Alcoholic Ketoacidosis (AKA)

Article Author:
Robert Howard
Article Editor:
Syed Rizwan Bokhari
4/1/2019 2:47:51 PM
PubMed Link:
Alcoholic Ketoacidosis (AKA)


Alcoholic ketoacidosis (AKA) is a clinical syndrome seen mostly in chronic alcoholics and frequently seen in patients who binge drink.  Typical patients are usually chronic drinkers who are unable to tolerate oral nutrition for a 1 to 3 day period.  Patients often have a recent bout of heavy drinking before the period of relative starvation, with persistent vomiting and abdominal pain contributing to their inability to tolerate PO intake. [1][2][3][4]


The etiology of Alcoholic ketoacidosis stems from the patient's inability to ingest, absorb and utilize glucose from their diet.  The vomiting and nausea prevent the patient from keeping foodstuffs in the GI tract that can cross over and provide nourishment. The alcohol further depressed gluconeogenesis in the body and keeps blood sugar levels low. An anxiety state and alcohol withdrawal further exacerbate the patient's ability to eat.  The lack of nutrients other than alcohol causes the creation of ketones and an elevated gap ketoacidosis in the absence of diabetes. [5][6]


The prevalence correlates with the incidence of alcohol abuse in a community. No racial or sexual differences in incidence are noted. AKA can occur in adults of any age; it more often occurs persons aged 20-60 years who are chronic alcohol abusers. Rarely, AKA occurs after a binge in persons who are not chronic drinkers.[7]


Patients present in a dehydrated state after a bout of heavy drinking and then an ongoing lack of oral intake. This period of poor PO intake lasts from 1 to 3 days. The pathophysiology of AKA starts with low glycogen stores and a lack of oral food intake, which shifts the metabolism from Carbohydrates to fats and lipids. The decreased PO intake causes decreased insulin levels and an increase in counter-regulatory hormones, Cortisol, Glucagon, and Epinephrine. The lack of insulin also allows an increase in the activity of hormone sensitive lipase. These changes are further enhanced, for as Ethanol is metabolized to Acetaldehyde and AcetylCOA, the NADH/NAD+ ratio increase.  The resultant increased NADH/NAD+ ratio increases lipid metabolism.  All of these changes increase the breakdown of lipids to Ketoacids. The elevated NADH/NAD+ ratio further encourage the conversion of Acetoacetate to Beta-Hydroxybutyrate.  Beta-hydroxybutyrate is the predominate ketoacid in AKA.  Ketoacids further accumulate as dehydration and decreased renal perfusion limit the removal of ketoacids. The differential diagnosis includes other causes of an increased anion gap metabolic acidosis. In a patient with diabetes, there must also be a consideration of DKA. A hemoglobin A1C may help in that consideration [8][9]


The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body. Ethyl alcohol oxidizes at a rate of 20 to 25mg/dl per hour in most individuals.  The accompanying lack of alcohol in the patient's body and the fact that for sometime the only source of calories that a patient has is ethanol both contribute to the clinical syndrome that we see.  

History and Physical

Diagnosis of AKA is made on a clinical basis.  Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain and are often agitated. Most patients will often have a ketone odor on their breath.

  • Tachycardia is common and due to several factors including:  (1) several days of ethanol ingestion, which blocks ADH and causes diuresis and increased urinary frequency, (2) nausea and vomiting which result in decreased PO intake 1 to 3 days prior to presentation, (3) abdominal pain which exacerbates decreased PO intake.  Patients develop acidosis, which causes an increase in respirations and fluid loss.
  • Dehydration causes an elevated heart rate and dry mucous membranes.  A degree of alcohol withdrawal and agitation are likely to present, resulting in an increased heart rate as well.
  • Patients are often become tachypneic due to acidosis, dehydration, alcohol withdrawal and abdominal pain.
  • Abdominal pain is commonly present although may be secondary to alcoholic gastritis or pancreatitis.  Rebound tenderness is not common, and the pain is commonly epigastric in nature.  If rebound tenderness or peritoneal signs are present, another cause should be sought for the pain.  

Neurologically, patients are often agitated, but may occasionally present lethargic on examination. Alcohol withdrawal, in combination with nausea and vomiting, makes most patients agitated.  However, if an AKA patient is lethargic or comatose, an alternative cause should be sought.


Laboratory findings are as follows:

  • CBC - The CBC may be elevated. The WBC, hemoglobin and the hematocrit may be elevated in a dehydrated patient.  An elevated mean corpuscular volume (MCV) is often seen in chronic alcoholics.
  • Metabolic Panel - The basic metabolic panel will likely be abnormal. Potassium levels can be normal or low, as dehydration and decreased PO intake frequently decrease the serum K level.  Bicarbonate or HCO3 will likely be decreased with the presence of a metabolic acidosis. The BUN to Cr ratio may be elevated if the patient is dehydrated.  Glucose levels are usually mildly elevated but are not generally above 250mg/dl.  The initial glucose levels are more likely to be in the normal range.
  • Beta - Hydroxybutyrate - The Beta-Hydroxybutyrate (B-OH) level will be significantly elevated. The degree of elevation of B-OH will be much greater than the elevation of lactate. If the lactate is greater than four mmol/L, another cause of the acidosis should be investigated. Serum alcohol levels are often low or absent.
  • ABG - The blood gas analysis will most likely reveal a pH that is low or normal. There will be a metabolic acidosis present with a decreased HCO3 level. If the patient is capable, a respiratory alkalosis will be mounted by the patient. The presence of a mixed disorder may also be present as significant vomiting can cause a metabolic alkalosis.
  • Urinalysis - Urinalysis may show an elevated specific gravity as the patient is usually dehydrated. The SG of the urine can be in the normal range if the patient has been drinking recently enough for the effect of ADH inhibition to be still present.  The patient may have been able to tolerate PO fluids over the last 24 hours, but no significant solid food.  
  • Nitroprusside Test - Ketonuria should be present as the Nitroprusside test will be positive with the present of Acetoacetate.  It may be weakly positive despite the presence of significant ketosis as the urine Nitroprusside test may vastly underestimate the presence of Beta-Hydroxybutyrate which is the major ketoacid present in AKA. Glucosuria will likely be absent.


  • The EKG will likely show sinus tachycardia, but atrial fibrillation or atrial flutter can be seen in a dehydrated alcohol abuser in AKA. The initial Chest x-ray is usually negative. 

Treatment / Management

Diagnosis of the condition of AKA is the first step in treatment. The patient should have an accucheck, or bedside POC testing was done on initial presentation.  The patients need to be treated with fluid and volume resuscitation. The patient will need IV normal saline volume replacement.  If the initial blood glucose level is normal or low, five%dextrose should be added to the IV fluids. The patient will need volume replacement to replenish circulating volume and to increase the elimination of ketoacids.  Dextrose will increase glycogen stores, diminish counterregulatory hormones and increase insulin secretion. Dextrose will help to suppress and eliminate ketoacid formation.  Hypokalemia needs to be treated, and dextrose containing fluids can be held until potassium levels are normalized. Intravenous saline will also diminish serum potassium levels. Thiamine administration should proceed with the IV fluids. Magnesium and Phosphate can be repleted if the serum levels are found to be low.  Intravenous Benzodiazepines should be given for seizure prophylaxis and to prevent full-blown alcoholic withdrawal.  An antiemetic such as Ondansetron or Metoclopramide may also be given to control nausea and vomiting.

AKA should be diagnosed clinically. The patients need fluid resuscitation, close monitoring of electrolytes and treatment to prevent alcohol withdrawal. They also need to have a complete history and physical for a complete differential diagnosis. [2][10][11]

Enhancing Healthcare Team Outcomes

Alcoholic ketoacidosis can affect many organs systems and is best managed by an interprofessional team of healthcare workers including a nurse and clinician. The key is to differentiate alcoholic ketoacidosis from starvation and diabetic-ketoacidosis. Starvation ketosis is more common than AKA, but starvation ketosis is not often complicated by acidosis. Diabetic ketoacidosis can be confused with AKA.  The glucose levels in AKA are rarely above 250mg/dl. In a hyperglycemic patient, Hemoglobin A1C should also be ordered to assess for the presence of uncontrolled blood glucose levels.

Also, in AKA, the Beta-hydroxybutyrate to acetoacetate ratio will be much higher with ratios of up to 8: 1, whereas in DKA B-OH to acetoacetate ratios are a 3: 1 ratio. The B-OH levels are higher in AKA. 

Other diagnoses that need to be considered are toxic alcohol ingestions; methanol and ethylene glycol ingestions can cause GI upset and an overwhelming acidosis.  Adding to the difficulty, the patient is often a chronic alcoholic.  Elevation of the osmolar gap < 20mOsm/kg is not often present in AKA but is present in ingestions of the toxic alcohols.  Always correct for the ethanol level in the osmolar gap calculation by dividing the ethanol level by 4.6. 


[1] Ghimire P,Dhamoon AS, Ketoacidosis null. 2018 Jan     [PubMed PMID: 30521269]
[2] Gerrity RS,Pizon AF,King AM,Katz KD,Menke NB, A Patient With Alcoholic Ketoacidosis and Profound Lactemia. The Journal of emergency medicine. 2016 Oct     [PubMed PMID: 27697197]
[3] Noor NM,Basavaraju K,Sharpstone D, Alcoholic ketoacidosis: a case report and review of the literature. Oxford medical case reports. 2016 Mar     [PubMed PMID: 26949539]
[4] Matsuzaki T,Shiraishi W,Iwanaga Y,Yamamoto A, Case of alcoholic ketoacidosis accompanied with severe hypoglycemia. Journal of UOEH. 2015 Mar 1     [PubMed PMID: 25787101]
[5] Suzuki K,Tamai Y,Urade S,Ino K,Sugawara Y,Katayama N,Hoshino T, Alcoholic ketoacidosis that developed with a hypoglycemic attack after eating a high-fat meal. Acute medicine     [PubMed PMID: 29930832]
[6] Heltø K, [Alcoholic ketoacidosis and lactic acidosis]. Ugeskrift for laeger. 2009 Jan 26     [PubMed PMID: 19176163]
[7] Yokoyama A,Yokoyama T,Mizukami T,Matsui T,Shiraishi K,Kimura M,Matsushita S,Higuchi S,Maruyama K, Alcoholic Ketosis: Prevalence, Determinants, and Ketohepatitis in Japanese Alcoholic Men. Alcohol and alcoholism (Oxford, Oxfordshire). 2014 Nov     [PubMed PMID: 25085997]
[8] McGuire LC,Cruickshank AM,Munro PT, Alcoholic ketoacidosis. Emergency medicine journal : EMJ. 2006 Jun     [PubMed PMID: 16714496]
[9] Caspar CB,Risti B,Iten PX,Jost R,Russi EW,Speich R, [Alcoholic ketoacidosis]. Schweizerische medizinische Wochenschrift. 1993 Oct 16     [PubMed PMID: 8259474]
[10] Allison MG,McCurdy MT, Alcoholic metabolic emergencies. Emergency medicine clinics of North America. 2014 May     [PubMed PMID: 24766933]
[11] Chandrasekara H,Fernando P,Danjuma M,Jayawarna C, Ketoacidosis is not always due to diabetes. BMJ case reports. 2014 Feb 25     [PubMed PMID: 24569261]