Despite improvements in anticoagulation monitoring, the majority of complications in extracorporeal membrane oxygenation (ECMO) continue to involve patient bleeding and circuit clotting.
The technology leading to the development of ECMO grew out of the experience with cardiopulmonary bypass, and unfractionated heparin (UNFH) has long been the anticoagulant of choice for both of these methods of support. Heparin was first used clinically in 1937 for the prevention of pulmonary embolisms in post-operative and postpartum patients.  UNFH continues to be widely used, widely available, and relatively inexpensive. As an intravenous infusion, it has a relatively short half-life, and it can be easily reversed with protamine.
Most of the anticoagulant effect of UNFH is due to its binding with antithrombin. The UNFH-antithrombin complex is approximately 1000-fold more effective than antithrombin alone.  The remaining anticoagulant effect comes from the increased release of tissue factor pathway inhibitor (TFPI) with UNFH administration.  As the effect of UNFH is largely dependent on antithrombin, it is difficult to achieve therapeutic anticoagulation with UNFH in patients with congenital or acquired antithrombin deficiency. Antithrombin can be replaced with commercially available concentrate or with fresh frozen plasma (FFP). However, antithrombin concentrate is very costly, and replacement of antithrombin with FFP exposes the patient to a large volume of blood product replacement. One milliliter of FFP contains approximately one unit of antithrombin.  Studies on the use of antithrombin concentrates for patients on ECMO have failed to demonstrate meaningful improvement in clinical outcomes. [5,6]
Another complication of UNFH is the potential of heparin-induced thrombocytopenia (HIT). The incidence of HIT is 0.9 to 4.9% in adult patients treated with heparin  and carries a mortality of 17% to 30%.  HIT is less commonly seen in pediatric patients. 
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