Seminars in thrombosis and hemostasis
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Semin. Thromb. Hemost. · Feb 2015
ReviewHemostasis and thrombosis in continuous renal replacement treatment.
During continuous renal replacement therapy, the delicate equilibrium of hemostasis is disturbed. Owing to a complex interaction of critical illness, uremia, use of an extracorporeal circuit and anticoagulation, patients exhibit both hypercoagulability and an increased risk of bleeding. Contact of blood with foreign material initiates coagulation by triggering the contact activation coagulation pathway, the tissue factor-factor VIIa pathway and activation of platelets and monocytes, which adhere to the membrane. ⋯ Its interference with anticoagulation is therefore unreliable during critical illness. Citrate provides regional anticoagulation and increases biocompatibility. It is better tolerated than heparin and confers less bleeding, less transfusion, and longer circuit life.
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Hemostasis and thrombosis in trauma patients consist of physiological hemostasis for wound healing and the pathological reaction of disseminated intravascular coagulation (DIC). Whole body trauma, isolated brain injury, and fat embolism syndrome, if extremely severe, can cause DIC and affect a patient's prognosis. Shock-induced hyperfibrinolysis causes DIC with the fibrinolytic phenotype, contributing to oozing-type severe bleeding. ⋯ Another type of pathological hemostatic change is acute coagulopathy of trauma shock (ACOTS), which gives rise to activated protein C-mediated systemic hypocoagulation, resulting in bleeding. ACOTS occurs only in trauma associated with shock-induced hypoperfusion and there is nothing to suggest DIC in this phenomenon. This review will provide information about the recent advances in hemostasis and thrombosis in trauma and will clarify the pathogeneses of the pathological processes observed in trauma patients.
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Semin. Thromb. Hemost. · Feb 2015
ReviewHeparin-induced thrombocytopenia in critically ill patients.
Many critically ill patients receive heparin, either before intensive care unit (ICU) admission (e.g., postcardiac surgery), for prophylaxis/treatment of thrombosis, for hemodialysis/filtration, or even incidentally (e.g., flushing of intravascular catheters), and are therefore at risk for developing immune heparin-induced thrombocytopenia (HIT), a prothrombotic drug reaction caused by platelet-activating antiplatelet factor 4 (PF4)/heparin antibodies. However, HIT explains at most 1 in 100 thrombocytopenic ICU patients (HIT frequency 0.3-0.5% vs. 30-50% background frequency of ICU-associated thrombocytopenia), and most patients who form anti-PF4/heparin antibodies do not develop HIT; hence, HIT overdiagnosis often occurs. This review discusses HIT-related issues relevant to ICU patients, including how to (1) distinguish HIT both clinically and serologically from non-HIT-related thrombocytopenia; (2) recognize HIT-mimicking disorders, such as the acute disseminated intravascular coagulation (DIC)/liver necrosis-limb necrosis syndrome; (3) prevent HIT in the ICU through use of low-molecular-weight heparin; and (4) treat HIT, including awareness of "PTT confounding" when anticoagulating patients with DIC.
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In the majority of patients with severe sepsis, systemic activation of coagulation is present. Increasing evidence points to an extensive cross-talk between coagulation and inflammation that may play an important role in the pathogenesis of sepsis. Inflammation not only leads to activation of coagulation, but coagulation also considerably affects inflammatory activity. ⋯ The cornerstone of the management of coagulation in sepsis is the specific and vigorous treatment of the underlying disorder. Strategies aimed at the inhibition of coagulation activation may theoretically be justified and have been found beneficial in experimental and initial clinical studies. Heparin may be an effective anticoagulant approach and alternative strategies comprise restoration of physiological anticoagulant pathways.
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The antiphospholipid syndrome (APS) is characterized by venous or arterial thrombosis and/or pregnancy morbidity in patients with persistent presence of antiphospholipid antibodies (aPL). Patients who are diagnosed with APS are identified to have a high risk of recurrent thrombosis, which can occur despite anticoagulant therapy. ⋯ Recognizing that patients with APS may potentially have different thrombotic risk profiles may assist clinicians in assessing the risks, benefits, and optimal duration of anticoagulation. Future studies that delineate thrombotic risk in APS and evaluate current and novel anticoagulants as well as nonanticoagulant therapies are required.