Emergent Treatment of Alcoholic Ketoacidosis
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Alcoholic ketoacidosis (AKA) is an acute metabolic acidosis seen in persons with a recent history of binge drinking and little or no nutritional intake.
Alcoholic ketoacidosis is characterized by high serum ketone levels and an elevated anion gap (see the Anion Gap calculator). 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. [1, 2]
Go to Alcoholic Ketoacidosis, Metabolic Alkalosis, and Pediatric Metabolic Alkalosis for complete information on these topics.
Assess the patient’s airway and manage as clinically indicated. Administer oxygen as indicated.
Obtain intravenous access and administer fluid resuscitation for volume depletion and/or hypotension. Consider and treat hypoglycemia. [3]
If the patient’s mental status is diminished, consider administration of naloxone and thiamine.
Note information about the patient’s social situation and the presence of intoxicating agents besides alcohol.
Suspect alcoholic ketoacidosis in any patient with recent binge drinking and an elevated anion gap. A history of alcoholism is not necessary for the development of alcoholic ketoacidosis. One episode of heavy alcohol intake combined with inadequate carbohydrate intake is sufficient to generate this disease state. Presenting symptoms may include nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension. [4]
Urine tests for ketones may be falsely negative or only trace positive in alcoholic ketoacidosis. This is because the relative excess of NADH to NAD+ created by the oxidative metabolism of ethanol creates a reducing environment. The ketoacids beta-hydroxybutyrate and alpha-ketoglutarate exist in dynamic equilibrium with one another; a reducing environment skews the proportions of these compounds towards an excess of beta-hydroxybutyrate, which may not be detected by routine assays for ketones. [5]
Although patients with alcoholic ketoacidosis have depleted glycogen stores, their serum glucose level is often within the normal range. An elevated lactic acid level and elevated osmolar gap due to acetone are typically seen. Significant lactic acidosis may be seen because of a combination dehydration and a metabolic redox state which favors pyruvate over lactate. [6]
An elevated osmole gap, though non-specific, should raise suspicion for toxic alcohol ingestion such as with methanol or ethylene glycol. If the anion gap (see the Anion Gap calculator) fails to close as resuscitation continues, it is important to consider other causes of an anion gap acidosis, such as methanol or ethylene glycol ingestion (co-ingestion). Although alcoholic ketoacidosis alone may increase the osmole gap, maintain a low threshold to treat suspected toxic alcohol ingestion with the alcohol dehydrogenase inhibitor, fomepizole. [7, 8] When considering other co-ingestants, note that alcoholic ketoacidosis can cause a mildly elevated osmolar gap (approximately 20 mmol/kg). [7]
Evaluate the patient for signs of alcohol withdrawal syndrome, which may include tremors, agitation, diaphoresis, tachycardia, hypertension, seizures, or delirium. Exclude other causes of autonomic hyperactivity and altered mental status. If the diagnosis of alcohol withdrawal syndrome is established, consider the judicious use of benzodiazepines, which should be titrated to clinical response.
Assess for clinical signs of thiamine deficiency (Wernicke-Korsakoff syndrome). Specifically look for nystagmus, confusion, ataxia, confabulation, and restriction of extraocular movements. Strongly consider providing thiamine supplementation to patients with alcohol dependence even without signs of thiamine deficiency.
Once the diagnosis of alcoholic ketoacidosis (AKA) is established, the mainstay of treatment is hydration with 5% dextrose in normal saline (D5 NS) to address the principal physiologic derangement, a lack of metabolic substrate (glucose). Carbohydrate and fluid replacement reverse this process by increasing serum insulin levels and suppressing the release of glucagon and other counterregulatory hormones and by providing metabolic substrate. Dextrose stimulates the oxidation of the reduced form of nicotinamide adenine dinucleotide (NADH) and aids in normalizing the ratio of NADH to nicotinamide adenine dinucleotide (NAD+).
Fluids alone do not correct AKA as quickly as fluids and carbohydrates together. Thiamine supplementation should also be given upon initiation of dextrose. Patients who can tolerate oral nutrition should be fed.
In general, exogenous insulin is contraindicated in the treatment of AKA, because it may cause life-threatening hypoglycemia in patients with depleted glycogen stores. In most cases, the patient’s endogenous insulin levels rise appropriately with adequate carbohydrate and volume replacement. Insulin may be required in patients with diabetes who have AKA. If the patient’s blood glucose level is significantly elevated, AKA may be indistinguishable from diabetic ketoacidosis (DKA). The disorders also may coexist.
As rehydration progresses and adequate renal function is established, consider electrolyte replacement, giving particular attention to potassium and magnesium.
Bicarbonate therapy should be considered only in the face of severe, life-threatening acidosis (ie, pH < 7.1) that is unresponsive to fluid therapy.
Patients with alcoholic ketoacidosis (AKA) may have various coexisting illnesses, especially those commonly associated with chronic alcohol abuse. A thorough history and physical examination must be obtained. Associated conditions include pancreatitis, hepatitis, cirrhosis, coagulopathy, gastritis, GI bleeding, pneumonia, cardiomyopathy, alcohol withdrawal, infection, anemia, seizures, cerebrovascular accident (CVA), myopathy, rhabdomyolysis, neuropathy, arrhythmias, vitamin deficiency (Wernicke-Korsakoff syndrome), and intoxication with alcohol or other substances. These associated illnesses and conditions may be a significant source of morbidity and mortality if not properly addressed.
Admit patients for continued treatment. Restoration of volume status and correction of the acidosis may be difficult to accomplish in the emergency department (ED).
Counseling and/or therapy for alcohol abuse should be part of the patient’s treatment regimen and should continue following discharge.
A requirement for any medications other than D5 NS and thiamine are uncommon. Fluid resuscitation, carbohydrate administration, and thiamine supplementation are the mainstays of treatment in alcoholic ketoacidosis (AKA). Fundamentally however, the patient must eat!
The need to correct pH actively depends on the severity of the pH imbalance, the compensatory capabilities of the patient, the patient’s overall clinical condition, and the potential harm caused by alkali administration. Sodium bicarbonate and other comparable solutions are usually unnecessary with adequate carbohydrate and fluid replacement. [9]
This is indicated to correct a thiamine deficiency.
These agents are rarely used for the management of severe metabolic acidosis.
Kraut JA, Kurtz I. Toxic alcohol ingestions: clinical features, diagnosis, and management. Clin J Am Soc Nephrol. 2008 Jan. 3(1):208-25. [Medline]. [Full Text].
Yokoyama A, Yokoyama T, Mizukami T, Matsui T, Shiraishi K, Kimura M, et al. Alcoholic Ketosis: Prevalence, Determinants, and Ketohepatitis in Japanese Alcoholic Men. Alcohol Alcohol. 2014 Aug 1. [Medline].
Matsuzaki T, Shiraishi W, Iwanaga Y, Yamamoto A. Case of alcoholic ketoacidosis accompanied with severe hypoglycemia. J UOEH. 2015 Mar 1. 37 (1):43-7. [Medline].
Nurulamin M. Noor, Krishna Basavaraju, and Dan Sharpstone. Alcoholic ketoacidosis: a case report and review of the literature. Oxford Medical Case Reports. March 2016. 3:31-33. [Full Text].
Smith SW, Manini AF, Szekely T, Hoffman RS. Bedside detection of urine beta-hydroxybutyrate in diagnosing metabolic acidosis. Acad Emerg Med. 2008 Aug. 15 (8):751-6. [Medline].
Gerrity RS, Pizon AF, King AM, Katz KD, Menke NB. A Patient With Alcoholic Ketoacidosis and Profound Lactemia. J Emerg Med. 2016 Oct. 51 (4):447-449. [Medline].
Schelling JR, Howard RL, Winter SD, Linas SL. Increased osmolal gap in alcoholic ketoacidosis and lactic acidosis. Ann Intern Med. 1990 Oct 15. 113 (8):580-2. [Medline].
Almaghamsi AM, Yeung CK. Osmolal gap in alcoholic ketoacidosis. Clin Nephrol. 1997 Jul. 48 (1):52-3. [Medline].
Kelly AM. The case for venous rather than arterial blood gases in diabetic ketoacidosis. Emerg Med Australas. 2006 Feb. 18(1):64-7. [Medline].
Adam Blumenberg, MD, MA Fellow Physician in Medical Toxicology, Assistant Clinical Instructor, Department of Emergency Medicine, Oregon Health and Science University School of Medicine
Adam Blumenberg, MD, MA is a member of the following medical societies: Alpha Omega Alpha, Gold Humanism Honor Society
Disclosure: Nothing to disclose.
Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; 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, Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen 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.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
Chaiya Laoteppitaks, MD Assistant Professor, Department of Emergency Medicine, Sidney Kimmel Medical College of Thomas Jefferson University
Chaiya Laoteppitaks, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians
Disclosure: Nothing to disclose.
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Mary Claire O’Brien, MD, and Roy Alson, MD, PhD, to the development and writing of the source article.
Emergent Treatment of Alcoholic Ketoacidosis
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