eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Alcoholic Ketoacidosis

Author: Chaiya Laoteppitaks, MD, Staff Physician, Department of Emergency Medicine, State University of New York Kings County Hospital Center
Coauthor(s): Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Contributor Information and Disclosures

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

References

  1. Manini AF, Hoffman RS, Nelson LS. Alcoholic ketoacidosis in an 11-year-old boy. Pediatr Emerg Care. Mar 2008;24(3):170-1. [Medline].

  2. Kelly AM. The case for venous rather than arterial blood gases in diabetic ketoacidosis. Emerg Med Australas. Feb 2006;18(1):64-7. [Medline].

  3. Mihai B, Lacatusu C, Graur M. [Alcoholic ketoacidosis]. Rev Med Chir Soc Med Nat Iasi. Apr-Jun 2008;112(2):321-6. [Medline].

  4. Adams SL. Alcoholic ketoacidosis. Emerg Med Clin North Am. Nov 1990;8(4):749-60. [Medline].

  5. Al-Sanouri I, Dikin M, Soubani AO. Critical care aspects of alcohol abuse. South Med J. Mar 2005;98(3):372-81. [Medline].

  6. Diltoer MW, Troubleyn J, Lauwers R, et al. Ketosis and cardiac failure: common signs of a single condition. Eur J Emerg Med. Jun 2004;11(3):172-5. [Medline].

  7. Fox JC, Whitcomb DC. Alcohol deficiency, stress hormones and bad acidosis: aka AKA. N C Med J. Feb 1991;52(2):69-73. [Medline].

  8. Halperin ML, Hammeke M, Josse RG, Jungas RL. Metabolic acidosis in the alcoholic: a pathophysiologic approach. Metabolism. Mar 1983;32(3):308-15. [Medline].

  9. Hoffman RS, Goldfrank LR. Ethanol-associated metabolic disorders. Emerg Med Clin North Am. Nov 1989;7(4):943-61. [Medline].

  10. Kearns T, Wolfson AB. Metabolic acidosis. Emerg Med Clin North Am. Nov 1989;7(4):823-35. [Medline].

  11. Moss M, Burnham EL. Alcohol abuse in the critically ill patient. Lancet. Dec 23 2006;368(9554):2231-42. [Medline].

  12. Palmer JP. Alcoholic ketoacidosis: clinical and laboratory presentation, pathophysiology and treatment. Clin Endocrinol Metab. Jul 1983;12(2):381-9. [Medline].

  13. Thomsen JL, Simonsen KW, Felby S, Frohlich B. A prospective toxicology analysis in alcoholics. Forensic Sci Int. Nov 10 1997;90(1-2):33-40. [Medline].

  14. Umpierrez GE, DiGirolamo M, Tuvlin JA. Differences in metabolic and hormonal milieu in diabetic- and alcohol-induced ketoacidosis. J Crit Care. Jun 2000;15(2):52-9. [Medline].

  15. Williams HE. Alcoholic hypoglycemia and ketoacidosis. Med Clin North Am. Jan 1984;68(1):33-8. [Medline].

  16. Wrenn KD, Slovis CM, Minion GE, Rutkowski R. The syndrome of alcoholic ketoacidosis. Am J Med. Aug 1991;91(2):119-28. [Medline].

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

Contributor Information and Disclosures

Author

Chaiya Laoteppitaks, MD, Staff Physician, Department of Emergency Medicine, State University of New York Kings County Hospital Center
Chaiya Laoteppitaks, MD is a member of the following medical societies: American College of Emergency Physicians and Emergency Medicine Residents Association
Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Howard A Bessen, MD, Professor of Medicine, Department of Emergency Medicine, UCLA School of Medicine; Program Director, Harbor-UCLA Medical Center
Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

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