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

This chapter has provided a review of available literature regarding alterations of hemostasis associated with CPB. The primary pathology of altered hemostasis during CPB appears to be two-fold: (1) a functional platelet defect of unclear etiology, which occurs in virtually all patients, and (2) a primary hyperfibino(geno)lytic defect which occurs in the majority of patients undergoing cardiopulmonary bypass. Significant thrombocytopenia does not appear to be a consistent problem, and is probably a function of perfusion technics; this may, however, be an important source of hemorrhage in some instances. Although hyperheparinemia, heparin rebound, and protamine excess have occasionally been incriminated as sources of hemorrhage during CPB, no well documented cases appear in the literature. Likewise, although DIC gained popularity in early reports of CPB hemorrahge, it appears that this syndrome rarely, if ever, arises as a consequence of CPB alone; it can be seen, however, in CPB patients who are provided a triggerin situation for DIC, such as shock, sepsis, or hemolytic transfusion reaction. It is likely that many reported alterations of hemostasis during CPB which were concluded to represent DIC actually were due to hyperfibino(geno)lysis. The key to prevention of CPB hemorrhage rests simply in obtaining an adequate preoperative workup. Of extreme importance is an adequate history with respect to bleeding tendencies in both patient and family; of equal importance is a careful history regarding antiplatelet drugs. A careful physical examination, searching for clues of a real or potential bleeding diathesis, also can often prevent catastrophic cases of CPB hemorrhage. Lastly, an adequate presurgical laboratory screen must be performed; in addition to the usual prothrombin time, partial thromboplastin time, and platelet count, a thrombin time and standardized template bleeding time must be added. The addition of these two simple modalities will insure against significant defects in fibrinogen, the fibrinolytic system, vascular function, and platelet function. When CPB hemorrhage occurs, simple laboratory screening will usually allow for a quick hemostasis evaluation. The parameters recommended in this review will distinguish between surgical and nonsurgical bleeding and should, therefore, allow for a quick decision regarding necessity for reexploration and the adequacy of hemostasis if reexploration is needed. In addition, this screen will distinguish between difficulties with heparin, protamine, and the fibrinolytic system. The vast majority of nonsurgical hemorrhages during CPB is due to a functional platlet defect, primary hyperfibrino(geno)lysis, or a combination of these. The quick administration of platelet concentrates, while awaiting laboratory evaluation, will control or significantly blunt most instances of CPB hemorrhage. If platelets fail to control bleeding, and reasonable laboratory evidence of primary hyperfibrino(geno)lysis is present, antifibrinolytics should then be used...
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PMID:Alterations of hemostasis associated with cardiopulmonary bypass: pathophysiology, prevention, diagnosis, and management. 79 78

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

An evaluation of the coagulation system has been conducted in vitamin E and/or selenium deficient swine. The partial thromboplastin time, plasma fibrinogen concentration, platelet lipid peroxides, as well as the fibrinogen/fibrin degradation products were not found to be significantly affected by either vitamin E deficiency, selenium deficiency, or deficiency of both. With selenium deficiency, the prothrombin time was shortened (p less than 0.05). The platelet count and platelet turnover were greatly decreased by both vitamin E (p less than 0.001) and selenium deficiency (p less than 0.005). Further-more, the survival of platelets labelled with 75Se-selenomethionine and the per cent isotope incorporated into platelets were reduced (p less than 0.05 and p less than 0.005) in association with vitamin E deficiency, but not with selenium deficiency. These results were interpreted as evidence of a platelet production defect and possibly a platelet function defect in vitamin E deficient animals. Selenium deficiency were also associated with decreased (p less than 0.05) survival of fibrinogen labelled with 75Se-selenomethionine and increased (p less than 0.05) turnover of fibrinogen. From these fibrinogen kinetic findings, it was considered that chronic low grade disseminated intravascular coagulation possibly occurs in selenium deficient animals, probably in relation to the development of hepatosis dietetica or widespread microvascular damage. However, other possibilities such as increased fibrinogenolysis in relation with hepatosis dietetica or an intrinsic fibrinogen defect due to selenium deficiency also need to be taken into consideration and have not been ruled out in the present study.
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PMID:Studies on vitamin E and selenium deficiency in young pigs. IV. Effect on coagulation system. 83 91

In experimental infections of guinea pigs with a virulent strain of Leptospira icterohaemorrhagiae widespread hemorrhages were observed. Thrombocytopenia, prolongation of prothrombin, thrombin, partial thromboplastin and coagulation times, decrease of plasma fibrinogen, factor V, factor VIII and the presence of fibrinogen degradation products were demonstrated. Treatment of infected guinea pigs with heparin prolonged life for two to three days. The histological observations revealed that the main lesion is a severe injury of the vasculature, mainly arteries, arterioles and capillaries. Most of the endothelial cells are affected or destroyed and the muscular fibers of arteries and arterioles are injured. With Martius-Scarlet-Blue, Weigert or Picro-Mallory stains it was demonstrated that the organization seen in the vessels is not all made of fibrin. The conclusion reached was that the hemorrhages observed in experimental leptospirosis in guines pigs are due to disseminated intravascular coagulation.
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PMID:The pathogenesis of leptospirosis I. Hemorrhages in experimental leptospirosis in guinea pigs. 86 35

The diagnosis of disseminated intravascular coagulation associated with intracranial pathology is discussed. This pathological entity is characterized by a diffuse bleeding diathesis. Laboratory studies suggest a consumption of all clotting and fibrinolytic factors with an elevation of fibrin split products as a sign of the fibrinolytic activity. The treatment consists of the administration of packed platelets and fresh frozen plasma to replace the consumed coagulation factors. Heparinization is recommended early to prevent further consumption of coagulation factors and epsilon-aminocaproic acid is recommended later after acute fibrinolysis is diagnosed. Constant coaguloanalytic monitoring is necessary. Although the etiology with massive injury to brain tissue is possibly secondary to autotransfusion of brain tissue thromboplastin, other causes such as hypotension, anoxia, acidosis and hemolysis must be considered.
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PMID:Disseminated intravascular coagulation. 89 1

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

The DIC syndrome is the most common cause of an abnormal hemorrhage tendency during pregnancy and the puerperium and reflects systemic activation of the coagulation cascade by circulating thromboplastic material, with secondary activation of the fibrinolytic system. Its presence in a pregnant patient almost invariably is evidence of an underlying obstetric disorder such as abruptio placentae, eclampsia, retention of a dead fetus, amniotic fluid embolism, placental retention or bacterial sepsis. Diagnosis of the DIC syndrome rests on the demonstration of reduced levels of fibrinogen and platelets, prolongation of the thrombin, prothrombin and partial thromboplastin times, and the presence of fibrin/fibrinogen degradation products (FDP) in the serum. Therapy consists of prompt removal of the source of procoagulant material, replacement of depleted clotting factors and, in some cases, anti-coagulation with heparin.
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PMID:Disseminated intravascular coagulation in pregnancy. 91 82

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


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