• A Tárnok and P Schneider.
• Pediatric Cardiology, Cardiac Center Leipzig, University of Leipzig, Germany.
• Shock. 2001 Jan 1;16 Suppl 1:24-32.

AbstractCardiovascular surgery with cardiopulmonary bypass (CPB) can lead to postoperative complications like postpericardiotomy syndrome (PPS), capillary leak syndrome, or multiple organ failure. In children, PPS morbidity is up to 30%, and intra- and immediate postoperative mortality is up to 4%. For these complications, the CPB is made responsible. Its etiology is not yet clarified in detail, but is thought to be of immunologic origin. The exact knowledge of these reactions is crucial for the selection of treatment strategies. The immune response to CPB surgery in children comprises of a cascade of pro- and anti-inflammatory events. Proinflammatory responses are indicated by the release of interleukin (IL)-6 and IL-8, and the activation of alternative complement pathway. This reaction is mainly a response to surgical trauma and medication and only activation of the alternative complement pathway is CPB specific. Antiinflammatory response during CPB surgery is serologically indicated by the systemic release of the immunosuppressive cytokine IL-10 already before that of proinflammatory cytokines. CPB surgery induces population shifts of the leukocyte subsets, changes their degree of activation, and contributes to the phenotype of a peripheral immune suppression. Circulating neutrophils are selectively filtered and inactivated. T-helper (Th) cells shift transiently to the Th2 phenotype, indicating the prevalence for a humoral immune response. These alterations start immediately after the onset of the CPB. Increased immunosuppression may be involved in PPS development and may be linked to an allergic/atopic predisposition. A generalized model of the immune sequela to pediatric cardiovascular surgery with CPB is drawn. CPB induces a systemic transient anti-inflammatory response by elimination of activated cells, by compensatory reaction to local, systemically not observable, proinflammatory responses, by IL-10 release, by anesthetics and medication, and by leukocyte extravasation. The subsequent proinflammatory reaction is the reaction to surgical trauma modulating the anti-inflammatory reaction. Possible therapeutic consequences of these findings may include treatment strategies that modulate the anti-inflammatory response. More studies are needed to test this hypothesis.

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