We report four patients with pandemic H1N1 2009 influenza virus and secondary bacterial infection who were treated with extracorporeal membrane oxygenation (ECMO) for cardiorespiratory failure. Three of the four patients had profound shock, necessitating support with venoarterial ECMO. Two patients died during ECMO support. The two survivors had prolonged hospital stays, which were complicated by renal failure and limb ischaemia.

Background: TSP2 and Akt1 exert opposite effects on tissue repair. Results: Akt1 KO mice display defects in fibroblast morphology and adhesion due to diminished Rac activation, which is a result of increased TSP2 expression. Loss of TSP2 rescues these defects. Conclusion: TSP2 contributes to compromised tissue repair in Akt1 KO mice. Significance: These data support a novel, NO-independent TSP2 regulatory mechanism in fibroblasts.

The novel severe acute respiratory syndrome coronavirus 2, SARS-CoV-2 (coronavirus Disease 19 (COVID-19)) was identified as the causative agent of viral pneumonias in Wuhan, China in December 2019, and has emerged as a pandemic causing acute respiratory distress syndrome (ARDS) and multiple organ dysfunction. Interim guidance by the World Health Organization states that extracorporeal membrane oxygenation (ECMO) should be considered as a rescue therapy in COVID-19-related ARDS. International registries tracking ECMO in COVID-19 patients reveal a 21%–70% incidence of acute renal injury requiring renal replacement therapy (RRT) during ECMO support. The indications for initiating RRT in patients on ECMO are similar to those for patients not requiring ECMO. RRT can be administered during ECMO via a temporary dialysis catheter, placement of a circuit in-line hemofilter, or direct connection of continuous RRT in-line with the ECMO circuit. Here we review methods for RRT during ECMO, RRT initiation and timing during ECMO, anticoagulation strategies, and novel cytokine filtration approaches to minimize COVID-19’s pathophysiological impact.

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