Inflammatory and Tissue Injury Responses to Cardiopulmonary Bypass in Children. Chew et al. (page 745)
To assess inflammatory response and resulting tissue injury after pediatric cardiopulmonary bypass (CPB), Chew et al. collected blood samples up to 48 h postoperatively from 13 children aged less than 12 months who were scheduled to undergo surgery with CPB for the repair of various congenital heart defects. Anesthesia was induced with halothane or ketamine and maintained with fentanyl and pancuronium. Furosemide (1 mg/kg) and methylprednisolone (30 mg/kg) were added to the pump prime. Dopamine or dobutamine was administered to all children from the beginning of rewarming. Modified ultrafiltration was performed after cessation of CPB. Average clamp and CPB times were 47.2 ± 26.9 and 93.8 ± 35.5 min, respectively.
At baseline and regular intervals thereafter until 48 h after surgery, blood samples were obtained. Concentration cytokines (interleukin [IL]-6, IL-1β, IL-1ra, tumor necrosis factor α), neutrophil elastase, complement split products (C3d, C4d), and coagulation system activation and tissue injury markers were measured later.
The authors noticed a clear-cut but widely variable cytokine response. Proinflammatory cytokine concentrations (IL-1β, tumor necrosis factor α, IL-6) were increased at baseline, but only IL-6 increased further, and then only after surgery. In contrast, antiinflammatory cytokines (IL-10, IL-1α) increased markedly. CPB activated the coagulation system, and a late release of C-reactive protein also was noted. Indicators of tissue injury, such as creatine kinase and lactate dehydrogenase concentrations, increased early during the perioperative period; lactate dehydrogenase did not return to baseline values even at 48 h postoperatively. Modified ultrafiltration had little impact on cytokine concentrations.
Although this work is entirely descriptive, it shows that neonates and infants can mount a cytokine response to CPB and surgery. However, the response was complex, suggesting some imbalances between inflammatory and antiinflammatory compounds. Further work will be needed to link these observations with clinical outcome or other markers of tissue injury. The balance of proinflammatory and antiinflammatory response may be key in determining the extent of tissue injury as well as clinical outcome, the investigators note.