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

Two cases of idiopathic adult hemolytic uremic syndrome in which deposits of IgM and C3 were identified in renal arterioles showing fibrinoid necrosis are reported. Fibrin was also identified in the lumina of the involved vessels, but there was no laboratory evidence of disseminated intravascular coagulation. In both cases, serum C3 was decreased and C4 was normal, suggesting involvement of the alternate pathway of complement activation. These two cases suggest that in some instances the adult hemolytic uremic syndrome may be immunologically mediated, and that renal vascular thrombosis is a secondary phenomenon.
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PMID:Adult hemolytic uremic syndrome with renal arteriolar deposition of IgM andC3. 15 58

Blood coagulation studies showed there was a pronounced thrombocytopenia and hypofibrinogenemia in Holstein calves infected with Trypanosoma congolense TREU 112. There was also ineffective thrombopoiesis characterized by an increased megakaryocytic mass, reduced uptake of 35S-methionine into peripheral blood platelets and a normal platelet lifespan. There was an increased uptake of isotopic label into fibrinogen and a shortened half life indicating a consumptive error with increased peripheral use of fibrinogen. No consistent abnormalities were found in ethanol gelation, partial thromboplastin time, clot retraction and lysis or plasminogen assay. Fibrin split products were rarely detected. These findings suggest that in the chronic form of bovine trypanosomiasis there is a partially compensated consumption coagulopathy.
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PMID:The pathogenesis of Trypanosoma congolense infection in calves. IV. The kinetics of blood coagulation. 44 53

Using the chromogenic substrate, Tos-Gly-Pro-Arg-pNA-HCl (Chromozym TH, Boehringer Mannheim) plasma thrombin was estimated in six cases of envenomation by Australian elapid snakes. All patients manifested findings characteristic of defibrination due to envenomation by these snakes. Fibrin-fibrinogen degradation products were grossly elevated, as was plasma thrombin in all cases. Following treatment with antivenene, all abnormal coagulation parameters returned rapidly towards normal by 24 hours and plasma thrombin disappeared.
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PMID:Plasma thrombin assay using a chromogenic substrate in disseminated intravascular coagulation due to snake bite envenomation. 46 21

Twenty cases of ischemic bowel disease were analysed to determine the frequency and significance of fibrin thrombi in this condition. Fibrin thrombi were present in all 10 patients with occlusive ischemic bowel disease and in 7 of the 10 patients with nonocclusive ischemic bowel disease. In addition, fibrin thrombi were noted in a wide variety of specific and nonspecific inflammatory bowel diseases and in acute appendicitis. We conclude that fibrin thrombi are a nonspecific feature of tissue necrosis and that their mere presence in the bowel should not be regarded as an expression of disseminated intravascular coagulation.
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PMID:The nonspecific nature of fibrin thrombi in ischemic bowel disease. 63 12

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

To test the possibility that a functionally abnormal fibrinogen may exist in some patients with liver disease, we studied the plasma and purified fibrinogens of five patients whose plasma thrombin times were prolonged at least 40% over normal controls. In no patient was there evidence of disseminated intravascular coagulation and/or fibrinolysis. No abnormalities were detected by immunoelectrophoresis of plasmas or purified fibrinogens. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of reduced patient fibrinogens showed normal mobility and amount of Aalpha, Bbeta, and gamma chains. Alkaline polyacrylamide gel electrophoresis and gradient elution, DEAE-cellulose chromatography of admixtures of radio-iodinated patient (125)I-fibrinogen and normal (131)I-fibrinogen showed identical mobility in the gel and simultaneous elution from the column, respectively. Thrombin and Reptilase (Abbott Scientific Products Div., Abbott Laboratories, South Pasadena, Calif.) times of purified patient fibrinogens were prolonged, and calcium ions improved but did not completely correct these defects. Increasing amounts of thrombin progressively shortened the clotting times of patient fibrinogens but not to the level of normal. Addition of equal amounts of patient fibrinogen to normal fibrinogen resulted in a prolongation of the thrombin time of the normal protein. Thrombin-induced fibrinopeptide release was normal. Fibrin monomers prepared from patient plasmas and purified fibrinogens demonstrated impaired aggregation at low (0.12) and high (0.24) ionic strength. These studies demonstrate that some patients with liver disease and prolonged plasma thrombin times have a dysfibrinogenemia functionally characterized by an abnormality of fibrin monomer polymerization.
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PMID:Dysfibrinogenemia associated with liver disease. 87 92

A critically ill patient with disseminated intravascular coagulation (DIC) secondary to gram negative septicemia is reported. Low dose (5-10 mu/kg/h) heparin by intravenous infusion promptly inhibited intravascular coagulation, as reflected by laboratory studies. Fibrin monomer (FM) became undetectable, concentration of fibrin degradation products (FDP) fell, fibrinogen rose, and the activated partial thromboplastin time (PTT) shortened. Unintentional, temporary interruption of heparin resulted in transient return of abnormal laboratory values. The patient went on to make a complete recovery. Although the therapeutic contribution of heparin could not be proven in this patient, the laboratory data suggested that it was a valuable adjunct and in the dosage given unlikely to potentiate bleeding. The monitoring of heparin therapy in DIC by measurement of FDP, FM, and fibrinogen rather than clotting time is recommended.
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PMID:Case report: low-dose intravenous heparin in the treatment of disseminated intravascular coagulation. 91 96

Plasma from cattle infected with Babesia bigemina contained soluble fibrin in monomer and high molecular weight complex forms. Fibrin(ogen) degradation products were not constantly detected and there appeared to be little or no evidence to suggest fibrinolysis or fibrin deposition. It is suggested that classical disseminated intravascular coagulation does not occur during B. bigemina infection.
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PMID:Acute Babesia bigemina infection: changes in fibrinogen catabolism. 91 87

In a review of 768 consecutive autopsies, 21 (2.7%) clinically unsuspected cases of disseminated intravascular coagulation (DIC) syndrome were diagnosed by histologic examination. DIC was diagnosed by the presence of fibrin thrombi in arterioles, capillaries, venules, and medium-sized veins. Fibrin thrombi were found, in the descending order of frequency, in the brain, heart, lungs, kidneys, adrenals, spleen and liver. Most patients had multiple visceral involvement, with three showing fibrin thrombi in as many as ten organs. The density of fibrin thrombi was greatest in the spleen, followed by kidneys, liver, lungs, adrenals, brain, and heart. A review of clinical data showed that infections were the most common underlying conditions in 13 cases, including nine with positive bacterial cultures from blood or cerebrospinal fluid, or both. The results suggest that, despite increasing clinical recognition of DIC, a great number of patients remain unsuspected of having the DIC syndrome prior to postmortem examination.
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PMID:Clinically unsuspected disseminated intravascular coagulation (DIC): an autopsy survey. 93 73

A prospective study was performed on 32 consecutive patients undergoing elective operations on the abdominal aorta. Dacron prosthetic grafts were used to replace resected abdominal aortic aneurysms or to bypass aorta-iliac occlusive disease. Complete coagulation studies were performed preoperatively, immediately postoperatively and 24 hours postoperatively. Twenty to 30 per cent of the patients had significant postoperative alterations in prothrombin time, partial thromboplastin time and platelet count. Fibrin monomer, fibrin split products and plasminogen were abnormal in 40 to 80 per cent of the patients postoperatively. Results of preoperative studies showed no significant abnormalities. One of the 32 patients had mild clinical evidence of disseminated intravascular coagulation postoperatively, which was treated with 5 units of heparin per kilogram per hour. Results of the study indicate that aortic grafting procedures frequently produce intravascular coagulation, either local or disseminated. In most patients, this is offset by activation of the fibrinolytic system. However, clinically significant sequelae may result, requiring prompt recognition and treatment.
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PMID:Intravascular coagulation in surgical procedures on the abdominal aorta. 98 52


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