From the Research
The approach to managing alcoholic ketoacidosis should prioritize fluid resuscitation with lactated Ringer's solution, thiamine administration, and glucose supplementation, as well as electrolyte replacement and monitoring for alcohol withdrawal symptoms, based on the most recent and highest quality evidence available 1, 2.
Key Components of Management
- Fluid resuscitation with lactated Ringer's solution (instead of normal saline) to correct volume depletion and improve renal perfusion, as it may reduce the risk of hyperchloremic acidosis and acute kidney injury 2
- Thiamine (100 mg IV) administration before glucose to prevent precipitating Wernicke's encephalopathy
- Glucose supplementation (D5W or D10W) to address hypoglycemia and provide substrate for metabolism
- Electrolyte replacement, particularly potassium, magnesium, and phosphate, guided by serum levels
- Monitoring for alcohol withdrawal symptoms and treatment with benzodiazepines (such as diazepam 5-10 mg or lorazepam 1-2 mg) as needed
Rationale
The underlying cause of alcoholic acidosis is ketoacid production (particularly beta-hydroxybutyrate) during alcohol metabolism combined with poor nutritional intake, leading to a complex acid-base disturbance 3, 4. The liver's preferential metabolism of ethanol depletes NAD+, shifting the redox state and promoting ketogenesis.
Additional Considerations
- Sodium bicarbonate (1-2 mEq/kg IV) may be considered in severe cases with pH < 7.1, although its use remains controversial
- Nutritional support and multivitamin supplementation are essential components of comprehensive care for these patients
- Serial monitoring of blood gases, electrolytes, and glucose levels is crucial to guide management and prevent complications.