Alcoholic ketoacidosis (AKA)
Alcoholic ketoacidosis is an acute, reversible high anion‑gap metabolic acidosis that typically affects chronic heavy drinkers who stop drinking and have little or no oral intake for hours to days. It is an important differential diagnosis for any patient with high anion‑gap acidosis in the emergency department.
With early recognition and supportive treatment - restoration of circulating volume, provision of carbohydrate and correction of electrolyte and micronutrient deficiencies - biochemical and clinical recovery is usually rapid.
Management should follow national alcohol‑care and nutrition guidance and local DKA/ketone pathways (Department of Health and Social Care - Alcohol care in acute hospitals; NICE CG32; NICE CG100; RCEM).
Pathophysiology (concise)
- Recent ethanol metabolism increases the hepatic NADH:NAD+ ratio, favouring conversion of acetoacetate to beta‑hydroxybutyrate (BHB) and suppressing gluconeogenesis.
- Starvation and low carbohydrate intake increase counter‑regulatory hormones and lipolysis, delivering free fatty acids for hepatic ketogenesis.
- Volume depletion (vomiting, poor intake) reduces renal clearance of ketones.
- The result is a BHB‑predominant ketosis with high anion‑gap metabolic acidosis and frequent electrolyte and micronutrient deficits (K+, Mg2+, PO43-, thiamine).
Typical presentation
- Recent binge alcohol use followed by several days of little or no food intake with progressive nausea, vomiting and anorexia.
- Symptoms commonly include nausea, vomiting, epigastric pain, malaise and weakness.
- Blood alcohol concentration may be falling or low at presentation.