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

Our previous studies suggested that disseminated intravascular coagulation (DIC) may be a sequel to saline-induced abortion. A hypothetical mechanism for the DIC is that hypertonic saline produces cellular disruption in the products of conception with the release of thromboplastic substances into the amniotic fluid. These substances, in turn, diffuse through the damaged membranes into the maternal circulation. To examine this hypothesis we obtained samples of amniotic fluid (AF) from 5 patients just prior to and at 1 hour, 6 hours, and 24 hours after intraamniotic instillation of hypertonic saline. The procoagulant and thromboplastic properties of the various AF specimens were quantitated using the prothrombin time (PT), partial thromboplastin time (PTT), and activated clotting time (ACT) as in vitro test systems. The results indicate that a change in the procoagulant and/or thromboplastic activity of AF following saline instillation is not afactor in the pathophysiology of DIC associated with saline abortion.
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PMID:Pathophysiology of disseminated intravascular coagulation in saline-induced abortion. 94 81

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

Intravascular coagulation was induced by two appropriately spaced doses of endotoxin and by infusion of thromboplastin. The resulting fibrin deposition was measured by a previously described quantitative technique. Evidence of thrombin elaboration was obtained indirectly by measurement of fibrin monomer (FM) and by the detection and isolation of a thrombin-induced anticlotting activity. Venous segments were isolated at intervals and examined for thrombus formation following 40 minutes of stasis. Endotoxin triggered thrombin elaboration was not detectable in the circulation for at least one hour and was not accompanied by any thrombosis in isolated venous segments. No thrombin elaboration was found in leukopenic rabbits given endotoxin. In the thromboplastin infused animals, the quantity of fibrin deposited in the organs was comparable to that found after endotoxin. However, thrombin was found in the blood immediately and was associated with thrombosis in the isolatet venous segments. Less thrombin-induced anticoagulant activity was found after thromboplastin than after endotoxin. The findings suggest that endotoxin-induced intravascular coagulation is probably not caused by a mechanism of systemic hypercoagulability due to the release of thromboplastic material into the blood stream. A focal process of thrombin elaboration involving leukocytes is postulated. The study is believed relevant to patients with disseminated intravascular coagulation in whom venous thromboembolism is rarely found despite evidence of extensive microvascular fibrin deposition.
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PMID:Thrombin elaboration in endotoxin-induced intravascular fibrin deposition. A leukocyte dependent process distinct from systemic hypercoagulability. 103 55

Total hemolytic complement activity and the third component of complement were found to be significantly depressed in vivo in rabbits following the induction of disseminated intravascular coagulation by both thrombin and thromboplastin. Production of severe thrombocytopenia by the administration of platelet antiserum prior to the infusion of thrombin or thromboplastin partially prevented complement activation. The data show that, when clotting is triggered, complement activation takes place and that platelets are required to some extent for this reaction.
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PMID:Effects of intravascular clotting on the activation of the complement system: The role of the platelet. 109 Nov 53

The therapeutic efficiency of two glucocorticoids (hydrocortisone and dexamethasone) on endotoxin-induced intravascular coagulation was investigated in the rat. Coagulation and platelet aggregation studies were performed and plaminogen was assayed. Our results indicate that pretreatment of the animals with large doses of these steroids within a few hours prior to endotoxin totally prevents the consumption in Hageman factor, measurable contact product activity, platelets, fibrinogen, plasminogen, and the loss in platelet aggregability and serotonin. In addition to this, the hypercoagulable state consecutive to endotoxin, characterized here by shortenings in the partial thromboplastin and recalcification times and by an increase in the availability of platelet procoagulant activity, was also totally prevented by the steroid pretreatment. On the other hand, it is shown that these glucocorticoids do not interfere in the normal rat with platelet aggregation (tested with thrombin,adenosine diphosphate, and collagen), but with the availability of platelet procoagulant activity. This last phenomenon, in addition to that of an interference in vivo with the mechanism of activation of Hageman factor, are believed to be responsible for prevention by glucocorticoids of endotoxin-induced disseminated intravascular coagulation.
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PMID:Prevention by glucocorticoids of disseminated intravascular coagulation induced by endotoxin: mechanisms. 109 78

Optical density measurements of plasma clot formation and lysis were recorded using a platelet aggregometer and strip chart recorder. It was discovered that, by adding standard solutions of ellagic acid-activated partial thromboplastin, urokinase, and CaCl2, and monitoring the reaction via the recorder, characteristic curves would be generated by normal human plasma. The curve segments were labeled Tc (clotting time), which correlated with the activated partial thromboplastin time, Fc (maximum optical density change), which paralleled fibrinogen concentration, and Tl (lysis time), which corresponded generally to plasminogen levels. Deviations from normal curve segments, observed in disseminated intravascular coagulation, hypo- and hyperfibrinogenemia, factor VIII deficiency, severe hepatocellular disease, juvenile rheumatoid arthritis, and neonates (normally low in plasminogen), indicated abnormalities which were substantiated by standard procedures. This new test, given the acronym "CLUE" for clotting and lysis, urokinase enzyme activated, appears to be sensitive, inexpensive and easily performed on a sample of 0.2 ml. of plasma in only 15 minutes.
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PMID:The CLUE test. A multiparameter coagulation and fibrinolysis screening test using the platelet aggregometer. 111 Dec 77

Disorders of blood coagulation were investigated before and during a cytostatic combination therapy with vincristine sulphate and iphosphamide (Asta Z 4942) in 12 patients with malignant tumours or haemoblastoses. Thromboplastin time, partial thromboplastin time, thrombin time, heat-dependent fibrin, clot retraction, and clotting factors II, V, VIII, IX, X, and the platelet count were determined. A change in the plasmatic coagulation system attributable to the combination therapy could not be demonstrated in any patient. The influence of the cytostatic combination on the platelet-dependent haemostasis was small; a decrease in platelet count could be observed in only one patient, in whom an additional causative damage to thrombopoiesis due to the underlying disease could be assumed. Regardless of the cytostatic therapy there were indications of a hypercoagulability in 10 patients. This explains the increased susceptibility of such patients for thromboses or consumption coagulopathy.
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PMID:[Influence of cytostatic combination therapy with vincristine sulphate and iphosphamide on blood coagulation]. 111 66

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

Blood coagulation tests were performed on admission to the hospital and on consecutive days after severe and moderate head injury in 34 patients. Platelet counts and fibrinogen were normal at admission and raised thereafter. The partial thromboplastin time was shortened at admission and lengthened in the following days. Fibrinolytic activity was enhanced at admission. The ethanol gelation test was negative in all patients during the post-traumatic time course. It was concluded that, in the first 24 hours after injury, activated coagulation was present after head injury. In contrast with data of other authors, disseminated intravascular coagulation did not occur in these series.
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PMID:Disseminated intravascular coagulation and head injury. 115 24

The effect of rapid decompression on the stress-accelerated blood coagulation system of male and fingerling coho salmon (Oncorhynchus kisutch) was examined after simulated 100- and 200-fsw dives. Blood samples taken either through a dorsal aorta cannula or from a severed caudal peduncle were analyzed for total plasma protein and fibrinogen concentrations, prothrombin times (PT), and partial thromboplastin times (PTT). The effect of mild decompression (100-fsw) on the hemostatic mechanism of both adult and fingerling coho salmon indicated an alternating fibrinogen concentration, declining from normal levels 1 min after decompression, followed by an increase 10 to 15 min later with an eventual loss of fibrinogen to one half the original level an hour after decompression. Partial thromboplastin times were found to increase 10 to 15 min after decompression occurred. Prothrombin times showed an increase 1 hour after decompression in adult salmon, whereas in fingerlings, prothrombin times increased almost immediately from normal levels. The effect of severe decompression (200-fsw) showed similar trends, but at an accelerated rate. It was concluded that both mild and severe decompression activates the hemostatic mechanism of fish which may eventually result in consumption coagulopathy at a greater rate than reported for experimental mammals.
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PMID:Changes in hemostatic parameters in fish following rapid decompression. 122 84


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