Hamostaseologie
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The severe impairment of the microcirculation plays a substantial role in the pathogenesis of severe sepsis and septic shock, and leads to multiple organ failure and death. Therapeutic strategies to resuscitate the microcirculatory blood flow and to improve the functional capillar density are therefore essential to surmount the microcirculatory pathology and to avoid tissue hypoxia. ⋯ Dobutamine is the first choice to improve cardiac output and to overcome myocardial depression in septic shock whereas phosphodiesterase-III-inhibitors and levosimendane are still experimental options. Furthermore selective inhibitors of iNOS, nitroglycerol, as well as vasopressin have to be investigated relating to their specific effects on the microcirculation and their influence on survival in seevere sepsis and septic shock.
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When no fresh frozen plasma is available, acute major blood loss is compensated above all with crystalloids, colloids and red blood cell concentrates, meaning that all plasma clotting factors are diluted. Consumption coagulopathy is almost always accompanied by dilutional coagulopathy. Formulas for calculating critical blood loss and standard coagulation tests are often not helpful in the case of massive transfusion. ⋯ If this is not available in sufficient quantity or within a reasonable time, coagulation factor concentrates must be used. Neither fresh frozen plasma therapy nor treatment with coagulation factor concentrates has been the subject of detailed clinical study. Further studies are needed to work out guidelines for coagulation management in the case of massive blood loss.
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Guidelines of official societies for diagnosis and therapy of intraoperatively occurring hypocoagulability rely mainly on data of patients receiving whole blood transfusions. They recommend--provided that laboratory evaluation shows deficiency (values>1.5 fold normal)--administration of fresh frozen plasma, cryoprecipitate and platelet concentrates (platelet count<50,000 or <100,000/microl). This article describes the pathogenesis of coagulopathy in the light of the special intraoperative setting, emphasizes recent changes of blood component preparation, transfusion triggers, effects of volume therapy and challenges standard laboratory assays as reliable guide for intraoperative hemostatic therapy. The role of thrombelastographic monitoring is discussed as well as an alternative strategy to compensate deficiencies by the use of coagulation factor concentrates instead of or in addition to transfusion of FFP, a new concept which is illustrated by the presentation of an actual case report.
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Thrombelastometry/-graphy provides information about clot strength and stability. Modified thrombelastometry/-graphy improved standardisation and diagnostic information using this system. Heparinase modified thrombelastometry/-graphy allows estimation of heparin. ⋯ Glanzmann. The correlation between coagulation time in thrombelastometry/-graphy (CT/r-value) to conventional coagulation may be low because of different activators used. The introduction of rotationthrombelastometry (ROTEM) provides a stable system suitable for bedside-monitoring.
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In trauma associated coagulopathy, the initial treatment consists of hypothermia and acidosis have to be treated aggressively. Already in in the emergency room, fibrinogen deficiency can be detected frequently, in addition, colloids interfere with fibrin polymerisation. Under these aspects, the early administration of fibrinogen seems to be justified. ⋯ The potential of using haemostatic agents like antifibrinolytics and DDAVP for this indication is only supported by few studies, although in individual cases it may be very helpful. The administration of recombinant FVIIa could not achieve sustainable amelioration of the outcome of trauma patients in a randomised controlled trial. Raising inhibitors of coagulation (antithrombin) simultaneously to antihaemorragic therapy is being discussed, but seems not reasonable in the acute phase of a life-threatening haemorrage.