Venous thromboembolism is considered one of the most preventable causes of in-hospital death. Venovenous extracorporeal membrane oxygenation (VV ECMO) utilization for severe respiratory failure has increased in the decade following the 2009 influenza A H1N1 pandemic and the publication of the CESAR trial.¹ The interaction between a patient’s blood and the ECMO circuit produces an inflammatory response that can provoke both thrombotic and bleeding complications. In a systematic review of patients with H1N1 treated with VV ECMO published in 2013, the incidence of cannula-associated deep venous thrombosis (CaDVT) was estimated to be as low as 10 percent; however, more recent data suggests the incidence of venous thrombosis after decannulation is much higher. Additionally, a significant proportion of CaDVT are distal thrombi located in the vena cava, which would be missed with a traditional ultrasound diagnostic approach after decannulation from VV ECMO.