Cases reported "Thromboembolism"

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1/61. Thromboembolic phenomena in patients with hereditary factor xi deficiency.

    factor xi deficiency is an hereditary coagulopathy that is usually associated with milder tendency to bleeding with comparison to hemophilia a. While the failure of stable fibrin clot formation may lead to bleeding, it is speculated that the same process may provide a protection against thrombosis of injured arteries due to atherosclerotic plaque rupture. Whereas 2 studies indicate that hemophiliacs have decreased mortality rate from cardiovascular diseases, there is no similar data regarding factor xi deficiency patients. In here we report about 3 patients with severe factor xi deficiency who have a long-standing history of thromboembolic phenomena: 2 patients with myocardial infarctions, and one patient with transient ischemic attacks. We discuss the possible role of factor XI in thrombosis, and whether its deficiency may protect patients from thromboembolic phenomena.
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2/61. Clinical therapeutic conference: recurrent venous thrombotic and thromboembolic disease.

    Recurrent venous thrombotic and thromboembolic disease, once thought to be an uncommon entity, is increasingly being recognized. Etiologies of recurrent deep venous thrombosis usually include elements of Virchow's triad. Venous stasis (e.g., immobilization, congestive heart failure, acute myocardial infarction, obesity), hypercoagulability (e.g., malignancy, inflammatory bowel disease, hyperhomocysteinemia, protein c resistance, antithrombin iii, protein c or S deficiency) and endothelial trauma (e.g., surgical trauma, venous trauma, in-dwelling venous instrumentation) are risk factors. diagnosis is dependent on objective testing, including venography duplex Doppler (color) ultrasonography and impedance plethysmography. Treatment is usually started with heparin or low-molecular-weight heparin and advanced to warfarin (adjusted to international normalized ratio). Prophylaxis may continue using low-molecular-weight heparin, warfarin, venacaval interruption (Greenfield filter), or concomitant use of the platelet-active agent indobufen and graduated compression stockings.
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3/61. Libman-Sacks endocarditis in a pregnant woman with acute respiratory distress syndrome.

    BACKGROUND: Sterile fibrinous vegetations on the mitral valve (Libman-Sacks endocarditis) might be found in one-third of patients with antiphospholipid antibodies. Usually of minor hemodynamic significance, these vegetations might complicate acute respiratory distress syndrome in pregnancy. CASE: Despite delivery and aggressive medical therapy, a 17-year-old primigravida with pyelonephritis and acute respiratory distress syndrome suffered rapid decompensation. echocardiography showed mitral valve vegetations with severe regurgitation. blood cultures were negative, but antinuclear antibody test and lupus anticoagulant were positive. The patient died of massive cerebral infarction and brainstem herniation. autopsy found a patent foramen ovale and Libman-Sacks endocarditis. CONCLUSION: With rapid decompensation of acute respiratory distress syndrome in pregnancy, despite aggressive medical therapy, complicating processes must be considered, especially with antiphospholipid antibodies, which can be associated with sterile heart vegetations and subsequent fatal thromboembolism.
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4/61. Disseminated mucormycosis caused by absidia corymbifera leading to cerebral vasculitis.

    An 18-year-old woman was admitted to hospital because of subcutaneous hematoma and fever of unknown origin. Acute myeloid leukemia was diagnosed and empirical antimicrobial treatment and induction chemotherapy were started. After initial defervescence, fever relapsed 2 days after the onset of neutropenia. The CT scan of the lung was consistent with an invasive fungal infection. Treatment with amphotericin b was started and antimicrobial treatment was continued with liposomal amphotericin b because of an increase in creatinine later. The fever persisted and the patient suddenly developed progressive neurological symptoms. CT scan of the head suggested cerebral infarction and angiography of the extra- and intracranial arteries showed signs of vasculitis. Six days after the onset of neurological symptoms cerebral death was diagnosed. autopsy revealed non-septate, irregularly branched hyphae in various histologic sections including brain. absidia corymbifera could be isolated from lung tissue confirming the diagnosis of disseminated mucormycosis. In this case, angiographic findings suggested severe cerebral vasculitis which was in fact caused by thromboembolic dissemination of fungal hyphae. This case underlines the fact that cerebral symptoms in febrile neutropenic patients are highly indicative for fungal infections of the brain.
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5/61. Acute renal infarction secondary to left ventricular thrombus, masquerading as a renal calculus--a case report and brief review of literature.

    Acute embolic renal infarction is an entity that is often misdiagnosed as a renal calculus because of similar presenting symptoms. This leads to delay in the initiation of treatment and to increased morbidity. Few case reports exist relating cardiac emboli to acute renal infarction. The authors present a patient with a renal embolism secondary to left ventricular thrombus. A brief review of the literature highlighting the importance of clinical suspicion in making an accurate diagnosis, the utility of various diagnostic studies, and comparison of various treatment options is presented.
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ranking = 6
keywords = infarction
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6/61. pheochromocytoma presenting as life-threatening pulmonary edema.

    Acute cardiogenic pulmonary edema as the first presentation of pheochromocytoma is uncommon and usually rapidly fatal. A 39-yr-old man presented in acute cardiogenic shock with global ventricular dysfunction that required high-dose iv inotrope support and an intraaortic balloon pump assist device. Abdominal imaging to exclude aortic dissection revealed a 6-cm right adrenal mass. Significant myocardial infarction (electrocardiographic changes and elevated cardiac enzymes) contributed to the cardiac decompensation. After withdrawal of inotrope support, 24-h urinary catecholamine levels revealed 2,155 nmol/d (<125) of adrenaline and 7,437 nmol/d (<560) of noradrenaline, confirming a pheochromocytoma. The tumor was successfully removed at laparotomy; however, the patient's course was complicated by a thromboembolic cerebrovascular accident with paraplegia. He recovered cardiac function almost completely within 3 wk of medical therapy alone. Although uncommon, this case highlights the need to consider pheochromocytoma early in the management of unexplained cardiogenic shock.
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7/61. Paradoxical brain embolism from thrombus associated with vena caval filter in a patient with cancer.

    A 71-year-old man experienced sudden onset of hemiparesis and aphasia. He had a 4-month history of gallbladder cholangiocarcinoma, complicated with a postoperative deep-vein thrombosis (DVT) that necessitated a vena caval filter placement. diffusion-weighted magnetic resonance imaging of the brain showed multiple hyperintense foci. magnetic resonance spectroscopy was compatible with cerebral infarction. Abdominal computed tomography showed a thrombus in the inferior vena cava extending through the filters. A transcranial Doppler bubble study revealed the presence of a right-to-left shunt. Paradoxical cerebral embolism must be considered in patients with DVT who have new onset neurologic deficits even in the presence of a caval filter.
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keywords = infarction
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8/61. portal vein thrombosis causing neonatal cerebral infarction.

    Neonatal cerebral infarction often occurs in the absence of known risk factors. Two such cases are described in which portal vein thrombosis was documented during two dimensional echocardiography. In both cases, infarcts were consistent with embolic events. A novel mechanism is proposed, which may explain some cases of "idiopathic" neonatal cerebral infarction.
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ranking = 6
keywords = infarction
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9/61. Two patients with arterial thromboembolism among 311 patients with adenocarcinoma of the pancreas.

    PURPOSE: To examine the prevalence and characteristics of arterial thromboembolism in patients with adenocarcinoma of the pancreas. methods: Retrospective review of charts of all patients with cancer of the pancreas diagnosed and followed at a regional teaching hospital over a decade. RESULTS: In total, 320 patients were diagnosed and 311 were available for evaluation. Two patients with arterial thromboembolism were identified (0.65%) and studied. Both had extensive metastatic disease on diagnosis and, soon after, developed an acute arterial occlusion of the iliac and femoral arteries, with no identifiable embolic source (case 1) or acute intestinal infarction due to mesenteric and multiple other embolic arterial occlusions associated with nonbacterial thrombotic endocarditis (NBTE) of the mitral valve (case 2). Both cases had laboratory evidence of disseminated intravascular coagulation and succumbed to their illnesses within a very short time. CONCLUSION: Arterial occlusion in pancreatic cancer is a rare preterminal event that may be caused by cardiogenic emboli from NBTE or to thrombosis in situ. The pathogenesis is briefly reviewed.
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keywords = infarction
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10/61. Protruding thrombus in the left atrium found 7 years after percutaneous transvenous mitral commissurotomy: report of a case.

    A 50-year-old man was transferred to our hospital for investigation of cerebellar infarction, thought to have been caused by cardiac thromboembolism. We assumed that the cardiac thromboembolism had occurred as a late complication of a percutaneous transvenous mitral commissurotomy (PTMC) performed 7 years earlier. An echocardiogram and thoracic computed tomography revealed a protruding thrombus in the left atrium and an emergency operation was performed. The protruding thrombus was found to originate from the scar that penetrated into the intra-atrial muscular septum caused by the PTMC. After removing the thrombus, the scar was covered with normal endothelium and the mitral valve was replaced with a 27-mm St. Jude Medical prosthetic valve. We think that the thromboembolism was caused by mitral valve restenosis, atrial fibrillation, and endothelial injury in the interatrial septum during PTMC. Therefore, long-term follow-up and appropriate medication is recommended after PTMC, since restenosis and thrombosis are likely to occur.
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keywords = infarction
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