Alcoholic ketoacidosis: Difference between revisions
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== 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 == | |||
Consider associated diseases (ie pancreatitis, rhabdo, hepatitis, infections) | |||
#Hydration - IVF should include 5% dextrose since there is a lack of glucose | |||
#Thiamine (100mg IV/PO) prior to glucose to decrease risk of Wernicke encephalopathy or Korsakoff syndrome | |||
#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 == | |||
#Most go 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 == | |||
:[[Anion Gap (High)]] | |||
:[[Acid-Base Disorders]] | |||
[[Category:FEN]] |
Revision as of 04:45, 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
- Ethanol metabolism depletes NAD stores
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
- Isopropyl alcohol
- Results in ketosis
- Methanol, ethylene glycol
- Do not produce ketosis
- Sepsis
- Salicylate ingestion
- DKA
- Starvation ketosis
- Uremia
Treatment
- Thiamine 100mg IV
- D5NS
- Glucose stimulates insulin which stops lipolysis
- Electrolyte repletion
Disposition
- Discharge home if resolution of acidosis and pt is able to tolerate PO
See Also
Source
Tintinalli's
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
Consider associated diseases (ie pancreatitis, rhabdo, hepatitis, infections)
- Hydration - IVF should include 5% dextrose since there is a lack of glucose
- Thiamine (100mg IV/PO) prior to glucose to decrease risk of Wernicke encephalopathy or Korsakoff syndrome
- 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
- Most go 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