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

An analysis was made of 346 cases of disseminated intravascular coagulation (DIC) diagnosed by utilizing a combination of laboratory tests which reflect the pathophysiology of the syndrome. The goals of the study were three fold: 1) to compare our clinical disease categories with those of other investigators, 2) to re-evaluate the diagnostic tests and, 3) most importantly, to report the results of tests infrequently performed when evaluating DIC. The patients fell into the following groups: 1) infection -- 26%, 2) malignancy -- 24%, 3) surgery and trauma -- 19%, 4) liver disease -- 8%, 5) miscellaneous -- 23%. Of the diagnostic tests, those for fibrin split products (FSP), fibrin monomer and antithrombin III were the most valuable. Of the clotting proteins, factors II, V, VII and X were the most frequently decreased. The factor VIII: C levels were in conflict with the prevailing dogma. Factor VIII:C levels were decreased in only 9% of patients studied and, in fact, were increased in the majority of cases. Factor VIIIR:Ag and F VIIIR:vW were elevated in 80% of the patients evaluated. An overall mortality of 68% further confirms the dismal prognosis previously associated with DIC.
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PMID:Disseminated intravascular coagulation. Findings in 346 patients. 677 70

Ten of 11 patients undergoing peritoneovenous (LeVeen) shunt placement for intractable ascites had disseminated intravascular coagulation (DIC) following the shunt procedure. Intraoperative ascitic fluid specimens revealed fibrin split products (FSP) in high titer (1:100-1:1600) in all patients. Endotoxin was found in 6 of 11 ascitic fluid samples but in no plasma samples. Activated clotting factors, clot inhibitors, excess protein, and fibrinolytic activity were not found in ascitic fluid. Clotting factor levels were much lower than in plasma. Bleeding occurred after operation in two patients; this appeared to be related to the severity of liver dysfunction as demonstrated by elevations of bilirubin, serum glutamic oxalocetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), and preoperative DIC. It is concluded that the LeVeen shunt coagulopathy is DIC, and may be related to exposure of the systemic circulation to FSP-rich ascitic fluid that may activate the coagulation mechanism. Bleeding complications do not appear to be related to the severity of the post shunt coagulopathy, but rather to the severity of liver dysfunction and presence of preoperative DIC (probably caused by the liver disease).
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PMID:Ascites-induced LeVeen shunt coagulopathy. 685 98

A 24-hours service was organized to study changes in the hemostatic system in surgical patients undergoing massive transfusion for excessive bleeding during operation or in the early postoperative period. Hemostasis tests gave normal results in only 12(7%) of the 172 patients, while in the remaining 160(93%) one or more tests gave abnormal results. The platelet count was the most frequently abnormal, followed by the prothrombin time and plasma fibrinogen. Well-defined hemostatic disorders (such as DIC, heparinization and liver disease) were ascertained in 82 patients (48%). 78 patients (45%) had less specific laboratory abnormalities, with a particularly high incidence of thrombocytopenia and less pronounced alterations in the coagulation tests. Unlike the patients with defined disorders, the strong inverse correlation in this group between platelet count, prothrombin time, plasma fibrinogen, and the number of transfusions suggests that the laboratory abnormalities were induced by massive blood replacement. Standard schemas involving the administration of platelet concentrates and/or fresh-frozen plasma without evaluation of hemostasis did not help to reduce the incidence of abnormalities. These measures also failed to decrease the requirements for whole blood and/or packed red cells. Therefore, indiscriminate administration in the massively transfused postoperative patient of blood components based on preestablished schemes appears to be unjustified. An approach based on hemostasis screening, identification of the underlying disorder, directed therapeutic intervention and laboratory monitoring is likely to be more effective.
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PMID:Hemostasis testing during massive blood replacement. A study of 172 cases. 704 20

Disseminated intravascular coagulation (DIC) is caused by a variety of underlying disorders, and criteria for diagnosis are not well defined. However, the most helpful are a low platelet count, positive plasma protamine test, and fibrinogen and fibrin degradation product levels viewed in the context of the patient's underlying disease. The cornerstone of therapy is prompt treatment of the underlying disease and elimination of the trigger mechanism. Additional treatment must be individualized, and generalizations are difficult to make. However, if the patient has low hemostatic factors and is actively bleeding or requires an invasive procedure, then replacement with the appropriate hemostatic factors should be tried. Heparin is indicated in patients with purpura fulminans and venous thromboembolism, but there is little evidence that heparin reverses organ dysfunction associated with DIC. In addition, heparin is also probably indicated in patients with retained dead fetus and hypofibrinogenemia prior to induction of labor, excessive bleeding associated with a giant hemangioma, and neoplastic disease, particularly promyelocytic leukemia. Although the use of heparin in acute forms of DIC remains controversial, the majority of studies suggest that it is not helpful. The role of antithrombin III (AT-III) concentrates is unknown, but they theoretically may be helpful when DIC is associated with very low AT-III levels, as is seen in liver disease.
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PMID:Diagnosis and management of disseminated intravascular coagulation: the role of heparin therapy. 704 45

Although the coagulopathies encountered in patients with liver disease can be multifactorial, the most common cause is underproduction of certain coagulation factors synthesized by the liver. Generally, vitamin K and replacement therapy are all that is necessary. In the rare instance in which the coagulopathy may be complicated by hyperfibrinolysis or disseminated intravascular coagulation, replacement therapy may not suffice and other means of correcting the defect may be necessary. The prothrombin time, partial thromboplastin time, platelet count, fibrinogen concentration, and a test for fibrinolysis are recommended as the initial workup for the bleeding patient with underlying liver disease. Other, more specific tests may be necessary to differentiate the various causes of the defects in the hemostatic mechanism in these patients.
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PMID:Diagnosis and therapy of coagulopathies in patients with liver disease. 722 37

Fresh frozen plasma is prepared within 6 hrs after collection in a double bag system. A second centrifugation at 4600 x g is necessary to obtain a platelet poor plasma. A special bag freezing system fitted to a conventional cryostat and cooled with ethanol to -50 degrees C was developed to reach the required cooling rate. It is possible to freeze 25 plasma bags simultaneously within 30 min in this new apparatus. Fresh frozen plasma prepared in this manner contains all coagulation factors and inhibitors with almost normal activities. Freezing at -40 degrees C in the air, prolonged storage of the starting material, or insufficient cooling of the frozen product deteriorate its quality. The influence of these variables with the discussed in detail. Indications of fresh frozen plasma, especially for dilution- and posttraumatic consumption coagulopathy as well as liver disease, are presented.
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PMID:[Deep frozen fresh plasma in blood component therapy: preparation--quality control--indications]. 730 26

The fibrinogen molecule is becoming increasingly understood. Amino acid sequencing has been undertaken and studies of abnormal fibrinogens are leading to a more functional concept of its structure. Acquired dysfibrinogenemia appears to be a more common problem than previously thought, and may be found in patients with liver disease, cancer, fibrinolysis, and disseminated intravascular coagulation (DIC). While previous evidence suggested that anti-thrombin activity and fibrin polymerization inhibitors were formed in these conditions, recent studies suggest that slow fibrin formation occurs as a result of structural changes induced in the fibrinogen molecule itself. These relatively minor, alterations in structure cause a functional dysfibrinogenemia simulating abnormalities seen in some congenital fibrinogenopathies. A case is presented illustrating such a dysfibrinogenemia in a patient with cirrhosis of the liver and evidence for DIC.
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PMID:Fibrinogen and dysfibrinogenemia. 744 88

To investigate the pathogenesis of fibrinolysis in liver disease, antithrombin III (AT III) activity, prothrombin fragment (F1 + 2) and d-dimer (D-DI) were measured in 50 patients with liver disease and in 17 healthy controls. Moreover, 4 patients with cirrhosis were randomly assigned to receive either an intravenous infusion of AT III (at two different dosages) or placebo, with a crossover design. Increased levels of D-DI were detected in patients with cirrhosis and hepatocellular carcinoma in comparison both with control subjects and with patients with acute hepatitis or mild chronic liver disease. An inverse correlation was observed between AT III and D-DI (r = -0.755, P < 0.001, simple linear regression), while no correlation was found between D-DI or AT III and F1 + 2. The correlation of the deficiency of AT III activity by infusion of human AT III did not result in any significant change (P0.10, analysis of variance for repeated measures) of the plasma concentration of either D-DI or F1 + 2, in comparison to placebo. Thus, advanced forms of chronic liver disease, but not acute hepatitis and mild forms of chronic liver disease, are associated with increased plasma concentrations of markers of fibrinolysis, which are inversely correlated with AT III activity. However, the correction of the deficient AT III activity does not affect the plasma concentration of either D-DI or F1 + 2, thence not supporting the hypothesis that enhanced fibrinolysis in advanced liver disease is the result of low-grade disseminated intravascular coagulation.
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PMID:Deficient antithrombin III activity and enhanced fibrinolysis in patients with liver disease: evidence against a cause-effect relationship. 757 84

When no specific factor concentrate is available fresh-frozen plasma (FFP) is indicated in the treatment of clinically relevant hemorrhagic diathesis. These disorders include congenital factor V and XI deficiencies, multiple factor defects, as disseminated intravascular coagulation and severe liver disease, and patients receiving massive transfusions, when bleeding occurs and severe abnormalities on coagulation testing are evident. FFP is beneficial when used with plasma exchange in thrombotic thrombocytopenic purpura and related disorders. Various virucidal treatments including solvent-detergent (SD), photoactivated dyes (methylene blue) or pasteurization have been evolved to improve virus safety of human plasma. More extensive studies to demonstrate efficient virus inactivation in plasma have been performed with SD compared to other methods. On the other hand, the use of single-donor FFP in methylene blue treatment is possibly superior to pooled plasma which is processed according to the SD procedure. Pasteurization enables the inactivation not only of lipid-enveloped but also of non-lipid-enveloped viruses. Virucidal treatment of plasma may cause alterations in clotting factors, fibrinolysis and protease inhibitors; however, the currently achieved recovery of procoagulant activities is approximately comparable with that found in untreated FFP. The toxicity of virucidal additives is reported to be negligible since manufacturing includes a removal procedure (SD) or comparably low amounts (methylene blue) are used in inactivation treatment.
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PMID:[Indications for fresh frozen plasma: evaluation of virus inactivating preparations]. 769 68

We studied the prevalence, clinical spectrum and epidemiologic features of thrombocytopenia among 442 (333 male, 109 female) HIV infected patients. Thrombocytopenia was defined as a platelet count < 100,000/mmc and severe if platelet count was < or = 30,000/mmc. Intravenous drug abusers were 83% (369/442). At the first clinical evaluation according to Walter-Reed (WR) classification, 90% (396/442) of patients were in stage 1-5 and 10% (45/442) in stage 6. Severe thrombocytopenia (platelet count < or = 30,000/mmc) was present in 24% (11/45) of the entire thrombocytopenic population. Forty percent (18/45) of the thrombocytopenic patients were positive to: HBV (6), HCV (7), HBV+HCV (5). Mild bleeding was present in 16% (7/45) of the patients but one case, with severe thrombocytopenia, died of intracranial hemorrhage. Major hemorrhagic sequelae with even fatal events are possible, especially when a low platelet count is associated with other hemostatic abnormalities (e.g. haemophilia, liver disease, disseminated intravascular coagulation). Zidovudine therapy (range 500-1250 mg/day) is effective in normalizing the platelet count (platelets > 100,000/mmc) only in 29% (9/31) of the patients.
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PMID:Thrombocytopenia in HIV infected patients. Prevalence and clinical spectrum. 775 81


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