J Extra Corpor Technol (The journal of extra-corporeal technology)
Although the systemic inflammatory response is recognized to contribute to patient morbidity and mortality after cardiopulmonary bypass, specific mechanisms linking cause and effect--linking a specific mediator with a defined adverse outcome--are lacking. The problem is partly because of the rarity of hard endpoints (stroke, myocardial injury, renal failure requiring dialysis), which studies are not always powered to measure, and partly one of definition; "systemic inflammatory response" wrongly suggests that the problem is confined to inflammation, whereas, in fact, it is characterized by systemic disturbances to a number of the body's natural defenses against injury and infection: fibrinolysis, coagulation, complement activation, immune cell activation, and oxidative stress in addition to inflammation. A better definition would be to think in terms of a "systemic host response" to surgery. End-organ injury results from the interplay of activated host defense systems with regional vessel wall injury, either because of physical trauma to the vein graft or ischemia/ reperfusion injury to susceptible vascular beds. Improved patient outcomes are going to take a concerted team effort to achieve, from the point of atraumatic vein harvest, to improved biocompatibility and shear resistance of circuits, monitoring, and minimizing of ischemia to organs, minimal cross-clamping trauma, optimized blood management, and combinatorial drug strategies. Surrogate endpoints for major organ dysfunction will play an important role to make sense of multiple interventions by the cardiac surgical team and to monitor continuous improvement to patient outcomes.
St. Paul, Minn., American Society of Extra-Corporeal Technology.