DJO VOLUME 14 NUM 7. JAN.-MARCH 2008

Role of Avastin in Management of Diabetic Retinopathy

Cataract Surgery in Patients with Diabetes Mellitus

Role of Systemic Acyclovir in Recurrent Cases of Disciform Keratitis"

The Science of Spirituality

Ocular Tuberculosis: Current Paradigms in Diagnosis and Management

Current treatment for Diabetic Macular Oedema

Fields in Neuroophthalmology

Editor Dr. Rajpal Insaan Delhi Journal of Ophthalmology

Editorial Board: DJO Advisor : Chief Editor : Rajvardhan Azad Rajpal Insaan Associate Editors: International Scientific Coordinator: Tanuj Dada, Dinesh Talwar Insaan, Sanjay Chaudhary, S. Bharti, Ashok Garg Shailesh G.M., Rajesh Sinha, Sonia Bhargav, Mohita Sharma, International advisory board: Ajay Aurora Samuel J.K. Abraham, NCRM Chennai, India Managing Editors : Suresh K. Chandra, USA Pradeep Sharma Insaan, Prashaant Chaudhry, Rohit Saxena, V.K. Raju, USA Sanjeev Gupta, Subhash Dadeya, Vishnu Gupta, Sharad Lakhotia, Punita K. Sodhi Howard Fine ,USA Deputy Editors: S.M. Betharia ,Muscat Aditya Insaan, Rajender Khanna, Subrata Mandal, Shibal Mateen Ahmed ,USA Bhartiya, Nita Gurha, Anuj Mehta, Manisha Rathi Rasik B. Vajpayee ,Australia Assistant Editors: Boris Malyugin ,Russia Avneesh Gupta Insaan, Rajeev Garg, Tinku Bali Razdan, Neeraj Mark J. Terry ,USA Manchanda, Sarita Beri, S.K. Sahu, G.K.Das, Rakesh Mahajan

Senior Executive Editors: S. Bharti, S.C. Lakhotia, Namrata Sharma, Amit Khosla, Sanjay Chaudhary, S K Khokhar, Rishi Mohan, Alkesh Chaudhary, Lalit Verma, Angshuman Goswami, Rajiv Gupta, Sanjeev Gupta,Rajender Prasad, Anita Sethi, Cyrus M. Shroff

Contributing Editors : Hemali Sharma Insaan, Umang Mathur, Suneeta Dubey, Prashant Nathani, Shashwat Ray, Shalini Mohan, Rasheena Bansal, Julie Pegu, Abhiyan Kumar, Murlidharan, Thirumalesh, Neeraj Sharma, Punita Sodhi, Siddarth, Sumeet Khanduja, Neha Khanduja, Saurabh Dileep, Zahir Abbas, Sunil, Nagindra Vashist, Ritesh Gupta, Lalit Alok, Munish Dhawan Abstract review editors: Ritika Sachdeva, Charu Mittal

Section editors: Cornea : Anita Panda, Ritu Arora, Radhika Tandon, Namarta Sharma Refractive surgery : Rasik B Vajpayee, Mahipal S. Sachdev, J.S. Titiyal, Rajinder Prasad Cataract : Abhay Vasavada, P.V. Chadha, Anil Tara, Vivek Pal, Sudipto Pakrasi ,A.K.Aggrawal Glaucoma : N.N.Sood, H.C.Agarwal, Ramanjit Sihota, Madhu Bhadauria, Usha Raina, Devender Sood J.K.S. Parihar, J.C. Das, Geeta Srinivasan Retina : P.N. Nagpal, Atul Kumar , Natarajan, A.K. Singh, R.B. Jain, Amod Gupta, B. Ghose, Y.R. Sharma, Manish Nagpal , M. Dogra, J.S. Guha, Rajpal Insaan Ocular Trauma : Brig.D.P. Vats, Lt. Col. J.K.S. Parihar, Shukla, D.K. Mehta , Mahesh Chandra Ocular Psychiatry : Ashok Sharma Insaan Oculoplasty : Ashok Grover, V.P. Gupta, Sushil Kumar, Mandeep Bajaj, Anita Sethi, Neelam Pushkar, Rachana Meel, Archana Sood Squint and Neuroophthalmolgy : Vimla Menon, Pradeep Sharma, Kamlesh, P.K Pandey, Gopal Das, Satya Karna, Subhash Dadeya Uvea : Rajpal Insaan, SP Garg, Vaishali Gupta,Pradeep Venkatesh, Biswas Jyoti May, Virender Sangwan Pediatric Ophthalmology : S. Ghose, S Khokhar, Anju Rastogi, Sarita Beri, Ocular Genetics : Jasbir Kaur, Rima Dada Insaan Stem Cell : Samuel JK Abraham,RV Azad, Lalit Kumar,Sujata Mohanty Medicolegal advisor : Madan Mohan,T.D. Dogra, P.C. Dixit, R.K. Sharma, Rajendra Prashad Ocular Pharamacology : T. Velpandian, Alok K. Ravi Ocular Microbiology : Geeta Satpathy, Niranjan Nayak Community Ophtha. : Rajkumar Gupta Insaan, R. Jose , G.V.S. Murthy, P. Vashisht, Monica Insaan, Ocular Anaesthesia : Punit Maheshwar Insaan, Yogesh Shukla Pandey, Renu Sinha Ocular Pathology : Seema Sen, Seema Kashyap Delhi Journal of Ophthalmology

Senior Academic Executive Editors: National advisory board: A S. Ghose, Chief, R.P. Centre, AIIMS, Delhi S. Sabharwal , Sharad Lakotia, R.K. Bhandari, A.K. Gupta, G. A K.P.S. Malik, HOD, Safdarjung Hospital, New Delhi Mukherjee, P.N. Nagpal, Meenakshi Thakkar, B.N. Khanna, A D. Rammurti, Director, Lasik Centre, Coimbatore V.Menon, R.B. Jain, P.V. Chaddha, A.K. Singh, Om Prakash, A B. Ghose, Director Prof., Guru Nanak Eye Centre, Delhi Jolly Rohatgi, Uprit Dhaliwal, Gaurav Y. Shah, S.P.S. Grewal, A P. D'souza, HOD, Lady Harding Medical College, Delhi Praveen Arora A V.P. Gupta, HOD, Guru Tegh Bahadur Hospital, Delhi A A.K. Khurana, P.G.I.M.S., Rohtak (Haryana) Regional Editors: A Hari Mohan, Mohan Eye Institute, Delhi A Aditya Insaan, Shah Satnam Ji Speciality Hospital, Sirsa A S. Vashist, HOD, Ram Manohar Lohia Hospital, Delhi A Neera Agarwal, Neera Eye Centre, Daryaganj, Delhi A Madan Mohan, Ex. Chief R.P. Centre A Sanjay Khanna, Khanna Eye Hospital, Delhi A P.K. Khosla, Ex. Chief R.P. Centre A N. Shroff, Shroff Eye Centre, Delhi A V.K. Dada, Centre for sight, Delhi; Ex. Chief R.P. Centre A Puneet Gupta, Sharnam Eye Centre, Ghaziabad A H.K. Tiwari, Centre for sight, Delhi; Ex. Chief R.P. Centre A H.C. Agarwal, Max Eye Hospital, Delhi A N.N. Sood, Glaucoma Imaging Center, New Delhi A Sushil Choudhry, Director, Eye Care, Noida A Brig. D. P. Vats, Army hospital (R & R), Delhi Cantt. A S. Singh, Tirupati Eye Hospital, Noida A S.C. Gupta, Medical Director, Venu Eye Institute, Delhi A Rajkumar Gupta Insaan, Gurusarmodia Hospital,Ganganagar A Amod Gupta, HOD, PGI Chandigarh (Rajasthan) A S. Sood, HOD, GMC, Chandigarh A Piyush Kapoor, Ganga Ram Hospital, Delhi A Sandeep Mittal, Medical College & Hospital, Meerut A Suneeta Dubey, Shroff Eye Hospital, Delhi A Shrikant, HOD (B.H.U) Varanasi A Charu Mittal, Meerut Medical College, Meerut A Kamal Jeet Singh, Medical College, Allahabad A S. Sood, HOD, GMC Chandigarh A Daljit Singh, Director, Amritsar Eye Hospital, Amritsar A Abhishekh Chandra, BHU, Varanasi A Lingam Gopal, Director, Shankar Nethralaya, Chennai A Devindra Sood, Glaucoma Imaging Center, Delhi A Natrajan, Mumbai, Aditya Jyot Foundation, Mumbai A M.C. Agarwal, Deen Dayal Upadhyay Hospital, Delhi A Amar Agarwal, Chennai A Yogesh Gupta, Hindurao Hospital, Delhi A Cyres K Mehta, Mumbai A Anil Mehta, ESI Hospital, Basai Darapur A R.B. Jain, Delhi A Harpreet Singh Insaan, Jalandhar A P.S. Sandhu, Principal, G.G.S Med. College, Faridkot, Punjab A P.S. Negi, HOD, Railway Hospital, New Delhi A Dr. G.C. Jain, Prof. & Head, S.P. Medical College, Bikaner A Arun Singhvi, ASG Eye Hospital, Jodhpur A Gur Satendra Singh, Prof., GMC, Patiala A Karamjeet Singh, GMC Amritsar A G.S. Bajwa, Prof. & Head, DMC, Ludhiana A Dr. Harpreet Kapoor, CMC, Ludhiana

Contribution Methodology: Delhi Journal of Ophthalmology (DJO) is a quaterly journal. Author/Authors must have made significant contribution in carrying out the work and it should be original. It should be accompanied by a letter of transmittal. The article can be sent by email to the Editor and the hard copy mailed. Articles received will be sent to reviewers whose comments will be e-mailed to the Author(s) within 4-6 weeks. The identity of the authors and the reviewers will not be revealed to each other by the editorial team. The contributors shall be responsible for statements in his /her/their work including the changes made during editing. Detailed instructions to the contributors and for advertisements are included at the end of the journal. Request for reprints or any queries should be addressed to the Editors office by email or post. Editorial Process: The DJO has Dr. Rajpal Insaan Additional Professor of ophthalmology Vitreo-Retina unit of R.P.centre AIIMS as its Editor who is assisted by a team of renowned ophthalmologists and an illustrious advisory board. The reviewers, who are leaders in their respective fields, form the back bone of the journal by setting standards for the published work. Editorial Office: Dr. Rajpal Insaan, Room No. 480, Dr. R.P. Centre, AIIMS, New Delhi-29, Tel. No. 011-26593180(D), 26588500,700, 26589900, Extn. 3180, 3188. Fax No. 011-26589380, 26588919, Mob. 09818598899,09868398421, e-mail [email protected], [email protected] Published by: Dr. Rajpal Insaan, Editor DJO, on behalf of Delhi Ophthalmological Society, Delhi Printed by: Unique Prints, B 68/1, Narayana Industrial Area Phase-2, New Delhi-28, Mob. 09910169596, 011-25897397,41417889 Page design by: Dr. Rajpal Insaan, Sajan Insaan, Dera Sacha Sauda, Sirsa, Haryana. Secretarial Assistance: Ghanshyam Dass (93121 30365), Mrs. Anju Vohra From Darkness to Light

Delhi Ophthalmological Society DOS Executive

PRESIDENT SECRETARY TREASURER Dr. S. Bharti Dr. Namrata Sharma Dr. Sanjay Chaudhary Ph.: (O) 25889900 (R) 25753400 Ph.: (O) 26588852(R) 95120-2572892 Ph.: (O) 23278423, (R) 23275893 (M) 9810060477 (M) 9810856988 (M) 9871411227 E-mail: [email protected] E-mail: [email protected] E-mail: [email protected]

VICE-PRESIDENT SECRETARIAT Room No. 474, 4th Floor JOINT SECRETARY Dr. S.C. Lakhotia Dr. R.P. Centre for Ophthalmic Sciences, Dr. Amit Khosla Ph.: (O) 29228828, 29228240 All India Institute of Medical Sciences, Ph.: (O) 26581171, (R) 25721800 (R) 29228985, (M) 9312255311 Ansari Nagar, New Delhi-110029 (M) 9811060501 E-mail: [email protected] Tel:-91-11-65705229, Fax: 91-11-26588919 E-mail: [email protected] E-mail: [email protected], EDITOR Website: www.dosonline.org EX-OFFICER MEMBER

Dr. Rajpal Insaan LIBRARY OFFICER Dr. Lalit Verma, MD Ph.: (O) 26588500 Extn. 3180 Ph.: (O) 41644000, (R) 26263636 (R)26589696 Dr. Vinay Garodia (M) 9811299934 (M) 9818598899, 9868398421 Ph.: (O) 41731777 E-mail: [email protected] E-mail:[email protected], (M) 9811084552 [email protected] E-mail: [email protected] Dr. Harbansh Lal EXECUTIVE MEMBER Ph.: 28741412 (R) 28743988 (M) 9810649942 Dr. Alkesh Chaudhary Dr. Sanjeev Gupta E-mail: [email protected] Ph.: (O) 29228101 (R) 29228924 Ph.: (O) 65293455 (M) 9810075900 (M) 9810077200 E-mail: [email protected] Dr. Dinesh Talwar Insaan E-mail: [email protected] Dr. Rajender Prasad Ph.:(O) 41644000 (R) 26961109 Dr. Zia Chaudhary Ph.: (O) 26895259 (M) 9810046823 (M) 9810302298 Ph.: (O) 22259613 (M) 9810645168 E-mail: [email protected] E-mail: [email protected] E-mail: [email protected] Dr. Anita Sethi DOS REPRESENTIVE TO AIOS Dr. Angshuman Goswami Ph.: (O) 41644000(R) 26932798 Ph.: (O) 95120-4266642 (R) 22619848 (M) 9810199636 Dr. S.K. Khokhar (M) 9810093809 E-mail: [email protected] Ph.: (O) 26588700, 26588852-65 E-mail: [email protected] Ext. 3037, (R) 26348693 Dr. Cyrus M. Shroff (M) 9810524238 Dr. Rajiv Gupta E-mail : [email protected] Ph.: (O) 22520480 (R) 22622855 Ph.: (O) 416333999(R) 26462449 (M) 9810243257 (M) 9811204241 Dr. Rishi Mohan E-mail: [email protected] E-mail: [email protected] Ph.: (O)24313262 (R) 24655493 (M) 9811107007 E-mail : [email protected] DJO is Distributed by : Chandan Health Care Ltd. -GATIDAN, VINIDAN Intas Pharmaceuticals Ltd. - Olopine Eye Drops Appasamy Associates Dortas-T Eye Drops Gflotas Eye Drops NRI - Tear-Aid, Zypred, Misty, Go-3( Eye Drops) C-NAC Eye Drops DERA SACHA SAUDA OPTHO - CCS, Zoline Plus, Flubrin

Delhi Journal of Ophthalmology

Contents of DJO

Editorial Page No.

Basics in ophthalmology Fields in neuroophthalmology 11 - 16 Dr. Swati, Dr. Rohit Saxena, Dr. Vimla Menon

Major Review Role of Avastin in management of Diabetic Retinopathy 17 - 19 Dr. Manisha Agarwal, Dr. S.P. Chaudhary, Dr. Cyrus M.Shroff

Major Review Cataract Surgery in Patients with Diabetes Mellitus 20 - 22 Dr. Jagat Ram , Dr. Jaspreet Sukhija

Major Review Ocular Tuberculosis: Current Paradigms in Diagnosis and Management 23 - 26 Dr. Rajpal Insaan , Dr. Shibal Bhartiya

Major Review Obesity and Eye Diseases Dr. Rajpal Insaan, Dr. Sonia Bhargav, Dr Shibal Bhartiya

Current Treatment Current treatment for diabetic macular oedema 27 - 31 Dr. Rajpal Insaan

Original Article Role of Systemic Acyclovir In Recurrent Cases Of Disciform Keratitis" 32 - 34 Dr. Kirti Jain. Dr. A.K. Sood , Dr. Suresh Chandra, Dr. Sandeep Kumar Dr. V. K. Malik, Dr. Sanjiv Kumar, Dr. Charu Jain, Dr. Reny Kamboj

The Science of Spirituality Prashaant Chaudhry, Rajpal Insaan, Vidya Nair, Vinod Kochupillai, 37 - 42 Dr. S.C. Manchanda, Dr. R.L. Bijlani

Case Report Hydrocephalus Requiring Shunt Surgery as an Initial Presentation of VogtKoyanagi-Harada Syndrome 43 -45 Dr. Subrata Mandal, Dr. Anusha V, Dr. Rajpal Insaan, Dr. Pradeep Venkatesh, Dr. Satpal Garg

Case Reort A case of giant choroidal tuberculoma misdiagnosed as amelanotic melanoma. 46 - 49 Dr. Anusha V, Dr. Rajpal Insaan, Dr. Pradeep Venkatesh, Dr. Satpal Garg, Dr. Subrata Mandal

Journal Abstract Dr. Shailesh G.M., MD, DNB, Dr. Munish Dhawan, MD 50 - 51

Instructions to Contributor Aims of the Journal 52

Forthcoming Events 53

Various Eye Bank 54

Training Programme 55 Editorial (DHAN DHAN SATGURU TERA HI AASRA)

Respected Members of the DOS family I would like to express my humble gratitude to all DOS members who have provided me help. I dedicate this issue of Delhi Journal Ophthalmology to Beparwah Shah Mastana ji who was the founder of Dera Sacha Sauda Sirsa. Mastana ji who dedicated his whole life in removing the cataract and cobwebs of the minds of people. He founded a spiritual organization which is unique in itself as it does not seek or accept donation in any form. Hai ghat main sujhe nahin Laanat aisi jind Tulsi is Sansaar ko Bhayo Motiya Bind. I am thankful to my Guru Hazoor Maharaj Saint Gurmeet Ram Rahim Singh Ji Insan of Dera Sacha Sauda for providing me strength, ability and self confidence in bringing this issue of DJO. For me, my Guru is everything because he has taught me the scientific method of doing practical research which no one has taught me. It is important to do some research within ourselves not only to understand the true meaning of life but also attain peace and harmony in our daily activities. I have tried to introduce article on meditations because directly or indirectly, it has got positive impact on our life. The gene expression of those who practices yoga and meditation in contrast to normal healthy controls was characterized by enhanced immunity, downregulation of cellular metabolism, and alteration of apoptotic genes in favour of a rapid resolution of inflammation. I have tried to highlighted the various eye banks which are doing good work in eye donations. Article by Dr. Manisha Agarwal has discussed the role of Avastin in management of Diabetic Retinopathy. Article by Prof. Vimla Menon at all has discussed Fields in Neuroophthalmology. Article by Dr. Jagat Ram on Cataract surgery in Patients with diabetes mellitus has emphasized the role of preoperative fundus examination to diagnose CSME and proper management before cataract surgery. Dear colleagues, I hope that you find the present issue of the djo both interesting and intriguing. It should serve the basic purpose enhancing your clinical skills as well as provide a basic frame work to incorporate new procedures in your armamentarium. I am thankful to Prof. S. Ghose for providing necessary help for DJO. Special thanks to Prof. L.P. Aggarwal, who was the founder of Dr. R.P. Centre for Ophthalmic Sciences

So, enjoy reading------and I sincerely look forward to hearing from you!

Dr Rajpal Insaan Additional Professor of Ophthalmology Vitreo-Retinal Services R.P. Centre for Ophthalmic Sciences Editor DJO E mail: [email protected] Telephone- 011-26589380, 26589696 Mob. : 9818598899 FIELDS IN NEUROOPHTHALMOLOGY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

BASICS IN OPHTHALMOLOGY

FIELDS IN NEUROOPHTHALMOLOGY Dr Swati, Dr. Rohit saxena, Dr. Vimla menon

The visual field is a three dimensional area which is Visual field of left eye Visual field of right eye visible through each eye when fixating at central target.

Extension: centered on fixation point Superior 70 Never forget that the image on the degrees retina is inverted. u Nasal Inferior 70 degrees Temporal half halves Temporal half u of left retina of of right retina Nasal 60 degrees retinas Optic nerve u Temporally 90 degrees Optic chiasma Optic tract There is binocular representation of visual fields for 60 degrees to the right and left common fixation point. Visual pathway: The visual pathway starts with stimulation of photoreceptors of retina and processing in ganglion cell whose axons converge to form optic nerve. Geniculo- Lateral calcarine tract geniculate The nasal fibres of optic nerve cross each other at body chaisma and then continue as optic tract which represents the one half visual field of each eye. The optic tract is relayed in ipsilateral lateral geniculate body where assortment of fibers occurs and optical radiation origin that terminate in visual cortex (area 17) of the occipital lobe. (fig 1)

The cerebral cortex INTERPRETATION OF VISUAL FIELD receives the encoded images of the contralateral visual fields of both eyes. Primary visual Terminologies Based on Kahle W. Frotsoher M: area (= striate Color Aves and Textbook of Human cortex) Anatomy. 5m ed. Stuffgavt. Theme. Isopter: is a line joining the retinal points of same Vol. 3 p.355. 2003. sensitivity Constriction: implies that there is generalized Figure 1: Visual Pathway decrease in sensitivity of retina and on kinetic perimetry it encloses smaller area than normal Hemianopia: when Scotoma: it is a localized area of decreased sensitivity. It one half of visual field is involved either in one or both may be absolute, when patient cannot see even the eyes brightest possible stimulus or it may be relative if some Homonymous: the defects that are persent in the visual stimuli are seen. They can be classified either by their fields of both eye and are on the same side of the vertical location or by shape. meridian. Congruency: the extent to which homonymous field Heteronymous: when the defects that are present in the defects in each resembles the other in shape, size depth visual fields of both eye but are on the opposite sides of and slope of margins. More distal a lesion in visual the vertical meridian. pathway more congruence field defect it produces. For example lesion of occipital lobe will produce more congruent field defect than that by a lesion of optic tract. Address for correspondence:- Dr. Swati Retina Dr. Rajendra Prasad Centre for Ophthalmic Science Anatomy: The light rays from visual field converge and All India Institute of Medical Sciences (AIIMS) form image on the opposite corresponding retinal area. New Delhi, India. Thus the light rays coming from the temporal visual field

11 FIELDS IN NEUROOPHTHALMOLOGY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008 from on the nasal retina. The 140 million photoreceptor cells have function of detecting light, the signal is then conveyed to ganglion cells in the inner retinal layer and the axons on these ganglion cells form nerve fibre layer. The nerve fiber bundles finally converge at optic nerve head and exit as optic nerve. Fields defects: the layer of retina that is affected by the disease process determines the pattern of field defect. Lesions in outer retina have no particular definite boundaries so it can produce field defects of varying shape and shape Optic nerve Anatomy: optic nerve is formed by the axons of retinal ganglion cells those converge in form of nerve fiber bundles. Its about 50 mm in length and can be divided in to four parts: ONH (intraocular part. 1mm), inraorbital part (25mm), intracanalicular part (10mm), intra cranial Figure 2: central scotoma in case of optic neuritis (15mm). The Chaisma Organization: The nerve fiber bundles converge in specific pattern to form optic nerve head. The Anatomy: Chaisma is a flat structure formed by the papillomacular bundle is formed by macular fibers that crossing of nasal fibres of each optic nerve. The chaism is enter the temporal aspect the disc. The arcuate nerve approximoately 4mm high 12mm wide and 8mm long. It is located over the diaphragm sella and posteriorly is fiber bundle contains the axons that arise from the related to wall of third ventricle. It continues as optic temporal to the fovea and arch superiorly and inferiorly tract. There may be variation in the location of chaisma to the fovea to enter the superior and inferior poles of the that may have important clinical significance. In 80% of disc respectively. The axons from the nasal retina enter its located directly over the sella (central) in such cases radially in to the optic nerve head as nasal nerve bundle. the pituitary lesions involve chaisma first; in about 10% Thus the macular fibers are centrally placed while fibers of normal its located more anteriorly over the from the upper part of retina lie superiorly and those tubercullum sellae (prefixed) in such cases the pituitary from lower retina are placed inferiorly in optic nerve. lesions will involve optic tract first or in rest 10% of cases Field defects: lesions affecting the axons produce a field it's located more posteriorly over the dorsum sella when defect corresponding to the particular pattern of the the pituitary lesions involve optic nerve first. nerve fiber bundle involved. These defects are well Relations of chaisma: Anteriorly chaisma is related to demarcated and respect the horizontal meridian and anterior cerebral arteries and their communicating either involve blind spot or point towards it. arteries.posteriorly it's related to hypophyseal stalk, Papillomacular bundle: involvement of this bundle of pituitary body. It forms the floor of third ventricle and nerve fibers results in Central scotoma (fig 2), lies above hypophysis. Laterally its related to internal Centrocecal scotoma or paracentral scotoma carotid artery and cavernous sinus. Arcuate nerve fiber bundle defects lead to: Bjerrum Organization: At chaisma the fibers representing the nasal visual field (temporal fibers) are present in the scotoma, Seidel scotoma, nasal step of Ronne. lateral part. The inferonasal fibres (superior temporal Involvement nasal fibers bundle leads to wedge shaped field) cross anteriorly in the chaisma and loop forward in defects to the contralateral optic nerve forming willbrand's knee and then continue in contralateral optic tract. The nasal Altitudinal defects are caused by involvement of axons macular fibers decussate most posteriorly. The upper at the superior or inferior pole of the optic disc. The nasal fibers (inferior temporal field) cross in the middle. arrangement of nerve fibers is maintained through out Thus right optic tract constitutes the right nasal field the optic nerve so even the lesion involving the posterior (right temporal axons) and left temporal field (left nasal part of optic nerve produce pattern corresponding to the decussated fibers) representing the right half of visual nerve fiber bundle involved. space.

12 FIELDS IN NEUROOPHTHALMOLOGY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Clinical features: the patient with chiasmal lesion ipsilateral eye) and temporal hemifield defect in presents with varying signs and symptoms depending contralateral eye (decussating nasal fibers of upon the type, size and site of lesions. Pituitary adenoma contralateral eye) (figure 4). Diseases like meningioma presents with signs of compression as well as other that arise form the dura of teberculum sellae and endocrinological abnormalities. There may be unilateral adjacent structure compress the optic nerve as well as or bilateral loss of vision as result of compression of optic chiasma. Depending upon their site and size they may nerve by a tumour. Relative afferent pupillary defect lead asymmetric involvement of both eyes. may be present in unilateral lesions. Lesions of Craniopharyngiomas can also lead to asymmetric visual cavernous sinus and large pituitary adenomas compress field defects. Meningiomas and carniopharyngiomas the motor nerves of the eye leading to ocular motility when small in size, lead to the compression of the disorders. See-Saw nystagmus and occilopsia is feature posterior part of the optic nerve or anterior part of of tumour or trauma. chiasma, leading to mono-ocular field defect in ipsilateral eye, most commonly in the superotemporal Field defects: The axons in the chaisma are arranged in quadrant (inferonasal decussating fibres). A proper and such a way that they are limited by a vertical meridian careful field evaluation will expose the subtle which passes through fovea of each eye; thus the lesion involvement of contralateral eye. of chaisma and distal visual pathway respect the vertical meridian. The lesion at chaisma and posterior to it would always produce the defect in both eyes. The field defect produced by a lesion involving chaisma depends upon the location of chaisma, site of lesion and part of chaisma affected. Bitemporal hemianopia: The lesions that affect the body of chaisma produce bitemporal hemianopia (Figure 3). In most of the cases the chaisma is central although in some cases it may be pre or post fixed. Pituitary tumours, Figure 4: Junctional scotoma inflammations, apoplexy are the main lesions that can affect the body of chaisma and produce classical Binasal field defects: A large mass lesion compressing bitemporal hemianopia. Inferior bitemporal hemianopia one side of the optic chiasma can on further enlargement is characteristic of craniopharyngioma. Saccular cause a midline shift of the chiasma with subsequent aneurysm of vessels in circle of Willi can also lead to compression of the other side as well, leading to a binasal bitemporal hemianopia. other ophthalmic conditions field loss presentation. This pattern of field loss can also that can cause similar field defect are bilateral glaucoma be seen with empty sella syndrome, arachnoiditis and as and other optic neuropathies, disc anamolies and a post-operative defect. psychogenic visual loss. Homonymous hemianopia: This type of field defect is commonly seen in cases where the chiasma is prefixed. Thus any lesion which affects chiasma can also affect the optic tract leading to homonymous hemianopia. Large p i t u i t a r y a d e n o m a s a n d craniopharyngiomas are the most common causes. Figure 3: Bitemporal hemianopia in a case of pituitary adenoma Lesions that affect the posterior part of chaisma cause central bitemporal Junctional scotoma: is produced when a lesion involves hemianopia. the junction of the optic nerve and chaisma leading to OPTIC TRACT AND LATERAL GENICULATE optic nerve defect in ipsilateral eye and superior BODY temporal (involvement of Willebrand's knee) defect in Anatomy: The optic tract runs superiorly and posteriorly the contralateral eye. A lesion involving hemichaisma from the optic chaisma and curves around brainstem to would cause total blindness in one eye (optic nerve of terminate in lateral geniculate body. Lateral geniculate

13 FIELDS IN NEUROOPHTHALMOLOGY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008 body is a part of thalamic body and is situated along the one side leads to macular splitting complete lateral aspect of the midbrain. Each geniculate body homonymous hemianopia while the partial consists of six layers of neurons and second order fibers involvement will cause incongruous field defect. tralvellling though optic tract relay here. Lateral Similarly a defect of one of LGB will produce complete geniculate body has dual blood supply from anterior homonymous hemianopia while the partial lesions of and lateral choroidal arteries, which nourish the LGB cause sectoral field defect. superior and inferior homonymous quadrants of the OPTIC RADIATIONS retina respectively. Anatomy: optic radiations are geniculocalcarine Relations: Optic tracts lie between the tuber cinereum pathways that extend from LGB to the visual cortex. and anterior perforated substance. They cross the Wernicke's area as optic peduncles and Organization: Each optic tract is formed by temporal travel in the retrolenticular part of the internal capsule. fibers of the ipsilateral eye while nasal fibres from the Organization: The fibers after exiting from the LGB contralateral eye. Thus each optic tract represents one rotate by 90 degrees again to regain their original half of binocular visual field. The arrangement of axons arrangement. Thus the superior fibers lie in the upper present in optic nerve takes a 90 degree turn through part of radiation, inferior fibers in the lower part and chaisma in to the optic tract. Thus the axons from lower macular fibers lie in the center. retina lie in the lateral aspect; the axons from upper lie in Arrangement of fibers in temporal lobe: the inferior the medial aspect while the macular fibers lie in the fibers from corresponding superior visual fields of both dorsolateral aspect. eyes start from anterolateral part of LGB sweep anterior The axons from ipsilateral eye are relayed in nuclei layer and then laterally along the temporal horn of the lateral 2, 3, 5 while axons from contralateral side relay in 1, 4 and horn to form Meyer's loop, then extend posteriorly to 6 nuclei layer. The fibers from upper part of retina end in the area below the calcarine fissure of occipital cortex. Arrangement of fibers in parietal lobe: The occupy the medial half of the anterior one third of the superior fibers that carry inferior field travel directly LGB. The lower retinal fibers occupy the lateral half of through the lower portions of parietal cortex below the anterior one third of the LGB, while the macular fibers sylvian fissure to occipital lobe area above calcarine are relayed in the posterior two third of LGB. fissure. Clinical features: The characteristic optic atrophy Field defects: Lesions involving the optic radiations pattern is seen in longstanding lesions of optic tract and produce field defects which are homonymous and more LGB in form of hemianopic atrophy or Bow tie congruous. configuration of arophy. The most useful sign of Features of temporal lobe involvement localizing a lesion between optic tract and LGB is involvement of pupil. The optic tract lesions are Temporal lobe lesions produce contralateral superior associated with various pupillary abnormalities in form homonymous field defects since temporal lobe carries of Wernicke's hemianopic pupil and Behr's pupil. While inferior fibers which form Meyer's loop. In more in lesions of LGB pupil reactions are spared. extensive lesions the defect may extend inferiorly but the hemianopia will be denser superiorly. The defects are Lesions affecting the optic tracts are craniophar- wedge shaped defects of varying sizes that are yngiomas, meningiomas, and large pituitary adenomas, homonymous, and incongruous. Temporal lobe lesions demyelinating diseases, vascular lesions such as cause seizures paragnosia, involuntary movement of aneurysms, arteriovenous malformations and mouth, visual and auditory hallucinations. Aphasia is hamartomas. Lesions affecting lateral geniculate body characteristic of left temporal lobe lesion. Most common can be infarctions of both anterior and lateral choroidal lobe lesion is tumour which includes glioma and arteries, tumors, trauma and inflammatory disorders. metastasis. Surgical resection of tumor (temporal lobe) when more than 8 cm, itself may produce field defects. Field defects: All retrochiasmal lesions lead to Anterior choroidal artery infarction may affect the optic contralateral homonymous macular splitting radiation in temporal lobe, as well as LGB. In such cases hemianopia with varying degrees of congruity. The hemianesthesia along with contralateral hemiplegia more posterior the lesion, the more likely that defect occurs. Other lesions are trauma, demyelination, and would be congruous. Complete optic tract disruption on abscess.

14 FIELDS IN NEUROOPHTHALMOLOGY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Features of parietal lobe involvement field in one eye have their corresponding points in other Lesions involving parietal lobe cause inferior eye thus there's overlapping of visual field of both eyes. homonymous field defect that is described as pie on In each eye there is an isolated temporal crescent in floor. These defects are usually more extensive and visual field for which they are no overlapping points in more congruous than temporal lobe defect. The other eye. This temporal crescent perceived by nasal homonymous hemianopia of parietal lobe is always retina is represented in the anterior most portion of associated with macular splitting (fig 5). The calcarine cortex. involvement of right parietal lobe leads to deficit of spatial orientation of left space, thus the patient may Clinical features: Occlusion of left posterior cerebral neglect left half of the body. The involvement of left artery leads to the infarction of calcarine cortex along parietal lobe lesions is associated with Grestmann's with splenium of the corpus collosum which leads to syndrome, word blindness, and visual agnosia. The two field defect in the right side and alexia without agraphia. most important localizing signs of parietal lobe lesion Other signs include headache, visual agnosia, are loss of normal optokinetic response and conjugate dyschmatopsia which are mainly secondary to the deviation of the eyes. The differential diagnosis of infarction. Tumours lead to isolated visual field defects lesions involving parietal lobe includes infaction, and palinopsia. The tumours affecting the occipital lobe haemorrhage, a-v malformations and tumours. are gliomas, meningionmas and metastasis. Bilateral occipital disease is usually due to the vascular lesions which include thromboembolism, hemorrhage, hyperviscosity syndromes, vasculititis. Fields defects: occipital lobe lesions produce field defects that are homonymous and highly congruous. Central homonymous: A lesion affecting the tip of occipital lobe would produce a field defect in the macular area which is homonymous. Atleast 5 degrees of central field must be spared in both eyes on the side of hemianopia. Figure 5: Right homonymous hemianopia in a case of left parietal lobe granuloma Complete homonymous hemianopia sparing macula: The macular area is watershed zone of anastomoses between the middle and posterior cerebral arteries Most VISUAL CORTEX of the occipital lobe lesion (ischemia) results in in which Anatomy: the primary visual cortex (area 17) is located central 3 to 5 degrees of the visual field is spared due to on the medial surface of the occipital lobe near the its dual blood supply (fig 6) calcarine fissure. Brodmann's area 18 and 19 are associated visual areas which help in further processing of visual information. Organization: the right visual cortex receives impulses from the left temporal field and right nasal field. The orientation of fibers in optic radiation is maintained in the visual Figure 6: Macular sparing right homonymous hemianopia cortex. The central field is represented in a case of left occipital lobe ischemia at the occipital tip and separated from the representation of peripheral fibers. The superior Quadrantic defects: The lesion of area below calcarine fibers (representing inferior field) are relayed in area fissure would give rise to homonymous superior superior to calcarine fissure while the inferior fibers quadrantic defect. Similarly a lesion involving are above (superior field) are projected to the area inferior to the calcarine fissure would lead to inferior homonymous fissure. The retinal points which represent the visual defect. Because of their anatomical and vascular 15 FIELDS IN NEUROOPHTHALMOLOGY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008 separation these defects always respect horizontal meridian and they should not be confused with optic Doctor Today's nerve related visual field defects. The former are always Request For homonymous and congruous and respect the vertical meridian as well. Involvement of bilateral occipital lobe may lead to bilateral homonymous hemianopia with MISTY sparing of central tubular vision. This should be EYE DROPS differentiated with other causes of constricted visual Sodium Carboxymethylcellulose IP 0.5%w/v field like malingering, glaucoma, retinitis pigmentosa. Stabilised Oxychloro Complex 0.005%w/v (as preservative) Lesions involving bilateral occipital tip would cause water for injection I.P. q.s. bilateral central homonymous hemianopia. A checkerboard pattern field defect results from MO-4 involvement of occipital lobe below the calcarine fissure EYE DROPS on one side and above the fissure on opposite side. There Moxifloxacin Hydrochlorida could be asymmetry in field defects in cases bilateral equivalent to Moxifloxacin 5mg. Sterile aqueous vehicle q.s. occipital lobe involvement. Temporal crescent: The binocular field of vision is formed by superimposition of corresponding visual GO-3 points of the central 60-deree visual field of both the EYE DROPS Gatifloxacin 3mg. eyes, but then in each eye there is a peripheral area which Benzalkonium Chloride NF 0.05mg. has no corresponding points in other eye. This area is (as preservative) perceived by nasal most retina of the eye and is Sterile aqueous vehicle q.s. represented in the anterior most portion of the calcarine cortex. Any lesion involving the anterior most part of ZENTOB-F the calcerine cortex leads to monocular temporal EYE DROPS crescentric field defect in the contralateral eye. Special Tobramycin 3mg. visual field defects (As Tobraymycin Sulphate USP) Fluorometholone U.S.P. 1mg. Baring of blind spot: when a small degree of field is Benzalkonium 0.1mg. mapped the isopter may be constricted and any scotoma Chloride NF q.s. outside the isopter may be continuous with blind spot gas preservative causing true baring of blind spot. False baring of the blind spot is seen when the isopter is just outside the BETOXID-PLUS blind spot. Softgel Capsules Pseudobitemporal hemianopia: field defects that do not Lycopene - 6% 10 mg respect the vertical meridian. Beta Carotene (30% Disp.) 10 mg Binasal hemianopia: bilateral nasal defects are usually Lutein 8 % 7 mg caused by involvement of arcuate fibers of both eyes. Zinc Oxide 7. mg Rarely it may be caused by pressure upon the temporal Vitamin E 25 mg aspect of the optic nerve or temporal portion of chaisma , Copper Sulphate 1 mg as in cases of aneurysm, pituitary tumour, vascular L-Arginine 20 mg infarction. Manganese Sulphate 1 mg Methyl Cobalamin 100 mcg. Selenious Acid 100 mcg. “ Other beings are serving their term for past deeds But a man has choices to the path he leads NR Vision Care Whether to join back the circle of 8.4 million A.O. : A-94, Sumti Nath Society, Kathawada Road, Or with Supreme Lord secure his union.” Naroda, Ahmedabad (Gujrat) – Shah Satnam Singh ji E-mail : [email protected]

16 ROLE OF AVASTIN IN MANAGEMENT OF DIABETIC RETINOPATHY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

MAJOR REVIEW Role of Avastin in management of Diabetic Retinopathy Dr. Manisha Agarwal,1 Dr. S.P. Chaudhary, 1 Cyrus M.Shroff1,2

Vascular endothelial growth factor (VEGF) plays a key Intravenous Avastin has been approved by the Food and role in the development of retinal neovascularization.1,2 Drug Administration for the treatment of metastatic 4 Various studies beyond doubt have proved the colorectal cancer. correlation between increased VEGF levels in the Avastin is currently having an off-label use in vitreous specimen and the severity of proliferative Ophthalmology, given as an intravitreal injection in the diabetic retinopathy (PDR). There has been a significant dosage of 1mg/0.04ml, 1.25mg/0.05ml or 2.5mg/0.1ml. reduction in the concentrations of VEGF after panretinal Avastin has a beneficial effect in patients of diabetic photocoagulation for PDR.3 retinopathy by the following mechanisms of action:- Bevacizumab (Avastin, Genentech) is a humanized 1. Diabetic macular edema (DME) monoclonal recombinant antibody that inhibits all the The major cause of vision loss in patients of diabetic active isoforms of VEGF.1 (Fig-1) VEGF is the main retinopathy is macular edema. Diabetic retinopathy factor responsible for neovasculariztion, increase in study5 has given guidelines for macular laser capillary permeability, inflammation and is also said to photocoagulation for clinically significant macular have a neuroprotective role. Avastin by inhibiting all edema (CSME).We are aware of the importance of good isoforms of VEGF blocks all these actions mediated systemic control of blood sugar levels, hypertension, through VEGF. lipid profile, renal functions prior to macular laser photocoagulation.6,7 Patients with persistent diabetic macular edema not responding to laser photocoagulation. Once the causes of DME such as vitreous macular traction and macular ischemia have been ruled out on optical coherence tomography and fundus fluorescein angiography respectively. We can treat these patients with intravitreal injection of avastin. Avastin helps in reducing DME by blocking the increased capillary permeability mediated through VEGF, without the associated side effects of laser photocoagulation such as macular burn, scotoma formation, decreased contrast senstivity ,choroidal neovascular membrane formation etc.

Figure - 1 Intravitreal triamcinilone is also effective against DME, however the advantage of avastin is that there is no risk Institutional Affiliation of authors:- of steroid induced glaucoma which is a very common 1. Dr.Shroff's Charity Eye Hospital side effect of triamcinolone.. 5027-Kedar Nath Road, Daryaganj, New-Delhi-110002. Many are now considering intravitreal avastin injection 2. Shroff Eye Centre as the first line of treatment for diffuse macular edema A-9 Kailash Colony, New-Delhi. after a good systemic control.

17 ROLE OF AVASTIN IN MANAGEMENT OF DIABETIC RETINOPATHY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

2. Regression of neovascularization Elsewhere(NVE) leakage from NVD in 73% eyes and from NVE in 59% of & neovascularization on disc (NVD) the treated eyes by blocking all isoforms of VEGF and it's Pan retinal photocoagulation has been the treatment of angiogenic effect on retinal neovascularization. choice for PDR, as suggested by the Diabetic However intravitreal injection of avastin in one eye Retinopathy Study. 5 Laser photocoagulation caused a milder regression of the neovascularization in remarkably regresses the neovascularization thus the contralateral eye also which signifies the fact that preventing severe visual loss in most of the patients. there is systemic absorption of the drug even after However in a few situations an adjunctive or alternative intavitreal injection. therapy to laser photocoagulation is required such as - 3. Regression of Iris neovascularization(NVI) & - Patients of PDR having undergone several sessions Neovascular glaucoma (NVG) of laser photocoagulation with complete ablation of Many patients of PDR progress to develop iris the retina showing persistence and proliferation of neovascularization leading to neovascular glaucoma new vessels. despite maximum laser photocoagulation. They present - Unable to perform laser photocoagulation due to a with corneal edema secondary to raised intraocular non-dilating pupil or media opacity such as cataract pressure (IOP) or hyphema which hampers further laser or vitreous hemorrhage. photocoagulation if not already completed .In such cases Intravitreal injection of avastin has shown benefit in Avastin injection has shown a very good regression of regressing neovascularization in such situations along NVI after intravitreal and intracameral injection in as with laser photocoagulation. (Fig.2) short a time as 24 hours ,again by blocking the angiogenic effect of VEGF.(Fig-3) A B Pre-Avastin

C D Early Phase Late Phase

Post-Avastin

Fig.2a&2b: Early and late phase fundus fluorescein angiogram of the left eye showing leakage from neovascularization elsewhere (NVE) in the superior quadrant prior to Avastin Fig.2c&2d: Early and late phase fundus fluorescein angiogram of Early Phase Late Phase the left eye showing decreased leakage from the same Figure - 3 neovascularization elsewhere (NVE) two weeks after intavitreal injection of Avastin. The case series of Robert LA et al,8 has shown resolution of leakage from NVI in 82% eyes of PDR patients treated In an interventional, consecutive, retrospective case with intravitreal Avastin injection, with recurrence of 8 series by Robert LA et al, intravitreal injection of iris neovascularization in one case 11 weeks after the Avastin has shown complete resolution of angiographic injection of avastin.

18 ROLE OF AVASTIN IN MANAGEMENT OF DIABETIC RETINOPATHY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

4. Preoperatively in Diabetic vitrectomy not possible, cases unresponsive to laser Intravitreal avastin injection given preoperatively about photocoagulation and lastly avastin may enhance the two weeks prior to a vitrectomy surgery in a patient of effect of laser photocoagulation by reducing the PDR helps in reducing intraoperative bleeding when concentration of VEGF thereby reducing the fibrovascular proliferation is segmented or delaminated, aggressiveness of neovascularization. thus helping in two ways-avoiding the loss of view References: during the surgery due to recurrent bleed making 1. Ferrara N. Vascular endothelial growth factor: basic membrane dissection easier and reducing the need to science and clinical progress. Endocr Rev 2004; 25: elevate the bottle height of the infusion bottle for the 581-611. purpose of hemostasis thereby reducing the risk of optic 2. Adamis AP, Shima DT. The role of vascular nerve ischemia in patients with already impaired endothelial growth factor in ocular health and retinovascular perfusion. disease. Retina 2005; 25:111-8. 5. Vitreous hemorrhage in PDR 3. Aiello LP,Avery RL,Arrigg PG,et al. Vascular PDR patients with vitreous hemorrhage or with endothelial growth factor in ocular fluid of patients recurrent vitreous hemorrhage after vitrectomy surgery with diabetic retinopathy and other retinal due to causes such as fresh bleed from persistent retinal disorders.N Eng J Med 1994;331:1480-7. neovascularization, anterior hyaloid proliferation or proliferation within sclerotomy sites. In such patients 4. Hurwitz H, Fehrenbacher L,Novotny W,et al. the vitreous hemorrhage hampers additional laser and Bevacizumab plus irinotecan,fluorouracil, and thus an intravitreal injection of avastin in such a situation leucovorin for metastatic colorectal cancer. N Engl J can help to regress the neovascularization and clear the Med 2004; 350: 2335-42. vitreous hemorrhage. In a recent report of two cases by 5. Diabetic Retinopathy Study Research Group. Spaide et al9 there was partial resolution of vitreous Preliminary report on effects of photocoagulation hemorrhage after 1 week and complete regression after 1 therapy. Am J Ophtahlmol 1976; 81: 383-96. month in two patients of PDR with vitreous hemorrhage 6. Gupta A, Gupta V, Thapar S, Bhansali. A. Lipid treated with intravitreal avastin injection. lowering drug Atorvastatin as an adjunct in the The role of the anti-VEGF avastin in the treatment of management of diabetic macular edema. Am J diabetic retinopathy is limited by the duration of action Ophthalmology 2004;137:675-682. of the drug and the need to repeat the injections .It still 7. Gupta A, Gupta V, Dogra MR, Pandav SS.Risk remains unclear how frequently avastin injections need factors influencing the treatment outcome in to be repeated to ensure permanent regression of diabetic macular oedema. Indian J Ophthalmol neovascularization. Laser photocoagulation despite its 1996;44: 145-148. associated side effects such as limitation of peripheral 8. Avery RL, Pearlman J, Pieramici DJ, Rabena MD et visual fields, decreased contrast sensitivity etc. still al. Intravitreal Bevacizumab (Avastin) in the remains an essential intervention for the treatment of Treatment of Proliferative Diabetic Retinopathy. PDR. Ophthalmology 2006;113:1695-1705. In future a combination of both intravitreal avastin and 9. Spaide, Richard F, Fisher, Yale L. Intravitreal laser photocoagulation may offer advantages such as Bevacizumab (Avastin) treatment of proliferative reduction in the requirement of multiple sessions of laser diabetic retinopathy complicated by vitreous photocoagulation, reduction in side effects of laser hemorrhage.Retina.26 (3): 275-278, March 2006. photocoagulation, treatment in situations when laser is

19 CATARACT SURGERY IN PATIENTS WITH DIABETES MELLITUS DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

MAJOR REVIEW

Cataract Surgery in Patients with Diabetes Mellitus Prof Jagat Ram and Dr Jaspreet Sukhija Advanced Eye Centre, Post Graduate Institute of Medical Education and Research, Chandigarh

Cataract Surgery in Patients with Diabetes Mellitus Prof PROGRESSION OF DIABETIC MACULOPATHY Jagat Ram and Dr Jaspreet Sukhija Advanced Eye AFTER CATARACT SURGERY Centre, Post Graduate Institute of Medical Education The preoperative status of retinopathy may influence its and Research, Chandigarh. susceptibility to surgical invasion. Diabetic patients with Cataract is a well recognised complication of diabetes any type of retinopathy should be advised that cataract and it has been estimated that up to 20% of all cataract extraction might increase the level of retinopathy. surgery is performed on diabetic patients. The overall (Figure 1) risk of developing cataract is two to four times higher in patients with diabetes compared with patients without diabetes, 1 and in patients under the age of 40 years, this risk may be 15 to 20 times higher. The risk of developing cataract increases with poor metabolic control and duration of the disease. Although the cataract has been reported to be reversible after metabolic control, by and large the lenticular changes are irreversible. The 1997 guidelines of the Royal College of Ophthalmologists state that all forms of diabetic retinopathy may become more severe following cataract surgery. Various authors have reported retinopathy progression rates15% to 70%. The rate of DR progression after cataract surgery is known to be influenced by the severity of the preoperative DR, the duration of diabetes, and the adequacy of glycaemic control. More than 90% of patients with diabetes without retinopathy attain a final Figure 1. Right eye fundus photograph shows non-proliferative visual acuity of 20/40 or better. Macular edema is as an diabetic retinopathy (NPDR) with clinically significant macular important cause of poor postoperative visual gain edema (CSME). Fundus fluorescein angiography (FFA) shows following cataract surgery. It is believed that leaking micro aneurysms (MAs) with late leakage corresponding inflammation consequent to cataract surgery leads to an to MAs.(A) Three weeks post phaco, no prior photocoagulation increased permeability more easily in patients with performed. Fundus photograph shows clear media with NPDR and CSME. FFA showed leaking MAs with late leakage from MAs diabetes, which in turn results in higher incidence of with diffuse leakage forming cystoid macular edema (CME). (B) CME. The incidence of surgical complications is same in (Courtesy: Prof Amod Gupta and Dr Ramandeep Singh) patients with diabetes without retinopathy and patients without diabetes. Clinically significant macular edema Diabetic nephropathy and retinopathy are present in diabetic eyes at the time of surgery is unlikely microangiopathic processes. Thus, those who have to resolve spontaneously, and the postoperative visual diabetic nephropathy are more prone to breakdown of acuity prognosis is not as good as in eyes without edema. the blood- retinal barrier (BRB), which may facilitate the Careful selection of cases and frequent follow-up may be progression of diabetic retinopathy. Preoperative laser needed in patients with preoperative CSME to reduce photocoagulation decreases the risk of progression of the progression of diabetic retinopathy and unresolved retionopathy after phacoemulsification. (Figure 2 &3). macular edema after cataract surgery. Gupta et al identified that the interval after cataract surgery was the most common risk factor for the Address for correspondence:- occurrence of maculopathy in the aphakic/ Prof Jagat Ram and Dr Jaspreet Sukhija pseudophakic eyes, and this had a significant negative Advanced Eye Centre, Post Graduate Institute of Medical correlate, thereby indicating that the macular edema in Education and Research, aphakic eyes tends to progress sooner after surgery than Chandigarh. the natural course in the nonoperated fellow eyes.2

20 CATARACT SURGERY IN PATIENTS WITH DIABETES MELLITUS DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

MANAGEMENT OF MACULAR EDEMA Macular edema tends to progress if caused by diabetes and improve if it is caused by Irvine-Gass Syndrome. There are no clear guidelines however regarding the optimum management of these eyes. Macular oedema that is not typical pseudophakic cystoid macular oedema can settle spontaneously in some patients. The early application of laser treatment for postoperative macula oedema in patients with diabetes would therefore mean over treating some patients. Generally, laser photocoagulation is deferred until 6 months or so to permit the resolution of Irvine-Gass syndrome. The angiographic CME following cataract surgery carries a Figure2. Right eye fundus photograph shows media haze with non-proliferative diabetic retinopathy (NPDR) with clinically favorable prognosis and seldom persists for more than a significant macular edema (CSME). Fundus fluorescein year. It is reasonable to expect a final visual acuity of at angiography (FFA) shows leaking micro aneurysms (MAs) with least 20/40 in nearly 90% of these eyes. In contrast, late leakage corresponding to MAs.(A) Six weeks after laser, he clinical CME that develops in eyes with pre-existing underwent uneventful phacoemulsifaction with intraocular lens implantation. Four weeks post phaco, fundus photograph shows retinopathy often persists. Exactly when laser can be clear media with NPDR and CSME. FFA showed reduction in applied in the postoperative edema is still not well leaking MAs with late leakage from MAs and minimal diffuse established. Such focal/grid treatment is best applied leakage in late phase.(B). (Courtesy: Prof Amod Gupta and Dr within the first 6 weeks after the surgery. In the series by Ramandeep Singh) Dowler's et al3 , macular edema secondary to cataract surgery occurred in nearly 50% of non CSME eyes, and it resolved in half of the eyes within 6 months and 75% within 1 year. Such eyes postoperatively do not require laser photocoagulation and may be managed conservatively. Preferably, diabetic retinopathy should be stabilized with appropriate laser treatment before cataract surgery. However, in patients where cataract density prevents appreciation of CSME or application of laser, laser photocoagulation should be applied as soon as the cataract wound is stabilized.

PHACOEMULSIFICATION/TYPE OF IOL/PCO IN PATIENTS WITH DIABETES The visual results and rate of maculopathy progression Figure 3. Right eye fundus photograph shows media haze with laser marks in macular area. The patient had been photocoagulated for are quite similar to those of techniques. Presence of pre- proliferative diabetic retinopathy (PDR) and macular edema in the existing retinopathy and surgical inexperience are risk past in this eye. Fundus fluorescein angiography (FFA) shows factors for progression of retinopathy. Those having transmission fluorescence with no leaking micro aneurysms (MAs) and new vessels.(A) Four weeks post phaco, fundus ECCE have also been noted to have an increased rate of photograph shows clear media with laser marks. FFA showed anterior segment complications including elevated transmission fluorescence minimal diffuse leakage in the foveal levels of fibrin and the development of posterior center.(B) (Courtesy: Prof Amod Gupta and Dr Ramandeep Singh)

21 CATARACT SURGERY IN PATIENTS WITH DIABETES MELLITUS DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008 synechias.4 Similarly, postoperative aqueous flare is References greater in diabetic patients having phacoemulsification 1. Ederer F, Hiller R, Tayler HR: Senile lens changes and occurs with increased intensity with advancing and diabetes in the population studies. Am J retinopathy.5 Dowler and coauthors report a prospective Ophthalmol 1981;91:381-395. series of 46 patients with diabetes and bilateral cataract 2. Gupta A, Bansal RK, Goel RC: Risk factors for in which they compared ECCE and phacoemul- asymmetric diabetic retinopathy following cataract 3 sification. They found that postoperative visual acuity surgery. Annals Ophthalmol 1996 ; 28:311-316 improved more after phacoemulsification than after 3. Dowler JGF, Sehmi KS, Hykin PG, Hamilton AMP: ECCE, especially in eyes with retinopathy. They The natural history of macular edema after cataract postulated that this finding may be a result of the lower surgery in diabetes. Ophthalmology 1999; 106:663- postoperative inflammation after phacoemulsification. 668. It is beneficial to consider phacoemulsification earlier in 4. Krupsky S, Zalish M, Oliver M, Pollack A. Anterior diabetic patients before vision-limiting diabetic segment complications in diabetic patients complications develop. Krepler et al did not find a following extracapsular cataract extraction and significant difference in flare values between the acrylic posterior chamber intraocular lens implantation. and HSM IOL groups.6 Thus, in terms of postoperative Ophthalmic Surg 1991; 22: 526-530. inflammation, the lenses seem equally suitable for 5. Zaczek A, Zetterstrom C. Aqueous flare intensity cataract patients with diabetic retinopathy. Variables after phacoemulsification in patients with diabetes other than surgical trauma and IOL type that may mellitus. J Cataract Refract Surg 1998; 24:1099-1104 influence flare after cataract surgery include the grade of 6. Krepler K , Ries E , Derbolav A, Nepp J, Wedrich A . diabetic retinopathy and the presence of CSME. Inflammation after phacoemulsification in diabetic However PCO rates have been shown to be least with retinopathy: Foldable acrylic versus heparin- Acylic hydrophobic IOL. Silicon IOl's should be avoided surface-modified poly (methyl methacrylate) in diabetics. Hayashi et al showed that diabetics intraocular lenses. J Cataract Refract Surg2001;27: developed greater PCO than nondiabetic patients after 7 233-238. cataract surgery. PCO in diabetic patients progressed in 7. Hayashi k, hayashi H, Nakao F, Hayashi F. Posterior the late postoperative period. The incidence of Nd:YAG laser capsulotomy was also higher in diabetic patients Capsule Opacification after Cataract Surgery in than in nondiabetic patients. There was no significant Patients with Diabetes Mellitus. Am J Ophthalmol correlation between PCO and stage of diabetic 2002;134:10-16. retinopathy. Since blood-aqueous barrier breakdown is more severe in eyes with more advanced retinopathy, some chemical mediators that stimulate the proliferation of lens epithelial cells must be present abundantly in eyes with advanced diabetic retinopathy, which may subsequently lead to extensive PCO. However, opacification in the peripheral posterior capsule most certainly precludes visualization of the fundus. Therefore, it is important to keep the entire posterior capsule transparent in the patients with diabetes, not only for visual acuity, but also for laser photocoagulation of the retina.

22 OCULAR TUBERCULOSIS DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

MAJOR REVIEW Ocular Tuberculosis: Current Paradigms in Diagnosis and Management Dr Rajpal Insaan , Dr Shibal Bhartiya, Dr Sonia Bhargav

In spite of advancement in various tests in diagnosis of CORROBORATIVE EVIDENCE intraocular tuberculosis clinical suspicious is the main in 1. Purified Protein Derivative/Mantoux Skin Test diagnosis of the same. We in our centre have not emphasized the various laboratory tests. Therapeutic The Mantoux test is commonly obtained in patients trial on suspected lesions is very effective The diagnosis suspected of ocular tuberculosis. The standard Mantoux of intraocular tuberculosis is difficult because of the test consists of an intradermal injection of 5 tuberculin large variations in clinical presentation and the lack of units (TU) of PPD to raise a wheal of 6-10 mm. The extent uniformity in diagnostic criteria .In most cases diagnosis of induration is read at 48-72 hours. An induration of less depends more on corroborative evidence, such as a than 5 mm is considered a negative result; an induration positive PPD and chest x-ray, and the exclusion of other of 5-10 mm is considered positive in persons with HIV causes. Direct evidence for the presence of the infectious infection, in those who are in close contact with a patient agent in the ocular cavity and/or ocular tissue is ideal for with infectious tuberculosis, and in those who have establishing the diagnosis, this could consist of the healed tuberculosis lesions on chest radiograph. A test demonstration of acid-fast organisms under the result of more than 10 mm is reported as positive for microscope or the detection of bacterial genome by those patients living in high incidence areas, for nucleic acid amplification procedures. employees of highrisk congregate settings (e.g., health CLINICAL MANIFESTATIONS care workers), and for residents of long-term facilities. Any result > 15 mm is considered a positive result. The varied manifestations of the disease have complicated efforts to name the clinical indicators that Mantoux skin test results can be negative in patients would suggest a diagnosis of intraocular tuberculosis. with severe tuberculous infection and in very moribund Miliary tubercles have a distinct clinical appearance but states. In addition the dosage of tuberculo-proteins tuberculomas can be confused with other diseases, such injected is important, as small doses might fail to incite a as syphilis, sarcoidosis, or brucellosis, and neoplasia reaction. such as as retinoblastoma, malignant melanoma, Vaccination with BCG poses a potential source of cross- lymphomas, or metastatic tumors. In the focal or diffuse reactions and false-positive results are attributed mostly forms of choroiditis, other conditions, such as to prior BCG vaccination. The probability that the toxoplasmosis, histoplasmosis, multifocal choroiditis reaction in PPD skin test is from the Mycobacterium with pan uveitis, or autoimmune serpiginous tuberculosis antigen and not due to BCG increases a) choroiditis, are included in the differential diagnosis. In with increase in size of reaction, b) with a patient who vasculitis with associated inflammation, snowball has been in contact with a person who has TB, c) with vitreous opacities, and neuroretinitis are possible clues family history of TB or patient's country of origin has a to a diagnosis of tubercular etiology. An intractable high incidence or prevalence of TB, and d) with an disease course with multiple recurrences on nonspecific increasing interval between vaccination and skin testing. treatment is a clue suggesting a possible tubercular etiology. Such patients should be investigated for 2. Interferon-gamma release assays (IGRA) tuberculosis. This test is based on the in vitro assays that measure interferon-gamma released by sensitized T cells after Address for Correspondence :- Dr. Shibal Bhartiya stimulation by Mycobacterium tuberculosis antigens. Senior Research Officer The newer versions of the test use antigens that are very Dr. R.P. Centre for Ophthalmic Sciences specific to Mycobacterium tuberculosis and include AIIMS, New Delhi early secreted antigen target (ESAT)6, culture filtrate

23 OCULAR TUBERCULOSIS DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008 protein (CFP)-IO, that are encoded by genes that are DIRECT EVIDENCE present in the region of difference segment of 1. Examination of Smear and Staining for Acid-Fast Mycobacetrium tuberculosis. These are much more Organisms specific than the earlier versions of this test where Examination of smears of infected tissue or fluid after purified protein derivative (PPD) was being used as a acid-fast staining is the most specific procedure for stimulating antigen. The newer antigens being more diagnosing tuberculosis. It has been estimated that at specific are not shared with BCG vaccine strains or other least 106 organisms/ml of sputum are required for species of Mycobacterium.ll Two kits are available detection on a smear. Because the yield of organisms commercially: T-SPOT.TB test (Oxford Immunotec Ltd, from intraocular fluids is low, direct microscopy of the Oxford, UK) and the QuantiFERON -TB GOLD (QFT- smears is not often helpful in the diagnosis of intraocular G:Cellestis Ltd, Carnegie, Australia). The CDC has tuberculosis. updated its guidelines suggesting that QFT-G can be used in place of tuberculin skin test for infection control 2. Culture of Intraocular Fluid/Tissue and survillence and conversion, that is, latent to manifest Cultures of M. tuberculosis on Lowenstein Jenson infection. The UK National Institute for Health and medium must be incubated for 8 weeks and the visible Clinical Excellence has recommended a two-step colonies are identified by Ziehl-Neelsen stain. The strategy for diagnosing latent tuberculosis, in which the process is prolonged and cumbersome, and may not tuberculin skin test is done first and those who are provide positive results because of the low yield of positive or in whom the test is unrealiable, should be organisms from intraocular fluids. further considered for IGRA. However, there are no 3. Polymerase Chain Reaction published studies yet on the IGRA and ocular tuberculosis. PCR is a sensitive and highly specific technique that works on the principle of amplification of mycobacteial 3. Chest Radiography and Tomography DNA several-fold for easy detection. This is especially Although ocular tuberculosis may occur without useful for intraocular fluids, because PCR can be evidence of pulmonary disease, the chest radiograph can performed with very small sample sizes. Samples can be still provide evidence of active or healed/primary or either aqueous, vitreous humor, subretinal fluid, or reactivated tuberculosis. Computerized tomography of rarely, tissue obtained by chorioretinal biopsy. The the chest and skeleton and cerebral MRI may be reported PCR-positivity for M. tuberculosis is 33.3% of undertaken if there is a high index of clinical suspicion as cases in retinal vasculitis and 66.6% in granulomatous these are more sensitive than radiograph panuveits.. 4. Serodiagnosis Use of real-time PCR technology can differentiate Serodiagnosis for detection of antibodies or antigens has commensals and contaminants from infecting microbes, been used for both pulmonary and ocular tuberculosis. but so far its use has not been reported in the diagnosis of The Middlebrook-Dubos test is a hemagglutinin ocular tuberculosis. Sensitivity may also be improved by reaction between sheep red blood cells treated with dot-blot hybridization of the PCR product by 32P- polysaccharide from M. tuberculosis extract and sera labeled specific probes. Gene sequencing of the PCR from tuberculosis patients. A positive reaction from the DNA product has confirmed the presence of the H37Rv serum in a dilution of 1:8 is thought to be specific for strain of M. tuberculosis in ocular specimens obtained tuberculous infection. ELISA using purified cord factor from intraocular tuberculosis patients using primers as the antigen has been found to be helpful for the targeting the IS 6110 sequence. The reliability of PCR diagnosis of ocular tuberculosis. The anti LAM-B depends on the sensitivity and specificity of a particular antibody consists of a nonprotein antigen of assay. These measures are difficult to establish in mycobacteria that becomes positive when a patient tuberculosis as the culture that is the gold standard for develops tuberculosis. Serodiagnostic tests are currently comparison itself has a poor yield from intraocular not preferred because of their low sensitivity and the specimen and histopathology is mostly not available high number of false-positive test results.

24 OCULAR TUBERCULOSIS DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

GUIDELINES FOR DIAGNOSIS 4. Exclusion of Other Uveitis Entities Based on laboratory investigations and clinical In the geographic regions where tuberculosis is low in parameters, follow-up examinations and therapeutic incidence, other causes of uveitis must be excluded by response to ATT, the following guidelines for the various laboratory investigations inclduing serology for diagnosis of intraocular tuberculosis enable the clinician syphilis, toxoplasmosism and others. to determine when to initiate ATT. Although these 5. Therapeutic trial criteria are based on clinical and laboratory A positive response to 4-drug ATT (isoniazid, investigations, cases can be divided into two groups, rifampicin, ethambutol, and pyrazinamide) over a confirmed cases and presumed intraocular tuberculosis. period of 4 to 6 weeks (under supervision of a TB expert, Anyone or more of the clinical signs in combination with therapeutic response to ATT in the eye evaluated by any of the positive tests could be considered a confirmed ophthalmologist) (definitive) case of intraocular tuberculosis. TREATMENT Anyone or more of the clinical signs listed in MEDICAL MANAGEMENT combination with any of the positive tests or a positive therapeutic trial in combination with exclusion of other 1. Drug Regimen uveitis entities could be considered presumed ocular It is imperative to obtain the opinion of an infectious tuberculosis and referred to a TB specialist to initiate a disease expert/pulmonologist/internistand to full course of ATT. comanage the case as the treatment of tuberculosis is 1. Clinical Signs complex even more so in the case of drug-resistant 1 . Anterior uveitis : Granulomatous tuberculosis. Non granulomatous Drug regimens for ocular tuberculosis are similar to Iris nodules those for pulmonary or extrapulmonary tuberculosis. Ciliary body granuloma For the treatment of ocular tuberculosis, a few studies 2. Intermediate uveitis : Granulomatous have described a course of chemotherapy consisting of Non granulomatous with isoniazid and rifampicin for 9 months. The J66'C organizing exudates recommends the use of all four drugs (isoniazid, 3. Posterior and pan uveitis: Choroidal tubercle rifampicin, pyrazinamide, and ethambutol) for an initial Choroidal tuberculoma 2month period followed by a choice of different options Subretinal abscess over next 4 to 7 months for treatment of tuberculosis. Serpiginous like choroiditis In patients from those regions where the incidence of 4. Retinitis and retinal vasculitis primary resistance to isoniazid is more than 4%, and in 5. Neuroretinitis and optic neuropathy those who come from regions with higher multidrug resistant strains, the use of a four-drug regimen should 6. Endophthalmitis and panophthalmitis be followed by consultation with an internist who has 7. Eale's disease expertise in the treatment of drug-resistant tuberculosis. 2. Ocular Investigations 2. Duration of Treatment a. Demonstration of AFB by microscope or culture of The exact duration of treatment and the endpoint for M. tuberculosis from the ocular fluids. stopping treatment for ocular tuberculosis is not known. b. Positive polymerase chain reaction from ocular Various authos have recommended four-drug therapy fluids for IS 6110 or other conserved sequences in M. for between 6 and 15 months, nearly 95% of patients tuberculosis genome. responding to treatment with the resolution of their 3. Systemic Investigations intraocular inflammation. The initial regimen consists of isoniazid, rifampicin, ethambutol, and pyrazinamide for a. Positive Mantoux reaction. 2 to 3 months and treatment with isoniazid and rifampin b. Evidence of healed or active tubercular lesion on continued for 9 to 12 months. Response to treatment is radiography of the chest. usually evident within 4 to 6 weeks. The CDC c. Evidence of confirmed active extrapulmonary recommends prolonged therapy for tuberculosis of any tuberculosis (either by microscopic examination or site that is slow to respond and thus the patients with by culture of the affected tissue for M. tuberculosis). intraocular TB may require prolonged therapy.

25 OCULAR TUBERCULOSIS DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

3. Immunosuppressive Agents 6. Ocular Side Effects of Anti-Tubercular Drugs Low-dose systemic corticosteroids used for 4 to 6 weeks, The ethambutol toxicity is dose-related and is rare if the along with multidrug ATT, may limit damage to ocular daily dose does not exceed 15 mg/kg. Of the patients tissues caused from delayed type hypersensitivity. receiving daily dose of 25 mg/kg or more, 1-2% Corticosteroids without concomitant ATT must be experience ocular toxicity.It l is known to cause optic avoided as they may promote multiplication of bacilli, neuritis, acquired red-green dyschromatopsia , central scotomas, disk edema, disk hyperemia, peripapillary leading to panophthalmitis or cause activation of latent splinter hemorrhages, optic atrophy and rarely, retinal systemic tuberculosis. edema and foveal pigmentary changes. The optic 4. Immunomodulatory Agents in Uveitis Patient neuritis is abrupt in onset and is generally seen at 3-6 with Positive PPD months of the onset of treatment .All patients should have a baseline ophthalmic examination including The positive tuberculin skin test indicates past (latent) or visual acuity, visual field, and color vision, If the dose present mycobacterial infection. A number of studies administered is more than 15 mg/kg/day, patients with have shown a high prevalence of Mantoux positivity in drug-resistant TB or TB requiring prolonged course of uveitis patients whose uveitis is unrelated to ethambutol should remain under ophthalmic tuberculosis. The anti TNF biological treatment for supervision. These patients should be examined every 2 uveitis or other autoimmune disorders can result in to 4 weeks, whereas for lower doses, follow-up every 3-6 flare-ups of the latent tuberculosis infection. months is adequate. In case of any ocular side effect, the The proposed treatment regimens for latent tuberculosis drug should be stopped immediately; following which (patients with positive PPD) are: 1) isoniazid 300 mg/ the vision usually improves. In cases where vision does not improve following discontinuation of therapy, day for 9 months,1 2) isoniazid twice weekly at a dose of parenteral hydroxycobalamine, 40 mg/ day over a 10- to 15 mg/kg where daily treatment is not possible, 3) 28-week period should be considered. Majority of rifampicin daily for 4 months where isoniazid cannot be symptoms resolve over a period of 3-12 months, used, and 4) rifampicin with pyrazinamide daily for 2 although permanent visual loss is also known to occur. months in situations where treatment period must be confined to 2 months. All these patients, irrespective of Isoniazid has been reported as a cause of optic neuritis age, need treatment if the reaction to 5 tuberculin units of and optic atrophy,albiet rarely. Recently rifampicin has been reported to induce neurodegredation in the optic PPD is > 10 mm or 2-5 mm in patients who are HIV nerve transection model. Rifabutin, a spiropiperidyl positive, who have recent contact with an infected derivative of rifamycin, is more effective than rifampicin person, or show evidence of old tuberculosis on chest x- against slow-growing mycobacteria, including M. ray.However, the treatment regimens for latent TB may avium-intracellulare, and has been extensively used in vary in geographical location and local physician should HIV-infected patients. This agent, especially when be consulted for the treatment. combined with clarithramycin or fluconazole, can cause 5. Drug-Resistant Tuberculosis severe acute anterior uveitis, including hypopyon uveitis, corneal endothelial deposits, and inflammatory There has been a decrease in the incidence of primary vitreous exudates and opacities. However, the drug- resistanct tuberculosis, but an increased occurrence of induced intraocular inflammation responds well to acquired resistance. Numerous factors, including poor topical corticosteroids. compliance, improper drug regimen, physician error in B. SURGICAL MANAGEMENT directing treatment or natural mutations, and often a combination of these factors may playa role in the Tubercular granulomas are quite amenable to medical development of drug-resistant tuberculosis. Use of management, provided it is initiated in timely manner. If multiple agents, with a minimum of three or four necessary local resection ,in case of anterior lesions ,and pars plana vitrectomy have proven to be efficacious in additional antituberculosis agents for a duration of 18 to non responsive lesions. 24 months, is recommended. The additional agents include rifabutin, fluoroquinolones, interferon-y, and linezolid; all of these agents have been tried for the “ Almighty first appeared as a mass radiant treatment of drug resistant tuberculosis. Recently the Every living being is his descendent CDC has published that during 2000-2004, of 17,690 TB We are all His flesh and blood, isolates, 20% were multidrug resistant and 2% were extensively drug resistant (XDR) that were resistant So how come some one is bad or good.” virtually to all second-line drugs, thus documenting the – Sant Kabeer Das existence of XDR TB as a emerging public health issue.

26 OBESITY AND EYE DISEASES DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

MAJOR REVIEW Obesity and Eye Diseases Dr. Rajpal Insaan, Dr. Sonia Bhargav, Dr Shibal Bhartiya

Obesity is a major public health problem, with reported a significantly positive association of IOP with prevalence increasing at staggering rates in many several factors including BMI 1 6 . A clear countries. The World Health Organization (WHO) pathophysiological explanation for the association of defines obesity as a body mass index (BMI) of 30 kg / m1 obesity with IOP and glaucoma is currently lacking. or greater, and overweight as individuals whose BMI Both the 'mechanical' and 'vascular' etiology theories of falls between 25 kg / m 1 and 29.9 kg/m1 . Different glaucoma may be related to obesity. With regards to the classification are used for some specific populations, mechanical theory, obesity has been postulated to exert such as Asian & children. In Asian populations, it has an effect on IOP by causing excessive intra orbital been proposed that a BMI of 25 kg/ m 1 or greater should adipose tissue, increased blood viscosity, increased be classified as obesity 1. episcleral venous pressure and impairment of aqueous outflow facility 17,18,19. On the other hand, the vascular The Current International Obesity Task Force estimates theory suggests that eyes with inherently poor vascular suggest at least 1.1 billion people are over weight world supply to the optic nerve head are more predisposed to wide, and 312 million of these are obese. The impact of damage by elevated or normal IOP 21. Increased obesity on health is widespread. Among different eye 2,3,4 oxidative DNA damage was found in the trabecular diseases, obesity has been associated cataract , age meshwork of glaucoma patients 22 and oxidative stress related maculopathy, diabetic retinopathy & glaucoma. has been postulated to cause proteasome failure and Obesity and Cataract :- induce trabecular meshwork degeneration leading to impairment of the ability of the tissue to modulate Obesity has been proposed to be risk factor for cataract outflow resistance 23. development, though the exact underlying mechanisms are unclear. Many studies have reported that over all Obesity and Age-Related Maculopathy: obesity, measured as BMI and abdominal adiposity, Age-Related Maculopathy remains the major blinding measured as waist to hip ratio (WHR) as independent condition in the elderly, despite the introduction of 2,3,4 risk factor for cataract . It was found that at any level of several new treatment modalities including BMI, a two unit higher level predicted a 12% increase photodynamic therapy, non - pharmacological 2 risk of cataract . Cortical and posterior subcapsular approaches to inhibit angiogenesis 24,25,26 and the use of cataracts have been most consistently associated with antioxidant supplement 27. The AREDS has reported 5,6,8 obesity . Several plausible pathophysiological cross-sectional association between higher BMI and mechanisms have been proposed to explain the more advanced ARM, as documented from fundus association of obesity and cataract. One theory suggests photographs 28. Obesity may increase systemic oxidative that leptin, a 16- kDa pleiotropic cytokine expressed and stress secondary to hyperleptinemia9,29,30. Oxidative 8 secreted mainly by adipocytes , is involved in the damage to lipids in the Bruch's membrane appears to be 7 molecular mechanisms underlying cataract formation. . important in the etiology of choroidal neovascular Individual with obesity exhibit hyperleptinemia and ARM31. In response to oxidative stress, the RPE cells 9,10 leptin resistance . The exact mechanist by which leptin may detach and migrate into the subretinal space or contributes in the process of cataractogenesis is still outer retina and secrete excessive vascular endothelial unclear. In Non-white population, lower BMI is also growth factor (VEGF), eliciting invasion of 11,12,13 associated with cataract formation . neovascularization in Bruch's membrane 31. Plasma Obesity and Glaucoma: fibrinogen and C-reactive protein are elevated in obese persons and may therefore be a potential link between Several studies have provided evidence in support of a obesity and ARM 32. positive association between obesity and intra ocular pressure, the strongest risk factor for glaucomatous optic Obesity and Diabetic Retinopathy: 14, 15 neuropathy (GON) . The Beaver Dam Eye Study Obesity (BMI > 31.0 kg/m1 for men and 32.1 kg/m1 for Address for Correspondence :- women) is found to be associated with progression and Dr. Rajpal Insaan severity of retinopathy in patients with type II DM 33. Additional Professor of Ophthalmology The concentration of VEGF has been found to be higher Vitreoretina Unit in the vitreous of eyes with proliferative diabetic Dr. R.P. Centre for Ophthalmic Sciences retinopathy 34. Serum VEGF and leptin levels has been AIIMS, New Delhi found to be elevated in obese persons 35.

27 OBESITY AND EYE DISEASES DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Obesity and other Eye Diseases: 18. Shiose Y: The aging effect on intraocular pressure in an apparently normal population. Arch Ophthalmol Various other ocular diseases associated with obesity 102:883-7, 1984. are central retinal vein occlusion, hypercoagulability 19. Shiose Y, Kawase Y: A new approach to stratified disorders, oculomotor nerve palsy, floppy eyelid normal intraocular pressure in a general population. syndrome. BIH, obstructive sleep apnea. Am J Ophthalmol 101:714-21, 1986. References: 20. Halpern DL, Grosskreutz CL: Glaucomatous optic neuropathy: mechanisms of disease. Ophthalmol Clin 1. James PT, Leach R, Kalamara E, et al: The worldwide North Am 15:61-8, 2002. obesity epidemic. Obes Res 9(Suppl 4):228S-33S, 2001. 21. Caulfield LE, West SK, Barron Y, et al: Anthropo status 2. Glynn RJ, Christen WG, Manson JE, et al: Body mass and cataract: the Salisbury Eye Evaluation. Am J Clin index. An independent predictor of cataract. Arch Nutr 69:237-42, 1999. Ophthalmol 113:1131-7, 1995. 22. Izzotti A, Sacca SC, Cartiglia C, et al: Oxidative deoxy- 3. Hiller R, Podgor MJ, Sperduto RD, et al: A longitudinal ribonucleic acid damage in the eyes of glaucoma study of body mass index and lens opacities. The patients. Am J Med 114:638-46, 2003. Framingham Studies. Ophthalmology 105:1244-50, 1998. 23. Caballero M, Liton PB, Epstein DL, et al: Protease 4. Jahn CE, Janke M, Winowski H, et al: Identification of inhibition by chronic oxidative stress in human metabolic risk factors for posterior subcapsular trabecular meshwork cells. Biochem Biophys Res cataract. Ophthalmic Res 18:112-6, 1986. Commun 308 52, 2003. 5. Kuang TM, Tsai SY, Hsu WM, et al: Body mass index 24. D' Amico DJ, Goldberg MF, Hudson H, et al: and age-related cataract: the Shihpai Eye Study. Arch Anecortave acetate as monotherapy for treatment of Ophthalmol 123:1109-14, 2005. subfoveal neo-vascularization in age-related macular degeneration: twelve-month clinical outcomes. 6. Leske MC, Wu SY, Hennis A, et al: Diabetes, Ophthalmology 110:2372-83, discussion 2384-5, 2003. hypertension, and central obesity as cataract risk factors in a black population. The Bardados Eye Study. 25. Ferris FL: A new treatment for ocular neovasculariz- Ophthalmology 106:35-41, 1999. ation. N Engl J Med 351:2863-5, 2004. 7. Gomez-Ambrosi J, Salvador J, Fruhbeck G: Is 26. Gragoudas ES, Adamis AP, Cunningham ET, et al: Pegaptanib for neovascular age-related macular hyperleptinemia involved in the development of age- degeneration. N Engl J Med 351:2805-16, 2004. related lens opacities? Am J Clin Nutr 79:888-9, author reply 889, 2004 8. Bengtsson B, Heijl A: A long-term 27. Hogg R, Chakravarthy U: AMD and micronutrient prospective study of factors for glaucomatous visual antioxidants. Curr Eye Res 29:387-401, 2004. field loss in patients ocular hypertension. J Glaucoma 28. Risk factors associated with age-related macular 14:135-8, 2005. degeneration. A case-control study in the age-related 9. Haynes WG: Role of leptin in obesity-related eye disease study: Age-Related Eye Disease Study hypertension. Exp Physiol 90:683-8, 2005. Report Number 3, Ophthalmology 107:2224-32, 2000. 29. Bouloumie A, Marumo T, Lafontan M, et al: Leptin 10. Narin F, Atabek ME, Karakukcu M, et al: The induced oxidative stress in human endothelial cells. association of plasma homocystenine levels with FASEB 1231-8, 1999. serum leptin and apolipoprotein B levels in childhood obesity. Ann Saudi Med 25:209-14, 2005. 30. Schorr U, Blaschke K, Turan S, et al: Relationship between angiotensinogen, leptin and blood pressure 11. Leske MC, Chylack LT, Wu SY: The Lens Opacities levels in young normotensive men. J Hypertens Case-Control Study, Risk factors for cataract. Arch 16:1475-80, 1998. Ophthalmol 109:244-51, 1991. 31. Spaide RF, Armstrong D, Browne R: Continuing 12. Chatterjee A, Milton RC, Thyle S: Prevalence and medical education review: choroidal neovascula- aetiology of cataract in Punjab. Br J Ophthalmol 66:35- rization in age-related macular degeneration-what is 42, 19 13. Mohan M, Sperduto RD, Angra SK, et al: the cause? Retina 23:595-614, 2003. India-US case-control study of age-related cataracts. 32. Valle V, Martos R, Gascon F, et al: Low-grade systemic India-US Case-Control Study Group. Arch inflammation, hypoadiponectinemia and a high Ophthalmol 107:670-6, 1989. concentration of leptin are present in very young obese 14. Jonas JB, Grundler AE, Gonzales-Cortes J, et al: children and correlate with metabolic syndrome. Pressure-dependent neuroretinal rim loss in normal- Diabetes Metab 3155-62, 2005. pressure glaucoma. Am J Ophthalmol 125:137-44, 1988. 33. Klein R, Klein BE, Moss SE: Is obesity related to 15. Leske MC, Wu SY, Hennis A, et al: Risk factors for microvascular and macrovascular complications in open-angle glaucoma. The Barbados Eye Study. Arch diabetes? The Wisconsin Epidemiologic Study of Ophthalmol 113:918-24, 1995. Diabetic Retinopathy. Arch Intern Med 157:650-6, 1997. 16. Klein BE, Klein R, Linton KL: Intraocular pressure in an 34. Aiello LP, Arrigg PG, et al: Vascular endothelial growth factor in ocular fluid of patients with diabetic American community. The Beaver Dam Eye Study. retinopathy and other retinal disorders. N Engl J Med Invest Ophthalmol Vis Sci 33:2224-8, 1992. 331:1480-7, 1994. 17. Bulpitt CJ, Hodes C, Everitt MG: Intraocular pressure 35. Uckaya G, Ozata M, Sonmez A, et al: Is leptin systemic blood pressure in the elderly. Br J associated with hypertensive retinopathy? J Clin Ophthalmol 717-20, 1975. Endocrinol Metab 85: 683-7, 2000.

28 CURRENT TRENDS IN MANAGEMENT OF AMBLYOPIA DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

CURRENT TREATMENT

Current Treatment for Diabetic Macular Oedema (DME) Dr. Rajpal Insaan

Abstract : Diabetic Retinopathy is an important cause of the Ophthalmologist. The Early Treatment Diabetes blindness in India and Indeed, the rest of the world.It is Retinopathy Study (ETDRS) defined CSME as the important to diagnose Diabetes Mellitus early so that following: early and proper control of blood sugar and other 1. Thickening of the retina at or within 500µm of the systemic factors can be done which will decrease the centre of the macula. complications related to DM .Inspite of advances in both pharmacological and surgical treatments of DR , it 2. Hard exudates at or within 500µm of the centre of continues to remain a threat to vision in epidemic the macula, associated with thickening of the retina, proportions..Management should include lifestyle any part of which is within 500µm of the centre of changes (yoga and meditation ) ,dietary change ,in the macula. (residual lipid exudates after addition to drugs and lasers . disappearance of retinal thickening is not CSME). Introduction: 3. Zone or zones of retinal thickening 1 disc diameter (DD) or larger, any part of which is within IDD of Macular oedema is the most common cause of moderate the center of the macula. visual loss in diabetic patients. Blindness due to diabetic retinopathy can be avoided if treated early. Complete management of DME involves thorough evalution, medical and ocular management. Frequency of DME is high in the diabetic population. According to the Wisconsin Epidemiological Study of EVALUTION Diabetic Retinopathy, the four-year incidences of Systemic Evalution clinically significant DME are 4.3 % for the younger onset It should be a routine practice to contact an group, 2.9% for the older onset and 5.1% for those taking endocrinologist. Blood glucose, serum lipids, blood insulin. pressure and HbA1C should be checked.Evaluation of Pathophysiology: kidney function is also essential because presence of Pathophysiology of DME is not known exactly ,although gross protienuria at baseline has been reported to be there are several hypothesis.Electrolyte imbalance associated with 95% increased risk of developing DME caused by the high aldose reductase levels leads to cell among Type I patients in the WESDR . death ,especially retinal pericytes which causes Ocular Evalution microaneurysm formation.Thickening of capillary Stereoscopic examination of the macular region at the basement membrane and increased deposition of slit lamp with a contact lens, Fluorescein angiography exracellular matrix also results in abnormal retinal and OCT are a must to evaluate a diabetic macular hemodynamics.Breakdown of the inner blood-retinal oedema patient. barrier results in acumulation of exreacellular fluid ,which manifests as DME. Diagnosis of DME is clinical, based on stereoscopic examination of the macula. Fluorescein angiography There has been various factors like VEGF which have helps to differentiate focal from diffuse macular oedema been implicated in inducing neovascularisation. and rule out macular ischemia. It is however not Clinically significant DME (CSME) requires combined required for making the diagnosis. OCT rules out or evaluation and management by the Endocrinologist and demonstrates macular traction and allows anatomic and objective evaluation of changes following therapy. Address for correspondence Correct evaluation of DME is not possible without an Dr. Rajpal Insan OCT examination. Best corrected visual acuity should be Additional professor of Ophthalmology recorded in each visit. Vitreoretina Unit. Dr. R.P. Centre for Ophthalmic Sciences Medical Treatment AIIMS, New Delhi It should be our routine practice to contact an E-mail: [email protected] endocrinologist to request optimization of the glycemic

29 CURRENT TRENDS IN MANAGEMENT OF AMBLYOPIA DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008 control and start local treatment of CSME only when the the macula, associated with thickening of the retina, HbA1C is 7.5% or less. any part of which is within 500µm of the centre of A) Blood glucose control- Optimum glycemic control is the macula. (residual lipid exudates after fundamental1 in the management of DME. In disappearance of retinal thickening is not CSME). Diabetes Control and Complications Trial (DCCT), 3. Zone or zones of retinal thickening 1 disc diameter intensive management of hyperglycemia decreased (DD) or larger, any part of which is within IDD of the risk of DME .Studies have also shown that the center of the macula. persons with type 2 diabetes and CSME refractory to Complete management of DME involves thorough treatment have higher HbA1C than patients who evalution, medical and ocular management. respond to the laser therapy. EVALUTION B) Serum lipids. In the ETDRS, elevated serum lipids were associated with higher prevalence of retinal Systemic Evalution hard exudates. Serum lipids should be checked and It should be a routine practice to contact an the patient should be referred in case of endocrinologist. Blood glucose, serum lipids, blood hyperlipidemia. Treatment of dyslipidemia pressure and HbA1C should be checked.Evaluaion of provides cardiovascular benefits in patients with kidney function is essential as gross protienuria is diabetes, but whether it provides vision benefits associated with a 95% prevalance of DME in Type I remains to be determined. patients in the WESDR.In WESDR ,hiher serum C) Blood pressure. The United Kingdom Prospective cholesterol has been associated with increased risk of Diabetes Study (UKPDS) demonstrated that the hard exudates.Lending further support to this is Gupta intensive treatment of arterial hypertension et al's observation that redution in edema,subfoveal reduced the deterioration of visual acuity in 47% lipid migration and severity of hard exudates following patients, mainly because the incidence of DME was use of lipid lowering drug atorvastatin as an adjuvant to lower in the intensive treatment group. This macular photocoagulation. beneficial effect was independent of the glycemic Ocular Evalution control. Stereoscopic examination of the macular region at the slit D) Aspirin therapy and smoking cessation also are lamp with a contact lens, Fluorescein angiography and recommended by some. OCT are a must to evaluate a diabetic macular oedema Ocular management patient. Based on binocular biomicroscopic examination, Diagnosis of DME is clinical, based on stereoscopic fluorescein angiography, OCT and best corrected visual examination of the macula. Fluorescein angiography acuity, DME can be classified in various categories for helps to differentiate focal from diffuse macular oedema treatment planning: and rule out macular ischemia. It is however not required for making the diagnosis. OCT rules out or Type 1. DME with focal leakage on fluorescein Macular demonstrates macular traction and allows anatomic and edema is the most common cause of moderate visual loss objective evaluation of changes following therapy. in patients and is the second cause of severe vision loss in Correct evaluation of DME is not possible without an patients with diabetes. OCT examination. Best corrected visual acuity should be Frequency of DME is high in the diabetic population. recorded in each visit. According to the Wisconsin Epidemiological Study of Medical Treatment Diabetic Retinopathy, the four-year incidences of clinically significant DME are 4.3 % for the younger It should be our routine practice to contact an onset group, 2.9% for the older onset and 5.1% for those endocrinologist to request optimization of the glycemic taking insulin. control and start local treatment of CSME only when the HbA1C is 7.5% or less. Clinically significant DME (CSME) requires combined evaluation and management by the Endocrinologist and A) Blood glucose control- Optimum glycemic control is 1 the Ophthalmologist .The Early Treatment Diabetes fundamental in the management of DME. In Retinopathy Study (ETDRS) defined CSME as the Diabetes Control and Complications Trial (DCCT), following: intensive management of hyperglycemia decreased the risk of DME. Studies have also shown that 1. Thickening of the retina at or within 500µm of the persons with type 2 diabetes and CSME refractory to centre of the macula. treatment have higher HbA1C than patients who 2. Hard exudates at or within 500µm of the centre of respond to the laser therapy.

30 CURRENT TRENDS IN MANAGEMENT OF AMBLYOPIA DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

B) Serum lipids. In the ETDRS, elevated serum lipids Clinically significant DME (CSME) requires combined were associated with higher prevalence of retinal evaluation and management by the Endocrinologist and hard exudates. Serum lipids should be checked and the Ophthalmologist .The Early Treatment Diabetes the patient should be referred in case of Retinopathy Study (ETDRS) defined CSME as the hyperlipidemia. Treatment of dyslipidemia following: provides cardiovascular benefits in patients with 1. Thickening of the retina at or within 500µm of the diabetes, but whether it provides vision benefits centre of the macula. remains to be determined. 2. Hard exudates at or within 500µm of the centre of C) Blood pressure. The United Kingdom Prospective the macula, associated with thickening of the retina, Diabetes Study (UKPDS) demonstrated that the any part of which is within 500µm of the centre of intensive treatment of arterial hypertension reduced the macula. (residual lipid exudates after the deterioration of visual acuity in 47% patients, disappearance of retinal thickening is not CSME). mainly because the incidence of DME was lower in the intensive treatment group. This beneficial effect 3. Zone or zones of retinal thickening 1 disc diameter was independent of the glycemic control. (DD) or larger, any part of which is within IDD of the center of the macula. D) Aspirin therapy and smoking cessation also are recommended by some. Complete management of DME involves thorough evalution, medical and ocular management. Ocular management EVALUTION Based on binocular biomicroscopic examination, fluorescein angiography, OCT and best corrected visual Systemic Evalution acuity, DME can be classified in various categories for It should be a routine practice to contact an treatment planning: endocrinologist. Blood glucose, serum lipids, blood Type 1. DME with focal leakage on fluorescein pressure and HbA1C should be checked. angiography and without vitreous traction on OCT. Ocular Evalution These patient usually show hard exudates organized in Stereoscopic examination of the macular region at the slit the form of circinate ring that involves or threatens the lamp with a contact lens, Fluorescein angiography and centre of the macula, with visible microaneurysms that OCT are a must to evaluate a diabetic macular edema leak on fluorescein angiography. patient. These patients are treated with focal laser Diagnosis of DME is clinical, based on stereoscopic photocoagulation according to the guidelines examination of the macula. Fluorescein angiography recommended by the Early Treatment Diabetes helps to differentiate focal from diffuse macular edema Retinopathy Study (ETDRS). and rule out macular ischemia. It is however not Type 2. Diffuse DME without vitreous traction on OCT. required for making the diagnosis. OCT rules out or demonstrates macular traction and allows anatomic and FA demonstrates diffuse leakage and may show a cystic objective evaluation of changes following therapy. pattern. The retina may be markedly thickened. Hard Correct evaluation of DME is not possible without an exudates may be absent and, if present, do not show a OCT examination. Best corrected visual acuity should be circinate pattern. Although the ETDRS recommended recorded in each visit. laser treatment for any type of clinically significant DME, most clinicians now believe and consider other Medical Treatment treatments for these patients. It should be our routine practice to contact an Macular edema is the most common cause of moderate endocrinologist to request optimization of the glycemic visual loss in patients and is the second cause of severe control and start local treatment of CSME only when the vision loss in patients with diabetes. HbA1C is 7.5% or less. A) Blood glucose control- Optimum glycemic control is Frequency of DME is high in the diabetic population. 1 According to the Wisconsin Epidemiological Study of fundamental in the management of DME. In Diabetic Retinopathy, the four-year incidences of Diabetes Control and Complications Trial (DCCT), clinically significant DME are 4.3 % for the younger intensive management of hyperglycemia decreased onset group, 2.9% for the older onset and 5.1% for those the risk of DME .Studies have also shown that taking insulin. persons with type 2 diabetes and CSME refractory to

31 CURRENT TRENDS IN MANAGEMENT OF AMBLYOPIA DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

treatment have higher HbA1C than patients who c) Intravitreal injection of anti-VEGF agents respond to the laser therapy. d) Vitrectomy-controversial B) Serum lipids. In the ETDRS, elevated serum lipids Type 3. Tractional diabetic macular edema. were associated with higher prevalence of retinal hard exudates. Serum lipids should be checked and The OCT will show anomalies at the vitreoretinal the patient should be referred in case of interphase, with vitreous traction ( anteroposterior or hyperlipidemia. Treatment of dyslipidemia tangential). Treatment for this type of DME is surgical provides cardiovascular benefits in patients with (vitrectomy with removal of the posterior hyaloid diabetes, but whether it provides vision benefits membrane, with or without peeling of the internal remains to be determined. limiting membrane). C) Blood pressure. The United Kingdom Prospective Type 4 . Ischemic macular edema. Diabetes Study (UKPDS) demonstrated that the This is an angiographic diagnosis. Fluorescein intensive treatment of arterial hypertension reduced angiography will show an irregular broadening of the the deterioration of visual acuity in 47% patients, foveal avascular zone. Late leakage of dye from the floor mainly because the incidence of DME was lower in of the avascular zone may be observed in some cases, the intensive treatment group. This beneficial effect probably generated at the level of the retinal pigment was independent of the glycemic control. epithelium. Some authors recommend laser D) Aspirin therapy and smoking cessation also are photocoagulation for these eyes. The treatment however recommended by some. remains controversial. 2,3,4 Ocular management Intravitreal injection of 4mg of Triamcinolone Based on binocular biomicroscopic examination, Intravitreal injection of 4mg of Triamcinolone (IVTA) is fluorescein angiography, OCT and best corrected visual effective in reducing DME in approximately 60% of acuity, DME can be classified in various categories for cases, usually with improvement in visual acuity. Its treatment planning: action may be the result of inhibition of the arachidonic acid pathway and down regulation of the production of Type 1. DME with focal leakage on fluorescein vascular endothelial growth factor. However, the angiography and without vitreous traction on OCT. beneficial effect of IVTA on vision and macular thickness These patient usually show hard exudates organized in is transitory and rarely persists beyond 3 months. the form of circinate ring that involves or threatens the It has been demonstrated that measurable centre of the macula, with visible microaneurysms that concentrations of triamcinolone last no more than 3 leak on fluorescein angiography. months in non vitrectomized eyes. Furthermore, is not These patients are treated with focal laser without complications, mainly raised intraocular photocoagulation according to the guidelines pressure and cataract. In the majority of cases, ocular recommended by the Early Treatment Diabetes hypertension can be managed with topical medication, Retinopathy Study (ETDRS). but some patients particularly the younger ones are Type 2. Diffuse DME without vitreous traction on OCT. refractory to glaucoma medication and may require FA demonstrates diffuse leakage and may show a cystic trabeculectomy. IVTA may be repeated, reproducing the pattern. The retina may be markedly thickened. Hard initial beneficial effect on vision and macular thickness, exudates may be absent and, if present, do not show a but with lesser efficacy. circinate pattern. Although the ETDRS recommended A small pilot study5 suggests that intravitreal injection of laser treatment for any type of clinically significant the solution of prednisolone sodium succinate may be a DME, most clinicians now believe and consider other good alternative in eyes with macular edema without treatments for these patients. intraocular pressure rise. Optimization of the glycemic control, treatment of Subtenon triamcinolone injections6 hypertension and lipid abnormalities are of most Subtenon triamcinolone injections are used by many for important in these patients. Therapeutic options(other the treatment of CSME. Although complications are than laser photocoagulation) for these patients are lower than those observed with intravitreal injection, its a) Intravitreal injection of 4mg of Triamcinolone effectiveness is also lower, since the intravitreal b) Subtenon triamcinolone injections injections provide a higher concentration of the drug at the retina.

32 CURRENT TRENDS IN MANAGEMENT OF AMBLYOPIA DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Intravitreal Bevacizumed (avastin)7,8 REFERENCES It is an humanized monoclonal antibody against VEGF. 1. Furlani BA, Meyer CH, Rodrigues EB, Maia M, Farah Avastin has been used with good and sometimes ME, Penha FM, Holz FG.Emerging pharmaco- spectacular results, in choroidal neovascularitization therapies for diabetic macular edema.Expert Opin associated with age-related macular degeneration and Emerg Drugs. 2007 Nov;12(4):591-603. Review. macular edema secondary to retinal vein thrombosis. Avastin has been used also in DME. Avastin could be 2. Nicolò M, Nasciuti F, Lai S, Ghiglione D, Borgia L, considered as initial treatment for diffuse diabetic Calabria Intravitreal triamcinolone acetonide as macular edema. primary treatment for diffuse diabetic macular 9,10 e d e m a : a p r o s p e c t i v e n o n c o m p a r a t i v e Vitrectomy. interventional case series.Eur J Ophthalmol. 2006 The role of vitrectomy in eyes with diffuse DME and no Jan-Feb;16(1):129-33 detectable anomalies at the vitreomacular interphase in OCT is controversial and should only be considered as a 3. Audren F, Lecleire-Collet A, Erginay A, Haouchine last resort in cases that did not respond to any of the B, Benosman R, Bergmann JF, Gaudric A, Massin therapeutic modalities mentioned previously. Surgery P.Intravitreal triamcinolone acetonide for diffuse can be affective even in eyes with posterior vitreous diabetic macular edema: phase 2 trial comparing 4 detachment, but this indication is controversial. It is mg vs 2 mg.Am J Ophthalmol. 2006 Nov;142(5):794- known that eyes with apparent total posterior vitreous 99. detachment may have remnants of vitreous cortex 4. Longo A.Intravitreal triamcinolone for diffuse adherent to the internal limiting membrane. ILM peeling is being considered recently in vitrectomy for diabetic diabetic macular oedema.Br J Ophthalmol. 2006 macular edema. Sep;90(9):1079-80. Future options 5. La Heij EC, Lundqvist IJ, Berendschot TT, Hardy E, Liem AT, Hendrikse F.Intravitreal prednisolone Several therapies, currently under investigation, may have role in treatment of DME in the future. sodium succinate reduces diabetic macular edema without intraocular pressure rise. Am J Ophthalmol. A) PORSUDEX (Allergan). This small device can be 2007 Jan; 143(1):176-8. easily implanted as an office procedure. The device provides extended release of dexamethasone, a 6. Toda J, Fukushima H, Kato S.Injection of glucocorticoid steroid several times more potent triamcinolone acetonide into the posterior sub-tenon than triamcinolone. IT has shown promising results capsule for treatment of diabetic macular in refractory DME. edema.Retina. 2007 Jul-Aug;27(6):764-9. B) Anti VEGF drugs for intravitreal administration 7. Kumar A, Sinha S.Intravitreal bevacizumab LUCENTIS (Genetech) and MACUGEN (pfizer). (Avastin) treatment of diffuse diabetic macular C) Inhibitor of protein Kinase C-B Ruboxistaurin. Oral edema in an Indian population.Indian J Ophthalmol. ingestion has demonstrated effective in limiting the 2007 Nov-Dec;55(6):451-5. progression of macular edema towards the center, in 8. Haritoglou C, Kook D, Neubauer A, Wolf A, comparison with controls. It is not cosualized as an Priglinger S, Strauss R, Gandorfer A, Ulbig M, effectiveness method for treatment established diffuse DME. Kampik A. Intravitreal bevacizumab (Avastin) therapy for persistent diffuse diabetic macular DME results from a series of biochemical and cellular edema.Retina. 2006 Nov-Dec;26(9):999-1005. changes, causing progressive leakage and exudation. Focal and grid photocoagulation remains the standard 9. Yanyali A, Horozoglu F, Celik E, Nohutcu AF.Long- care for diabetic maculopathy. However, the availability term outcomes of pars plana vitrectomy with of new agents raises the possibility of improvements, if internal limiting membrane removal in diabetic significant benefits can be validated in randomized macular edema.Retina. 2007 Jun; 27(5):557-66. clinical trials. Posterior vitreous attachments play a 10. Helbig H. Surgery for diabetic retinopathy. critical role through several mechanical or physiological mechanisms. Vitrectomy without ILM removal seems to Ophthalmologica. 2007; 221(2):103-11. Review. be effective in reducing the retinal thickness and Bloomgarden ZT Screening for and managing improving visual acuity. A combination of laser, diabetic retinopathy: current approaches.Am J pharmacological and surgical treatment modalities may Health Syst Pharm. 2007 Sep 1; 64(17 Suppl 12):S8-14. be necessary to maintain central vision in eyes with DME.

33 ROLE OF SYSTEMIC ACYCLOVIR IN RECURRENT DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

ORIGINAL ARTICLE

THE ROLE OF SYSTEMIC ACYCLOVIR IN RECURRENT CASES OF DISCIFORM KERATITIS

Dr. Kirti Jain, Dr. A.K. Sood, Dr. Suresh Chandra, Dr. Sandeep Kumar, Dr. V. K. Malik, Dr. Sanjiv Kumar, Dr. Charu Jain, Dr. Reny Kamboj

Subharti Institute of Medical Sciences, Delhi Haridwar by Pass Road, N.H. 58 Meerut (U.P)

Abstract Background & Objectives: The role of systemic acyclovir, if any, in recurrent cases of Disciform Keratitis, in addition to topical steroids and antiviral was assessed in this study. Material & Methods: We examined the recurrence rate of herpetic disciform keratitis in 15 patients (group A) treated prophylactically with long-term systemic acyclovir (400 mg twice a day) for a period of one year and compared it with that of 15 patients with no prophylactic therapy (group B). These groups of patients were followed up for a further period of 1 year after stopping treatment for any evidence of recurrence. Results: Patients of Group A, who were kept on systemic acyclovir therapy 400 mg twice a day for a period of 1 year, only one patient experienced a single recurrent episode of disciform keratitis while other remained clinically asymptomatic. However, recurrence rate increases to 4 (26.66%) during follow up period of 1 year in the same group of patient. In striking contrast 5 recurrences (30%) occurred in the 15 patients of group B receiving placebo therapy; which increases to 10 (66.66 %) recurrences during follow up period of 1 year. Discussion & Conclusion: The long-term use of oral acyclovir may be of benefit in the prevention of recurrences, and hence may reduce the blinding complications of this disease. Systemic acyclovir therapy has a potential role in the management of recurrent cases of disciform keratitis. A study with a larger sample size is needed to validate the above results. Key words: acyclovir, dexamethasone, Disciform Keratitis, Herpes simplex virus.

Introduction: dormant in the trigeminal ganglion and the other Recurrent corneal infection by the herpes simplex virus ganglion, until unknown triggers reactivates it, causing a (HSV) is a leading cause of corneal blindness, not only in recurrence of epithelial, stromal or lid disease. To assess the developed countries but also in the developing whether antiviral treatment can prevent recurrences of world1, 2. The prevalence of HSV keratitis, reported by disciform keratitis, we conducted a randomized clinical Pramod et al2 in south India is 7.8%.Dendritic keratitis trial in which oral acyclovir, 400 mg twice daily for 1 (68%) was the commonest presentation followed by year, was compared with placebo in immunocompetent disciform keratitis (28%). Often, the primary herpetic individuals who had a history of an episode of HSV lesions disappear, leaving the cornea clear. The virus lies disciform keratitis. Material and method: Address for Correspondence :- Dr. Kirti Jain In medical record of 30 consecutive patients referred to Department of Ophthalmology eye OPD of Subharti Medical College, Meerut, between Subharti Institute of Medical Sciences Delhi Haridwar By Pass Road, N.H. 58, Meerut (U.P) January 2004 to Dec 2006 and subsequently diagnosed as E-mail:jainmanish45@yahoocom recurrent disciform keratitis; on the basis of prior

34 ROLE OF SYSTEMIC ACYCLOVIR IN RECURRENT DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

episode of herpetic disciform keratitis within the Table 1. Recurrence of Stromal Keratitis Within Patient preceding year; were analyzed. The diagnosis is made Subgroups During 12-Month Treatment Period Among Patients With History of Stromal Keratitis clinically by the presence of characteristic disc like or diffuse stromal edema, folds in descemet's membrane Subgroup Acyclovir group Placebo group with or without keratic precipitates (KPs) or loss of Total no. of Total no. of No. Recurrence No. Recurrence corneal sensation and the absence of other causes of stromal keratitis. Patients were treated with topical Sex: corticosteroids (Dexamethasone 0.1%) eye drops four Male 9 0 8 3 times daily and acyclovir eye ointment 5% five times Female 6 1 7 2 daily. All these patients who had an episode of active Age: herpetic disciform keratitis within a year after the 15 - 24 2 0 1 0 primary episode were divided into two group's .Group 25 - 34 5 1 4 2 A patients received oral acyclovir, 400 mg twice a day for one year versus placebo therapy for group B. These 35 - 44 5 0 5 2 groups of patients were followed up for a further period 45 - 54 2 0 3 1

of 1 year after stopping treatment for any evidence of –> 55 1 0 2 0 recurrence. Result: Table 1. Recurrence of Stromal Keratitis Within Patient Subgroups During Follow-up Period of 1 year Among 30 patients were diagnosed with recurrent disciform Patients With History of Stromal Keratitis keratitis during the study period. There were 22 males Subgroup Acyclovir group Placebo group (73.33 %) and mean age of the entire group was 34 yrs (15-60 yrs) , thus majority of patient were young, adult Total no. of Total no. of No. Recurrence No. Recurrence males. In our study there was no clear seasonal pattern. The male female ratio being 2.7:1. 70 % of patients give Sex: history of fever malaise followed by gradual Male 9 2 8 6 diminutions of vision .The clinical features was typically Female 6 2 7 4 stromal oedema, epithelial oedema, and descemet's Age: membrane folds. As the intense stromal oedema can 15 - 24 2 0 1 0 mask KPs they were observed only in 10 eyes. Patients of Group A who were kept on systemic acyclovir therapy 25 - 34 5 2 4 4 for a period of 1 year, only one patient experienced a 35 - 44 5 1 5 5 single recurrent episode of disciform keratitis while on 45 - 54 2 1 3 1 400 mg twice a day of acyclovir therapy, while other > 55 1 0 2 0 remained clinically asymptomatic during the period of – systemic antiviral therapy. However, total 4 (26.66%) By applying z- test for proportion, significant difference recurrences noted during follow up period of 1 year in (p<0.5) was observed for each age group between patients of group A. While group B patient's show 5 acyclovir group and placebo group during 12 months recurrences (30%) within a period of 1 year after the treatment period and follow up period of 1 year. initial episode and 10 recurrences (66.66%) during Discussion: follow up period of 1 year..Table 1 Recurrent herpes simplex viral infection of the eye is an

35 ROLE OF SYSTEMIC ACYCLOVIR IN RECURRENT DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

important cause of ocular morbidity. The diagnosis of developing recurrent attack of disciform keratitis, the HSV disciform keratitis is purely clinical3. In routine form of herpetic eye disease associated with loss of visual clinical practice virological investigations like acuity. The clear benefit of oral acyclovir in preventing polymerase chain reaction are not easily available or disciform keratitis among patients with a history of prior feasible to the patient. stromal. The exact pathogenesis of HSV disciform keratitis is The role of systemic acyclovir in recurrent cases of debatable but it is believed to result from either a direct disciform keratitis keratitis identifies these patients as an infection of the endothelial cells or because of a delayed important target population for suppressive therapy. hypersensitivity reaction to HSV antigen expressed on Thus, although preventive antiviral therapy could be 4 offered to all patients who are at risk of a recurrence, endothelial cells . The management of HSV disciform targeting younger people with prior stromal disease keratitis is with topical Corticosteroids and antiviral might be the most cost-effective way to reduce the agents. Corticosteroids prevent the immunological national and global burden of visual loss caused by HSV destruction of endothelial cells while acyclovir prevents disciform keratitis. reactivation of epithelial cells. Power et al5 demonstrated REFERENCES: a faster healing with a combination of acyclovir (3%) eye 1. Liesegang, TJ.Classification of herpes simplex virus ointment and betamethasone (0.01%) eye drop, compare keratitis and anterior uveitis.Cornea 1999;18:127- to acyclovir and a placebo in herpetic disciform keratitis. 43. In adult recurrence rate of herpetic keratitis are about 2. Pramod NP, Rajendran P, kannan KA. Herpes 25% within a year and 33% within 2 years 6. saini et al7 simplex keratiris in South India.Aclinico-virological demonstrated recurrence rate of herpetic keratitis 37.5% correlation.jp J Ophthalmology 1999:43:303-7. at one year after first episode and 50% at 2 years. In the 3. Pepose JS. Herpes Simplex keratitis: role of viral present series recurrence rate of disciform keratitis in infection versus immune response.Surv acyclovir treated patients (6.66%) versus placebo (30%) Ophthalmol 1991; 35:345-52. within one year. However, total 4 (26.66%) recurrences 4. Leibowitz HM, Koleini B.Herpes Simplex noted during follow up period of 1 year in acyclovir keratitis.Clinical diagnosis and management.Ed group and 10 recurrences (66.66%) in placebo group. Leibowitz HM Waring GO 111.Philadelphia This was comparable with other study. Rodrequez et al8 1998:662. showed prevention of recurrence on long term use of 5. Power WJ, Hilleri MP, Benedict-Smith A, Column acyclovir 600-800 mg/ day. Herpetic eye disease study - LM. Br J Ophthalmology.1992 Dec; 76 (12):711-3. acyclovir. A pilot study to assess the role of systemic 6. klein RJ. Pathogenetic mechanisms of recurrent acyclovir in recurrent cases of disciform keratitis herpes simplex virus infection.Arch Virol 1976; 51:1- prevention trial9, demonstrated oral acyclovir twice 3. daily for a period of 1 year or longer reduces the rate of 7. Saini JS, Agarwala R. Clinical pattern of recurrent recurrence of stromal keratitis by about 50%. This trial of herpes simplex keratitis. Indian J Ophthalmol 1999; 30 patients demonstrated that oral acyclovir safely and 47:11-14. effectively suppresses recurrences of HSV eye disease 8. Herpetic Eye Disease Study Group. Acyclovir for during a 12-month treatment period and during follow the prevention of recurrent herpes simplex virus eye up period of 1 year. In summary, patients who have had disease. N Engl J Med. 1998; 339:300-306. stromal keratitis may have the greatest opportunity for 9. Rodriguez A, Power WJ, Neves RA, Foster CS. Doc benefit. These individuals are at the greatest risk for ophthalmology.1995; 90 (4):331- 40.

36 THE SCIENCE OF SPIRITUALITY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

THE SCIENCE OF SPIRITUALITY

The Science of Spirituality Dr Prashaant Chaudhry1, Dr Rajpal Insaan1, Dr Vidya Nair1, Dr Vinod Kochupillai2, Dr S C Manchanda3, Dr R L Bijlani4 1Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS 2Ex Chief IRCH, AIIMS 3Ex HOD, Cardiology Dept., AIIM 4Ex HOD, Dept of Physiology, AIIMS

India has a large heritage of spirituality of which we are the relaxation response may reduce adrenergic end- all proud. The past decade has seen a rapid spread of organ responsiveness. The mechanism for such a change spirituality, yoga and its healing effects into our living in this responsiveness is not clearly identified. These rooms. More and more people, especially youngsters, data are consistent with an earlier study suggesting that are taking to spirituality to deal with an increasingly subjects eliciting the relaxation response may be less stressful lifestyle. But have these techniques stood the responsive to stress. test of the rigorous scientific research done on them? We A landmark research on the physiological correlates of a aim to shed more light on this debate and present some Meditation technique was published in Science in 1972. of the published scientific data that has been researched This research found that the Transcendental Meditation at renowned institutions on this topic. technique produces a physiological state of restful Overview: How these practices differ from sleep or alertness. During the technique the physiology becomes simply closing eyes and relaxing deeply rested, as indicated by significant reductions in A frequently asked question is "how are the spiritual respiration, minute ventilation, tidal volume, and blood practices (yoga, meditation etc) different from our usual lactate, and significant increases in basal skin resistance forms of 'relaxing'?" (an index of relaxation). At the same time the physiology is alert rather than asleep, as indicated by an increased The state attained by these practices has been referred to abundance of alpha waves in the EEG. These findings as the "relaxation response"; defined by a set of led researcher Dr. Keith Wallace to conclude that restful integrated physiological changes that are elicited when a alertness is a fourth major state of consciousness, termed subject assumes a relaxed position in a quiet transcendental consciousness, which is physiologically environment, closes his or her eyes, engages in a distinct from ordinary waking, dreaming, and deep repetitive mental action, and passively ignores sleep. distracting thoughts , , , . These behaviors are associated with physiological changes that include decreased EEG patterns obtained in practitioners of Sudarshan oxygen consumption, heart rate (HR), arterial blood Kriya recorded a significant increase in beta activity in pressure (BP), respiratory rate, and arterial blood lactate the left frontal, occipital and midline regions. These , . In addition, there are slight increases in skeletal muscle findings are indications of heightened alertness. blood flow. All of these changes are different from those reported during sleep or quiet sitting. Beta•1 (12.5•18 Hz.) Physiological changes associated with the relaxation response In subjects eliciting the relaxation response more nor- epinephrine is required to produce the normal Mean Spectral Power in Various Bands in Control group compensatory increases in HR and BP. The elicitation of Beta•2 (18.5•30 Hz.)

Address for correspondence:- Dr Prashaant Chaudhry Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences (AIIMS), New Delhi - 110029 Bands in Control group Sudarshan Kriya Practitioners

38 THE SCIENCE OF SPIRITUALITY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Research has also been conducted to study the effect of practice of a yoga technique on Gene expression. Himani Sharma et al investigated the effect of regular practice of Sudarshan Kriya and Pranayam (SK&P- a type of Pranayama) on antioxidant enzymes, genes involved in oxidative stress, DNA damage, cell cycle control, aging, and apoptosis. Their results are summarized in the table below. Table -1 Parameter Controls (Mean ±S.E.M) (n=19) Practitioners (Mean ±S.E.M) (n=23). Glutathione (antioxidant) 76.7±4.06 nmol/ml 96.5±4.41 GSH-Peroxidase 5516±415 U/l 6923±382.3 U/l Superoxide Dismutase 173.6±7.6 U/ml 214.7±12.2 U/ml Glutathione S-transferase Higher (P=.034) Expression of antioxidant Significantly higher Cu-Zn SOD, Mn SOD, glutathione peroxidase, and catalase genes Antiapoptotic Cox-2 and HSP-70 Significantly higher (P=.035) and (P=.044) Life span of lymphocytes Prolonged by up-regulation of antiapoptotic genes

This study provided evidence suggesting that SK Plasma cortisol is a stress hormone. A study showed practice may exert effects on immunity, aging, cell that plasma cortisol decreased during Transcendental death, and stress regulation through transcriptional Meditation, whereas it did not change significantly in regulation. control subjects during ordinary relaxation. (Figure 2) Similarly, Li QZ et al studied the gene expression and EFFECT ON SYSTEMIC ILLNESSES gene regulation by mind-body interaction in Asian Qigong practitioners (pilot study). The gene expression Hypertension and Cardiovascular Disease of practitioners in contrast to normal healthy controls was characterized by enhanced immunity, As our lives become more stressful, we have seen an downregulation of cellular metabolism, and alteration abrupt increase in diabetes, hypertension and coronary of apoptotic genes in favor of a rapid resolution of artery disease. A number of researchers have studied the inflammation. Correlating with enhanced immunity effect of the relaxation response on established systemic reflected by microarray data, neutrophil phagocytosis diseases. Manchanda SC et al conducted a randomized, was significantly increased in Qigong practitioners. controlled trial of yoga (yoga, control of risk factors, diet Cortisol levels control and moderate aerobic exercise) versus conventional methods (i.e. risk factor control and 6.0 American Heart Association step I diet) in 42 )

l EyEyeses-C-Clolosesed Resest d / 5.5

g angiographically proven coronary artery disease male o m (

5.0

l patients. At one year, the yoga groups showed o s i t

r 4.5 significant reduction in number of anginal episodes per

o TM C

a 4.0 week, improved exercise capacity and decrease in body m s a l weight. Serum total cholesterol, LDL cholesterol and

P 3.5 triglyceride levels also showed greater reductions as 3.0 Before During After compared with control group. Revascularisation p < .01 procedures (coronary angioplasty or bypass surgery) (Figure 2) were less frequently required in the yoga group (one

39 THE SCIENCE OF SPIRITUALITY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008 versus eight patients; relative risk = 5.45; P = 0.01). Aivazyan TA et al in a randomized study on mild Coronary angiography repeated at one year showed that essential hypertension showed the treatment group to significantly more lesions regressed (20% versus 2%) have a significant reduction in systolic and diastolic and less lesions progressed (5% versus 37%) in the yoga blood pressures, peripheral vascular resistance, and group (chi-square = 24.9; P < 0.0001). hypertensive response to emotional stress, and an improvement in psychological adaptation, quality of Yogendra J et al also noted similar reductions in the LDL life, and capacity for work. cholesterol and triglyceride levels and increase in the HDL cholesterol levels, again in patients with There have however been a few studies that have not angiographically proven coronary artery disease. They shown a benefit. Van Montfrans GA et al reported 8 too noted regression of coronary lesions and weeks of relaxation therapy (one hour per week training improvement in myocardial function. These findings in muscle relaxation, yoga exercises, and stress have been confirmed by various other authors , . management) as being an ineffective method of Another study done by Chandra Patel el al on 194 lowering 24 hour blood pressure, being no more patients with two or more risk factors (BP > 140/90 mm beneficial than non-specific advice, support, and Hg, plasma cholesterol > 243 6 mg/100 ml and smoking reassurance--themselves ineffective as a treatment for >10 cigarettes/day) attempted to see the effect of the hypertension. This may have been due to a sub-optimal relaxation response in preventing cardiovascular intervention (only 1hr/week) failing to elicit the disease. They were randomly allocated to a group for relaxation response adequately. modification of behaviour or to serve as controls. The DIABETES treatment group had group sessions of one hour a week for eight weeks in which they were taught breathing Yoga asanas for 30-40 minutes a day were found to have exercises, relaxation, and meditation and about a beneficial effect on glycaemic control and improve managing stress. After eight weeks and eight months, nerve function in mild to moderate Type 2 diabetes with there was a significantly greater reduction in both sub-clinical neuropathy by Malhotra V et al . Right hand systolic and diastolic blood pressures in the group and left hand median nerve conduction velocity taught to relax compared with the control group, which increased significantly in the treatment group while the was maintained at four years follow up. Plasma nerve function parameters deteriorated in control group cholesterol concentration and the number of cigarettes over the period of study. smoked were lower in the treatment group at eight Studies on stress and psychiatric illnesses weeks and eight months, but not at the four year follow up. At four years, more subjects in the control group Nearly half of the world's population has some kind of reported having had angina and treatment for sleep disorder, with insomnia being the most common. hypertension and its complications. Incidence of Worry, anxiety, unconscious tensions and major or ischaemic heart disease, fatal myocardial infarction, or minor health problems can all affect the quality of sleep. electrocardiographic evidence of ischaemia was Sat Bir S Khalsa in his study of 'Treatment of Chronic significantly greater in the control group, thus Insomnia with Yoga' found a statistically significant establishing the beneficial effect of the intervention. improvement in the sleep parameters (Sleep efficiency Patel C et al compared the plasma rennin, plasma (SE), total sleep time (TST), total wake time (TWT), sleep angiotensin levels and blood pressure in untreated onset latency (SOL), wake time after sleep onset hypertensives between a group receiving biofeedback (WASO), number of awakenings, and sleep quality (relaxation and stress management techniques) and a measures were derived from sleep wake diary entries) control group. Both the biochemical parameters showed with yoga, comparable to that seen with somatic or a greater reduction in the biofeedback compared with cognitive relaxation techniques. the control group at eight weeks follow-up. The greater In India, people are known to turn to religion and reduction in blood pressure in the subjects in the biofeedback group compared with the control group prayer when disturbed or depressed. The efficacy of (11.0 mm Hg systolic and 8.8 mm Hg diastolic), Sudarshan Kriya (SK&Y) in melancholic depression persisting eight months after the training, suggests that was studied in a randomized fashion by N. relaxation-based behavioral methods might be offered Janakiramaiah et al . They hospitalized 45 patients and as a first-time treatment to patients with mild treated them with ECT, Imipramine or SKY. Remission hypertension.

40 THE SCIENCE OF SPIRITUALITY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008 rates at the end of the trial were 93, 73 and 67% in the severe anxiety attacks as well as suffering from ECT, IMN and SKY groups, respectively. Within the depression. Many of them were using alcohol as a form limitations of the design (lack of double blind of self medication, and were suffering from conditions), it was concluded that, although inferior to hypertension, diabetes, fatigue, anger, frustration and ECT, SKY was as efficacious as drugs in melancholia confusion. There was a highly significant drop in the and was an alternative as a first line treatment. Center for Epidemiology- Depression Scale (CED-S) scores were seen in all the participants. It was concluded In an attempt to demonstrate the effect of the relaxation that yoga provides a cheap, safe treatment, can be self response in depression at a molecular level, Nai-Ling administered, and provides a sense of self mastery, and Pan measured the serum cortisol, Brain-derived the benefits are broader than most areas tested. The neurotrophic factor (BDNF) levels and the Beck comorbidites of depression and alcohol dependence are Depression Inventory (BDI) scores in patients before and also addressed. after a 6 day course during which they practiced Sudarshan Kriya (SKY). BDNF is a key molecule in the Alcohol dependence neurotrophic hypothesis of depression in the recent A Vedamurthachar et al of NIMHANS studied the decade. Increase of BDNF levels in the brain and serum effect of Sudarshan Kriya and Yoga (SKY) on alcoholics seems to relate to antidepressive treatments in animal after a week of detoxification management. The patients models and human subjects. Results revealed that BDI and controls both completed the Beck Depression scores significantly decreased after the 6-day SKY Inventory and their plasma ACTH and cortisol (stress courses, and the decrease maintained for 12 weeks. The hormones) were measured before and at the end of 2 percent changes of serum BDNF levels after the courses weeks. In both groups, reductions in BDI scores were negatively correlated with serum BDNF levels occurred but significantly more so in SKY group. Likewise, in both groups plasma cortisol as well as before the course, indicating the normalization effects of ACTH fell after two weeks but significantly more so in the SKY courses. One episode of SKY group practice was SKY group. Reduction in BDI scores correlated with that found to increase serum BDNF levels but decrease in cortisol in SKY but not in control group. Reduction in serum cortisol levels. Increase of serum BDNF levels stress-hormone levels (cortisol and ACTH) along with sustained for at least 4 weeks and was not due to the BDI reductions were thought to possibly support a circadian rhythm. It concluded that the intervention of biological mechanism of SKY in producing beneficial SKY courses and practices has profound antidepressant effects. effects and the effects are highly correlated with its Tobacco deaddiction function in normalization of serum BDNF levels. In a study on tobacco de-addiction by Kochupillai V et al Post Traumatic Stress Disorder , 82 tobacco users were taught SK and P and advised to This is a state in which one is extremely over-whelmed practice regularly. Complete cessation of tobacco use by circumstances such as wars or natural calamities. was achieved in 17 of the 34 individuals who could be followed up to 6 months of practice. The Victim Services Center of Miami (VSCM) and the National Institute of Mental Health and Neuroscience CANCER conducted a collaborative study on the effects of It is believed that stress, a psychophysiological process, Sudharshan Kriya, on post-traumatic stress as applied to acts through the immune-neuroendocrine axis and survivors of the December 2004 Tsunami at a refugee affects cellular processes of body and immune functions, camp in Nagapattinam, India. All the yoga users leading to disease states including cancer. Cancer experienced a huge drop in scores for posttraumatic patients who had completed their standard therapy performed Sudarshan Kriya and Pranayam (SK&P). SK stress disorder and depression after just four days with and P increased natural killer (NK) cells significantly (P no change in the control group. Counseling provided <0.001) at 12 and 24 weeks of the practice compared to had no added benefits over the yoga training alone . baselinexxvi. Increase in NK cells at 24 weeks was An Australian Psychiatrist, Dr Janis Carter, studied the significant (P <0.05) compared to controls. The authors benefits of yoga on PTSD in 8 Australian Vietnam war feel that when confirmed in large and randomized veterans , aged between 50-60yrs old. At the beginning, studies, this result could mean that the regular practice the veterans were extremely stressed, and most could of SK and P might reduce the incidence and progression not sleep for more than a few hours at a time. They had of cancer.

41 THE SCIENCE OF SPIRITUALITY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

OPHTHALMOLOGY hypertension, coronary heart disease, diabetes mellitus, The head-stand (shirshasana) has been shown to cause a cerebrovascular disease, obesity, psychiatric illnesses transient and highly significant rise (doubling) of the like PTSD, insomnia, anxiety, depression and possibly in Intra Ocular Pressure (IOP). However, Mani Baskaran et cancer. These benefits have been shown both clinically al could not demonstrate a higher prevalence of ocular and at a genetic level. hypertensives in yoga practitioners regularly practicing It has been described by the practitioners to give an the head-stand, nor did the risk factors contributing to experience of joy, enthusiasm, love, belongingness and glaucoma show any correlation with magnitude of IOP fulfillment. In addition, they feel better able to cope with raise during the posture. On the other hand, Dimiter stress and have an increased concentration. These may Robert Bertschinger et al in a case report, showed be difficult to demonstrate in a randomized controlled progression of glaucoma in a 46 year old lady with fashion due to its more subjective nature, but is arguably Juvenile Open Angle Glaucoma (JOAG) who had just as important in attaining the WHO definition of recently started doing the headstand. This reversed on health (a state of physical, mental, social and spiritual cessation of the yoga asana. Glaucoma has been accepted well-being). by Yoga therapists as a contraindication to head-stand and they do not recommend this asana in these patients. The claims made by people who perform spiritual The effect of meditation and relaxation on glaucoma has practices and the wealth of data presented above put a not been well established. Stuart Brody et al strong case for adopting these practices in our lives. demonstrated and increase of 1.3 mmHg of IOP with Many of these results, you may agree, are almost too psychological stressors. Since meditation and relaxation good to be true. Maybe this is why our ancient yogi's and have been shown do decrease the stress response and learned ones put so much emphasis on adopting such a also increase the anti-oxidant levels, it was postulated lifestyle. It seems like we are making a full circle and the that meditation practices may be beneficial in glaucoma. way forward may indeed be by returning to our roots! Gert Kaluza et al studied the effect of a practice which Reference: involved special exercises in ocular relaxation and imagination of aqueous humor drainage in 23 patients of 1. H. Benson, J. F. Beary, M. P. Carol, Psychiatry 37, 37 Primary Open Angle Glaucoma. They detected a (1974). significant decrease in IOP. Twenty-four-hour profiles as 2. H. Benson, The Relaxation Response (Morrow, New well as the water drinking test also showed significant York, 1975). reductions of IOP across time. Medication dosage 3. R. K. Wallace and H. Benson, Sci. Am. 226, 84 decreased for 56% of the initially treated patients. The (February 1972). findings suggest that relaxation and visual imagery techniques can be beneficial in reducing elevated IOP 4. A. F. Wilson, Am. J. Physiol. 221, 795 (1971). levels in patients with open angle glaucoma. 5. R. K. Peters, H. Benson, J. M. Peters, Am. J.Public Yoga exercises for the eye improved the symptoms of Health 67, 954 (1977). dry eye significantly in computer users in a study by 6. H. Benson, N. Engl. J. Med. 296, 1152 (1977). Shirley Telles et al within 60 days of intervention. Yoga exercises were done for an hour, 5 days a week in subjects 7. Wallace, R. K. Physiological effects of and included yoga postures (asanas, 15 minutes), Transcendental Meditation.Science 167: 1751-1754, regulated breathing (pranayamas, 10 minutes), exercises 1970. for the joints (sithilikarana vyayama, 10 minutes), visual 8. M. Bhatia et al. Electrophysiologic evaluation of cleansing exercises (trataka, 10 minutes), and guided sudarshan kriya : an EEG, BAER, P300 study. Indian relaxation (15 minutes). The controls noted a worsening J Physiol Pharmacol 2003; 157 - 163. of symptoms in the same period. 9. Himani Sharma et al. Gene expression profiling in SUMMARY practitioners of Sudarshan Kriya. Journal of To summarize, the beneficial effects of yoga, pranayam Psychosomatic Research 64 (2008) 213-218. and meditation has been demonstrated at a molecular 10. Jevning, R.et al. Adrenocortical activity during level and it has been found to be useful in many diseases meditation, Hormones and Behavior 10(1): 54-60, believed to have a psychosomatic component including 1978.

42 THE SCIENCE OF SPIRITUALITY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

11. Manchanda SC et al. Retardation of coronary 21. Yoga: The Strongest Stretch. Psychology Today atherosclerosis with yoga lifestyle intervention. J Magazine, May/Jun 2007. Assoc Physicians India. 2000 Jul;48(7):687-94. 22. Carter J.J. et al. Two year study of four pilot studies Yogendra J et al. Beneficial effects of yoga lifestyle on using yoga as an adjunct to ordinary psychiatric reversibility of ischaemic heart disease: caring heart treatment in war veterans suffering from PTSD. project of International Board of Yoga. 2004. Vivekananda Yoga Research Institute and 12. Mahajan AS et al. Lipid profile of coronary risk RMIT University, Melbourne, Australia. subjects following yogic lifestyle intervention. 23. A. Vedamurthachar et al. Antidepressant efficacy Indian Heart J. 1999 Jan-Feb;51(1):37-40. and hormonal effects of Sudarshana kriya Yoga 13. Bijlani RL et al. A brief but comprehensive lifestyle (SKY) in alcohol dependent individuals. Journal of education program based on yoga reduces risk Affective Disorders 94 (2006) 249-253. factors for cardiovascular disease and diabetes 24. Kochupillai V et al. Effect of Rhythmic Breathing mellitus. J Altern Complementary Med. 2005 (Sudarshan Kriya and Pranayam) on Immune Apr;11(2):267-74. Functions and Tobacco Addiction. Annals of the 14. Chandra Patel et alTrial of relaxation in reducing New York Academy of Sciences. Volume 1056 coronary risk: four year follow up. British Medical Natural Products and Molecular Therapy Page 242- Journal Volume 290. 1103-6. 252, November 2005. 15. Patel C et al. Controlled trial of biofeedback-aided 25. Mani Baskaran et al. Intraocular Pressure Changes behavioural methods in reducing mild and Ocular Biometry during Sirsasana (Headstand hypertension.British Medical Journal 1981 Jun Posture) in Yoga Practitioners. Ophthalmology, 20;282(6281):2005-8. Aivazyan TA et al. Efficacy of Volume 113, Issue 8, Pages 1327-1332. relaxation techniques in hypertensive patients. 26. Dimiter Robert Bertschinger et al. Yoga can be Health Psychol. 1988;7 Suppl:193-200. dangerous-glaucomatous visual field defect 16. Van Montfrans GA. Relaxation therapy and worsening due to postural yoga. British Journal of continuous ambulatory blood pressure in mild Ophthalmology 2007;91:1413-1414. hypertension: a controlled study. BMJ 1990 May 27. Stuart Brody et al. Intraocular pressure changes: the 26;300(6736):1368-72. influence of psychological stress and the Valsalva 17. Malhotra V et al. Effect of Yoga asanas on nerve maneuver. Biological Psychology Volume 51, Issue 1 conduction in type 2 diabetes. Indian J Physiol October 1999, Pages 43-57. Pharmacol 2002 Jul;46(3):298-306. 28. Gert Kaluza et al. Stress reactivity of intraocular 18. Sat Bir S. Khalsa. Applied Psychophysiology and pressure after relaxation training in open-angle Biofeedback, Vol. 29, No. 4, December 2004. glaucoma patients. Journal of Behavoural Medicine. Volume 19, Number 6 / December, 1996. 19. N. Janakiramaiah et al. Antidepressant efficacy of Sudarshan Kriya Yoga (SKY) in melancholia: a 29. Shirley Telles et al. Effect of yoga on self-rated visual randomized comparison with electroconvulsive discomfort in computer users. Head Face Med. 2006; therapy (ECT) and imipramine. Journal of Affective 2: 46. Disorders 57 (2000) 255-259. 20. Nai-Ling Pan. The Role of Brain-Derived “Spiritual saints wherever they be Neurotrophic Factor in the Antidepressant Effects of Pray for every beings prosperity Sudarshan Kriya Yoga. Electronic Thesis and They love every one Dissertation System, P 72. http://etds.ncl.edu.tw/ And have enmity with none.” theabs/english_site/detail_result_eng.jsp?id=095 – Sant Gurmeet Ram Rahim Singh Insaan NCKU5116008.

43 HYDROCEPHALUS REQUIRING SHUNT SURGERY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

CASE REPORT Hydrocephalus Requiring Shunt Surgery as an Initial Presentation of Vogt-Koyanagi-Harada Syndrome Subrata Mandal, Anusha V, Rajpal Insaan, Pradeep Venkatesh, Satpal Garg Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS

Abstract: We report a female patient who presented with fever, chills and rigor and headache. On neurological consultation meningitis with hydrocephalus was diagnosed. Ophthalmological examination showed only bilateral disc edema. She underwent ventriculo-peritoneal shunt surgery for hydrocephalus. In postoperative period she developed signs of uveitis and after ophthalmological evaluation Vogt-Koyanagi-Harada syndrome was diagnosed. Inflammation as well as vision improved after treatment with pulse and oral corticosteroids.

Key words: Hydrocephalus; ventriculo-peritoneal shunt; Vogt-Koyanagi-Harada syndrome.

Vogt-Koyanagi-Harada syndrome (VKH) is an examination revealed bilateral disc edema. Noncontrast uveomeningoencephalitic syndrome involving the eye, computerized tomography scan of brain showed mild ear, meninges and integumentary system for which no dilated lateral and third ventricles. Third ventricle confirmatory diagnostic tests are available.1, 2 It usually transverse diameter was 8.2 mm and ventricular size affects persons in 2nd to 4th decades of life. Natural index was 37%. Computerized tomography scan course of VKH comprises of four different stages. Firstly, findings were suggestive of mild ventriculomegaly there is a prodromal stage manifested as headache, (Figure: 1A). She was diagnosed to have postmeningitic flulike symptoms, auditory symptoms and aseptic hydrocephalus and a ventriculo-peritoneal shunt meningitis. Then follows the ocular stage characterized surgery was performed on the 3rd week of illness for the by panuveitis with exudative retinal detachment and same. She was put on antibiotics and anticonvulsant. optic disc edema. In convalescent stage poliosis, vitiligo Post shunting surgery cranial CT scan showed of skin and limbal area, depigmentation of retinal pigment epithelium (RPE), alopecia appears. Lastly resolution of ventriculomegaly (Figure: 1B). In post chronic or recurrent stage manifests. We herein report a operative period she developed redness of the both the patient who underwent shunt surgery for eyes with pain and progressive dimness of vision. A hydrocephalus secondary to meningitis of unknown diagnosis of uveitis was made and referred to our uvea etiology and who subsequently developed typical clinic. features of VKH. Case Report A 27 year old female without any known systemic illness developed sudden onset fever with chills and rigor associated with headache, nausea and vomiting. She sought neurology consultation elsewhere. A series of investigations were done to rule out tuberculosis and connective tissue disorders. Ophthalmological Figure 1A, B: pre and post shunt surgery CT scan of brain showing decrease in ventricular size. Subrata Mandal, Anusha V, Rajpal Insaan, Pradeep Venkatesh, Satpal Garg Dr. Rajendra Prasad Centre for Ophthalmic Sciences, During first ophthalmological examination best AIIMS corrected visual acuity was 6/18 in both eyes. Poliosis New Delhi was present in both the eyes (Figure: 2).

44 HYDROCEPHALUS REQUIRING SHUNT SURGERY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Fundus fluorescein angiography revealed multiple pinpoint areas of hyperfluorescence suggestive of serous detachment along with disc leakage (Figure: 5A, B). On systemic examination, alopecia but no skin lesion was found. She was diagnosed to have complete VKH syndrome and was treated with pulse dexamethasone therapy (1000mg OD intravenously for three days) to which she responded. After three days, systemic oral steroid (1 mg/kg body weight) was prescribed. One week after treatment initiation BCVA was OD-6/9 and Figure 2: Poliosis OS-6/12. Ocular inflammation also reduced to the extent of occasional anterior chamber and retrolental cell.

Anterior segment examination revealed medium sized keratic precipitates and 3+ cells, flare and posterior synechiae (Figure: 3).

Figure 5A, B: fundus fluorescein angiography showing multiple pin point leakages.

She was discharged on topical steroids and cycloplegics and systemic steroids and advised regular follow up. In Figure 3: Anterior segment examination photographs showing the last visit (3 months) she is maintaining her vision on posterior synechiae and posterior subcapsular cataract. 20 mg oral steroid daily and fundus showed RPE depigmentation (Figure: 4C, D). Discussion Independently, Vogt, Koyanagi, and Harada described Iris nodules or iris neovascularization were absent. Mild several patients during a 20-year period with bilateral posterior subcapsular cataract was noted in both the uveitis, exudative retinal detachments, neurological eyes. Posterior segment examination shows bilateral abnormalities, and disorders of the integument. Despite disc edema and multiple small yellowish white lesions differences in their patients, the manifestations scattered diffusely all over the fundus (Figure: 4A, B). appeared to represent a spectrum of disease and several authors suggested that the disorder should be termed Vogt-Koyanagi-Harada syndrome. The revised criteria defined 3 categories of disease: complete VKH, incomplete VKH, and probable VKH. Common to all forms of VKH disease are the requirements that: patients have no prior history of ocular trauma or surgery, patients have no evidence of another ocular disease based upon clinical or laboratory evidence, and patients have bilateral ocular involvement. Patients with complete VKH disease must also have evidence of neurological and auditory findings as well as integumentary signs. However, the neurological and auditory manifestations which include meningismus, cerebrospinal fluid pleocytosis, and tinnitus may have resolved before an ophthalmic examination. To be diagnosed with incomplete VKH disease, patients must have either the neurological and auditory manifestations or the integumentary signs. The most Figure 4: fundus picture showing disc edema (A & B) frequently encountered neurological associations of followed by depigmented blonde looking fundus (C & D).

45 HYDROCEPHALUS REQUIRING SHUNT SURGERY DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008 uveitis are VKH disease, primary CNS lymphoma, examined for anterior chamber and vitreous reaction multiple sclerosis, and herpes virus infections.3 Others and if suspected fundus fluorescein angiography should are sarcoidosis, cytomegalovirus infection, collagen be done to rule out multiple areas of pin point leakage vascular diseases, disorders associated with suggestive of exudative detachment. disseminated intravascular coagulopathy, and Reference: malignant hypertension.4 The inflammatory aspects of VKH syndrome are attributed to the autoimmune 1. Sugiura S. Vogt-Koyanagi-Harada disease. Jpn J destruction of melanocytes through immunological Ophthalmol 1978;22: 9-35 mechanisms. This mechanism would account for the 2. Snyder DA, Tessler HH. Vogt-Koyanagi-Harada high incidence of Harada's disease in dark-skinned syndrome. Am J Ophthalmol 1980; 90:69-75 patients.5 It may affect any organ containing 3. J R Smith, J T Rosenbaum. Neurological melanocytes and if not treated early can cause advanced concomitants of uveitis. Br J Ophthalmol 2004; damage to the organ. Neurological signs in VKH 88:1498-1499 syndrome are usually mild, the main finding being atypical headache,6 and this particularity delays 4. Wolfensberger TJ, Tufail A. Systemic disorders diagnosis. Symptoms of meningitis usually do not need associated with detachment of the neurosensory any active intervention. To our knowledge this is the first retina and retinal pigment epithelium. Curr Opin case report of VKH associated meningitis requiring Ophthalmol. 2000; 11(6):455-61 ventriculo-peritoneal shunt surgery. In our case 5. Ghipponi JP, Boitte JP, Rosier S et al. Harada's symptoms of meningitis were so prominent that disc disease. Report of a case. Med Trop (Mars). 1995; edema was considered as a result of increased intra 55(4 Pt 2):459-61 cranial pressure by neurologist. We think if the disease could be diagnosed early and treated it may not 6. Beniz J, Forster DJ, Lean JS et al. Variations in clinical developed hydrocephalus. In conclusion, all cases of features of the Vogt-Koyanagi-Harada syndrome. bilateral disc edema and meningitis should be carefully Retina. 1991;11(3):275-80

46 A CASE OF GIANT CHOROIDAL TUBERCULOMA MISDIAGNOSED DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

CASE REPORT

A case of giant choroidal tuberculoma misdiagnosed as amelanotic melanoma. Anusha V, Rajpal Insaan, Pradeep Venkatesh, Satpal Garg, Subrata Mandal Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS.

Madhav ratti, 30 yr old male presented with sudden painless loss of vision, especially the nasal field of the left eye within a duration of one month. The patient was seen at a private hospital and was diagnosed to a have total retinal detachment, a vitreo-retinal surgery was contemplated and the patient was referred to RPC for the same. The diagnosis was revised at another private hospital and the patient was referred to R.P.centre with a diagnosis of amelanotic melanoma for further management and enucleation if deemed necessary. The patient presented to our centre with the same complaints. He did not give a history of photopsia ,floaters or metamorphopsia. There was no history of ocular trauma. A detailed enquiry of his past revealed a (Figure - 1b) history of tuberculous pleural effusion at the age of 8 years for which he had received anti-tuberculous Fundus examination of the right eye showed a yellowish treatment under supervision for 8 months. lesion along the inferotemporal arcade with no associated vitritis. On examination, the patient had a vision of 20/20 in the right eye and PL+ PR inaccurate in two quadrants in the left. Slit lamp examination of the left eye showed the presence of pigment deposits on the corneal endothelium with 3+ cells and flare in the anterior chamber and 3+ retrolental cells suggesting an inflammatory etiology. Fundus examination of the left eye revealed a mass arising from the supero-temporal quadrant that was diffusely elevated with overlying blood vessels and haemorhages. There was an associated retinal detachment with shifting fluid pointing towards an exudative cause for the same.

(Figure - 2) Ocular and systemic investigations were planned.

Address for correspondence:- Dr. Anusha V. Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences (AIIMS), New Delhi - 110029 (Figure - 1a)

47 A CASE OF GIANT CHOROIDAL TUBERCULOMA MISDIAGNOSED DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

The ocular ultrasound of the left eye confirmed the FFA of the other eye was however inconclusive. presence of a mass in the posterior segment that showed moderate to high amplitude spikes with associated retinal detachment.

(Figure - 3) (Figure - 5) Fluorescein angiography showed early hyper- Systemic investigations: Haemogram revealed a high flourescence with increasing hyperflourescence and ESR (57 mm/hour), the other parameters being normal. leakage in the late phases suggesting inflammation in Peripheral blood smear was normal. The renal function the left eye. testa and the liver function tests were unremarkable except for a mild elevation if the SGOT and SGPT liver enzymes. Mantoux was 15mm. HIV screening was done and was negative. Chest X-ray showed the presence of paratracheal widening suggestive of mediastinal lymphadenopathy.

(Figure - 4a)

(Figure - 6) (Figure - 4b)

48 A CASE OF GIANT CHOROIDAL TUBERCULOMA MISDIAGNOSED DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

MRI orbit showed the presence of a hyperintense lesion CECT chest and abdomen showed the presence of large on T-1 and a hypointense non-homogenous lesion on T-2 necrotic rim enhancing mediastinal lymph nodes: weighted image with enhancement of the borders of the possibly tuberculous in etiology. lesion with contrast suggesting an inflammatory abscess.

(Figure - 8a)

(Figure - 7a)

(Figure - 8b)

PET scan showed an increased FDG uptake in large orbital leson in the posteror part of the globe and multiple lymph nodes suggestive of disseminated (Figure - 7b) tuberculosis. USG guided FNAC from the lt. supraclavicular lmyph node shows necrosis in which few Acid Fast Bacilli were detected. Features were consistent with TB. In the presence of a past history of tuberculosis, and with the above investigations suggesting a definite tubercular etiology a diagnosis of choroidal tuberculoma with exudative retinal detachment was made and the patient was started on anti tuberculosis treatment- category 2. (the case being one of relapse.) The age of the patient , the findings on the MRI and the presence of anterior chamber and retrolental activity with a systemic involvement refutes the diagnosis of amelanotic melanoma in this patient. The patient is now following up at a local DOTS centre. (Figure - 7c)

49 A CASE OF GIANT CHOROIDAL TUBERCULOMA MISDIAGNOSED DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Discussion: Choroidal tuberculoma results from - Optic disc granuloma ± neuroretinitis hematogenous seeding from the primary complex or - Sub retinal abscess secondary lesions that may develop, where the bacilli may remain dormant for many years before reactivation. B. Ocular investigations: Progressive caseation necrosis, and rapid multiplication - Demonstration of AFB from ocular fluids of the tubercular bacilli and tissue destruction lead to the - Positive PCR formation of these tubercles C. Systemic investigations: It is seen in 1.4% to 60% in patients with different form of - Positive mantoux test TB. The most characteristic clinical presentation of - Evidence of healed/active TB on chest X-ray ocular TB is in the form of multifocal choroidal tubercles. It may occasionally present as solitary - Evidence of extra pulmonary TB (TB granuloma, elevated mass like lesion(4-14mm). The tubercles appear AFB, culture) as yellowish sub retinal mass with exudative D. Therapeutic test: positive response to ATT over 4-6 detachment, rapid progression and sometimes even as weeks. ocular perforation.Patients with military TB and AIDS The presence of any one or more of the clinical signs with may present with sub retinal abscess. any one of the positive tests (B) is confirmatory for Investigations: The investigation considered as Gold Ocular TB. standard in ocular TB is the isolation of mycobacteria by In the presence of any one or more of the clinical signs sub retinal fluid analysis that can help in the detection of with any one of the positive tests (C) or positive TB foci . therapeutic trial(D): ocular TB is presumed. Others investigations to be undertaken are Mantoux, Management: There are no large studies available on the Chest X-ray and culture for tuberculosis if any specimen treatment of ocular TB. However, a multi drug therapy is obtainable. for atleast 6 months-15 months depending upon the Ocular investigations: Ultrasound examination of the patient's immune status and response to treatment has posterior segment may show a low reflectivity on A-scan an efficacy of 95%. but may show a solid elevated mass lesion in B-scan. The recommendations by the american thoracic society Ocular fluid positivity for IS 6110 sequence in PCR is also and CDC and infectious disease society of america and suggestive of ocular TB. by the WHO are as follows: Category 1: 2(HRZE) +4(HR) Angiographic studies of large size tuberculomas show an early hyperfluorescence within and around the Category 2: 2(HRZES) +4(HRZE) lesion that increases in intensiy and size over the Category 3: 2(HRZES) +1(HRZE) +5(HRE) subsequent phases as the dye leaks into the surrounding The drug dosages are as follows: RD with late leakage from the lesion . FFA can also be drug Daily dosage Thrice weekly used to assess response to treatment which shows decreasing hyperfluoroscence of the lesion with INH 5mg/kg 15mg/kg treatment. The initial phases are said to have a ring of fire rifampicin 10mg/kg 10mg/kg appearance. The late hyperfluorescence hasd been pyrazinamide 15-30mg/kg 50-70mg/kg attributed to the presence of retinal pigment epithelitis. ethambutol 15-25mg/kg 25-30mg/kg ICG angiography is also a useful method to determine streptomycin 15 mg/kg 25-30mg/kg. the extent of the lesion. Ocular side effects: Ethambutol can cause optic Diagnosis : There are definite guidelines for the neuritis,photophobia, extraocular muscle paresis. Visual diagnosis of ocular TB: field and colour vision testing every 4 weeks(>15mg/ A. Clinical signs: kg); 3-6 months for lower doses is recommended. The complaints usually resolve by 3-12 months, otherwise - Cellular reaction in AC/vitreous ± posterior parentral hydroxy cobalamin is indicated. synechiae - Vitreous snow ball opacities The response to treatment is evident within 2-4 weeks. - Perivascular cuffing of inflammatory exudates The use of low dose steroids, though controversial, for 4- - Solitary or multiple choroidal granulomas ± 6 weeks with ATT may limit damage to the ocular tissues exudative RD from delayed hypersensitivity.

50 JOURNAL ABSTRACTS DJO VOLUME 14 NUM 7 . JAN-MARCH 2008

JOURNAL ABSTRACTS

Dr. Shailesh G.M., MD, DNB, Dr. Munish Dhawan, MD Laser-assisted subepithelial keratectomy for anisometropic amblyopia in children: outcomes at 1 year. Comparison of preoperative and postoperative anterior segment measurements with Pentacam in horizontal Astle WF, Rahmat J, Ingram AD, Huang PT. muscle surgery. J Cataract Refract Surg. 2007 Dec;33(12):2028-34. Emre S, Cankaya C, Demirel S, Doganay S. Vision Clinic, Alberta Children's Hospital, University of Eur J Ophthalmol. 2008 Jan-Feb;18(1):7-12. Calgary, Calgary, Alberta, Canada. william.astle@ calgaryhealthregion.ca Department of Ophthalmology, School of Medicine, Inonu University, Malatya, Turkey. mdsinanemre@ PURPOSE: To assess the refractive, visual acuity, and yahoo.com binocular results of laser-assisted subepithelial keratectomy (LASEK) for anisomyopia, anisohyperopia, PURPOSE: To evaluate the effect of horizontal muscle and anisoastigmatia in children with various levels of surgery (recession or recession plus resection) on the amblyopia secondary to the anisometropic causes. anterior chamber parameters in patients after strabismus surgery. SETTING: Nonhospital surgical facility with follow-up in a hospital clinic setting. METHODS: The Scheimpflug of 18 eyes of 12 patients with horizontal deviations were recorded just before METHODS: This retrospective review was of 53 surgery and 1 month after surgery. The power of children with anisometropia who had LASEK to correct anterior surface of cornea in horizontal and vertical axis, the refractive difference between eyes. All LASEK thinnest corneal thickness, anterior chamber depth, procedures were performed using general anesthesia. anterior chamber volume, and cornea volume were Patients were divided into 3 groups according to their analyzed. The clinical characteristics of patients, the size anisometropia as follows: myopic difference greater than of the deviations, the surgical doses, and observed 3.00 diopters (D), astigmatic difference greater than 1.50 responses to surgery were reviewed. D, and hyperopic difference greater than 3.50 D. The children were followed for at least 1 year, and their RESULTS: There were six male and six female patients refractive status, visual acuity, and binocular vision were with an average age of 11.4 years (range, 4 to 22 years). assessed and recorded at 2 and 6 months as well as 1 year. Mean preoperative deviation was 47.91 PD (range, 20 to 75 PD), eight patients had esotropia with 57.5 PD RESULTS: The mean age at treatment was 8.4 years average deviation (range, 40 to 75 PD), and four patients (range 10 months to 16 years). The mean preoperative anisometropic difference was 6.98 D in the entire group, had exotropia with 28.75 PD average deviation (range, 9.48 D in the anisomyopic group, 3.13 D in the 20 to 35 PD). Of these 18 eyes, 12 eyes had horizontal anisoastigmatic group, and 5.50 D in the anisohyperopic muscle recession and 6 eyes had recession plus resection group. One year after LASEK, the mean anisometropic surgery. At the end of 1 month, three patients were difference decreased to 1.81 D, 2.43 D, 0.74 D, and 2.33 D, orthophoric and eight patients had residual deviations respectively, and 54% of all eyes were within +/-1.00 D of varying between 16 and 35 PD. Preoperative and the fellow eye, 68% were within +/-2.00 D, and 80% were postoperative comparison of the whole study group within +/-3.00 D. Preoperative visual acuity and documented insignificant changes in anterior chamber binocular vision could be measured in 33 children. parameters and in keratometer readings. However, after Postoperatively, 63.6% of children had an improvement dividing patients into two groups-recession or recession in best corrected visual acuity (BCVA) and the remainder plus resection group-only one parameter, anterior had no noted change. No patient had a reduction in chamber volume, was significantly reduced in recession BCVA or a loss in fusional ability after LASEK. Of the 33 plus resection group. children, 39.4% had positive stereopsis preoperatively CONCLUSIONS: Patients with strabismus who and 87.9% had positive stereopsis 1 year after LASEK. undergo recession plus resection procedure are prone to CONCLUSION: Laser-assisted subepithelial change in anterior chamber volume. Study with larger keratectomy is an effective surgical alternative to groups and long follow-up is necessary for clearer improve visual acuity in anisometropic children unable documentation of alterations at anterior chamber to tolerate conventional methods of treatment or in parameters. whom these methods fail.

50 JOURNAL ABSTRACTS DJO VOLUME 14 NUM 7 . JAN-MARCH 2008

JOURNAL ABSTRACTS

Effect of preoperative stability of alignment on Computer-assisted dosage calculation for strabismus outcome of strabismus surgery for infantile esotropia. therapy in myopic patients.

Lueder GT, Galli ML. Koch M, Priglinger S, Hoerantner R, Haslwanter T. J AAPOS. 2008 Feb;12(1):66-8. Epub 2007 Dec 21. Acta Ophthalmol (Oxf). 2008 Feb;86(1):53-7. Epub 2007 Departments of Ophthalmology and Visual Sciences and Aug 6. Pediatrics, St. Louis Children's Hospital at Washington University School of Medicine, St. Louis, Missouri, USA. Department of Ophthalmology, University Hospital Graz, Graz, Austria. INTRODUCTION: Some strabismus surgeons wait until the angle of deviation stabilizes prior to operating PURPOSE: The published dosage recommendations for on patients with infantile esotropia. This study the surgical correction of horizontal strabismus in non- evaluated whether a preoperative increase in the angle myopic patients show large, unexplained differences. of deviation affected surgical outcomes. For patients with high myopia, the situation becomes even more complex because the increase in the size of the METHODS: This was a retrospective comparative case bulb also affects the geometry of the oculomotor series in which records of patients with infantile esotropia, who had surgery performed before age 2 muscles. In this study, we wanted to investigate whether years and who were followed for at least 2 years computer simulations of the oculomotor plant can be postoperatively, were reviewed to identify two groups used to find accurate surgical parameters. for comparison: the first had /=10(Delta) increase in the patients affected by convergent (seven patients) or angle of deviation prior to surgery. In the latter group, divergent (six patients) strabismus and high myopia. surgery was performed for the angle present at the time Postoperative checks were made 1 day, 1 week, 3 months of surgery. Outcomes were considered successful if the and 1-6 years after the operation. For each patient, we patients had microtropias. simulated the presurgical strabismus pattern with RESULTS: Fifteen patients were identified in each SEE++ (see 'Further Information' for manufacturer group. The interval between the first office visit and time details), a biomechanical simulation program of the of surgery was the same in both groups (mean, 2 oculomotor plant. The individual results of the months). Outcomes were successful in 11 of 15 (73%) in simulations were then compared to the measured each group (no significant difference, p = 0.659). postoperative strabismus patterns.

CONCLUSIONS: There was no difference in outcome RESULTS: We found a trend of under-correction in the between children whose angles of deviation were stable postoperative situation, resulting in four patients having and those whose angles increased prior to surgery. This a large remaining strabismus angle of more than 5 indicates that strabismus surgery does not need to be degrees. The computer simulations were able to delayed while waiting for the angle of deviation to reproduce this under-correction, and suggested an stabilize. Surgical correction may therefore be achieved increase in dosage. at an earlier age, which may have a beneficial effect on CONCLUSION: We conclude that realistic biomechanical outcome. simulations of the oculomotor plant can predict the postoperative result for myopic patients accurately. The results of the computer simulation correlate well with the postoperative outcome of the patient.

51 INSTRUCTION TO CONTRIBUTORS DJO VOLUME 14 NUM 7 . JAN-MARCH 2008

INSTRUCTION TO CONTRIBUTORS

Aims of the Journal at the time submitting their manuscript for submission Delhi Journal of ophthalmology (DJO) is the quarterly of the manuscript. journal published by Delhi Ophthalmological Society. Submission of the manuscript The DJO aims to become an easily readable fully Authors are requested to read these instructions referenced journal which will provide the specialists carefully before submitting manuscripts with up to date information and the residents with All manuscripts/ contribution should be sent by post to articles that give expert's opinions that are backed with th references. The journal aims to provide : Dr. Rajpal Insan: Editor DJO, Dr. R.P. Centre, AIIMS 4

1. The views of experts on current advances in the Floor, Room No- 480. Ansari Nagar New Delhi-29 India. field, in a clear and readable format. All manuscript and illustrations must be submitted in 2. Case Reports and clinical enigmas. 3. Original articles preferable of clinical relevance . triplicate along with a CD. The authors should retain a

4. Articles on Diagnostic and surgical techniques. copy for their future reference. To speed the process of 5. Selections, annotated by experts, of the most review the manuscripts may be submitted interesting papers from the great wealth of original publications. electreonically be email to Dr. Rajpal Insan at 6. New ideas and innovations, new devices, [email protected], drrajpal_editordjo instruments. @yahoo.co.in or on a disc. These should be in MS-Word 7. Book reviews and letters to editor. format and the images should be in jpeg format (email) All correspondence shall be acknowledged within six a n d T i f f f o r m a t ( D i s c ) . G r a p h s a n d l i n e weeks of receipt by the editorial board. Authors shall be intimated about the acceptance of their articles for drawing/diagrams must be sent in graphic format, i.e. publication within six weeks of the acknowledgement. EPS, LOTUS/EXCEL Spreadsheet files, PICT/CHART The journal expects each contributor to have made a files, or Harvard graphic. Do not send graphs and significant contribution in writing the article. diagrams in freehand. The authors must take full responsibility to ensure that The disk should be labeled with the title of the article, the manuscript contains no matter that is, to the best of contributors, knowledge, and libetous or unlawful, or author's name, the file name, software used including infringes upon any Indian copyright laws. All accepted version. The disk should be sent in proper packaging to manuscripts are subject to editing. The contributors are avoid damage and corruption of the information during responsible for the statements in his/her/their work including the changes made during editing. All transit. Unreadable disks will be returned to the author contributors are requested to sign a letter of transmittal' for substitution.

Armeta Essenz (Refreshing eye wash)

52 FORTHCOMING EVENTS DJO VOLUME 14 NUM 7 . JAN-MARCH 2008

FORTHCOMING EVENTS

April, 2008 11-14 CANADA 4-9 CHICAGO (USA) Canadian Ophthalmological Society ACSRS (American Society of Cataract & Fairmont Chateau Whistler Refractive Surgeons) Whistler, BC, Canada CHICAGO, IL, USA 19-22 WURZBURG, GERMANY 12-16 CHICAGO 21st Annual Congress of the German Retina ASCRSI ASOA Symposium and Congress Society/8th Symposium of IntI Society of Ocular CHICAGO, IL, USA Trauma, Main Topic: Ocular Trauma Contact: ASCRS Wurzburg, Germany http://www.retinologie.de Tel: + 1 703 591 2220, Fax: + 1 703 591 0614 Web: www.ascrs.org 28 June - 2 July, HONG KONG WOC (World Ophthalmology Congress) 19-20 GERMANY Secretariat Frankurt Retina Meeting Ms. Angela Cho Mainz, Germany Department of Ophthalmology & Visual Sciences The Chinese University of Hong Kong 27 Apr.-1 May USA 3/F, Hong Kong Eye Hospital, 147K, Argyle Street, Kowloon, Hong Kong ARVO (Association for Research in Vision & Tel: (852) 2762-3128, Fax: (852) 2194-0695 Ophthalmology) Email: [email protected] Greater Fort Lauderdale/Broward Country Convention Center Fort Lauderdale, FL, USA July, 2008 7-10 MONTREAL, CANADA May, 2008 9th International Conference on Low Vision 21-24 JAPAN Rehabilitation - Vision 2008 Montreal, Province: QC (Canada) 18th International Visual Field & Imaging Symposium (IPS2008) Contact: Beatrice Laham Nara, Japan Phone: 514-906-1979, Fax: 514-395-1801 Contact: Chota Matsumoto E-Mail: [email protected] Phone: 81-72-366-0221 ext 3335 Fax: 81-72-368-2559 September, 2008 E-Mail: [email protected] 5-7 NEW DELHI, INDIA Biennial Meeting SAARC Academy of Ophthalmology 22-25 VIENNA, AUSTRIA India Habitat Centre, New Delhi Euretina (European Society of Retina Specialist) Contact: Dr. Namrata Sharma Austria Centre, Vienna, Austria Phone: 011-26589810, E-Mail: [email protected] 28-31 BELGIUM XI International Orthoptic Congress 2008 13-16 CZECH REPUBLIC ANTWERP, BELGIUM EVRS (European Vitreo-Retinal Soceity) Contact: Daisy Godts Prague, Czech Republic Tel: +32 3 8214845, Fax: +32 3 8251926 Email: [email protected] Web: www.ioacongress2008.org 13-17 GERMANY ESCRS Berlin, Germany June, 2008 1-6 GERMANY December, 2008 European Glaucoma Society National update on Ophthalmology at Organizing Secretariat Shah Satnam Ji Super Speciality Hospital, Viale G. Matteotti, 7 - 50121 Firenze, Italy Dr. Shaane-meet, Phone ++39/055/50351 Chairman Shah Satnam Ji Healthcare Society Fax ++39/055/5001912-570227 Contact : Dr. Aditya Insaan, Dr. Rajpal Insaan, Dr. E-mail: [email protected] Pradeep Sharma Insaan, Dr. Dinesh Talwar Insaan, Website: www.eugs.org Prof. V.K. Dada E-mail : [email protected].

53 INSTRUCTION TO CONTRIBUTORS DJO VOLUME 14 NUM 7 . JAN-MARCH 2008

MOTIVATE FOR ORGAN DONATION

Contact organizations which are helping eye donation, blood donation and body donation campaign.

Prof. S. Ghose, Dr. Shaane-meet Jee Chief RP Centre, President, Shah Satnaam Jee Health Care Wing Prof. Radhika Tandon, Shah Satnam Ji Super Speciality Hospital, Dera Dr. Namarta Sharma Sacha Sauda, Sirsa National Eye Bank, Ph. 01666-245588,245688 Dr. R.P. Centre (AIIMS) E-mail: [email protected] No waiting list Ansari Nagar, New Delhi-110029 Ph:26589461/26588500/26588700/ Dr. Umang Mathur 26593444 Dr. Shroff's Charity Eye Bank Dr. Shroff's Charity Eye Hospital Prof. B. Ghose Dr. Umang Mathur Prof. Ritu Arora 5027, Kedar Nath Road, Guru Nanak Eye Centre Eye Bank Darya Ganj Maharaja Ranjit Singh Marg, New Delhi-110002 New Delhi-110002. Ph: 41564300-11 Extn 268, 9873208336/26 Ph: 23234612/22, 23235145/23232400 Email: sceh.org

Prof. KPS Malik Dr. Ashok Grover Safdarjung Hospital Eye Bank, Delhi Central Rotary Eye Bank Safdarjung Hospital, Sir Ganga Ram Hospital, Ansari Nagar, New Delhi-110029. Rajendra Nagar, Ph: 26198126/26707217 New Delhi-110060 Ph: 42251356/ 25861463 Extn 1356, 9811771213 Prof. Madan Mohan Dr. Rishi Mohan Dr. S C Gupta Sewa Eye Bank, Rotary Regency Gift of Sight Coordination & MM Eyetech processing Centre 29 Link Road, Lajpat Nagar-III Venu Eye Institute & Research Centre New Delhi-110024 1/31, Sheikh Sarai, Phase-II, Ph: 29841919/ 9212035119 New Delhi- 110017

Donation of blood, eye or other body organs is a noble deed which shall go a long way in helping the suffering humanity. It may be interesting to note that Dera Sacha Sauda, Sirsa (Haryana) under the spiritual guidance of Hazoor Maharaj Saint Gurmeet Ram Rahim Singh Ji Insaan has got the Guinness world record in blood donations and is now working for eye and other organ donations. Let us help motivate more people for this noble deed.

For more information contact: 1. ORBO, Organ Retrieval Banking Organisation 2. International Blood & Organ Donation Bank All India Institute of Medical Sciences Shah Satnam Ji Super Speciality Hospital, Ansari Nagar, New Delhi-110029 Dera Sacha Sauda, Sirsa (Haryana) Ph.: 1060 (24 hours helpline), 2659 3444, 2658 8360 Ph. 01666-245588,245688 Fax: 91-11-2658 8402 E-mail: [email protected] E-mail: [email protected] Website : www.derasachasauda.org Website: www.orbo.org

54 TRAINING PROGRAMME DJO VOLUME 14 NUM 7 . JAN-MARCH 2008 TTrainingraining pprogrammesrogrammes

Institute Ant. Segment Glaucoma, Orbit & Pediatric Retina General Shot Term Observer Cornea/cataract Uveitis Plastics Ophthal. Vitreous Ophthal. Fellowship ship 1. Aditya Jyot Eye Hospital, 1(DNB) 1(DNB) Mumbai 2 2. Aravind Eye Hospital, 3, 12= 4.1 2 4 7 10 72t, 49++24|| Madurai 24 , 20*, 12 Several shot term paramedical courses 3. Aso-Palov Eye Hospital, 6 12 Ahmedabad 48* 4. Bangalore West Lions Eye Hospital, 1 10 6 Bangalore 4(DNB) 5. Bombay City Eye Institute, 6 6 16+, 16t 52 Mumbai 6. Disha Eye Hospital, Barrackpore 104 7. Giridhar Eye Institute, Kochi 1 1 24* 1 12++,12+o 8. Grewal Eye Institute 1 9. Lions NAB Eye Hospital, Mid Miraj 1 6+, 6oo,24+

10. L.V. Prasad Eye Institute, 6 2 1 4 3 8 64 100¶ Hyderabad 11. Mahatme Eye Bank & Eye Hospital, 3§ 4(DOMS) 2§ Nagpur 3+ 1 2+ 2$ 12. Prakash Netra Kendr 1 1 13. Rajan Eye Care Hospital, Chennai 6 24+ 12+ 14. Shankar Nethralaya, Chennai 2 1 2 4 15. Sri Sankaradeva Nethralaya, Guwahati 2 6 20 16. Dr. S.B. Sohan Singh Eye Hospital, 2 Amritsar 17. Shri Ganapathi Netralaya, Jalna 1 1 2 4 18. Shroff’s Charity Eye Hospital, New Delhi 1+1 1 3+3 4 Optometry fellowship (2yrs + 1yr internship) 5+5/ observership in cornea, glaucoma, med retina, ped. Ophthal. 19. Suraj Eye Institute, Nagpur 3+ 3 1 20. Venu Eye Institute, 4 years BSc in Optometric Practices, 30seats 1 2 6+, 12 . 6++, 12+ New Delhi 3 years Bsc in Optometric Practices, 10seats 24+ , 24, 4*+, 6 24* 21. Dr. R.P. Centre, New Delhi A total of 18 observerships of varing duration are available in all subspecialities 22. Choudhary Eye Care, New Delhi A total of 18 observerships of varing duration are available in all subspecialities * Indirect ophthalmoscopy; tIOL microsurgery; +phacoemulsification; § Cornea; Glaucoma; ¶4 every 2 weeks, ++Lasers in diabetic retinopathy +ºContact lens, ºInstruments maintenance; *Community outreach;00 low vision; **Manual SICS; **1 every 2 Weeks in phacoemulsification & refactive surgery, +Eye banking, 0Counselling, 00Paediatric ocular anaesthesia.

1. Aditya Jyot Eye Hospital 7. Giridhar Eye Institute 15. Sankara Nethralaya Plot No. 153, Road No. 9 28/2576, A. Kadavanthra Medical Research Foundation Opp. SIWS College Kochi - 682 020, Kerala 18 College Road Near Five Gardens, Wadala 8. Grewal Eye Institute Chennai - 600 006 Mumbai - 400 031 Sector 9C, Madhya Marg 16. Sri Sankaradeva Nethralaya 2. Aravind Eye Hospital Chandigarh 160009 Beltola - 28, Guwahathi Anna Nagar 9. Lion NAB Eye Hospital 17. Dr. S.B. Sohan singh Eye Hospital, Madurai - 625 020 Plot No. P-31, Mide Miraj- 416 410 Katra Sher Singh 3. Aso-Palov Eye Hospital Sangli Dist Amritsar - 143 006 Near Under Bridge 10. L.V. Prasad Eye Institute 18. Shri Ganapati Netralaya Rajbhavan Road, shahibag L.V. Prasad Marg, Banjara Hills Head Post Office Road Ahmedabad - 380 004 Hyderabad - 500 034 Jalna - 431 203 4. Bangalore West 11. Mahatma Eye Bank & Hospital 19. Dr. Shroff's Charity Eye Hospital Lions Eye Hospital 16, Central Excise Colony 5027, Kedar Nath Road, Daryaganj, and Cornea Grafting Centre Ring Road, Nagpur - 440 015 New Delhi- 110002 56/2, H Siddaiah Road 12. Prakash Netra Kendr 20. Suraj Eye Institute Bangalore - 570 002 N H 2, Vipul- Khand IV 559, new colony 5. Bombay City Eye Institute Gomti Nagar 226010 Nagpur - 440 001 5, Babulnath Road 13. Rajan Eye Care Hospital 21. Venu Eye Institute Mumbai - 400 007 No. 5, Vidyodaya East ll Street 1/31 Institutional Aera 6. Disha Eye Hospital T Nagar, Chennai - 600 017 Sheikh Sarai Phase- ll & Research Centre 14. Dr. R.P. Centre for Ophthalmic New Delhi- 110 017 Barrackpore, North 24 Parganas sciences AIIMS, Ansari Nagar 22. Choudhary Eye Care West Bengal - 743 120 New Delhi - 110 029 New Delhi

55