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

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Abstract

A 49-year-old male developed bronchospasm and severe lactic acidosis after exposition to fire smoke. The correction of lactic acidosis following β-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 β-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 β-mimetic agents.

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Correspondence to P. Taboulet.

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Taboulet, P., Clemessy, J.-., Fréminet, A. et al. A case of life-threatening lactic acidosis after smoke inhalation — interference between β-adrenergic agents and ethanol?. Intensive Care Med 21, 1039–1042 (1995). https://doi.org/10.1007/BF01700670

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Key words

  • Smoke inhalation
  • Bronchospasm
  • Lactic acidosis
  • Salbutamol
  • Theophylline