Alcoholic ketoacidosis: Difference between revisions

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


===Pathophysiology===
===Pathophysiology===
*Ethanol metabolism depletes NAD stores
*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
**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
**High NADH:NAD also results in increased lactate production
***Lactate higher than normal but not as high as in shock or sepsis
***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==
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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]]


==Diagnosis==
==Differential Diagnosis==
*Binge drinking ending in nausea, vomiting, and decreased intake
*[[Isopropyl Alcohol]]
*Wide anion gap metabolic acidosis (ketonemia, lactic acidosis)
**Results in ketosis
*Positive serum ketones
*[[Methanol]], [[Ethylene Glycol]]
*Wide anion gap metabolic acidosis without alternate explanation
**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]]


==Differential Diagnosis==
*'''ECG'''
#[[Isopropyl Alcohol]]
**May show dysrhythmias or QT interval/QRS changes secondary to electrolyte abnormalities
##Results in ketosis
 
#[[Methanol]], [[Ethylene Glycol]]
*'''Imaging'''
##Do not produce ketosis
**Consider [[CXR]] if concern for aspiration pneumonia
#[[Sepsis]]
**Consider [[CT head]] if presentation associated with trauma
#[[Salicylate Toxicity]]
#[[DKA]]
#Starvation Ketosis
#[[Uremia]]


==Management==
==Management==
Consider associated diseases (ie pancreatitis, rhabdo, hepatitis, infections)  
Consider associated diseases (ie [[pancreatitis]], [[rhabdomyolysis]], [[hepatitis]], infections)  
#Thiamine (100mg IV)  
*[[Thiamine]] (100mg IV or IM)  
##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
##Glucose stimulates insulin which stops lipolysis
**Large IVF admin does not predispose to cerebral edema
#Oral nutrition if able to tolerate
**Glucose stimulates insulin which stops lipolysis
#Electrolyte replacement
*Oral nutrition if able to tolerate
## K, Mag and Phos
*[[Electrolyte abnormalities|Electrolyte replacement]]
#Monitor for signs of alcohol withdrawal
**K, Mag and Phos
#Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy
*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]]
*[[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:Tox]]
[[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.