alcoholic ketoacidosis

**Pathophysiology** - Typical patient: chronic heavy drinker with a recent binge, then decreased food intake and vomiting for days. Volume depletion and starvation follow. - Starvation lowers insulin and raises glucagon, cortisol, catecholamines, and growth hormone. This causes lipolysis, and free fatty acids go to the liver for β-oxidation, which produces acetyl-CoA. - Ethanol metabolism by alcohol dehydrogenase and aldehyde dehydrogenase generates a large amount of NADH. The high NADH/NAD+ ratio shifts acetoacetate to β-hydroxybutyrate (BHB), so BHB is the predominant ketone. - The same high NADH/NAD+ ratio shifts pyruvate to lactate, which can add a lactic acidosis. It also impairs gluconeogenesis, leading to hypoglycemia. - Volume depletion decreases renal ketoacid excretion and worsens the acidosis.

**Clinical features** - Nausea, vomiting, abdominal pain, tachypnea (Kussmaul respirations), tachycardia, and volume depletion. Mental status is often relatively preserved, although patients may be intoxicated or in withdrawal. - Often accompanied by alcoholic gastritis, pancreatitis, or withdrawal.

**Labs** - High anion gap metabolic acidosis, with a normal or low-normal serum ethanol level. - Glucose is low, normal, or mildly elevated. Marked hyperglycemia suggests DKA. - **The nitroprusside test can be falsely negative or weak.** It detects acetoacetate and acetone, not BHB. Because BHB predominates, measure serum BHB directly. - Acid-base status may be mixed. Vomiting causes metabolic alkalosis, so the pH can be near normal or high, and lactic acidosis can coexist. - Electrolytes: hypokalemia, **hypophosphatemia, and hypomagnesemia** are common. Phosphate falls further with refeeding. - Calculate the osmolar gap to exclude toxic alcohols (methanol, ethylene glycol), which are the key differential diagnosis for high anion gap acidosis in an alcoholic.

**Differential diagnosis** - DKA (very high glucose, positive nitroprusside test). - Toxic alcohol ingestion (elevated osmolar gap). - Lactic acidosis. - Starvation ketosis (milder, with bicarbonate usually >18). - Salicylate toxicity. - Uremia.

**Management** - IV isotonic saline with **dextrose (D5NS)**. Dextrose stimulates insulin, which suppresses lipolysis and ketogenesis. Fluids correct the volume depletion. - **Give thiamine before or with glucose** to prevent precipitating Wernicke encephalopathy. - Replete K+, Mg2+, and phosphate. Monitor for refeeding syndrome. - Insulin is usually not needed and is risky because of hypoglycemia and hypokalemia. Use it only if glucose is high. - Bicarbonate is generally not needed. - Treat withdrawal with benzodiazepines, and treat any precipitating illness such as pancreatitis or GI bleeding. - The acidosis usually resolves within 12–24 hours.

**Boards high-yield** - Buzzword stem: alcoholic, binge, then vomiting and abdominal pain, with high anion gap acidosis, normal or low glucose, and a negative or weak urine ketone test. - Key mechanism: increased NADH/NAD+ ratio, so BHB is greater than acetoacetate. - Key treatment: D5NS and thiamine.