consolidation in the orbit fracture treatment with scarce Implants inflammatory reaction, and may be a good Many materials are available for repair of orbital wall alternative in orbit fracture reconstruction. fractures. They include: Radiological studies suggested intramem- A. Autogenous bone branous and progressive cavitation and Cancellous bone grafts cannot be used due to high ossification without a reduction in implant size absorption rate, 60-80% of the volume may be lost. and with signs of calcium deposition; these Split thickness calvarial or membranous bones such events were confirmed by histological analysis. as ribs, iliac crest or the cranium have less absorption rate; 15-30%. This material needs a second surgical Surgical Procedures site with incidence of morbidity such as hematoma, All are done under general anesthesia and forced infection. Harvesting them needs proper and formal duction test is performed initially to confirm the degree training. The graft is usually placed with the cortical of tissue entrapment. side towards the recipient bone and it may need to Incision: Variable incisions can be used to expose the be secured by micro or miniplates. inferior orbital rim as well as inferior part of the medial B. Alloplastic material wall. a. Porous polyethylene: It is porous integrated a. Subciliary approach: It is similar to that used in biocompatible implant with average pore size lower lid transcutaneous blepharoplasty. The lid is 200-240 microns. It is easy to mold manually infiltrated with 1% lidocaine with 1:100:000 or the help of heat yet it is structurally stable. epinephrine and a horizontal incision 2 mm below b. Silicone: A non porous material that is easy to the lid margin is made. It should not extend too fashion, inert, safe and effective with low rate far laterally to avoid compromise of lymphatic of migration, infection and extrusion. It is pre- drainage. A skin muscle flap is created and retracted ferred in cases of orbital volume augmentation. inferiorly using Desmarres retractor. This approach c. Methyl methacrylate polymer (cranioplastic): It is more associated with postoperative lower lid is mixed with copolymer to form a mixture that malpositions namely ectropion. have a doughy consistency and can be placed b. Lower transconjunctival approach: The inferior to augment orbital volume. This material fornix is incised 4 mm below the lower edge of remains malleable for 3-5 minutes so that it can the tarsus. Lateral canthotomy and inferior be shaped. If it hardens before molding is com- cantholysis can be done to widen the exposed field. plete, a pneumatic drill is used to fashion it. The conjunctiva, Müller‘s muscle and the 116 Clinical Diagnosis and Management of Ocular Trauma capsulopaplepbral fascia are severed and the plane pupil and noting the optic nerve perfusion by the between the orbicularis and the capsulopaplpebral ophthalmoscope. head is reached. Tissues are dissected till the inferior Forced duction should be repeated to ensure that orbital rim is reached. A 4-0 silk tractional suture no more incarcerated tissues are present. Any bone is passed through conjunctiva and lower lid fragments or blood should be aspirated from the retractors. This approach is preferred as it is simple, maxillary antrum before the defect is covered. provides excellent exposure with no visible scar and A sterile alloplastic material is fashioned to cover it has minimal risk for postoperative lid malpositions. the defect completely and overlapping the surrounding However, there is a rare risk of entropion due to intact bone by 3-4 mm circumferentially. This sheet scarred posterior lamina. should not be too large or too thick. The edges are c. Antral (Caldwell-Luc) approach: An incision is made smoothened to avoid trauma to adjacent structures in the gingival margin of the canine fossa. Periostium or erosion through the covering periostium. The is elevated and separated from the anterior surface alloplastic material should be soaked in antibiotic of the exposed maxilla. A periosteal elevator is used before it is inserted. The thickness of the plate usually to create an osteotomy opening into the maxillary range from 0.4-0.6 mm. Thicker implants are indicated sinus. Bone fragments and blood are then in cases of significant enophthalmos and evacuated from the sinus. In conjunction with orbital hypophthalmos yet they have the risk of limiting approach, the herniated tissues are gently reposited extraocular muscles. The more posterior the implant superior to the orbital floor. The maxillary sinus is placed, the more it reduces enophthalmos. The more may then be packed with either petroleum gauze anterior it is, the more it reduced hypophthalmos. The imbricated with antibiotic or a catheter balloon. choice of the material depend on the nature of the The other end of the gauze or catheter is brought fracture as well as the surgeon preference and training, out through an antrostomy to facilitate its removal. When the defect is large or multiple walls are This approach has limited visualization, poor access involved, plates and screws are preferred; bone grafts for placement and securing the floor implant, poor may be a good choice in experienced hands. Titanium hemostasis, higher infection rate, lack of permanent mesh may be used if the residual bone is not enough globe support and hazards of forcing bony fragments to support an implant. It is not enough by itself and into the globe and optic nerve. That is why this it usually needs to be covered by bone or alloplastic approach is seldom used for fracture floor repair unless material. there is complete absence of orbital floor. The implant can be fixated by either placing it Exposure of the orbital floor behind the orbital rim and the mere periosteal closure Dissection is carried out till the inferior orbital rim using will keep it in place or two small fixation holes are blunt and sharp dissection keeping the orbital septum drilled in the infraorbital rim just anterior to the defect intact to avoid fat herniation. Then the periostium is as well as the anterior edge of the implant. Then the opened 1.5 mm below the orbital rim and elevated implant is secured to the orbital floor anteriorly by from the orbital floor. With the help of periosteal Supramid 2-0 sutures. elevator, the periostium is separated from the floor Forced duction test is repeated. Coexistent medial posteriorly; the fracture is localized and exposed, first wall fracture can be repaired at the same time. the lateral border then the medial and posterior limits. Hemostasis is secured and the periostium is closed over The infraorbital bundle should be identified. Any the implant. Lateral canthus is repaired in case of unattached bone fragments should be removed. cantholysis and canthotomy. The opened layers are Incarcerated tissues are freed from the fracture using then closed anatomically. hand on hand maneuver with the periosteal elevator Eye patch is better avoided and the patient should and the metal suction tip or malleable retractors. This be watched for bleeding, pupillary reaction and visual is easy in cases of recent fractures yet if the tissues are acuity postoperatively. Systemic antibiotics, anti- swollen, the extraction becomes difficult and the bone inflammatory drugs as well as cold foments are proven can be depressed into the maxillary antrum. In case useful. of hinged fractures or in some selected cases, the fracture may be enlarged to achieve atraumatic release. Complications Care should be taken to avoid undue bleeding and Diplopia may persist or worsen after the surgery. This trauma to the nearby optic nerve. can occur due to fibrosis of the muscle, orbital fat or Optic nerve should be checked every now and then connective tissue septa either present prior to surgery by detecting the pupillary light reaction or dilating the or secondary to inflammation induced by the surgery. Management of Orbital Trauma and Fractures 117 It can be due to unidentified nerve injury before NASO-ORBITAL AND MEDIAL ORBITAL WALL surgery. Diplopia may worsen due to improperly placed FRACTURES implant or residual tissue entrapment. A muscle These fractures result from a force delivered to the procedure is better deferred 6-12 months after surgery nasal bridge or medial orbital rim. These are the during which the diplopia may improve or the patient weakest in the midface bones and usually injured by can wear prisms. If a surgery is to be done it is better the dashboard in cases of automobile accidents. They to be with adjustable sutures. are commonly associated with fracture floor and Overcorrection may occur due to thick implant augmented by postoperative edema that usually contribute to the presenting enophthalmos. resolves after a month. On the other hand, residual In mild cases, the injury is limited to the nasal bone enophthalmos may be present due to inadequate and the frontal process of the maxilla. In more severe restoration of orbital volume, bone graft absorption, cases, the lacrimal and ethmoid bones (Fig. 21.9) migrating implant or orbital fat atrophy. It can be mild may crack and splay laterally causing traumatic requiring no further intervention. In some cases, telecanthus, flattening and widening of the midface, minimal ipsilateral upper lid elevation using Fasenella rounding of the medial canthus, epistaxis, periorbital Servat procedure or contralateral upper lid blepharo- ecchymosis, subcutaneous emphysema (if the ethmoid plasty to deepen the superior sulcus can be enough is fractured), with bony nasolacrimal duct injury to camouflage the appearance. In more extensive causing epiphora. The medial rectus is rarely entrapped cases, the implant may be exchanged for a thicker in the fracture with less common horizontal gaze one. limitation. The orbital implant may become infected. It may CSF rhinorrhea suggests a cribriform plate fracture. be oversized and extruding. In both conditions the Most of cases are managed conservatively. The patient implant should be removed and replaced with a proper is treated by bed rest, intravenous antibiotics and sized one. If fibrous tissue sufficient to cover the defect instructed not to blow the nose or smoke. If the condi- has formed since the original surgery, the implant may tion persists, neurosurgical interference is required. not require any replacement. Chronic lid swelling with Hemorrhage may be severe if the anterior and or superior globe displacement may indicate the presence posterior ethmoidal arteries are injured. The bleeding of a fluid filled cyst formed around the implant. The implant should be removed and the cyst excised. usually stops promptly. However, nasal packing or Ectropion, lower lid retraction or chronic edema direct ligation may be required. Any coexistent upper may result when the skin approach is used. Retraction airway obstruction should be relieved. can occur due to adhesions between the orbital septum If the fracture extends to the lacrimal bone and and the inferior orbital rim. This can be corrected by ethmoid, traumatic telecanthus may result (Figs recessing the lower lid retractors. 21.10A and B). This usually requires repositioning Persistent infraorbital nerve anesthesia may occur. of the bony fragments and transnasal wiring combined It may be injured or just compressed by the implant. with canthal Y-V plasty. If there is enough bone support If the nerve is not cut, function usually returns within Y miniplate is inserted and used for the telecanthus 1 year. Sometimes the implant can be exchanged with repair. widening the foramen decompressing the nerve. In some cases, the patient may get tolerant to the numbness in this area. Blindness may occur in 1 : 1500 cases. It can be secondary to compression of the optic nerve by the implant, orbital edema or hemorrhage. This can be prevented by avoiding undue pressure on the globe during surgery, continuous optic nerve monitoring, screening patients for clotting abnormalities preoperatively, using intra and postoperative steroids, complete hemostasis before wound closure, avoiding compressive ocular dressing postoperatively and continuous monitoring of the pupil and visual acuity. It should be remembered that the optic nerve may be damaged from the original injury with delayed visual loss from edema and vascular occlusion and may appear coincidently with surgery and mistakenly blamed on the surgical procedure. Fig. 21.9: Medial wall fracture 118 Clinical Diagnosis and Management of Ocular Trauma A Wright needle or 16 gauge trocar is passed from the surgically drilled opening (normal side) through the nasal septum, emerging at the fracture site. Some pressure is needed to penetrate the septum. Care should be taken to prevent momentum from carrying the needle immediately through the fracture site with the possibility of globe injury which lie in close proximity to the medial wall. Malleable retractors are placed to protect the globe. The supramid or wire suture are placed within the eyelet of the Wright needle or within the trocar after removing the stylet and this material becomes properly positioned as the needle/torcar is withdrawn. The two ends are tightened around 8 mm metal bloster pin on the sound side and the traumatized canthus is quantitatively drawn medially as the Supramid or wire is secured. The deeper layers are closed with 5-0 Vicryl mattress suture, followed by skin closure with running 7-0 silk suture.If nasal pads are to be placed, this should be done before the trocar is removed. A second loop of Figs 21.10A and B: Cases of traumatic telecanthus. There wire is passed through the trocar after the transnasal is flattening of the nose, scar at the site of fracture. The case on the left side was associated with severe ptosis while wiring is completed but before the skin closure, the both suffered from nasolacrimal duct obstruction loop is cut leaving two free skin wires. The end of each is passed through one of two silicone pads. The wires from each side are twisted together over a dental roll If dacryostenosis is present, dacryocystorhinostomy to compress the skin in the canthal region. The nose may be required. Nasal bone fractures should be pads and the skin sutures are left in place for 7-10 repaired by otolaryngeologist or plastic surgery. If days, then the skin wires and pads are removed. associated with fracture floor, the floor should be B. Bilateral naso-orbital fractures: repaired first with the implant the usually forms a If bilateral naso-orbital fractures, the bone may be platform for the medial wall implant insufficient on either side to support the reconstruction. Transnasal Wiring: Surgical Technique In this condition, standard transnasal wiring technique takes place where two medial canthal incisions are A. If the contralateral nasal bone is intact: made; bone penetration should be done at the Under general anethesia, a vertical incision is made posterior lacrimal crest level leaving intact bone anterior nasal to the medial canthus. This may take a V-Y or to this site to avoid forwards migration of the wire. C-U configuration if skin muscle advancement is also The trocar is passed and two looped 32 gauge required in the reconstruction. The incision is carried stainless steel wires are passed; one loop with the ends to the fracture site adjacent to medial canthal tendon of the other are tagged with the hemostat and they avoiding the lacrimal drainage system. The splayed will become the skin wires, the other fixates the canthal bone at the posterior lacrimal crest is thinned using tendons bilaterally. The medial canthal tendon is cutting burr. Either a 2-0 supramid suture or 27 gauge secured to the loop by 4-0 non-absorbable suture. stainless steel wire is used to engage the superficial head The two ends of the wire are twisted on themselves of the tendon. If insufficient tendon remains, the forming a second loop that is also secured to the medial supramid or wire may be positioned in the medial canthal tendon on this side. The looped wire is portion of the upper and lower tarsi. tightened pulling the medial canthal angles towards On the intact side, a 15 mm vertical incision is made the nasal septum. The skin wires are tied over nose into the skin and subcutaneous tissues just anterior to pads to restore the concavity of tissues at the medial the insertion of the superficial head of the medial canthal area and removed in a similar time to the canthal tendon. The periostium is opened vertically above. at the anterior lacrimal crest and reflected anteriorly. C. Lateral wall fractures: A 5 mm opening is made by a drill through the bone The orbital plate of the zygoma is less able to absorb and nasal mucosa anterior to the attachment. the trauma impact. It often fractures with orbital fat Management of Orbital Trauma and Fractures 119 herniation into the temporal or malar regions. Lateral zygomaticofrontal suture superior to the lateral canthus. wall fractures are usually associated with fractures of Hypothesia over the infraorbital nerve distribution is the zygoma and corrected with replacement of the a common association. Difficulty to open the mouth zygoma. Large defects usually need split cranial grafts can be present due to displaced fragment impinging with semi-rigid fixation to the orbital rim. on the temporalis muscle yet extraocular muscle imbalance is usually absent. D. Trimalar (Tripod/Tripartite) fractures: The incompletely displaced zygoma is hinged either It results form a lateral blow to the cheek resulting in at the frontal or maxillary attachment. If hinged to the a fracture of the zygomatic bone. Most commonly, frontal bone, there is usually no canthal displacement the zygoma is fractured at its sutural junction with the as the lateral canthal tendon and Lockwood’s ligament frontal bone superiorly, the zygomatic arch laterally are still attached to the lateral orbital tuberculum. The and maxilla medially. This can happen in different main displacement is at the zygomaticomaxillary suture combinations. Trimalar fractures may present with causing lower lid retraction inferolaterally and increased bone fragments either displaced or properly positioned. scleral show while the globe remains in its place. There Non-displaced zygoma fractures do not require surgery. is a step deformity at the inferior orbital rim and inferior In cases of completely displaced fracture (Figs rectus may be entrapped in the fracture site resulting 21.11A and B), the bone fragment may be displaced in diplopia. posteriorly. This causes a step like deformity of the If the zygoma is hinged at the maxilla, the lateral infraorbital rim at the zygomaticomaxillary suture, a tubercle is usually displaced inferiorly associated with flattened malar process and depression of the outer canthus and globe displacement. There is a palpable gap in the lateral orbital wall. Sometimes the lateral orbital rim becomes displaced superiorly and posteriorly causing malar flattening associated with a bulge in the lateral orbital rim and the lateral canthal angle may be displaced superiorly. In either condition, there is no step deformity of the inferior orbital rim nor diplopia as there is no muscle entrapment.

Management The fracture is reduced under general anesthesia and fixed in its place.

Surgical Technique Closed reduction: that can be either done by: a. Towel clip that grasps the central portion of the fractured bone, elevating it into position until the fragment is felt to “ pop” into place. b. An intraoral buccal sulcus incision where a blunt instrument is placed beneath the zygoma then upward and outward pressure is applied to restore the bone in place (Fig. 21.12). c. Gillis approach which is commonly used (Fig. 21.13). A 4 cm incision is placed at the temporal fossa hairline and carried down through the temporalis fascia and muscle to the periostium. A periosteal elevator is inserted beneath the temporalis fascia and gently passed downwards till a point below the zygoma. Leverage is applied to the elevator in an upward and outward direction reducing the fracture. The fragment can be guided by the surgeon’s other hand. In fresh fractures, the zygomatic bone once in place, Figs 21.11A and B: Axial scans showing varieties of it usually maintains its position. The temporalis fascia zygoma complete fractures is closed with 4-0 Vicryl while the subcutaneous layer 120 Clinical Diagnosis and Management of Ocular Trauma

Fig. 21.14: Incision and wiring in open reduction

Fig. 21.12: Lateral view for intraoral buccal approach ticofrontral and zygmoaticomaxillary sutures while protecting orbital structures during drilling. The screws are advanced until the head is firmly supporting the plate. Other methods of fixation include intramaxillary inflatable balloon and direct interosseus wiring where the bone fragments are united by 27-gauge wire that is tightened by wire twister without excessive tightening. It is effective in relatively stable fractures. The wire ends are cut leaving nearly 5 mm long and reposited in a drill hole or pressed flat against the bone to avoid injury to overlying structure. If sufficient periostium remains, it should be closed by 5-0 interrupted Vicryl sutures. Muscles and sub- cutaneous layers are also closed with 5-0 Vicryl. Skin is closed by 6-0 silk sutures. If the malar flattening persists after reduction which usually occurs with comminuted fractures, the malar eminence can be augmented by alloplast or bone graft placed in a subperiosteal pocket via inferior fornix or Fig. 21.13: Gillis approach Caldwell-Luc incision. Le Fort fractures (Fig. 21.15) is approximated by 5-0 Vicryl in vertical mattress. The Le Fort fractures involve the maxilla and are usually skin is finally closed by 6-0 silk sutures. If the zygoma complex, asymmetric and incomplete. Pure Le Fort is unstable, open and direct interosseus wiring is done. fractures are uncommon. Le Fort I is a low transverse Open reduction (Fig. 21.14) maxillary fracture that does not extend to the orbit. A superolateral eye brow incision and a horizontal The fragment of the maxilla containing the teeth is incision directly over the inferior orbital rim fracture separated from the remainder of the facial bones. site are fashioned. Dissection is carried to the fracture In severe cases, it may be free floating. sites then a periosteal elevator is inserted via the inferior Le Fort II fractures are pyramidal, involving the incision and the zygoma is rotated up into its position. maxilla, nasal bone and medial orbital floor. This All tissues entrapped within the fracture line should fracture begins at the lower portion on the nasal bones, be released. across the naso-orbital margin above the nasolacrimal Specially designed miniplates and microplates are canal through the medial orbital floor (sometimes used to approximate the fractured bones. Small drill associated with blow out fracture) over the infraorbital holes are placed on each side of the fractured zygoma- rim through the inferior orbital canal involving the Management of Orbital Trauma and Fractures 121

Fig. 21.15: Le Fort fractures I, II and III respectively from left to right anterior and posterior walls of the maxillary sinus. This fracture crosses the posterior pillar of the upper jaw, the pyramidal and pterygoid processes, and pterygomandibular fissure ending at the medial orbital margin and lateral wall of the nose. This fracture may be partially displaced or free floating. Le Fort III fractures create a craniofacial dysjunction involving both orbits, separating the maxilla from the skull; the facial skeleton is free floating attached to the cranium by only soft tissue. This fracture extends from the upper portion of the nasal bone, across the orbital margin near the frontomaxillary suture through the ethmoid bone passing posteriorly and inferiorly below the optic foramina to the inferior orbital fissure. It then separates into two segments; one extends upwards along the zygomaticosphenoid suture between the orbital roof and the lateral orbital wall crossing the Fig. 21.16: Coronal scan showing fracture roof of the orbit lateral orbital rim at the zygomaticofrontal suture. The second portion extends inferiorly and posteriorly results from third nerve affection, direct muscle injury crossing the pterygoid process. The zygomatic arch is or muscle entrapment. The fracture may extend to also involved. the superior orbital fissure and optic canal with resultant Le Fort II and III may extend to the orbital apex damage to the optic, oculomotor, trochlear and affecting the optic nerve and reducing vision. abducent nerves. In rare occasions with large or Management of these fractures require open reduction depressed fracture it may present with globe usually with arch bars. They may be associated with displacement, secondary menigeocele or encephalocele skull fracture thus requiring conjoint work with with and pulsatile proptosis. neurosurgery. Superior orbital rim, frontal sinus and glabellar Orbital roof fractures (Fig. 21.16) fractures either remain extracranial or communicate Isolated roof fractures are uncommon due to the with the intracranial compartment. If air is detected strength of the superior orbital rim. They can be seen in the anterior cranial fossa in case of orbital roof with wounds inflicted by sharp objects, gun shots or fracture, this signifies a dural tear. Unless a significant in association with Le Fort III fractures. displacement is found, superior orbital rim fractures It may be associated with brow and eyelid don’t need surgical reduction, displaced fractures of ecchymosis, forehead hyposthesia, ptosis and diplopia. small size without involving the orbital roof and did The latter is secondary to superior rectus or oblique not violate the intracranial space can be repositioned affection as well as damage to the trochlea. Ptosis and wired under the microscope. All other superior 122 Clinical Diagnosis and Management of Ocular Trauma rim or roof fractures should be evaluated and managed with orbital rim fractures. It has also been tested for by a neurosurgeon. repair of delayed cases with promising results. It offers a hidden incision, improved fracture visualization, and Orbital blow-in fractures: avoidance of post-operative eyelid malposition, Any of the four walls may be fractured and displaced however, specific knowledge of endoscopic anatomy towards the centre reducing the orbital volume and is required. causing edema, proptosis and optic nerve compression Via an endoscopic endonasal approach, a wide either directly or by secondary increase of intraorbital middle meatal antrostomy in case of floor fractures pressure. Diplopia and mechanical restriction of or intransal ethmoidectomy in case of medial wall extraocular muscle movements as well as globe injuries fracture is created. Adhesions between the protruded can also be detected. The most common in fractured periorbita and the paranasal sinus mucosa are dissected walls are the roof and the lateral wall (Fig. 21.17). and the bone fragments are removed. The orbital floor Cases with optic neuropathy or marked proptosis is supported by a saline filled balloon, which is causing exposure should be managed as soon as connected with an infant feeding catheter and passed possible. through the middle meatal antrostoma. After confirming the reduction of the orbital floor by postoperative CT, the catheter is ligated and cut in short to keep it in the nasal cavity. A silastic or Medpore implant sheet soaked in antibiotic solution can also be used for the floor or medial wall fracture repair. Temporary supporting of the orbital wall with a detachable temporary balloon, or a silastic sheet and Merocel packing was removed 4 weeks after surgery in the out-patient clinic (Figs 21.18A and B).

Management of Old Standing Orbital Trauma The patient is evaluated in a manner similar to acute cases with more stress on the globe position, ocular Fig. 21.17: Fractured zygoma incarcerated motility, forced duction testing as well as diplopia fields. behind the intact globe If globe reposition is indicated, it should be done before muscle or eyelid surgeries. Bony orbit may be restored by osteotomies and open reduction or volume Role of Endoscopy in Management of Orbital augmentation by placing an implant in the subperio- Fractures steal space. Soft tissues incarcerated in the sinus should Endoscopic repair of orbital fractures could become be carefully removed however, fibrosis render this step a predictable and efficient treatment alternative to difficult with more possibility of tissue injury. Adjustable traditional method. It is can be used for repair of suture technique is better used for muscle surgery in isolated floor or medial wall fractures not associated such cases. Sometimes, glasses with plus lenses can

Figs 21.18A and B: Endoscopic view of floor fracture A: before surgery, B: after repair Management of Orbital Trauma and Fractures 123 be prescribed for blind eyes to reduce the apparent hyaluronic acid can be injected to augment the volume enophthalmos. in eyes with mild enophthalmos and intact vision. Hyaluronic acid was described to be injected intraconal. Orbital contour deformity: The surgeon should always compare to the sound This may arise from old trauma that was not or poorly side for globe position, restoration of the supratarsal repaired. If the defect is small, no further management sulcus as well as alignment with the sound side. will be needed. In case of large defects, subperiosteal Correction of the condition may result in aggravating custom made implants are used. The extent of the existing ptosis that requires surgical intervention. deformity is defined by radiological studies and the ocularist takes mold of the affected region incorporating Late persistent handicapping diplopia: the defect. A positive impression is fashioned from the Muscle surgery is advocated after the motility and mold using the desired alloplastic material. This can diplopia measurements are stabilized. Orbital floor be designed using special computer programs. Methyl surgery can improve it when it is performed up to methacrylate and proplast implants are usually 5 weeks post trauma yet the extraocular muscle effective. motility rarely improves after that. The surgery is individualized according to the degree of ocular Surgical technique: Under general anesthesia, one or imbalance. Adjustable sutures are preferred two small incisions are placed adjacent to but not Most of patients suffer from diplopia on downgaze overlying the deformity in conformity with Langer’s interfering with reading. If the eye can move up lines. The incision is carried down till the deformity normally with normal forced duction test on upgaze, using sharp and blunt dissection. If the periostium is A reverse Knapp procedure is performed in which the intact, a periosteal pocket is created to receive the medial and lateral recti are placed at or several implant. Alloplastic materials soaked in antibiotic millimeters behind the original inferior rectus insertion. solution are mildly modified using scissors. The If the eye cannot move upwards normally with surrounding bone may be modified using a drill with positive forced duction test, inferior rectus is recessed fine burr head. The alloplastic material is placed within till the eye can be normally moved upwards during the periosteal socket and secured in place using 2-0 surgery. Then a modified reverse Knapp procedure Supramid sutures is performed 3-6 months later; thus avoiding working The wound is closed in two or three layers with on three muscles at the same time for fear of anterior interrupted sutures. segment ischemia. Late hypophthalmos or enophthalmos: Fadom operation can be done attaching the Implantation of various materials in the subperiosteal inferior rectus to the sclera in the sound eye. This space along the orbital floor can augment this area decreases diplopia in down-gaze yet it inhibits thus raising the globe and moving it anteriorly. Materials downwards movement and makes the patient tilt his/ used for orbital floor fractures are used to correct globe her head on reading. malpositions yet they are thicker especially posterior. Beads and pellets forms of these materials can be used Telecanthus and they require smaller incisions. The floor exposure A Y shaped miniplates can be used to correct is very similar to the approaches described for orbital telecanthus when there is enough bony support. In floor fracture repair. The periostium is incised elevated case of bone destruction, transnasal wiring is the from the floor using periosteal elevator and malleable procedure of choice. retractors. The implant is placed in the created space Surgical Technique with the same precautions taken for floor fracture implants, i.e. pupil and forced duction test. Some A medial orbitotomy incision is made just medial to authors inserted porous polyethylene (Medpor) the medial canthus and anterior to the lacrimal drainage particles diced about 1 × 1 cm diameter through a system. Soft tissue and scar are debulked, any lateral canthal incision to orbital floor with successful displaced bone fragments are either reduced or results. The advantages of this technique are limited removed. A Y shaped miniplate is attached to the nasal incision, decreased postoperative edema, volumetric bone or frontal bone with screws keeping the long adjustability, and applicability under local anesthesia. limb directed posteriorly. Soft tissue fillers have been tried to correct The medial canthal tendon is engaged by a wire enophthalmos, They include autologous fat, cross on a free needle then passed through the linked collagen (Zyplast) and self inflating hydrogel corresponding hole of the plate mirroring the place pellets. The latter should not be used in cases with of the posterior lacrimal crest. One of the previously visual potential as they may induce high pressures. placed screws is loosened and the wire is wrapped Calcium hydroxyapatite gel (Radiesse) as well as around its head. 124 Clinical Diagnosis and Management of Ocular Trauma

The wire is tightened while the assistant keeps 7. Ferraz FH, Schellini SA, Schellini RC, Pellizon CH, Hirai medial traction on the canthal tendon aiming at over FE, Padovani CR: BMP implant associated with platelet- correction. Then the ends of the wire are cut, twisted rich plasma in orbit fracture repair. Curr Eye Res. 2008 and bent back into the miniplate Mar;33(3):293-301. 8. Frodel JL Jr. Computer-designed implants for fronto- The tissues are closed in anatomical layers and orbital defect reconstruction. Facial Plast Surg. 2008 finally the skin is closed using 6-0 silk sutures. Jan;24(1):22-34. 9. Garibaldi DC, Iliff NT, Grant MP, Merbs SL. Use of porous polyethylene with embedded titanium in orbital Summary reconstruction: a review of 106 patients. Ophthal Plast Reconstr Surg. 2007 Nov-Dec;23(6):439-44. Orbital and globe injuries are common in maxillofacial 10. Gossman MD and Pollock RA. Acute orbital trauma: In traumas. Proper and systematic assessment is oculoplastic surgery 3rd edition McCord CD, Tanenbaum mandatory to detect any subtle lesion and should be M and Nunery WR (eds). Raven press, New York. 1995; done as soon as life-saving measures are taken. Proper 17:515-51. 11. Hinohira Y, Yumoto E, Hyodo M, Shiraishi A. Reduction understanding of the anatomy, possible problems and surgeries for delayed cases with isolated blowout their mechanisms is of utmost importance for proper fractures. Otolaryngol Head Neck Surg. 2008 management. Early reconstruction is desirable yet late Feb;138(2):252-4. repair is a challenge requiring many and staged 12. Jeon SY, Kwon JH, Kim JP, Ahn SK, Park JJ, Hur DG, procedures. The treatment is individualized according Seo SW. Endoscopic intranasal reduction of the orbit in to the patient’s condition. Proper assessment and isolated blowout fractures. Acta Otolaryngol Suppl 2007 Oct;(558):102-9. planning is the key for obtaining good results. 13. Kaufman Y, Stal D, Cole P, Hollier L Jr. Orbitozygomatic fracture management. Plast Reconstr Surg. Apr 2008; 121(4):1370-4. Bibliography 14. Koltus BS, Dryden RM. Correction of anophthalmic enophthalmos with injectable hydroxyapatite (Radiesse). 1. Barry C, Coyle M, Idrees Z, Dwyer MH, Kearns G. Ocular Ophthal. Plast Reconstr Surg 2007;23:313-4. findings in patients with orbitozygomatic complex 15. Moore CC, Bromwich M, Roth K, Matic DB. Endoscopic fractures: A retrospective study. J Oral Maxillofac Surg. anatomy of the orbital floor and maxillary sinus. 2008 May;66(5):888-92. J Craniofac Surg 2008 Jan;19(1):271-6. 2. Bilyk JR, Shore JW, Ward JB and Mckeown CA. Late 16. Nesi FA, Walz KL (eds). Orbital fractures and medial orbital trauma: Diagnosis and treatment In oculoplastic canthal reconstruction. Smith’s practical techniques in surgery 3rd edition McCord CD, Tanenbaum M and ophthalmic plastic surgery. 2nd edition, Mosby St Louis, Nunery WR (eds). Raven press, New York. 1995;18: Missouri Chapter 18; 1994;227-37. 553-80. 17. Putterman AM, Smith BC and Lisman RD: Blow out 3. Coban YK, Kabalci SK: Surgical treatment of posttraumatic fractures In Smith‘s ophthalmic plastic and reconstructive surgery, 2nd edition Nesi FA, Lisman RD and Levine MR enophthalmos with diced medpor implants through mini- (eds), Mosby St Louis, 1998, Chapter 8; 209-240. lateral canthoplasty incision. J Craniofac Surg 2008 18. Sargent LA. Nasoethmoid orbital fractures: Diagnosis and Mar;19(2):539-41. treatment. Plast Reconstr Surg. 2007 Dec;120(7): Suppl 4. Eppley BL, Dadvand B. Injectable soft tissue filers, clinical 2):16S-31S. overview. Plast Reconstr Surg 2006;118:98e-106e. 19. Tay E, Oliver J. Intraorbital hyaluronic acid for 5. Farwell DG, Sires BS, Kriet JD, Stanley RB Jr: Endoscopic enoph-thalmos. (letter to the editor). Ophthalmology repair of orbital blowout fractures: use or misuse of a 2008;115 (6):1101. new approach? Arch Facial Plast Surg 2007 Nov- 20. Tenzel RR. Orbital and periorbital fractures. Textbook of Dec;9(6):427-33. ophthalmic plastic and reconstructive surgery. Steven M, 6. Fernandes R, Fattahi T, Steinberg B, Schare H: Podos and Yanoff M (eds). 1st edn. 1993. Gower Endoscopic repair of isolated orbital floor fracture with medical publications, New York. Chapter 16 pp 322-37. implant placement. J Oral Maxillofac Surg 2007 21. Tse R, Allen L, Matic D: The white-eyed medial blowout Aug;65(8):1449-53. fracture. Plast Reconstr Surg. 2007 Jan;119(1):277-86. CHAPTER

Management of Anterior Segment Trauma: An Update 22 CS Dhull, Sumit Sachdeva (India)

Conjunctival, Corneal, and complete history and perform complete examination to rule out scleral rupture, foreign body or laceration. Scleral Injuries The condition itself requires no specific treatment, Evaluating the anterior segment encompasses a very except reassurance to the patient. important aspect in the proper diagnosis and manage- ment of ocular trauma. By anterior segment trauma we mean to evaluate the structures of the eye in front of the crystalline lens (including the lens itself), but in this chapter we will discuss only injuries related to conjunctiva, cornea and sclera with special reference to penetrating injuries.

CONJUNCTIVAL INJURIES Conjunctiva is the most superficial layer of eye and the inner eyelids. The role of conjunctiva though is neither visual nor structural, but it does offer first line of ocular defence against chemical agents and low velocity foreign bodies. It is generally the first to be involved in cases of blunt trauma to eye and orbit. As it is highly vascularized, therefore, its wounds heal Fig. 22.1: Subconjunctival hemorrhage rapidly. The injuries to conjunctiva are generally not as painful as those of cornea. Erosion: Loss of the conjunctival epithelium is much less painful than that of the cornea, and healing occurs Types of Injuries fast. When de-epithelialization occurs as a result of a chemical injury and is accompanied by ischemia, the Hemorrhage: Subconjunctival hemorrhage (Fig. condition should be considered very serious and 22.1) though alarming is generally of no intrinsic requires immediate treatment. Antibiotic ointment can consequence. It can be due to any of the following be applied as a lubricant and as an anti-infective agent. reasons: a. Idiopathic (spontaneous) Chemosis: Conjunctival edema is a pathology that may b. Minor trauma (finger nail injury) accompany virtually any type of eye trauma. It is c. Major trauma (scleral rupture) basically due to dysfunction of its vascular endothelium. d. Systemic conditions (hypertension, bleeding While itself insignificant, it may point towards conditions dyscrasias, physical exertion, valsalva maneuvers like chemical injury, endophthalmitis, orbital etc.) hemorrhage, orbital fracture, insect bite, retained The significance of the condition lies not in the intraocular foreign body, or more serious carotid- presence of blood, which generally absorbs sponta- cavernous fistula. The severity of the underlying neously within 2 weeks and without adverse conse- pathology and the degree of chemosis may not be quences. The real danger is a thick layer of blood proportional. There is no specific treatment: the concealing an underlying wound signifying occult scleral causative condition must be addressed. Topical rupture. The examiner must, therefore, obtain corticosteroids may help reduce the edema. 126 Clinical Diagnosis and Management of Ocular Trauma Emphysema: It occurs when air gets entrapped in or a. Reduces the cornea’s transparency underneath the conjunctiva. More commonly, the b. Alters the cornea’s shape causing astigmatism and source is a paranasal sinus in the presence of an orbital halo formation fracture. Blowing the nose or coughing exacerbates c. Makes the normally smooth surface uneven, so the emphysema and should strongly be discouraged leads on to symptoms of dry eye. until the etiology is treated. Removal of the air is not d. Leads to significant and permanent structural necessary; once the resupply is cut off, the air quickly weakness. absorbs. Foreign body: Conjunctival bodies generally adhere Evaluation of Corneal Injury to the upper palpebral conjunctiva (most commonly History: If the injury is caused by a chemical agent, in the sulcus subtarsalis) and lower fornix. These history-taking must be limited to asking a few crucial generally cause pain and discomfort due to continuous questions before treatment is started: type of the agent; rubbing of cornea with each blink. Superficial objects time of the incident; and the therapy already applied. are usually easy to recognize and remove. The FBs In all other cases, history should be detailed, so as to embedded superficially may be removed with a cotton learn about the circumstances and consequences of tipped applicator while those embedded deeper require the injury, the risk factors, etc. some type of a sharp instrument like a 26 G disposable needle and often topical anesthesia has to be given Inspection: Careful inspection should be performed before its removal. Glass foreign bodies (like from after the eyelids have been gently pulled apart to allow broken spectacles) may be difficult to identify. Proper viewing the cornea completely. Utilizing focal, illumination may reveal erosions, blood vessels, scars, slit lamp examination with dyes help in delineating the edema, infiltration, foreign bodies, and lamellar or full- FB. thickness wounds. It is preferable to use some Laceration: The conjunctiva is elastic and mobile and magnification (like a loupe) while examining the cornea. therefore very resistant to trauma from blunt objects, Changing the angle of illumination also increases the but a sharp object like broken glass can cause chance of detecting the abnormality. conjunctival laceration as easily. Slit lamp is the most appropriate equipment for As with foreign bodies, a complete history has to detecting pathologies of cornea. Magnification along be taken and a detailed slit lamp examination must with different illumination techniques are invaluable be performed to rule out any retained foreign body in reaching the correct diagnosis. Sometimes, a local and ruptured globe. Fundus examination should also anesthetic agent (like proparacaine 0.5%) is required, be carried out to rule out deeper injury. Generally if the pain is intense and patient is squeezing the lacerations less than 1 cm do not require any repair, eyelids. This is more so in patients with foreign bodies. but more than that have to be repaired with an All topical anesthetics are toxic, however, and their absorbable suture like 8-0 vicryl. Care should be taken longer-term use is contraindicated. not to incarcerate Tenon’s capsule into the wound. Application of certain dyes like Fluorescein (Fig. Simple wounds generally heal within a week and no 22.2) and Rose Bengal can help in identifying erosions treatment is required, except antibiotic ointment. and the damaged epithelial tissue respectively.

CORNEAL INJURIES The cornea is frequently involved in facial and ocular trauma. Corneal injuries comprise a very important aspect of ocular trauma as they are directly responsible for the visual outcome in the patient. Management of corneal injuries requires great skills of observation, diagnosis and planning, especially in children as they are more susceptible to such injuries and have a larger part of life lead with ocular morbidity. Corneal trauma can be extremely painful: the epithelium, only 50 μm thick, has a large number of unmyelinated nerve endings. Trauma deeper than the epithelium, breaching the Bowman’s membrane causes scar formation, which: Fig. 22.2: Corneal abrasion stained by fluorescein dye Management of Anterior Segment Trauma: An Update 127

Flow Chart 22.1: Various slit lamp examination techniques are helpful in examining the cornea completely

1. With direct illumination, the object is viewed 3. And finally there is formation of hemidesmosomal via light scattered from its anterior surface. But, due attachments to the underlying basement mem- to the complex optical nature of the cornea and the brane. multiple interactive surfaces, clear foreign bodies (e.g. Limbal stem cells play an important role in the glass, plastic) and even lacerations may be difficult to process, and their injury can lead to significant healing appreciate. difficulties. • Under retroillumination, the object is illuminated Symptoms from behind; the light can be reflected from the • Intense pain iris or the fundus, providing a light from back of • Lacrimation cornea, highlighting the opacities. • Photophobia • Sclerotic scatter is based on the principle of internal reflection. Light entering the cornea from the limbus is totally internally reflected from the epithelial and endothelial surfaces; any interruption in the light path results in light scattering. This is very helpful in detecting corneal foreign bodies as well as structural abnormalities. 2. In indirect illumination, the illuminating beam is at 45°, the biomicroscope is focused on cornea. The area examined is lateral to the illuminated area and receives illumination from the neighboring area. It is helpful in detecting microcystic edema and infiltrates in anterior cornea.

Specific Injuries Fig. 22.3: Corneal abrasion Examination CORNEAL ABRASION (FIG. 22.3) Examination of patients with corneal abrasion is It accounts for nearly 10% of patients who present generally difficult because of the pain, watering and with ocular injuries in the emergency. photophobia. A drop of topical anesthetic (e.g. In this only the epithelial layer is damaged. The proparacaine 0.5%) can be of great benefit, permitting abrasion can be partial or full thickness, and as long proper evaluation. as Bowman’s layer is not disturbed, healing generally Examine the face of the patient first to evaluate follows without scarring. Healing of the abraded any associated injuries and then specifically the cornea epithelium occurs in several stages: is inspected. 1. Initially, there is a migration of peripheral cells onto Slit lamp examination is done followed by fluo- the area of denuded basement membrane; rescein dye staining to delineate the abrasion. The 2. This is followed by proliferation of the epithelial underlying stroma should be examined for any deeper cells to restore epithelial thickness; pathology. 128 Clinical Diagnosis and Management of Ocular Trauma Treatment • Stromal micropuncture:3 The rationale behind this • Antibiotic ointment: To cover the sensitive surface treatment is that, due to inadequate adhesion, the and to prevent infection. Once the integrity of a epithelium is not anchored to its basement healthy epithelial surface has been reestablished, membrane. The micropunctures are aimed at there is no further need for topical antibiotics. attaching the epithelium by taking advantage of • Cycloplegic drops to alleviate the pain resulting the normal scarring following injuries to Bowman’s from reactive spasm of the sphincter muscle. The layer. drug should be short-acting (like cyclopentolate • Eximer laser ablation of basement membrane and 4,5 0.5%) superficial Bowman’s membrane. • Bandage soft contact lens may also be used; this • YAG-laser treatment of Bowman’s membrane. does not interfere with the external oxygen supply or the patient’s ability to use the eye during the FOREIGN BODIES healing process. Corneal foreign bodies are second most common form Note: The use of tight pressure-patching is not of eye trauma (Fig. 22.4). These can result from recommended as it interferes with the external oxygen minor trauma, like an insect wing falling into the eye, supply to cornea, raises the surface temperature, and or small iron foreign body from a grinder. These prolongs healing. Risk of infection is also increased. generally embed superficially in corneal epithelium and generally do not reach the Bowman’s membrane, RECURRENT EROSION while high velocity foreign bodies can embed deeply into the stroma. Multiple foreign bodies should be Recurrent erosion occurs in 7 to 8% cases.1 It occurs suspected if the etiology is explosion. probably due to abnormal adhesion complex formation in the base of epithelial defect. This results in delayed sloughing of the healed epithelial surface. Recurrent erosions are especially common if the trauma is caused by: finger nail, sheet or edge of paper and vegetative matter.

History The patient gives a typical history of intense lacrimation and photophobia in eyes upon wakening up and the symptoms improve by mid-day. Sometimes if the erosion is large, the symptoms persist for days.

Treatment The treatment is aimed at allowing the adhesion complexes to form and allowing the hemidesmosomal anchoring fibers to extend into the basement Fig. 22.4: Corneal foreign body (arrow) membrane to secure the epithelium firmly in place. • Topical hyperosmotic agent (e.g. 5% sodium Evaluation chloride ointment) is applied at night, immediately before retiring. In the majority of cases, a topical The patient should be examined initially with a torch hyperosmotic agent applied nightly for 8 weeks light, looking for foreign material on the skin or results in resolution of the condition. This reduces conjunctiva, which if present should alert the examiner the epithelial edema and helps the epithelium to to the possibility of a corneal foreign body. The slit adhere to Bowman’s layer.2 lamp, however, remains the most effective method of • Extended-wear bandage contact lens, changed detection. All the different techniques of slit lamp every two weeks and worn day and night for up examination should be employed while examining the to 8 weeks. patient as some transparent foreign bodies like glass • Surgical debridement to remove the loose epithe- and plastic can be difficult to visualize in diffuse lium and scrubbing the basement membrane illumination but stand out in retro-illumination. without damaging the Bowman’s layer. Remove The patient presents with symptoms of irritation any hypertrophy using a cotton-tip applicator or and pain, though the pain is not so much as in corneal a surgical blade. erosion. Management of Anterior Segment Trauma: An Update 129 Treatment injury is deeper then the intraocular contents can • The cornea must be properly anesthetized with prolapse out upon slightest pressure on the globe. If drops (0.5% proparacaine). the lids are swollen then lid retractors can be used to • Superficial FBs are best removed using a cotton- separate them. tip applicator or a 26G needle. The foreign body Slit-lamp examination is mandatory to evaluate the should be gently lifted so as to minimize the trauma wound completely. All the different techniques of slit to neighboring tissue. Rust rings, which can develop lamp examination can be employed to come to a as early as within a few hours should also be proper diagnosis. 6 removed, using a sharp needle. Once the FB has Partial thickness lacerations: Small, self-sealing, clean been extracted, the condition should be treated wounds require no intervention other than as an erosion. prophylactic antibiotics and mild cycloplegics for a few • Deep-seated FBs should be dealt with care. If the days. depth of foreign body in stroma cannot be Larger flaps if displaced need suturing, while still ascertained then the removal should not be larger, self-sealing, clean wounds need a bandage attempted. The patient should then be taken to contact lens or glue. operation theatre for proper evaluation and removal. Special instruments like fine tipped forceps Full-thickness wound (Fig. 22.5): When the diagnosis should be used to remove any foreign body is confirmed, unless the wound is tightly sealed, the protruding deep in stroma (e.g. splinter). Care wound has to be repaired. should be taken to remove it through the same track that it had entered. • Unless there is tissue loss, most wounds resulting from FBs are self-sealing, although occasionally the utilization of bandage soft contact lenses or a corneal glue can be required.

CORNEAL LACERATIONS AND RUPTURE Corneal lacerations may be full or partial thickness wound caused by a sharp object and typically involves the stroma. Most of the lacerations are full thickness.7

Evaluation Proper history is must in such cases as it helps the clinician in deciding not only the course of action to Fig. 22.5: Open globe injury: Full thickness wound at be taken, but also if there is any deeper pathology limbus with iris prolapse (like retained IOFB). Corneal Tear Repair Timing: The tear has to be repaired as early as possible Signs of Global Perforation in the operation theatre so as to prevent any chances Any one or combination of the following suggests of infection. possible perforation of the globe: The basic principles of wound repairing are:8 • Markedly decreased visual acuity. 1. The wound should be sutured preferably under • Hypotony (decreased IOP). general anesthesia under all aseptic conditions. • Shallowing or flattening of the anterior chamber 2. The wound should be made watertight. or hyphema. 3. Depth of sutures is very important in giving best • Alteration in pupil size, shape, or location.. results. Ninety percent suture depth is recommen- • Focal iris-corneal adhesion. ded. • Corneal, lens, or vitreal track. 4. Suture bites should be equal on both sides, unless • Acute onset lens opacity. the wound is oblique. Sutures should be equidistant • Marked conjunctival edema (chemosis) or and should have equal tension in all of them. subconjunctival hemorrhage. 5. If the limbus is involved, first suture is applied there, Inspection of the area is done first with a torch light then the cornea is sutured and then sclera. If the after carefully separating the lids. Care should be taken wound is zig zag type, then sutures are applied at not to apply deeper pressure on globe because if the angles first (Fig. 22.6A). 130 Clinical Diagnosis and Management of Ocular Trauma lamp to identify the type of injury. Subconjunctival hemorrhage and chemosis can make the visualization difficult so imaging studies like ultrasonography and CT scan should be ordered to rule out any occult pathology and also to evaluate the condition thoroughly.

Specific Conditions Foreign bodies: If the FB is anterior then it has to be removed by freeing the tissues around it. This is relatively simple unless the object is partially inside the globe. If that is the situation then it requires great skill Fig. 22.6A: Zig-zag tear repaired with sutures to free the FB from sclera. The depth of the FB has applied at angle first to be identified and injury to adjacent structures has to be taken into consideration. If the foreign body is posterior, then a judicious consideration is made that whether the foreign body is accessible or not. If accessible the scleral cutdown is advisable and if not then it should be left to VR surgeon for taking the foreign body from inside. Lacerations: The lacerations can be full thickness or partial thickness. I. Partial thickness lacerations: If small can be left as such but if large may require suturing. The technique of suturing is similar to the one for full thickness wounds. II. Full thickness lacerations: Full thickness lacerations have to be sutured and suturing technique differs Fig. 22.6B: Schematic representation of how sutures are according to the situation applied on cornea. Note that sutures at the periphery are • First assess the general condition of patient to rule longer than those at center out any life-threatening condition. • Always prefer general anesthesia to local or topical. 6. The suture arms in the optical area are kept smaller • If the wound is corneoscleral, then first suture is than those at the periphery to minimize scarring in applied at the limbus and then cornea is sutured that area (Fig. 22.6B). In the visual center no followed by the sclera (Fig. 22.7). sutures should be placed unless absolutely • If the wound is scleral only then firstly the conjunc- necessary. tiva and Tenon’s capsule is separated and the full 7. Knots should be buried so as to cause less discomfort and less chances of vascularization if knots cannot be buried for some reason then bandage contact lens should be applied.

SCLERAL INJURIES Scleral injuries account for about 30% of all ocular injuries. Although unlike cornea, sclera does not play a direct role in the visual process, but it accounts for most of the globe stability and rigidity. The proximity of the sclera to vital tissues such as the choroid, ciliary body, and the retina gives it significant clinical implications.

Evaluation Proper evaluation of sclera is must before proceeding Fig. 22.7: Corneoscleral wound: First suture applied at for management. The sclera is examined under slit- limbus then cornea and then sclera Management of Anterior Segment Trauma: An Update 131 length of the wound is exposed. Then 50% rule is applied to close the wound. In this the initial suture is placed at halfway mark of the wound (50%) and next suture at 25% and the third at 75% mark and so on. Alternatively closure can be started from the proximal end to the distal, with close as you go technique. This technique is helpful in those tears too in which the distal end is not visualized (Fig. 22.8).

Fig. 22.9B: Wound closed after disinserting the muscle and securing it properly

• Care should be taken that at no stage undue pressure is applied on the globe as it will lead on to tissue and vitreous prolapse. Also while closing the wound care should be taken not to incarcerate any tissue in the suture tract. • If the posterior limit of the tissue is not identified, then the wound is closed as far as possible without Fig. 22.8: First suture at the limbus and then go from undue force, and the remaining wound is left as anterior to posterior such, to be healed by natural process of scarring • If the wound goes beneath the muscle then, firstly or should be left for VR surgeon to manage from the assistant should try to move the muscle aside inside. with a retractor, but if it is not possible then the • Conjunctiva is carefully closed over the repaired muscle is first carefully secured and then cut at the sclera to avoid any chances of infection. insertion, the scleral wound is then sutured and the muscle reattached to its original place (Figs 22.9A and B). References • 8-0 nylon sutures are preferably used in closing 1. Weene LE. Recurrent corneal erosion after trauma: a the sclera as they have a good tensile strength. The statistical study. Ann Ophthalmol 1985;17:521–24. depth of the bites can be upto 80% of the tissue 2. Kenyon KR. Recurrent corneal erosion: pathogenesis and thickness. therapy. Int Ophthalmol Clin 1979;19:169–95. 3. McLean EN, MacRae SM, Rich LF. Recurrent erosion: treatment by anterior stromal puncture. Ophthalmology 1986;93:784–88. 4. Dausch D, Landesz M, Klein R, et al. Phototherapeutic keratectomy in recurrent corneal epithelial erosion. Refract Corneal Surg 1993;9:419–24. 5. John ME, Van der Karr MA, Noblitt RL, et al. Excimer laser phototherapeutic keratectomy for treatment of recurrent corneal erosion. J Cataract Refract Surg 1994; 20:179–81. 6. Zuckerman B, Lieberman TW. Corneal rust ring. Arch Ophthalmol 1960;63:254-64. 7. Duke-Elder S, MacFaul PA. Lacerations of the cornea. In: Duke-Elder S (Ed). System of Ophthalmology. Vol XIV. Part 1. St. Louis: Mosby; 1972. 8. Beatty RF, Beatty RL. The repair of corneal and corneo- scleral lacerations. Semin Ophthalmol 1994;9:165–76. 9. Ferenc Kuhn. In Ocular Traumatology; 1st (edn). Springer Fig. 22.9A: Scleral wound extending below the muscle 2008. CHAPTER

Glued IOL 23 Amar Agarwal, Dhivya A, Soosan Jacob, Athiya Agarwal Chandresh Baid, Ashok Garg (India)

Introduction Surgical Technique We devised a new surgical technique for implantation After inserting the infusion cannula or anterior chamber of a posterior chamber intraocular lens (IOL) in eyes maintainer, localized peritomy is done. Two partial with deficient or absent posterior capsule with the use thickness limbal based scleral flaps about 4 × 4 mm of biological glue. We used a quick acting surgical fibrin are created exactly 180 degrees diagonally apart sealant derived from human blood plasma, with both (Fig. 23.1) and about 1.5 mm from the limbus. This hemostatic and adhesive properties. is followed by vitrectomy via pars plana or anterior route to remove all vitreous traction. Two straight sclerotomies with a 22G needle are made about Scleral Fixated IOL 1.5 mm from the limbus under the existing scleral flaps. The sclerotomies are positioned such a way that the Intraocular lens implantation (IOL) in eyes that lack superior one lies close to the upper edge of the flap posterior capsular support has been accomplished in and the inferior one close to the lower edge of the 1,2 the past, by means of iris fixated IOL, anterior flap. A scleral tunnel incision is then prepared about chamber intraocular lens and transscleral IOL 2 mm from the limbus for introducing the IOL. While 3-12 fixation through the ciliary sulcus or pars plana. the IOL is being introduced with the left hand of the Surgical expertise, prolonged surgical time, suture surgeon using a McPherson forceps, an end gripping induced inflammation, suture degradation, and 25G micro-rhexis forceps (Micro Surgical Technology, delayed IOL subluxation or dislocation due to broken USA) is passed through the inferior sclerotomy. The suture are some of the limitations in sutured scleral tip of the leading haptic is then grasped with the micro fixated intraocular lenses (SFIOL). It is also difficult rhexis forceps, pulled through the inferior sclerotomy and time consuming requiring minute and perfect adjustment of suture length and tension to ensure good centration of SFIOL.

Fibrin Glue Fibrin glue13-15 has been used previously in various medical specialities as a hemostatic agent to arrest bleeding, seal tissues and as an adjunct to wound healing. The fibrin kit we used was ReliSeal™ (Reliseal, Reliance Life Sciences, India). It is available in a sealed pack, which contains freeze dried human fibrinogen (20 mg/0.5 ml), freeze dried human thrombin (250 IU/0.5 ml), aprotinin solution (1500 kiu in 0.5 ml), one ampoule of sterile water, four 21G needles, two Fig. 23.1: Scleral flaps prepared 180 degrees diagonally 20G blunt application needles and an applicator with apart. Note the infusion cannula fixed in and eye without two mixing chambers and one plunger guide. any capsule Glued IOL 133

Fig. 23.2: Tip of the haptic grabbed by the 25 gauge mirco- Fig. 23.4: Fibrin glue applied. Note the rhexis forceps (MST, USA) and then that haptic is haptic which is externalized externalized under the scleral flap

Fig. 23.3: Superior haptic grabbed by the 25 gauge micro Fig. 23.5: PC IOL well positioned and centered rhexis forceps (MST, USA) and then externalized under the scleral flap following the curve of the haptic (Fig. 23.2) and is externalized under the inferior scleral flap. Similarly, the trailing haptic is also externalized through the superior sclerotomy under the scleral flap (Fig. 23.3). Then, the reconstituted fibrin glue thus prepared is injected through the cannula of the double syringe delivery system under the superior (Fig. 23.4) and inferior scleral flaps. Local pressure is given over the flaps for about 10 to 20 seconds for the formation of fibrin polypeptides (Fig. 23.5). The anterior chamber maintainer or the infusion cannula is removed. Conjunctiva is also closed with the same fibrin glue. In case of those patients who had a luxated IOL, similar lamellar scleral flaps as described earlier were made and the luxated IOL haptic was then grasped with the 25 gauge rhexis forceps and exteriorized and Fig. 23.6A: Subluxated IOL. Note the infusion cannula glued under the scleral flaps (Figs 23.6A to E). The fixed and scleral flaps prepared. Vitrectomy being done 134 Clinical Diagnosis and Management of Ocular Trauma

Fig. 23.6B: Haptics externalized under the scleral flaps and IOL well centered

Fig. 23.6E: Fibrin glue seals the conjunctiva

Fig. 23.6C: Fibrin glue applied and scleral flaps seal the haptic of the IOL

Fig. 23.7: IOL haptic tucked through a scleral tunnel

Fig. 23.8A: Anterior segment OCT of scleral flap

Fig. 23.6D: IOL haptic now glued by the fibrin glue

haptic of the IOL if protruding beyond the scleral flap can be tucked in a tunnel created in the sclera (Fig. 23.7). Our follow-up anterior segment OCT (Figs 23.8A and B) showed postoperative perfect scleral flap adhesion as early as day 1 and continues to Fig. 23.8B: Anterior segment OCT of the IOL. remain well maintained at one week and one month. Note IOL well centered Glued IOL 135 Discussion derivatives, there is always a theoretical possibility of transmission of viral infections,25 therefore, it is This fibrin glue assisted sutureless PCIOL implantation mandatory to get informed consent from the patient technique as described by us would be useful in a before the procedure. Though the use of fibrin glue myriad of clinical situations where scleral fixated IOLs in ophthalmology is considered off-label, it has been are indicated, such as, luxated IOL, dislocated IOL, successfully used in the eye since long. Its various uses zonulopathy or secondary IOL implantation. In in the eye include repair of lacerated canaliculi28 to dislocated posterior chamber PMMA IOL, the same seal full thickness macular holes,26,27 to seal cataract IOL can be repositioned thereby reducing the need incisions,32-35 corneal perforations, and traumatic lens for further manipulation. Externalization of the greater capsule perforations,29 It has also been used for part of the haptics along its curvature stabilizes the axial temporary closure of scleral flaps31 after trabeculectomy positioning of the IOL and thereby prevents any IOL 30 16 in eyes with hypotony, conjunctival fistula closure , tilt. In the 12 eyes of our 12 patients, no complications conjunctival autografts,31 and amniotic membrane like postoperative inflammation, hyphema, decen- transplantation.36,37 teration, glaucoma or corneal edema were seen after Gabor et al38 have shown sutureless scleral IOL a regular follow-up till now. We expect less incidence fixation by placing the IOL haptic in a scleral tunnel. of UGH syndrome in fibrin glue assisted IOL Our technique differed from other sutureless implantation as compared to sutured scleral fixated methods,38,39 by use of the fibrin glue which enhances IOL. This is because, in the former the IOL is well the rate of adhesion with hemostasis. We also used stabilized and stuck onto the scleral bed and thereby, scleral flaps as in conventional sutured SFIOLs and has decreased intraocular mobility whereas in the latter, this makes the learning curve very simple. There is there is increased possibilty of IOL movement or also no danger of intra-ocular infection gaining entry persistent rub over the ciliary body. Visually significant 17 through the tunnel as the fibrin glue hermetically seals complications due to late subluxation which has been the flaps leaving behind no possible entry route for known to occur in sutured scleral fixated IOL may also microbes. There was no glue induced intraocular be prevented as sutures are totally avoided in this inflammation in any of our patients and all 12 eyes 18 technique. Moreover, the frequent complications of had clear media on the postoperative visits. Scleral secondary IOL implantation like secondary glaucoma, indentation performed in the operated eyes showed cystoid macular edema or bullous keratopathy were no change in the axial positioning of the IOL. After not seen in any of our patients. Another important one month of follow-up, we found no IOL advantage of this technique is the prevention of suture decentration or any other complications in any of the 19-21 related complications like suture erosion, suture knot operated 12 eyes. exposure or dislocation of IOL after suture disintegration or broken suture. Chances of scleral melt22-24 and haptic exposure is not increased by this technique except Summary possibly, in high risk patients like rheumatoid arthritis. The other advantage of this technique is the rapidity Fibrin glue assisted sutureless PC IOL implantation is and ease of surgery. Since all the steps of tying the appropriate for eyes with deficient or absent posterior difficult to handle 10-0 prolene suture to the IOL capsule and this can be performed easily with the haptic eyelets, the time required to ensure good available IOL designs, instruments and with less surgical centration before tying down the knots as well as time time. However, a longer duration follow-up might be for suturing scleral flaps and closing conjunctiva are necessary to judge the long-term functional and done away with, the total surgical time is significantly anatomical results of the procedure. reduced. It is also easier and does not require much surgical expertise to use the 25 gauge forceps to grasp and exteriorize the haptic. Fibrin glue takes only 20 References seconds to act in the scleral bed and it helps in adhesion 1. Zeh WG, Price FW. Iris fixation of posterior chamber as well as hemostasis. Fibrin glue has been shown to intraocular lenses. J Cataract Refract Surg 2000;26: provide airtight closure and by the time the fibrin starts 1028–34. degrading, surgical adhesions would have already 2. Lorencova V, Rozsival P, Urminsky J. Clinical results of occurred in the scleral bed. the aphakia correction by means of secondary implan- tation of the iris-fixated anterior chamber intraocular lens. The commercially available fibrin glue that we used Cesk Slov Oftalmol 2007;63(4):285-91. is virus inactivated and is checked for viral antigen with 3. Bleckmann H, Kaczmarek U. Functional results of polymerase chain reaction, hence the chances of posterior chamber lens implantation with scleral fixation. transmission of infection is very low. But with tissue J Cataract Refract Surg 1994;20:321–26. 136 Clinical Diagnosis and Management of Ocular Trauma 4. Holland EJ, Djalilian AR, Pederson J. Gonioscopic 23. Mamalis N, Johnson MD, Haines JM, et al. Corneal- evaluation of haptic position in transsclerally sutured scleral melt in association with cataract surgery and posterior chamber lenses. Am J Ophthalmol 1997; intraocular lenses: a report of four cases. J Cataract 123:411–13. Refract Surg 1990;16:108–15. 5. Factors contributing to retinal detachment after 24. Watson PG, Hayreh SS. Scleritis and episcleritis. Br J transscleral fixation of posterior chamber intraocular Ophthalmol 1976;60:163-91. lenses. J Cataract Refract Surg 1998;24:697–702. 25. Schlegel A, Immelmann A, Kempf C. Virus inactivation 6. Solomon K, Gussler JP, Gussler C, Van Meter WS. of plasma-derived proteins by pasteurization in the Incidence and management of complications of presence of guanidine hydrochloride. Transfusion 2001; transsclerally sutured posterior chamber lenses. J Cataract 41:382-9. Refract Surg 1993;19:488–93. 26. Tilanus MAD, Deutman T, Deutman AF. Full-thickness 7. Teichmann KD, Teichmann IAM. Haptic design for macular holes treated with vitrectomy and tissue glue. continuous-loop, scleral fixation of posterior chamber Int Ophthalmol 1994/1995;18:355-58. lens. J Cataract Refract Surg 1998;24:889–92 27. Olsen TW, Sternberg P Jr, Capone A Jr, et al. Macular 8. Chang S, Coll GE.Surgical techniques for repositioning hole surgery using thrombin-activated fibrinogen and a dislocated intraocular lens, repair of iridodialysis, and selective removal of the internal limiting membrane. secondary intraocular lens implantation using innovative Retina 1998;18:322-29. 25-gauge forceps AJO 1995;120(!):126. 28. Steinkogler FJ. Fibrin tissue adhesive for the repair of 9. Mensiz E, Avtulner E, Ozerturk Y. Scleral fixation suture lacerated canaliculi lacrimales. In: Schlag G, Redl H, eds, technique without lens removal for posteriorly dislocated Fibrin Sealant in Operative Medicine, vol 2: Ophthal- intraocular lenses. Can J Ophthalmol 2002;37(5):290-4. mology-Neurosurgery. Berlin, Springer, 1986;92-94. 10. Mittelviefhaus H, Witschel H. Transscleral suture fixation 29. Buschmann W. Progress in fibrin sealing of eye lens and of posterior-chamber lenses after cataract extraction conjunctiva. In: Schlag G, Ascher PW, Steinkogler F associated with vitreous loss Ger Jr Ophthalmol 1995; 4(2):80-5. Stammberger H, eds, Fibrin Sealing in Surgical and 11. Scleral fixation technique using 2 corneal tunnels for a Nonsurgical Fields, vol 5: Neurosurgery, Ophthalmic dislocated intraocular lens J Cataract Refract Surg 2000; Surgery, ENT. Berlin, Springer-Verlag, 1994;97-106. 26(10):1439-41. 30. Grewing R, Mester U. Fibrin sealant in the management 12. Oh H, Chu Y, Woong known O. Surgical technique for of complicated hypotony after trabeculectomy. suture fixation of a single-piece hydrophilic acrylic Ophthalmic Surg Lasers 1997;28:124-27. intraocular lens in the absence of capsule support J 31. Cohen RA, McDonald MB. Fixation of conjunctival Cataract Refract Surg 2007;33:962-65. autografts with an organic tissue adhesive [letter]. Arch 13. Fink D; Klein JJ; Kang H et al. Application of biological Ophthalmol 1993;111:1167-68. glue in repair of intracardiac structural defects The ann 32. Grewing R, Mester U. Radial suture stabilized by fibrin of thoraxic surg 2004;77(2):506-11. glue to correct preoperative against-the-rule astigmatism 14. AF Matar, JG Hill, W Duncan et al. Use of biological glue during cataract surgery. Ophthalmic Surg 1994;25:446- to control pulmonary air leaks Thorax, Vol 45:670-74. 48. 15. P. D. Mintz, L. Mayers, N. Avery, H et al.Fibrin Sealant: 33. Mester U. Wound closure with fibrin adhesive in cataract Clinical Use and the Development of the University of surgery. In: Schlag G, Ascher PW, Steinkogler FJ, Virginia Tissue Adhesive CenterAnn. Clin. Lab. Sci., Stammberger H, eds, Fibrin Sealing in Surgical and January 1, 2001;31(1):108-18. Nonsurgical Fields, vol 5: Neurosurgery, Ophthalmic 16. Teichmann KD, Teichmann IAM. The torque and tilt Surgery, ENT. Berlin, Springer-Verlag, 1994;123-32. gamble. J Cataract Refract Surg 1997;23:413-18. 34. Rauber M, Mester U, Zuche M. Fibrin adhesive for 17. McCluskey P, Harrisberg B. Long-term results using wound closure in small-incision cataract surgery. In: scleral-fixated posterior chamber intraocular lenses. J Schlag G, Ascher PW, Steinkogler FJ, Stammberger H, Cataract Refract Surg 1994;20:34-39. eds, Fibrin Sealing in Surgical and Nonsurgical Fields, 18. Biro Z. Results and complications of secondary vol 5: Neurosurgery, Ophthalmic Surgery, ENT. Berlin, intraocular lens implantation. J Cataract Refract Surg. Springer-Verlag, 1994;116-22. 1993;19:64-7. 35. Henrick A, Kalpakian B, Gaster RN, Vanley C. Organic 19. Heilskov T, Joondeph BC, Olsen KR, Blankenship GW. tissue glue in the closure of cataract incisions in rabbit Late endophthalmitis after transscleral fixation of a eyes. J Cataract Refract Surg 1991;17:551-55. posterior chamber intraocular lens. Arch Ophthalmol 36. Lagoutte FM, Gauthier L, Comte PRM. A fibrin sealant 1989;107:1427. for perforated and preperforated corneal ulcers. Br J 20. Mowbray SL, Chang S-H, Casella JF. Estimation of the useful lifetime of polypropylene fiber in the anterior Ophthalmol 1989;73:757-61. chamber. Am Intra- Ocular Implant Soc J 1983; 9:143-47. 37. Duchesne B, Tahi H, Galand A. Use of human fibrin glue 21. Jongebloed WL, Worst JFG. Degradation of poly- and amniotic membrane transplant in corneal perfora- propylene in the human eye: a SEM-study. Doc tion. Cornea 2001;20:230-23. Ophthalmol 1986;64:143-52. 38. Gabor SG, Pavilidis MM. Sutureless intrascleral posterior 22. Ahmed TY, Carrim ZI, Diaper CJM, Wykes WN. chamber intraocular lens fixation. J Cataract Refract Surg Spontaneous\ intraocular lens extrusion in a patient with 2007;33(11):1851-4. scleromalacia secondary to herpes zoster ophthalmicus. 39. Maggi R, Maggi C. Sutureless scleral fixation of intraocular J Cataract Refract Surg 2007;33:925-26. lenses. J Cataract Refract Surg 1997;23(9):1289-94. Posterior Segment Ocular Trauma

CHAPTER Management of Traumatic Hemorrhages to the Posterior Segment 24 Javier A Montero, Jose M Ruiz-Moreno (Spain)

Introduction penetration or rupture. Two types of injuries may disrupt the continuity of the sclera: penetration by Ocular trauma is a significant cause of visual impairment relatively sharp objects, and rupture caused by massive in the United States and the leading cause of unilateral blunt trauma. blindness worldwide. Ocular trauma is more frequent The visual prognosis is more favorable when the among adult males mainly due to occupational reasons, primary mechanical damage caused by sharp though females and children may also present ocular penetration is limited to the anterior segment of the damage secondary to trauma. Isolated damage to the eye. Modern microsurgical techniques permit better anterior segment occurs in more than half of the cases wound closure and reconstruction of the anterior and isolated damage to the posterior segment is ocular structures. Penetrating injuries involving the uncommon.1 posterior segment carry a less favorable prognosis. The Approximately 2.5 million injuries occur annually, primary mechanical damage of vital structures by such 40,000 of which cause serious visual loss. Vision is lost injuries may be so great that useful vision is instantly because of primary mechanical damage of vital ocular destroyed. However, the application of appropriate structures and secondary complications, such as vitreoretinal surgery to prevent or treat secondary infectious endophthalmitis and retinal detachment due complications may result in the preservation of eyes to intraocular fibrous proliferation and contraction.1 that would otherwise be lost. The presence of marked vitreous hemorrhage is Both eyes should always be examined. Visual acuity associated with poor visual prognosis in ocular trauma determination should be performed in the first place; involving the posterior segment. Poor prognostic factors if standardized charts are not available we should at include presenting visual acuity of light perception or least be able to determine finger counting and reading lower, hyphema, and traumatic cataract. Severe abilities and the distance of these exams should be vitreous hemorrhages after closed-globe injury are recorded. If none of these abilities can be reached, frequently associated with various anterior and the light perception and projection abilities should be recorded. The evaluation of the direct and consensual posterior segment pathologies, and early vitrectomy pupillary reflexes is of great prognostic value. Decreased is considered to improve early visual rehabilitation and visual acuity is usually a sign of severity. Over 40% management of any potentially treatable posterior of the cases report marked visual acuity loss (lower pathology.2 than 20/200) associated with severe ocular trauma. Ocular hemorrhage associated with trauma may Anterior segment examination may disclose corneal occur after blunt and penetrating injuries. A careful lacerations, traumatic iritis, hyphema, damage to lens and complete ophthalmic examination is required in and vitreous opacities among others, which may limit every case since injuries causing minimal signs of the examination of the posterior segment (Fig. 24.1). damage to one part of the eye may cause a significant Ocular examination should be extremely careful until injury in another part of the eye with severe the absence of ocular perforation has been established, consequences for the patient and occasionally to the avoiding pressure on the eye ball and administration ophthalmologist who has misdiagnosed the trauma. of drops or ointments (Fig. 24.2). Blunt injuries are more common and cause more In the presence of hyphema posterior segment cases of visual impairment than penetrating injuries, examination should be gently performed in order to although the frequency of severe damage, blindness, prevent further bleeding and scleral indentation should and loss of the globe itself is greater with ocular be avoided for 2-3 weeks. 140 Clinical Diagnosis and Management of Ocular Trauma The size, location and characteristics of hemorrhages should be recorded. Vitreous hemorrhages may vary in size, location and density. Initially they are usually close to the damaged area, though they may later spread and occupy the whole vitreous cavity precluding examination of posterior segment structures. If posterior segment examination is not satisfactory due to the presence of anterior segment or vitreous hemor- rhages contact A-scan and B-scan ultrasonography are helpful for detecting posterior vitreous detachment and differentiating it from retinal detachment (Fig. 24.3). The symptoms associated with posterior hemor- rhages will depend on the locations and size of the Fig. 24.1: Subconjunctival hemorrhage after severe blunt hemorrhage. Peripheral retinal hemorrhages may be trauma masking scleral rupture. The patient presented asymptomatic; retinal, choroidal or retrohyaloidal vitreous hemorrhage with choroidal rupture hemorrhages affecting the posterior pole will present as central scotomata (Fig. 24.4); and patients with vitreous hemorrhages will complain of floaters, blurred vision or even light perception vision, depending on the amount of blood present.

Fig. 24.2: Retroequatorial intraocular foreign body which penetrated through the lower lid

A careful examination of the vitreous, posterior pole and peripheral retina under pharmacologic mydriasis is mandatory, since anterior or posterior hemorrhage may later mask damage to the posterior segment. Indirect ophthalmoscopy is a useful tool to evaluate Fig. 24.3: Ultrasonography A and B scan reveals a damage to the posterior segment allowing a fast marked choroidal hemorrhage with vitreous blood binocular examination of the vitreous and the retina and verification of the presence of intraocular foreign bodies (IOFB). Posterior pole biomicroscopy using contact and non contact lenses will improve the detailed examination of the macula, though non contact lenses are more useful reducing the risk of squeezing an injured eye. Scleral depression may increase the risk of intraocular bleeding and should only be performed once ocular rupture has been discarded. Anterior, central and posterior vitreous examination should be performed and the presence of any hemorrhage or vitreous opacity recorded. The location and size of the opacities should be recorded, as well as the presence of posterior vitreous detachment. Pigment clusters may appear floating in the peripheral or anterior vitreous following detachment of the vitreous base from the pars plana. Fig. 24.4: Grade I vitreous hemorrhage Management of Traumatic Hemorrhages to the Posterior Segment 141 Pathogenesis penetration may cause visual impairment. They include the toxic effects of IOFB, such as copper and iron, Blunt trauma may cause damage to the eye by three and the introduction of bacteria and fungi with different mechanisms: coup, contrecoup and ocular consequent infectious endophthalmitis. Retained lens compression. Coup refers to local damage at the site material and blood and the incarceration of vitreous of impact, whereas contrecoup refers to injuries at the and uvea causes chronic inflammation that may play opposite side of the eye caused by shock waves that an important role in the stimulation of intraocular traverse the eyeball with foci of tissue damage along fibrocellular proliferation. At a later stage, blood and the path of the shock waves, especially at interfaces lens material in the presence of large scleral wounds of tissues of different density. may induce formation of fibrocellular proliferation The ocular compression mechanism is determined which, upon contraction may cause traction retinal by the inextensibility of the eyeball and the detachment, retinal breaks, rhegmatogenous retinal incompressibility of intraocular fluids so that when the detachments, proliferative vitreoretinopathy, cyclitic eye is compressed along its anterior-posterior axis, it membranes, ciliary body detachments, hypotony, and expands in its equatorial plane causing severe traction phthisis bulbi. at the vitreous base. Ocular compression may cause scleral rupture even in eyes which have not undergone previous surgery. In these cases the two most common locations for scleral rupture are at the limbus and Classification parallel to the muscle insertions between the insertion Even though these lesions seldom appear isolated, and the equator. The hallmarks of scleral rupture are hemorrhages to the posterior segment may be classi- severe reduction in visual acuity, an afferent pupillary fied for a didactic purpose as: defect, hypotony, abnormally deep anterior chamber, • Vitreous hemorrhages decreased ocular ductions, severe subconjunctival • Retrohyaloidal hemorrhages edema, hyphema, and vitreous hemorrhage. Scleral • Retinal hemorrhages rupture can rarely be confirmed by ophthalmoscopy • Choroidal hemorrhages because severe vitreous hemorrhage and/or hyphema • Papillary and peripapillary hemorrhages nearly always accompany scleral rupture. Ultrasono- • Hemorrhages associated with indirect trauma graphy and computed tomographic scanning may show a shrunken globe, retinal detachment, partial or VITREOUS HEMORRHAGES complete posterior vitreous detachment and vitreoretinal adherences. The visual prognosis of The presence of vitreous hemorrhage has been ruptured globes is usually very poor. associated with retinal detachment and surgical removal The aetiologies and the mechanisms of damage of of the blood seems to reduce the frequency of retinal 3 penetrating injuries are highly variable and cause a detachment. The role of the presence and manage- wide spectrum of acute structural alterations and ment of vitreous hemorrhage has been reported by 4, 5 secondary complications. several series, as well as the role of the quantification Penetration of the eye by relatively blunt objects of the hemorrhage. Brinton et al reported functional causes compression of the globe resulting in recovery in 48% of the eyes presenting moderate to iridodialysis, subluxation and dislocation of the lens, severe vitreous hemorrhage vs 67% of the eyes with traumatic cataract, choroidal rupture, retinal breaks mild or no vitreous hemorrhage.6 at the vitreous base borders and vitreous detachment. Blood proteins may be involved in vitreous proli- Ruptures of the uvea produce anterior chamber, feration mediated by hemorrhages. Fibronectin is a choroidal, subretinal, and vitreous hemorrhage. high molecular weight glycoprotein with a chemotactic Massive blunt trauma causes corneal and scleral action on retinal pigment epithelium (RPE), fibroblasts ruptures and may avulse the optic nerve. and giant cells and mediates in the interaction between Penetrating objects cause lacerations of the cornea, collagen and the RPE. Fibronectin has been detected iris, lens, sclera, ciliary body, choroid, retina, and optic in epiretinal membranes in human eyes following nerve, usually combined with anterior chamber, retinal detachment repair after ocular trauma.7, 8 Platelet choroidal, subretinal, and vitreous hemorrhages and derived growth factor (PDGF), complement and occasional prolapse and incarceration of the lens, uvea, interleukins also induce intravitreal fibrosis. retina, and vitreous. Cleary and Ryan reported on the It is necessary to quantify the amount of vitreous increased frequency of retinal detachment following hemorrhage. One accepted classification for this penetrating ocular trauma associated with vitreous quantification was proposed at the Vitrase for Vitreous hemorrhage.3 The secondary complications of ocular Hemorrhage study9 as Grade I when retinal detail is 142 Clinical Diagnosis and Management of Ocular Trauma

Fig. 24.6: Retrohyaloidal hemorrhage

of vitreoretinal traction or transit of subretinal blood (Fig. 24.6). Retrohyaloidal or preretinal hemorrhages Fig. 24.5: Grade 3 vitreous hemorrhage are usually thick, masking retinal vessels and may show a characteristic boat-shape with a superior horizontal visible with some hemorrhage present and laser level. Even though retrohyaloidal blood tends to photocoagulations is possible; Grade 2 with large retinal disappear spontaneously, treatment has been proposed vessels visible but central retinal is not visible enough in order to reduce the contact of blood with the retina 14-16 to perform adequate posterior laser treatment; Grade and decrease its toxic effect. 3 with red reflex and no retinal vessels are seen behind the equator; and Grade 4 with no red reflex. INTRARETINAL HEMORRHAGES The symptoms of vitreous hemorrhage are visual Intraretinal hemorrhages may appear under different acuity loss, perception of mobile dark spots in the visual circumstances associated with ocular or distant trauma. field. Associated signs are visualization of erythrocytes The location of the blood will determine the presence floating in the anterior vitreous behind the lens with of symptoms. Extrafoveal blood is usually dilated pupil. Intense vitreous hemorrhage may lead asymptomatic. Juxtafoveal and subfoveal blood may to loss of pupillary reflex and blurring of retinal details present as paracentral or central scotomata. (Fig. 24.5). Retinal tear and detachment should be Subretinal blood is toxic for the retina and the RPE17 disclosed in all cases of traumatic vitreous hemorrhage. and thick hemorrhages worsen visual prognosis. B scan ultrasonography is a useful tool to perform Additionally, it is considered that the presence of examination of vitreoretinal adherences. hemorrhage limits the closure of the retinal or Vitreous hemorrhages may appear secondary to choroidal tear. blunt trauma following scleral rupture, vitreous The image of retinal hemorrhages may vary detachment, tears in the iris, ciliary body, choroid, or depending on how deep the retina is affected. Blood retina. We should assume that a retinal break is present affecting the retinal nerve fibre layer appears as flame until proved otherwise. Blood from choroidal ruptures shaped hemorrhages, whereas hemorrhages affecting accumulates beneath the neurosensory retina passing the nuclear layers appear as irregular shaped spots through the retina into the vitreous cavity. (Figs 24.7 to 24.9). Retinal hemorrhages usually do Vitrectomy is indicated for vitreous hemorrhage not mask retinal vessels. caused by ocular contusion when a retinal detachment is suspected because of sudden additional loss of vision, CHOROIDAL HEMORRHAGES when a retinal detachment is detected through a Posterior choroidal ruptures are probably caused by window in the hemorrhage, when a large retinal break anterior-posterior compression and equatorial or retinal detachment is diagnosed by ultrasound, or expansion. Blunt trauma may produce hemorrhage when there is no improvement after a reasonable into the choroid secondary to Bruch’s membrane period of observation.10-13 rupture and tear of the overlying RPE and underlying choriocapillaris. Patients with angioid streaks and other RETROHYALOIDAL HEMORRHAGES conditions known to be associated with an inelastic Retrohyaloidal hemorrhages usually appear following and fragile Bruch’s membrane are especially vulnerable incomplete posterior vitreous detachment as a result to choroidal rupture. Management of Traumatic Hemorrhages to the Posterior Segment 143 Choroidal hemorrhages may vary in intensity from small subretinal hemorrhages associated with Bruch’s membrane ruptures to huge suprachoroidal hemorrhages that may complicate corneal or scleral lacerations leading to expulsive hemorrhages. Choroidal hemorrhages may be massive leading to ocular hypotony and choroidal detachment, usually associated with vitreous hemorrhage or mask subretinal hemorrhages.18 Direct choroidal ruptures are uncommon and usually anterior and oriented parallel to the ora. Indirect ruptures are more common and tend to occur away from the site of impact. A choroidal rupture may be initially obscured by a subretinal hemorrhage caused by tearing of the choriocapillaris. Later, after the blood Fig. 24.7: Submacular hemorrhage has resorbed, a white curvilinear streak concentric to causing central scotoma the optic disc is seen. Only rarely is a rupture oriented radially with respect to the optic disc. Most are temporal to the disc and single, although nasal and multiple ruptures can also occur (Fig. 24.10). Typical small choroidal hemorrhages are rounded, dark red-blue and frequently take many weeks to resorb and may leave areas of pigment alteration. Visual prognosis is generally good unless the choroidal rupture is under the foveola, or an associated subretinal hemorrhage extends under the foveola). The overlying nerve fiber layer is almost never torn. Therefore, a rupture can be located between the disc and the macula and yet not affect the visual acuity. Choroidal ruptures can, months to years later, be complicated by the development of a choroidal neovascular membrane, with serous or hemorrhagic retinal detachment and loss of central vision.19 In these cases photodynamic therapy20 and more recently Fig. 24.8: Spontaneous resorption of intravitreal antiangiogenic therapy may be useful. submacular hemorrhage PAPILLARY AND PERIPAPILLARY HEMORRHAGES Papillary and peripapillary hemorrhages may appear following optic nerve damage by blunt trauma. Possible

Fig. 24.9: Complete spontaneous resorption of macular hemorrhage. Visual acuity was 20/20 Fig. 24.10: Choroidal ruptures 144 Clinical Diagnosis and Management of Ocular Trauma mechanisms include compression by intrasheath and venules. The aetiology of the white retinal hemorrhage and oedema and direct shock-wave lesions resulted is controversial. Extravasated lymph trauma to the nerve fibers. The management involves from retinal vessels, reflux venous shock waves, high-dose intravenous steroids, especially if they can arteriolar and fat emboli and blood product emboli be started within 8 hours, surgical decompression of formed after complement activation have been optic nerve sheath hematoma and neurosurgical proposed. Clinically, the retinal lesions resolve over decompression of the optic canal. Avulsion of the optic a period of weeks to a few months followed nerve may be accompanied by severe damage to other occasionally by pigment migration and optic ocular tissues or be the sole manifestation of apparently atrophy. Visual acuity may return to normal or near minor direct trauma. normal. • Valsalva retinopathy is characterized by preretinal HEMORRHAGE ASSOCIATED WITH (retrohyaloidal) hemorrhages in the macular area, INDIRECT TRAUMA and is secondary to Valsalva manoeuvres associated with vomiting, coughing. Visual function usually • Shaken baby syndrome may be associated in one returns to normal spontaneously. Hemorrhages third of the cases with ocular manifestations, above located on the macula may present as decreased all subconjunctival and retinal hemorrhages. visual acuity, but the syndrome is usually Intraocular hemorrhages are considered to be a asymptomatic. predictive of intracranial bleeding and the severity • Retinitis sclopetaria is defined by the rupture of the of the latter is related to that of the neurological choroid or retina caused by shock waves generated lesion. Funduscopic examination usually reveals by passage of a high-velocity missile through the retinal hemorrhages, perimacular folds, cotton orbit without directly striking the eye. Initial clinical wool spots, optic disk edema, and venous stasis. manifestations may be a subretinal or vitreous Less frequently, vitreous hemorrhages, retinal hemorrhage with decreased visual acuity. As the detachment, retinoschisis and chorioretinal atrophy blood clears, breaks in the Bruch’s membrane and are seen. in the choriocapillaris are frequently seen as well • Terson syndrome is characterised by a preretinal hemorrhage associated with subarachnoidal as fibrous tissue proliferation into the eye. Retinal hemorrhage. The intraocular hemorrhage has been detachment rarely occurs because of fibrous tissue classically attributed to transit of blood through the proliferation binding the retina to the choroid. optic nerve sheaths. Presently, intraocular blood is considered to be secondary to rupture of peripapillary and epipapillary capillaries caused by Medical Management increased intracranial pressure. Ophthalmoscopy Intravitreal ovine hyaluronidase has been used to usually reveals a preretinal hemorrhage in the promote resorption of intravitreous blood. 1125 peripapillary and macular area located exterior to patients with vitreous hemorrhage and visual acuity the inner limiting membrane (ILM). However, blood worse than 20/200 during more than one month were may go through the ILM and appear as a vitreous randomized 55 IU or 75 IU ovine hyaluronidase or hemorrhage. The most frequent complication of saline. Clearance of blood was achieved at months Terson syndrome is the appearance of epiretinal 1, 2 and 3 in 13%, 26%, and 33% of patients injected membranes. with 55 IU compared with 6%, 16%, and 26% of • Purtscher retinopathy is a haemorrhagic vasculo- saline-treated patients.9 pathy characterized by multiple retinal Tissueplasminogen activator has been used in hemorrhages, areas of retinal pallor around the combination with surgery,21 with intravitreal injection optic disk and decreased visual acuity. A serous of gas (in patients with traumatic choroidal rupture)22 macular detachment may appear associated with or as isolated therapy23 with favorable results, vascular dilation and tortuosity and optic disk improving vision and occasionally deferring the need oedema. Purtscher retinopathy is secondary to for vitrectomy. These procedures have been used in blunt head trauma and thoracic compression. This cases of subfoveal21, 22, 24 and retrohyaloidal23 thick syndrome is usually bilateral and the symptoms hemorrhages. After a mean follow-up of 10.5 months usually appear 48 hours after the trauma. The final visual acuity improved by 2 lines or greater in peripheral retina is commonly spared. Fluorescein 10 (67%) of 15 eyes and measured 20/80 or better angiography can reveal focal areas of arteriolar in 6 (40%) of 15 eyes in on series with complications obstruction, capillary nonperfusion, disc edema, including breakthrough vitreous hemorrhage in three and dye leakage from retinal arterioles, capillaries, eyes and endophthalmitis in one eye.24 However the Management of Traumatic Hemorrhages to the Posterior Segment 145 reported series were short and randomized clinical trials because of the removal of nonclearing vitreous are missing. hemorrhage. Vitreoretinal surgery is also of great value Krypton, Argon and Nd-YAG laser treatment have in the repair of penetrating injuries with retained been performed in patients with intraocular nonmagnetic foreign bodies and selected cases of hemorrhages to improve visual acuity by removing magnetic IOFB that are difficult or dangerous to extract preretinal blood permitting its transit to the vitreous with an electromagnet and in the management of eyes cavity. Dellaporta reported on the use of argon laser with posttraumatic endophthalmitis. Secondary retinotomies to the posterior pole of one patient with complications, including traction and rhegmatogenous thick submacular hemorrhage permitting escape of retinal detachments, are minimized by the timely subretinal blood into the vitreous.25 A less aggressive removal of hemorrhage, disrupted lens, and damaged approach using Nd-YAG laser was tried on patients vitreous. with retrohyaloidal hemorrhages.14 Visual acuity in all Additionally, the presence of vitreous hemorrhage, cases before laser treatment was hand movement. as well as delay in IOFB removal, preoperative retinal After laser treatment, the hemorrhage instantly drained detachment and primary surgical repair combined with into the vitreous cavity, resulting in rapid improvement the IOFB removal have been significantly associated of vision. After a mean follow-up of 26.3 months no with the postoperative retinal detachment and a poorer retinal damage or rebleeding occurred due to the laser visual outcome.27 treatment, and vitrectomy was not required in any The aim of vitrectomy is to remove vitreous eye. However most of the reports lack long term opacities. A standard three-port 25 or 23 G vitrectomy follow-up. Ulbig et al reported on the the effects of technique is preferred for nonclearing vitreous drainage of premacular subhyaloid hemorrhage into hemorrhage. Initially, a central core of opaque vitreous the vitreous with an Nd-YAG laser in a large series of is removed, beginning sufficiently close to the lens that 21 patients with a circumscribed premacular subhyaloid the tips of the cutter and endoilluminator can be hemorrhage of various causes with long-term follow- visualized, while maintaining the cutting orifice of the up. Even though in 16 eyes visual acuity improved probe under visual control in order to be able to within 1 month, four eyes had persistent, dense, examine the aspirated material. The excision is nonclearing vitreous opacity for at least 3 months and progressively carried posteriorly until the anticipated finally required vitrectomy. One case with clotted plane of the posterior hyaloid is approached. A small hemorrhage did not drain into the vitreous. Final visual opening is made in the detached posterior hyaloid, outcome was determined by the underlying diagnosis, through which unclotted blood is aspirated by use of such as Valsalva retinopathy (7 eyes), diabetic active suction from a soft-tipped cannula. Once the retinopathy (7 eyes), branch retinal vein occlusion (4 retina has been visualized, it is best to remove as much eyes), and retinal macroaneurysm, Terson syndrome, retrohyaloidal blood as possible to prevent dispersion or blood dyscrasia (1 eye each). Eyes with Valsalva into the vitreous cavity with consequent loss of visual retinopathy fared the best. Complications included a control. macular hole in 1 eye and a retinal detachment from Recently opacified vitreous may be red, yellow or a retinal break in a myopic patient. The authors mild green whereas old blood looks brown and dirty. concluded that drainage of premacular subhyaloid While removing dense haemorrhagic vitreous we may hemorrhage into the vitreous with an Nd-YAG laser find areas with old liquefied blood that may obscure is a viable treatment alternative for eyes with recent visualization of the retina. In such cases we should bring bleeding, but the risks and benefits have to be weighed the probe forward in order to be able to visualize its in a randomized trial and compared with those of tip until visualization of the vitreous cavity has become deferral of treatment or primary vitrectomy. clearer. Actively bleeding foci in the iris, ciliary body Nd-YAG laser has been reported to complete or retina are treated by raising the intraocular pressure vitreous hemorrhages in order to achieve vitreolysis and using endodiathermy if necessary. If visualization and permit spontaneous resorption of the vitreous of the bleeding foci is not possible, a fluid-air blood.26 interchange can be performed to permit endodiathermy and the eye is refilled with liquid in SURGICAL MANAGEMENT order to proceed with vitrectomy. Fresh blood tends Vitreoretinal surgery is helpful in the management of to clot and firmly adhere to the retina, whereas old subluxation or dislocation of the lens, vitreous blood liquefies in a few days and is more easily hemorrhage, and retinal detachment caused by ocular aspirated. trauma, permitting identification and treatment of Significant vitreous hemorrhages occurring weeks retinal breaks created at the time of blunt injuries before surgery are usually associated with sponta- 146 Clinical Diagnosis and Management of Ocular Trauma neously detached posterior vitreous. In these cases the extrusion cannula is placed through the retinal tear posterior hyaloid is removed. Peripheral, adhered towards the surface of the clot. In those cases where opacified vitreous can be trimmed using the vitrectome not tear can be detected, endodiathermy is performed under scleral depression. This procedure is performed to create a retinotomy in an area that does not affect with the cutting orifice of the probe aiming forward much visual function and suction is performed over and taking care to not to damage the pars plana. the clot. In those cases with organized hemorrhages, If the posterior vitreous cortex is not detached, it the clot can be removed using an extrusion cannula can be separated from the retina by gentle suction and moving the clot to and fro to release adherences with a soft-tipped cannula at the edge of the optic to the RPE, and the clot is carefully removed, disc. The elevated cortex is penetrated with a hooked occasionally with the aid of intraocular forceps or the needle creating a window through which a pick is vitrectomy probe. The retinotomy is later treated by introduced to enlarge the area of cleavage. With the laser and a gas bubble is injected in order to flat the plane between hyaloid and retina established, the retina. surgeon attempts to remove the entire cortical vitreous It is necessary to expose as much peripheral retina except for the firmly attached portion at the anterior and vitreous base as possible in order to be able to vitreous base. Cortex that does not separate with gentle locate retinal breaks caused by ocular contusion. All manipulation is isolated from surrounding vitreous to retinal breaks should be treated: endolaser is used for eliminate traction on the retina. It is important to posterior breaks, whereas peripheral breaks are treated remove the cortical vitreous from areas adjacent to with indirect laser assisted by scleral depression or retinal breaks. Failure to do so may result in subsequent transscleral cryoretinopexy. Cryotherapy is preferred tangential traction and retinal detachment. A scleral when residual opaque vitreous partially obscures the buckle should be considered if retinal breaks cannot targeted break. be freed from surrounding vitreous cortex. Encircling scleral buckles are ususally not necessary Blood remnants deposited behind the posterior after vitrectomy for nonclearing vitreous hemorrhage hyaloid are easily removed using an extrusion tip, even caused by ocular contusion when a clear view of the though they may form whirlpools. fundus periphery reveals no peripheral retinal tears Sclerotomies placed close to the 3 o’clock and or signs of traction, such as vitreous base avulsion. A 9 o’clock positions facilitate maximal excision of the buckle is usually not needed for treated retinal breaks hemorrhagic anterior vitreous skirt improving visuali- without retinal detachment. A local scleral buckle zation of the peripheral retina and pars plana. With should be used when there is residual traction on a use of coaxial illumination and scleral depression, the posterior break. The peripheral retina should be peripheral vitreous on the temporal side of the globe supported by an encircling scleral buckle when traction is trimmed with the cutter placed in the temporal on breaks in the oral zone persists or the periphery sclerotomy, reaching both the superior and inferior is poorly visualized because of residual opaque quadrants, after which it is transferred to the nasal vitreous. sclerotomy, and the process is repeated. Patients with penetrating ocular trauma may present The crystalline lens may be damaged if the fiberoptic endoilluminator is used internally to illuminate the with severe vitreous hemorrhage and associated retinal peripheral vitreous on the opposite side of the globe. detachment. Removing the hemorrhage and repairing This may be avoided by directing the cone of light the retinal detachment can be a surgical problem. from the through the cornea to augment or replace Besides the limited surgical view due to the the coaxial light source. hemorrhage, an incomplete separation of the posterior Hemorrhagic retrolenticular vitreous can be hyaloid membrane can allow the detached retina to stripped from the posterior capsule of the lens by gentle be drawn towards the port of the vitrectomy aspiration into the cutting port followed by withdrawal instrument, producing an inadvertent retinal tear. of the probe and simultaneous activation of the cutting Perfluoroperhydrophenanthrene (Vitreon®) has been mode, though this procedure may be dangerous in used to manage penetrating ocular trauma with young children because the retrolenticular vitreous is concurrent retinal detachment and a partial vitreous adherent to the lens, and may lead to cataract detachment, either at the time of surgery or as noted formation. It is usually preferable to preserve an intact ultrasonographically. The perfluorocarbon liquid clear lens than to perform a complete removal of helped to separate the partially detached posterior peripheral and retrolenticular vitreous. hyaloid membrane and flatten the detached retina Removal of subretinal blood requires the simplifying removal of the vitreous hemorrhage and elimination of the vitreous surrounding the clot. An management of the retinal detachment.28 Management of Traumatic Hemorrhages to the Posterior Segment 147 Prophylactic treatment of most traumatic retinal References breaks is indicated. Breaks at the point of impact are one exception because they are frequently self-sealing 1. Fact Sheet. National Society to Prevent Blindness. New and the surrounding necrotic retina and choroid often York, 1980. 2. Yeung L, Chen TL, Kuo YH, et al. Severe vitreous unite in a common scar. In those cases when scleral hemorrhage associated with closed-globe injury. Graefes depression reveals a slight elevation and movement Arch Clin Exp Ophthalmol 2006;244:52-7. of their edges and the surrounding retina, prophylactic 3. Cleary PE, Ryan SJ. Method of production and natural treatment is advised. Traumatic macular holes also are history of experimental posterior penetrating eye injury not treated to prevent additional loss of central vision. in the rhesus monkey. Am J Ophthalmol 1979;88: They seldom cause retinal detachments when left 212-20. alone. 4. Barr CC. Prognostic factors in corneoscleral lacerations. Arch Ophthalmol 1983;101:919-24. Despite the advanced surgical techniques the 5. de Juan E, Jr., Sternberg P, Jr., Michels RG. Timing of prognosis of massive suprachoroidal hemorrhages vitrectomy after penetrating ocular injuries. remains guarded and the visual outcome is poor.29 Ophthalmology 1984;91:1072-4. Massive suprachoroidal hemorrhages following ocular 6. Brinton GS, Aaberg TM, Reeser FH, Topping TM, trauma have been managed by secondary surgical Abrams GW. Surgical results in ocular trauma involving intervention with radial sclerotomies combined with the posterior segment. Am J Ophthalmol 1982;93: vitrectomy, use of perfluorocarbon, and silicone oil.30 271-8. 7. Weller M, Fischbach R, Heimann K, Wiedemann P. Pre and post operative ophthalmoscopy and B-scan [Significance of fibronectins in proliferative retinal ultrasonography, as well as visual acuity measurement diseases]. Fortschr Ophthalmol 1988;85:263-6. are required. In all cases, anatomic restoration of ocular 8. Xu H. [Pathogenesis of traumatic proliferative vitreoretino- structures was achieved. Distance visual acuity pathy]. Yan Ke Xue Bao 1992;8:80-2. improved in all cases (preoperative Snellen visual acuity 9. Kuppermann BD, Thomas EL, de Smet MD, Grillone LR. ranged from light perception to hand motions; Pooled efficacy results from two multinational postoperative Snellen visual acuity ranged from 20/ randomized controlled clinical trials of a single 400 to 20/60) after a mean follow-up period of 17 intravitreous injection of highly purified ovine hyaluronidase (Vitrase) for the management of vitreous months. hemorrhage. Am J Ophthalmol 2005;140:573-84. Another series reported the outcome of 10. Wirth MG, Helbig H. Vitreous hemorrhage in children. hemorrhagic choroidal detachment with retinal and Klin Monatsbl Augenheilkd 2006;223:440-2. adherence of the “kissing” retina, where surgery was 11. Manuchehri K, Kirkby G. Vitreous hemorrhage in elderly delayed one to three weeks to allow liquefaction of patients: management and prevention. Drugs Aging the blood clot.31 All eyes had complete ocular 2003;20:655-61. 12. Chiquet C, Zech JC, Gain P, Adeleine P, Trepsat C. Visual evaluation including ultrasound, and were treated with outcome and prognostic factors after magnetic extraction steroids before surgical treatment. The procedure of posterior segment foreign bodies in 40 cases. Br J consisted of anterior chamber fluid infusion, posterior Ophthalmol 1998;82:801-6. drainage sclerotomies, and primary total pars plana 13. Winthrop SR, Cleary PE, Minckler DS, Ryan SJ. vitrectomy with posterior hyaloid removal. Mean Penetrating eye injuries: a histopathological review. Br J follow-up was 9.4 months. Visual acuity after surgery Ophthalmol 1980;64:809-17. 14. Celebi S, Kukner AS. Photodisruptive Nd:YAG laser in improved in all eyes from light perception to 20/60. the management of premacular subhyaloid hemorrhage. One patient without light perception improved to 20/ Eur J Ophthalmol 2001;11:281-6. 200. Secondary surgical treatment with combined 15. Ulbig MW, Mangouritsas G, Rothbacher HH, Hamilton radial sclerotomies and vitrectomy should be AM, McHugh JD. Long-term results after drainage of considered in order to minimize the damaging effect premacular subhyaloid hemorrhage into the vitreous with a pulsed Nd:YAG laser. Arch Ophthalmol 1998;116: and maximize the anatomic and functional restoration. 1465-69. The natural history of traumatic posterior segment 16. Kroll P, Busse H. [Therapy of preretinal macular hemorrhages depends on the underlying cause and hemorrhages]. Klin Monatsbl Augenheilkd 1986;188: is generally more favorable in eyes without underlying 610-2. disease. Ocular hemorrhage may not resolve sponta- 17. Glatt H, Machmer R. Experimental subretinal neously and early vitrectomy surgery is necessary and hemorrhage in rabbits. Am J Ophthalmol 1982;94: 762-73. beneficial, especially in cases where other ocular 18. Weis A, Kodsi SR, Rubin SE, et al. Subretinal hemorrhage 32 damage is involved. New strategies for the treatment masquerading as a hemorrhagic choroidal detachment of vitreous hemorrhage, such as pharmacologic in a case of nonaccidental trauma. J Aapos 2007;11: vitreous liquefaction, may be important in the future. 616-7. 148 Clinical Diagnosis and Management of Ocular Trauma 19. Dolan BJ. Choroidal neovascularization not associated 26. Ivanov AN, Degtiareva EM, Maliuta GD. [YAG-laser with age-related macular degeneration. Optom Clin 1996; treatment for traumatic hemophthalmia]. Vestn Oftalmol 5:55-76. 2007;123:22-5. 20. Harissi-Dagher M, Sebag M, Gauthier D, et al. 27. Erakgun T, Egrilmez S. Prognostic factors in vitrectomy Photodynamic therapy in young patients with choroidal for posterior segment intraocular foreign bodies. J neovascularization following traumatic choroidal rupture. Trauma 2008;64:1034-7. Am J Ophthalmol 2005;139:726-8. 28. Desai UR, Peyman GA, Harper CA, 3rd. Perfluorocarbon 21. Laatikainen L, Mattila J. Tissue plasminogen activator liquid in traumatic vitreous hemorrhage and retinal (tPA) to facilitate removal of post-traumatic submacular detachment. Ophthalmic Surg 1993;24:537-41. hemorrhage. Acta Ophthalmol Scand 1995;73:361-2. 29. Dong X, Yuan G, Wang W. [Surgical treatment of 22. Holland D, Wiechens B. Intravitreal r-TPA and gas traumatic suprachoroidal hemorrhage]. Zhonghua Yan injection in traumatic submacular hemorrhage. Ke Za Zhi 2002;38:654-6. Ophthalmologica 2004;218:64-9. 30. Feretis E, Mourtzoukos S, Mangouritsas G, et al. 23. Chung J, Kim MH, Chung SM, Chang KY. The effect of Secondary management and outcome of massive tissue plasminogen activator on premacular hemorrhage. suprachoroidal hemorrhage. Eur J Ophthalmol 2006; Ophthalmic Surg Lasers 2001;32:7-12. 16:835-40. 24. Hassan AS, Johnson MW, Schneiderman TE, et al. 31. Quiroz-Mercado H, Garza-Karren CD, Roigmelo EA, Management of submacular hemorrhage with intra- Jimenez-Sierra JM, Dalma-Weiszhausz J. Vitreous vitreous tissue plasminogen activator injection and management in massive suprachoroidal hemorrhage. Eur pneumatic displacement. Ophthalmology 1999;106: J Ophthalmol 1997;7:101-4. 1900-6; discussion 1906-7. 32. Simon J, Sood S, Yoon MK, et al. Vitrectomy for dense 25. Dellaporta AN. Evacuation of subretinal hemorrhage. Int vitreous hemorrhage in infancy. J Pediatr Ophthalmol Ophthalmol 1994;18:25-31. Strabismus 2005;42:18-22. CHAPTER

Traumatic Retinal Detachments 25 Neeraj Sanduja, Ajay Aurora, Gaurav Luthra (India)

Introduction eye. Traumatic injuries to such eyes irrespective of the nature of trauma needs a meticulous screening of the Traumatic retinal detachment is assuming more and peripheral retina to look for the presence of retinal more importance in present day era of rapid industria- defects and retinal detachment. These eyes should be lization of our country. The role of trauma in the periodically observed even if no vitreo-retinal causation of retinal detachment has been recognised pathology is observed in the initial examination soon for long. Coopers (1859) first described traumatic after trauma, because there is a latent period between retinal detachment. Leber1 in 1916 observed that the time of trauma and the development of retinal ocular contusions played an important role in the detachment.2-4. etiology of retinal detachment in 16.18% of cases. All Traumatic retinal tears development takes place types of injuries, i.e. ocular contusions, perforating because of equatorial expansion of the globe. It is ocular injuries and concussion injuries to lead can cause uncommon for a patient to develop an acute retinal detachment. rhegmatogenous retinal detachment after blunt Traumatic retinal detachments have been classified trauma. Most trauma victims are young with solid into two groups due to blunt trauma and due to per- vitreous, providing internal tamponade to the retina forating trauma. Blunt trauma related retinal despite retinal tears or dialyses. However, with time detachment is more common while the one due to the vitreous liquefies, allowing fluid to form in the perforating injury is comparatively rare. vitreous cavity, which can pass through the retinal breaks and detach the retinal. The incidence of traumatic retinal detachments has been found to be Blunt Trauma Related Retinal around 20%.Cox5 studied 160 patients with traumatic retinal detachments; 60% of these were found to have Tears and Retinal Detachments “oral” types of retinal breaks. Another study on post- traumatic retinal detachments found that 84% of these Traumatic retinal detachment constitute a special group were associated with retinal dialyses, 8% with giant of retinal detachment on account of certain important retinal tears, 3% with horseshoe tears, and 5% with clinical features. Young males and small children are round holes. more vulnerable to ocular trauma because of their Ross6 evaluated 50 eyes with trauma related detach- outdoor activities. The commonest type of trauma ments and found that myopia was present in 12.5% responsible for the occurrence of retinal detachment of these eyes and 41% of the patients were first is in the form of blunt injuries to the eye which diagnosed more than 1 year after their injury. He commonly include sports injuries, fist blow injuries and attributed the higher risk of the inferotemporal dialysis automobile injuries. to lack of protection of the superotemporal globe, Bell’s The force of the injury is an important factor in phenomenon, and being the weakest point of the determining the extent of vitreo-retinal damage and peripheral retina. The associated ocular abnormalities subsequent formation of retinal breaks. A peripheral were vitreous base avulsion, demarcation lines, pars retinal degeneration with associated vitreous traction plana detachments, retinal cysts, vitreous hemorrhage, is likely to develop retinal break and retinal detachment angle recession, and traumatic cataracts. following a direct or indirect trauma to the eye. Cases Goffstein and Burton7 noted that the most common having risk factors like high myopia, aphakia or fellow locations for posttraumatic retinal dialysis (in descen- eyes of retinal detachment, are more prone to develop ding order) are inferotemporal (27-73%), superonasal retinal detachment following a traumatic injury to the (2-46%), superotemporal, and inferonasal. Retinal 150 Clinical Diagnosis and Management of Ocular Trauma dialyses may have a slow progression and onset of Traumatic retinal breaks without detachment may symptoms, as they often occur in young patients be treated with laser or cryoretinopexy alone. Most without vitreous syneresis. Thus, the accumulation and traumatic retinal detachments can be treated with progression of the subretinal fluid is often very slow conventional scleral buckling techniques. Because of and pigmented demarcation lines are often noted. the potential for retinal damage 180 degrees from the Goffstein and Burton7 noted that “pathognomonic” impact site, an encircling element is recommended as features of previous injury include retinal detachments this gives the entire vitreous base support and helps with superonasal dialyses, large necrotic retinal holes, relieve anteroposterior traction. Principles of scleral and fibrous growth. Cox5 also noted avulsions of the buckling are same as in a nontraumatic detachments. vitreous base (virtually pathognomonic for a contusion- Johnston8 reported 77 eyes with retinal breaks after related retinal detachment)and equatorial holes 36% contusive injury; 65 developoed rhegmatogenous cases in post trauma cases. Equatorial holes were either detachment. Surgical intervention maintained retinal small, round multiple retinal breaks, or were large, apposition in 96% of the eyes. irregular tears with “ragged” edges. Cox attributed these larger holes to retinal hemorrhage and necrosis Traumatic Giant Retinal that occurred at the time of impact. The anatomic results after scleral buckling surgery Tears (GRT) in these eyes are excellent; the overall reattachment A giant retinal tear is a tear that extends for 90 degrees rate is approximately 95%, with 87 to 94% of the cases or more of the globe circumference. This tear may reattached after one operation. Good visual outcome be circumferential or may show radialization and is achieved in most of the cases, as one surgical series extension posteriorly. The differentiating feature reported a final visual acuity of 20/40 or better in 44% between retinal dialysis and giant retinal tears is that of eyes, 20/50 to 20/100 in 24% and 20/200 or worse there is a free, mobile posterior retinal flap that may in 32%. or may not become inverted posteriorly in the latter.

Preop

Postop

Fig. 25.1: A large HST at edge of a lattice with total retinal detachment produced by blunt trauma. Patient underwent scleral buckling surgery with intraocular SF6 gas injection. Postoperatively retina is on with good buckle effect Traumatic Retinal Detachments 151

Fig. 25.2: Blunt trauma induced macular hole with peripheral HSTs with retinal detachment

Fig. 25.3A: Post Blunt trauma — Temporal GRT with posterior extension of GRT edge with bare choroid

Fig. 25.3B: Postop– Attached retina with GRT edge covered with old laser marks

Fig. 25.3C: Post traumatic GRT in a high myopic young patient 152 Clinical Diagnosis and Management of Ocular Trauma

Fig. 25.3D: Postop fundus photograph showing attached retina with laser marks at edge of GRT

Most cases of GRT are idiopathic and are associated carbon liquid to the margin of the tear. The with a high incidence of myopia. Trauma is the second perfluorocarbon liquid and silicon oil direct exchange most common cause of giant retinal tears (25% of is done at the end of the case. Aylward and associates9 cases) and many of them have associated myopia. In reported the results of 38 cases of traumatic giant retinal traumatic GRTs, there may not be an immediate tear; 37% were due to penetrating trauma and 63% accumulation of subretinal fluid or a posterior to nonpenetrating trauma. Reattachment was achieved inversion of the flap as the vitreous remains solidified in 89% of the eyes at 12 months follow-up. and liquefied over days. Scleral buckling alone does not suffice for the management of GRTs as the detachment is large and Penetrating Injuries-related also vitreous needs to be removed so as to relieve any traction on the anterior flap and edges of GRT. Retinal Incarcerations and Although these detachments have been repaired Retinal Detachments successfully in the past with a variety of scleral buckling techniques, modern vitreoretinal surgery has signifi- There is a frequent failure in localisation of retinal cantly increased the rat of anatomic reattachment. breaks following penetrating ocular injury on account The surgical technique used in the repair of of poor visibility of retina due to associated lenticular traumatic giant retinal tears include a pars plana opacities, uveitis and/or fibrous tissue changes in the vitrectomy with complete base excision and a low, vitreous. The morphological and functional results after broad encircling scleral buckle to support the vitreous retinal surgery in traumatic retinal detachment are not base. A lensectomy may be needed depending on the spectacular probably on account of a longer duration amount of cataractous changes or in cases of of retinal detachment, frequent macular involvement subluxated lens or in cases of anterior peripheral GRT. and a common occurence of proliferative vitreo- The perfluorocarbon liquids are an important retinopathy. It would thus be reasonable to understand intraoperative tool for managing GRTs as it keeps the that an early diagnosis of traumatic retinal detachment posterior retina in place while working on anterior may have great bearing on the surgical results of these retina and also allows unfolding of the inverted cases. posterior flap with the patient in a supine position. Ultrasonography is an important diagnostic tool for After the core vitrectomy, approximately 0.5 ml of the cases where the retinal details are not visible on first perfluorocarbon liquid is injected over the optic nerve examination, for assessment of the state of vitreous head to unfold and reposition the tear. All traction on and retina in such cases.The role of ultrasonography edges of GRT are removed befor putting more PFCL in such cases is immense and can help design better so as to avoid subretinal migration of PFCL. The management of retinal detachment by indicating anterior flap of the tear should be removed, as it may emergency of the treatment of posterior segment retract anteriorly, causing traction on the ciliary body pathology. In cases with intraocular foreign body use or covering it with secondary hypotony or iris of ultrasonography can be made for detection of neovascularization. More perfluorocarbon liquid is intraocular foreign body and presence or absence of injected slowly until the level of the liquid is just posterior retinal detachment besides vitreous changes. to the margin of the tear. The wide angle systems are very helpful in giving a panormic view and managing PATHOPHYSIOLOGY GRT cases. Indirect laser photocoagulation or Penetrating injuries cause varying amount of initial endolaser photocoagulation is done under perfluoro- mechanical damage. The most important secondary Traumatic Retinal Detachments 153 change is vitreous contraction and organization due considerable disagreement about the appropriate to nonvascularized intravitreal fibrocellular prolifera- timing of surgery. Some experienced surgeon favor tion. These changes, in most cases, result from operating within the first 48 to 72 hours, and others intravitreal fibrovascular and fibroglial proliferation, prefer delaying surgery for 4 to 10 days or 10 to 14 which leads to traction on the ciliary body and the days after injury. retina. This proliferation seems to occur more Delaying vitreous surgery beyond 72 hours after commonly in injuries with lacerations of the ciliary body the injury permits further diagnostic evaluation, and retina and in injuries with vitreous hemorrhage. including utralsonography and electrophysiology. It also This causes both posterior-to-anterior and circum- 10,11 permits the operation to be performed under ferential traction on the adjacent peripheral retina. conditions more favorable than emergency circum- The peripheral retina is dragged anteriorly and centrally stances. Occurrence of a posterior vitreous detachment and may progress to total traction retinal detachment. is important because this makes achievement of the The pathoanatomic changes after penetrating injuries are observed in both experimental animal surgical objectives easier and safer. models and human eyes.10,11 In the rhesus monkey, In addition, several authors have noted the a large pars plana wound involving the vitreous gel problems of severe hemorrhage when attempting early and combined with intravitreal injection of blood was vitrectomy,20 presumably secondary to uveal often followed by a marked local inflammatory congestion associated with acute penetrating injury. response, fibrocellular proliferation, and then cyclitic Hemorrhagic choroidal detachment can accompany membrane formation with secondary tradition retinal a penetrating injury, which makes it difficult to insert detachment due to contraction of cellular membranes an infusion cannula or other vitrectomy instruments in the anteroperipheral part of the vitreous cavity. properly without damaging the retina. Delaying surgery Ultrastructural study of the fibrocellular membranes may decrease the risk of uncontrollable intraoperative demostrated myofibroblasts, perhaps accounting for hemorrhage, as well as allow choroidals to resolve and 12 the contractile nature of the proliferative tissue. making the drainage easier. Serum components fobronectin and platelet- First of all, Iris tissue, vitreous gel, and lens material derived growth factor stimulate cell migration and incarcerated in an anterior segment wound are proliferation.13,14 These factors are probably present in reposited or excised by conventional methods, or by high concentration when dense vitreous hemorrhage using a vitrectomy probe through a limbal or pars plana occurs. The trauma may cause breakdown of the incision. The placement of scleral buckle offsets traction blood-aqueous barrier, and serum components may diffuse into the damaged viteous gel. Several authors forces in the anterior periphery that occur despite made these observations in the animal model (1) vitrectomy and is intended to prevent peripheral occurrence of a posterior vitreous detachment 1 or detachment from spreading to involve the posterior 2 weeks after the injury and intravitreal blood injec- retina. Secondary fibrous proliferation and traction in tion,10 (2) a substantial population of myofibroblasts the posterior half of the posterior segment are largely noted between 12 and 21 days after the injury,15 and prevented by removing the posterior cortical (3) only minimal fibrous proliferation when the experi- vitreous.21,22 mental injury was repeated and combined with Retinal detachment secondary to retinal incarcera- intravitreal injection of emulsified lens material rather tion requires complete relief of the traction at the incar- than blood.16 certation site.The technique of relaxing retinotomies Cleary and Ryan17 described an experimental was later described by Machemer and associates23 and model for penetrating ocular injury with vitreous was found to be extremely useful in relieving the hemorrhage. Invariably, a traction retinal detachment traction at the incarceration, freeing the retina and thus seen clinically after penetrating ocular injuries. In allowing retinal reattachment. When performing a subsequent studies they demonstrated that vitrectomy relaxing retinotomy for traumatic incarceration, the performed at either day 1 or day 14 after injury could retinotomy should be extended onto “normal”, reduce the risk of traction retinal detachment at a nonincarcerated retina to ensure a complete relaxation. statistically significant level.18,19 These observations The incarcerated retina, which lies anterior to the supported the clinical impression that by removing the scaffold for intraocular proliferation, vitrectomy may retinotomy, should be completely excised if at all reduce the incidence of severe visual loss after possible, as this may be a future scaffold for penetrating injuries. reproliferation and/or traction of the ciliary body. Chang and associates24 have described the use of the SURGICAL PRINCIPLES FOR VITRECTOMY perfluorocarbon liquids to reattach and stablize the Vitrectomy for penetrating ocular trauma was first retina while performing the relaxing retinotomy for advocated by Coles and Haik in 1972. There is anterior retinal incarcerations. The perfluorocarbon 154 Clinical Diagnosis and Management of Ocular Trauma liquid is slowly injected over the optic nerve head until 6. Ross WH: Traumatic retinal dialyses. Arch Ophthalmol just posterior to the incarceration site, allowing 1981;99:1371. stabilization and reattachment of the retina. The 7. Goffstein R, Burton TC: Differentiating traumatic from relaxing retinotomy is then performed just anterior to nontraumatic retinal detachment. Ophthalmology 1982;89:361. the perfluorocarbon liquid bubble, taking care to avoid 8. Johnston PB: Traumatic retinal detachment, Br J any subretinal migration of the perfluorocarbon liquid. Ophthalmol 1991;75:18-21. After the mechanical objectives of vitrectomy have 9. Aylaward GW, Cooling RJ, Leaver PK: Trauma-induced been achieved, any remaining intraocular foreign retinal detachment associated with giant retinal tears, bodies are removed. Foreign bodies are first mobilized Retina 1993;13:136. by removing the surrounding vitreous get and lysing 10. Cleary PE, Ryan SJ: Method of productio and natural any adhesions to the retina. If an inflammatory capsule history of experimental posterior penetrating eye injury is present, it is incised with a hooked needle or MVR in the rhesus monkey, AM J Ophthalmol 1979;88:212. 11. Cleary PE, Ryan SJ: Histology of wound, vitreous, and blade. If the foreign body is small and magnetic, it retina in experimental posterior penetrating eye injury can be engaged with a magnet introduced into the in the rhesus monkey, Am J Ophthamol 1979;88:221. vitreous cavity. The foreign body may be grasped with 12. Cleary PE, Minckler DS, Ryan SJ: Ultrastructure of traction forceps in the vitreous cavity with hand shake retinal detachment in rhesus monkey eyes after a technique, after being elevated from the retina with posterior penetrating ocular injury, Am J Ophthalmol a magnet.Air fluid exchange is performed to flatten 1980;90:829. the retina. Retinal breaks are treated by transscleral 13. Campochiaro PA, Jerdan JA, Glaser BM: Serum contains cryotherapy or by endolaser photocoagulation/indirect chemo attractants for human retinal pigment epithelial laser ophthalmoscope. Most cases require silicon oil cells, Arch Ophthamol 1984;102:1830. 14. Campochiaro PA, Glaser BM: Platelet-derived growth as an intraocular tamponade agent. factor is chemotactic for human retinal pigment epithelial cells, Arch Ophthalmol 1985;103:576. 15. Ussmann JH, Lazarides E, Ryan SJ: Traction retinal Summary detachment. A cell-mediated event, Arch Ophthamol 1981;99:869. Early diagnosis of retinal detachment in a case of 16. Cleary PE, Jarus G, Ryan SJ: Experimental posterior perforating injury is not easy as these cases invariably penetrating eye injury in the rhesus monkey. Vitreous- present with lot of anterior segment changes in the lens admixture, Br J Ophthamol 1980;64:801. form of corneal edema, hyphema and traumatic 17. Cleary, PE, and Ryan, SJ: Method of production and cataract. Retinal detachment associated with per- natural history of experimental posterior penetrating eye forating injuries revealed a younger age group, a injury in the rhesus monkey, AM J Ophthalmol smaller latent period, a poor anatomical and functional 1979;88:212-220. 18. Cleary, PE, and Ryan, SJ: Vitrectomy in penetrating eye prognosis particularly if there has been gross vitreous injury: results of a controlled trial of Vitrectomy in an insult after the removal of intraocular foreign body. experimental posterior penetrating eye injury in the Management of traumatized eyes has dramatically rhesus monkey, Arch Ophthalmol 1981;99:287-292. changed over the years. Introduction of newer 19. Conway, BP, and Michels, RG: Vitrectomy techniques in microsurgical instruments and techniques has made the management of selected penetrating ocular injuries, possible better care of previously unsalvaged eyes. Ophthalmology 1978;85:560-583. 20. Abram, GW, Topping, TM, and Machemer, R: Vitrectomy for injury, Arch Ophthalmol 1979;97:743. 21. Topping TM, Abrams GW, Machemer R: Experimental References double-perforating injury of the posterior segment in 1. Leber Graife-Saemisch hb.d.ges Augenheilk, 15th ed. rabbit eyes. The natural history of intraocular Leipzig 1916;5:693. proliferation. Arch Ophthamol 1979;97:735. 2. Schepens CL, Marden D, Amer J. Ophthalmol 22. Abrams GW, Topping TM, Machemer R: Vitrectomy for 1966;61:213. injury. The effect on intraocular proliferation following 3. Schepens CL. Traumatic retinal detachments : Clinical and performation of the posterior segment of the rabbit eye, experimental study. In Retina and Retinal Surgery. C.V. Arch Ophthamol 1979;97-743. Mosby Company: St Louis, 1969;302. 23. Machemer R, Aaberg TM: Vitrectomy, ed 2, New York, 4. Shukla M, Ahuja OP, Bajaj RP. Proc All Ind Ophthalmol 1979, Grune & Stratton. Soc 1980;38:212. 24. Chang S, Reppucci V, Zimmerman NJ, et al: 5. Cox MS, Schepens CL, Freeman HM: Retinal detachment Perfluorocarbon liquids in the management of traumatic due to ocular contusion. Arch Ophthalmol 1966;76:678. retinal detachments, Ophthamology 1989;96:785. CHAPTER

Retained IOFB 26 Neeraj Sanduja, Ajay Aurora, Gaurav Luthra (India)

Introduction determine the structure and magnetic properties of the object. Penetrating ocular trauma with a foreign body is a rare • A corneal or scleral entry wound and a hole in the but serious ophthalmic emergency. Intraocular foreign iris provide trajectory information. bodies (IOFB) can be inert,20 but often cause serious • The slit lamp findings may show chemical effects damage inside the eye and must be removed promptly. related to metallic foreign body or exudation The final resting place of and damage caused by an suggestive of infection or hyphema. IOFB depend on several factors, including the size, • The indirect ophthalmoscope through a dilated the shape, and the momentum of the object at the pupil may allow direct visualization of the IOFB time of impact, as well as the site of ocular penetration. and to look for presence of vitreous hemorrhage, In addition to the initial damage caused at the time retinal breaks or retinal detachment. Direct obser- of impact, the risk of endophthalmitis and subsequent vation of the foreign body is the best method of scarring play an important role in the planning of the localization. surgical intervention. • Gonioscopy and scleral depression are not recommended in an open globe. Many factors influence ultimate visual recovery. Mode of Injury These include the size, material, and location of the Hammering and using power tools are the most IOFB; the associated ocular injuries; and the develop- important causes for retained IOFBs. In most of the ment and management of late complications after cases, tiny metal particles are seen as intraocular foreign IOFB removal.6,7 Williams and associates8 studied 105 bodies, which often get chipped free while hammering eyes with retained intraocular foreign bodies and found on metal.1-3 In a retrospective study conducted on that the factors associated with a poor visual outcome patients of retained IOFBs,4 protective safety goggles were a wound 4 mm or greater in length, regardless were not worn by any of the 235 patients who sustained of location, and an initial visual acuity of less than intraocular foreign body injuries in this manner. This 5/200. The most commonly encountered intraocular study indicates the need to emphasize the value of foreign body material are iron and copper. Both are safety glasses in health education programs. reactive inside the eye and have the potential to cause Williams and associates5 compared penetrating significant damage if not removed.9 ocular injuries with retained foreign bodies in patients Iron can cause siderosis bulbi. Retinal pigment aged 18 years or less and in adults. The most common epithelial cells take up iron and migrate perivascularly cause of intraocular foreign bodies was a projectile producing a clinical picture resembling retinitis weapon or explosion (60%) in the younger patients pigmentosa. Iris becomes brownish resulting in versus hammering (84%) among the adults. heterochromia. Iron is also deposited in the dilator and sphincter muscles resulting in early mydriasis. In Clinical Manifestations the advanced stage the iris becomes atrophic. Deposi- tion of iron in the lens occurs initially in the lens capsule A complete examination of both eyes is necessary, and imparts brownish spots on the anterior lens capsule. including the visual acuity. Copper and copper-containing alloys, such as brass • The patient should be carefully questioned about and bronze, may cause chalcosis. Ocular changes are the circumstances of the injury. The source of the caused by the affinity of the basement membrances foreign body, if known, should be considered to of ocular structure for copper. Involvement of 156 Clinical Diagnosis and Management of Ocular Trauma Descemet’s membrane results in a Kayser-Fleischer identifies multiple foreign bodies.14-16 It is a noninvasive ring, which appears as a peripheral greenish blue ring. technique requiring minimal patient cooperation and Deposition in the lens capsule forms greenish blue ring. can be used to image radioluscent and radiopaque Deposition in the lens capsule causes a greenish brown foreign bodies. CT scanning does have limitations, in sunflower cataract. Deposits of copper have been that metallic IOFBs often create significant scattering demonstrated in the internal limiting membrance of artifact that may obscure their precise location. This the retina and intraretinal glial tissue. can be particularly bothersome when attempting to determine whether a foreign body is intraretinal or intrascleral. In addition, identify some of the lower Localization of IOFB density foreign bodies, such as wood, may be difficult Thirty-two percent of all intraocular foreign bodies are with CT scanning.17 located in the anterior segment. Fifteen percent of Magnetic resonance imaging (MRI) has proved intraocular magentic foreign bodies are found in the useful for imaging intraocular tumors and other lesions. anterior chamber, 8% in the lens, 70% in the posterior However, the magnetic fields and heat generated segment, and 7% in the orbit as a result of perforation. during MRI scanning preclude examination of patients When IOFBs are retained, their precise localisation with potential intraocular of intraorbital metallic foreign is important in surgical decision-making. For many bodies. MRI’s main role is in accurately and safely years, the standard technique of localizing of foreign localizing wood and plastic intraocular foreign bodies. bodies involved special applications of conventional radiographic imaging. These methods were inaccurate Management and difficult, could cause iatrogenic damage to the globe, and were not useful in detecting radioluscent Patient should be put on frequent topical steroid foreign bodies. Now a days, radiographic localization antibiotic combination drops with intravenous broad of intraocular foreign bodies has been replaced by spectrum antibiotics. The management of an ultrasonography and CT scan. intraocular foreign body begins with primary repair Ultrasound B scan can accurately localise of the perforated globe. Primary surgery, when intraocular foreign bodies in majority of cases. The appropriate, must include closure of entrance wounds examination often must be performed gently through and repositioning or removal of incarcerated uvea to closed lids in open globe. The usefulness of echography prevent risk of endophthalmitis. is limited by shadowing caused by highly reflective Removal of an IOFB is recommended at the time surfaces such as air, reverberation artifacts creating by of repair of the entry site or soon afterward as soon some intraocular foreign bodies. Ultrasonography is as corneal clarity permits. IOFBs cause inflammation not accurate in determining whether a foreign body and often are rapidly surrounded by a fibrous capsule is intraocular or extraocular or if it is embedded in that can make delayed surgical removal more difficult. the eye wall when the foreign body is located within Foreign bodies may contain copper, which can cause 1 mm of the sclera.10 immediate severe inflammatory changes, or iron, which Ultrasound biomicroscopy (UBM), a high- can cause chronic siderotic damage to the eye.18 In frequency (50 MHz), high-resolution imaging techni- addition, traumatic endophthalmitis, particularly que, offers cross-sectional images of the anterior associated with the Bacillus cereus, is more commonly segment to a depth of 5 mm and is helpful in localizing seen with IOFBs than with other forms of penetrating aneriorly placed intraoular foreign bodies. However, injuries. B-scan ultrasound cannot be used to assess anterior Vitreous hemorrhage associated with an intraocular segment structures as its resolution is not sufficiently foreign body can result in the development of fibrotic high.11-13 bands that may detach the retina. Tolentino and CT scan has emerged as the imaging technique of colleagues demonstrated in rabbits that vitreous choice in the evaluation of IOFBs. CT scan can hemorrhage in the presence of an intraocular foreign demonstrate a perforation of the globe and localize body resulted in a proliferative fibroblastic reaction that metallic and nonmetalic foreign bodies. The CT scan caused retinal detachment and phthisis bulbi. Animals also provides valuable information about intraocular with intraocular foreign bodies but without vitreous structural alterations, including the presence of a hemorrhage did not develop these changes. Early dislocated lens or choroidal hemorrhage 2 mm sections vitrectomy in eyes with foreign bodies and vitreous on CT scan are able to localize IOFB as small as 0.7 mm hemorrhage can either prevent or eliminate these in size. The CT scan is noninvasive and can be changes before significant intraocular damage has performed on uncooperative patients and easily occurred. In a series by Percival19 on late complications Retained IOFB 157 from intraocular foreign bodies, retinal detachment was present in 42% of patients with vitreous hemorrhage but only 4% of those without hemorrhage. The incidence of retinal detachment was only slightly higher if the foreign body was embedded in the retina rather than lying in the vitreous. Foreign bodies in the anterior segment of the eye are usually easy to remove. The pupil should be constricted before removal is attempted. IOFBs located in corneal stroma can be removed by cutting down directly over the foreign body. Magnetic foreign bodies located in the anterior chamber or on the iris can be taken out through a limbal incision with a magnet or foreign body forceps or a toothed forceps. The posterior segment intraocular foreign bodies whether magnetic or nonmagnetic should be removed as their retention may severely damage the eye. Two types of magnets are used to remove magnetic intraocular foreign bodies. The Electromagnets are heavy, bigger in size and exert a substantially stronger force. These magnets can pull a foreign body at great speeds, and when misaligned, the foreign body can strike intraocular structures or the eye wall with damaging effect. Other type of magnet commonly used these days are Rare Earth magnets, and their magnetic pole is located at the tip. The magnetic pull of these instruments is coaxial with the tip. The pulling force only affects the magnetic foreign body when the instrument closely approaches it, which minimizes unwanted movements of the foreign bodies. Different tips sizes of rare earth magnets are available which can be introduced through the 20 gauge sclerotomy opening. For posterior segment IOFBs, removal by external approach may be adopted when a small magnetic IOFB is present in region of pars plana. Accurate localization is necessary to mark the incision point. Conjunctival peritomy is performed and if necessary, rectus muscles are isolated and looped with sutures to allow adequate exposure. Either partial thickness scleral flap or full thickness sclerotomy is performed. IOFB is removed with help of magnet (metallic IOFB) or toothed forceps. In most of the cases, IOFB is difficult to remove with magnet because of fibrotic strands or encapsulation of IOFB. Shock and Adams reported good anatomic and visual results following attempted pars plana external magnetic extraction in 13 patients with retained intraocular foreign bodies. In most of the cases of posterior segment IOFBs, a primary vitrectomy is indicated when a foreign body is associated with media opacities, IOFB is in vitreous Figs 26.1A to D: Retained IOFB with traumatic endo- cavity or adherent to the retina or vitreous strands or phthalmitis (A) At presentation: PL +, (B) 1 week after located intraretinally. A Standard 3 port vitrectomy is vitrectomy, IOFB removal and silicon iol injection, (C and D) done. At 3 months after surgery 158 Clinical Diagnosis and Management of Ocular Trauma

Figs 26.2A and B: (A) IOFB impacted superior to macula in right eye, (B) Postop at 1 month—Scar at FB impaction site BCVA – 6/18

Clear all vitreous strands away from IOFB to reduce risk of traction on the retina when IOFB is removed. Figs 26.3A to C: (A and B) Site of IOFB entry through Retrieval of IOFB done with forceps or magnet. Using sclera, (C) Postop—Retina on, Buckle effect shake hand technique. If IOFB is large then enlarge sclerotomy circumferentially. Vitreous base should not extrude through enlarged sclerotomy to reduce risk Second forceps is introduced through limbal incision of iatrogenic retinal tear formation. to grasp IOFB and extract the IOFBt.Care is taken not The surgeon must have the foreign body grasped to increase retinal injury site or to create hemorrhage. firmly when removing it through the sclerotomy. If Retinal break treatment consists of removing all the foreign body is dropped, it will likely strike the vitreous traction, cryopexy or laser photocoagulation macula and bring about poor visual consequences. and intraocular tamponade with silicon oil. Injection of liquid perfluorocarbon has been A prophylactic encircling scleral buckle is recommended as a means to protect the macula. recommended in all eyes receiving vitrectomy for Very large IOFB (more than 3 mm size) should management of penetrating injuries with IOFB. be removed through a limbal incision. Lensectomy is required in such cases. Summary IOFB is grasped with a magnet or IOFB forceps Prognosis in cases of retained IOFBs is dependent on and brought into the anterior chamber. Infusion line the location and size of the injury as well as the substance is turned off to reduce iris prolapse. involved and the time of removal. Overall, patients Retained IOFB 159

2. Armstrong MFJ: A review of intraocular foreign body injuries and complications in N. Ireland from 1978-1986. Int Ophthalmol 1988;12:113-17. 3. Khan D, Kundi N, Mohammed Z, et al: A 6½ years survey of intraocular and intraorbital foreign bodies in the North- west Frontier Province, Pakistan. Br J Ophthalmol 1987;71:716-19. 4. Trevor-Roper PD: The later results of removal of intraocular foreign bodies with the magnet. Br J Ophthalmol 1944; 28:361-65. 5. Williams DF, Mieler WF, Abrams GW: Intraocular foreign bodies in young people. Retina 1990;10(suppl):S45-49. 6. O’Neill E, Eagling EM: Intraocular foreign bodies: Indications for lensectomy and vitrectomy. Trans 1954;38:727-33. 7. Ballantyne JF: Siderosis bulbi. Br J Ophthalmol 1954;38:727-33. 8. Williams DF, Mieler WF, Abrams GW, et al: Results and prognostic factors in penetrating ocular injuries with retained intraocular foreign bodies. Ophthalmology 1988;85: 911-16. 9. Knave B: Electroretinography in eyes with retained intraocular metallic foreign bodies: A clinical study. Acta Ophthalmol 1969;100(suppl):1-63. 10. Loffredo A. Cennamo G. Sammartino A, et al: The value of the association of radiological methods with echographic examination in the study of intraocular foreign bodies, Ophthalmologica 1979;179:18-24. 11. . Laroche D, Ishikawa H, Greenfield D, Liebmann J M, Ritch R. Ultrasound biomicroscopic localization and evaluation of intraocular foreign bodies. Acta Ophthalmology Scand 1998;76:491-95. 12. Barash D, Goldenberg-Cohen N, Tzadok D, Lifshitz T, Yassur Y, Weinberger D. Ultrasound biomicroscopic detection of anterior ocular segment foreign body after trauma. Am J Ophthalmol 1998;126:197-202. 13. Berinstein DM, Gentile RC, Sidoti PA, Stegman Z, Tello C, Liebmann JM, et al. Ultrasound biomicroscopy in anterior ocular trauma. Ophthalmic Surg Lasers 1997; 28: 201-07. 14. Lobes LA Jr, Grand MG, Reece J, et al: Computerized axial tomography in the detection of intraocular foreign bodies. Ophthalmology 1981;88:26-29. 15. Gaster RN, Duda EE: Localization of intraocular foreign bodies by computed tomography. Ophthalmic Surg 1980;25-29. Figs 26.4A to C: (A,B) Preop photo-red glass IOFBs with 16. Leone CR Jr. Wilson FC: Computerized axial tomography subretinal altered hemorrhage, (C) 2 months postop of theorbit. Ophthalmic Surg 1976;7(2):34-44. following vitrectomy and IOFBs removal vision-6/18 17. Opilow, HW, Ackerman, AL, and Zimmerman, RD: Limitations of computerized tomography in the localization with IOFBs have an excellent prognosis, with 75% of intraocular foreign bodies, Arch Ophthalmol regaining visual acuity of 5/200 or better in one series, 1986;104:1477-82. as opposed to only 58% for those patients having a 18. Neubauer, H: Ocular metallosis, Trans Ophthalmol Soc UK 1979;99:502-10. penetrating injury without an IOFB. 19. Percival SPB: Late complications from posterior segment intraocular foreign bodies: With particular reference to References retinal detachment. Br J Ophthalmol 1972;56:462-68. 1. Behrens-Baumann W, Praetorius G: Intraocular foreign 20. De Juan, E, Sternberg, P, and Michels, RG: Penetrating bodies: 297 consecutive cases. Ophthalmologica injuries: types of injuries and visual results, Ophthalmology 1989;198:84-88. 1983;90:1318-22. CHAPTER

Penetrating Posterior Segment Trauma 27 T Mark Johnson(USA)

Epidemiology • Blunt trauma: Blunt trauma leads to compression of the globe.6 Anterior posterior compression of The incidence of open globe injury is estimated at the globe is associated with equatorial stretching 1 3/100 000 person years. Open globe injuries have during the initial deformation. This is followed by a bimodal distribution with the highest rates in young recovery resulting in overshoot with anterior persons and the elderly. The National Eye Trauma posterior elongation and equatorial contraction. Registry in the US (1985-1991) reported that 83% Finally there is a rebound phase of repeated of penetrating trauma occurred in men with a median oscillations. Globe rupture can result occur at 2 age of 27 years. several points of anatomic weakness including the The inciting event varies with the demographics of limbus, previous surgical wounds and posterior to the study. In a case series of penetrating injuries in the rectus muscle insertions. a single a tertiary care US hospital 33% of penetrating • Penetrating trauma: The complications of traumas were the result of gunshot wounds and 21% penetrating trauma result from progressive 1 were secondary to motor vehicle accidents. The contraction of vitreous membranes leading to National Eye Trauma Registry in the US (1985-1991) secondary retinal detachment, ciliary body injury noted that penetrating eye trauma occurred at home and secondary hypotony. Vitreous membranes (28%), workplace (21%), recreational activities (11%) develop within 2 to 3 weeks of initial trauma. The 2 and associated with transportation (8%). membranes often radiate to the initial laceration Explosive injuries have a high rate of open trauma. site. In a series of 74 eyes with retinal detachment In a case series of 57 explosive injuries 96% of cases following penetrating injury showed that the had open globe injuries and 76% had intraocular detachment resulted from contraction of vitreous foreign body (IOFB).3 In a case series of 797 severe membrane at perforation site.7 Animal models of ocular injuries occurring during the war in Iraq (2003- penetrating trauma describe the cellular events of 2005) 438 injuries were open globes including 49 healing that lead to secondary membrane bilateral injuries.4 formation.8 In the initial phase of healing (3 days) Many risk factors for occupational open globe injury is characterized by infiltration of the inner aspect are modifiable. In a case series of work place open of the wound by leukocytes and macrophages. globe injuries from 1994-1998 it was noted that 77% Proliferation of fibroblasts from the episclera, uvea of patients were not using recommended protective and non pigmented ciliary epithelium follows at eye wear and 14% of patients were under the influence day 6. The fibroblasts proliferate along vitreous of alcohol.5 The National Eye Trauma Registry noted strands and form membranes leading to alcohol to be a factor in the injury in 24% of cases progressive retinal detachment at day 12. and illicit drug use in 8%.2 Several factors that influence the healing response to trauma include the presence of blood and foreign bodies. Blood and its components contribute the membrane formation and proliferation. In rabbit models Pathophysiology of trauma autologous blood injection, compared with Several mechanisms of trauma have been described saline injections, seems to be critical to development in ocular trauma and lead to characteristic patterns of secondary vitreous membranes and detachment.9 of injury. These include: Serum derived proteins such as fibronectin may play Penetrating Posterior Segment Trauma 161 an important role in the stimulation of intravitreal Investigations proliferation. The presence of foreign material also complicates the nature of the trauma. Foreign bodies Radiology investigations are important in the determi- contribute to trauma in the following ways: (1) direct nation of the presence of an intraocular foreign body. tissue injury; (2) increased risk of secondary infection Various methods of evaluation include plain film or inflammation and (3) secondary late ocular toxicity X-rays and CT scan. CT scan is currently considered the including toxicity caused by oxidative reactions to some preferred technique for evaluation of IOFB. It is useful for imaging radiolucent and radiopaque foreign bodies. reactive metals (iron, copper). The absorption characteristics of IOFB can be quantified in Hounsfield units.11 Wood appears least dense on CT followed by plastic and then glass. Metallic foreign bodies Classification all have the same absorption and, therefore, CT scan 1996 OCULAR TRAUMA CLASSIFICATION10 cannot differentiate the type of metal present. Ultrasonography is also useful in evaluating the Term Definition traumatized globe. It allows visualization of posterior Eyewall Sclera and cornea segment through opaque media. It can be utilized in Closed globe No full thickness wound the determination of the presence of posterior vitreous Open globe Full thickness wound Rupture Full thickness due to blunt trauma detachment (PVD), retinal detachment or foreign body. Laceration Full thickness due to sharp trauma Penetrating Single laceration Perforating 2 full thickness lacerations Intraocular foreign body Retained foreign body Management Successful management of penetrating trauma requires meeting several specific objectives of management. The LOCATION primary objectives are: (1) clear optical media; (2) – Zone I prevent future retinal tears and detachment by • Cornea / corneoscleral removing the vitreous scaffold at the laceration site – Zone II and prevent formation of pre retinal membranes and • Anterior 5 mm of sclera (3) remove foreign body. – Zone III There are several principles of management that • More than 5 mm posterior to limbus influence the ease of vitrectomy. Water tight primary repair of globe during primary repair is crucial. Secondary vitrectomy techniques require that the initial Clinical Features traumatic wounds be watertight to maintain the While obtaining history is often critical in the diagnosis integrity of the globe. The timing of vitrectomy appears and management of patients it is often difficult to obtain to be important in outcome. Studies suggest that a clear history in the traumatized patient. This is often surgery undertaken within 14 days of trauma reduces related to factors such as secondary injuries and the the rate of retinal detachment in experimental influence of alcohol. The mechanism of injury is impor- models.12,13 Surgery at 14 days is technically easier due tant to understanding the nature of the ocular injury, to the development of posterior vitreous detachment. especially the possibility of intraocular foreign body. 3 port vitrectomy with wide field visualization is the Important aspects of the clinical examination standard method of management of complex posterior include: segment ocular trauma. There are several technical • Visual acuity: Visual acuity is an important prognostic considerations in surgical repair. factor • Presence of a relative afferent pupillary defect Infusion Port • Intraocular pressure: The IOP is often low but a Intraocular infusion is a key component of vitrectomy normal or elevated IOP does not rule out rupture as it is required for maintenance of intraocular pressure of the globe. during surgical manipulation. Port should be placed • Anterior Segment examination: Occult globe in healthy sclera and well secured to the globe to rupture results from scleral rupture posterior to the prevent it being dislodged during surgical limbus. Anterior segment features suggestive of manipulation. Infusion port must be free of occult globe rupture include chemosis and an incarceration and able to free flowly in the vitreous asymmetrically deep anterior chamber in the cavity to avoid secondary retinal or choroidal traumatized eye. detachment. Standard 4 mm cannulas are typically 162 Clinical Diagnosis and Management of Ocular Trauma adequate, however, longer 6 mm cannulas are that in case of retinal injury it occurs away from the available for cases with anterior vitreous contraction macula. PVD creation can be difficult in the eyes of or choroidal detachments. In cases where the infusion younger patients. The posterior hyaloid can be cannot be visualized initially an anterior infusion in the engaged with active suction and elevated. In difficult anterior segment of limbus can be employed. A 20 cases a bimanual technique employing suction and a gauge needle on a separate infusion line can often lighted membrane pick can be helpful. The posterior be helpful as an alternate infusion until the pars plana hyaloid is elevated with the suction instrument and infusion can be visualized. the pick is used to engage the hyaloid and lift it from the retinal surface. Vitreous skirt is peeled anteriorly Visualization of the Posterior Segment is Essential to the vitreous base and trimmed as much as safely possible, avoiding anterior retinal injury. Anterior segment hemorrhage should be cleared using passive washout techniques or cutting instruments. Corneal management can be difficult in traumatized Vitreous Bands eyes. In cases of severe corneal trauma a temporary Vitreous bands may appear white and can be dense, keratoprosthesis can be employed. Alternatively elastic membranes. Vitreous bands lead to secondary endoscopic visualization systems allow posterior traction on the retina. Vitreous bands can be divided segment manipulation without need for a clear anterior and truncated with the vitrectomy instrument or segment media. Cataract or traumatic disruption of intraocular scissors. the lens may prevent visualization. Lens material can be removed using the vitrectomy instrument or the Pre-retinal Membranes pars plana ultrasonic fragmentation instrument Various techniques of removal of pre-retinal depending on the density of the lens material. The membranes have been described including vitreoretinal decision to preserve the lens capsule for intraocular picks, barbed MVR blades and intraocular forceps. lens placement will vary with the nature and complexity Subretinal membrane removal is typically only of the trauma. In cases with high risk of vitreous necessary if the organized bands prevent complete proliferation complete removal of the lens capsule is retinal flattening. often preferred to avoid leaving scaffolding for membrane formation. Removal of the lens capsule should be complete with scleral depression being of Retinal Incarceration assistance to visualize and remove the peripheral lens Retinal incarceration can produce traction on the retina material and capsule. or prevent complete retinal flattening. Retinotomy is often required in the management of incarceration.14 Vitrectomy Endodiathermy is placed around the incarceration site and the retina is divided with intraocular scissors or Vitrectomy is accomplished with high speed cutting the high speed cutter. instruments. The vitreous of the traumatized eye is typically blood stained. The appearance of the blood will vary with the timing of surgery with acute blood Choroidectomy appearing red but older blood having an ochre Anecdotal evidence for removal of devitalized choroidal appearance. Older vitreous hemorrhage is often tissue at the time of vitrectomy to reduce the rate of associated with a denser, more congealed vitreous gel secondary PVR and redetachment. than acute hemorrhages. The objectives during vitrectomy include: (1) removal of blood to allow Foreign Body Removal visualization of the retina and (2) creation of a complete The objective of surgery is complete and atraumatic posterior vitreous detachment. Constant visualization removal of the IOFB. Methods for removal include of the vitrectomy port is key to avoiding secondary external magnets and direct removal. External magnets trauma, particularly in cases where visualization is have been used for over 100 years in ophthalmology difficult. The vitrectomy port should be anteriorly for the removal of foreign bodies, however, they have oriented and constantly visualized. In cases of extensive been increasingly replaced by direct removal techni- vitreous hemorrhage the surgeon should be constantly ques. Electromagnetic current is used to draw the looking for signs of retinal vessels to avoid inadvertent foreign body to the eye wall where it can be removed retinal trauma. In dense hemorrhages exploration of via a prepared sclerotomy. Direct removal via direct the vitreous cavity begins centrally and then progresses visualization is preferred method for IOFB removal, peripherally. If the location of the retina is in question, thus avoiding secondary iatrogenic trauma. Foreign then posterior dissection is often initiated nasally so bodies may be encased in an inflammatory capsule Penetrating Posterior Segment Trauma 163 that must be incised prior to removal. Intraocular vitreous hemorrhage after closed globe injury magnets and specialized forceps can be used to underwent PPV/PPL.20 In a non-randomized manipulate the foreign body and allow extraction comparative review of 15 patients with prophylactic through a limbal sclerotomy. scleral buckle and 18 without. No difference in retinal detachment rate (24% with scleral buckle and 17% Retinal Detachment without) was observed. Once all traction from vitreous or pre-retinal membranes is relieved the retina can be flattened. The Perfluorocarbon Liquid retina is flattened with air-fluid exchange or use of Perfluorocarbon liquids can be useful for manipulation perfluorocarbon liquids. Perfluorocarbon liquid is often and stabilization of detached retina. They may also preferable in trauma cases due to easier visualization be useful in the manipulation of IOFB.21 of the retina during the application of retinopexy. Endolaser or indirect laser retinopexy is applied to any Silicone Oil retinal breaks observed. Tamponade is typically required for cases with retinal detachment. Tamponade can be achieved with intra- Scleral Buckle ocular gas or silicone oil. No comparative trials of gas Encircling scleral buckles support the vitreous base and versus silicone oil in the context of penetrating ocular may be useful in preventing later retinal detachment. trauma exist. the Silicone Oil study excluded patients Animal models of retinal injury with randomized with retinal detachment in the setting of prior trauma. placement of episcleral buckle at the site of the Silicone oil tamponade may be useful in cases of severe laceration suggested that the buckle reduced vitreous ocular trauma. A case series of 23 patients with IOFB traction and reduced the degree of fibrovascular with placement of silicone oil at the time of initial repair proliferation at the injury site.15 Some studies suggest showed utility.22 61 % had retinal detachment at the that placement of a scleral buckle significantly reduces time of initial surgery. 78% had silicone oil removed the risk of later retinal detachment. A series of eyes after average of 9.1 months. Complete retinal reattach- undergoing vitrectomy with and without scleral buckle ment was achieved in 83% of eyes. Only 30% achieved suggested that the encircling buckle reduced the rate reattachment with one procedure with 70% of subsequent detachment.16 27% developed a detach- developing PVR. Visual acuity stabilized with an average ment without a prophylactic buckle compared with acuity of 20/640 and 55% achieving better than 20/ 8% that received a prophylactic buckle. Other series 400. Another case series of 13 eyes undergoing PPV have found that the detachment rate without a after trauma examined the role of silicone oil prophylactic buckle was 23% compared to 13% with tamponade.23 Cases had lacerations greater than 4 disc a buckle.17 In a prospective controlled clinical trial of diameters, primary RD greater than 2 quadrants or prophylactic scleral buckle with PPV in patients with persistent intrasurgical hemorrhage. 11 eyes underwent retained IOFB without retinal detachment 28 patients silicone oil removal at average of 5.8 months with visual underwent surgery.18 Rate of secondary retinal acuity ranging from 20/25 to 20/200. 2 eyes developed detachment was 6.6% with prophylactic scleral buckle PVR. and 30.8% without scleral buckle. While suggesting benefit to prophylactic scleral buckle the results did Antibiotics not meet statistical significance. In a matched Endophthalmitis is a potentially devastating compli- retrospective series of patients undergoing prophylactic cation of penetrating trauma. Antibiotic prophylaxis scleral buckle placement at the time of open globe seems reasonable though there is little evidence that repair.19 19 patients with prophylactic scleral buckle clarifies the preferred route of administration or the placement and 19 patients without scleral buckle were matched by visual grade, zone of injury and true efficacy of these measures. mechanism of injury. Patients with scleral buckle had significantly better visual outcome (20/270 versus hand Complications motions). There was a trend towards lower retinal detachment rate with prophylactic scleral buckle ENDOPHTHALMITIS placement (26% versus 53%) that did not meet statistical significance. Some series do not suggest a Epidemiology significant benefit to prophylactic scleral buckle. In a Two to seven percent of penetrating injuries result in series of 33 patients with retinal detachment and culture proven endophthalmitis.24 164 Clinical Diagnosis and Management of Ocular Trauma Risk Factors segment trauma. Studies conducted between 1952 The presence of IOFB increases the risk of secondary and 1970 showed that only 6 % of patients with infection. A delayed primary repair increases risk of ruptured globes achieved better than 5/200 visual 30 infection significantly. A 24 hour delay in primary repair acuity. Later studies conducted between 1985 and increases the risk of infection from 3.5 to 13.4%.25 1993 found that 36% of patients achieved better than 31 Disruption of the lens also increases the risk of infection 20/40. 15.8 times.26 In a case series of 110 eyes in Southern Several prognostic factors influence the outcome India with open globe injuries that underwent culture of open globe injuries. Poorer initial visual acuity of aqueous or prolapsed ocular tissue at the time of predicts a poorer outcome. A case series of 453 patients injury 56 patients had contamination (42 bacterial and with penetrating injuries showed that chance of 14 fungal).27 19 patients developed endophthalmitis regaining visual acuity better than 5/200 was 97% if with 18 having initial contamination noted. Multivariate the initial acuity was better that 5/200 and only 36% 31,32 analysis demonstrated that delayed surgical intervention if the initial acuity was worse than 5/200. The size greater than 72 hours, uveal tissue prolapse and of laceration is also important prognostically with corneoscleral laceration were associated with an lacerations greater than 10 mm carrying a poorer visual 31 increased risk of positive culture. prognosis. The location of laceration has been associated with outcome with more posterior lacerations having a poorer prognosis, presumably due to more Etiology The spectrum of organisms causing post-trauma endophthalmitis differs from those observed in post- operative endophthalmitis. Bacillus cereus is often observed in traumatic endophthalmitis, particularly in cases of IOFB contaminated with soil. Organisms observed in one series of post-traumatic endophthal- mitis include:28 • Staph epidermidis 24%. • Bacillus cereus 22% • Strept 13% • Gram negative 11% • Staph aureus 8% • Fungi 8%

SIDEROSIS Fig. 27.1: Right eye of young male following trauma from Siderosis results from retention or iron containing IOFB a homemade projectile device. Visual acuity was no light perception at presentation. He underwent primary repair. leading to oxidation and cellular damage. The clinical Post day 1 acuity was light perception features include: iris heterochromia with the affected eye becoming brownish; a mid dilated, non-reactive pupil; brown lens deposits; secondary open-angle glaucoma and peripheral pigmentary degeneration of the retina associated with vascular sclerosis. A decreased b wave on ERG is frequently noted.

CHALICOSIS Chalicosis results from retention of copper containing foreign bodies. The clinical features include: Kayser Fleischer ring; blue green peripheral corneal ring; sunflower anterior subcapsular cataract; refractile metallic aqueous particles and greenish iris discoloration.

Prognosis Fig. 27.2: Left eye of the same patient was light perception at presentation. The eye underwent primary repair. Day 1 Improvements in surgical management have resulted acuity was no light perception. At day 3 the eye became in better visual outcomes in patients suffering posterior inflamed and phthsical and underwent enucleation Penetrating Posterior Segment Trauma 165

2. Parver LM, Dannenberg AL, Blacklow B, et al. Characteristics and causes of penetrating trauma eye injuries reported to the National Eye Trauma System Registry, 1985-1991. Public Health Reports 1993;108: 625-32. 3. Bajaire B, Oudovitchenko E, Morales E. Vitreoretinal surgery of the posterior segment for explosive trauma in terrorist warfare. Grafes Arch Clin Exp Ophthalmol 2006;244:991-95. 4. Thach AB, Johnson AJ, Carroll RB et al. Severe eye injuries in the war in Iraq, 2003-2005. Ophthalmol 2008;115:377-82. 5. Vasu U, Vasnaik A, Battu RR, et al. Occupational open globe injuries. Ind J Ophthalmol 2001;49:43-47. 6. Delori F, Pmerantzzeff O, Cox MS. Deformation of the Fig. 27.3: Patient underwent secondary repair of the rupture globe under high speed impact: its relation to contusion right eye on day 4. Surgery involved vitrectomy, 360° retinotomy and peeling of membranes, temporary injuries. Invest Ophth Vis Sci 1969;8:290-301. keratoprosthesis and corneal transplantation with silicone 7. Cox MS, Schepens CL, Freeman HM. Retinal detachment oil tamponade. Five years later visual acuity was 20/200 due to ocular contusion. Arch Ophthalmol 1966;76: with aphakic spectacles 678-85. 8. Cleary PE, Ryan SJ. Experimental posterior posterior penetrating injury in the rabbit. II. Histology of wound, vitreous and retina. Br J Ophthalmol 1979;88:221-31. 9. Cleary PE, Ryan SJ. Experimental posterior posterior penetrating injury in the rabbit. I. Method of production and natural history. Br J Ophthalmol 1979;63:306-11. 10. Kuhn F, Morris R, Witherspoon CD, et al. A standardized classification of ocular trauma. Ophthalmol 1996;103:240-43. 11. Zinreich SJ, Miller NR, Aguayo JB, et al. Computed tomographic three-dimensional localization and compositional evaluation of intraocular and orbital foreign bodies. Arch Ophthalmol 1986;104:1477-82. 12. Gregor Z, Ryan SJ. Combined posterior contusion and penetrating injury in the pig eye. III. A controlled treatment trial of vitrectomy. Br J Ophthalmol 1983;67:282-85. 13. Gregor Z, Ryan SJ. Complete and core vitrectomy in the treatment of experimental posterior penetrating eye injury in the rhesus monkey. Br J Ophthalmol 1983;101: Fig. 27.4: Fundus photo of the right eye shows attached 441-45. posterior pole under silicone oil with extensive laser 14. Han DP, et al. Management of traumatic retinal incarceration with vitrectomy. Am J Ophthalmol extensive retinal injury. In a series of 453 traumatized 1988;106:640-45. eyes 60% of eyes with lacerations anterior to the muscle 15. Men G, Peyman GE, Kuo PC, et al. The role of scleral insertions achieved functional vision in comparison to buckle in experimental posterior penetrating eye injury. 28% where the lacerations extended posterior to the Retina 2003;23:202-08. muscles and only 4% where the laceration extended 16. Brinton GS, Aaberg TM, Reeser FH, et al. Surgical results in ocular trauma involving the posterior segment. Am J posterior to the equator.31 The prognostic effect of an Ophthalmol 1982;93:271-78. IOFB varies with the size and shape of the foreign body 17. Hutton WL, Fuller DG. Factors influencing final visual and the location of injury. In general the presence of results in severely injured eyes. Am J Ophthalmol an IOFB does not necessarily indicate a poor prognosis 1984;97:715-22. with approximately 1/3 of eyes in most series achieve 18. Azad RV, Kumar N, Sharma YR, et al. Role of prophylactic 20/40 or better acuity. scleral buckling in management of retained intraocular foreign bodies. Clin Exp Ophthalmol 2004;32:58-61. 19. Arroyo JG, Postel EA, Stone T, et al. A matched study of primary scleral buckle placement during repair of References posterior segment open globe injuries. Br J Ophthalmol 1. Smith D, Wrenn K, Stack LB. The epidemiology and 2003;87:75-78. diagnosis of penetrating injury. Acad Emerg Med 20. Ersanli D, Sommez M, Unal M et al. Management of 2002;9:209-13. retinal detachment due to closed globe injury by pars 166 Clinical Diagnosis and Management of Ocular Trauma

plana vitrectomy with and without scleral buckling. Retina 26. Thompson WS, Rubsamen PE, Flynn HW, et al. 2006;26:32-36. Endophthalmitis after penetrating trauma: Risk factors and 21. Sudhalkar HA, Johnson MW. Perfluorocarbon liquid visual acuity outcomes. Ophthalmol 1995;102: manipulation of high-density intraocular foreign bodies. 1696-1701. Retina 1998;18:460-65. 27. Gupta A, Srinivasan R, Kaliaperumal S, et al. Microbial 22. Szurman P, Roters S, Grisant S, et al. Primary silicone oil cultures in open globe injuries in Southern India. Clin tamponade in the management of severe intraocular Exp Ophthalmol 2007;35:432-38. foreign body injuries: An 8 years follow-up. Retina 28. Parrish CM, O’Day DM. Traumatic endophthalmitis. Int Ophthalmol Clin 1987;27:112-19. 2007;27:304-11. 29. Cherry PHM. Rupture of the globe. Arch Ophthalmol 23. Spiegel D, Nasemann J, Nawrocki J, et al. Severe ocular 1972;88:498-507. trauma managed with primary pars plana vitrectomy and 30. Pieramici DJ, MacCumber MW, Humayun MU, et al. silicone oil. Retina 1997;17:275-85. Open globe injury: Update on types of injuries and visual 24. Brinton GS, Topping TM, Hyndiuk RA, et al. results. Ophthalmol 1996;103:1798-1803. Posttraumatic endophalmitis. Arch Ophthalmol 31. de Juan E, Sternberg P, Michels RG. Penetrating ocular 1984;102:547-50. injuries: Types of injuries and visual results. Ophthalmol 25. Thompson JT, Parver LM, Enger CL, et al. Infectious 1983;90:318-22. endophthalmitis after penetrating injuries with retained 32. Sternberg P, de Juan E, Green WR, et al. Multivariate intraocular foreign bodies. National Eye Trauma System. analysis of prognostic factors in penetrating ocular Opthalmol 1993;100:1468-74. injuries. Am J Ophthalmol 1984;98:467-72. CHAPTER

Traumatic Retinopathies 28 Scott Pfahler, T Mark Johnson (USA)

Commotio Retinae The term commotio retinae (latin for retinal contusion) was coined by Berlin in 1873.1

ETIOLOGY AND PATHOLOGY Commotio is primarily observed following blunt ocular trauma (anterior contra-coup injury). Electrical injuries have also been described with similar findings. In both animal and human histological reports, the areas of retinal whitening have been shown to be frag- Fig. 28.1: OCT of patient with commotio retinae with mented outer segment photoreceptors. Later changes increased reflectivity at the level of the photoreceptors include swelling of photoreceptor inner segments and breakdown of the outer blood-retinal barrier.2 Other pathologic findings include cystic spaces, disruption of level of the photoreceptor outer segments in the area 7,8 RPE plasma membranes and loss of RPE apical of retinal whitening (Fig. 28.1). processes.3 Experimental models suggest that the outer blood-retinal barrier is re-established 7 to 14 days post- TREATMENT AND PROGNOSIS injury and that outer segments show evidence of The natural history of commotio retinae has shown regeneration. Clinical methods of evaluation of the to resolve in about 2-3 days, usually with return of foveal cone pigment has suggested impairment at the visual acuity. If injury occurs in the macula, reports time of the acute injury with resolution by 3 months of permanent visual loss has been reported. follow-up visits.4 CLINICAL FEATURES Traumatic Macular Hole Ophthalmoscopic examination reveals an area of retinal The first report case of traumatic macular hole whitening which can be found in both peripheral retina secondary to blunt ocular trauma was reported by as well as the posterior pole. If the retinal whitening occurs Knapp in 1869.9 in the posterior pole, the term Berlin’s edema is used.1 In both animal and human histological reports, the areas of retinal whitening have been shown to be fragmented ETIOLOGY AND PATHOLOGY outer segment photoreceptors. Other pathologic findings The mechanism of traumatic macular hole formation include cystic spaces, disruption of RPE plasma has been thought to be the result of ocular deformation membranes and loss of RPE apical processes.3,5 of the posterior pole at the time of trauma. This appears to lead to secondary retinal edema with cystoid DIAGNOSTIC TESTING changes in the outer retina10,11 (Fig. 28.2). Fluorescein angiography often reveals early hypo- fluorescence with late leakage, described by Gass as CLINICAL FEATURES “acute pigment epithelial edema.”6 Recent reports Macular holes in patients suffering blunt trauma often using OCT have described increased reflectivity at the have different features from the more common 168 Clinical Diagnosis and Management of Ocular Trauma Direct trauma can result in contusion necrosis of the choroid with a rupture oriented parallel to the ora serrata. Indirect choroidal ruptures result in a posterior rupture that is concentric to the optic nerve. This occurs following a compressive force upon the posterior pole combined with the anchoring effect of the optic nerve.

CLINICAL FEATURES Fig. 28.2: OCT of patient with traumatic macular hole Typical findings include intrachoroidal, subretinal and intraretinal hemorrhages. Commotio retinae is often idiopathic macular hole. Given that the pathogenesis accompanied with the choroidal rupture.20-22 Following is related to ocular deformation at the time of trauma choroidal rupture the local area of injury undergoes rather than abnormal progression of posterior vitreous bleeding, fibrovascular tissue proliferation and then detachment a PVD is rarely encountered in these RPE hyperplasia. Retinal tissue injury is variable and patients. In one series only 15% of cases had an can range from no direct injury to full thickness associated PVD at diagnosis.12 fibrovascular proliferation with vitreo retinal Traumatic macular holes are more typically elliptical proliferation20 (Figs 28.3A and B). with irregular edges. Traumatic holes tend to be larger The most common secondary complication of in size ranging from 0.2 to 0.5 DD.12 At diagnosis the choroidal rupture is development of choroidal neovas- holes are often associated with other features of trauma cularization. Reports of CNV following choroidal rupture including hyphema, commotion retina and vitreous have been reported as early as one month post-injury hemorrhage. Secondary retinal detachment may occur.

TREATMENT AND PROGNOSIS Spontaneous closure of traumatic macular holes is well described. Studies of mERG in patients with spontaneous closure of traumatic macular holes show improved func- tion with closure though recovery is often incomplete.13 In cases with persistent macular hole vitrectomy is typically recommended. Creation of a posterior vitreous detachment can be challenging in pediatric patients. Autologous plasmin has been used as a surgical adjunct to assist in creation of PVD.14 Removal of the internal limiting membrane may be useful to improving the rate of hole closure though no comparative studies exist in the context of traumatic Fig. 28.3A: Post-blunt trauma patient has acute 15,16 macular holes. Surgical closure rates have been subretinal hemorrhage reported to range from 87 to 100%.14-17 Visual recovery is variable and is influenced by the underlying ocular injury. Approximately 50% of patients achieve better than 20/50 acuity.18

Choroidal Rupture Choroidal ruptures can occur after blunt trauma (compression/contusion injuries). The incidence of this type of injury is between 5-10% of all blunt ocular trauma.19

ETIOLOGY AND PATHOGENESIS Positioned between the elastic scleral and retina, the inelastic Bruch’s membrane/RPE/Choriocapillaris Fig. 28.3B: Two weeks later clearance of subretinal complex is susceptible to rupture and tearing.20-22 blood shows evidence of choroidal rupture Traumatic Retinopathies 169 to four years later.23-26 A study of 111 patients with choroidal rupture showed that older age and macular choroidal rupture where strongly associated with CNV formation.27 Another study identified proximity to the fovea and length of the rupture as risk factors for developing CNV.28

DIAGNOSTIC TESTING Indocyanine green angiography and fluorescein angiography may aid in the visualization of ruptures not seen clinically.23,24 Optical coherence tomography may be a useful adjunct in following patients with choroidal ruptures.

TREATMENT AND PROGNOSIS Fig. 28.4: Extensive subretinal hemorrhage and retinal Current options for treatment of CNV associated with edema following blunt trauma with a paintball gun choroidal rupture are thermal laser photocoagulation, are often serrated. Due to the extensive fibrosis photodynamic therapy, photodynamic therapy with associated with this injury, retinal detachment is a rare adjuvant feeder vessel therapy, anti-VEGF intravitreal occurrence associated with this condition36 (Fig. 28.4). injections, submacular surgery. No comparative trials of therapy exist.29-32 The visual prognosis associated with choroidal TREATMENT AND PROGNOSIS rupture depends upon the location and the presence No treatment has been described to date. Visual prog- of neovascularization. A long-term study (4 years, 32 nosis is dependent upon the location of the injury, with eyes) of patients with choroidal ruptures secondary in the worst visual prognosis involving the posterior pole. the foveal region, juxtafoveal, and extrafoveal regions had final visual acuities of 20/68, 20/35, and 20/60 respectively over a period of 4.5, 3.5, and 4.4 years.33 Purtscher’s Retinopathy The term “Purtscher’s retinopathy” was derived from Otmar Purtschers original description of with multiple Chorioretinitis Sclopetaria retinal white spots scattered throughout the posterior pole after trauma in 1912. He suspected that these The term chorioretinitis sclopetaria has been used to white spots were caused by lymphatic extravasations describe chorioretinal injury from high velocity vehicle, associated with increased intracranial pressure typically a bullet or other high velocity projectile. This associated with head trauma.37 phenomenon was first described by Goldzieher in 1901.34 ETIOLOGY AND PATHOGENESIS ETIOLOGY AND PATHOGENESIS Purtscher’s retinopathy arises following severe head trauma or chest compression without direct globe Classically these injuries occur following a high velocity injury. It is generally considered to be a rare missle injury to the orbit. This has been attributed to phenomenon with the incidence of Purtscher’s shock waves within the orbit resulting in ruptures of retinopathy estimated at 0.24 cases per million choroidal and retinal layers with or without hemorrhage. population per year in the United Kingdom. The projectile does not contact the globe structures. The pathogenesis of Purtscher retinopathy has been The proximity to the globe, the size of the projectile widely debated, possible causes include fat emboli, air and its velocity may influence the nature of the injury. embolization, venous reflux with endothelial swelling, Following the initial injury, observational and pathologic and severe angiospasm.38-43,45 A common link between accounts have described a fibrovascular and pigmentary 35 many cases has been leukocyte aggregation by acti- proliferation with loss of photoreceptors. vated complement factor 5 (C5a) which can occur in the conditions mentioned previously. Despite the wide CLINICAL FEATURES range of opinions regarding the etiology the apparent At the time of the acute injury there is extensive retinal occlusion of capillaries on IVFA suggest an emboli edema and hemorrhage. The borders of the injury nature.40, 43,44 170 Clinical Diagnosis and Management of Ocular Trauma CLINICAL FEATURES have been described for large subhyaloid hemorrhages Typically findings in Purtscher retinopathy are bilateral that obscure the macula. Treatment options include but there have been reports of unilateral cases. Visual Nd:YAG laser hyaloidotomy, krypton laser membro- 55,56 acuity typical ranges from 20/200 to CF with possible tomy, or vitrectomy with membrane peel. The visual recovery to pre-event levels. Findings often prognosis in this condition is good, with vision often include inner retinal whitening polygonal in shape returning following resolution of the hemorrhage. which spare areas near the vasculature. Often upon resolution of the retinal edema/cotton-wool spots, there is nerve fiber layer dropout, mottling of the RPE in Shaken Baby Syndrome/ the involved areas and possible optic atrophy.45 Child Abuse DIAGNOSTIC TESTING ETIOLOGY AND PATHOGENESIS IVFA findings can vary from staining and leakage of The presence of retinal hemorrhages in a child is highly the vasculature early in the course of the disease to suspicious for abuse and non accidental head trauma. capillary non-perfusion late in the disease. ICGA can Retinal hemorrhages are a common finding in reveal choroidal hypofluorescent areas. childhood abuse cases and are the most common ocular finding in children with manifestations of child TREATMENT AND PROGNOSIS abuse occurring 11-23% of abused children and 50- 80% of shaken babies.57 Conversely direct, accidental Some reports suggest high dose corticosteroids as head trauma in children rarely produces intraocular therapy for Purtsher’s retinopathy but there are no hemorrhages.58 In a series of 241 infants hospitalized randomized trials to evaluate this treatment.45 with subdural hematomas 77.5% of children with shaken baby syndrome had intraocular hemorrhage compared with 0% with a history of direct, accidental Valsalva Retinopathy trauma.58 The likely cause of these hemorrhages are the ETIOLOGY AND PATHOGENESIS sudden, severe acceleration/deceleration head and Retinopathy caused by a sudden increase in venous neck movementts. Children are usually age three or pressure in the retinal capillary network has been younger in age.60 Similar ophthalmic findings have been reported. With the valveless nature of the venous described in abused children that are older.61 Macular system in the head and neck, increases in abdominal retinoschisis is a characteristic autopsy finding that is or intrathoracic pressure can be transmitted to the not observed with other forms of head trauma.62 head and neck resulting in a sudden increase in the capillary venous pressure with subsequent retinal CLINICAL FEATURES hemorrhage.46 Reports of this phenomenon have been associated with the Valsalva maneuver, heavy lifting, Involvement of ophthalmologists in the screening for childbirth, motor-vehicle airbags, sexual activity, shaken baby syndrome is of paramount importance. choking, vigorous dancing, refractive surgery.50-54 55 % of non-ophthalmologists involved in shaken baby cases fail to examine the retina.59 External signs of shaking or child abuse may be absent with only retinal CLINICAL FEATURES hemorrhages and subdural/subarachnoid hemorrhages Visual loss can occur with hemorrhages in the macular present. In one case series of 75 cases of shaken baby region. Peripheral hemorrhages are often asympto- syndrome 93 % had subdural hematoma, 44 % cerebral matic. More extensive hemorrhages can occur with edema and 16 % subarachnoid hemorrhage.63 Clinical sub-internal limiting membrane hemorrhages and the features include intraretinal, preretinal and sub ILM possibility of breaking through and becoming sub- hemorrhages (Fig. 28.5). hyaloid or vitreous hemorrhages.47 One published case report using OCT showed that the anatomic location DIAGNOSTIC TESTING 48, 49 was likely sub-ILM. All cases of suspected abuse need to be evaluated by a multi-disciplinary team. Neuroimaging is important TREATMENT AND PROGNOSIS due to the frequent association with intracranial Most Valsalva hemorrhages are minimally symptomatic hemorrhage. and do not require treatment. Many symptomatic Recent studies involving optical coherence tomo- hemorrhages will resolve spontaneously. Treatments graphy have shown evidence of vitreomacular traction Traumatic Retinopathies 171 ment is possible. Animal models of high velocity projectiles suggest that direct corneal trauma tended to produce tenting of the nasal retinal while peripheral trauma produced direct retina effects.69 High speed cinematography describes four phases of globe deformation from high velocity trauma: (1) compression of the globe with decreased axial length and equatorial expansion; (2) decompression with an increase in axial length and a decrease in equatorial diameter; (3) overshoot with a rebound in axial lengthening and equatorial shortening and (4) oscillation of small movement of the eye.70 Retinal breaks appear to develop via two mechanisms: (1) vitreous base contraction with traction on the anterior retina or (2) contusion necrosis Fig. 28.5: Extensive preretinal hemorrhages in of the retina secondary to direct trauma. shaken baby syndrome CLINICAL FEATURES associated with preretinal blood. In addition evidence Traumatic retinal detachments differ from routine of perimacular folds and hemorrhagic macular retino- rhegmatogenous detachments by the nature of the schisis were documented.64 pathologic retinal break. Traumatic detachments are more likely to arise from dialyses (55% of traumatic TREATMENT AND PROGNOSIS detachments versus 5% of rhegmatogenous detach- ments) or giant retinal tears (16 % of traumatic detach- Management of this condition necessitates prompt noti- ments versus 2 % of rhegmatogenous detachments).71 fication of children services authorities in the community Lattice degeneration is much less commonly observed and treatment of underlying retinal hemorrhagic and in traumatic retinal detachment series. neurologic sequelae. In one series of 241 infants 82% of intraocular hemorrhages resolved within 4 weeks.58 In cases of premacular hemorrhage that obscure the TREATMENT AND PROGNOSIS visual axis vitrectomy should be considered to reduce The preferred treatment of retinal breaks and detach- the risk of ambyopia. ments secondary to trauma vary but include laser retinopexy, cryopexy, pneumatic retinopexy, scleral buckle, pars plana vitrectomy, or combinations of these treatments. The prognosis depends up the extent and Retinal Tears, Retinal Dialysis duration of the retinal break or detachment.68 Treatment and Detachments options for traumatic retinal dialysis can include laser demarcation for small inferior temporal dialysis, while ETIOLOGY AND PATHOGENESIS scleral buckling has been shown to be successful in 96- In many case series, blunt force trauma causes the 98% of eyes with trauma associated retinal dialysis .72-75 majority of traumatic retinal detachments (70-86%) The most common age and sex demographic is young References males, who overall account for the majority of trauma cases.65-67 A large case series consisting of 160 patients 1. Berlin R. Zur sogenauten commotion retinae. Klin with retinal detachment showed that signs of detach- Monatsbl Augenheilkd 1873;1:42-78. ment manifested within two years of injury in most 2. Bunt-Milam AH, Black RA, Bensinger RE. Breakdown of the outer blood-retinal barrier in experiemental cases, however, a wide range exists. 12% of detach- commotion retinae. Experimental Eye Res 1986;43; ments are noted within 24 hours. Some presentations 397-412 may be delayed by many years.68 3. Blight R, Hart JCD. Structural changes in the outer retinal The pathological mechanism thought to cause layers following blunt mechanical non-perforating retinal tears and detachments is the rapid anterior- trauma to the globe: An experimental study. Br J posterior compression of the globe/vitreous structure Ophthalmol 1977;61:573-87. 4. Liem AT, Keunen JE, van Norren D. Reversible cone which causes a degree of vitreous base traction and photoreceptor injury in commotion retinae of the macula. subsequent retinal tears. If the vitreous has not liquefied Retina 1995;15;58-61. the break may remain stable but if liquid vitreous 5. Mansour AM, Green WR, Hogge C. Histopathology of accumulates near the break, a future retinal detach- commotion retinae. Retina 1992;12;24-28. 172 Clinical Diagnosis and Management of Ocular Trauma 6. Gass JDM. Stereoscopic atlas of macular diseases: 26. Smith RE, Kelly JS, Harbin TS. Late macular Diagnosis and treatment. St Louis: Mosby 1987. complications of choroidal ruptures. Am J Ophthalmol 7. Sony P, Venktash P, Gadaginamath S et al. Optical 1974;77:650-58. coherence tomography findings in commotion retina. 27. Ament CS, Zacks DN, Lane AM, el at. Predictors of visual Clin Experiment Ophthalmol 2006;34;621-23. outcome and choroidal neovascular membrane 8. Meyer CH, Rodrigues EB, Mennel S. Acute commotio formation after traumatic choroidal rupture. Arch retinae determined by cross-sectional optical coherence Ophthalmol 2006;124 (7):957-66. tomography. Eur J Ophthalmol 2003;13;816-18. 28. Secretan M, Sickenberg M, Zografos L, et al. Morphometic 9. Woldter JR. Coup-contrecoup mechanism of ocular characteristics of traumatic choroidal ruptures associated injuries. Am J Ophthalmol 1963;56:785-96. with neovascularization. Retina 1988:18;62-66. 10. Oehrens AM, Stalamns P. Optical coherence tomography 29. Mehta HB, Shanmugam MP. Photodynamic therapy of documentation of the formation of a traumatic macular a post-traumatic choroidal neovascular membrane. hole. Am J Ophthalmol 2006;142;866. Indian J. Ophthalmol 2005;53(2):131-32. 11. Frangieh GT, Green WR, Engel HM. A histopathologic 30. Harissis-Dagher M. Sebag M. Gauthier D, Marcil G. study of macular cysts and holes. Retina 1981;1: LabelleP, Arbour JD. Photodynamic therapy in young 311-36. patients with choroidal neovascularization following 12. Yanagiya N, Akiba J, Takahashi M, et al. Clinical traumatic choroidal rupture. Am J Ophthamol characteristics of traumatic macular holes. Jpn J 2005;139(4):726-28. Ophthalmol 1996;40;544-47. 31. Mennel S, Hausmann N. Meyer CH, Peter S 13. Chen H, Zhang M, Huang S, et al. OCT and multi focal Photodynamic Therapy and indocyanine green guided ERG findings in spontaneous closure of bilateral feeder vessel photocoagulation of choroidal neovas- traumatic macular holes. Documenta Ophthalmol cularization secondary to choroids rupture after blunt 2008;116;159-64. trauma. Graefes Arch Clin Exp Ophthalmol 2005;243(1): 14. Wu WC, Drenser KA, Trese MT et al. Pediatric macular 68-71. hole:results of autologous plasmin enzyme assisted 32. Gotzaridis EV, Bakalis AN, Sethi CS, Charteris DG. vitrectomy. Am J Ophtalmol 2007;144;668-72. Surgical removal of sequential epeiretinal and subretinal 15. Kuhn F, Morris R, Mester V, et al. Internal limiting neovascular membranes in a patient with traumatic membrane removal for traumatic macular holes. choroidal rupture. Eye 2003;17(6):790-91. Ophthalm Surg Lasers 2001;32:308-15. 33. Raman SV, Desai UR, Anderson SR, Samuel, MA. Visual 16. Kumar A, Wagh VB, Prakash G, et al. Visual outcome prognosis in patients with traumatic choroidal rupture. and electron microscopic features of indocyanine green Can J Ophthalmol 2004;39(3):260-66. assisted internal limiting membrane peeling from 34. Goldzieher W. Beitrag zur Pathologie der oritaln macular hole of various aetiologies. Ind J Ophthalmol 2005;53;159-65. Schussverletzugen. Z Augenheilkd 1901;6:277. 17. Chen YP, Chen TL, Chao AN, et al. Surgical management 35. Maguluri S, Hartnett M. Radial choroidal ruputures in of traumatic macular hole-related detachment. Am J sclopetaria. J Am Coll Surg 2003;197:689-90. Ophthalmol 2005;140;331-33. 36. Benson WE, Shakin J, Sarin LK. Blunt trauma. In: Tasman 18. Johnson RN, McDonald HR, Lewis H, et al. Traumatic W, Jaeger EA (Eds) Clinical ophthalmology, vol. 3. macular hole: Observations, pathogenesis and results of Philadelphia: JB Lippincott 1988. vitrectomy surgery. Ophthalmol 2001;108;853-57. 37. Purtscher O. Noch unbekannte Befunde nach 19. Benson WE, Shakin J, Sarin LK. Blunt trauma. In: Tasman Schadeltrauma. Berl Dtsch Ophthal Ges 1910;36: W, Jaeger EA, (Eds.) Clinical ophthalmology, Vol. 3. 294-301. Philadelphia: JB Lippincott 1988. 38. Kelley JS. Purtscher’s retinopathy related to chest 20. Aguilar JP, Green WR. Choroidal rupture: A compression by safety belts: Fluorescein angiographic histopathologic study of 47 eyes. Retina 1984;4: findings. Am J Ophthalmol 1972;74:278-83. 269-275. 39. Blodi B, Johnson MW, Gass JDM, et al. Purtscher’s-like 21. Hilton GF, Late serosanguinous detachment of the macula retinopathy after childbirth. Ophthalmology 1990; after traumatic choroidal rupture. Am J Ophthalmol 1975; 97:1654-59. 79:997-1000. 40. Burton TC. Unilateral Purtscher’s retinopathy. 22. Wyszynski RE Grossniklaus HE, Frank KE. Indirect Ophthalmology 1980;87:1096-1105. choroidal rupture secondary to blunt ocular trauma: a 41. Patel M, Bains A, O’Hara JP, et al. Purtscher retinopathy review of eight eyes. Retina 1988;8:237-43. as the initial sign of thrombotic thrombocytopenic 23. Har JCD, Natisikos VE, Raistrick ER, et al. Indirect purpura/hemolytic uremic syndrome. Arch J Ophthalmol choroidal tears at the posterior pole: a fluorescein 2001;119:1388-90. angiographic and perimetric study. Br J ophthalmol 1980; 42. Fischbein F, Safir A. Monocular Purtscher’s retinopathy: 64:59-67. a fluorescein angiographic study. Arch Ophthalmol 24. Kohno T, Miki T, Shiraki K, et al. Indocyanine green 1971;85:480-84. angiographic features of choroidal rupture and choroidal 43. Shah GK, Penne R, Grand MG. Purtscher’s retinopathy vascular injury after contusion ocular injury. Am J secondary to airbag injury. Retina 2001;21:68-69. Ophthalmol 2000;129:38-46. 44. Jacob HS, Craddock PR, Hammerschmidt DE, et al. 25. Fuller B, Gitter KA. Traumatic choroidal rupture with later Complement-induced granulocyte aggregation: An serous detachment of macula: report of successful argon unsuspected mechanism of disease. N Engl J N Engl J laser treatment. Arch Ophthalmol 1973;89:354-55. Med 1980;302:789-94. Traumatic Retinopathies 173

45. Agrawal A, McKibbin, M, Purtscher’s retinopathy: 60. Forbes BJ, Christian CW, Judkins AR, et al. Inflicted Epidemiology, clinical features and outcome. Br J childhood neurotrauma (shaken baby syndrome): Ophthalmol 2007;91;1456-59. Ophthalmic findings. J Pediatr Ophthalmol Strabismus 46. Ravin JG, Meyer RF. Fluorescein angiographic findings 2004;41:80-88. in a case of traumatic asphyxia. Am J Ophthalmol 1973; 61. Salehi-Had H, Brandt JC, Rosas AJ et al. Findings in older 75:643-47. children with abusive head injury: Does shaken-child 47. Duane TD. Valsalva hemorrhagic retinopathy. Trans Am syndrome exist? Pediatrics 2006;117:1039-44. Ophthalmol Soc 1972;70:298-311. 62. Gnaanaraj L, Gilliland MG, Yahya RR, et al. Ocular 48. Tatlipinar S, Shah SM, Nguyen QD. Optical coherence manifestations of crush head injury in children. Eye tomography features of sub-internal limiting membrane 2007;21;5-10. hemorrhage and preretinal membrane in Valsalva 63. Morad Y, Kim YM, Armstrong DC, et al. Correlation retinopathy.Can J Ophthalmol 2007;42;129-30. between retinal abnormalities and intracranial 49. Shukla D, Naresh KB, Kim R. Optical coherence abnormalities in the shaken baby syndrome. Am J tomography findings in valsalva retinopathy. Am J Ophthalmol 2002;134;354-59. Ophthalmol 2005;140;134-36. 64. Sturm V, Landau K, Menke MN. Optical Coherence 50. Friberg TR, Braunstein RA, Bressler NM. Sudden visual Tomography Findings in Shaken Baby Syndrome. Am loss associated with sexual activity. Arch Ophthalmol J Ophthalmol 2008. 1995;113:738-42. 65. Giovinazzo VJ, Yannuzzi LA, Sorenson JA, et al. The 51. Ladjimi A, Zaouali S, Messaoud R, et al. Valsalva ocular complications of boxing. Ophthalmology 1987; retinopathy induced by labour. Eur J Ophthalmol 2002; 94:587-96. 12:336-38. 66. Goffstein R, Burton TC. Differentiating traumatic from 52. Ho LY, Abdelghani WM. Valsalva retinopathy associated nontraumatic retinal detachment. Ophthalmology 1982; with the choking game. Semin Ophthalmol 2007;22; 89:361-68. 63-55. 67. Malbran E, Dodds R, Hulsbus R. Traumatic retinal 53. Bar-Sela SM, Moisseiev J. Valsalva retinopathy associated detachment. Mod Probl Ophthalmol 1972;10:479-89. with vigorous dancing in a discotheque. Ophthalmic Surg 68. Cox MS, Schepens CL, Freeman HM. Retinal detachment Lasers Imaging 2007;38;69-71. due to ocular contusion. Arch Ophthalmol 1966; 54. Moshfeghi AA, Harrison SA, Reinstein DZ, Ferrone PJ. 76:678-85. Valsalva-like retinopathy following hyperopic laser in situ 69. Weidenethal DT, Schepens CL. Peripheral fundus changes keratomileusis. Ophthalmic Surg Lasers Imaging. associated with ocular contusion. Am J Ophthalmol 2006:37;486-88. 1966;62;465-77. 55. Khan MT, Saeed MU, Shehzad MS, et al. Nd:YAG laser 70. Delori F, Pomerantzeff O, Cox MS. Deformation of the treatment for Valsalva premacular hemorrhages: 6 month follow-up: Alternative management options for preretinal globe under high speed impact: Its relation to contusion premacular hemorrhages in Valsalva retinopathy. Int injury. Invest Ophthalmol Vis Sci 1969;8;2901-301. Ophthalmol 2007. 71. Goffstein R, Burton TC. Differentiating traumatic from 56. Shen YJ, Kou HK. Krypton laser membranotomy for nontraumatic retinal detachment. Ophthamol premacular hemorrhage. Ophthalmologica 2004;218; 1982;89;361-68. 368-71. 72. Kennedy CJ, Parker CE, McAllister IL. Retinal detachment 57. Buys YM, Levin AV, Enzenauer RW, et al. Retinal findings caused by retinal dialysis. Aust NZ J Ophthalmol 1997; after head trauma in infants and young children. 25:25-30. Ophthalmology 1992;99:1718-23. 73. Bonnet M, Moyenin P, Pecoldowa C, et al. Retinal 58. Pierre-Kahn V, Roche O, Dureau P, et al. Ophthalmologic detachment caused by a tear at the ora serrata. J Francais findings in suspected child abuse victims with subdural d’Ophthalmol 1986;9:231-42. hematomas. Ophthalmol 2003;110;1718-23. 74. Ross WH. Traumatic retinal dialyses. Arch Ophthalmol 59. Morad Y, Kim YM, Mian M, et al. Nonophthalmogists 1981;99:1371-74. accuracy in diagnosing retinal hemorrhages in the shaken 75. Johnston PB. Traumatic retinal detachment. Br J baby syndrome. J Pediatrics 2003;142:431-34. Ophthalmol 1991;75:18-21. CHAPTER

Management of Endophthalmitis

29 Pei-Chang Wu, Hsi-Kung Kuo (Taiwan)

Introduction PROPHYLAXIS In recent evidence-based literature, Cillua et al found Endophthalmitis is defined by marked inflammation preoperative irrigation with povidone-iodine (PI) to of intraocular fluids and tissues. When caused by be a most strongly recommended technique based microorganisms, endophthalmitis often results in severe on the current clinical evidence (Table 29.2).1 PI is visual loss. The broad categories of endophthalmitis a potent antiseptic with a wide spectrum of activity include postoperative (acute-onset, chronic or delayed against both gram-positive and gram-negative bacteria, onset, bleb-associated), post-traumatic, endogenous fungi and viruses. Antimicrobial activity contributes to and miscellaneous, such as intravitreous triamcinolone the 1% free iodine released that occurs after contact associated endophthalmitis, microbial keratitis and with the skin for 30 seconds to 1 minute, and this suture removal (Table 29.1). These categories are effect will last for 1 hour.2, 3 Iodine penetrates the cell important in predicting the causative organism and wall and reacts with amino acids and nucleotides, which guiding therapeutic decisions before microbiological ultimately disrupt the cell’s protein synthesis. Despite confirmation. the wide use of PI solutions as disinfectants in hospitals, TABLE 29.1: Classification of endophthalmitis these solution have been reported to be susceptible and most frequent organisms to contamination with Pseudomonas cepacia, which could be passed on to the patient.4 1. Postoperative a. Acute-onset: coagulase (-) staphylococci (Staph. Preoperative preparation with 5% PI solution Epidermidis), Staphylococcus aureus, Entero- dropped into the conjunctival sac followed by a skin coccus species, Streptococcus species, gram- preparation of 10% PI solution has been recom- negative bacteria (Pseudomonas) mended.5 Our retrospective, case-controlled study b. Chronic: P. acnes, coagulase (-) staphylococci, fungi found that patients who received 10% PI skin disinfec- c. Bleb-associated: Streptococcus species, Hemo- tion combined with 5% PI conjunctival disinfection had philus influenza, Staphylococcus species significantly less risk of developing post-cataract surgery 2. Post-traumatic: Bacillus species, Staphylococci endophthalmitis. However, a modified preparation 3. Endogenous: Candida species, gram-negative bacteria (Klebsiella pneumoniae), S. aureus 4. Miscellaneous a. Corneal ulcer perforation: Pseudomonas, Staphy- TABLE 29.2: Prophylactic methods to prevent bacterial 1 lococcus species endophthalmitis after cataract surgery b. Intravitreous triamcinolone associated Prophylacitic intervention Clinical c. Suture removal associated. recommended Postoperative subconjunctival antibiotics C Preoperative lash trimming C Preoperative saline irrigation C Acute Postoperative Preoperative povidone-iodine antisepsis B Preoperative topical antibiotic therapy C Endophthalmitis Irrigating solutions containing antibiotics C Acute postoperative endophthalmitis is defined as the Intraoperative heparin C occurrence of intraocular infection within 6 weeks after Grade ‘A’ is considered very important or crucial to clinical surgery by the Endophthalmitis Vitrectomy Study outcome, grade ‘B’ as moderately important, and grade ‘C’ is (EVS). of questionable use Management of Endophthalmitis 175 method of 5% PI on both the skin and conjunctiva ceftazidime carries a lower risk of retinal toxicity and has been used in many institutes and for simple ocular a broader therapeutic index. However, intravitreous surgery, such as intravitreous injection.6,7 Caution should ceftazidime was not evaluated in the EVS and it has be taken to avoid touching the lid margin and lashes been shown that in-vitro ceftazidime precipitates in when the needle is inserted into the eye. vitreous humor at body temperature, irrespective of the presence of vancomycin.12 In clinical studies, INTRAOCULAR ANTIBIOTICS ceftazidime has been demonstrated to precipitate in inflamed eyes resulting in possible subtherapeutic Intravitreal antibiotic therapy could reach far greater concentration. Reconstitution with normal saline as intraocular antibiotic concentration than any other opposed to balanced salt solution produced less method of administration. It is the main stay of precipitation. Intravitreous ceftazidime is typically treatment for infective endophthalmitis. In instances injected at a concentration of 2.25 mg/0.1 mL.13 Like of instant and prompt treatment required in order to vancomycin, half-life is decreased in aphakic, save the vision, inaccuracies of gram-staining results vitrectomized and inflamed eyes. and unavailable culture results, broad-spectrum intravitreal antibiotics covering almost all the gram- positive and gram-negative bacteria are necessary. A Aminoglycosides few selected drugs are currently recommended, Aminoglycosides have a bactericidal effect through including vancomycin, ceftazidime and amikacin. In ionic interaction with the cell surface, energy the EVS, the antimicrobial sensitivity profile of amikacin dependent uptake phases and binding to ribosomes. and ceftazidime was similar at 89% against gram- Amikacin has a strong bactericidal effect against aerobic negative organism, and all gram-positive cocci were and facultative gram-negative bacilli. It has a synergistic sensitive to vancomycin.8 effect with vancomycin and other cell wall active antimicrobials (penicillins and cephalosporins). Aminoglycosides such as amikacin and gentamicin Vancomycin have been used for intravitreous injection. Gentamicin Vancomycin is the drug of choice for gram-positive has been reported to cause macular toxicity.14 bacteria in acute postoperative endophthalmitis. It is Aminoglycoside-induced macular infarction is thought a bactericidal drug whose primary mode of action is to result from an increased concentration by the inhibiting synthesis and assembly of the bacterial cell gravity-induced accumulation of drugs on the macula wall. It has a strong antimicrobial effect against gram- in a supine patient. Although animal experiments15 positive bacteria, especially Staphylococcus aureus, have shown that amikacin is safer than gentamicin, Staphylcoccus epidermidis and enterococcus, including a potential for macular toxicity might still exist. Amikacin methicillin-resistant Staphylococcus aureus. In has been shown to cause macular infarction with loss intraocular use, concentrations of up to 2 mg/0.1 mL of macular capillaries and pre-retinal hemorrhage.16-18 have been demonstrated to be non-toxic to the retina.9 The standard intravitreous dose of amikacin is 0.4 The EVS recommended a dose of 1.0 mg/0.1 mL.10 mg/0.1 mL. This is the dose used in the EVS. The half-life of the drug is reduced in inflamed eyes Pharmacokinetic studies in animals were similar to and prolonged in normal vitreous.11 Even in inflamed vancomycin pharmacokinetics in the vitreous cavity. eyes, therapeutic levels are still detected up to 72-84 However, levels measured 24 hours after injection were hours after injection. Vancomycin is also cleared more equal to or less than the minimal inhibitory concen- rapidly in aphakic, vitrectomized eyes.9, 11 tration (MIC) for most organisms sensitive to amikacin.19 Lower concentrations in the vitreous may necessitate the need for repeat injections of amikacin Ceftazidime if there is no response. No toxicity has been contributed Ceftazidime is a third-generation cephalosporin that to a single injection but repeated injections should be has a bactericidal effect by disrupting cell wall synthesis. undertaken with caution due to the possible risk of Third-generation cephalosporins have strong macular infarction.18, 19 Nasal side recumbency for antibacterial effects against gram-negative bacilli. They about 30 minutes might be suggested after intravitreous also have an added effect against Streptococcus injection of amikacin. pneumonia, pyogenes and other streptococci. Repeated vitreous tapping and injection of Cephalosporins have little effect against Staphylococcus antibiotics, together with pars plana vitrectomy, should aureus but a strong effect against Pseudomonas be consider if there is no clinical improvement or if aeruginosa. In contrast to the aminoglycosides, the condition deteriorates within 48 to 72 hours.20 176 Clinical Diagnosis and Management of Ocular Trauma SYSTEMIC ANTIBIOTICS after periocular antibiotic injection have been 29 The systemic antibiotics that cross the blood retinal reported. In addition, subconjunctival injection is barrier include cefazolin, ceftazidime and cipro- more painful and could not be as frequently floxacin.21-23 In the EVS, intravenous ceftazidime and administrated as topical antibiotics. A risk of macular amikacin were evaluated, and it was concluded that infarction when using gentamicin has also been 14 these antibiotics did not alter final visual acuity or media reported. Of the currently used antibiotics, the third- clarity.10 However, subsequent to the publication, this generation cephalosporins (ceftazidime and conclusion has come under question. First, these two ceftriaxone) achieve the highest vitreous levels. drugs did not cover the most common micro-organisms Topical application is associated with very poor of gram-positive bacteria in postoperative endoph- vitreous penetration. However, significant intraocular thalmitis. Second, intravenous amikacin has little levels of antibiotics can be achieved with frequent 30 intraocular penetration. The recommendation against administration of highly concentrated solutions , intravenous antibiotic use was not warranted and might especially if the corneal epithelium has been damaged. be based on inadequate data. For acute-onset postoperative endophthalmitis, topical Intravenous vancomycin has been suggested as an vancomycin (50 mg/mL) with amikacin (20 mg/mL) alternative therapy to systemic ceftazidime and amika- or ceftazidime (50 mg/mL) administered hourly is cin because of its superior gram-positive coverage. recommended. This regimen can then be adjusted for However, vancomycin penetrates poorly into the the specific organism after culture and sensitivity results vitreous yielding an inadequate antibacterial effect.24,25 are available. Oral ciprofloxacin might be an effective drug against many common infecting organisms causing endoph- STEROID TREATMENT thalmitis.26 However, older-generation fluoroquino- The early use of corticosteroids, in addition to antibiotics, lones (ciprofloxacin, ofloxacin and levofloxacin) are reduces inflammation and subsequent retinal damage increasingly ineffective against some of the pathogens in endophthalmitis. Corticosteroid therapy may be most commonly responsible for postoperative administered topically, intravitreally or systemically. In endophthalmitis. In contrast, the newer-generation the EVS, oral prednisone was used at a dose of 30 mg fluoroquinolones (gatifloxacin and moxifloxacin) show orally twice a day for 5 to 10 days. promising results; they not only display effective activity Intravitreous dexamethasone has been increasingly against gram-negative bacteria, as do the older- employed as an alternative to systemic therapy. generation fluoroquinolones, but also demonstrate Dexamethasone sodium phosphate is typically used enhanced potencies against gram-positive bacteria.27 in an intravitreous concentration of 0.4 mg/0.1 mL. Orally administered gatifloxacin was able to penetrate This is equivalent to 40 mg of oral prednisone. into the non-inflamed human eye, and reach Experimental studies have shown that intravitreal therapeutic levels in the aqueous and vitreous dexamethasone has a large safety window and that humors.28 Gatifloxacin has a broad spectrum of it prolongs the half-life of intravitreal vancomycin.31,32 coverage over the bacteria involved in endophthalmitis. Triamcinolone acetonide (4 mg/0.1 mL) is more potent It also has a low MIC of 90, good tolerability and and equivalent to 50 mg of oral prednisone. Recently excellent bioavailability after oral administration. Oral it has been reported that intravitreal triamcinolone gatifloxacin has the ability to achieve rapid, effective combined with intravitreal antibiotics appear to have levels in the aqueous and vitreous, with the notable exceptions of not achieving effective levels against Enterococcus or Pseudomonas. Gatifloxacin may thus TABLE 29.3: Recommended doses of initial management represent a good adjunctive treatment for certain types of infective postoperative endophthalmitis of endophthalmitis. Route Drug Dose Intravitreal Vancomycin 1 mg in 0.1mL SUBCONJUNCTIVAL AND TOPICAL Ceftazidime 2.25 mg in 0.1mL ANTIBIOTIC THERAPY Amikacin 0.4 mg in 0.1mL Dexamethasone 0.4 mg in 0.1mL Subconjunctival and topical antibiotics are often used Subconjunctival Vancomycin 25 mg in 0.5mL to supplement intravitreal injections in attempt to Ceftazidime 100 mg in 0.5mL increase the concentration of antibiotics within the Topical Vancomycin 50 mg/mL drop q1h anterior segment of the eye. Subconjunctival Amikacin 20 mg/mL drops q1h administration can reach therapeutic concentrations Systemic Fluoroquinolones 400 mg bid in the eye, especially in the aqueous humor. However, (oral) Gatifloxacin conflicting data regarding the intravitreal penetration Management of Endophthalmitis 177 a safety profile similar to current modalities, with a vitrectomy in conjunction with intraocular antibiotic favorable effect on visual recovery and function in acute injection. Culture of vitreous fluid from a vitreous tap postoperative endophthalmitis.33 or vitrectomy is essential for microbiology sensitivity patterns. The flow-chart for management of acute VITRECTOMY endophthalmitis is shown in Figure 29.1. For intravitreous antibiotic injection, we prefer intravitreal Vitrectomy debulks the vitreous cavity, reduces the load vancomycin (1 mg) and ceftazidime (2.25 mg) or of bacteria and toxins, and makes space for amikacin (0.4 mg) combined with intravitreal dexamet- intravitreous antibiotics. Only core vitrectomy is hasone (0.4 mg). The rationale and choice of systemic recommended, due to fear of causing retinal break antibiotics is best left to the treating physician. Systemic as the vitrector is near to the fragile, inflamed retina fluoroquinolone is suggested (Tables 29.3 to 29.5). in a cloudy vitreous. In addition, it is always combined with intravitreous antibiotic injection. The EVS concluded that immediate vitrectomy was not beneficial Chronic Postoperative for patients with an initial visual acuity of hand movement or better.10 Among patients with initial light- Endophthalmitis perception-only vision, it was three times more likely There are two different types of chronic postoperative that a visual acuity of 20/40 or better would be achieved endophthalmitis, one is caused by Propionibacterium after vitrectomy. Complications of pars plana acnes and the other is caused by fungus. These vitrectomy include infection, bleeding, cataract, microorganisms should be considered especially when glaucoma and retinal detachment. the initial culture result is negative. The culture plates In summary, the authors recommend the following should be investigated for at least 2 weeks. However, for management of acute postoperative endophthal- the culture rate is very low. Polymerase chain reaction mitis. Noting the patient’s unusual symptoms, carefully (PCR) detection of bacterial DNA with specific primers examining signs associated with infection and a highly from vitreous samples may prove a useful means of alert mind in the physician are important in early diagnosing delayed postoperative endophthalmitis.34 intervention, especially for immunocompromised and There are two important retrospective studies by diabetic patients. It is good to initiate topical antibiotics Aldave et al35 and Clark et al36 on P. acnes induced and cycloplegics immediately during close follow-up postoperative endophthalmitis. The choice for when there is suspicion of infection. The current choice intravitreous antibiotic injection is vancomycin (1 mg of drugs is ciprofloxacin 0.3% or ofloxacin 0.3%. If in 0.1 mL). However, intravitreous injection of infection is strongly suspected, the presenting vision antibiotics alone is associated with a very high rate is important in deciding between a vitreous tap and recurrence. Pars plana vitrectomy, partial capsulectomy

TABLE 29.4: Antimicrobial agents: dosages for ophthalmic use Drug Topical Subconj. Intravitreal Intravenous Oral dosage (in 0.5ml) (in 0.1ml) dose

Aminoglycosides Gentamicin 14 mg/ml 20 mg 0.1 mg 1.4 mg/kg q8-12hr Tobramycin 14 mg/ml 20 mg 0.1 mg 1.4 mg/kg IV, IV, q8-12hr Amikacin 20 mg/ml 25-50 mg 0.4 mg 7.5 mg/kg q12hr Cephalosporins Cefazolin 50 mg/ml 50 mg 2.0 mg 1 g q8h Cefotetan 3.0 mg 1 g q12h Ceftriaxone 2.0 mg 1-2 g q8h Ceftazidime 50 mg/ml 100 mg 2.25 mg 1-2 g q8h Penicillins Oxacillin 50 mg/ml 0.5 mg 2 g q4h 500 mg qid Miscellaneous Clindamycin 20 mg/ml 15-40 mg 1 mg 600 mg q8h 150-450 mg qid Ciprofloxacin 0.3% 0.1 mg 400 mg q12h 500-750 mg bid Gatifloxacin 400 mg bid Chloramphenicol 5 mg/ml 2 mg 750 mg q6h 250-750 mg qid Erythromycin 10 mg/ml 0.5 mg 500-1000 mg q6h 250-500 mg qid Vancomycin 50 mg/ml 25 mg 1-2 mg 1 g q12h 178 Clinical Diagnosis and Management of Ocular Trauma and intravitreous antibiotic injection without intraocular lens (IOL) exchange are usually successful on long- term follow-up. For patients with recurrent intraocular inflammation, pars plana vitrectomy, total capsular bag removal, intravitreous antibiotic injection and IOL exchange or removal is a uniformly successful strategy. Recommended treatment for chronic fungal endophthalmitis is pars plana vitrectomy and intravitreal injection of amphotericin B (5-10 μg in 0.1 mL).37 Effective systemic amphotericin concentration is still unknown. In cases of yeast endophthalmitis (i.e. Candida species), high doses of oral fluconazole (400- 600 mg/day) are recommended.38

BLEB-ASSOCIATED ENDOPHTHALMITIS It is important to distinguish between a localized bleb infection (blebitis) and true bleb-associated endoph- thalmitis. In cases of blebitis, topical antibiotics and subconjunctival antibiotics, such as vancomycin and ceftazidime, can usually be given in an out-patient setting.39 Bleb-associated endophthalmitis is typically characterized by a delayed onset, more virulent pathogens and poor visual prognosis. Due to the more virulent microorganisms (Streptococcus species and Haemophilus influenzae) and resulting poor visual prognosis, immediate pars plana vitrectomy, and intravitreal injection of vancomycin and ceftazidime are recommended.40 Topical and systemic antibiotics (vancomycin and ceftazidime) should be used.

POST-TRAUMATIC ENDOPHTHALMITIS Due to the initial injury, delay in primary wound repair and more virulent organisms (Bacillus or Staphylo- IOAB: Intraocular antibiotics coccus species), post-traumatic endophthalmitis Fig. 29.1: Flow-chart for the manage of acute generally has a worse visual outcome than other postoperative endophthalmitis categories. Endophthalmitis caused by Bacillus species

TABLE 29.5: Antifungal dosages in ophthalmic use Drug Topical Subconj Intravitreal Usual intravenous Oral dosage (in 0.5 ml) (in 0.1 ml) dose Polyenes Amphotericin B 2.5-10 mg/ml 300 µg 5-10 µg/ml 1mg/kg/day Natamycin 5% Nystatin 100,000 U/g ointment Imidazoles Fluconazole 2% 400 mg/day Clotrimazole 1% 5-10 mg 60-150 mg/kg/day

Econazole 1% 30 mg/kg/day 200 mg tid Ketoconazole 1-5% 200-400 mg/day Miconazole 1% 5-10 mg 0.25 mg 25 mg/kg/day in 2-3 divided doses Thiabendazole 4% 25 mg/kg/day Pyrimidines Flucytosine 1% 50-150 mg/kg/day Management of Endophthalmitis 179 is characterized by a rapidly progressive course, ring phthalmitis” that resolves without invasive treatment, corneal infiltrates and, generally, a poor visual which might be caused by triamcinolone crystal in the outcome, even with prompt therapy.41 Prophylactic anterior chamber or an inflammatory reaction to the intravitreal broad spectrum antibiotic injection solvent toxin. Infectious endophthalmitis usually decreases the risk of post-traumatic endophthalmitis.42 manifests acutely or subacutely with pain. It was In addition, systemic antibiotics are usually concluded that in certain eyes injected with administered.43 triamcinolone, the differential diagnosis should include a sterile, toxic endophthalmitis and it may be appropriate to observe the patient closely every 8 to Endogenous Endophthalmitis 12 hours to determine if the inflammation is worsening or improving. However, if new symptoms develop Endogenous endophthalmitis is more commonly more than several days after injection, infectious diagnosed in immunocompromised and debilitated endophthalmitis should be presumed and treatment patients. Once the diagnosis of endophthalmitis is initiated immediately.48 suspected, blood or urine cultures should be obtained and other organ involvement must be sought by consultation with an infectious disease specialist or internist. The use of systemic antibiotics is also usually Conclusion undertaken. Early recognition of endophthalmitis, together with Candida albicans is the most common organism appropriate and timely treatment, can often reduce causing endogenous fungal endophthalmitis and visual loss. Aspergillus species is the second most common fungal cause.44 The management of endogenous Candida endophthalmitis is generally tailored to the clinical References situation. When chorioretinal infiltrates are present with no or minimal vitreous involvement, systemic therapy 1. Ciulla TA, Starr MB, Masket S. Bacterial endophthalmitis prophylaxis for cataract surgery: an evidence-based alone is recommended. With moderate or severe vitritis, update. Ophthalmology 2002;109(1):13-24. or deterioration in spite of systemic therapy, vitrectomy 2. Saggers BA, Stewart GT. Polyvinyl-Pyrrolidone-Iodine: and intraocular amphotericin B are recommended. An Assessment of Antibacterial Activity. J Hyg (Lond) Endogenous bacterial endophthalmitis often is an 1964;62:509-18. initial finding leading to the diagnosis of bacterial 3. Connell JF, Jr., Rousselot LM. Povidone-Iodine. Extensive endocarditis, sepsis and liver abscess in Asians. In Surgical Evaluation of a New Antiseptic Agent. Am J Surg patients with diabetes and liver abscess, endogenous 1964;108:849-55. 4. Berkelman RL, Lewin S, Allen JR, et al. Klebsiella pneumoniae endophthalmitis is endemic in Pseudobacteremia attributed to contamination of 45 the Chinese population. It is a very fulminant infection povidone-iodine with Pseudomonas cepacia. Ann Intern and often results in poor visual outcome. Prompt Med 1981;95(1):32-36. diagnosis and vigorous treatment with intravitreous 5. Johns KJ, Feder RS, Hamill MB, Miller-Meeks MJ. injections of vancomycin, amikacin and dexametha- Surgery for Cataract. In: Johns KJ, Feder RS, Hamill MB, sone within 24 hours can save the patient’s eyes and Miller-Meeks MJ, eds. Basic and Clinical Science Course vision.46 Systemic antibiotics and intraocular antibiotics Section 11: Lens and Cataract: American Academy of Ophthalmology 2003-04. are recommended. Early vitrectomy for endogenous 6. Ferguson AW, Scott JA, McGavigan J, et al. Comparison Klebsiella pneumoniae endophthalmitis might be of 5% povidone-iodine solution against 1% povidone- beneficial.47 However, debilitation and confinement in iodine solution in preoperative cataract surgery antisepsis: bed because of the sickness in these patients often a prospective randomised double blind study. Br J results in it being unlikely that anesthesia and surgery Ophthalmol 2003;87(2):163-67. can be performed in the operating room. 7. Ta CN. Minimizing the risk of endophthalmitis following intravitreous injections. Retina 2004;24(5):699-705. 8. Han DP, Wisniewski SR, Wilson LA, et al. Spectrum and susceptibilities of microbiologic isolates in the Endo- Intravitreous Triamcinolone- phthalmitis Vitrectomy Study. Am J Ophthalmol 1996;122(1):1-17. associated Endophthalmitis 9. Pflugfelder SC, Hernandez E, Fliesler SJ, et al. Intravitreal Triamcinolone injection has become popular for vancomycin. Retinal toxicity, clearance, and interaction with gentamicin. Arch Ophthalmol 1987;105(6):831-37. treating macula edema in many diseases. Although 10. Results of the Endophthalmitis Vitrectomy Study. A some patients appear to have an infectious endo- randomized trial of immediate vitrectomy and of phthalmitis, many reports detail a “pseudoendo- intravenous antibiotics for the treatment of postoperative 180 Clinical Diagnosis and Management of Ocular Trauma bacterial endophthalmitis. Endophthalmitis Vitrectomy 29. Foster RE, Rubsamen PE, Joondeph BC, et al. Study Group. Arch Ophthalmol 1995;113(12):1479-96. Concurrent endophthalmitis and retinal detachment. 11. Coco RM, Lopez MI, Pastor JC, Nozal MJ. Pharmaco- Ophthalmology 1994;101(3):490-98. kinetics of intravitreal vancomycin in normal and infected 30. Barza M. Antibacterial agents in the treatment of ocular rabbit eyes. J Ocul Pharmacol Ther 1998;14(6):555-63. infections. Infect Dis Clin North Am 1989;3(3):533-51. 12. Kwok AK, Hui M, Pang CP, et al. An in vitro study of 31. Kwak HW, D’Amico DJ. Evaluation of the retinal toxicity ceftazidime and vancomycin concentrations in various and pharmacokinetics of dexamethasone after intravitreal fluid media: implications for use in treating endophthal- injection. Arch Ophthalmol 1992;110(2):259-66. mitis. Invest Ophthalmol Vis Sci 2002;43(4):1182-88. 32. Park SS, Vallar RV, Hong CH, et al. Intravitreal 13. Tanabe J, Kitano K, Suzuki T, et al. Nontoxic concen- dexamethasone effect on intravitreal vancomycin tration of ceftazidime and flomoxef sodium for intravitreal elimination in endophthalmitis. Arch Ophthalmol use—evaluated by in-vitro ERG. Lens Eye Toxic Res 1999;117(8):1058-62. 1990;7(3-4):677-83. 33. Falk NS, Beer PM, Peters GB, 3rd. Role of intravitreal 14. Campochiaro PA, Conway BP. Aminoglycoside toxicity— triamcinolone acetonide in the treatment of postoperative a survey of retinal specialists. Implications for ocular use. endophthalmitis. Retina 2006;26(5):545-48. Arch Ophthalmol 1991;109(7):946-50. 34. Hykin PG, Tobal K, McIntyre G, et al. The diagnosis of 15. D’Amico DJ, Caspers-Velu L, Libert J, et al. Comparative delayed post-operative endophthalmitis by polymerase toxicity of intravitreal aminoglycoside antibiotics. Am J chain reaction of bacterial DNA in vitreous samples. J Ophthalmol 1985;100(2):264-75. Med Microbiol 1994;40(6):408-15. 16. Campochiaro PA, Lim JI. Aminoglycoside toxicity in the 35. Aldave AJ, Stein JD, Deramo VA, et al. Treatment treatment of endophthalmitis. The Aminoglycoside strategies for postoperative Propionibacterium acnes Toxicity Study Group. Arch Ophthalmol 1994;112(1): endophthalmitis. Ophthalmology 1999;106(12):2395- 48-53. 401. 17. Kumar A, Dada T. Preretinal haemorrhages: an unusual 36. Clark WL, Kaiser PK, Flynn HW, Jr., et al. Treatment manifestation of intravitreal amikacin toxicity. Aust N Z strategies and visual acuity outcomes in chronic J Ophthalmol 1999;27(6):435-36. postoperative Propionibacterium acnes endophthalmitis. 18. Seawright AA, Bourke RD, Cooling RJ. Macula toxicity Ophthalmology 1999;106(9):1665-70. after intravitreal amikacin. Aust N Z J Ophthalmol 37. Ciulla TA. Update on acute and chronic endophthalmitis. 1996;24(2):143-46. Ophthalmology 1999;106(12):2237-38. 19. Mandell BA, Meredith TA, Aguilar E, et al. Effects of 38. Luttrull JK, Wan WL, Kubak BM, et al. Treatment of ocular inflammation and surgery on amikacin levels in the fungal infections with oral fluconazole. Am J Ophthalmol vitreous cavity. Am J Ophthalmol 1993;115(6):770-74. 1995;119(4):477-81. 20. Shaarawy A, Grand MG, Meredith TA, Ibanez HE. 39. Chen PP, Gedde SJ, Budenz DL, Parrish RK, 2nd. Persistent endophthalmitis after intravitreal antimicrobial Outpatient treatment of bleb infection. Arch Ophthalmol therapy. Ophthalmology 1995;102(3):382-87. 1997;115(9):1124-28. 21. Aguilar HE, Meredith TA, Shaarawy A, et al. Vitreous 40. Kangas TA, Greenfield DS, Flynn HW, Jr., et al. Delayed- cavity penetration of ceftazidime after intravenous onset endophthalmitis associated with conjunctival administration. Retina 1995;15(2):154-59. filtering blebs. Ophthalmology 1997;104(5):746-52. 22. Keren G, Alhalel A, Bartov E, et al. The intravitreal pene- 41. Foster RE, Martinez JA, Murray TG, et al. Useful visual tration of orally administered ciprofloxacin in humans. outcomes after treatment of Bacillus cereus endophthal- Invest Ophthalmol Vis Sci 1991;32(8):2388-92. mitis. Ophthalmology 1996;103(3):390-97. 23. Martin DF, Ficker LA, Aguilar HA, et al. Vitreous cefazolin 42. Narang S, Gupta V, Gupta A, et al. Role of prophylactic levels after intravenous injection. Effects of inflammation, intravitreal antibiotics in open globe injuries. Indian J repeated antibiotic doses, and surgery. Arch Ophthalmol Ophthalmol 2003;51(1):39-44. 1990;108(3):411-14. 43. Reynolds DS, Flynn HW, Jr. Endophthalmitis after 24. Ferencz JR, Assia EI, Diamantstein L, Rubinstein E. Vanco- penetrating ocular trauma. Curr Opin Ophthalmol mycin concentration in the vitreous after intravenous and 1997;8(3):32-38. intravitreal administration for postoperative endophthal- 44. Weishaar PD, Flynn HW, Jr., Murray TG, et al. Endogen- mitis. Arch Ophthalmol 1999;117(8):1023-27. ous Aspergillus endophthalmitis. Clinical features and 25. Souli M, Kopsinis G, Kavouklis E, et al. Vancomycin levels treatment outcomes. Ophthalmology 1998;105(1):57-65. in human aqueous humour after intravenous and 45. Chen YJ, Kuo HK, Wu PC, et al. A 10-year comparison subconjunctival administration. Int J Antimicrob Agents of endogenous endophthalmitis outcomes: an east Asian 2001;18(3):239-43. experience with Klebsiella pneumoniae infection. Retina 26. Das T, Sharma S. Current management strategies of acute 2004;24(3):383-90. post-operative endophthalmitis. Semin Ophthalmol 46. Chou FF, Kou HK. Endogenous endophthalmitis 2003;18(3):109-15. associated with pyogenic hepatic abscess. J Am Coll Surg 27. Mather R, Karenchak LM, Romanowski EG, Kowalski RP. 1996;182(1):33-36. Fourth generation fluoroquinolones: new weapons in the 47. Yoon YH, Lee SU, Sohn JH, Lee SE. Result of early arsenal of ophthalmic antibiotics. Am J Ophthalmol vitrectomy for endogenous Klebsiella pneumoniae 2002;133(4):463-66. endophthalmitis. Retina 2003;23(3):366-70. 28. Hariprasad SM, Mieler WF, Holz ER. Vitreous and 48. Roth DB, Chieh J, Spirn MJ, et al. Noninfectious aqueous penetration of orally administered gatifloxacin endophthalmitis associated with intravitreal triamcinolone in humans. Arch Ophthalmol 2003;121(3):345-50. injection. Arch Ophthalmol 2003;121(9):1279-82. CHAPTER

Management of Pediatric Ocular Trauma 30 Yog Raj Sharma, Ritesh Gupta, Rajni Sharma (India)

Introduction information if they feel that their negligence contributed to the accident. Some of the key information that needs Ocular trauma is a leading cause of unilateral blindness to be gathered is given below: in children. The American Academy of Pediatrics (AAP) • Mechanism of injury (1987) reported that 66% of all ocular injuries occur in • Exact time and place of injury persons 16 years of age or younger, with the highest • Visual status before the trauma frequency between 9 and 11 years of age. Virtually all • Any history of strabismus, congenital abnormalities studies of pediatric ocular trauma show a male to female ocular surgery, injury, patching or glasses predominance of approximately 4:1 attributed in part • Child’s general medical status before trauma to boys more frequently choices of sharp and pointed • Child’s tetanus immunization status 1-6 play objects. Sports equipment especially cricket ball, • Loss of vision, floaters or flashes of light. stones, wooden sticks (Gilli danda),1 fire-crackers,2 bow and arrow,1etc. are the items most often implicated. EXAMINATION Pediatric ocular trauma occurs most often during play It is important to establish a routine to assure a complete that is not supervised by an adult (AAP1987). assessment. Examination of a child who has sustained Other ocular disorders may be noticed first after ocular trauma is often difficult and frightening for both even subtle trauma. An injury may bring to light pre- the child and the ophthalmologist. Patience, gentle existing leukocoria, strabismus or proptosis. Therefore technique, careful preparation and attention to detail one should always consider nontrauma etiologies in provide the best outcome for everyone. Noncontact the evaluation of injured child. parts of the examination should be performed first. Caring for children with ocular trauma involves No external pressure should be exerted on the globe several distinctive aspects such as: at any time during the examination. • The possibility of prenatal injuries If an infant or toddler is extremely uncooperative, • Diagnostic challenges due to limitations experienced restraining in a papoose board may become necessary. during history taking and examination A wire eyelid speculum may be needed to retract the • The developing visual system and the potential for eyelids. It should be used only when it is certain that amblyopia the globe is not ruptured or lacerated. • An orbit that is immature (cosmesis following Toddlers may be restrained in a position in which enucleation and evisceration) parent and assistant hold the child and the ophthal- • Predisposition to certain types of trauma (e.g. fire- mologist examines the child. crackers or toys related). In cases where above measures do not allow adequate examination, appropriate sedation (e.g. Chloral hydrate 25-100 mg/kg, p.o.) should be used. Evaluation Sedation of the pediatric patient may be complicated by vomiting, anaphylaxis, seizure, airway obstruction HISTORY or cardiorespiratory arrest. Sedation should only be Evaluation of ocular trauma requires a thorough performed in a facility where the child’s vital signs are history, preferably from the child. Keep in mind that monitored and resuscitation and ventilatory equipment a child may fabricate a history if involved in a forbidden are at hand. It is advisable that an anesthetist or a activity when injured. Likewise, parents may withhold pediatrician be present while sedating a child. 182 Clinical Diagnosis and Management of Ocular Trauma Visual Acuity Management—in most cases the injury is self limited, Determination of visual acuity is the single most requiring no treatment. Persistent eyelid closure may important aspect of the ocular examination. Measure produce monocular amblyopia. The patient should the visual acuity of each eye separately. With a co- be followed periodically to assess visual development operative child, a Snellen chart, tumbling E , or illiterate and presence of astigmatism. Correction of refractive eye chart is used. In younger children, visual acuity error may be necessary to prevent amblyopia. is assessed by fixation and ability to follow target. Corneal Damage (Breaks in Descemet’s Membrane) Ocular Examination Corneal trauma is usually caused by the use of forceps during delivery. The resulting corneal edema is localized Estimate visual fields by bringing an object into the to the area of the break and usually clears within weeks child’s view from multiple angles. without intervention. Although there generally is vision Examine the eyelids and lacrimal drainage system loss with this condition caused by amblyopia and high to detect possible injuries. Gently palpate the orbital refractive errors,8 corneal transplantation is usually not rim for any irregularities or crepitus. Examine and necessary. record each pupil’s size, shape and reaction to light. Examine the conjunctiva and sclera to identify Retinal Hemorrhages lacerations, perforations or foreign bodies. If an open globe is suspected, examination should Retinal hemorrhages are seen in about 20% of 9 be stopped at this point to prevent further injury to newborn infants within 24 hours of birth. These the eye. A large eye shield or pad and bandage (not hemorrhages usually resolve quickly—and are seen pressure patch) should be applied over the eye. The in fewer than 3% of infants by day 5 of life. These remainder of the examination should be performed are more likely to be seen after forceps or vacuum under general anesthesia. extraction deliveries. And are seen in fewer than 1% Assess intraocular pressure with Goldmann of cesarean deliveries. applanation tonometer, Perkins tonometer, tono-pen These should be observed to assure resolution. This or careful finger tip palpation. Stain the cornea with usually occurs within a month. Diagnostic or fluorescein paper and examine with slit lamp to identify therapeutic intervention is usually not necessary. Child abrasions. Examine anterior chamber fro hyphema, abuse should be ruled out if it’s found after baby is hypopyon or other abnormalities. Evaluate the motility at home. of both eyes after excluding globe perforation. A dilated fundus exam (with or without scleral depression, EYELID LACERATIONS as appropriate), is also essential during the trauma Lid lacerations may present with significant disfigure- examination. ment. Laceration involving medial side of the lid Obtain radiologic evaluation for injuries consistent (Figs 30.1A and B) may damage the lacrimal with orbital fractures or retained foreign body. drainage system. For superficial lacerations, clean the wound and surrounding skin with povidone iodine and irrigate thoroughly with saline, and remove any Specific Eye Injuries foreign material that may still be present. Then apply an antibacterial ointment and sterile dressing. Common eye injuries in children are discussed below For deeper lacerations, suturing with 8-0 silk or in brief. nylon is required. Complicated lacerations require an oculoplastic surgeon consult. These are lacerations that BIRTH TRAUMA have extensive tissue loss or have damaged the lacrimal Delivery may be associated with ocular and periocular drainage system, levator aponeurosis, and/or the injuries.7 These include lid edema, subconjuctival hemor- medial canthus tendon. rhage, corneal edema, corneal abrasion, hyphema, vitreous and retinal hemorrhage. The use of forceps CORNEAL AND CONJUNCTIVAL FOREIGN during delivery increases the chances of injury. BODIES (FIGS 30.2 AND 30.3A AND B) Patients can be completely asymptomatic, but generally Periorbital Ecchymosis and Edema foreign bodies cause mild to moderate eye pain Periorbital ecchymosis and edema are present after depending on their composition, location, and the birth. One needs to rule out other causes of lid closure patient’s pain tolerance. When examining a patient or swelling, e.g. congenital ptosis or conjunctivitis. with a possible foreign body, it is always important to Management of Pediatric Ocular Trauma 183

Figs 30.3A and B: A large foreign body located medial to limbus. It was found to be superficial and there was no Figs 30.1A and B: Lid laceration involving the medial canthal penetrating trauma area. Lacrimal drainage system was unaffected in this patient object should be considered an open-globe injury and co-managed with an anterior segment or corneal sub- specialist, when available. Superficial corneal foreign bodies are removed with a moistened cotton-tipped applicator or with the help of 26G needle after putting a drop of topical anesthetic solution. Patients may continue to report the sensation of a persistent foreign body even after removal of foreign body. This is usually because of small associated corneal epithelial defect. After the foreign body is removed, patch the eye for 12 to 24 hours with a topical antibiotic to allow the epithelium to heal.

SUBCONJUCTIVAL HEMORRHAGE Fig. 30.2: Corneal foreign body It can be caused by blunt trauma, forceful sneezing or eye rubbing. It usually results from breakage of the inspect the fornices thoroughly and evert the eyelids fragile conjunctival blood vessels. Whenever a trauma- to look for occult palpebral conjunctival foreign bodies. tic subconjunctival hemorrhage occurs, a more severe Before removing a corneal foreign body, always underlying ocular injury, e.g. an occult scleral perfora- attempt to localize its depth because a penetrating tion or retained foreign body, etc. should be ruled out. 184 Clinical Diagnosis and Management of Ocular Trauma CORNEAL PENETRATION (FIGS 30.4A AND B) The Seidel test can be crucial in determining whether the patient has a full- or partial-thickness laceration. When examining these patients, gentle digital pressure may enhance the Seidel test and will allow a general assessment of the IOP if the depth of the laceration is uncertain.

Fig. 30.5: Hyphema

Grading of hyphema Grade Percentage of anterior chamber filled with blood Fig. 30.4A: Large corneoscleral penetrating wound with hyphema and iris prolapse Microscopic Circulating red blood cells only I < 1/3 II 1/3-1/2 III 1/2- near total IV Total (eight-ball)

The main goals of treatment are to normalize intraocular pressure and to minimize the likelihood of rebreeding. Rebleeding of a hyphema occurs in 5-33% of untreated eyes with hyphema and it typically occurs 2 to 5 days after the injury (when clot retraction and lysis are occurring).10, 11 Complications after hyphema are more common after rebleeding which may include corneal blood staining, optic atrophy, central retinal artery occlusion and peripheral anterior synechiae. The management of traumatic hyphema Fig. 30.4B: Prolapsed iris excised and wound repaired is controversial. But generally hospitalization with using 10-0 monofilament nylon moderate restriction of physical activities is often recommended. Topical steroids are started to decrease TRAUMATIC HYPHEMA anterior chamber inflammation. Atropine ointment1% Blunt ocular trauma can disrupt the vessels of iris and or eye drops hommatropine 2% is given to keep the ciliary body resulting in hyphema (blood in the anterior pupil in fixed and dilated position. (Short acting chamber, Fig. 30.5). Hyphema without history of cycloplegic such as tropicamide is avoided as it may significant trauma should raise the suspicion of bleeding precipitate rebleeding.) Aminocaproic acid (antifibrino- diatheses, leukemia, juvenile xanthogranuloma, iris lytic agent) can stabilize clot formation at the site of neovascularization, retinoblastoma or fictitious history hemorrhage and thus reduce the incidence of by the child. During the slit-lamp examination, it is rebleed.12,13 It is given as 50 mg/kg, p.o., every 4 hourly of the utmost importance to grade the hyphema, for five days. Commonly encountered side effects are because this will dictate both the management and nausea, vomiting and postural hypotension. It is follow-up of the condition. contraindicated in pregnant women. Management of Pediatric Ocular Trauma 185 Surgical drainage of hyphema is indicated if: 1. To prevent optic atrophy: If IOP is more than 50 mm Hg for 5 days. If IOP is more than 35 mm Hg for 7 days. 2. To prevent corneal blood staining I eyes with a large hyphema: If IOP is more than 25 mm Hg for 6 days. If there is any indication of blood staining. 3. To prevent peripheral anterior synechiae. If total hyphema persists for 5 days. Various surgical techniques have been described to remove the blood. These include paracentesis, anterior chamber washout with one needle irrigation or irrigation-aspiration technique and clot evacuation with a forceps. Automated hyphemectomy (Figs 30.6A to C) using vitrectomy instruments inserted through limbal incisions permits controlled removal of blood in the anterior chamber.14, 15

TRAUMATIC CATARACT It can be caused by both blunt and penetrating trauma. Blunt ocular trauma typically leads to stellate or rosette- shaped opacification which is usually axial in location and involves the posterior capsule. In perforating trauma, direct compromise of the lens capsule by penetrating object leads to cortical opacfication at the site of injury. If the perforation is small, then it may get sealed off and cataract remains localized whereas if the capsular tear is large, the entire lens can rapidly opacify. Primary cataract extraction is indicated if there is obvious capsular rupture with lens matter in anterior chamber (Fig. 30.7) or when there is posterior segment injury (retinal detachment, endophthalmitis or intraocular foreign body) and the cataract disallows the proper management of these conditions. In all other cases, cataract surgery is deferred so that intraocular inflammation and hemorrhage subsides. The anterior approach (scleral tunnel or limbal or corneal incision) is the method of choice for cataract surgery. It should preferably be done by phaco- emulsification with or without IOL implantation. This should be followed-up by rapid employment of optical correction and occlusion therapy to prevent amblyopia if the child is less than 8 years old. Figs 30.6A to C: Hyphemectomy using vitrectomy instruments VITREOUS AND RETINAL CONDITIONS One should particularly look for a self-sealing That can be caused by trauma are as follows: penetrating wound, iris hole, lens opacities, shallow anterior chamber, or low IOP in suspected IOFB cases. Intraocular Foreign Body In many cases, IOFB can be identified by slit-lamp Intraocular foreign body (IOFB) should be considered biomicroscopy or indirect ophthalmoscopy for all high-velocity ocular injuries, particularly those (Fig. 30.8). However, if the media is hazy or if foreign resulting from metal-on-metal activities. body is suspected but not visualized, imaging 186 Clinical Diagnosis and Management of Ocular Trauma Commotio Retinae Commotio retinae is also known as Berlin’s edema or concussion edema. It is caused by blunt trauma (a contrecoup injury), with the force being transmitted through the vitreous and finally onto the retina and choroids. With this condition, there will be a confluent area of retinal whitening due to outer photoreceptor disruption and RPE damage, but not edema. Blood vessels are seen distinctly and are undisturbed under the retinal whitening. The retinal opacification gradually subsides over several weeks and visual function usually returns to its pretrauma level. However, a permanent loss of vision is not unusual and can be associated with changes in the retinal pigment epithelium.

Choroidal Rupture Choroidal rupture is detectable as a yellow or white Fig. 30.7: Traumatic cataract with rupture of anterior crescent-shaped subretinal streak that is often capsule and lens matter in anterior chamber concentric with the optic nerve. The rupture can be single (Fig. 30.9) or multiple and may be obscured for several days to weeks by overlying pre- or sub- retinal hemorrhage. Patients with this condition are at a greater risk for developing a choroidal neovascular membrane, so they should be followed every 3 to 6 months. They should also be instructed to monitor their vision daily with an Amsler grid and to report any significant changes.

Fig. 30.8: Foreign body impacted in retina temporal to fovea

modalities are necessary. CT scan has emerged as the imaging modality of choice to rule out IOFB. Modern spiral CT scanning with 1mm cuts is effective in detecting a 0.5 mm metallic, glass or stone in 100% of cases.16 MRI is contraindicated if a metallic foreign body is suspected. Endophthalmitis occurs in up to 48% of eyes with an IOFB injury and only the timing of surgery (>24 Fig. 30.9: Post-traumatic choroidal rupture hours) and the type of FB (e.g. wood) are associated with macular hole with higher rates. The clinical findings include retinal periphlebitis, marked anterior chamber reaction or hypopyon, and severe vitreal inflammation. Retinitis Sclopeteria Metallic IOFBs can cause toxic retinal metallosis, Retinitis sclopeteria or chorioretinitis sclopeteria is a but even inert IOFBs can cause proliferative vitreo- rare condition in which the patient sustains both a retinopathy and/or debilitating ocular inflammation. choroidal and retinal rupture. It is a concussive injury The treatment is prompt surgical removal via pars plana to the posterior segment and results from shock waves vitrectomy (with or without lensectomy) involving produced by orbital penetration of a high-velocity magnetic and/or forceps assisted IOFB removal. object. The object does not penetrate the sclera but Management of Pediatric Ocular Trauma 187 ruptures the choroid and retina in the area adjacent to its path. The visual acuity is almost always poor. This condition occurs when a high-velocity object grazes the globe, but does not rupture the sclera. Patients with retinitis sclopeteria require a prompt retinal consult because surgical intervention may be necessary.

Traumatic Macular Hole Traumatic macular hole (Fig. 30.10) is clinically similar to the idiopathic variety in appearance. It can follow commotio retinae, subretinal hemorrhages and cystoid macular edema. Postcontusion necrosis may result in macular edema and macular cyst formation. Over months to years, rupture of cyst layer/s can lead to formation of lamellar or full thickness macular hole. Acute lamellar or full thickness macular hole is usually caused by contrecoup vitreofoveal traction. Fig. 30.11: Post-traumatic retinal detachment with early macular pucker

A patient with a macula-on RD (i.e. the macular region of the retina is intact) should receive a retinal consultation and undergo surgery within 1 to 2 days of diagnosis. These patients should be confined to bed rest until surgery. A macula-off RD (i.e. the macular region has detached) is less urgent and these patients should have a retinal consultation and surgery within approximately one week. Children’s lack of cooperation with postoperative positioning influences the surgeon’s decision during retinal detachment surgery. It’s very difficult to separate the nondetached posterior hyaloid in pediatric eye; nonetheless, vitreous removal should be as complete as possible as leaving behind the posterior hyaloid Fig. 30.10: Post-traumatic large macular hole increases the risk of proliferative vitreoretinopathy. Plasmin may have a future role in these cases. Silicon Pars plana vitrectomy with removal of internal limi- oil is preferred over gases as tamponading agent as ting membrane (ILM) and gas/ silicon oil tamponade former requires minimal positioning and immobility. has been found to be successful (anatomical closure) in more than 90% of cases.17 Visual improvement has been reported in 69-94% of cases.17-19 Surgical adjuvant such as autologus plasmin enzyme may improve the Child Abuse 20 rate of anatomic success . However, because a Child abuse must always be considered in a child significant number of cases of traumatic macular hole younger than 3 years of age who presents with may close spontaneously, it may be wise to just follow intraocular hemorrhages, cataract or subluxated lens, up these patients for initial 3 months or so. retinal detachment or retinischiasis, or periorbital ecchymosis. The ocular findings in shaken baby Traumatic Retinal Detachment syndrome may occur without any obvious external Traumatic retinal detachment (RD) (Fig. 30.11) is a injury. Retinal hemorrhages have been described in rhegmatogenous detachment that can be caused by shaken baby syndrome in which repeated acceleration retinal dialysis or a retinal tear. B-scan ultrasonography and deceleration is supposed to damage intraocular is necessary to rule out an RD if media is hazy and and intracranial blood vessels and thereby results in one is unable to visualize fundus. When appropriate, intraocular and intracranial hemorrhage. Typically the utilize scleral depression after trauma to help rule out retinal hemorrhages are bilateral, but may be retinal dialysis. asymmetric or even unilateral. Other causes of retinal 188 Clinical Diagnosis and Management of Ocular Trauma hemorrhage such as leukemia, accidental trauma, 4. Moreira CA Jr, Ribeiro MD, Belfort R Jr. Epidemiological leukemia, thrombocytopenia, anemia, etc. should be study of eye injuries in Brazilian children. Arch ruled out. Severe visual morbidity with shaken baby Ophthalmol 1988;106:781-84. 5. Rapoport I, Romem M, Kinek M, et al. Eye injuries in syndrome may be due to retinal detachment, optic children in Israel. A National Collaborative Study. Arch nerve atrophy or cortical blindness. Ophthalmol 1990;108:376-79. 6. Canavan VM, O’Flaherty MJ, Archer DB, et al. A ten year survey of eye injuries in Northern Ireland. Br J Eye Injury Prevention Ophthalmol 1980;64:618-25. 7. Holden R, Morsman DG, Davidek GMB, O’Conner GM. The vast majority of eye injuries are preventable. Key External ocular trauma in instrumental and normal components of prevention include parental deliveries. Br J Obstet Gynecol 1992;99:132. supervision, education of children and protective 8. Angell LK, Robb RM, Berson FG. Visual prognosis in eyewear. Ophthalmologists and parents must reinforce patients with ruptures in Descmet’s membrane due to forceps injury. Arch Ophthalmol 1981;99:21-37. the importance of not playing with objects like 9. Sezen F. Retinal hemorrhages in new born infants. Br J gillidanda, fire-crackers and bow and arrow. Health Ophthal 1970;55:248. education on the preventive aspects of ocular trauma 10. Volpe NJ, Larrison WI, Hersh PS et al Secondary in schools as well as through mass media like television hemorrhage in traumatic hyphema. Am J Ophthalmol can help in achieving this goal. 1991; 112: 507-13. Protective eyewear is the most important measure 11. Thomas MA, Parrish RK, Feuer WJ. Rebleeding after to prevent eye injuries in children. Plano polycarbonate traumatic hyphema. Arch Ophthalmol 1986 Feb; 104(2):206-10. goggles with a 2-3 mm center thickness are 12. McGetrick JJ, Jampol LM, Goldberg MF, et al. recommended for sports. Aminocaproic acid decreases secondary hemorrhage after traumatic hyphema. Arch Ophthalmol 1983 Jul; 101(7):1031-33. 13. Kutner B,Fourman S, Brein K Aminocaproic acid Summary reduces the risk of secondary hemorrhage in patients Ocular trauma is an important cause of monocular with traumatic hyphema. Arch Ophthalmol 1987 Feb; blindness in children. Due to young age, inability to 105(2):206-08. cooperate with examination and the potential for 14. Stern WH, Monclal KM. Vitrectomy instrumentation for surgical evacuation of total anterior chamber hyphema development of amblyopia, children presenting with and control of recurrent anterior chamber hemorrhage. eye injuries are evaluated and treated slightly differently Ophthalmol Surg 1979; 10: 34-37. from adults. Proper communication should be 15. McCuen BW, Fung WE. The role of vitrectomy maintained between the ophthalmologist and family instrumentation in the treatment of severe traumatic throughout the course of treatment. hyphema. Am J Ophthalmol 1979;88:930-34. 16. Dass AB, Ferrone PJ, Chu RY etal. Senstivity of spiral computed tomography scanning for detecting intraocular foreign bodies. Ophthalmology 2001; 108: 2326-28. References 17. Kuhn F, Morris R,Mester V, et al. Internal limiting membrane removal for traumatic macular holes. 1. Jaison SG, Silas SE, Daniel R, Chopra SK.A review of Ophthalmic Surg Lasers 2001 Jul-Aug;32(4):308-15. childhood admission with perforating ocular injuries in 18. Amari F, Ogino N, Matsumura M et al. Vitreous surgery a hospital in north-west India. Indian journal of for traumatic macular holes. Retina. 1999; 19(5):410-13. ophthalmology 1994;42(4):199-201. 19. Chow DR, Williams GA, Trese MT et al. Successful closure 2. Sarda RP, Mehrotra AS, Ratnawat PS, et al. Ocular injuries of traumatic macular holes. Retina 1999;19(5):405-09. in childhood. Indian J Ophthalmol 1971;19:67-70. 20. Margherio AR, Margherio RR, Hartzer M et al Plasmin 3. Niiranen M, Raivio I. Eye injuries in children. Br J enzyme-assisted vitrectomy in traumatic pediatric macular Ophthalmol 1981;65:436-38. holes. Ophthalmology 1998 Sep;105(9):1617-20. CHAPTER

Management of Blunt Retinal Trauma 31 Arturo Pérez-Arteaga, Yuri Flores (Mexico)

Introduction in cases of minor trauma. Maybe this is the first concept that the attending surgeon must keep in mind when As part of the ocular traumatology, the damage caused observing and evaluating a traumatized eye. by an impact directly or indirectly to the retina, can In this order of ideas, the possibilities are enormous; be smooth, and with total visual recovery, or in some blunt ocular trauma, orbital trauma and systemic other cases, can cause a severe visual impairment, with trauma may cause a variety of posterior segment tremendous consequences for the life of the patient. abnormalities (our matter in this chapter); trauma may The visual prognosis after ocular trauma depends cause damage to the retina (commotio retinae), retinal on a number of factors; a large proportion of eyes pigment epithelium (retinal pigment epithelial edema), with severe and irreversible visual loss due to trauma choroid (choroidal rupture) and optic nerve (optic almost always exhibit posterior segment injuries. These nerve evulsion) alone or in combination; traumatic injuries lead to vitreoretinal complications that may macular holes and retinal detachment or dialysis; occur immediately, days, weeks, or even years after trauma to the orbital tissues adjacent to the globe can the initial trauma. Recent advances in microsurgical cause concussive forces with damage to multiple techniques, as well as an improved understanding of structures within the eye (chorioretinitis sclopetaria); the pathophysiology of these vitreoretinal systemic trauma may result in diffuse retinopathy complications, may minimize the visual loss, even in (Purtscher’s retinopathy, shaken baby syndrome) or the more severely affected eyes. Therefore, although localized retinal abnormalities (whiplash retinopathy, prevention remains the ultimate goal, the adequate fat embolism syndrome). Alterations in intravascular diagnosis and “state of the art” management of (Valsalva retinopathy) or intracranial pressure (Terson’s posterior segment injuries are important factors in syndrome) due to a variety of causes may result in reducing the magnitude of visual loss in injured eyes. If well the traumatic lesions to the posterior segment preretinal or vitreous hemorrhage and associated visual of the eye too often are not alone, it means that an loss. ocular trauma is able to cause damage in many other The purpose of this chapter is to review the structures of the globe, we will try in this chapter, to mechanism of posterior segment injury in blunt establish didactic classifications in order to cover the trauma, the initial evaluation and a perspective of some broad spectrum of possible lesions, and so improve of the most important entities involved in the trauma the clinical evaluation, allowing the physician, to decide to the posterior segment. an adequate option of treatment for each particular patient. We have also to remember, that very often the Mechanism of Damage in impact to the retina, in particular in cases of blunt, trauma is not frequently a direct impact, it is a result Blunt Trauma of the transmission of forces inside the eye, and the The transfer of blunt forces to the globe is the wave of impact goes frequently from the anterior mechanism seen in the majority of ocular injuries. Even segment, to the posterior segment of the eye; the in high-speed projectile injuries, in which the implications of this physical concept are that sometimes mechanism of injury is primarily due to penetrating the damage caused in the retina not always correlate or sharp forces, associated blunt forces are involved. with the force of the impact and the mechanism of Blunt forces involve the posterior segment in several trauma; this can lead to underestimate the damage ways: 190 Clinical Diagnosis and Management of Ocular Trauma First there is direct contusion tissue damage at the globe status is obvious, careful documentation of these site of impact. This is known as a coup injury, and circumstances, as well as the use and type of safety includes retinal edema, necrotic changes, and glasses or other protective devices, has medical and choroidal hemorrhage at the site of impact. legal relevance. The history should determine the Second, injury can occur distant from the impact preinjury ocular status and the possibility of extraocular site as the force is transferred through the globe trauma; the ocular baseline should include preinjury to a contralateral site. This is called the contracoup vision, refractive status (myopic eyes are affected with injury; examples of it include retinal edema and more severity with minor traumas), preexisting ocular choroidal contusions in the posterior pole; in these diseases (e.g. retinal diseases, pseudoexfoliation, lesions the posterior pole was not impacted directly, glaucoma), and previous ocular surgery (e.g. cataract, but the transmission of forces affect it in different retinal surgery). The note of circumstances that should degree. raise suspicions of open globe injuries is mandatory, Finally, there are injuries caused by the globe high-speed projectile injuries, use of power tools, high- deformation; some authors have documented by speed grinding of metal, leak from high-pressure high-speed cinematography, globe deformation hydraulic system, metal-on-metal impact, sharp following the application of blunt forces to the penetrating injuries and severe blunt injury (racquetball cornea. In these movies we can see initially how or golf ball, stick or bat injury to orbit). the anteroposterior axis is compressed; then the anteroposterior axis is decompresses and so a rebound expansion occurs. Then the equatorial Individual Pathologies Description axis begins to expand as the anteroposterior axis COMMOTIO RETINAE compresses but doesn’t reach maximum expansion until after the anteroposterior axis begin its rebound Definition and Clinical Findings decompression. This tremendous change of intra- Commotio retinae is also known as Berlin’s edema, but ocular forces of compression and decompression the latter term is not completely appropriate. The clinical within different axis of the globe, creates shearing characteristic of this condition is a confluent area of forces within the eye at tissue interfaces that are retinal whitening due to outer photoreceptor disruption especially concentrated at the vitreous base. and RPE damage, but not edema. Blood vessels are seen Choroidal rupture, vitreous base avulsion, iris root distinctly and are undisturbed under the retinal disinsertion, retinal dialysis and tears, and posterior whitening. Commotio retinae results in retinal vitreous separation are examples of injuries caused opacification following blunt trauma. Mild commotio by these shearing forces. retinae usually settles spontaneously with minimal After reading this, the clinical comprehends that sequelae but more severe cases are associated with visual he must be aware of damage caused by ocular blunt loss. Commotio retinae can occur anywhere in the trauma at any site of the eye; so a complete evaluation retina, but it is usually maximal in the area opposite to of all structures is mandatory, even in case of an the blow (countracoup injury). So, explaining the “pretended minor trauma”. pathophysiology of the condition, the retinal changes are caused by a contrecoup that is created by blunt Initial Evaluation trauma, with the force being transmitted through the vitreous and finally onto the retina and choroid Proper identification and management of patients with (Figs 31.1 and 31.2). posterior segment injury begin with a systematic approach to obtaining a complete history and conduc- ting a thorough ophthalmic examination. The reader Histopathology will be able to see more details in some other chapters Immediately after injury, the only abnormality is of this book, but some important points will be disruption of the receptor outer segments. From one featured regarding the posterior segment blunt trauma; to six days after trauma, many receptor cells undergo because open and closed globe injuries are approached degeneration. The retinal pigment epithelium phago- differently it is important for the ophthalmologist to cytoses the degenerating outer segments, occasionally make this determination as soon as possible. migrating into the retina. There is no extracellular retinal The circumstances surrounding the trauma are edema. The opacity of commotio retinae seems to important and should be obtained directly from the represent disrupted receptor cells. Visual loss may result patient and/or an eyewitness in particular if the patient from permanent loss of receptors. The pigment is unable to communicate. Even in cases in which the epithelial response to traumatic receptor damage is Management of Blunt Retinal Trauma 191 spontaneously. However, they should also be adverted that in some instances visual acuity remains disabled. Concurrent treatment of any resultant uveitis should include a topical cycloplegic and, when appropriate, a topical corticosteroid. Cystoid macular edema (CME) is a classical complication of ocular inflammation. CME can result from a rupture of the inner or outer blood- ocular barrier, and it responds poorly to topical and surgical modalities. Topical nonsteroidal and steroidal preparations along with oral carbonic anhydrase inhibitors and injected steroidal depots have been used, but with varied results; sometimes these medication makes a placebo effect in the patient but also in the physician.

TRAUMATIC MACULAR HOLE Initial Concepts The first macular holes reported by Knapp, in 1869, Fig. 31.1: Commotio retinae and Noyes, in 1878, were traumatic in nature. Traumatic macular holes are reported to occur in about 6% of eyes with blunt trauma. The mechanism of traumatic macular hole formation may not be singular. Idiopathic macular holes are believed to be caused by tangential vitreoretinal traction at the fovea; so, traumatic macular holes may be caused by a similar mechanism. In fact, surgical repair of traumatic macular holes is identical to that for idiopathic macular holes, with removal of the posterior hyaloid and peeling of epiretinal or internal limiting membranes, and yields similar anatomic and visual results. There is no doubt that some of these traumatic macular holes may be caused by cystoid degeneration following postcontusion commotio and RPE edema. Under these circumstances the visual prognosis would be more guarded and surgical repair may not be as Fig. 31.2: Berlin`s edema effective. similar to that observed in experimental retinal Pathogenesis detachment and light-induced retinal damage. Macular holes have become the focus of much interest and controversy in ophthalmology. Much of this Management renewed interest stems from new theories of There is usually no treatment required because pathogenesis and the development of a possible surgical commotio retinae tends to resolve without sequela. treatment for macular holes. Despite the numerous The management consists of repairing the traumatic proposed theories, the pathogenesis of these lesions collateral damage and emotionally supporting of the is still not well understood. Most current investigators patient, especially if vision is poor. Visual acuity believe that tangential vitreous traction plays an monitoring, Amsler grid testing, and measurement important role in their pathogenesis, as we described of retinal thickness can provide data indicating the in the section of mechanism of blunt trauma. However, progress of recovery; however, no known topical, there are several mechanisms by which this tangential oral or surgical solution has been offered as a traction may be produced. Gass mentioned that treatment for the commotion it self. If patients initially condensation and contraction of the prefoveal cortical have decreased acuity, they should be informed that, vitreous with glial cell proliferation in this condensed in the majority of cases, improvement takes place vitreous may generate tangential traction. Guyer and 192 Clinical Diagnosis and Management of Ocular Trauma Green suggested that fluid movements of the liquefied macular holes. This sudden traction exerted on the vitreous in an enlarged premacular bursa can exert anatomically thin fovea results in an immediate traction on the remaining formed cortical vitreous, with formation of a macular hole in most cases (Fig. 31.3). that traction transmitted tangentially to the fovea. These finding suggests that the named mechanisms Treatment are important in the generation of tangential traction Vitrectomy surgery for idiopathic macular holes has leading to the macular hole formation, and cellular been shown to improve vision in some eyes. Current proliferation may not play a major role in their techniques include removal of the posterior hyaloids pathogenesis. Studies also found that retinal fragments and all epiretinal membranes from the macular area are a rare feature of the vitreous in these patients; they and prolonged postoperative macular gas tamponade. are thus unlikely to be a constituent of macular hole However, the role of vitrectomy surgery for a macular opercula. Opercula are therefore better termed hole caused by blunt ocular trauma is not still well pseudo-opercula, as has been previously suggested. established. A mild chronic inflammatory infiltrate (lymphocytes) The results of different series are encouraging. is present in some cases of macular holes. Inflammation Despite significant blunt trauma of different types, and cellular or fibrocellular membrane fragments are vitrectomy surgery for macular holes can result in a more frequent in traumatic holes than in idiopathic high likelihood of improved vision and a risk of comp- holes. The significance of this difference is unclear, but lications, that seems no greater than with vitrectomy it is likely a direct result of the initial trauma. surgery for idiopathic macular holes. Further, studies of different approaches with posterior vitrectomy are Studies of Mechanical Forces needed to establish a consistent result for this condition; Evidence from animal studies and biomicroscopic and meanwhile different approaches are being performing surgical observations of patients with a traumatic according the case, the criteria and the resources macular hole strongly suggest that vitreous traction is worldwide. important in their pathogenesis. Experimental observation shows that sudden compression of the TRAUMATIC RETINAL TEARS globe produces an immediate stress on the retina at (RETINAL BREAKS) points of vitreous attachment. High-speed photography Despite the surgical management (enough material to of blunt trauma reveals indentation of the cornea fill an entire book), we will describe in this stage some followed by expansion of the globe at the equator. features that can differentiate a Traumatic retinal Tear This outward expansion of the equator is followed by from those Non-Traumatic and the clinical features to flattening of the posterior pole and then posterior evaluate during the initial examination. displacement of the posterior pole of the eye. It seems likely that with this trampoline-like movement of the Peripheral retinal breaks occur at sites of strong posterior pole, traction forces may in fact be along vitreoretinal adhesions. During blunt trauma vitreo- the surface of the retina, that is tangential, not unlike retinal traction may occur by the forceful displacement what occurs in a more gradual manner with idiopathic or separation of the vitreous. Globe deformation also causes various shearing forces that further amplify the vitreoretinal traction (coup and countercoup). Retinal breaks resulting from trauma can be horseshoe-shaped flap tears or operculated holes. Formed vitreous is often attached to the elevated flap of a horseshoe tear and the free-floating operculum of the hole. These tears can occur along the vitreous base or at the edge of lattice degeneration or chorioretinal adhesions. If a retinal vessel is involved in the tear, a dense vitreous hemorrhage can occur; the attending surgeon must always remember that a vitreous hemorrhage can advice about a retinal rupture, that sometimes is covered by the blood at the initial examination. Giant retinal tears are retinal breaks that extend 3 or more clock hours. They occur at the edge of the Fig. 31.3: Traumatic macular hole vitreous base, which remains attached to the anterior Management of Blunt Retinal Trauma 193 flap; their formation will depend upon the transmission true in traumatic detachments associated with of forces inside the globe, but also upon some previous subretinal or vitreous hemorrhage, giant retinal tears, retinal damage (e.g. high myopia). or severe ocular contusions in which there has been A retinal dialysis is a discontinuity or separation an opportunity for RPE and other fibroglial cells to of the retina from the pars plana at the ora. It is most gain access to the vitreous cavity. Even a condition frequently traumatic in nature and is characterized like vitreitis can lead to retinal detachment because by attachment of the vitreous to the posterior retinal of its inflammatory condition. flap. This is in contradistinction to retinal tears, in Some studies conducted to study phakic retinal which the vitreous usually adheres to the anterior detachments have characterized some of the implied flap; anyhow, vitreo-retinal traction is present in almost features and have helped to establish improved all the times. Traumatic retinal dialysis occurs most guidelines for medicolegal determinations. Myopes often in either the inferotemporal or superotemporal typically developed giant tears and nasal dialyses; quadrant. The risk of progression to retinal emmetropes frequently developed inferotemporal detachment is significant. dialyses. It also has been noticed that lattice degene- Therefore, all traumatic retinal tears and dialyses ration did not increase post-traumatic detachments risk. are treated prophylactically with photocoagulation or Dialyses and giant tears caused 69% of traumatic cryotherapy. Giant retinal tears that continue to tear detachments in comparison with 6% of the cause of despite photocoagulation also can be treated with nontraumatic detachments. Experience has shown that scleral buckling. the overwhelming majority of traumatic retinal detachments are rhegmatogenous in origin. Retinal breaks are predominantly located within the vitreous TRAUMATIC RETINAL DETACHMENT base region but may occur at sites of focal scleral impact Like in the previous section, the retinal detachment or from posterior vitreous avulsion. can include entire books; we will describe only some features regarding the traumatic etiology of this Management condition. Although the use of scleral buckling techniques alone may be sufficient, closed microsurgery may be required Mechanism of Pathology in some cases to relieve retinal traction and to facilitate Traumatic retinal detachments occur primarily as the the identification and permanent closure of the retinal result of retinal changes at the vitreous base. Goffstein breaks. Prophylactic measures including the use of and Burton, reported that 53% of traumatic retinal closed microsurgery, play a vital role in the manage- detachments were caused by retinal dialyses, 16% by ment of traumatic retinal breaks and prevention of giant retinal tears, 11% by horseshoe flap tears, and complex retinal detachment. 8% by tears at the edge of lattice. Retinal detachments Traumatic retinal detachments are treated primarily can also happen secondary to traumatic tears of the by scleral buckling. The results and visual outcomes ciliary epithelium. Sometimes during the clinical evalua- are quite favorable. As previously mentioned, most tion is difficult to identify the specific cause. of these patients (young patients) have well-formed The majority of these traumatic tears and detach- vitreous with posterior hyaloid attachment. Sometimes ments occur in younger individuals. The vitreous often during a pars plana vitrectomy a posterior vitreous is quite well formed and has not yet undergone a detachment may be difficult to create and the morbidity associated with the vitrectomy may be posterior vitreous detachment (PVD). This well-formed greater than that seen with scleral buckling. vitreous often limits the progression of retinal detach- Because of these reasons, some authors attempt ment, especially if it is caused by an inferior dialysis. to avoid an intraocular approach in the repair of these As time progresses and the vitreous becomes more detachments. However, there are several well known liquid or separates further, the detachment can then indications for a primary repair of retinal detachment progress more rapidly. This explains why many by pars plana vitrectomy; vitreous hemorrhage traumatic detachments do not present until several obscuring visualization, posteriorly dislocated crystalline months or even years after the original trauma. At this lens, giant retinal tear with everted flap, proliferative point the physician must remember that after an initial vitreoretinopathy, subretinal hemorrhage and a large trauma, the patient must be educated to follow irregular posterior retinal tear. multiple evaluations, even without symptoms; this In these traumatic cases it is useful sometimes to condition can imply even some legal issues. combine the vitrectomy with an encircling element to Detachments also can be associated with support the vitreous base on a broad, shallow buckle. proliferative vitreoretinopathy (PVR). This is especially The final decisions must be taken by the attending 194 Clinical Diagnosis and Management of Ocular Trauma surgeon according the case, the experience and the VITREOUS BASE AVULSION available resources. The vitreous base represents the region of strongest adhesion between the retina and vitreous. The vitreous VITREOUS HEMORRHAGE base’s strong adhesion continues anteriorly beyond Vitreous hemorrhage can occur through a variety of the ora into the pars plana and ciliary epithelium.These different mechanisms and sometimes is not becoming adhesions are stronger in the young eye. the main trouble; in fact many times it is only the advice Avulsion of the vitreous base is characteristic of of some other disturbances occurring in the posterior blunt ocular trauma. It is the result of ocular segment because of the blunt trauma. It can be the deformation and shearing forces caused by the blunt clinical manifestation of iridodialysis, ciliary body trauma mentioned previously in this chapter. Frequently the avulsed vitreous base may be trauma, avulsion or tear of a retinal vessel, and associated with a retinal dialysis or giant retinal tear breakthrough of subretinal blood from a choroidal because the same shearing forces (coup and counter- rupture between the most important. coup).Therefore, the presence of an avulsed vitreous Visually significant vitreous hemorrhages should be base should alert the examiner to the possibility of followed closely; within the days after the trauma, the associated retinal or ocular injuries. These injuries can hemorrhage can change, but also can change the occur later in time than the initial trauma. In fact, some circumstances of the posterior segment it self. There studies reported that an avulsed vitreous base was may be peripheral retinal pathology and eyes with associated with a dialysis or giant tear in 26% of traumatic retinal detachments, a particular high percentage; this condition should aware the surgeon to observe frequently the retina for days and weeks, in particular in younger patients.

CHOROIDAL RUPTURE Definition and Cinical Findings Choroidal ruptures are breaks in the choroid, the Bruch membrane, and the retinal pigment epithelium (RPE) that result from blunt ocular trauma and can be secondary to indirect or direct trauma. Cases secondary to direct trauma tend to be located more anteriorly and at the site of impact and parallel to the ora serrata, whereas those secondary to indirect trauma occur more posteriorly (countercoup). These ruptures Fig. 31.4: Vitreous and pre-retinal hemorrhage have a crescent shape and are concentric to the optic disc. Indirect choroidal ruptures are almost 4 times retinal tears and vitreous hemorrhage are at increased more common than direct ruptures. risk for detachment due to fibroglial proliferation. Sometimes the changes in the retina can not be seen Histopathology through the blood, so frequent ultrasonography is After blunt trauma, the ocular globe undergoes mecha- recommended to rule out the development of retinal nical compression and then sudden hyperextension. detachment and to follow up the vitreous hemorrhage Because of its tensile strength, the sclera can resist this it self (Fig. 31.4). insult; the retina is also protected because of its elasticity. It is preferable to treat vitreous hemorrhages The Bruch membrane does not have enough elasticity expectantly; a conservative behavior should be the or tensile strength; therefore, it breaks! Concurrently, initial rule. Delayed clearing of the vitreous hemorrhage the small capillaries in the choriocapillaris are damaged, without the presence of other retinal abnormalities, leading to subretinal or sub-RPE hemorrhage. presence of retinal tears that cannot be adequately Hemorrhage in conjunction with retinal edema may visualized for treatment (corroborated with obscure the choroidal rupture during the acute phases, ultrasonography and sometimes even the clinical so frequently observation of retinal hemorrhages is suspect), development of retinal detachment, and mandatory. erythroclastic glaucoma are some indications for the As the blood clears, a white, curvilinear, crescent- surgical removal of the vitreous hemorrhage. shaped streak concentric to the optic nerve is seen. Management of Blunt Retinal Trauma 195 Direct choroidal ruptures are characterized by a angiography may be a useful adjunct to detect CNV; complete absence of choroid and RPE. The overlying if CNV is absent, hypofluorescence occurs during the retina is intact but atrophic because the lack of nutrition. early phase of the angiogram due to disruption of the In indirect choroidal ruptures, choroidal neovasculari- choriocapillaris. During later stages, hyperfluorescence zation (CNV) is a common finding during the early occurs from the adjacent healthy choriocapillaris; if healing phases. Most CNV is in the subretinal space. CNV is present, early hyperfluorescence followed by With time, most CNV involutes spontaneously. In a late leakage is present on the angiogram. small number of cases, a disciform scar or fibrous tissue may grow into the retina and vitreous cavity. During Management the healing phase, choroidal neovascularization Conservative treatment is recommended for most occurs, but in most cases, it involutes spontaneously; choroidal ruptures. During the healing phase of a good, and long-term follow-up is mandatory in these virtually all choroidal ruptures, CNV is present, with lesions. spontaneous resolution in the majority of the cases. In 15-30% of patients, CNV may recur and lead to Diagnosis a hemorrhagic or serous macular detachment with The physical findings are retinal edema (Berlin‘s concomitant visual loss. disease), hemorrhagic detachment of the macula, The treatment of CNV will depend upon the locali- serous detachment of the macula, subretinal hemor- zation; if CNV is extrafoveal, it may be treated success- rhage and a white curvilinear crescent-shaped streak fully with laser photocoagulation; if CNV is subfoveal concentric to the optic nerve (Figs 31.5 and 31.6). or juxtafoveal, consider pars plana vitrectomy with The imagines studies helping the diagnostic of membrane extraction, with all the implicating risks choroid hemorrhage and associated lesions; fluorescein because of working near the fovea. Most patients with choroidal ruptures do not reach a final visual acuity of 20/40 or better; poor visual acuity is associated with macular involvement. If the rupture does not involve the fovea, good vision is expected. Most CNV occurs within the first year. However, CNV has been reported to occur as late as 35 years after the choroidal rupture. For legal reasons the surgeon must always remember that choroidal neovascularization can occur again, and so periodic examinations are necessary.

Prognosis Fig. 31.5: Choroid fracture If the rupture does not involve the fovea, good vision is expected. In 15-30% of patients, CNV may arise again and lead to a hemorrhagic or serous macular detachment with concomitant visual loss. This usually occurs during the first year but can also occur decades later. Older age and macular rupture, the length of the rupture, and the distance of the rupture to the center of the fovea may be risk factors for CNV and so important factors in the long term prognosis.

OPTIC NERVE AVULSION Definition and Clinical Findings Traumatic optic neuropathy (TON) refers to an acute injury of the optic nerve secondary to trauma. The optic nerve axons may be damaged either directly or indirectly and the visual loss may be partial or complete. An indirect injury to the optic nerve typically occurs Fig. 31.6: Choroidal rupture from the transmission of forces to the optic canal from 196 Clinical Diagnosis and Management of Ocular Trauma blunt head trauma. This is in contrast to direct TON, which results from an anatomical disruption of the optic nerve fibers. Patients can present with a variable degree of vision loss (decreased visual acuity, visual field abnormalities, or loss of color vision). Most cases (up to 60%) present with severe vision loss of light perception (LP) or worse. In the acute phase, the optic nerve usually appears normal on funduscopic examination, but optic nerve atrophy is often seen 3-6 weeks after the injury; so the clinical must be aware to perform periodical revisions of the traumatized eye during a long period of time. Fig. 31.7: Optic nerve avulsion

Mechanisms of Injury There are two known forms of optic nerve injury: Indirect injury: In indirect TON cases, the injury to the axons is thought to be induced by shearing forces that are transmitted to the fibers or to the vascular supply of the nerve. Studies have shown that forces are transferred and concentrated in the area near the optic canal. The tight adherence of the optic nerve’s dural sheath to the periosteum within the optic canal is also thought to contribute to this segment of the nerve being extremely susceptible to the deformative stresses of the skull bones. Such injury leads to ischemic injury to the retinal ganglion cells within the optic canal. Direct injury: A secondary mechanism can result in optic nerve swelling after the occurrence the acute injury. The optic nerve swelling can exacerbate retinal ganglion cell degeneration by further compromising Fig. 31.8: Optic nerve atrophy the vascular blood supply, either through a rise in intraluminal pressure or reactive vasospasm. These of a bilateral TON, both pupils may be dilated and secondary mechanisms, in theory, form the rationale nonreactive to light if the injury is profound. for optic canal decompression via medical (e.g.steroids) At the funduscopic, because the location of the or surgical means (e.g. bony decompression). injury in most of the cases is within the posterior orbit or the optic canal, the optic disc typically appears Diagnosis normal on funduscopic examination on initial diagnosis. Even in an acute trauma setting, patients should have Optic nerve atrophy usually appears 3-4 weeks after a visual acuity assessment as soon as possible. If the the traumatic event, and the disc acquires a diffuse patient cannot read the top letter on the eye chart, pallor. Rarely, optic nerve changes can be seen with the visual acuity may be recorded with the following direct injuries to the retrobulbar section of the optic nomenclature; counting fingers vision, hand motion nerve, presenting as an avulsed optic nerve head or perception, light perception (LP), or no light perception optic disc swelling with surrounding hemorrhage (NLP), sometimes are the obtained lectures. (Figs 31.7 and 31.8). The pupil examination assesses for a relative or Computed Tomography of orbits, comparing both complete afferent pupillary defect. An eye with a optic nerves anatomy, are sometimes of great value, unilateral optic nerve injury will demonstrate an but even so, sometimes even in the presence of severe afferent papillary defect, verifying the presence of TON, optic nerve damage, the funduscopic and the radiologic but not excluding other diagnosis. In the rare cases findings can be normal. Management of Blunt Retinal Trauma 197 Management velocity missile; it is the result of traumatic chorioretinal Steroids have been used in TON since the early 1980s; rupture followed by marked fibrovascular proliferation they are thought to provide neuroprotection in with variable replacement of the choroid and retina traumatic central nervous system injury through their with no retinal detachment. antioxidant properties and inhibition of free radical- Contusion force may lead to choroidal ruptures induced lipid peroxidation. Recent studies have with hyperplasia and migration of the retinal pigment demonstrated that the therapeutic role for cortico- epithelium into the retina and choroid, epiretinal steroids in the management of TON is unsubstantiated. membrane formation, loss of photoreceptors and If steroids are considered to be used in cases with marked atrophy of the optic nerve. concomitant traumatic brain injury, it must not be a decision of the ophthalmologist by it self; dangerous Diagnosis circumstances involving the central nervous system can The diagnosis should be established only based on be mascared. The use high or lower doses of steroids clear objective findings, a relative afferent pupillary is also not clearly defined by the literature as useful defect or an evoked visual response. The most for optic nerve protection. May be, as has been seen important factor in determining the force of injury is in other sections of this chapter, they can provide a the velocity. As higher the speed of the projectile object, placebo effect in the patient, family, but also in the the greater the tissue disruption at the impact zone physician. due to the delivered kinetic energy. The shock wave The indication for surgical therapy in indirect optic nerve trauma is to decompress it at the site of injury, energy released by the projectile object is considered which is often the intracanalicular segment. Surgical as the main cause of choroidal and subsequently retinal decompression is thought to help reduce optic nerve injury (Fig. 31.9). compression and subsequent vascular compromise that may occur as a result of the indirect injury. Another Treatment probably benefit of surgery that has been postulated, Retained intraorbital metallic foreign bodies may is to remove bone fragments that may be injuring on accompany chorioretinitis scleopetaria, commotio the optic nerve within the optic canal. However, no retinae, vitreous hemorrhages, or some other times randomized, controlled studies have been performed this entity can be presented alone; treatment of to evaluate the role of surgery in this disease. concomitant damage should be done. In the case of bullets, gun pellets, the usual management is Conclusions conservative due to the inert nature of this type of Traumatic optic neuropathy (TON) can lead to pro- metallic foreign bodies. There are considerable found visual loss from either indirect or direct reported cases with chorioretinitis sclopetaria due to mechanisms. The diagnosis can be made with bullet gun injuries; the characteristic pattern of accurate history taking and clinical examination, based choroidal and retinal changes caused by a high on the presence of visual loss and an accompanying velocity projectile object passing through the orbit, relative afferent pupillary defect. The optimal treatment in close proximity to the globe is usually seen in this for TON, however, remains debated among physicians. condition. Corticosteroids should not be used in cases with concomitant traumatic brain injury or in patients who present 8 hours or more after initial injury. Based on the available evidence, surgical decompression of the optic canal is not routinely recommended. If treatment with either steroids, surgical intervention or both is considered, appropriate information and informed consent should be given to the patient and their family; they should know (and sign) the potential benefits and the risks.

CHORIORETINITIS SCLOPETARIA Definition It is a proliferation of fibrous tissue in the choroid and retina as the result of contusion of the sclera by a high Fig. 31.9: Retinitis sclopetaria 198 Clinical Diagnosis and Management of Ocular Trauma The role of steroids is also in debate with no demons- tration of real benefit in their application.

PURTSCHER RETINOPATHY Definition and Causes Purtscher retinopathy is a hemorrhagic and vaso- occlusive vasculopathy, which, in 1912, was first described as a syndrome of sudden blindness associated with severe head trauma. These patients had findings of multiple white retinal patches and retinal hemor- rhages that were associated with severe vision loss. Since its original description, Purtscher retinopathy has been associated with traumatic injury, primarily blunt thoracic trauma and head trauma, but also with Fig. 31.10: Purtscher retinopathy numerous non-traumatic diseases; it is seen in diverse conditions, including acute pancreatitis, fat emboli- zation, amniotic fluid embolization, and vasculitic include serous detachment of the macula, preretinal diseases. Bilateral manifestations are seen most hemorrhages, dilated vessels, and optic disc edema. commonly in systemic conditions, but unilateral Confluent cotton-wool spots in the central macula may findings have been also reported. Decreased vision simulate the cherry-red spot that is seen in central retinal occurs in the affected eyes, generally in the range of artery occlusion. Retinal microinfarcts that are observed 20/200 to counting fingers. Vision can often improve in patients with fat embolization are usually smaller within several months to a range of 20/30 to 20/200, in size and located in the peripheral, not central, retina. depending on the severity of the retinal findings. Pigment migration and optic atrophy have been reported as late findings in the disease (Fig. 31.10). Angiogram with fluoresceine is very useful to Hystopathology corroborate the ischemic damage, but many times the The exact pathophysiology remains somewhat only characteristic clinical pattern, is enough to controversial, and different mechanisms have been determine the diagnosis. Without history of trauma, described; the main mechanism purposed is vascular physician should consider fat embolization, amniotic occlusion. The characteristic white lesions are known fluid embolization, retinal vasculitis, system lupus as cotton-wool spots, and correspond to retinal erythematosus, dermatomyositis, scleroderma and microinfarcts at the level of the nerve fiber layer, caused radiation retinopathy, between others. by the ischemic lesion. Fluorescein angiogram reveals leakage, and it can suggests that an acute endothelial cell injury is caused by trauma; possibly this is the Management predisposing factor that lead the retinal vessels to No proven treatment exists for Purtscher retinopathy occlusion. Other possible sources of emboli include that occurs after traumatic injury. In patients with fat emboli in cases of long bone fractures and perhaps retinopathy due to systemic vasculitis, steroid therapy pancreatitis from enzymatic digestion of omental fat, is theoretically beneficial. amniotic fluid embolization during childbirth and post- Visual prognosis is guarded, although initially partum, air emboli from traumatic chest compression, decreased vision may improve over a period of months. and granulocyte aggregation resulting from The most important prognostic finding that is associated complement activation. with a poor visual prognosis is central macular infarction, due to the ischemic condition. Diagnosis In a funduscopic view, macular cotton-wool spots and Bibliography intraretinal hemorrhages in patients with this history of trauma are diagnostic of the condition. Patients with 1. Abrams GW, Topping TM, Machemer R. Vitrectomy for injury: The effect on intraocular proliferation following traumatic Purtscher retinopathy present with a recent perforation of the posterior segment of the rabbit eye. history of blunt chest trauma or head trauma. The Arch Ophthalmol 1979;97:743. severity of chest trauma is not always correlated with 2 Alapatt J, Hutchins R. Retinal detachments due to the incidence and/or severity of retinopathy, which is traumatic tears in the pars plana ciliaris. Retina observed in these patients. Some other findings can 1998;18:506. Management of Blunt Retinal Trauma 199

3. Barr CC. Prognosis factors in corneoscleral lacerations. 19. Gass JDM. Stereoscopic Atlas of Macular Disease: Arch Ophthalmol 1994;101:919. Diagnosis and Treatment. ed 3. St. Louis: CV Mosby 4. Barr CC, Vine AK, Martonyi CL. Unexplained hetero- 1987. chromia. Intraocular foreign body demonstrated by 20. Goffstein R, Burton TC. Differentiating traumatic from computed tomography. Surv Ophthalmol. 1984;28:409. nontraumatic retinal detachment. Ophthalmology 5. Berlin R. Zur sogenannten commotio retinae. Klin 1982;89:361. Monatsbl Augenheilkd 1873;11:42. 21. Hart JCD, Frank HJ. Retinal opacification after blunt 6. Blight R, Hart JCD. Structural changes in the outer nonperforating concussional injuries to the globe: A retinal layers following blunt mechanical nonperforating clinical and retinal fluorescein angiographic study. Trans trauma to the globe: An experimental study. Br J Ophthalmol Soc UK. 1975;95:94. Ophthalmol Soc UK. 1978;98:270. 22. Hilton GF. Late serosanguineous detachment of the 7. Brinton CS, Topping TM, Hyndiuk RA, et al. Post- macula after traumatic choroidal rupture. Am J traumatic endophthalmitis. Arch Ophthalmol 1984; Ophthalmol 1975;79:997. 102:547. 23. Kaufer G, Zimmerman IE. Direct rupture of choroid. 8. Chang S. Low viscosity liquid fluorochemicals in Arch Ophthalmol 1966;75:384. vitreous surgery. Am J Ophthalmol 1987;103:38. 24. Kohno T, Ishibashi T, Inomata H, et al. Experimental 9. Chang S, Reppucci V, Zimmerman NJ, et al. Perfluoro- macular edema of commotio retinae: Preliminary report. carbon liquids in the management of traumatic retinal Jpn J Ophthalmol 1983;27:149. MEDLINE detachments. Ophthalmology 1989;96:785. 25. Lewis H, Blumenkranz M, Chang S. Treatment of 10. Cogan DG. Pseudoretinitis pigmentosa: Report of two dislocated crystalline lens and retinal detachment with traumatic cases of recent origin. Arch Ophthalmol perfluorocarbon liquids. Retina 1992;12:299. 1969;81:45. 26. Martin DF, Awh CC, McCuen BW, et al. Treatment and 11. Coleman DJ. Early vitrectomy in the management of the pathogenesis of traumatic chorioretinal rupture severely traumatized eye. Am J Ophthalmol 1982; (Sclopetaria). Am J Ophthalmol 1994;117:190. 193:543. 27. Noyes HD. Detachment of the retina, with laceration of 12. Cox MS, Schepens CL, Freeman HM. Retinal detach- the macula lutea. Trans Am Ophthalmol Soc 1871;1:128. ment due to ocular contusion. Arch Ophthalmol MEDLINE. 1966;78:678. 28. Ross WH. Traumatic retinal dialyses. Arch Ophthalmol 13. Crouch ER, Apple DJ. Post-traumatic migration of retinal 1981;99:1371. pigment epithelial melanin. Am J Ophthalmol 29. Rubsamen PE, Cousins SW, Winward KE, et al. 1974;78:251. Diagnostic ultrasound and pars plana vitrectomy in 14. deJuan E, Sternberg P, Michels RG, et al. Penetrating penetrating ocular trauma. Ophthalmology 1994; ocular injuries: Types of injuries and visual results. 101:809. Ophthalmol 1983;90:1318. 30. Smith RE, Kelley JS, Harbin TS. Late macular 15. Delori F, Pomerantzeff O, Cox MS. Deformation of the complications of choroidal ruptures. Am J Ophthamol globe under high-speed impact: Its relation to contusion 1974;77:650. injuries. Invest Ophthalmol 1969;8:290. 31. Thompson JT. Traumatic retinal tears and detachments. 16. Dumas JJ. Retinal detachment following contusion to the In: Shingleton BJ, Hersh PS, Kenyon KR editor. Eye eye. Int Ophthalmol. 1967;7:19. Trauma. St Louis: Mosby–Year Book 1991;195. 17. Eliott D, Avery RL. Nonpenetrating posterior segment 32. Weidenthal DT, Schepens CL. Peripheral fundus trauma. Ophthalmol Clin North Am 1995;8:647. changes associated with ocular contusion. Am J 18. Fuller B, Gitter KA. Traumatic choroidal rupture with late Ophthalmol. 1966;62:465. serous detachment of macula: Report of successful argon 33. Zion VM, Burton TC. Retinal dialysis. Arch Ophthalmol. laser treatment. Arch Ophthalmol 1973;89:354. 1980;98:1971. CHAPTER

Applications of Stem Cell Therapy in Ophthalmology 32 Rajpal Vohra (India)

Introduction Embryonic stem cells are typically isolated from blastocysts and have pluripotency.they can give rise In Ophthalmology, there are various conditions where to virtually any adult tissue cell type under appropriate there is no treatment available like Retinal degene- conditions. Truly pluripotent embryonic stem cells have rations, and total deficiency of stem cells which occurs been identified that can give rise to a multitude of in alkali burns in cornea. Stem cells are recent advances differentiated cell types. Stem cell is the origin of life. in Ophthalmology, which has given newer therapeutic Ultimate the stem cell, fertilized egg, is formed from modalities in the management of retinal diseases, which fusion of the haplid progeny of germinal stem cells.The were thought to be incurable. Stem cell therapy is an fertilized egg is totipotent. upcoming new mode of treatment in present time. Adult derived stem cells typically reside in adult tissue Stem cell research offers hope to countless patients in a quiescent, undifferentiated state and under whose conditions have here to fore been deemed appropriate stimuli will divide and differentiate into incurable. Better understanding of stem cell behaviors the cell types of tissue in which they reside or if and functions will lead to insights into biological appropriately stimulated into other cell types. Normal mysteries encompassing the fields of angiogenesis, tissue renewal is accomplished by the differentiating development, tissue homeostasis, wound healing, and progeny of the stem cells, the so called transit- carcinogenesis. amplifying cells. The potential use of stem cells in the treatment of During early embryonic development, each cell a variety of human retinal disease remains divides and gives rise to two daughter cells with the tremendously exciting. There is by ethical controversy same potential:symmetric division. During normal tissue in use of fetal tissue so the actual potential use of such renewal in the adult, each progenitor cell gives rise approaches remains yet unexplored. Adult tissue is less to one daugther cell that remains a progenitor cell, controversial and more readily available, holds promise and one daugther cell that begins the process of but the pluripotency and actual utility of stem cells determination to a terminally differentiated cell leading obtained from this source remains uncertain. Clearly, to termination- asymmetric division. During normal populations of progenitor cells exist in the ciliary margin tissue renewal in adult organs, tissue stem cells give and bone marrow and each may have significant utility rise to progeny that differentiated into mature as we seek to repair and rebuild damaged retinas. Even functioning cells of that tissue. Stem cell with less than if such complex tissue reconstruction could be totipotentiality are called Progenitor Cells. successfully completed, re-establishing functional visual The Ivanova et al are doing large scale genomic pathways will be an even greater challenge. analysis and Ramalho– Santos M et al are doing transcriptional profiling of stem cells. At present there is a controversy whether adult Definition of Stem Cells tissue containing pluripotent stem cells will serve as a Stem cells are pluripotent cells capable of differentiating source of regenerative tissue. into variety of cell types. There are two sources of stem Lee MS et al, has done recent clinical trial using cells: adult bone marrow (BM) derived stem cells to 1. Stem cells from adult tissue regenerate infracted myocardium have reported 2. Stem cells from fetal material – called embryonic success in improving cardiac functions. Presuming on stem cells. the basis of bone marrow stem cells differentiating into Applications of Stem Cell Therapy in Ophthalmology 201 myocardium is not supported by experimental data mammal does not show regenerative capacity after by Murry CE et al. According to Balasam LB et al damage, there is a possibility for the reinitiation of stem hematopoietic stem cells adopt mature hematopoietc cell potential at the peripheral retinal margin, from fates in ischemic myocardium. According to Anderson the RPE or from the Muller glial cells. The application DJ, et al these clinical observations cannot be of information derived from the studies of retinal invalidated but raises many questions regarding progenitor cells in developing organisms should soon interpretation and emphasizes that there is a need to provide a test of these possibilities. establish rigorous standards by which such clinical This regenerative capacity derives from quiescent studies are evaluated. stem cells that reside in the adult retina of these species. Very limited work has been done regarding retinal Similar regenerative capacity has been demonstrated stem cells.There has been extensive literature work in mammalian retina. For a population of retinal stem done an stem cells giving rise to vascular, muscle cells to exist in the adult retina, it would have been nervous hemopoietic tissue. Very limited work has necessary for such a population of progenitor cells to been done on the retinal stem cells. remain quiescent after the retina has fully differentiated. There are four basic population of cells that may Livesey FJ et al has done large scale Genomic anlysis. contain dormant progenitor cells. Blackshaw S et al has done Genomic analysis of mouse 1. Retinal stem cells that can give rise to retinal development. photoreceptors The work of livesey and Blackshaw can serve as 2. Muller/glial stem cells the starting point for the evaluation of numerous genes 3. Retinal pigment epithelial [RPE]; and endothelial and their potential role in the regulation of retinal cell progenitor cells [EPC] developmental determination. How genes are Recently adult bone marrow-derived HSCs progressively switched on and off in an orderly fashion containing EPC is an intresting areas of research. during the generation of specific retinal cell types, and how this overlaps with gene sets utilized during the establishment of other, nonretinal neuronal cell types, Role of Retinal Stem Cells and will contribute significantly to our understanding of retinal progenitor biology. Dyer MA et al has done Muller Glial Cells study in regulation of cell proliferation in retinal Reh TA et al. has shown that regenerative capacity development. Das AV et al has done identification of exists in retina of amphibians and chicken embryos c-KIT receptor as a regulator of adult neural stem cells after injury. The vertebrate retina is derived from paired in the mammalian eye and the role of various evaginations from the neural tube in embryonic transcription factor and signaling molecules during this development and is initially produced by progenitor process have provided insight into putative cells similar to those that generate the neurons and mechanisms whereby the mammalian retina holds in glia of other areas of the central nervous system. In reserve a subset of progenitor cells that theoretically some amphibians and fish, the retina continues to grow could be used to regenerate damaged issued in the along with the eye throughout the life of the animal. in the adult. Clearly, James J et al has studied the the The new retinal cells are added at the ciliary margin development state of the retina and the context in of the eye from the mitotic activity of neural/glial stem which a specific cell finds itself will determine how a cells in a region known as the germinal zone and are particular retinal progenitor cell behaves: whether it seamlessly incorporated into the existing retinal circuitry. will terminally differentiate or maintain a quiescent state Little is known about the cell or molecular biology of from which it can letter emerge to give rise to cells these stem cells; however, studies of retinal progenitor useful in repair of a damaged retina will depend not cells in chick and mammalian embryos have led to only on its own developmental programme, but the the identification of several factors that control their microenmorvironment in which it finds it self. proliferation. Moreover, studies of retinal regeneration James J et al has done cellular and molecular have shown that retinal stem cells can also be derived characterization of early and late retinal stem cells/ from two or perhaps three additional sources after progenitors: differential regulation of proliferation and retinal damage: (a) the retinal pigmented epithelium context dependent roll of notch signaling. (RPE) in amphibians and embryonic chicks and James J et al has done transcriptional profiling mammals; (b) a specialized rod progenitor in fish; and studies of retina at different states of development (c) the Muller glial cells. While there is currently no coupled with in vitro studies of progenitor cell evidence for a neural/glial stem cell in the adult populations should provide the information necessary mammalian retina, and the retina of the mature to begin such an analysis and determine what 202 Clinical Diagnosis and Management of Ocular Trauma conditions help maintain quiescence and what activation of intrinsic genes. These studies are most conditions stimulate proliferation and subsequent provocative, could provide additional insight into differentiation of retinal progenitor cell populations. retinal regeneration in mammals, and provide a Konobu T et al have shown that cells with rationale for the targeting of Muller glial in certain characteristics of retinal neuron have been obtained inherited and acquired retinal degenerative disorders. from a number of embryonic tumor cell line, including If we isolate retinal stem cells from the adult neuroblastoma, gliaoblastoma, but because of the mammalian eye and then using them to regenerate malignant potential of these cells they are not likely diseased retina then it will have a great therapeutic to be useful. effect. There have been some reports suggesting that Martinez-Serrano A et al, have cultured virally if multipotent progenitor cells isolated from retina of transformed, immortalized neuronal precursors were neonatal mice retina are used in the early, then some evaluated for their ability to differentiate into retinal level of visual function may be obtained in animal eyes neurons after intraocular implantation. with retinal degeneration. At cellular level it is very Bain G et al have attempted at inducing in vitro difficult to establish functional neuronal connection differentiation of embryonic stem cells into retinal between implanted progenitor cells or sheets of neuronal phenotypes were done using a variety of photoreceptor and the host’s nerve fiber layer prior factors, including retinoic acid. to reestablishing visual pathways that would lead to Tropepe V, et al has identified Retinal progenitor functional vision. stem cells in the adult mammalian eye. Ahmad I, et al have done Identification of neural progenitors in the adult mammalian eye. Retinal progenitor cells have Role of Retinal Pigment been identified in ciliay margin. These cells were not isolated from central or peripheral pigmented Epithelial Stem Cells epithelium. These cells are clonally expanded in culture RPE cells and photoreceptors enjoy an close to give rise to a variety of retinal cells types, including relationship both anatomically and functionally. Where rod photoreceptors, bipolar neurons, and muller glia. is the principal underlying defect in many inherited The differentiation of these cells from the ciliary margin retinal degenerations is still a question: the pigmented cell progenitors is not due to photoreceptor or RPE cells ?. Although with the advent transdifferentiation of the ciliary margin cells, but rather, of molecular genetics this confusion has become less, clonal proliferation and defferentiation as observed in but the interdependency between these two cells types a true stem cell. remains and there is often concomitant degeneration Fischer AJ et al have shown that in chicken an adult of both cell types observed in a variety of inherited differentiated muller gila can serve as a source of stem and acquired degenerative disease of the retina. In cells that will, in response to injury, or cytokinenes, this regard—RPE cell transplantation has been differentiate, proliferate and redifferentiate into evaluated both for its potential to replace diseased RPE additional glial cells or neurons. as well as to provide a source of cells whose phenotypic Turner DL, et al have identified common progenitor differentiation may be manipulated by various cells that gives rise to both Muller glia and retinal cytokines and trophic substances. Thus, RPE cell lines neurons. have been developed for use as RPE cell transplants, Thus, the concept that Muller glia of the adult retina cell-based drug delivery platforms, and “photoreceptor can serve as potential source of retinal stem cells is stem cells”. consistent with molecular profiling of developing Transplantable RPE cell lines may serve as stem mammalian retinas that shown a high degree of cells of sorts to replenish diseased RPE cells themselves. similarity between the gene expression profiles of Muller In a number of macular and retinal degenerative glia and mitotic retinal progenitor cells in the mouse. disorders there is atrophy of the RPE and associated Since the Muller glia are the cells that commonly malfunctioning in the phototransducing cellular proliferate in response to retinal injury, it would not machinery. Damaged RPE cells and associated atrophy be surprising that these cells also retain the potential are hallmarks of age-related macular degeneration and to defferentiate along a number of pathways, some heroic surgical approaches have been considered to of which may lead to retinal neuronal replacement. provide photoreceptors in such individuals with Ooto S et al have done a recent study significantly healthier, RPE-rich regions of the retina through retinal expanded this concept: amarcine, horizontal, and translocation and the insertion of RPE sheets. photoreceptor phenotypes were mammalian retina in Human RPE cell lines enjoy an extended life span the presence of extrinsic factors (e.g. retinoic acid) or after being stably transfected with a plasmid encoding Applications of Stem Cell Therapy in Ophthalmology 203 the simian virus 40 large T antigen and many of the circumstances, provide a transplantable pool of cells factors expressed by functional RPE cells in vivo are to rescue diseased photoreceptors and, as such, have observed to be expressed by these transformed cell utility in the treatment of retinal degenerations. lines. When these cells are transplanted subretinally into a rat model of retinal degeneration (the RCS rat), loss of visual function is attenuated and cortically Role of Bone Marrow: Derived dependent visual function is preserved long-term. These RPE cell lines can be transferred with plasmids Stem Cells encoding a variety of trophic factors shown to have BONE MARROW HEMATOPOIETIC protective effects on photoreceptors and then STEM CELLS encapsulated into polymer devices that permit diffusion In 1917, Pappenhein postulated the existensce of an of cell products into the tissue into which they are undifferentiated stem cell for blood cells. The hema- transplanted. When transformed RPE cell lines are topoietic or blood forming cells are located in the bone transfected with a plasmid encoding one such factor, marrow. The lineage of blood cells extends from a ciliary neurotrophic factor (CNTF), and transplanted resting stem cell, to transit- amplifyilng precursor cells, directly into the vitreous of dogs with retinal to mature circulting blood cells. Untill recently, most degeneration, photoreceptor degeneration is reduced. primitive bone marrow progenitor cell was believed Further more, production of this factor and to be pluripotent, giving rise to stromal cells and implantation of the encapsulation device into the lymphocytic cells, as well as RBCs, WBCs. In addition vitreous of normal rabbits did not lead to toxic effects to hematopoietic precursor, bone marrow also on either the electroretinogram or retinal histology in contains a mesenchyamal progenitor cell can give rise these animals at doses that protect photoreceptors in to many other cell types such as muscle cells, astrocytes, dogs with retinal degeneration. Such cell-based and neurons,as well as stromal cells that support delivery devices may be used to provide trophic factors hematopoiesis. However, the accumulating evidence for the treatment of a variety of retinal degenerative is that, not only does the bone marrow contain a pluri/ diseases and, in fact have recently been used in a multipotent blood forming stem cell, but it also contains human clinical trial evaluating the efficacy of CNTF a cell that has the capacity to circulate to other organs in the treatment of retinal degeneration. In this respect, and replace different nonhematopoietic tissues. the implanted encapsulated cell devices function as a Although these bone marrow-derived cells have stem cell, providing factors critical to the prevention markers of the hematopoietic stem cell [HSC], it has of, or recovery from, retinal degenerative disease. not been ruled out that this multipotent cell may be Spontaneously differentiating human embryonic of stromal origin. Serial transplantation indicates that stem cell lines having many molecular and functional a single bone marrow cell may give rise to many characteristics of RPE cells have been touted as a different tissue types and suggest that a common potential source of transplantable RPE cells for precursor must exist, not only for stromal and subretinal transplantation into human retinas. Large- hematopoietic lineages, but also other germ layer- scale genomic analysis was used to compare these cells derived cell types. It is this putative totipotent bone to primary human RPE cell lines and they were found marrow cell that has stimulated the great revival of to resemble more closely the molecular signature of interest in adult stem cells in the last few years. There are still some caveats to the generally accepted primary RPE cells than previously reported, established assumption of pluripotentiality of tissue stem cells human RPE cell lines. If these cell lines can be including HSCs. maintained in cell banks and altered so as to facilitate immune acceptance, they may represent a source of transplantable tissue. Studies done over a decade ago evaluated the Role of Adult Bone Marrow: potential use of RPE cells as stem cells of sorts: when Derived Endothelial Progenitor RPE cells were injected subretinally into the eyes of mice with inherited retinal degeneration, rescue of (Stem) Cells photoreceptors was observed. It was found that Abnormalities in the retinal or choroidal vasculature: exogenously injected basic fibroblast growth factor macular edema, retinal and vitreous hemorrhage, and could mimic this rescue. This led to the concept that fibrovascular scarring commonly contribute to visual RPE cells may, under appropriate conditions, serve loss in diseases such as age retinal macular degene- as a form of cell-based therapy and may, under certain ration, diabetic retinopathy, retinopathy of prematurity, 204 Clinical Diagnosis and Management of Ocular Trauma and neovascular glaucoma. Retinitis pigmentosa are anywhere but in or near blood vessels since these cells commonly thought of as neuronal degenerations, but are derived from green fluorescent protein. How this most also exhibit vascular abnormalities traditionally is going to be used in human is still in question? attributed to loss of neuronal elements and accompan- ying decreased metabolic demand leading to vascular atrophy. Otoni A et al have describe a newly emerging Role of Bone Marrow: Derived paradigms: the existence of trophic “cross-talk” Stem Cells in Retinal and between local vascular networks and the tissues they supply and such interactions almost certainly help to Choroidal Neovascularization maintain a functional differentiated state in a variety It was Grant and colleague who has first directly

of organ systems. Shen Q et al have shown that, demonstrated that systemically administered HSC endothelial cells are also now known to provide trophic (Hematic stem cell can function as Hemangioblast substance that greatly stimulate self-renewal and during hypoxia stimulated retinal neovascularization).

expand neural differentiation of neural stem cells.Given Hematopoetic stem cells contains a pool of EPCs such interdependency of vascular endothelial cells and (endothelial progenitor cells) capable of incorporating surrounding tissues, it may be possible to use one cell into retinal vasculature has recently been demonstrated type to rescue the other in the face of severe stress by several groups. Grant and colleague have such as hypoxia or genetically encoded cell-specific demonstrated that circulating, undifferentiated degenerations. Under such conditions it would be precursor cells can be recruited to sites of retinal desirable to have available populations of progenitor neovascularization and, along with proliferation of local cells useful for such protection. endothelial cells, can contribute to new blood vessel growth and development. The relative contribution BONE MARROW: DERIVED STEM CELLS of circulating precursor cells and endogenous retinal CAN EXERT A NEUROTROPHIC RESCUE IN vascular endothelial cells to newly forming vasculature RETINAL DEGENERATION in human disease remains unknown; the experiments Humphries P et al has done molecular genetics of of Grant and colleagues demonstrate that circulating retinitis pigmentos and has identified mutations in over cells can incorporate into laser-stimulated retinal 110 different genes, accounting for only a relatively neovascularization, but the role of these cells in small percentage of the known affected individuals nonirradiated hosts where the proliferation of local many of these mutations are associated with enzymatic inflammatory, precursor, and endothelial cells is not and structural components of the phototransduction impaired by lethal irradiation remains unclear. Studies machinery, including rhodopsin. Most inherited human from several groups have demonstrated, using the retinal digenerations same irradiation/bone marrow reconstitution model Otoni A et al have shown that bone marrow – that circulating stem cells can also contribute to laser- derived stem cells exert vasculotrophic properties. stimulated choroidal neovascularization. These cells have also recently been reported to Dorrell MI, et al have demonstrated a role for the completely prevent retinal vascular degeneration adhesion molecule, R-Cadherin, in the targeting of ordinarily observed in mouse models of retinal HSC to the retinal vasculature when small molecule degeneration, and the vascular rescue correlates with antagonizes or function blocking antibodies to neuronal rescue. The inner nuclear layer remains nearly R-Cadherin are used to pretreat Lin-HSC prior to normal and the outer nuclear layer containing intravitreal injection, the cells no longer target sites of photoreceptors is significantly preserved, with the angiogensis and participate in the formation of new rescued mice being predominantly cones. Detectable, retinal blood vessels. Integrin alpha 4 beta 1, a albeit severely abnormal electroretinogram recordings adhesion molecules may play a role in targeting are observed in rescued mice at time when they are circulating EPCs to sites of abnormal angiogenesis never observed in control treated, or untreated, rd/ during vascularization of tumor, and that these integrin rd eyes. This rescue effect is also observed when human may be potential therapeutic target if, indeed circulating bone marrow-derived Lin- HSCs are used to treat EPCs contribute to pathological ocular angiogenesis. severe combined imnunodeficient mice with retinal Interfering with the function of such targeting molecule degeneration. Large-scale genomic analysis of rescued used by EPCs to target sites of pathological eyes revealed significant upregulation of antiapoptotic neovascularization in combination with cell based gene. It is important to note that the injected bone therapies to produce angiostatic molecues locally could marow-derived progenitor cells are never observed significantly reduced abnormal angiogenesis. Applications of Stem Cell Therapy in Ophthalmology 205 BONE MARROW—DERIVED STEM CELLS CAN derived cells, placenta-derived cells, and mesenchymal EXERT A VASCULOTROPHIC RESCUE EFFECT stem cells were studied; dermal fibroblasts served as Otoni A at al have injected Lin- HSCs directly into cell controls. At various ages up to 100 days, the eyes of newborn mice while they were forming electroretinogram responses, spatial acuity and their retinal vasculature; in this environment, these cells luminance threshold were measured. Both umbilical- can target activated astrocytes, a hallmark of many derived and mesenchymal cells significantly reduced ocular vascular and degenerative diseases. Once the degree of functional deterioration in each test. The targeted to this template of activated astrocytes, the effect of placental cells was little better than controls. Lin HsCs participate in normal developmental Umbilical tissue-derived cells gave large areas of angiogenesis in both neonatal mice or injury-induced photoreceptor rescue; mesenchymal stem cells gave neovascularization in the adult. only localized rescue. Fibroblasts gave sham levels of The HSC fraction used in these studies not only rescue. Donor cells were confined to the subretinal inhibited angiogenesis when engineered to express an space. There was no evidence of cell differentiation antiangiogenic, but also resued and stabilized into neurons, of tumor formation or other untoward (e.g. matured) degenerating vessels. More surprisingly, pathology. Since the umbilical tissue-derived cells it was also observed that by preventing vascular demonstrated the best photoreceptor rescue and degenertion there is a trophic rescue effect on the unlike mesenchymal stem cells were capable of photoreceptors themselves, suggesting that autologuous sustained population doublings without karyotypic bone marrow grafts of HSC fractions containing EPC changes, it is proposed that they may provide utility may provide trophic effects on associated neural tissue as a cell source for the treatment of retinal degenerative that goes beyond simple nutrition. Such observations diseases such as retinitis pigmentosa. could provide a rationale for the use of HSC in the treatment of a variety of inherited retinal degenerations such as retinitis pigmentosa. Recent Advances The use of stem cells are difficult and it is also very Atmaca-Sonmez P et al have investigated whether difficult to transfer and, it will be necessary to improve hematopoietic stem cells (HSC) given systemically can transfection efficiency. The use of human stem cell for home to the damaged subretinal space and express cell base therapy in the eye present a technical markers of RPE lineage. They have shown that challenge. systemically injected HSC homed to the subretinal Another enigma in the circulating stem cell filled space in the presence of RPE damage and that FC is the issue of HSC “Homing”, R-Cadherin is clearly promoted survival of these cells. Furthermore, the RPE- involved, but all of the molecular signals have not yet specific marker RPE-65 was expressed on adoptively been identified. Identification of these signals would transferred HSC in the denuded areas. be of immense benefit in terms of exploiting the Harris JR et al have shown that HSCs/HPCs can potential use of HSC in therapeutic angiogenesis as migrate to the RPE layer after physical or chemical well as directed cell therapy. Finally, which shall type injury and regenerate a portion of the damaged cell in adult bone marrow actually adheres to astrocytes layer. Bone marrow-derived cells home to and and incorporate into the developing vasculature. regenerate retinal pigment epithelium after injury. Lund RD et al have shown cells isolated from The wet form of ARMD is characterized by umbilical cord tissue rescue photoreceptors and visual choroidal neovascularization (CNV). A prior study has functions in a rodent model of retinal disease. shown that adult hematopoietic stem cells (HSCs) Progressive photoreceptor degeneration resulting from contribute to approximately 50% of newly formed genetic and other factors is a leading and largely vasculature in CN. Sengupta N et al have shown that untreatable cause of blindness worldwide. The object stromal-derived factor (SDF)-1 is involved with homing of this study was to find a cell type that is effective of HSCs from bone marrow to target tissue. Vascular in slowing the progress of such degeneration in an endothelial cadherin (VE-cadherin, or CD144) is animal model of human retinal disease, is safe and involved in endothelial cell adhesion. Preventing could be generated in sufficient numbers for clinical homing and/or adhesion of progenitor cells to application. We have compared efficacy of four damaged choroid could reduce CNV. human-derived cell types in preserving photoreceptor integrity and visual functions after injection into the METHODS: Adult C57BL/6J mice. subretinal space of the Royal College of Surgeons rat RESULTS: CNV lesions from eyes treated with anti- early in the progress of degeneration. Umbilical tissue- CD144 showed significantly less incorporation of gfp+ 206 Clinical Diagnosis and Management of Ocular Trauma cells compared with those treated with anti-SDF-1. Corneal epithelial stem cells reside in the basal region Antibody treatment generally reduced the degree of of the limbus, and are involved in renewal and gfp+ stem cell recruitment and incorporation into the regeneration of corneal epithelium. Following injury, CNV lesions, compared with the control. Treatment with basal stem cells are stimulated to divide and undergo either antibody also significantly reduced the size of the differentiation to form transient amplifying cells (TAC). CNV lesions. These results indicate that homing and Subsequent cell divisions result in non-dividing post- adhesion of progenitor cells to CNV may be targeted mitotic cells (PMC),which migrate towards the central differentially or in combination to prevent CNV. cornea and superficially forming terminal differentiated cells (TDC). The first step is the isolation of healthy corneal Role of Corneal Stem Cell in epithelial cell, and these are collected from the unaffected eye of the individual to be treated if the Pediatric problem is in one eye only, or from donor material Stem cell research offers hope to countless patients if the problem is bilateral. These cells are then cultivated whose conditions have here to fore been deemed in the laboratory for a couple of weeks under carefully incurable. Better understanding of stem cell behaviors monitored conditions, so that they grow into a nicely and functions will lead to insights into biological stratified cellular multi-layer, which resembles corneal mysteries encompassing the fields of angiogenesis, epithelium, in situ. This can then be used for the surgical development, tissue homeostasis, wound healing, and repair of the ocular surface. One problem, however carcinogenesis. Clarity of vision requires smooth ocular is that cells grown in this way on regular cell culture surface on which the corneal epithelial cells undergo dishes are difficult to detach from the underlying plastic continuous turnover every 3 to 10 days.Tragically, without damaging them in some way. Now, however, many patients are blinded and devastated by severe evolving research has provided a way to obtain intact, ocular surface diseases due to limbal stem cell isolated corneal epithelial cell sheets with minimal deficiency even though, besides opaque cornea, their harm. The secret lies in the use of a novel temperature- eyes are otherwise healthy. Corneal stem cell responsive culture surface, which readily supports cell transplantation offers hope by creating clear windows growth, but also allows easy cell release. for these eyes; unfortunately, the long-term successful outcome remains limited. The nature of corneal OCULAR SURFACE STEM CELLS (FIG. 32.1) epithelial stem cell is poorly understood, but many More than two decades ago, Thoft and Friend described circumstantial evidences suggest the presence of the X,Y and Z hypothesis which explained how corneal “source cells” in the limbal region of the eye. epithelial cells are continuously shed from the surface Nonetheless, the precise biomarker of corneal stem and regenerated by cells from the periphery. The limbal cell remains elusive. The stem cell puzzle can be solved stem cell residing in the alisades of Vogt are now with application of the fundamental scientific method- believed to be the never-ending source of corneal asking salient questions at the right time and finding epithelial cells. Adult corneal and conjunctival stem cells answers using keen observations and proper tools. represent a small, quiescent subopulation of epithelial Readily accessibility and structural simplicity of the cells of the ocular surface. The limbus is a 1.5 mm- cornea lend themselves to study of the stem cell biology. to-2 mm-wide area that straddles the cornea and The ability to identify and isolate corneal stem cell will be a gateway to meaningful investigation into its biology. This advance will also have direct impact on improving the efficacy of promising stem-cell-based therapies, including limbal stem cell transplantation. Technical advances in the surgical reconstruction of severely injured or diseased ocular surfaces have improved the quality of the life for many of those affected. An ever-present hurdle, however, is the limited availability of suitable donor material, partly because of this, the concept has emerged of fabricating transplantable tissue constructs by expanding small biopsies of corneal epithelial cells taken from the limbs. Conjunctival stem cells represent a small quiescent subpopulation of epithelial cells of ocular surface. Fig. 32.1: Ocular surface stem cells Applications of Stem Cell Therapy in Ophthalmology 207 bulbar conjunctiva. Corneal epithelial stem cells reside HOPE OF STEM CELLS FOR UNTREATABLE in the basal region of the limbus, and are involved EYE DISEASE in the renewal and regeneration of the corneal There are practical and ethical issues to the use of epithelium. Following injury, these limbal basal stem embryonic stem cells and the alternative of using cells are stimulated to divide and undergo somatic or adult stem cells has major advantage in differentiation to form transient amplifying cells (TACs) terms of immediate clinical application. The adult (Fig. 32.2). Subsequent cell divisions result in non- human eye harbors stem cells in the limbal region, dividing post-mitotic cells (PMCs), which then in the conjunctiva, the pars plana and plicata of the terminally differentiate and migrate towards the central retinal ciliary margin and adult human retina. cornea and superficially, taking on the final corneal phenotype as terminal differentiated cells (TDCs). Their IDENTIFICATION OF STEM CELLS presence allows continued replacement and Several putative stem cells markers have been regeneration of tissues following injury, thereby proposed, although no single molecular marker that maintaining a steady-state population of healthy cells. is specific for stem cells has been identified. Conjunctival and corneal epithelial cells have been Taking advantage of the slowcycling characteristic shown to belong to two separate, distinct lineages. of stem cells, an indirect method of labelling stem cells Unlike corneal epithelium, conjunctival epithelium was developed. consists of both non-goblet epithelial cells as well as Another characteristic of stem cells is their capacity to remain highly proliferative in vitro. Cells that have mucin-secreting goblet cells. Wei et al showed that both the highest proliferative capacity (holoclones-with less these populations of cells arise from a common than 5% of colonies being terminal) are considered bipotent progenitor cell. The conjunctival forniceal stem cells. Pelligrini et al showed by clonal analysis that region appears to be the site that is enriched in nuclear P63 was abundantly expressed by epidermal conjunctival stem cell, although stem cells are also likely and limbal holocolones, but were undetectable in to be present in other regions of the conjunctiva. paraclones, suggesting that P63 might be a marker of keratinocyte stem cells.

Disease Arising from Stem Cell Deficiency due to Ocular Surface Causes Ocular surface failure may be of two types according to Tseng et al depending on the epithelial phenotype as identified by impression cytology. Type 1 failure characterized by squamous metaplasia where the non- keratinized corneal epithelium is converted to a keratinized epithelium. Type 2 failure is characterized by limbal stem cell deficiency where the normal corneal epithelial is replaced by conjunctival epithelium. Limbal stem cell deficiency can be caused by the variety of hereditary or acquired disorders. Inherited disorders include aniridia keratitis and kratitis associated with multiple endocrine deficiency, in which limbal stem cells may be congenitally absent or dysfuntional. Acquired conditions that may result in limbal stem cell deficiency include Stevens-Johnson syndrome, chemical injuries, ocular cicatricial pemphigoid, contact lens-induced keratopathy, multiple surgeries or cryotherapies to the limbal region, neurotrophic keratopathy and peripheral ulcerative keratitis. Acquired disorders from the majority of cases seen in the clinical setting. Limbal stem cell deficiency is characterized by persistent or recurrent epithelial defects, ulceration, Fig. 32.2: Limbal epithelial stem cell therapy corneal vascularization, chronic inflammation, scarring, 208 Clinical Diagnosis and Management of Ocular Trauma

Fig. 32.3: Limbol stem cell deficiency

and conjunctivization (conjunctival epithelial ingrowth), with resultant loss of the clear demarcation between corneal and conjunctival epithelium at the limbal Fig. 32.4 region (Fig. 32.3). The diagnosis of the presence of limbal deficiency can be transplanted, either as intact annular ring or is crucial as these patients are poor candidates for in several contagious segments. Limbal allograft may conventional corneal transplantation alone. Conven- also be obtained from HLA matched living – related tional corneal transplantation alone. Conventional donors, to reduce risk of immunologic rejection corneal transplantation does not address the problem (Fig. 32.4). of inadequate corneal epithelial replacement, and Limbal stem cell transplant may be combined with subsequent conjunctival ingrowth, vascularization and penetrating keratoplasty which may be in same setting an inflammation ultimately results in grant rejection or in a staged manner. Severe ocular surface disorders and failure. are often associated with conjunctival or lid pathology Chronic instability of the corneal epithelium and which may require adjunctive surgical procedures in ulceration may lead to progressive melting of the reconstruction of ocular surface such as fornicela cornea and subsequent perforation. The pathgnomic reconstruction with symblepharon release, correction feature is conjunctival epithelial ingrowth over the of cicatrising lid disease. cornea. Limbal stem cell deficiency may be localized The use of allogenic grafts is associated with risk or generalized, localized stem cell deficiency is of graft rejection and there may be need for long- characterized by some sectors of normal and some term systemic immunosuppression with cyclosporin, sectors showing conjunctivization in regions devoid of FK 506 or mycophenolate mofetil. Inspite of good healthy epithelium. Impression cytology confirms the early success in several studies,subsequent reports presence of conjunctival goblet cells. suggest that approximately 50% of these grafts fail with Diagnosis of limbal stem cell deficiency is crucial in 3 to 5 years. as these patients are poor candidates for conventional LIVE-RELATED VS CADAVERIC LIMBAL corneal transplantation, as conventional corneal TRANSPLANTATION (LT) transplantation does not address the problem of In the unilateral and bilateral cases of LSCD, fresh inadequate corneal epithelial replacement which leds donor tissue may be harvested either from the healthy to subsequent conjunctival ingrowth, vascularization fellow eye in the former, or from a live-related donor and inflammation finally resulting in graft failure and or corneo-scleral rim or enucleated eye of a cadaver rejection. in case of the latter. Limbal autograft transplantation, first described in It is essential to screen the donor thoroughly prior

detail by Kenyon and Tseng, was limited to unilateral to surgery for evidence of limbal stem deficiency. Close cases or bilateral cases with localized limbal deficiency, monitoring of the donor is advised after surgery, as where sufficient healthy tissue was available for it is yet unknown how these eyes will respond to an harvesting. epithelial insult in the future and there may be stem Inpatients with bilateral diffuse disease, allogenic cell attrition due to inflammation and sub-clinical donor limbal graft is required, which when obtained from disease. The other alternative in bilateral cases is cadaveric donors, the entire 360° annulus of limbus cadaveric limbal allo-transplantation. Applications of Stem Cell Therapy in Ophthalmology 209 CULTIVATED VS DIRECT LIMBAL Hisatomi T et al have provided direct and novel TRANSPLANTATION evidence for the migration of BM and HSC cells into The potential problems with direct limbal trans- the sclera differentiating into macrophages and plantation include harvesting a relatively large amount dendritic cells.Vast infiltration of BM and HSC cells was of limbal tissue (upto 6 clock hours) from healthy found to be part of inflammatory process in EAU. donor eyes. Pellegrini et al were the first to describe Corneal epithelial stem cells are known to be culturing of limbal stem cells ex vivo thereby spear- localized to the basal layer of the limbal epithelium, heading ophthalmology into the field of regenerative providing a model system for epithelial stem cell medicine. Technically cultivated stem cells have the biology; however the mechanisms regarding the disadvantages of the long procedure. maintenance of these stem cells in their specialized 1. It takes 10 days to 2 weeks for the cells to grow. niche remain poorly understood. N-cadherin is a 2. A dedicated stem cell laboratory is required. member of the classical cadherin family and has previously been demonstrated to be expressed by Bioengineered Ocular Surface Equalents for hematopoietic stem cells. In the present study Hayashi Transplantation (Fig. 32.5) R, et al have demonstrated that N-cadherin is expressed by putative stem/progenitor cells as well as melanocytes Limbal autograft overcomes the problem of in the human limbal epithelial stem cell niche. immunologic rejection, but because large segments are Additionally, they have demonstrated that upon in vitro required this places the donor eye at the risk of surgically induced donor stemcell deficiency. The use of culture using 3T3 feeder layers, loss of N-cadherin autologus cultivated limbal stemcell has overcome this expression occurs with cell proliferation. These results problem. for this procedure only a small limbal biopsy indicate that N-cadherin may be a critical cell-to-cell is needed (approximately 2mm2),which minimizes the adhesion molecule between corneal epithelial stem/ risk of damage to the donor eye. This is then cultivated progenitor cells and their corresponding niche cells in on various substrates, such as human amniotic the limbal epithelium. membrane or fibrin based substrates, which results in Sun CC demonstrated that intact human AM may a composite graft which is then transplanted on the prevent cultured human limbal epithelial cells from diseased eye. With this procedure reasonable success undergoing apoptosis. IL-1RA might be a candidate upto one year of follow-up has been achieved. More mediator to exert as an anti-apoptotic molecule during recently Tan DT et al demonstrated the development the interaction between human limbal epithelial cells of serum-free derived conjunctival tissue- equalents. and intact human AM. The use of bioengineered tissue replacements Li W et al after dissolution of original amniotic BM, represents the future for replacement and regeneration new BM formed by ex vivo expanded human limbal of various tissues and organs. corneal epithelial cells on iAM deposits much faster and is more mature,resulting in regeneration of a limbal epithelial phenotype. In contrast, BM deposition is delayed and remains immature on dAM, resembling wound healing by a corneal epithelial phenotype. Thus, BM resynthesis may be used as another objective readout for assessing the success of ex vivo expansion of limbal epithelial progenitor cells on AM. Recently, Prof Yuichi Mori, dr Hiroshi Yoshioka of Waseda and Dr Samuel JK Abraham (Cardiac surgeon, Yamanashi University Hospital, Japan) in collaboration with M/S Nichi-In Biosciences (P) Ltd has started a joint venture program in india with G Sitalakshmi from Sankara Nethralaya and are in the process of collaborating with dr Rajpal from RP Centre using non- biological (Totally synthetic) material called Mebiol Gel.

First time in the world: This is the first time in the world that a nonbiological (Totally synthetic) material has been used as a substrate Fig. 32.5 to grow (cultivate) corneal limbal stem cells thereby 210 Clinical Diagnosis and Management of Ocular Trauma paving a way for avoiding biological materials for this normal rabbit:dose-dependent effects on ERG and retinal purpose and avoiding viral and other dangerous histology. Invest Ophthalmol Vis Sci 2004;45:2420-30. known and unknown contamination in such biological 16. Cahill MT, Freedman SF, Toth CA. Macular translocation with 360 degrees peripheral retinectomy for geographic materials as well as chances of rejections. The invention atrophy. Arch Ophthalmol 2033;121:132-33. has been proven with all the latest scientific parameters 17. Cai J, Weiss ML, Rao MS. In search of “stemness” Exp that the cells are stem cells and upon confirmation of Hematol 2004;32-585-98. the same by our co-researchers in Japan, a joint patent 18. Chen JJ, Tseng SC. Abnormal corneal epithelial wound through PCT (Patent Cooperation Treaty) has been healing in partial-thickness removal of limbal epithelium. filed. Invest Ophthalmol Vis Sci 1991;32:2219-33. 19. Coffey PJ, Girman S, Wang SM et al. Long-term preservation of cortically dependent visual function in RCS rats by transplantation. Nat Neurosci 2002; 5: Bibliography 53-56. 20. Coster DJ, Aggarwal RK, Williams KA. Surgical 1. Acland GM, Aguirre GD, Ray J et al. Gene therapy management of ocular surface disorders using restores vision in a canine model of childhood blindness. conjunctival and stem cell allografts. Br J Ophthalmol Nat Genet 2001;28:92-95. 1995;79:977-82. 2. Ahmad I, Das AV, James J et al. Neural stem cells in the 21. Cotsarelis G, Cheng SZ, Dong G, Sun TT, Lavker RM, mammalian eye types and regulation Semin Cell Dev Existence of slowcycling limbal epithelial basal cells that Bio 2004; 15:53-62. can be preferentially stimulated to proliferate: Implications 3. Ahmad I, Tang L, Pham H. Identification of neural on epithelial stem cells. Cell 1989;57:201-09. progenitors in the adult mammalian eye. Biochem 22. Csaky KG, Baffi JZ, Byrnes GA et al. Recruitment of Biophys Res Commun 2000;270:517-21. marrow-derived endothelial cells to experimental 4. Ali RR, Sarra GM, Stephens C et al. Restoration of choroidal neovascularization by local expression of photoreceptor ultra-structure and function in retinal vascular endothelial growth factor. Exp Eye Res 2004; degeneration slow mice by gene therapy. Nat Genet 78:1107-16. 2000;25:306-10. 23. Das AV, James J, Zhao X et al. Identification of c-Kit 5. Anderson DJ, Gage FH, Weissman IL. Can stem cells receptor as a regulator of adult neural stem cells in the cross lineage boundaries? Nat Med 2001;7:393-95. mammalian eye: Interactions with Notch signaling. Dev 6. Ang LP, Tan DT, Beuerman R, Phan TT, Lavker RM. The Biol 2004;273:87-105. development of a conjunctival epithelial equivalent with 24. Dorrell MI, Otani A, Aguilar E et al. Adult bone marrow- improved proliferative properties using multistep serum- derived stem cells utilize R-cadherin to target sites of free culture system. Invest Ophthalmol Vis Sci neovascularization in the developing retina. Blood 2004; 2004;45:1789-95. 103:3420-27. 7. Asahara T, Murohara T, Sullivan A et al. Isolation of 25. Dryja TP, McGee TL, Reichel E et al. A point mutation putative progenitor endothelial cells for angiogenesis. of the rhodopsin gene in one form of retinitis pigmentosa. Science 1997;275:964-67. Nature 1990;343:364-66. 8. Asakura A. Stem cells in adult skeletal muscle. Trends 26. Dua HS, Azuara-Blanco A. Allo-limbal transplantation in Cardiovasc Med 2003;13:123-12. patients with limbal stem cell deficiency. Br J Ophthalmol 9. Bain G, Kitchens D, Yao M et al. Embryonic stem cells 1999;83:414-19. express neuronal properties in vitro. Dev Biol 1995; 27. Dua HS, Azuara-Blanco A. Limbal stem cells of the 168:342-57. corneal epithelium. Surv Ophthalmol 2000;44:415-25. 10. Balsam LB, Wagers AJ, Christensen JL et al. 28. Dua HS, Saini JS, Azuara-Blanco A, Gupta P Limbal Haematopoietic stem cells adopt mature haematopoietic Stem cell deficiency: Concept, aetiology, clinical fates in ischaemic myocardium. Nature 2004; 228:668- presentation, diagnosis and management Indian J 73. Ophthalmol 2000;48:83-92. 11. Barrandon Y, Green H. Three clonal types of keratinocyte 29. Dua HS. Stem cells of the ocular surface: Scientific with different capacities for multiplication. Proc Natl Acad principles and clinical applications. Br J Ophthalmol Sci U S A 1987;84:2302-06. 1995;79:968-69. 12. Berson EL, Rosner B, Sandberg MA et al. A randomized 30. Dyer MA, Cepko CL. Regulating proliferation during trial of vitamin A and vitamin E supplementation for retinal development. Nat Rev Neurosci 2001; 2:333-42. retinitis pigmentosa. Arch Ophthalmol 1993;111:761-72. 31. Espinosa-Heidmann DG, Caicedo A, Hernandez EP et 13. Blackshaw S, Harpavat S, Trimarchi J et al. Genomic al. Bone marrow-derived progenitor cells contribute to analysis of mouse retinal development. PloS Biol 2004; experimental choroidal neovascularization. Invest 2:E247. Ophthalmol Vis Sci 2003; 44:4914-49. 14. Bowes C, Li T, Danciger M et al. Retinal degeneration 32. Faktorovich EG, Steinberg RH, Yasumura D et al. in the rd mouse is caused by a defect in the beta subunit Photoreceptor degeneration in inherited retinal dystrophy of rod cGMP-phosphodiesterase. Nature 1990;347: delayed by basic fibroblast growth factor. Nature 677-80. 1990;347:83-86. 15. Bush RA, Lei B, Tao W et al. Encapsulated cell-based 33. Farrar GJ, Kenna PF, Humphries P. On the genetics of intraocular delivery of ciliary neurotrophic factor in retinitis pigmentosa and on mutation-independent Applications of Stem Cell Therapy in Ophthalmology 211

approaches to therapeutic intervention Embo J and context dependent role of notch signaling. J 2002;21:857-64. Neurobiol 2004; 61:359-76. 34. Filip SMJ, Karbanova J, Vavrova J et al. Local 51. James J, Das AV, Bhattacharya S et al. In vitro generation environmental factors determine hematopoietic of early-born neurons from late retinal progenitors. J differentiation of neural stem cells. Stem Cells Dev Neurosci 2003;23:8193-203. 2004;13:113-20. 52. Kajiwara K, Hahn LB, Mukai S et al. Mutations in the 35. Fischer AJ, Reh TA. Potential of Muller glia to become human retinal degeneration slow gene in autosomal neurogenic retinal progenitor cells. Glia 2003:43:70-76. dominant retinitis pigmentosa. Nature 1991;354:480-83. 36. Frasson M, Picaud S, Leveillard T et al. Glial cell line- 53. Kalka C, Tehrani H, Laudenberg B el al. VEGF derived neurotrophic factor induces histologic and genetransfer mobilizes endothelial progenitor cells in functional protection of rod photoreceptors in the rd/rd patients with inoperable coronary disease. Ann Thorac mouse. Invest Ophthalmol Vis Sci 1999;40:2724-34. Surg 2000;70:829-34. 37. Frasson M, Sahel JA, Fabre M et al. Retinitis pigmentosa: 54. Kanuga N, Winton HL, Beauchene L et al. rod photoreceptor rescue by a calcium-channel blocker Characterization of genetically modified human retinal in the rd mouse. Nat Med 1999; 5:1183-87. pigment epithelial cells developed for in vitro and 38. Gill M, Dias S, Hattori K et al. Vascular trauma induces transplantation studies. Invest Ophthalmol Vis Sci 2002; rapid but transient mobilization of VEGFR2(+)Ac133 (+) 43:546-55. endothelial precursor cells. Circ Res 2001;88:167-74. 55. Kenyon KR, Tseng SC. Limbal autograft transplantation 39. Grant MB, Caballero S, Brown GA et al. The contribution for ocular surface disorders. Ophthalmology of adult hematopoietic stem cells to retinal 1989;96:709-22. neovascularization. Adv Exp Med Biol 2003;522:37-45. 56. Klassen H, Sakaguchi DS, Young MJ. Stem cells and 40. Grant MB, May WS, Caballero S et al. Adult retinal repair. Prog Retin Eye Res 2004; 23:149-81. hematopoietic stem cells provide functional 57. Klimanskaya I, Hipp J, Rezai K et al. Derivation and hemangioblast activity during retinal neovascularization. comparative assessment of retinal pigment epithelium Nat Med 2002;8:607-12. from human embryonic stem cells using transcriptomics. 41. Gu SM, Thompson DA, Srikumari CR et al. Mutations Cloning Stem Cells 2004;6:1-28. in RPE65 cause autosomal recessive childhood-onset 58. Kocker AA, Schuster MD, Szaboles MJ et al. severe retinal dystrophy. Nat sci 1997;17:194-97. Neovascularization of ischemic myocardium by human 42. Hayashi R, Yamato M, Sugiyama H, Sumide T, Yang J, bone-marrow derived angioblasts prevents Okano T, Tano Y, Nishida K.Tohoku University School cardiomyocyte apoptosis reduces remodeling and of Medicine, Sendai, Japan Stem Cells. 2006 Sep 28; improves cardiac function. Nat Med 2001;7:430-36. [Epub ahead of print] N-cadherin is expressed by 59. Koizumi N, Inatomi T, Suzuki T, Sotozono C, Kinoshita putative stem/progenitor cells and melanocytes in the S. Cultivated corneal epithelial stem cell transplantation human limbal epithelial stem cell niche. in ocular surface disorders. Ophthalmology 43. Hill JM, Zalos G, Halcox JP et al. Circulating endothelial 2001;108:1569-74. progenitor cells, vascular function,and cardiovascular risk. 60. Konobu T, Sessler F, Luo LY et al. The h NT human N Engl J Med 2003;348:593-600. neuronal cell line survives and migrates into rat retina. 44. Hisatomi T, Sonoda KH, Ishikawa F, Qiao H, Nakamura Cell Transplant 1998; 7-549-58. T, Fukata M, Nakazawa T, Noda K, Miyahara S, Harada 61. Krause DS, Theise ND, Collector MI et al. Multi-organ, M, Kinoshita S, Hafezi-Moghadam A, Ishibashi T, Miller multi-lineage engraftment by a single bone-marrow- JW.Br J Ophthalmol. 2006 Oct 11; [Epub ahead of print] derived stem cell. Cell 2001; 105:369-77. Identification of resident and inflammatory bone marrow 62. La Vail MM, Yasumura D, Matthes MT et al. Protection derived cells in thesclera by bone marrow and of mouse photoreceptors by survival factors in retinal hematopoietic stem cell transplantation. degenerations. Invest Ophthalmol Vis Sci 1998;39:592 45. Huang AJ, Tseng SC. Corneal epithelial wound healing 602. in the absence of limbal epithelium. Invest Ophthalmol 63. Lai JC, Lapolice DJ, Stinnett SS et al. Visual outcomes Vis Sci 1991;32:96-105. following macular translocation with 360-degree 46. Huang JC, Ishida M, Hersh P et al. Preparation and peripheral retinectomy. Arch Ophthalmol 2002; transplantation of photoreceptor sheets. Curr Eye Res 120:1317-24. 1998;17:573-85. 64. Lavker RM, Dong G, Cheng SZ, Kudoh K, Cotsarelis G, 47. Humphries P, Kenna P, Farrar GJ. On the molecular Sun TT. Relative proliferative rates of limbal and corneal genetics of retinitis pigmentosa. Science 1992;256:804- epithelia: Implications of corneal epithelial migration, 08. circadian rhythm, and suprabasally located DNA- 48. Ilari L, Daya SM. Long-term outcomes of keratolimbal synthesizing keratinocytes. Invest Ophthalmol Vis Sci allograft for the treatment of severe ocular surface 1991;32:1864-75. disorders. Ophthalmology 2002;109:1278-84. 65. Lavker RM, Wei ZG, Sun TT. Phorbol ester preferentially 49. Ishida M, Lui GM, Yamani A et al. Culture of human stimulates mouse fomical conjuctival and limbal epithelial retinal pigment epithelial cells from peripheral scleral flap cells to proliferate in vivo. Invest Ophthalmol Vis Sci biopsies. Curr Eye Res 1998;17:392-402. 1998;39:301-17. 50. James J, Das A, Rahnenfuhrer J et al. Cellular and 66. LeCouter J, Moritz DR, Li B et al. Angiogenesis molecular characterization of early and late retinal stem independent endothelial protection of liver:role of cells/progenitors: Differential regulation of proliferation VEGFR-1. Science 2003;299:890-93. 212 Clinical Diagnosis and Management of Ocular Trauma 67. Lee MS, Makkar RR. Stem-cell transplantation in inhibit retinal angiogenesis. Nat Med 2002;8:1004-10. myocardial infarction: A status report. Ann Intern Med 84. Pellegrini G, Dellambra E, Golisano O, Martinelli E, 2004;140:729-37. Fantozzi I, Bondanza S, et al. P63 identifies keratinocyte 68. Lehrer MS, Sun TT, Lavker RM. Strategies of epithelial stem cells. Proc Natl Acad Sci U S A 2001;98:3156-61. repair. Modulation of stem cell and transit amplifying cell 85. Pellegrini G, Golisano O, Paterna P, Lambiase A, Bonini proliferation. J Cell Sci 1998:111:2867-75. S, Rama P. et al. Location and clonal analysis of stem 69. Li W, He H, Kuo CL, Gao Y, Kawakita T, Tseng SC. cells and their differentiated progeny in the human ocular Basement membrane dissolution and reassembly by surface. J Cell Biol 1999;145:769-82. limbal corneal epithelial cells expanded on amniotic 86. Pellegrini G, Traverso CE, Franzi AT, Zingirian M, membrane: Invest Cancedda R, De Luca M. Long-term restoration of 70. Lindberg K, Brown ME, Chaves HV, Kenyon KR, damaged corneal surfaces with autologous culvivated Rheinwald JG. In vitro propagation of human ocular corneal epithelium. Lancet 1997;349:990-93. surface epithelial cells for transplantation.Invest 87. Rafii S, Lyden D. Therapeutic stem and progenitor cell Ophthalmol Vis Sci 1993;34:2672-79. transplantation for organ vascularization and 71. Livesey FJ, Young TL, Cepko CL. An analysis of the gene regeneration. Nat Med 2003;9:702-12. expression program of mammalian neural progenitor 88. Ramalho-Santos M, Yoon S, Matsuzaki Y et al. cells. Proc Natl Acad Sci USA 2004; 101:1374-79. “Stemness”: transcriptional profiling of embryonic and 72. Lund RD, Adamson P, Sauve Y et al. Subretinal adult stem cells. Science 2002;298:597-600. transplantation of genetically modified human cell lines 89. Reh TA, Fischer AJ. Stem cells in the vertebrate retina. attenuates loss of visual function in dystrophic rats. Proc Brain Behav Evol 2001; 58:296-305. Natl Acad Sci USA 2001;98:9942-47. 90. Reh TA, Levine EM. Multipotential stem cells and 73. Martinez-Serrano A, Rubio FJ, Navarro B et al. Human progenitors in the vertebrate retina. J Neurobiol 1998; neural stem and progenitor cells: in vitro and in vivo 36: 206-20. properties, and potential for gene therapy and cell 91. Rosenzweig A. Endothelial progenitor cells. N Engl J Med replacement in the CNS. Curr Gene Ther 2001;1:279- 2003;348:581-82. 99. 92. Schwab IR, Reyes M, Isseroff RR. Successful 74. Matic M, Petrov IN, Chen S, Wang C, Dimitrijevich SD, transplantation of bioengineered tissue replacements in Wolosin JM. Stem cells of the corneal epithelium lack patients with ocular surface disease. Cornea 2000;19:421-26. connexins and metabolite transfer capacity. Differentiation 93. Sengupta N, Caballero S, Mames RN et al. The role of 1997;61:25-60. adult bone marrow-derived stem cells in choroidal 75. Matsumoto K, Yoshitomi H, Rossant J et al. Liver neovasculari-zation. Invest Ophthalmol Vis Sci organogenesis promoted by endothelial cells prior to 2003;44:4908-13. vascular function. Science 2001;294:559-63. 94. Shen Q, Goderie SK, Jin L et al. Endothelial cells stimulate 76. McKay RD. Stem cell biology and neurodegenerative self-renewal and expand neurogenesis of neural stem disease. Philos Trans R Soc Lond B Biol Sci 2004; cells. Science 2004;304:1338-40. 359:851-56. 95. Solomon A, Ellies P, Anderson DF, Touhani A, Grueterich 77. Meller D, Pires RT, Mack RJ, Figueiredo F, Helligenhaus M, Espana EM, et al. Long-term outcome of keratolimbal A, Park WC, et al. Amniotic membrane transplantation allograft with or without penetrating keratoplasty for total for acute chemical or thermal burns. Ophthalmology limbal stem cell deficiency. Ophthalmology 2000;107:980-9; discussion 990. 2002;109:1159-66. 78. Meller D, Pires RT, Tseng SC, Ex vivo preservation and 96. Sridhar MS, Vemuganti GK. Bansal AK, Rao GN. expansion of human limbal epithelial stem cells on Impression cytology-proven corneal stem cell deficiency amniotic membrane cultures. Br J Ophthalmol in patients after surgeries involving the limbus. Cornea 2002;86:463-71. 2001;20:145-48. 79. Mohand-Said S, Deudon-Combe A, Hicks D et al. 97. Sun CC, Su Pang JH, Cheng CY, Cheng HF, Lee YS, Ku Normal retina releases a diffusible factor stimulating cone WC, Hsiao CH, Chen JK, YangCM. Interleukin-1 receptor survival in the retinal degeneration mouse. Proc Natl antagonist (IL-1RA) prevents poptosis in ex vivo Acad Scl USA 1998;95:8357-62. expansion of human limbal epithelial cells cultivated on 80. Murry CE, Soonpaa MH, Reinecke H et al. human amniotic membrane. Stem Cells. 2006 Haematopoietic stem cells do not transdifferentiate into Sep;24(9):2130-9. Epub 2006 Jun 1. cardiac myocytes in myocardial infarcts. Nature 98. Takahashi M, Miyoshi H, Verma IM et al. Rescue from 2004;428:664-68. photoreceptor degeneration in the rd mouse by human 81. Ooto S, Akagi T, Kageyama R et al. Potential for neural immunodeficiency virus vector-mediated gene transfer. J regeneration after neurotoxic injury in the adult Virol 1999; 73:7812-16. mammalian retina. Proc Natl Acad Sci USA 2004; 99. Tam DT, Ang LP, Beuerman R. Reconstruction of the 101:13654-59. ocular surface by equivalent. Transplantation 82. Otani A, Dorrell MI, Kinder K et al. Rescue of retinal 2004;77:1729-34. degeneration by intravitreally injected adult bone marrow- 100. Tan D. Conjunctival grafting for ocular surface disease. derived lineage negaive hematopoietic stem cells. J Clin Curr Opin Ophthalmol 1999;10:277-81. Invest 2004;114:765-74. 101. Tani H, Morris RJ, Kaur P. Enrichment for murine 83. Otani A, Kinder K, Ewalt K et al. Bone marrow-derived keratinocyte stem cells based on cell surface phenotype. stem cells target retinal astrocytes and can promote or Proc Natl Acad Sci U S A 2000;97:10960-65. Applications of Stem Cell Therapy in Ophthalmology 213

102. Tao W, Wen R, Goddard MB et al. Encapsulated cell- 110. Tsubota K. Corneal epithelial stem-cell transplantation based delivery of CNTF reduces photoreceptor lancet 1997;349:1556. degeneration in animal models of retinitis pigmentosa. 111. Turner DL, Cepko CL. A common progenitor for neurons Invest Ophthalmol Vis Sci 2002;43:3292-98. and glia persists in rat retina late in development. Nature 103. Thoft RA, Wiley LA, Sundarraj N. The multipotential cells 1987;328:131-36. of the limbus. Eye 1989:3:109-13. 112. Wagers AJ, Sherwood RI, Christensen JL et al. Little 104. Tropepe V, Coles BL, Chiasson BJ et al. Retinal stem cells evidence for developmental plasticity of adult in the adult mammalian eye. Science 2000;287: hematopoietic stem cells. Science 2002;297:2256-59. 2032-36. 113. Wei ZG, Lin T, Sun TT, Lavker RM. Clonal analysis of 105. Tsai RJ, Li LM, Chen JK. Reconstruction of damaged the in vivo differentiation potential of keratinocytes. Invest corneas by transplantation of autologous limbal epithelial Ophthalmol Vis Sci 1997;38:753-61. cells. N Engl J Med 2000;343:86-93. 114. Wei ZG, Sun TT, Lavker RM, Rabbit conjunctival and 106. Tseng SC, Prabhasawat P, Barton K, Gray T, Meller D. corneal epithelial cells belong to two separate lineages. Invest Ophthalmol Vis Sci 1996;37:523-33. Amniotic membrane transplantation with or without 115. Wei ZG, Wu RL, Lavker RM, Sun TT. In vitro growth and limbal allografts for corneal surface reconstruction in differentiation of rabbit bulbar, fornix, and palpebral patients with limbal stem cell deficiency. Arch Ophthalmol conjunctival epithelia. Implications on conjunctival 1998;116:431-41. epithelial transdifferentiation and stem cells. Invest 107. Tseng SC, Regulation and clinical implications of corneal Ophthalmol Vis Sci 1993;34:1814-28. epithelial stem cells. Mol Biol Rep 1996;23:47-58. 116. Yamashita JK. Differentiation and diversification of 108. Tseng SC. Concept and application of limbal stem cells. vascular cells from embryonic stem cells. Int J Hematol Eye 1989;3:141-57. 2004;80:1-6. 109. Tsubota K, Satake Y, Kaido M, Shinozaki N, Shimmura 117. Zieske JD, Bukusoglu G, Yankauckas MA, Wasson Me, S, Bissen-Miyajima H, et al. Treatment of severe ocular- Keutmann HT. Alpha-enolase is restricted to basal cells surface disorders with corneal epithelial stem-cell of stratified squamous epithelium. Dev Biol transplantation. N Engl J Med 1999;340:S1697-703. 1992;151:18-26. CHAPTER

Primary Globe Repair 33 Rupesh V Agrawal (India)

Introduction The basic objective of globe repair should be DO NOT HARM. Trauma to the sclera and cornea are common. Review of data of United States Eye Injury Registry and Indian Eye Injury Registry revealed that approximately 10% Strategic Planning for Primary of all reported serious eye injuries involve cornea and sclera. Males are predominantly affected and more Globe Repair common in younger age. However, more than half No two ocular trauma cases are alike and irrespective of the injuries occur at home. of the configuration or etiology of ocular trauma, the It can occur secondary to penetrating injury or following four pronged approach to ocular trauma blunt trauma. The open globe injury secondary to blunt patient will help in optimizing anatomical and visual trauma is termed as globe rupture and those secondary results in ocular trauma patients. The four pronged to penetrating injury is termed as lacerating injuries. approach is: It can be partial thickness or full thickness laceration. • Minimizing possibility of further trauma to the eye: Regardless of the object and nature of injury, the Further trauma to the eye can be minimized by management algorithm is similar in all cases with open trying to operate at the earliest possible, protecting globe injuries. The four pronged approach in manage- the eye with rigid eye shield and avoiding ment of open globe injuries is: manipulation of the traumatized eye in emergency a. Prevent further trauma to the eye out patient clinic. b. Minimize risk of infection • Minimizing infectious risks: Infectious risks to the c. Prevent psychological trauma to the patient and eye can be prevented by operating the eye as early his family as possible and by giving broad spectrum d. Minimize legal problems to oneself and to his intravenous antibiotics. institute. • Minimizing psychological trauma to the victim and victim’s family can be minimized by gentle but frank counseling of trauma victim and his family. Guarded Objectives of Globe Repair visual prognosis should be explained to the patient and all the consequences should be gently PRIMARY explained. Need for prolonged postoperative • Restoration of structural integrity follow-up and compliance is warranted to the • Achieve watertight closure patient at initial setting. • Prevent infection • Minimizing legal problems to oneself and to self’s • Smooth and optically effective refractive surface institute by proper documentation and filling up • Spherical cornea to minimize astigmatism and better medicolegal forms as and when required. contact lens fitting • Reduce scarring Algorithm for Management of SECONDARY Open Globe Injury • Removal of disrupted lens and vitreous • Avoid uveal and vitreous incarceration • Complete evaluation of the eye and adnexa. • Removal of intraocular foreign bodies • Ancillary testing as necessary. Primary Globe Repair 215 • Identification of any factors that could confound removing the loose or necrotic tissue and then apply the management. the thin layer of cyanoacrylate glue with help of cotton • Development and execution of the therapeutic tip applicator. The glue is allowed to get dry and if plan. required another thin layered film of glue is applied on the previously layered glue. Bandage contact lens COMPLETE EVALUATION OF THE needs to be applied on surface of glue and cornea EYE AND ADNEXA following tissue adhesive application. Detailed history including details about the incidence and objects causing the injury should be elucidated SURGICAL MANAGEMENT from the patient or informant and documented in the The different surgical options which can be contemp- file. Relative afferent papillary defect or consensual lated depending on the case to case basis: reflex of the light in fellow eye should be assessed for • Corneal laceration repair optic nerve integrity. External examination and diffuse • Corneoscleral laceration repair slitlamp examination should be carried out to assess • Scleral laceration repair the complete extent of damage to the eye without • Limbal laceration repair causing further trauma to the eye and intraocular • Patch grafts structures. Fundus examination should be carried out • With or without iris abscission or repositioning at the earliest sitting if fundus view is not precluded • With or without lens aspiration because of media haze. • With or without vitrectomy and intraocular antibiotic injections ANCILLARY TESTING AS NECESSARY • With complete pars plana vitrectomy with other vitreoretinal procedures Ultrasound examination of the eye with gentle standoff The management of these injuries is thus a thought technique can be employed to assess the posterior out process, rather than a reflexive response to an segment status and to rule out intraocular foreign body obvious injury. The present chapter will highlight on in suspected cases. X-rays or CT scans can be employed the surgical principles for corneal and scleral laceration in selective cases to rule out intraocular foreign body repair. and/or bony status of the orbit/optic canal. Anesthesia IDENTIFICATION OF ANY FACTORS THAT The recommended anesthesia in all open globe injuries COULD CONFOUND THE MANAGEMENT should be general anesthesia, but the cases with small To watch out for infection, intraocular foreign bodies lacerations can be managed under local anesthesia. or other factors which can have impact on final visual The patient is prepared for surgery as soon as possible outcome. and should be medically and neurosurgically cleared. For general anesthesia, the time of the last meal or DEVELOPMENT AND EXECUTION OF THE drink determines when surgery is scheduled. To prevent THERAPEUTIC PLAN aspiration, at least 6 hours should have elapsed since The planning in cases of open globe injury could be the last meal. Once the physician decides to repair the of broad spectrum comprises. laceration, the patient should be kept NPO. Anesthesia should be achieved without any increase in intraocular pressure, which can occur during intubation or because Surgical vs Nonsurgical of anesthetic agents. Depolarizing agents (e.g. succinyl- Management choline) are not used. Although succinylcholine possesses several advantages, it contracts extraocular NONSURGICAL MANAGEMENT muscles and increases intraocular pressure. External Nonsurgical management can be considered in cases pressure from the mask can also increase intraocular with self sealed corneal laceration or those which can pressure. be sealed with help of tissue adhesives and small conjunctival lacerations. Cyanoacrylate glue is the tissue Preparing the Eye adhesive which can be of great help in providing The eye should be prepared and draped with care. support lasting for several days to several weeks. Pressure should not be applied to the globe. The eye Cyanoacrylate glue on exposure to air starts getting is irrigated with a sterile balanced salt solution (BSS) polymerized. Dry the surface of the cornea after to remove any superficial foreign bodies. The eye is 216 Clinical Diagnosis and Management of Ocular Trauma gently examined to evaluate the extent of damage. shelved wounds, the placement of sutures should be If the globe appears unstable, sutures are first applied equidistant with respect to internal aspect of the wound prior to exploration of the wound. and tied without undue tension to optimize tissue apposition. On the other hand, wounds with Most Corneal Lacerations macerated or edematous edges require longer sutures for security. Most corneal lacerations require suture placement. Prompt, secure wound closure is especially important in children who are at greater risk of inadvertently rubbing Suture Bites through the Visual Axis the eye with consequent reopening of a tissue adhesive Suture bites through the visual axis should be avoided. or contact lens supported wound. Large corneal If suture needs to be taken through the visual axis, laceration, sclera laceration, corneoscleral laceration, a number of techniques can be used to minimize displaced wound, wounds with tissue incarceration such scarring. Sutures near to visual axis should be shorter, as iris or lens or vitreous incarceration should be taken superficial and relatively loose as against the peripheral up for primary wound repair at the earliest possible. sutures which should be longer, deeper and tighter. So, also the visual axis can be straddled by sutures Small Corneal Laceration with Reasonably placed at each side of, but not directly through the Formed Anterior Chamber axis itself. More importantly, No Touch Technique is employed wherein the globe is stabilized away from Suture the corneal wound directly with 10-0 nylon the site of corneal wound and sutures are directly suture, need not enter into anterior chamber. passed through the corneal wound without holding the corneal wound edges which will prevent tissue Less Stable Wound with Shallow or Flat Anterior damage in visual axis thereby preventing scarring at Chamber visual axis. Wound cleaning with normal saline, formation of anterior chamber with help of viscoelastic. Viscoelastic can be injected through side port made with help of Number of Suturing Techniques MVR blade, but in cases of collapsed globe it might be Number of suturing techniques has been discussed and difficult to make the side port and form the chamber described in the literature. In cases with straight with viscoelastic and hence in such cases viscoelastic can lacerations, a running shoestring closure may minimize be injected directly through the corneal wound and astigmatism and scarring, however at times the wound chamber can be completely or partly formed. The integrity may not be achieved as perfectly as it could eventual aim in corneal laceration repair is definitive have been with interrupted sutures. If a running suture placement of corneal sutures to make the wound is used, the bites should be placed perpendicular and watertight, minimize scarring, and reconstruct the native equidistant to a best fit imaginary line through the nonastigmatic corneal contour. One can start by taking wound, irrespective of laceration itself. However, while superficial temporary sutures in order to approximate using an interrupted suture technique for curvilinear the wound edges and subsequently those sutures can or irregular lacerations, all sutures should be placed be replaced with definite deep sutures at end of surgery. perpendicular to the wound to avoid transverse shifting of the wound margins. Monofilament 10-0 Nylon Suture Material Monofilament 10-0 nylon suture material on a fine Corneoscleral Laceration spatulated design microsurgical needle is used for In cases with corneoscleral laceration, first, a suture corneal suturing. Some surgeons even prefer use of is applied to the limbus, and the wound is tightly 11-0 nylon sutures especially for wounds involving secured. This suture helps to anatomically approximate visual axis. A number of strategies for corneal suturing the wound. After the first suture is applied, an iris are available. The simplest involves progressively prolapse or a vitreous prolapse is treated. In the halving the wound with simple interrupted sutures. presence of an iris prolapsed depending on the viability These definitve corneal sutures should be approximated of iris tissue it is either repositioned or absiccised. In 1.5 mm long, approximately 90% deep in the stroma, the presence of a vitreous prolapse, a vitrectomy is and of equal depth on both sides of the wound. performed with cellulose sponges or an automated Shallow sutures will cause internal wound gape; sutures vitrector. During the vitrectomy, traction on the vitreous that are asymmetric or of unequal depth will result should be avoided. Any vitreous in the anterior in wound override. On the contrary, full thickness segment may be removed using a vitrectomy machine. sutures can act as conduit for microbial invasion. In After the corneal wound is repaired, the scleral wound Primary Globe Repair 217 is explored. This exploration is achieved by performing a limbal peritomy at the site of the limbal wound. The sclera wound is secured with help of interrupted or continuous 7-0 vicryl suture or 8-0 vicryl suture. Segments of scleral laceration are explored and repaired. This method helps to stabilize the eye and to prevent uveal or vitreous prolapse.

Scleral Laceration Scleral laceration should be repaired as far posteriorly as possible; far posterior scleral ruptures may be left unsutured. While repairing scleral lacerations, care must be taken to not exert pressure on the globe. In the presence of uveal prolapse, the prolapsed tissue is reposited. The preferred method of sclera wound Fig. 33.1: Corneal laceration operated elsewhere closure over prolapsed uveal tissue is a zippering technique wherein the sclera wound is closed from anterior end, i.e. limbal end with interrupted sutures placed successively proceeding posteriorly. One should never do excision of the prolapsed uveal tissue unless it is necrotic because it causes excessive bleeding. Vitreous prolapse is managed by performing a vitrectomy with cellulose sponges and scissors or by using an automated vitrector. At every step, care should be taken to prevent iatrogenic damage. The sutures are placed closely together and tied to achieve a watertight closure. The conjunctiva is sutured using 8- 0 or 9-0 Vicryl.

Posterior Scleral Laceration Scleral laceration without corneal involvement may occur in a variety of settings. Posterior sclera dehiscence or occult sclera dehiscence can be suspected based on history and mode of ocular trauma, poor visual Fig. 33.2: Corneal laceration repaired under acuity, conjunctival chemosis, deep or shallow anterior topical anesthesia chamber, low intraocular pressure, hyphema and/or subconjunctival pigmentation. Lacerations extending beyond equator of the globe can be left unsutured if attempting suturing is causing more trauma to the globe, this sclera perforations will be taken care by delayed secondary healing.

Patch and a Shield A patch and a shield are applied to the eye. Postopera- tively, patients should be carefully monitored for signs of infection. Pain, photophobia, redness, tearing, or a deterioration of vision should alert the physician to look for signs of endophthalmitis. Conjunctival injection, chemosis, corneal edema, and elevated intraocular pressure may be present but are not diagnostic of infection. A more than expected anterior chamber reaction and cells in the vitreous are most suggestive of endophthalmitis. Fig. 33.3: Corneal laceration repaired with hypopyon 218 Clinical Diagnosis and Management of Ocular Trauma

Fig. 33.4: Corneal laceration with eye lash in wound Fig. 33.7: Corneal wound revision done

Fig. 33.5: Corneal laceration with infection of Fig. 33.8: Open globe injury repaired wound edges

Fig. 33.6: Corneal laceration with traumatic cataract Fig. 33.9: Open globe injury with iris prolapse Primary Globe Repair 219 wound should be carefully explored and should be addressed by doing atraumatic sclera laceration repair.

Bibliography 1. Beatty RF, Beatty RL. The repair of corneal and sclera lacerations. Semin Ophthalmol 1994;9(3):165-76. 2. Coumhaire-Poutchinian Y. Management of the repair of scleral and corneal injuries. Bull Soc Belge Ophtalmol 1996;260:81-88. (Article in Ffrench) 3. Drews RC. Sodium Hyaluronate (Healon) in the repair of perforating injuries to the eye. Ophthalmic surg 1986;17:23-29. 4. Eisner G: Eye surgery: an introduction to operative technique, New York, 1980 Springer-Verlag. Fig. 33.10: Post-corneal tear repaired with SFIOL 5. Hamill BM. Corneal and Scleral trauma. Ophthalmol Clin N Am 15(2002):185-94. 6. Hersh PS, Shingleton BJ, Kenyon KR. Management of Summary corneoscleral lacerations. Eye Trauma. 1991. Mosby's Publications 143-58. Corneal and sclera wounds commonly present to the 7. Lamkin JC, Azar DT. Simultaneous corneal laceration emergency clinic and management of this cases should repair, cataract removal and posterior chamber intraocular be prioritize to optimize visual potential in traumatized lens implantation. Am J Ophthalmolo. 1992 Jun 15; eyes. Management of corneal and sclera laceration 113(6):626-31. requires careful evaluation and planning prior to closure. 8. Lin DT, Webster RG Jr, Abbott RL. Repair of corneal The globe must be closed so that it is watertight with lacerations and perforations. Int Ophthalmol Clinics. the original anatomy restored and the original function 1988 Spring 28(1):69-75. 9. Rowsey JJ, Hays JC, Refractive reconstruction for acute can be as approximated as possible. Closure of the eye injuries, Ophthalmic Surg 1984;15:569-74. cornea and sclera is different from the typical skin 10. Russel SR, Olsen KR, Folk JC. predictors of sclera rupture technique of halving the wound. Corneal wound is and the role of vitrectomy in severe blunt ocular trauma. closed based on the principles explained whereas sclera Am J Ophthalmol 1984;102:547-50. Iatrogenic Ocular Trauma and its Complications Management

CHAPTER

Management of Iatrogenic Inflammation of the Eye 34 NR Biswas, GK Das, Viney Gupta (India)

Introduction to their use. In experimental studies the available 0.1 percent dexamethasone further diluted as 1:10 or 1:20 For the treatment of any type of inflammation dilution had no virus or fungal replications enhancing including iatrogenic, both the steroids and non-steroidal effect when instilled 10 times a day, while 1:5 dilution anti-inflammatory drugs may be used. or undiluted available dexamethasone drops (0.1%) The corticosteroids are essential drugs in ophthal- enhanced virus and fungal growth. Moreover, mological diseases. It is a boon to the patients when adequately diluted corticosteroid does not increase the it is used with proper indications. It is a two-edged risk of enhancing the collagenase effect. sword, and can cause serious complications and side effects if it is used unwisely. Are we using corticosteroids c. Corticosteroid therapy in vernal conjuncti- judiciously? This question must always be kept in mind vitis and allergic disorders: The use of cortico- and answered before instituting this therapy. Before steroids locally has a beneficial effect in vernal conjunctivitis. But prolonged use is attended by planning the corticosteroid therapy, we must keep in unwanted side effects like cataracts, glaucoma and mind its ocular hazards. In clinical practice secondary keratoconus. corticosteroids are often used as shotgun therapy or as a placebo when all is not going well. This practice d. Use of corticosteroids in alkali burns of must be discouraged. cornea and conjunctiva: The use of corticosteroids in alkali burns is obligatory and seems beneficial. e. Use of corticosteroids in pseudophakic Topical Application bullous keratopathy (PBK): The effects of 5% The route of administration of corticosteroids depends hypertonic sodium chloride drop and deturgescent primarily on the site of involvement. Topical therapy drops, prepared by mixing betamethasone eye drops is effective in anterior segment diseases, including (0.1%) 1 ml; glycerin, 1 ml and artificial tear drops disorders of lids, conjunctiva, cornea, iris and ciliary 8 ml, achieving 10% glycerin and 1:0 betamethasone body. Ease of application, relatively low cost, and eye drops (0.1%), were compared in a controlled absence of systemic complications strongly favor local clinical trial in 50 cases of PBK. These were instilled routes whenever they are effective. 10 times a day. The deturgescent drops were The course of posterior segment disease (chorio- significantly superior in subjective as well as objective retinitis, optic neuritis, and posterior scleritis) is not parameters like discomfort, foreign body sensation, appreciably affected by topical corticosteroids and corneal clarity and improvement in vision, etc. as compared to 5% hypertonic saline. requires systemic therapy. f. Ocular hypertensive effect of corticosteroids: a. Are diluted corticosteroid drops effective in Surgical trauma causes inflammation which demands controlling intraocular inflammation? the use of corticosteroids to prevent the trabecular It was demonstrated that diluted corticosteroids have meshwork, corneal endothelium and other inner therapeutic anti-inflammatory effect in strengths of structures of the eye from damage by inflammatory 0.01 and 0.005 percent. response as well as its debris. But, ocular hypertension b. Corticosteroids in infective corneal diseases: inducing effects restrict their wide usage. In this regard, Local installation of corticosteroids in frank suppurative 1:10 or 1:20 diluted steroid did not have any ocular conditions are generally considered as contraindications hypertensive effect. 224 Clinical Diagnosis and Management of Ocular Trauma The use of 1:10 or 1:20 dexamethasone (0.1%) Indications for specified periods is safe to be used in glaucoma patients after intraocular surgery or when there is an In general, corticosteroid therapy may be helpful for associate uveitis, as there should be negligible risk of all allergic ocular diseases, for most non-pyogenic producing hypertension. inflammations (episcleritis, scleritis, uveitis, interstitial keratitis, optic neuritis and the like), and for the reduction of immunologic responses. Systemic Therapy Prednisone has become a corticosteroid of choice USE IN OCULAR SURGERY because it is inexpensive, short acting, and relatively 1. Cataract free from sodium retention. It may be used in divided 2. Corneal graft rejection doses, a single daily dose, or a single alternate day 3. Glaucoma surgery dose. 4. Retinal detachment Single daily dose: For long-term low-dosage 5. Vitreous surgery maintenance (as for chronic uveitis), a single, morning, 6. Strabismus daily dose of prednisone may be optimal. 7. Intraocular foreign body. Alternate day therapy: The undesirable side effects of systemic corticosteroid therapy can be substantially reduced by using alternate day therapy rather than Contraindications and divided dosage. Briefly stated, the entire total dose of corticosteroid that would have been given during a Complications 2-day period is administered as a single dose every other morning. SYSTEMIC COMPLICATIONS • Peptic ulceration • Osteoporosis Repository Injection • Femoral head ischemia necrosis The ophthalmologist who wishes to administer cortico- • Pseudotumor cerebri steroids by “subconjunctival” injection should consider • Exophthalmos. use of the repository form of methyl-prednosolone acetate (Depo-Medrol). Thus suspension form of pre- LOCAL CONTRAINDICATION AND dnisolone provides a constant source of corticosteroid COMPLICATIONS that lasts for 2 to 4 weeks. • Superinfection • Activation of tuberculosis • Uveitis Intravitreal Injection • Glaucoma Intravitreal 0.1 ml (Dose 50 mg/ml) is injected to • Corticosteroid mydriasis prevent proliferation of fibroblast. It seems helpful to • Corticosteroid induced cataract. combat proliferative vitreoretinopathy. The severe scleritis associated with rheumatoid arthritis, an example of immunological disorder does Controlled Release Vehicles respond to corticosteroid treatment but the patient may suffer structural loss of sclera upto more severe Ocusert devices delivering 10 mg of hydrocortisone scleromalacia as a result of treatment. acetate/hr were used to treat allergic conjunctivitis. Sympathetic ophthalmia is a classic example of a disease responsive to corticosteroid therapy, but requires prolonged therapy. Pulse Therapy Non-specific iridocyclitis and chorio-retinitis, as well Slow intravenous infusion of 100 mg Prednisolone daily as herpetic keratitis do seem to benefit from cortico- for consecutive three days shows good response in steroid therapy. Harada’s disease. If needed, repeat dose can be given Posterior ocular effects require systemic adminis- after 14 days. tration or retrobulbar injection. Management of Iatrogenic Inflammation of the Eye 225 Responsive Diseases TOXOPLASMOSIS It can be treated with high corticosteroid doses (upto BOECK’S SARCOID UVEITIS 100 mg prednisone per day for a prolonged period The response of Boeck’s sarcoid uveitis to with specific antitoxoplasmic therapy). corticosteroid therapy may be very gratifying. Topical use of corticosteroids and mydriatics is often OTHER INDICATIONS insufficient to arrest the disease. Addition of systemic Corticosteroid is found to be useful in cysticercosis. corticosteroid therapy has frequently given prompt subjective relief, followed within a few weeks by considerable objective improvement. Upto 200 mg Use of Nonsteroidal Anti- daily was used and produced a consistently favorable symptomatic effect. inflammatory Drugs in Inflammation ORBITAL MYOSITIS In the treatment of ocular inflammation, the appeal Acute inflammation of one or more extraocular muscles of nonsteroidal anti-inflammatory drugs (NSAIDs) may be a sequel to upper respiratory infections. These hinges on the complications associated with the more painful restrictions of movement may respond promptly to corticosteroid therapy. established therapy for ocular inflammation, i.e. corticosteroids. Although an overlap exists between the mechanisms of action of both, the use of NSAIDs OCULAR PEMPHIGOID may be safer than the use of corticosteroids, as the Although pemphigoid is characteristically a slowly latter may produce adverse effects such as glaucoma, progressive chronic subepithelial scarring process, opportunistic infections, and posterior subcapsular episodes of acute inflammation may occur. These cataracts. In sharp contrast, topical NSAIDs are known typically are nonresponsive to topical corticosteroid to cause only minor adverse effects such as burning, therapy. Systemic corticosteroids in dosage of 60 to stinging and hyperemia of the conjunctiva. 100 mg/day have caused remission of the disease. OCULAR INFLAMMATION HERPES ZOSTER A simple definition of ocular inflammation would be In a small series of 11 patients with herpes zoster, very inflammation of any part of the eye. Intraocular favorable results were reported from the systemic inflammation can be subdivided into inflammation of administration of cortisone or ACTH. the anterior and posterior segments of the eye. The cardinal signs of ocular inflammation are hyperemia, NEOPLASMS increased vascular permeability, oedema, and cellular Hemangiomas, intracranial plasmacytoma, medullo- (leukocytes, mast cell, platelets, etc.) infiltration into blastoma, ewings tumors respond well to corticosteroid ocular fluids and tissues. In experimental anterior therapy. uveitis, miosis and a rise in intraocular pressure which is usually due to the breakdown of the blood-aqueous TOLOSA-HUNT SYNDROME barrier with subsequent release of protein and fibrin Recurrent unilateral, painful, acute ophthalmoplegia into the aqueous humor, but not of cellular infiltration, responds dramatically to corticosteroid therapy within is observed. Inflammation after paracentesis usually 2 to 3 days. A daily dosage of 60 mg prednisone was disappears within 2-3 hrs. used. To understand the history of NSAID use in ophthalmology, one must appreciate the relevance of ANTERIOR SEGMENT ISCHEMIA prostaglandins in the eye. In 1971, Vane and Smith Prednisolone 1% was used four times daily, with established the connection between the clinical effect gradual clearing of the corneal edema and anterior of acetylsalicylate and inhibition of prostaglandin chamber cellular reaction. systesis1,2. It is now well-known that aspirin and other NSAIDs produce their clinical efficacy by inhibiting PSEUDOTUMOR CEREBRI cyclooxygenase and thus inhibiting prostaglandin Dexamethasone 0.5 mg is prescribed three doses daily synthesis (Fig. 34.1). Specific drugs belonging to each for 3 weeks. class are listed in Tables 34.1 and 34.2. 226 Clinical Diagnosis and Management of Ocular Trauma

TABLE 34.1: Systemic nonsteroidal anti-inflammatory agents Drug Drug name How supplied Typical adult daily dose (mg) (mg) Salicylates Aspirin 325-925 650 q4th Diflunisal 250, 500 250-500 bid Fenamates Mefenamate 250 250 qid Meclofenamate 50, 100 50-100 qid Indoles Indomethacin 25, 50, 75 25-50 tid-qid, (slow release) 75 bid Sulindac 150, 200 150-200 bid Tolmetin 200, 400, 600 400 tid Phenylacetic acids Diclofenac 35, 50, 75 35-75 bid Pheynylalkanoic acids Fenoprofen 200, 300, 600 300-600 tid Ketoprofen 25, 50, 75 75 tid, - 50 qid Piroxicam 10, 20 10 bid, 20 daily Flurbiprofen 50, 100 100 tid Ketorolac 10 10 qid Naproxen 250, 375, 500 250-500 bid 275-550 275-550 bid 200, 300, 400 Ibuprofen 600, 800 400-800 tid Pyrazolones Phenylbutazone 100 100 tid-qid Oxyphenylbutazone 100 100 tid-qid Para-aminophenols Acetaminophen 80, 325, 500, 650 650 q4th

TABLE 34.2: Topical nonsteroidal anti-inflammatory agents Name Strength Typical doses Flurbiprofen 0.03% solution 1 drop every 30 minutes for 2 hrs Preoperatively (Total dose: 4 drops) Suprofen 1.0% solution 2 drops at 1.2 and 3hours preoperatively or every 4 hours while awake on the day of surgery. Diclofenac 0.1% solution qid Ketorolac 0.5% solution tid Indomethacin 0.5%-1.0% qid suspension

an increase in vascular permeability, breakdown of the blood-aqueous barrier and induction of miosis.

Cystoid Macular Edema (CME) Fig. 34.1: Mechanism by which nonsteroidal anti- Topical NSAIDs are effective in preventing postsurgical inflammatory drugs produce their clinical effect angiographic CME when topical or subtenon’s corticosteroid injections are given concurrently. Only MECHANISM OF ACTION one study (involving 50 patients) has demonstrated NSAIDs act mainly as anti-inflammatory agents by similar effect with a topical NSAID in the absence of inhibiting cyclooxygense and lipo-oxygenase enzymes concurrent corticosteroid therapy.4 Several studies have which lead to inhibition of products like prostaglandins, demonstrated that prophylactic treatment with a thromboxane and leukotrienes which induce topical NSAID has a beneficial effect on visual function. inflammation. Ocular actions of prostaglandins include In one study, this effect was shown even in the absence Management of Iatrogenic Inflammation of the Eye 227 of concurrent corticosteroid therapy. Topical NSAIDs US food and Drug Administration (FDA) has approved also are effective in the treatment of angiographically the use of the diclofenac 0.1% four times daily, starting documented subclinical CME, and this can translate 24 hours after cataract surgery for this purpose. Thus, into improved visual function. Oral NSAIDs have also it is possible to substitute a topical NSAID for a topical been shown to be effective in both the prevention corticosteroid to control postoperative inflammation, and treatment of CME after cataract surgery. However, especially in eyes with significant steroid responsive a study demonstrating a positive effect on visual glaucoma. function with oral promote one NSAID still is lacking. There is no strong evidence to promote one NSAID Uveitis over another. In contrast to post-surgical inflammation, many forms of uveitis require prolonged steroid therapy to control Postoperative Inflammation inflammation. At times, the therapeutic effort must be Fluorophotometric analysis has made available a escalated to the use of subtenon injections or oral quantitative means of studying anterior chamber administration of corticosteroid. Of course, the risk of inflammation. With this tool, it has been possible to iatrogenic glaucoma and cataract becomes substantial evaluate, in a reproducible fashion, the effect of in these situations. Therefore, NSAIDs are gaining a NSAIDs on postoperative inflammation. By using both more secure position in the treatment of certain forms slit lamp and fluorophotometric analysis as a part of of uveitis. randomized double-masked placebo-controlled studies, several topical NSAIDs like indomethacin Scleritis and Episcleritis 1.0%,5 flurbiprofen 0.03%,6 ketorolac 0.5%7,8 and Topical NSAIDs have no proven efficacy in the diclofenac 0.1%9 have been shown to reduce treatment of episcleritis. In fact, they appear to be postoperative inflammation. The positive effect of less effective than topical corticosteroids in reducing NSAIDs was seen in both intracapsular and episcleral injection and pain associated with extracapsular cataract surgery. It is important to note episcleritis12. In contrast, systemic NSAIDs are the that whereas in most of the studies, corticosteroids were agents of choice in the treatment of non-necrotizing given concurrently, two of these studies were simple, diffuse, and nodular scleritis.13 One may have conducted without concurrent corticosteroid therapy7,8. to proceed sequentially through several different In these studies, topical ketorolac 0.05% proved to NSAIDs until one finds the one that works. be better than placebo in controlling inflammation Furthermore, when a steroid is needed, the duration after cataract surgery. and dose of the steroidal may be reduced with the In the treatment of postsurgical inflammation, the adjunctive use of an NSAID. superiority of NSAID over placebo has led to a comparison of NSAIDs with corticosteroid. Ketorolac 0.5%10 and diclofenac11 were compared to Allergic and Giant Papillary Conjunctivitis dexamethasone and prednisolone, respectively. In both Vernal keratoconjunctivitis most commonly occurs in studies, there was no significant difference in the children and young adults. It shares with contact lens- reduction of postoperative inflammation by slit-lamp associated giant papillary conjunctivitis (GPC) the examination between patients on NSAIDs and those common finding of giant papillary conjunctivitis (GPC) on corticosteroid topical therapy. However, it should on the upper palpebral conjunctiva. The standard be noted that in the ketorolac study, a subtenon treatment for both is topical steroids until a topical mast injection of corticosteroid was given to all the patients cell stabilizer takes effect. and this may have contributed to the lack of difference between the two treatment groups. Concurrent corticosteroid therapy was not a factor in the study comparing diclofenac with prednisolone. When Side Effects of NSAIDs fluorophotometry was used in both comparative Common adverse effects following instillation of topical studies, it was found that control of inflammation in NSAIDs include burning, stinging, and hyperemia of the topical NSAID treatment group was better achieved conjunctiva. Allergic and hypertensive reactions are than in the corticosteroid groups. also reported following use of topical NSAIDs. Systemic Regardless of the preceding findings, it is a common side effects following use of NSAIDs mainly include practice to use topical corticosteroid alone to control gastritis, but are unlikely to occur with topical post-cataract surgery inflammation. Nevertheless, the administration. 228 Clinical Diagnosis and Management of Ocular Trauma 5. Sanders DR, Kraff ML: Steroidal and nonsteroidal anti- Conclusion inflammatory agents. Effects on postsurgical inflammation NSAIDs have wide potential for use in various ocular and blood-aqueous barrier breakdown. Arch. disorders, though the effects vary from one individual Ophthalmol 1984;102:1453-56. 6. Sabiston MB, Tessler D, Summersk H, et al: Reduction to another and the effect is unpredictable. More of inflammation following cataract surgery by flurbiprofen. research is required to develop newer NSAIDs which Ophthalmic Surg 1987;18:873-77. can be used for various inflammatory disorders of the 7. Flach AJ, Graham J, Kruger LP, et al: Quantitative eye with more effective action with minimal ocular assessment of postsurgical breakdown of the blood- toxicities. aqueous barrier following administration of ketorolack tromethmine solution. A double-masked, paired Currently corticosteroids are still the drugs of choice comparison with vehicle-placebo solution study. Arch. in the treatment of ocular inflammation. However, Ophthalmol 1988;106:344-47. because their prolonged use may result in severe ocular 8. Flach AJ, Lavelle CJ, Olander KW, et al. The effect of side effects, it would be therapeutically beneficial to ketorolac 0.5% solution in reducing postsurgical develop nonsteroidal anti-inflammatory drugs that inflammation following ECCE with IOL. Double masked, parallel comparison with vehicle. Ophthalmology. have similar or greater efficacy than steroids but not 1988;95:1277-84. their ocular side effects. 9. Vickers FF, McGuigan LJB, Ford C, et al. The effect of diclofenac sodium ophthalmic drops on the treatment of postoperative inflammation. Invest. Ophthalmol. Vis. Sci. (ARVO suppl) 1991;32:793. References 10. Flach AJ, Kraff MC, Sanders DR, et al. The quantitative effect of 0.5% ketorolac tromethamine solution and 0.1% 1. Flck AJ: Cyclo-oxygense inhibitors in Ophthalmology. dexamethasone sodium phosphate solution on Surv. Ophthalmol 1992;36:259-84. postsurgical blood aqueous barrier. Arch. Ophthalmol 2. Gilman AG, Rall TC, Nies AS, Taylor P: The 1988;106:480-83. pharmacologic basis of therapeutics. Elmsford: Pergamon 11. Kraff MC, Sanders DR, McGuigan L, et al. Inhibition of 1990:638-81. blood aqueous humour barrier breakdown with 3. Abramson SB, Weisman G: The mechanism of diclofenac. A fluorophotometric study. Arch. Ophthalmol nonsteroidal anti-inflammatory drugs. Arthritis Rheum 1990;108:380-83. 1989;32:1-9. 12. Lyons CH, Hakin KN, Watson PG. Topical flurbiprofen: 4. Flach AJ, Jampol LM, Weinberg D, et al: Improvement an effective treatment for epoiscleritis? Eye 1990;4: in visual acuity in chronic aphakic and pseudophakic 521-25. cystoid macular edema after treatment with topical 0.5% 13. Vitale A, Foster CS: Nonsteroidal anti-inflammatory ketorolac tromethamine. Am. J. Ophthalmol 1991; drugs. In: Zimmerman TJ, ed. Textbook of ocular 112:514-19. pharmacology, New York: Lippincott-Raven, 1995. CHAPTER

Management of Postrefractive Keratitis 35 Eric D Donnenfeld (USA)

Introduction performed by physicians returning the questionnaire in 2004. The increase in incidence of infections is Laser in situ keratomileusis (LASIK) is the most presumably due to an increase in gram-positive resistant commonly performed surgical procedure to correct organisms, most likely due to methicillin resistant refractive errors and is the most common elective Staphylococcus aureus. Culture results revealed procedure performed in the United States. LASIK opportunistic infections and gram-positive bacteria as offers many benefits over photorefractive keratectomy, the most common organisms in 2001 (Fig. 35.1A). including increased visual rehabilitation, decreased In contrast, as noted above, in 2004 gram-positive stromal scarring, less postoperative pain, less irregular bacteria have increased in incidence while opportunistic astigmatism, minimal regression, and the ability to treat infections, specifically atypical mycobacteria, have seen 1,2 a greater range of refractive disorders. Compared a marked reduction (Fig. 35.1B). to other refractive procedures, LASIK preserves the integrity of Bowman’s membrane and the overlying epithelium, thus decreasing the risk of microbial keratitis. However, microbial keratitis following LASIK has become an increasingly recognized, sight- threatening complication of refractive surgery.3-10 The incidence of infectious keratitis following LASIK is unknown and can vary widely depending on the study. One large, retrospective study investigating the complications associated with LASIK surgery found an incidence of two infections in 1,062 eyes,7 and another similar study found an incidence of one infection in 1,019 eyes.8 A more recent case series of LASIK- associated infections encountered at a single institution Fig. 35.1A: ASCRS 2001 culture results of post-LASIK quotes an estimated incidence between 1:1000 and infectious keratitis 1:5000.9 Based on a comprehensive review and analysis of the published literature on infections following LASIK, Chang and colleagues5 also noted that the incidence of infection after LASIK can vary widely (0-1.5%). The American Society of Cataract and Refractive Surgery (ASCRS) Cornea Clinical Committee developed a post-LASIK infectious keratitis survey and conducted a survey of the organization’s members in 2001 and again in 2004.10 In the 2001 survey, there was an incidence of 1 infection for every 2919 procedures performed by physicians returning the questionnaire (116 post-LASIK infections were reported by 56 LASIK surgeons who had performed an estimated 338,550 procedures). These results are Fig. 35.1B: ASCRS 2004 culture results of post-LASIK contrasted to 1 infection for every 2131 procedures infectious keratitis 230 Clinical Diagnosis and Management of Ocular Trauma In 2004, the epidemic of atypical mycobacteria that the cornea for 1-2 minutes to improve flap adherence was seen in 2001 (Fig. 35.1B) ended. Cases from and then apply antibiotic directly on the dehydrated atypical mycobacteria decreased from 48 to 5%. This flap to improve antibiotic absorption into the cornea. decrease is presumably due to the use of fourth- With PRK, we place the antibiotic directly onto the generation fluoroquinolones and improved sterile stromal bed and soak the bandage contact lens in technique. It was interesting to note that no patient antibiotic for 30 seconds prior to placing the contact who received a 4th generation fluoroquinolone as lens on the eye. Postoperatively, patients receive a prophylaxis developed an atypical mycobacteria fourth generation fluoroquinolone four times a day infectious keratitis in the 2004 survey. However, the for 5 days with LASIK and for one day after the overall incidence of infectious keratitis increased in epithelial defect has closed with PRK. 2004 from 2001. We divide infectious keratitis following LASIK into The results of these surveys and an analysis of the rapid onset within the first two weeks of surgery and trends seen in the data can help to guide prophylaxis late onset which can occur from 2 weeks to 3 months and treatment of infections keratitis following LASIK. following surgery.13 The organisms seen in early onset Infectious keratitis is a potentially devastating infectious keratitis within the first two weeks are complication of LASIK. A high degree of suspicion common bacterial pathogens such as staphylococcal coupled with a rapid diagnosis and appropriate therapy and streptococcal species. Gram-negative organisms can result in visual recovery. For prophylaxis against are rare. The organisms seen in late onset infectious a post-LASIK infectious keratitis there are several steps keratitis after two weeks are usually opportunistic such which can be implemented. Preoperatively, all patients as fungi, nocardia and atypical mycobacteria. The considering refractive surgery should have a thorough published literature review of LASIK-associated examination of their eyelids and lacrimal apparatus. infections by Chang and colleagues supports this Treatment of infectious lid disease prior to LASIK with classification of infection.5 Based on their study, gram- hot compresses and a topical antibiotic ointment applied positive organisms were more likely to present within three times daily to the lid margin may decrease the 7 days of surgery (p = 0.001) while mycobacterial risk of a bacterial keratitis. A small minority of clinicians infections were more likely to present 10 or more days recommend performing monocular surgery or the use after surgery (p < 0.001).5 of separate instruments when performing bilateral Since the organisms responsible for infectious surgery.11 Some clinicians recommend the use of sterile keratitis following LASIK often will not respond to drapes, gowns, gloves and masks by the treating empiric therapy, as with the results from the previous physician and assisting technician. A10% betadine survey, we recommend lifting the flap, scraping, and solution lid prior to cataract surgery has been shown culturing all suspicious cases, and selecting appropriate to decrease the incidence of endophthalmitis following culture media including blood agar, chocolate agar, cataract surgery and is recommend by many clinicians Sabouraud’s agar and thioglycolate broth.13 For when performing LASIK.12 Proper sterilization infectious keratitis after two weeks, we recommend a techniques can prevent the use of contaminated growth media for atypical mycobacteria such as instruments. As several epidemics of atypical Lowenstein-Jensen or Middlebrook 7H-9 media in mycobacteria have been associated with the use of addition to the previous culture media. If these special non-sterile water to clean instruments or the use of media are unavailable, we recommend using blood ice during LASIK surgery, all fluids applied to the eye agar as atypical mycobacteria grow quite well on these before, during and after LASIK should be sterile.13 plates. At the time of culture we also recommend Antibiotic prophylaxis for LASIK should emphasize scraping the infiltrate and performing a Gram stain, the need to provide broad-based spectrum coverage Gomori-methenamine silver stain, and Ziehl-Neelsen with gram-positive emphasis. The antibiotic should be stain to rule out unusual pathogens such as nocardia, non-toxic to promote epithelial healing and should atypical mycobacteria, and fungi. In cases in which provide coverage against atypical mycobacteria which cultures are negative and the infection continues to is the most common opportunistic organism responsible a corneal biopsy or PCR should be considered. for post-LASIK infections. Finally, the antibiotic should For the treatment of both rapid-onset and delayed- penetrate effectively into the cornea and achieve onset infectious keratitis, it is recommended to elevate therapeutic levels in the mid stroma. Fourth generation the flap and culture. Irrigation of the flap interface with fluoroquinolones (gatifloxacin 0.3% and moxifloxacin an appropriate antibiotic solution (fortified vancomycin 0.5%) for antibiotic prophylaxis of LASIK and PRK are 50 mg/ml for rapid-onset keratitis and fortified amikacin recommended as they best meet the criteria listed 20 mg/ml for delayed-onset keratitis) may be helpful. above.13 We begin topical therapy 1 hour prior to For rapid - onset keratitis, we recommend a fourth- surgery and at the conclusion of LASIK we dehydrate generation topical fluoroquinolone such as gatifloxacin Management of Postrefractive Keratitis 231 0.3% or moxifloxacin 0.5% be given in a loading dose misdiagnosis at initial presentation may result in every 5 minutes for 3 doses and then every 30 minutes significant vision loss. Antibiotic prophylaxis for LASIK alternating with an antimicrobial which is rapidly should emphasize the need to provide broad-based bacteriocidal and has increased activity against gram- spectrum coverage with gram-positive emphasis. For positive organisms, such as cefazolin 50 mg/ml every treatment, we do not recommend empiric therapy as 30 minutes.13 In patients who work in a hospital most organisms are opportunistic and do not respond environment or have been exposed to a hospital to conventional therapy. A high degree of suspicion surgical setting or health care environment, there is with flap elevation and culturing should be performed an added risk of methicillin-resistant Staphylococcus on all eyes suspected of infectious keratitis following aureus (Solomon R, Donnenfeld E, Perry H, et al. LASIK. methicillin resistant Staphylococcus aureus infectious keratitis following refractive surgery. Presented as a paper at the American Society of Cataract and References Refractive Surgery Symposium on Cataract, IOL, and Refractive Surgery, San Diego, Calif, 2004). In those 1. Hersh PS, Brint SF, Maloney RK, et al. Photorefractive patients who work in a hospital environment or have keratectomy versus laser in situ keratomileusis for had exposure to a health care environment, we moderate to high myopia: A randomized prospective study. Ophthalmology 1998;105:1512-23. recommend the substitution of vancomycin 50 mg/ml 2. Azar DT, Farah SG. Laser in situ keratomileusis versus every 30 minutes instead of cefazolin to provide more photorefractive keratectomy: An update on indications effective therapy against MRSA. In addition, we and safety. Ophthalmology 1998;105:1357-58. advocate the use of oral doxycycline 100 mg twice 3. Garg P, Bansal AK, Sharma S, Vemuganti GK. Bilateral daily (to inhibit collagenase production) and also infectious keratitis after laser in situ keratomileusis: A case report and review of the literature. Ophthalmology recommend discontinuing corticosteroids. 2001;108:121-25. For delayed-onset keratitis, which is commonly due 4. Solomon A, Karp, CL, Miller D, et al. Mycobacterium to atypical mycobacteria, nocardia and fungi, we interface keratitis after laser in situ keratomileusis. recommend beginning therapy with amikacin 35 mg/ Ophthalmology 2001;108:2201-08. ml every 30 minutes alternating with vancomycin 5. Perry HD, Doshi SJ, Donnenfeld ED, et al. Herpes 50 mg/ml every 30 minutes, starting oral doxycycline simplex reactivation following laser in situ keratomileusis and subsequent corneal perforation. CLAO J 100 mg BID, and discontinuing corticosteroids. 2002;28:69-71. Alternative therapy for delayed-onset keratitis, which 6. Chang MA, Jain S, Azar DT. Infections following laser in would cover atypical Mycobacteria, includes situ keratomileusis: An integration of the published clarithromycin and fourth-generation fluoro- literature. Surv Ophthalmol 2004;49:269-80. quinolones. This treatment will not cover fungal 7. Stulting RD, Carr JD, Thompson KP, et al. Complications infections, and therefore, treatment for all cases of of laser in situ keratomileusis for the correction of myopia. Ophthalmology 1999;106:13-20. infectious keratitis should be modified based on culture 8. Lin RT, Maloney RK. Flap complications associated with and scraping results and response to therapy. lamellar refractive surgery. Am J Ophthalmol 1999; Infectious keratitis after LASIK frequently presents 127:129-36. with inflammation in the corneal interface, which can 9. Karp CL, Tuli SS, Yoo SH, et al. Infectious keratitis after mimic diffuse lamellar keratitis (DLK). DLK usually LASIK. Ophthalmology 2003;110:503-10. 10. Solomon R, Donnenfeld ED, Azar DT, Holland EJ, occurs within the first few days following LASIK, unless Palmon FR, Pflugfelder SC, Rubenstein JB. Infectious 14 there is postoperative ocular trauma. The appearance keratitis after laser in situ keratomileusis: Results of an of an interface inflammation more than one week ASCRS survey. J Cataract Refract Surg 2003;29: following LASIK should be presumed to be infectious 2001-06. unless proven otherwise. Since DLK usually presents 11. Kohnen T. Infections after corneal refractive surgery: Can with a diffuse appearance while infectious keratitis has we do better? (editorial). J Cataract Refract Surg 2002; 28:569-70. focal area of infiltration, any focal infiltrate surrounded 12. Speaker MG, Menikoff JA. Prophylaxis of by inflammation following LASIK should be considered endophthalmitis with topical povidone-iodine. infectious until proven otherwise. Ophthalmology 1991;98:1769-75. In conclusion, infectious keratitis is a potentially 13. Donnenfeld ED, Kim T, Holland E, et al. Management devastating complication following LASIK. Culture of infectious keratitis following laser in situ keratomileusis. results reveal gram-positive bacteria as the most J Cataract Refract Surg 2005;31:2008-11. 14. Stulting RD, Randleman JB, Couser JM, Thompson KP. common organisms. Infectious keratitis may present The epidemiology of diffuse lamellar keratitis. Cornea as late as months following LASIK, and its frequent 2004;23:680-88. CHAPTER Optimized NSAIDs and Antibacterial Prophylaxis in Cataract Surgery 36 Ashok Garg (India), Ian Bell (USA)

Introduction Our preoperative routine is three doses of drops starting 30 to 60 minutes before surgery. Cataract surgery is one of the most commonly Some surgeons prefer to start the drops 24 hours performed ocular surgery in the world. Given the ability preoperative while others start the drops three days of ocular surface flora to enter the eye during surgery, preoperative. many of the prophylactic techniques aim is to suppress There are select indications where anti- their number and to limit the growth of those inflammatory drug dosing should begin a week organisms that do enter the eye during intraocular preoperative including high-risk cases for inflammation surgery. Antimicrobial prophylaxis is an essential and secondary macular edema. Such patients includes component of both cataract and refractive surgeries. those with a long-term, history of chronic uveitis and Choosing an antibiotic for surgical prophylaxis in the diabetes mellitus and patients with pigmentary clinical setting can also be challenging. retinopathy and macular edema, and those who The key surgical prophylaxis paradigm shift in recent developed macular edema in the first eye after cataract years for long practicing ophthalmologists is the surgery. growing evidence for preoperative use of both topical With high-risk patients such as those who are antibiotics and anti-inflammatory drops. The second immunocompromised or prone to infection, we can shift is the realization that we should discontinue start the antibiotic three days preoperative rather than antibiotics more quickly and ensure use of anti- just on the table. inflammatory for the full course of therapy. These In our routine cases, I load the entire drop regimen changes are key for limiting post-cataract (iatrogenic) in the eye in the operating room, but the high-risk inflammation and infection while they prevent the cases you may start, three to seven days preoperative. development of antibiotic resistance in patients. In the There is not yet a consensus, but you may want to preoperative period a fourth-generation fluoroquino- go a little longer and by more intense on the high- lone such as Moxifloxacin 0.5% solution, a non- risk patients. steroidal anti-inflammatory such as topical Nepafence The research evidence does not clearly identify 0.1%, suspension, and a topical steroid such as whether drug delivery shortly preoperative or several prednisolone acetate 1% should all be administered. days preoperative is better. However, as the patients Loading the eye with an antibiotic prior to the become higher risk, We tend to have a slightly longer surgical insult reduces the risk of endophthalmitis. and more intense course of antibiotic and anti- Furthermore studies have shown that the inflammatory drops. non-steroidal, anti-inflammatory drugs (NSAIDs) and Routine patients that never had a problem the steroids are synergistic and both work better if the generally start to receive the drug in the operating room eye is loaded preoperative. prior to surgery because it is easiler on the patient. There are two basic ways to approach the preoperative loading. One approach provides the drops within the three-to-four dose delating resimen Postoperative Schedule for in the surgical induction area. We can add Neosynephrine 10% Cyclogyl solution (1% Cyclo- Cataract Patients pentolate HCl), an antibiotic, steroid, non-steroidal, The major changes in recent years from previous so actually they get loaded up with five different drops. antibiotic experience is the perioperative and short Optimized NSAIDs and Antibacterial Prophylaxis in Cataract Surgery 233 postoperative course of the drugs. We now limit The incidence of very mild macular edema without antibiotic use because the risk of endophthalmitis drops an NSAID, even in a good surgeon’s hands, is about with in a week when the wound seals. It is the long- 12% and adding as NSAID takes it down to less than term, low-dose use of these drugs that leads to resistant 1% so you get a hug reduction in one of the most organisms. common sight threatening complications of cataract Our approach is to administer antibiotics and anti- surgery just by adding an NSAID and using it properly. inflammatory drops (steroid and NSAID) at the end Proper dosing of antibiotics, NSAIDs, and steroid of the case. My staff administer them agains in the plays a very important role in preventing complications recovery area before the patient goes home. such as infection or CME. We have patients use the antibiotic drops three Minimizing these complications with effective agents times a day for one week. Other surgeons have them and proper therapeutic dosing regimens will improve take the antibiotic for as few as five days. our surgical outcomes. However, the anti-inflammatory drug is required Surgeons can greatly improve their chances of a for longer use. Evidence suggests the blood aqueous successful surgical outcome if they keep in mind three barrier breakdown that occurs after cataract surgery key criteria in selecting antibiotics: potency, penetration, persists for four to eight weeks. Because the average and safety. A good balance of these aspects – especially breakdown lasts about six weeks, we should treat with potency and penetration – provides the best patient protection. anti-inflammatory drops for one to two months in An antibiotic that is highly potent and effective at routine cases. This will prevent any rebound of kiling infections at lower concentrations would lose inflammation or other secondary issues. much of its efficacy if it was unable to penetrate the We need to have patients use the anti-inflammatory tissue. Conversely, a medication that penetrates drops a big longer than some surgeons think is extremely well but lacks potency also would not be necessary because often the eyes are quiet and very functional. comfortable by two to three weeks after surgery, but Clinicians are best served by an effective combi- there is still some risk for cystoid macular edema up nation of penetration and potency. to six weeks postoperative. Although researchers are frequently asked whether For example, for at-risk patients preoperative dosing potency or penetration is more important, the only is recommended for one week and postoperative clear answer is the most effective approach is to dosing is recommended for four weeks to several combine these factors. months.

Measuring Potency Drug Dosages Identifying an antibiotic’s strength in penetration and The dosing regimen we use instillation of the topical potency is important, but surgeons should be aware Nevanac, which is a TID drop, a three-times daily drop. that potency definitions vary. The most common We use Moxifloxacin, Nepafenac, and a topical steroid, assessment of an antibiotic’s potency, the minimum which seems more than adequate, as these drugs have inhibitory concentration (MIC), traces whether demonstrated efficacy in contributing to good surgical organisms growth has been stopped. However, the outcomes. definition still alows viable organisms to remain. This Ophthalmologists should be aware of adding most common term may not be the most important. NSAID drug to their regimen. Most patients recover Another standard, minimum bactericidal concentration without complications when surgeons only use an (MBC), tracks whether 99.9% of the organism is killed antibiotic and a steroid. However, there are indications (MBC is approximately 4x the MIC). The final measure- that over 10% of patients will develop a very mild ment, mutant prevention concentration (MPC), gauges macular edema without an NSAID. That’s a risk that whether the organism was killed with mutations NSAIDs can eliminate. prevented (MPC is approximately 8x the MIC). We have pretty minimally invasive cataract surgery Drugs with the lowest potency numbers in MIC, today, and people work really hard at their surgical MBC or MPC are among the most potent. With technique, but probably the one thing that could have postoperative infections being potentially sight the greatest impact on their outcomes would be to threatening, it is ideal to exceed these levels with the add an NSAID to their regimen. antibiotic concentrations in the target tissues. 234 Clinical Diagnosis and Management of Ocular Trauma Penetration Tracking tested against a Staph. aureus ocular isolate using disk- diffusion analysis. The moxifloxacin achieve a 24 mm Antibiotic tissue penetration plays a key role in zone of inhibition, and Gatifloxacin had no zone of protecting against infection. inhibition. This surrogate model accounts for tissue This issue arises when examining the research on penetration and potency at the potential site of various antibiotics; some may have good potency infection, thus defining protection. statistics in vitro, but we fail to identify the in vivo performance of the antibiotic. The latter will tell ophthalmologists what levels of the drug our patients Safety Evaluation actually will get in the cornea, the anterior chamber, and the vitreous. Our research administering In addition to potency and penetration, a solid fluoroquinolones to a cornea transplant model prior evaluation of antibiotics for surgical prophylaxis should to corneal transplant and then examining the antibiotic assess whether the drug is non-toxic. Efforts to prevent levels in the cornea showed Moxifloxacin had three the use of non-toxic medication should look for times the concentration of Gatifloxacin. epithelial problems or endothelial problems. Similar research at various International Research As a class of drugs, the Fluoroquinolones have Centres on aqueous concentrations of antibiotic proven to by very safe and non-toxic. applied a series of drops preoperative and measured Our experience with all fourth-generation Fluoro- aqueous concentration at the time of cataract surgery. quinolones has found that they are very safe. Research Those researchers identified the same three-fold comparing corneal epithelial healing postoperative greater penetration of Moxifloxacin. Protection can be when Moxifloxacin or Gatifloxacin are used have defined by overlaying these concentrations with the found very similar would healing rates. In fact, an MICs for potential pathogens. independent well-controlled study evaluating wound In vivo potency after tissue penetration is a better healing post-PRK for Moxifloxacin and Gatifloxacin measure of antibiotic efficacy than speed of kill in vitro. were conducted in USA. The conclusion was that both The latter removes all of the factors that determine the drugs are safe. Generally, they found that eyes how the antibiotic performs in human tissue. These treated with Moxifloxacin healed faster and had smaller studies disrergard the reality of penetration of the defects than those treated with Gatifloxacin. antibiotic through human tissue. For these reasons Rabbit model studies that created epithelial defects in vivo potency and penetration studies will always and tracked healing when the two antibiotics are used have more real-world resonance than in vitro speed found similar results. Clinical trials looking at healing of kill research. The aqueous humor concentrations after PRK also identified similar healing. Both achieved in the International Resarch Centres were Fluoroquinolones are safe and non-toxic. CHAPTER Optimizing Visual Outcomes with NSAIDs Therapy in Cataract and Refractive Surgery 37 Eric D Donnenfeld, Henry D Perry (USA)

Introduction prostaglandins, and leukotrienes (McColgin). Clinical symptoms of prostaglandin production include Ophthalmic nonsteroidal anti-inflammatory drugs hyperemia miosis, poor vision, pain, and cystoid (NSAIDs) are becoming a cornerstone for the macular edema (CME), management of ocular pain and inflammation. Their It is well accepted that inhibition of prostaglandin well-characterized anti-inflammatory activity, analgesic synthesis and release reduces the inflammatory property, and established safety record have also made response induced by surgery and allergies, thereby NSAIDs an important tool to optimize surgical reducing the clinical symptoms of prostaglandin outcomes. Ophthalmic NSAIDs currently play four production (McColgin). Prostaglandin synthesis can be principle roles in ophthalmic surgery including the suppressed by inhibiting phospholipase A2, which prevention of intraoperative miosis during cataract inhibits the release of arachidonic acid from the surgery, management of postoperative inflammation, intracellular stores, or by inhibiting the conversion of the reduction of pain and discomfort following cataract arachidonic acid to prostaglandin via the cyclooxy- and refractive surgery, and the prevention and genase pathway. Multiple portions of this pathway can treatment of cystoid macular edema following cataract be blocked and different classes of anti-inflammatory surgery. medications have differing effects on this pathway. Ocular inflammation is characterized by redness, For example, corticosteroids interfere with the swelling, and/or pain associated with irritation or trauma to the eye. Common triggers of ocular activity of phospholipase A2, thereby inhibiting the inflammation include allergies, meibomian gland release of arachidonic acid and the production of all dysfunction, ocular diseases (traumatic iritis, peripheral arachidonic acid metabolites including prostaglandins. corneal inflammatory keratitis, episcleritis, and (Polansky and Weinreb, 1984). unilateral nongranulomatous idiopathic iritis) and most In contrast, the nonsteroidal anti-inflammatory importantly ophthalmic surgical procedures. agents (NSAIDS) specifically and irreversibly inhibit the The strict regulation of inflammatory reactions synthesis of prostaglandins by interfering with the within the eye is vital in maintaining both anatomical activity of cyclo-oxygenases (COX-1 and COX-2). integrity and visual function. Left unregulated, (Polansky and Weinreb, 1984). inflammation within the eye may lead to extensive ocular damage, resulting in impaired vision. Ocular inflammatory pathways commence with the Rationale for Treating Ocular triggering of the arachidonic acid cascade. The cascade is triggered either by mechanical stimuli (such as the Inflammation case of surgically-inflicted trauma) or by chemical Reducing ocular inflammation is critical because failure stimuli (such as foreign substances or allergens). to do so may cause patients’ discomfort, pain, visual Prostaglandins are generated in most tissues by loss, and increase the risk for the development of CME. activation of the arachidonic acid pathway. CME is potentially the most adverse ocular outcome Phospholipids in the cell membrane are the substrate of prostaglandin production. CME is caused by cystic for the enzyme phospholipase A to cause generation accumulation of intraretinal fluid in the outer plexiform of arachidonic acid and, in turn, the enzymes cyclo- and inner nuclear layers of the retina, as a result of oxygenases and lipoxygenases act on arachidonic acid breakdown of the blood-retinal barrier. It is the most to produce a family of chemically distinct common following intraocular surgery, and in patients 236 Clinical Diagnosis and Management of Ocular Trauma

Fig. 37.1: Prostaglandin synthesis

with venous occlusive disease, diabetic retinopathy, and group that got the NSAID just 1 hour prior for anti- posterior segment inflammatory conditions (Quin). miosis had a rate of 12% CME as detected by OCT However, CME can develop in surgeries with no (Donnenfeld). CME frequently has a late onset, obvious complications. The condition is often asymp- occurring 4-6 weeks postoperatively. CME often tomatic and may only be detected with fluorescein presents with blurred or decreased central vision or angiography or optical coherence tomography (Quin, painless retinal inflammation or swelling. Visual loss is Roberts). Although the exact incidence of CME is still usually temporary but may be irreversible in refractory unclear, CME is a frequent cause of visual loss to conservative treatment. In high risk patients such following even uncomplicated cataract surgery. Studies as diabetics the risk of CME and permanent vision loss suggest that the rate of clinical CME ranges from 1- is even greater. 2% (Ray), while the incidence of angiographic CME NSAIDs are also frequently used to inhibit may be as high as 9-19% (Ursell, Mentes). In a recent intraoperative miosis during cataract surgery. Miosis study, patients using ketorolac tromethamine 0.4% pre- may restrict the surgeon’s field of view during cataract operatively 1-3 days prior to surgery had no instances surgery, thereby hindering the progression of the of CME, whereas the steroid-only group and the procedure, and increasing the risk of complications and posterior capsule rupture (Guzek, Stewart). The NSAIDs prevent miosis by limiting prostaglandin synthesis within the tissues by inhibiting cyclooxygenase and reducing inflammation. They also help to maintain increased pupillary size during the surgical procedure thereby helping to reduce complications.

Pharmacologic Therapy for Ocular Inflammation Ocular inflammation is currently treated with either topical corticosteroids or NSAIDs. The corticosteroids, considered the gold standard for the treatment of ocular inflammation, are associated with an increased incidence of adverse events that warrant their judicious Fig. 37.2: Background diabetic retinopathy use. These adverse events include cataract formation, increases the risk of CME a rise in intraocular pressure, increased susceptibility Optimizing Visual Outcomes with NSAIDs Therapy in Cataract and Refractive Surgery 237 for the treatment of for the reduction of ocular pain and burning/stinging following corneal refractive surgery.

NSAIDs for Control of Pain Following PRK The recently reported pooled analysis of 2 multicenter, randomized, double-masked, vehicle-controlled, parallel-group studies of 313 patients with unilateral photorefractive keratectomy (PRK) evaluated the safety and analgesic efficacy of ketorolac tromethamine 0.4% ophthalmic solution in postoperative patients (Solomon). After surgery, patients were treated with 1 drop of ketorolac tromethamine 0.4% ophthalmic Fig. 27.3: Preoperative NSAIDs reduce pupil solution (n = 156) or vehicle (n = 157) four times constriction during cataract surgery (Donnenfeld) daily for up to 4 days. Pain intensity, pain relief, use of escape medication, and severity of ocular symptoms to microbial infections due to a suppressed host were assessed and adverse events, epithelial healing, immune-response, retardation in corneal epithelial and and visual acuity recorded. Patients in the ketorolac stromal wound healing. Steroids are not safe for group reported significantly less pain intensity than periods of extended use as prolonged use is associated patients in the vehicle group (P<.001). During the with development of glaucoma, visual acuity defects first 12 hours post PRK, 50% fewer patients in the and loss of visual field, and posterior subcapsular ketorolac group than in the vehicle group had severe cataract formation. to intolerable pain [41.6% (64/154) and 84.5% (131/ A safer alternative to corticosteroids for the 155), respectively]. The median time to no pain was treatment of ocular inflammation are the NSAIDs. 30 hours in the ketorolac group and 54 hours in the There are four classes of NSAIDS available for topical vehicle group (P<.001). Ketorolac patients reported ophthalmic use: indoles, phenylacetic acids, an significantly greater pain relief than vehicle patients arylacetic acid pro-drug, and phenylalkanoic acids. throughout the study (P<.001) and used significantly Indomethacin 1% aqueous suspension is an indole less escape medication than vehicle patients for 48 derivative that is available outside of the United States hours post-PRK (P<.008). The authors concluded that (O’Brien). Diclofenac 1% is a water-soluble ketorolac 0.4% ophthalmic solution is safe and effective phenylacetic derivative approved by the FDA as a in reducing ocular pain when used 4 times daily for treatment to minimize inflammation related to cataract up to 4 days post-PRK. surgery and as a therapeutic option for the reduction of pain and photophobia after cataract surgery. Bromfenac 0.09% is a recently approved twice-daily NSAIDs vs Steroids topical phenylacetic compound indicated for the A recent study compared the efficacy, safety and patient treatment of postoperative cataract inflammation. comfort of two topical steroids (prednisolone 1% and Originally available as a systemic medication, the rimexolone 1%) with ketorolac tromethamine 0.5% product was removed from the market in the United after extracapsular cataract extraction in a prospective, States because of potentially fatal liver toxicity but has randomized, double-masked study of 45 patients. been available as an ophthalmic agent in Japan for Patients were assigned to receive topical treatment with several years. Nepafenac 0.1% is approved as a three prednisolone, rimexolone or ketorolac tromethamine times a day treatment for pain and inflammation ophthalmic solution after phacoemulsification for associated with cataract surgery. This agent is an cataract extraction. Although there were no significant arylacetic acid pro-drug. Flurbiprofen 0.03% and between-group differences in inflammatory cell counts, suprofen 1% are water-soluble phenylalkanoic acids (P=0.165), flare readings in the anterior chamber were approved by the FDA for intraoperative use during lowest (P=0.008) in the ketorolac group. One patient cataract surgery for inhibition of excessive miosis during in the prednisolone group experienced elevated IOP cataract surgery. Ketorolac tromethamine 0.4% is also and had to be excluded. The authors concluded that a water-soluble phenylalknaoic acid and is approved ketorolac tromethamine provides good control of 238 Clinical Diagnosis and Management of Ocular Trauma intraocular inflammation after cataract extraction miosis during phacoemulsification cataract surgery. without the risk of a steroidal IOP increase (Herneiss). Mean horizontal pupillary diameter measurements for Holzer and associates reported that ketorolac both medications were similar at the start of surgery. tromethamine ophthalmic solution 0.5% was is However, a consistent trend of larger pupillary effective as loteprednol etabonate ophthalmic diameter was seen in all subsequent surgical intervals suspension 0.5% in reducing inflammation after routine in the ketorolac-treated group. Changes from baseline phacoemulsi-fication and IOL implantation, suggesting measurements also indicated a more significant that ketorolac tromethamine 0.5% is a safe and inhibition of miosis at all subsequent intervals, and a effective antiinflammatory alternative to steroids after more stable mydriasis throughout the procedure in cataract extraction. the ketorolac-treated group (Solomon 1997). Similarly, Solomon and associates reported ketorolac tromethamine 0.5% is a safe and effective anti-inflammatory alternative to steroids after cataract NSAIDs and Topical Steroids extraction. In that study, ketorolac tromethamine 0.5% It is well accepted that combination topical therapy was as effective as rimexolone 1% in reducing with a corticosteroid and a NSAID is more effective inflammation after cataract surgery. There were no than either agent dosed individually for treatment of between-group differences in signs and symptoms of CME following cataract surgery, and a recent study inflammation, intraocular pressure, or Kowa cell and by Rho and associates supports this paradigm. The flare measurements in this double-masked, prospective authors compared combination therapies of diclofenac evaluation of 36 patients (Solomon and Vroman sodium 0.1% and prednisolone acetate 1%, with 2001). ketorolac tromethamine 0.5% and prednisolone acetate 1%, for treatment of CME in 68 patients following uncomplicated cataract surgery. Complete NSAIDs for the Inhibition of resolution of CME was noted in 28% of diclofenac patients and in 25% of ketorolac patients. Final vision Miosis improved three or more lines in 58% and 53% of Srinivisin and associates reported that topical ketorolac patients, respectively. None of the patients showed signs was a more effective inhibitor of miosis than topical of corneal toxicity or significant intraocular pressure diclofenac during extracapsular cataract extraction and rise during the treatment period. The authors IOL implantation. Ketorolac also provided a more concluded that combination therapy with NSAIDs and stable mydriatic effect throughout surgery. In a study steroids was effective in reducing the severity of of 51 patients who were prospectively randomized to pseudophakic CME and in improving final vision. receive ketorolac 0.5% or diclofenac 0.1% at 3 The findings of Rho and associates are supported intervals preoperatively. In this study, the ketorolac by another recent study by Heier and associates (Heier, group showed a consistent trend toward larger pupil 2000). That study evaluated the efficacy of ketorolac, diameters at subsequent surgical intervals as well as prednisolone acetate 1.0%, and ketorolac and greater inhibition of miosis in the ketorolac group. prednisolone combination therapy in the treatment Similarly, Snyder and associates reported that the of acute, visually significant, clinical CME following use of ketorolac as a single agent negated the need cataract extraction surgery in a randomized, double- for use of a combination of preoperative NSAID masked, prospective trial of 28 patients. Treatment was (flurbiprofen) and postoperative cosrticosteroid for the continued until CME resolved or for 3 months, prevention of intraoperative miosis and postoperative whichever occurred first and then tapered over 3 weeks. inflammation in cataract surgery. In their study of 26 The average improvements in Snellen visual acuity patients, there were no statistically significant differences were 1.6 lines with ketorolac monotherapy, 1.1 lines in dilation (preoperative versus postoperative) or cell with steroid monotherapy, and 3.8 lines with and flare postoperatively. The authors concluded that combination therapy. More patients in the combination the use of ketorolac as a single agent could eliminate group achieved at least a two-line improvement (89% the expense of using separate anti-inflammatory and of combination patients versus 67% of ketorolac and antimiotic preparations preoperatively and post- 50% of steroid patients). Moreover, these patients operatively, thereby enhancing surgeon convenience improved faster with combination therapy than with and patient convenience and compliance (Snyder). monotherapy with either agent (1.33 months for Recently, a large study (n=118) compared the combination therapy compared with 1.43 months for effects of topical ketorolac with topical 0.03% ketorolac patients and 2.75 months for steroid flurbiprofen on the inhibition of surgically induced patients). Improvements in contrast sensitivity and Optimizing Visual Outcomes with NSAIDs Therapy in Cataract and Refractive Surgery 239 leakage on fluorescein angiography tended to mirror concluded that macular edema decreases the quality improvements in Snellen acuity. The authors concluded of postoperative vision and that the use of pre- that treatment of acute, visually significant operative and postoperative NSAIDs decreases the pseudophakic CME with ketorolac and prednisolone amount of postoperative macular edema. combination therapy appears to offer benefits over Many clinicians are hesitant to prescribe topical monotherapy with either agent alone. NSAIDs for long-term use because of prior reports of A study by Arshinoff et al evaluated postoperative corneal melting associated with topical NSAIDs (Flach, pain in 97 PRK patients using different topical NSAID Gaynes). However, analysis of NSAID-associated protocols. In their study, treatment with topical corneal events implicates the now defunct generic homatropine hydrobromide, either diclofenac sodium diclofenac product, diclofenac sodium ophthalmic or ketorolac tromethamine, and a soft contact lens solution as the agent primarily responsible (Gaynes). was most effective in achieving post-PRK analgesia. The demonstrated safety of ketorolac throughout They also found that NSAIDs added to topical steroid numerous studies, some as long as 6 weeks duration, protocols had a significantly greater effect than steroids suggests that this drug is safe for extended use. If fact alone on reducing myopic regression for one year ketorolac has actually been recommended for the postoperatively (Arshinoff, 1994). treatment of post-cataract inflammation in a patient with systemic steroid treated rheumatoid arthritis post- phacoemulsification. In this patient the fear of “melting” Prevention of CME led the physician to avoid topical NSAIDs. However, the severe reaction postoperatively led him to using All available evidence demonstrates that ketorolac is it successfully in the second eye with excellent results an effective treatment for acute and chronic CME. (Caronia). Several studies, however, suggest that ketorolac is also The available evidence demonstrates that NSAIDs able to prevent CME in postoperative patients. A study are highly effective analgesics for pain associated with by Flach and associates (1990) suggested that ketorolac cataract and refractive procedures. The ability to prevents CME without the risks associated with provide relief of patient pain is critical because patients concomitant topical steroid treatment. In that study, have high expectations and expect almost no pain with 50 patients with bilateral cataracts were enrolled in a ophthalmic surgeries. Patients who experience ocular placebo-controlled, paired-comparison, double- pain or discomfort may therefore believe that their masked study. Eleven patients had evidence of surgeon may have substandard surgical skills and the angiographic (angiographic aphakic CME) ACME on resulting patient dissatisfaction and potential for postoperative day 40. Two of these patients demons- negative word of mouth to the patient’s colleagues trated bilateral ACME, one patient had ACME in the and friends may have adverse consequences for a NSAID-treated eye, and eight patients had ACME in surgical practice. Choosing the most effective topical the placebo-treated eye. This was a statistically agent for relief of ocular inflammation and pain significant difference favoring drug treatment. In postoperatively is therefore. addition, the signs of anterior ocular inflammation were The adjunctive use of NSAIDs with steroids optimizes greater in the eyes with ACME. surgical outcomes as numerous studies have Roberts presented data from a clinical study at the demonstrated that the combination of an NSAID and 2005 meeting of ASCRS that demonstrated that steroid is more effective for the treatment of post- patients using preoperative and postoperative NSAIDs operative inflammation, CME, and improving visual had less postoperative increase in macular thickness acuity than either NSAID or steroid monotherapy. than those who did not use NSAIDs. In that study, Perhaps the most important effect to surgeons is 200 patients undergoing phacoemulsification were the increased amount of dilation preoperatively and randomized to two pharmaceutical treatment the tendency for the dilation to remain for the entire regimens, differing only by the inclusion/exclusion of procedure. Some surgeons have likened this effect as ketorolac 0.4% into the standard treatment regimen. like having a third hand during surgery. Other studies Outcome measures included macular thickness by OCT point out the direct relationship between pupil size and at preoperative and 4 weeks postoperative, contrast rate of surgical complications (Donnenfeld). sensitivity by FACT, and Snellen visual acuity. After 4 In recent years, there has been a substantially weeks, the change in macular thickness was amount of debate in the ophthalmic community substantially greater without NSAIDs than with regarding the use of NSAIDs prior to surgery to prevent (10.4 μm compared with 4.2 μm, respectively). There the formation of CME. We understand and accept that were no differences in visual acuity. The author increased inflammation postoperatively is associated 240 Clinical Diagnosis and Management of Ocular Trauma with an increased risk of developing CME. In fact, a 2. Caronia RM, Perry HD, Donnenfeld ED, J Cataract and study by Ursell and associates reported that patients Refractive Surg 2002;28:1880-81. who had angiographic CME at day 60 were more likely 3. Donnenfeld ED, Perry HD, Wittpenn JR, Solomon R, to have had more postoperative inflammation than Nattis A, Chou T. Preoperative ketorolac tromethamine 0.4% in phacoemulsification outcomes: pharmacokinetic- patients who did not develop CME. (Ursell) It follows, response curve. J Cataract Refract Surg 2006 therefore, that preventing inflammation with pro- Sep;32(9):1474-82. phylactic dosing would decrease the risk of developing 4. Evans RE, Bucci FA Jr, Amico LM. Efficacy of Ketorolac CME. A recent study by Donnenfeld and associates 0.5% versus Ketorolac 0.4% Following Cataract Surgery. (Donnenfeld) does provide us with evidence Presented at ARVO 2005. supporting the use of ketorolac 0.4% as surgical 5. Flach AJ, Stegman RC, Graham J, Kruger LP. Prophylaxis prophylaxis against CME. The study was a prospective of aphakic cystoid macular edema without corticosteroids. A paired-comparison, placebo-controlled double-masked evaluation of 100 patients randomized in a double- study. Ophthalmology 1990;97:1253-58. masked fashion prior to phacoemulsification into 4 6. Flach AJ. Corneal melts associated with topically applied groups: one group received preoperative ketorolac nonsteroidal anti-inflammatory drugs. Trans Am tromethamine 0.4% four times daily for 3 days and Ophthalmol Soc. 2001;99:205-10; discussion 210-12. three doses every 15 minutes immediately surgery, 7. Gaynes BI, Fiscella R. Topical nonsteroidal anti- another received four doses on the day before surgery inflammatory drugs for ophthalmic use: a safety review. ketorolac 0.4% and three doses every 15 minutes Drug Saf. 2002;25:233-50. immediately surgery, another received ketorolac only 8. Goyal R, Shankar J, Fone DL, Hughes DS. Randomized controlled trial of ketorolac in the management of corneal 3 times (every 15 minutes) in the hour immediately abrasions. Acta Ophthalmol Scand. 2001 Apr;79(2): surgery, and the fourth group was randomized to 177-79. control. In that study, use of ketorolac for 1 or 3 days 9. Guzek JP, Holm M, Cotter JB, et al. Risk factors for reduced the incidence of CME. No patients in these intraoperative complications in 1000 extracapsular groups had CME at week 2, compared with 12% (3/ cataract cases. Ophthalmology 1987;94:461-66. 25) of control patients and 4% (1/25) of patients in 10. Heier J, Cheetham JK, Degryse R, et al. Ketorolac the 1 hour group. This study suggests that three day tromethamine 0.5% ophthalmic solution in the treatment of moderate to severe ocular inflammation after cataract preoperative dosing with ketorolac effectively prevents surgery: a randomized, vehicle-controlled clinical trial. Am CME. Other findings of that study demonstrated that J Ophthalmol 1999;127:253-59. ketorolac maintained pupil size, reduced discomfort, 11. Hirneiss C, Neubauer AS, Kampik A, Schonfeld CL. limited reductions in epithelial cell counts, and reduced Comparison of prednisolone 1%, rimexolone 1% and patient need for additional anesthesia. Ketorolac also ketorolac tromethamine 0.5% after cataract extraction. A provided substantial reductions in the amount of time prospective, randomized, double-masked study. Graefes needed to perform surgery, making it a cost-effective Arch Clin Exp Ophthalmol 2005 Mar 9; [Epub ahead of print]. pharmaceutical for cataract surgery. Most of these data 12. Kaiser PK, Pineda R 2nd. A study of topical nonsteroidal followed a clear dose-response pattern, suggesting that anti-inflammatory drops and no pressure patching in the maximum prophylaxis can be expected with the three treatment of corneal abrasions. Corneal Abrasion days dosing regimen, though even 1 day of ketorolac Patching Study Group. Ophthalmology 1997;104: was consistently superior to 1 hour of ketorolac or to 1353-59. control. Flach and Roberts that ketorolac is an effective 13. McColgin AZ, Heier JS. Control of intraocular prophylaxis against CME. inflammation associated with cataract surgery. Curr Opin Ophthalmol 2000;11(1):3-6. If a 3-day dosing regimen of ketorolac is effective 14. Mentes J, Erakgun T, Afrashi F, Kerci G.Incidence of surgical prophylaxis, what is the most appropriate cystoid macular edema after uncomplicated postoperative dosing regimen? In my experience, 4 phacoemulsification. Ophthalmologica 2003 Nov- weeks of QID dosing with ketorolac 0.4% is optimal Dec;217(6):408-12. for most patients, in patients with diabetes mellitus we 15. O'brien TP. Emerging guidelines for use of NSAID therapy use at least 6 weeks of therapy and most important to optimize cataract surgery patient care. Curr Med Res in patients with diabetic retinopathy we use ketorolac Opin 2005 Jul;21(7):1131-38. 0.4% for at least three months to help protect this 16. Polansky JR, Weinreb RN. Steroids as anti-inflammatory agents. In: Sears ML, ed. Pharmacology of the Eye. New most susceptible group from developing CME. York, NY: Springer-Verlag 1984;460-538. 17. Price FW Jr, Price MO, Zeh W, Dobbins K. Pain reduction after laser in situ keratomileusis with ketorolac Bibliography tromethamine ophthalmic solution 0.5%: a randomized, 1. Arshinoff S, D'Addario D, Sadler C, Bilotta R, Johnson double-masked, placebo-controlled trial. J Refract Surg. TM. Use of topical nonsteroidal anti-inflammatory drugs 2002 Mar-Apr;18(2):140-44. in excimer laser photorefractive keratectomy. J Cataract 18. Price FW, Tonon E, VanDenburgh AM, Stern K, Refract Surg. 1994;20:216-22. Cheetham JK, Schiffman RM. Safety and Efficacy of Optimizing Visual Outcomes with NSAIDs Therapy in Cataract and Refractive Surgery 241

Reformulated Ketorolac Tromethamine 0.4% Ophthalmic antimiotic and anti-inflammatory in cataract surgery. J Solution in Post-Photorefractive Keratectomy Patients. Cataract Refract Surg 2000;26:1225-27. Presented at ARVO 2003. 31. Snyder RW, Siekert RW, Schwiegerling J, Donnenfeld E, 19. Price MO, Price FW. Efficacy of topical ketorolac Thompson P. Acular as a single agent for use as an tromethamine 0.4% for control of pain or discomfort antimiotic and anti-inflammatory in cataract surgery. J associated with cataract surgery. Curr Med Res Opin 2004 Cataract Refract Surg. 2000;26:1225-27. Dec;20(12):2015-19. 32. Solomon KD, Donnenfeld ED, Raizman M, et al. Safety 20. Quinn CJ. Cystoid macular edema. Optom Clin and efficacy of ketorolac tromethamine 0.4% ophthalmic 1996;5(1):111-30. solution in post-photorefractive keratectomy patients. J 21. Ray S. D'Amico DJ. Pseudophakic macular edema. Cataract Refract Surg. 2004 Aug;30(8):1653-60. Semin Ophthalmol 2002;17:167-80. 33. Solomon KD, Donnenfeld ED, Raizman M, et al. Safety 22. Rho DS, Soll SM. Combination Therapy for and efficacy of ketorolac tromethamine 0.4% ophthalmic Pseudophakic Cystoid Macular Edema: Diclofenac solution in post-photorefractive keratectomy patients. J Sodium 0.1% and Prednisolone Acetate 1% Versus Cataract Refract Surg 2004 Aug;30(8):1653-60. Ketorolac Tromethamine 0.5% and Prednisolone Acetate 34. Solomon KD, Turkalj JW, Whiteside SB, Stewart JA, 1%. Presented at ARVO 2004. Apple DJ. Topical 0.5% ketorolac vs 0.03% flurbiprofen 23. Rho DS. Treatment of acute pseudophakic cystoid for inhibition of miosis during cataract surgery. Arch macular edema: Diclofenac versus ketorolac. J Cataract Ophthalmol 1997 Sep;115(9):1119-22. Refract Surg 2003 Dec;29(12):2378-84. 35. Solomon KD, Turkalj JW, Whiteside SB, Stewart JA, 24. Roberts CW. Comparison of the Ocular Comfort of Acular Apple DJ. Topical 0.5% ketorolac vs 0.03% flurbiprofen LS with Acular PF in Healthy Volunteers. Presented at for inhibition of miosis during cataract surgery. Arch ARVO 2004. Ophthalmol 1997;115:1119-22. 25. Roberts CW. Pretreatment with topical diclofenac sodium 36. Solomon KD, Vroman DT, Barker D, Gehlken J. to decrease postoperative inflammation. Ophthalmology Comparison of ketorolac tromethamine 0.5% and 1996;103:636-39. rimexolone 1% to control inflammation after cataract 26. Rossetti L, Autelitano A. Cystoid macular edema extraction. Prospective randomized double-masked following cataract surgery. Curr Opin Ophthalmol study. J Cataract Refract Surg 2001 Aug;27(8):1232-37. 2000;11:65-72. 37. Srinivasan R, Madhavaranga. Topical ketorolac 27. Sandoval HP, Fernandez de Castro LE, Vroman DT, tromethamine 0.5% versus diclofenac sodium 0.1% to Solomon KD. Comparison of 0.4% Ketorolac Tromethamine Ophthalmic Solution vs 0.5% Ketorolac inhibit miosis during cataract surgery. J Cataract Refract Tromethamine Ophthalmic Solution to Prevent Surg 2002 Mar;28(3):517-20. Inflammation After Phacoemulsification and Intraocular 38. Stewart R, Grosserode R, Cheetham JK, et al. Efficacy and Lens Implantation: A Prospective, Randomized, Double- safety profile of ketorolac 0.5% ophthalmic solution in Masked, Clinical Trial. Presented at ARVO 2005. the prevention of surgically induced miosis during 28. Schechter BA, Wittpenn JR. Evaluation of Ketorolac cataract surgery. Clin Ther 1999;21:723-32. (Acular LS) During the Induction Phase of Cyclosporine 39. Ursell PG, Spalton DJ, Whitcup SM, Nussenblatt RB. a (Restasis) Therapy to Improve Patient Comfort. Cystoid macular edema after phacoemulsification: Presented at ARVO 2005. relationship to blood-aqueous barrier damage and visual 29. Singal N, Hopkins J. Pseudophakic cystoid macular acuity. J Cataract Refract Surg 1999 Nov;25(11): edema: ketorolac alone vs. ketorolac plus prednisolone. 1492-97. Can J Ophthalmol. 2004 Apr;39(3):245-50. 40. Waterbury LD, Flach AJ. Efficacy of low concentrations 30. Snyder RW, Siekert RW, Schwiegerling J, Donnenfeld E, of ketorolac tromethamine in animal models of ocular Thompson P. Acular as a single agent for use as an inflammation. J Ocul Pharmacol Ther. 2004;20:345-52. CHAPTER

Management of Cystoid Macular Edema 38 Arturo Pérez-Arteaga, René Cano-Hidalgo (Mexico)

Introduction Etiology Cystoid macular edema (CME) is an inflammatory POST-SURGICAL, PRIMARY OR SECONDARY condition of the central retina that can be produced (CAPSULOTOMY) for many causes, since drugs for other ophthalmic It was first described as the Irving-Gass syndrome; a diseases until surgical intervention of the eye. If well pathologic condition where Irving in 1953 mentioned the initial descriptions of the disease can be found as a decrease in the visual acuity with vitreoretinal a surgical complication, now we know much more alterations after the intracapsular surgery of the lens, conditions that can produce these clinical and para- and Gass and Norton described the typical fluorangio- clinical findings, so that we can talk about a multi- graphic changes of this condition. At that time 77% factorial disease. of the eyes operated with intracapsular cataract surgery Many drugs are involved in the treatment of this developed some degree of CME, even sometimes sub- condition. The choose of each one is according the clinical. etiology of the inflammatory process, preference of the During the days of the extracapsular cataract physician, response of the patient, underlying disease, extraction the incidence decreased because the severity of visual loss and anatomic findings. Even surgical preservation of the posterior capsule and the decrease treatment has been described, and so the use of specifical of vitreous loss. Even so, this incidence increase when drugs during and after the procedure; so it is a very there is posterior capsule rupture in an extracapsular good way to review the drugs involved in the treatment technique. With the entrance of phacoemulsification of this pathologic condition according to the physioscopy techniques for cataract surgery the incidence was even of this book, the use of anti-inflammatory drugs in less, but again, it was demostrated that the main goal ophthalmology. In fact several proven treatment to decrease this condition is the conservation of the modalities are available and so on new therapies are posterior capsule and to avoid the vitreous loss. It is continuing to expand our horizons. still to be proved that the newest technologies of First the reader will find in this chapter a brief minimally invasive cataract surgery can produce a description of CME definition, etiology, clinical findings statistical reduction of post-cataract surgery CME. and diagnostic strategies. Then the drugs that are The posterior capsulotomy is also a very well-known involved in the treatment of this condition, including procedure that can lead to CME, and it is also related those used in the surgical treatment will be described. to the rupture of the retinal and accuous barriers; so in this field new technologies and evolution of Definition intraocular lenses that can reduce the incidence of posterior capsule opacification are very important. CME is a pathologic condition of the macula with Any kind of intraocular surgery can produce swelling where multiple cyst-like (cystoid) areas of fluid sometime some degree of CME. At the end the cascade appear in the central retina, mostly in the outer of events become from the rupture of the intraocular plexiform layer. It is a painless disorder that according barriers. The initial trauma (damage, surgery, etc.) to the cause and severity can be fully reversed or can produce the liberation of the chemical mediators of cause permanent visual loss. Sometimes this condition the inflammation to the accuous and vitreous; mainly has clinical manifestations from low to severe, but also prostaglandins are produced by the damaged tissue can occur in the sub-clinic plane. and the traumatized epithelial cells, but many other Management of Cystoid Macular Edema 243 factors like the complement, the platelet activation of risk factors like cataract surgery, uveitis, posterior factor, lisozomal enzymes, cytoquines, nitric oxide, capsulotomy and diabetic retinopathy. endothelin and interleukin. We can conclude that any This concepts must be taken in count by the factor that contributes to the rupture of the barriers physician at the time to prescribe this medications in blood-accuous and blood-retinal is going to increase particular if some risk factors are present in some patient. the possibility to develope CME. If the therapy can be done with another medication it will be better, but if it must be continued for some MICROVASCULAR DAMAGE reason, the utilization of non-steroidal anti- This is commonly found in diabetic retinopathy, inflammatory drugs can avoid the development of occlusive diseases like retinal vein occlusions, and other CME without loss of the hypotensor effect of the anti- less commonly diseases like idiopathic juxtafoveal glaucoma drugs. Also a constant follow-up with the capillary telangiectasia. The main factor is again the explanation to the patient of specific symptoms of rupture of the intraocular barriers that this vascular macular disease and Amsler test in each visit for alterations produce and the liberation of the mentioned glaucoma control, are mandatory. mediators during the acute vascular event. Some other factors like the VEGF and IGF-1 liberated by the PERIPHERAL RETINAL LESIONS ischemic tissues, have been involved in the rupture A peripheral lesion, can lead by itself, to the rupture of the intraocular barriers and so in the production of the intraocular barriers and so the development of of CME. Any syndrome associated with sub-retinal CME. It is a good behavior to explorate the periphery neovascularization can have the same effect. of the retina in a case when we find CME and we are trying to know the cause. INFLAMMATORY DISEASES The most well-known form of uveitis that can produce TUMORAL DISEASES CME is pars planitis; in fact CME is the main cause Because of acummulation of leakage and rupture of of visual loss in this inflammatory process, but many the barriers, many ocular tumors, like malignant other forms of uveitis like Behçet´s disease, Crohn´s melanomas, peripheral capillary hemangiomas and disease, rheumatoid arthritis, sarcoidosis and some Coat´s disease can be also cause of CME. other forms of non-specifical uveitis can produce some degree of CME. The cause is as mentioned before, EYE HYPOTONY the liberation of the inflammatory mediators. It can be post-traumatic, with or without rupture of the globe, it can be followed cataract surgery, glaucoma POST-MEDICATION (ANTIGLAUCOMA DRUGS procedures or choroidal effussions of any cause. At AND PRESERVATIVES) the end, the low intraocular pressure is the cause for The first reference about the relation between an anti- the rupture of the intraocular barriers and so the glaucoma medication and the development of CME liberation of mediators. was described by Becker in 1967 and was with the use of epinephrine; was noted years after, that this OPTIC NERVE DISEASES incidence was more in the aphakic patient. It is well Optic nerve inflammations like true papilledema, known at this time, that the topical epinephrine neuropathy or some ischemic diseases can produce increase the prostaglandins in the eye, in particular CME. in the aphakic one, and so the rupture of the intraocular barriers. Some other medications were described to RETINAL TRACTION produce this effect like dipivalylepinephrine, timolol Peripheral traction, macular traction, epiretinal and benzalconium chloride. Recently with the arise of membranes, and traction produced by diabetic new pharmacologic groups of anti-glaucomatous retinopathy (even without direct macular traction) are medication, in particular prostaglandins, the incidence common entities that can produce CME. of post-medication CME has increase. A lot of studies have been conducted in this field and what we know FINAL COMMON PATHWAY OF UNDERLYING currently is that latanoprost, travoprost, bimatoprost DISEASES and unoprostone can produce some degree of CME and that this incidence can increase with the association Ischemic, tractional, inflammatory, toxic and genetic. 244 Clinical Diagnosis and Management of Ocular Trauma Histopathology poor visuality like 20/400 or less in severe cases. Like some others macular diseases the patients can The breakdown of the inner blood-retinal barrier due experience some degree of metamorphopsia. to vasogenic and/or cytotoxic causes is the initial event At the clinical examination the evidence of surgery, in CME. There is a leaking of the perifoveal capillaries trauma, vascular retinal diseases and others like leading the formation of edema. The fluid collects in glaucoma diseases must be achieved. Of course the the loosely arranged outer plexiform layer of Henle; main study is the fundoscopy where the macular in this layer the fibers are arranged in an horizontal thickening and/or swelling can be found. It also can pattern. This is the cause of the petalloid flower be found in many degrees depending upon the severity appearance that is seen as characteristic of this disease of the disease, and can go since a loss of foveolar reflex in the angiogram (cystic pattern) (Fig. 38.1). with out clinical evidence of edema, to a characteristic Electronic microscopy has shown acummulation of cystic appearance. This is the typical clinical finding in intracelullar fluid within expanded Müller cell processes. the ophthalmoscopy, radiating cystic spaces emana- ting from the macula. Of course, in these cases, there is a complete loss of the red reflex. The red free light examination is mandatory, where a “honeycombed” appearance is seen, and it corresponds to the fluid filled cyst (Fig. 38.2). In severe cases these cyst may coalesce into a macular cyst and then form a hole.

Fig. 38.1: Cystic pattern

Clinical Findings Fig. 38.2: Loss of red reflex There is always an history of previous ocular disease, surgery, medication, vitreous pathology or another PARACLINICAL APPROACH condition in the patient that developes CME. No laboratory studies are necessary to establish the Sometimes it can be very easy to obtain, like previous diagnosis of CME. The main study in the establishment cataract surgey or posterior capsulotomy, but in some of this diagnosis is the fluorescein angiogram (FA). others, the physician must be very accurate like in In the FA parafoveal retinal capillary leakage is seen glaucoma medications, posterior vitreous detachment in the early and mid phases. These phases are not or peripheral tears that may lead to the break of the characteristic of CME because the acummulation of inner blood-retinal barrier. fluid in certain conditions is delayed, so the late phase The main symptom of CME is the reduction of has a particular importance, and it is about 20 minutes visual acuity, even so, here are many forms of CME and sometimes can be more, to find the characteristic that goes free of visual symptoms. Many patients that petaloid pattern of leakage in the macula. undergo a cataract surgery can develop some degree Another related conditions can be seen in the FA of sub-clinical CME, and the only one evidence can according the underlying disease: If likeage micro- be found in a retinal fluorogram. The degree of the aneurysms are present, diabetic retinopathy can be disease and so the severity of symptoms frequently the cause; vascular collaterals can be due to retinal correlates with the degree of complications during the oclussion; optic nerve findings are also useful in the cataract surgery, if this is the case. So the reduction final etiologic diagnosis establishment. of visual acuity may undergo from a minimal degree, Optical coherence tomography (OCT) is a non- like 20/25 and be not notice by the patient, until very invasive method also very useful in the final diagnosis Management of Cystoid Macular Edema 245 of CME because the fluid-filled spaces in the retina NON-SURGICAL APPROACH are easily seen. This cross-sectional image of the retina Many drugs have been involved for the treatment of can also be helpful in the monitoring over time of the CME during the time. Some of them are used as a disease by quantifying the amount of fluid inside the traditional fashion and some others are emerging as retina in serial studies. A non-invasive study can be new therapeutic resources. the ideal modality in monitoring the response to treatment. Nonsteroidal Anti-inflammatory Drugs (NSAIDs) In particular cases an electroretinogram can also be helpful but not mandatory (Figs 38.3 to 38.5). The main effect of this group of drugs is to estabilize the blood-retinal barrier. This effect is because they inhibit the enzyme cyclo-oxygenase. They can be used by systemic way and also in the form of eyedrops. The main examples of this group of medications are: 1. Indomethacin 2. Ketorolac 3. Diclofenac They inhibite the prostaglandin synthesis by decreasing the activity of the enzyme cyclo-oxygenase. These drugs in the topical form must be used as a medication in the preoperative and postoperative period of some intraocular procedures like cataract Fig. 38.3: Macular quistic edema surgery, posterior capsulotomy and peripheral iridectomy for example, to reduce the incidence of CME. This profilactic form also helps to reduce the postoperative inflammatory process. As has been said before, the development of CME in some way correlates with the degree of manipulation during the ocular surgery and some factors have been demonstrated in the development of CME like the time of light microscope exposure, posterior capsule rupture and vitreous manipulation. Of course, a real “clean” surgery can decrease the incidence of CME, but anyway, the use of NSAIDs is mandatory. New operative devices that avoid the use of direct light exposure during the ocular surgery are promising in Fig. 38.4: CME plus epiretinal membrane the near future to decrease the incidence of CME in uncomplicated surgery cases. The use of systemic NSAIDs is only reserve for the cases of complete diagnosis of CME; even so some surgeons are using them as a profilactic medication. There is not a recomended time for the use of systemic NSAIDs for the treatment of CME; the time of use will depend upon the response of each patient in particular according the follow-up. Because sometimes it is a long-term medication, secondary effects of NSAIDs must be always taken in count. In the systemic medication, gastric effects should be monitoring during the visits of the patient. A history Fig. 38.5: Epiretinal membrane plus macular cystic edema of gastric diseases including ulcerative disease and bleeding is mandatory when oral indomethacin is in use. If some of these effects are present the Treatment therapeutic must be suspended and replaced by other The treatment of CME can be divided in two medication. approaches that finally in the practice are combined Local NSAIDs have also some secondary effects; but in the theory we are going to describe separately. long-term use may delay wound healing and has been 246 Clinical Diagnosis and Management of Ocular Trauma reported cases of corneal stromal thinning or melting of the blood-ocular barrier. They can be useful in some in some particular patients receiving diclophenac forms of uveitic CME. Nevertheless the secondary eyedrops for extended period of time. If symptoms effects of systemic corticoid medication must be like blurred or diminished vision and signs of corneal avoided, and this is why recently the medication of deposits, retinal changes and scotoma are present, the CME is trying to move to the ocular space instead the medication must be suspended. systemic route.

Corticosteroids Carbonic Anhydrase Inhibitors (CAIs) Steroidal medication is very useful in the treatment Carbonic anhydrase is an enzyme present in the apical of CME and also in the prevention of it. The routine and basal surfaces of the retinal pigment epithelium use of steroids in the eyedrops form before and after cell membrane. Its action is to pump and produce a surgical procedures, has decrease the incidence of change in the ion flux. CAIs enhance this pumping postsurgical CME, even in complicated cases. action of these cells, and helps to improve this ion flux The most frequent form of steroid medication for that affects the cellular environment of the retina. CME is topical, in the form of prednisolone acetate; CAIs are commonly used in ophthalmology, in it is indicated in several conditions of steroid-responsive particular in the glaucoma cases, where the topical intraocular inflammation. The presentation is at 1% medication is not enough to control the intraocular solution and can be used several times in a day pressure, so it is a well-known resource. Also the according the severity of the inflammation. The amount physician is close to side effects of the CAIs, like the and time of administration must be measured according alteration in the ionic composition of blood, increase the response of the disease to the treatment. in urine excretion, and in large doses hepatic and Monitoring of the side effects of topical steroids like, metabolic problems. So it is known that it is not a raise in the intraocular pressure and an increased risk chronic medication, it has to be used according the of secondary ocular infections, must be evaluating severity and response to treatment of CME and the during the time of therapy and this should be physician has to advice the patient the side effects, the discontinued if some of these effects are found. Not mode to contrarest them and the total communication all patients have the same response to steroids they both have to mantain in order to manage the according the rise in the intraocular pressure; some dose in good response, but also in good levels of side patients can tolerate large periods of time without effects. This medication should be suspended as soon changes in the pressure, but some others cannot as possible according the evolution of CME. tolerate too much medication. If the topical steroid The presentation of acetazolamide is in tablets of therapy is really needed in these cases, the physician 250 mg and can be given until three to four times can add some glaucoma therapy; medications that can a day. Close monitoring of antiinflammatory and side increase the CME should be avoided (e.g. latanoprost, effects is mandatory. travoprost, epinephrine); the best adjunctive anti- glaucoma medication is dorsolamide that also can have Intravitreal Medication some benefit effects in the macula. Other side effects of long-term topical steroids like subcapsular cataract Recently new drugs are appearing in the retinal medi- formation must be addressed. cation field for intravitreal injection, like Bevacizumab The use of injections of long acting depot-steroids (Avastin) and Pegaptinib, also called Macugen. These (e.g. triamcinolone) into the sub-Tenon space has also drugs are promising results in many retinal vascular a role in the treatment of CME. This external way of disorders like occlusive diseases and diabetic administration that can have more penetration to the retinopathy. The side effects are not completely known, retina; the drug delivery to the retina is superior by and many trials around the world are in progress at this route in comparison to peribulbar. In some cases this time to achieve consistent results. of uveitic CME refractory to conventional treatment, The apparently positive action seen in some vascular the triamcinolone has been used in intravitreous disorders lead the possibility to use them in CME. Some injection alone or in combination with some other of them are including only diabetic patients, some drugs. Triamcinolone alone has been effectively in others only postoperative cataract patients and some reducing CME and improving vision; some studies are others are combining the avastin with triamcinolone. currently underway in the combination of this steroidal During the middle of year 2007 these trials will be drug with other drugs, like bevacizumab (Avastin). finish and we will be able to know the safety, efficacy Oral steroids play also an important role in the and probably side effects of these drugs in the treatment of CME because the effect in the stabilization treatment of CME. Management of Cystoid Macular Edema 247 SURGICAL APPROACH AND DRUGS RELATED NSAIDs according the case. After all we know about The surgical treatment is not the first choice in the this disease, prevention and treatment we believe this treatment of CME; nevertheless, some particular should be mandatory. Also in patients with glaucoma situations can lead to the indication of pars plana control with prostaglandines, this therapy should be vitrectomy (PPV): avoided and the control must be followed with another • Cases of uveitis related CME. anti-glaucoma medication, during the pre, trans and • Remove of vitreous strands that can cave an effect postoperative period. If it is not possible to eliminate of “pull the retina”, from anterior and posterior the prostaglandin and NSAIDs should be started in segment structures. addition. Of particular importance is the glaucoma • Remove inflammatory mediators from the vitreous patient, who is receiving medication that can produce (e.g. memory cells, cytoquines), that can be CME; the physician must be alert to any kind of sign mantaining an inflammatory response. that can advice the presentation of CME. The adjuntive • Remove of retained lens fragments. NSAIDs therapy can be helpful in cases where is • Remove of epiretinal membrane. impossible to avoid prostaglandins. Because the rupture of the blood-retinal barrier, New medications are promising good results, even after the PPV there is an increase in the peneration alone or in combination, for the treatment of refractory of topical and oral steroids. Also some surgeons are CME. Like all new products, we are specting some happy with the use of triamcinolone during the surgical new non-reported adverse effects; the test of time, approach, achieving so the benefit effect of both, like always, will lead us to the complete knowledge vitrectomy and intravitreal medication. We believe at of their specific indications. this time, that the PPV by itself is not enough for the treatment of CME; we agree that it must be accompanied by intravitreal medication. Bibliography The side effects of steroids in the vitreous cavity 1. Antcliff RJ, Standorf MR, Chauhan DS et al. Comparison must be addressed continuously because the possibility between optical coherence tomography and fundus of changes in IOP; in this particular case sometimes fluorescein angiography for detection of cystoid macular it is very difficult to achieve a good IOP because the edema in patients with uveitis. Ophthalmology deposit effect of the steroid. Even so, sometimes 2000;107:593-9. 2. Ayyala RS, Cruz DA, Margo CE, et al. Cystoid macular without steroid medication in the vitreous cavity, PPV edema associated with latanoprost in aphakic and it self, is able to produce an increase in IOP of difficult pseudophakic eyes. Am J Ophthalmol 1998;126:602- control. 04. The final decision to perform a PPV must be carefully 3. Becker B. Topical epinephrine in the treatment of evaluated and consented between the surgeon and the glaucomas. In New Orleans Glaucoma Symposium: patient, because of the possible side effects. 152-9. The CV Mosby Company. St Louis 1967. 4. Bhattacherjee P, Kulkarny PS, Eakins KE. Metabolism of arachidonic acid in rabbit ocular tissues. Invest Ophthalmol Vis Sci 1979;18:172-8. Conclusion 5. Callanan D, Fellmann RL, Savage JA. Latanoprost associated cystoid macular edema. Am J Ophthalmol At the end of the day a lot of factors are going to 1998;126:134-5. influence the prognosis of a patient who develops CME. 6. Clinical Trials Gov. US. National Institutes of Health. Effect The main factor of all is the inherent cause of the of prophylactic ketorolac on CME after cataract surgery. disease; it will not be the same a patient who develops Queens university. May, 2006. Trial ongoing. CME because of a glaucoma treatment (in this case 7. Clinical Trials Gov. US. National Institutes of Health. The Effect of Macugen in Patients with chronic, Postoperative the suspension of the prostaglandin and the medical cystoid macular edema. John Hopkins University. July, treatment with NSAIDs can be enough to reverse by 2006. Trial ongoing. complete the disease without any permanent loss of 8. Clinical Trials Gov. US. National Institutes of Health. To vision), that a CME caused by a chronic pars planitis compare therapeutic effect of intravitreal bevacizumab of difficult treatment (in this case a chronic CME can and triamcinolone in resistant uveitic cystoid macular lead to severe decrease of vision). edema. Shaheed Beheshti Medical University. Patients who are going to be operated, in particular September, 2006. Trial ongoing. 9. Flach AJ, Jampol LM, Weinberg D et al. Improvement anterior segment procedures, must be medicated since in visual acuity in chronic aphakic and pseudophakic the preoperative period, through the operation and cystoid macular edema after treatment with topical 0.5% during the postoperative time, with drugs that can ketorolac tromethamine. Am J Ophthtalmol 1991; decrease the development of CME, like steroids and 112:514-9. 248 Clinical Diagnosis and Management of Ocular Trauma 10. Furuichi M, Chiba T, Abe K, Kogure S, Iijima H, Tsukahara 28. Miyake K, Ibaraki N. Prostaglandins and cystoid macular S, Kashiwagi K. Cistoid macular edema associated with edema. Surv Ophthalmol 2002; 47(Suppl 1):S203-18. topical Latanoprost in glaucomatous eyes with a normal 29. Miyake K, Kayazawa F, Manabe R, et al. Indomethacin functioning blood-ocular barrier. J Glaucoma 2001; and the epinephrine-induced breakdown of the blood- 10:233-6. ocular barrier in rabbits. Invest Ophthalmol Vis Sci 11. Gass JDM, Norton EDW. Cystoid macular edema and 1988;29:332-4. papilledema following cataract extraction. A fluorescein, 30. Miyake K, Mibu H, Horiguchi M, et al. Inflammatory funduscopic and angiographic study. Arch Ophthalmol mediators in postoperative aphakic and pseudophakic 1966;76:646-61. baboon eyes. Arch Ophthalmol 1990;108:1764-7. 12. Handa J, Henry JC, Krupìn T et al. Extracapsular cataract 31. Miyake K, Miyake Y, Kuratomi R. Long-term effects of extraction with posterior chamber lens implantation in topically applied epinephrine on the blood-ocular barrier patients with glaucoma. Arch Ophthalmol 1987;105: in humans. Arch Ophthalmol 1987;105:1360-3. 7659. 32. Miyake K, Miyake Y, Maekubo K et al. Incidence of 13. Hanna C, Sharp JD. Ocular absorption of indomethacin cystoid macular edema after retinal detachment surgery by the rabbit. Arc Ophthalmol 1972;88:196-8. and the use of topical indomethacin. Am J Ophthalmol 14. Heier JS, Steinert RF, Frederick AR. Cystoid macular 1985;100:510-9. edema associated with latanoprost use. Arch Ophthalmol 33. Miyake K, Ota I, Ibaraki N et al. Enhanced disruptionof 1998;116:680-2. the blood-ocular barrier and the incident of angiographic 15. Irvine SR. A new defined vitreous syndrome following cystoid macular edema by topical timolol and its cataract surgery interpreted according to recent concepts preservative in early postoperative pseudophakia. Arch of the structure of the vitreous. Am J Ophthalmol Ophthalmol 2001;119:387-94. 1954;36:599-619. 34. Miyake K, Ota I, Maekubo K, Ichihashi S, Miyake S. 16. Jaffe NS, Clayman HM, Jaffe MS. Cystoid macular edema Latanoprost accelerates disruption of the blood-aqueous after intracapsular and extracapsular cataract extraction barrier and the incidence of angiographic cystoid macular with and without an intraocular lens. Ophthalmology edema in early postoperative pseudophakias. Arch 1982;89:25-9. Ophthalmol 1999;117:34-40. 17. Jampol LM, Sanders DR, Kraff MC. Prophylaxis and 35. Miyake K, Shirasawa E, Hikita M, et al. Synthesis of therapy of aphakic cystoid macular edema. Suv prostaglandin E in rabbit eyes with topically applied Ophthalmol 1984;28:535-9. epinephrine. Invest Ophthalmol Vis Sci 1988;29:332-4. 18. Kass MA, Holmberg NJ. Prostaglandin and thronboxane 36. Miyake K, Sugiyama S, Norimatsu I et al. Prevention of synthesis by microsomes of rabbit ocular tissues. Invest cystoid macular edema after lens extraction by topical Ophthalmol Vis Sci 1979;18:166-71. indomethacin. Albrecht von Graefes Arch Klin Exp 19. Kent D, Vinores SA, Campochiaro PA. Macular Ophthalmol 1978;209:83-8. oedema:The role of soluble mediators. Br J Ophthalmol 37. Miyake K. Prevention of cystoid macular edema after lens 2000;84:542-5. extraction by topical indomethacin. A preliminary report. 20. Kolker AE, Becker B. Epinephrine maculopathy. Ach Albrecht Von Graefes Arch Klin Exp Ophthalmol 1977; Ophthal 1968;79:552-62. 203:81-8. 21. Liesegang TJ, Bourne WJ, Ilstrup DM. Secondary surgical 38. Mondino BJ, Nagata S, Glovsky MM. Activation of the and neodimium: YAG laser discussions. Am J alternative complement pathway by intraocular lenses. Ophthalmol 1985;100:164-8. Invest Ophthalmol Vis Sci 1985;26:905-8. 22. Lima MC, Paranhos A, Salam S, et al. Visually significant 39. Nishi O, Nishi K, Imanishi M. Synthesis of interleukin- cystoid macular edema in pseudophakic and aphakic 1 and prostaglandin E2 by lens epithelial cells of human patients with glaucoma receiving Latanoprost. J of cataracts. Br J Ophthalmol 1992;76:338-41. Glaucoma 2000;9:317-24. 40. Ohrloff C, Schalnus R, Rothe R, et al. Role of the posterior 23. Malecaze F, Chollet P, Cavrois E et al. Role of interleuquin capsule in the aqueous-vitreous barrier in aphakic and 6 in the inflammatory response after cataract surgery. An pseudophakic eyes. J Cataract Refract Surg 1990;16: experimental and clinical study. Arch Ophthalmol 1991; 198-201. 109:1681-3. 41. Ozaki H, Hayasi H, Vinores SA et al. Introvitreal sus- 24. Mehelas TJ, Kollarits CR, Martin WG. Cystoid macular tained release of VEGF causes retinal neovascularization edema presumably induced by dipivefrin hydrochloride in rabbits and breakdown of the blood-retinal barrier in (Propine). Am J Ophthalmol 1982;94:682. rabbits and primates. Exp Eye Res 1997;64:505-17. 25. Meredith TA, Kenyon KR, Singerman LJ, et al. Perifoveal 42. Pollack A, Leiba H, Bukelman A, et al. Cystoid macula vascular leakage and macular edema after intracapsular oedema following cataract extraction in patients with cataract extraction. Br J Ophthalmol 1976;60:765-76. diabetes. Br J Ophthalmol 1992;76:221-4. 26. Michels RG, Maumenne AE. Cystoid macular edema 43. Rossetti L, Chaudhuri J, Diickersin K. Medical profilaxis associated with topically applied epinephrine in aphakic and treatment of cystoid macular edema after cataract eyes. Am J Ophthalmol 1975;80:379-88. sugery. The results of a meta-analysis. Ophthalmology 27. Miyake K, Ibaraki N, Goto Y, Oogiya S, Ishigaki J, Ota 1998;105:397-405. I, Miyake S. ESCRS Binkhorst lecture 2002: Pseudopha- 44. Schumer RA, Camras CB, Mandahl AG. Putative side kic preservative maculopathy. J Cataract Refract Surg effects of prostaglandin analogs. Sur Ophthalmol 2002;47 2003;29:1800-10. (Suppl 1):S219-30. Management of Cystoid Macular Edema 249

45. Schumer RA, Camras CB, Mandalh AK. Latanoprost and 51. Wand M, Gaudio AR, Shields MB. Latanoprost and cystoid macular edema: Is there a causal relation? Current cystoid macular edema in high risk aphakic or pseudo- Opin Ophthalmol 2000;94-100. phakic eyes. J Cat Refract Surgery 2001;27:1397-1401. 46. Sjoquist B, Almegard B, Khalilef V, et al. The 52. Wand M, Gaudio AR. Cystoid macular edema associated bioavailability of Xalatan in the human eye. Invest with ocular hypotensive lipids. Am J Ophthalmol Ophthalmol Vis Sci 1997;38:S248. 2002;133:403-5. 47. Solomon LD. Efficacy of topical flubriprofen and 53. Wand M, Shields BM. Cystoid macular edema in the era indomethacin in preventing pseudophakic cystoid of ocular hypotensive lipids. Am J Ophthalmol 2002; macular edema. Flubiprofen-CME Study Group I. J 133:393-7. Cataract Refract Surg 1995;21:73-81. 54. Warwar RE, Bullock JD, Deepti B. Cystoid macular 48. Thomas JV, Gragoudas ES, Blair NP et al. Correlation edema and anterior uveitis associated with latanoprost of epinephrine use and macular edema in aphakic use. Experience and incidence in a retrospective review glaucomatous eyes. Arch Ophthalmol 1978;96:625-8. of 94 patients. Ophthalmology 1998;105:263-8. 49. Ursell PG, Spalton DJ, Withcup SM et al. Cystoid macular edema after phacoemulsification: Relationship to blood- 55. Weisz JM, Bressler NM, Bressler SB, et al. Ketorolac aqueous barrier damage and visual acuity. J Cataract treatment of pseudophakic cystoid macular edema Refract Surg 1999;25:1492-7. identified more than 24 months after cataract extraction. 50. Vinores SA, Sen H, Campochiaro PA. An adenosine Ophthalmology 1999;106:1656-9. agonist and prostaglandin E1 cause breakdown of the 56. Yousufzai SYK, Abdel-Latif AA. Prostaglandin F2α and blood-retinal barrier by opening tight junctions between its analogs induce release of endogenous prostaglandins vascular endothelial cells. Invest Ophthalmol Vis Sci in iris and ciliary muscles isolated from cat and other 1992;33:1870-78. mammalian species. Ex Eye Res 19996;63:305-10. CHAPTER

Managing Intraoperative Floppy Iris Syndrome 39 David F Chang (USA)

Introduction Alpha-1 receptors also mediate contraction of the iris dilator muscle, and we proposed that loss of dilator In 2005, John Campbell and I first described a new muscle tone and rigidity was the cause of the floppy small pupil syndrome associated with systemic iris. Furthermore, we postulated a semi-permanent tamsulosin that we named intraoperative floppy iris effect because of several cases of IFIS in patients who 1 syndrome (IFIS). In addition to a tendency for poor had discontinued tamsulosin several years before pupil dilation, we identified a triad of intraoperative surgery. Indeed, in a prospective trial, stopping signs that characterize IFIS—iris billowing and tamsulosin preoperatively did not prevent or decrease floppiness, iris prolapse to the main and side incisions, the severity of IFIS.2 1 and progressive intraoperative miosis (Fig. 39.1). Since our initial report, it has become clear that Particularly when such iris behavior is unexpected, the other systemic alpha-1 blockers such as doxazosin rate of complications such as posterior capsule rupture, (Cardura), terazosin (Hytrin), and alfuzosin (Uroxatral) 1,2 vitreous loss, and iris trauma is increased with IFIS. can also cause IFIS. However, the frequency and Tamsulosin (Flomax), a systemic alpha-1 severity of IFIS is much less with these non-specific antagonist, is the most widely prescribed treatment alpha-1 antagonists, as compared with tamsulosin.3 worldwide for benign prostatic hyperplasia (BPH), This difference may relate to the much greater affinity which is characterized by increased urinary frequency. and specificity of tamsulosin for the alpha-1A receptor Systemic alpha-1 antagonists improve the lower urinary sub-type that predominates in both the prostate and tract symptoms of BPH by relaxing the smooth muscle the iris dilator muscle.2,4 in the prostate and lower bladder wall. By allowing IFIS can be classified as being mild (good dilation; more complete emptying of the bladder, these some iris billowing without prolapse or constriction), medications decrease night time urinary frequency. moderate (iris billowing with some constriction of a moderately dilated pupil), or severe (classic triad and poor preoperative dilation). In a prospective study of 167 eyes in patients taking tamsulosin, the distribution of IFIS severity using this scale was as follows: 10% no IFIS, 17% mild, 30% moderate, and 43% severe.2 There can be significant variability in the severity of IFIS between different patients, and even between two eyes of the same patient. This makes it difficult to determine whether one pupil management strategy is superior to another. In fact, the various IFIS techniques discussed in this chapter can be combined and it is therefore helpful to master several complimentary approaches. As general surgical principles for IFIS patients, one should make a well-constructed shelved incision, Fig. 39.1: Intraoperative floppy iris syndrome in a patient taking tamsulosin. In addition to iris prolapse to the phaco perform hydrodissection more gently than usual, and and side port incision, the pupils has constricted limiting reduce the irrigation and aspiration flow parameters visibility if possible. Bimanual microincisional cataract surgery Managing Intraoperative Floppy Iris Syndrome 251 may be helpful, particularly for mild to moderate IFIS.1 This technique utilizes water tight incisions and allows the surgeon to dissociate the irrigation and aspiration currents. Keeping the irrigation inflow anterior to the iris can lessen the iris billowing and prolapse. In our original report, we noted that mechanical pupil stretching, performed with or without partial sphincterotomies, did not prevent iris prolapse or pupil constriction with IFIS.1 Excessive iris manipulation may in fact worsen the iris prolapse in IFIS. Instead, we found that mechanical pupil expansion, such as with iris retractors, was far more effective. Subsequently, several other strategies for the surgical management of IFIS have been suggested, and are outlined below. Because IFIS results from alpha-1 receptor blockade of the iris dilator muscle, a variety of pharmacologic strategies for managing IFIS have been proposed.2, 4-10 As first suggested by Sam Masket, preoperative atropine drops (e.g., 1% t.i.d. for 1-2 days preoperatively) can provide sufficient cycloplegia to prevent intraoperative miosis2,5,6. However, as a single strategy atropine alone is often ineffective for more severe cases of IFIS.2 Stopping tamsulosin preoperatively is of unpredictable and questionable value, and has the potential to cause acute urinary retention in patients with severe BPH. This is particularly true if preoperative atropine is used. Direct intracameral injection of alpha agonist drugs is an excellent pharmacologic strategy for preventing or mitigating IFIS. Richard Packard first reported using intracameral phenylephrine,7, 8 and Joel Shugar Figs 39.2A and B: Pupil diameter in tamsulosin patient before subsequently suggested using epinephrine for this (A) and after (B) injection of 0.2 ml of intracameral epinephrine solution (bisulfite-free 1:1000 mixed 1:3 with BSS) purpose.9 By presumably saturating the alpha 1-A receptors, these agents can further expand the pupil (Figs 39.2A and B). Alpha agonists may also prevent billowing and prolapse by increasing iris dilator smooth muscle tone and maximizing iris rigidity. Preserved solutions should be avoided and one should use a diluted mixture (e.g., 1:1000 bisulfite-free epinephrine (American Regent) mixed 1:3 with BSS or BSS+) in order to buffer the acidic pH of the commercial preparation. Finally, Sam Masket reported excellent results with the synergistic combination of preoperative topical atropine with intracameral epinephrine in a small series patients taking tamsulosin.6 As first described by Bob Osher and Doug Koch, Healon 5 (Advanced medical optics) is a maximally cohesive ophthalmic visco-surgical device that is particularly well-suited for viscomydriasis and for Fig. 39.3: Healon 5 viscomydriasis in a patient with IFIS following removal of the cortex blocking iris prolapse in IFIS2, 10 (Fig. 39.3). However, to avoid immediately aspirating Healon 5 the surgeon proposed injecting Healon 5 peripherally over the iris, must employ low flow and vacuum parameters (e.g. and then filling the central chamber with a dispersive < 175-200 mmHg; < 26 ml/min). This strategy is agent such as viscoat (Alcon) to create a Healon 5 therefore less suitable if a surgeon wishes to use high “donut”. The viscoat will better resist aspiration and vacuum settings for denser nuclei. Wendell Scott has delay the evacuation of Healon 5. For surgeons 252 Clinical Diagnosis and Management of Ocular Trauma the Milvella Perfect Pupil are disposable PMMA pupil expansion rings whose grooved contours are threaded alongside the pupillary margin using metal injectors (Figs 39.4A to C). In contrast, a disposable plastic injector is used to insert Eagle Vision’s Graether disposable silicone pupil expansion ring. All of these rings are more difficult to position if the pupil is less than 4 mm wide or if the anterior chamber is shallow. Iris retractors are a more popular mechanical strategy for pupil expansion in IFIS. Placement of the hooks in a diamond configuration has several significant advantages11 (Figs 39.5A and B). The subincisional hook retracts the iris downward, and out of the path of the phaco tip. This maximizes exposure in front of the phaco tip while the nasal hook facilitates chopper placement. One millimeter limbal paracenteses are made in each quadrant, including a separate stab incision made just posterior to the temporal clear corneal incision. In this way, the subincisional hook and the

Figs 39.4A to C: Management of IFIS using a Morcher PMMA pupil expansion ring. (A): Ring is inserted with an injector. (B): Ring is threaded along pupil margin to maintain a constant diameter. (C): Following removal of the ring, iris prolapse and pupil constriction occur during removal of the viscoelastic Figs 39.5A and B: Management of IFIS using 4-0 prolene favoring high vacuum and flow settings, DisCoVisc iris retractors in a patient taking tamsulosin. (A): retractors (Alcon) has been advocated by Satish Modi. placed in a “diamond” configuration, with the sub-incisional A final set of strategies utilizes devices to retractor placed directly behind the clear corneal phaco mechanically expand and maintain the pupil diameter incision. (B): Pupil constriction and iris prolapse occurring during surgery. Both the Morcher 5S Pupil Ring and after removal of the iris retractors Managing Intraoperative Floppy Iris Syndrome 253 phaco tip access separate entry tracks. If the pupil is mechanical expansion devices insure the most reliable fibrotic, overstretching it with iris retractors can cause and optimal surgical exposure for severe IFIS, and bleeding, sphincter tears, and permanent mydriasis. should be considered when other complicating risk This typically does not occur with the IFIS pupil, which factors (e.g. dense nuclei, narrow angles, posterior is so elastic that it readily springs back to physiologic synechiae, weak zonules, pseudoexfoliation, etc.) are size despite being maximally stretched. Options include present. 6-0 nylon disposable retractors (Alcon) or reusable 4- 0 polypropylene retractors (Katena, FCI). Being of the same size and rigidity as an IOL haptic, the latter are References easier to manipulate and can be repeatedly autoclaved making them more cost effective to use. 1. Chang DF, Campbell JR. Intraoperative floppy iris syndrome associated with tamsulosin (Flomax). J Cataract It is much easier and safer to insert iris retractors Refract Surg 2005;31:664-73. and pupil expansion rings prior to creation of the 2. Chang DF, Osher RH, Wang L, Koch DD. A prospective capsulorhexis. If the pupil dilates very poorly or billows multicenter evaluation of cataract surgery in patients during injection of intracameral lidocaine, one should taking tamsulosin (Flomax). Ophthalmology 2007;114: suspect severe IFIS and consider using these 957-64. mechanical devices. Often, the pupil dilates reasonably 3. Blouin M, Blouin J, Perreault S, et al. Intraoperative well-preoperatively, and it is not until after floppy iris syndrome associated with Alpha-1 adrenoreceptors. Comparison of tamsulosin and hydrodissection or during phaco that the prolapse and alfuzosin. J Cataract Refract Surg 2007;33:1227-34. miosis occur. Healon 5 and intracameral epinephrine 4. Chang DF. Chapter 10: Intraoperative floppy iris are excellent “rescue” techniques in this situation where syndrome. In Agarwal A, ed. Phaco Nightmares. it is difficult to visualize the capsulorhexis edge. If one Conquering Cataract Catastrophies. Slack Publishing Inc. chooses to insert iris retractors at this point, one should 2006. retract the pupil margin with a second instrument to 5. Bendel RE, Phillips MB. Preoperative use of atropine to avoid hooking the capsulorhexis margin with the prevent intraoperative floppy-iris syndrome in patients retractors. taking tamsulosin. J Cataract Refract Surg 2006; 32:1603-5. Eliciting a history of current or prior alpha-blocker 6. Masket S, Belani S. Combined preoperative topical use should alert surgeons to anticipate IFIS and to atropine sulphate 1% and intracameral nonpreserved employ these alternative strategies either alone or in epinephrine hydrochloride 1:2500 for management of combination. A prospective, multi-center prospective intraoperative floppy iris syndrome. J Cataract Refract trial using these techniques in 167 consecutive eyes Surg 2007;33:580-82. from patients on tamsulosin demonstrated excellent 7. Gurbaxani A, Packard R. Intracameral phenylephrine to outcomes and only a 0.6% posterior capsular rupture prevent floppy iris syndrome during cataract surgery in 2 patients on tamsulosin. Eye 2005: Nov 11; [Epub ahead rate. Because of the variability in IFIS severity of print]. associated with tamsulosin and other alpha-1 blockers, 8. Manvikar S, Allen D. Cataract surgery management in surgeons may consider using a staged approach in patients taking tamsulosin. J Cataract Refract Surg 2006; dealing with this condition.8 Pharmacologic measures 32:1611-4. alone are often adequate for managing the pupil in 9. Shugar, JK. Intracameral epinephrine for prophylaxis of mild to moderate IFIS cases. Even if they fail to expand IFIS [letter]. J Cataract Refract Surg 2006; 32: 1074-5 the pupil, intracameral alpha agonists can reduce or 10. Arshinoff SA. Modified SST-USST for tamsulosin- associated intraocular floppy iris syndrome. J Cataract prevent iris billowing and prolapse by increasing iris Refract Surg 2006;32:559-61. dilator muscle tone. If the pupil diameter is still 11. Oetting TA, Omphroy LC. Modified technique using inadequate, viscomydriasis with Healon 5 can further flexible iris retractors in clear corneal surgery. J Cataract expand it for performing the capsulorhexis. Finally, Refract Surg 2002;28:596-98. CHAPTER

Toxic Anterior Segment Syndrome 40 Simon P Holland, Douglas W Morck, Richard Mathias, Tracy L Lee, Gina Chavez, Yumi G Ohashi (Canada)

Introduction first day postoperatively, whereas IE presents later, usually day 3 to 7, accompanied by pain and vitreal Toxic anterior segment syndrome (TASS) is increasingly involvement.10-13 Figure 40.1 shows a case of TASS recognized and reported as an early complication of with characteristic features presenting on the day of 1-9 cataract surgery. Postoperative inflammation of surgery, and Figure 40.2 shows a case of IE. Rarely unknown cause was previously considered as a sterile low grade vitritis may be seen in severe cases of TASS endophthalmitis although vitritis is uncommon. Multiple probably from some spillover from the anterior outbreaks have recently been reported stimulating segment. In such cases the vitritis is a result of culture- extensive research and the creation of a task force. negative or sterile endophthalmitis rather than The understanding of TASS is thus rapidly evolving infectious endophthalmitis.10,11 Vitreous taps and more and will likely lead to improved prevention and recently PCR can be used to differentiate the two management of outbreaks. conditions.14 When the diagnosis is unclear the practi- tioner should treat as IE due to the severity of its sequelae.15,16 Diagnosis and Clinical Features DIAGNOSIS TASS presents as early and severe postoperative inflammation following anterior segment surgery. • Postoperative Symptoms include fibrin formation, corneal edema, • Anterior segment inflammation minimal or no pain, and the absence of vitreous • Unknown cause. involvement.10 Differentiation from conditions such as infectious endophthalmitis (IE) is critical. Table 40.1 DIFFERENTIAL DIAGNOSIS summarizes the key differences between TASS and IE. Pain and/or vitritis usually indicates infectious TASS usually presents on the day of surgery or the endophthalmitis.

TABLE 40.1: Differential diagnosis TASS vs infectious endophthalmitis Presentation TASS Infectious endophthalmitis

Onset (usual) 6 to 24 hours 3 to 7 days postoperatively postoperatively Symptoms Blurred vision Pain, blurred vision Cornea Edema Edema Anterior chamber Cells Cells Fibrin, membranes Fibrin variable Hypopyon Hypopyon External findings None Variable: Lid swelling Discharge Conjunctival chemosis Vitreous Clear, rarely vitritis Vitritis (primarily Response to topical (culture negative) culture positive) steroids Rapid improvement to No improvement resolution within days Toxic Anterior Segment Syndrome 255 • Fibrin/membranes • Corneal edema • No or minimal pain.

Pathology Changes to the pH and osmolality or the inadvertent introduction of an antigen can initiate a cellular response. The histological examinations of corneal buttons taken from patients with TASS showed an almost absent endothelial cell layer, with the epithelium thinned and the stroma diffusely thickened.8 The massive damage to the endothelial layer is a result of its sensitivity to toxic agents.11 Fig. 40.1: TASS on the first postoperative day (Courtesy: SLACK Inc)10 Epidemiology and Etiology The epidemic in the United States prompted the American Society of Cataract and Refractive Surgery (ASCRS) to assemble a special task force to deal with the growing problem.19 The task force reported that over 100 centers experienced an outbreak of TASS prior to May 2006 and this only included clinics that chose to self report.20 Many outbreaks may be unreported given the potential for poor publicity, and regulatory and liability issues. The increasing incidence of TASS is likely due to an actual rise in numbers rather than simply an increased awareness. Growing interest in TASS is resulting in the rapid expansion of knowledge regarding the cause and therefore the management Fig. 40.2: Early endophthalmitis presenting on the day and prevention of the condition. of surgery (Courtesy: SLACK Inc)10 The etiology of TASS is speculative, although there is increasing acceptance of its multifactorial causation. Toxic Endothelial Cell Destruction Syndrome The ASCRS task force, and several other researchers (TECDS) is a related syndrome that specifically have complied a list of possible risk factors and potential indicates localized corneal endothelial damage and is 3,5-8,20-23 2,5,7,17 causes of TASS. These potential etiology factors considered to be within the continuum of TASS. 10 The clinical features of TASS have been well are listed in Table 40.2. It is likely that individual described in previous literature.1,2,5,7,10,11 Most patients TASS cases not occurring in an outbreak are due to are asymptomatic but may have blurred vision and complications during surgery such as iris stretching, 10 redness within 24 hours of surgery . Pain is almost retained cortex and a prolonged surgery. Multiple never a feature although there may be mild factors have been associated with TASS outbreaks discomfort. Characteristic clinical features include a ranging from inappropriate chemical composition of severe anterior chamber cellular response with fibrin, irrigating solutions to the presence of endotoxins on membrane formation and the occasional hypopyon. poorly sterilized instruments.13 Corneal edema, described as limbus to limbus, is frequently present.10,11,18 When patients present INTRAOCULAR MEDICATIONS, IRRIGATING predominantly with corneal edema and less marked SOLUTIONS AND BALANCED SALT SOLUTION anterior chamber inflammation the cause is more likely Many TASS outbreaks have been attributed to to be toxic agents (e.g. preservatives, ointments). contaminants, endotoxins and preservatives gaining access to the anterior chamber during or following FEATURES surgery.5,7,12 Outbreaks have been linked to external • Within 48 hours eye rinses, such as Eye Stream (Alcon, Ft. Worth, Texas) • Cellular reaction 2-4+ due to the preservative content.5 Ointments applied 256 Clinical Diagnosis and Management of Ocular Trauma

TABLE 40.2: Potential etiology factors associated Etiology with TASS (previously published: SLACK Inc).10 • Edema—toxic, e.g. preservatives Intraocular causes • Inflammation—endotoxin. Incomplete cortex removal, pupil stretching, and possible immunological differences (as with DLK in atopic Causation patients). • Sterilization issues most common Intraocular medication • Beware of re-usable cannulas. Dosing errors with antibiotics, preservatives, ointments8, and pH imbalance. Treatment Instrument contamination Bacterial endotoxins, dried debris, e.g. inadequate Conventional treatment is focused on the suppression cleaning of cannulas, persistence of detergents, irrigating of the inflammatory immune response and includes solutions, endotoxins in irrigating fluids (Endosol),10,24 topical steroids given every half hour to hour for the incorrect pH or composition of irrigating fluids. first three days followed by gradual tapering.10 During this acute period the patient should be monitored closely for anterior segment inflammation, corneal edema, and intraocular pressure (IOP). In particular postoperatively also have the potential to gain access monitor for an IOP increase several days following the to the anterior chamber. One study described a TASS initial presentation due to damage to the trabecular outbreak following the application of postoperative meshwork.11 Improvements are generally seen within ointments and tight eye patching.8 The use of the first 24 to 48 hours of steroid commencement. contaminated balanced salt solution (BSS) has also Anterior chamber washout has been reported but been associated with TASS outbreaks. Endotoxin was outcomes are uncertain and it is not generally recom- discovered in balanced salt solution (BSS) manufac- mended.10,11 When there is corneal and endothelial tured by Cytosol Laboratories (Lenoir, NC).10,24 toxicity a penetrating keratoplasty may be necessary. Points INSTRUMENT CONTAMINATION Rapid response to frequent steroid drops. Detergent residues left on reusable instruments have the potential to cause corneal toxicity.2,21 Prolonged cycle sterilization is needed to deactivate enzymes and Outcomes other active ingredients in detergents.11 TASS outbreaks have been associated with the dried residue on reusable Early diagnosis and treatment usually result in an cannulas.10 excellent outcome. Most mild cases clear within several 21 Impurities can also be present in sterilizer steam.9,22 days to weeks. Glaucoma is a potential complication An outbreak of TASS was associated with inadequate due to either initial trabeculitis or fibrin membrane 10 maintenance of steam sterilizer systems with resulting formation. Severe TASS can result in permanent copper, zinc, nickel, sulfate and silica impurities.9 endothelial damage, cystoid macular edema and Instruments can also become contaminated with permanently dilated pupil requiring corrective 21 endotoxin following short cycle steam sterilization.25 surgery. The sterilization process kills bacteria but does not inactivate endotoxin, which can be a potent initiator COMPLICATIONS of an inflammatory immune response and has been • Misdiagnosis associated with TASS outbreaks.10,11,22,26 • Glaucoma Ultrasound baths may also be a source of contami- • Corneal edema nation. Klebsiella pneumonia and bacterial endotoxin • Cystoid macular edema. were identified in the ultrasonic cleaning bath during one TASS outbreak.3 TASS is often associated with IOL implantation, but Investigation and Reporting more recently has also been observed following Outbreak investigation is difficult with the multifactorial placement of phakic IOL.18 It is important to consider etiology although sterilization issues usually IOL polishing compounds, as well as the chemical predominate. Consequences to an affected clinic structure of the lens as possible causes of TASS.6,23 may be severe with voluntary or mandated closure. Toxic Anterior Segment Syndrome 257 Proactive reporting to local regulatory authorities and Conclusion seeking support from colleagues, as well as academic and public health resources is advisable.10,27 TASS outbreaks have become of major concern in the ophthalmology community. The assembly of the CASE AND OUTBREAK DEFINITION TASS task force and the numerous recent studies on the subject has assisted in controlling TASS outbreaks. Postoperative anterior segment inflammation of The final task force report concluded that there was unknown cause occurring within 48 hours of surgery no one factor attributable to TASS outbreaks but rather with one or more of the following features: anterior multiple potential etiological factors. It appeared that chamber response 2+ or greater, fibrin, membranes, cleaning and sterilization of instruments for cataract 10 corneal edema without significant vitritis. Criteria for surgery was the most important of the identified factors. a TASS outbreak have not been established as they It is recommended that all reusable cannulas and 28 have for conditions such as DLK. However, any instruments be thoroughly flushed with sterile, occurrence of more than two affected patients should deionized/distilled water after cleaning at the conclusion raise concerns and merit investigation since this may of each case.29 rapidly escalate. Although TASS outbreak reports, at least in the United States, now appear to be declining it is DATA COLLECTION important to constantly monitor and improve cleaning Suggested data include; demographics, VA before and and sterilization protocols. Growing awareness resulting after surgery, symptoms, clinical features, day of in early diagnosis and treatment, with prompt surgery, day of onset and diagnosis, any associated dissemination of new information will hopefully conditions, subsequent management and outcome. It eliminate TASS as a significant complication of modern is important to record details of the surgical procedure cataract surgery. including instrument preparation and specifically any staffing or procedural changes made prior to the onset. Retrospective collection of data is difficult and it is References recommended to collect data and note changes as they 1. Monson MC, Mamalis N, Olson RJ. Toxic anterior happen making the creation of an epidemic curve less segment inflammation following cataract surgery. J problematic. Cataract Refract Surg 1992;18:184-9. 2. Breebaart AC, Nuyts RMMA, Pels E, et al. Toxic MICROBIAL INVESTIGATIONS endothelial destruction of the cornea after routine Bacterial culturing, biofilm sampling and analysis of extracapsular cataract surgery. Arch Ophthalmol 1990; 108:1121-5. steam distillate and BSS for endotoxin may help 3. Kreisler KR, Martin SS, Young CW, et al. Postoperative determine the cause of the outbreak. The sterilizer inflammation following cataract extraction caused by reservoir, internal tubing of the sterilizer, ultrasound bacterial contamination of the cleaning bath detergent. baths, cannulas and air and water supplies have proved J Cataract Refract Surg 1992;18:106-10. to be useful sampling areas.10,12,13 4. Nelson DB, Donnenfeld ED, Perry HD. Sterile TASS investigations are often difficult and require endophthalmitis after sutureless cataract surgery. careful planning. It is usually best to designate one Ophthalmolgy 1992; 99:1655-7. 5. Liu H, Routley I, Teichmann KD. Toxic endothelial cell staff member to manage the outbreak, including data destruction from intraocular benzalkonium chloride. J collection and media consultation. Another important Cataract Refract Surg 2001; 27:1746-50. issue to consider is the disclosure of TASS as a further 6. Jehan FS, Mamalis N, Spencer TS, et al. Postoperative risk of cataract surgery, particularly during a TASS sterile endophthalmitis (TASS) with the MemoryLens. J outbreak. Cataract Refract Surg 2000; 26:1773-7. Once an investigation has been concluded dissemi- 7. Eleftheriadis H, Cheong M, Saneman S, et al. Corneal nation of the findings will help other practitioners solve toxicity secondary to inadvertent use of benzalkonium chloride preserved viscoelastic material in cataract their TASS outbreaks or hopefully avoid them. The surgery. Br J Ophthalmol 2002; 86:299-305. TASS task force is one example of how this sharing 8. Werner L, Sher JH, Taylor JR, et al. Toxic anterior of knowledge has likely reduced the risk of further segment syndrome and possible association with outbreaks. ointment in the anterior chamber following cataract surgery. J Cataract Refract Surg 2006; 32:227-35. INVESTIGATION 9. Hellinger WC, Hasan SA, Bacalis LP, et al. Outbreak of toxic anterior chamber syndrome following cataract Suspect everything. surgery associated with impurities of autoclave steam 258 Clinical Diagnosis and Management of Ocular Trauma moisture. Infect Control Hosp Epidemiol 2006; www.ascrs.org/press_releases/Toxic-Anterior-Segment- 27(13):294-8. Syndrome-Outbreak-Preliminary-Report.cfm. 10. Holland SP, Morck DW, Chavez G, Lee, TL. Toxic anterior 20. The American Society of Cataract and Refractive Surgery segment syndrome. In Agarwal A (Ed). Refractive Surgery (ASCRS) (2005). Press release May 22, 2006: TASS Nightmares: Conquering Refractive Surgery Catastrophes. Outbreak Update. Retrieved June 1, 2006, from http:/ Thorofare, NJ: SLACK Incorporated. In press. /www.ascrs.org/press_releases/upload/Update 11. Mamalis N, Edelhauser HF, Dawson DG, et al. Toxic Briefing.doc. anterior segment syndrome. Review/update. J Cataract 21. Parikh C, Sippy BD, Martin DF, Edelhauser HF. Effects Refract Surg 2006; 32:324-33. of enzymatic sterilization detergents on the corneal 12. Holland SP, Chavex G, Morck D, Mathias. Toxic Anterior endothelium. Arch Ophthalmol 2002; 120:165-72. Segment Syndrome After Cataract Surgery Associated 22. Whitby JL, Hitchins VM. Endotoxin levels in steam and with Short-Cycle Sterilization presented at the ASCRS reservoirs of table-top steam sterilzers. J Cataract Refract Symposium on Cataract, IOL and Refractive Surgery, San Surg 2002; 18:51-2. Francisco, USA , March 17-22, 2006. Available at 23. Meltzer, DW. Sterile hypopyon following intraocular lens www.ascrs.org. Accessed June 12, 2006. surgery. Arch Ophthalmol 1980; 98:100-4. 13. Holland SP, Morck D, Lee T. Update on toxic anterior 24. US Food and Drug Administration. (2006). Patient segment syndrome. Current Opinion in Ophthalmology. advisory Feb 13th 2006; FDA-Requested Recall - Cytosol In press. Laboratories, Inc. Product Contains Dangerous Levels of 14. Van Gelder RN. Applications of the polymerase chain Endotoxin. Retrieved Feb. 14, 2006, from http:// reaction to diagnosis of ophthalmic disease. Surv www.fda.gov/bbs/topics/news/2006/NEW01315.html. Ophthalmol 2001; 45(3):248-58. 25. Holland SP, Mathias RG, Morck DW, et al. Diffuse 15. West ES, Behrens A, McDonnell PJ, et al. The incidence lamellar keratitis related to endotoxins released from of endophthalmitis after cataract surgery among the US medicare population increased between 1994 and 2001. sterilizer reservoir biofilms. Ophthalmol 2000; 107(7): Ophthalmology 2005; 112:1388-95. 1227-33. 16. Wallin T, Parker J, Jin Y, et al. Cohort study of 27 cases 26. Rietschel ET, Brade H. Bacterial endotoxins. Sci Am 1992; of endophthalmitis at a single institution. J Cataract 267:54-61. Refract Surg 2005; 31:735-41. 27. Mamalis, N. TASS outbreaks: What should we do? 17. Duffy RE, Brown SE, Caldwell KL, et al. An epidemic of Cataract and Refractive Surgery Today, July 2006;53-5. corneal destruction caused by plasma gas sterilization; 28. Bigham M, Enns CL, Holland SP, et al. Diffuse lamellar the toxic endothelial cell destruction syndrome team. keratitis complicating laser in situ keratomileusis; Arch Ophthalmology 2000;118:1167-76. postmarketing surveillance of an emerging disease in 18. Moshirfar M, Whitehead G, Beutler BC, et al. Toxic British Columbia, Canada, 2000-2002. J Cataract Refract anterior segment syndrome after Verisyse iris-supported Surg 2005; 31:2340-44. phakic intraocular lens implantation. J Cataract Refract 29. The American Society of Cataract and Refractive Surgery Surg 2006; 32(7):1233-7. (ASCRS). (2005). Press release September 22, 2006: 19. The American Society of Cataract and Refractive Surgery Toxic Anterior Segment Syndrome (TASS) Outbreak Final (ASCRS) (2005). Press release June 22, 2006: TASS task Report. Retrieved September 22, 2006, from http:// force. Retrieved August 15, 2006, from http:// www.ascrs.org/press_releases/Final-TASS-Report.cfm. CHAPTER

Small Pupil Phaco: An Innovative Technique 41 Boris Malyugin (Russia)

Introduction the cornea. The technique of pupillary membranec- tomy with the forceps presented by R.Osher6 is also In spite of several recent innovations in cataract surgery effective in some cases. patients with small pupils are always challenging. The second method—mechanical stretching of the Poor pupil dilation we can be observed in cases pupil was introduced by Miller and Keener.8 It is usually complicated by pseudoexfoliation syndrome, uveitis, effective for small pupils with the rigid iris tissue which posterior synechiae, trauma or previous intraocular is usually caused by prior miotic use, pseudoexfoliation, surgery.1-6 or posterior synechiae. Stretching can be achieved with Significant amount of patients who present for the spatula, Sinskey hook or special instrument. Beehler phacoemulsification cataract surgery have pupils that pupil dilator.2 Usually a pair of hooks is introduced do not respond adequately despite several through 2 stab incisions in the cornea engage the iris pharmacological attempts with different mydriatic sphincter. After that the hooks are pulled in opposite agents. Inadequate pupil dilation can decrease directions. This maneuver creates microscopic sphincter visualization during all stages of the phacoemulsification tears which enlarge the pupil aperture. The main including capsulorhexis, hydrodissection, lens nucleus advantage of this procedure is that it is relatively simple disassembly and IOL insertion. This compromises the and requires no special instruments. Mechanical surgery and increases the risk for complications. stretching of the pupil usually provides sufficient access Pharmacological therapy with the use of nonsteroi- to the lens and maintains the pupil diameter dal eyedrops or strong mydriatics such as phenylephrine intraoperatively. 10% sometimes lead to unwanted ocular and systemic Sometimes iris stretching technique leads to instabi- side effects. Intracameral mydriatics is an effective, and lity of it’s papillary margin, which can compromise safe addition to topical mydriatics in phacoemulsifica- cataract surgery. In some eyes and stretching technique tion.7 In some cases their use can simplify preoperative fails to adequately expand the pupil.9 The drawback patients preparation and in certain high-risk groups, of this technique is that it is creating permanent damage may reduce the risk for cardiovascular side effects. of the iris sphincter. The micro tears of the sphincter Unfortunately present pharmacological approaches muscle are usually clinically asymptomatic but of managing a small pupil during cataract surgery have sometimes result in bleeding and pigment dispersion limitations. Most surgeons decide to dilate the pupil postoperatively. In a study of stretch pupilloplasty by mechanically at the time of the surgery if pharmaco- Dinsmore10 10% of 50 patients developed an enlarged logical agents fail. atonic pupil postoperatively. All patients had a history There is no general recommendation or solution of injury or inflammatory disease. to the small pupil problem because the strategies for Partial-thickness iris sphincter cuts made with micro pupil enlargement greatly depend on surgeon skill and scissors is a common pupil enlargement technique.11 preferences, as well as on intraoperative situation. The cutting method is more controlled but requires There are four main dilation methods: the first is the multiple maneuvers of the scissors inside the anterior synechiolysis, the second is mechanical stretching, the chamber which can result in corneal endothelial third is the cutting method and the fourth is the iris damage. The disadvantages are the same as those with retraction. the stretching method. In the first method—the surgeon separates the Suboptimal pupil dilation in response to the adhesions between the iris, the lens capsule and/or preoperative mydriatic protocols and minimal efficacy 260 Clinical Diagnosis and Management of Ocular Trauma of pupil stretching techniques is a usual indication to Masket19 and Yuguchi and coauthors20 recommends the intraoperative use of iris hooks or other mechanical the pupil not be stretched by the hooks to larger than pupil dilation devices. For the iris retraction several a 5.0 mm square because overstretching produces devices have been introduced in the clinical practice. irregular atonic pupils postoperatively. Novak21 suggests The main disadvantages of these devices include the the use of hooks with rigid pupils smaller than 3.0 mm bulkiness and rigidity. They are difficult to insert, (4.0 mm with a hard nucleus) and smaller than 4.0 remove, and manipulate through a small incision. to 5.0 mm for an inexperienced surgeon. In extremely Graether12 developed a pupil expander that small and rigid pupils he prefers combining the use according to his data is superior to other methods of of hooks with a radial sphincterotomy. pupil enlargement, causing less sphincter trauma and During engagement of the pupillary edge with the fewer cases of permanent pupil size alteration. Pupil iris hook, it may catch and damage the capsule, leading dilation technique with the hydrogel ring reported by to an anterior capsule tear that may extend to the Siepser6 has a potential benefits but very limited clinical periphery. To avoid this problem, a drop of viscoelastic use. The Perfect Pupil device (Milvella) is a disposable material should be injected between the iris and the polyurethane ring with the 0.24 mm flanged groove capsule before the hook is inserted. The other useful throughout the length of the ring and an integrated technique is to keep the hook parallel to the iris plane arm that allows insertion and removal from the anterior during the insertion and to tilt it slightly posterior right chamber at the end of surgery.11 near the pupillary edge to engage the iris only. The Retracting the iris tissue rather than cutting it as iris hooks may become loosened during surgery. Their in a classic sector iridectomy is much simpler and results tips may become dislocated, no longer holding the in a much better postoperative pupil appearance. pupillary edge. This can cause some problems including Mackool13 was the first one who described a 4-point iris aspiration and chafing from contact with the iris retractor configuration for phacoemulsification. He phacoemulsification needle. developed metal iris retractors connected to small Small degrees of pupil dysfunction are common blocks of titanium. The latter allows for stabilization place after cataract surgery with and without iris mani- of the hooks during the retraction of the iris. This pulation but usually this causes no subjective method was enhanced with the introduction of the symptoms. Halpern and coauthors22 found an flexible iris retractor by de Juan and Hickingbotham.14 incidence of postoperative atonic pupil of 1.1% after Traditionally, 4 evenly spaced retractors are placed phacoemulsification, with pupil diameters ranging from through limbal paracentheses 90 degrees apart from 6.0 to 8.0 mm. one another. The corneal incision is centered on 1 of Most of the surgical maneuvers for enlarging the the 4 sides of the square.15 Some surgeons use iris pupil and preventing its intraoperative constriction are retractors in a triangular pattern decreasing the number not safe enough. They can lead to an increased risk of additional corneal incisions. The use of the iris hooks of iris sphincter tear, bleeding, iris damage, posterior may lead to the damage of the pupillary margin capsule tears, and loss of the vitreous body. The intraoperatively producing a semimydriatic non- postoperative complications can include an atonic pupil reacting pupil postoperatively. of irregular shape with poor cosmetic result, and Modification of the original square retractor photophobia. configuration is described by16 the rotation of the square The rate of occurrence of iris prolapse has been improves lens access in clear corneal phacoemulsification reported between 0.3% and 1% in complicated cataract by orienting the phacoemulsification needle along the cases.23 Allan24 described one of the critical factors of diagonal. This was called by Dupps and Oetting iris prolapse during phaco which relates to fluid velocity. “diamond configuration” of retractors.17 Advantages Allan’s model considers the Bernoulli principle as the of this technique include ease of conversion from most important because when the velocity of fluid phacoemulsification, optimal orientation of the maxi- passing through the anterior chamber increases, the mum pupil diameter nucleus expression or intracapsular force exerted on the iris increases by the square of lens removal, and conservation of iris tissue. the velocity. Birhall18 assessed the effect on pupil shape and We calculated the speed of the emulsion in the circumference of various flexible iris hook positions. anterior chamber during the phaco procedure with the He confirmed that malpositioned iris hooks may Millenium CCS (Bausch and Lomb) for US handpiece increase pupil stretching with possible deleterious effects settings: 1.0 mm Microflow US needle, vacuum 300 mm on postoperative pupil function. He recommends Hg, bottle height 85 cm, and I/A handpiece settings: using additional fifth hook to create a pentagonal pupil coaxial handpiece, 0.3 mm opening, vacuum 550 mm that reduces pupil stretching by 17%. Hg, bottle height 90 cm. For the calculation we utilized Small Pupil Phaco: An Innovative Technique 261

Fig. 41.1: Fluid velocity distribution along the line connecting the opposite points of the anterior chamber angle (X1–X2) in case when the US handpiece location in the middle of the anterior chamber at the iris plane

Fig. 41.2: Fluid velocity distribution along the line connecting the opposite points of the anterior chamber angle (X1–X2) in case when the US handpiece is location in the middle of the lens nucleus the equation of Navie-Stocks. The calculations were zones of high (more than 120 cm/sec) medium (80- performed for the two positions of the handpiece: in the 120 cm/sec) and low (80 cm/sec) fluid velocities are center of the anterior chamber at the iris plane represented. (Fig. 41.1) in the middle of the capsular bag The pupil often dilates poorly in atrophic irises, with (Fig. 41.2) and close to the center of the posterior significantly decreased iris tone unable to withstand capsule (Fig. 41.3). the fluidic currents in the anterior chamber and Figures 41.4 and 41.5 represent the color coded maintain the correct position of the iris. These map of fluid velocity distribution around the US and calculations give us some conclusions. In small pupil irrigating-aspirating handpiece. The areas of the highest iris tissue is located closer to the zone of the high fluidic currents are located in the angle of 40 to 60 degrees currents that is why it is more likely to be aspirated with the apex at the end of the aspiration orifice. Three into the US or IA handpiece. Decreasing of flow 262 Clinical Diagnosis and Management of Ocular Trauma

Fig. 41.3: Fluid velocity distribution along the line connecting the opposite points of the anterior chamber angle (X1–X2) in case of US handpiece location close to the center of the posterior capsule

Fig. 41.4: Fluid velocity distribution around the Fig. 41.5: Fluid velocity distribution around the tip of handpiece tip of the US irrigating-aspirating handpiece

parameters is an important factor of preventing iris tamsulosin (Flomax). The intraoperative diagnostic damage during phacoemulsification. Not only reducing triad of this symptom is fluttering and billowing of the the flow can make an appreciable difference in these iris stroma, a tendency to iris prolapse through the cases, but also central positioning and minimal main and/or side-port incisions, and progressive movements of the handpiece are also important to constriction of the pupil during surgery. Stretching of prevent iris damage. Endocapsular lens nucleus the pupil is ineffective in IFIS because the iris pupil fragmentation is much safer because the areas of the margin remains elastic and the pupil immediately highest fluidics currents are located inside the capsular snaps back to its original size following attempts at bag away from the corneal endothelium and iris. stretching it. Chang and Campbell25 recently described the Viscomydriasis with high viscosity OVDs such as intraoperative floppy-iris syndrome (IFIS) associated Healon5 are very useful in small pupil phaco cases. with systemic administration of the Ü-1A antagonist S.Arshinoff26 described a technique using ophthalmic Small Pupil Phaco: An Innovative Technique 263 viscosurgical devices to perform cataract surgery in patients taking tamsulosin. This method uses a combination of the two OVDs. The lower-viscosity dispersive OVD which is highly retentive despite the presence of moderate fluid turbulence is injected in the periphery of the anterior chamber and covers the endothelial layer and the iris. The viscoadaptive central layer of Healon5, according to S.Arshinoff adds a relatively rigid OVD roof above the surgical space and adds rigidity to the OVD structure to keep the iris from moving and the Viscoat in place. The BSS layer just over the pupillary space and below viscoadaptive central layer provides working space for the phaco tip. The Fig. 41.7: The principle of iris pupillary margin fixation surgeon is working in the endocapsular space and with the curl of IQ-ring Healon5 is not attracted into the phaco tip and the The insertion of IQ-ring is carried out through the OVD shell structure remains intact throughout the case. This technique gives satisfactory iris stability and permits main incision. The pupil expander is positioned uneventful surgery. centrally and gently pushed at each angle with the Cataract surgery in cases of iridoschisis may result help of a Sinskey hook to trap the iris in the four curls. in aspiration of iris fibers flowing in the anterior Once in place, the ring expands the pupillary opening chamber.5, 11 In these cases stretching the iris with various to 6.0 mm. The IQ-ring provides stable mydriasis with instruments or dilating the pupil with iris retractors may no trauma to the iris tissue and no need for additional not prevent the danger contact of US needle with the paracentheses. It retracts the iris away from the flow iris tissue and aspiration of fibers. currents and thus helps to prevent its incarceration Intaoperative iris manipulations may lead to severe into the US and I/A handpieces. As the result of the postoperative fibrinoid reaction especially in eyes with IQ-ring implantation we obtain a square, 6 mm pupil pseudoexfoliation syndrome, chronic uveitis, glaucoma dilation that allows for safe and comfortable maneuvers or diabetes. Tat is why cataract surgery in the presence during phacoemulsification. of a small pupil remains one of the most difficult and The ring is usually inserted at the beginning of the challenging cases. phaco procedure through an unenlarged 2.8 mm clear corneal incision into the pupillary aperture. The IQ-ring surgeon can control the iris without significant changes “To enhance phaco surgery in complicated small-pupil of his accustomed technique. The capsulorhexis, cases we designed the new device which was called hydrodissection, phacoemulsification, and injection of IQ-ring (Fig. 41.6). It is used in cases of pupil miosis the intraocular lens are performed through the refractory to dilation protocols. The device is a square, expanded pupil with the device in place. In case of O-shaped, temporary implant with four circular curls necessity the ring can be inserted at any stage of the that holds the iris at equidistant points. One-piece operation. design with the curls at each angle of the ring provides Cadaver eye study using scanning electronic micro- balanced stretching and gentle holding of the iris tissue. scopy showed that much less damage to the pigmented The main principle of iris pupillary margin fixation with iris tissue was caused by the new instrument than by the curl is represented on Figure 41.7.” conventional iris retractors (Figs 41.8 and 41.9).

Surgical Technique Topical anesthesia is applied using 2% lidocain, and the paracenthesis is done at 12 o’clock. A 2.8 mm temporal clear corneal incision is performed using the disposable metal blade. A dispersive ophthalmic viscosurgical device (OVD) is injected in the anterior chamber to stabilize it and protect the corneal endothelium. The IQ-ring is introduced into the AC through the clear corneal phacoincision using forceps and Sinskey hook (Fig. 41.10). The device is placed Fig. 41.6: The general view of IQ-ring in the AC and laid flat on the iris. It is then attached 264 Clinical Diagnosis and Management of Ocular Trauma

Fig. 41.8: IQ-ring implantation in the cadaver eye Fig. 41.10: IQ-ring is inserted through the main clear corneal incision

Fig. 41.9: Scanning electronic microscopy of the pupillary Fig. 41.11: The iris is fixated in the loops of the device margin of the cadaver eye after implantation of the IQ-ring and conventional iris hooks

to the pupillary margin in a circular manner, resulting in a pupillary opening approximately 6.0 mm wide (Fig. 41.11). Capsulorhexis is performed using forceps or a bent needle. Hydrodissection and hydrodelineation are performed with BSS until the nucleus could be rotated freely inside the capsular bag. Phacoemulsification is done with the Millenium CCS phacoemulsifier (Bausch and Lomb) using a modified quick-chop technique (Microflow or Kelman US needle; 36% of linear US power; pulse 10 pps, duty cycle 80%; vacuum settings at 350 mm Hg; bottle height 85 cm). A deep but short central trench is made in cases of the hard nucleus Fig. 41.12: Phacoemulsification of the nucleus with the cases. The step-by-step chop in situ and lateral IQ-ring in place separation technique allows nucleus division with minimal stress on the capsular bag (Fig. 41.12). inserted using injector through unenlarged incision. Coaxial or bimanual irrigation/aspiration is used to “Forceps flexible IOL insertion usually requires incision clean residual cortical fibers from the capsular bag enlargement from 3.5 to 3.75 mm”. (Fig. 41.13). The capsular bag is then filled with the Then the device is loosened from the pupillary margin cohesive OVD and foldable intraocular lens (IOL) is using a Sinskey hook and laid on the iris (Fig. 41.12). Small Pupil Phaco: An Innovative Technique 265

Fig. 41.13: Irrigation-aspiration after IOL implantation Fig. 41.15: The ring is removed from the anterior chamber and removal of the device through the clear corneal incision with the forceps

Fig. 41.14: The ring is cut with the Vannas scissors Fig. 41.16: Final situation after surgery

The ring is cut with the Vannas scissors and retracted from with zonular weakness and capsular inadequacy. We the anterior chamber through the clear corneal incision believe that our iris retraction technique with IQ-ring with the forceps (Figs 41.14 and 41.15). Aspiration has several advantages. is performed to remove the residual OVD. After First, the IQ-ring does not require additional inci- viscoelastic removal, the clear corneal incision is hydrated sions. This instrument is inserted through main incision, with balanced salt solution (BSS) (Fig. 41.16). thus reducing surgical trauma and minimizing the risk On the first postoperative day, the eyes presented of contamination and postoperative inflammatory with minor cell and flare in the anterior chamber. The reaction. pupillary margin was minimally disturbed or undama- Second, the device is applying pressure to the ged and the IOL well centered. We usually treat patients sphincter muscle over an area which is wider than in with small pupils after the surgery more aggressively than cases of iris hooks. It is particularly useful in patients uncomplicated patients with topical steroids, in which cutting or tearing of the iris tissue should be cycloplegics, and sometimes systemic steroids Patients avoided. Especially in the presence of rubeosis, chronic receive local antibiotic and steroid treatment for 4-6 anterior uveitis, or systemic coagulopathy. Iris rim is weeks. safely fixed in the loops of the ring and there is no risk of iris aspiration during phacoemulsification. Third, compared to other long-in-use iris retractors Conclusion IQ-ring has the advantage of being friendlier with the Adequate transpupillary access to the lens is essential eye, due to the well-distributed stretching and gentle to the success of phaco procedures especially in cases holding of the delicate iris tissue, and to the easier and 266 Clinical Diagnosis and Management of Ocular Trauma less traumatic implantation. It has no sharp or pointed 6. Vasavada A, Singh R. Phacoemulsification in eyes with a endings that can damage the eye. small pupil. J Cataract Refract Surg 2000; 26:1210–18. Fourth, equidistant position of the loops that holds 7. Lundberg B, Behndig A Intracameral mydriatics in phacoemulsification cataract surgery J Cataract Refract Surg the iris tissue ensure correct position of the iris and 2003; 29:2366–71. prevents the effect of overstretching of the pupil 8. Miller KM, Keener GT Jr. Stretch pupilloplasty for small pupil observed in incorrect iris hooks position. phacoemulsification (letter). Am J Ophthalmol 1994; Fifth, IQ-ring provides sufficient room for nucleus 117:107–08. fragmentation and removal. The device configuration 9. Chang DF. Phaco strategies for complicated cataracts. In: and plate design allows surgeon to work in the deep Chang DF, ed, Phaco Chop; Mastering Techniques, Optimizing Technology, and Avoiding Complications. lens layers below the iris plane and the square-shaped Thorofare, NJ, Slack 2004;173–98. pupil formed by the ring. This provides enough space 10. Dinsmore SC. Modified stretch technique for small pupil for grooving and cutting the nucleus and increased phacoemulsification with topical anesthesia. J Cataract peripheral visualization during the chopping phase of Refract Surg 1996; 22: 27–30. the procedure. 11. Auffarth G, Reuland AJ., Heger T, Volcker HE, Cataract In summary, different techniques of nucleus surgery in eyes with iridoschisis using the Perfect Pupil iris disassembly in small-incision cataract surgery requires extension system J Cataract Refract Surg 2005; 31:1877– 80. wide and unobstructed view of the anterior portion of 12. Graether JM. Graether pupil expander for managing the the lens as well as the instruments inserted in the anterior small pupil during surgery. J Cataract Refract Surg 1996; chamber. The other important factor is sufficient 22:530–35. manipulability of the instruments which is critical for the 13. Mackool RJ. Small pupil enlargement during cataract successful completion the surgery. A pupil that fails to extraction; a new method. J Cataract Refract Surg 1992; dilate makes cataract removal more difficult with added 18:523–26. 14. de Juan E Jr, Hickingbotham D. Flexible iris retractor [letter]. risk. The IQ-ring adequately dilates the pupil, prevents Am J Ophthalmol 1991; 110:776–77. iris sphincter damage. It is easy to insert and remove. 15. Nichamin LD. Enlarging the pupil for cataract extraction The ring expands the pupil to 6.0 mm, protects the iris using flexible nylon iris retractors. J Cataract Refract Surg sphincter during surgery, and allows the pupil to return 1993; 19:793–96. to its normal shape, size, and function after the operation. 16. Oetting TA, Omphroy LC. Modified technique using flexible IQ-ring is an important tool in phacoemulsification iris retractors in clear corneal cataract surgery. J Cataract Refract Surg 2002; 28:596–98. surgery. Careful intraoperative manipulation and inser- 17. Dupps WJ., Oetting TA. Diamond iris retractor configuration tion of the IQ-ring with liberal use of OVD can help for small-pupil extracapsular or intracapsular cataract prevent complications. After the surgery most of our surgery J Cataract Refract Surg 2004; 30:2473–75. patients had pupils almost indistinguishable from the 18. Birchall W, Spencer AF. Misalignment of flexible iris hook appearance before surgery with the preserved func- retractors for small pupil cataract surgery: effects on pupil tional activity. We consider IQ-ring among the most circumference. J Cataract Refract Surg 2001; 27:20–24. effective methods to increase the size of even very rigid 19. Masket S. Avoiding complications associated with iris retractor use in small pupil cataract extraction. J Cataract small pupils during phacoemulsification surgery. We use Refract Surg 1996; 22:168–71. it in cases with IFIS syndrome with a great success. The 20. Yuguchi T, Oshika T, Sawaguchi S, Kaiya T. Pupillary functions use of this method is highly recommended as it is likely after cataract surgery using flexible iris retractor in patients to reduce postoperative abnormalities in pupil size and with small pupil. Jpn J Ophthalmol 1999; 43:20-24. function. 21. Novak J. Flexible iris hooks for phacoemulsification. J Cataract Refract Surg 1997; 23:828–31. 22. Halpern BL, Pavilack MA, Gallagher SP. The incidence of References atonic pupil following cataract surgery. Arch Ophthalmol 1. Drolsum L, Haaskjold E, Davanger M. Results and 1995; 113:448–50. complications after extracapsular cataract extraction in eyes 23. Rho DS, Kahn M, Obstbaum SA. Complications of cataract with pseudoexfoliation syndrome. Acta Ophthalmol surgery. In: Charlton JF, Weinstein GW, eds, Ophthalmic (Copenh) 1993; 71:771–76. Surgery Complications: Prevention and Management. 2. Fine IH. Pupilloplasty for small pupil phacoemulsification. Philadelphia, JB Lippincott Co., 1995; 95–116. J Cataract Refract Surg 1994; 20:192–96. 24. Allan BD. Mechanism of iris prolapse: a qualitative analysis 3. Gimbel HV. Nucleofractis phacoemulsification through a and implications for surgical technique. J Cataract Refract small pupil. Can J Ophthalmol 1992; 27:115–19. Surg 1995; 21:182–86. 4. Kershner RM. Management of the small pupil for clear 25. Chang DF, Campbell JR. Intraoperative floppy iris syndrome corneal cataract surgery. J Cataract Refract Surg 2002; associated with tamsulosin. J Cataract Refract Surg 2005; 28:1826–31. 31:664–73. 5. Smith GT, Liu CSC. Flexible iris hooks for phacoemulsi- 26. Arshinoff S. Modified SST–USST for tamsulosin-associated fication in patients with iridoschisis. J Cataract Refract Surg intraocular floppy-iris syndrome. J Cataract Refract Surg 2000; 26:1277–80. 2006; 32:559–61. Current Concepts and Recent Advances in Management of Ocular Trauma

CHAPTER

Trauma after Refractive Surgery 42 D Ramamurthy, Chitra Ramamurthy (India)

Introduction US Eye Injury Registry in 19991 assessed closed Vs open globe injury in 173 patients who had undergone Refractive surgeries gained momentum from 1960’s refractive surgery prior to injury. 165 of these eyes with inception of RK followed a decade later by developed traumatic wound dehiscence. Only 20.6 evolution of excimer laser and PRK, had a crescendo % recovered 20/200 or better vision. The primary in 1990’s with Lasik gaining footage and the revolution has been ever on with increasing vigor and growing concern which arises from this study data is the effect understanding. of trauma on ocular integrity. The other possibility is On an average, over 17 million have undergone the probability of closed globe injury getting converted LASIK so far. More than 2 million LASIK procedures to an open globe injury, in a setting of post-refractive have been performed each year. Over 22 % with a surgery. refractive error of –5 D to – 7 D have undergone LASIK in US. A further revelation tells us that 19 % of the US refractive surgeons have themselves undergone Trauma in Radial Keratotomy refractive surgery. Radial keratotomy (Fig. 42.1) was introduced in 60’s If one reflects on the popularity and demand of and 70’s. It maintained its stand as a popular refractive a surgical procedure on the human body, refractive procedure till 90’s. procedures claim the 2nd position, next only to cataract Cassey et al 2 came up with the analysis of the tensile surgery. strength of corneal wounds. The conclusion derived The primary concerns which needs reflection is was that the weakest point in the eye in a post incisional occurrence of trauma of the refractive surgery per se surgery is the site of incision. After complete healing, and trauma after refractive surgery. the tensile strength is only 50% of normal. Trauma in LASIK could range from flap related complications, rare instances of corneal perforations, corneal infection, macular hemorrhage, interface deposits, epithelial ingrowth and irregular astigmatism. The increasing concern following LASIK is that the force that the residual untreated cornea could resist decreases as a result of a thinner stromal bed and can lead to Iatrogenic Keratectasia. Trauma from RK could range from perforation to residual refractive error, would response unpredictability, hyperopic shifts, starburst phenomenon and drop in BCVA. PRK could complicate issues with its varying wound response trends with incremental need for topical steroids, residual nebular haze, residual refractive error, etc. But the burgeoning problem is the propensity of late onset trauma impact in any of these eyes and the Fig. 42.1: Radial keratotomy risk: benefit ratio. If we look at the profile of refractive surgery Pin heiro et al3 further assessed corneal integrity patients, it’s largely a young, active and working after refractive surgery. The analysis indicated that population in the prime of their productive life. following blunt injury in a normal eye, rupture 270 Clinical Diagnosis and Management of Ocular Trauma occurred at limbus or sclera. Post RK, rupture occurred – 42 D treatment. There has been no reported cases through the incision (Fig. 42.2). Deeper, larger or to date of rupture occurring in the cornea at the site more the incisions, higher the risk. of ablation after PRK.

Trauma in LASIK The stromal wound healing after LASIK occurs at the flap edges and is minimal compared to the PRK group. This may support in part our clinical observation that less corneal haze was noted after LASIK then after PRK as a result of less disorganized stromal collagen fibers from wound healing process.

POSSIBLE MECHANISMS Theoretically, the force that the cornea would resist is directly proportional to the thickness of the residual untreated stroma after lasik9, i.e. thinner the thickness, Fig. 42.2: Rupture through incision the more vulnerable to blunt ocular injury it will be. According to Munnerlyn’s formula: Probably in this setting, mini RK gained acceptance. Ablation depth in microns (μm) = Reducing incision length4 appears to reduce the likelihood of corneal rupture, a more advantageous Optical zone in mm×diopters of myopia position in patients predisposed to ocular trauma. 3 Histological evidence on examination of corneal To prevent ectasia, a minimal residual stromal bed buttons post RK shows that wound healing of incisions is not completed several years after the procedure. thickness of at least 250 μ is advocated. Following injury Epithelial plugs of various size still incompletely fill the in a LASIK flap, there are 2 probable sites of injury. somewhat dehiscent wound margins. Fibroblastic A shearing force could act at the junction between the activity 5 in the surrounding stroma remains incomplete. flap and the corneal bed which separates the flap from Mc Knight et al’s6 report on corneal rupture following the bed. In addition, a perpendicular penetrating force RK in cats subjected to BB gun injury. They conclude perforates the residual thinner cornea. Most complica- that for the same intensity of injury rupture occurs in tions associated with LASIK are flap related. They RK treated eyes with hyphema occurred in untreated include intra-operative flap complications like shifted eyes. flap, button hole formation, free flap, wrinkled flap We cannot however conclude that post RK eyes and postoperative complication like micro and macro are condemned to rupture. The risk ratio is higher in striae and flap slippage and dislocation. all probability and demands for a continued usage of The mechanisms10 postulated for early flap protective eye wear in instances of exposure to trauma. adherence includes endothelial pumping, capillarity, Slade SG et al report7 on ocular integrity after fiber interlacing, intra-corneal suction, intra-corneal refractive procedures makes a comparative study on molecular attraction and ionic bonding and strength RK, PRK, LASIK and normal eyes. The conclusions of the epithelium. Whatever the mechanism, the derived are that RK eyes ruptures at significantly lower anecdotal ease with which a flap can be lifted years stress levels. PRK and LASIK eyes are not significantly after surgery for retreatments is a definite indication different from normal eyes. The sites of rupture are that the flap actually never heals fully (Fig. 42.3). the same as normal eyes in PRK and LASIK. Trauma to LASIK Flap Trauma in PRK Early flap complications occur in the first 24 hours. Burnstein et al report8 on PRK ablations in human The sequence of events declines after one week. The cadaver eyes indicate that these eyes following PRK flap slippage and displacement most commonly occur ablations of – 6.00 to –54 D were infused with nitrogen in the early postoperative period and presumably as gas to build high pressure in the eye and the ablation a result of mechanical disruption such as forceful zones responded to pressure trauma only after a blinking, lid squeezing and eye rubbing (Fig. 42.4). Trauma after Refractive Surgery 271

Fig. 42.3: Enhancement 5 years after LASIK Fig. 42.6: Late flap dislocation

The longer the time interval between occurrence and intervention, probability of intractable micro and macro striae (Fig. 42.7) drop in BCVA, irregular astigmatism and even onset of DLK is likely.

Fig. 42.4: Flap dislocation within 24 hours

Fig. 42.7: Macro striae in post-LASIK trauma

These flaps need to be lifted, both surfaces of the flap hydrated thoroughly, stretched to the gutter and ironed out in a direction perpendicular to the direction of the striae. The interface also needs to be thoroughly irrigated and if in an eventuality of a long wait to inter- vention, possibility of epithelial ingrowth increases and appropriate debridement is indicated. Recalcitrant macrostriae demand removal of the overlying epithe- Fig. 42.5: DLK after foreign body removal lium, hydrate, stretch and ironing of the flap. Lin et al report11 on complications with lamellar refractive A mere foreign body removal with a spud or a surgery indicates flap adhesion and bonding occurs needle on a LASIK flap acts like a shearing force, could between 5 to 100 days with peak strength between cause flap slippage or DLK (Fig. 42.5). Recent or late ¼ and ½ of the original strength. dislocation of flap demand immediate attention Reports of late flap complications following LASIK (Fig. 42.6). has been reported from 10 days to 5 years - playing 272 Clinical Diagnosis and Management of Ocular Trauma with basket ball, dog, motor vehicle accident with airbag injury, playing in snow, army field training, peck by pet bird and multiple trivial injuries of this fashion. Diffuse lamellar keratitis (DLK) can be precipitated by the least of trauma and needs to be kept in mind and be treated vigorously (Fig. 42.8).

Fig. 42.9: Phakic IOL disenclavated after trauma

References 1. US Eye Injury Registry in 1999. Fig. 42.8: Diffuse lamellar keratitis 2. A. R. Gasset; C. H. Dohlman The tensile strength of corneal wounds. Arch Ophthalmol 1968;79:595-602. 3. MN Pinheiro, MR Bryant, R Tayyanipour. Corneal Trauma in Surface Treatments integrity after refractive surgery: effects of radial keratomy and mini-radial keratotomy Ophthalmology 1995; Surface ablations are by and large more risk free 102:297-301. related to trauma although the refractive outcomes 4. Casebeer JC, Shapiro DR , Phillips S. Severe ocular would be compromised without adequate wound trauma without corneal rupture after radial keratotomy: modulators. The absence of the thick flap created in case reports. J Refract Corneal Surg 1994; Jan-Feb: 10 LASIK makes surface treatment more bio-mechanically (1): 31-33. stable and makes it less vulnerable to trauma. 5. Pinheiro MN , Bryant MR, Tayyanipour R et al. Corneal integrity after refractive surgery. Effects of radial keratotomy and mini-radial keratotomy. Ophthalmology 1995 Feb; 102 (2): 297-301. Trauma in Phakic IOL Implants 6. McKnight SJ, Fitz J, Giangiacomo J.et al .Report on corneal rupture following RK. Ophthalmic Surgery 1988; Iris supported Phakic IOLs have multiple reports of 19:165-67. disenclavation of haptics and decentration of phakic IOL 7. Peacock LW, Slade SG, Martiz J, et al. Ocular integrity (Fig. 42.9) which could lead to progressive endothelial after refractive procedures Ophthalmology 1997;104: loss if immediate intervention is not forth coming. 1079-83. 8. Burnstein Y, Klapper D, Hersh PS Experimental globe rupture after excimer laser photorefractive keratectomy. Arch ophthalmol 1995;113:1056-59. Conclusion 9. Sun CC, Chang SW, Tsai RF. Traumatic Corneal The conclusive ideas which emerge from this chapter Perforation With Epithelial Ingrowth After Laser In Situ Keratomileusis. Arch Ophthalmol 2001;119:907-09. is that one needs to practice abundant caution. 10. Cda RP, Narvaez J, King JA, et al. Late-onset traumatic Wearing shatter proof protective glasses is a necessary dislocation with central tissue loss of laser in situ precaution. Literature reports are few, clinical keratomileusis flap. Cornea 2006 Oct;25(9):1107-10. experience rare but awareness of such occurrences 11. Lin RT, Maloney RK. Flap complications associated with and educating our patients would be preventive at lamellar refractive surgery Am. J Ophthalmology 1999; large. 127:129-136. CHAPTER

Complication and Contusion after Phakic IOL 43 Jerome Bovet (Switzerland)

Introduction The implantations of IOLs in the phakic eye (phakic IOLs) is a relatively old technique to correct ametropia, they have been used in clinical practice in refractive surgery for 15 years. The early problems are related to the design of the lens and the meticulous details of surgery. The late postoperative complications are related to the interaction of the IOL and the intimate ocular tissues during the lifetime of the patient. Lifelong, regular follow-up care is essential in all cases. Explantation of the lens may ameliorate some of the complications. Later in life, if the patient develops a cataract, it should be possible to do an atraumatic Fig. 43.1: Eye care IOL (corneal) explantation, followed by cataract extraction and implantation of another appropriate IOL. Development of a newer, safer technology to correct preoperative examination should exclude those ametropia may necessitate explantation of the IOL. patients with low endothelial cell count or those with However, the presence of the IOL inside the eye shallow anterior chambers because the risk of cell loss has been associated with complications specific to the increases as the distance between phakic IOL and the type of phakic IOLs involved. Some of these compli- endothelium decreases. cations have led to changes in design of some lenses We know today that a minimum of 1.5 mm and to discontinuing of others.9 between the IOL and the corneal endothelium is Currently, only a few long-term studies are available needed to long-term safety. This explains the damage with phakic IOLs the complication spectrum appear to the endothelium, if not explanted early to slowly and some lenses become forbidden to insert endothelial decompensation.3,11,12 in some European country.8 Meticulous long-term follow-up of each patient is We will describe the most frequent late complica- at the moment necessary for any AC phakic IOL to tions and traumatisme associated with implantation of detect those individuals with significant damage to the phakic IOLs. endothelium and to explant the phakic IOL before clinically necessary.

Anterior Chamber Phakic IOLs PIGMENT DISPERSION AND LENS (Fig. 43.1) DEPOSITS Although no definite incidence for these conditions is ENDOTHELIAL COMPLICATIONS AND reported in the literature, these conditions are seen ANTERIOR CHAMBER DEPTH in clinical practice. They normally do not negatively The main concern about AC Phakic IOLs is loss or affect visual acuity and thus no futher procedure— damage to the endothelial integrity. An Exact except for regular clinical observation—is necessary. 274 Clinical Diagnosis and Management of Ocular Trauma CHRONIC INFLAMMATION AND UVEITIS As the angle-supported AC phakic IOL is positioned directly in front of the iris, chronic inflammation and pigment dispersion are possible .

SIZE-RELATED COMPLICATIONS PUPIL OVALIZATION AND IRIS RETRACTION (FIG. 43.2) Angle supported anterior chamber phakic IOLs need to have the same size of the anterior chamber in order to fit there exactly without causing damage to the ocular Fig. 43.3: The Visante OCT (Carl Zeiss Meditec) tissues. Anterior chamber

Fig. 43.4: Pentacam Oculus AG. Anterior chamber and pachymetry

Fig. 43.2: Anterior chamber aphakic IOL with ovalisation of the pupilla

This is now possible with the visante OCT (Carl Zeiss Meditec) or with the Pentacam (Oculus AG) which give you the exact morphology and sizing of the anterior chamber (Figs 43.3 and 43.4). If an anterior chamber angle-supported phakic IOL is too short, the IOL will rotate in the anterior chamber causing important glare. Rotation of the angle- supported phakic IOLs might occur due to undersizing. In fact, 80% of eyes showed rotation greater than 15 degrees.8 A more frequent and serious complication is the pupil ovalisation. Ovalization of the pupil is a specific complication of angle-AC phakic IOLs. The position Fig. 43.5: Anterior chamber Phakic IOL NuVita of haptics in the sclerocorneal angle and their size might Bausch and Lomb Permanent mydriasis lead to mild deformation of the iridosclerocorneal architecture, resulting in iris retraction and pupil ovalization. INDUCED ASTIGMATISM Pupil distortion starts after 12 to 18 months of Surgically induced astigmatism is of significance because implantation, the pupil showing ovalisation, the longer patients request acceptable unaided postoperative axis being always the axis of the IOL. visual acuity. Iris retraction with oval pupil deformation remains a concern of the angle-supported phakic IOLs. This mater together with potential damage to endothelial GLARE AND HALOS cells, is the major objection against the current lens One disadvantage of AC phakic IOLs is that they are designs (Figs 43.5 and 43.6). positioned in front of the pupil, with edge affects as Complication and Contusion after Phakic IOL 275

Fig. 43.7: Iris fixated lens: iris claw

Fig. 43.6: Pupillary bloc with anterior phakic IOL a potential source of optical aberrations. Furthermore, the relatioin of pupil size and center to the optic of the lens is a crucial factor that should be evaluated and discusses preoperatively.

GLAUCOMA The risk of acute angle glaucoma is well known from aphakic anterior chamber IOLs therefore a peripheral Fig. 43.8: Decentration of the lens with not enough iris iridectomy is recommended for this IOL. tissue grasp: Iris claw Artisan

CATARACT FORMATION As the AC phakic IOL is positioned away from the lens, cataract formation is of less significance when compared to posterior chamber phakic IOLs.

Iris-fixated Anterior Chamber Phakic Intraocular Lenses (Fig. 43.7) The iris-fixated IOL is marketed in Europe as the Artisan has been used since 1978 for pseudophakic IOLs, mainly for secondary implantation in aphakic eyes. Fig. 43.9: Iris claw Artisan, decentration Since 1986, the Worst-Fechner IOL has been implanted in phakic eyes for the correction of high minor trauma. However, this complication is always myopia and subsequently hyperopia. The original the consequence of the so called “weak grasp”, that design was modified in 1991 to assure a sufficient vault is insufficient amount iris tissue grasped in the claw between the IOL optic and the iris. (Figs 43.8 and 43.9). We will related an eye trauma with an artisan which COMPLICATIONS OF IRIS-SUPPORTED induce a intumescent cataract, retinal detachcment and PHAKIC IOLS5 loss of vision. One frequent complication is the loosing of the IOL There are in fact very few complications related from the iris. This can occur spontaneously or after to Artisan/Artiflex. 276 Clinical Diagnosis and Management of Ocular Trauma ENDOTHELIAL CELL LOSS AND ANTERIOR GLARE AND HALOS CHAMBER DEPTH Phakic IOLs are often implanted in eyes of compara- Damage to the endothelium can occur mostly because tively young patients with a large scotopic pupil of the IOLs direct contact with the inner surface of diameter. This can result in glare phenomena if the the cornea, either during implantation or by pupil is larger than the IOL optic. postoperative changes in IOL position. The height of the Artisan lens and the potential closeness to the cornea increase with the dioptric GLAUCOMA power. Therefore, a sufficient anterior chamber depth Because the anterior chamber angle is not affected (ACD) for the calculated IOL is necessary. The distance by the haptics of the iris-claw IOL, lens size-related between the implant and the corneal endothelium secondary glaucoma is not pratically possible. A should not be less than 1.5 mm. This may be a problem peripheral iridectomy or iridotomy is necessary for the more for the hyperopic than the myopic iris-claw prevention of a papillary block. phakic IOL.

CHRONIC INFLAMMATION AND UVEITIS CATARACT FORMATION The possiblility of chronic inflammation has always Cataract formation due to the iris-claw lens is very been a major concern with the iris-claw lens, as this unlikely with myopic eye because it is inserted over IOL is fixated directly in the iris tissue and causes a miotic pupil without contacting the crystalline lens. pressure or shear forces when the eye is moving. Cataract formation has been reported in association Careful postoperative monitoring of inflammatory with the iris-claw lens and hypermetropia on a long- signs is necessary. If persistent intraocular inflammation term basis. occurs that is not sufficiently treatable with drugs, the The increasing size of the crystalline lens with age removal of the implant must be considered. and the formation of cataract, especially of an PUPIL OVALIZATION AND DECENTRATION intumescent type, will greatly disturb the tissue Pupil ovalization or irregularity can occur if the fixation relations. An early management of cataract, including of the haptics is perfomed asymmetrically. No the explantation of the implanted phakic lens, will be pregressive pupil ovalization has been reported so far. needed. This can lead to difficulties if the pupil itself is Implantation of a phakic lens in a hyperopic eye decentered and if the optical axis is not in the middle of ought to be a small event for the operated eye; the pupil. Postoperative decentration is possible if the unfortunately, it is not so. Therefore, lifelong regular enclavation is not sufficient. follow-up care is essential. Postoperative dislocations due to blunt ocular trauma have been described. In the author’s experience, they CASE REPORT (FIGS 43.11 AND 43.12) observed only case of possible phakic IOL dislocation in a patient with very thin iris tissue (Fig. 43.10). A 41-year-old worker presented with a sudden loss of vision in the left eye after trauma. He reportedly had receive a cable on his left eye. The patient had had uneventful bilateral implantation of Artisan toric phakic IOLs 1 year earlier to correct RE S-19.5 C -2.5 respectively LE S-14.0 C-3.0 the vision after one week was VAWC 0.5/0.6 On presentation at the emergency room, the left eye visus light perception. The globe presented no open wound. Anterior chamber had an hyphema, The Artisan phakic IOL were not found on examination. An intumescent white cataract with ruptured capsule and 180 degrees zonulolyse prolapsed inside the AC. No vitreous prolapse in AC. Eye pressure on the left eye was 38 mm Hg. On the echo B the retina seem on place and the Fig. 43.10: Dislocated iris claw iris-claw lens seem on the retina. Complication and Contusion after Phakic IOL 277

Discussion This case show that the old initial corneal wound of 6 mm was strong enough and no dehiscence appear. The iris claw give a rigidity to the anterior chamber and prevent the natural elasticity of the globe, result of the rupture of the zonule lens subluxation and dislocation. The contusive injury was strong enough to dislocate the artisan lens and to push the lens all through the posterior chamber where a claw pinch the retina and do a retina tears. Traumatic dislocation of an Artisan IOL is a rare complication, with only 5 reports in the clinical literature.1,2,4,6,7,13 Most dislocations resulted in the haptic claw tearing free from the iris at one point, which could be easily corrected by reenclavation. Based on the reports, it seems probable that the enclavation force of the haptic claw is insufficient or the iris tissue is not Fig. 43.11: Schematic trauma and iris claw inside the strong enough to hold the Artisan IOL during ordinary vitreous chamber trauma. This case stresses the need for protection in eyes with previous eye surgery and may reduce the risk, particularly when the patient is involved in activities such as hard worker,contact sports, e.g. football, tennis, squacrh. Despite five operations,when the eye develop a proliferative vitreoretinopathy (PVR) under silicone oil, it is very difficult not to finish with a phthisic eye.4

Posterior Chamber Phakic Intraocular Lenses14 Fig. 43.12: Schematic trauma and iris claw inside the vitreous chamber (Figs 43.13 and 43.14)

In urgency the cataract was phacoemulsified and The specific complications of PC phakic IOLs are caused an anterior vitrectomy under topical anesthesia with by their position between the iris and the natural lens. propofol general anesthesia, was performed to remove The most common complications—cataract formation, the hemorrhage and to diminish the pressure. papillary block, and glaucoma—are dependent on the Four days later a 23 gauges 3 ports posterior lens position, material, and original design. vitrectomy was done to remove the Artisan aphakic lenses which was enclaved by the claw on the retina. A retinal tears was found at the place of the claw of the lens full vitrectomy, 180 degrees of endolaser and exchange Dkline-air-silicone was done. A phakic artisan lens was replace on the iris. One week after the second operation the visus BCVA was 3/10. Two months postoperatively, he develloped a PVR posterior and anterior a second 23 gauges 3 ports posterior vitrectomy was performed with a full shawing, 360 degrees retinotomy and panphotocoagulation. Silicone was injected at the end of procedure. One year later, he developed a neovacularised cornea and a ophthisic eye. Fig. 43.13: Posterior phakic IOL ICL (Staar) 278 Clinical Diagnosis and Management of Ocular Trauma no damage occurs. The crystalline lens, IOP, and endothelial cell status are important guides to the continued good health of the eye. The operated eye needs to be protected from rubbing and trauma because they tend to upset the delicate balance between the implanted IOL and the adjacent ocular tissues. Yearly eye examination is an essential ingredient of Aphakic IOL follow-up, and as soon as a trauma occurs. References 1. Asano-Kato N, Toda I, Hori-Komai Y, et al. Experience with the Artisan phakic intraocular lens in Asian eyes. J Cataract Refract Surg 2005;31:910–15. 2. Ball JL, McLeod BK. Traumatic wound dehiscence following cat- aract surgery: a thing of the past? Eye 2001; 15:42–44 3. Baikoff G, Arne JL, Bokobza Y, et al. Anglefixated Anterior Fig. 43.14: Visian ICL (Staar) Chamber Phakic Intraocular Lens for Myopia of -7 to -19 diopters. J Refract Surg 1998;14:282-93. 4. Banta JT, Cebulla CM, Quinn CD. Closed globe CATARACTS HAVE ALWAYS BEEN Injuries:anterior segment. In Banta JT (Ed): Ocular trauma THE MAIN CONCERN Sauders Elsevier, 2007. Cataracts related to posterior chamber phakic IOLs 5. Benedetti S, Casamenti V, Marcaccio L, et al. Correction are anterior subcapsular opacities. The phakic IOLs of myopia of 7 to 24 diopters with the Artisan phakic intraocular lens: two- year follow-up. J Refract Surg 2005; induced cataracts typically start between 12 and 18 21:116–26 months after surgery with some anterior subcapsular 6. Ioannidis A, Nartey I, Little BC. Traumatic dislocation and opacities, progressing later causing sometimes the need successful re-enclavation of an Artisan phakic IOL with of cataract surgery. analysis of the endothelium. J Refract Surg 2006; The reason, why these cataracts develop, is not 22:102–3. well established, although it is widely believed that 7. Lee JS. Traumatic aniridia and aphakia after Artisan intraocular lens implantation. J Cataract Refract Surg depends mainly on the space (vault) between the IOL 2007;33:1341–42. and the natural lens. 8. Kohnen T, Mirshahi A, BŸhren J, Kasper T, Baumeister M. Complications of phakic Intraocular lenses (Chap 9). PUPILLARY BLOCK, ACUTE GLAUCOMA AND In Hardten DR (Eds): Phakic Intraocular lenses. Slack Eds MALIGNANT GLAUCOMA 2007. 9. Marinho A, Salgado R. Complications of phakic IOLs Because of the PC phakic IOLs the iris can be pushed (Chap 18). In Garg A (Ed): Mastering the Techniques of forward and narrow the anterior chamber angle, so Lens based Refractive Surgery (Phakic IOLs). Jaypee a pupillary block with acute glaucoma can appear, Brothers, 2005. especially in hyperopic eyes. This problem can be 10. Marinho A. New generation Phakic IOL implant for myopia provides good vision quality. Euro Times prevented by creating an intraoperative surgical 1998;3(6):26. iridectomy. 11. Mimouni F, Colin J, Koffi V, et al. Damage to the corneal For hyperopic treatement, the preoperative endothelium from anterior chamber intraocular lenses in iridotomy is even more important in preventing early phakic eyes. Refract Corneal Surg 1991;7:277-81. pupillary block. 12. Saragoussi JJ, Cotinat J, Renard J, et al. Damage to the corneal endothelium by minus power anterior chamber intraocular lenses. Refractive Corneal Surgery 1991;7:282-85. Conclusion 13. Yoon H, Macaluso DC, Moshirfar M, Lundergan M. Traumatic dislocation of an Ophtec Artisan phakic Good results are obtained as much by surgical skill intraocular lens. J Refract Surg 2002;18:481–83 as by the lens design chosen. A regular detailed follow- 14. Zaldivar R, Davidorf JM, Oscherow S. Posterior Chamber up examination is essential for all operated cases to phakic IOL for myopia of -8 to -19 diopters. J Refract detect and treat any untoward problem early, so that Surg 1998;14:294-305. CHAPTER

Management of Corneal Lacerations 44 SH Lee (Canada)

Introduction Flow chart 44.1: Management of corneal laceration Laceration of cornea is one of the leading causes of ocular morbidity. The management of such injury, whether medical or surgical, is directed primarily at the restoration of normal ocular anatomy. The ultimate goal is to prevent secondary complication and maximize the patient’s visual prognosis.

Injury Assessment A meticulous injury assessment is important in determining the extent of injury. This should include detection of presence or absence of intraocular foreigner body, orbital bony injury or adnexal tissues injury such as lacrimal duct injury. A quick history must be obtained, how it happened, when it happened, past ocular history, past medical history, including current topical and oral medications and allergy. A short but focused ocular examination should be If in doubt, it is best to suture the wound especially conducted. Visual acuity, ocular mobility, external if the wound edge is not in good apposition. examination, anterior and posterior segment It is a good principal to follow the Flow chart examination, including intraocular pressure if possible 44.1. should be documented. Auxiliary tests such as X-rays, CT scans will help to determine the extent of the injury. All documented details should be neatly written on patient’s chart not only for medical record, but for Medical Management medical legal purpose if required in the future. All suspected nonperforating corneal laceration must be carefully examined to rule out perforation, such as microscopic leak. Perforating or Nonperforating Seidel testing with 2% fluorescein will be helpful, Gentle digital pressure may reveal it is indeed a self Corneal Laceration sealing wound. The primary goal is to determine whether it is a All self sealing corneal lacerations may be treated perforating or nonperforating corneal laceration, as with eye patch or bandage contact lens, with broad the former type of injury is always surgically managed, spectrum antibiotic eye drop frequently. Patient has and the latter may be medical or surgically managed. to be monitored daily on out- patient basis. Any 280 Clinical Diagnosis and Management of Ocular Trauma symptom or sign of infection such as infectious keratitis Other incorrect corneal suturing should be avoided; or endophthalmitis should admit the patient to the shallow suturing –leads to internal wound gape, suture hospital for more intense treatment. Any sign of with unequal depth will create wound override anterior chamber becomes progressively shallow, or (Fig. 44.2). the corneal wound becomes unstable, suturing of the wound must be considered. Every effort must be made to minimize scarring and surface irregularity. The bandage contact lens should not be removed until the wound is stable, and complete re-epithelialization has occurred.

Surgical Management If the corneal laceration is perforating, it should be determined whether it is: simple or complex laceration, with or without uveal. Crystalline lens vitreous, retinal or scleral involvement. It is important to detect any corneal tissues loss, and whether it is irrepairable severely damaged globe. The primary goal in repairing corneal laceration is to achieve a water tight globe with structural integrity. Fig. 44.2: Positions of corneal suturing. (A) Correct. (B) Wrong—suturing too shallow and lead to Other secondary goals will be removal of any lens internal gape. (C) Wrong—suturing through and fragments, vitreous incarceration, uveal tissue through.100% depth, creating a conduit. (D) Wrong— incarceration or prolapse and intraocular foreigner unequal distant from each side of the wound lead to wound body if they are detected during the surgery. To restore distortion. (E) Wrong—suture with unequal depth and the normal or near normal anatomical relationship is distance will cause wound over ride. (F) Correct the final goal. Placement of sutures through the visual axis should Simple Corneal Laceration be avoided. If the laceration affecting the visual axis, Stable wound, with watertight laceration, and formed suturing should avoid the central cornea, by placing anterior chamber, 10-0 monofilament nylon may be it on either side of the wound but not through the placed directly across the wound without entering the axis, and by making sure the suture bites close to the anterior chamber, The suture has to be 90% depth visual axis short (Fig. 44.3). through the stroma, 1.5 mm in length, and equal depth on each side of the wound (Fig. 44.1). Some corneal surgeons would think 100% depth through the stroma will be better, but at least in theory, such suturing would provide a conduit for allowing micro organism from external surface to enter the eye.

Fig. 44.3: Placement of sutures. (A) Correct, central cornea —no suture, (B) wrong, as suturing run through the visual axis

Unstable wound with shallow or no anterior chamber. A viscoelastic is used to recreate the anterior chamber through a newly created side port (Fig. 44.4). Any incarcerated ocular tissues into the Fig. 44.1: After suturing of corneal laceration wound should be either excised or repositioned. At Management of Corneal Lacerations 281 time that anterior chamber cannot be formed, because of leaking, temporary suture to close the wound may be required, and subsequent removal will be required once the wound become stable. Once the wound become stable, the accurate appositional way of correct suturing should be carried out.

Fig. 44.6: Stellate laceration close by (A) bridging sutures, (B) purse string suture, and (C) multiple interrupted sutures and tissue adhesive in the center Corneal Laceration with Tissue Loss The wound can be divided into central, paracentral, peripheral. Central with tissue loss will be treated with corneal Fig. 44.4: Recreation of anterior chamber with viscoelastic. Viscoelastic material is injected into anterior chamber graft (Fig. 44.7). through the side port Paracentral with tissue loss will be treated with suturing or tissue glue or combination of the two. Complex Corneal Laceration Peripheral with tissue loss will be treated with patch Wound graft (Fig. 44.8). The goal is to achieve good wound apposition with minimal distortion. An irregular wound is first subdivided into straight Use of Tissue Glue segments with interrupted sutures. Long deep and In most cases of corneal laceration, use of tissue glue relatively tight peripheral sutures and short, shallow, is only for adjunct treatment to suturing. appositional sutures near the central corneal may restore the normal corneal dome and surface corneal topography. Some of those complex corneal laceration wound are shown in Figures 44.5 and 44.6:

Fig. 44.5: Complex corneal laceration. A T-or Y- shaped Figs 44.7A and B: Penetrating keratoplasty for central laceration often leaks at the apex and may be difficult to corneal laceration with tissue loss, removal of lacerated close. A purse string suture is generally effective in closing cornea. Curved scissor and supra sharp knife are used such laceration instead of trephine 282 Clinical Diagnosis and Management of Ocular Trauma

Fig. 44.8: Final appearance of cornea after patch graft after peripheral corneal laceration with tissue loss It is useful in small puncture wound with leaking, selected small perforated laceration, and paracentral laceration with suturing. When deciding to use tissue adhesive, the corneal surface is dried with a cellulose sponge and the epi- thelium surrounding the perforation is debrided, tissue adhesive (cyanoacrylate) is applied to the edge of the perforation with 25-gauge needle on a tuberculum syringe with least amount or in the form of a bead Figs 44.9 A to C: (A) Puncture corneal wound with leaking. (Fig. 44.9). (B) #25 gauge needle on tubercular syringe with tissue glue in the form of bead. (C) Final appearance of corneal A bandage contact lens is placed for comfort and wound after tissue glue, the bandage contact lens had been to protect the adhesive from being lodged by the eyelids removed and the corneal surface has been re- Frequent following up is necessary to ensure the epitheliumized perforation is sealed. suturing to minimizing the corneal scarring, to stabilize Corneal Laceration with the wound and to re-establish normal or near normal anatomical relationship is vital. Involvement of Other Ocular A clearer understanding of corneal laceration and Structure the use of appropriate surgical approaches may permit the reduction the rate of ocular morbidity and enhance With lens involvement, depending upon the extent visual rehabilitation after trauma. of involvement, lensectomy may be required. Any lens fragment has to been removed, and anterior vitrectomy has to be performed. Bibliography 1. Cowden JW, Hu BV. A new surgical technique for With uveal tissue involvement, incarceration of posterior chamber lens fixation during penetrating uveal tissues have to be repositioned or excised. keratoplasty in the absence of capsular or zonular With vitreous or retinal tissue involvement, service support. Cornea 1988;7:231. 2. Hersh PS, Kenyon KR. Anterior segment reconstruction of retinal subspecialist will be required, and it will be following ocular trauma. Int Ophthalmol Clin 1988; multispeciality approach. 28:57. With intraocular foreign body, it has to be removed 3. Mackenson G, Faulborn J. Primary and secondary with any means possible. reconstruction of the eyeball after extensive lacerations. Ophthalmic Surg 1974;5:43. 4. Refojo MF, Dohlman CH, Ahmad B, et al. Evaluation of Conclusion adhesives for corneal surgery. Arch Opthalmol 1968; 80:645. It is important to manage corneal laceration according 5. Smiddy WE, et al. Contact lenses for visual rehabilitation to the flow chart for management of corneal after corneal laceration repair. Ophthalmology 1989; laceration; Use of appropriate surgical techniques of 96:293. CHAPTER

Sports Injuries in Eye 45 B Shukla, Binoo Nayar (India)

Introduction per 100,000.3 Hyphaema has been mentioned as a special feature of sports trauma4 (Fig. 45.1). From The word ‘Sports’ includes many entities. It includes USA baseball and basket ball are reported as common all types of game (indoor and outdoor) and all types sports injuries.5-6 US eye injury registry has reported of athletic events. Some authors have used the word sports injury upto 12%.7 The author in a study of 1744 ‘Recreational’ instead of sports and that would include eyes found 12.27% sports injuries.8 many more diverse activities found in different parts of the world and to account for all of them is no easy job. Classification This problem can be looked at from various angles. There can be age wise distribution, regionwise, Broadly speaking most of the sports injuries could be seasonwise and from the point of view of the agent classified on the basis of the source of injury as follows: causing injury. In the present chapter sports injuries 1. Ball injuries will be considered from the last point of view with 2. Physical contact injuries passing reference to other modes of injury. 3. Miscellaneous injuries. Since there has been no standardization in the terminology of ocular trauma for a long time nor any BALL INJURIES uniformity in study design it is by no means easy or Perhaps this is the commonest type of sports injury valid to make any comparison. In one study at Boston as most of the children, youngsters or even adults play 34% ruptured globes were reported from trauma.1 In with some type of ball. The main advantage here is another study from Stockholm 23% of perforating that as a ball is a rounded structure it is not likely to injuries were found due to sports.2 The incidence of cause very severe injury unless it hits with a great force. paediatric injuries from Maryland was reported as 15.2 From the formula E= ½ mv2 it can be reasoned that harder balls will hit with greater force and are more likely to cause greater damage. Cricket ball and hockey ball can be included in this category. However a third factor is also important and that is the curvature of the ball. The greater is radius of curvature (bigger in size) the less they would cause damage as the brunt of the force will be taken up by the orbital rim and less damage is likely to occur to the eyeball. On the contrary balls with lesser radius of curvature (smaller balls) can cause greater harm as that they can enter the orbital cavity and directly hit the eyeball. Thus ball injuries could be large, medium or small ball injuries. a. Small balls like golf and squash balls can cause severe eye injuries because of their curvature, some mass and great velocity. Out of 29 cases of golf ball injuries USEIR9 has reported 12 (41%) as open Fig. 45.1: Traumatic hyphaema RE globe injury which has a very poor prognosis. Table 284 Clinical Diagnosis and Management of Ocular Trauma PHYSICAL CONTACT INJURIES In many sport there is close physical contact which can lead to eye injuries. Boxing and wrestling are common games in this group. In India ‘Kabaddi’ is a popular game in rural areas where also there is close physical contact between players. In a report from New York out of 74 boxers about two third had some evidence of eye injury.10 Black eye is commonly seen in boxing. Free style wrestling is also a dangerous game. In other games also like basketball, football and soccer contact with hand or foot can cause either a direct injury or after a fall. There are other types of ball injuries also.

Fig. 45.2: Cricket ball injury MISCELLANEOUS There many other types of sports and games in different parts of the world which can lead to ocular trauma. Some of them include fishing, hunting, water sports, motor sports, Bungee cord and fireworks. The last one is quite common in many countries during festivals and can cause a burn or blast injuries sometimes to both the eye balls.11 Air gun injuries are also common in young boys. As in all types of injury males are four times prone to sports injury and the incidence is highest in 11-15 age group.12 The incidence of sports trauma also depends on the craze of a particular game in a particular country. Thus cricket is very popular in South Asia (India, Pakistan, Ceylone and Bangla Desh). In Europe football and soccer are extremely popular. In USA boxing and Fig. 45.3: Hockey ball injury tennis are very common games apart from baseball and basketball. tennis ball can cause no injury because of its very light weight. b. Medium size balls like cricket and hockey balls can References also cause very severe injuries because of their hardness and velocity. In cricket right handed 1. Schein OD, Hibbers PL, Shingleton BJ, et al. The Spectrum and burden of ocular injury. Ophthalmology, batsmen can get their left eye more affected and 1988;95:300-05. vice versa (Fig. 45.2). In hockey the goal keeper 2. Blomdahi S, Norell S. Perforating eye injury in the is at great risk (Fig. 45.3). However due to helmet Stockolm population, An epidemiological study, Acta such injuries have become rare. Tennis ball though Opthalmol 1984;62:378-90. of lesser weight also causes severe eye injury 3. Strahlman E, Elman M, Baker S. The incidence and because of high velocity. Thus a tennis ball weighs causes of pediatric ocular trauma, a population based study, Invest Opthalmol Vis Sci 29 (ARVO Suppl). only 58 grams but its velocity is 132’/second.10 1988;63. c. Large size balls include football, volleyball, 4. Kennedy RH, Brubaker RF. Traumatic hyphaema in a basketball and others. Though these games are very defined population. Am J Ophthalmol 1988;106: commonly played usually they do not cause a severe 123-30. injury. Thus in a report from USEIR out of the 13 5. Karloson T, Klein B. The incidence of acute hospital cases of football and 24 cases of soccer none treated eye injuries. Arch Ophthal 1986;104:1473-76. received an open globe injury though in basketball 6. White M, Morris R, Feist R, et al. Eye Injury, prevalence and prognosis by setting. South Med J 1989;82:151-58. out of 66 cases 11 had open globe injury. In 7. Ference K, Mester V, Mann L, et al. Eye injury epidemilogy basketball physical contact with hand and fist can and prevention of ophthalmic injuries. Kuhn F, Pieramici also add to the severity of injury. So is true with DJ (Eds). In: Ocular Trauma, Tieme Publication, baseball. New York 2002;19. Sports Injuries in Eye 285

8. Shukla B. Sports Injuries. Shukla B, Natarajan S (Eds). 10. Giovinazzo VJ, et al. The ocular complications of boxing, In: Management of ocular Trauma, CBS Publishers, New ophthalmology 1987;587-95. Delhi 2005;322. 11. Wilson RS. Fireworks blindness: A co-operative study. 9. Vinger PF. The need for standardization for protec- South Med J 1980;73:728-31. tive eyewear in sports. Kuhn F, Pieramici DJ (Eds). In: 12. Laroche GR, McIntyre L, Schertzer RM. Epidemiology of Ocular Trauma, Thieme Publication, New York severe eye injuries in childhood. Opthalmology 1988; 2002;456-57. 95:1603-07. CHAPTER

Management of Travel Eye Injuries 46 Leonardo Toledo Netto, Belquiz A Nassaralla (Brazil)

Introduction Prevention and Management There are approximately 2.4 million ocular and orbital NON-CONTACT EYE INJURIES injuries in the US per year, 20,000 to 68,000 of which The use of spectacles, even those with impact-resistant are vision-threatening injuries, and some 40,000 lenses, is not enough to protect your eyes during your persons sustain significant vision loss each year.1 The summer trip. In fact, they can increase the risk by Eye Injury Registry of Alabama (EIRA) has published shattering under high impact. However, they are of a study with 514 serious eye injuries of which 5% have slight value in the presence of small splash hazards or resulted from travel accidents.2 After an accident, the case history should be the flight of small insects. directed particularly to details of the trauma, pre-injury On travels, it is common to have dirt or grit in the vision, previous ocular surgery, medical history, current eye. It can be harmless, but it can also scratch the medications, and allergies. Since many periorbital and eyeball and cause infection. In this case, it is important eyelid injuries can also involve the globe, a history of to take the time to flush the eye clean. any change in visual acuity or severe ocular pain after Other frequent condition on travels is sun super the injury should be obtained. exposition. High intensities of UVB light are hazardous Visual acuity may be difficult to ascertain and topical to the eyes, and exposure can cause welder’s flash anesthesia may be necessary to facilitate this task. (photokeratitis or arc eye) and may lead to cataracts,

Detailed history is fundamental to the selection of pterygium, and pinguecula formation. Protective appropriate investigative procedures and for the eyewear is beneficial to those who are exposed to planning of therapy. In addition, any serious ocular ultraviolet radiation, particularly short wave UV. Given trauma may involve medicolegal action, and that light may reach the eye from the sides, full coverage consequently the importance of taking and carefully eye protection is usually warranted if there is an increased recording a detailed history cannot be overemphasized. risk of exposure, as in high altitude mountaineering. External examinations should always include Mountaineers are exposed to higher than ordinary levels pupillary testing, extraocular motilities measurements, of UV radiation, both because there is less atmospheric and confrontation visual fields. If the patient has filtering and because of reflection from snow and ice. sustained blunt ocular trauma, a cover test (or Maddox Exposition to new groups of allergens in different rod testing) should be performed, the eyelids and countries, cities and hotel rooms may also affect orbital margins should be palpated, and forehead and travelers.3 When traveling by auto, bus or train, potential cheek sensitivity should be evaluated. irritants or allergens can include dust mites, indoor Slit-lamp examination should include fluorescein molds, pollens and other substances. Common staining, which is necessary for Seidel testing and allergens such as mites and molds can lurk in the applanation tonometry, but tonometry should be carpeting, upholstery and ventilation systems of deferred if there is a known open globe injury. A dilated vehicles. Before beginning a lengthy auto trip, it is fundus exam (with or without sclera depression, as important to turn on the air conditioner or heater and appropriate) is also essential during the trauma open the windows for at least 10 minutes prior to examination. entering the car. This will help remove dust mites and/ Travel eye injuries may be divided in non-contact or molds that may be in the system. Outdoor allergens, or direct traumatic injuries and most of them are such as pollens and molds, are also potential hazards, preventable. especially when traveling with open windows. Management of Travel Eye Injuries 287 Cigarette smoke or outdoor air pollution can 3. If you are a frequent flyer, avoid using high water worsen allergy symptoms. To avoid excess air pollution contact lenses because this type of lens dries and when traveling by automobile, it is better to travel in distorts easier. Materials such as silicone hydrogel early morning or late evening, when the air quality or rigid gas permeable lens may help. is better and it is possible to avoid heavy traffic. 4. Contact lens care systems which contain Air quality on planes can greatly affect the allergic moisturizing agents as HPMC and Propylene Glycol patient. While all domestic flights are now smoke free, can create a shield of moisture between the lens many international flights are not. If traveling abroad, and the eye, to ensure prolonged lubrication. For allergic patients should make sure they are seated as sensitive eyes, a hydrogen peroxide system may far as possible from the smoking section when getting help in reducing irritation. a seat assignment. 5. Use lubrication drops during the flight. A lubricating Many travelers stay at hotels. Hotel rooms, eye drop containing sodium hyaluronate, has been however, often contain large concentrations of dust proven to effectively reduce dry eye symptoms. mites and molds in carpeting, mattresses and Use a preservative-free formula for sensitive or upholstered furniture that can worsen allergy allergy-prone eyes. symptoms. Irritant fumes from cleaning products may 6. Carry a pair of spectacles with you. If dryness also cause problems. When making hotel reservations, persists, remove the lenses and wear the spectacles. it is important to ask if there are allergy-proof rooms 7. Under new flight security regulations, there are available. If the patient is sensitive to molds, it is better limitations on carrying liquid over 100 ml per to request a sunny, dry room away from areas near container in hand baggage. In this case, you can indoor pools. Also, for those who have allergies to any carry a contact lens case containing fresh multi- animals, it is important to inquire about the hotel’s purpose contact lens solution. If you experience pet policy, and request a room that has been pet-free. any discomfort, simply remove your lenses and According to Aslam et al4, at the emergency place them in the lens case. department of the Chelsea and Westminster Hospital 8. In desert, beaches and tropical countries it is very in London, UK, 12% of the emergencies involving the important to use sunglasses with U-V protection. ocular surface are related to contact lens wearers. The Make sure the label states that the lenses block 99 main environmental factor in pressurized cabins that to 100 percent of both UVA and UVB rays. When can affect eyes is low humidity.3 The optimum humidity you are driving the sunlight can reflect from the range for comfort is between 40% and 60%. However, road pavement, or when you are shipping, the cabin humidity may drop to 11% after takeoff. The water like the snow in skiing, can burn the eyes low cabin humidity during air travel increases aqueous surface. tear evaporation and can cause ocular discomfort such as dryness, especially for contact lens wearers. The DIRECT TRAUMATIC INJURIES presence of a contact lens in the eye can produce a In a study published in 1998 by the Flight Safety condition called contact lens-induced dry eye (CLDE), Foundation,5 there are an estimated 4,500 incidents in an otherwise normal individual. Contact lenses may of injuries from falling baggage each year in the U.S. disrupt normal tear physiology through thinning and and about 10,000 such events worldwide. Baggage breakup of the tear film, interrupt tear film reformation can emerge uncontrolled from overhead and rupture the lipid layer with consequent increase compartments if the contents shift in flight or if the in tear film evaporation. The symptoms include compartments were loaded beyond their capacity. This grittiness, scratchy eyes, lens intolerance, and blurred study was based on a survey of 462 falling baggage vision. Therefore, contact lens wearers should know events on the 757 aircraft of an unnamed major U.S. preventive measures as follows: airline. Of these 462 events, which occurred during 1. Beverages containing alcohol or caffeine and certain the mid-1990s, a person was struck in 397 cases. In medications can exacerbate dryness. If lenses are those cases where a person was struck, there were 67 worn during air travel, avoid alcohol and coffee injuries involving bruising, 53 injuries involving consumption. lacerations, and 277 cases resulting in no injuries. More 2. Lens deposits reduce lens wetting and increase tear than 90 percent of the injury cases involved head evaporation. Clean the lenses thoroughly before injuries to aisle seat passengers. the journey. If you are a disposable lens wearer, In automobile trips we have to consider the air bag, insert new fresh lenses. If you are a yearly an inflatable device designed to decrease the morbidity replacement lens wearer, use a protein remover associated with high speed vehicle collisions. Front air in addition to your normal lens cleaning regime bags, for the driver and right-front passenger, mainly before the journey. provide protection against head contact with the 288 Clinical Diagnosis and Management of Ocular Trauma steering wheel and dashboard. They are designed as type of corneal injuries may result from two supplementary restraint systems (SRS), meaning that mechanisms. The first is a chemical keratitis resulting the protection they provide is in addition to that offered from exposure to the alkaline sodium azide gas that by the use of a regular lap-and-shoulder seat belt. is used to inflate the air bag. The second mechanism Because air bag deployment happens so rapidly, is blunt impact between the eye and the air bag.8 it is extremely important that vehicle occupants should Figure 46.1 shows a blunt eye trauma after air bag not be too close to the air bag modules. These are deployment.9 generally located in the steering wheel hub and the It is difficult to determine the true incidence and upper right-front dashboard. There would be significant range of severity of these ocular injuries for two reasons. risk of head, neck and chest injury if an occupant were First, patients involved in motor vehicle accidents may to be struck by the flaps of the air bag cover as they have multiple systemic injuries, and ocular trauma may open (punch out), or by the rapidly expanding fabric therefore not be recognized. Second, a bias of of the bag as it is inflated (membrane loading). Most ascertainment exists, in that severe ocular injuries are agencies recommend that occupants should be at least more likely to be reported than the minor injuries. 25 cm (10 inches) away from the air bag module. Few case series of air bag-related ocular injuries have Child passengers in the right-front seat of vehicles been reported, and these also are biased towards severe equipped with air bags are of particular concern. Rear- injury.10 Such injuries range from relatively mild (e.g. facing infant carriers should never be installed in the corneal abrasions, eyelid ecchymosis) to severe (e.g., right-front seat when there is an air bag. This would hyphema, lens injury, retinal detachment and angle place the child’s head much too close to the passenger’s recession).11 Figure 46.2 shows a case of a man who air bag module. Many children have been killed or sustained an airbag-induced face and periorbital injury. seriously injured in this manner. Similarly, most agencies It highlights the potential harm that can be caused by recommend that children aged 12 and under should airbags.9 be seated in the rear of the vehicle with an age- appropriate restraint system (infant carrier, child seat, booster cushion and seat belt). Children frequently don’t sit still in vehicles. They will often sit on the edge of their seat, lean forward, and may even slip their body out of the seat belt or child restraint harness. If a child were to do this in the right-front passenger’s seat at the very instant that a collision occurred, they would be out of position and too close to the air bag, and this could easily result in serious injury or fatality.6 Corneal injuries have been frequently reported in adults in association with air bag deployment.7 This

Fig. 46.2: Airbag-induced face and periorbital injury (From: Spoor TC)

Fukagawa et al12 demonstrated corneal endothelial cell damage in an animal model of blunt ocular air bag injury. In this model, porcine eyes were placed in the orbits of a crash-test dummy and exposed to deploying air bags at different distances, air bag weights, and bag inflation powers. Histopathologic examination of the corneas after air bag inflation revealed damage to the corneal endothelial cell membranes and exposure of Descemet’s membrane, consistent with detachment of Descemet’s membrane or endothelial cell loss. Air bag associated ocular injuries have only rarely been described in children. In a retrospective study, 10 Fig. 46.1: Airbag-related blunt eye trauma Lueder reviewed the medical records of seven (From: Spoor TC) children who were injured by air bags and concluded Management of Travel Eye Injuries 289 Conclusion Eternal vigilance is the price of safety. The greatest deterrent to ocular injury is educated awareness of risk and careful avoidance procedures. Trauma, usually needless, continues to be one of the major causes of lost eyes. Automobile crashes continue to be one of the most common causes of death from age 1 to 24 years. Males distinctly predominate in the statistics of ocular injury and are increasingly represented in motor vehicle crash. Proper and complete assessment of any patient with ocular trauma is the basic prerequisite for anatomical and visual rehabilitation of a patient with Fig. 46.3: Operating microscope view of a corneal laceration ocular trauma. in the right eye of a 4-year-old boy after a lateral car crash. There was a significant hyphema (iris details are obscured), soft globe, expulsion of the lens and iris extrusion References that serious ocular injuries may result, although most 1. Rappon JM. Ocular Trauma Management for the Primary injuries heal without detrimental long-term effects. Care Provider. In: www.opt.pacificu.edu. Accessed June 15, 2008. However, there can be serious consequences if the 2. White MF Jr, Morris R, Feist RM, Witherspoon CD, Helms child is too close to the air bag when it deploys. The HA Jr, John GR. Eye injury: Prevalence and prognosis most serious injuries in these children were cataracts by setting. South Med J 1989;82(2):151-8. and glaucoma. Other injuries were blood in the front 3. Wong Gunter.In: Leaving on a Jet Plane- Tips for chamber of the eye, alkali bum, temporary loss of contact lens wearers who travel on a plane. consciousness and visual acuity, eyelid laceration, black In:www.useronline.org. Accessed June 15, 2008. eye, swelling and hemorrhaging of the blood vessels 4. Aslam SA, Sheth HG, Vaughan AJ. Emergency manage- ment of corneal injuries. Injury 2007;38(5):594-7. under the outer surface of the eyeball, corneal lesions 5. Rozmaryn L. Head Injury risks from overhead luggage. and abrasions, and iris inflammation. Figure 46.3 The AirSafe J 1999;13. shows the right eye of a 4-year-old boy seriously 6. Braver ER, Ferguson SA, Greene MA, Lund AK. injured after a vehicle (Fiat Uno) lateral crash. The Reductions in deaths in frontal crashes among right front child was unbelted and seated in the rear of the car. passengers in vehicles equipped with passenger air bags. His eye was hit by fragments of glass from the broken JAMA 1997;278:1437-9. side window. 7. Smally AJ, Binzer A, Dolin S, Viano D. Alkaline chemical keratitis: eye injury from airbags. Ann Emerg Med Chemical eye injuries may also affect travelers, and 1992;21:1400-2. they are potentially blinding injuries. If chemicals are 8. Ingraham HJ, Perry HD, Donnenfeld ED. Airbag Keratitis. splashed into the eye, the eye and the conjunctival N Engl J Med 1991;324:1599-600. sacs (fornices) should be washed out immediately with 9. Spoor TC. An Atlas of Ophthalmic Trauma. Editora copious amounts of water. Alkali injuries are more Manole Ltda, Sao Paulo, Brasil, 1999;3:35-44. common and can be more deleterious. Bilateral 10. Lueder GT. Airbag-associated ocular trauma In children. chemical exposure is especially devastating, often Ophthalmology 2000;107:1472-75. 11. Driver PJ,Cashwell LF,Yeatts RP. Air bag associated resulting in complete visual disability. Immediate, bilateral hyphemas and angle recession. Am J prolonged irrigation, followed by aggressive early Ophthalmol 1994;118:250-51. management and close long-term monitoring, is 12. Fukagawa K, Tsubota K, Kimura C. Corneal endothelial essential to promote ocular surface healing and to cell loss induced by air bags. Ophthalmology 1993;100: provide the best opportunity for visual rehabilitation. 1819-23. CHAPTER

Ocular Injuries after Vehicular Accident and Possible Prevention 47 Bojan Pajic, Brigitte Pajic-Eggspuehler, Jasna Ljubic (Switzerland)

Introduction which contains a combustible solid-state powder, usually sodium azide (NaN3), and an oxidizing agent.21 Constructional improvement of passengers safety in The combustion of sodium azide produces mostly inert cars alone did not result in a significant decline of open nitrogen gas, but other byproducts include ammonia, globe injuries in traffic accidents. Only after compulsory carbon dioxide, nitric oxide, carbon monoxide, an seat belt legislation was introduced, a 60-70% alkaline aerosol containing sodium hydroxide, and reduction in ocular injuries was observed. Emerging various metallic oxides. An inert talc powder used in statistics have revealed seat belts to be the primary packaging also is discharged. Heat is an additional by- occupant safety system, and use of seat belts along product of the combustion process. The expanding with airbags has provided a cumulative reduction in bag splits the plastic casing and is propelled out of the adult accident injuries and fatalities. Airbags gained storage compartment at 160 to 320 km/h, depending widespread popularity as an effective means of on the manufacturer. The entire inflation sequence is reducing severe injury and death during motor vehicle completed within 0.05 seconds (Table 47.1). The accidents in the late 1980s. Airbags on both the driver airbag capacity varies widely, but most fully inflated and passenger side are mandatory on all 1998 and bags contain 60 L of gas on the driver’s side and 140 later-model cars and in 1999 and later light trucks. L on the passenger’s side. The driver-side airbag With use of both airbags and seat belts, fatalities have expands to a depth of 25 to 30 cm. The passenger- been reduced 50% in all types of crashes. Fatalities side airbag expands to a greater depth. Some bags have been attributed to the airbag deployment, many are tethered, others are not. A tethered bag contains occurring during slow-speed crashes. The purpose of one or more straps that limit its anterior-posterior this investigation is to examine data reported in the expansion. The airbag quickly begins to deflate through numerous case studies of ocular injuries attributed to vents directed away from the occupant. Systems vary airbag deployment in order to gain a better widely between vehicle models. The purpose of the appreciation of the scope of ocular damage and to airbag is to cushion the occupant from the rigid identify individuals more susceptible to such injuries. components of the vehicle interior. In order to provide When travelling in the right front passenger seat during the desired cushion, the airbag should expand with frontal crashes, adults have a significantly lower sufficient speed to be fully inflated before the occupant mortality risk when airbags are deployed, but children moves forward following impact. Occupants who are 1 have a substantially increased mortality risk. Ocular positioned too close to the wheel may be caught within injuries associated with airbag deployment have been the envelope of the expanding airbag. Even when reported in many adults.2-19 TABLE 47.1: Airbag inflation sequence The Airbag System Time (sec) Action 0 Frontal impact The airbag is a coated nylon bag housed within the 0.015 Sensors signal to cartridge NaN3 ignited steering column on the driver side and within the dashboard on the passenger side.20 Sensors located Bag inflation begins within the vehicle structure are activated when a crash 0.05 Bag fully deployed occurs at 19.3 km/h or faster and within a 60° frontal 0.06 Occupant strikes fully inflated bag arc. An electrical signal is sent to the airbag cartridge, 1-2 Bag deflates Ocular Injuries after Vehicular Accident and Possible Prevention 291 properly belted, occupants will move forward, although TABLE 47.2: Anterior segment injuries to a lesser degree. In any motor vehicle accident there are at least 2 collisions: the vehicle with the object of No of patients % patients impact and the occupant with the airbag or car interior. Usually a third, or “rebound,” collision also occurs. Corneal Abrasio 163 31.5 Hyphema 105 20.3 Eyelid laceration, burn, periorbitale contusion 39 7.5 Methods Iritis 13 2.5 The investigators performed an exhaustive review of Iris tear 13 2.5 the literature of peer-reviewed papers published Cataract 151 29 Angle recession 21 4 between 1991 and 2008 that described ocular injuries Corneal/scleral laceration/ related to airbag inflation or car accident. Furthermore, ruptured globe 63 12.2 own experience are insert in this review study. Each Chemical keratitis 12 2.3 of the paper, inclusively the own data, that formed Lens dislocated/subluxated 101 19.5 the database for this study was reviewed, and Orbital fracture 15 2.9 information pertaining to the following variables was Facial nerve palsy 1 0.2 extracted from each article and recorded on a SPSS spread sheet: patient age, sex, position in the vehicle 101 of patients. Angle recession was found in 21 and (driver or front-seat passenger), patient height, eye chemical keratitis in 12. The integrity of the globe was wear (if any) worn by the patient at the time of the compromised in 63 of patients. Most of these ruptured accident, eyes injured, last reported visual acuity, seat- globes sustained significant damage to many ocular belt use at the time of the accident, the object of impact, structures with resultant poor vision. As might be speed of the vehicle at impact, and all ocular injuries anticipated, injuries to the periorbital area (7.5%) were resulting from the accident. Heights reported in inches common and included lacerations, burns, and were converted to centimeters, and speeds reported contusions. Some lacerations required skin grafting and in mph were converted to km/h. plastic repair. Other anterior segment injuries included traumatic iritis (2.5%), iris tear (2.5%), orbital fracture (2.9%), and facial nerve palsy (0.2%). Results POSTERIOR SEGMENT INJURIES Review of the literature from 1991 to 2008 and own data identified describing 518 patients with ocular Retinal or vitreous hemorrhage occurred in 15.5% of injuries accident deployment during a motor vehicle injured occupants (Table 47.3). Retinal tear or accident.1-51 detachment (11%) and commotio retinae (3.1%) were also common. Other traumatic injuries reported were PATIENT PROFILE macular hole (0.8%), choroidal rupture (1%), traumatic maculopathy (2.9%), and optik disc edema 343 (66.2%) of the injured occupants were male, and (0.2%). Most likely, these patients also sustained 175 (33.8%) were female. The age of the patients anterior segment injuries, but they were not docu- varied between 1 and 83 years, with a mean age of mented. 25.5 years. 70.5% of patients were wearing three-point seat belts, 29.5% were known to be not belted. VISUAL ACUITY Best-corrected visual acuity at the last examination with OCULAR INJURY PROFILE a mean follow-up time of 6.5 months was as follows. 55.3% of occupants sustained injuries limited to the In 9.19% a enucleation had to be performed. 13% anterior segment of the eye, 31.7% to both anterior and posterior segments and 13% to the posterior TABLE 47.3: Posterior segment injuries segment. No of patients % patients Vitreous/retina hemorrhage 80 15.4 ANTERIOR SEGMENT INJURIES Retina tear/detachment 57 11 Commotio 16 3.1 Corneal abrasion occurred in 163 of the total database Macular hole 4 0.8 of 518 patients, and hyphema was reported in 105 Choroidal rupture 5 1 of occupants (Table 47.2). A cataract was present Traumatic maculopathy 15 2.9 Optic disc edema 1 0.2 in 151, and the lens was dislocated or subluxated in 292 Clinical Diagnosis and Management of Ocular Trauma

TABLE 47.5: Estimated effectiveness of occupant protective systems in reducing injury Injury severity System used front damage

Moderate Air bag+lap-shoulder belt 61% Air bag alone 6% Manual lap-shoulder belt 56% Serious Air bag+lap-shoulder belt 69% Fig. 47.1: Visual acuity distribution after injuries Air bag alone –8% Manual lap-shoulder belt 74% had no light perception. 4.81% there was light perception. 7.79% of patients had a visual acuity of less than 0.05. 2.41% had a final visual acuity of 0.01, NHTSA reported 113 fatalities attributed to airbag 57 12.63% had a best-corrected visual acuity of less than deployment as of September 1,1998. Forty-seven 0.4, 24.32% had less than 0.7 and 25.85% had a were adults, only 13 of whom were properly restrained. final visual acuity of less than 1.0 (Fig. 47.1). Fifteen infants in passenger-side rear-facing car seats In the age group of 18 to 22 years old has the were killed. The infants head was too close to the highest risk of injury. The most number of accidents expanding bag. Fifty-one children aged 1 to 12 were (85%) were during the night, it is said between 18.00 killed, none of whom were properly restrained. and 06.00 o’clock and during winter time, from Children should be in the back seat and belted! The October to March. 17.9% patients admitted that, at Insurance Institute for Highway Safety updates these 58 the time of the accident, they were under the influence statistics periodically. Spontaneous deployment of 59 of alcohol. airbags also has been reported. Several large-scale recalls have occurred because of the potential threat Discussion of spontaneous airbag deployment. Occupants positioned within 25 centimeters of the wheel or A 58 to 73% reduction of penetrating ocular injuries dashboard cannot avoid being injured. occurred when use of a car seat belt became obli- NHTSA has permitted manufacturers to “depower” gator.54-56 The seat belt protects the eye from injury the airbag by 20 to 35%.20 Depowering the bag should as it prevents the forward movement of the body and reduce airbag-induced injuries in smaller and average- consequently the possible hit of the head against the sized occupants but may place larger individuals at windshield of the car. increased risk of injury, particularly during high-speed Airbags are most effective in preventing fatal driver crashes. Side airbags already have been placed in the injury in pure frontal crashes but also are effective in newer car models. Concern has been expressed for 10 o’clock to 2 o’clock frontal arc crashes. They play passenger-side children as well as adults resting against no role in side, rear, or rollover crashes. In crashes the door. So-called “smart bags” are being developed. of all types, the airbag and seat belt combination The next generation of sensors will enable the airbag reduced fatalities 50 compared with unbelted drivers to deploy according to the severity of the impact, the in a passenger car without an airbag (Table 47.4). proximity of the occupant to the bag, and the weight The airbag alone reduced driver fatality 13%, and the and height of the occupant. The development of this seat belt alone, 45%.20 NHTSA has calculated the effectiveness of occupant protective systems in reducing technology is ongoing and will be phased in over the moderate and serious driver injury in frontal crashes next few years. compared with unbelted drivers with no airbag Seat-belt performance varies greatly between (Table 47.5). The airbag is less effective than a manufacturers. The configuration of airbags and their combination of seat belt and airbag or the seat belt speed and pattern of deployment vary by model and alone. manufacturer. These factors, which are very important to the safety engineer, could not be documented in these cases. Although the airbag deployment and the TABLE 47.4: Estimated effectiveness of occupant eye injury seem to be cause and effect in most cases, protection system in reducing fatality risk for passengers and drivers in all types of crashes other elements, such as collision with the rear-view mirror, side window, or loose articles within the car System used Fatality Reduction interior, may have played a role. These precautions Air bag+lap-shoulder belt 50% not withstanding, this investigation serves to increase Air bag alone 13% the awareness of the role of occupant safety systems Manual lap-shoulder belt 45% in motor vehicle accidents and to document air-bag- Ocular Injuries after Vehicular Accident and Possible Prevention 293 related eye injuries and the factors associated with their clinically.14, 29, 65 In one patient with irreversible bullous occurrence. keratopathy, a corneal transplant was required.13 Burns The majority of the ocular injuries in this series are have been estimated to occur in 7.8% of all injuries the result of blunt trauma between the occupant and associated with airbag deployment.25, 66 Burns may be the airbag, in either its expanding phase or its fully due to vented hot nitrogen gas or melting of clothing inflated status. Obviously, a greater impact force will or may be chemical in origin.67 Chemical keratitis is be generated when a forward-moving eye strikes an the result of corneal contact with the ammonia, sodium expanding bag. Penetrating injuries and alkali burns hydroxide, and the alkaline aerosol that are emitted 27, 32, are exceptions to the blunt trauma mechanism. as by-products of the combustion of sodium azide, 47 Severe blunt trauma has been shown experimentally which is used to inflate the airbag.2, 68 While the hot to decrease the anterior-posterior diameter of the globe nitrogen gas and the by-products are vented away 60 by 41%. Reduction of the anterior-posterior diameter from the occupant, accident circumstances may bring 61 of the globe beyond 60% will result in rupture. The the alkali into contact with the eyes. Resulting burns flattening of the anterior chamber may cause the will depend on the amount and duration of corneal corneal endothelium to come in contact with the iris exposure to the alkali. and anterior surface of the lens. There is an expansion Hyphema injury, along with angle recession, is the of the equatorial diameter of the globe. Severe traction result of the sudden increase in pressure created by on the vitreous base develops during the initial phase the flattening of the anterior chamber following. The following impact.61 This has been demonstrated experimentally with pellet guns and is believed to aqueous has nowhere to go and dissects the angle 63 explain much of the ocular damage sustained in and iris root. Most hyphemas absorbed. The long- nonperforating BB gun injuries.62 Most of the ocular term potential complication of angle recession injuries to the iris, angle, lens, vitreous, retina, and glaucoma should be discussed with patients. choroid documented in this study are compatible with The majority of developed cataract were described a blunt trauma injury mechanism.63 It has been shown as an opacification of the anterior capsule and cortex. that the airbag dramatically decreases brain injury in They are the result of contact between the corneal motor vehicle accidents.20, 24 The combination of airbag endothelium and the anterior lens surface. The integrity plus a lap-shoulder belt reduces the risk of moderate of the lens capsule was compromised in other cases, and serious head injury to drivers in frontal crashes leading to more severe opacification. Dislocation and by 75%, compared with a 38% reduction for seat belts subluxation of the lens are the result of zonular rupture alone. However, the brain is fully encased by rigid secondary to deformation of the globe. Bilateral lens bone. The eye has an open surface. dislocation occurred in one case.38 A great deal of publicity has been given to the The rapid horizontal expansion of the globe at the increased risk of airbag injury to individuals of small- vitreous base creates traction that results in retinal breaks stature who, presumably, are positioned closer to the and dialysis in this area.62, 64 Several clinical studies have steering wheel. Many of the reports reviewed in this demonstrated the preponderance of retinal damage investigation mention this circumstance. NHTSA’s associated with blunt trauma to occur at the ora serrata comprehensive report contains information suggesting and vitreous base.69-71 The position of the retinal tears that occupants of small-stature are at greater risk of and detachments in this study was not described in injury.20 While this sounds very reasonable, hard data sufficient detail to allow further speculation on an are lacking. Driver position in relation to the steering airbag trauma pattern. All patients with air-bag-related wheel is more important than actual stature. injuries should have a thorough indirect ophthalmo- The corneal abrasions are the result of impact with scopic examination when possible and ultrasound the airbag, either directly or in an abrasive “slap” examination in those cases in which vitreous hemor- motion from an unfolding bag. Most of the corneal rhage or hyphema prevents adequate visualization. surface often is involved. Generalized stromal edema Commotio retinae and macular holes injuries are the and folds in Descemet’s membrane frequently are result of a countercoup-type force commonly found present. One investigator described the imprint of the in blunt trauma to the globe.63 airbag on the cornea. The imprint of an open eye, Likewise, those patients who have undergone complete with eye shadow, mascara, and lashes has refractive surgeries, including RK, PRK and LASIK, are been seen on the airbag. The airbag deploys quicker also more at risk for development of severe ocular than a blink. Fortunately, most corneal abrasions heal injuries, secondary to compromised corneal integrity.72,73 without sequellae, although a decreased endothelial The airbag is appropriately labeled SRS (Supple- cell count has been demonstrated experimentally and mental Restraint System). The best way to reduce the 294 Clinical Diagnosis and Management of Ocular Trauma risks of injury from the car interior or the airbag in 19. Ghafouri A, Burgess SK, Hrdlicka ZK, Zagelbaum BM. a motor vehicle accident is to wear a seat belt and Airbag-related ocular trauma. Am J Emerg Med 1997; be properly positioned 25 centimeters or more from 15: 389-92. 20. National Highway Traffic Safety Administration. the wheel. Children should be in the back seat and Effectiveness of Occupant Protective Systems and Their belted. Use. Third Report to Congress. Washington, DC: US Department of Transportation; December 1996. 21. Kuhn F, Morris R, Witherspoon CD. Eye injuries and the References airbag. Curr Opin Ophthalmol 1995,111:38-44. 22. Ingraham HJ, Perry HD, Donnenfeld ED. Airbag keratitis. 1. Braver ER, Ferguson SA, Greene MA, Lund AK. N Engi J Med 1991;34:1599-1600. Reductions in deaths in frontal crashes among right front 23. Hueike DF, Moore JL, Ostrom M. Airbag injuries and passengers in vehicles equipped with passenger airbags. occupant protection. J Trauma 1992:33:894. JAMA 1997;278:1437-9. 24. Campbell JK. Automobile airbag eye injuries. Nebraska 2. Smally AJ, Binzer A, Dolin S, Viano D. Alkaline chemical Med J 1993,78:306-07. keratitis: eye injury from airbags. Ann Emerg Med 25. Swanson-Bierman B, Mrvos R, Dean BS, et al. Airbags: 1992;21:1400-2. Lifesaving with toxic potential? Am J Emerg Med 1993; 3. McDermott ML, Shin DH, Hughes BA, Vale S. Anterior 11:38-39. segment trauma and airbags [letter]. Arch Ophthalmol 26. Braude LS. Passenger side airbag ocular injury while 1995;113:1567-8. wearing sunglasses. Br J Ophthalmol 1995:79:391. 4. Scott IU, John GR, Stark WJ. Airbag-associated ocular 27. Gault JA, Vichnin MC, Jaeger EA, et al. Ocular injuries injury and periorbital fractures [letter]. Arch Ophthalmol associated with eyeglass wear and airbag inflation. / 1993;111:25. Trauma 1995;38:494-97. 5. Whitacre MM, Pilchard WA. Airbag injury producing 28. Goldberg MA, Valluri S, Pepose JS. Airbag related comeal retinal dialysis and detachment [letter]. Arch Ophthalmol rupture after radial keratotomy. ATM/ Ophthalmol 1993;111:1320. 1995,10:800-802. 6. Lesher MP, Durrie DS, Stiles MC. Corneal edema, 29. McDermott ML, Shin DH, Hughes BA, et al. Anterior hyphema, and angle recession after airbag inflation segment trauma and airbags. Arch Ophthalmol 1995; [letter]. Arch Ophthalmol 1993; 111:1320-2. 113;1567-68. 7. Rosenblatt MA, Freilich B, Kirsch D. Airbag-associated 30. Sastry SM, Copeland RA Jr, Mezghaba H, et al. Retinal ocular injury [letter]. Arch Ophthalmol 1993;! 11:1318. hemorrhage secondary to airbag-related ocular trauma/ Trauma 1995;38:82. Comment on: Arch Ophthalmol 1993;111:25. 31. Vichnin MC, Jaeger EA, Cault JA, et al. Ocular injuries 8. Han DP. Retinal detachment caused by airbag injury related to airbag inflation. Ophthalmic Surg Lasers [letter]. Arch Ophthalmol 1993;111:1317-8. 1995;26:542-48. 9. Rimmer S, Shuler JD. Severe ocular trauma from a 32. Walz FH, MacKay M, Gloor B. Airbag deployment and driver’s-side airbag [letter]. Arch Ophthalmol 1991; eye perforations by a tobacco pipe. J Trauma 109:774. 1995,38:498-516. 10. Driver PJ, Cashwell LF, Yeatts RP. Airbag-associated 33. White JE, McClafTerty K, Orton RB, et al. Ocular alkali bilateral hyphemas and angle recession [letter]. Am J bum associated with automobile airbag activation. CMAJ Ophthalmol 1994; 118:250-1. 1995;153:933-34. 11. Mishler KE. Hyphema caused by airbag [letter]. Arch 34. Baker RS, Flowers CW Jr, Singh P, et al. Comeoscleral Ophthalmol 1991; 109:163 5. Comment on: Arch laceration caused by airbag trauma. Am/ Ophthalnwl Ophthalmol 1991;109:774. 1996;121:709-11. 12. Larkin GL. Airbag-mediated comeal injury. Am J Emerg 35. Geggel HS, Griggs PB, Freeman MI. Irreversible bullous Med 1991;9:444-6. keratopathy after airbag trauma. CLAOJ 1996;2:148-50. 13. Geggel HS, Griggs PB, Freeman MI. Irreversible bullous 36. Michaeli-Cohen A, Neufeld M, Lazar M, et al. Bilateral keratopathy after airbag trauma. CLAO J 1996;22:148- comeal contusion and angle recession caused by an 50. airbag. Brj Ophthalnwl 1996;80:487. 14. Fukagawa K, Tsubota K, Kimura C, et al. Comeal 37. Molia LM, Stroh E. Airbag injury during low impact endothelial cell loss induced by airbags. Ophthalmology collision. Br J Ophthalmol 1996;80:487-88. 1993;100:1819-23. 38. Onwuzuruigbo CJ, Fulda GJ, Lamed D, et al. Traumatic 15. Zacovic JW, McGuirk TD, Knoop KJ. Bilateral hyphemas blindness after airbag deployment: Bilateral lenticular as a result of airbag deployment [letter]. Am J Emerg Med dislocation./ Trauma 1996;40(2):314-16. 1997;15:323-4. 39. Scott IU, Greenfeld DS, Parrish RK. Airbag-associated 16. Rosenblatt M, Freilich B, Kirsch D. Airbags: trade-offs injury producing cyclodialysis cleft and ocular hypotony. [comment]. N Engi J Med 1991;325:1518-9. Comment Ophthalmic Surg Lasers 1996;7:955-57. on: N Engl J Med 1991;324:1599-600. 40. Bedell JR, Malik V. Facial nerve paresis involving 17. Manche EE, Goldberg RA, Mondino BJ. Airbag-related passenger airbag deployment: A case report./ Emerg Med ocular injuries. Ophthalmic Surg Lasers 1997;28: 1997; 15:475-76. 246-50. 41. Bhavsar AR, Chen TC, Goldstein DA. Comeoscleral 18. Duma SM, Kress TA, Porta DJ, et al. Airbag-induced eye laceration associated with passeger-side airbag inflation. injuries: a report of 25 cases. J Trauma 1996; 41:114-9. Br J Opthalmol 1997;81:514-15. Ocular Injuries after Vehicular Accident and Possible Prevention 295

42. Cacciatori M, Bell RW, Habib NE. Blow-out fracture of 57. Safety fact sheet. National Highway Traffic Safety the orbit associated with inflation of an airbag: A case Administration Web site. Available at http:// report. Br J Oral Maxillofac Surg 1997:35:241-42. www.nhtsa.dot.gov/airbags/factsheets/numbers.html. 43. Dubinsky I, McGowan H. Case report: Retinal tear as a Accessed March 20, 1999. consequence of airbag inflation. Can Fam Physician 58. Airbags. Insurance Institute for Highway Safety Web site. 1997;43:1576-77. Available at http://www.highwaysafety.org/airbags/ 44. Madreperia SA, Benetz BA. Formation and treatment of airbag.htm. Accessed March 20, 1999. a traumatic macular hole. Arch Ophthalmol 1997; 59. Adams Sl, Petri RW. Injury with spontaneous deployment 115(9):1210-11. of an automobile airbag. Acad Emerg Med 1996;3: 45. Zabriskie NA, Hwang IP, Ramsey JF, et al. Anterior lens 179-80. capsule rupture caused by airbag trauma. Am J 60. Delori F, PomerantzeffO, Cox MS. Deformation of the Ophthalmol 1997;123:832-33. globe under high speed impact: Its relation to contusion 46. Goldblum D, Fleischhauser J, Bachmann HU, et al. injuries. Invest Ophthalmol 1969;8:290-301. Augenverletzungen (lurch airbag. Klin Monatsbl 61. Weidenthal DT, Schepens CL. Peripheral fundus changes Augenheilkd 1998;212:376-78. associated with ocular contusion. Am J Ophthalmol 47. O’Halloran HS, Draud K, Stevens JL. Priinary enucleation 1966;62:465-77. as a consequence of airbag injury. Trauma 1998; 62. Sternberg P, De Juan E, Green R, et al. Ocular BB 44:1090. injuries. Ophthalmology 1994;91:1269-77. 48. Ruiz-Moreno JM. Airbag associated retinal tear. Eur J 63. Benson W. Blunt trauma. In: Tasman W, Jaeger EA, eds. Ophthalmol 1998;8:52-53. Clinical Ophtlialmology. Vol III. Philadelphia: Lippincott 49. Totten VY, Fani-SaIek MH, Chandramohan K. Hyphema Williams and Wilkins;1998;chap 31. associated with airbag deployment in a pediatric trauma 64. Jagger J, Vemberg D, Jane JA. Airbags: Reducing the patient. Am J Emerg Med 1998;16:102-03. brain trauma. Neurosurgery 1987;20:815-817. 50. Schmitt-Bemard CF, Amaud B. Traumatisme oculaire et 65. Slingsby JG, Forstot L. Effect of blunt trauma on the brulure caustique par airbag. J Fr Ophthalmol 1998: comeal endothelium. Arch Ophthalmol 1981,99:1041- 43. 21:220-222. 66. Antosia RE, Partridge RA, Virk AS. Airbag safety. Ann 51. Kenney KSK, Fanciulio LM. Automobile airbags: friend Emerg Med 1995;25:794-98. or foe? A Case of ire bag-associated ocular trauma and 67. Hallock GG. Mechanisms of bum injury secondary to related literature review. Optometry 2005; 76: 382-86. airbag deployment. Ann Plast Surg 1997,39:111-13. 52. Panagiotidis DN, Theodossiadis PG, Petsias CB, Kyriaki 68. Schreck RM, Rouhama SW, Santrock J, et al. Physical TE, Marakis TR, Friberg TR, Moschos MN. Ocular injuries and chemical characteristics of airbag effluents. J Trauma secondary to motor vehicle accidents. Eur J of Ophtha- 1995;38:528-32. lmol 2003;14:144-48. 69. Cox MS, Schepens CL, Freeman HM. Retinal detachment 53. Schrader W, Gramer E, Goldmann F, Marcus U. due to ocular contusions. Arch Ophthalmol 1966; Penetrierende und perforierende Augenverletzungen bei 76:678-685. PKW-Unfällen von 343 Patienten vor und nach 70. Tasman W. Peripheral retinal changes following blunt Einführung des Bussgeldes für „Gurtenmuffel“. Klin trauma. Trans Am Ophthalmol Soc 1972;70:190-198. Monatsbl Augenheilkd 2000;217:23-29. 71. Welch RB. Peripheral retinal changes following blunt 54. Hall NF, Denning AM, Elkington AR, Cooper PJ. The eye trauma (Discussion). Trans Am Ophthalmol Soc and the seat belt in Wessex. Br. J Ophthalmol 1985; 1972,70:196-197. 69:317-19. 72. Uchio E, Kadonosono K. Are airbags a risk for patients 55. Johnston PB, Armstrong MF. Eye injuries in Nothern after radial keratotomy? Br J Ophthalmol 2001;85: Ireland two years after seat belt legislation. Br. J. 640-642. Ophthalmol 1986;70:460-62. 73. Uchio E, Watanabe Y, Kadonosono K, et. Al. Simulation 56. Vernon SA, Yorston DB. Incidence of ocular injuries from of airbag impact on eyes after photorefractive keratectomy road traffic accidents after introduction of seat belt by finite element analysis method. Graefe’s Arch Clin legislation. J R Soc Med 1984;77:198-200. Exper Ophthalmol 2003;241:497-504. CHAPTER

Bottle Cork Injury to the Eye 48 Gian Maria Cavallini, Matteo Forlini, Cristina Masini Luca Campi, Simone Pelloni (Italy)

Introduction the compression phase, a decompression can be observed and the antero-posterior diameter becomes In the field of blunt ocular trauma the bottle cork injury longer than the original one due to oscillatory forces of the eye can cause severe damage to the globe with depending on various factors such as the intrinsic secondary loss of visual function that can be permanent elasticity of the tissues involved. In this phase, the eye as we observed in the literature and in the series we structures are stretched and if the elasticity is lower report. than the oscillating forces the eye tissues may rupture. Various studies show the dangerous effect of An acute increases in vitreo-retinal traction is pressurized fluid, well-known even under normal produced from the expansion, which often results in 1,2 3 circumstances. Sellar and Jonhston highlight the retinal dialysis. Traumatic retinal dialysis most serious nature of these injuries in Britain pointing out commonly occurs inferotemporally and superonasally. the danger of glass bottles containing carbonated It can occur at the anterior margin of the vitreous base drinks, especially to young children. In his review of in the pars plana at the junction of the ciliary epithelium the databases of the United States (USEIR), Hungarian and neural retina, or in the retina at the posterior (HEIR), and Mexican (MEIR) eye injury registers, margin of the vitreous base.8 4 Kuhn reports that whilst most eye injuries caused by In another situation a direct contusion injury to the bottles containing carbonated drinks improved, in 26% globe can lead to disruption of the retina and necrotic of cases the patient remained legally blind. Another breaks. One common finding with blunt injuries, which work describes ocular injuries caused by bottle caps may lead to acute visual loss is Berlin’s edema in Israel.5 (Commotio retinae).9 The scleral spur is also involved Archer and Galloway6 reviewed the medical records and intraocular pressure (IOP) is raised. of nine patients consecutively diagnosed with This type of domestic injury is considered as being champagne cork eye injuries over a 4-year period. unusual and is often underestimated, however it can A cork ejected from an upright bottle can reach a be the cause of disabling functional sequelas. height of 12 meters and strikes the eye at a speed The incidence seems to be higher in regions with of about 15 meters per second. When the diameter large-scale production and sale of sparkling wine. This of a blunt object is smaller than that of the orbital rime, kind of wine induces fermentation inside the bottle, as in the case of a bottle cork, the full impact of the shock wave is borne by the globe, without any of it resulting in a rise in pressure that can reach 4 being absorbed by the orbital bony structures. atmospheres, high enough to release an expulsion Shooting a bullet of 0.345 grams of weight against speed of at least 15 m/sec; this means that the cork a pig eye at a speed of 66.44 m/sec (chosen in order reaches the eye in less than 0.1 sec (faster than blinking to gain a kinetic energy lower than that able to rupture reflex), from an average distance of 40-50 cm with 6 the globe) the anteroposterior diameter can decrease a strength of impact of about 100 atmospheres. to 59% during the compression phase and simul- A bottle cork can damage the ocular structures of taneously an expansion of the equatorial diameter can the anterior and posterior segments, both directly in reach 128% of the normal length and a flattening of the impact area and also through a counterblow effect. the posterior pole occurs (Delori and Pomerantzeff This particular type of eye injury is characterized experiments).7 During this compression phase huge by a compression phase and rapid decompression with tractional forces develop at the vitreous base, at the lengthening of the antero-posterior axis beyond the periferic retina and at the macular region. Following physiological range, causing sudden distortion of the Bottle Cork Injury to the Eye 297

Fig. 48.1: Compression > decompression > passing beyond primary position intraocular structures that can result in various different lesions (Fig. 48.1). From an analysis of different kinds of bottle corks, the plastic ones were found to ensure good tightness on account of their inherent tension, so that when the bottle is opened a kind of explosive discharge of energy is released. On the contrary, the natural cork expands inside the bottle because of the inner damp ambient and its discharge is consequently less violent. A particular type of sparkling wine is manufactured in the province of Modena, which ferments, generating pressure inside the bottle that can cause the ejection of the cork similar to that of a bottle of champagne. In Modena University we collected a series of 34 consecutive cases of bottle–cork eye injury admitted to the Ophthalmology Institute of Modena in the last 8 years that needed hospitalization. We assessed the anatomic and functional consequences of the injury in a retrospective study.10 Of the cases of eye injury admitted to our department in this 8-years period, 11% were bottle Fig. 48.2: Month-by-month distribution of cork injuries, 13% were occupational accidents, 5% bottle cork eye injuries were road accidents, 13% were sport injuries, 23% were domestic accidents, and other types accounted for 35%. Clinical Features In all cases the bottle cork or cap hit the eye of The clinical features more frequently observed are: the person opening the bottle, did not involve • Hyphema (79%) (Figs 48.3 and 48.4) bystanders in any case. Sparkling wine was involved • Corneal edema (59%) in all cases: white in 71%, and red in 29%; 38% of • Periferic retinal edema (24%) the bottles were homemade wine and 62% were • Subluxation of the crystalline lens (21%) commercial. The types of cork were as follows: 38% (Fig. 48.5) stoppers without wire, 32% corks and 30% metal • Retinal hemorrhage (18%) crown caps. • Iridodialysis (15%) (Fig. 48.6) About seasonal distribution, there’s a greater • Retinal tear (9%) incidence in January, on account of the holiday period, • Posterior pole retinal edema with macular involve- and in October, due to wine fermentation which ment causing a poor vision acuity (6%) influences the internal pressure of the bottle • Retinal detachment (6%) (Fig. 48.2). All cases are closed–globe injury according • Complete displacement of the IOL (3%) to Kuhn’s classification.11,12 • Traumatic cataract (3%) 298 Clinical Diagnosis and Management of Ocular Trauma

Fig. 48.6: Iridodialysis

Fig. 48.3: Hyphema Treatment In most of the cases the treatment consists of general medical practice and use of local anti-hemorragic and anti-inflammatory medication. In some cases it can be necessary to treat the ocular hypertension with carbonic anhydrase inhibitors administered generally and with beta-blockers administered locally. Surgical treatment is necessary in the most severe cases: If a lens luxation occurs it is necessary to perform a complete Via Pars Plana Vitrectomy, preferably with Posterior Hyaloid removal, and make a secondary IOL scleral fixation. Recently, the approach can be done Fig. 48.4: Hyphema with transconjunctival mini-invasive (25, 23G) strategies. In these cases a Iris fixation secondary implantation could be the gold standard, avoiding in this way to open the conjunctiva. In case of traumatic cataract, a phacoemulsification could be difficult depending on the grade of subluxation. If vitreous is in anterior chamber, a vitrectomy is necessary, via limbus or via pars plana, using preferably a mini-invasive (25, 23G) approach. In presence of retinal detachment, after an accurate examination we can choose for an episcleral approach or for internal approach with vitrectomy: in the last situation the choice of the tamponade agent depends on the retinal situation and the preferences of the surgeon. The iris injuries need adequate iris plastic surgery, even if many cases of iridodialysis, usually well limited, don’t need surgical treatment. Fig. 48.5: Lens subluxation

Sequelas are: • Pupil motility anomalies (21%) Prevention • Traumatic cataract (21%) In most of the cases visual acuity on admission was • Post-traumatic ocular hypertension (6%) generally very low, and although most patients made • Maculopathy (3%) an almost complete recovery, very severe visual • Optic neuropathy (3%) impairment was observed in others. Bottle Cork Injury to the Eye 299 These cases prove that bottle cork eye injury can 5. Koval R, Teller J, Belkin M, Romem M, Yanko L, Savir involve very severe traumas, although most patients re- H. The Isaraeli ocular injuries study. A nationwide cover almost totally with appropriate medical treatment. collaborative study. Arch Ophthalmol 1988;106:776-80. More information and prevention is needed, 6. Archer D, Galloway NR. Champagne-cork injury to the particularly in certain periods of the year and in specific eye. Lancet 1967;2:487-9. areas of the country. It is advisable to fit bottles with 7. Delori F, Pomerantzeff O, Cox MS. Deformation of the safety devices and/or include captions describing the globe under high-speed impact: its relation to contusion hazard posed by bottle caps/corks.4 Moreover, the injuries. Invest Ophthalmol 1969;8:290-301. introduction of a standardized type of screwable cork 8. Greven CM. Retinal Breaks. In: Yanoff M, Duker JS (eds) could be effective in preventing ejection. Alternatively Opthalmology. Mosby, Philadelphia, section 8, the use of a contention system, connecting the cork 1999;38.2. to the bottle neck with a wire, could represent another 9. Rubsamen PE. Posterior Segment Ocular Trauma. In: preventive possibility. Yanoff M, Duker JS (eds) Opthalmology. Mosby, Philadelphia, section 8, 1999;43.2-3. 10. Cavallini GM, Lugli N, Campi L, Pagliani L, Saccarola P. References Bottle –cork injury to the eye: a review of 13 cases. Eur 1. Al Salem M, Sheriff SMM. Ocular injuries from carbonated J Ophthalmol 2003;13(3):287-91. soft drink bottle explosions. Br J Ophthalmol 1984; 11. Kuhn F, Morris R, Witherspoon CD, Heimann K, Jeffers 68:281-3. JB, Treister G. A standardized classification of ocular 2. Gupta AK, Nadiger M, Moraes O. Ocular injury from a trauma. Ophthalmology 1996;103(2):240-3. carbonated beverage bottle. J Pediatr Ophthalmol 12. Pieramici DJ, Sternberg P Jr, Aaberg TM Sr, Bridges WZ Strabismus 1980;17:394-5. 3. Sellar PW, Johnston PB. Ocular injuries due to exploding Jr, Capone A Jr, Cardillo JA, de Juan E Jr, Kuhn F, bottles of carbonated drinks. BMJ 1991;303:176-7. Meredith TA, Mieler WF, Olsen TW, Rubsamen P, Stout 4. Kuhn F, Mester V, Morris R, Dalma J. Serious eye injuries T. A system for classifying mechanical injuries of the eye caused by bottles containing carbonated drinks. Br J (globe). The Ocular Trauma Classification Group. Am J Ophthalmol 2004;88:69-71. Ophthalmol 1997;123(6):820-31. CHAPTER

Ocular War Injuries 49 Jaroslaw Kulinski, Karol Stasiak, Marek Prost (Poland)

Introduction Percentage of soldiers who experienced ocular injuries is increasing with the consecutive wars and In our times of global terrorism the occurrence of military conflicts. Inaccurate data indicate that this injuries caused by the explosives is not limited only percentage accounted for about 1.5 to 2% during the to the battlefields but also to the countries which do I World War, about 2 to 3.3% during the II World War, not wage war. Very often civilians in seemingly peaceful 3 to 8% during the Korean War, 5 to 9% of casualties cities are more frequently victims of such a trauma in Vietnam, about 10% in Arab-Israeli War and 13% than military personnel on the modern battlefield. So speaking about “war injuries” that this description of Iraqis operations. (Ari 2006, Homblass 1981, Heier should be nowadays applied not only the soldiers but et al, 1993, La Plana et al 1997, Mader et al 1993). also to the civilians. Various authors state that ocular injuries connected Eyes occupy only 0.29% of the body surface and with military operations (wars, terrorist actions, 4% of the face surface. However, ocular injuries are landmine clearing) accounts for 16% of all injuries. extremely important health problem, because of their It is due to an increase in head trauma by about 40% predominating role in perception. Despite the fact that in 1982-2005, compared to an increase of all injuries eyeballs are relatively small organ, their direct injuries and wounds by 12% (Rustemeyer et al 2007). are usually extensive and severe. It is due to the short One should bear in mind that the first specialist distance and proximity of the explosives. They are ophthalmologic aid may be delayed during the war. mainly caused by the explosive wave and objects of Despite usually efficient medical evacuation medical different size colliding with the human body with very help is not always possible immediately after trauma. high speed and kinetic energy. Even with small Moreover, war injuries frequently involve several diameter such factors may produce severe ocular organs, additionally delaying ophthalmologic damages. They results not only in extensive injuries examination and treatment. but also in severe functional outcomes (Fig. 49.1). Field hospital should be equipped with basic It is estimated that ocular injuries are bilateral in 15 ophthalmologic devices, enabling examination of the to 25% of cases. globe anterior segment and eye fundus in the slit lamp. Physician-ophthalmologist, ophthalmologic technician or optometrist should carry out examination of the eyes. Very important is access to the split lamp in examination room of the field hospital. This lamp enables preliminary evaluation of the degree and severity of trauma and decision on the further diagnostic and therapeutic procedures. Some field hospitals are also equipped in teleconsultaion system. Help of specialists from other health care centers is possible in some difficult cases. Demographic characteristics of patients reporting to the field hospital with eye diseases depend on the type of military operations in the said region. Bancroft Fig. 49.1: Eye-bulb atrophy in a soldier after blunt and Lattimore saw only 48 (3%) patients with ocular ocular trauma during Iraqi operation injuries out of 1471 patients who reported to the Ocular War Injuries 301 ophthalmologic service in the transportation base Mechanical Ocular War Injuries support hospital during 9 months in 1995 (Bancroft et al 2001). Remaining 168 (11%) patients presented GLOBE AND ADNEXAL INJURIES with ocular diseases, requiring an intensive treatment. Global and adnexal injuries may be classified in several Nine patients required evacuation from the military ways. First of all, they may be classified by causative operation region but not necessary surgical treatment factor as: incised, punctured, crushed, lacerated, and in other specialist centers. However, this hospital was contused injuries. Ocular injuries may also be classified located some hours of drive from the front line. by anatomical structures involved. To unify the classi- Statistics cited by the authors working in vicinity fication of mechanical ocular injuries the International of the military operations are far worse. Thach et al Trauma Classification was approved in 1996 (Table noted 797 severe ocular injuries, including as many 49.1) (Fryczkowki et al 2003), Kuhn et al 1996, as 438 open globe injuries, in the war in Iraq during Pieramici et al 1997). 34 months (from March 2003 to December 2005) (Thach et al 2008). Enucleation was performed in 116 TABLE 49.1: International ocular trauma classification cases, including 6 patients with bilateral enucleation. Heier reported 108 (14%) patients with ocular injuries Open Closed out of 767 wounded, including 20 patients had to be Type A Rupture A Contusion evacuated for further specialist treatment, during B Penetrating B Laceration Operation Desert Storm (1990-1991) (Heier et al C IOFB C Superficial FB D Perforating D Mixed 1993). Retrospective study carried out by Muzaffar E Mixed - - et al. a total of 91 eyes of 51 men, clearing landmines in the aftermath of the Russo-Afghan war, were Degree 1 >20/40 1 >20/40 by visual 2 20/50–20/100 2 20/50–20/100 operated within 39 months (from November 1992 acuity 3 19/100–20/800 3 19/100–20/800 to January 1996) (Muzaffar et el 2000). Total blindness 4 19/800–LP 4 19/800–LP (NPL) was seen in 37.5% of the eyes, and visual acuity 5 NLP 5 NLP was below cfbe. in further 20.8%. Only 16.4% of Zone I Cornea to I External injuries were classified as mild with VA over 0.3. Eyelids corneoscleral plasty (50% of eyes), evisceration (23.1%), and limbus vitrectomy (17.6%) predominated in the treatment. II Within 5 mm of II Anterior segment It should be mentioned that all these patients the limbus worked without any eye protection. Bajaire et al III Sclera more than III Posterior segment published data on performed vitreo-retinal surgeries 5 mm from limbus during a 8-year follow-up period (from January 1995 Marcus Positive Positive to June 2003) (Bajaire et el 2006). As much as 40% Gunn Negative Negative of injuries involved zone I to the corneal limbus, 44% – zone II from the corneal limbus to 5 mm behind Below ocular injuries that may result from the it, 16% of injuries were localized in zone III in the military operations are briefly discussed. However, the posterior globe pole. Visual acuity in 98% eyes was authors focus on the specific ocular war injuries. Sequels below 1/40. During vitrectomy, silicone oil was used of the globe injuries by anatomical structures presents in 65% of cases, perfluorocarbons in 21%, lensectomy Table 49.2. in 82%, IOFB was removed in 72% of cases, and Management varies in dependence on the type of endolaser was used in 81% of cases. Improvement injury. As it is seen in the table, the treatment is was seen in 43%, stabilization in 41%, and sight frequently surgical. Therefore, knowledge, experience, worsening in 15% of cases. Factors of poor prognosis proper equipment in the wards and OR are required. included: lesions in zone III, retinal detachment, Applied procedures do not differ from these used in intraocular inflammation, and perforating trauma. any ophthalmologic center. From the above listed data, it results that ocular injuries constitute serious problem, not only medical but also social and economic. Americans estimated that Open Globe Injuries the cost of one soldier exclusion from the service due Open globe injuries are one of the most severe ocular to ocular injury for 5.9 days on average amounted injuries. They are most frequently produced by to $6295 (Buckingham et al 2001). Ocular injuries landmine blasts or hand grenades. It is estimated that may be classified as multiorgan, when the eye is only such injuries constitute 50 to 80% of trauma in the one of many damaged organs, and uniorgan, involving contemporary battlefields with penetrating and the eye and adnexa only. perforating wounds with IOFB predominance, often 302 Clinical Diagnosis and Management of Ocular Trauma

TABLE 49.2: Globe injuries by anatomical structures Anatomical structure Type of injury Sequel Treatment Prognosis Eyelids Abrasion, closed or open Upper lid ptosis, lacrimal tract S Good global injury disruption, hemorrhage Lacrimal apparatus Dislocation Edema S Good Lacrimal ducts Disruption Lacrimation, inflammation S Good Conjunctiva Abrasion, rupture Hemorrhage, defects S Good Cornea Epithelial abrasion Recurrent defects C Good Rupture of the Scars, keratoconus, C Poor posterior limiting corneal edema, membrane of the cornea anterior adhesions Sclera Rupture Uveal prolapse, vitreous prolapse, C Poor retinal impaction, hypotonia, loss of vision, inflammation, retinal detachment, glaucoma Abrasion Hemorrhage C Good Anterior chamber Rupture of the iris sphincter Photophobia C/S Good Iridodialysis Inflammation C/S Good Iridoschisis Edema C Good Angle recession Inflammation C Hyphema Corneal incrustation, C/S Favorable secondary glaucoma Pupillary muscles paralysis Photophobia C Good Traumatic iritis Adhesions, secondary glaucoma C Good Refraction disorders Hypermetropia, myopia C Good Vitreous hernia Vitreous base avulsion, retinal C Good detachment Lens Opacities (Vossius’ Cataract C, Good rings, subcapsular, sometimes disseminated, diffused) awaiting Luxation Deterioration of sight C Poor Subluxation Refraction disorders C/S Poor Rupture of the Opacity – cataract S Good lenticular capsule Vitreous Hemorrhage Opacities, sparkling floaters, C/S Poor photoreceptors damage, retinal pigmentation Posterior vitreous C Good detachment Retina Tear, detachment Complete retinal detachment S Poor from the limbus Retinal detachment Worsening, loss of vision S Poor Commotio retinae (Berlin’s edema, Terson syndrome, Purtscher’s angiopathic retinopathy, peripheral retinal edema) Vision deterioration C Favorable Hemorrhage Vision deterioration, proliferations, retinal detachment C Poor Macular hole Vision deterioration Laser Poor therapy Choroid Rupture Retinal detachment C Poor Detachment of the Intraocular pressure drop – papilledema, C Poor ciliary body retinal edema, choroidal detachment Post-traumatic inflammation Scotoma C Good Lesions to the ciliary Accommodation disorders, lens dislocation, muscles or nerves ciliary muscle spasm C Good Orbit Hemorrhage Optic nerve and orbital structures compression S Soft tissues edema Optic nerve and orbital structures compression S/C Poor Fracture of the orbital walls Orbital structures and eyeball damage S Poor Optic nerve Rupture of the optic Partial damage C Good nerve II vessels Detachment Vision loss C Poor Legend: S – surgical treatment ; C– conservative treatment. Ocular War Injuries 303 multiple (about 80%). Foreign bodies, both metallic vitreous opacities, macular holes, orbital walls fractures, and non-metallic may penetrate to the ocular adnexa, post-traumatic cataract surgery, keratoplasty, anti- eyeball, orbit or even maxillary sinusal structures or glaucoma surgeries) may be delayed until partial healing brain (Biehl et al 1999). Therefore, detailed diagnostic of the post-traumatic wound have been achieved or procedures with possible ultrasound, X-ray and CT make the decision on surgical operation time are very important in the field hospital already. Open dependent on the course of therapy (Gos et al 2001). globe injuries damage ocular adnexa (eyelids, As it was already mentioned, the outcome of conjunctiva, cornea, and sclera) in nearly all instances. treatment is sometimes unsatisfactory for the patient Copious hemorrhage, edema, and pain are usually but adequate visual acuity may be preserved. The seen. Plastic, gunpowder, sand, dust, and bacterial treatment is always surgical in such cases and should pathogens are deposited in the eye following open be carried out in the specialist centers, following globe injuries. Each ocular war open injury is medical evacuation from the regions of direct military considered infected and requires antibiotic therapy as operations. It is always connected with the necessary soon as possible. Therefore, an incidence of intraocular hospitalization, surgical treatment, and sometimes inflammation after any injury is rare because an early discharge. administration of antibacterial agents. Closed Globe Injuries It is different in case of the closed globe injuries. As ocular wounds usually force the victim to seek medical aid, contusions (especially mild) are often ignored. Some authors estimate that contusions constitute about 50% of all ocular injuries (Kozuchowska 1986). Symptomatology of these injuries varies from no symptoms and signs to the immediate blindness of the injured eye, depending on the severity of trauma. The following symptoms usually accompany the contusion: blurred vision, reddening, hemorrhage, pain, photophobia, sensation of veils, dots, “curtains” in the front of eye, sight instability (Szaflik et al 1998). All these symptoms are usually the reason of early reporting to the ophthalmologic clinic, enabling an Fig. 49.2: Scar after corneoscleral wound caused by landmine shrapnel in a soldier of Iraqi operation early diagnosis and proper treatment which is often less invasive (e.g. in retinal detachment) than that The treatment is frequently two-staged. The firs stage delayed. Post-traumatic sequels may develop takes place as soon as possible after reporting to the asymptomatically or the symptoms may be scare, slow doctor. It comprises post-traumatic wounds care with (e.g. retinal peripheral injuries), and may easily be anatomical structures reconstruction and intensive anti- overlooked by the patient (Waclawiak-Dabrowska et inflammatory therapy with antibiotic therapy. Foreign al 2007). It may be the case of peripheral retinal bodies are removed and eyelids, conjunctival, scleral, detachment, which may lead to complete detachment and retinal wounds are sutured. of retina (Fig. 49.3). Similar situation concerns sequels Then, the patient should be evacuated to the of the peripheral hemorrhages into the retina. centers, where the treatment aimed at proper sight Fibroproliferative changes leading to the secondary functioning reconstruction is possible. Timing plays an retinal detachment may develop after months following important role in the treatment of the open globe the injury (Bajaire et al 2006). Properly performed injuries. The majority of surgeries should be carried laser therapy mainly protects the patient against such out soon after injury, as remote outcome frequently complications. However, the patient should regularly depend on the time of surgery. It is especially true in report to follow-up visits in order to not overlooking case of retinal detachment, IOFB and intraorbital preventable complications. foreign bodies removal, perforating eyeball wounds, intraocular inflammation, prophylactic retinal MULTIORGAN INJURIES photocoagulation. Other injuries may (and sometimes The firs group is usually related to multiorgan injuries, should) wait until partial healing of the post-traumatic mainly craniofacial. Ophthalmologists are participating wound have been achieved. The treatment of some to the specialist team dealing with the treatment and open globe injuries (e.g. eyelids plasty, hemorrhagic patients care. Prospective studies have shown that 304 Clinical Diagnosis and Management of Ocular Trauma incidence of post-traumatic nerve damage is shown in the Table 49.3 (Mariak et al 2002).

TABLE 49.3: Post-traumatic nerve damage Damaged nerve Percentage of injuries Optic nerve II 1.2 to 16% Oculomotor nerve III 2.4 to 15.8% Trochlear nerve IV 0.15 to 20% Trigeminal nerve V 1.3 to 4.2% Abducent nerve VI 2 to 26% Facial nerve VII 2.0 to 60%

Fig. 49.5: Post-traumatic lens subluxation in a soldier of Iraqi operation Figs 49.3A and B: Choroidal ruptures, subretinal hemorrhage and peripheral retinal dialysis (black arrows) Post-traumatic damage of these nerves, especially after blunt trauma of eyeball in soldier during service in Iraq. partial, may be overlooked during patient’s hospita- Yellow arrows indicate barrage retinal laser coagulation lization immediately after injury. Such patients are usually hospitalized in emergency wards, their health status is severe and there is no possibility to perform complete ophthalmologic examination. These patients frequently report to the ophthalmologist with some delay. Delayed treatment of the ocular injuries poses quite a problem. Treatment in such cases do not differ from these used in any ophthalmologic center.

Fig. 49.4: Total retinal detachment with superior retinal laceration after blunt trauma

craniocerebral trauma involved the damage of at least one cranial nerves connected with the organ of vision (cranial nerves II–VII). Risk factors of these nerves damage include: severity of trauma (it should be noted that these nerves damage occurred also in mild injuries in about 10%), causative factor and its energy, skull Fig. 49.6: Post-traumatic optic nerve atrophy base fractures, and intracranial hematomas. An in a soldier of Iraqi operation Ocular War Injuries 305 PROPHYLAXIS OF THE OCULAR INJURIES IN agents is determined by its localization, identity, and THE BATTLEFIELD neutralization. This action may be related to both Prophylaxis is of utmost importance due to such military and terrorist operations. In general, mass serious complications of the ocular injuries. It is, destruction weapon is divided into chemical warfare, however, quite limited in the battlefield. Nevertheless, biological warfare, and nuclear warfare. Mass destruc- an incidence of ocular diseases may be partially reduced. tion weapons may be transported by artillery shells, It is justified by the health and economic reasons. ballistic missiles or bombs. Chemical and biological The most important is eye protection (special warfare agents may additionally be thrown down in protective goggles) during all military operations, which containers or dispersed from aircrafts. protect the eyes against dust and other contaminants and all minor ocular injuries. Glasses of eye protective Chemical Warfare devices should be made of polycarbons of 2.3 or History of sulphur fumes and hot pitch use is as old 3 mm thick. They may protect against injuries of kinetic as history of wars. These agents were used in Greece energy up to 18 J or even higher, depending on the (Peloponnesian Wars) and in China already in the 5th direction of action. Eye protective devices should be century BC. Chemical warfare was extensively used safe, comfortable, disperse an impact on the large as battlefield weapons during the I World War. In 1914, craniofacial surface, not limiting the field of vision, and French and Germans use chlorine, and in 1915, not to stem up. Sometimes such goggles are made Germans used hydrogen cyanide (prussic acid) and individually for every soldier, taking his sight defects, Yperite (mustard gas). Ever since, an international needs, habits, craniofacial anatomy, and type of effected community elaborated various agreements that aimed operations into consideration (Chizh et al 1999). at disarming under strict and effective control. In 1925, Moreover, wearing of contact lenses should be chemical warfare was banned by the Geneva Protocol. banned. Their proper cleaning and observation of rules The Polish government put a motion on biological concerning the wear of these lenses are difficult during warfare ban, which was added to this Protocol. In military operations. Between military operations, 1972, Biological and Toxic Weapons Convention was recommendations depend on the climatic conditions agreed upon and ultimately signed by 108 countries and environment. Military operations in the deserts in 1975. In 1993, Chemical Weapons Convention on require wearing sunglasses with side shield, protecting the Prohibition of the Development, Production, not only against excessive insolation but also against Stockpiling and Use of Chemical Weapons and on sand. It the tropics, special attention should be paid Their Destruction came into force. Unfortunately, there to insects as their bites may produce not only diseases are cases of unobserving these agreements. but also allergic reactions. Chemical warfare agents can be grouped into military toxic agents (military gases, volatile liquids dispersed as aerosols), and military auxiliary agents Non-mechanical Ocular War (incendiary agents, defoliants, tear gas). Toxic effect Injuries of these agents always depends on the dose, i.e. concentration and duration of action of the said OCULAR WAR INJURIES RESULTING FROM substance. THE USE OF MASS DESTRUCTION WEAPONS Military toxic agents Use of the mass destruction weapons aims—from the Depending on the effect, military toxic agents are tactic point of view—at attaining the best possible grouped into nervous system damaging agents (nerve military effect without engaging a lot of means and agents), blister agents, suffocating, choking, and number of soldiers. Unfortunately, such an effect is hallucinogenic compounds. Remaining agents may related to not only maximum enemy loss but also civil produce only transient ocular irritation manifested by population and complete destruction of non-military reddening and lacrimation. objects and environmental pollution in case of nuclear weapon use. However, maximum effect on the eyes 1. Phosphororganic compounds (nervous system has chemical warfare agents, out of all types of damaging agents, nerve agents): Phosphororganic weapons. These agents significantly decrease ability to compounds are volatile liquids. They absorbed from carry military actions due to visual disturbances and airways and conjunctiva as well as from the skin, if accompanying ailments. contaminated clothes were not earlier removed. They Presenting an effect of chemical warfare agents on were primarily used as insecticides (pesticides), i.e. plant the organ of vision, we propose to use military and protection agents. However, it was found that they not medical terminology. An action of chemical warfare are highly toxic for humankind. As chemical warfare 306 Clinical Diagnosis and Management of Ocular Trauma the following compounds are used: tabun (GA), sarin 2. Blister agents: These agents serve to decrease (GB), soman (GD), cyclosarin (GF), and X gases (VX military capability by the local burning effects or forcing or AX). Recent reports on the use of these agents come wearing the protective clothes, which markedly reduce from Iran-Iraq conflict in 1987. These agents act by mobility. Such agents include: sulphur mustard gas blocking acetylcholinesterase (AchE). Accumulation of (HD), nitrogen mustard gas (HN), lewisite (L), acetylcholine in the parasympathetic nerves endings phosgene oxime (CX). These agents produce chemical produce muscarinic effect in the iris and ciliary body, ocular burns, burns of airways, skin, intestines, and lacrimal gland and conjunctival blood vessels. Effects affect circulatory system. of nerve agents are also visible in the bronchi, bladder, gastrointestinal tract, and heart. Nicotine effect is i. Mustard gas (Yperite): Sulfur mustard (sulfur connected with acetylcholine accumulation in the Yperite) is one of the oldest and best-known chemical postsynaptic part of the myoneural junction and some weapons. It was used for the first time by Germans sympathetic ganglia. Laboratory confirmation of near the city of Ypres (Belgium; it took its name after intoxication is a decrease in erythrocyte AchE. the name of this city) in 1915. Later, it was used by Ocular symptoms are the earliest and occur at the Italians in Ethiopia in 1936, Japanese during the war lowest dose. They include: Maximum miosis (lasting with China in 1937, Iran-Iraq conflict in 1985-1988; up to 14 days), sensation of pressure and weight in Iraq used it also against Kurdish minority in 1988. the eyeballs, ocular pain, injection of the conjunctiva. Nitrogen mustard, manufactured for the first time in Miosis may be accompanied by sight disorders, 1935, is a new generation of the burning chemical especially peripheral, whereas ciliary body stimulation warfare agents. One should remember that it might – transient accommodation myopia. There may occur be used in the contemporary battlefields. intraocular pressure (IOP) disorders: decrease in IOP Mustard gas is a liquid used in the form of an related to the reduction in aqueous production or an aerosol. It easily penetrates through military uniforms, increase in IOP from the papillary block. Then, a ordinary clothes, skin, and mucous membranes. This sequence of general symptoms follows, including: pain compound may also persist in humid soil and water of the frontal region, rhinorrhea, hypersalivation, in the colloidal form for days. Mechanism of its action sweating, bradycardia, chest pain, bronchospasm and on the tissues is not fully explained. However, it is dyspnea, nausea, vomiting, abdominal cramps, known that DNA, RNA, cellular membranes, enzymes involuntary miction, and defecation, somnolence, and proteins are damaged by the alkilation with speech disorders, muscular tremor, convulsions, particular affinity to guanine. This leads to cytotoxic, parestesis, pulmonary edema, blood pressure drop, cytostatic, and mutagenic effects (Dabrowska et al paralysis of the respiratory muscles, respiratory arrest, 1994). Characteristic feature of mustard gas is latency, and death. General symptoms may persist for some lasting for several to dozens hours. Then, progressing days. High doses cause death within some minutes. lesions develop, producing irreversible damage. Medical management of intoxication with phos- The eye is the organ most sensitive to mustard gas. phororganic agents includes so-called pretreatment, Threshold of its stimulation is 10-fold lower than that i.e. pyridostigmine administration. It reversibly binds for skin and airways. Even if characteristic odor of AChE for about 12 hours, blocking this way an entry Yperite (mustard) is not detectable, the first ocular of phosphororganic agents. Pyridostigmine symptoms of contamination may appear within one administration should immediately be discontinued, hour. These ocular symptoms occur most frequently if contamination was detected. Protection against chemical attack in the battlefield includes wearing a in about 4 to 6 hours in the form of burning sensation, facemask, which protects the eyes and airways for photophobia, blurred vision, and painful blepharo- about 30 minutes. Within aid procedures, prefilled spasm. Simultaneously, mustard gas is penetrating the syringes with atropine should used (it has muscarinic skin, leading to the general poisoning. anticholinergic activity), oxime drug (nicotinic In order of incidence, the following symptoms are cholinergic action), and benzodiazepine observed: mild conjunctivitis (75%), severe conjunc- (anticonvulsant). Drugs should be injected tivitis with superficial keratitis – a symptom of orange subcutaneously or intramuscularly. Atropine dose is rind, edema and eyelids reddening (15%), superficial repeated every 5 to 15 minutes, depending on the corneal abrasions – erosions, and inflammation with degree of poisoning and achievement of the general injection in the corneal limbus, lesions to the eyelids atropinization. Next phase of management is victim epithelium (10%), deep corneal injury with ulceration, evacuation from the battlefield, removal of the neovascularization, necrosis of conjunctiva, and deep contaminated clothes, skin decontamination, airways burns of eyelid skin (Solberg et al 1997). Ocular cleaning (suction), oxygen therapy, and transportation response to the contamination may include also to the medical station. adherence of the iris to the cornea, leading ultimately Ocular War Injuries 307 to the secondary glaucoma. Latent and rare and these features are its virtue from the military point complication of mustard gas action may be irreversible of view. Usually impurities give it brown coloring and superficial corneal opacification, requiring keratoplasty, odor similar to that of geraniums. Which can be and/or recurrent conjunctivitis, keratitis, and blepharitis undetectable in the battlefield. Lewisite, similarly to (AmedP-6). An effect on the cornea is tetraphasic: mustard gas, penetrates clothes, mucous membranes, loosening of the epithelial intercellular junctions, and skin. As it contains arsenic atom, lewisite disturbs damage of stromal collagen, stimulation of the stromal cellular energetic processes, blocking –SH groups in neovascularizing factor, and apoptosis of endothelial pyruvate dehydrogenase and inhibiting acetylco- cells. enzyme A synthesis. Ocular symptoms herald other consequences of Lewisite produces severe ocular injuries. The first the contamination. They include: chemical skin burns sign of ocular injury is painful blepharospasm, followed with blisters, rhinorrhea, vocal cords injury with by: chemosis and blepharoedema, keratitis and iritis hoarseness or aphonia, increased mucus secretion in with hypopyon within 1 hour after the contact. the airways, bronchospasm, persisting cough, nausea Inflammation usually resolves but the necrosis of and vomiting, diarrhea. Other squeals include: skin conjunctiva, corneal opacification, corneal pannus, hyperpigmentation or discoloration, painful ulcerations secondary glaucoma, and cataract may persist after of the skin, aphonia or chronic hoarseness, chronic severe injury. obturative pulmonary disease (COPD), intestinal Intensive pain of eyeballs, skin and blisters filled hemorrhage and perforation, aplastic anemia, with liquid toxic for not only surrounding tissue but leucopenia, depression, loss of libido, anxiety. It was also for medical staff is characteristic for lewisite also found that mustard gas increases the risk of contamination. It exerts a severe irritating effect on pulmonary carcinoma in chemical causalities and the airways, forcing the immediate use of anti-gas manufacturers (Norman 1975, Woda et al 1968). It facemask. Lewisite absorbed to the circulating blood, should be born in mind that general symptoms, such mainly through the respiratory tract, causes hemolytic as headache and abdominal pain, nausea and anemia, increased capillary permeability, pulmonary vomiting, anemia, and leucopenia may be identical edema, damage of both liver and kidneys, and with those in radiation sickness. hypovolemic shock. Basic medical management of chemical causalities The treatment includes copious eye irrigation with is careful washing of skin and irrigation of eyes as well water and normal saline. Topical antibiotic ointments, as removal of the contaminated clothes. Eyes and strong mydriatics (atropine solutions) are used. An mucous membranes are washed with water or normal important element of the treatment is BAL – British saline and sodium bicarbonate for at least 2 minutes, Anti Lewisite (dimercaptol) – chelating arsenic and immediately after contamination with mustard gas liberating –SH groups of pyruvate dehydrogenase. It (Wilems 1989). Delayed eye irrigation is useless as is used topically in the form of ophthalmic ointment, mustard gas is already absorbed. Mustard gas is skin ointment, and systematically in intramuscular removed from the skin wooden spatula, when injections. contaminated clothing was removed, and powdered with anti-gas powder (calcium chloride or magnesium iii.Phosgene oxime: Phosgene oxime, being oxide). Activated carbon and synthetic resins may also classified as blister agent (vesicant), has an irritating be used for this purpose(Smith et al 1991). Then, action without producing the blisters. It is solid exposed skin is washed with water and soap and compound dispersed in the form of aerosol for military normal saline. Treatment of ocular injuries include purposes. Mechanism of its action is not clearly application of topical antibiotic ointments, explained, but most probably it damage protein and corticosteroids, and mydriatics for dozens weeks to enzyme structures. Contact with the eyes causes edema several months (Safarinejad et al 2001). Then, the of the conjunctiva and keratitis, leading to its patients are followed-up for months to detect possible opacification and marked decrease in visual acuity. corneal and anterior chamber symptoms. Wartime Typical for phosgene oxime action are skin lesions in practice indicates, however, that for the treatment the form of reddening and urticaria progressing to the severity of injuries, depending on the dose and rapid skin necrosis with suprainfections. Medical management decontamination is more important than medical includes decontamination with water and sodium procedures. bicarbonate. Then, topical antibiotics and preparations accelerating the healing of cornea and skin are applied. ii. Lewisite: Lewisite was synthesized in by WL Lewis in USA in 1918 (it was named after him). Most 3. Remaining military toxic agents: One should probably it was not used as chemical warfare agent remember that each case of the conjunctival irritation up-to-now. Pure lewisite is colorless and odorless liquid manifested by reddening, burn sensation or lacrimation 308 Clinical Diagnosis and Management of Ocular Trauma requires facial mask wearing and detecting procedures. These plants may serve as food or shelter in the natural Such symptoms may be the first sign of battlefield terrain configuration. The most toxic proved purple contamination with deadly substances. These agent and orange agent, containing high levels of substances include: lung damage agents (phosgene, dioxins. diphosgene, chlorine, chlorpicrin), cyanide compounds 3. Incendiary agents: They serve to eliminate (hydrogen cyanide, cyanogen halides, cyanogens mankind and damaging the equipment and objects chloride, cyanogens bromide). Every case of paralyzing (flammable aluminum and phosphorous compounds, agents use – both depressants, tranquillizers and hydrocarbon fuels: gasoline, refuel, fuel oil, kerosene). stimulants, hallucinogens (LSD, amphetamines) – These agents cause ocular, skin and mucous mem- papillary dilatation is seen together with typical branes burns, and combustion gases are additionally neurological symptoms. toxic for respiratory tract and central nervous system. Military auxiliary agents i. Thermal ocular burns: In wartime, thermal To this group of agents belong: lacrimators, defoliants, ocular burns result from the use of incendiary agents, incendiary agents, and smoke screen. In general, these incendiary bombs, flames of exploding shells and fire. agents do not cause direct irreversible immobilization Military thermal burns do not differ from the typical of the enemy and according to the international law eye burns, described elsewhere, except the presence are approved for use, except defoliants, dioxan, and of gunpowder remnants or foreign bodies connected incendiary bombs. with the explosion. However, ocular burns with 1. Lacrimators and smoke screens: Lacrimators phosphorus need separate discussion. (tear gas, pepper gas) are military gases irritating the ii. Burns caused by phosphorus: White phos- eye and upper respiratory tract. They rapidly and phorus is used in the phosphorus incendiary bombs. transiently cause stinging sensation and, tearing (for It is self-ignition agent, which produces white fumes about 15 minutes), and reddening (for about 30 in the air. White phosphorus is a cause of numerous minutes) of the eyes, reddening of the eyelids (for about and deep burns of the skin and eyes. Therefore, 1 hour) without toxic consequences. Rarely, the immediate decontamination is of utmost importance. corneal epithelium is damaged. Ocular symptoms are The particles of white phosphorus are mechanically accompanied by the cough and rhinorrhea. Similar removed from the eyelids, conjunctiva and cornea. but weaker effects are produced by the smoke screens, The eye and exposed skin are abundantly washed with used to mask location of the military troops or in shock 1% copper sulfate solution or 5% sodium bicarbonate, tactics. These agents serve not only as warfare agents which neutralize phosphorus. Then, abundant irrigation but also as riot control agents used by police forces. with water or normal saline is necessary. It not only Medical management includes: eye irrigation with water cleans and cools the tissue but also removes copper and possible use of topical antibiotics. Chlorine compounds, preventing general intoxication. Medical derivatives (calcium hypochlorite) are banned as their treatment involves topical antibiotic use, epidermization chemical reactions with lacrimators may produce toxic preparations, mydriatics, and corticosteroids later. effects. 2. Dioxins and defoliants: Dioxins chemically Biological Warfare damage the skin, mainly on the face and hands, Biological warfare agents consist of microorganisms and manifested as chloracne, leaving deep, sometimes their toxins. These agents serve for permanent elimina- disfigurating scars. As far as the eyes are concerned, tion of the enemy, quite often with mortal effect. dioxins may produce deformity of the eyelids, leading International agreements concerning the ban of to the recurrent conjunctivitis and marginal blepharitis. biological weapons are similar to that concerning Skin lesions persist for years and may be accompanied chemical weapons and were agreed upon in 1925 and by the lesions to pancreas, liver, and immunological 1972. Despite of biological weapons ban, several system, anemia, and neurological diseases. The best- countries still experiment with biological weapon, which known dioxin is TCDD. Its mechanism of action and is also within the interest of terrorist organizations (so- treatment of poisoning are unknown. Actually, cases called bioterrorism). of Dixon poisoning are rare and are related only to The following warfare agents are considered mortal: terrorist attacks or intelligence actions. During the wars botulin toxin (BTX), SEB toxin (staphylococcal entero- in Korea and Vietnam, several cases of poisoning with toxin type B – cadaveric poison), antrax, tularemia. dioxins being added to defoliants were noted in both Brucellosis, Q fever, VEE fever incapacite the enemy. participants of the conflict. Defoliants are phytotoxic Out of all types of the biological warfare agents, chemicals used to remove plants in the battlefields. characteristic ocular signs are produced by the botulin Ocular War Injuries 309 toxin, produced by Clostridium botulinum. It inhibits absorbed energy. Penetrating radiation is produced acetylcholine release in the myoneural endings and during nuclear explosion, lasts for dozen seconds, and parasympathetic nerves. Ocular symptoms include: is composed of electromagnetic gamma rays and papillary dilatation, accommodation disorders and neutron radiation. Radioactive pollution is related to double vision. The general symptoms include: mouth the radioactive dust fallout after explosion and dryness, peristalsis impairment, speech and swallowing radioactive substances formation by the neutron disorders, breathing muscles paralysis. Antitoxin is used radiation. It results in X, gamma, alpha, beta, and in the treatment. Mortality rate in untreated subjects proton rays emission, the most intense during a few is about 65% in about 18 to 36 hours. days but persisting for years. Radiation sickness may develop within hours after Nuclear Warfare nuclear explosion. However, it should be born in mind Nuclear weapon is characterized by the most that now, when the nuclear weapons are banned, destructive action, out of all types of weapons. Its effect symptoms of radiation sickness may result from on the vision is connected with five elements of inappropriate storage of the radioactive substances, explosion: blast, thermal radiation, shock wave, leak of nuclear reactors cooling water, overheating or penetrating radiation, and radioactive pollution. Data explosion in the nuclear power plants. General on the nuclear warfare effects on the human body symptoms of the radiation sickness include: headache, come from the end of the II World War, when USA abdominal pain, nausea, vomiting, gastrointestinal dropped the atomic bombs on the Japanese cities hemorrhage, skin burns. Later, anemia and leucopenia Hiroshima and Nagasaki (on the 6th and 9th August develop. Ocular effects of the radiation sickness include 1945). Other nuclear explosions were related to the edema and reddening of eyelids with madarosis. nuclear weapons testing carried out by several countries Blisters on the eye lids skin, necrotic conjunctival during so-called Cold War. It should be assumed that ulceration, corneal erosion, and corneal stroma such tests did not involve experiments on human infiltrations follow. Ultimately, eye lids scar deformities, beings. The Cold War arming was followed by the conjunctival adhesions, corneal defects with perforation period of nuclear disarmament. In 1963, United States, are observed. Typical sequel is postradiation cataract Soviet Union, and Great Britain Kingdom signed an that may develop from 3 months, already (Sinskey agreement which banned testing in the atmosphere, 1955). It begins with punctate dot opacification in the outer space, and underwater. However, tests front of the posterior lens capsule, progressing to the underground tests were permissible. In 1968, an subcapsular discoid changes, and finally involves the agreement on nuclear weapons non-proliferation, whole lens (Ham et al 1953). Patients with general signed by 178 countries, and prolonged open-ended symptoms of the radiation sickness manifested by in 1995. A comprehensive test ban was approved by hematopoietic disorders but without visible ocular UN General Assembly in 1996; 170 nations have now problems require periodical eye fundus examination signed. Actually, China, France, Russia, United States, to detect possible intraretinal and preretinal Great Britain, India, and Pakistan have nuclear hemorrhages, hemorrhages into vitreous. weapons. Moreover, it is stored in post-Soviet regions: Bielarus, Kazkhstan, and Ukraine. It is probable that OCULAR WAR INJURIES RELATED TO THE also Israel and Iran have nuclear weapons. LASER LIGHT AND EXPLOSION BLASTS There are several typical ocular injuries in nuclear Accidental laser use and explosion blasts produce explosion survivors. Intensive light during nuclear electromagnetic wave of the visible light, similar to explosion causes transient central vision disturbances. infrared light harmful for the macula. It results in the Thermal radiation, related to the blast, produces eye central vision disturbances, manifested by the visual burns and lens opacification. This problem is discussed acuity decrease, central scotoma and color sensitivity in detail within the effects of explosion blast and laser disorders. Mechanism of these pathologies involves light. Shock wave means translocation of air with photochemical macular metabolism disorders with supersonic speed and it is not produced in case of accompanying small foci of the internal structures neutron bomb explosion. Shock wave may cause edema and intraretinal blood extravasation. Listed mechanical injuries related to the foreign bodies in the disorders may persist for about 1 to 3 months. Lesions eye and circulatory disorders due to the sudden change to the macular pigmentary epithelium and its outer of the air pressure (Flick 1948). structures are also possible (Harris et al 2003). The Nuclear explosion produces penetrating radiation later occur, if the electromagnetic wave mainly consist and radioactive pollution. Both may produce similar infrared light, being a component of laser light, falling disorders known as radiation sickness. Ocular and vertically on the eye. Laser light falling on the eye under systemic clinical effect will depend on the dose and certain angle causes local skin, conjunctival and corneal 310 Clinical Diagnosis and Management of Ocular Trauma lesions. Explosion blast is accompanied by thermal 14. Heier JS, Enzenauer RW, Wintermeyer SF, et al. Ocular radiation which causes eyelids skin, conjunctival and injuries and diseases at combat hospital in support of corneal burns as well as lens opacification (Harris Operations Desert Shields and Desert Storm, Arch et al 2003, Pariselle et al 1988). Prophylactic measures Ophthalmol. 1993; 111(6): 795-8. 15. Homblass A. Eye injuries in the military. Int Ophthalmol include wearing of goggles, first of all. In the treatment Clin 1981; 21: 121-38. topical anti-inflammatory agents are applied. One 16. Ko¿uchowska I. Injuries of globe and adnexa. In: Witold should also consider the administration of anti- Or³owski (Ed): Modern Ophthalmology vol. II, PZWL, edematous drugs, such as carbonic anhydrase Warsaw, 1986. inhibitors. In more severe cases corticosteroids are 17. Kuhn F, Morris R, Witherspoon D, Heimann K, Jeffers injected periorbitally. Periodical ophthalmologic follow- J, Treister G. A standardized classification of ocular up central vision examinations are also necessary, trauma. Ophthalmology. 1996; 103:240–243. 18. Mader TH, Aragones JV, Chandler AC, et al. Ocular and including visual acuity, color and contrast sensitivity, ocular adnexal injuries treated by United States military Amsler test, computer-assisted perimetry. Additional ophthalmologists during Operations Desert Shield and tests and examinations should also be considered: Desert Storm, Ophthalmology. 1993; 100 (10): 1462-7. fluorescein angiography, optical coherence 19. Mariak Z, Mariak Z, Stankiewicz A, ¯ywalewski J. The tomography, electrophysiological tests. occurence of posttraumatic lesions of cranial nerves. Okulistyka, 2002, 2:143–47. 20. Muzaffar W, Khan MD, Akbar MK, et al. Mine biust injuries; Ocular and social aspects, Brit J Opthalmol, Bibliography 2000, 84, (6); 626-31. 1. AMedP-6(C) Vol. III (NATO Handbook on the Medical 21. Norman JE. Lung cancer mortality in World War I veterans Aspects of NBC Defensive Operations), 2006. with mustard gas injury, J Natl Cancer Inst. 1975; 54; 311. 2. Ari AB. Eye injuries on the battlefields of Iraq and 22. Pariselle J, Sastourne JC, Bidaux F. Eye injuries caused Afghanistan: public health implications, Optometry. 2006; by lasers in military and industrial environment. Apropos of 13 cases, J Fr Ophthalmol. 1988; 21 (9): 661-9. 77 (7): 329-39. 23. Pieramici D, Sternberg P Jr, Aaberg TM, Bridges WZ Jr, 3. Bajaire B., Oudovitchenko E, Morales E. Vitreoretinal Capone A Jr, Cardillo JA, de Juan E Jr, Kuhn F Meredith surgery of the posterior segment for explosive trauma in TA, Mieler WF, Olsen TW, Rubsamen P, Stout T. A system terrorist warfare, Graefe’s Arch Clin Exp Ophthalmol, for classifying mechanical injuries of the eye (globe). Am 2006 (244): 991-5. J Ophthalmol. 1997: 123:820–83. 4. Bancroft D, Lattimore M. Initial 67th Combat Support 24. Rustemeyer J, Kranz V, Bremerich A. Injuries in combat Hospital optometry services in Taszar. Hungary, during from 1982-2005 with particular reference to those to the Operation Joint Endeavor. MlUt Med 2001; 166: 71-4. head and neck: A review, Br J Oral Maxillofac Surg. 2007; 5. Biehl JW, Valdez J, Hemady RK, Steidl SM, Bourke DL. 45(7): 556-60. Penetrating eye injury in war, Mil Med. 1999; 164 (11): 25. Safarinejad MR, Moosavi SA, Montazeri B. Ocular injuries 780-4. caused by mustard gas: diagnosis, treatment and medical 6. Buckingham RS, Whitwell KJ, Lee RB. Department of defense, Military Medicine; 2001; 166, 1, 67-70. defense eye injuries from fiscal year 1988-1998, 26. Sinskey RM. Status of lenticular opacities caused by Optometry. 2001; 72(10): 653-60. atomic radiation, Am J Ophthalmol. 1955; 39; 285-293. 7. Chizh IM, Pluzhnikov NN, Shishkin MM et al. Eye 27. Smith WJ, Dunn MA. Medical defense against blistering protection for servicemen under battle conditions by the chemical warfare agents, Arch Dermatol, 1991; 127; use of special glasses, Voen Med Zh. 1999 Sep; 320(9): 1207-13. 4-9, 96. 28. Solberg Y, Alcalay M, Belkin M. Ocular injury by mustard 8. Dabrowska Ml. Sulfur mustard induces apoptosis and gas, Surv Ophthalmol. 1997; 41(6): 461-6. necrosis in endothelial cells, Toxicol Appl Pharmacol. 29. Szaflik J, Langwiñska-Woœko E, Kiciak Z. Blunt okular 1994; 141; 568-83. trauma. Okulistyka, 1998, 4:11-15. 9. Flick J.J. Ocular lesion following the atomic bombing of 30. Willems JL. Clinical management of mustard gas Hiroshima and Nagasaki, Am J Ophthalmol. 1948; 31; casualties, Ann Med Milit Belg, 1989; 3(suppl): 1-61. 137-54. 31. Thach AB, Johnson AJ, Carroll RB. Severe eye injuries 10. Fryczkowski P, Kmera-Muszyñska M, Kamiñska A. in the war in Iraq, 2003-2005, Ophthalmology. 2008; Classification of mechanical ocular trauma. Birmingham 115(2): 377-82. Eye Trauma Terminology (BETT), Okulistyka 2003, 4: 32. Wac³awiak-D¹browska M, Prost M, Kuliñski J. 9-15. Posttraumatic choroidal ruptures and retinal dialysis in 11. Goœ R, Goœ A. Ocular war injuries. Lekarz Wojskowy, technician during service in Iraq – case report. Polski 2001, 77 (2): 115-17. Przegl¹d Medycyny Lotniczej, 2007, 13: 445-454. 12. Ham WT, Richmont VA. Radiation cataract, Arch 33. Ward DL, Gorie C. Occupational eye injuries in soldiers, Ophthalmol. 1953; 50; 618-43. J Occup Med 1991; 33(5): 646-50. 13. Harris MD, Lincoln AE, Amoroso PJ, At al. Laser eye 34. Woda S, Nishimoto Y, Miyanish M. Mustard gas as a injuries in military occupations, Aviat Space Environ Med, cause of respiratory neoplasia in man, Lancet. 1968, 1: 2003; 74(9): 947-52. 1191. CHAPTER

Trauma of Anterior Eye Segment: An Update 50 Boris Malyugin(Russia)

Introduction Orbital roof fractures can also be associated with liquior-rhinorrhea. Clinical suspicion of a blowout The division of the eye trauma to anterior and posterior fracture is based on diagnosing one or more of the is rather relative. Not infrequently anterior segment following symptoms: anesthesia of the nose and the trauma is associated with the damage of the posterior skin of the lower lid, diplopia, pain at the upward gaze, eye structures including vitreous body, retina, choroid, displacement of the globe (downward or inward). sclera and optic nerve. More over traumatic influence leading to the anterior segment damage can INVESTIGATIONS compromise the eye but facial muscles, bones, brain, and other structures as well. That is why all traumatic As a first step the physician has to collect the history. cases require comprehensive examination of the eye Second step include the determining of the injury extent. and surrounding structures. In many cases of the eye Particular attention should be drawn to the underlying injuries require urgent examination by physician and globe. therapy. X-ray examination should be performed if the fracture of the orbit is suspected.

Injuries of the Lids DIFFERENTIAL DIAGNOSIS Lid hemorrhages usually does not have serious INTRODUCTION consequences but they can signal the injury of the Lid injuries of various etiologies can be isolated or orbital content which can be much more serious, for combined with traumatic changes of the eye and instance fracture of the roof of the orbit. Lid hematomas surrounding tissues. Lid lacerations are usually caused can also be associated with contusion injuries of the by bytes, or by sharp objects. eye.

CLINICAL SIGNS AND SYMPTOMS TREATMENT Direct blow to the eyelids cause blood infiltration of Treatment is greatly depends of the extent of the injury. the lid tissues, echymosis, and may be associated with In cases of lid hemorrhage without damaging of the subconjunctival and orbital hemorrhages. In some eye and other orbital structures optimal tactics will be cases, blood moves with the gravity from the lid to the to wait a period of time necessary for the for the check area. spontaneous resorbtion of blood. In cases of laceration if it contains fat that means Bites (from humans or animals) should be cleared that the orbital septum has been perforated. The of the debris and irrigated with antiseptics and then absence of the lid fold and blepharoptosis are the signs allowed to heal with secondary tension. The use of of the levator muscle damage. prophylactic antibiotics is strongly recommended. In Special attention should be pointed to the diagnosis cases of animal bites (dogs, foxes, etc.) prophylaxis of the orbital fractures. The latter is typically signaled against rabies must be considered. by ecchymosis, lid swelling, proptosis, an in some cases For lid lacerations primary repair with suturing ophthalmoplegia, subcutaneous emphysema from should be performed. Careful reapproximation of all fracturing of the sinuses causing crepitation during ruptured tissue planes and reconstruction of defects will palpation. ensure functional and cosmetic result. 312 Clinical Diagnosis and Management of Ocular Trauma Repair of the lid lacerations requires knowledge of INVESTIGATIONS the anatomy. The lid is a triple-layered structure The examination can be performed with the penlight composed of skin (anterior layer), orbicularis muscle or under the slit lamp. Fluorescein drops or paper strips (middle layer) and tarsus and palpebral conjunctiva are very helpful in detecting the presence and extent (posterior layer). All three layers of the lids should be of epithelial defect. closed separately. During the lid reconstruction it is extremely DIFFERENTIAL DIAGNOSIS important to save as much of the natural lid margin as possible. Special attention should be directed not A careful history must also be elucidated in order to only to obtain the complete lid closure but also to repair find out the possibility of the presence of foreign bodies the functional passage of tears with blinking into the and perforations. lacrimal canaliculi and the lacrimal sac. In cases of In corneal epithelial defects differential diagnosis damaged medial parts of the lids canaliculi should be should be performed with recurrent erosion due to the carefully explored and reconstructed if necessary. damage of the epithelial basement membrane, herpes If medial or lateral tarsal tendons were cut at the simplex keratitis, dry eyes, neurotrophic kertitis, atopic time of trauma they should be identified and repaired. disease, ocular surface inflammation, damage to the In the cases of conjunctival deficiency mucous limbal stem cells due to the chemical burns and limbal membrane grafts taken from the contralateral eye or ischemia. buccal cavity can be used with great success. An orbital fracture in the absence of the physical TREATMENT symptoms in many cases does not require operative Patients should be treated with antibiotics and intervention. The most frequent indications for the cycloplegics. A broad-spectrum antibiotic ointment surgery are disabling dyplopia and severe should be placed in the eye followed by placement enophthalmos. Surgical intervention in orbital floor of a semi-pressure patch on the eye. Use of ocular fracture is not considered and emergency and usually surface lubricants in small erosions may be enough to delayed for 2 or more weeks. improve patient comfort and support the healing process at the same time preventing infection. In eyes PROGNOSIS with corneal abrasions corticosteroids are strictly Lids tissue is a richly vascularized that is why it heals contraindicated. rapidly. Primary repair of lid lacerations will produce In cases of foreign bodies located in the upper fornix a very good cosmetic result. The latter depends on the the patient is seated and a drop of anesthetic is instilled. extent and direction of the formed scar. On the other Then patient is asked to look down, the examiner hand in delayer repair, presence of necrotic tissue and perform lid eversion and remove FB from the after bites can delay healing and result in compromised conjunctival sac. cosmetic appearance. Secondary reconstructive surgery can be considered if this clinical situation arises. PROGNOSIS In small corneal abrasions the prognosis is favorable. Abrasions of the Globe Epithelization is usually achieved in 24 to 48 hours. INTRODUCTION Corneal erosions are caused by eye scratching with Blunt Injuries of the Globe fingernails, hairbrushes, sand blowing in the air, incorrect handling of the contact lenses, etc. The other INTRODUCTION cause is the foreign body (FB) located under the upper lid. Blunt injuries of the globe can be caused by a variety of objects that strikes the eye and disrupts its content. CLINICAL SIGNS AND SYMPTOMS Right after injury there is sudden onset of pain, CLINICAL SIGNS AND SYMPTOMS lacrimation and blepharospasm. Eye motions as well Conjunctival hemorrhage is the most common sign of as blinking can aggravate pain syndrome. Even at the ocular trauma (Fig. 50.1). By itself it has no absence of the FB, a foreign-body sensation is consequences. In some cases severe bleeding can cause produced. ballooning of the conjunctiva. Trauma of Anterior Eye Segment: An Update 313

Fig. 50.1: Post-traumatic conjunctival hemorrhage Fig. 50.3: Traumatic iridodialysis secondary to blunt injury

Fig. 50.2: Appearance of hyphema following blunt trauma Fig. 50.4: Traumatic cataract and iridodialysis secondary to blunt injury

Hyphema is the other characteristic sign of the blunt of forceful impact of the iris against the anterior surface eye trauma (Fig. 50.2). This term refers to blood of the lens. This sign is rather diagnostic and has no retained in the anterior chamber. Some hyphemas are clinical significance and it is usually gradually resolves small and located in the inferiorly, while the others may with time. fill the entire anterior chamber. Blunt injury can cause acute or late cataract The extent of visual loss depends on the level of formation. Contusion cataract may form even in the hyphema. In total hyphema when the entire anterior absence of detectable damage of the capsule. Opacities chamber is filled intraocular pressure is invariably usually localized in the anterior and/or posterior elevated. subcapsular region. Rosette-shaped cataract is often an In the early post-traumatic period the aqueous early manifestation of lens contusion. It is located axially, humor contains cells and protein. Mild inflammation involves posterior lens capsule, and can either improve of uveal tissue may typically follow any trauma to the spontaneously or progress to opacification of entire lens. eye. Blunt injury of the eye can also cause lens dislocation Hard blows of the eye typically produce iris sphincter and subluxation (Fig. 50.6). The leading mechanism rupture with traumatic mydriasis. The latter can be of this is the compression of the globe in axial direction transitory or permanent. Traumatic iridodialysis of with expansion in the equatorial plane leading to various extents may be one of the consequences of zonular rupture. The lens may be dislocated in the the blunt trauma (Fig. 50.3). Not infrequently anterior chamber or in the vitreous cavity. iridodialysis is associated with traumatic cataract Location of the lens in the anterior chamber impedes (Fig. 50.4). the aqueous humor outflow and causes pupillary block In blunt trauma pigment epithelium can be glaucoma (Fig. 50.7). Iridodonesis is observed in cases imprinted in the anterior surface of the lens forming of lens posterior dislocation when the patient moves a Vossius ring (Fig. 50.5). It is produced as the result the eye quickly. 314 Clinical Diagnosis and Management of Ocular Trauma INVESTIGATIONS Medical history is a very important issue. Specific ophthalmic tests include: refraction, visual acuity, keratometry, biometry, B-scan ultrasonography, gonioscopy. Slit-lamp microscopy is a major method of eye examination. During examination pupil should be maximally dilated. In all cases of blunt trauma particular attention should be paid to fundus examination. Physician has to evaluate not only affected eye but also the fellow eye when possible.

DIFFERENTIAL DIAGNOSIS Fig. 50.5: Vossius ring on the anterior capsule of the In blunt trauma scleral ruptures can be present without eye with history of blunt trauma being visible to the examiner. Rupture is being suspected when the eye is soft.

TREATMENT A medication in conjunctival hemorrhage does not speed up blood resorption. The latter usually occurs within several days or weeks depending on the amount of blood. In conjunctival ballooning it has to be kept lubricated with ointment until the swelling diminishes. In hyphemas medications inducing mydriasis and cycloplegia are indicated together with sedation and patching of the traumatized eye. In severe hyphemas systemic aminocapronic acid in a dose of 50 mg/kg can sharply decrease the incidence of rebleeding. In the hemorrhage does not resorb promptly, anterior Fig. 50.6: Dislocated cataractous lens following blunt trauma chamber lavage should be performed in order to prevent blood staining of the cornea. Careful monitoring of the intraocular pressure and prompt treatment of ophthalmic hypertension are mandatory. Beta-blockers, carbonic anhydrase inhibitors and osmotic agents are widely used. In cases of lens dislocation into the anterior chamber leading to glaucoma emergency surgery is usually indicated. Dislocation of the lens in the vitreous cavity never requires emergency lens extraction. These patients are managed surgically after inflammation decrease. The main treatment method of visually disabling cataract is extraction. In general, traumatic cataracts can be safely removed with phacoemulsification Fig. 50.7: Lens dislocated into anterior chamber followed by posterior chamber intraocular lens implantation. Indications for the surgical tactics in each In blunt injuries even in cases when conjunctiva particular case vary extensively. remains intact, rupture of sclera may occur. The most Risks of the modern small incision cataract surgery common sites of the rupture are: limbal area, rectus are few if technically performed well. So the main source muscle insertion and equator of the globe. of complications is the ocular comorbidity. Special In patients with previous surgery (corneal trans- surgical techniques (vitrectomy, capsular tension rings, plantation, radial keratotomy, cataract extraction) after pupil expansion devices) and alternative methods of blunt trauma postoperative wound dehiscence can IOL fixation (i.e. scleral and iris fixation) should be occur. considered since zonular dehiscence, loss of capsular Trauma of Anterior Eye Segment: An Update 315 integrity, small pupils and some other clinical findings segment are: conjunctival fornix of the upper or lower and intraoperative events are not uncommon in lid, corneal epithelium and stroma, anterior chamber traumatic cataract cases. and lens. In corneal wound dehiscence, urgent surgery is Foreign body located on the corneal surface can indicated. Suture placement can be combined with iris be single or multiple, clearly visible or detected only reposition, cataract extraction, and hyphema washout with meticulous slit-lamp. Different biological or physical if necessary. objects can be found (fragments of glass or metal, fragments of insects, etc.). From the metal foreign bodies PROGNOSIS rust, pieces of metal from grinding wheel, etc. are one Hyphemas usually clear spontaneously. In some cases of the most often discovered. In metal objects a rust of hyphemas rebleeding can occur. The highest ring can surround the foreign body. frequency of rebleeding is between 3 and 5 days after In perforating or penetrating injury aqueous humor initial trauma. In severe traumatic hyphemas glaucoma enters the lens through the capsular defect. This results and corneal blood staining are the matters of concern. in lens swelling, local opacification rapidly progressing The latter can lead to persistent corneal opacity. to complete cataract formation (Fig. 50.8). If the If total hyphema is the result of the secondary capsule defect is small it sometimes can heal spontaneously or can be blocked by the iris. In this hemorrhage the prognosis is unfavorable. In cases when cases localized lens opacity develops. the lens is involved the prognosis of vision is reduced. Perforating ocular injuries may lead to In surgical reconstruction final visual acuity depends endophthalmitis (Fig. 50.9). Characteristic clinical on the retinal function. signs of this condition are: lid edema, corneal haze, Cataract removal usually leads to visual aqueous inflammation, vitreous opacification, rehabilitation. Nevertheless, ophthalmic co-morbidity conjunctival hyperemia, edema and pain. may prejudice good visual outcome. The final visual acuity of patients with traumatic cataracts who undergo surgery depends on a couple of factors including amount of the initial eye damage, surgical trauma of the ocular structures, and degree and duration of postoperative inflammation. Proper medical management of operated patients is essential for a successful outcome of treatment.

Perforating Injuries of the Globe Intraocular Foreign Bodies INTRODUCTION The physician must suspect the presence of the retained Fig. 50.8: An intralenticular metallic foreign body intraocular or intraorbital foreign body (FB) in all cases when periorbital or ocular tissues are lacerated.

CLINICAL SIGNS AND SYMPTOMS Patients usually complain on the pain, photophobia, foreign body sensation, loss or decrease of vision. Lid swelling, tearing, eye redness, tissue defects at the wound entry site, corneal erosion, hyphema are the most common but not the only symptoms physician can observe. Local corneal defect and edema signals the site of perforation. Small sharp particles may pass through the cornea and sink inferiorly into the angle of the anterior chamber. Clinical symptoms greatly depend on the localization of the FB. With the most common sites in the anterior Fig. 50.9: Bacterial endophthalmitis after ocular trauma 316 Clinical Diagnosis and Management of Ocular Trauma INVESTIGATIONS all relevant factors. The risks of inflammation, toxic Patient’s history and detailed description of the injury chemical effects and fibrovascular proliferation should should be obtained. be taken into consideration. Single or double eversion of the lid is important These effects largely depend on the chemical nature in the search and visualization of the FB located in the of the FB. If the foreign body contains iron or upper lid fornix. Direct visualization is very useful in particularly copper treatment tactics should be determining the presence and location of the foreign aggressive and early surgery is mandatory. The opposite body. It is sometimes very difficult to visualize small is true in small non-magnetic FB containing no or and transparent foreign bodies (for instance small minimal concentrations of aggressive substances. particles of glass or plastic) even with the slit lamp. FB located in the anterior segment is not difficult Iris defects due to perforation may be visible under to remove. In many cases anterior segment foreign direct light or with transillumination. Examination of bodies can be removed through the wound of entry. the anterior chamber angle with the gonioscope can If the object is small (2-3 mm in diameter) extraction be useful in detecting small FB lying in the angle. with magnet through the entry route may be considered. Gonioscopy should be performed with caution not to Larger object can be removed utilizing the limbal produce aqueous humor leak through the site of approach. penetration. Ophthalmoscopy after maximal pupil Tears in the lens capsule of 2 mm in size can seal dilation should be used in cases of suspected FB in without causing cataractous changes. Thus small foreign the vitreous or on the retina. bodies can be left in the lens. Bigger FB causing diffuse In cases of opaque ocular media (extensive corneal cataracts should be managed during cataract extraction. edema, hyphema, cataract and vitreous hemorrhage) Intensive antibiotic treatment (topical, oral or IV) A- and B-scans, X-ray examination, computerized should be administered in all cases of intraocular FB. tomograms must be performed in suspected cases. With metal FB in the superficial corneal layers, after Some of these examinations can also determine topical anesthesia is being applied, the patient is brought whether or not the FB is magnetic. under slit lamp and the metal fragment is lifted with the 25G needle on a syringe or a special instrument. DIFFERENTIAL DIAGNOSIS Foreign body located in the deep corneal layers should be removed under the operating microscope. In cases Main differential diagnosis relates to the fact whether of full thickness corneal penetrations suturing of the intraocular FB is present or not. Physician should keep wound should be done in order to achieve watertight in mind that multiple foreign bodies are not uncommon. The latter is characteristic to the explosions and blasting seal. Postoperatively patients should be treated with injuries (multiple intracorneal rocks), shotgun blasts and antibiotics and cycloplegics. the like. PROGNOSIS Once the presence of the FB in the eye has been TREATMENT established, the prognosis depends on the variety of In cases of perforating ocular injuries prompt factors. In the eye with the injury limited to the anterior therapeutic intervention is justified. Local and systemic eye segment prognosis is favorable in most cases and wide spectrum antibiotics should be given. depends of the effectiveness of the surgical repair and Corticosteroids are administered in order to limit the antibiotic treatment. In cases without good light destructive effect of inflammation that accompanies projection the prognosis is not infrequently poor. Foreign infection. bodies containing cooper or iron are particularly dange- In most cases of globe lacerations urgent surgery rous due to the chalcosis and siderosis development. with the suturing of the wound site should be performed. Traumatic perforations of the cornea lead to scar Clinical management in cases of FB largely depends formation (Figs 50.10 and 50.11). of the judgment of the following factors: localization Consideration of the potential development of of the foreign body, its shape, size and composition, sympathetic ophthalmia in perforating globe injury is extent of the trauma of surrounding tissues and the absolutely necessary. Sympathetic ophthalmia is more decision of whether remove it or leave in place. likely in severe globe injury with excessive damage The ophthalmologist must decide for or against of the uveal tissue leading to eye globe atrophy (Fig. removal of the foreign body after careful judgment of 50.12). Trauma of Anterior Eye Segment: An Update 317 CLINICAL SIGNS AND SYMPTOMS In ultraviolet corneal burns there is typically a delay in the onset of the symptoms. Interval after the exposure can reach up to 5-8 hours. A patient complains of eye irritation, photophobia, pain, and foreign body sensation. These symptoms can progress to severe pain and blepharospasm.

INVESTIGATIONS Careful history and slit-lamp examination should be performed. Topically applied fliorescein can reveal punctuate corneal staining. Fig. 50.10: Corneo-scleral scar involving iris and lens DIFFERENTIAL DIAGNOSIS In ultraviolet corneal burns differential diagnosis should be performed with ocular surface inflammation, dry eye, chemical burns.

TREATMENT Patients should be treated with antibiotics and ocular surface lubricants.

PROGNOSIS The prognosis is usually favorable. Rehabilitation is usually achieved in 24 to 48 hours.

Fig. 50.11: Complete cataract after perforating corneal Chemical and Thermal Burns of injury with iris and lens capsule damage the Eye INTRODUCTION Burns of the eye are one of the most urgent ocular emergencies. The extent and severity of damage are determined by the nature and concentration of the chemical agent as well as the time of contact with the tissue. The damage caused by acids is progressive but longs only within the first few hours. Their buffering with tissue proteins lead to the tendency of damage localization at the area of the contact with the agent. Alkali can penetrate rapidly into the tissue. This effect is determined by their ability to damage cellular membrane lipids, causing disruption of cells and melting Fig. 50.12: Eye globe atrophy of tissue. Tissue penetration of alkali occurs quickly and their effect may lasts for days. Exposure to flame rarely affects the cornea and eye Ultraviolet Corneal Burns globe, but more likely to cause the lid damage. INTRODUCTION Ultraviolet corneal burns can be caused by the use of CLINICAL SIGNS AND SYMPTOMS sunlamps or welding lamps without use of proper eye Patient complains on the severe pain and loss of vision. protection. Main symptoms include: necrosis of the skin, lids 318 Clinical Diagnosis and Management of Ocular Trauma swelling, blepharospasm, necrosis of conjunctiva, Chemical matter and debris should be removed with corneal opacification (the severity is judged upon the irrigation, cotton swabs, and forceps. possibility to visualize the anterior chamber structures). In moderate and severe alkali burns immediate In the most severe cases corneal perforation may occur. paracenthesis of the anterior chamber should be Strong alkalis cause ischemia and coagulative performed. Aqueous humor drainage is done with the necrosis of conjunctiva and sclera. The extent and purpose to lower aqueous pH. severity of damage is judged by the severity of corneal Medications: topical antibiotics, cycloplegics, opacification and degree of perilimbal ischemia. corticosteroids, hypotensive medications if necessary. In thermal burns marked edema and tissue necrosis Surgical treatment including mucous membrane or of the lids are usually present. conjunctival grafts can be used in cases of symbleopharon and delayed epithelisation. Lamellar or penetrating corneal transplantations in acute INVESTIGATIONS chemical burns are limited to the cases of corneal In chemical burns steps in evaluation and treatment perforation. Limbal stem cells transplantation with or include: anamnesis, identification of the nature of the without lamellar corneal grafting recently showed their chemical agent, visual acuity evaluation. Determination efficiency in restoration of the optical clarity of the media of the conjunctival pH should be done if the nature in long-term period after corneal burns. of the chemical agent is unknown. For this matter pH In thermal burns the treatment of shock and pain paper touched to the affected tissue will show whether as well as infection control are of primary importance. chemical is acidic or basic. In burns of lid antibiotic ointments are prescribed, topical steroids remains controversial.

DIFFERENTIAL DIAGNOSIS PROGNOSIS The examiner should be looking for the presence of Alkaline materials penetrate more rapidly into the ocular perforating injuries and intraocular foreign cornea and anterior chamber. That is why the results bodies. The nature of the chemical agent should be of alkali burns are more severe then those of burns differentiated. caused by acids. Moderate and severe chemical burns may lead to TREATMENT scarring of conjunctiva with symblepharon formation. The eye should be irrigated immediately after injury Cataracts are common consequence of severe chemical with minimum of 1.0 liter of water. The only very rare burns, especially alkali. Alkali penetration into the exception – is the chemicals that react violently with anterior chamber and coagulation of the anterior water. The use of the neutralizing agents is feasible in chamber angle structures can result in glaucoma. case they are available. Fornices of the conjunctival Skin scarring of the lids can cause cosmetic defects sac should be washed thoughtfully. The latter can but also chronic epiphora, trichiasis, exposure keratitis, require application of local anesthetic agents to prevent corneal opacification. Damage of the tear ducts and patient’s squeezing. lacrimal glands may lead to severe dry eye. CHAPTER

Management of Ocular Trauma with Plasma (Fugo) Knife 51 Ranjit Singh, Indu R Singh, Kiranjit Singh, Harmit Kaur, KK Bhalla, Daljit Singh (India)

Introduction Plasma can be found in a variety of everyday contexts, including plasma displays, fluorescent lamps, Ocular trauma throws up interesting and varied clinical neon signs, plasma balls, photolithographic etching situations, some of which really make us scratch our machines, flames, lightning, aurora borealis and more. brains and make us wish we had something more than The cutting abilities of plasma can be gauged from our regular instrumentation to deal with the problems the fact that Plasma cutters are used in the industry at hand. for precision cutting of steel. In this chapter we are going to discuss the Fugo’s plasma knife is a surgical device that uses management of some such peculiar situations as a result plasma (focused electromagnetic energy) to perform of ocular trauma, which we feel are either difficult or precision cutting of ocular tissues. In the Fugo’s plasma outrightly impossible to be tackled. knife, the plasma generating engine has been bundled We are going to discuss the role of a new surgical into a small unit, which creates enough energy to be instrument known as the Plasma Knife in the safely used for ophthalmological applications. management of such problems. Plasma generation is done in a filament fixed to While traditional definition of trauma brings to our a hand piece and connected to the plasma generating mind, accidents involving injuries to the eyes, we engine. The filament is barely thicker than a human strongly feel that iatrogenic reasons of ocular trauma hair (100 micron). The tip can be made in different cannot be evaded while discussing this subject. So lengths and can be bent as required. Only the extreme badly operated eyes have also been included in this tip gets activated for cutting. An electronic charge pump textbook of ocular trauma. causes the upper layer of atoms in the filament (about a micron deep) to transform from the solid state into the activated plasma state. A focused electromagnetic field is used to control, contour and shape these plasma What is Plasma (Fugo) Knife? particles into a plasma cloud around the filament. Before we go any further with this chapter, it is (Fugo, 1999). imperative to understand the nature of the instrument The temperature at the tip as measured with a that is going to be referred to most frequently during thermocouple is as high as 4500 degrees centigrade, the course of this article, i.e., the Plasma Knife. Designed though the amount of total heat produced is very little by Dr.Richard Fugo, in USA, this device has been tuned because the surface area of the plasma produced is for ophthalmic use. very small. The atomic particles that make up this The plasma, which we refer to, is also known as plasma cloud are in such a high state of agitation that the fourth state of matter. Plasma is distinctly different they literally dissolve the molecular bonds of the from, solids, liquids and gases. It is also the most material they come in contact with. The tiny filament abundant phase of matter in the universe as both stars doesn’t bend, even when cutting through something and interstellar dust consist of plasma. Plasma is often as strong as cow-hide, because it never touches the referred to as ionized gas. This is similar to normal material. The plasma cloud dissociates the material gas except that electrons have been stripped from their faster than the hand can move the instrument. (Fugo, respective nucleons and float freely within the plasma. 1999). Plasma is electrically conductive and can be Cutting with even the sharpest diamond knife needs manipulated by magnetic fields. at least some counter pressure but the plasma knife 320 Clinical Diagnosis and Management of Ocular Trauma can cut through without any tactile feedback. This fact has been tested by floating an enucleated eyeball(fixed to piece of foam) in water and then trying a diamond knife and the plasma knife to cut. The eyeball would just float away when the diamond knife would touch it and cutting was not possible at all. On the other hand the activated plasma knife filament would effortlessly pass through the eyeball with minimum push. However, the characteristics of a cut created by a diamond knife and a plasma knife are fundamentally different because of obvious reasons.

Fig. 51.1C: Magnified view of the plasma knife tip. Plasma generation takes place on the extreme tip of the exposed filament

The plasma blade tip is essentially an electrically conducting needle, which ends into a 100 micron fiber. All except the extreme tip of the 100 micron fiber is insulated and waterproofed. The tip can be made up to any required length or bent into any desirable shape.

Fig. 51.1A: Fugo’s plasma Knife Unit, including the console, activation footswitch and the handpiece

The Fugo’s plasma knife unit essentially consists of a console, a foot switch and a handpiece, to which disposable plasma delivery tips are attached. The machine runs on rechargeable batteries. A single charge delivers up to one hour of continuous plasma energy. There are two setting switches on the machine. One knob adjusts between low medium and high energy while the other knob selects the intensity of cutting energy.

Fig. 51.1D: Activated plasma knife filament seen under magnification. The yellow part is the plasma and the orange part is the photon cloud.It is the plasma which cuts, not the photon cloud. If plasma is generated in a dark room,it emits bright flashes of light

An uncharged plasma blade filament has no cutting ability at all. It is the plasma that creates the incision. The inactivated tip has difficulty even in abrading corneal epithelium. (Fugo, 1999). The activated tip easily cuts through a 50 micron stainless steel wire. The Fugo’s Plasma Knife has been approved by US FDA for performing capsulotomy and trans-ciliary filteration for glaucoma. Already things are underway Fig. 51.1B: Low magnification picture of the Plasma knife for the introduction of this fundamental technology tip attached to the hand piece with a bayonet mount in general surgery and dentistry. Management of Ocular Trauma with Plasma (Fugo) Knife 321 Though originally designed capsulotomy device we found limited usage of this for the said purpose, but found it to be invaluable as a cutting instrument for thick irido-capsular membranes, something which is difficult/impossible to be cut with a capsulotomy needle, a vanna’s scissor or a vitrectomy cutter. It is this ability that finds this machine a place in the management of tough cases of ocular trauma.

Key Properties of Plasma Knife a. Cuts effortlessly. b. There is no tissue drag. Fig. 51.2C: The plasma blade was activated and a round circle c. Coagulates as it cuts. was traced in the optical axis in an effort to cut the dense d. Ease of use. membrane. You can very well visualize the process of cutting and the formation of cavitation bubbles in the figure above

Fig. 51.2A: A 22-year-old male patient suffered injury in a road accident 6 months ago. Left eye was lost and the right Fig. 51.2D: The plasma knife membranectomy was eye suffered bad injuries. Cornea had been repaired. The completed with the cut out part of the membrane resting ruptured cataract had absorbed on its own, leaving behind in the centre.This piece was removed with a forceps and a thick membrane in the pupil formed by the fusion of the limited anterior vitrectomy done anterior and the posterior capsule and imprisoned lens material. It was planned to clear the visual axis with the plasma knife and implant an Iris Claw Lens

Fig. 51.2B: The plasma knife tip was introduced into the Fig. 51.2E: An Iris Claw Lens implant is fixed to the anterior chamber through a 2.8m keratome incision while anterior surface of the iris a cannula was introduced from the left paracentecis to deliver continuous methyl cellulose irrigation 322 Clinical Diagnosis and Management of Ocular Trauma

Fig. 51.2F: A 10-month post operative picture of the patient with corrected visual acuity of 6/18 Snellen’s. Patient had to wear high cylindrical glasses because of corneal scarring. As of now, the patient is mobile

Fig. 51.3A: Intraoperative picture of an encapsulated metallic foreign body in the retina.During the pre-operative evaluation, it was the B-scan and the CT scan which confirmed the presence of the foreign body cocooned inside the fibrous tissue.During vitrectomy the fibrosis was found to be so thick that it could not be split open with the tip of a vitrector or 24-gauge needle. We even tried using a diamond blade, mounted on a 20-gauge tip to cut the Figs 51.3C to E: Showing the various stages of the shell open but of no avail.So the services of the plasma exposure of the foreign body while the fibrotic tissue is knife were sought. The endo-laser marks can be seen being sliced with the plasma knife.There was no push applied to the retina all around the foreign body generated by the plasma knife during the cutting of the fibrous tissue, unlike the needle and the diamond blade

Fig. 51.3B: A special plasma knife tip, long enough to reach the retinal surface was utilized to expose the hidden foreign Fig. 51.3F: This is a picture of the extracted foreign body body. You can see the tip of the foreign body getting being held with an intraocular foreign body removal forceps, progressively exposed which will be removed via pars plana Management of Ocular Trauma with Plasma (Fugo) Knife 323

Fig. 51.4A: A 9-year-old female child suffering from Fig. 51.4D: A very thick membrane (posterior capsule) could Iatrogenic trauma having been operated for congenital be visualized very clearly under the intraocular lens.A gap cataract 4 years ago.The parents were unaware whether was created between the posterior chamber intraocular lens implantation had been done or not. The pupil was slit Lens and the posterior capsule so that the plasma knife like and closed off with a layer of pigment.Patient was taken tip could be slipped into the gap up for exploratory surgery because of strongly positive perception and projection and a normal B-Scan ultrasound

Fig. 51.4B: Iris hooks were used to keep the pupil Fig. 51.4E: The plasma knife was pushed under the expanded after dissecting the adhesions of the posterior intraocular lens. It was then activated and a circle was surface of the entire iris to the tissues below.Below the iris, traced on the fibrosed posterior capsule we discover a intraocular lens encapsulated between a thick anterior and posterior capsule

Fig. 51.4C: The plasma knife was first used to cut the anterior Fig. 51.4F: A perfect opening was created in the centre of capsule while the anterior chamber was continuously the thick posterior capsule. The cut out piece of the irrigated with methyl cellulose.The plasma knife tip was posterior capsule was removed with a forceps and limited traced on the fibrotic anterior capsule and within no time anterior vitrectomy was performed the thick capsule was inundated 324 Clinical Diagnosis and Management of Ocular Trauma

Fig. 51.4G: Picture at the end of the procedure with a Fig. 51.6A: Picture of a child’s eye aged 6, post penetrating clear visually axis ocular trauma, having been repaired elsewhere along with implantation of a posterior chamber lens. A thick vascularized membrane was visible in the pupil and the intraocular lens formed a part of this complicated mess. Perception and projection of light was strongly positive and B-Scan ultrasound revealed a clear posterior segment, therefore we decided to clear the visual axis

Fig. 51.4H: A 4-month post-operative picture of the same eye showing a nicely created opening in the centre in the visual axis.The immediate visual result was poor because of amblyopia and pleoptics were started

Fig. 51.6B: Since the implantation of the intraocular lens was far from satisfactory, it was decided to explant the lens after dissecting it carefully from its surrounding tissues. Plasma knife was then used to slice through the membrane after retracting the pupil. This one day post-operative picture of the patient after membranectomy along with limited anterior vitrectomy

Fig. 51.5: Picture of a posterior chamber IOL which went on to progress to optic capture into the pupil, cheese wiring of the haptics through the iris tissue and complete closure of the pupil with irido - capsular tissue. Vain attempts to clear the pupil with a yag laser are visible as pits on the optic of the lens. Since the tissues were strongly fused to each other, the plasma knife was used to cut through the stubborn tissue, which obliged by creating a round pupil in the middle. The rest of the abnormalities continue to exist but the patient can see now and has no other major Fig. 51.6C: Two months’ post-operative picture of the problem same eye showing a clear visual axis Management of Ocular Trauma with Plasma (Fugo) Knife 325

Fig. 51.7A: Intraoperative picture of an eye in an 11-year Fig. 51.7D: Implantation of the intraocular lens into the old child after blunt trauma with a fire cracker.There was capsular bag could be done. The capsulotomy performed mature traumatic cataract with fibrosed and thickened within the fibrosed capsule is clearly visible. It seems that anterior capsule and traumatic mydriasis. We decided to in the absence of the plasma knife, optimal surgical do the capsulorrhexis with the plasma knife outcome may not have been possible

Fig. 51.8A: A typical case of blunt trauma with add on Iatrogenic ocular trauma in a 12-year-old girl operated for traumatic cataract and lens implantation elsewhere. The intraocular lens visible in the anterior chamber had seemingly migrated from the posterior chamber into the anterior chamber.While one haptic was still behind the iris, the optic was in front of the iris and the second haptic was seen missing, having broken off near the haptic-optic junction.Whether this was accidentally broken while implanting or deliberately done will never be known.In addition, there was an intimidating vascularized iridocapsular membrane in the pupillary area. Since B-Scan Figs 51.7B and C: Pictures showing plasma knife revealed a normal looking posterior segment and capsulotomy in progress while the viscoelastic was being perception and projection of light was good,we decided to injected through the side port explant the lens and perform pupilloplasty 326 Clinical Diagnosis and Management of Ocular Trauma

Figs 51.8B and C: After explantation of the broken Figs 51.8D and E: Then we pressed the plasma knife into intraocular lens, we tried to do pupilloplasty with a service. A perfect pupilloplasty could be performed with the vitrectomy cutter as well as with a capsulotomy needle.Both plasma knife with minimal bleeding and fuss.Limited of these instruments were not only ineffective but also led anterior vitrectomy followed the pupilloplasty to bleeding from the tissues

Fig. 51.8F: Postoperative outcome of the surgery, 20 days later shows a quiet eye with a clear visual axis. We can certify that without the plasma knife, this case would have been impossible to perform Management of Ocular Trauma with Plasma (Fugo) Knife 327 Technique of Using the Plasma • Case 4 (Figs 51.5) • Case 5 (Figs 51.6A to C) Knife • Case 6 (Figs 51.7A to D) Basically plasma knife cuts whatever tissue it comes • Case 7 (Figs 51.8A to F) in contact with but for working in a closed anterior chamber, the following technique has been evolved. Whenever plasma knife tip is activated in a fluid Conclusion medium, cavitation bubbles are produced and these The plasma knife is a capable cutting instrument which bubbles can lead to poor visibility by sticking to the has been approved as a device that can be safely used endothelium. To counter this problem, we use a simple inside the eye. Its impeccable cutting ability along with device to continuously inject a viscoelastic material property of hemostasis makes it a capable machine. (usually methyl cellulose)through the side port. The I will not be too off the mark in saying that this surgeon inserts a 24 gauge cannula attached to a machine deserves a place inside every ophthalmic syringe filled with a viscoelastic. The assistant is operating set-up. We may not come across cases like responsible for injecting the viscoelastic while the the ones described here everyday, but the presence plasma knife is activated. This serves a dual purpose of this device in the operating room provides us with of keeping the anterior chamber deep at all times as additional capabilities and allows us to undertake well as pushes the cavitation bubbles away from the surgeries which normally may be turned away from working tip and out through the main incision. This the outpatient room itself. leads to precise cutting and minimum time spent inside As of now there are not too many users of this the anterior chamber. machine, hence the experience is just very limited. When one buys an expensive machine you expect certain specific indications where it is supposed to be Clinical Examples of used. While a couple of indications have been outlined Management of Cases of there is much more that is still to be figured out. What you have just gone through are but just a few examples. Trauma with the Plasma Knife I am sure that with time, more indications are bound • Case 1 (Figs 51.2A to F) to evolve. • Case 2 (Figs 51.3A to F) Disclaimer: The authors have no financial interest in • Case 3 (Figs 51.4A to H) the device(s) mentioned here. CHAPTER Chandelier Illumination and Bimanual Vitrectomy Used to Remove a Dislocated IOL 52 Amar Agarwal, Soosan Jacob, Athiya Agarwal Sunita Agarwal, Ashok Garg (India)

Introduction Numerous advances in microsurgical techniques have led to highly safe and effective cataract surgery. Two of the current trends in the evolution of modern cataract techniques include increasingly smaller surgical incisions associated with phacoemulsification (e.g. sub 1.4 mm incisions as in Phakonit with rollable IOL implantation)1, as well as the movement from retrobulbar and peribulbar anesthesia to topical anesthesia, and even “no anesthesia” techniques.2 Despite such advances, the malpositioning or dislocation of an intraocular lens (IOL) 3-5 due to capsular rupture or zonnular dehiscence remains an infrequent but important sight-threatening complication for contemporary cataract surgery. The key to the prevention of poor visual outcome for this complication is its proper management. Fig. 52.1: Dislocated IOL on the retina

Management of a Malpositioned IOL Disturbing visual symptoms such as diplopia, metamorphopsia, and hazy images are associated with a dislocated intraocular lens (IOL) (Fig. 52.1). If not properly managed, a malpositioned IOL may also induce sight-threatening ocular complications, including persistent cystoid macular edema, intraocular hemorrhage, retinal breaks, and retinal detachment. Contemporaneous with advances in phakonit microsurgical techniques for treating cataracts, a number of highly effective surgical methods have been developed for managing a dislocated IOL.

Chandelier Illumination Fig. 52.2: IOL lying over the macula. Notice the wide field Visualization is done using a Chandelier illumination view of the retina. This is because of the wide field contact in which xenon light is attached to the infusion cannula. lens being used and the Chandelier illumination which is This gives excellent illumination and one can perform seen in the upper left hand corner Chandelier Illumination and Bimanual Vitrectomy Used to Remove a Dislocated IOL 329 a proper bimanual vitrectomy as an endoilluminator is not necessary for the surgeon to hold in the hand. (Fig. 52.2). A Reinverter system has to be used if one is using a wide field lens (Volk or Oculus). The supermacula lens (Fig. 52.3) helps give better steropsis so that one will not have any difficulty in

Fig. 52.6: Handshake technique. Using two forceps one can hold the IOL comfortably and bring it anteriorly

Fig. 52.3: View using the super macula lens. This gives better steropsis

Fig. 52.7: IOL brought out anteriorly through the limbal route. Notice in the upper right and left corners infusion cannulas fixed. One is for infusion and the other for the Chandelier illumination. One can also have the same infusion cannula with the Chandelier illumination holding the IOL with a diamond tipped forceps (Fig. 52.4). When one is using the Chandelier Fig. 52.4: Diamond tipped forceps lifting a looped IOL illumination system one hand can hold the IOL with lying on the retina after a vitrectomy the forceps and the other hand can hold a vitrectomy probe to cut the adhesions of the vitreous thus doing a bimanual vitrectomy (Fig. 52.5). One can also use two forceps to hold the lens thus performing a hand shake technique (Fig. 52.6). The lens is then brought out anteriorly and removed through the limbal route (Fig. 52.7).

Reinverter System When we use the wide field indirect contact vitrectomy lenses we have to use a reinverter as the image is seen inverted. The reinverter again makes the image erect Fig. 52.5: Forceps holding the IOL and the vitrectomy probe so that the surgeon does not have difficulty in cutting the vitreous adhesions. This is bimanual vitrectomy operating. The one we use is the one from Zeiss which is possible due to the Chandelier illumination microscopes which has a foot switch connection. In 330 Clinical Diagnosis and Management of Ocular Trauma other words on pressing the footswitch button the is free and so one can use two instruments to reinverter works. manipulate the dropped IOL. The Chandelier The Volk Reinverting operating lens system is also illumination system we used was from Synergetics present. It has a unique single-element prism design. (USA) and the machine was the Photon. Sophisticated This installs in the Zeiss and other microscopes. It offers filtering techniques within the Photon and its associated surgical visualization ranging from high magnification fiberoptics are used to provide higher illumination of the macula to panoramic viewing upto and including levels. the ora serrata.

Wide Field Indirect Contact References 1. Agarwal A, Agarwal S, Agarwal A. Phakonit: Lens Vitrectomy Lenses removal through a 0.9 mm incision. In: Agarwal A These are essential for performing proper bimanual Phacoemulsification, Laser Cataract Surgery and Foldable vitrectomy. When one is doing vitrectomy for dropped IOL’s First edition. Jaypee Brothers 1998. IOL we use the Mini Quad Volk lens or the Oculus 2. Agarwal A, Agarwal A, Agarwal S. No Anesthesia Cataract lens. These lenses give the view of the retian upto the surgery. In: Agarwal A Phacoemulsification, Laser ora serrata. When one wants to pick up the IOL with Cataract Surgery and Foldable IOL’s Second edition. the diamond tipped forceps then we use the Jaypee Brothers 2000. Supermacula Volk lens. This lens gives very high 3. Chang S. Perfluorocarbon liquids in Vitreo-retinal surgery. magnification. Another advantage of this lens is the International Ophthalmology Clinics-New approaches to better steropsis so that you know exactly where the vitreo-retinal surgery: Vol32, No.2, Spring 92: 153-63. 4. Chan CK, An improved technique for management of IOL haptic is in relation to the retina. These lenses come dislocated posterior chamber implants. Ophthalmol with a handle so that the assistant can hold the lens 1992; 99:51-57. comfortably. 5. Chan CK, Agarwal A, Agarwal S, Agarwal A. Management of dislocated intraocular implants. In: Ophthalmology Bimanual Vitrectomy Clinics of North America, Posterior Segment Complications of Cataract Surgery, December 2001; The advantage of the bimanual vitrectomy set-up is editors: P.N. Nagpal, I. H. Fine; W. B. Saunders, that the hand which normally holds the endoilluminator Philadelphia 681-93. CHAPTER

Principles and Management of Ocular Trauma 53 Syed Asghar Hussain, Amol Mhatre, Kanupriya Mhatre Supriya Dabir, Saumil Sheth, Vandana Jain, S Natarajan (India)

Introduction DIFFERENT TERMS USED IN OCULAR TRAUMA • Closed globe: Eye wall does not have a full thickness Ocular trauma classification groups has classified wound. mechanical injuries to the eye into 2 categories. • Open globe: Eye wall has a full thickness wound. 1. Open globe: Full thickness defect in corneoscleral • Laceration: Full thickness wound caused by a sharp coat of the eye and object. 2. Closed globe : Ocular injuries without full thickness • Penetrating injury: Single full thickness wound defect of the globe caused by a sharp object. • Intraocular foreign body (IOFB): Retained foreign body causes a single entrance wound. Classification • Perforating injury: Two full thickness wounds- entry Mechanical Eye injury can be classified as follows and exit wound. (Table 53.1). • Contusion: Closed globe injury resulting from a blunt object.

TABLE 53.1: Classification of mechanical eye injuries

1. Open Globe Injury Classification 2. Closed Globe Injuries Classification Type Type A. Rupture A. Contusion B. Penetrating B. Lamellar laceration C. Intraocular foreign body C. Superficial foreign body D. Perforating D. Mixed E. Mixed Grade Grade Visual acuity Visual Acuity 1. ≥ 20/40 1. ≥ 20/40 2. 20/50-20/100 2. 20/50-20/100 3. 19/100-5/200 3. 19/100-5/200 4. 4/200 to light perception 4. 4/200 to light perception 5. No light perception 5. No light perception Pupil Pupil Positive: relative afferent pupillary defect present in Positive: relative afferent pupillary defect present in affected eye. affected eye. Negative: relative afferent pupillary defect absent in Negative: relative afferent pupillary defect absent in affected eye. affected eye. Zone Zone I. External (limited to bulbar conjunctiva, sclera, I. Isolated to cornea( including corneoscleral cornea) limbus). II. Anterior segment (involving structures in anterior II. Corneoscleral limbus to a point 5 mm posterior segmentinternal to the cornea and including the posterior lens capsule; also includes pars plicata into the sclera. but not pars plana) III. Posterior to the anterior 5 mm of sclera. III. Posterior segment ( all internal structures posterior to the posterior lens capsule) 332 Clinical Diagnosis and Management of Ocular Trauma • Lamellar laceration: Closed globe injury of the eye Then, the cornea is scraped with the help of a 26 wall or bulbar conjunctiva caused by a sharp object. G needle and the foreign body is removed. Following this, the eye is instilled with antibiotic ointment and EPIDEMIOLOGY OF OCULAR TRAUMA eye pad is applied. The common complications encountered with are The general incidence reported is variable both in India corneal ulcer, corneal perforation and traumatic and abroad. In India, the reported incidence varies cataract. Then, flurbiprofen should be added as an from 1-5%. In almost all studies, the incidence of anti-inflammatory. Vitamin C may be supplemented injuries is higher in males than females. Male to promote re-epithelisation. Regular follow up, preponderance is understandable as they are more protective goggles for 24 hrs and review is advised. exposed to outdoor activities. Maximum incidence of A deep corneal foreign body may cause corneal injuries occur in 21-30 years of age. Shukla and Verma opacity abscess. have found 29.2% incidence as occupational.

PROGNOSTIC FACTORS Lamellar Corneal Lacerations History: The patient usually presents with history of Despite of advances in ocular imaging, instrumentation, injury or unconsciousness, convulsions, bleeding from materials, and surgical procedures, the management nose, ears, etc. of open globe injuries continue to pose difficult management dilemmas. Prognosis depends on various Evaluation: The patient is subjected to a complete factors such as initial visual acuity, presence or absence general and ophthalmic examination, including Slit of relative afferent pupillary defect, type and zone of Lamp Examination, which is a must. Determination injury, time elapsed between the injury and surgery, of visual, acuity and Siedel’s Test should be performed cataract formation or dislocation of lens and also in all cases of occult injury. presence or absence of retinal detachment or Siedel's Test: This test is performed to rule out occult endophthalmitis. perforation of Descemet's Membrane. In positive cases, there is a high risk of endophthalmitis and hypotony. Closed Globe Injuries Traumatic hyphema ANTERIOR SEGMENT TRAUMA CORNEAL Traumatic hyphema generally occurs in young active INJURIES people, predominantly males, and also children, This is one of the most common ophthalmic emer- accounting for nearly 50% of all eye injuries. gencies. The mechanism could either be due to direct impact, The most common presentations are: compressive wave force, reflected compressive wave 1. Corneal Foreign Bodies or rebound compressive wave. It is usually caused by 2. Lamellar Corneal Lacerations a high velocity projectile or an object which strikes the 3. Vossius Ring exposed portion of the eyeball, the total extent of the 4. Traumatic Hyphema damage depending upon the nature, size, anatomical 5. Traumatic Cataract location and force of impact. The most common causative factors are balls, rocks, Corneal Foreign Bodies toys, human fists and gun pellets, etc. The usual effect Clinical features of a blunt compressive force onto an eyeball results • Foreign Body Sensation in the sudden decrease in the antero posterior • Conjunctival Congestion dimensions of the eyeball, thus causing a compensatory • Watering of Eyes increase in the anterior equatorial circumference of • Photophobia the globe. This leads to the posterior displacement of Ocular examination may reveal edematous lids. Slit the iris-lens diaphragm, with scleral expansion in the Lamp examination shows foreign body embedded in equatorial zone. This, in turn leads to shearing and the corneal epithelium. disruption of the circulus arteriosus iridis major, arterial branches of the ciliary body, and / or recurrent choroidal Management: After informing the patient about the arteries and veins, crossing between the ciliary body procedure, instill topical anaesthetic drops into the eye. and episcleral venous plexus, resulting in hyphema. Also explain to the patient about infection and In cases where no layering of blood is visible in the sensation of foreign body in the affected eye. anterior chamber, but few red blood corpuscles are Principles and Management of Ocular Trauma 333 seen, it is called as microhyphema. In later stages, this event, the whole suspensory ligament apparatus is has propensity to develop into a hyphema. If the whole drawn behind the iris. The lens may remain in the anterior chamber is filled with a massive organized patellar fossa, retained by its attachment to the vitreous hyphema constituting clotted blood, it is called as "Eight or the ligamentum hyaloideocapsularis. The lens Ball Hyphema". becomes tremulous, and its position is determined by The anterior chamber bleed usually results from the traction of the intact zonulae and the effect of tears or splits in the iris, ciliary body, trabecular gravity. The patient presents with myopia and meshwork, zonule, lens and peripheral retina, in impairment of accommodation as well as astigmatism, response to blunt ocular trauma. which is usually impossible to correct. The anterior segment manifestations usually include When the lens is completely dislocated from the corneal abrasion, endothelial denudation, corneo- patellar fossa, it may be seen incarcerated in the pupil, scleral rupture, scleral rupture, iris sphincter tears, in the anterior chamber, in the vitreous (either free iridodialysis, angle recession, cyclodialysis, iris floating - lens natans) or fixed - lens fixata, in the sub meshwork tears, vossius ring, zonular rupture, cataract, conjunctival space - phacocele, in the sub scleral space lens subluxation, etc. or sub retinal space or may be wandering forwards The posterior segment manifestations include into the AC and backwards into the vitreous, through vitreous hemorrhage, retinal edema, retinal dialysis, the pupil. retinal hemorrhages, horseshoe tear, choroidal The usually associated complications include Lens rupture, sclopeteria retinitis, optic nerve avulsion, etc. Particle Glaucoma, Phacolytic Glaucoma, Lens induced If left untreated, a total hyphema of over six days angle closure, Rubeosis iridis, uveitis, keratitis, retinal with more than 25 mm Hg of intraocular pressure detachment and sensory deprivation amblyopia. tends to develop blood staining of the cornea. In The investigations include Macular Function Tests, addition, the raised intraocular pressure over long IOP, Angle Study, B-Scan Ultrasonography and periods of time can cause optic nerve damage. electrophysiological tests (ERG, VEP) and The line of management is medical and surgical. Radiographic studies (X-ray, OCT, CT Scan and MRI). The patient is advised hospitalisation, sedation, bed The techniques of lens removal are Anterior Limbal rest, elevated head position to 30°, eye shield, 1% Route (Bimanual Lenticular aspiration, Epilenticular Atropine eye drops b.i.d. (controversial), topical cortic- IOL implantation, ECCE, Phacoemulsification and the osteroids (1% prednisolone q.i.d.), oral prednisolone delamination technique). These may be followed by (0.75mg/kg per day). Some surgeons recommend oral IOL implantation (in the capsular bag, sulcus fixated, Aminocaproic acid (50mg/kg q.i.d.) or tranexamic acid iris fixated). The posterior route techniques are (Pars which are both antifibrinolytic agents. Plana Lensectomy, Pars Plana recovery of a posteriorly Associated secondary glaucoma (IOP>30 mmHg) dislocated lens). is treated aggressively with topical beta blockers (0.5% timolol b.i.d.), alpha agonist (0.2% brimonidine t.i.d.), carbonic anhydrase inhibitor (2% topical dorzolamide CLOSED GLOBE INJURY TO THE IRIS AND t.i.d.) or 50 mg oral methazolamide t.i.d.) and 20% CILIARY BODY IV mannitol (1 gm/kg to 2 gm/kg over 45 mins). The uvea may be involved in both contusion and con- Surgical interventions have also been advocated cussion injuries. In rare instances the generated force such as paracentesis, irrigation and aspiration, clot overcomes the resilience of the outer scleral coat and expression, clot excision with automated vitrectomy causes a laceration or perforation with uveal incarcera- apparatus. tion. The effects of blunt injury on the uvea are traumatic LENS AND TRAUMA miosis, traumatic mydriasis, vossius ring, hyphema, iris sphincter tears, iris laceration, iridoschisis, iridodialysis, Trauma affects the human lens in different ways such anteflexion of the iris, iris avulsion, retroflexion of iris as vossius ring, discrete sub epithelial opacities, rosette and traumatic iridocyclitis. shaped opacities, zonular cataracts, concussion Blunt trauma to the ciliary body results in ciliary cataracts, capsular tears, swelling, zonular dehiscence body laceration, iridodialysis, angle recession, without lens displacement, lens displacement and cyclodialysis and ciliochoroidal detachment. dislocation. Blunt trauma in an anterior-posterior direction causes shortening in that meridian with stretching of Investigations the equator which may cause zonular disruption with Ancillary Tests: Plain X-ray, Orbit, USG, OCT, CT Scan resultant subluxation or dislocation of the lens. In this and MRI, Electrophysiological Tests (VEP, ERG). 334 Clinical Diagnosis and Management of Ocular Trauma POSTERIOR SEGMENT TRAUMA may allow secondary choroidal neovascularisation Blunt injuries to the ocular, periocular and cranial which needs to be monitored. regions can produce ocular damage by Contrecoup The etiology of Commotio Retinae is unknown. mechanism where the injury is at a site opposite to Sipperly, Quigley and Gass' experimental model site of injury. suggests that the visual outcome of an eye with Anterioposterior compression results in horizontal Commotio retinae is dependent on the number of displacement of intra ocular structures. location of damaged photoreceptors.

COMMOTIO RETINAE (BERLIN'S EDEMA) TRAUMATIC MACULAR HOLE (FIG. 53.2) Commotio Retinae was first described by Berlin in Trauma accounts for 9% of Full Thickness Macular 1873. It is seen as a greyish white Opacification of the Holes. They may occur due to posterior contusion outer retina. It always typically occurs opposite to the necrosis, following subfoveal hemorrhage or due to site of impact and may occur anywhere in the posterior acute vitreo retinal traction. The size varies from 300μ segment. Visual acuity is usually affected if macular - 500μ with a sharp irregular margin and a cuff of edema is involved. Histological examination shows that neuro sensory detachment. It rarely leads to a retinal there is edema in the outer retinal layers along with detachment. OCT is the best method to demonstrate some photoreceptor loss. Fluorescein Angiography a macular hole. Surgical anatomic closure is achieved shows no breakdown in the Blood Retinal Barrier. Later in 93% cases following vitrectomy with membrane in the course, RPE mottling shows areas of hyper and peeling and fluid gas exchange. They show good visual hypofluorescence. The prognosis is usually good with recovery perhaps due to the younger age of the the lesions resolving completely or with varying degrees patients and early diagnosis. of RPE mottling.

CHOROIDAL RUPTURE (FIG. 53.1) Indirect choroidal ruptures result from compressive injury to the posterior pole of the eye.11 With the horizontal expansion of the globe, the elastic retina and tough sclera resist tearing, but the Bruch's membrane is prone to rupture. Classically, the ruptures at the site of trauma may also be seen, which tend to be anterior and parallel to the ora. Choroidal ruptures are typically singular, concentric to the disc and temporal. Initially they may be obscured by overlying hemorrhage and become visible later. The visual acuity is affected if it passes through the fovea. FFA may be of use to detect small ruptures and the location in relation to the foveal centre. The ruptures Fig. 53.2: Traumatic macular hole

PUTSCHER'S RETINOPATHY Severe head trauma or chest compression in the absence of direct trauma to the globe results in Putscher's Retinopathy. Its frequency is unknown. It is characterised by multiple patches of superficial retinal whitening and retinal hemorrhage surrounding a hyperaemic Optic Nerve Head. It is seen in subjects with head injury, chest compression injury, acute pancreatitis, childbirth, connective tissue disorders and retrobulbar anaesthesia. Though the pathogenesis is not well understood, the entire picture above has in common, the ability to activate massive amounts of complement. The resultant leukoemboli may be a source of retinal arteriolar embolization. A similar picture is seen in the Fat Embolism Fig. 53.1: Choroidal rupture Syndrome in patients with fractured medullated bones. Principles and Management of Ocular Trauma 335 RETINAL TEARS AND TRAUMATIC RETINAL Indirect choroidal ruptures result from compressive DETACHMENT (FIG. 53.3) injury to the posterior pole of the eye. Blunt Trauma is the commonest cause of traumatic retinal detachment, more common in young males TERSON'S SYNDROME (78%-87%). Myopes are more likely to develop retinal It is a syndrome of vitreous hemorrhage in association detachment after blunt trauma. with any form of intra cranial hemorrhage. It is seen in 3%-8% of individuals with subarachnoid hemorrhage commonly due to a ruptured aneurysm. Usually bilateral, there may be associated intra- retinal, sub-retinal and pre retinal hemorrhages. A peculiar dome shaped pre-retinal hemorrhage is sometimes seen within the vascular arcades between the internal limiting membrane (ILM) and Posterior Hyaloid Face (PHF). Late sequelae may include Epiretinal Membranes (ERMs) and macular abnormalities. The pathogenesis is unknown but may be due to an acute rise in intracranial pressure which is transmitted down the intra vaginal space of the optic nerve. The venous stasis due to compression and stretching of the intraorbital veins lead to a rapid increase in intraocular venous pressure causing distension and Fig. 53.3: Traumatic retinal detachment rupture of fine causing distension and rupture of fine papillary and retinal capillaries. Ocular contusion produces a forceful anteriopos- Surgical management hastens visual rehabilitation terior compression of globe, with a resultant lateral and may avoid potential complications of persistent expansion of the equatorial region and disinsertion or blood in the vitreous. tearing of the retina. Blunt trauma is the cause of 70%- 80% of traumatic retinal detachment, 80% occurring within two years of the injury. Retinal dialysis is the VALSALVA RETINOPATHY most common retinal break produced by blunt trauma. Raised intra-thoracic pressure causes decreased venous Other breaks seen are also usually anterior produced retina which may be associated with pre-retinal by traction at the borders of the vitreous base. hemorrhages. Visual loss occurs due to a hemorrhagic Contusion results in retinal detachment which is detachment of the ILM, pre-retinal hemorrhage, pathogenically due to vitreous base avulsion. Some vitreous hemorrhage and dissection of blood under breaks are a result of tissue necrosis seen directly at the retina. the site of trauma, especially in the inferotemporal Part of the blood may turn yellow after several days. quadrant, which is the most exposed. Traumatic Serous detachment may replace the resorbing blood. syneresis of the vitreous gel then leads to a retinal Recovery of normal vision with spontaneous reattach- detachment. Myopes are more susceptible to develop ment is the rule. retinal detachment especially along with nasal dialysis and giant tears. OPTIC NERVE AVULSION (FIG. 53.4) It occurs typically when an object intrudes between CHORIORETINITIS SCLOPETERIA the orbital wall and globe and displaces the eye or Sclopeteria is a simultaneous full thickness rupture of there is sudden rotation or abduction of the globe. the retina and choroid when a highly velocity missile The optic nerve is disinserted from the retina, choroid penetrates the orbit and travels in close proximity to and vitreous. The lamina cribrosa is retracted from the globe. Shock waves cause a rapid deformation of the scleral rim. There is a total or partial visual loss the globe. The retina and choroid rupture exposing depending on the degree of avulsion. Initially, the optic the underlying sclera, once the overlying hemorrhages nerve is covered by hemorrhage. When the media clear. Retinal detachment is rarely seen due the clears a striking cavity is seen where the optic nerve extensive scarring. A pars plana vitrectomy may be has retraced into its dural sheath. required for non-clearing vitreous hemorrhage. The There is no known effective medical or surgical site of involvement determines the final visual acuity. treatment. 336 Clinical Diagnosis and Management of Ocular Trauma cautious exploration of the site and extent of wound. It is preferable to repair tear as it is being uncovered to prevent further uveal or vitreal prolapse; and then explore further. Dilated fundoscopy followed by intraoperative cryo-photocoagulation can be done to prevent future retinal detachments. Alternatively, corneo-scleral repair can be done in two sittings. Initial repair of tear to close the globe and volume replacement, followed by vitrectomy within 10 days if required for retinal tears, endo drainage of subretinal blood or fluid, internal tamponade, scleral buckle with encirclage and endolaser or external cryotherapy.

Fig. 53.4: Optic nerve avulsion Corneoscleral Laceration with TRAUMATIC OPTIC NEUROPATHY Tissue Loss Damage to one or both nerves may occur with blunt trauma to the head. Prognosis for recovery of vision Small punctured wounds may simply be sutured tightly. is poor. Treatment with high dose corticosteroids has For large tissue loss, tissue replacement techniques such been advocated along with surgical decompression in as full thickness and lamellar patch graft are more selected cases. appropriate for restoration of structural integrity without astigmatism inducing distortion. Primary penetrating keratoplasty with anterior segment reconstruction are the definitive treatment for complex Corneoscleral Laceration injuries with extensive tissue loss. with Lens and Vitreous Involvement Irreparable Scleral Rupture Large corneal lacerations or small penetrating injuries caused by projectiles can cause significant lens damage. Badly ruptured eyes with extensive tissue loss and no The decision about lens removal depends on critical visual function should be enucleated in the interest pre and intra-operative assessment. If lens capsule is of the other eye. ruptured and surgical visualization is adequate, it is preferable to complete all operative interventions at one session. In cases with posterior capsular rupture Postoperative Management with vitreous involvement, lensectomy with pars plana Appropriate medical therapy comprising of systemic vitrectomy are advisable. Primary IOL insertion should and topical antimicrobials to control infection and not be performed if there is vitreous in AC or surgical corticosteroids to minimize inflammation and scarring, visualization is poor. Wound should be watertight and should be instituted. Anti-glaucoma therapy for IOP free of vitreous incarceration at the conclusion of control and lubricants or bandage contact lens for surgery. ocular surface stabilization may be required.

Posterior Scleral Laceration Conclusion Scleral lacerations without corneal involvement may The management of open globe injuries continues to be difficult to diagnose due to relatively formed eyeball pose difficult management dilemmas. The standard and anterior chamber. Signs of posterior rupture practice worldwide in these cases should be to include bullous sub-conjunctival hemorrhage, poor undertake a primary surgical repair to restore the vision, shallow or very deep anterior chamber, low structural integrity of the globe at the earliest IOP, rarely high IOP due to choroidal hemorrhage, opportunity regardless of the extent of the injury and hyphema and distorted pupil. Their management the presenting visual acuity. Despite microsurgical requires a 360°. Conjunctival peritomy, followed by improvements in management in this devastating Principles and Management of Ocular Trauma 337 setting, there remain many eyes that cannot be A. Inert: Metals like gold, silver and platinum are salvaged. A primary enucleation is usually only inert in nature and are tolerated well in the eye considered in eyes that are beyond primary repair. for long periods. Delayed repair, lens disruption, extent of wound, B. Toxic: Metals like iron copper and lead are toxic vitreous prolapse, posterior location of the wound, in nature and requires immediate removal. foreign body and rural setting are the known risk Copper is the most injurious metal to the eye. factors for poor visual outcome in ocular trauma. In 2. Inorganic non-metals: Stone, glass, porcelain an Indian study by Narang et al incidence of open are relatively inert and may be tolerated by the globe injuries and the outcome in children, and the eye. risk factors for post-traumatic endophthalmitis was 3. Organic: Wood and vegetable matter of foreign studied. It was concluded from the study that delayed bodies are commonly associated with agricultural repair, bow and arrow injuries and household injuries trauma and result in severe endophthalmitis and were associated with significantly higher risk of poor visual outcome. endophthalmitis. The incidence of endophthalmitis can be reduced by early referral of trauma cases and EVALUATION OF A PATIENT WITH IOFB parental supervision. To conclude, open globe injuries can be present History in varying severity and though the overall prognosis A few direct questions should be sufficient for the is grave, prompt surgical intervention can result in ophthalmologist to suspect the presence of an IOFB better visual outcome. in eyes with an open globe injury. In case of doubt, it is advisable to err on the side of an IOFB presence. The most common cause for litigation against the Intraocular Foreign Body ophthalmologist in a trauma case is a missed IOFB. It is important to remember that the patient may be Intraocular foreign body represents a subset of open unaware of any object entering (even striking) the eye, globe injury that involves both anterior and posterior and the vision may be unaffected initially. Sometimes segments of the eye. An intraocular foreign body may the circumstances (e.g. polytrauma cases) divert traumatize the eye mechanically, introduce infection primary attention towards systemic evaluation and or exert toxic effects intraocularly. Foreign body may management sidelining the ocular assessment, e.g. be lodged anywhere from anterior segment to retina road traffic accident, blast injuries, which commonly and choroid. Notable mechanical effects include result in multiple IOFBs' (Fig. 53.5). cataract formation, vitreous hemorrhage, retinal tears and hemorrhage. Due to their high velocity, most of Ocular Examination the IOFB's come to lie in the posterior segment of the eye. A complete examination of both the eyes is necessary, Intraocular foreign bodies occur in 18 to 41% of including the visual acuity and the presence of relative the open globe injuries. Most patients are young males afferent pupillary defect. When pupil in the traumatized eye cannot be examined, a reverse RAPD in the fellow in 3rd and 4th decades. Commonest case is an occupa- tional hazard involving hammering metal or stone. Sharp particles require less energy to penetrate the eye as compared to blunt particles resulting in lesser degree of damage to ocular tissues. In contrast blunt objects like gun pellets require much more energy to penetrate the eye resulting in severe ocular tissue destruction. Smaller size is difficult to detect but easier to remove. Proliferative vitreoretinopathy is common with larger IOFB's.

COMPOSITION IOFB's may be grouped into 3 types according to their composition 1. Metallic: 80-90% of IOFBs' out of which 55-80% are magnetic in nature. Fig. 53.5: Fundus photograph showing Metallic IOFB 338 Clinical Diagnosis and Management of Ocular Trauma eye is a poor prognostic sign. A corneal entry wound • Ultrasound is a useful tool in localizing IOFB's, and and a hole in the iris provide trajectory information. its careful use is possible even if the globe is still Localized conjunctival chemosis strongly suggests open; alternatively, intraoperative use after wound perforation. Most common site of entry for IOFB is closure can be attempted. USG is very effective cornea (65%) followed by sclera (25%) and limbus in detecting radiolucent IOFB, assessing the status (10%). A corneal passage is usually accompanied by of retina, vitreous, choroids and optic nerve and iris hole and traumatic cataract which reduces the detecting globe perforation. IOFB appears as high velocity of IOFB and decreases the damage potential. density echo which persists at a low gain and A scleral entry allows the foreign body to retain its shadowing of the retina choroids sclera complex. momentum which therefore causes more damage. Ringing bell phenomenon may be seen. The ultra- Most eyes have a single IOFB. Multiple IOFB's are sound biomicroscope may help with IOFB's in the usually associated with firearm or blast injuries. The anterior segment or angle of anterior chamber. slit lamp is extremely useful in detailing all anterior segment pathologies. The indirect ophthalmoscope Other Tests through a dilated pupil may allow direct visualization Electroretinography is useful if a chronic IOFB is found of the IOFB, which gives the most useful information and siderosis is either suspected or present. Four stages for the surgeon. Gonioscopy and scleral depression are recognized: initially, a and b waves are normal or are not recommended unless the entry wound has supernormal. Later, a wave is larger and b wave been surgically closed. smaller. Still later, b wave becomes subnormal in amplitude. Eventually, ERG becomes non-recordable. Lab Studies These changes can be reversed by IOFB removal Culture an IOFB or a sample of vitreous if an infection before the b wave amplitude is significantly reduced. is suspected. Remember that a positive result does not mean that an infection is occurring and that a negative PATHOPHYSIOLOGY result does not preclude the possibility of endophthal- The final resting place of and the severity of damage mitis. caused by an IOFB depend on several factors, including the size, the shape, and the momentum of Imaging Studies the object at the time of impact, as well as the site They are useful to detect the presence and localization of ocular penetration. of IOFBs' in presence of opaque media such as cataract IOFB primarily damages the ocular tissue mecha- or vitreous hemorrhage. nically. The injuries include corneal/scleral perforation, • Plain X-ray of orbit is the simplest and readily cataract formation, vitreous hemorrhage, retinal tears available tool for IOFB detection. It is useful if a and hemorrhage. In addition to the initial damage metallic IOFB is present and a CT scan is unavailable. caused at the time of impact, the risk of endophthalmitis However, it is difficult to ascertain the intra/extra and subsequent scarring play an important role in the ocular location of foreign body. Another dis- planning of the surgical intervention. Retained metallic advantage of plain X-ray is that small metallic and IOFB additionally results in a delayed chemical injury, nonmetallic IOFB are frequently missed. metallosis bulbi, caused by electrolytic dissociation of • CT scans are the test of choice for IOFB localiza- metal ions. These ions react with the tissues and cause tion. It allows detection of IOFB 0.5 mm or more oxidative damage that interrupts cell function by in diameter. Though 3 mm cuts allow rapid altering cell membrane permeability and lysosomal detection of foreign bodies; wood plastic and small breakdown. The common metals that dissociate in this metallic foreign bodies may be missed. A manner are iron and copper. consultation with the CT technician is helpful in selecting the optimal section so as to reduce the Siderosis risk of a false-negative result. Helical CT scans have Iron is the most common intraocular foreign body. a very high identification rate. Limitations of CT- It undergoes dissociation resulting in deposition of iron scan are in detecting an inorganic IOFB and ocular intraocularly, notably the lens epithelium and the soft tissue damage. retina. It results in toxic effects on cellular enzyme • MRI generally is not recommended for metallic systems resulting in cell death. Signs involve reddish IOFB's as the strong magnetic fields may move brown discolouration of iris, deposits on anterior the IOFB causing intraocular damage capsule, secondary glaucoma and pigmentary Principles and Management of Ocular Trauma 339 retinopathy. Pigmentary retinopathy has most • A posterior segment IOFB requires a pars plana profound effect on vision. ERG manifests progressive vitrectomy, unless the tissue damage is minimal. The attenuation of the b-wave over time. posterior hyaloid should always be removed, and any deep impact should be prophylactically treated. Chalcosis For the actual removal, the best tool to extract a Severe ocular reaction occurs due to an intraocular ferrous IOFB is a strong intraocular magnet. For foreign body with high copper content, leading to an non-magnetic IOFBs; a proper forceps may be endophthalmitis like presentation followed by phthisis used. External electromagnets should not be used bulbi. When the copper content of intraocular foreign since they do not allow controlled extraction. Rarely, body is low, it results in chalcosis. In these cases a scleral cut-down is used. Corneo-scleral tear electrolytically dissociated copper is deposited repair and removal of traumatic cataract are intraocularly, forming a Kayser-Fleischer ring and frequently required at the same sitting. As a rule- anterior sunflower cataract similar to those seen in all IOFB's should be removed except in certain Wilson's disease. circumstances. • A chronic, inert, encapsulated or intralenticular IOFB without clinical / electrophysiological evidence MANAGEMENT of toxixcity in a quiet eye may be left alone, after Primary Care Guidelines proper patient counseling. A periodic follow up with Since most of FB's come to rest in the posterior segment, ERG monitoring is necessary. the attending ophthalmologist should refer the case • Large IOFB's in a phthisical irreparably damaged for tertiary care, if the expertise and equipment eye with no perception of light are better left alone. required for comprehensive globe reconstruction is not • Once ERG is extinguished in an eye with established available. Before referral, the primary ophthalmologist metallosis, the ocular damage is almost irreversible should use systemic medications to control pain and and IOFB removal is unlikely to improve the anxiety. The injured eye should be patched and outcome. covered with a shield before referring the patient. A tetanus booster may also be appropriate. Surgical Techniques The posterior segment intraocular foreign bodies are Principles of Management removed by vitrectomy or via trans-scleral route. The timing of intervention is primarily determined by Magnetic IOFB Extraction: This approach is non- whether the risk of endophthalmitis is high. If the risk invasive but largely uncontrolled. External electro- is high, immediate (emergency) surgery is indicated; magnets like the permanent hand magnet and the in most other cases, the surgeon has the option of newer Broson Magnion instrument can be used to exert deferring intervention for a few days to reduce the powerful magnetic pull after scleral cut down. In case risk of intraoperative hemorrhage. If endophthalmitis of an anterior IOFB, magnet can be applied directly occurs, it is present at the time of patient presentation over the IOFB. For a posterior intravitreal IOFB which in over 90% of the cases. Broad spectrum systemic is away from the retina, magnet can be applied antibiotics can be started though their effectiveness is indirectly through pars plana. The indirect approach not proven. Intravitreal antibiotics may be useful in may damage the retina or crystalline lens by IOFB high risk cases like IOFB of vegetable matter, rural movement. This technique is useful in small (< 3 mm), injury. anterior, visible, intravitreal, magnetic IOFB in a fresh • IOFBs in the anterior chamber are typically case. removed through a paracentesis (not through the Non-magnetic IOFB Extraction: Requires extraction original wound) performed at 90-180° from where with intraocular forceps combined with vitrectomy and the IOFB is located. Viscoelastics should be used if required lensectomy. to reduce the risk of iatrogenic damage to the corneal endothelium and the lens. • An intralenticular IOFB does not necessarily cause Pars Plana Vitrectomy (PPV) cataract. Unless there is a risk of siderosis or the Vitrectomy is indicated for large, posterior, invisible, loss to follow-up is high, the IOFB and the lens nonmagnetic, intra/subretinal or encapsulated IOFB's may be left in situ. Otherwise, usually, the IOFB is or those associated with retinal detachment, endoph- extracted first, the lens is extracted second, and an thalmitis or vitreous hemorrhage. PPV nowadays has intraocular lens (IOL) is implanted simultaneously. become the standard modality for foreign body 340 Clinical Diagnosis and Management of Ocular Trauma management due to greater control and less risk of are found to be the predominant cause for fulminant iatrogenic injury. Induction of posterior vitreous onset, Gram-positive bacillus (28.4%) for acute onset, detachment, wherever possible, is now a standard step and fungi (52.3%) for chronic onset of infections. The in PPV to eliminate ERM and PVR. Endolaser incidence of post-traumatic endophthalmitis varies photocoagulation is done around site of FB impaction from 3.3 to 16.5%. Several predisposing factors to prevent future retinal detachment. Perflurocarbon increase the risk of endophthalmitis following ocular liquids (PFCL) can be used to float the IOFB and trauma such as delayed primary repair, retained prevent iatrogenic macular damage. PFCL may not intraocular foreign body, disruption of lens. These eyes be able to support heavy metallic IOFB. The foreign require immediate surgical repair. Most of the body is picked up from retina or vitreous after infections in post-traumatic endophthalmitis are removing its adhesions, with an intraocular magnet polymicrobial with high culture positivity. Bacillus or forceps depending upon its magnetic properties. elaborates several enzymes and exotoxins leading to For medium sized IOFB, sclerotomy is enlarged for rapid onset fulminant endophthalmitis with systemic removal. For large IOFB's (> 5 mm) limbal incision features like fever and leukocytosis. Vitreous biopsy or Open Sky Approach may be required. If corneal shows blood stained purulent material. B. cereus is damage is present, corneal button is removed and commonly found in cases with retained intraocular temporary keratoprosthesis is used followed by corneal foreign body. grafting. Special forceps like Stroinko forceps or ureter stone forceps can be used for large non-magnetic IOFB CLINICAL FEATURES (e.g. glass). Primary silicone oil tamponade is used in Symptoms like pain, photophobia, redness, visual loss patients with severe intraocular foreign body (IOFB) are present both due to trauma itself and endophthal- injuries and high risk of proliferative vitreoretinopathy. mitis also. It is of utmost importance to rule out endo- Primary silicone oil stabilizes the retina during the critical phthalmitis if pain and visual loss is not proportionate period of active PVR and limits the visual loss in the to clinical signs. long term. Prophylactic 360 degrees encircling scleral Clinical signs include lid edema, circumcorneal buckle placed at the time of pars plana vitrectomy congestion, corneal edema, hypopyon, vitritis, retinal reduces the risk of retinal detachment in future. periphlebitis or hazy view of fundus. Fungal endophthalmitis though rare, can be present late after PROGNOSIS initial trauma repair, presenting as persistent or Postoperative anatomic and visual outcome after IOFB worsening vitritis and snow ball opacities in vitreous removal is limited by proliferative vitreoretinopathy, (Figs 53.6 and 53.7). RD and endophthalmitis. Endophthalmitis occurs in 16-45% of eyes with IOFB depending upon time delay Management of Post-traumatic Endophthalmitis in removal of IOFB, type of IOFB (inorganic or organic Prophylaxis: Prophylactic systemic antibiotics covering vegetative) or self contaminated injuries. The main risk the common causative organisms of traumatic factors for PVR and RD are the size of IOFB, retinal endophthalmitis (especially Staphylococcci and Bacillus injury and traumatic cataract. The recent advances in cereus) and good intraocular penetration should be surgical techniques have been associated with a significant improvement in prognosis.

Post-traumatic Inflammation TRAUMATIC ENDOPHTHALMITIS Post-traumatic endophthalmitis is a rare but catastro- phic event associated with open globe injuries. Traumatic endophthalmitis, a type of exogenous endophthalmitis, is unique in having a high incidence of Bacillus species especially B.cereus. These eyes have more intense symptoms and signs than eyes with acute postoperative endophthalmitis, perhaps due to more virulent organisms and in addition trauma itself. The diagnosis of traumatic endophthalmitis depends on a Fig. 53.6: Anterior segment photograph of post-traumatic high index of suspicion followed by vitreous biopsy endophthalmitis showing corneal wound (white arrow) and and culture techniques. Gram-negative bacilli (65.2%) hypopyon Principles and Management of Ocular Trauma 341 12 hourly) are ideal for initial therapy. The same combination is preferred for intravitreal injections: Vancomycin 1 mg in 0.1 ml and ceftazidime 2.25 mg in 0.1 ml. Vancomycin covers the gram positive oraga- nisms that usually cause post-traumatic endophthalmitis whereas ceftazidime covers gram-negative organisms. In case of suspicion of fungal etiology intravitreal amphotericin B 0.005 mg in 0.1 ml can be given. Topical therapy is started with hourly administration of fortified antibiotic solutions (cefazolin, gentamicin) or fluroquinolone (ciprofloxacin or gatifloxacin) eye drops. Use of adjunctive steroids in the form of intra- vitreal or topical dexamthasone or topical prednisolone eye drops is important to decrease the tissue destructive effects of the inflammation. Fig. 53.7: Fundus photograph showing vitreous haze Surgical management: Vitrectomy is generally required in cases of post-traumatic endophthalmitis, started in all cases of traumatic open globe injuries. due to severity of the infection and the associated Oral Fluroquinolones have good intravitreal trauma. Essentially a core vitrectomy should be penetration and are the drug of choice. Tetanus performed to reduce the microbial load. Peripheral prophylaxis should be considered in all open globe vitreous is better left alone as the retina is very friable injuries especially the contaminated cases. The role of and can lead to iatrogenic tears and detachment. A prophylactic intravitreal antibiotics is controversial due lensectomy may be required in cases of traumatic to their toxicity. Prophylactic intravitreal antibiotics cataract or severe pars plana exudates sticking the back should be given in cases with high risk of infection of the lens leading to poor visualization of vitreous. such as intraocular foreign body, lens disruption, soil Any associated pathologies like IOFB or retinal contamination and injuries in rural setting at the time detachment can be tackled during vitrectomy. of primary repair. Perflurocarbon liquid (PFCL) helps in removal of IOFB Microbiology: In addition to complete clinical and also protects the retina from damage. The retinal examination, a complete microbiologic work up is detachment is repaired with vitrectomy, fluid-air essential for confirmation of endophthalmitis and the exchange and endolaser followed by intravitreal gas causative agents. The various specimens taken are or silicon tamponade and intravitreal antibiotics and vitreous tap or biopsy, AC tap, corneal scraping, steroids. Intravitreal injections are repeated after 48 vitrectomy cassette fluid or removed IOFB. Smears to 72 hours of first injection depending on the response of specimens are sent for staining( Gram, Giemsa and to therapy or half life of the drugs. fungal stains) and inoculated on various agar like Patient should be made aware of the guarded chocolate agar, blood agar for bacteria and nature of visual prognosis and need for repeat Sabauroud's agar for fungi. Microbiologic work up procedures like intravitreal injections or vitrectomy in should include antibiotic susceptibility testing of isolates view of worsening of the condition. Among eyes with which would help in any alteration of antibiotic therapy positive intraocular cultures after open globe injury, in future. the visual prognosis is guarded. Clinical features B-scan Ultrasonography: It is useful in evaluating associated with better visual acuity outcomes include posterior segment status in hazy media. USG will show better presenting visual acuity, culture of a non-virulent moderate density echoes in vitreous cavity suggestive organism, lack of a retinal detachment, absence of of exudation or membranes. We can detect any clinical endophthalmitis, and shorter wound length. associated retinal or choroidal detachment.USG also Prevention of infection by prompt primary repair of detects related conditions such as IOFB and dropped the wound and detection of earliest signs of infection nucleus. is of utmost importance. Medical Management: Mainstay of medical therapy are systemic, intravitreal and topical antibiotic drops with or without steroids. Steroids help in reducing the inflammation associated damage to the intraocular Sympathetic Ophthalmitis structures. It is a bilateral granulmatous panuveitis occurring Systemic therapy is usually by intravenous route. subsequent to penetrating trauma involving uveal tissue Intravenous ceftazidime and vancomycin (both 1 gm prolapse or intraocular surgery. The traumatized eye 342 Clinical Diagnosis and Management of Ocular Trauma is known as the exciting eye and the fellow eye which 5. Al-Omran AM, Abboud EB, Abu El-Asrar AM. also develops uveitis is known as the sympathizing eye. Micro-biologic spectrum and visual outcome of post- Presentation is usually between two weeks to three traumatic endophthalmitis. Retina 2007;27(2):236-42. 6. Azad RV; Kumar N; Sharma YR; Vohra R. Role of months, with 90% of cases occurring within first year of prophylactic scleral buckling in the management of injury. Injuries account for 47% of patients while ocular retained intraocular foreign bodies. Clin Experiment surgery 44% of patients. Patient may also have systemic Ophthalmol 2004; 32(1): 58-61. manifestations similar to VKH syndrome, like headache, 7. B Shukla, S Natarajan: Management of Ocular Trauma tinnitus, dysacousis, aloepecia, vitiligo and poliosis. 2005, PP. 3-12, 89-151, 167-252. The exciting eye has signs of initial trauma, besides 8. Barr CC: Prognostic factors in corneoscleral lacerations, being irritable. The fellow eye is also inflammed and Arch Ophthalmol 1983;101:919-24. 9. BastekJV, FoosRY, HeckenliveyJ.: Traumatic Pigmentary photophobic, and shows anterior granulmatous uveitis, Retinopathy. Am. J Ophth. 1981; 92:621-624. vitritis and multifocal choroidal infiltrates in the mid 10. Beatty S, Smyth KL, Au Eong KG, Lavin MJ. periphery. Histology shows sub RPE infiltrates Chorioretinitis Sclopeteria. Injury 2000; 31:55-60. corresponding to the Dalen Fuchs nodules. Severe 11. Bradford J. Shingelton, Eye Trauma; clinical evaluation. cases may show choroidal thickening or exudative In: Shingleton BJ, Hersh PS, Kenyon KR, editors. Eye retinal detachment on ultrasonography. trauma. St Louis: Mosby, 1991;3-24. 12. Brinton GS, Topping TM et al: Post traumatic FFA shows multifocal leaks at the RPE level, with endophthalmitis. Arch Ophthalmol 102:547, 1984. subretinal pooling in presence of exudative detach- 13. Brinton GS, Topping TM, Hyndiuk RA, Aaberg TM, ment.Dark spots seen in ICG are suggestive of active Reeser FH, Abrahams GW, Post traumatic endophthal- disease. mitis. Arch Ophthalmol 1984; 102(4): 547-50. Enucleation of the traumatized eye, if severely and 14. Bryden FM, Pyott AA, Bailey M, McGhee CN. Real time irreversibly damaged with no visual potential, should ultrasound in the assessment of intraocular foreign be performed within ten days of injury to prevent risk bodies. Eye. 1990; 4 (Pt 5):727-31. of sympathetic ophthalmitis. Uveitis may require 15. Bustros SD. Posterior segment intraocular foreign bodies. In: Shingleton BJ, Hersh PS, Kenyon KR, editors. Eye treatment in the form of topical and systemic steroids trauma. St Louis: Mosby, 1991.pp.226-237. that should be continued for at least a year with gradual 16. Castiblanco CP, Adelman RA. Sympathetic ophthalmia. tapering to reduce the risk of relapse. Immunosup- Graefes Arch Clin Exp Ophthalmol. 2008 Sep 16. pressive therapy with high dose systemic steroids such 17. Cekiç O, Batman C, Yasar U, Basci NE, Bozkurt A, Kayaalp as intravenous methylprednisolone and steroid-sparing SO. Human aqueous and vitreous humour levels of agents such as cyclosporin A and azathioprine have ciprofloxacin following oral and topical administration. improved the prognosis. Eye. 1999 Aug;13 ( Pt 4):555-58. 18. Chiquet C, Zech J, Gain P, Adeleine P, Trepsat C. Visual outcome and prognostic factors after magnetic extraction ENUCLEATION of posterior segment intraocular foreign bodies in 40 Primary enucleation should be considered for severe cases. Br J Ophthalmol 1998; 82:801-06. irreparable injuries with no visual potential. Secondarily, 19. Committee on Trauma and Committee on Shock. Accidental death and disability: the neglected disease of enucleation can be attempted if the severely damaged modern society. Washington: National Academy Press; lost eye is unsightly or uncomfortable. This should be 1966:5. performed within ten days of injury to prevent risk 20. Cruvinel Issac DL, Ghanem VC, Nascimento MA, Toriqoe of sympathetic ophthalmitis. M, Kara Jose N. Prognostic factors in open globe injuries. Ophthalmologica. 2003; 217 (6); 431-5 21. Danis RP Endophthalmitis.Ophthalmol Clin North Am 2002;15(2): 243-248. Bibliography 22. Das T, Jalali S, Gothwal VK, Sharma S, Naduvilath TJ. 1. Affeldt JC, Flynn HW Jr, Forster RK, Mandelbaum S, Intravitreal dexamethasone in exogenous bacterial Clarkson JG, Jarus GD.Microbial endophthalmitis endophthalmitis: results of a prospective randomised resulting from ocular trauma. Ophthalmology. 1987 study. Br J Ophthalmol. 1999 Sep;83(9):1050-55. Apr;94(4):407-13. 23. Dass AB, Ferrone PJ, Chu YR, Esposito M, Gray L. 2. Aaberg TM. Macular Holes. Survey of Ophth. 1970; Sensitivity of spiral computed tomography scanning for 15:139-62. detecting intraocular foreign bodies. Ophthalmology. 3. Aguilar JP, Green WR. Choroidal rupture: A 2001 Dec; 108(12):2326-28. histopathologic study of 47 cases. Retina. 1998; 4:269- 24. Drews RC: Sodium hyaluronate in repair of perforating 75. eye injuries. Ophthalmic Surg 1986;17:23 4. Alfaro DV, Roth D, Liggett PE. Posttraumatic 25. Duke-Elder S., Mac Faul PA. Injuries, Part I:Mechanical endophthalmitis. Causative organisms, treatment, and Injuries. In:Duke-Elder. System of Ophthalmology. prevention. London: Henry Klimpton; 1972. Principles and Management of Ocular Trauma 343

26. Eagling, E.M.: Ocular damage after blunt trauma to the 46. Lieb Df, Scott IU, Flynn HW Jr, Miller D, Feuer Wj. Open eye. Its relationship to the nature of injury. globe injuries with positive intraocular cultures: Factors BJO.1974;58:126-140 influencing final visual acuity outcomes. Ophthalmology. 27. Edwards WC, Layden WS: Traumatic hyphema. AmJ 2003 Aug;110(8):1560-65. Ophthalmol 1973;75:110 47. Madreperla SA, Bentz BA. Formation and treatment of 28. Erakgun T, Egrilmez S. Prognostic factors in vitrectomy a traumatic macular hole. Arch. Ophthal. 1997; 115: for posterior segment intraocular foreign bodies. 1210-1211. J Trauma. 2008 Apr; 64(4):1034-37. 48. Management of corneoscleral lacerations. In Shingleton 29. Ersanli D, Unal M, Avdin A, Gulecek O, Kalemoqlu M. BJ, Hersh PS, Kenyon KR, editors. Eye trauma. St Louis: Results of pars plana vitrectomy in closed globe injuries. Mosby, 1991.pp143-168 Ophthalmic Surg Lasers Imaging. 2005; 36(3):182-88. 49. McNicholas MM, Brophy DP, Power WJ, Griffin JF. Ocular 30. Fred M. Wilson II: Basic and Clinical Science Course trauma: evaluation with US.Radiology. 1995 May; 1990-91, AAO, Section 8, “Glaucoma, Lens and Anterior 195(2):423-27. Segment Trauma”, PP.162-165. 50. Mehta DK, Tuli D: New classification systems for ocular 31. Glaser Bm, Carter JB, Kuppermann BD et al. Perfluoro- trauma. In: Management of Ocular Trauma Shukla octane in treatment of giant retinal tears with proliferative B,Natrajan S; 1st Ed; Jaypee brothers Medical publisher, vitreo-retinopathy. Ophthalmology 1991;98:1613-21. New Delhi, 2005. pp 9 32. Greven CM, Engelbrecht NE, Slusher MM, Nagy 51. Meier P, Wiedemann P. Endophthalmitis—clinical picture, SS.Intraocular foreign bodies: Management, prognostic therapy and prevention Klin Monatsbl Augenheilkd. factors, and visual outcomes. Ophthalmology. 2000 Mar; 1997 Apr;210(4):175-91. Review. German. Erratum in: 107:608-12. Klin Monatsbl Augenheilkd 1998 Mar;212(3):162. 33. Gupta A, Srinivasan R, Gulnar D, Sankar K, Mahalakshmi 52. Mester V, Kuhn F, Intraocular foreign bodies. Ophthalmol T. Risk factors for post-traumatic endophthalmitis in Clin Am 2002; 15:235- 42. patients with positive intraocular cultures.Eur J 53. Muga R, Maul E: Management of lens damage in Ophthalmol. 2007 Jul-Aug;17(4):642-47. perforating corneal laceration. Br J Ophthalmol 34. H. Mackenzie Freeman: Ocular Trauma 1979, Chapter 1978;62:784 17, “Traumatic Hyphema” Merrill Grayson and Fred M. 54. Narang S, Gupta V, Gupta A, Dogra MR, Pandav SS, Wilson II, PP.145-149 Das S. Role of prophylactic intravitreal antibiotics in open 35. Hersh PS: Anterior segment reconsruction following globe injuries. Indian J Ophthalmol. 2003 Mar;51(1):39- ocular trauma. Int Ophthalmol Clin 1988;28:57 44. 36. JH Krachmer: The requisites in Ophthalmology - Anterior 55. Narang S, Gupta V, Simalandhi P, et al. Paediatric open Segment Trauma. 2000, Christopher J. Rapuono, Jodie globe injuries. Visual outcome and risk factors for I. Luchs, Terry Kim PP.299-303. endophthalmitis. Indian J Ophthalmol 2004;52:29-34 37. Jonas JB, Knorr HL, Budde WM.Prognostic factors in 56. Negrel AD, Thylefors B. The global impact of eye injuries. ocular injuries caused by intraocular or retrobulbar Ophthalmic Epidemiol 1998;5:143- 69. foreign bodies. Ophthalmology. 2000; 107(5):823-28. 57. Ottavio Bernasconi, Carlos Auer, Leonidas Zografos and 38. Keates RH, Lichtenstein SB: The management of anterior C. P. Indocyanine green angiographic findings in sympa- sement trauma with multiple small incisions. thetic ophthalmia. Herbort Graefe’s Archive for Clinical Ophthalmology 1980;87:887 and Experimental Ophthalmology, Volume 236, Number 39. Keren G, Alhalel A, Bartov E, Kitzes-Cohen R, Rubinstein 8 / July, 1998 E, Segev S, Treister G.The intravitreal penetration of orally 58. Pavlovic S, Schmidt KG, Tomic Z, Dzinic M. Management administered ciprofloxacin in humans. Invest Ophthalmol of intra-ocular foreign bodies impacting or embedded in Vis Sci. 1991 Jul;32(8):2388-92. the retina. Aust N Z J Ophthalmol. 1998 Aug; 40. Konstantinidis L, Borruat FX, Wolfensberger TJ. Long- 26(3):24142. term stability of retinal function despite retained 59. Pieramici DJ, Sternberg P et al. A system for classifying intraocular metallic foreign body. Klin Monatsbl Mechanical injuries of the eye. Am J Ophthalmol. 1997; Augenheilkd. 2008 May;225(5):482-5. Links 123: 820-831. 41. Kuhn F, Morris R et al. A standardized classification of 60. Postel EA, Mieler WF. Management of posterior segment ocular trauma. Ophthalmology. 1996; 103: 240-243. intraocular foreign bodies. In: Guyer Dr, Yanuzzi LA, 42. Kuhn F, Morris R: Posterior segment IOFB-management Chang S, Shields JA, Green WR, editors. Retina-Vitreous- in the vitrectomy era. Ophthalmology 2000; 107:821- Macula, vol2.Philadelphia: WB Saunders Company; 22. 1999.pp 1395-1406. 43. Kunimoto DY, DasT, Sharma S, et al. Microbiologic spec- 61. Potts AM, Distler JA. Shape factor in the penetration of trum and susceptibility of isolates: Part II. Postoperative intraocular foreign bodies. Am J Ophthalmol. 1985 Jul endophthalmitis. Am J Ophthalmol 1999;128:242-44. 15;100(1):183-87. 44. Lakits A, Prokesch R, Scholda C, Bankier A. Orbital 62. Rahman I, Maino A, Devadason D, Leatherbarrow B. helical computed tomography in the diagnosis and Open globe injuries : factors predictive of poor outcome. management of eye trauma. Ophthalmology. 1999 Dec; Eye. 2006;20(12): 1335. 106(12):2330-35. 63. Ramakrishnan R, Bharathi MJ, Shivkumar C, Mittal S, 45. Levin MR, D’Amico DT: Traumatic endophthalmopathy. Meenakshi R, Khadeer MA, Avasthi A. Microbiological In: Shingleton BJ, Hersh PS, Kenyon KR, editors. Eye profile of culture-proven cases of exogenous and trauma. St Louis: Mosby, 1991.pp.242-52. endogenous endophthalmitis: a 10-year retrospective 344 Clinical Diagnosis and Management of Ocular Trauma study. Eye. 2008 Jul 4.Centre for Excellence in with retained intraocular foreign bodies. National Eye Glaucoma, Aravind Eye Hospital & Postgraduate Trauma System. Ophthalmology. 1993 Oct; 100(10): Institute of Ophthalmology, Tirunelveli, Tamil Nadu, 146874. South India. 80. Tran TP, Le TM, Bui HT, Nguyen TM, Küchle M, Nguyen 64. Rao NA, Tso MO, Rosenthal AR.Chalcosis in the human NX. Post-traumatic endophthalmitis after penetrating eye. A clinicopathologic study. Arch Ophthalmol. 1976 injury in Vietnam: risk factors, microbiological aspect and Aug; 94(8):1379-84. visual outcome Klin Monatsbl Augenheilkd. 2003 65. Refojo MF, Dohlman CH et al: Evaluation of adhesive Jul;220(7):481-5. German. for corneal surgeries. Arch Ophthalmol 1968;80: 645 81. Vote BJ, Hall A, Cairns J, Buttery R. Changing trends in 66. Rosenthal AR, Marmor MF, Leuenberger P, Hopkins Sympathetic ophthalmia. Clin Experiment Ophthalmol. JL.Chalcosis: a study of natural history.Ophthalmology. 2004 Oct;32(5):542-45. 1979 Nov; 86(11):1956-72. 82. W.A.J. van Hueven, Johan T. Zwaan: Decision Making 67. Rowsey JJ, Hays JC: Refractive reconstruction for acute in Ophthalmology” PP. 48-49; “Eye trauma” Mark eye injuries. Ophthalmic Surg 1984;15:569 Haywood, Lina Marouf. PP. 58-59. 68. Ryan SJ, Allen LW: Pars plana vitrectomy in ocular 83. Wani VB, Al-Ajmi M, Thalib L, Azad RV, Abul M, Al- trauma. Am J Ophthalmol 1979;88:483 Ghanim M, Sabti K. Vitrectomy for posterior segment 69. Secrets in Ophthalmology 1999, Chapter 21, “Traumatic intraocular foreign bodies: visual results and prognostic Hyphema and Glaucoma”, Annette k. Terebuh & Martha factors. Retina. 2003 Oct; 23(5):654-60. Motuz Leen, PP.151-161. 84. Weiss MJ, Hofeldt AJ, Behrens M, Fisher K.Ocular 70. Shiedow TG, Gonder JR. Macular Hole secondary to siderosis. Diagnosis and management. Retina. retrobulbar needle perforation. Retina 1998; 178-180 1997;17(2):105-8. 71. Shingleton BJ, Hersh PS: “Traumatic Hyphema”: Eye 85. Wickham L, Xing W, Bunce C, Sullivan P. Outcomes of Trauma 1991, Pages 104-116. surgery for posterior segment intraocular foreign 72. Shukla B, Management of Ocular Trauma, chapter 11; bodies—a retrospective review of 17 years of clinical page no. 93-102. experience. Graefes Arch Clin Exp Ophthalmol. 2006 73. Shukla B; Epidemiology of Ocular Trauma, 1st Ed; Dec; 244(12):1620-26. Jaypee brothers Medical publisher, New Delhi, 2002. 86. Williams DF, Mieler WF, Abrams GW, Lewis H. Results 74. Smiddy WE, Stark WJ: Anterior segment intraocular and prognostic factors in penetrating ocular injuries with foreign body. In: Shingleton BJ, Hersh PS, Kenyon KR, retained intraocular foreign bodies.Ophthalmology editors. Eye trauma. St Louis: Mosby, 1991.pp.169-174 1988;95:911-16. 75. Smith D, Wrenn K, Stack LB. The epidemiology and 87. Williams DF, Mieler WF, Abrams GW. Intraocular foreign diagnosis of penetrating eye injuries. Acad Emerg Med bodies in young people. Retina 1990: 10: S45-9. 2002; 9: 209-213. 88. Wirostko WJ, Mieler WF, McCabe CM, Diekert JP. 76. Steinert RF: Iris trauma. In: Shingleton BJ, Hersh PS, Intraocular foreign bodies In: Albert DM, Jakobiee FA, Kenyon KR, editors. Eye trauma. St Louis: Mosby, editors. Principles and practice of Ophthalmology, vol 6, 1991.pp.95-103 2nd edition. Philadelphia: WB Saunders Company; 77. Szurman P, Roters S, Grisanti S, Aisenbrey S, Rohrbach 2000.pp 5241-50. JM, Warga M, Gelisken F, Spitzer MS, Bartz-Schmidt KU. 89. Wirostko WJ, Mieler WF, McCabe CM. Removal of Primary silicone oil tamponade in the management of intraocular foreign bodies. In Peyman GA, Meffert SA, severe intraocular foreign body injuries: an 8-year follow- Conway MD, editors. Vitreoretinal surgical techniques. up. Retina. 2007 Mar;27(3):304-11. London: Martin Dunitz Ltd, 2001. pp. 443-56. 78. Thach AB, Lopez PF, Snady-McCoy LC, Golub BM, 90. Wolter JR: Coup-contrecoup mechanism of ocular Framach DA. Accidental Nd:YAG LASER injuries to the injuries. AJO.1963;56:785-796. macula. AJO 1995; 119:767-773 91. Woodcock MG, Scott RA, Huntbach J, Kirkby GR. Mass 79. Thompson JT, Parver LM, Enger CL, Mieler WF, Liggett and shape as factors in intraocular foreign body injuries. PE. Infectious endophthalmitis after penetrating injuries Ophthalmology. 2006 Dec; 113(12):2262-69. CHAPTER

Eyelid Injuries and Reconstruction: An Update 54 Quresh Maskati, Sunil Vasani (India)

Introduction The anterior lamella is broadly made up by skin (thinnest in the body) and orbicularis oculi muscle. Most eyelid defects, full thickness or otherwise, come The posterior lamella is broadly made up by the tarsal from cancers such as basal cell carcinoma or otherwise. plate, conjunctiva, Muller’s muscle and the levator In traumatic defects, the defect may be partial or full aponeurosis in its posterior part. thickness and a simple inspection of the trauma site An important surface anatomy landmark is the eyelid often reveals that slowly piecing the remnants together crease in the upper eyelid, which is formed by the like a jigsaw puzzle will correct the defect. Most ophthalmic or oculoplastic surgeons must know the attachment of a few fibres of the levator aponeurosis consistency and limitation of periorbital tissues to begin to the skin. A recession of the eyelid crease with ptosis eyelid reconstruction. The same knowledge can also and a good levator function may signify levator be applied for cosmetic surgery. dehiscence. Also important are the medial and central pads of fat that lie on and are important landmarks in finding Eyelid Injuries the levator aponeurosis. The palpebral portion of the lacrimal gland replaces the lateral fat pad in the upper A careful history to evaluate the circumstances under eyelid. which the injury was caused is mandatory. Some injuries are simple with only superficial lacerations of the lid while other facial trauma may involve injuries to the EXAMINATION head and neck regions along with severe lid injury. All examination should begin with a thorough search The latter should be dealt with immediately as they may be life threatening. Hence it is imperative to establish for any damage to the globe. In a conscious patient, that the injury is localized only to the eyelid and visual acuity, intra-ocular pressure check, slit lamp bio surrounding adnexa before beginning management. microscopy and fundus examinations are mandatory. It is important to include assessment of ocular motility CLASSIFICATION in the initial exam. Remember, even seemingly trivial eyelid injuries may be associated with underlying globe The authors prefer to classify eyelid injuries into: 1. Simple lacerations injuries. In patients with altered sensorium, a complete 2. Complex injuries eye examination should be still carried out. 3. Full thickness margin defects (a) with tissue loss (b) without tissue loss Assessment of Adnexal Injuries 4. Damage to levator aponeurosis In conscious patients complete and thorough 5. Associated with eye/orbital injuries evaluation of the eyelids and lacrimal system should 6. Canalicular lacerations. be carried out. The levator muscle can be assessed ANATOMY REVIEW by the eyelid crease, the margin reflex distance (MRD) The upper eyelid can be broadly broken up into: and the levator function test. Medial lacerations may a. Anterior lamella cause canalicular tears or canthal tendon disinsertion. b. Posterior lamella. The punctum may be displaced laterally. 346 Clinical Diagnosis and Management of Ocular Trauma Evaluation of the Orbit Sometimes severe injuries may cause significant eyelid edema, which may hamper proper eye examination. Manipulation of the eyelids in these cases may exacerbate pre-existing globe damage. Such patients should be examined under anesthesia. Orbital injuries can be evaluated with CT scan with axial and coronal cuts to rule out associated orbital fractures and foreign bodies. CT scan may also help in assessing optic nerve compression or damage. A further MRI examination, after ruling out metallic foreign bodies in the orbit can be carried out if necessary for further optic nerve / muscle/adnexal studies. Figs 54.1A and B: (A) Incorrect closure with lid notch, If facial/nasal or head neck regions are affected, (B) Correct closure additional help from the concerned specialists should be sought.

MANAGEMENT The aim of all management is to restore function, vision and cosmesis to as close to normal as possible. If the patient is intoxicated or unconscious and immediate surgery cannot be performed, tissues should be washed and repositioned as close to normal as possible. A light dressing with topical antibiotics can be given. Intravenous steroids and antibiotics or oral antibiotics should be Figs 54.2A and B: (A) Devitalized apex, administered. Intra-muscular tetanus toxoid injection (B) Y-shaped flap should also be administered. The surgeon can safely wait 24-48 hours before attempting surgical intervention. • To avoid lid notching, try to close wounds horizontally i.e. parallel to lid margin in the upper Anesthesia eyelid and vertically in the lower lid, i.e. Minor lacerations can be repaired in the outpatient perpendicular to lid margin (Figs 54.1A and B). department itself under local anesthesia. 2% lidocaine • Simple eyelid laceration can be closed directly with with epinephrine 1:100,000 can be infiltrated locally slight margin eversion. Care should be taken to before closure. General anesthesia should be adminis- avoid tension on wound edges. The authors prefer tered for complex or deeper injuries. However, sedation to close vertical lacerations in layers with 6/0 with monitored care along with local infiltration with polyglactin and skin with 6/0 polypropylene. or without a regional nerve block will suffice in most Horizontal lacerations spontaneously reapproxi- cases. mate themselves due to orbicularis sphincter Surgical Tips action. Disfigurement of the anterior lamella can cause • Examine globe thoroughly for perforations and complex lacerations. We try to undermine the edges injuries – if necessary, explore. • Wash all wounds with saline and a solution of 1gm to mobilize the tissue to aid anatomically perfect cefazolin in 250 ml saline. apposition. Debridement should be minimal. After • Prepping can be done with diluted solution of debridement, a “V” shaped laceration can be converted povidone-iodine. to a “Y” shaped configuration after removal of the • Remove all foreign bodies after thorough devitalized apex (Figs 54.2A and B). exploration of all affected tissues. • Check anterior and posterior lamella LID MARGIN REPAIR • Look for lid laxity, indicative of canthal tendon Proper and immaculate closure of lid margin injuries injury should be sought for rewarding results. Failure to do • Examine upper and lower canaliculi, lacrimal gland so will cause lid disfigurement and notching and may and levator muscle. lead to corneal drying and complications. Eyelid Injuries and Reconstruction: An Update 347 type rotational flap in moderate tissue loss can be carried out (Fig. 5). For upper eyelid, the arc of the circle is below the lateral canthus and for lower it is above the canthus. For severe tissue or lid loss, Mustarde type flaps or lid sharing procedures can be used. While attempting closure of small lid margin lacerations, the wound has to be modified to avoid formation of lid notch. The entire vertical portion of Figs 54.3A and B: (A) First silk suture through the tarsal the tarsus has to be removed corresponding to the plate is tied first. Second through the grey line. Third and fourth behind and in front of the lash lines. (B) Skin and width of the deficit. The tarsal excision is carried out muscles closed in layers. perpendicular to the lid margin. A “V” shaped defect is converted into a pentagon shaped defect before closure.

LEVATOR MUSCLE DEHISCENCE In levator muscle disinsertion cases, the patient may present with mild to moderate ptosis with or without the presence of a laceration. If the orbital fat is seen in the wound, the same signifies damage to the orbital septum. Exploration is sought in such cases. The orbital septum is identified, exposed and fully opened and the levator aponeurosis is explored. Tears in the muscle can be repaired with 6/0 polyglactin sutures. The disinserted aponeurosis can be sutured to the tarsal plate with 3 6/0 polypropylene sutures. Care should Fig. 54.4: Tenzel rotation flap be taken to preserve the lid contour. All prolapsed lacrimal gland tissue should be repositioned before closure. There should be no ectropion or lagophthalmos after closure is complete.

CANALICULAR LACERATIONS • Commonly missed injuries. • Look carefully for the severed edges.

Fig. 54.5: Technique for lateral canthotomy and lid closure

Evaluate lid tissue loss by trying to approximate the cut edges of the margins and see if closure can be achieved without tension. If this is possible, the marginal defect has to be closed in layers separately, i.e. the anterior and posterior lamellae (Figs 54.3A and B). If there is tissue loss and the wound cannot be closed without tension, a lateral cantholysis or canthotomy (Fig. 54.4) in mild cases and a Tenzel Fig. 54.6: Canlicular repair with stent 348 Clinical Diagnosis and Management of Ocular Trauma

Fig. 54.7: Eyelid avulsion preoperative Fig. 54.9: Eyelid injury with zygoma fracture 4

Fig. 54.8: Eyelid injury with canalicular injury Fig. 54.10: Eyelid injury with zygoma fracture 7

• Irrigation from the ipsilateral punctum with Conclusion fluoroscein stained saline or injection of air may help identify the cut edge of the punctum. Though eyelid trauma has myriad manifestations, • Authors prefer to use bicanalicular stents, left in general surgical principles are to be followed in repair. place for 6 months for repair (Fig. 54.6). Repair is to be attempted once the general condition • The surrounding lid margin and adventitia can be of the patient permits; meticulous cleaning of the repaired as described earlier. injured area, maintenance of asepsis is essential. In • In our opinion the pigtail probe should be avoided. most cases one can manage edge to edge apposition • Before repairing the canaliculi it is important to as the lids are fairly forgiving of minor tissue loss. determine the presence of any canthal tendon However, in cases of major tissue loss or where there avulsion. is concurrent injury to canaliculi or canthal tendons, • Repair of the posterior horn of the medial canthal plastic repair as outlined above will yield very tendon is necessary to maintain the lacrimal pump satisfactory results in terms of function andcosmesis. function. • Approximation and suturing of the 2 cut edges of the tendon with 6/0 polypropylene is sufficient to Bibliography maintain function. • The tendon can also be sutured directly to the 1. Color Atlas of Ophthalmic Plastic Surgery: A.G.Tyers, periosteum. J.R.O.Collins. • If both are absent micro-plating can be considered. 2. Oculoplastic Surgery: William P Chen. 3. Ophthalmic Plastic and Reconstructive Surgery: Frank • Care must be taken to avoid inadvertent damage A Nesi, Richard D Lisman, Mark Levine. to the lacrimal sac during repair. CHAPTER

Prevention of Ocular Trauma 55 B Shukla, P Dutta (India)

Introduction is linked to the epidemiology of ocular trauma in a given population or region. This is bound to alter from “Prevention is better than cure” is an often quoted country to country and within a large country from phrase. It can not be over-emphasised in ocular one region to another. This study on one hand will trauma. However it has remained more of a precept give the magnitude of the problem and on the other than practice. In ocular trauma it can be seen from hand it would help in deciding the priority areas of Table 55.1. prevention. In one study on epidemiology on ocular However this scarcity on prevention can be trauma in Northern India the incidence of avoidable defended in a way as primary prevention in ocular injuries is stated as 67%.6 Although it is believed that trauma is not easy and secondary prevention can be many eye injuries are preventable7 actual data for the managed by early and efficient treatment which has same is scarce. been discussed in detail in most of the books. Primary prevention is a little difficult as it is basically a problem of children and young adults many of whom are bound to indulge in all types of sports, fight, fast driving, etc. Occupational Injuries Secondary prevention depends on availability of good In most of the Western studies work related or hospitals and efficient doctors at a convenient distance 8-10 and cost. Tertiary prevention is basically rehabilitative occupational eye injuries are very common. In a and ameliorative. report from MP, India 40.7% injuries were work related The subject of prevention of ocular trauma can be including labourers, farmers, industrial and sedentary 11 looked at by several ways. Mention has already be workers. In many factories the workers are at high made about primary, secondary and tertiary preven- risk of getting eye injuries. In many cases flying splinters tion.5 It can also be considered from environmental and particles are a big hazard. Not only protective point of view whether occurring during the profession, glasses should be provided but the machines should during sports, driving, in criminal assault, agricultural, also be guarded from emitting particles. Ordinary in war or at home. The third way would be to avoid glasses or goggles usually do not provide much in specific risk groups and lastly educational and protection and in some cases can cause damage after legislative. All these views are not mutually exclusive breaking.12 Toughened or laminated glasses are better. and combination is possible. We shall however deal However polycarbonate lenses with variable central the subject mainly from the environment point of view. thickness depending on degree of safety required are It may also be stated that the subject of prevention considered very satisfactory.13 However, at many places

TABLE 55.1: Ocular trauma coverage in various books No. Year Name of book Author Total pages On prevention % age 1. 1972 System of Oph. Vol. 14, Injuries Duke-Elder S1 1350 0 0% 2. 1991 Eye Trauma Singhleton BJ et al2 410 3 0.7% 3. 2002 Ocular Trauma Kuhn F et al3 445 2 0.45% 4. 2005 Management of Ocular Trauma Shukla B et al4 324 5 1.5% 350 Clinical Diagnosis and Management of Ocular Trauma

APPENDIX: RECOMMENDATIONS OF INDIAN INSTITUTE OF STANDARDS.16 Classification of hazards related to eye, face and ear protection equipment. Hazards against which protection equipment for eyes, face and ear should be used are given in Table 1.

TABLE 1: Hazards against which protection equipment for eyes, face and ear should be used Code No. Protection against hazard Typical Industrial operations of Hazard H-1 Impact Clipping, caulking, sealing, grinding of metals. Stone dressing, turning of case iron and non-ferrous metals, etc. H-2 Dust Sealing, grinding, handling of cement, clay, etc. H-3 Splashes from metals Babbiting, pouring of lead in joints, die casting, dipping in hot metals, pouring of molten metals and foundry work H-4 Splashes of liquids Handling of acids, alkalis and other chemicals H-5 Irritating gases and vapours - H-6 Reflected light and glare Testing of lamps, sheet metal and lathe work H-7 Injurious radiant energy Oxy-acetylene welding and cutting furnace work; electric arc welding; open hearth, bessemer and crucible steel making H-8 Noise -

Selection of equipment for different hazards Different types of eye, face and ear protection equipment should be selected keeping in view the hazards they can protect against. Guidance may be taken from the information given in Table 2.

TABLE 2: Selection of different types of eye, face and ear protection equipment keeping in view the hazards they can protect against Code No. Brief description of Recommended against Remarks of equipment equipment hazard code number E-1 Safety spectacles with side H-1, H-6 and H-7 Spectacles may be fitted with shields, safety lenses mounted clear, tinned, blue or welding in spectacle-type frame filter gas lenses. E-2 Cup-type goggle. Two pieces H-1, H-3, H-6 and H-7 Goggle may be fitted with clear, holding safety lenses and tinted, blue or welding filter connected across the nose, glass lenses and provided with head-band or harness E-3 Goggles (a) With ventilation H-4 - (b) Without ventilation H-4 and H-5 - E-4 Dust goggles H-2 - E-5 One piece eye protectors H-1, H-2, H-3, H-4, H-6 and H-7 Should be capable of being (Monogoggles) used over prescription glasses E-6 Face shields H-1, H-3, H-4, H-6 and H-7 - E-7 Wire mesh goggles H-3 -

there is no quality control and the goggles or face masks proportion to mass and velocity (E=1/2 mv2). Hence are cumbersome to wear. In a study it was found that hard balls like cricket and hockey balls can cause severe only 10% of those injured at work were wearing some injury. However in eye injuries the radius of curvature kind of protective device.8 Wearing of safety devices of a ball is also important as smaller balls can enter is not strictly enforced at many places. the orbit easily causing severe damage to eye ball like the squash or golf balls. On the contrary larger balls like basketball, volleyball and football are unlikely to Recreational Injuries cause severe injury unless they strike with great force. Various types of sports and games are common causes Various devices like pads, abdominal guards, wrist and of eye injuries. In Western countries boxing is a very elbow guards are now available to minimize sport common cause of eye injury.14 Damage is usually in injuries. Helmets by cricket players and hockey goal Prevention of Ocular Trauma 351 keepers are very useful devices to minimize eye injuries. Proper education, awareness and strict In some countries like India bow and arrow are enforcement of traffic rules can go a long way to common games and many eyes are lost due to sharp prevent eye injuries. However as stated earlier arrow injury. Gilli danda is another such game secondary prevention by early reporting and treatment commonly played in rural areas. Children should be can also prevent a more severe damage. advised and prevented from playing such dangerous games. Even a passer-by can get hurt. References Travel Injuries 1. Duke-Elder S : System of Ophthalmology, vol. IVX, Injuries Henry Kimpton, London 1972. The quality and the width of roads are not increasing 2. Shingleton BJ, Hersh PS, Kenyon KR :Eye Trauma, Mosby in proportion with the alarming increase in cars and year Book, St.Louis 398-400. two wheelers. In addition the fast life in cities and 3. Ocular Trauma : Kuhn F, Pieramici DJ : Ocular Trauma, indulgence in liquor and smoking are also factors Thieme Publication, New York, 2002;19-20. contributing to increasing number of road accidents. 4. Shukla B, Natarajan S : Management of Ocular Trauma, CBS Publishers, New Delhi, 2005;317-21 Use of cell phone while driving is not yet prohibited 5. Park K : Park’s Text Book of Preventive and Social in many places which may also be a causative factor Medicine, 14th Ed., Banarsidas Bhanot Publishers, in road accidents. Wearing of seat belts and helmets Jabalpur 1995, 6. can minimize such injuries. In some places animals are 6. Shukla, B : Epidemiology of Ocular Trauma, Jaypee also freely roaming adding to disaster. Strict regulations Brothers Medical Publishers, New Delhi, 2002;91. should be enforced by the concerned authorities. 7. Vinger PF : The eye in sports medicine. In : Duane TD, Jaeger, EA, Edit.Clnical Ophthalmology, Vol. 5, Harper and Row 1985. 8. Schein OD, Hibberd PL, Shingleton BJ et al :The Other Injuries spectrum and burden of ocular injury, Ophthalmology Other eye injuries can occur during a difficult labour, 1988;95:300-05. criminal assault and in domestic setting. Adequate 9. Glynn R, Seddon J, Berlin B : The incidence of eye injuries in New England adults, Arch Ophthalmol, 1988; precautions, education and legislation can minimize 106:785–89. these injuries. Domestic or casual injuries are quite 10. Saari M, Parvi V : Occupational eye injuries in Finland, common. Acta Ophthalmol Suppl. 1984;161:17-28. It has been seen that children are more at risk for 11. Shukla, B : Epidemiology of Ocular Trauma, Jaypee injuries hence they should never be given pointed toys Brothers Medical Publishers, New Delhi 2002;33-34. or any type of fire work. They should also be not left 12. Keeney A, Fintelmann E, Renaldo D : Clinical alone. In a recent report it was found that all injuries mechanism of non industrial trauma, Am J Opthalmol 1972;74:662. occurring in children below 16 years were unsuper- 13. Schein OD, Vinger PF : Epidemiology and Prevention, 15 vised. In : Eye Trauma, Edit. Shingleton BJ, Hersh PS, Kenyon Similarly though injuries decline with advance in KR, Mosby Year Book, St. Louis 1991, Chapter 36, p. age there is again a rise in the very old. They are more 399-401. prone to fall due to weakness, walking difficulties or 14. Giovinazzo VJ et al : The ocular complications of boxing, poor sight. A one eyed person is also at great risk Ophthalmology 1987;94:587-95. because of restricted field of vision and needs special 15. Vats S, Murthy GVS, Chandra M et al :Epidemiological protection. Those who have undergone previous eye study of ocular traumain an urban slum population in Delhi, India, Indian J Ophthalmol 2008:56:313– surgeries like cataract, keratoplasty and radial 16. keratotomy are at a greater risk as relatively minor 16. Shukla B, Dutta P. Prevention of ocular trauma. In : injuries can cause rupture of the globe due to Shukla B, Natarajan S Edit, Management of ocular dehiscence at the operative site. trauma, CBS Publishers, New Delhi 2005;320-21. CHAPTER

Endophthalmitis Prevention Strategies 56 John D Sheppard (USA)

Introduction New data have extended our understanding of the pathogenesis and prevention of postoperative Perfected treatment strategies depend on a surgeon’s endophthalmitis since the completion of the EVS. preferences and individual patient needs. Postcataract infections originate by one of three routes: Infectious complications following routine cataract (1) introduction through instrumentation at the time surgery are the most feared of all ophthalmic infections, of surgery; (2) inoculation through the wound after due to the high expectations for cataract operations cataract surgery; and (3) (although extremely rarely) in the 21st century. Endophthalmitis complicates by endogenous spread from concurrently infected approximately one in every 1,000 cataract operations. extraocular tissues, such as a tooth abscess or infected With clear corneal incisions, this rate may be rising. diverticulum. Material presented at the 2002 ARVO Risk factors cited in the peer-reviewed literature include meeting in Fort Lauderdale, Florida, in particular extracapsular surgery, intracapsular surgery, clear offered insight into bacteriologic factors relevant to corneal incisions, diabetes mellitus, prolonged surgical cataract surgery. time, previous or concurrent trabeculectomy, repeated instrument entry and exit, chronic blepharitis, chronic conjunctivitis, keratitis sicca, ocular surface disease, Existing Literature capsular rupture, vitreous prolapse, and vitrectomy surgery. The potential for this risk may rise to one in With experience and consideration of extensive every 100 cases with vitreous loss. Although rapid laboratory data, most surgeons now believe that diagnosis and expeditious surgical intervention can postcataract infections are introduced into the eye from preserve excellent visual function in many patients with the ocular surface. This belief brings into question the endophthalmitis, preventive measures are the traditional use of topical perioperative aminoglycosides cornerstone of any surgical management strategy. for cataract patients, especially when most endoph- thalmitides are Gram-positive and aminoglycosides are so insoluble. In our analysis, Gram-positive isolates from 163 patients with bacterial conjunctivitis were only New Concepts in 85% sensitive to tobramycin, while 97% were sensitive to levofloxacin, a third-generation fluoroquinolone, Endophthalmitis Treatment 83% to sulfasoxazole, 77% to ciprofloxacin, and only The landmark Endophthalmitis Vitrectomy Study 75% to trimethoprim, commonly used in combination (EVS), conceived by Dr Bernard Doft and completed with the Gram-negative agent, polymyxin B.2 in 1995, found that 70% of endophthalmitis cases were Franco Recchia of Vanderbilt University and caused by coagulase-negative, Gram-positive micro- colleagues clearly showed that an increasingly higher cocci, overwhelmingly Staphylococcus epidermidis.1 percentage of postcataract infections are due to Gram- This study has revolutionized our treatment algorithm positive organisms.3 In a study of 493 consecutive patients for postcataract surgery endophthalmitis, recognizing with postcataract endophthalmitis, researchers cultured the essential aspects of vitreous-tap diagnosis and an organism from the vitreous in 318 cases (65%). expeditious injection of intravitreal antibiotics, while During the last decade of the 20th century, gram- surprisingly raising the threshold for pars plana vitrec- positive isolates increased from 92 to 97%. Furthermore, tomy for patients with light perception or worse-quality resistance rates to commonly used prophylactic vision. antibiotics increased; resistance among all isolates to Endophthalmitis Prevention Strategies 353 ciprofloxacin rose significantly (23 to 38%), while irrigating solutions during cataract surgery, a group of resistance to ciprofloxacin and cefazolin rose among researchers in Arizona, led by Robert Snyder, MD, do coagulase-negative staphylococci (18 to 38%). not see the efficacy of this approach.7 Dr Snyder and In his new study from Stanford University, his colleagues noted that antibiotics chosen for infusion Christopher Ta and associates compared the ability of should be fast-acting, due to the limited time exposure 21 different antibiotics to cover coagulase-negative to purported intracameral bacterial contaminants. The Staphylococcus organisms.4 Researchers took fluoroquinolones showed dose-dependent killing. On preoperative conjunctival swabs from 66 patients prior the other hand, vancomycin killing did not correlate to applying antibiotics or antiseptic. Their analysis with drug concentration relative to the MIC of concluded that, among the four fluoroquinolones Staphylococcus species tested. Fluoroquinolones may tested, levofloxacin had the highest antistaphylococcal be more suitable for killing bacteria seeded into the susceptibilty (91%) compared to norfloxacin (79%), anterior chamber than vancomycin. Because ofloxacin (75%), and ciprofloxacin (73%). Conversely, vancomycin concentration decreases rapidly in the resistance patterns also favored levofloxacin at only anterior chamber following surgery completion, 5%, whereas norfloxacin was 18%, ciprofloxacin 20%, residual surviving organisms with exposure to this and ofloxacin 23%. antibiotic of last resort could have a high likelihood of vancomycin resistance. Those who advocate Practical Clinical Practice aminoglycoside antibiotic infusion during routine surgery ignore both the severe potential retinal toxicity Revealing in vivo data from Frank Bucci, MD, in of this class, and waning Gram-positive sensitivity. Wilkes-Barre, Pennsylvania, demonstrate that levofloxacin reaches therapeutic aqueous concentrations, therefore exceeding the mic90 for both Staphylococcus and Streptococcus.5 Dr Bucci found Microbial Antibiotic Resistance that 0.5% levofloxacin reached four- to sevenfold Careful clinical analysis customized to each prospective higher aqueous concentrations than 0.3% ciprofloxacin cataract patient by a knowledgeable, conscientious when administered according to identical preoperative surgeon provides the best solution to endophthalmitis regimens. The ciprofloxacin levels were below the risk. There is no single agent capable of killing every established NCCLS MIC90 for both Staphylococcus microbe known to cause postoperative infections.8 and Streptococcus. Dr Bucci also noted that, higher Even in this brief review of recent ARVO abstracts, intracameral levofloxacin concentrations could be epidemiologic patterns differ between hospitals, cities, achieved with a regimen of administering five drops and regions, a fact that renders each surgeon uniquely every 10 minutes immediately prior to surgery, when capable of understanding the peculiarities of their own compared to administering the drug four times per bacteriologic environs. Although newer fourth- day for 2 days preoperatively. He achieved an generation fluoroquinolones, such as moxifloxacin and additional 50% increase in aqueous levels by combining gatifloxacin, may demonstrate increased potency for the two regimens. Gram-positive bacteria over second- and third- Starr, Jensen and Fiscella6 showed that, of 24 generation drugs, the fourth-generations demonstrated endophthalmitis cases in 9,079 patients, eyes receiving no advantage for Gram-negative coverage in a keratitis topical ofloxacin postoperatively developed study conducted by Kowalski et al.9 Gram-negative endophthalmitis significantly less often than those receiving topical ciprofloxacin (P<.0009). According resistance appears to cross all fluoroquinolone to these investigators, this difference in endophthalmitis generations. Thus, miniscule but significant holes have rates may reflect differences in pharmacological and appeared in the once-invincible fluoroquinolone bioavailability properties that exist among family’s Gram-negative coverage spectrum. The best fluoroquinolone antibiotics. Ciprofloxacin, the least protection of all may be a thorough povidone-iodine 10 soluble of available topical fluoroquinolones, achieves preparation, including the periorbital skin, lids, lashes, the lowest intraocular levels. Levofloxacin, with 3.3 and conjunctival cul-de-sac. times more active drug per drop than ofloxacin, might Consistent routines, meticulous iodine preparation be the preferred choice at this time because of superior and reliable surgical technique, coupled with highly Gram-positive coverage and solubility. effective and penetrating topical antibiotics given Even though some surgeons have popularized the frequently prior to surgery, provide our patients with use of antibiotic infusion through balanced saline- the best defense against infection. 354 Clinical Diagnosis and Management of Ocular Trauma 7. Snyder RW, Krueger T, Nix DE: Kill curves for vancomycin References versus 3rd generation quinolones. IOVS 2002 (abstr 1. Han DP, Wisniewski SR, Wilson LA, et al: Spectrum and 4452) (suppl). susceptibilities of microbiologic isolates in the 8. Benz MS, Scott IU, Flynn HW, et al: In vitro susceptibilities Endophthalmitis Vitrectomy Study. Am J Ophthalmol to antimicrobials of pathogens isolated from the vitreous 1998;122:1-17. cavity of patients with endophthalmitis. IOVS 2002 (abstr 2. Sheppard JD, Oefinger PE, Wegerhoff PE: Susceptibility 4428) (suppl). patterns of conjunctival isolates to newer and established 9. Kowalski RP, Karenchak LM, Romanowski EG, et al: An anti-infective agents. IOVS 2002 (abstr 1588) (suppl). in vitro comparison of 2nd, 3rd, and 4th generation 3. Recchia FM, Busbee BG, Pearlman RB, et al: Changing fluoroquinolones against bacterial keratitis isolates. IOVS trends in the microbiologic aspects of post-cataract 2002 (abstr 1585) (suppl). endophthalmitis. Arch Ophthalmol 2005;123:341-46. 10. Ciulla TA, Starr MB, Masket S: Bacterial endophthalmitis 4. Ta CN, Mino de Kaspar H, Chang RT, et al: Antibiotic prophylaxis for cataract surgery: an evidence-based susceptibility pattern of coagulase-negative staphylococci update. Ophthalmology 2002;109(1):13-24. in patients undergoing intraocular surgery. IOVS 2002 11. John D. Sheppard, MD, MMSc, serves as Professor of (abstr 4444) (suppl). Ophthalmology, Microbiology and Immunology, as well 5. Bucci FA: An in vivo comparison of the ocular absorption as Program Director for Ophthalmology Residency of levofloxacin versus ciprofloxacin prior to Training at the Eastern Virginia Medical School in phacoemulsification. IOVS 2002 (abstr 1579) (suppl). Norfolk, Virginia. He is also Clinical Director of the 6. Starr MB, Jensen MK, Fiscella RG: A retrospective study Thomas R. Lee Center for Ocular Pharmacology. Dr. of endophthalmitis rates comparing quinolone antibiotics, Sheppard may be reached at (757) 622-2200; Am J Ophthalmol 2005:140;769-71. [email protected] Index

A prevention 298 chronic inflammation and treatment 298 uveitis 274 Abrasions of the globe 312 glare and halos 274 clinical signs and symptoms 312 glaucoma 275 differential diagnosis 312 induced astigmatism 274 investigations 312 C pigment dispersion and lens prognosis 312 Causes of postoperative non- deposits 273 treatment 312 improvement of BCVA in size-related complications Acute postoperative endophthalmitis traumatic cataract 75 pupil ovalization and 174 Chandelier illumination 328 retraction 274 intraocular antibiotics 175 Chemical and thermal burns of the iris-fixated anterior chamber aminoglycosides 175 eye 317 phakic intraocular lenses ceftazidime 175 clinical signs and symptoms 318 275 vancomycin 175 differential diagnosis 318 cataract formation 276 prophylaxis 174 investigations 318 chronic inflammation and steroid treatment 176 prognosis 318 uveitis 276 subconjunctival and topical treatment 318 complications of iris-supported antibiotic therapy 176 Chemical injuries of the eye 50 phakic IOLs 275 systemic antibiotics 176 management 50 endothelial cell loss and anterior vitrectomy 177 general principles 50 chamber depth 276 Algorithm for management of open recent advances in therapy 52 glare and halos 276 globe injury 214 pathogenesis 50 glaucoma 276 acids 50 pupil ovalization and alkalis 50 B decentration 276 classification 50 posterior chamber phakic Bimanual vitrectomy 330 Chorioretinitis sclopetaria 169 intraocular lenses 277 Birth trauma 68 clinical features 169 Complications of corneal injury 46 Blunt eye trauma 80 etiology and pathogenesis 169 astigmatism 48 Blunt injuries of the globe 312 treatment and prognosis 169 corneal infection 46 clinical signs and symptoms 312 Choroidal rupture 168 iris/capsular incarceration 46 differential diagnosis 314 clinical features 168 posterior segment complications 47 investigations 314 diagnostic testing 169 post-traumatic endophthalmitis 47 prognosis 314 etiology and pathogenesis 168 secondary glaucoma 46 treatment 314 treatment and prognosis 169 sympathetic ophthalmia 47 Blunt retinal trauma 189 Chronic postoperative endophthalmitis traumatic cataract 46 individual pathologies description 177 Complications of SFIOL 97 190 bleb-associated endophthalmitis choroidal detachment 98 chorioretinitis sclopetaria 197 178 cystoid macular edema 97 choroidal rupture 194 post-traumatic endophthalmitis 178 endophthalmitis 98 commotio retinae 190 Clinical evaluation of ocular trauma 10 glaucoma 97 purtscher retinopathy 198 general examination 10 lens decentration and lens tilt 97 traumatic macular hole 191 structural examination 10 retinal detachment 97 traumatic retinal detachment functional examination 11 193 ocular adnexa 10 suture erosion 98 traumatic retinal tears 192 Closed globe injuries 332 uveitis 98 vitreous base avulsion 194 Commotio retinae 167 Conjunctival injuries 125 vitreous hemorrhage 194 clinical features 167 types 125 initial evaluation 190 diagnostic testing 167 Corneal injuries 126 mechanism of damage 189 etiology and pathology 167 evaluation 126 Blunt trauma of anterior segment 67 treatment and prognosis 167 Corneal laceration 279 Blunt trauma related retinal tears and Complication and contusin after complex corneal laceration wound retinal detachments 149 phakic IOLs 273 281 Bottle cork injury to the eye 296 anterior chamber phakic IOLs 273 corneal laceration with tissue loss clinical features 297 cataract formation 275 281 356 Clinical Diagnosis and Management of Ocular Trauma injury assessment 279 prognosis 37 mortality/morbidity 100 medical management 279 treatment 37 pathophysiology 100 perforating or nonperforating Hyphema 68 treatment 101 corneal laceration 279 complications 69 conservative treatment 101 simple corneal laceration 280 ophthalmic examination 68 holistic approach 102 surgical management 280 severity grades 69 surgical care 101 use of tissue glue 281 raised intraocular pressure 69 Irreparable scleral rupture 336 Corneoscleral laceration with lens and secondary hemorrhage 69 vitreous involvement 336 L Corneoscleral laceration with tissue I Late post-traumatic glaucoma 64 loss 336 international incidence 64 Cultivated vs direct limbal Iatrogenic 223 indian incidence 65 transplantation 209 complications 224 slit lamp findings 65 Cystoid macular edema 242 contraindications 224 gonioscopic findings 65 clinical findings 244 controlled release vehicles 224 pathology 65 etiology 242 indications 224 Luxation and subluxation to the histopathology 244 intravitreal injection 224 crystalline lens 80 treatment 245 pulse therapy 224 repository injection 224 clinical evaluation 81 responsive diseases 225 intracapsular extraction 83 E anterior segment ischemia 225 IOL placement considerations 84 Electrical injuries 57 Boeck’s sarcoid uveitis 225 phacoemulsification and IOL clinical lesions 57 herpes zoster 225 placement in subluxated lighting injury 57 neoplasms 225 crystalline lens 83 Endogenous endophthalmitis 179 ocular pemphigoid 225 prognosis and long-term Endophthalmitis prevention strategies orbital myositis 225 considerations 84 352 pseudotumor cerebri 225 surgical approach 82 Evaluation of a patient with ocular Tolosa-Hunt syndrome 225 trauma 13 toxoplasmosis 225 M approach in emergency 14 systemic therapy 224 Management of a malpositioned 328 examination 15 topical application 223 Management of acute corneal injury 41 history 14 Indications of SFIOL 95 corneal laceration with tissue loss approach to a patient with ocular Initial management of ocular trauma 43 trauma 14 patient 20 management of injury to lens 44 Eye injury prevention in children pearls 20 postoperative treatment 45 188 Injuries of the lids 311 principles of repair 43 Eyelid injuries 345 clinical signs and symptoms 311 slit-lamp biomicroscopy 42 anatomy review 345 differential diagnosis 311 anesthesia 43 canalicular lacerations 347 investigations 311 anterior chamber 42 classification 345 prognosis 312 conjunctiva 42 examination 345 treatment 311 cornea 42 levator muscle dehiscence 347 Intraoperative floppy iris syndrome 250 lens 42 lid margin repair 346 Intravitreous triamcinolone associated sclera 42 management 346 endophthalmitis 179 traumatic wound dehiscence 46 IOFB 155 type of sutures 45 viscoelastic materials 44 F clinical manifestations 155 localization 156 Management of corneal injuries 41 Fugo’s plasma knife 319 management 156 classification 41 key properties 321 mode of injury 155 terminology 41 technique 327 Iridodialysis 102 Management of eyelid injuries 28 causes 102 evaluation of lid injury 28 examination 28 G complications 105 principles of iris repair 103 history 28 Glued IOL 132 iris implants 103 principles of wound repair 28 fibrin glue 132 repair of iridodialysis 103 wounds associated with canthal scleral fixated IOL 132 suture placement 103 tendon injuries 31 surgical technique 132 suture tying 103 wounds with no or minimal signs 102 tissue loss 29 wounds with significant tissue H surgical planning 102 symptoms 102 loss 30 Hyphema 35 treatment and management 102 Management of lacrimal injuries 33 associated exam findings 36 Iris prolapse 100 evaluation of lacrimal injuries 33 examination 35 clinical profile of a patient with examination 33 history 35 iris prolapse 100 history 33 Index 357

Management of traumatic cataract 74 Orbital injuries 108 Post-traumatic strabismus 106 causes 75 anatomic considerations 108 direct trauma 107 complications 76 carotid cavernous fistula 111 entrapment of muscle 107 medical care 75 orbital foreign bodies 112 intramuscular hemorrhage 107 pathophysiology 74 septic cavernous sinus traumatic disinsertion 107 physical examination 74 thrombosis 111 Practical clinical practice 353 surgery 75 evaluation of acute orbital and Prevention of CME 239 types 75 periorbital injuries 109 Primary globe repair 214 Medical management of blunt trauma problems associated with orbital management 215 69 trauma 110 nonsurgical 215 Mode of lens injury in ocular trauma orbital hemorrhages 110 surgical 215 and its presentation 94 surgical emphysema 110 objectives 214 Muller glial cells 201 traumatic optic neuropathy 110 strategic planning 214 Principles and management of ocular trauma 331 N P Purtscher’s retinopathy 169 New classification of ocular trauma 7 Pediatric ocular trauma 181 clinical features 170 New concept in endophthalmitis evaluation 181 diagnostic testing 170 treatment 352 examination 181 etiology and pathogenesis 169 NSAIDs and topical steroids 238 history 181 treatment and prognosis 170 NSAIDs for the inhibition of miosis 238 specific eye injuries 182 NSAIDs vs steroids 237 birth trauma 182 R corneal and conjunctival Radiational injuries to the eye 59 O foreign bodies 182 injuries due to infrared radiation 61 corneal penetration 184 injuries due to ultraviolet radiation Occupational injuries 349 eyelid lacerations 182 60 Ocular injuries after vehicular accident subconjunctival hemorrhage cornea 60 290 183 lens 61 air bag system 290 traumatic cataract 185 injuries due to visible radiation 61 methods 291 traumatic hyphema 184 mechanical injuries 61 results 291 vitreous and retinal conditions photic injuries 61 Ocular surface stem cells 206 185 thermal injuries 61 Ocular trauma 3 Penetrating injuries related retinal injuries of the eye due to ionizing epidemiology 3 incarcerations and retinal radiation 60 new classification 4 detachments 152 conjunctiva 60 Ocular war injuries 300 pathophysiology 152 lens 60 mechanical 301 surgical principles vitrectomy 153 lids 60 non-mechanical 305 Penetrating posterior segment trauma Rationale for treating ocular Optimized NSAIDs and antibacterial 160 inflammation 235 prophylaxis in cataract classification 161 Recreational injures 350 Reinverter system 329 surgery 232 clinical features 161 Retinal tears, tetinal dialysis and drug dosages 233 complications 163 detachments 171 measuring potency 233 chalicosis 164 clinical features 171 penetration tracking 234 endophthalmitis 163 postoperative schedule for cataract etiology and pathogenesis 171 siderosis 164 treatment and prognosis 171 patients 232 epidemiology 160 Role of adult bone marrow in safety evaluation 234 investigations 161 endothelial progenitor Orbital fracture 113 location 161 (Stem) cells 203 naso-orbital and medial orbital management 161 Role of bone marrow in stem cells wall fractures 117 pathophysiology 160 203 management 119 prognosis 164 Role of bone marrow in stem cells in surgical technique 119 Perforating injuries of the globe retinal and choroidal transnasal wiring 118 intraocular foreign bodies neovascularization 204 orbital floor and blow out 315 Role of corneal stem cell in pediatric fractures 113 clinical signs and symptoms 315 206 pathogenesis 113 differential diagnosis 316 Role of retinal pigment epithelial stem clinical presentation 113 investigations 315 cells 202 complications 116 prognosis 316 Role of retinal stem cells 201 implants 115 treatment 316 management 114 Pharmacologic therapy for ocular procedure 115 inflammation 236 S surgical procedure 115 Posterior scleral laceration 336 Scleral fixated IOL vs anterior timing 114 Postrefractive keratitis 229 chamber iol 94 358 Clinical Diagnosis and Management of Ocular Trauma Scleral injuries 130 diagnosis 254 etiology and pathology 167 evaluation 130 epidemiology 255 treatment and prognosis 168 specific conditions 130 etiology 255 Traumatic retinal detachments 149 Shaken baby syndrome child abuse investigation 256 Travel eye injuries 286 170 pathology 255 prevention and management 286 clinical features 170 treatment 256 direct traumatic injuries 287 diagnostic testing 170 Trauma in LASIK 270 non-contact eye injuries 286 etiology and pathogenesis 170 Trauma in phakic iol lmplants 272 treatment and prognosis 171 Trauma in PRK 270 Small pupil phaco 259 Trauma in radial keratotomy 269 U IQ-ring 263 Trauma in surface treatments 272 Ultrasonic injuries 56 surgical technique 263 Trauma to LASIK flap 270 clinical lesions 56 Specific injuries 127 Traumatic angle recession glaucoma 64 Ultrasound biomicroscopy in ocular corneal abrasion 127 history 64 trauma 25 examination 127 Traumatic cataract in children 86 assessment of zonules 27 symptoms 127 epidemiology 86 foreign bodies 27 foreign bodies 128 examination 87 iris and ciliary body status 27 evaluation 128 pathophysiology 86 Ultraviolet corneal burns 317 treatment 129 postoperative complications 91 clinical signs and symptoms 317 recurrent erosion 128 postoperative medication 91 differential diagnosis 317 history 128 preoperative evaluation 87 investigations 317 treatment 128 surgical details 88 prognosis 317 Sports injuries in eye 283 timing of surgery 88 treatment 317 classification 283 visual outcome 92 Use of nonsteroidal anti-inflammatory ball injuries 283 Traumatic giant retinal tears 150 drugs in inflammation 225 physical contact injuries 284 Traumatic hemorrhages to the Stem cell therapy in ophthalmology 200 posterior segment 139 mechanism of action 226 classification 141 ocular inflammation 225 side effects of NSAIDs 227 T choroidal hemorrhages 142 hemorrhage associated with Technique of insertion of SFIOL 95 indirect trauma 144 V Thermal injuries 55 intraretinal hemorrhages 142 hyperthermal injuries 55 papillary and peripapillary Valsalva retinopathy 170 contact burns 55 hemorrhages 143 etiology and pathogenesis 170 flame burns 55 retrohyaloidal hemorrhages 142 clinical features 170 scalds 55 vitreous hemorrhages 141 treatment and prognosis 170 hypothermal injuries 56 management 144 Visual rehabilitation 48 accidental hypothermia 56 medical 144 Vitrectomy lenses 330 cryosurgery 56 surgical 145 surgical hypothermia 56 pathogenesis 141 W Toxic anterior segment syndrome 254 Traumatic macular hole 167 clinical features 254 clinical features 167 Welding arc injuries 62