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Propranolol Does Not Increase Inflammation, Sepsis, or Infectious Episodes in Severely Burned Children

Jeschke, Marc G. MD, PhD; Norbury, William B. MD; Finnerty, Celeste C. PhD; Branski, Ludwik K. MD; Herndon, David N. MD

Journal of Trauma-Injury Infection & Critical Care: March 2007 - Volume 62 - Issue 3 - pp 676-681
doi: 10.1097/TA.0b013e318031afd3
Original Articles

Background: Propranolol, a nonselective β1–2 antagonist, attenuates hypermetabolism and catabolism in severely burned patients. However, recent data suggest that propranolol impairs immune function and enhances inflammation. The purpose of the present study was to determine the effect of propranolol administration on infection, sepsis, and inflammation in severely burned pediatric patients.

Patients: A prospective, intent-to-treat study was performed; patient demographics (age, gender, burn size, and mortality); infectious episodes (colony count greater then 105); and sepsis (guidelines by the society of critical care medicine) were determined. Hypermetabolic response was determined by resting energy expenditure (REE), and the inflammatory response was determined by measuring serum cytokine expression.

Results: Two hundred forty-five patients (143 controls, 102 propranolol) were included into the study. There were no differences between the control and propranolol groups for age, gender distribution, burn size, third degree burn, and length of stay. Mortality was 6% in the control group and 5% in the propranolol group. Propranolol significantly decreased REE and predicted REE during acute hospital stay. Forty-three patients developed infections in the control group (30%), whereas 21 developed infections in the propranolol group (21%). The incidence of sepsis was 10% for controls and 7% for propranolol. Analysis of the cytokine expression profile in 20 patients in each group revealed that propranolol significantly decreased serum tumor necrosis factor and interleukin-1β compared with controls (p < 0.05).

Conclusion: Propranolol treatment attenuates hypermetabolism and does not cause increased incidence of infection and sepsis.

© 2007 Lippincott Williams & Wilkins, Inc.