II. Pathophysiology

  1. See Ketoacidosis
  2. 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

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. Hyponatremia
      2. Hypomagnesemia
      3. Hypokalemia
      4. 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)

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. Give Thiamine 100 mg before dextrose (Wernicke Encephalopathy)
    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

Images: Related links to external sites (from Bing)

Related Studies