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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anterior segment ischemia changes can occur without detachment of any muscles. The most common cause of such ischemic changes of the anterior segment is the removal of too many rectus muscles in one operation. Twenty dog eyes and eight monkey eyes were subjected to the disinsertion and detachment of various combinations of extraocular muscles. They were sacrificed at intervals from 30 to 90 days. During the observation period, they were observed for gross and slit lamp changes. The enucleated eyes were studied microscopically for signs of ischemic and necrotic changes. Two patients who were studied, observed, and treated for anterior segment ischemia following muscle surgery are described. The changes which occur after muscle surgery are extensive and include corneal edema, cataract, chemosis, corneal changes, decreases in intraocular pressure, decreases in outflow or glaucoma and frank necrosis. The variables which lead to this reaction is described in detail. Also, some unanswered queries, such as the duration of the reaction and the time interval of the reaction after multiple muscle surgeries, are discussed.
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PMID:Production of anterior segment ischemia. 10 21

Anterior segment ischemic changes can occur without detachment of any muscles. The most common cause of such ischemic changes of the anterior segment is the removal of too many rectus muscles in one operation. Twenty dog eyes and eight monkey eyes were subjected to the disinsertion and detachment of various combinations of extraocular muscles. The dogs were sacrificed at intervals from 30 to 90 days. During the observation period, they were observed for gross and slit-lamp changes. The enucleated eyes were studied microscopically for signs of ischemic and necrotic changes. Two patients who were studied, observed, and treated for anterior segment ischemia following muscle surgery are described. The changes which occur after extraocular muscle surgery are extensive and include corneal edema, cataract, chemosis, corneal changes, decreases in intraocular pressure, decreases in outflow or glaucoma, and frank necrosis. The variables which lead to this reaction are described in detail. Also, some unanswered queries, such as the duration of the reaction and the time interval of the reaction after multiple muscle operations are discussed.
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PMID:Production of anterior segment ischemia. 41 49

We morphologically investigated what kinds of inflammatory cells infiltrate the corneoscleral limbus by light and electron microscopy and what manner of keratocytes and vascular endothelial cells appear at the corneal limbus, when the corneal edema was aggravated severely and clinical corneal new vessels were found initially, i.e. until three days after anterior segmental ischemia in rabbit eyes. The majority of infiltrating inflammatory cells were polymorphonuclear leukocytes and the others were lymphocytes and histiocytes etc. Peripheral keratocytes around limbal vessels were stimulated and transformed to fibroblastic cells as a result of anterior segment ischemia. Proliferating endothelial cells of comparatively minor limbal vessels invaded between corneal lamellar layers toward the corneal center. Polymorphonuclear leukocytes were often found near activated keratocytes proliferating vascular endothelial cells, hear and there. Consequently, it is considered that the stimulated polymorphonuclear leukocytes play an important role when corneal neovascularization occurs after anterior segmental ischemia.
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PMID:[Morphological study of experimental corneal neovascularization after anterior uveal ischemia]. 247 4

This experiment was performed to investigate the correlation between morphological changes of the corneal endothelium and clinical corneal edematous opacities after a procedure causing obstruction of bilateral long posterior ciliary arteries of the albino-rabbits. Shortly after the procedure, corneal endothelium became irregular on the anterior-chamber side and there were numerous lysosomal granules in the cytoplasm of corneal endothelial cells. On the third day, endothelial cells became necrotic and collapsed and a part of the cells peeled into the anterior chamber. Fibroblast-like cells and inflammatory cells were piled up in severely damaged areas of the endothelium. On the 11th day, the corneal endothelium developed again as a single layered structure on Descemet's membrane. It's seemed that corneal edema was induced as a result of severe damage corneal endothelium exposed to biochemical mediators such as prostaglandins released into the aqueous humor because the severity of corneal edema indicated some relation to changes in the concentration of prostaglandins in aqueous humor after anterior segmental ischemia.
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PMID:[Morphological study of corneal edema after anterior segment ischemia]. 281 80

In a 79-year-old woman with temporal arteritis, an attack of corneal edema coincided with an ischemic attack of the anterior eye segment. Specular microscopy 17 months after the acute attack demonstrated a 72% endothelial cell loss on the side with previous edema as compared to the other side without corneal involvement. The development of endothelial damage is assumed to be caused by ischemia of the endothelial cells during the acute phase, which, in turn, caused the corneal edema.
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PMID:Corneal edema as a result of ischemic endothelial damage: a case report. 709 39

The involvement of platelet-activating factor (PAF) in the development of anterior segment necrosis after occlusion of the bilateral long posterior ciliary arteries was investigated in rabbits. With the progression of anterior segment necrosis, which was characterized by corneal edema and neovascularization, the contents of protein and total phospholipids increased in the cornea and aqueous humor, but not in the iris. PAF acetylhydrolase activity was significantly increased on the first postoperative day in the peripheral cornea and on the second day in the central cornea prior to the development of marked corneal edema and neovascularization, but it did not increase in the iris. The accumulation of newly synthesized PAF in the cornea reached a plateau level on the third postoperative day, which coincided with the progression of the corneal lesion. In the aqueous humor, PAF acetylhydrolase activity was increased by the induced ischemia, but no PAF was detected. The increased PAF acetylhydrolase activity may reflect adaptation to the participation of PAF in the progression of anterior segment necrosis.
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PMID:Corneal PAF acetylhydrolase increases in anterior segment ischemia in rabbits. 840 66

A retrospective study was performed to determine the complications that occurred after cyclophotocoagulation. The condition of 33 eyes in 25 patients was observed from 1 month to 1 year after application of cyclophotocoagulation with a neodymium:YAG (Nd:YAG) laser for open-angle glaucoma. The number of treatment burns ranged from 16 to 50, and laser output energy ranged from 3 to 7 J. Complications included anterior uveitis in 14 eyes (42%), conjunctival injection in 12 eyes (36%), pain in 9 eyes (30%), and conjunctival hemorrhage in 5 eyes (15%). Corneal edema, intraocular pressure spikes, and corneal epithelial defects were each noted in three (9%) of the eyes treated, whereas cataracts developed in four (12%) of the eyes. Two eyes (6%) developed anterior segment ischemia with subsequent phthisis bulbi. Seven eyes (21 %) demonstrated no adverse reactions.
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PMID:Complications of neodymium:YAG cyclophotocoagulation in the treatment of open-angle glaucoma. 1052 83

Vasospasm can have many different causes and can occur in a variety of diseases, including infectious, autoimmune, and ophthalmic diseases, as well as in otherwise healthy subjects. We distinguish between the primary vasospastic syndrome and secondary vasospasm. The term "vasospastic syndrome" summarizes the symptoms of patients having such a diathesis as responding with spasm to stimuli like cold or emotional stress. Secondary vasospasm can occur in a number of autoimmune diseases, such as multiple sclerosis, lupus erythematosus, antiphospholipid syndrome, rheumatoid polyarthritis, giant cell arteritis, Behcet's disease, Buerger's disease and preeclampsia, and also in infectious diseases such as AIDS. Other potential causes for vasospasm are hemorrhages, homocysteinemia, head injury, acute intermittent porphyria, sickle cell disease, anorexia nervosa, Susac syndrome, mitochondriopathies, tumors, colitis ulcerosa, Crohn's disease, arteriosclerosis and drugs. Patients with primary vasospastic syndrome tend to suffer from cold hands, low blood pressure, and even migraine and silent myocardial ischemia. Valuable diagnostic tools for vasospastic diathesis are nailfold capillary microscopy and angiography, but probably the best indicator is an increased plasma level of endothelin-1. The eye is frequently involved in the vasospastic syndrome, and ocular manifestations of vasospasm include alteration of conjunctival vessels, corneal edema, retinal arterial and venous occlusions, choroidal ischemia, amaurosis fugax, AION, and glaucoma. Since the clinical impact of vascular dysregulation has only really been appreciated in the last few years, there has been little research in the according therapeutic field. The role of calcium channel blockers, magnesium, endothelin and glutamate antagonists, and gene therapy are discussed.
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PMID:Vasospasm, its role in the pathogenesis of diseases with particular reference to the eye. 1128 96

A 52-year-old man had loss of vision and black discoloration of the lids of the right eye after a retrobulbar injection of 3 mL lidocaine hydrochloride 2% (Xylocaine). Examination of the right eye revealed no light perception with extensive necrosis of the lids. Anterior segment examination revealed conjunctival pallor, corneal edema, and necrosis of the sclera. This is a previously unreported complication of retrobulbar anesthesia comprising ophthalmic artery occlusion with scleral melt, ocular ischemia, and eyelid necrosis.
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PMID:Necrosis of the eyelids and sclera after retrobulbar anesthesia. 1268 60

Clinical aspects and prognosis of corneal burns mainly depend on the agent responsible for the trauma. The most severe burns are caustic burns, which should be classified as burns caused by basic agents, associated with deep and prolonged injuries, and burns caused by acidic agents, associated with more superficial injuries. At the acute stage, caustic burns induce epithelial defects, corneal edema, and ischemic necrosis of the limbus, conjunctiva, iris and ciliary body. At the early stage, reepithelialization occurs and is often associated with corneal vascularization and stromal infiltrates, followed by corneal scar formation. At the chronic stage, the following complications are possible: corneal scars, limbal stem cell insufficiency, lachrymal insufficiency, irregular astigmatism, ocular surface fibrosis, cataract, glaucoma, decreased intraocular pressure, and ocular atrophy. The Ropper-Hall classification is based on the extent of limbal ischemia. Thermal burns induce epithelial defects at the acute stage, with the more severe forms giving the same complications as caustic burns. Radiation-related burns can be caused by ultraviolet radiations (acute epithelial keratitis, pterygium, droplet-like keratitis), microwaves, infrared radiations, ionizing radiations or, laser radiations. Electrical burns are often a result of torture and give corneal stroma opacification.
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PMID:[Clinical aspects of corneal burns]. 1568 32


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