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

An assay technic for measuring heparin cofactor activity in which antithrombin activity can be assessed without plasma attenuation even in the presence of therapeutic levels of heparin is presented. Heparin-activated anti-thrombin activity was markedly depressed in plasmas of four patients with disseminated intravascular coagulation and in ten patients with cirrhosis. Residual activity in those plasmas appeared qualitatively normal, and no inhibitor (platelet factor IV activity) was observed. Plasmas from patients with disseminated intravascular coagulation and cirrhosis required more heparin to obtain in vitro clotting time prolongation equivalent to normal.
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PMID:Minimal heparin cofactor activity in disseminated intravascular coagulation and cirrhosis. 6 Aug 79

Bleeding is common in acute myeloblastic leukemia (AML). At the time of diagnosis, the danger of bleeding cannot be predicted by laboratory means. However, the following factors represent increased risks: Promyeloblastic leukemia, high blast count, low fibrinogen, low plasminogen. From coagulation studies performed at the time of bleeding complications, the pathomechanism leading to bleeding complications usually cannot be detected. The question whether impairment of production, consumption coagulopathy, or primary fibrinolysis causes the bleeding complications can only be answered by controlling frequently clinical and hemostatic criteria, which include the thrombocytic stystem as well as plasmatic coagulation and fibrinolysis. At the present time, the therapy of bleeding complications in AML is symptomatic. It consists of transfusion with thrombocytes or fresh whole blood, respectively. Coagulation factor concentrates should only be given in combination with Heparin to prevent the deterioration of consumption coagulopathy.
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PMID:[Bleeding complications in acute myeloblastic leukemia (author's transl)]. 28 49

In a prospective, randomized study 35 patients with multiple injuries were examined for early changes of blood coagulation. Parameters suggesting a consumption coagulopathy were lower in patients who died subsequently than in survivors. No therapeutic influence of low dose Heparin therapy or of the proteinase inhibiting substance TrasylolR could be demonstrated.
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PMID:[Early changes of the coagulation system in multiple injuries and their modification with heparin and Trasylol]. 37 36

Anticoagulants in the form of heparin, dipyridimole, steroids, prostaglandin E1, Macrodex, and antithrombin III were administered in separate experiments prior to endotoxin infusion in the dog. The pattern of disseminated intravascular coagulation (DIC) developed consistently when endotoxin alone was administered. Heparin dosages from 1 to 10 mg/kg did not influence the appearance of thrombocytopenia but effectively eliminated the decrease in fibrinogen levels ordinarily found. Antithrombin III (AT III), obtained from the National Red Cross, administered in a dose designed to provide a doubling of the circulating AT III, reduced the fibrinogen utilization to a similar degree as heparin without affecting the platelet loss. Dipyridimole, as administered, was ineffective in this model, and did not alter the development of thrombocytopenia or the hypofibrinogenemia. Steroids, Macrodex, and prostaglandin E1 had minimal effect on the coagulopathy. Our finding would suggest that the endotoxin effect on dog platelets id direct, and not mediated by thrombin, and that the role of heparin in the clinical management of DIC should be considered only in instances in which renal complications exist.
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PMID:Endotoxin-induced intravascular coagulation (DIC) and its therapy. 40 May 81

Clinical studies in the treatment of 54 children suffering from DHF with a combination of dipyridamole and ASA as an adjuvant of our standard therapy consisted of fluid, electrolytes, blood, plasma and plasma expanders were evaluated. Heparin was administered in cases of DIC. It appeared that dipyridamole and ASA did not change the mortality significantly, but it prevented the progress of the severity of the disease from grade I and II to grade III and IV.
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PMID:Dipyridamole in the treatment of dengue haemorrhagic fever. 51 1

The correlation between disseminated intravascular coagulation (DIC) and pulmonary insufficiency following trauma and shock was studied in patients. Serial coagulation tests were performed on nine patients suffering from adult respiratory distress syndrome (ARDS), and six of nine showed the evidence of consumption coagulopathy. Heparin infusion was effective in two patients with the improvement of platelet counts, other coagulation factors and the concomitant improvement of lung function.
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PMID:Disseminated intravascular coagulation in the pathogenesis of adult respiratory distress syndrome: 1. Clinical study. 60 92

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

A case of histiocytic medullary reticulosis in a 45-year-old man is described. The presentation with a swinging pyrexia is typical. Associated features were very low levels of all immunoglobulins and proved disseminated intravascular coagulation. Heparin therapy was given and the difficulties of controlling such treatment are demonstrated. It is concluded that an increased awareness of the condition as a cause of pyrexia might lead to an improvement in prognosis.
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PMID:Histiocytic medullary reticulosis with hypogammaglobulinaemia and disseminated intravascular coagulation. 87 15

Platelets contain heparin neutralizing activity, which is released into plasma following aggregation. This material is probably identical to platelet factor 4. We describe a technic to measure heparin neutralizing activity in platelet-poor plasma based on the serial heparin dilution technic of Harada and Zucker. Heparin neutralizing activity was depressed in thrombocytopenia due to immune thrombocytopenia and bone marrow depression, and elevated in thrombocytopenia due to disseminated intravascular coagulation. Secondary thrombocytosis is characterized by markedly elevated heparin neutralizing activity, while thrombocytosis associated with myeloproliferative disorders has normal heparin neutralizing activity.
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PMID:Plasma heparin neutralizing activity. Its use in the evaluation of thrombocytopenia and thrombocytosis. 94 87

The coagulation and fibrinolytic systems play a key role in maintaining the integrity and patency of the vascular compartment. Pregnancy induces extensive physiological changes in these systems, thus creating an enhanced capacity to produce fibrin and a diminished ability to remove it. Fibrin deposition localized to the uteroplacental circulation is a feature of normal pregnancy. In women with fatal eclampsia, disseminated intravascular coagulation with fibrin deposition in the renal glomeruli is well documented. The condition of preeclampsia is not well defined. Nonetheless, evidence of intravascular coagulation, as shown by elevated levels of fibrin degradation products and reduced platelet counts, has been found in many women with preeclampsia. Serial studies showed that thrombin generation, as indicated by the ratio of factor VIII-related antigen to factor VIII coagulant activity, is considerably in excess of that which occurs in normal pregnancy, and its appearance coincides with the development of the clinical features of preeclampsia. Heparin therapy has bot been proven of value in established preeclampsia, but this fact does not disprove that role that intravascular coagulation may play in the pathogenesis of the disease. A controlled trial ina high-risk group of low-dose he;arin and an antiplatelet agent from the 16th to the 18th weeks of pregnancy onwards is required to elucidate the role of intravascular coagulation in preeclapmsia and its effect on the fetus.
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PMID:The role of coagulation and fibrinolysis in preeclampsia. 100 56


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