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Alcoholic Ketoacidosis
Updated: Jul 28, 2009
Introduction
Background
Alcoholic ketoacidosis (AKA) is an acute metabolic acidosis seen in those with a recent history of binge drinking and little or no nutritional intake. It was first described by Dillon et al in 1940. Previously, diabetes mellitus was the most common cause of a severe ketoacidosis. Dillon described 5 patients with ketoacidosis and normal or slightly elevated blood glucose concentrations. Four of the 5 patients were alcoholics with a recent marked increase in their ethanol intake and a decrease in their normal dietary intake.
Alcoholic ketoacidosis is characterized by high serum ketone levels and an elevated anion gap. A concomitant metabolic alkalosis is also common, resulting from vomiting and volume depletion. Although AKA most commonly occurs in adults with alcoholism, alcoholic ketoacidosis has been reported in less-experienced drinkers of all ages.
Pathophysiology
Alcoholic ketoacidosis (AKA) is a result of starvation with glycogen depletion and counter-regulatory hormone production, an increased nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+) ratio related to ethanol metabolism, and volume depletion, resulting in ketogenesis.
The body decreases insulin activity in the starvation state and increases the production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone. Hormone-sensitive lipase is inhibited by insulin, and, when insulin levels fall, lipolysis is up-regulated causing the release of free fatty acids from peripheral adipose tissue. Free fatty acids are either oxidized to CO2 or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid. Carnitine acyltransferase (CAT) is responsible for transporting the free fatty acids into the mitochondria and therefore regulates the entry of fatty acids into the oxidative pathway. The decreased insulin-to-glucagon ratio that occurs in starvation indirectly reduces the inhibition on CAT activity, thereby allowing more free fatty acids to undergo oxidation and ketone body formation.
Prolonged vomiting leads to dehydration, which decreases renal perfusion, thereby limiting urinary excretion of ketoacids. Moreover, volume depletion increases the concentration of counter-regulatory hormones, further stimulating lipolysis and ketogenesis.
Ethanol is oxidized to acetaldehyde, which is itself oxidized to acetate. Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide (NADH). The decreased ratio of NAD + to NADH has several implications: (1) impaired conversion of lactate to pyruvate with an increase in serum lactic acid levels, (2) impaired gluconeogenesis because pyruvate is not available as a substrate for glucose production, and (3) a shift in the hydroxybutyrate (β-OH) to acetoacetate (AcAc) equilibrium toward β-OH. Unlike diabetic ketoacidosis, the predominant ketone body is -OH. Routine clinical assays for ketonemia test for AcAc and acetone but not for -OH. Clinicians underestimate the degree of ketonemia if they rely solely on the results of laboratory testing.
Frequency
United States
The prevalence of alcoholic ketoacidosis (AKA) in the United States correlates with the incidence and distribution of alcohol abuse within a given community.
Mortality/Morbidity
Mortality is rare; however, alcoholic ketoacidosis (AKA) has been reported as the cause of death in a number of alcoholics. Morbidity more often results from associated complications, such as liver dysfunction, acute pancreatitis, seizures, rhabdomyolysis, hypoglycemia, lactic acidosis, heart failure, or systemic infection.
Race
No specific distribution of this disorder has been identified based on race or ethnicity.
Sex
Males and females are affected equally.
Age
Alcoholic ketoacidosis usually occurs in persons aged 20-60 years who are chronic abusers of alcohol. Alcoholic ketoacidosis occurs only rarely after a binge in persons who are not chronic drinkers. Recently, a case report was published of an 11 year-old boy who presented in AKA after drinking ethanol-based mouthwash.1
Clinical
History
Example case of alcoholic ketoacidosis: A 35 year-old man who chronically abuses alcohol presents with abdominal pain and intractable emesis for 2 days. After 5 days of heavy drinking, he developed the pain and emesis and has stopped eating and drinking altogether. He complains of epigastric pain that radiates through to his back. He is afebrile, tachycardic, and borderline hypotensive. He is sleepy, but awakens easily to verbal stimuli.
Typical symptoms of alcoholic ketoacidosis (AKA) and related conditions may include the following:
- Nausea, vomiting, and abdominal pain (each found in 60-75% of patients)
- Dyspnea, tremulousness, and/or dizziness (10-20% each)
- Muscle pain, diarrhea, syncope, and seizure (1-8% each)
Physical
Generally, the physical findings relate to volume depletion and chronic alcohol abuse. The fruity odor of ketones may be present on the patient's breath. The patient's mental status may be impaired. Physical findings may include the following:
- Tachycardia, tachypnea, and/or abdominal tenderness (30-40% each)
- Hypotension, hypothermia, fever, abdominal distention, rebound tenderness, hepatomegaly, ascites, and/or heme-positive stools (These are less common, with each found in 1-15% of patients.)
Causes
Most cases of alcoholic ketoacidosis (AKA) are related to poor nutritional status due to long-standing alcohol abuse. AKA is often precipitated by another medical illness such as infection or pancreatitis. The diagnostic evaluation of AKA should search for potential precipitating factors when not clearly identified by history.
More on Alcoholic Ketoacidosis |
 Overview: Alcoholic Ketoacidosis |
| Differential Diagnoses & Workup: Alcoholic Ketoacidosis |
| Treatment & Medication: Alcoholic Ketoacidosis |
| Follow-up: Alcoholic Ketoacidosis |
| References |
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References
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Further Reading
Keywords
alcoholic ketoacidosis, AKA, alcoholic acidotic coma, alcohol withdrawal, acute metabolic acidosis, metabolic alkalosis, alcohol abuse, glycogen depletion, lipolysis, ketogenesis, ethanol consumption, ketonemia, alcoholism, chronic alcoholism, chronic alcohol abuse, ketones, substance abuse, ketosis, binge drinking, Wernicke encephalopathy, Wernicke's encephalopathy
