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

Stereophotographs of the optic disc were reviewed in 78 patients with ischemic optic neuropathy (ION). Only 10% (6) of 61 nonarteritic (idiopathic) ION eyes developed optic disc cupping similar to that seen in glaucomatous eyes. Five of ten eyes with ION due to giant cell arteritis had cupping simulating glaucoma; however, two had elevated intraocular pressure, and the other three had large physiologic cups in the opposite eye. Optic disc pallor was proportionately more severe in ION eyes than in glaucomatous eyes of similar cup size. While there are similarities in the type of visual field loss in ION and glaucoma, the two disorders differ in the usual appearance of the disc after field loss has occurred and in the portion of the field most frequently affected. These observations suggest that if both disorders have an ischemic mechanism, there is a difference in the nature or distribution of the ischemia. There should be little difficulty under most circumstances in making the clinical differentiation between a disc that has suffered ION and a disc that has suffered pressure-induced damage, although occasional instances of ION may be classified as low-tension glaucoma on the basis of field loss and cupping without elevated intraocular pressure.
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PMID:Cupping of the optic disc in ischemic optic neuropathy. 92 94

Eight patients with proliferative diabetic retinopathy developed extensive retinal arteriolar and capillary obstruction. Ophthalmoscopy showed many white, thread-like retinal arterioles associated with capillary and venous dilatation. Widespread retinal arteriolar and capillary nonperfusion was demonstrated by fluorescein angiography. Ischemic maculopathy resulted in severe loss of visual acuity in some eyes. The severe degree of retinal ischemia was accompanied by optic disc pallor and neovascularization and a high incidence of rubeosis iridis with neovascular glaucoma. Patients with this variety of diabetic retinopathy have a poor prognosis of retaining useful vision.
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PMID:Retinal ischemia in diabetic retinopathy. 120 Aug 95

We examined 11 brains of human immunodeficiency virus (HIV) seropositive cases who died from unnatural causes (10 intravenous drug abusers who died from heroin overdose and 1 homosexual dead from a gunshot injury); 10 brains of HIV seronegative heroin addicts who died from overdose and 1 seronegative drug abuser who died from gunshot injury served as controls. Complete postmortem examination did not show evidence of acquired immune deficiency syndrome (AIDS) or AIDS related complex. Terminal changes including nerve cell ischemia, edema and diffuse vascular congestion were observed in all cases. Perivascular pigment deposition with macrophages was a constant finding in drug addicts and was probably related to chronic intravenous injection. In contrast, cerebral vasculitis was significantly more frequent and marked in HIV seropositive cases and was often associated with lymphocytic meningitis. Granular ependymitis, myelin pallor with reactive astrocytosis and microglial proliferation were also more frequent and more severe in HIV seropositive cases. Immunocytochemistry was negative for HIV antigens. Our study further supports the view that early central nervous system changes occur in HIV infection.
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PMID:Early brain changes in HIV infection: neuropathological study of 11 HIV seropositive, non-AIDS cases. 153 41

Acute embolic occlusion of a peripheral artery requires rapid and precise diagnosis in order to provide the appropriate treatment without delay. The symptoms and findings of acute arterial occlusion are characterized by "the six Ps": pain of sudden onset in the hypoperfused extremity, paleness, pulselessness, paresthesias, paralysis and, in the extreme case, prostration with the symptoms of shock. With embolization in arterial segments with only minimal residual perfusion via collaterals (for example, the femoral bifurcation), a complete ischemic syndrome is usually incurred manifesting the six Ps as delineated. If preformed collateral systems provide some perfusion distal to an arterial occlusion (for example, in the common iliac artery), there is frequently an incomplete ischemic syndrome observed which is characterized by pain, paleness and pulselessness. Peripheral arterial embolism has a predilection for the femoral bifurcation, the superficial femoral artery and the popliteal artery. In principle, however, embolization can occur in every arterial segment. The diagnosis of the acute ischemic syndrome can generally be established on the basis of the history and physical examination. Diagnostic aid can be provided by electronic segmental oscillography to demonstrate diminished or absent oscillations and with the Doppler sonographically-determined systolic arterial pressure at the ankle which, in the case of severe ischemia, is less than 50 mmHg. Arteriography provides the most accurate morphological information. Abrupt occlusion of the vessel and no collateral perfusion especially in the absence of arteriosclerotic changes are strongly indicative of embolism but not conclusive. If the clinical diagnosis is unequivocal, arteriography need not be performed prior to embolectomy with a Fogarty catheter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The diagnosis of peripheral arterial embolism]. 176 45

Acute arterial occlusion in an extremity must be treated as a medical-surgical emergency since not only the affected limb is endangered, but the life of the patient as well. The cause of the acute occlusion is an embolism or in situ thrombosis. The most common source of embolism is the heart from which about 30% of the cardiac emboli obliterate the bifurcation of the femoral artery and about 4/5 of all emboli involve the extremities. Arterio-arterial emboli arise from aneurysms or from nonocclusive, ulcerated atheromatous plaques. Acute in situ thrombosis occurs mostly at the site of stenotic arteriosclerotic lesions. Aneurysms and dilated forms of atherosclerosis can be both the cause of in situ thrombosis as well as the source of an embolism. Differentiation between thrombosis and embolism can be extremely difficult but for acute treatment, however, it is of little relevance. There is a peak of both events in the seventh and eighth decades. On complete occlusion without adequate collaterals, the presentation is characterized by "the six Ps": pain, pallor, pulselessness, paresthesia, paralysis and prostration. With acute occlusion of central points such as the aortic bifurcation or the femoral artery bifurcation, there is complete ischemia with onset of rhabdomyolysis after four to six hours which can lead to severe local and generalized symptoms due to the dangerous metabolites released. In contrast, occlusion of isolated lower leg arteries usually only lead to transient symptoms. If arterial occlusion is suspected, prior to transportation to the hospital, 5000 I.E. heparin should be given intravenously. Acute thrombotic occlusion of large arteries is the surgical domain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy of acute peripheral arterial occlusion]. 183 82

Medical personnel should be able to recognize vascular injuries. Knowing the key signs of ischemia, namely pallor, pulselessness, pain, paresis, and paresthesia and the soft signs of vascular injury will help to prevent limb loss.
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PMID:Recognition of vascular injury in the trauma patient. 211 86

Oxygen affinity of hemoglobin, erythrocyte 2,3-diphosphoglycerate (DPG) and adenosine triphosphate (ATP) concentrations were compared before and after oral administration of vinpocetine (TCV-3B) (15 mg/d), a primarily vasodilating agent, for three weeks in eight patients with vascular dementia of the Biswanger type which is characterized by diffuse myelin pallor and multiple lacunes in the cerebral white matter. After vinpocetine administration, oxygen affinity of hemoglobin (P50) was significantly increased (26.5 +/- 0.55 to 27.6 +/- 0.62 mmHg; mean and standard deviation, p less than 0.05), red blood cell (RBC) ATP concentrations were significantly increased (846 +/- 168 to 1,158 +/- 130 mumol/l RBC, p less than 0.05), while DPG concentrations were unaltered (4.46 +/- 0.48 to 4.59 +/- 0.57 mmol/l RBC). There was a significant positive correlation between the increase of P50 and the increase of erythrocyte ATP concentrations (r = 0.67, p less than 0.05). The effect of vinpocetine of enhancing oxygen release of hemoglobin may offer an additional benefit to its primary vasodilating action in the treatment of vascular dementia of the Binswanger type due to chronic ischemia.
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PMID:Effect of vinpocetine on oxygen release of hemoglobin and erythrocyte organic polyphosphate concentrations in patients with vascular dementia of the Binswanger type. 239 97

Unilateral transient cerebral ischemia was produced in Mongolian gerbils by clipping the left common carotid artery for 1 h. About 60% of the gerbils with neurological symptoms had post-ischemic seizures. The majority of those that had seizures died within a few days, and sections of their cerebral cortices contained many dark and shrunken neurons. However, the gerbils that did not have seizures survived without any severe complications. In the cerebral cortex of the latter, the neurons with diffuse or peripheral pallor of the perikarya were seen along with a small number of dark and shrunken neurons. Diffuse pallor occurred within a few hours following ischemia in layers III, V, and VI, and disappeared 1 or 2 days after recirculation. Electron microscopically, these neurons showed dispersion of ribosomes, simple and elongated profiles of rough endoplasmic reticulum (r-ER), clustered vacuoles, and mild to moderate mitochondrial swelling. Occasional net-like tubulomembranous structures, probably derived from r-ER, were observed. On the other hand, peripheral pallor became apparent after 5 days following ischemia, usually involving layer II first and gradually extending to the deeper layers. Concomitantly, the amount of neuropil decreased and the dendrites exhibited tortuosity and irregularity in layer II. Electron microscopically, these neurons showed marked swelling of peripheral perikarya and polyribosomes and organelles were located peripherally to the nuclei. In addition, numerous degenerated axon terminals and distended dendrites were observed around the neurons. These observations indicate that diffuse pallor represents damage directly induced by ischemia and subsequent recirculation, while peripheral pallor is the delayed and remote effect of ischemia, probably due to degeneration of neuronal processes.
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PMID:Morphological studies on cerebral cortical lesions induced by transient ischemia in Mongolian gerbil--diffuse and peripheral pallor of the neuronal perikarya. 273 84

Arterial embolism is usually caused by cardiac disease, and atherosclerotic coronary vascular disease is the primary precursor. Other cardiac states, as well as several uncommon causes, are part of the etiologic spectrum. The earliest signs are pain, paresthesias, pallor, and pulselessness. Severe ischemia is indicated by paralysis, a late feature. Arterial embolism and acute thrombosis can be difficult to distinguish, and deep venous thrombosis may also be suspected in the differential diagnosis. To restore arterial flow, anticoagulation treatment with heparin (Lipo-Hepin, Liquaemin) is given and surgical embolectomy is performed. Heparin infusion is continued until the patient is ambulatory, and then warfarin sodium (Coumadin, Panwarfin) is given over the long term. Fibrinolysis has also been used to treat acute arterial occlusion. Complications of embolism must be carefully guarded against, and additional procedures are sometimes necessary.
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PMID:Management of arterial emboli. Gleanings from 20 years of experience. 357 97

Eight baseball players developed digital ischemia as a result of repetitive ball impact. Symptoms and signs were coolness, numbness, cyanosis, paleness, and a positive reaction to the digital Allen's test. Seven of the eight players developed digital ischemia between the ages of 16 and 17. Angiograms of four patients with an occluded index digital artery are presented. Thermograms of four patients with a cool area of the left index finger are also presented. We investigated the incidence of digital ischemia by administration of a questionnaire. The respondents were 578 players belonging to clubs in junior high schools, high schools, and colleges. No digital ischemia was found in 207 junior high school baseball players. The incidence increased in high school (66 of 299) and college (29 of 72). The probability of developing digital ischemia corresponded to the accumulated playing time. Digital ischemia occurred characteristically in the left index finger.
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PMID:Digital ischemia in baseball players. 372 87


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