Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism.
Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Growth hormone, epinephrine, cortisol, and glucagon are all increased. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs.
Typically, an alcohol binge leads to vomiting and the cessation of alcohol or food intake for ≥ 24 hours. During this period of starvation, vomiting continues and abdominal pain develops, leading the patient to seek medical attention. Pancreatitis may occur.
Diagnosis requires a high index of suspicion; similar symptoms in a patient with alcohol use disorder may result from acute pancreatitis, methanol or ethylene glycol poisoning (see table Symptoms and Treatment of Specific Poisons), or diabetic ketoacidosis (DKA). Often, blood alcohol levels are no longer elevated when patients present with alcoholic ketoacidosis. In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), blood urea nitrogen (BUN) and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement.
The absence of hyperglycemia makes diabetic ketoacidosis improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated hemoglobin (HbA1C).
Typical laboratory findings include
Detection of acidosis may be complicated by concurrent metabolic alkalosis due to vomiting, resulting in a relatively normal pH; the main clue is the elevated anion gap. If history does not rule out toxic alcohol ingestion as a cause of the elevated anion gap, serum methanol and ethylene glycol levels should be measured. Calcium oxalate crystals in the urine also suggests ethylene glycol poisoning. Lactic acid levels are often elevated because of hypoperfusion and the altered balance of reduction and oxidation reactions in the liver.
Patients are initially given thiamin 100 mg IV to prevent development of Wernicke encephalopathy or Korsakoff psychosis. Then an IV infusion of 5% dextrose in 0.9% saline solution is given. Initial IV fluids should contain added water-soluble vitamins and magnesium, with potassium replacement as required.
Ketoacidosis and gastrointestinal symptoms usually respond rapidly. Use of insulin is appropriate only if there is any question of atypical diabetic ketoacidosis or if hyperglycemia > 300 mg/dL (> 16.7 mmol/L) develops.
Alcoholic ketoacidosis is caused by the combined effects of alcohol and starvation on glucose metabolism; it is characterized by hyperketonemia and elevated anion gap metabolic acidosis without significant hyperglycemia.
Measure serum and urine ketones and electrolytes and calculate a serum anion gap.
Treat initially with IV thiamin to prevent Wernicke encephalopathy or Korsakoff psychosis, then follow up with IV dextrose in 0.9% saline.