Alcoholic Ketoacidosis: Signs, Symptoms, and Treatment

Patients can have a long-standing history of alcohol use and may also present following binges. Acetic acid is a product of the metabolism of alcohol and also a substrate for ketogenesis. The conversion to acetyl CoA and subsequent entry into various pathways or cycles, one of which is the ketogenesis pathway is determined by the availability of insulin in proportion to the counter-regulatory hormones, which are discussed in more detail below. If you chronically abuse alcohol, you probably don’t get as much nutrition as your body needs. Going on a drinking binge when your body is in a malnourished state may cause abdominal pain, nausea, or vomiting. Infection or other illnesses such as pancreatitis can also trigger alcoholic ketoacidosis in people with alcohol use disorder.

• As mentioned above, the direct measurement of serum beta-hydroxybutyrate is more sensitive and specific than the measurement of urine ketones.
• Low insulin levels are seen inherently in as either an absolute or relative deficiency in type I diabetes or a relative deficiency with insulin resistance in type 2 diabetes.
• The reversal of ketosis and vigorous rehydration are central in the management of AKA.
• On arrival, he is tachycardic and tachypneic, and physical examination findings include dry mucous membranes, decreased sakin turgor, epigastric tenderness, and a tremor in both hands.

Given the frequency with which the condition is seen in other countries, the possibility exists that many cases may be unrecognised and misdiagnosed in UK EDs. AKA should be included in the differential diagnosis of alcohol dependent patients presenting with acute illness. Management is based around exclusion of serious pathology and specific treatment alcoholic ketoacidosis smell for AKA where it is present. A possible link between AKA and sudden death in chronic alcoholism has been proposed but remains unconfirmed. In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption.

Moderate drinkers: fundamentally different?

The clinically relevant ketoacidoses to be discussed include diabetic ketoacidosis (DKA), alcoholic ketoacidosis (AKA), and starvation ketoacidosis. DKA is a potentially life-threatening complication of uncontrolled diabetes mellitus if not recognized and treated early. It typically occurs in the setting of hyperglycemia with relative or absolute insulin deficiency. The paucity of insulin causes unopposed lipolysis and oxidation of free fatty acids, resulting in ketone body production and subsequent increased anion gap metabolic acidosis. Alcoholic ketoacidosis occurs in patients with chronic alcohol abuse, liver disease, and acute alcohol ingestion.

If the patient’s blood glucose level is significantly elevated, AKA may be indistinguishable from diabetic ketoacidosis (DKA). Hypomagnesemia and hypophosphatemia are common problems seen in the laboratory evaluation due to decreased dietary intake and increased losses. As mentioned above, the direct measurement of serum beta-hydroxybutyrate is more sensitive and specific than the measurement of urine ketones. Starvation ketoacidoses patients may again have multiple electrolyte abnormalities due to chronic malnutrition, along with vitamin deficiencies. The pH may not be as low as in DKA or AKA, and the glucose levels may be relatively normal. Under normal conditions, cells rely on free blood glucose as the primary energy source, which is regulated with insulin, glucagon, and somatostatin.

Signs and symptoms of alcoholic ketoacidosis

You can prevent alcoholic ketoacidosis by limiting your alcohol intake. You can learn how to reduce your alcohol intake or eliminate it altogether. Joining a local chapter of Alcoholics Anonymous may provide you with the support you need to cope.

• Note information about the patient’s social situation and the presence of intoxicating agents besides alcohol.
• The high ratio of NADH to NAD+ also favors the reduction of acetoacetate to beta-hydroxybutyrate.
• Group meetings provide support for people trying to quit drinking.
• Blood glucose levels and electrolytes should be monitored on an hourly basis during the initial phase of management.

Acetic acid (an acyl group carrier) is linked with coenzyme A (a thiol) to produce Acetyl-CoA. This process is catalyzed by the enzyme acetyl-CoA synthetase. The metabolism of alcohol itself is a probable contributor to the ketotic state. Alcohol dehydrogenase (ADH), a cytosolic enzyme, metabolizes alcohol to acetaldehyde in hepatocytes.