Alcoholic ketoacidosis: Difference between revisions
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==Evaluation== | ==Evaluation== | ||
*[[Anion gap acidosis]] | *'''Labs''' | ||
**Typically ''wide'' anion gap | **[[Anion gap acidosis]] | ||
**Positive serum ketones + [[lactic acidosis]] | ***Typically ''wide'' anion gap | ||
***Lab measured ketone is acetoacetate | ***Positive serum ketones + [[lactic acidosis]] | ||
***May miss beta-hydroxybutyrate | ****Lab measured ketone is acetoacetate | ||
***Urine ketones may be falsely negative or low | ****May miss beta-hydroxybutyrate | ||
*Typically normal osmolal gap | ****Urine ketones may be falsely negative or low | ||
*Alcohol level usually zero or not considerably high | **Typically normal osmolal gap | ||
*BMP, Mg/phos | **Alcohol level usually zero or not considerably high | ||
**Often have concomitant [[electrolyte abnormalities]] | **BMP, Mg/phos | ||
***Often have concomitant [[electrolyte abnormalities]] | |||
*'''ECG''' | |||
**May show dysrhythmias or QT interval/QRS changes secondary to electrolyte abnormalities | |||
*'''Imaging''' | |||
**Consider [[CXR]] if concern for aspiration pneumonia | |||
**Consider [[CT head]] if presentation associated with trauma | |||
==Management== | ==Management== | ||
| Line 53: | Line 61: | ||
**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 | **[[IVF]] should include 5% dextrose to treat starvation ketosis | ||
**Large IVF admin does not predispose to cerebral edema | **Large IVF admin does not predispose to cerebral edema | ||
**Glucose stimulates insulin which stops lipolysis | **Glucose stimulates insulin which stops lipolysis | ||
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==Disposition== | ==Disposition== | ||
* | *'''Admission''' | ||
*Consider admission for those with severe volume depletion | **Consider admission for those with severe volume depletion, acidosis, or persistent nausea/vomiting | ||
*[[Hypoglycemia]] is poor prognostic feature, indicating depleted glycogen stores | **[[Hypoglycemia]] is poor prognostic feature, indicating depleted glycogen stores | ||
*'''Discharge''' | |||
**Discharge home after treatment if able to tolerate POs and acidosis resolved | |||
==See Also== | ==See Also== | ||
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*[[Anion Gap (High)]] | *[[Anion Gap (High)]] | ||
*[[Acid-Base Disorders]] | *[[Acid-Base Disorders]] | ||
==External Links== | |||
*[https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/diabetes-mellitus-and-disorders-of-carbohydrate-metabolism/alcoholic-ketoacidosis?query=alcoholic%20ketoacidosis Merk Manual - Alcoholic Ketoacidosis] | |||
*[https://www.emra.org/emresident/article/alcoholic-ketoacidosis/ EMRA - Alcoholic Ketoacidosis: Mind the Gap, Give Patients What They Need] | |||
==References== | ==References== | ||
Latest revision as of 12:55, 23 July 2021
Background
- Seen in patients with recent history of binge drinking with little/no nutritional intake
- Anion gap metabolic acidosis associated with 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 (toxic alcohols, salicylates)
- Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis, so a normal blood pH may be found
Pathophysiology
- Ethanol metabolism depletes NAD stores[1]
- Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
- Suppresses gluconeogenesis and may result in hypoglycemia
- 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%)
- Typically, history of binge drinking ending in nausea, vomiting, and decreased intake
- Not hyperosmolar as opposed to DKA
Differential Diagnosis
- Isopropyl Alcohol
- Results in ketosis
- Methanol, Ethylene Glycol
- Do not produce ketosis
- Sepsis
- Salicylate Toxicity
- DKA
- Hyperosmolar hyperglycemic state
- Starvation Ketosis
- Uremia
- Ethanol toxicity
- Alcohol use disorder
- Alcohol withdrawal
- Electrolyte/acid-base disorder
Evaluation
- Labs
- Anion gap acidosis
- Typically wide anion gap
- Positive serum ketones + lactic acidosis
- Lab measured ketone is acetoacetate
- May miss beta-hydroxybutyrate
- Urine ketones may be falsely negative or low
- Typically normal osmolal gap
- Alcohol level usually zero or not considerably high
- BMP, Mg/phos
- Often have concomitant electrolyte abnormalities
- Anion gap acidosis
- ECG
- May show dysrhythmias or QT interval/QRS changes secondary to electrolyte abnormalities
- Imaging
Management
Consider associated diseases (ie pancreatitis, rhabdomyolysis, hepatitis, infections)
- Thiamine (100mg IV or IM)
- Prior to glucose to decrease risk of Wernicke encephalopathy or Korsakoff syndrome
- Hydration (D5NS)
- IVF should include 5% dextrose to treat starvation ketosis
- Large IVF admin does not predispose to cerebral edema
- 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 bicarbonate if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy
Disposition
- Admission
- Consider admission for those with severe volume depletion, acidosis, or persistent nausea/vomiting
- Hypoglycemia is poor prognostic feature, indicating depleted glycogen stores
- Discharge
- Discharge home after treatment if able to tolerate POs and acidosis resolved
See Also
External Links
- Merk Manual - Alcoholic Ketoacidosis
- EMRA - Alcoholic Ketoacidosis: Mind the Gap, Give Patients What They Need
References
- ↑ McGuire LC, Cruickshank AM, Munro PT. Alcoholic ketoacidosis. Emerg Med J. 2006 Jun;23(6):417-20.