1/20. Neurotrophic corneal endothelial failure complicating acute horner syndrome.PURPOSE: The authors report the clinical findings of a unique case of rapid corneal endothelial decompensation in association with acute horner syndrome. STUDY DESIGN: Case report and literature review. methods: The authors followed a 38-year-old woman who developed horner syndrome after right jugular vein catheterization during cardiac valvular surgery. Shortly after the operation, horner syndrome accompanied by conjunctival hyperemia and stromal corneal edema developed in the right eye. Over the course of 4 months, the eye became painful, the corneal endothelial cell count dropped precipitously, and the stromal edema worsened, causing a difference of 100 microm in central corneal thickness compared to the unaffected eye. Deep stromal vascularization started at the limbus, resembling interstitial keratitis. RESULTS: A 3-week course of topical steroid treatment resulted in a dramatic improvement in the stromal corneal edema and regression of the deep stromal vascularization. Ocular and right hemicranial pain subsided shortly thereafter. CONCLUSION: The authors hypothesize that corneal endothelial failure in this unique case may have resulted from traumatic sympathectomy. According to experimental evidence in the reviewed ophthalmologic literature, sympathetic innervation may have a neurotrophic role in the cornea. Corneal pathology similar to the authors' case has been described in hemifacial atrophy (Parry-Robson syndrome), a disorder that is assumed to result from sympathetic denervation and that can be produced in animals by cervical sympathectomy. The authors therefore hypothesize that sympathetic denervation of the cornea may rarely cause endothelial decompensation and corneal edema. To the authors' knowledge, this is the first reported case of corneal endothelial failure in horner syndrome.- - - - - - - - - - ranking = 1keywords = keratitis (Clic here for more details about this article) |
2/20. Acute hydrops in the corneal ectasias: associated factors and outcomes.PURPOSE: To identify factors associated with the development of hydrops and affecting its clinical outcome. methods: Chart review of all patients with acute hydrops seen by a referral cornea service during a 2.5-year period between June 1996 and December 1998. RESULTS: Twenty-one patients (22 eyes) with acute hydrops were seen. Nineteen patients had keratoconus, 2 had pellucid marginal degeneration, and 1 had keratoglobus. Twenty-one of 22 (95%) eyes had seasonal allergies and 20 of 22 (91%) eyes had allergy-associated eye-rubbing behavior. Six of 22 (27%) had a diagnosis of Down's syndrome. Six patients were able to identify a traumatic inciting event: vigorous eye rubbing in 4 and traumatic contact lens insertion in 2. The affected area ranged from 7% to 100% of the corneal surface area and was related to disease duration and final visual acuity. Proximity of the area of edema to the corneal limbus ranged from 0 to 2.3 mm and was also related to prognosis. Three serious complications were observed: a leak, an infectious keratitis, and an infectious keratitis and coincidental neovascular glaucoma. Various medical therapies did not differ significantly in their effect on outcome, and ultimately 4 (18%) of 22 patients underwent penetrating keratoplasty. Best-corrected visual acuity was equal to or better than prehydrops visual acuity in 5 of the 6 patients in whom prehydrops visual acuity was known, without corneal transplantation. CONCLUSIONS: Allergy and eye-rubbing appear to be important risk factors in the development of hydrops. Visual results are acceptable in some patients without surgery. Close observation allows for the early detection and treatment of complications such as perforation and infection.- - - - - - - - - - ranking = 2keywords = keratitis (Clic here for more details about this article) |
3/20. Differential diagnosis of corneal oedema assisted by in vivo confocal microscopy.The purpose of this study was to demonstrate microstructural differences between clinically similar, but aetiologically different, cases of corneal oedema in four subjects. In vivo confocal microscopy highlighted oedema of the basal epithelium, prominent nerve-keratocyte interactions, and typical 'epithelialization' of the endothelium in a case of iridocorneal endothelial syndrome; however, a similar microstructural appearance was observed in a case of presumed herpetic disciform keratitis. The latter diagnosis was subsequently revised on this basis. Confocal examination of fuchs' endothelial dystrophy demonstrated oedema of the basal epithelium, prominent wing cells, anterior stromal alterations, fibrosis of Descemet's membrane and a typical 'strawberry' appearance of the endothelium. In contrast, in vivo microstructural examination of bilateral keratoconus with hydrops confirmed oedema mainly involving the epithelium and anterior stroma. In vivo confocal microscopy allows the clinician to observe the living cornea at a microstructural level and to better diagnose and differentiate borderline or unusual cases of corneal oedema.- - - - - - - - - - ranking = 1keywords = keratitis (Clic here for more details about this article) |
4/20. herpes simplex virus bullous keratitis misdiagnosed as a case of pseudophakic bullous keratopathy with secondary glaucoma: an unusual presentation.PURPOSE: To report an unusual case of herpetic bullous keratitis misdiagnosed as a case of pseudophakic bullous keratopathy with secondary glaucoma. RESULTS: A retrospective analysis of the case record of a 60-year-old man who had earlier undergone bilateral cataract surgery, was done. He presented with a complaint of decrease in vision in the right eye of 20 days duration. On examination, cornea showed epithelial bullae all over the surface with stromal and epithelial edema. intraocular pressure was 30 mm of Hg in RE. He was treated with anti-glaucoma medications. Two dendritic lesions were seen in the cornea during a subsequent visit four days later. Virological investigations confirmed a diagnosis of herpes simplex keratitis. He was treated with topical acyclovir. CONCLUSIONS: This case highlights the fact that herpes simplex keratitis can present initially as a more diffuse corneal stromal and epithelial edema with epithelial bullae mimicking bullous keratopathy. Herpetic bullous keratitis, although unusual, should be considered in the differential diagnosis under such circumstances.- - - - - - - - - - ranking = 8keywords = keratitis (Clic here for more details about this article) |
5/20. Interface fluid after laser in situ keratomileusis.We report a case in which raised intraocular pressure (IOP) was associated with interface fluid after uneventful bilateral laser in situ keratomileusis (LASIK). The patient presented with diffuse lamellar keratitis in both eyes 3 weeks postoperatively that was treated aggressively with topical corticosteroids. A steroid-induced rise in IOP resulted in interface fluid accumulation and microcystic edema. Measurements with the Goldmann tonometer revealed an IOP of 3.0 mm Hg in both eyes. However, Schiotz tonometry recorded a pressure of 54.7 mm Hg in both eyes. Reduction in the dosage of topical corticosteroid and medical treatment of the raised IOP resulted in resolution of the microcystic edema and interface fluid accumulation. This case highlights the inaccuracies of IOP measurement after LASIK and the resulting complications.- - - - - - - - - - ranking = 1keywords = keratitis (Clic here for more details about this article) |
6/20. Steroid-induced glaucoma after laser in situ keratomileusis associated with interface fluid.PURPOSE: To report the ocular manifestations and clinical course of eyes developing interface fluid after laser in situ keratomileusis (LASIK) surgery from a steroid-induced rise in intraocular pressure. DESIGN: Retrospective, noncomparative interventional case series. PARTICIPANTS/INTERVENTION: We examined six eyes of four patients who had diffuse lamellar keratitis develop after uneventful myopic LASIK surgery and were treated with topical corticosteroids. PRINCIPAL OUTCOME MEASURE: Slit-lamp findings, intraocular pressure measurements, and visual field loss. RESULTS: All eyes had a pocket of fluid develop in the lamellar interface between the flap and the stromal bed associated with a corticosteroid-induced rise in intraocular pressure. However, because of the interface fluid, intraocular pressure was normal or low by central corneal Goldmann applanation tonometry in all eyes. The elevated intraocular pressure was diagnosed by peripheral measurement in several cases after months of elevated pressure. All six eyes had visual field defects develop. Three eyes of two patients had severe glaucomatous optic neuropathy and decreased visual acuity develop as a result of undiagnosed steroid-induced elevated intraocular pressure. CONCLUSIONS: A steroid-induced rise in intraocular pressure after LASIK can cause transudation of aqueous fluid across the endothelium that collects in the flap interface. The interface fluid leads to inaccurately low central applanation tonometry measurements that obscure the diagnosis of steroid-induced glaucoma. Serious visual loss may result.- - - - - - - - - - ranking = 1keywords = keratitis (Clic here for more details about this article) |
7/20. Interface fluid after laser in situ keratomileusis.PURPOSE: To describe a case of interface fluid after laser in situ keratomileusis (LASIK) and review the literature on this rare complication after LASIK. methods: We present a case report and literature review. Articles for this review were chosen from electronic database and manual literature searches. medline searches were made from 1990 to April 2002, using the key words "interface fluid" and "LASIK." RESULTS: A 40-year-old man had uneventful LASIK for residual refractive error from previous penetrating keratoplasty in his right eye. Diffuse lamellar keratitis began 1 day postoperatively. Topical corticosteroids were administered. Six weeks after LASIK, a layer of interface fluid developed. intraocular pressure was 9 mmHg when measured centrally by Goldmann applanation tonometry and 30 mmHg by Tono-pen tonometry. The interface fluid resolved with antiglaucoma agents and corticosteroids combined with cyclosporine. CONCLUSIONS: This case, along with other reported cases, demonstrate the clinical features of interface fluid after LASIK.- - - - - - - - - - ranking = 1keywords = keratitis (Clic here for more details about this article) |
8/20. Delayed onset of varicella keratitis.Although varicella is one of the most common infectious diseases in the united states, systemic and ocular complications are rare. We report a patient who developed disciform edema followed by microdendritic keratitis 1 and 2 months, respectively, after resolution of the acute phase of varicella. Cultures were negative, but serologic analysis found positive antibodies against varicella zoster virus and negative antibodies against herpes simplex virus. Based on this case and on a review of the literature, we believe that this delayed onset of keratitis represents a distinct category of varicella corneal complications.- - - - - - - - - - ranking = 6keywords = keratitis (Clic here for more details about this article) |
9/20. Severe late-onset recurrent epithelial erosion with diffuse lamellar keratitis after laser in situ keratomileusis.A 39-year-old woman had laser in situ keratomileusis that was complicated by intraoperative epithelial erosion in both eyes. Seven months after surgery, the patient returned, complaining of pain and blurred vision in the left eye. Slitlamp examination revealed corneal epithelial erosion with severe diffuse lamellar keratitis (DLK). Reepithelialization was complete in several days. However, severe inflammation remained until systemic steroids were administered. Recurrent erosions can lead to a serious inflammatory reaction such as DLK because of the presence of the flap-stroma interface.- - - - - - - - - - ranking = 5keywords = keratitis (Clic here for more details about this article) |
10/20. Characteristic clinical findings and visual outcomes.PURPOSE: To describe a potentially serious complication of laser in situ keratomileusis (LASIK) that can masquerade as a persistent epithelial defect. SETTING: Refractive surgery centers in academic institutions. methods: charts of 4 eyes in which epithelial-defect-masquerade syndrome was diagnosed were reviewed to determine the time to diagnosis and the presence of associated features that may have contributed to the delay in diagnosis. Clinical findings and outcomes of medical and surgical intervention were recorded. RESULTS: All eyes developed an epithelial defect involving the edge of the flap during surgery. The diagnosis of epithelial ingrowth was delayed because of the presence of stromal edema (n = 4), diffuse lamellar keratitis (n = 3), and contraction of the flap leading to gutter widening (n = 4). Epithelial ingrowth was diagnosed 5, 7, 15, and 60 days after LASIK. All eyes satisfied the following criteria: convexity of the peripheral epithelium at the edge of the flap associated with light reflections at the end of the flap, fluorescein pooling in the gutter, stromal edema, reduced best spectacle-corrected visual acuity (<20/60 in 3 eyes), and partial healing of the epithelial defect limited to the flap hinge. One eye developed stromal scarring and ulceration that required fortified antibiotics. Surgical repair included epithelial scraping after the flap was lifted and ironing followed by placement of a contact lens after surgery. The epithelial defect healed 5, 7, 21, and 24 days after surgery. The final uncorrected visual acuity ranged from 20/15 to 20/100. CONCLUSIONS: Epithelial ingrowth following LASIK-associated epithelial defects may masquerade as stromal edema associated with a persistent epithelial defect. A high index of suspicion for epithelial ingrowth is essential to avoid a delayed diagnosis, which can result in irreversible visual loss due to stromal melting and infectious keratitis.- - - - - - - - - - ranking = 2keywords = keratitis (Clic here for more details about this article) |
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