Protein S-100, inflammatory and haemostatic mediators in paediatric open heart surgery. Influence of clinical variables and a biocompatible cardiopulmonary bypass system

Abstract

Cardiopulmonary bypass (CPB) is used in most operations when correcting congenital heart malformations. Postoperative neurological problems (temporary or permanent) are complications of the procedure. These neurological injuries, especially if they are minor, are difficult to recognise in small children. CPB gives rise to activation of the inflammatory response. This response can, in extreme cases, result in hypotension, fever, coagulopathies, oedema, tissue injury and organ failure. Protein S-100 , a possible biochemical marker for neurological injury measurable in blood, was studied in paediatric general surgery patients and patients operated on for congenital heart malformations. Markers indicating activation of the inflammatory response: complement factors, pro-inflammatory cytokines, PMN elastase and factors from the coagulation and fibrinolytic systems were described. Relations between measured variables and clinical variables were tested. The possibility of influencing the response in activation of inflammation and haemostasis when using a biocompatible perfusion system compared with a conventional system was investigated. All children who participated in the studies were below three years of age. Young children unlike adults have age dependent (inverted correlation) measurable concentrations of S-100 in blood before operation. Both heart surgery and general surgery increase S-100 during surgery which cast doubt on the neuro-specificity of the marker in connection with surgery. Open heart surgery with CPB leads to activation of the complement system and the release of PMN elastase and pro-inflammatory cytokines. Pre-and peroperative clinical variables are related to the inflammatory response, which is related to the postoperative course. The use of a biocompatible perfusion system as compared with a conventional perfusion system reduces complement activation and measurable levels of PMN elastse, but does not influence activation of pro-inflammatory cytokines. It also leads to less activation of fibrinolysis during CPB.