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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 studies showed there was a pronounced thrombocytopenia and hypofibrinogenemia in Holstein calves infected with Trypanosoma congolense TREU 112. There was also ineffective thrombopoiesis characterized by an increased megakaryocytic mass, reduced uptake of 35S-methionine into peripheral blood platelets and a normal platelet lifespan. There was an increased uptake of isotopic label into fibrinogen and a shortened half life indicating a consumptive error with increased peripheral use of fibrinogen. No consistent abnormalities were found in ethanol gelation, partial thromboplastin time, clot retraction and lysis or plasminogen assay. Fibrin split products were rarely detected. These findings suggest that in the chronic form of bovine trypanosomiasis there is a partially compensated consumption coagulopathy.
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PMID:The pathogenesis of Trypanosoma congolense infection in calves. IV. The kinetics of blood coagulation. 44 53

Seven patients, aged 12 to 19 years, had atypical measles. Prodromal symptoms of fever, malaise, myalgia, headache, nausea, and vomiting were commonly followed by coryza, sore throat, conjunctivitis, photophobia, nonproductive cough, and pleuritic pain. The characteristic rash was erythematous, maculopapular, and progressed frequently to vesicular, petechial, or purpuric lesions. It initially involved palms and soles with subsequent spread to proximal extremities and the trunk, sparing the face. Six of six chest roentgenograms showed infiltrates. Findings not previously described in atypical measles included liver enzyme elevations, thrombocytopenia, disseminated intravascular coagulation, possible transmission among three siblings, and suspected cardiac involvement. Measles complement fixation titers compatible with recent infection were seen in all patients. All patients had previously received killed measles vaccine. A substantial number of persons who are older adolescents or young adults may be at risk of developing atypical measles.
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PMID:Atypical measles in adolescents and young adults. 44 83

Twenty-seven patients requiring massive transfusions were studied prospectively to determine whether administration of stored, modified whole blood induced a primary disorder of hemostasis evidenced by generalized microvascular oozing. Platelet counts fell in proportion to the number of units of blood transfused. In contrast, the levels of factors V and VIII correlated poorly with the units of blood transfused, 85% of the total variation in the levels being due to influences other than transfused blood. Levels of all other clotting factors were unrelated to the number of units of blood given. Eight patients developed abnormal bleeding. The cause appeared to be dilutional thrombocytopenia in five patients, and DIC in three. In six of the eight, bleeding was controlled with platelet concentrates alone. Two patients were given cryoprecipitate also. The most useful laboratory test for predicting abnormal bleeding was the platelet count. Fibrinogen levels should be followed as an aid in the diagnosis of DIC. The BT, PT, and PTT were not helpful in assessing the cause of bleeding, unless they were greater than 1.5 times the control value. We recommend that any patient receiving massive transfusions who develops diffuse microvascular bleeding be given platelet concentrates. Platelet counts as high as 100,000 may be required to control bleeding from surgical wounds. It is not necessary to supplement transfusions of stored, modified whole blood with fresh blood or fresh frozen plasma.
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PMID:Hemostasis in massively transfused trauma patients. 46 85

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

We describe a microtechnology for the study of the coagulation system in newborn infants. Interpretation of results demands an understanding of the techniques used and the nature of the control population from which normal values are drawn. We have examined two syndromes which represent the majority of hemostatic disorders of sick newborn infants. The first is thrombocytopenia resulting from bacterial infections in which there are minimal changes in the levels of blood coagulation factors and little tendency to bleed. The second is a syndrome of disseminated intravascular coagulation in which there is a profound disturbance in the coagulation mechanism, relatively little change in platelet counts, a severe hemorrhagic diathesis, and widespread ischemic necrosis.
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PMID:Clinical and laboratory diagnosis of hemostatic disorders in newborn infants. 54 15

Disseminated intravascular coagulation is described as a complication of Babesia canis infection in the dog. B. canis infection in the dog is characterized as a mild (uncomplicated) or severe (complicated) disease. The clinical, coagulation and haematological, pathological and histopathological findings of the severe disease are described. Thrombocytopenia is reported as occurring in both the mild and severe forms of B. canis infection in the dog.
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PMID:Disseminated intravascular coagulation: a complication of Babesia canis infection in the dog. 55 64

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

With clinical vigilance and laboratory tests of platelet and coagulation factor function, the clinician can promptly recognize and treat hemostatic disorders in leukemic patients. For example, laboratory values are strikingly abnormal in disseminated intravascular coagulation. Prompt neutralization of the underlying cause of the coagulopathy is essential. Platelet and coagulation factors may have to be replaced if the disorder is severe. Diffuse petechiae, purpura, mucous membrane bleeding, and hemorrhage around venipuncture or infusion sites indicate thrombocytopenia. Vigorous platelet replacement is necessary to prevent massive intracranial of gastrointestinal hemorrhage. Platelet dysfunction may cause spontaneous bleeding or immediate or delayed hemorrhage after surgery. The abnormality is often evident in peripheral blood smear or indicated by bleeding time or aggregation studies. If possible, sufficient autologous platelets should be infused to return the bleeding time to normal. Immune thrombocytopenic purpura may be easy to diagnose when the reduction in the circulating platelet count is compared with the normal number of marrow megakaryocytes. But attempts to increase platelet count by platelet transfusions may be frustrating. Treatment involves high doses of corticosteroids, followed by splenectomy if necessary.
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PMID:Hemostatic complications in leukemic patients. 56 14

A prospective study of 104 patients receiving heparin obtained from porcine intestinal mucosa for 4 or more days was conducted to determine the frequency of associated significant thrombocytopenia (platelet count less than 100 x 10(9)/I on 2 consecutive days). No episodes of significant thrombocytopenia were identified in the 13 patients receiving heparin by continuous intravenous infusion for a mean of 8.0 days or in the 38 patients receiving heparin subcutaneously for a mean of 9.9 days. In 1 of the 26 patients receiving heparin as intermittent intravenous boluses for a mean of 8.2 days significant thrombocytopenia developed; this patient had laboratory evidence of disseminated intravascular coagulation. In none of the 17 patients receiving uninterrupted heparin therapy for 4 or more days by more than one route of administration but for less than 4 days by any single route did significant heparin-associated thrombocytopenia develop. Of the 104 patients 13 had one or more platelet counts of less than 150 x 10(9)/I, but in most it was not possible to definitely relate the thrombocytopenia to the heparin therapy. Platelets in normal platelet-rich plasma did not aggregate when heparin and serum from patients with thrombocytopenia were added. The frequency of heparin-associated thrombocytopenia noted in this study was considerably lower than that reported previously.
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PMID:Heparin-associated thrombocytopenia: low frequency in 104 patients treated with heparin of intestinal mucosal origin. 57 55

Experiments were made to evaluate the potential role played by thrombogenic factors on the hematogenous arrest of circulating tumor cells in mice with demonstrable coagulopathies associated with the presence of a primary tumor, by administration of "therapeutic" doses of anticoagulants. The effects of warfarin, aspirin and heparin administration on the early arrest patterns of 125IdUrd-labelled TA3 carcinoma and Gardner lymphosarcoma cells injected intravenously into tumor-bearing mice were examined. Several hematologic parameters of carcinoma- and lymphosarcoma-bearing animals were measured prior to anticoagulation experiments and the results indicated that mice had coagulopathies similar to those found in cancer patients with disseminated intravascular coagulation syndrome, i.e., thrombocytopenia and elevated fibrinogen levels. Despite the presence of coagulation abnormalities and effective anticoagulation in recipient animals, all three agents were without effect on localization patterns of both tumor types. It was concluded that the proposed involvement of thrombogenesis in metastasis was probably not due to any role played by those clotting factors inhibited by aspirin, warfarin and heparin in early intravascular tumor cell arrest.
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PMID:Initial tumor cell arrest in animals of defined coagulative status. 58 Sep 32


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