Abstract
Multiple factors affect how a patient responds to extracorporeal life support (ECLS) including the patient’s age, size, underlying problem, clinical condition, genetic differences and clinical progress. To better understand this highly variable response, we must separate what is happening in the patient versus the ECLS circuit. Pre-ECLS risk factors, including disseminated intravascular coagulation and recent surgery, increase the risk of platelet loss and bleeding during ECLS. Exposure of blood to artificial surfaces in the circuit activates the contact system which in turn activates coagulation. High shear in the cannula, tubing and pumps, along with coagulation activation, damages and activates platelets, red cells, endothelial cells and leukocytes. Platelets and red cells are lost during ECLS through bleeding, phlebotomy, activation, hemolysis, sub-lethal injury induced extravascular clearance, and other causes. Activation of coagulation and platelets leads to circuit thrombus formation. Clinically important circuit thrombi include arterial tubing thrombi associated with arterial embolism, oxygenator surface membrane thrombosis resulting in oxygenator failure/circuit replacement and venous pump emboli leading to severe hemolysis. The variability in response means some patients require almost continuous transfusion support while others receive almost no transfusions. This review summarizes what is known and what research is needed to improve ECLS.