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 pts with recent h/o binge drinking with little/no nutritional intake | ||
*Anion gap | *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 | **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
- 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
Differential Diagnosis
- Isopropyl Alcohol
- Results in ketosis
- Methanol, Ethylene Glycol
- Do not produce ketosis
- Sepsis
- Salicylate Toxicity
- DKA
- Starvation Ketosis
- Uremia
Management
Consider associated diseases (ie pancreatitis, rhabdo, hepatitis, infections)
- Thiamine (100mg IV)
- Prior to glucose to decrease risk of Wernicke encephalopathy or Korsakoff syndrome
- Hydration (D5NS)
- IVF should include 5% dextrose since there is a lack of glucose
- Glucose stimulates insulin which stops lipolysis
- Oral nutrition if able to tolerate
- Electrolyte replacement
- K, Mag and Phos
- Monitor for signs of alcohol withdrawal
- Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy
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
Source
Tintinalli's