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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 role of various chemical mediators in the development of complications after major surgery was investigated. Phospholipase A2 activity (PLA2), and the levels of pancreatic secretory trypsin inhibitor (PSTI), polymorphonuclear leukocyte elastase (PMNE), thromboxane B2 (TxB2), 6-keto-PGF1 alpha (6-KF), leukotriene (LT) B4, C4, D4, interleukin-beta (IL-1 beta), tumor necrosis factor (TNF), and endotoxin (Et) in the serum were measured in 134 surgical patients of whom 36 developed postoperative complications. PLA2, arterial TxB2 and 6-KF showed significant changes in the patients with post-operative complications, associated with elevated Et levels. The majority of these patients had a significantly higher ratio of TxB2/6-KF. These results suggest TxB2 and 6-KF, and the TxB2/6-KF ratio are useful indices of outcome in critically ill patients with hepatic failure. Our findings revealed marked production of prostanoids in sepsis and indicate a severity of the complication in balance of the thromboxane/prostacyclin axis. It was also suggested that the opsonin and eicosanoid levels are closely related to the serum endotoxin level. LTB4, C4 and D4 were increased in the patients with postoperative sepsis or DIC, especially at the initial onsets. The increased levels of IL-1 beta or TNF were observed in some patients with postoperative complications, especially those with severe postoperative complications.
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PMID:[The relationship between opsonin, endotoxin and chemical mediators in postoperative complications after surgery]. 194 9

The Wisconsin Division of Health (DOH) began surveillance for severe illnesses associated with group A beta-hemolytic streptococcus (GABS) infections in late 1989 to describe the current epidemiologic features and clinical spectrum of these infections in the state. Severe illness was defined by the isolation of GABS from the blood or by the development of one or more of the following in a patient infected with GABS: shock, extensive tissue injury, desquamating rash, disseminated intravascular coagulation, renal failure, adult respiratory distress syndrome, or death. Case reports involving 28 patients with severe GABS-related illnesses with onset from November 1989 through October 1990 were received by the DOH. The majority of the case-patients had sepsis (57%), cellulitis (50%) or both. Nine (32%) cases were fatal. Those who died were older than those who survived (median age 74 years v 43 years, p = 0.002) and were more likely to have clinical diagnoses that included pneumonia (relative risk [RR] 3.0, 95% confidence interval [CI] 1.2, 7.3) or necrotizing fasciitis/myositis (RR 3.7, 95% CI 1.5, 9.0). The median interval from illness onset to hospitalization was similar for fatal cases (1 day) and non-fatal cases (2 days), suggesting that early intervention after the appearance of clinical illness may not improve the outcome.
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PMID:Severe illness associated with group A-hemolytic streptococcal infections. 194 73

The plasma kallikrein-kinin system is activated in Gram-negative sepsis and typhoid fever, two diseases in which bacterial products have been shown to initiate inflammation. Because a single intraperitoneal injection of bacterial cell wall peptidoglycan-polysaccharide polymers from group A steptococci (PG-APS) into a Lewis rat produces a syndrome of relapsing polyarthritis and anemia, we investigated changes in the role of the kallikrein-kinin system in this model of inflammation. Coagulation studies after injection of PG-APS revealed an immediate and persistent decrease in prekallikrein levels. High-molecular-weight kininogen levels decreased significantly during the acute phase and correlated with the severity of arthritis. Factor XI levels were decreased only during the acute phase. Antithrombin III levels remained unchanged, indicating that neither decreased hepatic synthesis nor disseminated intravascular coagulation caused the decreased plasma contact factors. Plasma T-kininogen (an acute phase protein) was significantly elevated during the chronic phase. PG-APS failed to activate the contact system in vitro. Thus the kallikrein-kinin system plays an important role in this experimental model of inflammation, suggesting that activation of this system may play a role in the pathogenesis of inflammatory bowel disease and rheumatoid arthritis in which bacterial products might be etiologically important.
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PMID:Role of kallikrein-kinin system in pathogenesis of bacterial cell wall-induced inflammation. 199 42

Disseminated intravascular coagulation (DIC) is a frequent complication of meningococcal sepsis in children. The clinical course variability, the severity of manifestations and the need of an early diagnosis for appropriate treatment, guides us to report a case of meningococcal sepsis and DIC. The patient, male, prematurely born, 11 months years old, presented himself with high fever of sudden onset, malaise, diarrhea, diffuse skin rash with abdominal petechiae, and no clinical evidence of meningitidis. Initial hematochemical findings, peripheral leukocytosis, quantitative and qualitative changes in plasma coagulation factors, liquoral hypocellularity together with the development of signs of meningeal irritation (stiff neck and back) were considered diagnostic clues for meningococcal sepsis associated with DIC. A gram-negative diplococcus was cultured from liquor. Primary goals of the treatment of this life-threatening clinical picture were the elimination of the bacterial component, the correction of clotting disorders and careful control of shock and metabolic acidosis often related with DIC. The patient then received a wide spectrum Cephalosporin, fresh frozen plasma, appropriate electrolyte solutions and eventually heparin, which led to a complete control and resolution of symptomatology.
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PMID:[Meningococcal sepsis and DIC in childhood: a report of a clinical case]. 205 63

Twenty cases of symptomatic patent ductus arteriosus (PDA) in preterm inborn infants were studied retrospectively. The diagnostic criteria were a systolic or a systolodiastolic murmur, tachycardia (greater than 160 per minute), hyperdynamic precordium, collapsing arterial pulses, cardiomegaly or a need for intermittent positive pressure ventilation or continuous distending airway pressure. The incidence was found to be 2.48/1000 live births and 1.5% of SCBU admission. All babies were less than 35 weeks gestation and 18/20 weighed less than 1750 g at birth. Ten babies were treated with indomethacin (0.2 mg/kg) and two of these babies died before the course of treatment was completed. Ten babies were treated with conservative therapy. They could not be administered indomethacin because two died of fulminant sepsis soon after the diagnosis was made; two babies had sepsis and DIC but recovered from it, three had thrombocytopenia, one had azotemia, two babies had hyperbilirubinemia requiring exchange transfusion. The two groups of babies matched in respect to gestational age, sex, age at presentation, birth weight and associated illnesses. Two babies in each group died soon after diagnosis. Of the eight babies in each group, six babies closed the ductus on indomethacin therapy as against two on conservative therapy. This difference was significant (p less than 0.05). The babies who responded to indomethacin were all treated within two weeks of age. None of them showed any complication of drug therapy or recurrence of PDA. We conclude that intragastric indomethacin given early in the management of symptomatic PDA in term infants is a safe and effective modality.
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PMID:Clinical profile and management of symptomatic patent ductus arteriosus in premature infants. 205 26

Disseminated intravascular coagulation (DIC) may complicate severe septicemia caused by Staphylococcus aureus. S. aureus can induce spontaneous platelet aggregation in vitro, the rapidity and degree of which correlates with the severity of DIC in patients with sepsis. Purified peptidoglycan from DIC isolates aggregated human platelets in the presence of staphylococcal protein A with significantly shorter aggregation times than did peptidoglycan from non-DIC isolates. Purified teichoic acid from DIC and non-DIC isolates failed to aggregate platelets in vitro, or in vivo in guinea pigs but inhibited the peptidoglycan-induced aggregation in a dose-response manner. These studies suggest that peptidoglycan may mediate S. aureus-induced spontaneous platelet aggregation in vitro and DIC in vivo. The variability among strains of S. aureus to induce DIC and platelet aggregation may depend on the unique composition of their peptidoglycan and perhaps also the extent of exposure or availability of cell wall teichoic acid.
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PMID:Disseminated intravascular coagulation associated with Staphylococcus aureus septicemia is mediated by peptidoglycan-induced platelet aggregation. 205 98

The plasma level of interleukin-1 beta (IL-1 beta) was determined in normal individuals, patients with disseminated intravascular coagulation (DIC), patients in the pre-DIC period (within 7 days before the onset of DIC), and non-DIC patients to examine the relationship between DIC and the plasma IL-1 beta level. The plasma IL-1 beta level was 0-0.085 ng/ml in normal individuals, with little difference being seen according to related age. It was significantly higher in the DIC group (0.19 +/- 0.19 ng/ml) than in the pre-DIC group (0.05 +/- 0.08 ng/ml) or the non-DIC group (0.09 +/- 0.01 ng/ml). The plasma IL-1 beta level was not markedly elevated in leukemia patients, even in the DIC group, but it was significantly increased in the DIC group of solid cancer patients and was generally elevated in patients with sepsis. It was markedly elevated to 0.39 +/- 0.26 ng/ml in patients with organ failure. When mononuclear cells were incubated with lipopolysaccharide, it was found that IL-1 beta, tumor necrosis factor, and tissue factor (TF) were released into the medium, and there was an increase of TF release from endothelial cells incubated with this medium. These results suggest that the increase in IL-1 beta reflected the activation of monocytes and may be an important factor in DIC and its associated organ failure.
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PMID:Plasma level of IL-1 beta in disseminated intravascular coagulation. 205 18

Disseminated intravascular coagulation (DIC) or renal damage associated with septicemia was induced in rats by ligating the cecum or by injecting endotoxin. In the septicemia model, the number of E. coli and Bacteroides spp in the blood increased concomitantly with an increase of endotoxin. In this model the development of hypercoagulability with mild fibrinolysis was observed. Histopathologic findings in the kidneys, including the formation of microthrombi in the glomeruli and the vacuolization and dilatation of renal tubular cells, suggest the development of mild DIC. In the endotoxin-induced DIC model, both remarkable state of hypercoagulability and fibrinolysis were observed with fibrin thrombi in glomeruli. The administration of the platelet-activating factor antagonist, CV-6209, or of human antithrombin III, ameliorated DIC significantly by limiting the increases in prothrombin time, activated partial thromboplastin time and fibrin degradation products. These agents significantly reduced the deposition of fibrin in the glomeruli and significantly prolonged the survival time of the endotoxin injected rats. These observations suggest that the PAF antagonist CV-6209 and ATIII merit clinical evaluation in the management of DIC caused by septisemia.
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PMID:Effect of a platelet activating factor antagonist and antithrombin III on septicemia and endotoxemia in rats. 206 2

Blood assay in patients with DIC-syndrome and thrombosis has shown different changes in red blood cell acid resistance: it is increased in acute noninfectious DIC-syndrome, and significantly decreased in the presence of sepsis, in patients with chronic DIC-syndrome and acute thrombophlebitis it is less lowered, while it is significantly elevated in the development of thromboembolism of the pulmonary artery. At the same time red blood cells damaged due to DIC-syndrome are characterized by increased acid resistance and high coagulation potential. This combination has proved the pathogenetic role of damaged red blood cells and the process of fragmentation in the development of intravascular blood coagulation.
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PMID:[Coagulative activity and acid resistance of damaged and intact erythrocytes in various types of intravascular blood coagulation]. 206 59

In order to elucidate a possible role of hypercoagulability leading to disseminated intravascular coagulation (DIC) in the pathogenesis of multiple organ failure (MOF), unfractionated heparin and the related agents were administered to septic rabbits which manifest DIC and MOF. Administration of heparin resulted in prevention of thrombocytopenia, leukopenia and elevation of plasma bilirubin and creatinine. The morphological hepatic damage was also ameliorated by heparin. Similar favorable effects were obtained by the administration of low molecular weight heparin. Dextran sulfate prevented the hepatic damage to some extent without improvement on other parameters. No significant effect was observed by the administration of a synthetic thrombin inhibitor (MD805). These results indicate that the favorable effect of heparin is due to its anticoagulant property, especially anti-Xa activity. Thereby, it is concluded that the hypercoagulable state leading to DIC is a prerequisite for the occurrence of MOF in sepsis.
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PMID:The effect of heparin on multiple organ failure and disseminated intravascular coagulation in a sepsis model. 208 91


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