Cases reported "Carotid Artery Diseases"

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1/14. Tracheocarotid artery fistula infected with methicillin-resistant staphylococcus aureus.

    Massive life-threatening haemorrhage from a fistula between the trachea and a major blood vessel of the neck is a rare complication of the tracheostomy procedure, well-recognized by anaesthetists and otolaryngologists. Although the lesion is likely to be encountered at autopsy, it is not described in histopathological literature. The possible causes are discussed together with the macroscopic and microscopic appearances of the lesion. Suitable procedures for its identification and for obtaining appropriate histopathological blocks are suggested. Presence of methicillin-resistant staphylococcus aureus (MRSA) has not been documented before and might have contributed to the genesis of the fistula in this case.
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2/14. Ruptured internal carotid aneurysm resulting from neurofibromatosis: treatment with intraluminal stent graft.

    PURPOSE: This report shows a method of treatment for life-threatening hemorrhage due to rupture of an aneurysm in the cervical internal carotid artery caused by neurofibromatosis. methods: Ten days after delivery of healthy twins, a 28-year-old woman with known neurofibromatosis had sudden massive swelling in the left neck. After initial tracheostomy, angiography confirmed rupture of the mid cervical internal carotid artery as well as contribution to the resultant pseudoaneurysm from external carotid branches. Treatment began with coil embolization of the external carotid branches. The internal carotid lesion, a defect approximately 1 cm in length, was then closed through use of two stent grafts, each made from Palmaz stents and 3-mm polytetrafluorethylene grafts predilated to 6 mm. The neck hematoma was then evacuated surgically. RESULTS: Completion angiography and computed tomographic scanning confirmed control of the hemorrhage. The patient survived neurologically intact with the exception of cranial nerve deficits caused by the hemorrhage. The tracheostomy tube was removed 3 weeks postoperatively. Follow-up computed tomographic scanning showed a gradual decrease in the size of the cervical soft tissue and no recurrent aneurysm. CONCLUSION: Neurofibromatosis is a rare cause of aneurysmal degeneration of blood vessels. Repair of a ruptured cervical internal carotid artery aneurysm, though feasible, is difficult with stent grafts; however, this is a better option than surgical intervention in inaccessible vessels.
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3/14. Aneurysms of the carotid arteries associated with von Recklinghausen's neurofibromatosis.

    Aneurysms of both common carotid arteries were seen in a patient with neurofibromatosis. Histologic examination of the involved arteries demonstrated a dense proliferation of spindle cells within the arterial walls accompanied by medial cystic degeneration and disruption of the tunica elastica. These changes were also observed in adjacent, grossly uninvolved segments of the blood vessels. Immunohistochemical analysis of the proliferating cells was positive with antibodies against desmin and muscle-specific actin. The findings demonstrate and confirm the smooth muscle origin of the aberrant proliferated cell population in arteries in a patient with von Recklinghausen's neurofibromatosis.
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4/14. Increased intraocular pressure following endarterectomy.

    Two patients are presented with neovascularization of the iris due to ischemia secondary to decreased blood flow through the carotid arteries. Panretinal photocoagulation was followed by regression of the new iris blood vessels to a greater extent in one patient than in the other. Following carotid endarterectomy, intraocular pressure increased, and, in one case, filtering surgery was required. Possible mechanisms for the rise in intraocular pressure following carotid endarterectomy are discussed.
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5/14. dissection of the thoracic aorta following partial clamping.

    A case is reported in which an extensive dissection of the thoracic aorta was observed after partial clamping during surgery on that blood vessel. The unfavourable outcome of the operation and the accurate investigation of the post-mortem material suggest a lesion of the artery wall secondary to tangential clamping by Satinsky's clamp. The possible pathogenetic mechanisms of lesions induced by vascular clamping are also discussed.
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6/14. diagnosis and management of isolated angiitis of the central nervous system.

    Isolated angiitis of the central nervous system (IAC) is usually a fatal inflammatory disease with a predilection for small blood vessels. Recurrent cerebral infarction leading to death within a few years is the usual course, but this may be significantly altered by aggressive immunosuppressive therapy with prednisone and cyclophosphamide. Other diseases may, however, present with similar clinical and angiographic features. Because antemortem diagnosis suggests a therapy, establishing the criteria for diagnosis is important. This report describes clinical, angiographic, and biopsy features, and therapy of five successfully treated patients with IAC. The following specific criteria are recommended for establishing an antemortem diagnosis of IAC: (1) clinical pattern of headaches and multifocal neurologic deficits present for at least 6 months, unless the deficits are severe at onset or rapidly progressive; (2) cerebral angiography demonstrating segmental arterial narrowing; (3) exclusion of systemic inflammation or infection; and (4) leptomeningeal/parenchymal biopsy demonstrating vascular inflammation or exclusion of alternate diagnoses. Based upon the successful management of these five previously unreported patients, as well as others in the literature, the following treatment regimens are recommended for the initial 6 weeks of therapy: (1) prednisone 40 to 60 mg/day, and (2) cyclophosphamide 100 mg/day.
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7/14. A xanthogranulomatous process encircling large blood vessels (erdheim-chester disease?).

    The case of a strange type of generalized xanthogranulomatosis, ending by a lethal kidney complication, is described in a woman aged 68. The clinical symptoms of the patient were not characteristic and did not lead to the actual diagnosis. The process was located along the basal brain arteries, it adhered to the adventitia of the descending thoracic aorta and of the coronary arteries. An identical xanthogranulomatous infiltrate was found in the peripelvic adipose tissue of both kidneys, where it led to stenosis of the proximal ends of both ureters; to a lesser extent such infiltrates appeared also in the periportal areas of the liver and in the bone marrow. Histological findings grant the possibility of the erdheim-chester disease. Differential diagnosis is subjected to discussion.
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8/14. Familial occurrence of spontaneous dissection of the internal carotid artery.

    Spontaneous dissections of the extracranial internal carotid artery are diagnosed more frequently as their clinical and angiographic features are more widely recognized. Familial occurrence of spontaneous dissection of the internal carotid artery has not been previously reported. We describe the occurrence of this entity in a mother and daughter and also in a father and son. The familial occurrence of spontaneous dissection of the internal carotid artery raised the possibility of an inherited disorder of the blood vessel wall that predisposes the artery to this disorder. fibromuscular dysplasia is suspected to be the underlying arterial disease, but other unknown arteriopathies cannot be excluded.
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9/14. pathology of spontaneous dissection of intracranial arteries.

    Spontaneous dissection of a major subarachnoid artery is an uncommon cause of stroke in young and apparently healthy individuals. Such dissection does not correlate well with systemic conditions such as emboli, thrombotic or hemorrhagic tendencies or hypertension, nor with disease of blood vessels such as atherosclerosis, fibromuscular dysplasia, cystic medial necrosis or Moya-Moya disease. Unusual exertion has been implicated as a factor in some cases. Gap defects were found in the internal elastic lamina near the site of dissection in three of four cases of spontaneous dissection reported here. It is suggested that such defects, because of their unusual size or number, may be responsible for initiating dissection in susceptible individuals. A detailed study of the major cerebral arteries in cases of dissection and control cases to document the size and frequency of such defects could shed light on the pathogenesis of spontaneous dissection. The subsequent course of events tends to differ in the internal carotid and vertebro-basilar systems. In most cases, the dissection in the internal carotid system is sub-intimal leading to thrombosis and cerebral infarction, while in the vertebrobasilar system dissection lies between the media and adventitia leading to subarachnoid hemorrhage. It is not known what structural differences of the two arterial systems may underlie this difference in the pattern of arterial dissection.
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10/14. Defective cerebrovascular autoregulation in regions proximal to arteriovenous malformations of the brain: a case report and topic review.

    We report the case of a patient with a large left subfrontal arteriovenous malformation (AVM) that was supplied by the right internal carotid artery. The anomalous blood supply developed because of complete occlusion of the left internal carotid artery. When the AVM was removed, the patient experienced a hemorrhage into the right basal ganglia. The possibility that this hemorrhage was related to a defect of autoregulation in blood vessels that lie proximal to a large AVM is discussed. Even though this is a unique case, the pathophysiological events that are documented are relevant to the preoperative preparation and surgical management of all patients with AVMs.
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