Alcoholic Ketoacidosis

Aka: Alcoholic Ketoacidosis, Alcohol Induced Ketoacidosis

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II. Pathophysiology

  1. See Ketoacidosis
  2. See Glucose Metabolism
  3. Develops in baseline chronic Alcohol Abuse and associated poor nutrition, in combination with an acute stressor
    1. Identifying the acute stressor is key to effective management (see causes below)
    2. Most common triggers are infection and Pancreatitis
    3. Often occurs with recent Alcohol cessation
  4. Alcoholism results in reduced glycogen and nutritional stores (starvation state)
    1. Occurs when most of daily calories are obtained from Alcohol
      1. Ethanol is a 2 carbon Alcohol that cannot be burned as fuel in the TCA Cycle, nor used for Gluconeogenesis
      2. Ethanol can only be metabolized to Ketone Bodies for fuel, or used to build Fatty Acids and Triglycerides
      3. Contrast with Glycolysis and Gluconeogenesis pathways, dependent on 3-carbon sugars (e.g. pyruvate)
    2. Glucose is depleted by decreased Gluconeogenesis and glycogenolysis
      1. Compounded by advanced liver disease, in which hepatic Gluconeogenesis is impaired
    3. Initial response to starvation is to increase hormonal factors that transiently increase Glucose levels
      1. These factors include Glucagon, Catecholamines, Cortisol and Growth Hormones
    4. Ketoacidosis results from increased lipolysis and Ketone generation when Glucose is unavailable
      1. Alcohol is metabolized to Ketones by hepatic Alcohol dehydrogenase
      2. Fatty Acids are also metabolized to Ketones for energy utilization
    5. Lactic Acidosis also develops
      1. Alcohol metabolism increases NADH to NAD+ ratio and a suppression of mitochondrial activity
      2. Lactic Acid accumulates with disrupted mitochondrial activity (pyruvate is unable to enter TCA Cycle)
      3. Lactic Acid further increases in advanced liver disease with impaired Gluconeogenesis
      4. Volume depletion (Dehydration) is frequently also present and compounds the Lactic Acidosis
  5. Images
    1. gluconeogenesis.png

III. Causes

  1. Intraabdominal Disorder
    1. Cholecystitis
    2. Appendicitis
    3. Pancreatitis
    4. Small Bowel Obstruction
    5. Bowel Perforation
    6. Mesenteric Ischemia
  2. Other Alcohol related disorder
    1. Alcohol Withdrawal
    2. Delirium Tremens
  3. Other metabolic disorder
    1. Diabetic Ketoacidosis
    2. Rhabdomyolysis
  4. Other Systemic Disorders
    1. Hypothermia
    2. Acute Coronary Syndrome
    3. Pulmonary Embolism
    4. Sepsis
  5. Toxic Ingestion
    1. Salicylate Toxicity
    2. Toxic Alcohol Ingestion (e.g. Ethylene Glycol Poisoning)

IV. Symptoms

  1. Nausea and Vomiting (frequently with volume depletion)
  2. Generalized Abdominal Pain

V. Signs: Red Flags

  1. Significant intraabdominal findings suggest a possible underlying trigger (see causes above)
    1. Peritoneal signs
    2. Abnormal bowel sounds
    3. Abdominal Distention or significant tenderness
  2. Significant Altered Level of Consciousness (expect only mild alteration in Alcoholic Ketoacidosis)
    1. See Altered Level of Consciousness
    2. Consider Unknown Ingestion (coingestion)
    3. Consider Wernicke Encephalopathy
    4. Toxic Alcohol Ingestion (e.g. Ethylene Glycol Poisoning)
      1. Consider in severe Lactic Acidosis, Altered Mental Status, Osmolal Gap

VI. Labs

  1. Comprehensive Metabolic Panel
    1. Increased Anion Gap
    2. Decreased serum bicarbonate
    3. Serum Glucose is typically low or normal (elevated in 10% of cases)
    4. Other Electrolyte abnormalities may be present
      1. Serum levels are unreliable in evaluating total body stores (esp. Phosphorus, Magnesium)
      2. Hyponatremia
      3. Hypomagnesemia
      4. Hypokalemia
      5. Hypophosphatemia
  2. Venous Blood Gas
    1. Metabolic Acidosis
    2. Mixed acid base findings are common (75% of cases)
  3. Serum Ketones
    1. Increased Beta Hydroxybutyrate in addition to other Ketones
    2. Ketones are elevated more than Lactic Acid in uncomplicated Alcoholic Ketoacidosis
  4. Serum Lactate
    1. Lactic Acid is mildly elevated (rarely >4 mmol/L) in uncomplicated Alcoholic Ketoacidosis
    2. Significantly increased (>4 mmol/L) in Toxic Alcohol ingestion (Methanol or Ethylene Glycol Poisoning)
  5. Osmolar Gap
    1. Consider Toxic Alcohol ingestion (Methanol or Ethylene Glycol Poisoning)
  6. Serum Alcohol Level
    1. Alcohol level is independent to Ketoacidosis development (may be high or low)
  7. Toxicology Screening
    1. Consider other causes of Metabolic Acidosis with Anion Gap (e.g. Salicylism, Toxic Alcohols, Rhabdomyolysis)

VII. Management

  1. Similar to Starvation Ketosis
  2. Most common cause of Metabolic Acidosis with Anion Gap in Alcoholics (poor nutrition)
    1. However, exclude Toxic Alcohol ingestion (e.g. Ethylene Glycol Poisoning)
  3. As with Diabetic Ketoacidosis, Serum Beta Hydroxybutyrate is increased
    1. Urine Ketones are unreliable for detection
  4. Administer IV fluids containing dextrose (e.g. D5LR)
    1. Emergent correction of Hypoglycemia (Serum Glucose <60 mg/dl)
    2. Before dextrose, give Thiamine 200 mg IV (500 mg IV if Wernicke Encephalopathy suspected)
    3. Dextrose infusions stop Ketone formation, whereas simple crystalloid will not
    4. However, assess Potassium and replace before significant dextrose aministered (Hypokalemia risk)
    5. Anticipate Ketone clearance and acidosis resolution within 8 to 12 hours of starting fluid and dextrose infusion
  5. Replace other Electrolytes as needed
    1. Potassium Replacement
    2. Magnesium Replacement
  6. Alcoholism Management
    1. See Alcoholism Management
    2. See Alcohol Dependence Management
    3. See Alcohol Withdrawal
    4. See Substance Addiction Aftercare

VIII. References

  1. Long and Swaminathan in Swadron (2022) EM: Rap 22(9): 13-5
  2. Thorson and Abboud (2024) Crit Dec Emerg Med 38(7): 16-7

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