title: The relationship between inflammatory activation and clinical outcome after infant cardiopulmonary bypass.
abstract: BACKGROUND
  Cardiopulmonary bypass (CPB) induces a systemic inflammatory response. The magnitude and consequences in infants remain unclear. We assessed the relationship between inflammatory state and clinical outcomes in infants undergoing CPB.
  
  
  METHODS
  Plasma concentrations of interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor α, IL-1β, and C-reactive protein (CRP) were measured pre-CPB and immediately post-CPB, and at 6, 12, and 24 hours post-CPB in infants ≤9 months old. Perioperative clinical data were collected prospectively.
  
  
  RESULTS
  Diagnoses of 93 patients included transposition of the great arteries (40), tetralogy of Fallot (28), ventricular septal defect (21), truncus arteriosus (2), and complete atrioventricular canal (2). The median age was 37 days (range = 2 to 264). Pre-CPB IL-6 and CRP were higher in younger infants but were not associated with postoperative inflammatory mediator concentrations or measured clinical outcomes. IL-6 increased post-CPB (median 3.2 pg/mL pre-CPB, 24.2 post-CPB, 95.4 at 6 hours, and 90.3 at 24 hours; all P < 0.001). CRP increased post-CPB, peaking at 24 hours (median 27.5 at 24 hours, 0.3 pre-CPB; P < 0.001). IL-10 and IL-8 increased immediately post-CPB. After adjusting for age and diagnosis, postoperative IL-6 and IL-8 correlated with intensive care unit length of stay and postoperative blood product administration and, for IL-8, 24-hour lactate.
  
  
  CONCLUSIONS
  Greater preoperative cytokine and CRP production in younger infants did not correlate with postoperative outcomes; correlation between postoperative inflammatory mediator production and clinical course was statistically significant but clinically modest. We conclude that in infants undergoing low-to-moderate-complexity cardiac surgery in a single high-volume center, the contribution of inflammatory mediator production to postoperative morbidity is relatively limited.
authors.affiliation: Department of Cardiology, Children's Hospital, Boston, MA 02115, USA. catherine.allan@cardio.chboston.org
authors.forename: Catherine K
authors.initials: CK
authors.lastname: Allan
authors.forename: Jane W
authors.initials: JW
authors.lastname: Newburger
authors.forename: Ellen
authors.initials: E
authors.lastname: McGrath
authors.forename: Jodi
authors.initials: J
authors.lastname: Elder
authors.forename: Charles
authors.initials: C
authors.lastname: Psoinos
authors.forename: Peter C
authors.initials: PC
authors.lastname: Laussen
authors.forename: Pedro J
authors.initials: PJ
authors.lastname: del Nido
authors.forename: David
authors.initials: D
authors.lastname: Wypij
authors.forename: Francis X
authors.initials: FX
authors.lastname: McGowan
mesh_terms: D015415:Biomarkers / Q000097:blood; D001900:Boston; D002097:C-Reactive Protein / Q000378:metabolism; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D006330:Heart Defects, Congenital / Q000601:surgery*; D006400:Hematocrit; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007249:Inflammation / Q000276:immunology*; D018836:Inflammation Mediators / Q000097:blood*; D007363:Intensive Care Units, Neonatal; D015278:Intensive Care Units, Pediatric; D016753:Interleukin-10 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D007902:Length of Stay; D016032:Randomized Controlled Trials as Topic; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D065227:Transfusion Reaction; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; C508606:CXCL8 protein, human; C508609:IL10 protein, human; C508600:IL6 protein, human; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D019344:Lactic Acid; D002097:C-Reactive Protein