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

Laser photocoagulation has changed the visual prognosis of diabetic patients affected by retinopathy. It aims to lower the risk of blindness of diabetic patients. The goal of photocoagulation is to reduce the tissue damage of microangiopathic origin expressed by nonperfusion areas and permeability abnormalities that are responsible for retinal ischemia and oedema respectively. Loss of visual acuity in the diabetic is due mainly to two causes : first, vitreous hemorrhage with its dramatic loss of vision; secondly, macular cystoid oedema, occuring more commonly and with progressive loss of central vision. The efficiency of pan-retinal photocoagulation in reducing the risk of vitreous hemorrhage and consequent blindness in patients with disc or preretinal newly formed vessels, has been ascertained by American and British randomised studies. The indications, technics and results of photocoagulation in non-proliferative diabetic retinopathy are the subject of many studies. Only photocoagulation for macular oedema due to intra-retinal microvascular abnormality has shown to be of benefit.
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PMID:[Treatment of diabetic retinopathy with laser photocoagulation (author's transl)]. 38 89

It is important to establish the diagnosis of temporal arteritis because the disease is treatable; treatment may prevent blindness and even death. Temporal arteritis usually occurs in people older than 51 years of age, although very rarely, histologically documented disease occurs in younger people. The onset may be occult, so that there are few findings. A multitude of signs and symptoms may occur such as fever, headaches, malaise, weight loss, anemia, stroke, cranial nerve palsies, polymyalgia rheumatica, aortitis and other large vessel involvement. The eye may suffer from ischemic optic neuropathy (anterior or posterior), central or cilio-retinal arterial occlusion, ophthalmic artery ischemia, or extraocular muscle palsies. An arterial biopsy showing giant cell arteritis establishes the diagnosis. However, a negative biopsy does not rule out the disease because of the occasional presence of skip areas. Arteriography has only rarely yielded a positive temporal artery biopsy when the initial biopsy done elsewhere was negative. As a diagnostic parameter, the erythrocyte sedimentation rate is nonspecific, being elevated in diseases other than temporal arteritis and sometimes being falsely lowered by technical factors. Furthermore, the temporal artery biopsy is occasionally positive despite a normal erythrocyte sedimentation rate. Treatment is aimed at relieving the patient's symptoms and normalizing the erythrocyte sedimentation rate. Because of the wide spectrum of clinical and laboratory finding in temporal arteritis, no one specific treatment regimen with systemic corticosteroids works for all patients. Temporal arteritis is a well known disease of the elderly which ir rarely fatal but results in significant visual morbidity (Hinzpeter & Naumann, 1976; Spencer & Hoyt, 1960). Since Hutchinson's (1890) description, more than a thousand articles have been written on the subject (Cohen & Smith, 1974). Despite this, many unanswered questions and controversies remain concerning the diagnosis, prognosis and treatment of temporal arteritis. My goal is to review these questions and areas of controversy.
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PMID:Controversies regarding giant cell (temporal, cranial) arteritis. 39 20

The pattern and pathogenesis of nonlocalizing visual disturbances, associated with optic disc edema (ODE). raised cerebrospinal fluid pressure, and intracranial space-taking lesions were investigated experimentally in rhesus monkeys with simulated progressive brain tumor and clinically in patients with benign intracranial hypertension. The visual disturbances occurring in one of both eyes were of three types: recurrent attacks of transient obscuration, permanent blindness, and various types of visual field defects. The studies indicate that the visual disturbances are usually due to two mechanisms. The most common is ischemia of the optic disc secondary to ODE. The other, rarer mechanism probably consists of the space-taking lesion causing downward herniation of the parahippocampal gyrus into the tentorial notch, producing compression of the lateral geniculate body and optic tract.
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PMID:Optic disc edema in raised intracranial pressure. VI. Associated visual disturbances and their pathogenesis. 40 82

A 24-year-old woman developed bilateral blindness after recovery from coma secondary to acute intermittent porphyria. Gradual return of vision in the right eye with a permanent unilateral visual field defect and optic atrophy followed. We believe the pathophysiologic mechanism was spasm of the vessels supplying the optic disk leading to ischemia and infarction of the optic nerve.
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PMID:Optic atrophy in acute intermittent porphyria. 43 76

A 10-year-old girl developed bilateral blindness and partial third nerve paresis immediately following a closed head injury. Bilateral optic atrophy developed subsequently. This is the first report of an association between second and third nerve injuries after minor head trauma in the absence of a preexisting lesion. The pathophysiology of indirect injury to the optic nerve under these circumstances is uncertain, but the lesions in this patient seemed to be due to ischemia.
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PMID:Total blindness after trivial frontal head trauma: bilateral indirect optic nerve injury. 57 Jun 62

Based on our close personal observation of several patients after blepharoplasty who developed retrobulbar hemorrhage progressing to blindness, the mechanism appears to operate through ischemia of the anterior optic nerve head. Relief of this blindness has followed prompt surgical intervention, with supportive medical therapy. The importance of close nursing observation for some hours after the operation is stressed, as it may be the only means of detecting this complication while the sight can still be saved.
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PMID:Blindness after blepharoplasty: mechanism and early reversal. 62 98

We report on three patients in whom ipsilateral blindness developed following carotid endarterectomy. Fundoscopic examination of the retina documented ischemia and the visual field defects were permanent. In one patient, the internal carotid artery was patent and thought to be the conduit for embolization to the eye. Two patients had chronic occlusion of the internal carotid artery, and blindness resulted from atheromatous emboli to the eye through the external carotid artery in one and from postoperative thrombosis of the external cartoid artery in the other. Our experience calls attention to this infrequently reported complication of carotid endarterectomy and emphasizes the importance of the external carotid artery, especially when the internal carotid artery is occluded.
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PMID:Ipsilateral blindness: a complication of carotid endarterectomy. 88 39

Amaurosis fugax (transient monocular blindness) is a symptom of retinal ischemia just as contralateral hemiparesis and sensory loss are symptoms of cerebral ischemia. These symptoms are produced by atherosclerotic stenosis of the carotid vessels at the ipsilateral carotid bifurcation and emboli from these areas causing focal, repetitive, retinal ischemia. A study of 31 endarterectomy patients was undertaken to see if eight patients with amaurosis fugax (25%) could be differentiated from 22 patients with transient cerebral ischemia. The patients with amaurosis fugax were found to be younger. They all had 75% or greater stenosis of the internal carotid artery at the bifurcation on the symptomatic side. They all had unilateral visual symptoms and these symptoms were relieved by surgery. The patients with amaurosis fugax were devoid of cardiac disease, while 45% of the cerebral ischemic patients had documented myocardial disease. Amaurosis fugax (transient monocular blindness) in the setting of clinically significant atheroslerosis of the carotid vessels is an indication for carotid endarterectomy.
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PMID:Amaurosis fugax: a clinical comparison. 117 55

Seven patients of temporal arteritis with eye involvement have been presented. These cases represent a spectrum of disease from intermittent diplopia with minimal 6th nerve weakness through mild retinal ischemia with recovery to permanent bilateral blindness. Temporal arteritis should be suspected when any form of ocular ischemia is suspected by history or found on examination of an elderly person. An early diagnosis may protect the vision in both eyes if vision is normal at the time of diagnosis. If vision in one eye is decreased because of ischemia, the vision in the other eye can usually be retained if proper therapy is instituted. Furthermore, adequate therapy may even result in improvement in vision in the involved eye. Patients with biopsy proven temporal arteritis should be continued on steroid therapy until the active disease is quiescent. Inactivity should be determined by carefully monitoring the ESR while steroids are being tapered. If the ESR rises, it is indicative of continued inflammation and if steroids are not continued, the eyes remain at risk as seen in Case 5. If the ESR remains elevated for a year or more despite continuation of high steroid levels, consideration should be given to repeating the temporal artery biopsy. Temporal arteritis should be considered in the differential diagnosis of any multisystem disease in older patients. Even central nervous system involvement may occur concomitantly, since the intracranial vessels are not immune from the disease process. Tuberculosis, systemic syphilis and more recently the collagen vascular diseases have been dubbed the "great imitators" and "the protean diseases." We suggest that the same terminology can be applied to temporal arteritis. Temporal arteritis can affect any organ. Moreover, there is a wide spectrum of variation in the degree of involvement of any particular tissue as illustrated by these 7 cases of ocular involvement.
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PMID:Temporal arteritis: a spectrum of ophthalmic complications. 118 Apr 60

In the industrialized countries, diabetic retinopathy represents the most frequent cause of blindness during the period of active life. It occurs as two distinct clinical entities: non proliferating retinopathy characterized by dilatation of the retinal capillary bed and alterations in their vascular wall responsible for an increase in permeability, and proliferating retinopathy characterized by the appearance of pre-retinal neovessels secondary to the presence of vast zones of retinal ischemia. Numerous risk factors are implicated in the development of diabetic retinopathy: the primordial factor is the optimal equilibration of blood glucose levels. The primum movens of these diabetic lesions could be intoxication of the pericipets and endothelial cells of the retinal capillaries by an accumulation of sorbitol and fructose in this region. Additionally, the hyperglycemia suppresses the functioning of the retinal blood flow feed back system. An increase in systemic blood pressure will therefore be transmitted directly to the damaged capillary bed. In type II diabetes (NID), worsening of the diabetic retinopathy correlates with elevation of the systolic blood pressure. In type I diabetes (ID), worsening of the diabetic retinopathy correlates with an elevated diastolic blood pressure. A diastolic pressure of less than 74 mm Hg is a statistically significant protective factor against the worsening of type I diabetic retinopathy.
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PMID:[Influence of arterial hypertension on diabetic retinopathy]. 149 59


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