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Side effects of pcp use

Know the facts and connect with support to help you address known or suspected substance use with your. Its sedative and anesthetic effects are trance-like.

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Originally developed in the s as a surgical anesthetic, the drug was soon discontinued after it was found to cause agitation and mania, hallucinations, and irrational thinking in patients following its use. The psychiatric effects vary widely, but it is considered dangerous, and its use has been linked to violent and aggressive actions, psychosisand a risk of accidental death. An overdose can be life-threatening.

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Try out PMC Labs and tell us what you think. Learn More. The acronym PCP stems from its organic name 1- 1-phenylcyclohexyl piperidine, which alludes to its relatively simple production from the arylcyclohexylamine piperidine. More than 60 deer analogs more toxic than PCP, but able to escape clinical detection, were common before the sale of piperidine and its derivatives became illegal in the United States in Ketamine is the only one authorized for medical use, and it was often stolen from veterinary offices for its PCP-like effects.

PCP has re-emerged as a drug of abuse in this decade since its decline after the s.

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In Regrettably, exposure to the smoke and butts of these cigarettes has resulted in many cases of occult pediatric PCP intoxication. A typical PCP-laced marijuana cigarette contains 1 to 10mg of the drug. The average tablet varies in weight from 1 to 6 mg. Effects may take 15 to 60 minutes when ingested orally. Walberg et al.

Additionally, no relevant data or literature could be found to correlate PCP concentrations in the cerebrospinal fluid CSF with the clinical effects of the drug. In animal experiments PCP-binding antibodies actually increased serum concentrations of PCP, indicating that they simply alter its distribution. Regardless of the method of administration, ificant amounts of the weakly basic PCP are actively secreted into the acid milieu of the stomach, accumulating to levels up to 50 times higher than serum levels, where it is then reabsorbed in the small intestine.

Phencyclidine is believed to have several sites of action in the central nervous system, all of which act synergistically to result in anesthesia and analgesia. It has greatest affinity for the NMDA N-methyl-D-aspartate receptor complexes in the hippocampus, neocortex, basal ganglia, and limbic system.

Pcp (phencyclidine)

The NMDA-Phencyclidine complex includes a calcium channel stimulated by excitatory neurotransmitters such as glutamate, glycine, and aspartate, but inhibited by phencyclidine at a PCP-specific binding site. Metabotropic receptors are G-protein rather than ion-gated channels.

PCP has contrary actions on the glutamate transmission, explaining its different effects. The clinical picture may wax and wane between extreme agitation and sedation, because PCP can produce CNS stimulation and depression through its different clinical effects in the CNS. Doses greater than 10 mg usually result in coma. Low doses of phencyclidine have produced patterns of metabolic and neurochemical changes in rodent brains that resemble those in brains of schizophrenic patients.

The very characteristics that made PCP ideal for anesthesia at moderate doses — absence of cardiorespiratory depression or muscle hypotonia — make it dangerous at higher recreational doses. It produces sympathomimetic s such as hypertension, tachycardia, and diaphoresis similar to cocaine, and cholinergic s like bronchospasm, salivation, urinary retention, flushing, and miosis, similar to opiates. The most common of these are tachycardia and hypertension.

PCP has also been shown to be a direct cardiac irritant, and may induce arrhythmias and vasospasm. In addition, muscle tone becomes exaggerated, and patients may exhibit hyperreflexia, and myoclonic, dystonic or choreoathetoid movements such as opisthotonos and torticollis. Respiratory depression requiring intubation is uncommon in PCP intoxication; however, patients may exhibit irregular breathing, with episodes of both apnea and tachypnea.

Non-traumatic causes of death include cardiopulmonary arrest, intracranial hemorrhage in hypertension, and hyperkalemia secondary to rhabdomyolysis. Patients have walked into traffic, jumped from buildings, and even enucleated their own eye. Patients recovering from PCP exposure may undergo an emergence reaction as the drug is eliminated, consisting of psychosis, bizarre behavior, or depression that may last from days to weeks. Depression, anxiety, irritability, restlessness, anergia, and disturbances of thought and sleep have been described in as little as a day of abstinence in chronic abusers.

Oculomotor hyperactivity, tremor, diarrhea, and piloerection were reported within 8 hours of abstinence in monkeys chronically administered PCP. Ikonomidou et al. Different brain regions display different age-dependent vulnerabilities to NMDA receptor-blocking drugs, leading to different patterns of neuronal loss depending on the time of exposure.

What is phencyclidine (pcp), or angel dust?

Thus, young children are very sensitive to PCP, and develop serious neurologic s with minimal exposure. They can become intoxicated from passive inhalation of secondhand smoke, or by ingesting the butts of PCP-impregnated cigarettes.

Seizures, apnea, and respiratory depression are documented more frequently in children than adults; however, they rarely require intubation. Violent behavior is less common in children, which may explain the lack of mortality reported in children. Phencyclidine intoxication is a diagnosis that must be suspected clinically so that the appropriate tests are ordered for confirmation.

The differential diagnosis of the clinical picture created by PCP includes other intoxications, schizophrenia, intracranial pathology, hypoxia, hypoglycemia, hyponatremia, sepsis, meningitis and encephalitis, thyroid storm, and neuroleptic malignant syndrome. PCP intoxication shares many features with overdoses of cocaine, amphetamines, anticholinergic agents, hallucinogens, effects withdrawal from benzodiazepines.

Therefore, a qualitative urine toxicologic screen has become mandatory standard of care for any patient, infant or adult, with altered mental status of unknown etiology. Bond et al. In this situation, saliva or gastric contents can be analyzed for PCP. Because PCP-induced seizures, myoclonic activity, and trauma may result in rhabdomyolysis, serum potassium, blood urea nitrogen, creatinine, and creatine phosphokinase CPK should be ordered any time it is suspected. Serum CPK is the preferred screening method for rhabdomyolysis, because the presence of urinary myoglobin may be transient. The management of PCP intoxication begins just as any other intoxication would.

The patient should then be restrained and sedated if necessary to prevent self-inflicted injury, which is the most common cause of morbidity and mortality in these patients. Chemical restraints are preferred over physical restraints, which may exacerbate the risk of rhabdomyolyis. The risks of lengthening of the QT interval, torsade de pointes and adverse neurologic effects limit the use of haloperidol in PCPintoxicated patients.

Due to their more favorable side effect profile, atypical antipsychotics like olanzipine or ziprazidone would be a better side than haloperidol when treating PCP-induced agitation and psychosis. Patients should then be closely observed in a dark and quiet environment, with minimal auditory and tactile stimuli so as not to provoke violent outbursts. Naloxone, to treat potentially coingested pcp, is not necessary in patients use adequate respiration.

Gastric lavage is controversial, and should only be used after consultation with a toxicologist. Patients must be on continuous cardiac monitoring because of the frequency and severity of cardiac symptoms. There are case reports of intracerebral hemorrhage secondary to hypertension. In the past, PCP elimination was thought to be enhanced by urinary acidification via ammonium chloride or ascorbic acid; however, this is no longer recommended because acidic urine increases the risk of acute tubular necrosis secondary to myoglobinuria in rhabdomyolysis.

Understand the risks

Hemodialysis is also ineffective because it simply removes the drug from the serum, clearing the path for redistribution from lipid stores. Hemodialysis is, however, a treatment option for renal failure caused by rhabdomyolysis. Renal failure is considered to be far more dangerous than PCP intoxication; therefore patients with rhabdomyolysis should be aggressively treated with fluids, sodium bicarbonate, mannitol and furosemide. Status epilepticus should be treated with airway protection and IV benzodiazepines or phenobarbital.

The patient should not be paralyzed after rapid sequence intubation RSI because it is then virtually impossible to monitor whether seizures are still ongoing, short of continuous EEG monitoring. Benzodiazepines are a useful adjunct to prevent shivering and provide sedation.

Patients with rhabdomyolysis, hyperthermia, altered mental status, seizures, ificant injuries, or pediatric age require hospitalization. Children require continuous monitoring to note fluctuations in consciousness, cardiorespiratory stability, and for suction of excess oral secretions. Mildly intoxicated patients should return to normal functioning four to eight hours after ingestion, whereas larger ingestions may require weeks. Infants have been reported to need from 48 hours to four days to recover.

Finally, it is important to investigate the source of intoxication, whether it be in an adult who is unknowingly inhaling PCPlaced marijuana cigarettes, or more tragically, who is unwillingly exposed to secondhand smoke.

In conclusion, phencyclidine is a unique, paradoxical drug that produces central nervous system depression and peripheral and central nervous system stimulation. Hallmark clinical findings of PCP intoxication are nystagmus, hypertension and a mental status, which is often described as dissociative anesthesia. In higher doses patients become unconscious and can succumb to pulmonary aspiration and cardiovascular collapse. The most disturbing behavioral effects of PCP are violent, aggressive and bizarre behavior with self-mutilation tendencies.

National Center for Biotechnology InformationU. Cal J Emerg Med. Author information Copyright and information Disclaimer. This article has been cited by other articles in PMC. Pharmacology of Phencyclidine PCP in the central nervous system.

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