Alcoholic ketoacidosis: Difference between revisions

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==Background==
==Background==
*Anion gap met acidosis a/w acute cessation of ETOH consumption after chronic abuse
*Seen in patients with recent history of binge drinking with little/no nutritional intake
*Pathophysiology
*Anion gap [[metabolic acidosis]] associated with acute cessation of EtOH consumption after chronic abuse
**Ethanol metabolism depletes NAD stores
*Characterized by high serum ketone levels and an elevated AG
***Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
**Consider other causes of elevated AG, as well as co-ingestants (toxic alcohols, salicylates)
***High NADH:NAD also results in increased lactate production
**Concomitant [[Metabolic Alkalosis|metabolic alkalosis]] can occur from dehydration (volume depletion) and emesis, so a normal blood pH may be found
****Lactate higher than normal but not as high as in shock or sepsis
 
===Pathophysiology===
*Ethanol metabolism depletes NAD stores<ref>McGuire LC, Cruickshank AM, Munro PT. Alcoholic ketoacidosis. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2564331/ Emerg Med J. 2006 Jun;23(6):417-20.]</ref>
**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
**Acetoacetate is metabolized to acetone so elevated osmolal gap may also be seen
[[File:AKA_crashingpatient.JPG|thumbnail]]


==Clinical Features==
==Clinical Features==
*Nausea (75%)
*[[Nausea]] (75%)
*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]]
 
==Differential Diagnosis==
*[[Isopropyl Alcohol]]
**Results in ketosis
*[[Methanol]], [[Ethylene Glycol]]
**Do not produce ketosis
*[[Sepsis]]
*[[Salicylate Toxicity]]
*[[DKA]]
*[[Hyperosmolar hyperglycemic state]]
*Starvation Ketosis
*[[Uremia]]
 
{{Ethanol DDX}}
 
==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
***Often have concomitant [[electrolyte abnormalities]]


==Diagnosis==
*'''ECG'''
*Binge drinking ending in nausea, vomiting, and decreased intake
**May show dysrhythmias or QT interval/QRS changes secondary to electrolyte abnormalities
*Wide anion gap metabolic acidosis (ketonemia, lactic acidosis)
*Positive serum ketones
*Wide anion gap metabolic acidosis without alternate explanation


==DDX==
*'''Imaging'''
#Isopropyl alcohol
**Consider [[CXR]] if concern for aspiration pneumonia
##Results in ketosis
**Consider [[CT head]] if presentation associated with trauma
#Methanol, ethylene glycol
##Do not produce ketosis
#Sepsis
#Salicylate ingestion
#DKA
#Starvation ketosis
#Uremia


==Treatment==
==Management==
#Thiamine 100mg IV
Consider associated diseases (ie [[pancreatitis]], [[rhabdomyolysis]], [[hepatitis]], infections)
#D5NS
*[[Thiamine]] (100mg IV or IM)
##Glucose stimulates insulin which stops lipolysis
**Prior to glucose to decrease risk of [[Wernicke encephalopathy]] or [[Korsakoff syndrome]]
#Electrolyte repletion
*Hydration (D5NS)
**[[IVF]] should include 5% dextrose to treat starvation ketosis
**Large IVF admin does not predispose to cerebral edema
**Glucose stimulates insulin which stops lipolysis
*Oral nutrition if able to tolerate
*[[Electrolyte abnormalities|Electrolyte replacement]]
**K, Mag and Phos
*Monitor for signs of [[Alcohol Withdrawal|alcohol withdrawal]]
*Consider [[bicarbonate]] if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy


==Disposition==
==Disposition==
*Discharge home if resolution of acidosis and pt is able to tolerate PO
*'''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==
*[[Metabolic Acidosis]]
*[[Anion Gap (High)]]
*[[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]


==Source==
==References==
Tintinalli
<references/>


[[Category:Endocrinology]]
[[Category:FEN]]
[[Category:FEN]]
[[Category:Toxicology]]

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.