Cases reported "Infarction"

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1/8. Idiopathic intimal hyperplasia of small arteries and arterioles affecting intestines and myocardium.

    We report the case of a 52-year-old woman dying from a noninflammatory, occlusive vasculopathy. histology showed marked intimal hyperplasia of small arteries of the intestines and myocardium with subsequent infarction of myocardium, large intestine and gallbladder. A comprehensive work up including laboratory studies, clinical investigations and postmortem failed to assign this condition to any of the known vascular diseases.
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keywords = arteriole
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2/8. Lupus vasculopathy combined with renal infarction: unusual manifestation of lupus nephritis.

    A 30-year-old woman with a 10-year history of systemic lupus erythematosus was admitted to our hospital because of the onset of hypertension and renal dysfunction. Renal arteriogram revealed multiple renal infarctions, and cut-off or tapering-stenosis in the interlobular arteries. Renal biopsy showed concentric intimal thickening with narrowed lumen in some arterioles and deposition of IgG/IgM/complement 3 in the wall of arteriole without any active lesions or immune complex deposition in glomeruli. The present case indicates that this type of renal vascular lesion in lupus nephritis, lupus vasculopathy, may cause renal infarction and the loss of renal function without active glomerular lesions.
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3/8. spinal cord infarction following intraaortic balloon support.

    infarction of the lumbar and sacral spinal cord was demonstrated at autopsy of a 72-year-old man in whom acute paraplegia developed following coronary artery bypass grafting and atrial septal defect repair with intraoperative insertion of an intraaortic balloon. autopsy findings showed that infarcts of the spinal cord and other key organs were caused by critical occlusion of small arterioles by cholesterol emboli. These emboli apparently arose as a result of the fragmentation of atheromatous plaques within the aorta during use of the intraaortic balloon pump with subsequent embolization and occlusion of small blood vessels.
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keywords = arteriole
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4/8. Bilateral macular infaction in SS disease.

    A 10-year-old Afro-American female with SS disease presented with a history of painless loss of vision (RE) of 26 hours duration. Sequential fluorescein angiography revealed bilateral parafoveal occlusions and evidence of prior vaso-occlusions in each eye. Initial hydration therapy with dextrose 5% and 1/4 normal saline was followed within eight hours by transfusion with two units of packed red blood cells. Patency was restored to the occluded arterioles with return of normal acuity in LE, though the vision remains at hand motions in the RE. Sudden loss of central acuity in sickle hemoglobinopathies may result from vaso-occlusion in terminal arterioles near the foveal avascular zone. Therefore a reduced number of permanently irreversibly sickled red blood cells may prevent these macular infarcts.
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5/8. spinal cord infarction in a patient with sickle cell anemia.

    The most common serious neurologic complication of sickle cell anemia is occlusive vascular disease with central nervous system infarction. The parenchymal lesions are most often located in the brain, chiefly within major cerebral arterial boundary zones. spinal cord infarction is extremely rare. We report a patient with sickle cell anemia who developed an acute cervical myelopathy. At autopsy, there was a spinal cord infarction with extensive involvement of the rostral cervical segments. Recanalized thrombi were present in the right vertebral artery and smaller subarachnoid arterioles adjacent to the infarcted cord. This is the first report of autopsy-confirmed spinal cord infarction associated with sickle cell anemia.
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keywords = arteriole
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6/8. pathology of the lung in Behcet's disease. Case report and review of the literature.

    Histopathologic changes in the lung in a patient with Behcet's disease are described and the literature dealing with pulmonary pathologic changes in this disease is summarized. The basic lesion is a lymphocytic and necrotizing vasculitis involving all sized pulmonary arteries, veins and septal capillaries. Complications include aneurysms of elastic pulmonary arteries, arterial and venous thromboses, pulmonary infarcts, and bronchial erosion by pulmonary artery aneurysms. Striking periadventitial fibrosis develops and is believed to be related to repetitive vascular inflammatory insults. Peculiar newly formed collateral vessels, lacking elastic lamellae and derived from smooth muscle metaplasia around arterioles, are found in the periadventitial fibrous tissues around thrombosed arteries and aneurysms. Cases of pulmonary artery aneurysms of obscure origin, including those found in the Hughes-Stoven syndrome, are reviewed and both clinical and pathologic findings in these reports are found to be remarkably similar to those observed in Behcet's disease. It is suggested that such cases represent unrecognized or incomplete expressions of Behcet's disease.
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7/8. Ischemic optic neuropathy in chronic papilledema.

    We evaluated the condition of a patient with chronic papilledema due to pseudotumor cerebri in whom a permanent, monocular, inferior, altitudinal, visual field defect suddenly developed. Clinical and fluorescein angiographic findings indicated that the loss of visual field was due to ischemic optic neuropathy. Ischemic optic neuropathy might occur in papilledema if the tissue pressure in the optic disc becomes sufficiently elevated to occlude the pressure-sensitive prelaminar arterioles.
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8/8. Histopathologic features of neovascularization in sickle cell retinopathy.

    PURPOSE: To examine the histopathologic and morphometric features of neovascular lesions in human proliferative sickle cell retinopathy. methods: Postmortem ocular tissue was obtained from three subjects (aged 20, 28, and 40 years) with SS hemoglobinopathy and prepared for adenosine diphosphatase flat-embedding. Morphometric analysis was performed before serial sectioning. RESULTS: Numerous active and autoinfarcted lesions were found that represented virtually all stages in the life cycle of preretinal neovascularization. These formations ranged from single small loops extending from arteries and veins along the retinal surface to the typical complex, elevated sea fan formations. Sea fans developed at hairpin loops and at arteriovenous crossings. There was an average of 5.6 connections between sea fans and retinal vessels; of these, 45% were arteriolar, 52.5% were venular, and 2.6% were at the capillary level. Six of eight sea fans were located at arteriovenous crossings. Autoinfarction appeared to occur initially within the sea fan capillaries. The average height of sea fans was 123 microns above the retinal surface. CONCLUSIONS: Preretinal neovascularization in sickle cell retinopathy can arise from both the arterial and venous sides of the retinal vasculature and can assume a variety of morphologic configurations. Multiple feeding arterioles and draining venules are common, and autoinfarction appears to occur initially at the preretinal capillary level rather than at feeding arterioles. Arteriovenous crossings may be a preferential site for sea fan development.
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