Hamostaseologie
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Fibrinogen plays an essential role in clot formation and stability. Importantly it seems to be the most vulnerable coagulation factor, reaching critical levels earlier than the others during the course of severe injury. A variety of causes of fibrinogen depletion in major trauma have been identified, such as blood loss, dilution, consumption, hyperfibrinolysis, hypothermia and acidosis. ⋯ Therefore, repeated measurements of plasma fibrinogen concentration are strongly recommended in trauma patients with major bleeding. Recent guidelines recommend maintaining plasma fibrinogen concentration at 1.5-2 g/l in coagulopathic patients. It has been shown that early fibrinogen substitution is associated with improved outcome.
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The plasma circulating zymogenic coagulation factor XIII (FXIII) is a protransglutaminase, which upon activation by thrombin and calcium cross-links preformed fibrin clots/fibrinolytic inhibitors making them mechanically stable and less susceptible to fibrinolysis. The zymogenic plasma FXIII molecule is a heterotetramer composed of two catalytic FXIII-A and two protective FXIII-B subunits. Factor XIII deficiency resulting from inherited or acquired causes can result in pathological bleeding episodes. ⋯ Recently however, with a growing understanding into the pleiotropic roles of FXIII, the fairly frequent milder form of FXIII deficiency caused by heterozygous mutations has become one of the subjects of investigative research. The acquired form of FXIII deficiency is usually caused by generation of autoantibodies or hyperconsumption in other disease states such as disseminated intravascular coagulation. Here, we update the knowledge about the pathophysiology of factor XIII deficiency and its therapeutic options.
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Some cases of thrombotic microangiopathy (TMA) are refractory to plasma exchange therapy (PE) with persistence or recurrence of thrombocytopenia. We report two patients suffering from TMA of different aetiologies (associated with disseminated malignancy, typical haemolytic uraemic syndrome) with recurrent or persistent thrombocytopenia despite adequate therapy including PE. Since both patients were exposed to unfractionated heparin, heparin-induced thrombocytopenia (HIT) was suspected as a cause. ⋯ TMA might represent a predisposition for HIT. This could be due to TMA-related platelet activation with increased PF4 release. In TMA patients exposed to heparin and with refractory or rapidly recurrent thrombocytopenia HIT should always be considered as a possible cause.
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Both, severe haemorrhage and blood transfusion are associated with increased morbidity and mortality. Therefore, it is of particular importance to stop perioperative bleeding as fast and as possible to avoid unnecessary transfusion. Viscoelastic test (ROTEM® or TEG®) allow for early prediction of massive transfusion and goal-directed therapy with specific haemostatic drugs, coagulation factor concentrates, and blood products. ⋯ The Essener Runde task force is a group of clinicians of various specialties (anaesthesiology, intensive care, haemostaseology, haematology, internal medicine, transfusion medicine, surgery) interested in perioperative coagulation management. The ROTEM diagnostic algorithm of the Essener Runde task force was created to standardise and simplify the interpretation of ROTEM® results in perioperative settings and to present their possible implications for therapeutic interventions in severe bleeding. To exemplify, this text mainly focuses on coagulation management in trauma.