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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
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PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Eighteen patients with idiopathic optic neuropathy lacked symptoms and signs of cardiovascular and cerebrovascular disease, especially when compared to three groups of patients with sudden visual loss caused by retinal infarction, transient ischemia, and cerebral infarction. Many patients in the latter groups had hypertension, carotid bruits, heart disease, transient ischemic attack, and stroke. But among the patients with ischemic optic neuropathy, hypertension was the only evidence of cardiovascular disease, affecting 44% of the patients. We argue that, in many cases, ischemic optic neuropathy represents a direct and early complication of hypertension arterial disease affecting small arterioles supplying the anterior part of the optic nerve. The pathologic process may thus be similar or identical to lacunar infarction of the brain.
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PMID:Ischemic optic neuropathy as a possible early complication of vascular hypertension. 51 8

Ischaemic optic neuropathy is a well recognised cause of sudden visual loss in middle and late life. It is characterised by painless visual impairment, pale swelling of the optic disc and nerve fibre bundle field defects. Although some cases are due to cranial arteritis, the majority of patients suffer from non-arteritic diseases, particularly hypertension. The present study consists of a reveiw of 22 cases of ischaemic optic neuropathy. Apart from cranial arteritis and vascular disease, migraine and trauma appear to have a causal relationship to the disorder.
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PMID:Ischaemic optic neuropathy. 55 Sep 42

A 62-year-old lady with hypertension and diabetes developed bilateral, sequential ischemic optic neuropathy, progressive in the right eye. Because of a reported association between amiodarone and optic neuropathy with disc edema, the patient discontinued taking this medication; however, her visual loss continued. The differential diagnoses of bilateral ischemic optic neuropathy--including infiltrative optic neuropathy and temporal arteritis--were exhaustively investigated in this patient.
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PMID:Getting to the heart of visual loss: when cardiac medication may be dangerous to the optic nerves. 156 39

Optic atrophy can often be a result of arterial blood flow insufficiency associated with systemic vascular disease (cardiovascular disease, hypertension, or diabetes mellitus). The lack of adequate blood perfusion pressure can create conditions leading to anoxia and death of the nerve fiber layer with a resultant visual field defect. A case of a 63-year-old white male is presented with optic atrophy resulting from anterior ischemic optic neuropathy 5 years earlier. A review of the literature concerning the more common causes of ocular vascular insufficiency (i.e., anterior ischemic optic neuropathy, internal carotid disease, central retinal artery occlusion, and branch retinal artery occlusion) as well as diagnostic testing and therapeutic management is discussed.
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PMID:Vascular implications of optic atrophy. 163 40

Four patients with isolated acute ocular ischemic syndromes also had circulating antiphospholipid antibodies. Two patients had vaso-occlusive retinopathy and two, anterior ischemic optic neuropathy (which was successive in one). Extensive clinical laboratory evaluation identified vascular risk factors in two patients. One patient had essential thrombocytosis, confirmed by bone marrow biopsy; the other had stable hypertension and a history of coronary artery disease. These cases suggest that small vessel thrombosis in situ may be a mechanism for antiphospholipid-associated ocular and cerebral ischemia.
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PMID:Ocular thrombosis associated with antiphospholipid antibodies. 174 13

Anterior ischemic optic neuropathy is an uncommon and devastating event that can result in unilateral or bilateral blindness. It has been reported as a complication of ophthalmologic or general surgical and cardiothoracic procedures as well as a spontaneous event in severe systemic disease. Aggravating intraoperative factors include anemia, hemorrhage, hypotension, preexisting small-vessel disease, and increased intraocular pressure. We present a case of anterior ischemic optic neuropathy as a complication in a 48-year-old man undergoing extensive resection of recurrent carcinoma of the head and neck. Possible contributing risk factors in our patient include preexisting hypertension, intraoperative blood loss, previous radical neck dissection with venous compromise, intraoperative head and neck edema, and the use of tightly adherent plastic bubble-type intraoperative eye protection. The possible pathogenesis of this devastating complication and recommendations for prevention and management of anterior ischemic optic neuropathy are described.
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PMID:Anterior ischemic optic neuropathy causing blindness in the head and neck surgery patient. 174 39

We studied the effects of intra-arterial chemotherapy (IAC) with a new nitrosourea (hydroxyethyl-chloroethyl nitrosourea: HeCNU) on the visual system of 68 patients with malignant gliomas. The intra-arterial chemotherapy was given as a complementary treatment of glioma after surgery (19 patients), after tumor recurrence (28 patients) and as the preliminary treatment before radiotherapy (21 patients). Eleven patients (16%) suffered a visual complication after two or more courses of chemotherapy. The main visual symptoms included mild to major decrease of visual acuity and in some cases ocular pain, palpebral edema and conjunctival injection. The delay in onset of ocular symptoms from the last course of IAC varied from 1 week to 9 months. From ophthalmoscopic findings, visual field testing and fluorescein angiography, the visual symptoms presented by our patients could be related to ischemic optic neuropathy or retinal vasculopathy. None of the patients had hypertension, diabetes, cardiopathy or hematological disease. Statistical analysis failed to demonstrate a relationship between the occurrence of visual toxicity and patient age, number of courses of HeCNU, the vascular axis treated, total systemic dose or dose by carotid artery, suggesting a possible specific sensitivity of some patients to chemotherapy. The pathophysiology and the therapeutic implications of this visual toxicity are discussed.
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PMID:Visual toxicity following intra-arterial chemotherapy with hydroxyethyl-CNU in patients with malignant gliomas. A prospective study with statistical analysis. 174 75

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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PMID:Mechanisms of visual loss in severe proptosis. 176 22

Clinical and Doppler sonographic findings on the internal carotid artery of 218 patients with acute central retinal artery obstruction (42), branch retinal artery obstruction (43), anterior ischemic optic neuropathy (AION) (51), amaurosis fugax (AF) (21), and retinal vein occlusions (61) were evaluated. The most prominent finding was that only 1 out of 51 patients with AION and none of 61 patients with retinal vein occlusions showed a relevant stenosis or occlusion of the internal carotid artery. In contrast, however, patients with acute central retinal artery obstruction and branch retinal artery obstruction and those with AF revealed stenoses or occlusions of the internal carotid artery in approximative one-third to one-fourth of the cases. No excavation of the optic disc (cup) occurred in patients' eyes affected by AION or in the other eye. Fourteen of 51 patients with AION showed a "stuttering progression" of their visual function. The patients with progressive loss of vision were significantly younger on average than patients with permanent visual loss due to AION. Some of these cases with progressive field defects revealed an increase in edema of the optic discs and in hemorrhages. Patients with acute central retinal artery obstruction showed very high blood pressure values more often than patients with AION. Retinal emboli (Holenhorst plaques) were very often seen in patients with branch retinal artery obstruction (in 29 of 43 patients; 67%). However, they rarely occurred in patients with acute central retinal artery obstruction (5 of 42 patients). Only 1 of 51 cases with AION showed retinal emboli.
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PMID:[Acute circulatory disorders of the eye. Clinical findings and results of Doppler sonography of the internal carotid artery]. 204 32


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