Asthma is one of the most prevalent chronic respiratory diseases, characterized by bronchial hyper-responsiveness and intermittent airflow obstruction. Short-acting β2 agonists (SABA) remain the cornerstone of acute asthma management due to its properties in smooth muscle relaxation and bronchodilatation. Rarely, these drugs might be associated with adverse effects, including the development of metabolic and hydro-electrolytic imbalances. We report a case of lactic acidosis secondary to β2 agonists in a young female patient admitted with severe acute asthma. After initial management and significant improvement of the respiratory distress with nebulized and subcutaneous salbutamol, the patient developed high anion gap metabolic acidosis due to hyperlactacidemia and hypokalemia. Alternative causes of lactic acidosis were discarded, such as severe hypoxemia, systemic hypoperfusion, sepsis, and organ dysfunction, and SABA-related lactic acidosis was suspected. This treatment was halted, and tachypnea, metabolic acidosis, and lactate levels rapidly resolved. The remainder of the hospital stay was uneventful, and the patient was discharged after a period of five days. Although rare, the development of unexplained lactic acidosis in a SABA-treated patient should alert the treating physician to this β2 agonist side-effect.
Keywords: asthma; hyperlactacidemia; intensive care; lactic acidosis; short-acting beta-2 agonists.
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