Alcoholic ketoacidosis: Difference between revisions
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==See Also== | ==See Also== | ||
*[[Alcohol (ETOH) Intoxication]] | *[[Alcohol (ETOH) Intoxication]] | ||
*[[Metabolic Acidosis]] | |||
==Source== | ==Source== |
Revision as of 07:14, 14 November 2011
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