Ethanol toxicity: Difference between revisions

 
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==Background==
==Background==
*Alcohol (ethanol) is a CNS depressant that can cause respiratory depression, coma, or death when consumed rapidly or in large quantities.
*Rate of ETOH elimination is 15-30mg/dL/hr (depending on degree of chronic alcohol intake)
*Rate of ETOH elimination is 15-30mg/dL/hr (depending on degree of chronic alcohol intake)
*Ethanol is involved in 30-50% of all traumatic injuries in the US<ref>American College of Surgeons Committee on Trauma. Statement on insurance, alcohol-related injuries, and trauma centers. Bull Am Coll Surg. 2006;91(9):29-30.</ref>


==Clinical Features==
==Clinical Features==
[[File:The Alcohol Flushing Response.png|thumb|Alcohol flushing reaction: before (left) and after (right) drinking alcohol.]]
===Classic Features===
===Classic Features===
*Diminished fine motor control
*Impaired judgement and coordination
*Slurred speech
*Slurred speech
*Nystagmus
*Nystagmus
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*Alcohol odor on breath
*Alcohol odor on breath
*Respiratory depression
*Respiratory depression
*Lethargy
*[[Coma]]
*[[Coma]]


===Other Features (if malnourished)===
===Other Features===
*[[Hypoglycemia]]
*[[Hypoglycemia]], particularly in young children due to gluconeogenesis inhibition by ethanol metabolism
*[[Alcoholic ketoacidosis|Ketoacidosis]]
*[[Alcoholic ketoacidosis|Ketoacidosis]]
*[[Lactic acidosis]]
*[[Lactic acidosis]]
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{{AMS DDX}}
{{AMS DDX}}


==Diagnosis==
==Evaluation==
''Clinical diagnosis. No specific workup required, but the following may be considered based on clinical picture/gestalt:''
''Clinical diagnosis. No specific workup required when there is clear evidence of alcohol intake, but the following may be considered based on clinical picture/gestalt:''
*Fingerstick glucose (recommended as minimum workup in all patients with AMS)
*Fingerstick glucose (recommended as minimum workup in all patients with [[AMS]])
*Blood alcohol level (BAL)
*Consider blood alcohol level (BAL) when a good history cannot be obtained or patient fails to improve as expected
**Correlates poorly with degree of intoxication<ref>Olson KN, Smith SW, Kloss JS, et al. Relationship between blood alcohol concentration and observable symptoms of intoxication in patients presenting to an emergency department. Alcohol Alcohol. 2013 Jul-Aug;48(4):386-9. doi: 10.1093/alcalc/agt042.</ref>
**Correlates poorly with degree of intoxication<ref>Olson KN, Smith SW, Kloss JS, et al. Relationship between blood alcohol concentration and observable symptoms of intoxication in patients presenting to an emergency department. Alcohol Alcohol. 2013 Jul-Aug;48(4):386-9. doi: 10.1093/alcalc/agt042.</ref>
*Thiamine deficiency can cause an elevated lactic acid level, and IV thiamine should be administered (in addition to considering other etiologies including toxic alcohol ingestions) <ref> Wardi G, Brice J, Correia M, Liu D, Self M, Tainter C. Demystifying Lactate in the Emergency Department. Ann Emerg Med. 2020 Feb;75(2):287-298. doi: 10.1016/j.annemergmed.2019.06.027. Epub 2019 Aug 29. Erratum in: Ann Emerg Med. 2020 Apr;75(4):557. PMID: 31474479. </ref>
*Maintain low threshold for imaging in intoxicated patient with signs of trauma
*Maintain low threshold for imaging in intoxicated patient with signs of trauma
{{Toxic Alcohols Anion/Osmolar Gaps}}


==Management==
==Management==
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**[[Benzodiazepines]] or [[haloperidol]] for agitation
**[[Benzodiazepines]] or [[haloperidol]] for agitation
*IV fluids are commonly used but do not hasten ETOH elimination or reduce length of stay<ref>Perez SR, Keijzers G, Steele M. Intravenous 0.9% sodium chloride therapy does not reduce length of stay of alcohol-intoxicated patients in the emergency department: a randomised controlled trial. Emerg Med Australas. 2013 Dec;25(6):527-34. doi: 10.1111/1742-6723.12151.</ref><ref>Li J, Mills T, Erato R. Intravenous saline has no effect on blood ethanol clearance. J Emerg Med. 1999 Jan-Feb;17(1):1-5.</ref>
*IV fluids are commonly used but do not hasten ETOH elimination or reduce length of stay<ref>Perez SR, Keijzers G, Steele M. Intravenous 0.9% sodium chloride therapy does not reduce length of stay of alcohol-intoxicated patients in the emergency department: a randomised controlled trial. Emerg Med Australas. 2013 Dec;25(6):527-34. doi: 10.1111/1742-6723.12151.</ref><ref>Li J, Mills T, Erato R. Intravenous saline has no effect on blood ethanol clearance. J Emerg Med. 1999 Jan-Feb;17(1):1-5.</ref>
{{Vitamin prophylaxis for ETOH}}


==Disposition==
==Disposition==
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==See Also==
==See Also==
*[[Toxic alcohols]]
*[[Beer Potomania Syndrome]]
*[[Beer Potomania Syndrome]]
*[[Alcohol (ETOH) Intoxication]]
*[[Alcoholic ketoacidosis]]
*[[Alcoholic ketoacidosis]]
*[[Alcohol withdrawal]]
*[[Alcohol withdrawal]]
*[[Alcohol withdrawal: Inpatient management]]
*[[Alcohol withdrawal: Outpatient management]]
*[[Alcohol withdrawal seizures]]
*[[Alcohol withdrawal seizures]]
*[[Altered mental status]]
*[[Altered mental status]]

Latest revision as of 17:05, 22 December 2023

Background

  • Alcohol (ethanol) is a CNS depressant that can cause respiratory depression, coma, or death when consumed rapidly or in large quantities.
  • Rate of ETOH elimination is 15-30mg/dL/hr (depending on degree of chronic alcohol intake)
  • Ethanol is involved in 30-50% of all traumatic injuries in the US[1]

Clinical Features

Alcohol flushing reaction: before (left) and after (right) drinking alcohol.

Classic Features

  • Diminished fine motor control
  • Impaired judgement and coordination
  • Slurred speech
  • Nystagmus
  • Ataxia
  • Nausea and vomiting
  • Alcohol odor on breath
  • Respiratory depression
  • Lethargy
  • Coma

Other Features

Mellanby effect

  • Impairment is greater at a given blood alcohol concentration when the level is rising than when it is falling. [2]

Differential Diagnosis

Ethanol related disease processes

Sedative/hypnotic toxicity

Altered mental status

Diffuse brain dysfunction

Primary CNS disease or trauma

Psychiatric

Evaluation

Clinical diagnosis. No specific workup required when there is clear evidence of alcohol intake, but the following may be considered based on clinical picture/gestalt:

  • Fingerstick glucose (recommended as minimum workup in all patients with AMS)
  • Consider blood alcohol level (BAL) when a good history cannot be obtained or patient fails to improve as expected
    • Correlates poorly with degree of intoxication[3]
  • Thiamine deficiency can cause an elevated lactic acid level, and IV thiamine should be administered (in addition to considering other etiologies including toxic alcohol ingestions) [4]
  • Maintain low threshold for imaging in intoxicated patient with signs of trauma

Toxic Alcohols Anion/Osmolar Gaps

Osmolar gap Anion gap Management
Ethanol + + if ketoacidosis Mainly supportive
Ethylene glycol + + Fomepizole, Thiamine, Pyridoxine, +/- Dialysis
Methanol + + Fomepizole or ethanol, Folinic acid, +/- Dialysis
Isopropyl alcohol + - Mainly supportive

Management

  • Supportive care is mainstay of ED treatment and is based on clinical presentation
  • IV fluids are commonly used but do not hasten ETOH elimination or reduce length of stay[5][6]

Vitamin Prophylaxis for Chronic alcoholics

  • At risk for thiamine deficiency, but no symptoms: thiamine 100mg PO q day
  • Give multivitamin PO; patient at risk for other vitamin deficiencies

Banana bag

The majority of chronic alcoholics do NOT require a banana bag[7][8]

Disposition

  • Caution should be taken when BAL is measured on arrival as clinical exam cannot be used alone for discharge
  • Can be discharged once patient at baseline mental status, able to tolerate PO and ambulate without assistance

See Also

References

  1. American College of Surgeons Committee on Trauma. Statement on insurance, alcohol-related injuries, and trauma centers. Bull Am Coll Surg. 2006;91(9):29-30.
  2. Wang MQ, Nicholson ME, Mahoney BS, et al. Proprioceptive responses under rising and falling BACs: a test of the Mellanby effect. Percept Mot Skills. 1993 Aug;77(1):83-8.
  3. Olson KN, Smith SW, Kloss JS, et al. Relationship between blood alcohol concentration and observable symptoms of intoxication in patients presenting to an emergency department. Alcohol Alcohol. 2013 Jul-Aug;48(4):386-9. doi: 10.1093/alcalc/agt042.
  4. Wardi G, Brice J, Correia M, Liu D, Self M, Tainter C. Demystifying Lactate in the Emergency Department. Ann Emerg Med. 2020 Feb;75(2):287-298. doi: 10.1016/j.annemergmed.2019.06.027. Epub 2019 Aug 29. Erratum in: Ann Emerg Med. 2020 Apr;75(4):557. PMID: 31474479.
  5. Perez SR, Keijzers G, Steele M. Intravenous 0.9% sodium chloride therapy does not reduce length of stay of alcohol-intoxicated patients in the emergency department: a randomised controlled trial. Emerg Med Australas. 2013 Dec;25(6):527-34. doi: 10.1111/1742-6723.12151.
  6. Li J, Mills T, Erato R. Intravenous saline has no effect on blood ethanol clearance. J Emerg Med. 1999 Jan-Feb;17(1):1-5.
  7. Krishel, S, et al. Intravenous Vitamins for Alcoholics in the Emergency Department: A Review. The Journal of Emergency Medicine. 1998; 16(3):419–424.
  8. Li, SF, et al. Vitamin deficiencies in acutely intoxicated patients in the ED. The American Journal of Emergency Medicine. 2008; 26(7):792–795.