Alcoholic Ketoacidosis

Basics

Description

  • Increased production of ketoacids due to:
    • Depleted glycogen stores in the liver after alcohol binge, malnutrition, and decreased food intake
    • Increased stress hormone production in response to starvation and/or alcohol withdrawal leads to amplification of ketone body production
    • Dehydration (nausea/vomiting, ADH inhibition)
    • 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
    • Leading to the cessation of caloric intake
  • Presentation usually occurs within 12–72 hr

Diagnosis

Signs and Symptoms

  • Nausea, vomiting, and abdominal pain: Most common symptoms
    • Usually diffuse with nonspecific tenderness
    • Epigastric pain is common
    • Uncommon: Rebound tenderness, abdominal distension, hypoactive bowel sounds
      • These findings mandate a search for an alternative, coexistent illness
  • Tachycardia (common) due to:
    • Dehydration with associated orthostatic changes
    • Concurrent alcohol withdrawal
  • Tachypnea
    • Common
    • Deep Kussmaul respirations may be present with significant acidosis
  • Decreased urinary output from hypovolemia
  • Fever absent unless there is an underlying infection
  • 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 (more common with severe acidosis)

History
Chronic alcohol use:
  • Recent binge
  • Abrupt cessation

Physical Exam
  • Findings of dehydration most common
  • May have ketotic odor
  • Kussmaul respirations
  • Palmar erythema (cirrhosis)
  • Abdominal tenderness without rebound or guarding

Essential Workup

  • Increased anion gap metabolic acidosis secondary to the presence of ketones:
    • Venous blood gas may be utilized in lieu of arterial
  • Differentiate from diabetic ketoacidosis (DKA), 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 sepsis, shock, seizures, and hypoxia
    • 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
    • β–hydroxybutyrate assay, if available, is more accurate in detecting ketoacids:
      • BHB in ↑↑↑ in AKA, and only ↑ in DKA
  • Electrolytes:
    • Decreased serum bicarbonate
    • Hypokalemia due to vomiting
    • Hypocalcemia
    • Hypophosphatemia (may worsen with treatment)
    • Hypomagnesemia:
      • Serum magnesium level may not accurately reflect total-body depletion
    • Initially, can potentially see hyperkalemia and/or hyperphosphatemia (despite total-body depletion):
      • Will correct with treatment of the acidosis
  • Glucose:
    • May be reduced, normal, or mildly elevated
    • Should be monitored frequently, as with DKA
  • Alcohol level may be negative
  • BUN and creatinine mildly elevated due to dehydration, unless underlying renal disease
  • Urinalysis:
    • Ketonuria without glucosuria
  • Lipase (more specific)/amylase:
    • May be elevated with associated acute pancreatitis
  • 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
  • LFTs:
    • May have mildly elevated LFTs
  • Hemoglobin A1C: May help differentiate AKA vs. DKA:
    • Hyperglycemia >250 mg/dL less common in AKA:
      • A normal A1C makes AKA more likely
    • Euglycemia with elevated A1C increases likelihood of euglycemic DKA (e.g., due to use of SGLT2 [sodium-glucose cotransporter 2] inhibitor)
  • CBC:
    • Mild leukocytosis: neither sensitive nor specific
    • Thrombocytopenia and anemia commonly due to chronic alcoholism

ECG
  • May demonstrate changes in QT interval and/or QRS duration secondary to electrolyte abnormalities and acid–base disturbances
  • Dysrhythmias may be seen, including atrial fibrillation and possible ventricular tachycardia, depending on electrolytes and underlying cardiac condition

Imaging
  • CXR if suspect associated pneumonia or aspiration
  • Abdominal x-rays to rapidly assess for free air if an acute abdomen is present, followed by CT imaging
  • CT 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
    • DKA:
      • Consider euglycemic DKA with use of an SGLT2 inhibitor
    • Paraldehyde, phenformin, propylene glycol
    • Iron, INH
    • Lactic acidosis
    • Ethylene glycol
    • Salicylate (aspirin), starvation ketosis
  • Hypovolemia:
    • GI bleeding
    • Sepsis
  • Abdominal pain, nausea, vomiting:
    • Pancreatitis
    • GI bleeding
    • Gastritis/esophagitis
    • Pneumonia
    • Hepatitis
    • Perforated ulcer
    • Alcohol withdrawal
    • DKA
    • Obstruction/Ileus
    • Spontaneous bacterial peritonitis
    • Viral illness

Treatment

Pre Hospital

  • Supportive measures including IV access with 0.9 NS, oxygen (if hypoxic), 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
  • Supplemental oxygen (if hypoxic)
  • Thiamine and dextrose if altered mental status
  • Consider naloxone if altered mental status
  • Initiate 0.9 NS IV fluids:
    • 1-L bolus
    • Fluid resuscitation as necessary
    • Promotes renal excretion of ketone bodies

Ed Treatment/Procedures

  • Antiemetic for vomiting: ondansetron, prochlorperazine, or promethazine
  • Benzodiazepines for symptoms of alcohol withdrawal
  • Start dextrose-containing solutions (D5NS):
    • More rapid resolution of the metabolic abnormalities than with saline alone
    • Rate higher than maintenance, as tolerated, until acidosis resolves
    • Avoid with significant hyperglycemia
    • Helps replete glycogen stores
    • Decreases production of ketone bodies by stimulating the production of endogenous insulin
  • Thiamine repletion (IV) prior to, or shortly after, glucose administration to avoid precipitating Wernicke encephalopathy—do not delay glucose administration
  • Sodium bicarbonate is not generally indicated:
    • No peer-reviewed evidence to support use
    • Consider in cases of severe acidemia (pH <7.0) with associated cardiovascular dysfunction or irritability
    • Must consider alternative/concomitant etiologies of severe acidemia
  • Electrolyte replacement:
    • Hypokalemia occurs with treatment and should be anticipated
    • Magnesium replacement as indicated for both hypokalemia and hypomagnesemia
    • Hypophosphatemia may occur with treatment:
      • May not require repletion unless critically low
  • Insulin is not indicated and may precipitate hypoglycemia, even in markedly hyperglycemic patients

Medication

  • D50W: 1 amp of 50% dextrose (25 g) IVP
  • Lorazepam (benzodiazepine): 2 mg IV, with additional doses titrated to effect
  • Ondansetron: 4–8 mg IVP
  • Prochlorperazine: 5–10 mg IVP slowly (not >5 mg/min)
  • Promethazine: 12.5–25 mg IM
  • 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
  • Most patients will require observation:
    • May consider management in observation unit over 12–24 hr
  • Tolerating oral fluids well
  • Resolution of metabolic abnormalities
  • No other associated illnesses requiring additional therapy

Follow-Up Recommendations

Counseling and referral for alcohol cessation resources

Pearls and Pitfalls

  • Aggressive volume repletion with dextrose-containing fluid is key
  • Easily missed diagnosis, can be confused with DKA (euglycemic DKA/hyperglycemic AKA)
  • Volume resuscitate with NS as necessary
  • Thiamine repletion
  • Monitor electrolytes before and after treatment
  • Unrecognized increased osmolal gap
  • Avoid insulin
  • Inadequate monitoring of glucose levels
  • Failure to recognize initial electrolyte abnormalities and electrolyte shifts caused by treatment
  • Must be placed on cardiac monitor:
    • Cases of sudden death in AKA:
      • Possible alcoholic cardiomyopathy
      • Dysrhythmias
      • Electrolyte derangements

Additional Reading

  • Allison MG, McCurdy MT. Alcoholic metabolic emergencies. Emerg Med Clin North Am. 2014;32(2):293–301.
  • Flannery AH, Adkins DA, Cook AM. Unpeeling the evidence for the banana bag: Evidence-based recommendations for the management of alcohol- associated vitamin and electrolyte deficiencies in the ICU. Crit Care Med. 2016;44(8):1545–1552.
  • Schabelman E, Kuo D. Glucose before thiamine for Wernicke encephalopathy: a literature review. J Emerg Med. 2012;42(4):488–494.
  • Sorkin T, Sheppard MN. Sudden unexplained death in alcohol misuse (SUDAM) patients have different characteristics to those who died from sudden arrhythmic death syndrome (SADS). Forensic Sci Med Pathol. 2017;13(3):278–283.

See Also

Authors

Nicholas M.V. Schulack
Ketan Patel
Ross P. Berkeley


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