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 | ||
*Ataxia | *[[Ataxia]] | ||
* | *[[Nausea and vomiting]] | ||
*Alcohol odor on breath | *Alcohol odor on breath | ||
*Respiratory depression | *Respiratory depression | ||
*Coma | *Lethargy | ||
===Other Features | *[[Coma]] | ||
*Hypoglycemia | |||
*Ketoacidosis | ===Other Features=== | ||
*Lactic acidosis | *[[Hypoglycemia]], particularly in young children due to gluconeogenesis inhibition by ethanol metabolism | ||
*Epigastric pain (pancreatitis) | *[[Alcoholic ketoacidosis|Ketoacidosis]] | ||
*[[Lactic acidosis]] | |||
*[[Epigastric pain]] ([[pancreatitis]]) | |||
===Mellanby effect=== | ===Mellanby effect=== | ||
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{{AMS DDX}} | {{AMS DDX}} | ||
== | ==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]]) | ||
* | *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]] | ||
*[[Alcoholic ketoacidosis]] | *[[Alcoholic ketoacidosis]] | ||
*[[Alcohol withdrawal]] | *[[Alcohol withdrawal]] | ||
*[[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
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
- Hypoglycemia, particularly in young children due to gluconeogenesis inhibition by ethanol metabolism
- Ketoacidosis
- Lactic acidosis
- Epigastric pain (pancreatitis)
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 toxicity
- Alcohol use disorder
- Alcohol withdrawal
- Electrolyte/acid-base disorder
Sedative/hypnotic toxicity
- Absinthe
- Barbiturates
- Benzodiazepines
- Chloral hydrate
- Gamma hydroxybutyrate (GHB)
- Baclofen toxicity
- Opioids
- Toxic alcohols
- Xylazine toxicity
Altered mental status
Diffuse brain dysfunction
- Hypoxic encephalopathy
- Acute toxic-metabolic encephalopathy (Delirium)
- Hypoglycemia
- Hyperosmolar state (e.g., hyperglycemia)
- Electrolyte Abnormalities (hypernatremia or hyponatremia, hypercalcemia)
- Organ system failure
- Hepatic Encephalopathy
- Uremia/Renal Failure
- Endocrine (Addison's disease, Cushing syndrome, hypothyroidism, myxedema coma, thyroid storm)
- Hypoxia
- CO2 narcosis
- Hypertensive Encephalopathy
- Toxins
- TTP / Thrombotic thrombocytopenic purpura
- Alcohol withdrawal
- Drug reactions (NMS, Serotonin Syndrome)
- Environmental causes
- Deficiency state
- Wernicke encephalopathy
- Subacute Combined Degeneration of Spinal Cord (B12 deficiency)
- Vitamin D Deficiency
- Zinc Deficiency
- Sepsis
- Osmotic demyelination syndrome (central pontine myelinolysis)
- Limbic encephalitis
Primary CNS disease or trauma
- Direct CNS trauma
- Diffuse axonal injury
- Subdural/epidural hematoma
- Vascular disease
- SAH
- Stroke
- Hemispheric, brainstem
- CNS infections
- Neoplasms
- Paraneoplastic Limbic encephalitis
- Malignant Meningitis
- Pancreatic Insulinoma
- Seizures
- Nonconvulsive status epilepticus
- Postictal state
- Dementia
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
- Manage ABCs
- Benzodiazepines or haloperidol for agitation
- 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]
- Thiamine 100mg IV
- Folate 1mg IV (cheaper PO)
- Multivitamin 1 tab IV (cheaper PO)
- Magnesium sulfate 2mg IV
- Normal saline as needed for hydration
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
- Toxic alcohols
- Beer Potomania Syndrome
- Alcoholic ketoacidosis
- Alcohol withdrawal
- Alcohol withdrawal seizures
- Altered mental status
- Delerium tremens
- EBQ:Outpatient use of benzodiazepines for the treatment of acute alcohol withdrawal
- Sedative/Hypnotic
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Krishel, S, et al. Intravenous Vitamins for Alcoholics in the Emergency Department: A Review. The Journal of Emergency Medicine. 1998; 16(3):419–424.
- ↑ Li, SF, et al. Vitamin deficiencies in acutely intoxicated patients in the ED. The American Journal of Emergency Medicine. 2008; 26(7):792–795.