Alcoholic ketoacidosisš„ {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 ā 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 ā NADH:NADāŗ ratio ā 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; āfruityā ketotic breath. |
Reduced oral intake, recent bingeāstop history. | Possible stigmata of chronic liver disease. |
Investigations
Test | Typical Result |
---|---|
Capillary glucose | Normal (3ā7 mmol Lā»Ā¹) or low. |
Arterial / venous blood gas | pH < 7.35,Ā high anion gap; low or normal lactate. |
Serum / urine ketones | β-hydroxybutyrate > 3 mmol Lā»Ā¹ or ++ ketones on dipstick. |
U&Es, Mg²āŗ, POā³⻠| Often ā Kāŗ, ā Mg²āŗ, ā POā³⻠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).
- WernickeāKorsakoff syndrome if thiamine deficient.
- Aspiration pneumonia, pancreatitis, death if untreated.
Management (Emergency Department / AMU)
- 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 ā„ 0.5 mL kgā»Ā¹ hā»Ā¹).
- Thiamine before glucose
- IV PabrinexĀ® 2 pairsĀ over 30 min to prevent Wernickeās encephalopathy.
- 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 ā 60 min; add dextrose bolus if < 4 mmol Lā»Ā¹.
- Electrolyte correction
- ReplaceĀ potassium, magnesium and phosphateĀ according to local IV protocols, monitoring levels 2-hourly initially.
- Address co-morbidities
- Treat alcohol withdrawal (chlordiazepoxide or lorazepam).
- Empirical antibiotics if sepsis suspected; CT abdomen / serum lipase if pancreatitis possible.
- Avoid insulin
- Not required unless concomitant DKA; insulin may precipitate profound hypoglycaemia and falls in potassium.
- 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 Wernickeās encephalopathy.
- If the patient experiences seizures or hallucinations, IV lorazepam or diazepam should be administered.
- Wernickeās 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.