Induction of transient immune suppression and Th1/Th2 disbalance by pediatric cardiac surgery with cardiopulmonary bypass

Cardiovascular surgery with cardiopulmonary bypass (CPB) can lead to postoperative complications like postpericardiotomy syndrome (PPS), capillary leak syndrome or multiple organ failure. PPS morbidity in children is up to 30%, mortality up to 4%. For these complications the CPB is made responsible. Their etiology is not yet clarified in detail, but it is thought to be of immunologic origin. The exact knowledge of these reactions is crucial for the selection of treatment strategies and is the issue of this overview. Cardiovascular surgery is accompanied by the release of proinflammatory cytokines (IL-6, IL-8) and the activation of the alternative complement pathway. This reaction is mainly a response to the surgical trauma and the medication. The exclusively CPB-specific response is the elevated activation of the alternative complement pathway. CPB also induces an antiinflammatory response. The immunosuppressive cytokine IL-10 is systemically released before the release of proinflammatory cytokines. Perioperatively T-helper (Th) cells shift transiently to the Th2 phenotype and indicate the prevalence for a humoral immune response. This shift starts immediately after the onset of the CPB. Increased immunosuppression may be involved in PPS development and seems to be linked to an allergic/atopic predisposition. CPB surgery induces population shifts of the leukocyte subsets, changes of their degree of activation and contributes to the peripheral phenotype of immune suppression. During CPB surgery, circulating neutrophils are inactivated and activated cells are selectively depleted by the CPB filters. In children, cardiovascular surgery with CPB induces a systemic antiinflammatory response. The following factors contribute to this response: elimination of activated cells; compensatory reaction to local, systemically not observable, proinflammatory responses; IL-10 release; anesthetics and medication; and leukocyte extravasation. The subsequent proinflammatory reaction is the reaction to surgical trauma and modulates the antiinflammatory reaction. Immune suppression seems to be an important response to CPB and PPS development and may lead to temporary anergy. Possible therapeutic consequences may include treatment strategies that modulate the antiinflammatory response. More studies in neonates and infants are needed to test this hypothesis. Novel microanalytical techniques have to be developed to achieve this goal.