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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 paper is concerned with four Marathon athletes who developed grave impairments in hemodynamics and microcirculatory disorders in the organs (collapse, acute renal failure, cerebral abnormalities) and signs of the grave acute syndrome of disseminated intravascular coagulation with thrombohemorrhage and bleeding after competitions carried out under unfavourable conditions (a temperature of 30 degrees C and high air humidity). Three patients died. The diagnosis of the syndrome of disseminated intravascular coagulation was supported at autopsy. One of the athletes suffered brain stroke. The clinical and laboratory examination of the other 19 Marathon athletes showed that after competitions 6 persons had subclinical hemostatic disorders characteristic of the syndrome of disseminated intravascular coagulation. It is recommended that control and correction of hemostatic disorders should be strictly exercised in athletes experiencing hard and prolonged physical exercise.
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PMID:[The syndrome of disseminated intravascular coagulation in marathon athletes]. 271 33

Four probable cases of amniotic fluid embolism (AFE) are reviewed. The outcome appeared to be determined by the severity of the insult, and possibly the gestation of the pregnancy, rather than the management of the AFE. Two cases occurred during early labour; neither patient recovered consciousness. One died two weeks later and the other suffered severe permanent cerebral damage. The other two cases occurred during dilatation and curettage, one for therapeutic abortion at fourteen weeks gestation and the other for missed abortion at twenty weeks gestation. Both patients made full recoveries. Disseminated intravascular coagulation (DIC) was a feature of all four cases. In the patients in labour it occurred almost immediately. In those undergoing dilatation and curettage it occurred after the patients had apparently recovered but were under observation in the intensive care unit. Amniotic fluid embolism can occur during an apparently uneventful labour. It should also be suspected when unexplained collapse occurs during second trimester dilatation and curettage. Because severe DIC may follow, such patients should be transferred immediately to a centre with full haemotology services.
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PMID:Amniotic fluid embolism: a report of four probable cases. 371 41

When Escherichia coli B6 lipopolysaccharide, 0.2 mg/kg of body weight, was infused into nonpregnant minipigs during a 5-hour period, the animals died after 12 to 16 hours as a result of endotoxic shock. When the same infusion was given to six pregnant minipigs at term, these animals died after only 3 1/2 hours. The decrease in the number of white blood cells, the number of platelets, hematocrit, and clotting factors was not significantly different between the two groups. The acid-base status, however, indicated a much more pronounced metabolic acidosis in the pregnant animals than in the nonpregnant controls. In the pregnant minipigs heart rate, cardiac output, mean arterial pressure, and total peripheral resistance indicated cardiovascular collapse, and the multiple wire, platinum surface electrode revealed a drastic reduction in uterine tissue oxygenation in the pregnant animals. The data support the hypothesis that pregnant animals at term are more susceptible to the harmful effects of lipopolysaccharide. Early death in the pregnant minipigs, however, was not associated with disseminated intravascular coagulation as it is in smaller animals (rat, rabbit, and hamster).
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PMID:Septicemia during pregnancy: a study in different species of experimental animals. 392 Sep 12

Three cases of hypotension are described that followed rapid evacuation of persistent unilateral pneumothorax. Common features included the presence of a pneumothorax for approximately one week before treatment commenced and profuse unilateral reexpansion edema, a rising hematocrit reading, hypotension, and anuria after evacuation of the pneumothorax in spite of a relatively normal pulmonary capillary wedge pressure. In one case, cardiac output was measured and found to be low (1.54 and 1.65 L/min/sq m), with a pulmonary capillary wedge pressure of 10 to 14 mm Hg. Death due to cardiovascular collapse occurred in one patient; ischemic colitis, acute renal failure, disseminated intravascular coagulation, and ischemic necrosis of both humeral heads occurred in another. The cases presented and the literature reviewed suggest that cardiovascular compromise was the end result of the combined effects of intravascular volume depletion and myocardial depression.
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PMID:Reexpansion hypotension. A complication of rapid evacuation of prolonged pneumothorax. 394 Jul 93

Described is the clinical course of a 26-year-old woman who died following an overdose of the MAO inhibitor phenelzine. Signs and symptoms of toxicity were delayed in onset. Initial findings of excessive neuromuscular activity were followed by severe hyperthermia, coma, cardiovascular collapse, acute renal failure, hemolysis, rhabdomyolysis, and disseminated intravascular coagulation. A review of the literature suggests that these features are not unusual following MAO inhibitor overdosage. The pathophysiology and management of MAO inhibitor poisoning are discussed.
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PMID:Monoamine oxidase inhibitor overdose. 639 5

The neuroleptic malignant syndrome (NMS), clinically manifested by hyperpyrexia, mental status changes, muscular rigidity, and autonomic dysfunction, is an idiosyncratic reaction to major neuroleptic pharmacologic agents. The reported causes of morbidity and mortality include respiratory insufficiency, cardiovascular collapse, arrhythmias, and renal failure. Coagulopathy does not seem to be a prominent component of the syndrome. We observed a case of NMS in which disseminated intravascular coagulation was a prominent feature.
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PMID:Neuroleptic malignant syndrome complicated by disseminated intravascular coagulation. 673 89

Thromboembolism of minor vessels in the lungs is almost constantly seen in posttraumtic lung insufficiency. Many investigators consider it as the primary factor in the pathogenesis of this condition. The present paper deals with screening of the coagulation system as part of a more extended project also investigating changes in the fibrinolytic system and the kallikrein-kinin system. The data are also to be compared with morphological findings during the development of experimental posttraumatic lung insufficiency. The experimental syndrome was evoked in Labrador retriever dogs by haemorrhagic hypotension combined with clamping of the portal triad. The surgical procedure was extended to additional thoracotomy in one group of dogs. Group I, without thoracotomy, were followed for 12 hours. Group II, with thoracotomy, were followed until they succumbed (3-14 hours). Thrombotest (TT) showed a steady prolongation of clotting time in both groups, whereas Cephotest did not reveal any alterations, except for a significant prolongation in group II just before collapse. Fibrinogen was markedly reduced in both groups. Platelets and leucocytes were significantly reduced, but only in group II. It is concluded that the present data are indicative of disseminated intravascular coagulation. The involvement of the intrinsic coagulation system is questioned.
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PMID:Blood cells and coagulation during experimental lung insufficiency in dogs. 693 93

Two young women with toxic shock syndrome are reported and compared with three previous New Zealand cases. Both presented with fulminant diarrhoea, confusion, collapse and an erythematous desquamating rash. One, complicated by disseminated intravascular coagulation, rhabdomyolysis, myoglobinuria and renal failure, recovered following peritoneal dialysis. At the onset of their illnesses both were menstruating and using tampons. Light growths of Staphylococcus aureus were cultured from the vagina in one case and the faeces in the other. Successful treatment depended on a vigorous intensive care regime.
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PMID:Staphylococcal toxic shock: two fulminant cases with recovery. 695 24

The data on one of sepsis variations, bacterial or endotoxin shock (BS) are presented. BS is caused by gram-negative flora among which the first place belongs to E. coli, but may also be caused by gram-positive bacteria. BS is characterized by an acute onset with chills, hyperthermia, leukocytosis and early development of circulatory collapse which may cause early death of the patient. The direct of mediated effect of endotoxin on the vascular wall causing paralytic distention of the microcirculatory bed with deposition of the blood in it is recognized in the pathogenesis of BS. Subsequently, under conditions of hypoxia and acidosis disorders of hemocoagulation develop in the form of disseminated intravascular coagulation which may result in cortical necrosis of the kidneys, necrosis and apoplexy of the adrenals, hypophysis, acute ulcers in the gastrointestinal tract, necroses and hemorrhages in some other organs.
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PMID:[Bacterial (endotoxic) shock]. 699 29

Twenty-four fatal cases of echo 11 infection in the eleven years 1968-78 are presented. All were children, and could be divided into two groups according to age at death and clinical presentation. The first group comprised 12 babies who died aged between 5 and 11 days after a short illness characterised by collapse, acidosis, and bleeding. At necropsy there was evidence of disseminated intravascular coagulation with haemorrhage into many organs including the renal medulla, suprarenal glands, gastrointestinal tract, and central nervous system. Six cases showed hepatic necrosis which was massive in three. Virus was present in many tissues. Infection was probably acquired from the mothers at delivery in 3 cases. Low maternal neutralising antibody titres and prematurity were thought to be adverse factors in the outcome. The second group consisted of 12 children aged between 9 weeks and 4 years 10 months who died suddenly. Pathological findings included upper respiratory tract infection, pneumonia, encephalitis, and gastroenteritis. Six of this group had been classified as 'cot deaths'. The role of echo 11 in the death of some of these older children is unknown. This report shows the danger of echo 11 to neonates, especially if unprotected by maternal antibody.
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PMID:Fatal infection with echovirus 11. 719 96


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