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 to 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 months to 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 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