Makindo Medical Notes

🍺 Alcoholic ketoacidosis (AKA) occurs when chronic or binge alcohol use impairs hepatic gluconeogenesis. This results in reduced insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis. Blood glucose is often normal or low, which can mislead diagnosis compared with diabetic ketoacidosis (DKA).

ℹ️ About

• Seen in patients with chronic alcohol excess, malnutrition, dehydration, and often after episodes of vomiting or starvation.
• Typically occurs after a recent alcohol binge followed by abrupt cessation of drinking with poor oral intake.
• Important because it may mimic DKA or sepsis but requires a different management approach.

🧪 Aetiology & Pathophysiology

• 🍷 Alcohol metabolism (ethanol → acetaldehyde → acetate) increases NADH in the liver, suppressing gluconeogenesis.
• ⬆️ Counter-regulatory hormones (catecholamines, glucagon, cortisol, GH) stimulate lipolysis → free fatty acids released.
• ⚡ Fatty acids undergo incomplete oxidation → accumulation of ketone bodies (β-hydroxybutyrate, acetoacetate, acetone).
• Blood glucose remains normal/low because insulin secretion is not completely absent.

🩺 Clinical Presentation

• Background of heavy alcohol use ± liver disease.
• Symptoms: nausea, vomiting, abdominal pain, poor oral intake, malaise.
• Signs: tachypnoea (Kussmaul breathing), tachycardia, hypotension, fruity ketotic breath.
• Look for complications: jaundice, ascites, encephalopathy (suggesting liver decompensation).

🔍 Investigations

• Bloods: U&E (look for AKI, ↓K, ↓Mg, ↓P, ↓Ca), FBC (anaemia, ↑WCC), LFTs (alcoholic hepatitis or cirrhosis).
• Coagulation: PT may be prolonged in liver dysfunction.
• ABG/VBG: Metabolic acidosis with a raised anion gap, often mixed with metabolic alkalosis from vomiting. Lactate may be raised.
• Glucose: Normal or low (distinguishes from DKA).
• Ketones: ↑ serum β-hydroxybutyrate, positive urine ketones.
• Ascitic tap if ascites present → exclude spontaneous bacterial peritonitis (SBP).

💊 Management

• 🔑 Rehydration: 5% dextrose IV to provide carbohydrate and suppress ketogenesis (avoid saline-only resuscitation).
• 💉 Vitamin support: IV Pabrinex (thiamine + B vitamins + C) before glucose to prevent Wernicke’s encephalopathy.
• ⚡ Correct electrolytes: replace K, Mg, and phosphate aggressively.
• 🍬 If hypoglycaemia: 10% dextrose infusion.
• 🧪 IV antibiotics if infection suspected (take cultures first: blood, urine, ascitic fluid, CXR).
• 📟 Monitor fluid balance, cardiac rhythm, and acid–base status closely.
• 🧠 Consider chlordiazepoxide if at risk of alcohol withdrawal seizures.
• 📞 Refer to alcohol support/addiction services once stabilised.

📚 References

• Review Article on Alcoholic Ketoacidosis, EMJ 2006

💡 Teaching Pearl: Always distinguish Alcoholic Ketoacidosis from DKA — both present with acidosis and ketones, but in AKA the glucose is usually normal/low. Giving dextrose with thiamine reverses ketogenesis rapidly, whereas in DKA insulin therapy is the mainstay.