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Pediatric emergency medicine trisk 3158 3158

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use or drug trade (which is most common in adolescents), but, commonly,
exposure is initiated through a physician’s prescription to a parent for insomnia or
anxiety.
The sedative-hypnotics reversibly depress the activity of all excitable tissues.
For most of these agents, CNS effects occur with little action on skeletal, cardiac,
or smooth muscle. Uncommonly, serious depression in cardiovascular and other
functions may occur. The pharmacologic characteristics of each drug are largely
determined by their specific chemical nature. For example, all barbiturates are
bound by plasma proteins. These characteristics have important implications in
affecting their renal elimination and the effectiveness of extracorporeal drug
removal techniques (hemodialysis, hemoperfusion). Because tolerance develops
to most of the actions of these drugs, no signs of chronic use may be apparent.
Clinical Considerations
After sedative-hypnotic use, the adolescent may exhibit sluggishness, difficulty in
thinking, dysarthria, poor memory, faulty judgment, emotional lability, and short
attention span. The classic presentation of oral sedative-hypnotic overdose is
lethargy or coma with relatively normal vital signs. Respiratory depression may
be seen, especially with combination sedative-hypnotic ingestions (i.e.,
benzodiazepines and ethanol). Toddlers who unintentionally ingest
benzodiazepines may present with acute ataxia.
With chronic use, these drugs also lead to dependence, so a picture of
abstinence may appear after their disuse, with clinical manifestations of apathy,
weakness, tremulousness, agitation, or convulsions. In its mildest form, the
abstinence syndrome may consist only of rebound increases of rapid eye
movement sleep, insomnia, or anxiety.
Direct initial attention to ensuring a patent airway and assessing an intact gag
reflex. Monitor end-tidal CO2 , if available, to detect worsening ventilation.
Cardiovascular disturbances are rare after sedative use, but because of the
possibility of drug coingestion, thorough hemodynamic assessment is necessary.
Many sedative-hypnotics are detectable on comprehensive toxin screens, so
specimens of serum and urine may be sent for analysis; however, these screens


rarely come back in real time, thus minimizing their importance at the bedside. GI
decontamination should be considered in select cases and can typically be
confined to administration of activated charcoal. Repeated doses of charcoal
enhance clearance of certain barbiturates and benzodiazepines. Urinary
alkalinization aids in the excretion of phenobarbital. In extreme cases, consider
charcoal hemoperfusion, but most patients will recover with supportive care.



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