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

Evidence of disseminated intravascular coagulation (DIC) was dought in normal baboons infused with autologous hemolyzed whole blood, preceded or followed by infusion of dextran (molecular weight, 70,000). Mean peak plasma hemoglobin following a rapid single injection was 370 mg/100 ml in 2 animals and 1,236 mg/100 ml in 1 animal, while levels during continuous 5 hour infusion in 2 animals averaged 326 and 474 mg/100 ml, respectively. Dextran infusion immediately preceded hemoglobin injection in 2 baboons and followed hemoglobin injection by 1 1/2 and 2 1/2 hours, respectively, in 2 baboons. Coagulation studies showed a moderate although significant fall in platelet count with prolongation of the partial thromboplastin time following hemoglobin infusion, and shortening of the thrombin time after dextran. Fibrin degradation products developed in four of five experiments after hemolysate injection. The induction of acute experimental hemoglobinemia results, therefore, in the development of coagulation changes consistent with milk DIC. Preliminary infusion of dextran (molecular weight, 70,000) may facilitate this response by either initiating the development or impeding the clearance of fibrin degradation products.
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PMID:Coagulation changes in baboons during acute experimental hemoglobinemia and dextran infusion. 80 56

Infusion of autologous hemolyzed blood in humans has served as a model for various experimental investigations for many years. Numerous studies have shown this model to be unattended by any adverse clinical reactions. In this study evidence of subclinical disseminated intravascular coagulation (DIC) was sought in normal humans infused with autologous hemolyzed blood. Hemoglobinemia was induced in 10 experiments by a single injection of frozen-thawed blood and in 4 experiments by such an injection of hemolysate followed by a 5-h maintenance infusion. Mean peak plasma hemoglobin following single dose injections was 540 mg/100 ml, while levels during continuous infusion averaged 240 mg/100 ml. The induction of hemoglobinemia was asymptomatic. Coagulation studies showed no significant alteration in prothrombin time, partial thromboplastin time, thrombin time, clottable fibrinogen, or WBC. Fibrin degradation products were not found. Platelet counts fell slightly in the 5-min postinfusion sample but returned to preinfusion levels within 30 min, suggesting a temporary sequestration of platelets rather than consumption. The induction of moderate brief experimental hemoglobinemia in normal subjects did not result in the development of demonstrable DIC.
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PMID:Coagulation studies during experimental hemoglobinemia in humans. 112 Jul 40

Three units of group A blood were inadvertently administered to a group O recipient during surgery without evidence of hemoglobinemia, hemoglobinuria, hypotension, disseminated intravascular coagulation, acute renal tubular necrosis, or other signs and symptoms of transfusion reaction. The recipient had normal concentrations of IgG, IgA, and IgM as well as complement (C3) prior to transfusion and anti-A agglutinins titered to 64 (titer of 128 by the antiglobulin technic). Seventeen hours following the transfusion, 28 per cent of the circulating red blood cells were group A (equivalent to 475 ml of packed cells); they were eliminated by day 5 without evidence of hemoglobinuria, hemoglobinemia or hyperbilirubinemia. Anti-A titers (antiglobulin) had risen from a posttransfusion low of 4 to 4,096 by day 10. After treatment of serum with 2-mercaptoethanol, however, hemolytic activity which was first noted on day 5 was lost and the antiglobulin titer dropped to 24 which suggested that most of the anti-A produced in response to the transfusion was IgM rather than IgG. The anti-A titer had dropped to essentialyy pretransfusion levels and the majority of anti-A present was IgM by day 91. The recipient suffered no untoward effects from the transfusion and was in good health three months following the transfusion.
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PMID:Unusual response to ABO incompatible blood transfusion. 119 85

ABO blood group incompatibility is of major concern because the antibodies frequently cause intravascular destruction leading to the most clinically severe complications. Irregular erythrocyte antibodies seldom cause intravascular destruction. However, when the antibodies bind complement and are present in high concentration the extravascular destruction occurs predominantly in the liver and may cause a clinically severe reaction with hemoglobinemia, shock and DIC. Those IgG class antibodies which do not bind complement cause a spleen-mediated, more or less drastically shortened life span of the red cells with unpleasant but usually not life threatening consequences for the patient. The transfusion reaction may occur with a delay of several days. Compatibility testing may consist of either a cross-match performed in such a way that both ABO incompatibility and irregular antibodies are detected, or a type-and-screen procedure. In the latter a computerized delivery control checking the patient's previous serological history and the donor/recipient compatibility is a recent improvement and rationalization. In an acute situation a reduction of the normal security measures may be necessary. The clinician responsible for the patient must know the time needed for carrying out an acute blood group determination and compatibility test in the hospital and must give instructions about what normal security measures that should be refrained from. Blood group incompatible transfusions have nowadays a much better prognosis than earlier, provided a rapid diagnosis can be made and appropriate treatment can be started promptly. Formation of antibodies against leukocyte/thrombocyte antigens is a frequent consequence of transfusion which, however, can be prevented by modern blood component therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunologic transfusion reactions. 306 89

Evidence of disseminated intravascular coagulation (DIC) was sought in New Zealand white rabbits infused with autologous, hemolyzed whole blood. Hemoglobinemia was induced in 17 rabbits by rapid intravenous injection of frozenthawed whole blood. Three dose regimens yielded mean peak plasma hemoglobin concentrations of 325, 615 and 860 mg/100 ml respectively (range 260 to 1050 mg/100 ml). Eleven control animals were infused with autologous, nonhemolyzed whole blood in similar doses. Rabbits were killed at either 15, 60, 120 or 180 minutes following infusion and multiple organ biopsies obtained immediately post-mortem. Coagulation studies demonstrated no significant alterations in prothrombin time, partial thromboplastin time, thrombin time or fibrinogen. Fibrin degradation products were not found. Histologic examination of lung, heart, liver, spleen and kidney revealed no fibrin deposition, thrombus formation or other abnormalities. We conclude from our study that induction of brief, experimental hemoglobinemia in New Zealand white rabbits, utilizing moderately large doses of autologous, hemolyzed whole blood, does not result in the development of DIC.
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PMID:Coagulation studies and correlative histology during experimental hemoglobinemia in rabbits. 481 1

The purpose of pretransfusion compatibility testing is to prevent incompatible red blood cell transfusions that could lead to immune mediated hemolytic transfusion reactions. Some hemolytic transfusion reactions may have serious sequelae including hemoglobinemia, disseminated intravascular coagulation, renal failure, and death. This article reviews the most comprehensive recent analyses of the laboratory methods used during pretransfusion compatibility testing in the United States. Most of the laboratory practice data have been published in the College of American Pathologists Transfusion Medicine Survey Sets and in a national survey called the Pre-Transfusion Testing Survey. This article couples and trends the data of these comprehensive surveys with an assessment of the literature to present the current practice of pretransfusion compatibility testing.
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PMID:Pretransfusion compatibility testing for red blood cell administration. 1160 82

The Food and Drug Administration (FDA) licensed Rh(o)(D) immune globulin intravenous (anti-D IGIV) on March 24, 1995, for treatment of immune thrombocytopenic purpura (ITP). A previous review described data on 15 patients who experienced acute hemoglobinemia or hemoglobinuria following anti-D IGIV administration for ITP or secondary thrombocytopenia. Eleven of those patients also experienced clinically compromising anemia, transfusion with packed red blood cells, renal insufficiency, dialysis, or death. That review suggested that patients receiving anti-D IGIV be monitored for those and other potential complications of hemoglobinemia, particularly disseminated intravascular coagulation (DIC). Through November 30, 2004, the FDA received 6 reports of DIC associated with "acute hemolysis" (or similar terms), 5 of which involved fatalities. The attending or consulting physicians assessed that acute hemolysis or DIC caused or contributed to each death. This review presents the first case series of DIC associated with acute hemoglobinemia or hemoglobinuria following anti-D IGIV administration for ITP. The purpose of this review is to increase awareness among physicians and other health care professionals that DIC may be a rare but potentially severe complication of anti-D IGIV treatment. Increased awareness of DIC as a diagnostic possibility may enable prompt recognition and medical intervention in affected patients.
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PMID:Disseminated intravascular coagulation associated with acute hemoglobinemia or hemoglobinuria following Rh(0)(D) immune globulin intravenous administration for immune thrombocytopenic purpura. 1755 71