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

Blood coagulation tests were performed in 93 newborn infants with different Apgar score at the 1st and 5th minutes of life. The laboratorial determinations were periodically performed at 0, 24 and 48 hours of life. The following tests were performed: bleeding time, whole blood clotting time, prothrombin time, kaolin-cephalin clotting time, thrombin time, dosage of factors I, V, VIII and X, clot retraction, platelet count, englobulin lysis time and the tourniquet test. Immediately after birth, the mean values of the blood coagulation factors were significantly different among the groups, with the exception of the whole blood clotting time and the platelet count. Those differences were due to the presence of the more depressed neonates. Although these results could indicate some degree of hepatic damage, it was apparent that an activation of the blood coagulation mechanisms took place, leading to a consumption coagulopathy. The infants who died (10) presented clinical and laboratorial data suggestive of disseminated intravascular coagulation (DIC). Necroscopic findings of microthrombosis in the liver and in the central nervous system were diagnosed in two infants.
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PMID:Apgar score and blood coagulation factors. 93 62

The infusion of thrombin in rats induced a disseminated intravascular coagulation (DIC) with haemolysis and schistocytosis. The number of schistocytes was found to be correlated to fibrinogen catabolism, plasma haemoglobin level and to the extent of fibrin deposition in the renal glomeruli in the early phase only. Later, no correlation could be observed, indicating a time-dependent behaviour of schistocytosis. The results suggest that a large number of schistocytes in blood smear is suspicious for DIC. These studies also support the concept that fibrin depositions in the blood vessels could play a role in the production of red cell fragmentation by mechanical destruction.
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PMID:The appearance of schistocytes in the peripheral blood in correlation to the degree of disseminated intravascular coagulation. An experimental study in rats. 95 Jan 76

The high incidence of consumption coagulopathy in active liver cirrhosis prompted us to introduce low-dosage heparin therapy (LDHT) in the management of this condition. An investigation was carried out on 109 patients with clinical and biochemical evidence of progressive liver cirrhosis, which was designed to evaluate whether in addition to basic LDHT, the administration of either vitamin K1, human fibrinogen or partial prothrombin complex (Prothromplex 500) enhanced the results obtained with LDHT alone. The normotest, PTT, thrombin coagulase activity, fibrinogen and platelet count were determined at regular intervals. A significant increase in fibrinogen and platelet count was obtained within 14 days of LDHT in about 75% of the patients and the consumption coagulopathy was halted. Additional treatment with vitamin K1 did not bring about any further increase in the prothrombin complex. Substitution therapy with factors II, IX, X and fibrinogen combined with LDHT brought the expected results. The results reported in the literature and the aims of, and indications for LDHT are discussed.
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PMID:[The therapeutic management of consumption coagulopathy in progressive liver cirrhosis: low-dosage heparin therapy (author's transl)]. 99 29

Disseminated intravascular coagulation was induced in rats by injection of a silver colloid suspension or thrombin. Ten min after the injection of colloid, fibrin deposits were observed light microscopically in all major organs. At 30 min, fibrin was no longer present. In rats treated with antifibrinolytics (epsilon-aminocaproic acid or Trasylol) fibrin was still present at 30 and 60 min. Interaction of fibrin with Kupffer cells was studied by electron microscopy. At 3, 10, and 20 min after the colloid injection, all fibrin occurred extracellularly, close to the surface of Kupffer cells. At 30 min, all fibrin had disappeared. In rats pretreated with antifibrinolytics, too, all fibrin was found extracellularly at 10, 30, and 60 min. Comparable results were obtained when thrombin was used to induce coagulation. It is concluded that removal of native fibrin from the circulation by Kupffer-cell phagocytosis is unlikely.
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PMID:Rat liver macrophages will not phagocytose fibrin during disseminated intravascular coagulation. 100 4

The coagulation and fibrinolytic systems play a key role in maintaining the integrity and patency of the vascular compartment. Pregnancy induces extensive physiological changes in these systems, thus creating an enhanced capacity to produce fibrin and a diminished ability to remove it. Fibrin deposition localized to the uteroplacental circulation is a feature of normal pregnancy. In women with fatal eclampsia, disseminated intravascular coagulation with fibrin deposition in the renal glomeruli is well documented. The condition of preeclampsia is not well defined. Nonetheless, evidence of intravascular coagulation, as shown by elevated levels of fibrin degradation products and reduced platelet counts, has been found in many women with preeclampsia. Serial studies showed that thrombin generation, as indicated by the ratio of factor VIII-related antigen to factor VIII coagulant activity, is considerably in excess of that which occurs in normal pregnancy, and its appearance coincides with the development of the clinical features of preeclampsia. Heparin therapy has bot been proven of value in established preeclampsia, but this fact does not disprove that role that intravascular coagulation may play in the pathogenesis of the disease. A controlled trial ina high-risk group of low-dose he;arin and an antiplatelet agent from the 16th to the 18th weeks of pregnancy onwards is required to elucidate the role of intravascular coagulation in preeclapmsia and its effect on the fetus.
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PMID:The role of coagulation and fibrinolysis in preeclampsia. 100 56

Alternations in the coagulation mechanism were looked for in a population of eclamptic women, most of when were young, nulliparous, and without evidence of chronic vascular disease, and all of whom survived. Thrombocytopenia was identified in 29% of these women. A prolonged plasma thrombin time was demonstrated in 51% yet elevated fibrinogen-fibrin degradation products in serum were uncommon, as was fibrin monomer in plasma. Overt microangiopathic hemolysis was rare. It is concluded that disseminated intravascular coagulation, when it does occur in eclampsia, is the consequence of the disease rather than the cause. Moreover, endothelial damage, rather contents, probably initiates the thrombocytopenia and other coagulation changes.
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PMID:Does coagulation have a causative role in eclampsia? 100 57

A study of coagulation disorders due to hepatitis A infection occurring during pregnancy was undertaken to determine if the unique coagulation status produced by pregnancy (elevated clotting factors and decreased fibrinolytic activity) was responsible for the increased severity of hepatitis A infections reported for pregnant women from various parts of the world. Of 49 patients studied, 12 (24%) developed hepatic failure and 9 (18%) died. A prolonged prothrombin time and low fibrinogen level were found to be as frequent as previously reported for nonpregnant patients with and without hepatic failure. Thrombocytopenia was less common and a long thrombin time was more common. Although intravascular coagulation was suggested by a lower mean fibrinogen level than expected in late pregnancy, mean platelet counts were similar to controls. The frequency of a positive protamine sulfate paracoagulation test for intravascular coagulation (DIC) was similar to that reported for uncomplicated pregnancy, and was of no prognostic value when performed on admission. We conclude that the severe clinical course of hepatitis during pregnancy in this epidemic was not attributable to a predisposition for DIC. However, once fulminant hepatitis occurred, DIC may have been a clinically significant factor.
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PMID:Coagulation studies of viral hepatitis occurring during pregnancy. 100 76

Intravascular coagulation was induced by two appropriately spaced doses of endotoxin and by infusion of thromboplastin. The resulting fibrin deposition was measured by a previously described quantitative technique. Evidence of thrombin elaboration was obtained indirectly by measurement of fibrin monomer (FM) and by the detection and isolation of a thrombin-induced anticlotting activity. Venous segments were isolated at intervals and examined for thrombus formation following 40 minutes of stasis. Endotoxin triggered thrombin elaboration was not detectable in the circulation for at least one hour and was not accompanied by any thrombosis in isolated venous segments. No thrombin elaboration was found in leukopenic rabbits given endotoxin. In the thromboplastin infused animals, the quantity of fibrin deposited in the organs was comparable to that found after endotoxin. However, thrombin was found in the blood immediately and was associated with thrombosis in the isolatet venous segments. Less thrombin-induced anticoagulant activity was found after thromboplastin than after endotoxin. The findings suggest that endotoxin-induced intravascular coagulation is probably not caused by a mechanism of systemic hypercoagulability due to the release of thromboplastic material into the blood stream. A focal process of thrombin elaboration involving leukocytes is postulated. The study is believed relevant to patients with disseminated intravascular coagulation in whom venous thromboembolism is rarely found despite evidence of extensive microvascular fibrin deposition.
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PMID:Thrombin elaboration in endotoxin-induced intravascular fibrin deposition. A leukocyte dependent process distinct from systemic hypercoagulability. 103 55

Total hemolytic complement activity and the third component of complement were found to be significantly depressed in vivo in rabbits following the induction of disseminated intravascular coagulation by both thrombin and thromboplastin. Production of severe thrombocytopenia by the administration of platelet antiserum prior to the infusion of thrombin or thromboplastin partially prevented complement activation. The data show that, when clotting is triggered, complement activation takes place and that platelets are required to some extent for this reaction.
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PMID:Effects of intravascular clotting on the activation of the complement system: The role of the platelet. 109 Nov 53

The therapeutic efficiency of two glucocorticoids (hydrocortisone and dexamethasone) on endotoxin-induced intravascular coagulation was investigated in the rat. Coagulation and platelet aggregation studies were performed and plaminogen was assayed. Our results indicate that pretreatment of the animals with large doses of these steroids within a few hours prior to endotoxin totally prevents the consumption in Hageman factor, measurable contact product activity, platelets, fibrinogen, plasminogen, and the loss in platelet aggregability and serotonin. In addition to this, the hypercoagulable state consecutive to endotoxin, characterized here by shortenings in the partial thromboplastin and recalcification times and by an increase in the availability of platelet procoagulant activity, was also totally prevented by the steroid pretreatment. On the other hand, it is shown that these glucocorticoids do not interfere in the normal rat with platelet aggregation (tested with thrombin,adenosine diphosphate, and collagen), but with the availability of platelet procoagulant activity. This last phenomenon, in addition to that of an interference in vivo with the mechanism of activation of Hageman factor, are believed to be responsible for prevention by glucocorticoids of endotoxin-induced disseminated intravascular coagulation.
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PMID:Prevention by glucocorticoids of disseminated intravascular coagulation induced by endotoxin: mechanisms. 109 78


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