• K Chaulier, S Chalumeau, C-E Ber, M Bret, and T Rimmelé.
• Département d'anesthésie-réanimation, pavillon P réanimation, hôpital Edouard-Herriot, 5, place d'Arsonval, 69003 Lyon, France. kevinchaulier@yahoo.fr
• Ann Fr Anesth Reanim. 2007 Apr 1;26(4):352-5.

AbstractIn a context of asthma, lactic acidosis may occur during beta2-agonist therapy. Several cases have been reported during its administration by intravenous and/or inhaled route. This side-effect seems rather unknown and the mechanism for compensation of metabolic acidosis by hyperventilation may worsen dyspnoea and mislead clinicians. Other causes of lactic acidosis such as a major hypoxemia, a cardiovascular collapse or sepsis may also be experienced in this context and must be ruled out before attributing the lactic acidosis to beta2-agonist treatment. We report the case of a 50-year-old man hospitalized for an acute major asthma, who received a salbutamol continuous infusion associated with inhaled terbutaline. A serum lactate level of 13 mmol/l was noted eight hours after the introduction of the bronchodilator treatment. After reducing doses of beta2-agonists, the evolution was favourable, regarding both respiratory and metabolic aspects, with a rapid decrease of the serum lactate level, which finally returned to normal level after 32 hours of hospitalization.

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