• R A Hayes, K Shekar, and J F Fraser.
• Critical Care Research Group, The Prince Charles Hospital and The University of Queensland, Brisbane, Queensland, Australia 4032. rylan.hayes@bigpond.com
• Perfusion. 2013 May 1; 28 (3): 184-93.

AbstractExtracorporeal membrane oxygenation (ECMO) facilitates organ support in patients with refractory cardiorespiratory failure whilst disease-modifying treatments can be administered. Improvements to the ECMO process have resulted in its increased utilisation. However, iatrogenic injuries remain, with bleeding and thrombosis the most significant concerns. Many factors contribute to the formation of thrombi, with the hyperoxaemia experienced during ECMO a potential contributor. Outside of ECMO, emerging evidence associates hyperoxaemia with increased mortality. Currently, no universal definition of hyperoxaemia exists, a gap in clinical standards that may impact patient outcomes. Hyperoxaemia has the potential to induce platelet activation, aggregation and, subsequently, thrombosis through markedly increasing the production of reactive oxygen species. There are minimal data in the current literature that explore the relationship between ECMO-induced hyperoxaemia and the production of reactive oxygen species - a putative link towards pathology. Furthermore, there is limited research directly linking hyperoxaemia and platelet activation. These are areas that warrant investigation as definitive data regarding the nascence of these pathological processes may delineate and define the relative risk of supranormal oxygen tension. These data could then assist in defining optimal oxygenation practice, reducing the risks associated with extracorporeal support.

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