• J J Sistino and J R Acsell.
• Program in Extracorporeal Circulation Technology, Medical University of South Carolina, Charleston 29401-5797, USA.
• J Extra Corpor Technol. 1999 Mar 1; 31 (1): 37-43.

AbstractA complication of emergency resuscitation is the development of the Systemic Inflammatory Response Syndrome (SIRS). In the past, this has been identified as multiple organ failure, with symptoms similar to sepsis. The hallmark of this syndrome is peripheral vasodilation, which is associated with a breakdown of capillary membranes and the accumulation of excess interstitial fluid. This case report discusses the development of SIRS in a patient following emergency cardiopulmonary bypass (CPB). The patient was a 53 year old male with significant left main coronary artery disease who developed sudden bradycardia and hypotension in the operating room and was emergently placed on cardiopulmonary bypass. During CPB, the patient was peripherally vasodilated, and required continuous alpha-adrenergic support to maintain normal systemic vascular resistance. In addition, metabolic acidosis was present despite high flow rates, high hematocrit, addition of colloids, and hemoconcentration. Despite excellent neurological and myocardial recovery following surgery, the patient died one week later in renal and hepatic failure. Several mechanisms for the development of this syndrome have been hypothesized. One of these theories is that the ischemic injury in the gastrointestinal tract disturbs the gut barrier function and allows enteric bacterial endotoxins to pass into the circulation producing sepsis-like symptoms. Other theories relate to the release patterns of cytokines associated with CPB. These mechanisms and the treatment of SIRS with new pharmacological agents and perfusion techniques are reviewed.

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