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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 53-year-old female patient with ovarian dermatoid cyst and lung tuberculosis had been treated with rifampicin. During repeated rifampicin treatment she developed an acute haemolytic syndrome with haemorrhagic diathesis. Laboratory findings showed that it was caused by disseminated intravascular coagulation. Death ensued despite intensive administration of heparin and Trasylol. It is assumed that the repeated rifampicin application had provoked massive haemolysis by an allergic mechanism leading to thrombofibrinolytic haemorrhagic diathesis.
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PMID:Disseminated intravascular coagulation (DIC) during superacute haemolysis in a patient with ovarian dermatoid cyst treated with rifampicin. 61 55

Disseminated intravascular coagulation (DIC), experimentally induced by endotoxin, caused severe hemorrhagic necrosis of the intestinal mucosa in dogs. Microscopic observation showed tortuous thrombus formation in the microcirculation of the villi. Ligation of the pancreatic and bile ducts, or administration of heparin protected the mucosa from hemorrhagic necrosis, while systemic administration of tranexamic acid increased the intestinal mucosal lesion. Local pretreatment of the intestinal mucosa by Trasylol or tranexamic acid reduced the degree of hemorrhagic necrosis. It is concluded that intravascular coagulation in the microcirculation of the intestinal mucosa, as well as pancreatic proteases, play a role in the pathogenesis of hemorrhagic necrosis in the intestine associated with DIC.
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PMID:Hemorrhagic necrosis of the intestinal mucosa associated with disseminated intravascular coagulation. 62 19

Disseminated intravascular coagulation was induced in rats by injection of a silver colloid suspension or thrombin. Ten min after the injection of colloid, fibrin deposits were observed light microscopically in all major organs. At 30 min, fibrin was no longer present. In rats treated with antifibrinolytics (epsilon-aminocaproic acid or Trasylol) fibrin was still present at 30 and 60 min. Interaction of fibrin with Kupffer cells was studied by electron microscopy. At 3, 10, and 20 min after the colloid injection, all fibrin occurred extracellularly, close to the surface of Kupffer cells. At 30 min, all fibrin had disappeared. In rats pretreated with antifibrinolytics, too, all fibrin was found extracellularly at 10, 30, and 60 min. Comparable results were obtained when thrombin was used to induce coagulation. It is concluded that removal of native fibrin from the circulation by Kupffer-cell phagocytosis is unlikely.
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PMID:Rat liver macrophages will not phagocytose fibrin during disseminated intravascular coagulation. 100 4

Two patients diagnosed as having acute promyelocytic leukemia (APL) and disseminated intravascular coagulation (DIC) were closely followed by serial fibrinolysis and coagulation studies from the day of admission until completion of the first course of chemotherapy. One patient was treated with intravenous heparin and Trasylol (Bayer AG, West Germany) and the other received heparin therapy without Trasylol. In Patient 1, hyperfibrinolytic activity, not observed during the administration of Trasylol, developed with its discontinuance. In Patient 2, hyperfibrinolysis was observed coincidentally with a decrease in APL cells due to chemotherapy. These results indicate that hyperfibrinolysis in APL is not associated with DIC.
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PMID:Fibrinolysis in patients with acute promyelocytic leukemia and disseminated intravascular coagulation during heparin therapy. 242 61

Abruptio placentae rarely produces severe maternal complications while the fetus is alive in utero. The advent of fetal death (grade III) indicates a severe form of abruptio placentae and a real risk that an overt coagulopathy might develop (grade IIIB). Overt coagulopathy associated with a live fetus is, however, uncommon. The advent of an overt coagulopathy should be viewed as ominous. Treatment of abruptio placentae with overt coagulopathy should be directed toward obtaining a rapid and atraumatic vaginal delivery. Once delivery has occurred, spontaneous reversal of the coagulopathy can be anticipated. In the opinion of one of the authors (G.S.), the advent of severe consumption coagulopathy and/or uterine inertia is an indication for intravenous therapy with aprotinin. It has been shown that such therapy will limit DIC, reverse fibrinolysis, reawaken uterine activity, and lead to rapid vaginal delivery within 6-8 hours. Aprotinin is not commercially available for clinical use in the United States. Prolongation of the abruption-delivery interval will worsen maternal prognosis. Accordingly, the advent of uterine inertia prior to complete cervical dilatation is an indication for immediate cesarean section in circumstances where aprotinin is not available. Following delivery, the physician should be on the lookout for postpartum hemorrhage, which may necessitate immediate transfusion, the administration of oxytocics, and/or uterine manipulation. Surgical intervention is rarely indicated in such cases. The patient should also be carefully observed over the ensuing days and weeks for the evolution and resolution of complications, such as renal failure, pulmonary insufficiency, and panhypopituitarism.
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PMID:Abruptio placentae with coagulopathy: a rational basis for management. 258 Jun 57

Significantly decreased levels of blood plasma clotting factor XIII (FSF) were found in the blood of 20 patients with acute myeloblastic leukemia as compared to the control values. It was found that after administration of cytostatic drugs (Cerubidyne and Cytosar) FSF deficiency was higher. This effect was associated with a proteolytic activity detectable in plasma which destroys FSF in vitro. This proteolytic activity was neither inhibited by EACA nor by Trasylol. These results indicate that in patients with acute myeloblastic leukemia beside DIC the treatment with cytostatic drugs as well as the presence of proteases from leukemic cells in the plasma will cause an impairment of transformation of soluble fibrin polymer into insoluble desmofibrin.
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PMID:Disturbances of desmofibrinogenesis in pateints suffering from acute myeloblastic leukemia. 615 14

With the aid of an asphyxia model in rabbit fetuses the possibility of diaplacental influence on the hypoxic effects of the fetal organism has been investigated. The trial to change the vasotonia during the asphyctic shock by sympathicomimetic or -lytic drugs (Dilatol, Obsidan, Ergocomb, Regitin) remained to be without any effect on the DIC in the fetal organism. Trying to seal the vascular wall by the high-molecular-weight basic polypeptide Aprotinin there seemed rather to be an increase of the intravascular fibrin sedimentation.
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PMID:[Diaplacental influence on the disseminated intravascular coagulation (DIC) in an asphyxia model. I. Influence on the vasal tonus and on the vasal wall (author's transl)]. 616 51

A patient undergoing subtotal pancreatectomy and intraportal islet tissue autotransplantation for chronic pancreatitis developed severe portal hypertension (49 cm of H(2)O) and acute disseminated intravascular coagulation (DIC). In an attempt to identify the cause of these problems, portal pressure and the activities of the coagulation and fibrinolytic systems were studied in dogs undergoing intraportal autotransplantation of islet tissue. Following intraportal injection of the pancreatic tissue in five control dogs, the portal pressure rose to a maximum of 43.2 cm of H(2)O +/- 2.4 and major coagulation abnormalities occurred. The mean hematocrit value fell to 18% +/- 8.6, the mean platelet count to 218,000 +/- 31,000, the mean plasma fibrinogen to 40 mg/dl +/- 18, and the mean euglobulin clot lysis time (ECLT) to 25 min +/- 4. Partial thromboplastin time (PTT) became prolonged (233 secs +/- 30) and significant quantities of fibrinogen-fibrin degradation products (FDP-fdp) (1:128 +/- 32) appeared. These changes indicate the development of DIC probably secondary to significant amounts of tissue thromboplastin detected in the tissue homogenate infused at time of autotransplantation. In a group of seven dogs in whom heparin and Trasylol (aprotinin) were added to the pancreatic tissue at the time of transplantation, portal pressure rose only to a peak of 28.3 cm of H(2)O +/- 3.6 and no significant abnormalities occurred in mean hematocrit value, plasma fibrinogen, platelet count or ECLT. Minor prolongation of PTT occurred secondary to the activity of heparin. FDP-fdp (1:16) were present transiently during tissue injection. Four patients in whom heparin and Trasylol were added to the pancreatic tissue at the time of autotransplantation developed only minor elevations of portal pressure (mean 15.5 cm of H(2)O) without intravascular coagulopathy.
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PMID:Disseminated intravascular coagulation and portal hypertension following pancreatic islet autotransplantation. 676 51

Leukocytes play an important role in the development of disseminated intravascular coagulation (DIC). In the reperfusion phase of OLT a DIC-like situation has been described and has been held responsible for the high blood loss during this phase. We investigated the role of leukocytes in the pathogenesis of DIC in OLT by measuring the leukocytic mediators released upon activation (cathepsin B, elastase, TNF, neopterin) and the levels of thrombin-antithrombin III (TAT) complexes, seen as markers of prothrombin activation. Arterial blood samples were taken at 10 different time points during and after OLT. Samples were also taken of the perfusate released from the liver graft vein during the flushing procedure before the reperfusion phase. Aprotinin was given as a continuous infusion (0.2-0.4 Mill. KIU/hr) and its plasma levels were determined. Significantly elevated levels of neopterin (15-fold; P < 0.01), cathepsin B (440-fold; P < 0.01) in the perfusate, as compared with the systemic circulation, as well as their significant increases in the early reperfusion phase suggested that they were released by the graft liver. This was paralleled by elevated levels of elastase (1.3-fold, P < 0.05), TNF (1.5-fold, P = NS), and TAT complexes (1.4-fold; P < 0.1) in the perfusate. Significant correlations could be identified between the parameters of leukocyte activation and TAT complexes, whereas no correlation was observed between any of the parameters investigated and the aprotinin levels. Our results strongly indicate a release of leukocytic mediators from the graft liver during its reperfusion which seems to be related to the parallely increased prothrombin activation. No correlation could be seen between levels of aprotinin and levels of leukocytic mediators.
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PMID:Mediators of leukocyte activation play a role in disseminated intravascular coagulation during orthotopic liver transplantation. 750 86

A patient undergoing intracranial surgery developed disseminated intravascular coagulation with life threatening peroperative bleeding. Thromboelastography established the diagnosis of hyperfibrinolysis, usually a fatal complication of a neurosurgical operation. With the administration of a high dose regimen of aprotinin (Trasylol) the haemorrhage was controlled and the hyperfibrinolytic state reversed. Evaluation of blood samples from the jugular bulb suggested that there was a pronounced local release of tissue plasminogen activator into the circulation.
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PMID:Hyperfibrinolysis during intracranial surgery: effect of high dose aprotinin. 752 19


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