Alcohol ketoacidosis: Difference between revisions
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[[Alcoholic Ketoacidosis]] | |||
== 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 | ||
Revision as of 04:45, 5 February 2014
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
