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A unique coagulopathy often manifests following traumatic brain injury, leading the clinician down a difficult decision path on appropriate prophylaxis and therapy. Conventional coagulation assays—such as prothrombin time, partial thromboplastin time, and international normalized ratio—have historically been utilized to assess hemostasis and guide treatment following traumatic brain injury. However, these plasma-based assays alone often lack the sensitivity to diagnose and adequately treat coagulopathy associated with traumatic brain injury. Here, we review the whole blood coagulation assays termed viscoelastic tests and their use in traumatic brain injury. Modified viscoelastic tests with platelet function assays have helped elucidate the underlying pathophysiology and guide clinical decisions in a goal-directed fashion. Platelet dysfunction appears to underlie most coagulopathies in this patient population, particularly at the adenosine diphosphate and/or arachidonic acid receptors. Future research will focus not only on the utility of viscoelastic tests in diagnosing coagulopathy in traumatic brain injury, but also on better defining the use of these tests as evidence-based and/or precision-based tools to improve patient outcomes.

Background: The treatment of COVID-19 patients with heparin is not always effective in preventing thrombotic complications, but can also be associated with bleeding complications, suggesting a balanced approach to anticoagulation is needed. A prior pilot study supported that thromboelastography and conventional coagulation tests could predict hemorrhage in COVID-19 in patients treated with unfractionated heparin or enoxaparin, but did not evaluate the risk of thrombosis. Methods: This single-center, retrospective study included 79 severely ill COVID-19 patients anticoagulated with intermediate or therapeutic dose unfractionated heparin. Two stepwise logistic regression models were performed with bleeding or thrombosis as the dependent variable, and thromboelastography parameters and conventional coagulation tests as the independent variables. Results: Among all 79 patients, 12 (15.2%) had bleeding events, and 20 (25.3%) had thrombosis. Multivariate logistic regression analysis identified a prediction model for bleeding (adjusted R2 = 0.787, p &lt, 0.001) comprised of increased reaction time (p = 0.016), decreased fibrinogen (p = 0.006), decreased D-dimer (p = 0.063), and increased activated partial thromboplastin time (p = 0.084). Multivariate analysis of thrombosis identified a weak prediction model (adjusted R2 = 0.348, p &lt, 0.001) comprised of increased D-dimer (p &lt, 0.001), decreased reaction time (p = 0.002), increased maximum amplitude (p &lt, 0.001), and decreased alpha angle (p = 0.014). Adjunctive thromboelastography decreased the use of packed red cells (p = 0.031) and fresh frozen plasma (p &lt, 0.001). Conclusions: Significantly, this study demonstrates the need for a precision-based titration strategy of anticoagulation for hospitalized COVID-19 patients. Since severely ill COVID-19 patients may switch between thrombotic or hemorrhagic phenotypes or express both simultaneously, institutions may reduce these complications by developing their own titration strategy using daily conventional coagulation tests with adjunctive thromboelastography.

Septic pulmonary emboli rarely cause respiratory failure that requires mechanical ventilation. The most common causes of septic pulmonary emboli are related to intravenous drug abuse, indwelling intravenous catheters, endocarditis and septic pelvic thrombophlebitis. In addition, soft tissue injury-related thrombophlebitis rarely causes septic pulmonary emboli. We describe a unique case of a 43-year-old man who developed septic thrombophlebitis of the femoral vein following soft tissue injury from trauma to the shin with ensuing septic pulmonary emboli which necessitated endotracheal intubation and mechanical ventilation. The patient required mechanical ventilation for eleven days, developed empyema and grew out methicillin-resistant Staphylococcus aureus on blood cultures. A transesophageal echocardiogram was normal, and there was no indication of bacterial endocarditis. In addition to eleven days of mechanical ventilation, the patient was treated with intravenous heparin, cefepime and clindamycin. These medications were then discontinued and the patient was treated with weight-adjusted vancomycin. Following the return of cultures, the patient was treated for six weeks with ceftaroline 600 mg IV twice a day. In addition, the patient received bilateral thoracentesis followed by chest tube drainage until resolution of the pleural effusions. The patient made a complete recovery. We describe this case and the implications for differential diagnosis and treatment of these two uncommon conditions.