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

DIC is a hemorrhagic syndrome frequently encountered as a complication in severe gram-negative bacterial sepsis. An animal model for sepsis-associated DIC was developed in order to permit study of the appearance and development of this syndrome in relation to the entire disease process. Rhesus monkeys (4 to 6 kg) were infected by intravenous injection of 10(9) Salmonella typhimurium organisms and studied for a period of 7 to 10 days following infection. Ten of 23 infected monkeys developed petechial rash characteristic of DIC, which appeared on days 1 to 2 infection and lasted 4 to 5 days. In the group of monkeys developing rash, activation of coagulation was suggested by an 80% decrease in platelet count and 20% to 30% increases in PT and APTT. Fibrinolytic system activation was indicated by the appearance of FDP. Kinin system activation was evidenced by decreases in both prekallikrein nad kininogen. Changes in laboratory tests suggestive of subclinical DIC were also noted in infected monkeys which did not develop a rash. Pathologic evidence of DIC was obtained through observation of numerous fibrin thrombi in the kidneys of the only monkey which died in the course of infection. Occurrence of DIC in association with this experimental infection in rhesus monkeys was established on the basis of clinical, laboratory, and pathologic criteria. Expression of the syndrome on days 1 to 2 following infection correlated with the period of increasing bacteremia.
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PMID:Model for disseminated intravascular coagulation: bacterial sepsis in rhesus monkeys. 9 3

Six rhesus and two vervet monkeys were infected intraperitoneally with Ebola virus. They developed an acute haemorrhagic fever with skin rash 4 days later and died 6--12 days after infection. Histopathological lesions of acute necrosis were present in the liver, spleen, lymph nodes, lungs and testes. The presence of fibrin thrombi in several organs was suggestive of the occurrence of disseminated intravascular coagulation during the infection.
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PMID:The pathology of experimental Ebola virus infection in monkeys. 10 47

Experimental infection of rhesus monkeys (Macaca mulatta) with Machupo virus produced a hemorrhagic disease similar to that of Bolivian hemorrhagic fever in humans. The disease in infected animals was also characterized by the development of hypotension and coagulation abnormalities as indicated by severe thrombocytopenia and prolongation of the activated partial thromboplastin time. Evidence for disseminated intravascular coagulation was inconclusive due to the presence of normal to elevated fibrinogen levels, relatively low levels of circulating fibrin split products, and the lack of widespread fibrin thrombus deposition. The most likely causes of the hemorrhagic tendencies of this disease in infected monkeys were thrombocytopenia and decreased synthesis of coagulation and other plasma proteins due to severe hepatocellular necrosis. Hypotension may also have been due to decreased plasma protein synthesis.
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PMID:Studies of the coagulation system and blood pressure during experimental Bolivian hemorrhagic fever in rhesus monkeys. 10 47

Coagulation studies were carried out in a group of non-human primates (rhesus monkeys) following envenomation with lethal and sublethal doses of Russell's viper venom. The envenomated animals showed significant fibrinogenopenia in association with or without disseminated intravascular coagulation. The findings offer a rational explanation for the bleeding manifestations seen in clinical cases of Russell's viper bite.
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PMID:Coagulation abnormalities induced by Russell's viper venom in the rhesus monkey. 11 72

Three cases of a new variety of acute leukemia have been reported. The main features were: hyperleukocytosis made of large-sized blasts with a double shaped nucleus, few or no granulations in the cytoplasm, and in a few cell faggots or unique Auer rods; mycloperoxydase reaction was positive. This feature was associated with disseminated intravascular coagulation syndrome and t(15;17)(q22;q21) translocation in the majority of mitoses.
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PMID:[A new variety of acute non-promyelocytic leukemia with t(15;17)]. 11 26

Five cases of disseminated meningococcal disease due to serogroup W135 Neisseria meningitidis are presented. The cases ranged in age from 16 months to 23 years, and spanned a clinical spectrum from mild meningitis without rash or evidence of meningococcal septicemia to severe meningoencephalitis with fulminant meningococcemia, disseminated intravascular coagulation, and death. These cases demonstrate that serogroup W135 N meningitidis is fully pathogenic for man and capable of producing the full spectrum of disseminated meningococcal disease associated with other serogroups. Since this serogroup has recently emerged as a significant cause of disease in Europe, attention should be focused on the correct serogroup designation of strains of N meningitidis isolated from clinical material and reported as "nongroupable" by clinical laboratories, so that additional clinical and epidemiologic information may be obtained.
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PMID:Disease due to serogroup W135 Neisseria meningitidis. 11 72

Serial prospective studies of coagulation status have been undertaken on 73 babies with a positive Coombs test. No abnormalities were detected in the babies with mild haemolytic disease, but seven of the 36 babies with severe haemolytic disease (cord Hb less than 11 g/dl or cord bilirubin greater than 85 mumol/1) showed evidence of transient defibrination 1 d after birth and another six had evidence of coagulation failure at birth with a platelet count of less than 150 x 10(9)/1 and a severe deficiency of multiple coagulation factors. The level of factor II and factor X was less than a fifth of the normal cord blood level in these six babies and the level of I, VII and IX was severely reduced; the factor VIII level was normal or high. Exchange transfusion started within 1 h of birth corrected the immediate factor deficiency in these six babies, but evidence of defibrination then became apparent with afibrinogenaemia, a marked fall in factors II and V, less constant falls in factors VII, IX and X, and a raised fibrin:fibrinogen degradation product level. One of these six babies died with severe pulmonary hypoplasia within an hour of birth; the other five died from haemorrhage into the lung or brain 1 1/2--6 d after birth. The very low vitamin-K dependent factor levels in the cord blood of the babies who died are presumably the result of liver damage in utero, but the subsequent changes are those of a comsumption coagulopathy. Simple screening tests at birth served to indicate which babies were at risk and it is concluded that death due to haemorrhage might be reduced by more intensive factor replacement before there is overt evidence of haemorrhage in these babies.
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PMID:Coagulation failure in babies with rhesus isoimmunization. 11 26

The development of transfusion medicine started from the attempts to transfuse blood in animals in the 17th century and the first fruits were seen in the second half of the 19th century. About 1800, however, Blundell introduced a new development which brought fundamental changes with the elucidation of the problems of defibrination, the phenomenon of hemolysis and coagulation. At the beginning of the 20th century the serological problems were solved by Landsteiner's discoveries. The introduction of anticoagulation permitted the conservation of blood and led to the discontinuation of direct blood transfusion in favour of indirect transfusion of conserved blood. This considerably enlarged the functions and possibilites of transfusion medicine which opened into the development of blood component therapy with its opportunities for optimal care of the patients.
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PMID:[The development of transfusion medicine (author's transl)]. 11 27

Clotting analysis in 30 patients with bleeding complications in malignant hematological diseases revealed the following troubles: The global tests, Quick's index and partial thromboplastin time markedly differed from normal. Activity of clotting factors revealed hypo- or hyperfibrinogenemia, disturbances of the prothrombin complex (factors II, VII, IX and X), decrease of factors V, VIII, XII. Factor XI (= PTA) was not diminished in any case. Regarding the fibrin-stabilizing factor (factor XIII), its activity was significantly decreased in 30 patients with solid tumors and in 30 patients with hemoblastoses. Faulty clotting balance was characterized by hyperfibrinolysis or disseminated intravascular coagulation (DIC) accompanied by reactive hyperfibrinolysis. About one quarter of the patients with malignant disturbances of the hematopoetic system demonstrated (mostly amegacaryocyte) thrombocytopenia. Finally, treatment of bleeding complications in malignant neoplastic diseases is pointed out.
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PMID:[Hemorrhagic diathesis in patients with malignant neoplasms (author's transl)]. 11 27

Human newborns have certain hemostatic "deficiencies" which seem to be peculiar to this period of life, such as reduced factors II, VII, IX, X, XI, and XII, reduced antithrombin III levels, and reduced plasminogen levels. However, they are capable of activating the coagulation mechanism to elicit either the entity of disseminated intravascular coagulation or the occurrence of localized and diffuse thrombotic events. The mechanisms involved have yet to be defined. Evidence has been presented to suggest that preterm infants may manifest a variant form of disseminated intravascular coagulation in which thrombocytopenia is not present.
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PMID:Activation of coagulation and disseminated intravascular coagulation in the newborn. 12 Jun 82


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