Alcoholic ketoacidosisšŸŽ„ {Free Video}

Alcoholic ketoacidosis

Introduction

Alcoholic ketoacidosis is an acute metabolic emergency seen in chronic, often binge, alcohol users after a period of heavy drinking followed by starvation and vomiting. It is characterised by a high-anion-gap metabolic acidosis with markedly raised ketone bodies butĀ normal or low blood glucose.


Epidemiology & Risk Factors

  • Presents most often in adultsĀ 30 – 60 yearsĀ with long-standing hazardous alcohol intake.
  • Precipitating factors: prolonged fasting, persistent vomiting, intercurrent sepsis or pancreatitis, abrupt reduction in alcohol (e.g. after binge).

Pathophysiology

  • Ethanol metabolism ↑ NADH:NAD⁺ ratio → inhibits gluconeogenesis and shunts free fatty acids toĀ ketone production (β-hydroxybutyrate > acetoacetate).
  • Vomiting and poor intake cause volume depletion andĀ hypoglycaemia.
  • Counter-regulatory hormones (glucagon, cortisol, catecholamines) further stimulate lipolysis and ketogenesis.

Clinical Features

Symptoms Signs
Nausea, repeated vomiting, general abdominal pain. Tachycardia, postural hypotension (dehydration).
Malaise, dizziness, tremor or agitation (withdrawal). Kussmaul-type deep breathing; ā€œfruityā€ ketotic breath.
Reduced oral intake, recent binge–stop history. Possible stigmata of chronic liver disease.

Investigations

Test Typical Result
Capillary glucose Normal (3–7 mmol L⁻¹) or low.
Arterial / venous blood gas pH < 7.35,Ā high anion gap; low or normal lactate.
Serum / urine ketones β-hydroxybutyrate > 3 mmol L⁻¹ or ++ ketones on dipstick.
U&Es, Mg²⁺, PO₄³⁻ Often ↓ K⁺, ↓ Mg²⁺, ↓ PO₄³⁻ from vomiting and osmotic diuresis.
FBC, CRP, amylase, lipase Screen for infection or pancreatitis.
Serum ethanol May be low or undetectable at presentation.

Always exclude diabetic ketoacidosis (DKA), lactic acidosis, sepsis and salicylate overdose.


Complications

  • Severe hypovolaemic shock.
  • Hypokalaemia-induced arrhythmias, seizures (hypomagnesaemia).
  • Wernicke–Korsakoff syndrome if thiamine deficient.
  • Aspiration pneumonia, pancreatitis, death if untreated.

Management (Emergency Department / AMU)

  1. Resuscitation
    • High-flow oxygen, cardiac monitoring and large-bore IV access.
    • 0.9 % sodium chloride 1 L over 60 min, then reassess (aim urine output ≄ 0.5 mL kg⁻¹ h⁻¹).
  2. Thiamine before glucose
    • IV PabrinexĀ® 2 pairsĀ over 30 min to prevent Wernicke’s encephalopathy.
  3. Glucose replacement
    • 5 % or 10 % dextrose infusion (e.g. 10 % dextrose 500 mL over 4 h) to switch off ketogenesis and correct hypoglycaemia.
    • Repeat capillary glucose every 30 – 60 min; add dextrose bolus if < 4 mmol L⁻¹.
  4. Electrolyte correction
    • ReplaceĀ potassium, magnesium and phosphateĀ according to local IV protocols, monitoring levels 2-hourly initially.
  5. Address co-morbidities
    • Treat alcohol withdrawal (chlordiazepoxide or lorazepam).
    • Empirical antibiotics if sepsis suspected; CT abdomen / serum lipase if pancreatitis possible.
  6. Avoid insulin
    • Not required unless concomitant DKA; insulin may precipitate profound hypoglycaemia and falls in potassium.
  7. Disposition
    • Admit to HDU/ICU if pH < 7.1, persistent hypotension, arrhythmia, or altered mental state (Glasgow Coma Scale < 12).

FAQ from our users

Why is thiamine used?
  • Thiamine is a B vitamin complex which is used to avoid the development of Wernicke encephalopathy or korsakoff syndrome.
What is the pathophysiology of alcoholic ketoacidosis
  • Chronic alcohol consumption can lead to poor nutrition.
  • This leads to to glycogen depletion and starvation.
  • Alcohol further inhibits gluconeogenesis & insulin secretion (leading to lower glucose availability)
  • The body shifts to fat metabolism for energy
  • Accumulation of ketones leads to ketoacidosis and metabolic acidosis

Common pitfalls in a clinical setting

Common pitfalls in a clinical setting
Common pitfalls in a clinical setting
  • Assess for alcohol withdrawal using the CIWA score.
  • Start chlordiazepoxide for alcohol withdrawal management if indicated.
    • Acute alcohol withdrawal (characterised by sweating, tremors, and altered mentation) is first treated with chlordiazepoxide along with thiamine (Vitamin B1) to prevent Wernicke’s encephalopathy.
    • If the patient experiences seizures or hallucinations, IV lorazepam or diazepam should be administered.
    • Wernicke’s encephalopathy is treated with IV Vitamin B1 (Thiamine), IV Pabrinex, or high-potency Vitamin B Complex.
    • A patient undergoing alcohol detoxification who wants a medication as a deterrent against alcohol consumption can be prescribed disulfiram.
    • A patient seeking to reduce alcohol cravings during detoxification may benefit from acamprosate.
    • A patient looking for a medication to reduce withdrawal symptoms during detoxification should be given chlordiazepoxide.
  • Check pancreatic function tests & liver function tests, especially in patients with long-term alcohol use.