Index
Module 20 • Toxicology
Toxicology
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Data Tables
Toxicology
Kyle Weant ~3 min read Module 20 of 20
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Toxicology

2Common symptoms include tremors, diaphoresis, nausea, vomiting, and abnormal vital signs, including
hypertension, tachycardia, hyperthermia, and tachypnea (Am J Emerg Med 2013;31:734-42).
3

Additional symptoms categorized as moderate to severe withdrawal include:

Alcoholic hallucinations – Auditory, visual, or tactile; may last up to 6 days

Alcohol withdrawal seizures (tonic-clonic) – Occur within 72 hours; however, it is highest in the

first 24 hours after the last drink.

Delirium tremens – Severe and potentially life-threatening symptom that may develop within 72

hours; presentation includes autonomic hyperactivity, confusion, delirium, psychosis, hallucinations,

and seizures.

C.Treatment
1

The goal of therapy is to keep the patient safe, alleviate and prevent the progression of symptoms,

and treat comorbidities (Crit Care Med 2010;38(suppl):S494-S501). Agents for the treatment of alcohol

withdrawal are listed in Table 5.

2Benzodiazepines are the primary agents used in treatment; they bind to the γ-aminobutyric acid

(GABAA) receptor, resulting in hyperpolarization and membrane stabilization.

Lorazepam and diazepam are preferred because of their advantageous pharmacokinetic and

pharmacodynamic profiles, most notably their longer durations of action compared with other

benzodiazepines.

Chlordiazepoxide is not recommended in the acute stabilization setting.

Symptom-triggered therapy is preferred because it reduces benzodiazepine use, duration of

mechanical ventilation, and duration of ICU stay.

A front-loading regimen (i.e., a single dose of preventative medication) is recommended for

patients at high risk for severe withdrawal (J Addict Med 2020;14:1-72).

d.Scheduled treatment may be necessary if symptoms are severe or difficult to control.
3

Use of ethanol to control alcohol withdrawal is controversial and is not routinely recommended.

4

Phenobarbital

Barbiturate with sedative, hypnotic, and antiseizure activity. Increases the binding of GABA to

GABAA receptor and prolonging the chloride channel opening. It may also concomitantly mitigate

neuronal stimulation through NMDA receptor antagonism. Potential advantage over benzodiazepines

in alcohol withdrawal because it does not require GABA to be effective (GABA may be depleted),

and a longer duration of action.

Historically considered a second-line agent if benzodiazepines fail to adequately control

symptoms. Current data suggests that phenobarbital appears to have equivalent outcomes as that

of benzodiazepines, and may be more advantageous for certain patients based on patient-specific

factors (Am J Emerg Med. 2023 Jul;69:65-75.)

May increase the efficacy of benzodiazepines when used in combination by increasing the binding

to the GABAA receptor.

5

Clonidine: α2-receptor agonist that helps control the catecholamine surge associated with withdrawal

(responsible for elevations in BP and HR); however, it will not prevent seizures.

6

Baclofen: Selective GABAB receptor agonist that reduces the signs and symptoms of alcohol withdrawal;

however, it will not prevent seizures.

7

Gabapentin: Increases GABA syntheses and concentrations; may reduce benzodiazepine requirements;

however, it may not effectively control seizures when used as monotherapy (Ann Pharmacother

2015;49:897-906).

8

Propofol

General anesthetic acting through GABAA receptor agonism and N-methyl-D-aspartate (NMDA)

receptor antagonism; chronic alcohol use is associated with an up-regulation of NMDA.

Useful for controlling delirium and preventing seizures; patients must be intubated to receive

propofol for this indication

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