Michael P. Kefer
EPIDEMIOLOGY
Alcoholic ketoacidosis (AKA) is a high anion gap metabolic acidosis that can occur after acute cessation of alcohol. It usually occurs in chronic alcoholics, but can occur in first-time drinkers.
PATHOPHYSIOLOGY
AKA results from heavy ethanol intake, either acute or chronic, and minimal to no food intake. Glycogen stores become depleted and insulin secretion is suppressed.
To maintain a supply of glucose, the counter-regulatory hormones glucagon, growth hormone, cortisol, and epinephrine are released.
Fat and ethanol oxidation become the body’s primary substrate for energy production, resulting in the formation of the ketone bodies β-hydroxybutyrate, acetoacetate, and acetone.
Acetone is rapidly excreted by the lungs. Acetoacetate and β-hydroxybutyrate accumulate, resulting in a metabolic acidosis.
β-Hydroxybutyrate is the reduced form of acetoacetate. In AKA, the reduction of acetoacetate to β-hydroxybutyrate is favored. As a result, in advanced cases, acetoacetate levels are low and β-hydroxybutyrate levels are high.
CLINICAL FEATURES
AKA presents with nausea, vomiting, orthostasis, and abdominal pain 24 to 72 hours after the last alcohol intake.
On examination, the patient is acutely ill and dehydrated with a tender abdomen. Abdominal tenderness is diffuse and nonspecific, or is a result of other causes associated with the use of alcohol, such as gastritis, hepatitis, or pancreatitis.
Presentation may be confounded by other complications of alcoholism, such as infection or alcohol withdrawal.
DIAGNOSIS AND DIFFERENTIAL
Laboratory investigation reveals an anion gap (Na+ – [Cl– + HCO3–] > 12 ± 4 mEq/L) metabolic acidosis.
Serum pH may be low, normal, or high, as these patients often have mixed acid–base disorders, such as a metabolic acidosis from AKA and a metabolic alkalosis from vomiting and volume depletion.
Blood glucose is low to mildly elevated.
Blood alcohol level is usually low or zero, as vomiting and abdominal pain limit intake.
Serum ketones (acetoacetate and β-hydroxybutyrate) are elevated. Although ketones are usually detected in significant amounts, the redox state may be such that most or all acetoacetate is reduced to β-hydroxybutyrate.
If the nitroprusside test is used to detect serum or urine ketones, results may be falsely low or negative because this test only detects acetoacetate and not β-hydroxybutyrate.
Diagnosis of AKA is established by criteria listed in Table 132-1.
Differential diagnosis includes other causes of an anion gap metabolic acidosis such as salicylate, methanol, ethylene glycol, iron, or isoniazid toxicity, diabetic ketoacidosis, uremia, and lactic acidosis.
TABLE 132-1 Diagnostic Criteria for Alcoholic Ketoacidosis*
Low, normal, or slightly elevated serum glucose
Binge drinking ending in nausea, vomiting, and decreased intake
Wide anion gap metabolic acidosis
Positive serum ketones*
Wide anion gap metabolic acidosis without alternate explanation
*The absence of ketones in the serum based on the nitroprusside test does not exclude the diagnosis.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Treat with IV infusion of D5NS. The crystalloid solution restores intravascular volume and glucose administration stimulates endogenous insulin release, which inhibits ketosis.
Unlike treatment for diabetic ketoacidosis, insulin administration is not necessary.
Thiamine 100 milligrams IV is recommended before glucose administration to, in theory, prevent precipitation of Wernicke’s disease.
Other electrolytes and vitamins should be supplemented as the condition warrants.
Treatment should be continued until the acidosis clears, which is usually within 12 to 24 hours.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 221, “Alcoholic Ketoacidosis,” by William A. Woods and Debra G. Perina.