Cases reported "Ischemia"

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1/33. Superior and inferior limb ischaemia in giant cell arteritis: angiography follow-up.

    giant cell arteritis most often affects the superficial temporal artery. Arterial territories such as the facial, carotid, myometrial and upper and lower limb arteries may be affected. In this paper we describe the case of a 52-year-old patient with upper and lower limb ischaemia who presented with grade III ischaemia in the left lower limb. giant cell arteritis was diagnosed as responsible for the symptoms. After treatment with corticoids, an angiographic improvement was evidence after 2-year period. The low number of reported cases, the diverse symptoms and varied course make diagnosis of GCA difficult. Therefore, GCA must be taken into consideration in the ischaemia of inferior and superior limbs whether isolated or simultaneous.
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2/33. rupture of pseudointima in an implanted vascular prosthesis: immunohistological study of plasminogen activators and matrix metalloproteinases.

    We investigated late-onset anastomotic stenosis in an implanted prosthetic graft. rupture of the pseudointima and hemorrhaging from the vasa vasorum were observed at the border of the collagenous tissue and fibrin layer. An immunohistological study showed that the fibrin layer was positive for tPA, but weakly positive for PAI-1. Some neutrophils and monocyte/macrophages in the fibrin layer were immunostained for tPA, uPA, uPAR, and MMP-1, -2 and -3. Some spindle-shaped cells surrounding the graft were immunostained for uPA, uPAR, MMP-1, -2, -3, -7 and -9, and TIMP-1 and -2. The endothelial cells of some microvessels were positive for MMP-1 and -2, and tPA. Some multi-nucleated giant cells were immunostained for MMP-7 and-9, tPA, PAI-1, uPA, and uPAR. Overexpressed MMPs and PAs possibly caused instability of the pseudointima.
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3/33. Atypical decubital fibroplasia with unusual histology.

    A case of atypical decubital fibroplasia with unusual histology arising in the buttock of a 68-year-old bed-ridden male in presented. The lesion measuring 5.4 cm in greatest dimension was histologically characterized by a proliferation of fibroblasts with oval to spindle nuclei and dense fibrous stroma with focal hyalinization and calcification. Ganglion-like fibroblastic cells and multinucleated giant cells of osteoclast type were also observed. There were numerous elastic fibers within and adjacent to the proliferating stromal cells. The proliferating stromal cells were positive for vimentin and collagen type iv but negative for CAM 5.2, epithelial membrane antigen, desmin, alpha-smooth muscle actin, muscle actin, HHF35, S-100 protein and CD34. Ultrastructurally, they were of a fibroblastic nature. The hypercellularity, lack of zones of fibrinoid necrosis, lack of lobulation and the presence of multinucleated giant cells were different from the originally described lesion. This condition represents a variant of atypical decubital fibroplasia. Pathogenic factors of this lesion are considered to be chronically repeated pressure and associated intermittent ischemia. The recognition of the lesion and its distinction from a sarcoma is essential.
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4/33. anterior spinal artery syndrome after total spondylectomy of T10, T11, and T12.

    Although radical resection is the best treatment for local aggressive benign tumors or malignant tumors of the spine, total spondylectomy for lower thoracic vertebrae may cause anterior spinal artery syndrome. There are few reports in the literature in which this syndrome has been documented in association with thoracic spondylectomy, although this syndrome is the most common neurologic complication after abdominal aortic surgery. A 50-year-old woman with a giant cell tumor of the thoracic vertebrae was treated by posterior and anterior surgery. Thoracic segmental arteries from T10 to T12 had to be resected bilaterally to dissect the aorta free from the tumor. After resection of all feeding arteries to the tumor, the tumor and entire parts of T10, T11, and T12 were removed. Postoperative neurologic examination disclosed flaccid paralysis of the lower extremities and sphincter incontinence. Although pain and temperature sensation were absent, vibration and position sense were intact, showing anterior spinal artery syndrome. Intraoperative somatosensory-evoked potential monitoring only showed that transient deterioration failed to adequately reflect this neurologic injury. Major reconstructive surgery involving lower thoracic regions may cause anterior spinal artery syndrome. Somatosensory-evoked potential monitoring might not reliably predict overall neurologic outcome involving the blood supply of the lower thoracic regions.
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5/33. Florid ischemic cholangitis due to leucocytoclastic vasculitis.

    ischemia-induced biliary tract lesions, called ischemic cholangitis, often lead to strictures of biliary ducts and cholestasis. Causes of ischemic changes of the biliary tract can be found in the arterial blood supply or in the peribiliary capillary plexus. Known examples are thrombosis after transplantation, intraoperative ligation, or the application of chemotherapeutic drugs. Rarely, such changes are due to inflammation of the blood vessels, such as occurs in polyarteritis nodosa or giant cell arteritis. We present a report of a 49-year old man with leucocytoclastic vasculitis after viral infection, influenza vaccination, and antibiotic treatment, leading to florid ischemic cholangitis. We conclude that hypersensitivity vasculitis must be included in the differential diagnosis of cholestasis and cholangitis.
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6/33. giant cell arteritis in the ocular ischemic syndrome.

    oculomotor nerve paresis, ocular hypotony, anterior segment ischemia, and the ocular ischemic syndrome are uncommon manifestations of giant cell arteritis. Four patients with these findings had giant cell arteritis documented by temporal artery biopsy. cerebral angiography or ultrasonography, or both, performed in three patients, excluded hemodynamically significant stenosis of the internal carotid artery as the cause of ocular ischemia and cerebral aneurysms as the cause of oculomotor nerve paresis. Corticosteroid treatment, administered to three patients, resulted in resolution of the oculomotor deficits and the clinical signs of ocular ischemia, although the visual acuity in one patient improved from 20/400 to 20/60. giant cell arteritis should be considered in the differential diagnosis of the ocular ischemic syndrome.
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7/33. giant cell arteritis manifesting as mesenteric ischemia.

    We report a case of giant cell arteritis in an 80-year-old woman who presented with chronic mesenteric ischemia to our vascular surgery service. Computed tomography, arteriography, and magnetic resonance angiography revealed long, smooth stenosis of the superior mesenteric artery and focal stenosis of the celiac artery. After the patient was found to have an elevated erythrocyte sedimentation rate and a positive temporal artery biopsy specimen, glucocorticoid therapy was initiated. giant cell arteritis is a rare and easily overlooked cause of vascular insufficiency that can result in a devastating clinical outcome if not recognized before surgical therapy or other interventions are attempted.
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8/33. Anterior segment ischaemia with giant cell arteritis.

    CASE REPORT: A 69-year-old male presented with bilateral blurred vision, left periocular pain, and headache. Ocular examination revealed a right optic neuropathy and left anterior segment ischaemia. An elevated erythrocyte sedimentation rate (ESR) and c-reactive protein (CRP) raised suspicion of giant cell arteritis (GCA), which was confirmed by temporal artery biopsy. Treatment with intravenous methylprednisolone followed by a gradually reducing dose of oral prednisolone improved vision in both eyes. COMMENTS: GCA typically affects large- and medium-sized vessels. It is a recognised cause of anterior ischaemic optic neuropathy. Anterior segment ischaemia is usually caused by disease of the anterior ciliary arteries not typically affected by GCA. This case illustrates that GCA can rarely cause anterior segment ischaemia, without posterior segment involvement in the same eye.
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9/33. Contemporaneous retinal and optic nerve infarcts, choroidal non-perfusion, and Hollenhorst plaque: are these all embolic events?

    A 76-year-old man developed a sudden painless superior field defect in the right eye, retinal whitening along the inferior temporal arcade, and fluorescein angiographic evidence of lobular choroidal non-perfusion. One week later, ophthalmoscopy revealed inferior optic nerve edema with splinter hemorrhages consistent with an anterior ischemic optic neuropathy (AION) and a new cholesterol plaque near the macula. There was no clinical, serologic, or pathologic evidence of giant cell arteritis. Carotid ultrasound revealed no evidence of significant stenosis but did show an echolucent soft plaque in the right carotid artery. Transthoracic echocardiography demonstrated normal left ventricular function with no source of emboli. The presumed cause of the clinical findings in this patient was embolism, a rarely reported cause of AION. An embolic origin may be considered in non-arteritic AION associated with choroidal non-perfusion.
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10/33. Ischemic chiasmal syndrome.

    Twenty-two patients with ischemic chiasmal syndrome (ICS) have been examined by means of magnification angiography and polytomographic encephalography. The causes of ICS may be divided into 5 categories: (1) mechanical compression of the chiasm by ectatic redundant anterior cerebral arteries, (2) atherosclerotic vascular occlusions, (3) optochiasmal arachnoidal fibrosis, (4) various forms of arteritis especially giant cell (cranial) arteritis, and (5) post-partum pituitary necrosis associated with ICS. The most common cause of ICS appears to be optochiasmal arachnoiditis which occasionally developed some time after a craniotomy and radiation therapy for pituitary or other juxta-sellar tumors; similar fibrotic change may develop following steroid treatment of granulomatous lesions.
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