Expert review of hematology
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Acute hemorrhage is a global healthcare issue, and remains the leading preventable cause of death in trauma. Acute severe hemorrhage can be related to traumatic, peripartum, gastrointestinal, and procedural causes. Hemostatic defects occur early in patients requiring massive transfusion. Early recognition and treatment of hemorrhage and hemostatic defects are required to save lives and to achieve optimal patient outcomes. ⋯ Patients with acute hemorrhage requiring massive transfusion commonly develop coagulopathy due to specific hemostatic defects, and accurate diagnosis and prompt correction are required for definitive hemorrhage control. Damage control resuscitation and massive transfusion protocols are optimal initial treatment strategies, followed by goal-directed individualized resuscitation using real-time coagulation monitoring. Distinct phenotypes exist in trauma-induced coagulopathy, including 'Bleeding' or 'Thrombotic' phenotypes, and hyperfibrinolysis vs. fibrinolysis shutdown. The trauma 'lethal triad' (hypothermia, coagulopathy, acidosis) has been updated to the 'lethal diamond' (including hypocalcemia). A number of controversies in optimal management exist, including whole blood vs. component therapy, use of factor concentrates vs. blood products, optimal use of tranexamic acid, and prehospital plasma and tranexamic acid administration.
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COVID-19 has similarities to the Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS) outbreaks, as severe patients and non-survivors have frequently shown abnormal coagulation profiles. Immune-mediated pathology is a key player in this disease; hence, the role of the complement system needs assessment. The complement system and the coagulation cascade share an intricate network, where multiple mediators maintain a balance between both pathways. Coagulopathy in COVID-19, showing mixed features of complement-mediated and consumption coagulopathy, creates a dilemma in diagnosis and management. ⋯ A tailored anticoagulant regimen, including intensification of standard prophylactic regimens with low-molecular-weight heparin is advisable for COVID-19 patients. Atypical manifestations and varying D-dimer levels seen in different populations bring forth the futility of uniform recommendations for anticoagulant therapy. Further, direct thrombin inhibitors and platelet inhibitors in a patient-specific manner should also be considered.