Difference between revisions of "Alcoholic ketoacidosis"

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****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
 +
 +
== Background ==
 +
*Seen in pts with recent h/o binge drinking with little/no nutritional intake
 +
**Starvation leads to excess glucagon and decreased insulin
 +
**Elevated NADH:NAD+ ratio due to ETOH metabolism
 +
**Volume depletion from emesis & poor PO intake
 +
*Characterized by high serum ketone levels and an elevated AG
 +
**Consider other causes of elevated AG, as well as co-ingestants
 +
**Concomitant metabolis alkalosis can occur from dehydration (volume depletion) and emesis
  
 
==Clinical Features==
 
==Clinical Features==
Line 36: Line 45:
 
#Electrolyte repletion
 
#Electrolyte repletion
  
==Disposition==
 
*Discharge home if resolution of acidosis and pt is able to tolerate PO
 
 
==See Also==
 
*[[Ethanol Toxicity | Alcohol (ETOH) Intoxication]]
 
*[[Metabolic Acidosis]]
 
 
==Source==
 
Tintinalli's
 
 
[[Category:Endo]]
 
 
 
== Background ==
 
*Seen in pts with recent h/o binge drinking with little/no nutritional intake
 
**Starvation leads to excess glucagon and decreased insulin
 
**Elevated NADH:NAD+ ratio due to ETOH metabolism
 
**Volume depletion from emesis & poor PO intake
 
*Characterized by high serum ketone levels and an elevated AG
 
**Consider other causes of elevated AG, as well as co-ingestants
 
**Concomitant metabolis alkalosis can occur from dehydration (volume depletion) and emesis
 
  
 
== Treatment ==
 
== Treatment ==
Line 67: Line 55:
 
#Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy
 
#Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy
  
== Disposition ==
+
==Disposition==
#Most go 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==
:[[Anion Gap (High)]]
+
*[[Ethanol Toxicity | Alcohol (ETOH) Intoxication]]
:[[Acid-Base Disorders]]
+
*[[Metabolic Acidosis]]
 +
*[[Anion Gap (High)]]
 +
*[[Acid-Base Disorders]]
  
 +
==Source==
 +
Tintinalli's
 +
 +
[[Category:Endo]]
 
[[Category:FEN]]
 
[[Category:FEN]]

Revision as of 04:49, 5 February 2014

Background

  • Anion gap met acidosis a/w acute cessation of ETOH consumption after chronic abuse
  • Pathophysiology
    • Ethanol metabolism depletes NAD stores
      • Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
      • 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

Background

  • Seen in pts with recent h/o binge drinking with little/no nutritional intake
    • Starvation leads to excess glucagon and decreased insulin
    • Elevated NADH:NAD+ ratio due to ETOH metabolism
    • Volume depletion from emesis & poor PO intake
  • Characterized by high serum ketone levels and an elevated AG
    • Consider other causes of elevated AG, as well as co-ingestants
    • Concomitant metabolis alkalosis can occur from dehydration (volume depletion) and emesis

Clinical Features

  • Nausea (75%)
  • Vomiting (73%)
  • Abdominal pain (62%)

Diagnosis

  • 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

  1. Isopropyl alcohol
    1. Results in ketosis
  2. Methanol, ethylene glycol
    1. Do not produce ketosis
  3. Sepsis
  4. Salicylate ingestion
  5. DKA
  6. Starvation ketosis
  7. Uremia

Treatment

  1. Thiamine 100mg IV
  2. D5NS
    1. Glucose stimulates insulin which stops lipolysis
  3. Electrolyte repletion


Treatment

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

  1. Hydration - IVF should include 5% dextrose since there is a lack of glucose
  2. Thiamine (100mg IV/PO) prior to glucose to decrease risk of Wernicke encephalopathy or Korsakoff syndrome
  3. Oral nutrition if able to tolerate
  4. Electrolyte replacement - K, Mag and Phos
  5. Monitor for signs of alcohol withdrawal
  6. Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy

Disposition

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

See Also

Source

Tintinalli's