RETOUR

HYPERBARIC OXYGEN THERAPY IN THE TREATMENT OF BURNS:
EVALUATION OF SYSTEMIC LIPID PEROXIDATION AND
ACTIVATION OF OXYGEN-RADICAL DEPENDENT INFLAMMATORY REACTIONS

P.Germonpré (1), I. Van Renterghem (1), P.Reper (2), L.Duinslaeger (2), A.Vanderkelen (2)
(1) Center for Hyperbaric Oxygen Therapy, Military Hospital Brussels
(2) Burn Center, Military Hospital Brussels

Introduction

In a previous study, we demonstrated the ability of Hyperbaric Oxygen Therapy (HBOT) to prevent at least partially the deepening of an experimental burn during the first days after injury. However, most of the distant complications of major burns seem to be related to the generation of Oxygen Free Radicals (OFR). Therefore, before proceeding to a clinical human study, we wanted to evaluate the possible toxic effects of HBOT in a more extensive burn injury.

Methods

A double-blind prospective study was undertaken. Male Wistar rats were subjected to a 40% TBSA thermal burn or sham burn by submersion, and were resuscitated with intraperitoneal Hartmann solution. After randomisation, half of the burned animals received one HBOT session (60 minutes, 2 ATA) starting 30 minutes after the burn. The animals were sacrificed at 30 minutes (sham burn and control burn groups), 120, 240 or 360 minutes (all groups). Lipid peroxidation products were measured by means of an optimised fluorometric measurement of Malondialdehyde (MDA). Systemic inflammation was evaluated using standard Complement Hemolytic Activity (CH50) and Tumor Necrosis Factor alpha (TNFa).

Results

There was a significant difference in the mortality rate at time points 240 and 360: 28% in the control burn group vs. 11% and 7% in the sham burn groups and HBOT groups respectively. The serum MDA content in the HBOT treated rats was similar to that of the sham burned rats, at all time points, whereas the control burn rats showed a moderate but significant rise at time points 120 and 240 (p<0.05). The HBOT group showed normal CH50 values at all time points, whereas the control burn group showed a stimulation of complement activation and production (but not depletion), reflected by a rise in CH50 (p<0.05). There was a small and statistically non-significant rise in serum TNFa content (p>0.05).

Conclusions

Early HBOT seems to diminish the generation of lipid peroxidation products after a 40% TBSA experimental burn. It seems moreover to have a positive effect on complement activation, and no significant influence on TNFa production. We conclude that, in this model, HBOT seems a safe therapeutic procedure.

(Supported by a grant from the Brussels Capital Region Energy Department)