Cases reported "Uveal Diseases"

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1/19. Expulsive choroidal effusion. A complication of intraocular surgery.

    Massive serous choroidal effusion may occur as an expulsive complication of intraocular surgery. The pathophysiology of expulsive hemorrhage involves rupture of the short posterior ciliary arteries, while that of effusion involves massive exudation through the walls of the choroidal vessels. Many of the predisposing factors may be shared including atherosclerosis, hypertension, and sudden surgical decompression. The treatment of both entities is the same--swift closure of the wound, drainage of suprachoriodal blood or effusion through a posterior sclerotomy site, and injection of a physiologic solution into the anterior chamber to tamponade the leaking vessels and restore normal intraocular anatomic relationships. The visual prognosis following expulsive choroidal effusion is much more favorable than that of expulsive hemorrhage.
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2/19. Uveal effusion and angle-closure glaucoma in primary pulmonary hypertension.

    PURPOSE: To report a patient with uveal effusion and intermittent angle-closure glaucoma associated with primary pulmonary hypertension. methods: Observational case report. RESULTS: A 78-year-old woman with primary pulmonary hypertension noticed pain and decreased vision in her right eye. Ocular examination disclosed excessive dilation of conjunctival and episcleral veins and uveal effusion with annular ciliochoroidal detachment in both eyes. The right eye revealed corneal edema with folds in the descemet membrane, congested iris vessels, and a markedly shallow anterior chamber with a partially closed angle, corresponding to a recent attack of angle-closure glaucoma. Systemic treatment of her congestive heart failure with an angiotensin-II receptor antagonist resulted in a partial resolution of the uveal effusion and complete normalization of the anterior chamber depth. CONCLUSION: Primary pulmonary hypertension may cause uveal effusion, leading to a forward displacement of the lens-iris diaphragm and intermittent angle-closure glaucoma.
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3/19. Ischemic optic neuropathy in a female carrier with Fabry's disease.

    We report ocular findings of a patient with anterior ischemic optic neuropathy (AION) and cilioretinal artery occlusion in a female carrier of Fabry's disease. fluorescein angiography revealed delayed filling of the upper and temporal part of peripapillary choroidal vessels and capillaries of the right optic disk and late filling of the cilioretinal artery. CT scanning was performed several times in early stages and demonstrated thickening of the intraorbital optic nerve due to ischemic edema. About 5 months later, the fellow eye showed optic disk edema, an early sign of AION, and was treated by systemic corticosteroid and urokinase whereby AION did not progress.
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4/19. Massive choroidal haemorrhage as a complication of krypton red laser photocoagulation for disciform degeneration.

    A 78-year-old man with perifoveal subretinal neovascularization originally treated with krypton red laser was re-treated. An attempt was made to produce a "chalky white" burn at the site of the neovascular frond. Immediately after a burn, a brisk choroidal haemorrhage followed, apparently from a ruptured choroidal vessel. Bleeding occurred subretinally and into the vitreous, blinding the patient. While the krypton red laser carries advantages over the argon laser in the treatment of subretinal neovascular fronds, this case indicates that hard burns with the krypton laser carry a risk of massive subretinal haemorrhage.
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5/19. Siegrist's streaks in hypertensive choroidopathy.

    The retinal and choroidal vasculatures are supplied by different systems of blood vessels, each having distinct anatomic and physiologic properties. In response to systemic hypertension, tissues supplied by each of these vascular systems of the eye are affected differently and reveal different manifestations. Siegrist's streaks are sequelae of hypertensive choroidopathy, associated with acute systemic hypertension, generally indicative of a poor prognosis for patients presenting with them. A case report of this uncommon clinical condition is described along with a discussion of the associated hisopathology to allow for a better understanding of how the eyes may change secondary to systemic vascular disease.
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6/19. An unusual macular lesion associated with malaria.

    A case of a young man afflicted with falciparum malaria is presented in which the primary ocular finding was a subpigment epithelial hemorrhage involving the macula. Previous reports in the literature concentrate on peripheral and central retinal hemorrhages, almost to the exclusion of choroidal vascular abnormalities. The value of this case lies in the recognition that the choroid can assume an important role in fundus abnormalities associated with malaria, probably on the basis of obstructive phenomena with subsequent ischemic degenerative changes, similar to the process which involves the retinal vessels and central nervous system.
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7/19. Autosomal dominant juvenile vitreoretinal degeneration and retinal detachment.

    To study the inheritance and clinical picture of a new form of vitreoretinal dystrophy I examined 18 family members of a family with six generations. Seven patients, three male and four female, in three consecutive generations were observed to be affected indicating autosomal dominant inheritance. The disease was characterized by juvenile degeneration of the vitreous with detachment of the vitreous body and some floating vitreous opacities, cystoid degeneration of the peripheral retina with whitish glistening stippled areas of superficial retinal degeneration, spotty hyperpigmentation, patches of retinal atrophy with pigmentations, occasional atrophic retinal holes, and in four family members at the age of 4 to 12 years, unilateral or bilateral retinal detachment with breaks in the peripheral retina. Most patients had hyperopia with or without astigmatism. In eyes without detached retina, the disease did not show any marked progression, the lens was clear, the posterior fundus and the retinal and choroidal vessels were normal, and the visual acuity, visual fields, dark adaptation, colour vision, electroretinograms, and visually evoked response findings were normal.
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8/19. Anterior segment fluorescein angiography in inflammatory diseases of the cornea.

    To study the vascular changes in inflammatory diseases of the cornea 22 patients with various corneal inflammations were examined by means of anterior segment fluorescein angiography. Simple avascular central and marginal corneal ulcers stained with fluorescein in the late phase of angiography. An inflamed limbus and an early microscopic pannus adjacent to the ulcer were seeen in simple corneal ulcers. Progressive pannus with pronounced fluorescein leakage was observed in chronic corneal ulcer, disciform keratitis, Mooren's ulcer, and complicated acute keratoconus. In sclerokeratouveitis and in gutter associated with rheumatoid arthritis the corneal vessels showed less leakage. The iris vessels showed fluorescein leakage as a sign of irritative iritis during the active stage of simple and chronic corneal ulcers, in disciform keratitis, Mooren's ulcer, and in graft rejection. It is concluded that anterior segment fluorescein angiography gives valuable information of the vascular architecture, flow and leakage in inflammatory diseases of the cornea.
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9/19. White thrombi in massive subchoroidal haemorrhage: indicators of the site of its origin and of the mechanism of its control.

    Sharply circumscribed white thrombi with well developed Zahn's lines resembling the free-floating ball thrombi occurring in the auricles of the heart are demonstrated histologically at the end of ruptured ciliary arteries, causing massive subchoroidal haemorrhages in two degenerated human eyes. Not only do white thrombi in subchoroidal haemorrhages, in principle, serve as indicators for the exact location of the bleeding vessel, but their formation also allows for an understanding of the natural control of arterial bleeding in the eye.
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10/19. Evidence for vasculitis in acute posterior multifocal placoid pigment epitheliopathy.

    A case of acute posterior multifocal placoid pigment epitheliopathy is presented with the unusual feature of the exposure of deep choroidal vessels which filled with dye in the early phase of the fluorescein angiogram in the center of many of the placoid lesions. Visualization of these vessels with surrounding hypofluorescence implies nonperfusion of choriocapillaris presumably due to inflammation, rather than retinal pigment epithelial blockage. The pathology of acute posterior multifocal placoid pigment epitheliopathy is probably a vasculitis of the choriocapillaries, which causes transient occlusion of these vessels and the initial hypofluorescence in the typical lesions during angiography. In many lesions the ischemia is mild enough to cause only temporary disturbance of visual function with subsequent recovery. Only in the center of some of the lesions is the inflammation severe enough to allow for the findings observed in the case presented and to account for the permanent visual defects found in some patients.
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