A case of life-threatening lactic acidosis after smoke inhalation - interference between beta-adrenergic agents and ethanol?
Autor: | A. Fréminet, P. Taboulet, J. L. Clemessy, F.J. Baud |
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Rok vydání: | 1995 |
Předmět: |
Male
Smoke inhalation Pharmacology Critical Care and Intensive Care Medicine chemistry.chemical_compound Theophylline Intensive care medicine Humans Albuterol Ethanol metabolism Bronchial Spasm business.industry Metabolic acidosis Drug Synergism Adrenergic beta-Agonists Middle Aged Smoke Inhalation Injury medicine.disease Lactic acid Bronchodilator Agents Alcoholism chemistry Anesthesia Lactic acidosis Salbutamol Acidosis Lactic business Severe lactic acidosis Alcoholic Intoxication medicine.drug |
Zdroj: | Intensive care medicine. 21(12) |
ISSN: | 0342-4642 |
Popis: | 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. |
Databáze: | OpenAIRE |
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