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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The statement that amniotic fluid embolism is the most dangerous and untreatable condition in obstetrics appears to be true. It must be suspected in any patient who collapses or bleeds excessively during labour or the immediate post-partum period. Attempts should be made to secure a definitive diagnosis in life by examination of blood obtained from the right side of the heart and the sputum for elements of amniotic fluid. Lung scanning is a useful aid to diagnosis. The principal factors that have been implicated in the clinical syndrome of amniotic fluid embolism are anaphylaxis, vascular obstruction by particulate matter, vascular spasm due to prostaglandins and possibly some other vasoactive substances, and the possibility that all the changes could be explained by disseminated intravascular coagulation as a primary event. Further work is required to elucidate the relative contributions of these various factors. Due to the suddeness of the catastrophe and the very high mortality, haemodynamic data in humans is virtually non-existent. With improved methods of resuscitation it is to be hoped that the mortality rate will be reduced and that such data will become available. In this way it might become possible to apply the results of animal research and indicate the most effective method of treatment.
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PMID:Amniotic fluid embolism. 37 60

Amniotic fluid embolism is a catastrophic event of the intra- and early postpartum period which may also be seen with cesarean delivery and during abortions. Presenting symptomatology includes respiratory distress with cyanosis, shock, and possibly tonic-clonic seizures. DIC frequently occurs. The pathogenesis may include entry of amniotic fluid through lacerations or ruptures of the uterus or cervix, through endocervical veins and through abnormal uteroplacental sites, such as with placental abruption, placenta previa, or placenta accreta. Amniotic fluid probably causes cardiovascular-respiratory symptoms by pulmonary vascular obstruction and through a vasoactive substance causing pulmonary vascular constriction. The lethality of amniotic fluid may be enhanced by a high particulate content or meconium staining. The diagnosis of amniotic fluid embolism may be made ante mortem by demonstrating amniotic fluid debris in central blood samples or expectorated sputum. Postmortem diagnosis often requires meticulous examination of the pulmonary microvasculature with the utilization of special stains. Treatment is directed towards symptoms of shock, arterial hypoxemia, and DIC. Acute renal failure may complicate the picture after shock. If the patient survives the embolic and coagulative problems, recovery is usually complete without long-term sequelae.
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PMID:Amniotic fluid embolism. Three case reports with a review of the literature. 402 76

The cardiovascular, coagulation and haematological effects of Tiger Snake (Notechis scutatus) venom were investigated in anaesthetized, mechanically ventilated dogs. Intravenous infusion of venom caused dose-related systemic hypotension, low cardiac output, pulmonary hypertension and raised pulmonary artery occlusion pressure. These effects occurred within several minutes of venom administration but recovered over 30 to 40 minutes. They were accompanied by prolongation of prothrombin and activated partial thromboplastin times and by depletion of serum fibrinogen. Fibrin degradation products were not detected. Thrombocytopenia and leucopenia were observed within minutes of venom administration but recovered over 30 to 40 minutes. The mechanism of systemic hypotension is probably pulmonary vascular obstruction and coronary ischaemia caused by disseminated intravascular coagulation, although the existence of a myocardial depressant in venom or release of vasoactive substances by venom cannot be excluded.
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PMID:The cardiovascular, coagulation and haematological effects of tiger snake (Notechis scutatus) venom. 980 9

Disseminated intravascular coagulation can cause multiple organ failure including adult respiratory distress syndrome by obstruction of visceral microcirculation by microclots. It was reasoned that if a clot causes vascular obstruction, lysing the clot by a plasminogen activator would be of value.
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PMID:The etiology and treatment of traumatic and septic shock. 1047 May 17

Hepatic vascular disorders are a set of conditions that may be acute, or may be insidious and subclinical for many years. They can be organized into 3 categories: obstruction to hepatic vascular inflow, obstruction to blood flow through the liver, and obstruction to hepatic vascular outflow. In the first category are portal vein thrombosis, hepatic artery thrombosis, and presinusoidal causes of vascular obstruction. In the second category are sickle cell disease, disseminated intravascular coagulation, intrasinusoidal malignancy, and infection. In the third category are macroscopic hepatic venous thrombosis, thrombosis of the retrohepatic inferior vena cava, and venoocclusive disease. There are 2 nodular conditions of the liver that are not neoplastic but the result of occlusion of hepatic vasculature with compensatory hyperplasia of well-vascularized parenchyma. Hepatic vascular disorders constitute a heterogeneous group of conditions that must be considered in the differential diagnosis of any patient with hepatic compromise.
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PMID:Vascular disorders of the liver. 2105 87