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

A gravida with intrauterine fetal death who developed progressive chronic consumption coagulopathy was treated with heparin. When serial fibrinogen levels fell below 100 mg% and the prothrombin time was significantly prolonged, intravenously injected heparin corrected hypofibrinogenemia. A safe delivery followed administration of oxytocin. The authors emphasize the infrequent need for heparin therapy in the majority of cases of the intrauterine fetal death syndrome. Therapeutic guidelines for its use in selected cases are reviewed.
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PMID:Consumption coagulopathy associated with intrauterine fetal death: the role of heparin therapy. 3 82

Coagulation studies were carried out in a group of non-human primates (rhesus monkeys) following envenomation with lethal and sublethal doses of Russell's viper venom. The envenomated animals showed significant fibrinogenopenia in association with or without disseminated intravascular coagulation. The findings offer a rational explanation for the bleeding manifestations seen in clinical cases of Russell's viper bite.
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PMID:Coagulation abnormalities induced by Russell's viper venom in the rhesus monkey. 11 72

This report concerns 20 patients with intrauterine fetal death. Blood samples for coagulation studies were obtained before, during and after delivery. No clinical defibrination or bleeding was noted. Coagulation defects were observed as follows: 2 biological defibrinations: The first case was a pregnancy of 32 wk with retention for more than 12 wk; hypofibrinogenemia was noted in all 6 samples, between 180 and 280 mg/100 ml. The second was a pregnancy of 32 wk with retention for more than 8 wk; fibrinogenemia was between 170 mg/100 ml and 140 mg/100 ml. 2 intravascular coagulations with normal fibrinogenemia, increase of fibrin degradation products and positive ethanol tests. 3 cases with slight coagulation defects that were difficult to explain. The coagulation defects appeared to be transient, and sometimes resolved themselves spontaneously. Induction of labour was made in 19 cases; quinine sulfate, used in 17 cases, was remarkably successful (1 intolerance, 1 failure). Study of the half-life of [125I]fibrinogen was made in 18 of the 20 cases. On average, it was reduced by half in comparison with the half-life of healthy men. The decrease was noted even in cases of fetal deaths without the coagulation defects detected by classical tests. The half-life of [125I]fibrinogen in 6 pregnant women before therapeutic abortion was also studied. The decrease of half-life was noted. Changes of metabolism of fibrinogen during pregnancy are discussed.
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PMID:Fetal death: coagulation defects and management. Report of 20 cases with study of the half-life of [125I]fibrinogen. 26 51

The evidence for intravascular coagulation in liver diseases is critically reviewed. Alternative mechanisms for hypofibrinogenemia and the accelerated disappearance of fibrinogen from blood are proposed, such as loss into extravascular compartments (e.g., ascites, areas of liver necrosis, etc.). Possible mechanisms other than DIC for the elevation of serum FDP are also considered, such as extravascular fibrinogen proteolysis with subsequent transfer of FDP to blood. Therapy is discussed with reference to the current knowledge on pathophysiology of the coagulation defect in liver diseases.
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PMID:Diffuse intravascular coagulation in liver disease? 33 13

When a dead fetus has remained in utero, an abnormality in haemostasis can be observed depending on the duration of retention. The most significant symptom is hypofibrinogenemia. Publications on the subject show in addition to a variety of symptoms a non-uniform pathogenetic pathway of the haemostatic disorder: Both an isolated hyperfibrinolysis and disseminated intravascular coagulation (DIC) with subsequent secondary activation of fibrinolysis have to be taken into consideration of the pathomechanism of the haemostasis defect. The triggering of DIC is possibly connected to the presence of the dead fetus and placenta, a primary hyperfibrinolysis seems to be induced by the mechanical factor of labors or curettage. The management of the haemostatic failure should be directed at the pathogenetic considerations; the appropriate treatment may be life-saving, when the haemostatic conditions become precarious inducing a bleeding tendency.
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PMID:[Disorders of hemostasis in intrauterine fetal death. Pathogenetic and therapeutic considerations]. 39 53

Anticoagulants in the form of heparin, dipyridimole, steroids, prostaglandin E1, Macrodex, and antithrombin III were administered in separate experiments prior to endotoxin infusion in the dog. The pattern of disseminated intravascular coagulation (DIC) developed consistently when endotoxin alone was administered. Heparin dosages from 1 to 10 mg/kg did not influence the appearance of thrombocytopenia but effectively eliminated the decrease in fibrinogen levels ordinarily found. Antithrombin III (AT III), obtained from the National Red Cross, administered in a dose designed to provide a doubling of the circulating AT III, reduced the fibrinogen utilization to a similar degree as heparin without affecting the platelet loss. Dipyridimole, as administered, was ineffective in this model, and did not alter the development of thrombocytopenia or the hypofibrinogenemia. Steroids, Macrodex, and prostaglandin E1 had minimal effect on the coagulopathy. Our finding would suggest that the endotoxin effect on dog platelets id direct, and not mediated by thrombin, and that the role of heparin in the clinical management of DIC should be considered only in instances in which renal complications exist.
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PMID:Endotoxin-induced intravascular coagulation (DIC) and its therapy. 40 May 81

Blood coagulation studies showed there was a pronounced thrombocytopenia and hypofibrinogenemia in Holstein calves infected with Trypanosoma congolense TREU 112. There was also ineffective thrombopoiesis characterized by an increased megakaryocytic mass, reduced uptake of 35S-methionine into peripheral blood platelets and a normal platelet lifespan. There was an increased uptake of isotopic label into fibrinogen and a shortened half life indicating a consumptive error with increased peripheral use of fibrinogen. No consistent abnormalities were found in ethanol gelation, partial thromboplastin time, clot retraction and lysis or plasminogen assay. Fibrin split products were rarely detected. These findings suggest that in the chronic form of bovine trypanosomiasis there is a partially compensated consumption coagulopathy.
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PMID:The pathogenesis of Trypanosoma congolense infection in calves. IV. The kinetics of blood coagulation. 44 53

An outbreak of chronic liver disease was investigated in a kennel of dogs. Anorexia, depression, polyuria, polydipsia, icterus and a terminal hemorrhagic diathesis were noted in clinically affected dogs. Thrombocytopenia, hypofibrinogenemia, elevated fibrinogen degradation products and prolonged activated partial thrombosplastin times (PTT) and one-stage prothrombin times (PT) were associated with the hemorrhagic crisis. Aflatoxicosis was confirmed by the presence of significant levels of aflatoxicosis was confirmed by the presence of significant levels of aflatoxin B in the commercial dog food being fed. A subacute hepatitis was found on necropsy. Disseminated intravascular coagulation was suspected as the cause of the hemorrhage in these cases and treatment was instituted.
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PMID:Disseminated intravascular coagulation complicating aflatoxicosis in dogs. 55 87

Patients with typhoid fever were studied to determine whether disseminated intravascular coagulation (DIC), circulating bacteria, and endotoxemia were responsible for the signs and symptoms of their illnesses. Coagulation tests in 28 patients detected thrombocytopenia in 17, hypofibrinogenemia in nine, and elevated titers of fibrinogen-related antigens in 20. Repeated testing during convalescence showed a return toward normal values. Intestinal bleeding, however, did not correlate with abnormalities of coagulation tests. Thus, DIC occurred commonly but appeared to be a subclinical event in these patients. In 25 patients with positive blood cultures for Salmonella typhi, quantitative cultures detected from less than 10 to 9 x 10(2) bacteria/ml. Limulus tests for endotoxin in plasma were negative in all 21 patients tested. These results indicated that the concentrations of circulating bacteria and endotoxin in typhoid fever are lower than in other Gram-negative bacterial infections and suggested that circulating bacteria and endotoxin do not play a major role in the pathogenesis of typhoid fever.
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PMID:Typhoid fever. Studies of blood coagulation, bacteremia, and endotoxemia. 62 35

Coagulation studies were performed in 61 patients of acute infective hepatitis. 18 with clinical signs of liver failure had bleeding and all succumbed. The 47 patients without liver failure showed no haemorrhagic diathesis and all of them had uneventful recovery. Though coagulopathy was present in most of the patients, the severity and frequency of coagulation defects were more in those with signs of hepatic failure. Hypofibrinogenemia, elevated serum fibrinogen degradation products and accelerated euglobulin lysis were conspicuous in patients with hepatic failure. It appears that while diminished synthesis of coagulation factors is the main basis for coagulopathy in patients without hepatic failure, additional factors like local or disseminated intravascular coagulation and increased fibrinolysis also contribute significantly to the coagulopathy in cases of liver failure.
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PMID:Blood coagulation in patients with acute infections hepatitis in India. 81 35


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