Alcoholic Ketoacidosis

Aka: Alcoholic Ketoacidosis

advertisement

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

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
  2. Vomiting
  3. 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. Hyponatremia
      2. Hypophosphatemia
      3. Hypokalemia
  2. Venous Blood Gas
    1. Metabolic Acidosis
    2. Mixed acid base findings are common (75% of cases)
  3. Serum Ketones
    1. Increased
  4. Serum Lactate
    1. 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. 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)

These images are a random sampling from a Bing search on the term "Alcoholic Ketoacidosis." Click on the image (or right click) to open the source website in a new browser window. Search Bing for all related images

Related Studies

Related Topics in Chemical Dependency

advertisement