Alcoholic ketoacidosis: Difference between revisions
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*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 met 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 metabolis alkalosis can occur from dehydration (volume depletion) and emesis


===Pathophysiology===
===Pathophysiology===
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***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
*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


==Clinical Features==
==Clinical Features==

Revision as of 05:02, 5 February 2014

Background

  • 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
  • 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

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

DDX

  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

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