From the FDA Drug Label
In metabolic acidosis associated with shock, therapy should be monitored by measuring blood gases, plasma osmolarity, arterial blood lactate, hemodynamics and cardiac rhythm. The amount of bicarbonate to be given to older children and adults over a four-to-eight- hour period is approximately 2 to 5 mEq/kg of body weight - depending upon the severity of the acidosis as judged by the lowering of total CO2 content, blood pH and clinical condition of the patient.
The treatment for alcoholic ketoacidosis involves administering bicarbonate (IV), with a dose of approximately 2 to 5 mEq/kg of body weight over a period of 4 to 8 hours, depending on the severity of the acidosis.
- Key considerations include:
- Monitoring blood gases, plasma osmolarity, arterial blood lactate, hemodynamics, and cardiac rhythm.
- Adjusting the dose based on the patient's clinical response.
- Avoiding full correction of low total CO2 content during the first 24 hours of therapy to prevent unrecognized alkalosis 1.
From the Research
The treatment for alcoholic ketoacidosis (AKA) should focus on addressing fluid deficits, electrolyte imbalances, and providing glucose, with initial management including intravenous fluid resuscitation with isotonic saline and dextrose administration, as well as thiamine and electrolyte replacement, as supported by the most recent study 2. The goal of treatment is to correct the underlying metabolic disturbances and prevent complications. Key components of treatment include:
- Intravenous fluid resuscitation with isotonic saline (0.9% NaCl) at rates of 15-20 mL/kg in the first hour, followed by maintenance fluids based on clinical response, as recommended by 2
- Dextrose administration, typically as D5W or D5NS, to reverse the ketogenic state caused by alcohol-induced hypoglycemia and starvation
- Thiamine (100 mg IV) should be given before glucose to prevent precipitating Wernicke's encephalopathy, as emphasized by 3
- Electrolyte replacement, particularly potassium, magnesium, and phosphate, is necessary as levels may drop during treatment, as noted by 4
- Bicarbonate therapy is rarely needed as the acidosis typically resolves with fluid and glucose administration, as stated by 2 Patients require close monitoring of vital signs, electrolytes, and glucose levels during treatment. The underlying pathophysiology involves alcohol consumption leading to increased NADH:NAD+ ratio, inhibiting gluconeogenesis and promoting ketone body formation, which is exacerbated by poor nutritional intake and dehydration, as explained by 2. Most patients respond rapidly to treatment, with resolution of ketoacidosis within 24 hours, as reported by 5.
It is essential to differentiate AKA from diabetic ketoacidosis (DKA) to prevent mismanagement, as highlighted by 3. A precise patient's medical history is crucial to prevent misdiagnosis, and thiamine and judicious fluid resuscitation, as well as electrolytes and malnutrition correction, should be promptly initiated in patients with AKA, as recommended by 3. Good family, social support, and rehabilitation programs are crucial to help patients with alcohol abuse, as noted by 3.
In terms of fluid administration, the rate of infusion may vary, but the goal is to correct volume depletion and provide adequate hydration, as discussed by 6. However, this study focused on diabetic ketoacidosis, and its findings may not be directly applicable to AKA. Therefore, the treatment approach should be individualized based on the patient's clinical presentation and response to therapy, with a focus on addressing the specific needs of patients with AKA, as emphasized by 2.