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

The injection of a sublethal bolus of E. coli into conscious swine produces an early increase in PAP and a decrease in LAP. This hemodynamic effect may be secondary to the pulmonary venous constriction seen in other species, or may relate to demonstrated multiple pulmonary microemboli. Hypoxemia developed in only four of 17 animals although all endotoxin-treated swine showed interstitial edema and elevated wet/dry weight ratios with normal pulmonary surfactant. In addition, endotoxin-treated swine developed signs of disseminated intravascular coagulation, with renal cortical infarcts in 44%, and coronary arterial thrombi in 28% including one transmural myocardial infarction. This effect was observed in the absence of prolonged hypotension in swine and should provide a useful model for further study of the relationship of endotoxin to disseminated intravascular coagulation.
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PMID:Hemodynamic and respiratory responses of conscious swine to E. coli endotoxin. 0 64

The appearance of lesional edema in the region of the alveolar wall constitues the initial phenomenon of involvement of the pulmonary parenchyma during shock lung, fat embolism, DIC and post perfusion lung syndrome. The alveolar septum reacts in a monomorphous manner to these various agressions, although the responsible physiopathological factors are numerous and varied. The lung in E.C.C. represents a vertiable experimental post-agressive lung. It has been studied in man from the clinical, radiological, hemodynamic and anatomopathological standpoints. The modifications found enable one to better understand the etiological factors intervening in the other post-agressive lungs.
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PMID:[Pulmonary edema due to shock, fat embolism, disseminated intravascular coagulation and post extracorporeal circulation]. 0 70

Disseminated intravascular coagulation (DIC) was induced in both normal and asplenic rhesus monkeys by intravenous challenge with Streptococcus pneumoniae. Our observations in the infected monkeys have led us to conclude that (1) pneumococcal capsular polysaccharide (PCP), immune complexes and complement may not have primary roles in the initiation of DIC; (2) intact pneumococci may be catalysts for the development of DIC; (3) the initial event in DIC may be activation of Hageman factor; and (4) evidence of activation of Hageman factor-dependent systems is present regardless of severity of infection.
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PMID:Disseminated intravascular coagulopathy during experimental pneumococcal sepsis: studies in normal and asplenic rhesus monkeys. 2 58

A chronic hemodialysis patient, previously splenectomized because of trauma in conjunction with gastrectomy, developed bacteremia with type 18 Streptococcus pneumoniae and died within 13 hours of onset of symptoms. Characteristics of this illness were severe hypoglycemia, pneumococci visible on peripheral blood smear, disseminated intravascular coagulation, neutropenia, and in vitro hemolysis. Splenectomy should be considered with caution in uremic patients and in renal transplant recipients because of the increased risk of fulminant bacteremia. Polyvalent pneumococcal vaccine may be helpful in preventing this syndrome in such asplenic patients.
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PMID:Fulminant pneumococcal bacteremia in an asplenic chronic hemodialysis patient. 3 5

A gravida with intrauterine fetal death who developed progressive chronic consumption coagulopathy was treated with heparin. When serial fibrinogen levels fell below 100 mg% and the prothrombin time was significantly prolonged, intravenously injected heparin corrected hypofibrinogenemia. A safe delivery followed administration of oxytocin. The authors emphasize the infrequent need for heparin therapy in the majority of cases of the intrauterine fetal death syndrome. Therapeutic guidelines for its use in selected cases are reviewed.
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PMID:Consumption coagulopathy associated with intrauterine fetal death: the role of heparin therapy. 3 82

A 58-year-old man who survived an episode of fulminant pneumococcal septicemia with disseminated intravascular coagulation had undergone splenectomy 23 years previously. In the literature there are 25 reported cases of fulminant septicemia and disseminated intravascular coagulation associated with asplenia in adults (excluding cases in which corticosteroid or immunosuppressive therapy was given). The pneumococcus was responsible for all of these cases as well. The mortality in this series was more than 90%, and death occurred within 24 hours of presentation at hospital in almost 70% of the fatal cases and was associated with high-density bacteremia and adrenal hemorrhage. Gram-staining of the buffy coat of the peripheral blood or the exudate from purpuric skin lesions was carried out in only 6 of the 26 cases but yielded positive results in all but 1. It is concluded that a diagnosis of septicemia in asplenic adults can be established within a short time of presentation on the basis of statistical probability and the results of Gram-staining of the peripheral blood and exudate from the skin lesions. Prevention appears to be the cornerstone of management because of the variable interval from splenectomy to the onset of the syndrome and the high mortality.
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PMID:The syndrome of pneumococcemia, disseminated intravascular coagulation and asplenia. 3 2

In 46 head-injured patients coagulation studies were performed immediately after admission. In 76% of all cases signs of disseminated intravascular coagulation (DIC) were found. DIC was related to the severity of the injury and outcome. It is suggested that DIC may be used as an important parameter in assessing craniocerebral trauma. In a previous report it was stated that disseminated intravascular coagulation (DIC) is met frequently in head-injured patients (2.5--15.3%), and is associated with a more severe grade of injury and an increased mortality. This paper explores in more detail the relationship between outcome after head-injury and signs of DIC, as detected by laboratory studies performed in the first few hours after injury.
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PMID:Disseminated intravascular coagulation related to outcome in head injury. 3 28

The striking mortality in viral hepatitis associated with pregnancy, regularly observed in developing countries, has shown a significant decrease in Saudi Arabia during a period of unprecedented economic growth. However, the risk of fatal hepatitis in the pregnant Saudi woman remains approximately four times that for the nonpregnant woman. The explanation for the observed mortality trend is not apparent, but is unlikely to be the result of improved nutritional status of the population alone, or because of treatment of severe hepatitis with adrenal corticosteroids. Disseminated intravascular coagulation may be one factor that decisively influences the outcome of hepatitis in the pregnant woman.
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PMID:Viral hepatitis complicating pregnancy: mortality trends in Saudi Arabia. 3 43

Complement activation as shown by increased clearance of radioactive C1q and reduction in serum-C3 level was found in fifteen (83%) of eighteen patients studied during Plasmodium falciparum infection. Six patients had haemostatic defects suggesting disseminated intravascular coagulation (D.I.C.), and five others had other clinical complications. A correlation was found between reduction of C3 and clinical complications as well as with the degree of anaemia and with thrombocytopenia. Moreover, the most severe thrombocytopenia and the most severe reduction of C3 levels were found in those patients with D.I.C. An immune reaction associated with complement activation in P. falciparum infection is believed to contribute to injury of red blood-cells and platelets and to promote the development of D.I.C. and other serious clinical complications.
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PMID:Complement changes and disseminated intravascular coagulation in Plasmodium falciparum malaria. 4 1

A prothrombin complex concentrate rich in factor VII has been used in the management of the clotting defect in thirteen patients with liver disease. Adequate correction of coagulation was achieved immediately after infusion in all cases. Within 4 hours there was some deterioration and by 24 hours the results approximated to pre-fusion values. Liver biopsies were performed without haemorrhagic complication in the immediate post-infusion period. There was no evidence of induced intravascular coagulation. Since other prothrombin complex concentrates have proved disappointing, both in their failure to correct the clotting defect and in their production of disseminated intravascular coagulation, this factor-VII-rich concentrate may be the treatment of choice in patients with liver disease who require temporary correction of their coagulation defect.
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PMID:Use of factor-VII-rich prothrombin complex concentrate in liver disease. 4 16


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