Patient Presentation

A 43-year-old female with a past medical history of bipolar disorder and hypothyroidism presented to the emergency department with three days of nausea, vomiting, and coffee-ground emesis. Her home medications were divalproex sodium and sertraline; she additionally reported starting semaglutide 0.25 mg by subcutaneous injection three days prior.

Patient vital signs showed blood pressure of 118/89, heart rate of 139, respiratory rate of 24, oxygen saturation of 99 percent on room air, and a temperature of 97.9°F. On exam she was ill-appearing, tremulous with dry mucous membranes, mildly tachypneic, and had mild diffuse abdominal tenderness.

Lab work was notable for normal lipase, white blood cell count of 14,000, creatinine of 1.59, aspartate aminotransferase level of 142, alanine aminotransferase level of 94, bicarbonate of 7, anion gap of 51, lactic acid of 2.6, beta-hydroxybutyrate of greater than 5 mmol/L, and venous blood gas with pH of 7.15. Ethanol was undetectable. CT imaging was suggestive of gastritis with hepatomegaly. On further questioning, the patient reported a history of alcohol use disorder, stating a recent relapse several weeks ago with heavy daily alcohol consumption until her last alcoholic drink three days prior concurrent with initiation of semaglutide.

Discussion

Anion Gap Acidosis

This patient had a severely elevated anion gap metabolic acidosis with a mild lactic acidosis and acute kidney injury. Considerations for metabolic acidosis commonly include lactate producing processes like sepsis, ketone producing processes like unregulated diabetes or starvation states, uremia, and toxic ingestions.¹ Patients experiencing recurrent emesis or large volume losses, especially when compounded by poor enteral hydration, may have notable decrease in serum bicarbonate levels associated with hypoperfusion and lactic acid production. Aggressive fluid resuscitation can be a confounder in serial interpretations of acidosis as large amounts of chloride containing fluids can reduce the ion difference and increase renal bicarbonate excretion, thereby compounding metabolic acidosis.²

Alcoholic ketoacidosis

Alcoholic ketoacidosis (AKA), a pathophysiological nutritional state, should be considered in patients such as this with alcohol dependence. AKA is due to the altered NADH/NAD+ (elevated NADH and lower NAD+) ratio from alcohol metabolism that ultimately disrupts normal routes of glucose utilization resulting in increased use of free fatty acids from adipose tissue.^3,4 Depletion of thiamine and pyruvate impairs gluconeogenesis. Overall, this constellation of metabolic and hormonal dysfunction produces elevated levels of serum ketones and lactate.

With an anion gap of 51 and renal dysfunction, other etiologies warrant exploration. If history is suggestive, or if no alternatives are identified in an otherwise undifferentiated patient, clinicians should work up the patient for toxic alcohol ingestion and initiate treatment.