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

Coagulation parameters were initially monitored in 8 patients receiving whole body hyperthermia (WBH). Patients were heated by the warm water blanket technique to 41.8 degrees C (Tmax), maintained at this temperature for 2 hours, then allowed to cool. A fall in platelets was apparent by the time Tmax was achieved and continued during the 18 hours after WBH. Levels of beta-thromboglobulin (BTG) and platelet factor 4 rose by 56% and 191% by the end of treatment but returned to baseline 18 hours later. Fibrinogen, plasminogen and alpha 2-antiplasmin levels declined and FDP and fibrinopeptide A (FPA) levels increased during WBH. Factor XII and Factor VIII:C fell moderately during WBH while Factors VIII R:Ag, VIII:RC and V did not change or showed a late rise. Factor VII levels fell in 7 of 8 patients, reaching levels of 30% of normal in four. To better define the sequence of these coagulations perturbations, earlier and more frequent timepoints were studied in an additional 3 patients. This revealed that decreases in fibrinogen and plasminogen and increases in FPA and BTG occur very early (by the time the patient reaches 39 degrees C). On the other hand, a decrease in Factor VII activity was not apparent until patients had reached Tmax. WBH is therefore associated with a consumption coagulopathy. Possible mechanisms are discussed and extrapolations to the situation seen in heat stroke are suggested.
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PMID:Activation of coagulation during therapeutic whole body hyperthermia. 373 68

Intravenous injection of homologous lung or brain tissue thromboplastin in dogs under general anesthesia induced changes of conventional hemostasis variables consistent with acute DIC (prolongation of prothrombin times, thrombin times, APTT, drop of fibrinogen and a transient reduction of the platelet count). The animals reacted with accelerated respiration and pulse rates. After recovery from anesthesia they resumed their normal activity as before. Fibrinogen reached a minimum within 40 min after the DIC trigger dose had been injected. Dependent on the size of the latter up to 80% of clottable fibrinogen was consumed. No consumption of antithrombin III and heparin cofactor II could be demonstrated by functional assays based on thrombin inhibition by diluted plasma in the presence of heparin or dermatan sulfate. Prothrombin measured amidolytically by an Echis Carinatus venom assay remained practically unchanged. These findings are consistent with free thrombin concentrations in the nanomolar range sufficient to clot fibrinogen rapidly without visibly affecting the up to 1,000 fold higher concentrations of inhibitors and prothrombin. Heparin administered before tissue thromboplastin virtually suppressed the evolution of DIC but its protective effect was overcome by higher trigger doses. Heparin injected after the induction of DIC had no protective effect. The reversible DIC model in dogs may be a promising tool to study activated coagulation in vivo at practically constant inhibitor concentrations. One dog can be used for several acute experiments with homologous tissue thromboplastin, thus the number of animals and their costs may remain within reasonable limits.
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PMID:Heparin-enhanced inhibitors during reversible disseminated intravascular coagulation. 386 25

Subnormal concentrations of alpha 2 Antiplasmin (alpha 2 AP) in liver cirrhosis may be due to an impaired hepatic synthesis and/or to a fibrinolysis activation in disseminated intravascular coagulation (DIC). In order to clarify this problem, in 26 cirrhotic patients (15 compensated and 11 decompensated) alpha 2 AP plasma activity and plasma Fibrinopeptide A (FPA) were measured. Serum albumin, p-Cholinesterase (p-CHE), Fibrinogen and Fibrinogen Degradation Products (FDP) were also carried out. Our data show that alpha 2 AP and FPA were equally abnormal in compensated and decompensated cirrhosis. The significant negative correlation obtained between alpha 2 AP and FPA as well as the lack of correlation between alpha 2 AP and albumin, alpha 2 AP and p-CHE in both groups suggests that, in our patients, alpha 2 AP decrease may be due to a fibrinolysis activation induced by a DIC which appears chronic since Fibrinogen and FDP were normal. These findings are in agreement with the results obtained in the four subgroups a posteriori selected on the basis of FPA levels: alpha 2 AP in subgroups with high FPA was significantly different from controls while it did not differ in subgroups with normal FPA.
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PMID:alpha 2 Antiplasmin and disseminated intravascular coagulation in liver cirrhosis. 397 73

The mechanism of thrombocytopenia in six patients with falciparum malaria has been studied. All the patients recovered after antimalarial therapy, and cerebral malaria was not a feature. Radioactive-labelled platelets and fibrinogen were injected into the patients during the phase of thrombocytopenia. In all cases recovery of injected platelets was notably subnormal, indicating excessive splenic pooling of platelets. Platelet life span was moderately shortened in all patients, and platelet turnover increased approximately two-fold. Fibrinogen catabolism was moderately increased in all patients, but coagulation tests failed to reveal evidence of disseminated intravascular coagulation. The results suggest that in uncomplicated cases of malaria thrombocytopenia is the result of splenic pooling of platelets aggravated by a moderate decrease in platelet life span. In such cases thrombocytopenia is thus not the result of disseminated intravascular coagulation (D.I.C.), and heparin therapy is not indicated unless there is unequivocal ancillary evidence of D.I.C.
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PMID:Mechanisms of thrombocytopenia in malignant tertian malaria. 471 66

Fibrinogen concentrations were determined in normal plasma and in plasma from patients with high and low levels. There was a good correlation between the results of a rapid semi-quantitative fibrinogen titre technique and those of a quantitative assay of coagulable fibrinogen. In normal subjects fibrinogen levels were not significantly influenced by taking blood into epsilon aminocaproic acid (EACA) or by the addition of protamine to plasma. In patients with the defibrination syndrome in whom increased plasma fibrinolysis was not detected, fibrinogen levels were not affected by taking blood into EACA but considerably increased levels were observed after the addition of protamine to plasma. In patients undergoing thrombolytic therapy the fibrinogen levels measured were increased both in blood taken into EACA and in plasma containing protamine. It is suggested that EACA acted by preventing lysis in vitro whilst protamine counteracted abnormal fibrin polymerization. The pattern of results may be of diagnostic importance.
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PMID:A study of two methods for estimating plasma fibrinogen and the effect of epsilon aminocaproic acid and protamine. 557 39

A model was experimentally made with 2 hours serial infusion of thromboplastin (Tp) into rabbits to examine the drug's effect on a hemorrhagic tendency and to elucidate the coagulation and fibrinolytic system in acute DIC encountered in obstetrics, and the system was periodically observed. Groups given the drug, given it during pregnancy, those which bled massively, and those with accelerated fibrinolysis were prepared. The results are as follows. 1) Fibrinogen, PT, APTT, TEG, ELT, AT-III, antiplasmin activity, and platelet count varied markedly from the initiation of Tp injection, and returned to normal following termination. 2) Blood from the heparin dose group showed non-coagulation but decreases in the platelet count and fibrinogen were inhibited. 3) In the aprotinin dose group, serial 2 hour administration induced inhibition of fibrinolysis despite the relatively delayed appearance of anti-fibrinolytic activity. 4) No fibrinolytic effects were seen in anti-plasmin activity or ELT in the tranexamic acid dose group. 5) Lowering of parameters examined was marked in the Tp dose group during pregnancy. 6) The mortality rate up to 6 hours after Tp infusion was 54.5% with solely given, and 10% with group given drug. 7) Death within one hour of Tp infusion in the mass bleeding group, being rated for 50%, was improved to 16.7% by the pre-administration of urokinase.
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PMID:[Treatment of obstetrical disseminated intravascular coagulation--sequential changes of coagulation and fibrinolytic system in DIC rabbits]. 618 25

Fibrinogen degradation, fibrin polymerisation, and the insertion of cross links into fibrin by fibrin stabilising factor lead to the appearance of new antigenic determinants. Antibodies against these antigenic sites may react specifically with the derivatives but not with the parent molecules. We have utilised a monoclonal antibody, which interacts with the cross linked fragment D dimer and related high molecular weight fibrin derivatives, to develop an enzyme immunoassay which measures cross linked fibrin derivatives in plasma and serum using D dimer as standard. Mean concentration in plasma from normal subjects was 75 ng/ml with an upper limit of about 144 ng/ml. Concentrations in patients with pulmonary embolism, deep venous thrombosis, arterial thromboembolism, and disseminated intravascular coagulation were raised in all cases. Confirmation of the specific increase of cross linked fibrin derivatives in patients with disseminated intravascular coagulation was obtained by parallel monitoring of their fibrin degradation products in serum using affinity chromatography and sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis. In many patients the plasma concentrations greatly exceeded the serum values of cross linked fibrin degradation products, suggesting that the procedure can measure fibrin derivatives in plasma which are absent from serum.
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PMID:Measurement of cross linked fibrin derivatives in plasma: an immunoassay using monoclonal antibodies. 620 97

Sequential coagulation tests were carried out in 13 children with acute nonlymphoblastic leukemia (ANLL) treated with the German cooperative protocols BFM 78 and 82. The test program included a PTT, Quick's Prothrombin time, Thrombin time, Fibrinogen (Clauss method and RID), coagulation factors II, V, VII, AT III, antiplasmin, plasminogen and FDP. Severe coagulation changes could be demonstrated in ANLL patients with FAB type M2 (myeloblastic leukemia with maturation) and FAB type M5 (monocytic leukemia). Usually they were found already at the time of diagnosis and improved during induction therapy. A variety of coagulation changes were observed, resembling classical DIC, typical hyperfibrinolysis or atypical proteolysis. It is allowed to question the concept of DIC as the typical coagulation disturbance in children with ANLL.
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PMID:[Blood coagulation changes in children with acute myelogenous leukemia: thrombin effect or proteolysis]. 659 Sep 23

Thrombin clotting times and fibrinogen levels were measured in plasma from patients on chronic coumadin therapy who had prolonged prothrombin times. Thrombin clotting times were usually prolonged. Fibrinogen concentrations were generally elevated, but some were normal or even low. There was no evidence for disseminated intravascular coagulation. Comparison of thrombin clotting times and fibrinogen levels in normal plasma demonstrates that as fibrinogen concentration increases the thrombin clotting time lengthens. A similar correlation was found in many of the patients tested.
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PMID:Thrombin clotting time and fibrinogen concentration in patients treated with coumadin. 661 96

To test the value of diagnostic and therapeutic data in obstetric DIC, 14 women were selected who presented a severe clotless haemorrhage with fibrin degradation products and/or soluble complexes, decreased fibrinogen (0.87 +/- 0.47 g X 1(-1)), platelet count (75.7 +/- 41 X 10(3) X ml-1) and prothrombin complex (33.7 +/- 12%). The hypovolaemia was treated at the same time as heparin was given in a bolus injection of 0.5 mg X kg-1 followed by a constant flow infusion of 1 mg X kg-1 X day-1 in all patients. Relevant obstetrical treatment was performed in 71.4% of patients. Fibrinogen, fresh frozen plasma, prothrombin complex concentrate and platelet concentrate were given if required. One patient, with severe toxaemia, died. Haemorrhage was stopped in 92.8% of patients after 4.5 +/- 0.8 h. Reversible visceral complications occurred in 28% of cases. The initial data used was easily obtained and seemed to give a reliable diagnosis in acute obstetrical DIC. Substitutive treatment was discussed in correlation with the evolution: PCC seemed pointless; the use of fibrinogen must become exceptional when fresh frozen plasma is available. Heparin remained necessary.
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PMID:[Disseminated intravascular coagulation. Retrospective study of 14 acute obstetrical cases]. 665 Sep 31


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