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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 laboratory tests of 38 patients in pediatric age with Disseminated Intravascular Coagulation (DIC) were retrospectively evaluated. In all patients were performed PT, aPTT, platelets count, FDP dosage and biological assay of Fibrinogen. In most of them the activity of FII, FV, FVII, FX and FVIII was assaied. According to the diagnostic criteria of FSP greater than 8 micrograms/ml, Platelets less than 150 10(9)/1 and Fibrinogen less than 150 ml/dl, in 16 patients the diagnosis of DIC was possible since first examination, while in 9 patients it became possible within 2-4 days; in 13 patients we never could diagnose DIC, although it was reasonably present, since the criteria above mentioned were never simultaneously satisfied. Looking back in our experience, we confirm that the platelets count and the quantitation of plasmatic Fibrin Degradation Products (FDP) are the most useful tests for the diagnosis of full blown DIC, and that the biological assay of plasmatic fibrinogen helps to follow the disorder. A low level of FVIII:C seems to be a forecast of failure. None of the other test performed give any useful information for diagnosis when it is not possible with the above mentioned tests.
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PMID:[Diagnostic usefulness and predictive value of laboratory tests in disseminated vascular coagulation]. 369 26

A clinicopathological study was undertaken in 15 cases of massive hepatic necrosis after shock. The GOT and GPT level exceeded 1000 units in 10 cases. The 15 cases consisted of 3 diagnosed as fulminant hepatitis clinically and 12 diagnosed as disseminated intravascular coagulation (DIC) or multiple systemic organ failure (MOF) from the unremarkableness of liver dysfunction. It was noteworthy that sepsis and surgery were closely associated with these lesions. The weight of the liver at autopsy ranged from 800 to 2,700 g. Liver necrosis was macroscopically characterized by clear demarcation of the necrotic areas sharply separated from the surrounding liver parenchyma, showing the appearance of so-called "map-like necrosis". Microscopically, the lesions in these subjects showed mainly the pattern of centrilobular necrosis. As observed in the burn shock case (case 12), the shock which provoked in different phases of time seemed to have repeated its attack. These liver necroses were considered to result from severe systemic circulatory disturbance or intrahepatic circulatory disturbance. The possibility is indicated that the generalized or univisceral Shwartzman reaction, and repeated and combined severe shock participated in the pathogenesis. Fibrin thrombi aggrevate tissue perfusion and accelerate anoxia. Heparin therapy seemed effective in these cases if administered at an appropriate time.
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PMID:Fatal hepatic necrosis after shock. 371 91

Disorders of the coagulation system in shock are caused by injuries of the endothelium, influx of thromboplastic material into the blood and stasis. In this way, the intrinsic and the extrinsic system is activated. Fibrin is generated in the blood stream and forms high molecular complexes together with fibrinogen (hypercoagulability). With progress of the shock fibrin can deposit in the small vessels with the consequence of impaired circulation. Finally clotting factors and inhibitors (e.g. antithrombin III) are consumed by disseminated intravascular coagulation. This results in a bleeding tendency (consumption coagulopathy). In this survey particular shock formes (endotoxin induced, cardiogenic, traumatic, hemorrhagic) are discussed with regard to the reflections of the blood coagulation. The therapy of shock-induced disorders of blood coagulation are focused on treatment of primary disease, prevention or elimination of microthrombi, substitution of blood respective plasma components.
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PMID:[Changes in the coagulation system in shock]. 371 3

Fibrin/fibrinogen degradation product (FDP) was measured in 270 cases with various carcinomas. An elevation of FDP (5 micrograms/ml or more) was observed in 68 cases (25%). Of the 68 elevated FDP cases, 5 (82%) were inoperable or received nonradical resection. Forty of those 56 cases (71%) showed hematogenous metastasis. FDP in those cases which showed hematogenous metastasis was found to be due to fibrinolysis accompanied by consumption coagulopathy.
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PMID:The significance of the fibrin/fibrinogen degradation product in serum of carcinoma patients with hematogenous metastasis. 374 66

Fibrin(ogen) degradation products, platelet counts, antithrombin III, and the components of the Factor VIII complex were studied in a total of 80 patients with Plasmodium falciparum, Plasmodium vivax or Plasmodium ovale infections. The haemostatic findings were correlated to the numbers of parasitized erythrocytes and to each other. The results indicate that haemostatic changes in malaria correlate with the degree of parasitaemia. Evidence for moderate hyperfibrinolysis was found in patients with high P. falciparum parasitaemias only. Thrombocytopenia closely corresponded to parasitaemia and to von Willebrand factor levels, but appeared not to be linked to a consumption of coagulation factors. It was concluded that thrombocytopenia in malaria is not indicative of disseminated intravascular coagulation (DIC) but may relate to endothelial damage.
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PMID:Haemostatic alterations in malaria correlate to parasitaemia. 393 96

A new method is described for identifying low concentrations of circulating derivatives of fibrinogen and fibrin, even when present in heterogeneous mixtures. This technique is applicable to plasma and serum and uses electrophoresis in 2% agarose in the presence of sodium dodecyl sulfate (SDS) followed by immunological identification of separated derivatives, using radiolabeled antifibrinogen antiserum and autoradiography. Unique electrophoretic patterns distinguish plasmic derivatives of crosslinked fibrin from those of fibrinogen and also identify crosslinked fibrin polymers produced by the combined action of thrombin and factor XIII on fibrinogen. The assay is sensitive to a concentration of 0.1 micrograms/mL of fibrinogen in serum or plasma. Fibrin polymers, plasmic degradation products of fibrinogen, and plasmic degradation products of crosslinked fibrin were detected in the plasma or serum of a patient with disseminated intravascular coagulation. Plasmic derivatives of both fibrinogen and crosslinked fibrin appeared in serum in the course of fibrinolytic therapy for pulmonary embolism, whereas during acute myocardial infarction a marked increase in the proportion of fibrin polymers in plasma was found in comparison with normal controls. Thus, the procedure can distinguish between the simultaneous processes of fibrin polymer formation, fibrinogenolysis, and fibrinolysis, and is sufficiently sensitive to detect relevant quantities of derivatives in pathologic conditions.
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PMID:Specific identification of fibrin polymers, fibrinogen degradation products, and crosslinked fibrin degradation products in plasma and serum with a new sensitive technique. 397 Oct 42

The anticoagulant effect of antithrombin III (AT-III) in the management of disseminated intravascular coagulation (DIC) was investigated. When AT-III concentrate (4 mg/0.2 ml) was added to pregnant whole blood (0.8 ml), r(21.0 +/- 0.6 mm) and K(7.2 +/- 0.3 mm) (Mean +/- SE) were prolonged as compared with the saline control (C) (r: 18.6 +/- 0.6, K: 4.6 +/- 0.2 mm), and ma was decreased from 68.8 +/- 1.2 mm (C) to 60.3 +/- 1.0 mm (AT-III) on the TEG (p less than 0.01). PT and aPTT were also prolonged by the addition of AT-III concentrate (p less than 0.01). DIC models in rabbits were induced by continuous infusion of endotoxin (E). AT-III concentrate was administered two hours after starting infusion of E. Anticoagulant activity was evident on the TEG. In the data on coagulative and fibrinolytic factors, there were no significant differences between the control and the group administered AT-III concentrate. Fibrin deposits in the renal glomeruli were reduced after administration of AT-III concentrate (control: 46.5 +/- 38.7%, AT-III: 13.4 +/- 27.9%). The decreasing rate of AT-III antigen was the same in E infusion and non-infusion groups. However, the rate of decrease in activity was higher in the former than in the latter (rate of decrease: 40.0% and 24.6% 8 hours after administration of the AT-III concentrate). This indicated that inactive AT-III combined with thrombin and Xa might remain in the blood in DIC.
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PMID:[Fundamental studies on the management of disseminated intravascular coagulation (DIC) with antithrombin III (AT-III) concentrate]. 398 38

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

Carcinoma of the prostate, above all when accompanied by bone metastases, may be associated with a disseminated intravascular coagulation syndrome. The problem was to determine whether even in the absence of metastases the coagulation state of prostatic carcinoma patients predisposes them to disseminated intravascular coagulation. The authors compared coagulation equilibrium in 13 patients with a prostatic adenoma and 21 with carcinoma of the prostate free of metastases or infection. Fibrin breakdown product levels were abnormally high in 85.7 % of the carcinoma patients (as against 46.2 % of the adenoma sufferers). Clotting factor XIII was decreased in 70 % of carcinoma patients (as against 48.5 % of those with an adenoma). One prostatic carcinoma patient in four shows evidence of latent intravascular coagulation even in the absence of bone metastases. This prevalence justifies thorough coagulation studies in all patients with carcinoma of the prostate.
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PMID:[Disseminated intravascular coagulation syndrome (D.I.C.) and carcinoma of the prostate (author's transl)]. 616 Jan 84

The purpose of these studies was to establish the validity of 125I fibrin autoradiography--SDS gel techniques for monitoring degradation products from whole plasma or blood clots. These methods can be used to study fibrin degradation not only in patients with congenital factor XIII deficiency, but also in patients with disseminated intravascular coagulation or deep vein thrombosis during the course of thrombolytic therapy. Such an assay might complement existing immunologic techniques to characterize fibrin degradation in vivo by providing an in vitro analysis of the rate and pattern of fibrin degradation in whole blood or plasma. Fibrin degradation was traced by Coomassie blue staining for protein and by autoradiography on SDS-PAGE of degradation products released from a 125I-labeled fibrin tracer. The degradation of non-crosslinked clots from purified fibrin supplemented with plasmin showed a typical release of X, Y, D, and E fibrin fragments. Subsequently, all X and Y fragments were digested to D and E fragments. The degradation of non-crosslinked washed clots prepared from plasma supplemented with plasmin reflected the same pattern. The degradation of non-crosslinked washed clots prepared from EDTA anticoagulated plasma without added plasmin also showed release of X, Y, D, and E fragments. However, in contrast to the non-crosslinked washed clots supplemented with plasmin, there was no additional degradation of the X and Y fragments. These studies established that the pattern of degradation of the 125I-radiolabeled fibrin tracer was similar to that of the total protein released from the fibrin clot as observed by protein staining.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of crosslinking on the structure of solubilized fibrin degradation products in whole plasma. 623 29


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