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 pts with recent h/o 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]] a/w 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
**Concomitant metabolis alkalosis can occur from dehydration (volume depletion) and emesis
+
**Concomitant [[Metabolic Alkalosis|metabolic alkalosis]] can occur from dehydration (volume depletion) and emesis
  
 
===Pathophysiology===
 
===Pathophysiology===
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**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
 
**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
  
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==Diagnosis==
 
==Diagnosis==
 
*Binge drinking ending in nausea, vomiting, and decreased intake
 
*Binge drinking ending in nausea, vomiting, and decreased intake
*Wide anion gap metabolic acidosis (ketonemia, lactic acidosis)
+
*Wide anion gap [[metabolic acidosis]] (ketonemia, [[lactic acidosis]])
 
*Positive serum ketones
 
*Positive serum ketones
*Wide anion gap metabolic acidosis without alternate explanation
+
*Wide anion gap [[metabolic acidosis]] without alternate explanation
  
 
==Differential Diagnosis==
 
==Differential Diagnosis==
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Consider associated diseases (ie [[pancreatitis]], [[rhabdo]], [[hepatitis]], infections)  
 
Consider associated diseases (ie [[pancreatitis]], [[rhabdo]], [[hepatitis]], infections)  
 
#Thiamine (100mg IV)  
 
#Thiamine (100mg IV)  
##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 since there is a lack of glucose
 
##Glucose stimulates insulin which stops lipolysis
 
##Glucose stimulates insulin which stops lipolysis
 
#Oral nutrition if able to tolerate
 
#Oral nutrition if able to tolerate
#[[Electrolyte replacement]]
+
#[[Electrolyte abnormalities|Electrolyte replacement]]
 
## K, Mag and Phos
 
## K, Mag and Phos
#Monitor for signs of [[alcohol withdrawal]]
+
#Monitor for signs of [[Alcohol Withdrawal|alcohol withdrawal]]
 
#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
  
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#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==

Revision as of 19:06, 6 February 2015

Background

  • Seen in pts with recent h/o binge drinking with little/no nutritional intake
  • Anion gap metabolic acidosis a/w 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
    • Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis

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

Clinical Features

Diagnosis

Differential Diagnosis

  1. Isopropyl Alcohol
    1. Results in ketosis
  2. Methanol, Ethylene Glycol
    1. Do not produce ketosis
  3. Sepsis
  4. Salicylate Toxicity
  5. DKA
  6. Starvation Ketosis
  7. Uremia

Management

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

  1. Thiamine (100mg IV)
    1. Prior to glucose to decrease risk of Wernicke encephalopathy or Korsakoff syndrome
  2. Hydration (D5NS)
    1. IVF should include 5% dextrose since there is a lack of glucose
    2. Glucose stimulates insulin which stops lipolysis
  3. Oral nutrition if able to tolerate
  4. Electrolyte replacement
    1. 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