Alcoholic Ketoacidosis

Basics

Description

  • Increased production of ketone bodies due to:
    • Dehydration (nausea/vomiting, ADH inhibition) leads to increased stress hormone production leading to ketone formation
    • Depleted glycogen stores in the liver (malnutrition/decrease carbohydrate intake)
    • Elevated ratio of NADH/NAD due to ethanol metabolism
    • Increased free fatty acid production
  • Elevated NADH/NAD ratio leads to the predominate production of β–hydroxybutyrate (BHB) over acetoacetate (AcAc)

Etiology

  • Malnourished, chronic alcohol abusers following a recent episode of heavy alcohol consumption:
    • Develop nausea, vomiting, or abdominal pain
    • Leading to the cessation of alcohol ingestion
  • Presentation usually occurs within 12–72 hr

Diagnosis

Signs and Symptoms

  • Dehydration
  • Fever absent unless there is an underlying infection
  • Tachycardia (common) due to:
    • Dehydration with associated orthostatic changes
    • Concurrent alcohol withdrawal
  • Tachypnea:
    • Common
    • Deep, rapid, Kussmaul respirations frequently present
  • Nausea and vomiting
  • Abdominal pain (nausea, vomiting, and abdominal pain are the most common symptoms):
    • Usually diffuse with nonspecific tenderness
    • Epigastric pain common
    • Rebound tenderness, abdominal distension, hypoactive bowel sounds uncommon
    • Mandates a search for an alternative, coexistent illness
  • Decreased urinary output from hypovolemia
  • Mental status:
    • Minimally altered as a result of hypovolemia and possibly intoxication
    • Altered mental status mandates a search for other associated conditions such as:
      • Head injury, cerebrovascular accident (CVA), or intracranial hemorrhage
      • Hypoglycemia
      • Alcohol withdrawal
      • Encephalopathy
      • Toxins
  • Visual disturbances:
    • Reports of isolated visual disturbances with AKA common

History
Chronic alcohol use:
  • Recent binge
  • Abrupt cessation

Physical Exam
  • Findings of dehydration most common
  • May have ketotic odor
  • Kussmaul respirations
  • Palmar erythema (alcoholism)

Essential Workup

  • Presence of an increased anion gap metabolic acidosis secondary to the presence of ketones
  • Differentiate from toxic alcohol ingestion and other causes of anion gap metabolic acidosis.

Diagnostic Tests and Interpretation

Lab
  • Acid–base disturbance:
    • Increased anion gap metabolic acidosis hallmark
    • Mixed acid–base disturbance common:
      • Respiratory alkalosis
      • Metabolic alkalosis secondary to vomiting and dehydration
      • Hyperchloremic acidosis
    • Mild lactic acidosis common
      • Due to dehydration and the direct metabolic effects of ethanol
      • Profound lactic acidosis should prompt a search for other disorders such as seizures, hypoxia, and shock.
    • Positive urine and serum nitroprusside reaction tests for ketoacids
      • May not reflect the severity of the underlying ketoacidosis, since BHB predominates and is not measured by this test.
      • May become misleadingly more positive during treatment as more AcAc is produced.
  • Electrolytes:
    • Decreased serum bicarbonate
    • Hypokalemia due to vomiting
    • Hypocalcemia
    • Hypophosphatemia may worsen with Tx
    • Hypomagnesemia
    • Initially, can see hyperkalemia and/or hyperphosphatemia which will correct with treatment of the acidosis
  • Glucose:
    • Usually mildly elevated
    • Should be monitored frequently as per DKA
    • Hypoglycemia may be present
  • Alcohol level may be negative
  • BUN and creatinine mildly elevated due to dehydration unless underlying renal disease.
  • CBC:
    • Mild leukocytosis—neither sensitive nor specific
    • Thrombocytopenia and anemia commonly due to chronic alcoholism
  • Urinalysis:
    • Ketonuria without glucosuria
  • Amylase/lipase:
    • Elevated with associated pancreatitis
  • LFTs:
    • May have mildly elevated LFTs
  • Osmolal gap:
    • May be elevated
    • Elevation >20 mOsm/kg should prompt evaluation for other ingestions (methanol and ethylene glycol)
    • Correct for ethanol level in osmolal gap by dividing ethanol level by 4.6

Imaging
  • CXR if suspect associated pneumonia
  • Abdominal films for free air if an acute abdomen is present
  • CT scan of the head if associated trauma or unexplained altered mental status

Differential Diagnosis

  • Elevated anion gap metabolic acidosis: ACAAT MUDPILES:
    • Alcoholic ketoacidosis
    • Cyanide, CO, H2S, others
    • Acetaminophen:
      • Rare in acute ingestion
      • Rare in chronic ingestion
      • Fulminant hepatic failure
    • Antiretrovirals (NRTI)
    • Toluene
    • Methanol, metformin
    • Uremia
    • Diabetic ketoacidosis
    • Paraldehyde, phenformin, propylene glycol
    • Iron, INH
    • Lactic acidosis
    • Ethylene glycol
    • Salicylate, acetylsalicylic acid (ASA; aspirin), starvation ketosis
  • Hypovolemia:
    • GI bleeding
    • Sepsis
  • Abdominal pain, nausea, vomiting:
    • Pancreatitis
    • GI bleeding
    • Gastritis
    • Hepatitis
    • Perforated ulcer
    • Alcohol withdrawal
    • DKA
    • Viral illness
    • Obstruction/Ileus

Treatment

Pre Hospital

  • Supportive measures including IV access with 0.9 NS, oxygen, and cardiac monitoring
  • Search for historical clues that may suggest other etiologies such as toxic ingestions or diabetic history, consider scene search
  • Attend to other possible coexistent illnesses such as GI bleeding.

Initial Stabilization/Therapy

  • Cardiac monitor and supplement oxygen
  • Naloxone, thiamine, and dextrose if altered mental status
  • Initiate 0.9 NS IV fluids
    • 500 mL–1 L bolus
    • Fluid resuscitation as necessary
    • Promotes renal excretion of ketone bodies

Ed Treatment/Procedures

  • Antiemetic for vomiting—ondansetron, promethazine, or prochlorperazine
  • Benzodiazepines for symptoms of alcohol withdrawal
  • Start dextrose containing solutions (D5NS):
    • More rapid resolution of the metabolic abnormalities than saline alone
    • Rate higher than maintenance as tolerated until acidosis resolves
    • Avoid with significant hyperglycemia
    • Help replete glycogen stores
    • Decreases production of ketone bodies by stimulating the production of endogenous insulin
  • Thiamine repletion (IV) prior to glucose administration to avoid precipitating Wernicke encephalopathy
  • Sodium bicarbonate rarely indicated:
    • Consider in severe acidosis with associated cardiovascular dysfunction or irritability
  • Electrolyte replacement:
    • Hypokalemia occurs with treatment and should be anticipated.
    • Hypophosphatemia may occur with treatment.
    • Magnesium replacement as indicated for both hypomagnesemia and hypokalemia
  • Insulin is not indicated and may precipitate hypoglycemia.

Medication

  • D50W: 1 ampule of 50% dextrose (25 g) IVP
  • Lorazepam (benzodiazepine): 2 mg IV and titrate to effect
  • Narcan: 2 mg IVP
  • Ondansetron: 4–8 mg IVP
  • Prochlorperazine: 5–10 mg IVP slowly (not >5 mg/min)
  • Promethazine: 12.5–25 mg IVP
  • Thiamine: 100 mg IVP

Ongoing Care

Disposition

Admission Criteria
  • Persistent metabolic acidosis
  • Persistent signs of hypovolemia
  • Persistent nausea and vomiting
  • Abdominal pain of uncertain etiology
  • Comorbid illness requiring admission for treatment
  • Need for monitored bed due to electrolyte abnormalities requiring continued treatment

Discharge Criteria
  • Many patients can be managed in observation unit over 12–24 hr.
  • Tolerating oral fluids well
  • Resolution of metabolic abnormalities
  • No other associated illnesses requiring additional therapy
  • Most will warrant at least observation

Follow-Up Recommendations

Counseling regarding alcohol cessation

Pearls and Pitfalls

  • Aggressive volume repletion with dextrose containing fluid is key.
  • Volume resuscitate with NS as necessary
  • Thiamine repletion
  • Monitor electrolytes before and after treatment.
  • Unrecognized increased osmolal gap
  • Inadequate monitoring of glucose levels
  • Failure to recognize initial electrolyte abnormalities and electrolyte shifts caused by treatment.
  • Must be placed on monitor:
    • Cases of sudden death in AKA:
      • Possible alcoholic cardiomyopathy
      • Dysrhythmias
      • Electrolyte derangements

Additional Reading

  • Cartwright MM, Hajja W, Al-Khatib S, et al. Toxigenic and metabolic causes of ketosis and ketoacidotic syndromes. Crit Care Clin. 2012;28(4): 601–631.  [PMID:22998993]
  • Diltoer M, Troubleyn J, Lauwers R, et al. Ketosis and cardiac failure: Common signs of a single condition. Eur J Emerg Med. 2004;11(3):172–175.  [PMID:15167181]
  • McGuire L, Cruickshank A, Munro P. Alcoholic ketoacidosis. Emerg Med J. 2006;23:417–420.  [PMID:16714496]
  • Yanagawa Y, Kiyozumi T, Hatanaka K, et al. Reversible blindness associated with alcoholic ketoacidosis. Am J Opthalmology. 2004;137(4):775–777.
  • Yanagawa Y, Sakamoto T, Okada Y. Six cases of sudden cardiac arrest in alcoholic ketoacidosis. Intern Med. 2008;47(2):113–117.  [PMID:18195501]

See Also

  • Acidosis
  • Diabetic Ketoacidosis

Codes

ICD-9

276.2 Acidosis

ICD-10

Acidosis

SNOMED

  • 55571001 alcoholic ketoacidosis (disorder)

Authors

Charles Garcia


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