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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 results of this paper indicate that cattle infected with B. bovis (argentina) have a markedly altered and activated coagulation system. A degree of thrombin activation occurs due partly to release of thromboplastin-like substances from lysed erythrocytes but due primarily to activation of kallikrein by babesial proteases. This produces a hyperfibrinogenaemia, particularly in intact cattle, with soluble fibrin complexes constituting up to one-third of the total fibrinogen concentration. High molecular weight non-coagulable fibrinogen-like proteins are detected terminally but more so in splenectomized cattle. Plasminogen concentration decreases in splenectomized but not intact cattle while low molecular weight fibrinogen degradation products are not easily detected. It is suggested that a hypercoagulable intermediate state with little or no fibrin deposition occurs rather than terminal disseminated intravascular coagulation.
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PMID:Babesia bovis (argentina): observations of coagulation parameters, fibrinogen catabolism and fibrinolysis in intact and splenectomized cattle. 60 70

Forty-five patients with multiple injuries treated at an intensive care unit were studied prospectively. The patients were divided into two groups: the severely injured (no mortality) and critically injured (56% mortality). Treatment was started within two hours from the accident in all cases. The following coagulation parameters were measured for eight days: euglobulin lysis time (ELT), thromboelastography (TEG), vecalcification time (RECA), partial thromboplastin time (PTT), factor V, factor VIII, Normotest, Thrombotest, thrombin time, fibrinogen and platelets. Severe coagulation disorders were observed in one-third of the patients 12-48 hours after trauma. The abnormalities were more pronounced in patients who had sustained very severe injuries and arrived in a state of shock. The ELT was shortened 0-6 hours after the accident and accelerated coagulation was indicated simultaneously by decreased PTT, RECA, and r-values as well as by elevated Thrombotest and factor VIII values. The factor V and fibrinogen levels were initially lowered. Low platelet values at 2-4 days, prolonged thrombin and r-times, secondary decrease of fibrinogen FV, FVIII, and low Thrombotest values suggested disseminated intravascular coagulation associated with complications, such as fat embolism and "shock lung" syndromes. General bleeding tendency with high mortality was observed in 16% of the patients.
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PMID:Coagulation disorders in severely and critically injured patients. 60 16

Autoprothrombin II-A anticoagulant was isolated from bovine prothrombin. Purified prothrombin was applied to DEAE-cellulose chromatography after incubation with thrombin. Four protein peaks were obtained where the third peak corresponded to the anti-coagulant effect. The fractions under the third peak were pooled together and the anticoagulant effect was evaluated with different methods. From 25,470 +/- 2,800 U of prothrombin, 5,800 +/- 1,400 U of inhibitor were obtained. The inhibitor was found to be most effective at pH 7.2--7.8. In vitro, the inhibitor inhibited the thrombin time and the plasma clotting time highly significantly but had no effect on euglobulin lysis time and fibrin plates. In vivo, when injected into rabbits, the inhibitor effect was also significant on the same tests. The autoprothombin II-A anticoagulant had a protective effect on DIC formation with rabbit brain thromboplastin administration. This protective effect was found to be statistically significant.
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PMID:Some properties of autoprothrombin II-A anticoagulant. 61 78

Thrombogenicity of the factor IX concentrate and its clinical use for stoppage of the bleeding in the case of hemophilia A with inhibitor were reported. (1) Factor IX concentrate contained the coagulation factors as prothrombin complex (factors II, VII, IX and X); Thrombin and factor Xa. (2) Prothrombin in the factor IX concentrate could be converted to thrombin without any additional procoagulant such as thromboplastin or factor V, but in just 2.5M glycine solution by the effect of factor Xa. (3) The infusion of factor IX concentrate into a rabbit induced DIC promptly which was proved by autopsy and coagulation-fibrinolytic studies. (4) Factor IX concentrate showed a great efficacy in stopping the bleeding in the case of hemophilia A with inhibitor.
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PMID:Characteristics and thrombogenicity of factor IX concentrate. 61 88

This is an investigation into thromboplastin time, partial thromboplastin time, plasma thrombin time, fibrinogen, and platelets in 30 patients with severe brain injury over 7--14 days. Platelets showed a very marked initial decrease and a slow return to normal around the seventh day. Fibrinogen was initially lowered in most of the cases, and raised from the second day onward. Changes in the other laboratory values were less definite. Latent signs of consumption coagulopathy were not accompanied by bleeding disorders, or by disseminated intravascular coagulation at autopsy. The severity of laboratory value changes clearly correlated with the extent of brain damage, and was significantly higher when the patient did not survive the first week after injury.
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PMID:Disturbances of the coagulatory system in patients with severe cerebral trauma. I. 70 71

Nine patients with severe classic hemophilia and inhibitors against factor VIII were treated for 156 bleeding episodes with 503 infusions of Proplex, Konyne, or Auto-Factor IX, three preparations of prothrombin complex concentrates (PCCs). Approximately two thirds of the bleeding episodes were managed successfully. Although the prothrombin time (PT) and partial thromboplastin time (PTT) were shortened after most PCC infusions, there was no evidence of disseminated intravascular coagulation. The degree of shortening of PT or PTT was not related to the particular PCC preparation used, dose, or cessation of hemorrhage. All PCC preparations contained activated clotting factors, as manifested by their ability to shorten the PTT of normal plasma, factor-VIII-deficient plasma, and factor-IX-deficient plasma. Shortening, which was greater with Auto-Factor IX than with the other products, was inhibited partially by a factor IX antibody and blocked completely by prolonged incubation with plasma. Although the nature of the procoagulant material in PCCs is uncertain, these products are of proven benefit to hemophilic patients with high-titer inhibitors. Side effects have been minimal and inhibitor titers have not risen.
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PMID:Use of prothrombin complex concentrates in hemophiliacs with inhibitors: clinical and laboratory studies. 72 19

We have reviewed 53 cases of disseminated intravascular coagulation (DIC) in the newborn, including 29 cases that were confirmed at autopsy. Factors predisposing to DIC included maternal complications (60%), low Apgar scores (30%), hyaline membrane disease (62%), and sepsis (26%). Diagnostic criteria common to autopsy-proved cases included presence of fibrin degradation products, low factor V activity, a prolonged prothrombin time, and a prolonged partial thromboplastin time and/or thrombocytopenia. There appeared to be no difference in coagulation response or in mortality among patients treated with different therapeutic regimens. Survivors were older gestationally, had higher birth weights, and higher Apgar scores.
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PMID:Disseminated intravascular coagulation in the newborn. 76 May 11

Gram-negative septicemia and metastatic prostatic cancer are frequent causes of disseminated intravascular coagulation. The clinical manifestations of this condition as well as the laboratory data vary considerably, depending on the patient's compensatory mechanisms in relation to the magnitude and duration of the thromboplastin or endotoxin release. Treatment centers primarily on correcting the underlying disorder. Secondly, deficient clotting factors and platelets should be replaced in the appropriate patient. Heparinization is often unnecessary. The use of drugs that inhibit the protective fibrinolytic mechanism is contraindicated in disseminated intravascular coagulation.
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PMID:Disseminated intravascular coagulation in the urologic patient. 77 99

The possible association between acute respiratory failure and disseminated intravascular coagulation was examined in eight patients with severe acute respiratory failure--a condition characterized by tachypnea, right to left intrapulmonary shunting of blood greater than 30 per cent of cardiac output, increased pulmonary artery pressure with low or normal pulmonary artery wedge pressure and roentgenologic interstitial pulmonary edema. Treatment consisted of mechanical ventilation with positive end expiratory pressure sufficient to minimize intrapulmonary shunting. There was no abnormality in platelet concentration fibrin split product concentration, fibrinogen concentration, prothrombin time or activated partial thromboplastin time during the period of most severe respiratory failure in any patient. However, mean platelet concentration fell to 90,000+/-9,000 per cubic millimeter, less than 0.001, and mean fibrin split product levels rose to 60+/-10 micrograms per milliliter, p less than 0.05, the fourth day after the onset of acute respiratory failure. No significant change occurred in other coagulation parameters. Disseminated intravascular coagulation developed in none of the patients nor was there any correlation between coagulation abnormalities and severity of acute respiratory failure that would suggest a cause and effect relationship.
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PMID:Acute respiratory failure and intravascular coagulation. 78 44

Levels of serum fibrin degradation products (FDP) were determined in patients with acute nephritis, chronic nephritis, lupus nephritis and toxemia of pregnancy by the passive hemagglutination inhibition test. Serum FDP levels were less than 10 mug/ml in normal control adults, averaging 3.2 +/- 1.2 mug/ml. The incidence of serum FDP positive patients (more than 10 mug/ml) in those with acute nephritis, chronic nephritis, lupus nephritis and toxemia of pregnancy was 28%, 73%, 100% and 100%, respectively. Their serum FDP levels averaged 8.4 +/- 5.6 mug/ml, 16.0 +/- 5.9 mug/ml, 21.4 +/- 7.6 mug/ml and 35 mug/ml, respectively. Plasma fibrinogen levels, prothrombin time, partial thromboplastin time, euglobulin lysis time and platelet counts were within normal limits in serum FDP positive patients with renal diseases, indicating that there was no severe disseminated intravascular coagulation. All FDP positive patients with renal diseases of immunological origin demonstrated the deposition of fibrin within glomeruli with complement and immunoglobulin deposits. However, FDP positive patients with toxemia of pregnancy demonstrated fibrin depositions within glomeruli without complement and immunoglobulin deposits. FDP D fragments of urine from lupus nephritis patients showed no changes in immunoelectrophoretic patterns by heat treatment, indicating that urine FDP was derived from secondary fibrinolysis.
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PMID:Fibrin degradation products in renal diseases. 78 95


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