The Coagulopathy Bleeding in Disseminated Intravascular Coagulation. Therapy by Heparin and Treatment Plasmapheresis

Apply

The Coagulopathy Bleeding in Disseminated Intravascular Coagulation. Therapy by Heparin and Treatment Plasmapheresis

Journal Title: Lviv Clinical Bulletin - Year 2015, Vol 4, Issue 12

Abstract

Introduction. The passing of some obstetric complications, intravascular haemolysis and destructive traumas are complicated by the syndrome of disseminated intravascular coagulation (DIC). DIC is caused by presence of thromboplastin (T) in the blood flow – pieces of cytoplasmic membranes or substances that are extracted from membranes. T causes formation of trombin, plasmin, kallikrein by activation of XII factor of heamocoagulation system. The activation of these enzymes disturbs the haemostasis system. It is known, that beginning of DIC is the phase of hypercoagulation with formation of disseminated microthrombosis. It activates the processes of fibrinolysis. The blood loses the ability to coagulate, and it is the phase of hypo-coagulation. As a result, haemorrhage, hypotension, thrombocytopenia appears. Aim. To investigate the dependence of clinical manifestations of DIC on the degree of dispersion of infused thromboplastin, as well as the effectiveness of its treatment with heparin and plasmapheresis. Materials and methods. It is ascertained that hyper-, hypocoagulation in case of DIC depends on the grade of dispersion of thromboplastin, which enters in bloodstream. It is proved, that pieces of cytoplasm membranes were shrouded by fibrin and platelet during 15-20 seconds after infusion. Fibrin-monomer and platelets adhere to the surface of pieces of cytoplasm membranes, which are recognized as ″alien″ and montage fibrin polymer. As a result, there is a formation of blood microthrombuses. The surface aria of the extractive substances T wasn`t sufficient for such montage and plasmin lyses free molecules of fibrin-monomer to degradation products (DP). DP has the anticoagulation properties and cause hypocoagulation and bleeding. Bradykinin, synthesized under kallikrein, causes hypotonia. Heparin, given bolus intravenousny in dose 300-350 U/kg of body mass, inhibited the activity of trombin, plasmin, kallikrein, DP, bradykinin. Results and discussion. It was found out that the manifestations of hyper-, hypocoagulation in case of DIC depended on the degree of dispersion of T. The microtubes arose due to sticking to the “other” surface of the cubes with the fibrin-monomer (FM) and platelets. The surface area of the extracted substances T was insufficient to stick to the FM molecules, and plasmin lysed them to degradation products (PDP). As anticoagulants, PDP caused hypocoagulation, bleeding. Bradykinin, formed by the action of calicreatin, predisposes hypotension. Heparin, injected intravenously bolus dose of 300-350 OD / kg of body weight, inhibited the activity of thrombin, plasmin, calicreatin, PDP, bradykinin. The blood flow T was removed by plasmapheresis. Conclusions. Heparin infusion stopped lysis of platelets, bleeding, normalized the blood pressure in clinical cases. The symptoms of DIC completely disappeared, clinical status of patients returned to normality.

Authors and Affiliations

M. Kurgan, D. Kurgan, V. Novak

Keywords

The Role of Tumor Necrosis Factor and ITS Soluble Receptors in Myelosuppression Developing in B-Cell Chronic Lymphocytic Leukemia

Introduction. Myelosuppression with severe anemia or thrombocytopenia refers to the adverse factors in clinical course of B-cell chronic lymphocytic leukemia (B-CLL). According to the existing data, in B-CLL patients (pt...

EP ID EP255008
DOI 10.25040/lkv2015.04.034
Views 126
Downloads 0