Cases reported "Ocular Hypertension"

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1/7. Glaucomatous optic nerve head changes with scanning laser ophthalmoscopy.

    PURPOSE: To determine whether there are angiographic differences among normal, preperimetric and advanced glaucoma eyes using indocyanine green angiography with SLO. This method was chosen because of its sensibility to detect peripapillary capillary vessels. methods: Scanning laser opthalmoscopy was preformed on normal eyes, preperimetric glaucomas and advanced glaucomas. MATERIAL: The authors used a confocal SLO (Heidelberg Retina Angiograph-HRA) CONCLUSION: Several changes may be seen on peripapillary capillary vessels at the different glaucomatous stages. DISCUSSION: In normal subjects HRT shows preservation of the disc/cup area ratio; indocyanine green angiography shows normal prepapillary plexus pattern on the neuroretinal rim and cup. Subjects on glaucomatous preperimetric stage reveal a decrease in the disc/cup area ratio as a result of an increase of the cup area secondary to a reduction of the neuroretinal rim area. ICG at this hipertensive stage shows an increase in prepapillary plexus visualization, which may be a consequence of increased blood flow while autoregulation is still operative. Subjects with advanced glaucoma show prominent decrease in the disc/cup area ratio as well as marked capillary droupout in ICG angiography.
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2/7. Retinal and choroidal vascular occlusion after posterior sub-tenon triamcinolone injection.

    PURPOSE: To report a case of retinal and choroidal vascular occlusion occurring as a complication after posterior sub-Tenon triamcinolone injection for treatment of uveitic cystoid macular edema. DESIGN: Interventional case report. methods: Retrospective study. A 32-year-old woman with uveitis and cystoid macular edema underwent a right posterior sub-Tenon injection of triamcinolone (40 mg/ml, 1 ml total) through a superotemporal approach after topical anesthesia. After the procedure, the patient experienced severe eye pain, orbital ecchymosis, and globe proptosis consistent with retrobulbar hemorrhage. RESULTS: Dilated fundus examination of the right eye (OD) demonstrated multiple intraretinal hemorrhages with particulate white emboli occluding the retinal and choroidal vessels. visual acuity was no light perception. Ocular massage and hypotensive therapy was initiated for an intraocular pressure of 50 mm Hg. Canthotomy and cantholysis were performed. A total of 39 months post-incident, her visual acuity improved to 20/100. CONCLUSION: Posterior sub-Tenon triamcinolone injection can rarely result in retinal and choroidal occlusion. Immediate intervention may preserve limited visual acuity.
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3/7. Mechanisms of visual loss in severe proptosis.

    Vision loss in orbital hypertension secondary to sudden space-occupying lesions is usually attributed to one of three causes: central retinal artery occlusion, direct compressive optic neuropathy, or compression of optic nerve vasculature. Accepted modes of decompressive therapy include lateral canthotomy and cantholysis; drainage of localized orbital air, hematoma, or abscess; and bony wall decompression. Five cases are presented in which orbital hypertension caused severe proptosis with traction on the optic nerve and tenting of the posterior globe. Another mechanism contributing to visual loss is proposed in these cases: ischemic optic neuropathy due to stretching of nutrient vessels. In these cases, rapid posterior decompression should theoretically be favored to reduce orbital pressure and relieve traction on the optic nerve vasculature.
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4/7. Familial amyloidotic polyneuropathy: ocular manifestations with clinicopathological observation.

    Clinical findings of ocular involvement in two patients with familial amyloidotic polyneuropathy are described. Both cases revealed irregular pupillary margin, white membranous material on the pupillary border and on the lens surface. Open-angle glaucoma was found in one case, and ocular hypertension in the other. Histopathological examination of the tissues obtained during trabeculectomy in Case 1 revealed a large amount of amyloid substance around the vessels of the conjunctiva and the iris and in the endothelial meshwork of the chamber angle. Electron microscopic observation revealed that amyloid fibrils had formed in the basement membrane of the endothelial cells of the blood vessels in the conjunctiva and the iris. However, no amyloid fibrils were observed in the endothelial cells of the trabecular meshwork. Crossed immunoelectrophoresis of the aqueous humor of Case 1 showed a high-protein content, especially of alpha 1-lipoprotein and ceruloplasmin. The findings described above suggest that glaucoma or ocular hypertension in association with familial amyloidotic polyneuropathy is a result of the accumulation of amyloid substance in the endothelial meshwork.
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5/7. Solitary silent venous papillary loops and ocular hypertension.

    A series of 24 eyes in 23 patients is described showing solitary silent venous papillary loops. These loops are usually associated with a considerable degree of ocular hypertension, presenting when this hypertension is being investigated. They are silent, usually with no previous ocular history, single with a large diameter, affecting veins at the optic disc and not extending into the vitreous. The optic disc is cupped, but usually not more than 0.6 disc diameter, there is good central vision and either a full visual field or only early field loss. fluorescein angiography shows the loops to be competent with no evidence of any other retinal vascular abnormality. Rarely loss of central vision may occur due to progression to advanced glaucoma. The condition is distinct from prepapillary vascular arterial papillary loops, neovascularization at the optic disc and optociliary shunt vessels. It is also distinct from the venous collateral vessels which develop at the optic disc after acute central or branch retinal vein occlusion. These collaterals are usually multiple, the accompanying ocular hypertension is of lesser degree, cupping of the disc and field loss are usually much more advanced and, while visual acuity may be normal, it is often grossly reduced. On fluorescein angiography all these cases of venous collaterals after retinal vein occlusion showed evidence of other retinal vascular dysfunction. Solitary silent venous papillary loops appear to develop from venules on the optic disc as a bypass to a low grade venous occlusion which is seldom clinically manifest. They form a distinct entity with a good prognosis if the accompanying ocular hypertension is carefully controlled.
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6/7. Choroidal ischemia after extracapsular cataract extraction by phacoemulsification.

    Three patients developed apparent choroidal ischemia after phacoemulsification. The outer half of the posterior retina appeared white after operation, with confluent lesions in the posterior pole and splotchy white areas in the midperiphery. The separate lesions appeared similar in pattern to the lobular division of the choriocapillaris, and the retinal vessels were not involved. The white lesions resolved in two to three weeks, leaving alterations in the pigment epithelium. Vision was transiently reduced in each eye but returned to a nearly normal level in two of three affected eyes, although paracentral scotomas persisted. In each case of phacoemulsification, the posterior lens capsule was either damaged or was removed. In all three cases, an investigational type of irrigating solution (BSS Plus) containing balanced salt, glutathione, and other constituents was used. Controlled ocular compression was performed before operation using a pneumatic device in two cases. However, the cause of retinal and choroidal damage now described was probably excessively elevated intraocular pressure during the operation.
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7/7. Visual field loss following vitreous surgery.

    OBJECTIVE: To assess possible causes of visual field loss following vitreous surgery. DESIGN: charts of 8 patients prospectively identified, who developed visual field loss following vitreous surgery, were reviewed to characterize this newly recognized syndrome and assess possible causes. RESULTS: Two patients had preexisting chronic open-angle glaucoma and 1 had ocular hypertension. Indications for surgery included 4 eyes with macular holes, 1 eye with epiretinal membrane, 2 eyes with rhegmatogenous retinal detachment, and 1 eye with retinal detachment and giant retinal tear. All patients received retrobulbar anesthesia. Seven of 8 patients had fluid/gas exchange with installation of long-acting bubbles. In 1 patient with a macular hole, a small hemorrhage was noted along a vessel coming off the nerve superotemporally while attempting to engage the posterior cortical vitreous intraoperatively. This patient developed an inferior visual field defect. No intraocular pressure (IOP) measurements greater than 26 mm Hg were recorded in any eye perioperatively. Visual field defects included 4 eyes with inferotemporal defects, 2 eyes with inferior altitudinal defects, 1 eye with a cecocentral scotoma, and 1 eye with a superonasal defect. Only 1 patient had worsened visual acuity. A relative afferent pupillary defect was observed in 4 eyes and disc pallor in 5 eyes. CONCLUSIONS: Central or peripheral visual field loss can now be recognized as a possible complication of vitreous surgery. In some cases, a relative afferent pupillary defect and optic disc pallor are present, suggesting that the optic nerve is the site of injury. Possible mechanisms include ischemia due to elevated IOP or fluctuations in IOP, optic nerve damage from retrobulbar injection, direct intraoperative mechanical trauma to the optic nerve, indirect injury from vigorous suction near the optic nerve leading to shearing of peripapillary axons or vessels, or a combination of these. Certain optic nerves may be more susceptible to injury because of preexisting compromise from glaucoma or vascular disease.
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