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

Eleven patients who developed thromboembolic complications while receiving heparin were studied for a possible adverse reaction to heparin as the cause of their progressive thrombosis. Fifteen additional patients who were receiving heparin for recurrent thromboembolism, but who did not develop signs of thrombotic complications, were studied as patient controls. The most significant finding was an abnormal in vitro aggregation response to heparin alone in all of the patients who developed complications who were tested for it (64 percent). None of the patient controls demonstrated this abnormality. In addition, thrombocytopenia was noted in all of the former but in only one of the latter. Results of prothrombin times, fibrinogens and fibrin split products eliminated disseminated intravascular coagulation as the cause of the thrombocytopenia in the majority of cases. Finally, an approach to the early detection of the abnormal heparin response is presented and guidelines for its therapeutic management are recommended.
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PMID:Heparin induced platelet aggregation: in vitro confirmation of thrombotic complications associated with heparin therapy. 51 11

A coagulation screen consisting of measurement of the prothrombin time, thrombin time, kaolin caphalin clotting time, platelet count, plasma fibrinogen level, fibrin degradation products and ethanol gelation test was performed on 24 patients with impairment of consciousness due to acute diabetic metabolic decompensation at the start of treatment and 24 hours later. 22 out of 24 patients showed at least one coagulation abnormality on admission of which the commonest were a prolonged prothrombin time, shortened kaolin cephalin clotting.time and raised plasma fibrinogen level. After 24 hours of treatment these values were more normal but 20 out of 22 patients still displayed some abnormality. 15 patients had two or more coagulation abnormalities on admission including 3 patients with haematological abnormalities suggestive of disseminated intravascular coagulation. This group was older and had higher blood ureas than those with fewer abnormalities, but plasma glucose, sodium, potassium and bicarbonate levels were similar in both groups of patients. All 5 patients with hyperosmolar non-ketotic coma and all 3 patients who died without recovering consciousness had two or more coagulation abnormalities on admission.
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PMID:Coagulation abnormalities in diabetic coma before and 24 hours after treatment. 53 72

An outbreak of chronic liver disease was investigated in a kennel of dogs. Anorexia, depression, polyuria, polydipsia, icterus and a terminal hemorrhagic diathesis were noted in clinically affected dogs. Thrombocytopenia, hypofibrinogenemia, elevated fibrinogen degradation products and prolonged activated partial thrombosplastin times (PTT) and one-stage prothrombin times (PT) were associated with the hemorrhagic crisis. Aflatoxicosis was confirmed by the presence of significant levels of aflatoxicosis was confirmed by the presence of significant levels of aflatoxin B in the commercial dog food being fed. A subacute hepatitis was found on necropsy. Disseminated intravascular coagulation was suspected as the cause of the hemorrhage in these cases and treatment was instituted.
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PMID:Disseminated intravascular coagulation complicating aflatoxicosis in dogs. 55 87

The exposure of rats to 100% oxygen at 1 atmosphere leads to a prolongation of prothrombin times and activated partial thromboplastin times. This development is associated with a consumption of factor XII, VIII, and VII activities and with the appearance of fibrin monomers and fibrinogen degradation products. Lead acetate enhances all oxygen-induced changes of the coagulation systems drastically. The O2 survival time of chicks which are naturally deficient in factor XII is greatly increased over that of rats and is not affected by lead acetate. Oxygen survival times of rats suffering from chronic respiratory disease (CRD) are also significantly increased when compared with normal rats. It appears that consumptive coagulopathy and disseminated intravascular coagulation are early events in oxygen exposure, and that their development is accelerated by lead ions.
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PMID:Oxygen-induced consumptive coagulopathy and its enhancement by lead acetate. 57 13

Coagulation and fibrinolysis were studied in a colony of aged Syrian hamsters with spontaneous atrial thrombosis, and the results are consistent with concomitant consumption coagulopathy. In comparison to age- and sex-matched hamsters from the same colony, those with atrial thrombi had significantly prolonged prothrombin and partial thromboplastin times, reduced levels of factors II, VII, VIII and X activities and plasminogen; and concentrations of fibrinogen-fibrin split products in excess of 80 microgram/ml. Hematocrits of the thrombosed animals were significantly decreased, total plasma proteins were increased, leukocyte counts were within normal limits, and platelet counts were about half those of the controls. Thrombosed hamsters had significantly reduced plasma albumin content, increased alpha1-, beta-, and gamma-globulins, and reduced A/G ratios. Aged sick hamsters demonstrable thrombi also had reduced coagulation and fibrinolytic activities and platelet counts, but their fibrinogen levels were markedly elevated, and fibrinogen-fibrin split products were either absent or present in trace amounts. This suggests an earlier and/or less acute form of the thrombotic process.
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PMID:Spontaneous atrial thrombosis in aged Syrian hamsters. II. Hemostasis. 57 88

The medical records of 118 cases who met laboratory criteria of DIC were studied. The most frequent etiologies were: Generalized infection (39.8%), trauma (16.9%), malignancy (6.8%) and surgical cases (6.8%). The main clinical manifestations which appeared to be related solely to DIC were (in a decreasing order of frequency): Bleeding (64.4%), renal dysfunction (24.6%), liver dysfunction (18.6%), respiratory dysfunction (16.1%), shock (14.4%), thromboembolic phenonmena (6.8%) and central nervous system involvement (1.7%). In 26 patients none of these manifestations were observed. In patients with infection, liver and renal dysfunction were frequent and respiratory dysfunction rare, whereas in trauma cases, liver and renal dysfunctions were rare and respiratory dysfunction frequent. This variability indicates that the clinical manifestations are affected not only by the process of intravascular coagulation but also by the underlying clinical disorders. The most impaired coagulation tests were prothrombin time, partial thromboplastin time, platelet count and thrombin time. The degree of abnormality of these coagulation tests was found to be related to the extensiveness of organ involvement. The mortality (overall 54.7%) increased independently with age, with the number of clinical manifestations and with the degree of abnormality of the above-mentioned four most impaired coagulation tests. In addition, older patients were more likely to have an increased number of clinical manifestations and more impaired coagulation tests. Mortality was similar in the various etiologies except for trauma patients in whom it was lower (30%).
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PMID:Clinical and laboratory aspects of disseminated intravascular coagulation (DIC): a study of 118 cases. 58 Apr 88

Autoprothrombin II-A anticoagulant was isolated from bovine prothrombin. Purified prothrombin was applied to DEAE-cellulose chromatography after incubation with thrombin. Four protein peaks were obtained where the third peak corresponded to the anti-coagulant effect. The fractions under the third peak were pooled together and the anticoagulant effect was evaluated with different methods. From 25,470 +/- 2,800 U of prothrombin, 5,800 +/- 1,400 U of inhibitor were obtained. The inhibitor was found to be most effective at pH 7.2--7.8. In vitro, the inhibitor inhibited the thrombin time and the plasma clotting time highly significantly but had no effect on euglobulin lysis time and fibrin plates. In vivo, when injected into rabbits, the inhibitor effect was also significant on the same tests. The autoprothombin II-A anticoagulant had a protective effect on DIC formation with rabbit brain thromboplastin administration. This protective effect was found to be statistically significant.
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PMID:Some properties of autoprothrombin II-A anticoagulant. 61 78

Thrombogenicity of the factor IX concentrate and its clinical use for stoppage of the bleeding in the case of hemophilia A with inhibitor were reported. (1) Factor IX concentrate contained the coagulation factors as prothrombin complex (factors II, VII, IX and X); Thrombin and factor Xa. (2) Prothrombin in the factor IX concentrate could be converted to thrombin without any additional procoagulant such as thromboplastin or factor V, but in just 2.5M glycine solution by the effect of factor Xa. (3) The infusion of factor IX concentrate into a rabbit induced DIC promptly which was proved by autopsy and coagulation-fibrinolytic studies. (4) Factor IX concentrate showed a great efficacy in stopping the bleeding in the case of hemophilia A with inhibitor.
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PMID:Characteristics and thrombogenicity of factor IX concentrate. 61 88

Coagulopathy, or non-mechanical hemorrhage, complicated the operative course of 17 of 33 (51.5%) patients suffering severe liver trauma. The highest incidence of non-mechanical hemorrhage (66.7%) occurred in patients undergoing anatomic lobectomy. Serial hemostatic parameters were assessed and thrombocytopenia was the most striking abnormality in patients with non-mechanical hemorrhage. The degree of thrombocytopenia was directly correlated with the number of blood transfusions administered. The mean operative blood transfusion requirement was significantly greater in patients with non-mechanical hemorrhage, 25.1 +/- 2.87 (S.E.M.) units, than in those without, 12.2 +/- 1.83 units (p < 0.001). The bulk of this transfusion was given before the onset of clinically overt coagulopathy. Massive transfusion of stored blood was felt to be the most important factor in causing non-mechanical hemorrhage. Convincing evidence for disseminated intravascular coagulation was lacking, and abnormal fibrinolysis was infrequent and mild when observed. Although uneventful in most, in six patients non-mechanical hemorrhage resulted in excessive blood transfusion, unnecessary operation or death. Infusions of platelet concentrate, fresh frozen plasma, and fresh blood were used to successfully treat most cases of non-mechanical hemorrhage. In all cases, these components were not started until non-mechanical hemorrhage was clinically apparent. The value of prophylactic use of blood components is stressed. Because of troublesome side effects associated with the use of prothrombin complex concentrates, these agents are contraindicated in patients with severe liver injury. After receiving concentrates, one patient developed severe hypotension leading to ventricular fibrillation, two developed transient thrombocytopenia and two others demonstrated multiple pulmonary microthrombi at autopsy, a finding not observed in autopsied patients not receiving the concentrates.
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PMID:Non-mechanical hemorrhage in severe liver injury. 64 75

Coagulation studies conducted on 42 patients with acute peritonitis of varying etiology revealed statistically significant prolongation of kaolin cephalin clotting time, decrease of platelets and elevation of plasma fibrinogen and serum fibrinogen degradation products. The relationship of the coagulopathy to bacterial invasion of peritoneal cavity was indicated by the absence of significant change in KCCT, prothrombin time, and bleeding time in patients with sterile peritoneal fluid. The results suggest a process of insidious defibrination intricately superimposed on the hypercoagulable state in these patients.
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PMID:Blood coagulation profile in patients with acute diffuse peritonitis. 71 10


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