Alcoholic ketoacidosis: Difference between revisions
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==Background== | ==Background== | ||
*Seen in | *Seen in patients with recent history of binge drinking with little/no nutritional intake | ||
*Anion gap [[metabolic acidosis]] | *Anion gap [[metabolic acidosis]] associated with acute cessation of EtOH consumption after chronic abuse | ||
*Characterized by high serum ketone levels and an elevated AG | *Characterized by high serum ketone levels and an elevated AG | ||
**Consider other causes of elevated AG, as well as co-ingestants | **Consider other causes of elevated AG, as well as co-ingestants (toxic alcohols, salicylates) | ||
**Concomitant [[Metabolic Alkalosis|metabolic alkalosis]] can occur from dehydration (volume depletion) and emesis | **Concomitant [[Metabolic Alkalosis|metabolic alkalosis]] can occur from dehydration (volume depletion) and emesis, so a normal blood pH may be found | ||
===Pathophysiology=== | ===Pathophysiology=== | ||
*Ethanol metabolism depletes NAD stores | *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 | **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 | **High NADH:NAD also results in increased lactate production | ||
***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 | ||
[[File:AKA_crashingpatient.JPG|thumbnail]] | |||
==Clinical Features== | ==Clinical Features== | ||
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*[[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]] | |||
==Diagnosis== | ==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== | ||
*[[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]] | |||
==Management== | ==Management== | ||
Consider associated diseases (ie [[pancreatitis]], [[ | 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 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 | |||
==See Also== | ==See Also== | ||
*[[Metabolic Acidosis]] | *[[Metabolic Acidosis]] | ||
*[[Anion Gap (High)]] | *[[Anion Gap (High)]] | ||
*[[Acid-Base Disorders]] | *[[Acid-Base Disorders]] | ||
== | ==References== | ||
<references/> | |||
[[Category: | [[Category:Endocrinology]] | ||
[[Category:FEN]] | [[Category:FEN]] | ||
[[Category: | [[Category:Toxicology]] |
Revision as of 00:27, 23 November 2019
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
- 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
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
- Discharge 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
See Also
References
- ↑ McGuire LC, Cruickshank AM, Munro PT. Alcoholic ketoacidosis. Emerg Med J. 2006 Jun;23(6):417-20.