Albuterol, Acidosis, and Aneurysms
Furthermore, the patient harbored an enlarged thoracic aortic aneurysm and remained hypertensive above the goal of BP 130/80 mm Hg for patients with thoracoabdominal aneurysms.9 Lactic acidosis in the context of hemodynamic instability for this patient might have indicated tissue hypoperfusion secondary to a ruptured aneurysm or aortic dissection. Fortunately, the patient did not manifest any signs or symptoms suggestive of a ruptured aortic aneurysm. Last, on discontinuing the nebulizer therapy, the patient’s hyperlactatemia resolved within 24 hours, highly indicative of albuterol-induced lactic acidosis as the proper diagnosis.
As a β-agonist, albuterol stimulates β-adrenergic receptors, which increases lipolysis and glycolysis. The biochemical reactions increase the product pyruvate, which is used in both aerobic and anaerobic metabolisms. With an increase in pyruvate, capacity for aerobic metabolism is maximized with increased shunting toward anaerobic metabolism, leading to elevated lactate levels and lactic acidosis.8,10,11
Regardless, albuterol-induced lactic acidosis is a diagnosis of exclusion.6 It is thus prudent to rule out life-threatening etiologies of hyperlactatemia, given the association with increased morbidity and mortality. This case illustrates the importance of ruling out life-threatening etiologies of hyperlactatemia and lactic acidosis in an older patient with multiple comorbidities. This case also recognizes the acute AEs of hyperlactatemia and lactic acidosis secondary to scheduled albuterol nebulization therapy in acutely ill patients. Of note, patients presenting with an acute medical illness may be more susceptible to hyperlactatemia secondary to scheduled albuterol nebulization therapy.
Conclusions
We encourage heightened clinical suspicion of albuterol-induced lactic acidosis in acutely ill patients with COPD on albuterol therapy on rule out of life-threatening etiologies and
