• A high degree of suspicion based on a patient’s history of significant alcohol use, and an anion gap metabolic acidosis with ketosis is key.
• Volume resuscitation (often with dextrose), electrolyte repletion, and reversal of underlying triggers and complications are the cornerstones of management.

•  Definition
  • Anion gap metabolic acidosis (AGMA) precipitated by an accumulation of ketone bodies, attributed to the combined effects of recent alcohol consumption and starvation.
  • Mild-moderate ketoacidosis (AKA) can develop during active alcohol consumption through the metabolism of excessive ethanol to acetoacetate and beta-hydroxybutyrate.
  • Classically severe kAKA can develop following cessation of alcohol consumption due to increased lipolysis in fasting conditions, exacerbated by alcohol withdrawal and associated sympathetic activation.
• Risk Factors
  • Baseline malnourishment, and long-standing alcohol use disorder.
• Complications
  • Complications from AKA are often due to delayed diagnosis, and involve severe volume depletion and electrolyte derangements, which can lead to cardiac dysrhythmias.
  • Patients can also decompensate due to other conditions in patients with severe alcohol use disorder.

The diagnosis of AKA requires a high index of suspicion based on clinical presentation, with an AGMA with ketosis being a hallmark feature.

It is important to exclude other conditions that can present with an AGMA (Useful mnemonic  = MUDPILES).

• Presentation: Clinical presentation varies, most commonly:
  • 1-2 day history of anorexia, nausea, vomiting, and abdominal pain following a prolonged alcohol binge. Typically have normal mentation,Kussmaul breathing and “fruity” scented breath.
  • Often present with signs and symptoms of hypovolemia, alcohol withdrawal.
  • May also present with other conditions related to severe alcohol use disorder.
• Investigations
  • Patients suspected of AKA should typically receive blood gas analysis (ABG/VBG), anion gap calculation, serum ketones (beta hydroxybutyrate) and urine ketones, lactate, osmolality, extended electrolytes, creatinine, BUN, LFTs, lipase, and glucose.
  • Common Laboratory Findings
    • AGMA
    • Ketonemia, ketonuria.
    • Low, normal, or mildly elevated plasma glucose.
    • Low or undetectable plasma ethanol.
    • Elevated osmolar gap.
    • Electrolyte derangements, including hypokalemia, hypomagnesemia, and hypophosphatemia.
• Pitfalls
  • Concomitant metabolic alkalosis due to vomiting, and may obfuscate the presence of acidosis.
  • AKA, in isolation, does not present with altered mental status; altered patients should be worked up for other etiologies.

• Management Considerations
  • Patients with alcohol use disorder should receive IV thiamine, often 500 mg IV although there is no compelling evidence to suggest that administration of dextrose solutions prior to thiamine will result in precipitation/exacerbation of Wernicke’s encephalopathy.
  • Patients should be resuscitated with D5NS infusion at an individualized rate; subsequent insulin secretion following dextrose infusion will inhibit ketogenesis, while saline will replete extracellular fluid lost to vomiting.
  • Dextrose should be avoided in those with overt hyperglycemia and severe hypokalemia; hyperglycemic patients should be managed with insulin therapy, and hypokalemia should be repleted prior to administration of dextrose.
  • Potassium, phosphate, and magnesium should be repleted as necessary.
  • Labs should be repeated every 1-2 hours, targeting closure of the anion gap, and monitoring electrolyte levels.
  • Antiemetics
  • CIWA protocol.

• Patients will require admission if they have ongoing biochemical derangements, hemodynamic instability, or poor tolerance of PO intake.
• Inpatient management is also commonly required for those with severe ketoacidosis, concomitant ailments, or significant alcohol withdrawal.

Patients with AKA typically do not require transfer, unless coexisting conditions require a higher level of care.

• Based on one study, approximately 50% of AKA cases will resolve within 12 hours, and these patients can be discharged from the ED. However, a significant number of patients will not require monitoring for this long. Patients that demonstrate resolution of ketoacidosis and electrolyte abnormalities, improvement of volume status, and ability to tolerate PO intake may be appropriate for discharge with follow-up.
• Patients with AUD should be offered specialist addictions referral for treatment.

1. https://www.uptodate.com/contents/fasting-ketosis-and-alcoholic-ketoacidosis#H506562870

   https://www.merckmanuals.com/en-ca/professional/endocrine-and-metabolic-disorders/diabetes-mellitus-and-disorders-of-carbohydrate-metabolism/alcoholic-ketoacidosis

   https://www.acep.org/siteassets/sites/acep/media/moc/moc-documents/alcoholic-ketoacidosis.pdf

   
   

1. Long, B., Lentz, S., Gottlieb, M. (2021). Alcoholic Ketoacidosis: Etiologies, Evaluation, and Management. The Journal of Emergency Medicine, 61(6), 658-665. https://doi.org/10.1016/j.jemermed.2021.09.007

   
   

2. Mehta, A., Emmett, M. (2023). Fasting ketosis and alcoholic ketoacidosis. UpToDate. Retrieved November 25^th, 2023 from https://www.uptodate.com/contents/fasting-ketosis-and-alcoholic-ketoacidosis#H506562870

   
   

3. Brutsaert, E.F. (2023). Alcoholic Ketoacidosis. Merck Manual Professional Version. Retrieved November 25^th, 2023 from https://www.merckmanuals.com/en-ca/professional/endocrine-and-metabolic-disorders/diabetes-mellitus-and-disorders-of-carbohydrate-metabolism/alcoholic-ketoacidosis