Alcoholic ketoacidosis: Difference between revisions
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==Background== | ==Background== | ||
*Anion gap | *Seen in patients with recent history of binge drinking with little/no nutritional intake | ||
*Pathophysiology | *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) | |||
***High NADH:NAD also results in increased lactate production | **Concomitant [[Metabolic Alkalosis|metabolic alkalosis]] can occur from dehydration (volume depletion) and emesis, so a normal blood pH may be found | ||
===Pathophysiology=== | |||
*Ethanol metabolism depletes NAD stores<ref>McGuire LC, Cruickshank AM, Munro PT. Alcoholic ketoacidosis. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2564331/ Emerg Med J. 2006 Jun;23(6):417-20.]</ref> | |||
**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 | **Acetoacetate is metabolized to acetone so elevated osmolal gap may also be seen | ||
[[File:AKA_crashingpatient.JPG|thumbnail]] | |||
==Clinical Features== | ==Clinical Features== | ||
*Nausea (75%) | *[[Nausea]] (75%) | ||
*Vomiting (73%) | *[[Vomiting]] (73%) | ||
*Abdominal pain (62%) | *[[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 DDX}} | |||
==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]] | |||
*'''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== | ||
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 abnormalities|Electrolyte replacement]] | |||
**K, Mag and Phos | |||
*Monitor for signs of [[Alcohol Withdrawal|alcohol withdrawal]] | |||
*Consider [[bicarbonate]] if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy | |||
==Disposition== | ==Disposition== | ||
*Discharge home if | *'''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== | |||
*[[Metabolic Acidosis]] | |||
*[[Anion Gap (High)]] | |||
*[[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/> | |||
[[Category:Endocrinology]] | |||
[[Category:FEN]] | [[Category:FEN]] | ||
[[Category:Toxicology]] |
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.