A case of life-threatening lactic acidosis after smoke inhalation - interference between beta-adrenergic agents and ethanol?

Intensive Care Med. 1995 Dec;21(12):1039-41. doi: 10.1007/BF01700670.

Abstract

A 49-year-old male developed bronchospasm and severe lactic acidosis after exposition to fire smoke. The correction of lactic acidosis following beta-adrenergic agents withdrawal, and the transitory increase in lactate after salbutamol reintroduction are consistent with hypersensitivity to salbutamol. However, the plasma lactate concentration (32.6 mmol/l) that we observed 9.5 h after admission is far above those currently seen after administration of beta-adrenergic agents. We searched 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/NAD+ ratios, thus reducing lactate liver clearance. This observation suggests that plasma lactate levels should be monitored closely in alcoholic patients treated with beta-mimetic agents.

Publication types

  • Case Reports

MeSH terms

  • Acidosis, Lactic / blood
  • Acidosis, Lactic / chemically induced*
  • Adrenergic beta-Agonists / adverse effects*
  • Albuterol / adverse effects*
  • Alcoholic Intoxication / blood
  • Alcoholic Intoxication / complications*
  • Alcoholism / blood
  • Alcoholism / complications
  • Bronchial Spasm / drug therapy*
  • Bronchial Spasm / etiology
  • Bronchodilator Agents / pharmacology
  • Drug Synergism
  • Humans
  • Male
  • Middle Aged
  • Smoke Inhalation Injury / complications*
  • Smoke Inhalation Injury / therapy
  • Theophylline / pharmacology

Substances

  • Adrenergic beta-Agonists
  • Bronchodilator Agents
  • Theophylline
  • Albuterol