Bioincompatibility of the extracorporeal circuit is a trigger-factor for the systemic inflammatory response in patients undergoing on-pump CABG. Blood contact with synthetic surfaces leads to activation of complement, neutrophils and subsequent cytokine expression. Corticosteroids were recommended to inhibit the activation of inflammation and reduce the reperfusion injuries. The present study aims to document the effect of prophylactic dexamethasone on myocardial, renal, intestinal, and hepatic injury associated with CPB.
20 patients scheduled for first-time CABG were prospectively, double-blind randomized in two groups receiving either dexamethasone (1mg/kg before anesthesia induction and 0.5mg/kg after 8 hours) or placebo. Inflammatory reaction was documented with plasma interleukins IL6,IL8,IL10. Organ-damage was assessed by measuring specific markers: troponinI (cTnI..myocardial damage), urine N-acetyl-β-D-glucosaminidase (NAG..kidney damage), urine intestinal-type fatty acid binding protein (IFABP..intestinal damage), plasma á-glutathione S-transferase (alphaGST..liver damage).
Significant lower values of IL6,8 and higher IL10 were measured as main effect of dexamethasone (Mann-Whitney p<0.001). cTnI peaked at 6h post-Ao declamping with significant higher concentrations in placebo-group (Mann-Whitney p=0.009).There was no main effect for dexamethasone on overall plasma cTnI concentration. Urine NAG peaked at 2hICU with no main effect for dexamethasone on overall urine NAG concentration (F=0.297,p=0.592) Urine IFABP: maximum difference with the base line was reached at 2hICU(Wilcoxon p<0.001);There was no main effect for dexamethasone (F=0.262,p=0.615). Significant independent predictors for IFABP and NAG at 2hICU were serum glucose at end-CPB (IFABP:R2=0.31,Sig.=0.015; NAG:R2=0.33,Sig.=0.008 ) and pump-perfusion time(IFABP:R2=0.23,Sig.=0.031; NAG:R2=0.25,Sig.=0.02). Plasma alpha-GST- peaked at end-CPB with no significant difference between groups at any time-point.
Transient, subclinical myocardial, renal, intestinal and hepatic injury was detectable even following uncomplicated CPB in low-risk patients.Prophylactic dexamethasone, even if active in inhibiting the inflammatory response, seemed to be ineffective in preventing abdominal organ-damage. Patients receiving dexamethasone had lower myocardial damage 6h post-Aorta declamping, as showed by significant lower plasma cTnI concentrations.
Therapeutic value of dexamethasone is evident postoperatively for the myocardium and it is of no importance in preventing ischemia/reperfusion injuries in kidneys, intestine and liver.
A.M. Morariu, None.