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]]


== Background ==
==Clinical Features==
*Seen in pts with recent h/o binge drinking with little/no nutritional intake
*[[Nausea]] (75%)
**Starvation leads to excess glucagon and decreased insulin
*[[Vomiting]] (73%)
**Elevated NADH:NAD+ ratio due to ETOH metabolism
*[[Abdominal pain]] (62%)
**Volume depletion from emesis & poor PO intake
*Typically, history of binge drinking ending in nausea, vomiting, and decreased intake
*Characterized by high serum ketone levels and an elevated AG
*Not hyperosmolar as opposed to [[DKA]]
**Consider other causes of elevated AG, as well as co-ingestants
**Concomitant metabolis alkalosis can occur from dehydration (volume depletion) and emesis


==Clinical Features==
==Differential Diagnosis==
*Nausea (75%)
*[[Isopropyl Alcohol]]
*Vomiting (73%)
**Results in ketosis
*Abdominal pain (62%)
*[[Methanol]], [[Ethylene Glycol]]
**Do not produce ketosis
*[[Sepsis]]
*[[Salicylate Toxicity]]
*[[DKA]]
*[[Hyperosmolar hyperglycemic state]]
*Starvation Ketosis
*[[Uremia]]


==Diagnosis==
{{Ethanol DDX}}
*Binge drinking ending in nausea, vomiting, and decreased intake
*Wide anion gap metabolic acidosis (ketonemia, lactic acidosis)
*Positive serum ketones
*Wide anion gap metabolic acidosis without alternate explanation


==DDX==
==Evaluation==
#Isopropyl alcohol
*'''Labs'''
##Results in ketosis
**[[Anion gap acidosis]]
#Methanol, ethylene glycol
***Typically ''wide'' anion gap
##Do not produce ketosis
***Positive serum ketones + [[lactic acidosis]]
#Sepsis
****Lab measured ketone is acetoacetate
#Salicylate ingestion
****May miss beta-hydroxybutyrate
#DKA
****Urine ketones may be falsely negative or low
#Starvation ketosis
**Typically normal osmolal gap
#Uremia
**Alcohol level usually zero or not considerably high
**BMP, Mg/phos
***Often have concomitant [[electrolyte abnormalities]]


==Treatment==
*'''ECG'''
#Thiamine 100mg IV
**May show dysrhythmias or QT interval/QRS changes secondary to electrolyte abnormalities
#D5NS
##Glucose stimulates insulin which stops lipolysis
#Electrolyte repletion


*'''Imaging'''
**Consider [[CXR]] if concern for aspiration pneumonia
**Consider [[CT head]] if presentation associated with trauma


== Treatment ==
==Management==
Consider associated diseases (ie pancreatitis, rhabdo, hepatitis, infections)  
Consider associated diseases (ie [[pancreatitis]], [[rhabdomyolysis]], [[hepatitis]], infections)  
#Hydration - IVF should include 5% dextrose since there is a lack of glucose
*[[Thiamine]] (100mg IV or IM)  
#Thiamine (100mg IV/PO) prior to glucose to decrease risk of Wernicke encephalopathy or Korsakoff syndrome
**Prior to glucose to decrease risk of [[Wernicke encephalopathy]] or [[Korsakoff syndrome]]
#Oral nutrition if able to tolerate
*Hydration (D5NS)
#Electrolyte replacement - K, Mag and Phos
**[[IVF]] should include 5% dextrose to treat starvation ketosis
#Monitor for signs of alcohol withdrawal
**Large IVF admin does not predispose to cerebral edema
#Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy
**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 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==
*[[Ethanol Toxicity | Alcohol (ETOH) Intoxication]]
*[[Metabolic Acidosis]]
*[[Metabolic Acidosis]]
*[[Anion Gap (High)]]
*[[Anion Gap (High)]]
*[[Acid-Base Disorders]]
*[[Acid-Base Disorders]]


==Source==
==External Links==
Tintinalli's
*[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/>


[[Category:Endo]]
[[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.
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