eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Alcoholic Ketoacidosis: Differential Diagnoses & Workup

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

Differential Diagnoses

Alcohol and Substance Abuse Evaluation
Pancreatitis
Cholecystitis and Biliary Colic
Toxicity, Alcohols
Diabetic Ketoacidosis
Wernicke Encephalopathy
Gastritis and Peptic Ulcer Disease
Withdrawal Syndromes
Mesenteric Ischemia
Metabolic Acidosis

Other Problems to Be Considered

Korsakoff psychosis

Workup

Laboratory Studies

  • Arterial blood gas determination
    • Arterial blood gas (ABG) measurement may show a low pCO 2 level, low bicarbonate level, and normal partial pressure of oxygen (pO 2 ) level in a pattern consistent with a metabolic acidosis with a respiratory compensation. 
    • Serum pH levels may be misleading because the patient with alcoholic ketoacidosis (AKA) often has a mixed acid-base disorder. In addition to metabolic acidosis due to ketone formation, a metabolic alkalosis may be present due to vomiting and volume depletion. A respiratory alkalosis may be present secondary to hyperventilation. The possibility of a double or triple acid-base disorder means serum pH levels may be near normal despite a severe acid-base disturbance. 
    • Venous blood gas measurements correlate very well with arterial measurements. One should consider using venous blood gas measurements in lieu of arterial blood gas measurements.2
  • Serum ketones
    • The nitroprusside reaction (Acetest) may be negative or only weakly positive for serum ketones because nitroprusside reacts with acetone and AcAc, but not with β–OH. Direct serum measurements of β–OH should be used when available.
    • In AKA, the β-OH/AcAc formation ratio is 5:1. Therefore, ketosis may be more severe than would be inferred from a nitroprusside reaction alone. With initial therapy, ketone formation shifts toward the production of AcAc so that measured ketone levels rise, although β-OH levels decrease. 
  • Glucose and electrolyte levels
    • Serum glucose level may be low, normal, or slightly elevated, which should help the clinician distinguish alcoholic ketoacidosis (AKA) from diabetic ketoacidosis (DKA). Usually, serum glucose levels are markedly elevated in cases of DKA.
    • Anion gap is elevated.
    • Lactate levels may be elevated.
    • Hyponatremia and hypokalemia have been reported in patients with alcoholic ketoacidosis.
    • Ethanol-enhanced urinary excretion, emesis, and antacid use may contribute to hypophosphatemia in people who have chronic alcoholism.
    • Hypomagnesemia may be caused by poor nutrition, decreased renal absorption of magnesium, or nasogastric suctioning. Serum magnesium levels are not reliable indicators of total body magnesium stores, however. Due to the linked excretion between potassium and magnesium, the presence of hypokalemia is a strong indicator of hypomagnesemia and can be used as a surrogate test to determine if magnesium replacement is needed.
    • BUN and creatinine levels are typically elevated.
  • Complete blood count
    • Anemia may be present secondary to nutritional deficiencies, alcoholic bone marrow suppression, or GI bleeding.
    • Hematocrit (Hct) may be falsely elevated from hemoconcentration in the presence of intravascular volume depletion
    • Thrombocytopenia may be present due to chronic liver disease.
  • Liver and pancreatic function test results, including hepatic enzymes (eg, serum glutamic-oxaloacetic transaminase [SGOT], lactate dehydrogenase [LDH], alkaline phosphatase), total bilirubin, and pancreatic amylase and lipase levels, may be elevated because of associated illnesses (eg, alcohol-induced hepatitis, pancreatitis).
  • Alcohol levels
    • Alcohol level may be absent or low due to anorexia and decreased drinking in the preceding 1-3 days. Blood alcohol levels do not typically change the management of AKA and are therefore not often necessary.

Imaging Studies

  • Chest radiography: Consider obtaining a chest radiograph because aspiration pneumonia is common in persons with alcoholism. Esophageal rupture may occur with prolonged retching, resulting in pneumomediastinum or subdiaphragmatic air.
  • Urgent abdominal series: Consider obtaining an urgent abdominal series in patients with significant vomiting and abdominal pain because these symptoms may indicate obstruction and/or perforation of a viscus.

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

  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].

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Further Reading

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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

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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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