Second edition

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threatens, flumazenil may be given (Brogden and Goa
1991); however, caution is needed here in cases in which
tolerance has developed, as flumazenil may precipitate a
withdrawal syndrome with seizures.
Sedative–hypnotic blackouts require only observation
until serial mental status examinations have revealed a
restoration of short-term memory, and the intoxication
itself has resolved.
Sedative–hypnotic withdrawal should probably be
treated with the same agent that the patient is addicted to.
This is particularly the case for barbiturate withdrawal,
which is not controlled by benzodiazepines, and alprazolam
withdrawal, which may not respond to other benzodiazepines
such as diazepam (Zipursky et al. 1985). For
benzodiazepine withdrawal, a strategy similar to that
described for the treatment of alcohol withdrawal in the
preceding section may be utilized, with equivalent doses
(e.g., lorazepam 2 mg, alprazolam 1 mg, diazepam 10 mg,
chlordiazepoxide 25 mg). In the case of barbiturate withdrawal
it is traditional to utilize phenobarbital, with doses
of 90–120 mg every 1–2 hours until symptoms are controlled,
after which the dose may, as with the benzodiazepines,
be gradually tapered.
An alternative to consider in the case of benzodiazepine
withdrawal is carbamazepine (Schweizer et al. 1991). Once
symptoms have been adequately controlled with the benzodiazepine,
one may add carbamazepine in a dose of 200 mg
three or four times daily, after which the benzodiazepine
may be rapidly tapered over a day or two. Importantly, carbamazepine
is not effective for barbiturate withdrawal and
may also be ineffective in the case of alprazolam.
Sedative–hypnotic withdrawal seizures should be
treated by rapidly reinstituting the sedative–hypnotic in
question, with the goal of completely controlling any concurrent
withdrawal symptomatology.
Sedative–hypnotic withdrawal delirium demands vigorous
treatment of the withdrawal syndrome, with the goal
of producing a light degree of sedation. Should hallucinations
and delusions persist in a troubling fashion, an
antipsychotic, as described in Section 5.3, may be required.
Once symptoms have been brought under control, the
sedative–hypnotic may be gradually tapered in daily decrements
approximately equivalent to 10 percent of the total
daily dose initially required to effect control.
Overall, the goal of treatment in the case of abuse or
addiction is abstinence. Those addicted to sedative–
hypnotics alone, or to a combination of a sedative–hypnotic
and alcohol, may do well in AA.
21.7 INHALENTS (SOLVENTS)
The volatile ingredients of many readily available products
are often inhaled for intoxication. These include airplane or
model glue, paint thinner, kerosene, gasoline, fingernail polish
remover, the propellants in aerosol sprays and spray
paints, and typewriter correction fluid. Each of these products
21.7 Inhalents (solvents) 669
contains various mixtures of aliphatic and aromatic hydrocarbons,
some of which may be halogenated; of all of these
intoxicating hydrocarbons, toluene appears to be the most
significant.
Clinical features
Intoxication is obtained either by soaking a rag in the
volatile substance and holding it to the face or by placing
the substance in a plastic or paper bag and then inhaling;
when a bag is used it may leave a telltale circular rash on the
face. The intoxication (Evans and Raistrick 1987) occurs
within minutes and is characterized by a dreamy euphoria,
drowsiness, dizziness, dysarthria, diplopia, nystagmus, and
ataxia. Some may also experience confusion and hallucinations,
which may be either visual or, less commonly, auditory,
and others may become irritable and impulsive.
Cardiac arrhythmias may occur and may be fatal (GS King
et al. 1985; Steffee et al. 1996). Convulsions, coma, and respiratory
depression may also be seen (King et al. 1981), as
may acute hepatitis and renal failure (Gupta et al. 1991;
Taverner et al. 1988). If leaded gasoline is sniffed, intoxication
may be accompanied by chorea and myoclonus
(Goldings and Stewart 1982).
Tolerance may develop and, when this occurs, withdrawal
may also appear. Withdrawal (Evans and Raistrick
1987; Watson 1979) occurs within 1–2 days of abstinence
and is characterized by irritability, sweating, tremulousness,
and insomnia, all of which generally remit within a
matter of days.
With long-term use a dementia may occur (discussed in
Section 22.12), as may a severe motor peripheral polyneuropathy
(Altenkirch et al. 1977; PJ King et al. 1985).
Course
Occasional, recreational use of inhalants is not uncommon
among adolescents; abuse and addiction appear to be far
less common. In many cases other substances are also used,
especially alcohol and opioids.
Etiology
Although the intoxicating hydrocarbons clearly have an
effect on lipid neuronal cell membranes, the precise mechanism
whereby intoxication occurs is not known.
Differential diagnosis
Intoxication with alcohol or sedative–hypnotics may yield
a somewhat similar clinical picture. The odor of solvents
on clothing or skin may be a clue, as may a rash on the face;
if toluene has been used it may be detected in the blood for
days (King et al. 1981).