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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 behavior of direct fibrinolytic (non-plasmin) proteinase activity and plasminogen-activator activity in the lung and spleen was investigated in rats after a single intravenous injection of bacterial endotoxin, and the influence of thrombin inhibitors on the effects of the endotoxin was assessed. The non-plasmin fibrinolytic activity was markedly increased following a decrease of plasminogen-activator in the lung. In addition, variations in hematological parameters, i.e. a decrease of platelet count, fibrinogen level and antithrombin III, and an increase of blood urea nitrogen and euglobulin fibrinolytic activity, were induced by the injection, indicating the occurrence of disseminated intravascular coagulation. In comparative studies on the effects of the endotoxin injection and thrombin infusion, in the lung and spleen an increase of fibrinolytic proteinase activity was induced in a similar manner; the plasminogen-activator activity in the lung was decreased by the endotoxin injection but not decreased by the thrombin infusion. In prevention studies with heparin and MD-805, the latter was found to prevent the decrease of either fibrinogen or platelet count. However, the former failed to prevent the decrease of platelet count although that of the fibrinogen level was prevented. Heparin and MD-805 exerted no preventive effect on the endotoxin-induced variations of proteinase activity and plasminogen-activator activity in the lung.
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PMID:Variation in activities of non-plasmin fibrinolytic proteinase and plasminogen-activator in the lung and spleen induced by bacterial endotoxin in rats with special reference to the effects of MD-805. 390 90

The thromboplastic activity of amniotic fluid (AF) from women in labor may be a significant factor in amniotic fluid embolism (AFE) and obstetric disseminated intravascular coagulation (DIC). Infusion of AF from women in labor into laboratory animals was found to depress the platelet count, as seen in DIC. In this study we also investigated the ability of heparin and aspirin to block the thromboplastic activity and thrombocytopenia subsequent to AF infusion. In animals, heparin prophylaxis before infusion of AF prevented thrombocytopenia, whereas aspirin prophylaxis did not. Heparin prophylaxis may be useful in the management of coagulation defects associated with AFE and labor.
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PMID:Amniotic fluid embolism: prophylaxis with heparin and aspirin. 398 57

Disseminated intravascular coagulation (DIC) is not uncommon in the obstetric patient, but DIC of sufficient severity to be of clinical importance is unusual. Treatment of DIC is directed primarily at its cause. Replacement of depleted blood components with packed red blood cells, fresh frozen plasma, cryoprecipitate, and platelets is sometimes required for treating hemorrhage. Heparin should be used only rarely, and only to help control life-threatening hemorrhage because DIC is refractory to vigorous and adequate blood-component therapy. With careful planning of treatment, adherence to a few general principles, and the combined approach of an obstetrician and a coagulationest, fatalities and major morbidity should be rare.
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PMID:Disseminated intravascular coagulation. 405 71

Two cases of abruptio placentae with disseminated intravascular coagulation (DIC) were treated with heparin, and coagulation was monitored by thromboelastography as well as the usual hematology tests. The cases demonstrated the vagaries of DIC and both showed decreased overt hemorrhage after heparin treatment was started. Heparin may be indicated for the management of abruptio placentae where delivery is not imminent, where significant disseminated intravascular coagulation exists, and when adequate serial coagulation studies are available.
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PMID:Heparin treatment in abruptio placentae. 482 41

Antithrombin III (AT III) is a plasma protein which acts as the principal inhibitor of thrombin and is a major modulator of intravascular coagulation. Hereditary deficiency of AT III leads to recurrent episodes of thromboembolism. Acquired deficiency of AT III occurs in persons with a variety of conditions, including severe liver disease and disseminated intravascular coagulation. Replacement of AT III may be important in some deficient persons. To determine if cryoprecipitate is a useful source of AT III, we measured the AT III content of cryoprecipitate prepared from citrate phosphate dextrose blood using coagulation and fluorogenic assays and immunoassays. Using the fluorogenic assay, we also determined the effect of adding heparin to blood on the cryoprecipitation of AT III. Functional and antigenic AT III levels were similar to those of normal plasma in all citrate phosphate dextrose blood units tested, indicating that AT III is not concentrated in cryoprecipitate. Heparin had no effect on the cryoprecipitation of AT III.
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PMID:The antithrombin III content of cryoprecipitate prepared from blood collected with and without heparin. 640 59

Purpura fulminans presents as a catastrophic illness with gangrene of the distal extremities and necrosis of skin. The clinical picture consists of septicemia, shock, and disseminated intravascular coagulation. The Shwartzman and Arthus reactions are thought to be responsible for the pathogenesis of purpura fulminans. The exact mechanisms of these reactions are not completely understood. Immediate resuscitation is the treatment for shock and sepsis. Heparin is recommended to reverse the disseminated intravascular coagulation component of this disease. Surviving patients require treatment of skin necrosis and digital and extremity gangrene. The former are managed in a fashion similar to the management of burns. Amputation should be delayed until maximal collateral circulation has developed. A series of 10 patients is presented and 58 cases from the literature are analyzed.
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PMID:Purpura fulminans. 646 Dec 69

A typical case of DIC presumably precipitated by cesarean section done for severe toxemia of pregnancy is reported. A laboratory study followed up the progress of DIC, especially of the drop in the consumptive platelet count and fibrinogen level as a result of excessive blood clotting. In this case the patient was a 29-year-old nulliparous gravida 1 who developed severe toxemia at 29 weeks and underwent a cesarean section for fetal distress at 33 weeks, although the baby died immediately after birth. On the following day of operation slight bleeding from the operative wound occurred and she had pertinent laboratory tests, which yielded a platelet count of 81,000/mm3, plasma fibrinogen level of 200mg/dl and FDP of 160 micrograms/ml and led to a diagnosis of DIC. While placing her on replacement and adjunctive therapies the laboratory tests were performed serially, which permitted a close follow-up observation of the subsequent progress of DIC with the detection of lowered platelet counts and fibrinogen levels as administration of Heparin resulted in an increase in the amount of bleeding, FOY, 800mg/day, was instituted and following this treatment the DIC disappeared.
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PMID:[A typical case of DIC precipitated by cesarean section done for severe toxemia of pregnancy and a follow up laboratory study of the progress of DIC]. 651 26

A 27-year-old man with acute monoblastic leukemia had clinical and laboratory evidence of disseminated intravascular coagulation (DIC), which was exacerbated by induction chemotherapy. Heparin therapy, adjusted according to the patient's clinical status and the results of coagulation studies, rapidly controlled the manifestations of DIC.
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PMID:Disseminated intravascular coagulation in acute monoblastic leukemia: response to heparin therapy. 658 92

To test the value of diagnostic and therapeutic data in obstetric DIC, 14 women were selected who presented a severe clotless haemorrhage with fibrin degradation products and/or soluble complexes, decreased fibrinogen (0.87 +/- 0.47 g X 1(-1)), platelet count (75.7 +/- 41 X 10(3) X ml-1) and prothrombin complex (33.7 +/- 12%). The hypovolaemia was treated at the same time as heparin was given in a bolus injection of 0.5 mg X kg-1 followed by a constant flow infusion of 1 mg X kg-1 X day-1 in all patients. Relevant obstetrical treatment was performed in 71.4% of patients. Fibrinogen, fresh frozen plasma, prothrombin complex concentrate and platelet concentrate were given if required. One patient, with severe toxaemia, died. Haemorrhage was stopped in 92.8% of patients after 4.5 +/- 0.8 h. Reversible visceral complications occurred in 28% of cases. The initial data used was easily obtained and seemed to give a reliable diagnosis in acute obstetrical DIC. Substitutive treatment was discussed in correlation with the evolution: PCC seemed pointless; the use of fibrinogen must become exceptional when fresh frozen plasma is available. Heparin remained necessary.
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PMID:[Disseminated intravascular coagulation. Retrospective study of 14 acute obstetrical cases]. 665 Sep 31

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12


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