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A6637 - Albuterol-Induced Lactic Acidosis, a Diagnosis Not to Be Overlooked
Author Block: A. Madanieh, C. Orabi, I. Acosta-Sanchez, F. Afridi; University of Central Florida College of Medicine, Orlando, FL, United States.
Introduction
Albuterol is a common short acting bronchodilator used in the acute treatment of obstructive lung disease. However, albuterol-induced lactic acidosis is often an overlooked diagnosis amongst patients using excessive amounts of albuterol and therefore recognizing this association is crucial.
Case Presentation
A 53-year-old gentleman with a history significant for mild chronic obstructive pulmonary disease (COPD) presented to the emergency department with complaints of dyspnea, wheezing and a non-productive cough for several weeks. He denied chest pain, fever, chills, or hemoptysis. His history was notable for excessive use of his albuterol inhaler (4-6 times a day) for the last six days and prednisone 40 mg orally twice daily. On examination, the patient was anxious, afebrile, tachypneic, SaO2 of 94% on room air and tachycardic. Lung examination was only remarkable for inspiratory and expiratory wheezing on chest auscultation. Initial lab work was remarkable for a leukocytosis of 14,100/mm3, and findings consistent with a high anion gap metabolic acidosis on arterial blood gas and basic metabolic profile. Lactic acid was noted to be elevated at 3.75 mmol/L (normal: 0.5-1 mmol/L). Further lab work including liver function tests, β-hydroxybutyric acid, LDH, TSH, urinalysis and toxic drug screen were unremarkable. Chest x-ray showed only hyperinflation. CT of the abdomen was negative for any evidence of acute intra-abdominal abnormality. In the absence of significant signs suggesting infection, malignancy, trauma, tissue hypoxia or hypoperfusion, albuterol was suspected as the culprit of the patient’s unexplained lactic acidosis in the setting of his acute COPD exacerbation. Albuterol inhalers were therefore discontinued and the patient was placed on non-invasive ventilation and ipratropium bronchodilators. Lactic acid levels decreased back to normal (0.96 mmol/L) within the following 48 hours.
Discussion
Lactic acidosis (LA) caused by albuterol is a type B LA in which there is an increased lactate production or decreased lactate removal without evidence of hypoxia. Albuterol as a cause of lactic acidosis remains a diagnosis of exclusion. The underlying mechanism remains not fully understood, but has been reported to be related to enhanced cyclic adenosine monophosphate (cAMP) mediated glycogenolysis, gluconeogenesis and lipolysis due to excessive activation of the beta-adrenergic receptors, leading to increased plasma concentration of glucose, which is converted to lactate via glycolysis. Recognition of albuterol-induced LA by healthcare providers can help prevent excessive and often unnecessary diagnostic interventions, antibiotic use, and imaging studies. Management involves discontinuation of β-agonist therapy and using alternative bronchodilators such as antimuscarinic bronchodilators.