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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 effects of intraamniotic instillation of saline solution for abortion induction on blood coagulation were studied in 81 women in the 16-24th week of pregnancy. Activity of blood coagulation system was estimated by changes in plasma fibrinogen concentration. Depending upon the time period between saline instillation and the onset of abortion, the women could be divided into 3 groups. Group 1 included 37 women in whom abortion occurred 24 hours after instillation, group 2 consisted of 28 women in whom abortion occurred 24-48 hours after instillation, and group 3 included 16 women in whom abortion occurred 48 hours after saline instillation. The women in all 3 groups showed decrease in fibrinogen concentration within the 1st 24 hours after saline administration. The maximum decrease in fibrinogen concentration was observed in group 1. Fibrinogen concentrations returned to normal values within 48-64 hours after abortion. It was concluded that transient hypofibrinogenemia induced by intraamniotic saline instillation can play a role in the pathogenesis of disseminated intravascular coagulation.
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PMID:[Changes in the fibrinogen level and the risk of defibrination after the intra-amniotic instillation of a saline solution used for abortion purposes]. 738 74

Venom activity in citrated plasma from a patient with a green pit viper bite was demonstrated by measuring its ability to decrease fibrinogen levels in normal plasma for six days after the bite. By in-vitro study, the minimal amount of crude venom to induce hypofibrinogenemia was 0.5 microgram/ml of normal plasma. The findings explained the continuing defibrination with bleeding and especially the failure of fresh-frozen plasma transfusion to correct hypofibrinogenemia in this patient. The most beneficial therapy should therefore be the neutralization of venom by antivenin, for as long as abnormal coagulation profiles are present, to discontinue the defibrinating process. The preparation of potent antivenin must be encouraged.
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PMID:Prolonged defibrination syndrome after green pit viper bite with persisting venom activity in patient's blood. 745 31

Hemostatic abnormalities are rather frequent in cancer patients either in hematological or in solid tumors. Acute disseminated intravascular coagulation (DIC) is a rare coagulopathy in cancer patients, but when it develops it becomes rapidly fatal. Between June 1988 and December 1992 we observed 8 cases of acute DIC occurring in gastric cancer (4 patients), breast cancer (3 patients) and high-grade non-Hodgkin lymphoma (1 patient). In 3 patients affected by gastric carcinoma, acute DIC was the first manifestation of the presence of the tumor, while in the other patients DIC occurred during the course of the disease. All the patients were treated with heparin, fresh frozen plasma and platelet support, but only in 1 patient was a short duration improvement of clinical conditions and coagulation tests recorded. Acute DIC can be the first manifestation of gastric tumors and the presence of the hemorrhagic syndrome associated with thrombocytopenia, hypofibrinogenemia and fibrin/fibrinogen degradation products should initiate a search for gastric carcinoma.
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PMID:Acute disseminated intravascular coagulation syndrome in cancer patients. 747 40

Thrombin and plasmin generation were assessed in patients with endemic hepatosplenic schistomiasis (15 hepatosplenomegalic, 15 splenomegalic, 15 with advanced hepatic fibrosis and ascites and 15 hepatosplenic patients with hematemesis). Prolongation of prothrombin time, partial thromboplastin time and thrombin time, thrombocytopenia, hypofibrinogenemia, a decrease in antithrombin III and protein C and S levels and elevation in fibrinopeptide A, D-dimer and thrombin-antithrombin complex levels were detected in all groups. The deficit in hemostatic parameters was more pronounced with the advancement of the disease and was maximal in the hematemesis group. Our data demonstrate an increase in both thrombin and plasmin generation and indicate that low grade disseminated intravascular coagulation may occur in association with endemic Egyptian hepatosplenic schistosomiasis even in the steady state without overt bleeding.
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PMID:Disseminated intravascular coagulation in endemic hepatosplenic schistosomiasis. 748 60

The Kasabach-Merritt syndrome of consumptive coagulopathy associated with massive hemangiomas is a potentially life-threatening problem in patients who sustain long bone fractures of the involved extremities. In this syndrome, platelet consumption is caused by their sequestration in the sinusoids and epitheloid chambers of large hemangiomas. Secondary fibrinolysis then occurs with resulting thrombocytopenia, hypofibrinogenemia, and increased fibrin degradation products that can lead to disseminated intravascular coagulation. This can result in massive bleeding even after minor trauma. In such patients, operative management of long bone fractures, including the placement of cutaneous pins for skeletal traction, may be contraindicated; nonoperative management may be necessary. Kasabach-Merritt syndrome must be suspected in patients with large hemangiomas and associated long bone fractures, and appropriate coagulation studies should be obtained before operative management or placement of percutaneous skeletal pins. Decreased hematocrit and fibrinogen levels associated with thrombocytopenia and prolonged prothrombin time and partial thromboplastin time should alert the orthopaedist to the possibility of Kasabach-Merritt syndrome, and prompt hematologic consultation should be obtained. If surgical treatment is deemed too dangerous because of the possibility of uncontrollable disseminated intravascular coagulation, the only prudent option may be a closed reduction and cast application after appropriate medical management of coagulation parameters.
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PMID:Kasabach-Merritt syndrome complicating treatment of a closed femoral fracture. 763 3

Experiments on dogs (n = 86) revealed that a combined injury led to marked disorders in the hemostasis, manifesting by third-degree syndrome of disseminated intravascular coagulation which develops as early as at the height of injury. Infusion therapy, particularly making use of intravenous polygluquin, led to progress of chronological and structural hypocoagulation and hypofibrinogenemia. Heparin in a dose of 25 to 30 U/kg b.w. reduced the severity of hypocoagulation shifts, this manifesting by a shorter time of some coagulation tests and suppression of intravascular platelet aggregation. A manifest trend to normalization of plasma and platelet hemostasis was observed 3 h after the onset of infusion therapy. This trend was more manifest if intraosseous infusion of isotonic NaCl solution was used.
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PMID:[Use of heparin in the early post-traumatic period in burns and hemorrhage]. 789 70

We describe the case of a 42-year-old woman with giant cavernous hemangioma and Kasabach-Merritt syndrome. The patient presented with consumption coagulopathy due to intravascular, intratumoral coagulation as revealed by low platelet levels, fibrinogenopenia and an increase in fibrinolysis with high levels of fibrinogen degradation products. She was scheduled to receive an orthotopic liver transplant because of three factors: respiratory distress caused by compression of the diaphragm by the giant tumor; the risk of bleeding caused by spontaneous rupture or trauma; and the presence of Kasabach-Merritt syndrome due to consumption coagulopathy. Before surgery fibrinogen deficit was corrected with 4 units of cryoprecipitates and low platelet level was treated with 10 units of platelets. Coagulopathy during surgery was corrected with fresh plasma (17 units), cryoprecipitates (6 U), aprotinin (1 x 10(6) U/kg) and antithrombin 3 (2000 U). Blood loss was compensated for with 9 units of packed red blood cells. This report describes the procedures used for anesthesia, for prevention of accidental bleeding during surgery, hemodynamic control and preoperative coagulation testing.
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PMID:[Orthotopic liver transplant for giant cavernous hemangioma and Kasabach-Merritt syndrome]. 789 56

BACKGROUND. Hypofibrinogenemia and increased fibrin(ogen) degradation products in acute leukemia have been attributed to intravascular thrombin generation triggered by leukemic cells. However, the strict relationship between fibrinogen catabolism and turnover of fibrinopeptide A (FPA), which is a sensitive and specific marker of thrombin activity, has not been evaluated in acute leukemia (AL) with or without disseminated intravascular coagulation (DIC) to see whether mechanisms other than thrombin activity could be responsible for fibrinogen consumption. We report here the 125I-fibrinogen kinetics and FPA measurements in 19 patients with AL, 6 of them with DIC. METHODS AND RESULTS. Radiolabelled fibrinogen kinetics were studied in all the patients concomitantly with the start of chemotherapy. Fibrinopeptide A was measured by a radioimmunoassay at time of diagnosis and during chemotherapy. The kinetics of disappearance of radiolabelled fibrinogen where biphasic, with a rapid phase in the first 1-3 days of chemotherapy and a subsequent slow phase associated with the reduction or disappearance of blast cells. Patients with DIC had a significantly shorter half-life and turnover than patients without DIC. The latter group had significant shortening of these parameters in comparison to normal subjects. The thrombin-dependent catabolic rate of fibrinogen, calculated from the mean level of FPA during the first phase of disappearance curve and by assuming 2 moles of FPA generated per mole of fibrinogen, was similar in patients without DIC and in normal subjects, whereas patients with DIC had a significantly higher catabolic rate, even though the increase was not sufficient to account for all the turnover of fibrinogen. No relationship was observed between fibrinogen turnover and FPA turnover.
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PMID:Fibrinogen survival and fibrinopeptide A in acute leukemia. 803 60

The dissolution by the fibrinolytic agent saruplase of microthrombi due to disseminated intravascular coagulation (DIC) has been studied in anesthetized rats. The intravenous infusion of E. coli lipopolysaccharide (endotoxin) for 4 hours (total dose: 25 mg/kg) induced marked thrombocytopenia and hypofibrinogenemia. DIC-related microthrombosis, detected as increased deposition of 125I-labelled human fibrin, was found in the liver and the kidneys, but not in the lungs, the heart, the mesenterium, the spleen and the M. rectus abdominis of endotoxemic rats. Treatment with 1-20 micrograms/kg.min saruplase, that was infused concomitantly with endotoxin, dose-dependently and significantly reduced endotoxin-induced microthrombosis in the liver and the kidneys by 85 resp. 88%. When saruplase (20 micrograms/kg.min) was administered only during the last two hours of endotoxin infusion, liver microthrombosis was still significantly dissolved by 69%, whereas renal microthrombosis was insignificantly reduced by 34%. The inhibition of endotoxin-induced microthrombosis took place in the same dosage range as the shortening of the euglobulin clot lysis time in normal rats by saruplase as a measure of its fibrinolytic activity. Saruplase did not modify thrombocytopenia and hypofibrinogenemia in endotoxemic rats. Saruplase per se did not affect plasma fibrinogen levels. Thus, in a fibrin-selective dose range saruplase is able to dissolve microthrombosis associated with DIC in endotoxemic rats.
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PMID:Fibrin-specific lysis of microthrombosis in endotoxemic rats by saruplase. 812 89

Disseminated intravascular coagulation (DIC) is uncommon in acquired immunodeficiency syndrome (AIDS), despite the high incidence of infectious diseases. We describe an HIV-infected patient presenting with disseminated cryptococcosis, who had clear-cut laboratory evidence of progressively worsening DIC (thrombocytopenia, prolonged prothrombin time and partial thromboplastin time, hypofibrinogenemia, increased fibrin(ogen) degradation products and D-Dimer, reduced antithrombin III), although the clinical signs of the disease were rather scarce. The patient died despite intense treatment, which included heparin and fresh frozen plasma, and DIC was confirmed histologically. It is suggested that, in a patient with AIDS presenting with an opportunistic infection, laboratory signs of DIC should be carefully checked to early recognize this complication and promptly initiate the required therapy.
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PMID:Disseminated intravascular coagulation associated with disseminated cryptococcosis in a patient with acquired immunodeficiency syndrome. 836 14


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