AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Phencyclidine, 1-(1-phenylcyclohexyl) piperidine (PCP), is a dissociative anesthetic that was originally synthesized for intravenous use in 1957 and was marketed under the trade name Sernylan. Because of its postoperative emergence reactions (ie, hallucinations, prolonged abnormal level of consciousness, agitation), it fell out of favor; its use as an anesthetic in humans was discontinued in 1963. Subsequently, it was used primarily as an animal tranquilizer and was distributed for veterinary use until 1978, when the US government added the drug to its list of controlled substances. Today, several of its congeners (eg, ketamine) are used in anesthesia or are under investigation for use as anesthetics.

PCP emerged as an oral drug of abuse, known as the PeaCe Pill on the streets of San Francisco in 1967. However, its reputation for bad trips (ie, unexpected and unpleasant reactions), coupled with its unpredictable effects, quickly filtered through the drug community and caused the drug to wane in popularity. In the early 1970s, smoking of PCP was recognized as an effective method of use because its mind-altering effects could be titrated.

Pathophysiology

PCP is a commonly abused street drug sold under many different names and in many different forms. It may be sold on the street in tablet or capsule form, as a powder, or as a solution. The PCP content in each form differs widely, commonly containing only 10-30% PCP. Angel dust, the powdered form of PCP, generally has a higher PCP content, occasionally reaching 100%. Angel dust may be sniffed, smoked, ingested, or injected intravenously. Percutaneous absorption has also been reported to occur in individuals handling PCP (eg, law enforcement officers). Smoking remains the desired method of use; the substance is commonly sprinkled onto dried leaf material (eg, marijuana, tobacco, oregano, mint) and then smoked.

PCP is easy to synthesize, and a number of its analogs or byproducts of synthesis may be found on the streets. These include phenylcyclohexylethylamine (PCE), thienylcyclohexylpiperidine (TCP), and phenylcyclohexylpyrrolidine (PHP), which have similar pharmacologic activity to PCP but may be more toxic. One byproduct, piperidinocyclohexane carbonitrile (PCC), can cause cyanide poisoning.

Pharmacokinetics

PCP is a dissociative anesthetic because it renders the patient motionless (ie, rigid muscles, flat facies, staring gaze) while maintaining a wakeful, although amnestic, state. The anesthetic effect results from PCP's ability to block selected sensory stimuli, such as pain. It produces profound analgesia and anesthesia while preserving spontaneous respiration and without major effects on the cardiovascular system.

PCP is an arylcyclohexylamine compound, and, like other arylcyclohexylamines, it interacts with most neurotransmitter systems, resulting in a combination of CNS stimulant and depressant effects. For example, it blocks the N-methyl-D-aspartic acid (NMDA)–type glutamate receptors located in both the cortex and limbic regions of the brain, it inhibits GABA, and it increases dopamine synthesis and release while inhibiting its presynaptic reuptake. PCP also blocks acetylcholine receptors, thus resulting in anticholinergic activity; however, PCP may also inhibit acetylcholinesterase, resulting in cholinergic activity. Additionally, PCP has some interaction with the sigma opiate receptors in the hippocampus and competitively inhibits norepinephrine and serotonin. While the predominant effect is sympathomimetic, a number of other effects may be observed to varying degrees in individuals who are intoxicated with PCP.

PCP is a weak base (pKa 8.6-9.4) that is absorbed well orally, nasally, and percutaneously, especially when in liquid form. When ingested, PCP has an oral bioavailability of approximately 50-90%, and it is absorbed best from the alkaline environment of the intestines. When smoked, almost all the PCP that reaches the alveoli is absorbed. Once in the blood, it undergoes extensive first-pass metabolism in the liver and extensive enterohepatic recirculation. PCP is also secreted into the stomach, where it is ionized and trapped by gastric acid, only to be released to the alkaline environment of the duodenum, where it is reabsorbed. This gastroenteric recirculation may help explain the waxing and waning effects of PCP as plasma levels decrease when PCP is secreted into the stomach and rise again when it is reabsorbed from the duodenum.

PCP is highly lipid-soluble and may be found in high concentrations in the brain and adipose tissue. It is ion-trapped and tightly bound in many tissues, particularly the liver and the brain. PCP has a volume of distribution of approximately 6.2 L/kg and is approximately 65-78% protein-bound.

The onset of action of PCP depends on the route of administration and may be as quick as a few minutes to 30 minutes, depending on the route. The onset of action is 2-5 minutes when inhaled or smoked and 15-30 minutes when ingested. Peak plasma levels occur in 5-30 minutes when inhaled or smoked and 2.5 hours when ingested orally. The half-life and the duration of clinical effects also vary and depend on the long-term nature of use and individual variations. Effects usually last from 4-6 hours but may last as long as a week in those who have used it long-term. Severe symptoms lasting longer than 24 hours should raise the possibility of continued absorption, as in the case of a ruptured body pack (eg, worn by smugglers).

PCP is metabolized by the liver via hydroxylation, which produces metabolites that are excreted by the kidneys. Approximately 9% of absorbed PCP is excreted unchanged in the urine. This may increase to approximately 50% with urinary acidification (pH 6.1-7.4). PCP and its metabolites remain in the urine for an average of 2 weeks after use but may persist for up to a month.

PCP is capable of crossing the placental membrane and has been found in amniotic fluid, umbilical cord blood, and neonatal urine. PCP also may be excreted in breast milk. While long-term intrauterine exposure has occasionally been linked to an increased incidence of cerebral palsy and facial dysmorphogenesis, these reports did not control for other substances of abuse and, therefore, are difficult to interpret. Long-term intrauterine exposure to PCP has been reported to lead to dependence, as evidenced by a withdrawal syndrome, similar to narcotic withdrawal.

Frequency

United States

According to the latest National Household Survey on Drug Abuse, 3.2% of persons aged 12 years and older have used PCP at least once in their lifetime.

According to data from the Drug Abuse Warning Network (DAWN), which examines the number of emergency department records that mention drug use in the diagnosis, for the third and fourth quarters of 2003, PCP was involved in 4,581 of all drug-related ED visits nationwide (n= 627,923), nearly 0.75% of all drug-related ED visits.

Mortality/Morbidity

In 2003, 785 exposures were reported to US Poison Control Centers, including 8 deaths and 83 cases with severe morbidity due to phencyclidine.

Morbidity and mortality from PCP are related directly to trauma sustained during intoxication. PCP may also cause status epilepticus, hyperthermia, rhabdomyolysis, intracranial hemorrhage, and respiratory arrest. A fatal dose is 1 mg/kg. Lethal PCP blood concentration is 100-500 mcg/dL.

Race

No racial or ethnic predilection is recognized among those who abuse PCP.

Sex

No sexual predilection is recognized among those who abuse PCP.

Age

PCP use is observed most commonly in older teenagers and in young adults.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

The clinical presentation of intoxication is highly variable and depends on the amount consumed, the route of administration, the presence of co-ingestants, and individual variations. Symptoms generally fluctuate and depend on the degree of sympathomimetic, serotoninergic, cholinergic, anticholinergic, and narcotic effects. These generally result in abnormal behavior and thought processes, along with an altered level of consciousness.

Most intoxications are without complications. Patients present for medical care when they are having a particularly bad trip or when they develop complications of PCP use. Life-threatening complications include those relating to major traumatic injuries, convulsions, and hyperthermia.

Physical

The clinical manifestations of PCP intoxication are also extremely variable. While no pathognomonic signs of PCP intoxication exist, nystagmus and hypertension are present in more than half of the patients. These physical findings, along with a history of an acute episode of bizarre behavior and urine toxicology screen results that are positive for PCP, are usually enough to make the diagnosis. Other symptoms present in those with PCP poisoning include the following:

• Central nervous system: Patients may be alert and oriented, comatose or catatonic, markedly agitated, and violent. They may exhibit amnesia, opisthotonos, torticollis, choreoathetoid movements, and seizures. Coma has been reported in as many as 10.6% of patients; seizures have been reported in 3.1% of patients and are more common in children. Cerebellar symptoms such as dysarthria and ataxia may also be present.
• Psychiatric: In a study of 1000 patients with PCP intoxication, 35% were violent, 34% were agitated, 29% exhibited bizarre behavior, 19% had delusions or hallucinations, and many were dysphoric. Paranoid delusions were especially common, and the hallucinations were both auditory and visual.
• Head, ears, eyes, nose, and throat: Nystagmus (horizontal, vertical, or rotary) is a hallmark of PCP intoxication and is present in more than half the patients studied. Patients also commonly exhibit a blank stare and occasionally have dysconjugate gaze, miosis, or mydriasis. Miosis is more common in children. Hypersalivation may also be observed.
• Respiratory: Tachypnea and irregular respiratory patterns have been reported. Apnea is rare and may be due to co-ingestants or to one of the complications of PCP intoxication. Bronchorrhea and bronchospasm have also been reported.
• Cardiovascular: Mild tachycardia is common (present in 30% of patients), but hypertension (systolic and diastolic) is a hallmark of PCP intoxication and is present in 57% of patients. It commonly resolves within 4 hours but may persist longer than 24 hours. The occurrence of hypertension beyond the first 24 hours should raise the possibility of an intracerebral complication. In the absence of trauma or preexisting heart disease, cardiac arrest is very rare.
• Musculoskeletal: Symptoms include muscle rigidity, dystonia, opisthotonos, torticollis, akinesis, and hyperkinesis.
• Skin: Diaphoresis is common in patients intoxicated with PCP.

Causes

PCP poisoning occurs when PCP is substituted for marijuana. Children may be poisoned by ingesting PCP solutions, PCP-laden leaves, PCP tablets, and sometimes by inhaling PCP smoke in a smoke-filled room. PCP poisoning has also been reported in body packers (ie, smugglers) who transport PCP across different territories.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Thyrotoxicosis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Glucose (hypoglycemia is possible)and electrolytes, osmolarity, and ketones.
• Complete blood cell count - Leukocytosis (common)
• Creatine kinase level especially if rhabdomyolysis is suspected
• Renal function tests - BUN and creatinine, uric acid
• Urine analysis, urine myoglobin level and urine pH
• Blood gas determination
• Liver function tests
• Toxicology screen - Blood alcohol level, acetaminophen, aspirin
• Urine toxicology screen
• • In general, quantitative assays for PCP levels are not clinically useful because serum levels do not correlate with clinical symptoms; all one needs to make the diagnosis of PCP intoxication is a proper clinical setting and a positive result from a qualitative immunoassay for PCP.

    Care must be taken when interpreting results from qualitative screens for PCP because the urine may test positive for up to a month after the agent was last used.Rarely, patients may have a negative urinary PCP screen result. This may be secondary to alkaline urine, which allows PCP to be reabsorbed back into the blood stream.

• Thyroid function tests
• Cerebrospinal fluid analysis
• Cultures

Imaging Studies

• Head CT scan
• Chest radiograph to investigate for a source of infection or for any resulting complications

Other Tests

• Electrocardiogram: The electrocardiogram findings may indicate abnormalities in rate or rhythm that may be secondary to the effects of PCP or to electrolyte disturbances.
• Compartment pressure measurements: In these patients, rhabdomyolysis is always a consideration. Rhabdomyolysis may lead to compartment syndrome and its known complications. If compartment syndrome is suggested, compartment pressure measurements should be taken and fasciotomy performed, when necessary.
• Electroencephalogram: Tracings may indicate diffuse slowing with theta and delta waves.

Procedures

• Lumbar puncture
• Intubation
• Mechanical ventilation
• Nasogastric tube insertion
• Urinary bladder catheterization
• Cooling methods - Ice, cooling blankets, fans, lavage (ie, gastric, thoracic, peritoneal, bladder)
• Neuromuscular blockade
• Pulmonary artery catheter insertion

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Because no specific antidote is available for PCP intoxication, treatment is generally supportive in nature, with meticulous attention to the airway, breathing, and circulation. Four major clinical patterns have been identified as potentially problematic and require admission to the hospital. These include coma, catatonia, toxic psychosis, and acute brain syndrome. Patients with reportedly minor symptoms, such as lethargy, stupor, mild-to-moderate agitation, violent behavior, and euphoria, generally do not require admission to the hospital.

Following a massive oral overdose, the effects may last for days, requiring intensive monitoring until the patient has stabilized. Assessment and stabilization of the airway must be performed early in the course of poisoning. The infusion of 50% dextrose solution and thiamine may be appropriate steps in the evaluation and treatment of all patients with abnormal mental status.

Major life-threatening complications should be actively sought and immediately corrected. These include hyperthermia, rhabdomyolysis, acute renal failure, hypertension, seizures, cardiovascular collapse, and self-inflicted trauma. Cardiovascular and respiratory status, temperature, and renal function must be monitored closely. A pulmonary artery catheter may be necessary to guide fluid therapy.

• Decontamination
• • Gastric lavage is recommended when a large amount of PCP has been ingested or when other life-threatening co-ingestions are possible. Gastric lavage should be performed only when the airway is secure. In the setting of PCP overdose, gastric lavage with continuous suctioning has been advocated by some authors because absorbed PCP is secreted into the stomach and trapped in its acid environment. When this method of decontamination is used, monitoring the patient's acid-base status and electrolytes closely is important. GI fluid losses must be replenished.
  • Some authors recommend pulse infusion of activated charcoal as a safer and more effective method of PCP decontamination compared to continuous gastric suction. Pulse charcoal is thought to work because of the extensive enterohepatic circulation of PCP. While pulse charcoal has not been studied in humans with PCP toxicity, it has been shown to reduce the number of seizures and the death rate in dogs.
  • Urinary acidification had been recommended in the past to enhance ion trapping and the elimination of PCP from the body. However, because most PCP is eliminated via liver metabolism (90%) and very little is eliminated via the kidneys (10%), urinary acidification is not expected to result in any significant effect on elimination. Furthermore, urinary acidification is fraught with dangers because it may result in a systemic acidosis and promote the precipitation of urinary myoglobin in cases of rhabdomyolysis, a known complication of PCP intoxication.
  • Hemodialysis and hemoperfusion are ineffective in persons with PCP poisoning because of a number of factors, including the large volume of PCP distribution, its high lipid solubility, its high protein binding, and its very limited renal excretion.
• Agitation
• • Agitated patients should be placed in a dark quiet room to minimize external stimuli.
  • Benzodiazepines are safe and effective in the control of agitation and should be used liberally to control agitation.
  • Phenothiazines and butyrophenone, while effective sedatives in patients who are psychotic, have a number of adverse effects that make them less desirable in the setting of PCP toxicity, including their association with malignant hyperthermia and neuroleptic malignant syndrome and their ability to lower the seizure threshold. In addition, they cause dystonic reactions.
• Hyperthermia
  • Hyperthermia should be treated with rapid cooling. Ice-water baths are the most effective method for reducing temperatures quickly, but other methods, such as spraying mist on the body and fanning the body may be as effective.
  • Shivering is common during rapid ice-water cooling and may be controlled with benzodiazepines.
  • Occasionally, neuromuscular blockade may be necessary.
• Seizures
  • Seizures, which occur more commonly in children, should be treated with intravenous benzodiazepines as a first-line choice.
  • Phenobarbital and, occasionally, phenytoin may be necessary to control seizures.
  • Status epilepticus, which is rare, may require neuromuscular blockade and barbiturate coma to avoid complications such as hypoxia, hyperpyrexia, hyperkalemia, metabolic acidosis, rhabdomyolysis, and acute renal failure.
• Rhabdomyolysis
  • Urine should be tested for blood, and concomitant samples should be sent for microscopic examination.
  • If rhabdomyolysis is suspected, serum creatine kinase levels should be evaluated. If confirmed, large amounts of intravenous fluids may be required, and alkalinization of the urine with sodium bicarbonate should be instituted immediately to an endpoint of urine pH between 7.5-8.0.
  • Alkalinization of the urine may increase reabsorption of PCP but will protect against rhabdomyolysis-induced renal failure.

Surgical Care

• Exploratory laparotomy may be necessary in persons who are body packers (ie, smugglers) with ruptured PCP-containing packets because symptoms may be severe and prolonged.
• Fasciotomy may be necessary in cases of rhabdomyolysis-induced compartment syndrome.

Consultations

• Consultation with a surgeon is indicated in cases of ruptured PCP packets because patients may experience severe prolonged symptoms. Consultation with a surgeon is also indicated in patients with possible compartment syndrome.
• Consultation with a nephrologist is indicated in patients with severe rhabdomyolysis and acute renal failure.
• Consultation with a toxicologist or personnel at the regional poison control center may be indicated.

Diet

• Patients may resume a normal diet when the GI tract is functional. Dietary restrictions may be required when renal failure occurs.

Activity

• Patients should be kept sedated until all symptoms of agitation have resolved. Patients may resume normal activity when their condition has stabilized.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Glucose supplements

Raise serum glucose level.

Drug Category: Vitamins

Cofactors required for aerobic cellular respiration.

Drug Category: Narcotic antagonists

Prevent or reverse opioid effects (ie, hypotension, respiratory depression, sedation).

Drug Category: Benzodiazepines

Mainstay of therapy for most toxic psychoses and agitated delirium; first-line drugs for treatment of convulsions.

Drug Category: Gastrointestinal decontaminants

Prevent absorption of PCP from GI tract.

Drug Category: Alkalinizing agents

Increase pH of blood and urine.

Drug Category: Osmotic diuretics

Once in kidneys, exert an osmotic diuresis.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Further inpatient therapy and care may be required in patients who sustained serious complications such as renal failure requiring long-term hemodialysis, hepatic failure, disseminated intravascular coagulation (DIC), CNS hemorrhage, and extensive traumatic injuries.
• Patients who ingest large amounts of PCP may exhibit bizarre behavior and may remain comatose for many days after the ingestion because of the high lipid solubility of PCP and because it is stored in adipose tissues. Additionally, patients may exhibit a vacillating course because of a combination of factors, including the high lipid solubility, gastroenteric circulation, enterohepatic circulation, and ion trapping of PCP.
• Long- and short-term physical and occupational rehabilitation therapy may be required.
• Inpatient psychiatric care may be indicated for patients who are suicidal or homicidal.

Further Outpatient Care

• Long-term outpatient therapy may involve physical and occupational rehabilitation in cases of neurovascular, cardiovascular, and traumatic complications.
• Long-term outpatient therapy may be required in patients who sustained serious long-term complications (eg, renal failure, hypertension).
• Long-term outpatient psychiatric therapy may be required in those who have abused PCP long-term who discontinued the use of PCP and who exhibit prolonged depression and other psychiatric symptoms.

In/Out Patient Meds

• Outpatient medications depend on the complications sustained during poisoning. Long-term antidepressant medications may also be required.

Transfer

• Transfer to a medical or psychiatric floor may be undertaken when the patient has stabilized and requires no further intensive therapy.

Deterrence/Prevention

• Enrollment in deterrence programs such as Narcotics Anonymous may benefit some patients.

Complications

• Trauma: The most common complications of PCP poisoning are related to trauma during the acute intoxication phase.
• Rhabdomyolysis: This is reported in approximately 2.2% of patients and may progress to renal failure.
• Aspiration pneumonia
• Intracranial hemorrhage
• Pulmonary embolus
• Hepatic necrosis and DIC

Prognosis

• During the initial phase, the prognosis of patients with PCP poisoning depends on the type and extent of traumatic injuries, the extent and duration of hyperthermia, the extent of rhabdomyolysis, the occurrence of renal failure, and the occurrence of liver failure and DIC.
• Patients who develop psychiatric symptoms, such as major depression, when withdrawn from PCP, have a grim psychiatric prognosis.

Patient Education

• Patients who use PCP should be educated regarding the dangers of the substance and should be referred to support centers.
• For excellent patient education resources, visit eMedicine's Substance Abuse Center, Poisoning - First Aid and Emergency Center, and Mental Health and Behavior Center. Also, see eMedicine's patient education articles Drug Dependence & Abuse, Club Drugs, Narcotic Abuse, Substance Abuse, Poisoning, and Activated Charcoal.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to diagnose and treat complications of acute PCP intoxication
• Failure to realize the waxing and waning effects of PCP and discharging patients prematurely
• Failure to quickly sedate agitated patients
• Failure to quickly cool patients with hyperthermia
• Failure to consider traumatic injuries in patients who are intoxicated with PCP
• Failure to diagnose and adequately treat rhabdomyolysis
• Failure to consider compartment syndrome when present
• Failure to consider co-ingestions

Special Concerns

• PCP can cross the placental membrane and has been found in amniotic fluid, umbilical cord blood, and neonatal urine. PCP may also be excreted in breast milk. While long-term intrauterine exposure has occasionally been linked to an increased incidence of cerebral palsy and facial dysmorphogenesis, these reports did not control for other substances of abuse and, therefore, are difficult to interpret. Long-term intrauterine exposure to PCP has also been reported to lead to dependence, as evidenced by a withdrawal syndrome that is similar to narcotic withdrawal.
• Children may develop PCP toxicity when they accidentally ingest the drug or when they inhale PCP in a smoke-filled room. The most common symptoms observed in children intoxicated with PCP include ataxia, stupor with a blank stare, nystagmus, and bizarre behavior. Convulsions, choreoathetoid movements, and respiratory arrest occur more frequently in children than in adults.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Aniline O, Pitts FN Jr. Phencyclidine (PCP): a review and perspectives. Crit Rev Toxicol. Apr 1982;10(2):145-77. [Medline].
• Armen R, Kanel G, Reynolds T. Phencyclidine-induced malignant hyperthermia causing submassive liver necrosis. Am J Med. Jul 1984;77(1):167-72. [Medline].
• Baldridge EB, Bessen HA. Phencyclidine. Emerg Med Clin North Am. Aug 1990;8(3):541-50. [Medline].
• Barton CH, Sterling ML, Vaziri ND. Rhabdomyolysis and acute renal failure associated with phencyclidine intoxication. Arch Intern Med. Apr 1980;140(4):568-9. [Medline].
• Burns RS, Lerner SE. Causes of phencyclidine-related deaths. Clin Toxicol. 1978;12(4):463-81. [Medline].
• Cook CE, Brine DR, Jeffcoat AR, et al. Phencyclidine disposition after intravenous and oral doses. Clin Pharmacol Ther. May 1982;31(5):625-34. [Medline].
• Ellenhorn MJ. Phencyclidine. In: Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, Md: Williams & Wilkins; 1997:. 389.
• Fallis RJ, Aniline O, Weiner LP, Pitts FN Jr. Massive phencyclidine intoxication. Arch Neurol. May 1982;39(5):316. [Medline].
• Gossel TA, Bricker JD. Phencyclidine. In: Principles of Clinical Toxicology. 3rd ed. New York, NY: Raven; 1994:. 422.
• Hoogwerf B, Kern J, Bullock M, Comty CM. Phencyclidine-induced rhabdomyolysis and acute renal failure. Clin Toxicol. 1979;14(1):47-53. [Medline].
• Jackson JE. Phencyclidine pharmacokinetics after a massive overdose. Ann Intern Med. Oct 1 1989;111(7):613-5. [Medline].
• Karp HN, Kaufman ND, Anand SK. Phencyclidine poisoning in young children. J Pediatr. Dec 1980;97(6):1006-9. [Medline].
• McCarron MM, Schulze BW, Thompson GA, et al. Acute phencyclidine intoxication: incidence of clinical findings in 1,000 cases. Ann Emerg Med. May 1981;10(5):237-42. [Medline].
• McCarron MM, Schulze BW, Thompson GA, et al. Acute phencyclidine intoxication: clinical patterns, complications, and treatment. Ann Emerg Med. Jun 1981;10(6):290-7. [Medline].
• Milhorn HT Jr. Diagnosis and management of phencyclidine intoxication. Am Fam Physician. Apr 1991;43(4):1293-302. [Medline].
• O' Brien CP. Drug addiction and drug abuse. In Goodman and Gilman’s. The Pharmacological Basis of Therapeutics. 10th Edi. 2001;638-640.
• Olmedo Rueben. Phencyclidine and ketamine. In Goldfrank's Toxicologic Emergencies. 7th Edition. 2002. McGraw Hill Compani. 2002;1034-1042.
• Patel R, Connor G. A review of thirty cases of rhabdomyolysis-associated acute renal failure among phencyclidine users. J Toxicol Clin Toxicol. 1985-86;23(7-8):547-56. [Medline].
• Schwartz RH, Einhorn A. PCP intoxication in seven young children. Pediatr Emerg Care. Dec 1986;2(4):238-41. [Medline].
• Shepherd SM, Jagoda AS. Phencyclidine and the hallucinogens. In: Sanders WB, Haddad LM, eds. Clinical Management of Poisoning and Drug Overdose. 2nd ed. WB Saunders Co;1990:749-60.
• Simpson GM, Khajawall AM, Alatorre E, Staples FR. Urinary phencyclidine excretion in chronic abusers. J Toxicol Clin Toxicol. Dec 1982;19(10):1051-9. [Medline].
• Strauss AA, Modaniou HD, Bosu SK. Neonatal manifestations of maternal phencyclidine (PCP) abuse. Pediatrics. Oct 1981;68(4):550-2. [Medline].
• U.S. Department of Health and Human Services, Substance Abuse and Mental Health. Drug Abuse Warning Network 2003: Interim National Estimates of Drug-Related Emergency Department Visits. 2004;December.
• Watson WA, Litovitz TL, Klein-Schwartz W. 2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2004;22(5):335-404. [Medline].
• Young JD, Crapo LM. Protracted phencyclidine coma from an intestinal deposit. Arch Intern Med. Apr 1992;152(4):859-60. [Medline].

Article Last Updated: Jun 21, 2006