ABSTRACT
Contact with synthetic polymer and metal surfaces of blood-contacting equipment (pumpoxygenators, dialyzers, ventricular assist devices, vascular prostheses, etc.) activates host defenses, including the coagulation and inflammatory pathways, and the fibrinolytic cascade [1]. In largesurface contact situations, especially with cardiopulmonary bypass (CPB) equipment, the end result of these reactions includes reduced platelet function and survival and increased postperfusion bleeding times [2]. The resulting organ dysfunction may be viewed as a direct complication of CPB. The generalized inflammatory response is multifactorial and includes activation of complement, the initiation of fibrinolytic, kallikrein, kinin, and coagulation cascades within the body. It also includes the activation of platelets and neutrophils. The activation of platelets may render them less effective for hemostasis, leading to postoperative bleeding problems. The activation of neutrophils may lead to sequestration of neutrophils within the pulmonary vasculature, contributing to postoperative complications, including capillary leak syndrome and microvascular lung injury.
