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

Disseminated intravascular coagulation (DIC) was induced in 84 rabbits by intravenous infusion of 20 micrograms/kg/h of endotoxin during 6 hours. The following treatments were administered simultaneously with endotoxin: heparin, 5, 10 and 20 UI/kg/h, antithrombin III (AT III), 10, 20 and 40 U/kg/h or as a 240 U/kg bolus dose, and heparin (10 UI/kg/h) plus AT III (20 U/kg/h). Blood samples were taken before endotoxin and 2 and 6 hours after endotoxin to perform screening coagulation assays, factors V, VIII and XII, AT III, fibrin monomers and fibrinogen degradation products. All treatments were able to modify some of the parameters related to DIC, but only AT III bolus dose and heparin plus AT III significantly reduced fibrin deposition in kidneys (p less than 0.05). All the therapeutic schedules significantly diminished the mortality rate. We conclude that AT III bolus dose and heparin plus AT III are useful in the treatment of endotoxin-induced intravascular coagulation in rabbits.
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PMID:[Effect of heparin and/or antithrombin III in a model of disseminated intravascular coagulation induced by endotoxin in rabbits]. 158 38

Spontaneous ICH is an unusual and potentially disastrous event that may complicate primary and secondary hemostatic abnormalities. Among the primary abnormalities, deficiencies of coagulation factors I, VII, VIII, IX and XIII as well as von Willebrand factor have been clearly associated with ICH. Specific factor replacement or supportive management to normalize the hemostatic defect is indicated in each case. Among secondary alterations in hemostasis, thrombocytopenia, platelet function abnormalities, or factor consumption contribute to the risk of ICH in patients with ITP, TTP, disseminated intravascular coagulation, myeloproliferative or myelodysplastic disorders, and exposure to certain medications. The precise incidence of spontaneous hemorrhage among these disorders is unknown but low. Platelet transfusion and fibrinogen replacement are appropriate in specific cases; however, treatment of the underlying cause is usually required. The association of hemorrhage with antithrombotic agents in several settings is better defined. Cessation of the medication is required in each instance. Fibrinogen replacement may be required after the use of fibrinolytic agents. In all cases, an assessment of the precise hemostatic defect is recommended.
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PMID:Hematologic causes of intracerebral hemorrhage and their treatment. 163 86

High-dose interleukin-2 (IL-2) immunotherapy can cause hypotension, respiratory distress, interstitial edema, and thrombocytopenia, similar to endotoxic shock. We have observed that IL-2 has no direct effect on coagulation factors in vitro, but it has been observed to alter the coagulant properties of vascular endothelium. Accordingly, we investigated the possibility that IL-2 infusions initiate plasma fibrinolysis and disseminated intravascular coagulation (DIC). We studied the clinical course, platelet count, and coagulation profile in response to IL-2 infusion in seven patients, two with metastatic melanoma and five with metastatic renal cell carcinoma. Every patient experienced hemodynamic instability and thrombocytopenia, and one patient suffered an unusual complication, mesenteric thrombosis. No patient had appreciable changes in the prothrombin time or the partial thromboplastin time, nor did factors V or VIII decline in the two patients observed. In four patients examined, we found decreased titers of Hageman factor (factor XII), high molecular weight kininogen, prekallikrein, and plasma thromboplastin antecedent, as if these had been consumed by reactions of the intrinsic pathway of thrombin formation. Circulating D-dimer fragments were found in the plasma of every patient at some point during each infusion cycle, and we observed decreased titers of plasminogen in the four patients just mentioned, suggesting that IL-2 infusions initiated fibrinolysis. Taken together, the clotting factor derangements and related toxicity phenomena cannot be ascribed firmly to DIC. Activation of the intrinsic (contact) system of coagulation, however, may provide one link between the vascular endothelial surface alterations caused by IL-2 infusions and the development of the systemic toxicity that resembles septic shock.
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PMID:Fibrinolysis, thrombocytopenia, and coagulation abnormalities complicating high-dose interleukin-2 immunotherapy. 198 12

Most infants with hemophilia have no bleeding in the neonatal period even if birth trauma occurs. The explanation for this lack of bleeding in the first few days of life in most hemophiliacs is unknown. Maternal factors VIII and IX fail to cross the placenta and cannot, therefore, protect the neonate. There have, however, been an increasing number of reports of severe neonatal bleeding in hemophiliac neonates. Herein, a case of severe neonatal bleeding responsible for hypovolemic shock and disseminated intravascular coagulation masking the hemophilia and delaying its diagnosis is reported. Transfusion of twice the total globular mass and exchange-transfusion were required. Hemorrhagic gastric necrosis occurred, requiring subtotal gastrectomy. The diagnosis of severe hemophilia A (factor VIII = 1%) was established only at 17 days of age. At the age of five months, the child developed a dumping syndrome which improved under appropriate dietary therapy and finally resolved. Outcome was favorable and at the evaluation at two years of age the child was leading a normal life. This case underlines the difficulty of the diagnosis of hemophilia at birth. When there is no family history of bleeding, the diagnosis of hemophilia is usually missed in the neonatal period and established only later or retrospectively. Factors VIII and IX should consequently be measured in male neonates with unusual bleeding and an increased activated partial thromboplastin time, even if disseminated intravascular coagulation is present. Prompt diagnosis and initiation of specific therapy may lessen acute morbidity and prevent long-term sequelae in affected infants.
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PMID:[Disseminated intravascular coagulation masking neonatal hemophilia]. 203 86

Rabbits were given polyclonal anti-tissue factor (TF) immunoglobulin G (IgG) before an injection of endotoxin to test the hypothesis that TF triggers disseminated intravascular coagulation (DIC) after endotoxin. The rabbits had been prepared with cortisone to develop DIC after one injection of endotoxin. Anti-TF IgG substantially reduced the falls in fibrinogen, factors V and VIII, and platelets noted in control rabbits given preimmune IgG before endotoxin. At autopsy 24 hours later, fibrin was present in glomerular capillaries of 4 of 5 control rabbits, but in none of 11 rabbits given anti-TF IgG. DIC was also induced in a second group of rabbits by the infusion, over 4 hours, of 1 microgram/kg of purified, reconstituted rabbit brain TF. This resulted in striking falls in plasma fibrinogen, factors V, and VIII that were diminished, but not prevented by prior treatment with anti-TF IgG. Circulating activated factor VII, induced by either TF infusion or endotoxin, could not be detected after DIC. Mean plasma extrinsic pathway inhibitor (EPI) activity did not fall significantly after endotoxin, and only to about 65% of the preinfusion after infusion of TF. Thus, DIC induced by both agents proceeded despite nearly normal plasma EPI levels. Because EPI neutralizes factor VIIa/TF in vitro only after a short lag period, the DIC that persisted for up to 6 hours after injection of endotoxin suggests that TF activity continued to be generated during this period on cells to which the circulating blood was exposed. All animals given endotoxin became ill with cyanosis, tachypnea, cold ears, and diarrhea, regardless of whether they had received anti-TF IgG to attenuate DIC. Infusion of TF caused some animals to die acutely with pulmonary arterial thromboses, but surviving animals did not appear ill. The findings support the hypothesis that exposure of blood to TF triggers DIC after endotoxin, but is not important for the pathogenesis of endotoxin-induced shock.
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PMID:Disseminated intravascular coagulation in rabbits induced by administration of endotoxin or tissue factor: effect of anti-tissue factor antibodies and measurement of plasma extrinsic pathway inhibitor activity. 231 59

Effects of non-lethal Sarcocystis miescheriana infections on the blood coagulation system were investigated. Nine pigs were inoculated orally with 2 X 10(5) sporocysts (Group A) and nine pigs (Group B) served as non-infected controls. Blood samples were taken from the vena jugularis externa every 2 or 3 days until 19 days post-infection (dpi). The following parameters were investigated: partial thromboplastin time (PTT), prothrombin time (PT), thrombin time (TT), thrombin coagulase time (TCT), fibrinogen (FIB), factor (F) VIII, F XI, F XII, antithrombin III (AT III), alpha 2 macroglobulin (alpha 2 MG), alpha 2 antiplasmin (alpha 2 AP), pre-kallikrein (PK), and the number of circulating thrombocytes. All infected pigs suffered from acute sarcocystiosis between 12 and 19 dpi. Clinical illness was most severe from 14 to 17 dpi. At this time, PTT and FIB increased, and TT and TCT decreased slightly. The activities of the clotting factors increased at 17 and 19 dpi. However, only F VIII activity was significantly higher in the infected pigs than in the controls at 17 and 19 dpi. PK was significantly lower in the infected pigs at 12, 14, and 17 dpi. Thrombocyte counts were reduced with the onset of the acute phase of illness and some pigs had marked thrombocytopenia. These results indicate low-grade disseminated intravascular coagulation (DIC) in the course of mild S. miescheriana infections in pigs.
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PMID:Hemostatic alterations in pigs fed sublethal doses of Sarcocystis miescheriana. 251 58

The pathophysiology of bleeding manifestations in hemorrhagic fever with renal syndrome (HFRS) was elucidated by serially evaluating coagulation and fibrinolytic profiles and complement alterations in patients with HFRS. In the early stage of the disease, platelet counts, platelet survival time, and platelet aggregation in vitro decreased. Prolongation of bleeding time, prothrombin time, and activated partial thromboplastin time was noted, with decreases in coagulation factors II, V, VIII, IX, and X. Levels of fibrinogen were decreased, and those of fibrinogen-fibrin degradation products in serum and urine were increased. Concentrations of plasminogen, alpha 2-plasmin inhibitor, and antithrombin III in plasma were depressed. Procoagulant activity was present in plasma. Circulating immune complexes were found, whereas serum levels of C3 were decreased. In the early stage of HFRS, thrombocytopenia, defects in platelet function, and disseminated intravascular coagulation may play central roles in the pathogenesis of bleeding manifestations. Vasculopathy and immunologic aberrations also may play a role.
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PMID:Coagulopathy in hemorrhagic fever with renal syndrome (Korean hemorrhagic fever). 256 77

Assessment of animals with a suspected hemorrhagic diathesis of unknown cause(s) should be methodical. Most acquired coagulopathies result from thrombocytopenia. A platelet estimate (from a blood smear) and/or a platelet count on a fresh blood sample therefore are useful first steps in case evaluation. If thrombocytopenia is present, the most likely causes are immune-mediated destruction of platelets, DIC, or megakaryocytic hypoplasia. These diagnoses can be pursued by further test, including antiplatelet antibody assays (for example, the platelet factor 3 tests or an ELISA test), measurement of FDP, and bone marrow biopsy, respectively. If the platelet count is normal, a buccal mucosa bleeding time test is a useful second step. If this is prolonged, most likely causes are vWD or a thrombocytopathy (functional platelet defect). von Willebrand's disease can be diagnosed by measurement of vWf concentration or activity. A normal bleeding time does not exclude a diagnosis of vWD, but suggests that the functional activity of vWf is not compromised markedly. If the bleeding time is normal, APTT and PT should be measured. A prolonged APTT with normal PT, in the clinical setting, implies a deficiency of factor XI, IX, or VIII. A prolonged PT with normal APTT indicates factor VII deficiency. Prolongation of both APTT and PT usually is caused by a deficiency of several factors and is seen most often in cases with vitamin K deficiency or antagonism. Obviously, if a particular cause is suspected from the case history or for other reasons, appropriate tests should be evaluated at the beginning. If these do not confirm the provisional diagnosis, the just-described protocol might be a useful one to follow.
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PMID:Laboratory evaluation of hemorrhagic coagulopathies in small animal practice. 267 37

Coagulation abnormalities with and without haemorrhagic manifestations have been frequently reported in newborn-infants affected by hypoxia. Particularly in postmature-infants and in those ones with acute asphyxia at birth, respiratory distress syndrome (RDS), intra-uterine growth retardation (IUGR) and cyanotic congenital heart disease (CCHD). A reduction of synthesis or a consumption of blood coagulation factors are the main causes of these abnormalities. The anomalies of platelet number and of their function, of haemostasis global tests, of coagulation factors and physiologic inhibitors levels, of fibrinogenesis and fibrinolysis are examined, including authors' studies and a review of literature too. The authors think platelet count, PT, PTT, fibrinogen, factor V and VIII, and PDF determinations are necessary laboratory investigations for newborn-infants with RDS or acute asphyxia for about the first week of life, because of the risk of consumption coagulopathy. In the other hypoxic newborns (IUGR, CCHD, postmature infants) platelets count, PT, PTT and serum PDF determinations could be enough in order to value any coagulation abnormalities presence.
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PMID:[Neonatal hypoxia and hemocoagulative changes]. 269 28

The course of haemostasis defects was investigated in dimethylnitrosamine (DMNA) acute liver necrosis. Before 18 hr there was no evidence of disseminated intravascular coagulation (DIC) nor of abnormal fibrinolysis. At 12 hr the level of the vitamin-K-dependent factors (factors II, VII, IX and X) was reduced to 25-63% of control. Factors V and VIII:C levels decreased to about 10 and 20% by 12 hr. Factor V was the only molecule which decreased significantly by 6 hr. The rapid decrease of these proteins might be related to an early parenchymal functional impairment attested by early structural lesions observed in the endoplasmic reticulum and nucleus. The isolated decrease of factor V in the absence of any significant change in serum transaminase (SGOT and SGPT) levels is proposed, at least in the rat, as an early criterion of hepatic failure.
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PMID:Experimental DMNA induced hepatic necrosis: early course of haemostatic disorders in the rat. 286 Oct 9


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