Cases reported "Cardiac Tamponade"

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1/9. erdheim-chester disease with prominent pericardial involvement: clinical, radiologic, and histologic findings.

    erdheim-chester disease (ECD) is a rare form of non-Langerhans cell histiocytosis. Herein we describe documented skeletal and pericardial involvement by ECD producing cardiac tamponade in a 30-year-old woman. The diagnosis of ECD was established by histopathology, immunocytochemistry, and by radiologic studies demonstrating diffuse, bilateral, symmetrical osteosclerosis of the long bones, sparing the epiphyses and axial skeleton. Scintography using methyl diphosphonate showed increased uptake in involved bone. The patient presented with jaundice and hepatic congestion produced by cardiac tamponade. Pericardial biopsy revealed xanthogranulomatous lesions comprised of foamy and lipid-laden macrophages, multinucleated giant cells, monocytes, and lymphocytes in a mesh of fibrosis. Immunohistochemical staining was positive for CD68 and negative for CD1a, consistent with ECD rather than with the much more common Langerhans cell form of histiocytosis.
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2/9. Giant metastatic myxoid liposarcoma causing cardiac tamponade: a case report.

    We report a case of a rapidly progressing isolated giant metastatic myxoid liposarcoma to the heart in a 54-year-old man, who presented with acute symptoms of cardiac tamponade. Surgery remains the best treatment option for this rare condition.
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3/9. Giant epicardial lipoma.

    A patient undergoing coronary artery bypass was found to have a giant epicardial lipoma weighing 1.36 kg which was excised uneventfully. The radiological and pathophysiological features are considered, and the options for management discussed.
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4/9. rupture of a giant coronary artery aneurysm due to Kawasaki disease.

    Coronary artery aneurysm requiring surgery is rare. We report a case of a ruptured giant coronary artery aneurysm due to Kawasaki vasculitis which presented with cardiac arrest and was successfully treated by emergency coronary artery bypass grafting. The controversies surrounding the management of this disease are also discussed.
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5/9. A fatal case of ruptured giant coronary artery aneurysm.

    A 5-year-old Japanese boy died because of a ruptured left coronary artery aneurysm (CAA). He was diagnosed as having Kawasaki disease (KD) on the 5th day from onset, with all of the principal signs. On the 7th day of illness, bilateral CAAs were already found via echocardiography, and he was treated with intravenous (IV) gamma globulin and oral ASA. However, the fever persisted and the CAA progressed rapidly. echocardiography on the 12th illness day showed a giant (18-mm) left anterior descending (LAD) artery aneurysm. Oral propranolol and nifedipine were administered, in conjunction with warfarin/aspirin anti-coagulation therapy. On the 13th day of illness, cardiac arrest developed abruptly, and, despite cardiopulmonary resuscitation (CPR), the patient remained unresponsive and died one hour later. The final pathological diagnosis was a ruptured LAD artery aneurysm and cardiac tamponade. Microscopic investigation of the ruptured vascular wall revealed marked neutrophilic infiltration, with fewer macrophages and lymphocytes. CAA ruptures are a very rare, but fatal, complication of KD. Based on a review of previous reports on CAA ruptures, we consider it useful to distinguish aneurysms which rapidly dilate and continue to expand beyond a diameter of 10 mm with ongoing vasculitis (these CAAs can be termed "super-giant") from the more common giant CAAs limited to a diameter of 8 or 9 mm, because a decision must be made as to whether to start intensive care or to intervene surgically, in order to ensure the survival of patients with such a potentially critical complication.
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6/9. Giant coronary artery fistula complicated by cardiac tamponade.

    A 30 year old female was admitted to the hospital with cardiogenic shock due to cardiac tamponade. A ruptured giant coronary artery fistula (CAF) originating from the left main coronary artery draining into the right atrium was identified as the cause. In this case report we describe the clinical course with emphasis on diagnostic work-up and imaging.
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7/9. Generalized granulomatous arteritis with aortic dissection.

    A 56 year-old Japanese woman died suddenly after complaining of abdominal pain. autopsy revealed typical aortic dissection with cardiac tamponade. Histologically, generalized granulomatosis with giant cells resembling sarcoidosis was found. The aorta was most strikingly affected so that granulomatous aortitis was regarded as the cause of the aortic dissection.
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8/9. cardiac tamponade secondary to giant lymph node hyperplasia (Castleman's disease)

    A unique association of giant lymph node hyperplasia (Castleman's disease) and cardiac tamponade is presented. Although pleural effusions have been previously described with Castleman's disease, the authors believe this to be the first report of pericardial effusion and tamponade with this entity. The development of effusions may be due to an inflammatory syndrome sometimes seen with the plasma cell variant of this disease.
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9/9. Leaking giant aneurysm of the aortic root due to cystic medial necrosis with pericardial tamponade mimicking type-A aortic dissection.

    The diagnosis of acute type-A aortic dissection is predominantly based on the demonstration of an intimal tear or a dissection membrane. We describe another pathogenetic mechanism in a patient with the typical features of acute aortic dissection with pericardial tamponade, and a giant aneurysm of the ascending aorta. However, no dissection membrane, rupture site, or intimal tear could be demonstrated by transesophageal echocardiography, intraoperatively, or histologically. The histological work-up showed an extreme form of cystic medial necrosis with intramural hemorrhages consistent with a leaking aneurysm. Hence, in a patient with a symptomatic aneurysm of the aortic root and pericardial tamponade, obvious intimal dissection or rupture does not always have to be present echocardiographically or intraoperatively. A different presentation can occur in the setting of an extreme medial necrosis, where blood leaks through the aortic wall causing intramural hemorrhages with intimal leaks invisible to the surgeon's or echocardiographer's eye. This process is clinically indistinguishable from type-A aortic dissection.
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