Hyphema Disease Entity
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Summary Benchmarks for Preferred Practice Pattern® Guidelines
SUMMARY BENCHMARKS FOR PREFERRED PRACTICE PATTERN® GUIDELINES TABLE OF CONTENTS Summary Benchmarks for Preferred Practice Pattern Guidelines Introduction . 1 Glaucoma Primary Open-Angle Glaucoma (Initial Evaluation) . 3 Primary Open-Angle Glaucoma (Follow-up Evaluation) . 5 Primary Open-Angle Glaucoma Suspect (Initial and Follow-up Evaluation) . 6 Primary Angle-Closure Disease (Initial Evaluation and Therapy) . 8 Retina Age-Related Macular Degeneration (Initial and Follow-up Evaluation) . 10 Age-Related Macular Degeneration (Management Recommendations) . 11 Diabetic Retinopathy (Initial and Follow-up Evaluation) . 12 Diabetic Retinopathy (Management Recommendations) . 13 Idiopathic Epiretinal Membrane and Vitreomacular Traction (Initial Evaluation and Therapy) . 14 Idiopathic Macular Hole (Initial Evaluation and Therapy) . 15 Posterior Vitreous Detachment, Retinal Breaks, and Lattice Degeneration (Initial and Follow-up Evaluation) . 17 Retinal and Ophthalmic Artery Occlusions (Initial Evaluation and Therapy) . 18 Retinal Vein Occlusions (Initial Evaluation and Therapy) . 19 Cataract/Anterior Segment Cataract (Initial and Follow-up Evaluation) . 20 Cornea/External Disease Bacterial Keratitis (Initial Evaluation) . 22 Bacterial Keratitis (Management Recommendations) . 23 Blepharitis (Initial and Follow-up Evaluation) . 24 Conjunctivitis (Initial Evaluation) . 25 Conjunctivitis (Management Recommendations) . 26 Corneal Ectasia (Initial Evaluation and Follow-up) . 27 Corneal Edema and Opacification (Initial Evaluation) . 28 Corneal Edema -
Repair of Open Globe Injury
Advances in Ophthalmology & Visual System Case Report Open Access Case report: repair of open globe injury Abstract Volume 3 Issue 1 - 2015 Globe rupture is a common sight-threatening ophthalmic emergency. We present a twelve-year-old girl with ocular trauma by sharp object resulting in corneal laceration, Nader Hussein Fouad Hassan Department of Ophthalmology, Benha University Hospital, hyphema, traumatic cataract and iris prolapse. This case illustrates the importance of early Egypt diagnosis, proper wound repair of ruptured globe as well as management of post-operative complications and value of early post-operative visual rehabilitation. Correspondence: Nader Hussein Fouad Hassan, Ophthalmology department, Benha University Hospital, Keywords: globe rupture, open globe injury, corneal laceration Kaliyobeya, Egypt, Tel +201224727982, Email Received: October 16, 2015 | Published: October 19, 2015 Abbreviations: FB, foreign body; VA, visual acuity; CT scan, patient then was given tetanus immunization, antiemetics, analgesics computerized tomography; RD, retinal detachment; INR, international and intravenous broad spectrum antibiotics and prepared for globe normalized ratio; GA, general anesthesia; D, diopter rupture repair under GA. Laboratory tests included a full blood count, liver function tests, INR, prothrombin time, partial thromboplastin Introduction time, kidney function tests, all were within normal. Ruptured Globe is a common ophthalmic emergency. It is a leading cause of blindness. Early examination with high level of suspicion is recommended in any patient with ocular trauma. Many signs may obscure detection of globe rupture, so the ophthalmologist should examine the patient thoroughly and treat the patient as early as impossible including early visual rehabilitation for young patients to prevent amblyopia. Globe rupture may be associated with traumatic hyphema, traumatic cataract, lens dislocation, vitreous hemorrhage, retinal detachment, uveal prolapse, scleral wound, orbital wall fractures, or optic nerve damage. -
URGENT/EMERGENT When to Refer Financial Disclosure
URGENT/EMERGENT When to Refer Financial Disclosure Speaker, Amy Eston, M.D. has a financial interest/agreement or affiliation with Lansing Ophthalmology, where she is employed as a ophthalmologist. 58 yr old WF with 6 month history of decreased vision left eye. Ache behind the left eye for 2-3 months. Using husband’s contact lens solution made it feel better. Seen by two eye care professionals. Given glasses & told eye exam was normal. No past ocular history Medical history of depression Takes only aspirin and vitamins 20/20 OD 20/30 OS Eye Pressure 15 OD 16 OS – normal Dilated fundus exam & slit lamp were normal Pupillary exam was normal Extraocular movements were full Confrontation visual fields were full No red desaturation Color vision was slightly decreased but the same in both eyes Amsler grid testing was normal OCT disc – OD normal OS slight decreased RNFL OCT of the macula was normal Most common diagnoses: Dry Eye Optic Neuritis Treatment - copious amount of artificial tears. Return to recheck refraction Visual field testing Visual Field testing - Small defect in the right eye Large nasal defect in the left eye Visual Field - Right Hemianopsia. MRI which showed a subacute parietal and occipital lobe infarct. ANISOCORIA Size of the Pupil Constrictor muscles innervated by the Parasympathetic system & Dilating muscles innervated by the Sympathetic system The Sympathetic System Begins in the hypothalamus, travels through the brainstem. Then through the upper chest, up through the neck and to the eye. The Sympathetic System innervates Mueller’s muscle which helps to elevate the upper eyelid. -
Differentiate Red Eye Disorders
Introduction DIFFERENTIATE RED EYE DISORDERS • Needs immediate treatment • Needs treatment within a few days • Does not require treatment Introduction SUBJECTIVE EYE COMPLAINTS • Decreased vision • Pain • Redness Characterize the complaint through history and exam. Introduction TYPES OF RED EYE DISORDERS • Mechanical trauma • Chemical trauma • Inflammation/infection Introduction ETIOLOGIES OF RED EYE 1. Chemical injury 2. Angle-closure glaucoma 3. Ocular foreign body 4. Corneal abrasion 5. Uveitis 6. Conjunctivitis 7. Ocular surface disease 8. Subconjunctival hemorrhage Evaluation RED EYE: POSSIBLE CAUSES • Trauma • Chemicals • Infection • Allergy • Systemic conditions Evaluation RED EYE: CAUSE AND EFFECT Symptom Cause Itching Allergy Burning Lid disorders, dry eye Foreign body sensation Foreign body, corneal abrasion Localized lid tenderness Hordeolum, chalazion Evaluation RED EYE: CAUSE AND EFFECT (Continued) Symptom Cause Deep, intense pain Corneal abrasions, scleritis, iritis, acute glaucoma, sinusitis, etc. Photophobia Corneal abrasions, iritis, acute glaucoma Halo vision Corneal edema (acute glaucoma, uveitis) Evaluation Equipment needed to evaluate red eye Evaluation Refer red eye with vision loss to ophthalmologist for evaluation Evaluation RED EYE DISORDERS: AN ANATOMIC APPROACH • Face • Adnexa – Orbital area – Lids – Ocular movements • Globe – Conjunctiva, sclera – Anterior chamber (using slit lamp if possible) – Intraocular pressure Disorders of the Ocular Adnexa Disorders of the Ocular Adnexa Hordeolum Disorders of the Ocular -
RETINAL DISORDERS Eye63 (1)
RETINAL DISORDERS Eye63 (1) Retinal Disorders Last updated: May 9, 2019 CENTRAL RETINAL ARTERY OCCLUSION (CRAO) ............................................................................... 1 Pathophysiology & Ophthalmoscopy ............................................................................................... 1 Etiology ............................................................................................................................................ 2 Clinical Features ............................................................................................................................... 2 Diagnosis .......................................................................................................................................... 2 Treatment ......................................................................................................................................... 2 BRANCH RETINAL ARTERY OCCLUSION ................................................................................................ 3 CENTRAL RETINAL VEIN OCCLUSION (CRVO) ..................................................................................... 3 Pathophysiology & Etiology ............................................................................................................ 3 Clinical Features ............................................................................................................................... 3 Diagnosis ......................................................................................................................................... -
A Case of Uveitis-Hyphema-Glaucoma Syndrome Due to Express Miniature Implantation
Henry Ford Health System Henry Ford Health System Scholarly Commons Case Reports Medical Education Research Forum 2020 5-2020 A Case of Uveitis-Hyphema-Glaucoma Syndrome due to ExPRESS Miniature Implantation Andrew Hou Henry Ford Health System, [email protected] Madeline Hasbrook Henry Ford Health System David A. Crandall Henry Ford Health System, [email protected] Follow this and additional works at: https://scholarlycommons.henryford.com/merf2020caserpt Recommended Citation Hou, Andrew; Hasbrook, Madeline; and Crandall, David A., "A Case of Uveitis-Hyphema-Glaucoma Syndrome due to ExPRESS Miniature Implantation" (2020). Case Reports. 135. https://scholarlycommons.henryford.com/merf2020caserpt/135 This Poster is brought to you for free and open access by the Medical Education Research Forum 2020 at Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Case Reports by an authorized administrator of Henry Ford Health System Scholarly Commons. A Case of Uveitis-Hyphema-Glaucoma Syndrome due to ExPRESS Miniature Implantation Andrew Hou MD, Madeline Hasbrook MD, David Crandall MD Department of Ophthalmology, Henry Ford Health System, Detroit, Michigan Purpose Results Discussion To report a case of a 69-year-old patient We believe etiology for the UGH who developed uveitis-glaucoma- syndrome the significant iridodonesis seen hyphema (UGH) syndrome after an on gonioscopy. In the interim between uneventful ExPRESS (Alcon, Fort Worth, surgery and presentation, the patient had TX) mini shunt surgery for advanced been prescribed tamsulosin for his benign primary open-angle glaucoma. To our prostatic hyperplasia. knowledge, this is the first case report Tamsulosin has been well established as describing glaucoma device induced UGH the cause of intraoperative floppy iris syndrome and its successful treatment syndrome secondary to iris dilator atrophy. -
Neovascular Glaucoma: Etiology, Diagnosis and Prognosis
Seminars in Ophthalmology, 24, 113–121, 2009 Copyright C Informa Healthcare USA, Inc. ISSN: 0882-0538 print / 1744-5205 online DOI: 10.1080/08820530902800801 Neovascular Glaucoma: Etiology, Diagnosis and Prognosis Tarek A. Shazly Mark A. Latina Department of Ophthalmology, Department of Ophthalmology, Massachusetts Eye and Ear Massachusetts Eye and Ear Infirmary, Boston, MA, USA, and Infirmary, Boston, MA, USA and Department of Ophthalmology, Department of Ophthalmology, Tufts Assiut University Hospital, Assiut, University School of Medicine, Egypt Boston, MA, USA ABSTRACT Neovascular glaucoma (NVG) is a severe form of glaucoma with devastating visual outcome at- tributed to new blood vessels obstructing aqueous humor outflow, usually secondary to widespread posterior segment ischemia. Invasion of the anterior chamber by a fibrovascular membrane ini- tially obstructs aqueous outflow in an open-angle fashion and later contracts to produce secondary synechial angle-closure glaucoma. The full blown picture of NVG is characteristized by iris neovas- cularization, a closed anterior chamber angle, and extremely high intraocular pressure (IOP) with severe ocular pain and usually poor vision. Keywords: neovascular glaucoma; rubeotic glaucoma; neovascularization; retinal ischemia; vascular endothe- lial growth factor (VEGF); proliferative diabetic retinopathy; central retinal vein occlusion For personal use only. INTRODUCTION tive means of reversing well established NVG and pre- venting visual loss in the majority of cases; instead bet- The written -
Traumatic Glaucoma: an Overview
Indian Journal of Clinical and Experimental Ophthalmology 2020;6(1):1–2 Content available at: iponlinejournal.com Indian Journal of Clinical and Experimental Ophthalmology Journal homepage: www.innovativepublication.com Editorial Traumatic glaucoma: An overview Rajendra Prakash Maurya1,* 1Regional Institute of Ophthalmology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India ARTICLEINFO © 2020 Published by Innovative Publication. This is an open access article under the CC BY-NC-ND Article history: license (https://creativecommons.org/licenses/by/4.0/) Received 11-03-2020 Accepted 12-03-2020 Available online 17-03-2020 of blunt trauma are (i) Trabecular meshwork disruption, Dear Friends (ii) Hyphaema: Accumulation of blood in the anterior chamber leads to obstruction of the trabecular meshwork Season’s Greeting!! with erythrocytes, fibrin, platelets and other inflammatory It is my humble privilege to present the special issue debris lead to prolonged increase in the IOP. 2 (iii) of IJCEO after successful journey of five years. This Inflammation: Trauma may also lead to direct inflammation issue of IJCEO has several interesting articles on vision of the trabecular meshwork (trabeculitis) causing decrease threatening morbidity, Glaucoma particularly on diagnosis in aqueous outflow. (iv) Choroidal hemorrhage: causing and management of primary glaucoma. a mass effect in the posterior segment leading to forward Traumatic glaucoma (TG) refers to a heterogeneous displacement of the lens-iris diaphragm and leads to acute group of post-traumatic secondary glaucoma with varying angle closure glaucoma. The pathophysiology of late underlying mechanisms. Traumatic glaucoma occurs onset TG are (i) Angle-Recession (tear which occurs commonly after mechanical injury of globe (blunt or between the longitudinal and circular layers of the ciliary penetrating injury). -
Acquired Colour Vision Defects in Glaucoma—Their Detection and Clinical Significance
1396 Br J Ophthalmol 1999;83:1396–1402 Br J Ophthalmol: first published as 10.1136/bjo.83.12.1396 on 1 December 1999. Downloaded from PERSPECTIVE Acquired colour vision defects in glaucoma—their detection and clinical significance Mireia Pacheco-Cutillas, Arash Sahraie, David F Edgar Colour vision defects associated with ocular disease have The aims of this paper are: been reported since the 17th century. Köllner1 in 1912 + to provide a review of the modern literature on acquired wrote an acute description of the progressive nature of col- colour vision in POAG our vision loss secondary to ocular disease, dividing defects + to diVerentiate the characteristics of congenital and into “blue-yellow” and “progressive red-green blindness”.2 acquired defects, in order to understand the type of This classification has become known as Köllner’s rule, colour vision defect associated with glaucomatous although it is often imprecisely stated as “patients with damage retinal disease develop blue-yellow discrimination loss, + to compare classic clinical and modern methodologies whereas optic nerve disease causes red-green discrimina- (including modern computerised techniques) for tion loss”. Exceptions to Köllner’s rule34 include some assessing visual function mediated through chromatic optic nerve diseases, notably glaucoma, which are prima- mechanisms rily associated with blue-yellow defects, and also some reti- + to assess the eVects of acquired colour vision defects on nal disorders such as central cone degeneration which may quality of life in patients with POAG. result in red-green defects. Indeed, in some cases, there might be a non-specific chromatic loss. Comparing congenital and acquired colour vision Colour vision defects in glaucoma have been described defects since 18835 and although many early investigations Congenital colour vision deficiencies result from inherited indicated that red-green defects accompanied glaucoma- cone photopigment abnormalities. -
Fibroblast Growth Factor-2 Drives and Maintains Progressive Corneal Neovascularization Following HSV-1 Infection
ARTICLES Fibroblast growth factor-2 drives and maintains progressive corneal neovascularization following HSV-1 infection HR Gurung1, MM Carr2, K Bryant2, AJ Chucair-Elliott2 and DJJ Carr1,2 Herpes simplex virus type 1 (HSV-1) infection of the cornea induces vascular endothelial growth factor A (VEGF-A)- dependent lymphangiogenesis that continues to develop well beyond the resolution of infection. Inflammatory leukocytes infiltrate the cornea and have been implicated to be essential for corneal neovascularization, an important clinically relevant manifestation of stromal keratitis. Here we report that cornea infiltrating leukocytes including neutrophils and T cells do not have a significant role in corneal neovascularization past virus clearance. Antibody- mediated depletion of these cells did not impact lymphatic or blood vessel genesis. Multiple pro-angiogenic factors including IL-6, angiopoietin-2, hepatocyte growth factor, fibroblast growth factor-2 (FGF-2), VEGF-A, and matrix metalloproteinase-9 were expressed within the cornea following virus clearance. A single bolus of dexamethasone at day 10 post infection (pi) resulted in suppression of blood vessel genesis and regression of lymphatic vessels at day 21 pi compared to control-treated mice. Whereas IL-6 neutralization had a modest impact on hemangiogenesis (days 14–21 pi) and lymphangiogenesis (day 21 pi) in a time-dependent fashion, neutralization of FGF-2 had a more pronounced effect on the suppression of neovascularization (blood and lymphatic vessels) in a time-dependent, leukocyte- independent manner. Furthermore, FGF-2 neutralization suppressed the expression of all pro-angiogenic factors measured and preserved visual acuity. INTRODUCTION corneal neovascularization is topical administration of steroid The cornea is an immune privileged tissue and its transparency is or non-steroid anti-inflammatory drugs, unwarranted side critical for optimal visual acuity. -
Intraocular Pressure During Phacoemulsification
J CATARACT REFRACT SURG - VOL 32, FEBRUARY 2006 Intraocular pressure during phacoemulsification Christopher Khng, MD, Mark Packer, MD, I. Howard Fine, MD, Richard S. Hoffman, MD, Fernando B. Moreira, MD PURPOSE: To assess changes in intraocular pressure (IOP) during standard coaxial or bimanual micro- incision phacoemulsification. SETTING: Oregon Eye Center, Eugene, Oregon, USA. METHODS: Bimanual microincision phacoemulsification (microphaco) was performed in 3 cadaver eyes, and standard coaxial phacoemulsification was performed in 1 cadaver eye. A pressure transducer placed in the vitreous cavity recorded IOP at 100 readings per second. The phacoemulsification pro- cedure was broken down into 8 stages, and mean IOP was calculated across each stage. Intraocular pressure was measured during bimanual microphaco through 2 different incision sizes and with and without the Cruise Control (Staar Surgical) connected to the aspiration line. RESULTS: Intraocular pressure exceeded 60 mm Hg (retinal perfusion pressure) during both standard coaxial and bimanual microphaco procedures. The highest IOP occurred during hydrodissection, oph- thalmic viscosurgical device injection, and intraocular lens insertion. For the 8 stages of the phaco- emulsification procedure delineated in this study, IOP was lower for at least 1 of the bimanual microphaco eyes compared with the standard coaxial phaco eye in 4 of the stages (hydro steps, nu- clear disassembly, irritation/aspiration, anterior chamber reformation). CONCLUSION: There was no consistent difference in IOP between the bimanual microphaco eyes and the eye that had standard coaxial phacoemulsification. Bimanual microincision phacoemul- sification appears to be as safe as standard small incision phacoemulsification with regard to IOP. J Cataract Refract Surg 2006; 32:301–308 Q 2006 ASCRS and ESCRS Bimanual microincision phacoemulsification, defined as capable of insertion through these microincisions become cataract extraction through 2 incisions of less than 1.5 mm more widely available. -
Hyphema. Part I. Pathophysiologic Considerations
University of Pennsylvania ScholarlyCommons Departmental Papers (Vet) School of Veterinary Medicine 11-1-1999 Hyphema. Part I. Pathophysiologic Considerations András M. Komáromy David T. Ramsey Dennis E. Brooks Cynthia C. Ramsey Maria E. Kallberg See next page for additional authors Follow this and additional works at: https://repository.upenn.edu/vet_papers Part of the Ophthalmology Commons, and the Veterinary Medicine Commons Recommended Citation Komáromy, A. M., Ramsey, D. T., Brooks, D. E., Ramsey, C. C., Kallberg, M. E., & Andrew, S. E. (1999). Hyphema. Part I. Pathophysiologic Considerations. Compendium on Continuing Education for the Practicing Veterinarian, 21 (11), 1064-1069. Retrieved from https://repository.upenn.edu/vet_papers/51 Dr. Komáromy was affiliated with the University of Pennsylvania from 2003-2012. Part II can be found at http://repository.upenn.edu/vet_papers/52/ This paper is posted at ScholarlyCommons. https://repository.upenn.edu/vet_papers/51 For more information, please contact [email protected]. Hyphema. Part I. Pathophysiologic Considerations Abstract Hemorrhage in the anterior chamber of the eye, or hyphema, results from a breakdown of the blood-ocular barrier (BOB) and is frequently associated with inflammation of the iris, ciliary body, or retina. Hyphema can also occur by retrograde blood flow into the anterior chamber via the aqueous humor drainage pathways without BOB breakdown. Hyphema attributable to blunt or perforating ocular trauma is more common than that resulting from endogenous causes. When trauma has been eliminated as a possible cause, it is prudent to assume that every animal with hyphema has a serious systemic disease until proven otherwise. Disciplines Medicine and Health Sciences | Ophthalmology | Veterinary Medicine Comments Dr.