Cases reported "Corneal Edema"

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1/15. 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.
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2/15. corneal edema after pediatric cataract surgery.

    INTRODUCTION: We have encountered idiopathic corneal edema in four patients (five eyes) after pediatric lensectomy. This problem has not been previously described in the pediatric ophthalmology literature. methods: Clinical and operative records were reviewed. The children, who ranged in age from 15 months to 6 years, underwent apparently uncomplicated limbal lensectomy without lens implantation. After surgery, all received subconjunctival hydrocortisone (12.5 mg) and 2 to 4 drops daily of topical prednisolone acetate. The corneal edema developed between 2 and 14 days after surgery. RESULTS: The condition cleared in all patients during a 5- to 14-day course of intensive topical steroids. No sequelae have been apparent. Final visual acuities are 20/30 or better in the three children (four eyes) old enough for recognition acuity testing. The fifth eye has excellent central fixation. CONCLUSIONS: We suspect that the corneal decompensation was a manifestation of sterile inflammation. Two of the children had a history of iritis. Difficulty measuring cellular response at the slit-lamp examination and instilling eyedrops at home may have contributed to the complication. Postoperative corneal decompensation can be responsive to topical steroids, which we now prescribe more intensively even in apparently quiet eyes.
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3/15. Corneal decompensation after laser in situ keratomileusis in fuchs' endothelial dystrophy.

    PURPOSE: To report corneal decompensation after laser in situ keratomileusis (LASIK) in a patient with fuchs' endothelial dystrophy.methods: Observational case report. RESULTS: A 47-year-old woman with cornea guttata without symptoms or findings of corneal edema had uneventful LASIK for -5.50 -0.50 x 150 in the right eye and -4.00 -1.25 x 170 in the left eye. Postoperatively, she developed corneal edema, with significant loss of best-corrected visual acuity in both eyes. Preoperative corneal thickness was 587 microm in the right eye and 549 microm in the left eye, measured by ultrasound pachymetry. These readings were 550 and 560 microm on day 67 postoperatively. Endothelial cell counts showed means of 1209 and 1661 cells/mm2 in the right and left eyes, respectively. CONCLUSION: Caution is suggested when considering LASIK in eyes with severe cornea guttata.
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4/15. Permanent corneal edema resulting from the treatment of PTK corneal haze with mitomycin: a case report.

    A 39-year-old man underwent phototherapeutic keratectomy via excimer laser for recurrent corneal erosions secondary to basement membrane dystrophy with the subsequent development of irregular astigmatism and central stromal opacity. The cornea was scraped and treated with 0.02% mitomycin C using a total of 14 drops over a period of 6 days. corneal edema developed as a consequence of low endothelial cell count with dysfunctional cells. A corneal transplant restored acuity of 20/20 with binocular vision. It is believed that the underlying endothelium was exposed to toxic doses of mitomycin C sufficient to damage and destroy vital cells. The author reports this case not to criticize the use of mitomycin C in visually disabling post-phototherapeutic keratectomy or photorefractive keratectomy haze but to apprize colleagues of a potential pitfall. The author believes that the use of mitomycin C as a 1-time application at the end of surgery is a safe and valuable adjunct to recover vision when no other is known. However, continued topical application of mitomycin C to the central cornea, in the face of an epithelial defect or an epithelium with inadequate barrier function, increases the risk of endothelial damage.
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5/15. calotropis procera (ushaar) keratitis.

    PURPOSE: To report a case of permanent endothelial cell injury after intracorneal penetration of milky latex from calotropis procera (ushaar). DESIGN: Interventional case report. methods: A 40-year-old patient developed painless corneal edema despite minimal epithelial injury after exposure to ushaar latex. RESULTS: Confocal and specular microscopy confirmed permanent endothelial cell loss with morphologic alteration after intracorneal penetration of ushaar latex. corneal edema resolved completely after 2 weeks, although reduced endothelial cell count and abnormal morphology persisted. CONCLUSION: Ushaar latex is capable of penetrating the corneal stroma and inducing permanent loss of endothelial cells. corneal edema resolves if sufficient endothelial cell viability is still present after resolution of ushaar keratitis.
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6/15. corneal edema and penetrating keratoplasty after anterior chamber phakic intraocular lens implantation.

    Phakic intraocular lens (IOL) implantation is an increasingly popular option in surgical correction of refractive error. To date, reports of long-term morbidity are infrequent in the literature. We encountered 3 patients who experienced corneal decompensation and cataract progression following angle-fixated anterior chamber phakic IOL placement.
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7/15. Long-term complications of iris-claw phakic intraocular lens implantation in weill-marchesani syndrome.

    PURPOSE: This study was designed to report the long-term complications of iris-claw phakic intraocular lens implantation in a patient with weill-marchesani syndrome. methods: Case report and literature review. RESULTS: A 26-year-old man with a history of glaucoma had bilateral phakic lens implantation for high myopia 10 years previously. Two years later, the left implant dislocated and was repositioned. Slit-lamp examination of both eyes revealed phakic implants of the iris-claw variety. There were moderate iridocorneal adhesions in the areas in which the lens haptics pinched the iris in both eyes and moderate epithelial and stromal edema over the temporal one-third of the left cornea. The crystalline lenses were clear with 3 phacodonesis OU. Dilated fundus examinations revealed bilateral severe optic nerve cupping. Crystalline lens diameters were measured at 7.5mm in the right eye and 8 mm in the left. anterior chamber depths were 2.63 mm OD and 2.40 mm OS. Specular microscopy revealed central endothelial cell counts of 1133 and 587 cells/mm OD and OS, respectively. Axial lengths were 23.3 mm OD and 25 mm OS. Gonioscopic examination revealed bilateral angle closure with marked peripheral anterior synechiae. Based on our findings of short stature, shortened and thickened fingers, relatively normal axial length, microspherophakia, high myopia, and glaucoma, we diagnosed the patient with weill-marchesani syndrome. CONCLUSION: iris claw-lens phakic lenses may be an effective surgical alternative to correct high myopia in select patients; however, it may produce long-term complications in eyes with specific features.
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8/15. Iatrogenic descemetorhexis as a complication of phacoemulsification.

    During clear corneal temporal phacoemulsification, an accidental iatrogenic descemetorhexis occurred. The entire cornea was hazy and edematous on the first postoperative day. By the 1-month postoperative review, the cornea had become clear with visible descemetorhexis margins; best corrected visual acuity was 20/25, and the pachymetry was 556 microm. The patient remained stable at the 2-years postoperative follow-up, and specular microscopy done at this time showed a cell density of 1301 cells/mm2 with evidence of pleomorphism and polymegethism. This is the first report of iatrogenic descemetorhexis in which the cornea had become clear and nonedematous by as early as 1 month postoperatively. This case highlights that a healthy endothelium can maintain corneal deturgescence despite a low endothelial cell count. Corneal thickness increases only when the number of endothelial cells has gone below a physiologic lower limit.
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9/15. Presumed herpetic endotheliitis following phacoemulsification surgery.

    The authors present an observational case series. Three cases of presumed herpetic endotheliitis presented as cases of pseudophakic bullous keratopathy many years after successful phacoemulsification surgery. All patients had reduction of vision in the involved eye, corneal oedema and secondary glaucoma. The patients were treated with medical therapy consisting of topical corticosteroids, antiviral and antiglaucoma drugs. Resolution of corneal oedema, control of glaucoma and restoration of visual acuity were achieved in all cases. Specular microscopy performed thereafter demonstrated relatively normal endothelial cell counts. The authors conclude that pseudophakic bullous keratopathy occurring after phacoemulsification surgery may be caused by herpetic endotheliitis.
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10/15. Interface fluid syndrome in laser in situ keratomileusis after complicated trabeculectomy.

    A 69-year-old man developed stromal edema and a pocket of fluid in the laser in situ keratomileusis (LASIK) interface wound in the left eye after acute endothelial cell loss from complicated trabeculectomy. He eventually required penetrating keratoplasty along with cataract surgery. Histologic examination of the corneal button showed an edematous 720 microm central residual stromal bed, a 54 microm empty space at the level of the central interface wound, and a 154 microm LASIK flap. The endothelial cell count was 0 to 2 cells per high-power field, corresponding to a cell density of 450 to 500 cells/mm(2). Four years after LASIK, the central interface wound was susceptible to forming a pocket of serous fluid after the corneal endothelial function was compromised.
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