[Complications of anticoagulant and thrombolytic treatment].
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Biomedical subjects
Publications and source records attributed to G Nitenberg.
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The authors report the case of a man of 62 who was admitted with a clinical and electrocardiographic picture of a posterior infarction which was very soon complicated by collapse and anuria. The findings on catheterisation of the right side of the heart were as expected. The cardiac index was very low, and the major abnormality was a type of adiastole with equal pressures in the right ventricle and the auricle of the right atrium. Despite an attempt to assist the circulation by an intra-aortic ballon, the patient died within a few hours. The postmortem examination confirmed the presence of a massive infarction of the left ventricle, but also of the right ventricle, together with rupture of the posterior papillary muscle of the mitral valve, and ischaemic rupture of one papillary muscle of the tricuspid valve.
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Twenty cases of hypovolemic shock of various etiologies in which initial diagnosis was massive pulmonary embolism are analyzed. The error was due to intensity of respiratory failure symptoms and electrocardiographic changes suggesting acute cor pulmonale. However, although constant, hypoxemia was mild and easily corrected by oxygen administration. Hypovolemia was confirmed by low central venous pressure (CPV EQUALS 1, 3 cm H20); in 7 patients, right heart catheterism showed lowered cardiac output associated to low ventricular filling pressures (VFP). Rapid blood volume expansion simultaneously corrected in all cases both shock and clinical signs of "respiratory failure", while CVP increased only slightly. These findings suggest that CVP must be carefully checked when faced with a clinical picture of massive pulmonary embolism and if low, rapid blood volume expansion must be performed under CVP monitoring, in order to rule out hypovolemic shock.
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Four out of 23 consecutive patients treated with high-dose Ara-C for lymphomas in our institution developed a strikingly similar syndrome during the perfusion. It was characterized by the onset of fever, diarrhea, shock, pulmonary edema, acute renal failure, metabolic acidosis, weight gain and leukocytosis. Thorough bacteriological screening failed to provide evidence of infection. Sequential biological assays of IL-1, IL-2, TNF and PAF were performed during Ara-C infusion to ten patients, including the four who developed the syndrome. TNF and PAF activity was found in the serum of respectively two and four of the cases, but not in the six controls. As TNF and PAF are thought to be involved in the development of septic shock and adult respiratory distress syndrome, we hypothesize that high-dose Ara-C may be associated with cytokine release.