Case Presentation: Here we present a case of a 63 year old female with a past medical history of COPD on 5L home oxygen and BiPAP with eight exacerbations in the past year who presented with shortness of breath and was admitted for acute hypoxic respiratory failure secondary to COPD exacerbation. When initially evaluated by EMS, she was saturating in the thirties and immediately placed on continuous BiPAP. Upon arrival to the emergency room (ER), she remained short of breath and was treated with ipratropium-albuterol nebulizers. Her hypoxia improved with continuous BiPAP usage and she stabilized on her home oxygen level. She was afebrile, with a negative infectious workup. Initial lactic acid was 5.9, consistent with her prior hypoxic presentations but later rose to 11.5, prompting immediate re-evaluation. Despite this, she was found to be breathing comfortably on 5L nasal cannula in no acute distress. The patient initially received a fluid bolus, which was stopped after thorough patient examination revealed no signs of hypoperfusion. Further review showed the patient had received several ipratropium-albuterol nebulizers, including three within 20 minutes totaling 12.5mg of albuterol. This made type B lactic acidosis more likely given the rising lactate level despite respiratory improvement. Beta-adrenergic agonists were discontinued and the patient’s lactate level declined without further intervention.
Discussion: Lactic Acidosis can be categorized based on etiology and mechanism of action. Type A lactic acidosis is caused by mismatch between oxygen supply and demand (eg, hypoperfusion, shock states, cardiopulmonary arrest, seizures, and shivering). Type D lactic acidosis is due to overgrowth of bacteria in the colon. Type B Lactic Acidosis is caused by disturbances in cell metabolism and has been attributed to diabetes mellitus, malignancy, alcoholism, toxins, HIV infection, medications, and mitochondrial dysfunction. In terms of medications, Type B lactic acidosis was most commonly attributed to intravenous epinephrine use rather than inhaled beta adrenergic agonists. Sparse cases have been reported of lactic acidosis in patients with severe bronchospasm who have been treated with inhaled beta agonists, as seen in our case. We present a unique cause where several administrations of ipratropium-albuterol nebulizer caused a significant rise in lactic acid levels, more than doubling lactic acid levels within five hours.
Conclusions: Frequent doses of inhaled beta-adrenergic agonists can induce type B lactic acidosis, even in patients with prior exposures to these medications. In this case, the lactic acidosis self-resolved without fluid resuscitation when further beta agonists were held. Identifying this phenomenon as a cause of lactic acidosis is crucial, especially those with respiratory symptoms and heart failure, to avoid unnecessary fluid overload as these patients may respond to other pharmaceutical interventions. This report also highlights the importance of a holistic approach to patient care and prioritizing clinical assessment over solely focusing on laboratory values. Further studies are required to identify the specific factors that predispose a subset of COPD and asthma patients to the development of type B lactic acidosis.