Pediatric emergency medicine trisk 3143 3143
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Pharmacologically, PCP acts as a dissociative anesthetic, meaning that it
interferes potently with association pathways that link the cerebral cortex with
deeper structures in the brain, thus diminishing the ability to integrate sensory
input into meaningful behavior. Its anesthetic actions also lead to a marked
diminution of pain sensation. In conjunction with bizarre behavior, this often
leads patients to have feelings of invulnerability and to attempt life-threatening
actions (e.g., stepping into automobile traffic).
Clinical Considerations. Small doses of PCP produce signs and symptoms of
inebriation with staggering gait, slurred speech, and nystagmus (vertical or
rotatory). Users may be diaphoretic and have catatonic muscular rigidity with a
blank stare. PCP often causes hypertension and tachycardia because of its
sympathomimetic actions. Dextromethorphan toxicity resembles the syndrome of
low-dose PCP exposure; nystagmus and myoclonus may help distinguish this
toxidrome from alcohol or sedative toxicity, and the urine drug screen may be
falsely positive for PCP. Moderate doses of PCP cause other signs of intoxication,
including hypersalivation, pyrexia, repetitive movements, and muscle rigidity.
Larger doses can cause seizures, coma, or respiratory arrest. The typical “high”
from a single dose lasts 4 to 6 hours and is followed by an extended “coming
down”; PCP-induced psychosis may be long lasting and may recur (flashbacks).
Tolerance develops to the behavioral and toxic effects of the drug. Chronic users
report persistent difficulties with recent memory, speech, and thinking that last
from 6 months to 1 year after the last dose; they also may be left with personality
changes such as withdrawal, isolation, anxiety, nervousness, and depression.
PCP is easily detected through a qualitative analysis of urine, though several
pharmaceuticals may cause a false-positive result and several novel analogs may
not be detected reliably with standard PCP immunoassays. Serum levels are
rarely available and do not correlate with clinical manifestations. Therefore,
management must often be based solely on a history of exposure or index of
suspicion. Initial treatment is directed at stabilizing vital signs and treating lifethreatening events such as seizures. If exposure is the result of ingestion, consider
GI decontamination with activated charcoal. A quiet room may be helpful as long
as it does not compromise the ability to monitor the patient. Physical restraints
should be avoided if possible because they may lead to significant
rhabdomyolysis with resulting myoglobinuria and renal injury. For chemical
restraint benzodiazepines are the preferred first-line agent; additional agents (e.g.,
haloperidol) are often necessary.
