Difference between revisions of "Alcoholic ketoacidosis"

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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==
*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]]
  
==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}}
  
==Differential Diagnosis==
+
==Evaluation==
#[[Isopropyl Alcohol]]
+
*[[Anion gap acidosis]]
##Results in ketosis
+
**Typically ''wide'' anion gap
#[[Methanol]], [[Ethylene Glycol]]
+
**Positive serum ketones + [[lactic acidosis]]
##Do not produce ketosis
+
***Lab measured ketone is acetoacetate
#[[Sepsis]]
+
***May miss beta-hydroxybutyrate
#[[Salicylate Toxicity]]
+
***Urine ketones may be falsely negative or low
#[[DKA]]
+
*Typically normal osmolal gap
#Starvation Ketosis
+
*Alcohol level usually zero or not considerably high
#[[Uremia]]
+
*BMP, Mg/phos
 +
**Often have concomitant [[electrolyte abnormalities]]
  
 
==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
+
*Discharge home after treatment if able to tolerate POs and acidosis resolved
#Consider admission for those with severe volume depletion and/or acidosis
+
*Consider admission for those with severe volume depletion and/or acidosis
 
+
*[[Hypoglycemia]] is poor prognostic feature, indicating depleted glycogen stores
:Hypoglycemia is poor prognostic feature, indicating depleted glycogen stores
 
  
 
==See Also==
 
==See Also==
*[[Ethanol Toxicity]]
 
 
*[[Metabolic Acidosis]]
 
*[[Metabolic Acidosis]]
 
*[[Anion Gap (High)]]
 
*[[Anion Gap (High)]]
 
*[[Acid-Base Disorders]]
 
*[[Acid-Base Disorders]]
  
==Source==
+
==References==
Tintinalli's
+
<references/>
  
[[Category:Endo]]
+
[[Category:Endocrinology]]
 
[[Category:FEN]]
 
[[Category:FEN]]
[[Category:Tox]]
+
[[Category:Toxicology]]

Latest revision as of 00:27, 23 November 2019

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

  • 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

Management

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

Disposition

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

See Also

References

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