Acute alcohol intoxication and alcoholism are two separate and unique entities that we see regularly in the emergency department. As ER physicians, our role for the acutely intoxicated patient should focus on ruling out life threatening disease and ensuring their safety for discharge.
Alcoholism, however, does predispose patients to many acute and chronic complications, in particular; Wernicke’s encephalopathy, alcoholic ketoacidosisand alcohol withdrawal.
· Legal Limit = 0.08% (80mg/dL); approximate conversion to IU may be calculated by dividing by 5 (mmol/L)
· Metabolism of alcohol:
o Zero order kinetics at low concentrations (via Alcohol Dehydrogenase)
o First order kinetics at high concentrations (via MEOS)
· Average rate of elimination is 3-9mmol/hr
· In terms of detoxification; charcoal binds alcohol, but due to rapid absorption, there is no role for acute decontamination.
· Consider alternative diagnoses, ie: alcohol induced hypoglycemia, trauma, substance withdrawal, etc.
· Incidence of vitamin deficiency is rare – no evidence for regular replacement in the acutely intoxicated patient.
o No treatment is able to increase the rate of alcohol elimination.
o There are no decision tools to help determine when a patient is safe for discharge, so this is best done via physician assessment. It is important to utilize caution during assessment as our ability to estimate blood alcohol concentration on physical exam alone is very poor. EtOH level is poorly correlated to level of intoxication, and should not be used alone as a guide in clinical decision making.
· Typically considered a chronic problem, however there are some useful ED screening tools, including; CAGE or AUDIT-C. ED interventions (even while brief) have been shown to reduce alcohol related injuries/complications.
- Alcoholic ketoacidosis should be suspected in the settings of acute stress/illness or lack of access to alcohol. Although treatment is relatively simple, the diagnosis is often missed due to failure of consideration.
- Distinct from starvation or diabetic ketoacidosis: occurs as a result of significant malnutrition with associated alcohol consumption, resulting in significant glycogen utilization.
- Urine dip will not test positive for ketones despite severe ketosis, but they will demonstrate a high anion gap metabolic acidosis. However, serum beta-hydroxybutyrate has a high sensitivity for ketoacidosis.
- Treatment: glucose, fluids (D5W!), antiemetics, treatment of the underlying cause as well as correction of electrolyte disturbances.
- Diagnosis based upon the Caine criteria, and requires the patient to have > 2 of the following: dietary deficiencies, oculomotor abnormalities, ataxia or altered level of consciousness. It is important to remember that Wernicke’s is an clinical diagnosis, and therefore investigations play a minimal role in the recognition and diagnosis of this entity.
- Thiamine is beneficial and required in doses much larger than 100mg
- There is little evidence that thiamine must be administered before glucose, and therefore if hypoglycemia is discovered, glucose administration should not be delayed.
- There is some evidence to suggest initiating a starting dose of Thiamine 500 mg IV q8h x 2 days before tapering down.
- Magnesium – required for Thiamine related kinetics, and is often low in alcoholics, replace magnesium when giving thiamine.
· Note that there is a duty to notify the Ministry of Transportation of patients with alcoholism.
- Spectrum consists of Early Withdrawal, Withdrawal Seizures, Alcoholic Hallucinosis, Delirium Tremens.
- Begins ~ 6hrs after cessation of alcohol consumption, peaks at ~24-36 hours, duration ~ 2-7 days.
- Occurs as a result of loss of GABA inhibition by alcohol + the persistence of Glutamate up-regulation.
- Early Withdrawal = symptoms of autonomic hyperactivity; tremor (postural and intentional, but not resting), sweating, tachycardia, hyperreflexia, anxiety, and nausea.
- Withdrawal Seizures:
- Occur at ~ 12-48hrs
- Typically preceded by tremor
- Typically tonic-clonic seizures
- Previous withdrawal seizure places the patient at higher risk
- Alcoholic Hallucinosis = clear cognition and hallucinations. High risk of progression to Delirium Tremens.
- Delirium Tremens = profound confusion, sympathetic overdrive and hallucinations. Mortality approaches 5-35%
- Benzodiazepines; Diazepam or Lorazepam
- Symptom based approach superior to scheduled dosing
- Considerations when choosing a benzodiazepine:
|Benzodiazepine considerations in alcohol withdrawal
|CIWA or SHOT protocols for mild to moderate withdrawal
- Anticonvulsants; limited evidence, no role for withdrawal treatment given potential for side effects and current safer alternative (benzodiazepines).
- Use care when considering the use of Haldol – potential to lower seizure threshold, potential to prolong QT and anticholinergic effects may worsen hyperthermia.
- Unable to use CIWA or SHOT tools for delirium tremens (due to altered mental status), however, a symptom based approach is still recommended.
- Refractory Delirium Tremens – consider barbiturates in an ICU setting.
- Other anticonvulsants have been studied extensively, however, the potential for side effects usually outweighs their benefits.
· Benzodiazepines are not effective for long term treatment
· If you still wish to prescribe benzodiazepines for brief symptom control, consider strategies to remove responsibility of control from the patient:
- Fax prescription to detox and write “Do not dispense remainder of meds at time of discharge”.
- Daily pharmacy dispensing.
Dr. Chris Fabian is a 5th year Emergency Medicine resident at the University of Ottawa with a special interest in Emergency Medical Services and Wilderness medicine.
Edited by Dr. Shahbaz Syed, 4th year Emergency Medicine Resident, University of Ottawa
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