Alcoholic ketoacidosis: Difference between revisions

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*[[Vomiting]] (73%)
*[[Vomiting]] (73%)
*[[Abdominal pain]] (62%)
*[[Abdominal pain]] (62%)
*Typically, history of binge drinking ending in nausea, vomiting, and decreased intake
*Not hyperosmolar as opposed to [[DKA]]
*Not hyperosmolar as opposed to [[DKA]]
*Large IVF admin does not predispose to cerebral edema


==Differential Diagnosis==
==Differential Diagnosis==
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==Evaluation==
==Evaluation==
*Binge drinking ending in nausea, vomiting, and decreased intake
*'''Labs'''
*Wide anion gap [[metabolic acidosis]] (ketonemia, [[lactic acidosis]])
**[[Anion gap acidosis]]
*Positive serum ketones
***Typically ''wide'' anion gap
*Wide anion gap [[metabolic acidosis]] without alternate explanation
***Positive serum ketones + [[lactic acidosis]]
*Urine ketones may be falsely negative or low
****Lab measured ketone is acetoacetate
**Lab measured ketone is acetoacetate
****May miss beta-hydroxybutyrate
**May miss beta-hydroxybutyrate
****Urine ketones may be falsely negative or low
*Typically normal osmolal gap
**Typically normal osmolal gap
*Alcohol level usually zero or not considerably high
**Alcohol level usually zero or not considerably high
**BMP, Mg/phos
***Often have concomitant [[electrolyte abnormalities]]
 
*'''ECG'''
**May show dysrhythmias or QT interval/QRS changes secondary to electrolyte abnormalities
 
*'''Imaging'''
**Consider [[CXR]] if concern for aspiration pneumonia
**Consider [[CT head]] if presentation associated with trauma


==Management==
==Management==
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**Prior to glucose to decrease risk of [[Wernicke encephalopathy]] or [[Korsakoff syndrome]]
**Prior to glucose to decrease risk of [[Wernicke encephalopathy]] or [[Korsakoff syndrome]]
*Hydration (D5NS)
*Hydration (D5NS)
**[[IVF]] should include 5% dextrose since there is a lack of glucose
**[[IVF]] should include 5% dextrose to treat starvation ketosis
**Large IVF admin does not predispose to cerebral edema
**Glucose stimulates insulin which stops lipolysis
**Glucose stimulates insulin which stops lipolysis
*Oral nutrition if able to tolerate
*Oral nutrition if able to tolerate
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**K, Mag and Phos
**K, Mag and Phos
*Monitor for signs of [[Alcohol Withdrawal|alcohol withdrawal]]
*Monitor for signs of [[Alcohol Withdrawal|alcohol withdrawal]]
*Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy
*Consider [[bicarbonate]] if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy


==Disposition==
==Disposition==
*Discharge home after treatment if able to tolerate POs and acidosis resolved
*'''Admission'''
*Consider admission for those with severe volume depletion and/or acidosis
**Consider admission for those with severe volume depletion, acidosis, or persistent nausea/vomiting
*[[Hypoglycemia]] is poor prognostic feature, indicating depleted glycogen stores
**[[Hypoglycemia]] is poor prognostic feature, indicating depleted glycogen stores
*'''Discharge'''
**Discharge home after treatment if able to tolerate POs and acidosis resolved


==See Also==
==See Also==
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*[[Anion Gap (High)]]
*[[Anion Gap (High)]]
*[[Acid-Base Disorders]]
*[[Acid-Base Disorders]]
==External Links==
*[https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/diabetes-mellitus-and-disorders-of-carbohydrate-metabolism/alcoholic-ketoacidosis?query=alcoholic%20ketoacidosis Merk Manual - Alcoholic Ketoacidosis]
*[https://www.emra.org/emresident/article/alcoholic-ketoacidosis/ EMRA - Alcoholic Ketoacidosis: Mind the Gap, Give Patients What They Need]


==References==
==References==

Latest revision as of 12:55, 23 July 2021

Background

  • Seen in patients with recent history of binge drinking with little/no nutritional intake
  • Anion gap metabolic acidosis associated with acute cessation of EtOH consumption after chronic abuse
  • Characterized by high serum ketone levels and an elevated AG
    • Consider other causes of elevated AG, as well as co-ingestants (toxic alcohols, salicylates)
    • Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis, so a normal blood pH may be found

Pathophysiology

  • Ethanol metabolism depletes NAD stores[1]
    • Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
    • Suppresses gluconeogenesis and may result in hypoglycemia
    • High NADH:NAD also results in increased lactate production
      • Lactate higher than normal but not as high as in shock or sepsis
    • Acetoacetate is metabolized to acetone so elevated osmolal gap may also be seen
AKA crashingpatient.JPG

Clinical Features

  • Nausea (75%)
  • Vomiting (73%)
  • Abdominal pain (62%)
  • Typically, history of binge drinking ending in nausea, vomiting, and decreased intake
  • Not hyperosmolar as opposed to DKA

Differential Diagnosis

Ethanol related disease processes

Evaluation

  • Labs
    • Anion gap acidosis
      • Typically wide anion gap
      • Positive serum ketones + lactic acidosis
        • Lab measured ketone is acetoacetate
        • May miss beta-hydroxybutyrate
        • Urine ketones may be falsely negative or low
    • Typically normal osmolal gap
    • Alcohol level usually zero or not considerably high
    • BMP, Mg/phos
  • ECG
    • May show dysrhythmias or QT interval/QRS changes secondary to electrolyte abnormalities
  • Imaging
    • Consider CXR if concern for aspiration pneumonia
    • Consider CT head if presentation associated with trauma

Management

Consider associated diseases (ie pancreatitis, rhabdomyolysis, hepatitis, infections)

Disposition

  • Admission
    • Consider admission for those with severe volume depletion, acidosis, or persistent nausea/vomiting
    • Hypoglycemia is poor prognostic feature, indicating depleted glycogen stores
  • Discharge
    • Discharge home after treatment if able to tolerate POs and acidosis resolved

See Also

External Links

References

  1. McGuire LC, Cruickshank AM, Munro PT. Alcoholic ketoacidosis. Emerg Med J. 2006 Jun;23(6):417-20.