Hemostatic abnormalities after trauma resuscitation: challenges and strategies in caring for the critically injured patient.

Severe polytrauma and hemorrhage is a common and life-threatening condition often leading to intensive care unit admission for those who survive their initial injury. The injury itself, hypoperfusion from hemorrhagic shock, and resuscitative efforts introduce a complex set of hemostatic derangements collectively referred to as trauma-induced coagulopathy (TIC). Although the trauma population is notoriously heterogenous, TIC can generally be divided into an "early" hypocoagulable phase and then a "late" hypercoagulable, prothrombotic phase. Existing literature on TIC focuses heavily on reversing and preventing hypocoagulation in the early, acute phase. However, intensivists commonly manage patients throughout the later post-acute resuscitation phase of TIC, during which thrombotic complications are common and may lead to major morbidity and mortality. Derangements in platelet activation, endothelial dysfunction, suppression of fibrinolysis, and crosstalk between the innate immune and coagulation systems all contribute to the prothrombotic late TIC phenotype. Deep venous thrombosis and other macrovascular thrombotic complications also commonly occur after trauma. Thrombosis prophylaxis and treatment present a challenge for patients still at high risk for bleeding. An in-depth understanding of risk factors specific to trauma patients, including iatrogenic contributions from resuscitation and hemostatic efforts in the pre-intensive care phase, can help stratify thromboembolic risk and optimize prophylaxis and surveillance efforts. We stress the importance of an individualized approach to assessment of hemorrhagic and thrombotic risks for each patient. Here, we summarize the underlying contributors to the prothrombotic phenotype in late TIC, including a description of emerging roles for HMGB1, extracellular vesicles, and endogenous inhibitors. Additionally, a general approach to thromboprophylaxis, monitoring, and anticoagulation in this patient population are discussed. Finally, we summarize relevant risk stratification systems and guidelines for clinical management of thromboembolic risk among trauma patients, and highlight limitations in these systems and guidelines as areas for future research.