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

A patient was transfused with a unit of red blood cells that had been frozen accidentally prior to transfusion. Although he had received approximately 60 gm of free hemoglobin intravenously, the patient's only clinical reaction was massive hemoglobinuria. The benign clinical response, in the presence of massive hemoglobinuria, is attributed to the absence of immunologic imcompatibility and, thus, failure to activate vasoactive mediators and disseminated intravascular coagulation. The case illustrates revised concepts of the pathophysiology of acute renal failure associated with hemolytic blood transfusion reactions.
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PMID:Benign hemoglobinuria following transfusion of accidentally frozen blood. 94 95

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

By damaging cell membrane integrity, acute rhabdomyolysis leads to electrolyte shifts according to the concentration gradients and the liberation of intracellular substances. Diagnosis is confirmed by the presence of a high serum creatinkinase activity (CK) and myoglobinuria. For clinical purposes myoglobinuria is demonstrated by a blood-positive dipstick in the absence of hematuria or hemoglobinuria. Rhabdomyolysis is usually acquired and is rarely due to hereditary enzyme defects. The authors report on 61 patients admitted in the last 15 years with rhabodomyolysis. In the past 4 1/2 years the diagnosis was suggested by CK greater than 5000U/1 in 49 patients, representing 1.6% of all admissions in the departments of medicine and surgery. Originally described in crush situations, rhabdomyolysis has been observed with increasing frequency as a consequence of muscular stress and self crush due to coma or hemi- and paraplegia during the last decades. 24% of the patients with this diagnosis had had an intoxication, and in 70% there were multiple simultaneous causes. Autoimmune diseases, infections of bacterial, viral and fungal origin, endocrinopathies, and thermic and ischemic injuries can also provoke rhabdomyolysis. As a consequence of fluid shift into the damaged muscle a compartment syndrome may lead to vascular or neural defects. In 80% of cases there is initial hypocalcemia, turning later into hypercalcemia. Other frequent electrolyte disorders accompanying rhabdomyolysis are hyperkalemia, hyperphosphatemia and a widened anion gap. 6 of 13 patients showed the typical blood changes found in patients with disseminated intravascular coagulation. Acute renal failure developed in 30 patients, 15 of whom underwent dialysis or hemofiltration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute rhabdomyolysis]. 395 76

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

A case is reported of hemolytic anemia following rifampicin administration and complicated by acute renal failure. Furthermore clotting analyses suggested a slight disseminated intravascular coagulation, very likely activated by hemolysis products. Both hemolysis and renal function impairment subsided spontaneously, after the sole withdrawal of rifampin. Direct antiglobulin test became negative within a few days, while an indirect Coomb's test was demonstrated persistently with the patient's serum using red blood cells sensitized in vitro with the drug. Otherwise from all reports in the literature, the patient developed an acute hemolytic anemia while on daily therapy and as many as twenty years after a previous treatment with rifampicin. Mechanisms of drug-induced immune hemolytic anemia and acute nephropathy are discussed (formation of drug-antibody complexes, which adhere on the red blood cells surface and are able to fix complement and induce intravascular hemolysis; tubular necrosis due to hemoglobinuria or immuno-mediated interstitial nephritis).
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PMID:[Immune hemolytic anemia and acute kidney failure due to rifampicin]. 818 1

The caval syndrome is a serious complication of chronic heartworm (Dirofilaria immitis) disease in dogs and cats. The syndrome is characterized by acute anorexia, respiratory distress, weakness, right-sided cardiac murmur, anemia, hemoglobinuria, hepatic and renal dysfunction, signs of forward and backward heart failure, and, possibly, disseminated intravascular coagulation (DIC). Retrograde migration of adult heartworms from the pulmonary arteries to the right ventricle, right atrium, and venae cavae causes disruption of the tricuspid apparatus. Valvular insufficiency, with concurrent pulmonary hypertension, reduces cardiac output thus resulting in forward and backward heart failure. Additionally, red blood cells are traumatized and hemolyzed as they flow through the mass of worms. Therapy consists of supportive care and the removal of the heartworm mass from the right ventricular inflow tract. Caval syndrome in dogs and cats is associated with high mortality rates and generally has a guarded to poor prognosis.
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PMID:Canine and feline caval syndrome. 975 97

Malaria remains an overwhelming problem in tropical developing countries, with 300 to 500 million new cases and 1.5 to 3.5 million deaths per year. Malaria is a potentially life-threatening disease for travelers to the tropics. Imported malaria is an important clinical problem in nonendemic areas of the world because of increasing numbers of travelers, overseas workers, and immigrants from endemic areas. According to the World Health Organization's criteria, the recognition of one or more of the following clinical features should raise the suspicion of severe malaria: cerebral malaria (unrousable coma), severe anemia (hemoglobin <5 g/dL), renal failure (serum creatinine >3 mg/dL), pulmonary edema or adult respiratory distress syndrome, hypoglycemia (glucose <40 mg/dL), circulatory collapse or shock, disseminated intravascular coagulation, repeated generalized convulsions, acidosis (pH <7.25), macroscopic hemoglobinuria, hyperparasitemia (>5 percent of the erythrocytes infested by parasites), or jaundice (bilirubin >3 mg/dL). Although only a small proportion of patients with malaria develops severe manifestations, these patients require the most urgent and intensive care. Mortality among patients with cerebral malaria, even when treated in modern intensive care units, exceeds 30%, and when complicated by the adult respiratory distress syndrome, it may approach 80%. Among travelers, mortality remains a serious issue because of failure to obtain and use preventive measures, delay in seeking medical attention, and misdiagnosis.
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PMID:Imported severe falciparum malaria in Israel. 977 25

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

Immune thrombocytopenia (ITP) is an acquired bleeding autoimmune disorder characterized by a markedly decreased blood platelet count. The disorder is variable, frequently having an acute onset of limited duration in children and a more chronic course in adults. A number of therapeutic agents have demonstrated efficacy in increasing the platelet counts in both children and adults. Anti-RhD immunoglobulin (anti-D) is one such agent, and has been successfully used in the setting of both acute and chronic immune thrombocytopenia. In this report we review the use of anti-D in the management of ITP. While the FDA-approved dose of 50 mg/kg has documented efficacy in increasing platelet counts in approximately 80% of children and 70% of adults, a higher dose of 75 microg/kg has been shown to result in a more rapid increase in platelet count without a greater reduction in hemoglobin. Anti-D is generally ineffective in patients who have failed splenectomy. Anti-RhD therapy has been shown capable of delaying splenectomy in adult patients, but does not significantly increase the total number of patients in whom the procedure can be avoided. Anti-D therapy appears to inhibit macrophage phagocytosis by a combination of both FcR blockade and inflammatory cytokine inhibition of platelet phagocytosis within the spleen. Anti-RhD treatment is associated with mild to moderate infusion toxicities. Rare life-threatening toxicities such as hemoglobinuria, acute renal failure and disseminated intravascular coagulation have been reported. Recommendations have been proposed to reduce the risk of these complications. Anti-D immunoglobulin can be an effective option for rapidly increasing platelet counts in patients with symptomatic ITP.
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PMID:Anti-RhD immunoglobulin in the treatment of immune thrombocytopenia. 1970 96

Malaria, the most important of the parasitic diseases of humans, is transmitted in 108 countries containing 3 billion people and causes nearly 1 million deaths each year. With the re-emergence of malaria various life-threatening complications of malaria have been observed. Unarousable coma/cerebral malaria, severe normochromic, normocytic anemia, renal failure, pulmonary edema/adult respiratory distress syndrome, hypoglycemia, hypotension/shock, bleeding/disseminated intravascular coagulation (DIC), hemoglobinuria and jaundice are few of the common complications of severe malaria. Symmetrical peripheral gangrene (SPG) has been reported as a rare complication of malaria. We report a rare and unique case of Plasmodium falciparum malaria complicated by DIC, severe normocytic normochromic anemia, and SPG.
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PMID:Symmetrical peripheral gangrene: A rare complication of plasmodium falciparum malaria. 2662 58


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