A CASE OF LIFE-THREATENING LACTIC-ACIDOSIS AFTER SMOKE-INHALATION - INTERFERENCE BETWEEN BETA-ADRENERGIE AGENTS AND ETHANOL

A 49-year-old male developed bronchospasm and severe lactic acidosis a fter exposition to fire smoke. The correction of lactic acidosis follo wing beta-adrenergic agents withdrawal, and the transitory increase in lactate after salbutamol reintroduction are consistent with hypersens itivity to salbutamol. However, the plasma lactate concentration (32.6 mmol/l) that we observed 9.5 h after admission is far above those cur rently seen after administration of beta-adrenergic agents. We searche d for causes able to potentiate the adverse effects of these drugs and we noticed that our patient had a high plasma ethanol level (2.4 g/l) . Alcohol metabolism in the liver results in generation of high NADH/N AD(+) ratios, thus reducing lactate liver clearance. This observation suggests that plasma lactate levels should be monitored closely in alc oholic patients treated with beta-mimetic agents.