Alcoholic ketoacidosis is a metabolic state characterized by elevated ketones and metabolic acidosis due to heavy and prolonged alcohol use. In contrast to the hyperglycemia seen in diabetic ketoacidosis, blood glucose levels are normal or low. Alcoholic ketoacidosis can cause severe metabolic derangement and be fatal if untreated.
Alcoholic ketoacidosis is caused by complex physiology that is the result of prolonged and heavy alcohol intake, usually in the setting of poor nutrition. Chronic alcohol use can cause depleted hepatic glycogen stores and ethanol metabolism further impairs gluconeogenesis. This can reduce glucose availability and lead to hypoglycemia and increased reliance on fatty acid and ketone metabolism. An additional stressor such as vomiting or dehydration can cause an increase in counterregulatory hormones such as glucagon, cortisol and growth hormone which may further increase free fatty acid release and ketone production. Ethanol metabolism can also increase blood lactic acid levels which may also contribute to a metabolic acidosis.
Signs and symptoms
Nausea, vomiting, and abdominal pain are commonly present and patients may also have tachypnea, tachycardia, and hypotension. In contrast to diabetic ketoacidosis, patients with alcoholic ketoacidosis are usually alert and lucid despite the severity of the acidosis.
A elevated anion gap metabolic acidosis is the classic presentation of alcoholic ketoacidosis. A mixed acid-base disorder may be present especially if vomiting is contributing to a hypochloremic alkalosis. Laboratory findings are usually similar to diabetic ketoacidosis except patients usually do not present with hyperglycemia or glycosuria. The ratio of beta- hydroxybutryate to acetoacetate is usually higher (~6:1) in contrast to diabetic ketoacidosis (3:1). This can cause false negative results when testing urine ketones as they only measure acetoacetate. Ethanol level may be negative despite a chronic alcohol use history. Lactate may be elevated and electrolyte disturbances including hypokalemia and hypomagnesemia may also be present.
Treatment includes administration of intravenous saline and dextrose as well as correction of electrolyte imbalances. Thiamine supplementation is often included to prevent Wernicke encephalopathy. Insulin is generally not used due to risk of hypoglycemia. Methanol and ethanol glycol poisoning as well as diabetic ketoacidosis should be ruled out before treating for alcoholic ketoacidosis.
Outcomes are generally favorable with treatment but up to 10% may develop cardiac arrest. It is proposed that alcoholic ketoacidosis is a significant cause of death among people with chronic alcoholism although the true prevalence is unknown. Estimation of prevalence and outcomes of this population is limited by difficulty in diagnosing the condition and the presence of multiple disorders at presentation.
In 1940, Edward S. Dillon, W. Wallace, and Leon S. Smelo, first described alcoholic ketoacidosis as a distinct syndrome. They stated that "because of the many and complex factors, both physiologic and pathologic, which influence the acid-base balance of the body, a multitude of processes may bring about the state of acidosis as an end result."
In 1971, David W. Jenkins and colleagues described cases of three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis.
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