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

Infusion of autologous hemolyzed blood in humans has served as a model for various experimental investigations for many years. Numerous studies have shown this model to be unattended by any adverse clinical reactions. In this study evidence of subclinical disseminated intravascular coagulation (DIC) was sought in normal humans infused with autologous hemolyzed blood. Hemoglobinemia was induced in 10 experiments by a single injection of frozen-thawed blood and in 4 experiments by such an injection of hemolysate followed by a 5-h maintenance infusion. Mean peak plasma hemoglobin following single dose injections was 540 mg/100 ml, while levels during continuous infusion averaged 240 mg/100 ml. The induction of hemoglobinemia was asymptomatic. Coagulation studies showed no significant alteration in prothrombin time, partial thromboplastin time, thrombin time, clottable fibrinogen, or WBC. Fibrin degradation products were not found. Platelet counts fell slightly in the 5-min postinfusion sample but returned to preinfusion levels within 30 min, suggesting a temporary sequestration of platelets rather than consumption. The induction of moderate brief experimental hemoglobinemia in normal subjects did not result in the development of demonstrable DIC.
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PMID:Coagulation studies during experimental hemoglobinemia in humans. 112 Jul 40

Blood coagulation screening profiles were performed in 512 patients who underwent open-heart surgery with extracorporeal circulation. Severe coagulation disorders were found in 29 (5.6 per cent) patients. The most common abnormalities were low one-stage prothrombin time (PT) activities and impaired whole blood clot retractions. In the majority of patients the discrepancy between low PT's and normal or only slightly depressed factor II, V, VII, and X activities was explained by the presence of an inhibitor of the extrinsic system. Eight patients demonstrated the heparin rebound phenomenon but only 1 bled excessively. The pattern of severe hepatic dysfunction was found in 4 and severe depression of vitamin K-dependent factors due to oral anticoagulants in 2. Two had disseminated intravascular coagulation. Seventeen patients with normal coagulation screening profiles bled excessively postoperatively. Of these, 2 had moderate thrombocytopenia associated with a marked platelet functional abnormality. Revision of the wound in 13 revealed a surgical hemostatic defect and in 2 the cause of bleeding could not be determined.
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PMID:The hemostatic mechanism after open-heart surgery. I. Studies on plasma coagulation factors and fibrinolysis in 512 patients after extracorporeal circulation. 115 4

The effect of rapid decompression on the stress-accelerated blood coagulation system of male and fingerling coho salmon (Oncorhynchus kisutch) was examined after simulated 100- and 200-fsw dives. Blood samples taken either through a dorsal aorta cannula or from a severed caudal peduncle were analyzed for total plasma protein and fibrinogen concentrations, prothrombin times (PT), and partial thromboplastin times (PTT). The effect of mild decompression (100-fsw) on the hemostatic mechanism of both adult and fingerling coho salmon indicated an alternating fibrinogen concentration, declining from normal levels 1 min after decompression, followed by an increase 10 to 15 min later with an eventual loss of fibrinogen to one half the original level an hour after decompression. Partial thromboplastin times were found to increase 10 to 15 min after decompression occurred. Prothrombin times showed an increase 1 hour after decompression in adult salmon, whereas in fingerlings, prothrombin times increased almost immediately from normal levels. The effect of severe decompression (200-fsw) showed similar trends, but at an accelerated rate. It was concluded that both mild and severe decompression activates the hemostatic mechanism of fish which may eventually result in consumption coagulopathy at a greater rate than reported for experimental mammals.
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PMID:Changes in hemostatic parameters in fish following rapid decompression. 122 84

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin-fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.
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PMID:Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation. 124 23

Disseminated intravascular coagulation (DIC) is a syndrome caused by the systemic generation of thrombin. Most cases are due to pathological activation of the intrinsic coagulation systems (e.g. in sepsis), and/or the extrinsic system (e.g. in malignancy and head trauma). Diagnosis is made by finding abnormalities in at least 3 of 4 laboratory values, namely prothrombin time, platelet count, fibrinogen and fibrinogen/fibrin degradation products. The most common clinical manifestation of DIC is bleeding, with thrombosis in less than 10% of acute cases but more frequently encountered in chronic DIC associated with malignancy. Acute DIC must first be treated by specific therapy of the underlying disease and general support measures. If serial clinical and laboratory monitoring improves, no further treatment is required. If severe or life-threatening haemorrhage occurs or a thrombotic event ensues, heparin anticoagulation followed by aggressive replacement with platelets, fresh plasma and possibly cryoprecipitate is indicated. Heparin doses should be 'therapeutic' (i.e. adequate to overcome the coagulant forces that may have produced a relative heparin-resistant state in the blood). Chronic DIC with haemorrhage, or more usually thrombosis, should also be treated with heparin; warfarin is ineffective. If DIC persists because, for example, a tumour does not regress, long term outpatient subcutaneous heparin therapy may be required.
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PMID:Disseminated intravascular coagulation. Approach to treatment. 128 66

Changes in the plasma thrombomodulin (TM) level were examined in endotoxin-infused rabbits. The plasma TM level in normal rabbits was 143.8 +/- 8.4 ng/ml (n = 67) and the molecular weight of the major TM was about 55 kd. Endotoxin (lipopolysaccharide, LPS, E. Coli B8:0127) was intravenously infused. LPS infusion increased the plasma TM level dose-dependently between 0.2 mg/kg and 5 mg/kg. When 5 mg/kg LPS was infused, the plasma TM level started to increase immediately and was 2.3 times higher than the control value within 1 hr. The molecular weight of the major TM was about 75 kd. This rapid increase in TM occurred before the decrease in fibrinogen content and the prolongation of prothrombin time. To examine the effect of circulating leukocytes on the TM increase in endotoxin-infused rabbits, 5 mg/kg LPS was infused into rabbits with leukocytopenia induced by X-ray irradiation. The maximum plasma level of TM was significantly lower than in the untreated rabbits given LPS. These data suggest that the increase in plasma TM is caused by LPS-stimulated leukocyte's prior to hemostaseological changes. It is well known that endothelial cells can be injured by stimulated leukocytes, so this increase in plasma TM probably reflects the deterioration of endothelial cells. This deterioration decreases the ability of endothelial cells to inhibit thrombosis, which would, in turn, contribute to the development of disseminated intravascular coagulation in endotoxin-infused rabbits.
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PMID:Changes in thrombomodulin level in plasma of endotoxin-infused rabbits. 131 90

Preoperative hemostatic data were obtained on 42 brain tumor patients and correlated with the subsequent occurrence of venous thrombosis detected with 125I-labeled fibrinogen leg scans. The occurrence of thrombosis correlated significantly with an increased prothrombin time, plasminogen, and total fibrinolytic activity and a decreased fibrinogen level. This overall trend in the group of patients with postoperative thrombosis indicates that the hemostatic disorder noted in brain tumor patients is most closely related to a subclinical form of chronic disseminated intravascular coagulation syndrome. Differences in hemostatic parameters seen with the various types of brain tumors suggest that biological factors specific to each tumor are likely responsible for the described hemostatic disorder and support the need for further research directed at the tumor tissue level.
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PMID:Postoperative venous thromboembolism and brain tumors: Part II. Hemostatic profile. 133 49

Hemostasis is intimately related to liver function, because most coagulation factors are synthesized by liver parenchymal cells and the liver's reticuloendothelial system serves an important role in the clearance of activation products. The extent of coagulation abnormalities depends upon the degree of disturbed liver function. Acute or chronic hepatocellular diseases may display decreases in the vitamin K-dependent factors (prothrombin; factors VII, IX, and X; proteins C and S), whereas other parameters remain normal. Patients with hepatic failure may present with the entire spectrum of factor deficiencies and may even develop disseminated intravascular coagulation (DIC). Patients with liver cirrhosis have a wide spectrum of abnormalities. Except for factor VIII:C and von Willebrand factor, all procoagulant and inhibitory factors are decreased, which is a reflection of impaired protein synthesis. Abnormal fibrinogen and prothrombin molecules can be identified. Platelets are quantitatively and qualitatively altered, and most patients develop DIC. Vitamin K deficiency leads to the production of abnormal vitamin K-dependent factors. The factors lack gamma-carboxy glutamic acid residues in the NH2-terminal part of their molecules. Surgery associated with the liver leads to major hemostasis alterations. The LeVeen shunt is invariably related to DIC. Bleeding with partial liver resection is mostly mechanically induced, but chronic DIC may be present. Orthotoptic liver transplantation is associated with severe hemorrhages. These are partly due to the pre-existing hemostasis defects and partly due to DIC with a marked fibrinolytic response. This is especially noted during the anhepatic phase and when the donor liver is perfused by the recipient's blood. Postoperative recovery is quick, provided the graft is not rejected. Postoperatively, there may be an initial hypercoagulable state, which could be related to the thrombosis occasionally encountered.
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PMID:Coagulation abnormalities in liver disease. 133 67

Plasma levels of prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin III complex (TAT) are thought to be specific indicators of thrombin generation. To assess whether these two parameters behave similarly in vivo, we compared the plasma levels of F1 + 2 with TAT in 41 patients with disseminated intravascular coagulation (DIC). Both F1 + 2 and TAT were markedly elevated in patients with DIC compared to healthy subjects. Although a positive correlation was found between F1 + 2 and TAT (r = 0.585, P < 0.001) there was a large scatter among individuals. In addition, plasma concentrations of TAT were much lower than F1 + 2. The correlation between the TAT/F1 + 2 ratio and antithrombin III was weak (r = -0.268, P = 0.09). The TAT/F1 + 2 ratio was positively correlated with TAT (r = 0.481, P = 0.002), indicating that the difference in molar concentrations between F1 + 2 and TAT decreased as the TAT value increased. Serial determinations of these parameters showed that plasma TAT values changed roughly in parallel with F1 + 2 in the majority of patients. Although further studies are required to further clarify the observed differences between F1 + 2 and TAT, both parameters would be equally useful for the precise detection of haemostatic activation in patients with DIC.
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PMID:Comparison of prothrombin fragment 1 + 2 with thrombin-antithrombin III complex in plasma of patients with disseminated intravascular coagulation. 133 86

Seven rabbits experimentally infected with rabbit haemorrhagic disease virus were examined haematologically and histologically. Haematologically, activated partial thromboplastin time and prothrombin time were markedly prolonged in the terminal phase of the disease, just prior to death (all the animals died between 27 and 40 hr after inoculation with rabbit haemorrhagic disease virus). There was an increase in the titre of fibrin degradation products and a decrease in antithrombin III activity during the same interval. Acute necrotic hepatitis and disseminated intravascular coagulation (DIC) in many organs, including the lung, kidney, spleen and heart were the characteristic histopathological changes. Thus, the haematological and histological changes suggested that DIC was induced by rabbit haemorrhagic disease virus infection. Severe liver necrosis was considered to be a factor causing DIC by inducing a hypercoagulable condition in the systemic blood circulation.
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PMID:Disseminated intravascular coagulation (DIC) in rabbit haemorrhagic disease. 133 94


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