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Alcoholic ketoacidosis
From WikEM
(Redirected from ETOH Ketoacidosis)
Contents
Background
- Seen in patients with recent history of binge drinking with little/no nutritional intake
- Anion gap metabolic acidosis associated with acute cessation of ETOH consumption after chronic abuse
- Characterized by high serum ketone levels and an elevated AG
- Consider other causes of elevated AG, as well as co-ingestants
- Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis
Pathophysiology
- Ethanol metabolism depletes NAD stores[1]
- Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
- High NADH:NAD also results in increased lactate production
- Lactate higher than normal but not as high as in shock or sepsis
- Acetoacetate is metabolized to acetone so elevated osmolal gap may also be seen
Clinical Features
- Nausea (75%)
- Vomiting (73%)
- Abdominal pain (62%)
- Not hyperosmolar as opposed to DKA
- Large IVF admin does not predispose to cerebral edema
Differential Diagnosis
- Isopropyl Alcohol
- Results in ketosis
- Methanol, Ethylene Glycol
- Do not produce ketosis
- Sepsis
- Salicylate Toxicity
- DKA
- Hyperosmolar hyperglycemic state
- Starvation Ketosis
- Uremia
- Ethanol toxicity
- Alcohol withdrawal
- Electrolyte/acid-base disorder
- Wernicke-Korsakoff syndrome
- Beer potomania syndrome
- Alcoholic ketoacidosis
Evaluation
- Binge drinking ending in nausea, vomiting, and decreased intake
- Wide anion gap metabolic acidosis (ketonemia, lactic acidosis)
- Positive serum ketones
- Wide anion gap metabolic acidosis without alternate explanation
- Urine ketones may be falsely negative or low
- Lab measured ketone is acetoacetate
- May miss beta-hydroxybutyrate
Management
Consider associated diseases (ie pancreatitis, rhabdomyolysis, hepatitis, infections)
- Thiamine (100mg IV)
- Prior to glucose to decrease risk of Wernicke encephalopathy or Korsakoff syndrome
- Hydration (D5NS)
- IVF should include 5% dextrose since there is a lack of glucose
- Glucose stimulates insulin which stops lipolysis
- Oral nutrition if able to tolerate
- Electrolyte replacement
- K, Mag and Phos
- Monitor for signs of alcohol withdrawal
- Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy
Disposition
- Discharge home after treatment if able to tolerate POs and acidosis resolved
- Consider admission for those with severe volume depletion and/or acidosis
- Hypoglycemia is poor prognostic feature, indicating depleted glycogen stores
See Also
References
- ↑ McGuire LC, Cruickshank AM, Munro PT. Alcoholic ketoacidosis. Emerg Med J. 2006 Jun;23(6):417-20.
