Cases reported "Corneal Edema"

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1/10. Cataract surgery in a patient with Brown-McLean syndrome.

    The Brown-McLean syndrome is defined by corneal edema that involves the peripheral 2.0 to 3.0 mm of cornea, sparing the central cornea. This syndrome is usually associated with previous cataract surgery but has been reported rarely in patients with other predisposing factors such as angle-closure glaucoma or spontaneous lens absorption with iridodonesis. We describe the clinical course of a 50-year-old man with myotonic dystrophy who had Brown-McLean syndrome with no identifiable predisposition for peripheral corneal edema. Although this syndrome appears to be the result of peripheral endothelial dysfunction, this patient was able to tolerate cataract extraction without developing central corneal edema.
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2/10. Corneal decompensation and graft failure secondary to a broken posterior chamber poly(methyl methacrylate) intraocular lens haptic.

    A 66-year-old man developed an unexplained corneal decompensation 7 years after extracapsular cataract extraction and implantation of a single-piece poly(methyl methacrylate) (PMMA) posterior chamber intraocular lens (IOL). He had penetrating keratoplasty (PKP). Two years later, he developed corneal graft failure secondary to an IOL haptic fragment in the anterior chamber angle. The patient had a repeat corneal graft and IOL exchange. The broken haptic was examined with scanning electron microscopy. The findings were consistent with late fracture of the haptic within the capsular bag, which was presumably weakened by an improper implantation technique. Fracture of a PMMA haptic should be suspected as a cause of corneal decompensation and corneal graft failure after cataract surgery. This case emphasizes the importance of safe implantation techniques.
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3/10. Clinical and pathologic findings of aphakic peripheral corneal edema: Brown-McLean syndrome.

    Twenty-two patients (36 eyes) are reported with Brown-McLean syndrome, which consists of peripheral corneal edema associated with peripheral endothelial pigment deposits, usually after intracapsular cataract extraction. This group, the largest reported to date, had a spectrum of corneal alterations, those at the more severe end of the spectrum being both progressive and symptomatic. Some patients required medical and surgical treatment, including keratoplasty. Four corneas (two obtained surgically, two postmortem) were examined by light and electron microscopy (EM). Centrally, the corneas were relatively normal, but peripherally there were disintegrated endothelial cells with an abnormal posterior collagenous layer of Descemet's membrane. Scanning EM showed a somewhat distinct junction between the normal central endothelium and the diseased peripheral endothelium.
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4/10. Recurrent corneal oedema following late migration of intraocular glass.

    This is a report of very late complications following intraocular penetration of numerous fragments of glass as a result of a test tube explosion. Fifteen years after the initial injury glass splinters began to migrate from the vitreous into the anterior chamber, causing acute episodes of corneal oedema. Four such episodes occurred over the past nine years, the corneal oedema each time disappearing within a few days following surgical extraction of the glass splinters. The literature on intraocular glass and its movement within the eye is reviewed.
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5/10. Spontaneous detachment of Descemet's membrane. Case report and literature review.

    Detachment of Descemet's membrane is an unusual cause of postoperative corneal edema. The typical detachment is small and usually limited to the area near the limbal wound. These peripheral detachments usually heal without sequelae as endothelium spreads over the area and secretes a new Descemet's membrane. We report an unusual case of spontaneous, extensive central separation of Descemet's membrane occurring 3 weeks following uncomplicated extracapsular cataract extraction with posterior chamber lens implant. Attempted reattachment of the membrane with intracameral air was only partially successful, but 12 weeks later the detachment spontaneously resolved with recovery of vision to 20/30. An anatomic predisposition may be implicated, because the fellow eye exhibits the diffuse thickening of Descemet's membrane. Descemet's detachment is a rare but potentially reversible cause of corneal edema following cataract surgery and should not be confused with early-onset pseudophakic bullous keratopathy.
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6/10. Linear endotheliitis.

    We treated six eyes of five patients with linear endotheliitis. This entity appears clinically as a line of keratic precipitates on the corneal endothelium that progresses centrally and is accompanied by peripheral stromal and epithelial edema. All five patients had ocular pain, redness, and photophobia. One eye had an episode of a dendritic lesion typical of herpes simplex. Two eyes had a history of cataract extraction before developing linear endotheliitis. We treated all patients aggressively with a combination of corticosteroids and antiviral agents. Complete resolution of inflammation and edema occurred in all cases. Four patients required the use of oral acyclovir to control the inflammation and prevent recurrence of the disease. Linear endothelitis is a distinct form of endotheliitis that may be associated with herpes simplex virus, and treatment included corticosteroid and antiviral therapy.
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7/10. Pars plana vitrectomy in the management of vitreous touch syndrome.

    The management of three patients with aphakic bullous keratopathy by means of pars plana vitrectomy is described. The patients had previously undergone uneventful intracapsular cataract extraction with intact vitreous face. Eventual herniation of the vitreous into the anterior chamber with resultant corneal endothelial touch caused the corneal edema in all three cases. Pars plana vitrectomy resulted in resolution of photophobia and irritation. The visual acuity improved from 20/200, 20/200 and 20/70 to 20/70, 20/60 and 20/40 respectively. The central cornea was cleared of edema in all three cases. The final vision was limited in two of the patients by the persistence of preoperative cystoid macular edema. Pars plana vitrectomy may be used in the management of selected cases of aphakic bullous keratopathy from vitreous touch.
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8/10. Brown-Mclean syndrome associated with corneal endotheliitis in a pseudophakic eye.

    A healthy 65-year-old woman had uncomplicated unilateral extracapsular cataract extraction followed by iridocapsular intraocular lens (IOL) implantation. Three and one half years after surgery, the inferior cornea developed marked edema with moderate retrocorneal precipitates, a phenomenon that recurred three more times during her eight-year postoperative course. Values obtained by laser flare cell meter coincided with each recurrence of corneal edema. Each occurrence was managed well by steroid therapy. Corneal endothelial cell density of the affected eye changed from a presurgical value of 3,260 cells/mm2 (central) to 553 (upper), 519 (central), and 363 (inferior). The intraocular lens was not touching the cornea, and there were no signs of general and local herpetic infections. The recurrent corneal edema responded well to steroid therapy, suggesting concurrent corneal endotheliitis and Brown-Mclean syndrome.
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9/10. Clinical findings in Brown-McLean syndrome.

    The Brown-McLean syndrome is a clinical condition with corneal edema involving the peripheral 2 to 3 mm of the cornea. The edema typically starts inferiorly and progresses circumferentially, but spares the central portion of the cornea. Additionally, the edema is associated with a punctate orange-brown pigmentation on the endothelium underlying the edematous areas. Central cornea guttata is frequently seen. This condition occurs most frequently after intracapsular cataract extraction, but may also occur after extracapsular cataract extraction and phacoemulsification, or pars plana lensectomy and vitrectomy. Surgical complications and multiple intraocular procedures are frequently observed in these patients. Less frequently, the Brown-McLean syndrome can occur in eyes that have not had surgery. We studied the clinical characteristics of 43 affected eyes of 32 patients. New findings included Brown-McLean syndrome occurring in two eyes of a phakic patient with intermittent angle-closure glaucoma. Two eyes developed Brown-McLean syndrome after phacoemulsification and one eye developed peripheral edema after pars plana vitrectomy and lensectomy. Additionally, severe, infectious keratitis occurred after rupture of peripheral bullae in two eyes. patients with this condition should be examined periodically and educated regarding the early clinical signs of corneal ulceration.
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10/10. Brown-McLean syndrome occurring in a corneal graft.

    PURPOSE: To present a case of Brown-McLean syndrome occurring in a transplanted cornea. methods: Retrospective case report. RESULTS: A patient had penetrating keratoplasty performed for bullous keratopathy 6 years after intracapsular cataract extraction in the right eye. She developed atypical Brown-McLean syndrome in the left eye 6 years after extracapsular cataract extraction with pupil-support intraocular lens (IOL) insertion and later IOL removal. The clear corneal graft in the right eye developed peripheral stromal and epithelial edema with pigmentation of the endothelium, consistent with Brown-McLean syndrome 9 years after keratoplasty. CONCLUSION: Brown-McLean syndrome can occur in a grafted cornea, although the features may differ from those seen in ungrafted corneas.
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