Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19) that manifests with variable severity. 1 A subset of symptomatic individuals develop proinflammatory or prothrombotic profiles requiring additional testing and interventions. [2][3][4][5] It is unclear which COVID-19 patients will ultimately develop severe disease that would have benefitted from early and aggressive interventions.A 63-year-old man was admitted with rapidly progressive COVID-19 pneumonia with hypoxia. Given the patient's worsening clinical status, laboratory coagulation analysis, including viscoelastic testing by rotational thromboelastometry (ROTEM delta, Instrumentation Laboratory Co., Bedford, MA), was performed immediately upon hospital admission. He subsequently developed acute respiratory distress syndrome and shock that required mechanical ventilation and vasopressor support.Routine coagulation testing demonstrated a prothrombin time (PT) of 12.2 seconds (normal 9.4-15.4 seconds), a partial thromboplastin time (PTT) of 30 seconds (normal 26-38 seconds), and D-dimers of 2143 ng/mL fibrinogen equivalent units (FEU; normal <600 ng/mL FEU), the last associated with severe COVID-19. 6 Viscoelastic testing demonstrated a hypercoagulable profile (see Fig. 1). 7 In particular, there was elevated maximum clot firmness observed on EXTEM (78 mm), INTEM Fig 1 Viscoelastic testing tracings from an intensive care unit patient with severe COVID-19. (A) EXTEM tracing; (B) INTEM tracing; (C) FIBTEM tracing; (D) APTEM tracing.