From the Research
The treatment for alcoholic ketoacidosis (AKA) should focus on fluid resuscitation, electrolyte correction, and glucose administration, as outlined in the most recent and highest quality study available 1. The pathophysiology of AKA involves depleted glycogen stores, elevated counter-regulatory hormones, and an increased NADH:NAD+ ratio from alcohol metabolism, which shifts metabolism toward ketone production. Key aspects of treatment include:
- Fluid resuscitation with intravenous isotonic fluids, typically normal saline, at a rate of 15-20 mL/kg in the first hour, followed by maintenance fluids based on clinical response
- Administration of dextrose 5% once fluid resuscitation has begun to address hypoglycemia or the risk of developing hypoglycemia
- Thiamine (100 mg IV) given before glucose to prevent precipitating Wernicke's encephalopathy
- Electrolyte replacement, particularly potassium, magnesium, and phosphate, as levels may drop during treatment
- Bicarbonate therapy is rarely needed as the acidosis typically resolves with proper hydration
- Prophylactic treatment for alcohol withdrawal with benzodiazepines if appropriate The goal of treatment is to reverse the underlying pathophysiological processes, restore volume status, provide glucose substrate, and allow the body to clear ketones naturally, as supported by recent studies 2, 1. It is essential to note that AKA can be confused with diabetic ketoacidosis, and a thorough diagnostic approach, including laboratory tests such as haemoglobin A1c, fructosamine level, and betahydroxybutyrate to acetoacetate ratio, can help differentiate between the two conditions 2. Overall, the treatment of AKA requires a comprehensive approach that addresses the patient's fluid, electrolyte, and glucose needs, as well as their underlying alcohol use disorder, to improve morbidity, mortality, and quality of life outcomes.