Difference between revisions of "Alcoholic ketoacidosis"

(Source)
(Management)
 
(45 intermediate revisions by 13 users not shown)
Line 1: Line 1:
 
==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]]
  
==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]]
  
==DDX==
+
{{Ethanol DDX}}
#Isopropyl alcohol
 
##Results in ketosis
 
#Methanol, ethylene glycol
 
##Do not produce ketosis
 
#Sepsis
 
#Salicylate ingestion
 
#DKA
 
#Starvation ketosis
 
#Uremia
 
  
==Treatment==
+
==Evaluation==
#Thiamine 100mg IV
+
*[[Anion gap acidosis]]
#D5NS
+
**Typically ''wide'' anion gap
##Glucose stimulates insulin which stops lipolysis
+
**Positive serum ketones + [[lactic acidosis]]
#Electrolyte repletion
+
***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]]
 +
 
 +
==Management==
 +
Consider associated diseases (ie [[pancreatitis]], [[rhabdomyolysis]], [[hepatitis]], infections)
 +
*[[Thiamine]] (100mg IV or IM)
 +
**Prior to glucose to decrease risk of [[Wernicke encephalopathy]] or [[Korsakoff syndrome]]
 +
*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
+
*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==
 +
*[[Metabolic Acidosis]]
 +
*[[Anion Gap (High)]]
 +
*[[Acid-Base Disorders]]
  
==Source==
+
==References==
Tintinalli's
+
<references/>
  
[[Category:Endo]]
+
[[Category:Endocrinology]]
 +
[[Category:FEN]]
 +
[[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.