Phencyclidine Toxicity 

Updated: Mar 28, 2022
Author: Patrick L West, MD; Chief Editor: Michael A Miller, MD 


Practice Essentials

Phencyclidine (PCP) is a hallucinogen—specifically, a dissociative anesthetic—that can produce a wide variety of physical and behavioral effects and has a high potential for abuse and dependence. Acute toxicity often resembles a psychotic episode. PCP is often taken in conjunction with other co-ingestants, including ethanol and marijuana. 

PCP is a white crystalline powder that is available in tablet or powder forms, or dissolved in a liquid. It can be snorted, ingested orally, or injected intravenously. It also can be smoked as a "joint" or "wet" ("embalming fluid") when sprinkled on cigarettes or applied to mint or marijuana leaves.[1]  

Newer designer versions such as 3-methoxyphencyclidine (3-MeO-PCP) and 4-MeO PCP now exist.[2]  3-MeO-PCP bonds more strongly to N-methyl-D-aspartate (NMDA) receptors than PCP or 4-MeO-PCP.  However, 4-MeO-PCP is toxic at lower concentrations than either PCP or 3-MeO-PCP.[3, 4]


Phencyclidine (PCP) was originally developed in the 1950s for use as a general anesthetic for surgery, under the trade name Sernyl. Its use was discontinued in humans in 1965 because it often produced postanesthetic delirium with psychotic features, dysphoria, and occasionally extreme agitation. PCP under the name Sernylan was used as a veterinary anesthetic until 1978, after which time it became illegal to use altogether.

In the 1960s, people began illegally manufacturing PCP in laboratories, and by the late 1970s it became a popular street drug. Common street names include the following:

  • Angel dust
  • Peace pill
  • Crystal joint
  • Hog
  • Rocket fuel
  • KJ
  • Elephant tranquilizer
  • Supergrass
  • Boat
  • Tic-tac
  • Zoom
  • Wet
  • Embalming fluid
  • Wack


PCP, also known as 1-(1-phenylcyclohexyl-piperidine), is classified as a dissociative anesthetic. PCP acts mainly in the central nervous system, producing both stimulation and depression. Its sympathomimetic effects are thought to be due to weak reuptake inhibition of norepinephrine and dopamine. PCP also exerts some cholinergic and anticholinergic effects and has some other actions at nicotinic and opioid receptors.

The dissociative properties of PCP are believed to be due to its actions as a glutamate antagonist at the N-methyl-D-aspartate (NMDA) receptors. NMDA antagonists have been known to produce behavioral effects similar to those observed in schizophrenia, and they are used to induce an animal model of schizophrenia for research. PCP also affects the actions of dopamine, which may cause the psychomotor effects seen with PCP.

Clinical effects occur within minutes and usually last several hours. These effects may last up to 48 hours in the event of significant overdose. However, even more prolonged effects may be seen in long-term users, either from enterohepatic recirculation or from delayed release of PCP from lipid stores. Because PCP is fat soluble, it accumulates in adipose tissue and the brain. Recurrent and fluctuating symptoms occur as PCP is remobilized from lipid stores, which can occur days, weeks, or months after the initial use.[5] The half-life of PCP is estimated at 17.4 hours; however, half-lives of 1-4 days have been reported.[6] PCP is primarily metabolized in the liver.


The Drug Abuse Warning Network (DAWN), which functioned from 1992 through 2011, estimated that PCP-related emergency department (ED) visits increased more than 400% from 2005 to 2011 (from 14,825 to 75,538 visits). PCP-related ED visits doubled from 2009 to 2011. DAWN estimates from selected metropolitan areas show geographic variation in trends, with PCP-related ED visits increasing in some areas (New York City, Chicago) while remaining stable in others (Seattle, San Francisco, Phoenix).[7]

Of PCP-related ED visits in 2011, 72% involved PCP combined with other drugs; in about half, PCP was combined with illicit drugs (32% involved marijuana and 20% involved cocaine), and in about a quarter PCP was combined with pharmaceutical agents such as pain relievers (16%) and anti-anxiety and insomnia drugs (13%).

The 2012 Monitoring the Future Survey of high school seniors showed 1.6% using PCP once in their lifetime (down from 2.13% in 2011), 0.9% had used PCP at least once in the last year, and 0.5% had used PCP at least once in the last 30 days.[8]

The 2017 National Survey on Drug Use and Health, polling persons 12 years of age and older, found that an an estimated 1.4 million people were current users of hallucinogens (LSD, PCP, peyote, mescaline, psilocybin mushrooms, MDMA (Ecstasy or Molly), ketamine, DMT/AMT/“Foxy,” and Salvia divinorum). Of adolescents aged 12 to 17, an estimated 114,000  (0.5%) were current users of hallucinogens. Adults aged 18-25 represented the largest group currently using hallucinogens, with an estimated 668,000 users (1.9%). Use among adults older than 25 was estimated at 0.3%, which represents 608,000 individuals.[9]

Doses of 20 mg or more of PCP may cause prolonged coma, seizures, and even death. One death has been reported from an ingestion of 150-200 mg in an acute overdose. In 2020, the American Association of Poison Control Centers reported 212 single exposures to PCP, with 20 major outcomes and 2 deaths.[10]

Since the identification of 3-MeO-PCP and 4-MeO-PCP as new psychoactive substances (NPS), in 2010, there have been a few case reports of  toxicity and death involving those drugs in the US and Europe.[11]  In a study of one non-fatal intoxication and 7 deaths involving 3-MeO-PCP, autopsy revealed the presence of other medications and drugs of abuse in 6 of the 7 fatal cases.[12]

DAWN estimated that males accounted for 69% of PCP-related ED visits in 2011. Approximately 45% of patients were aged 25 to 34 years. Persons aged 18 to 24 years accounted for 19% of visits, as did those aged 35 to 44.[7]


Morbidity and mortality are usually associated with rhabdomyolysis, acute kidney injury, hypertensive crises, accidental trauma, and self-destructive behavior. The outcome in cases of PCP toxicity tends to be worse in patients who present with any of the following:

  • Rhabdomyolysis
  • Acute kidney injury
  • Seizures
  • Hyperthermia
  • Hypertensive crisis
  • Traumatic injuries

Chronic PCP toxicity results in cognitive deficits and mood disorders. Patients can develop speech impediments and also suffer from dysphoria, depression, anxiety, and psychosis.[13, 14]

Patient Education

For patient education information, see the First Aid and Injuries Center and Mental Health Center, as well as Drug Dependence & Abuse, Poisoning, Club Drugs, and Activated Charcoal. Further information is available on the following Web sites:




Because of the numerous routes of administration, variations in dosage, and possibility of co-ingestants, phencyclidine (PCP) produces a wide variety of physical and behavioral effects. Most commonly, witnesses may report agitation, bizarre actions, or violent behavior. Users of PCP often appear to be having a psychotic episode and may or may not report to the physician that they have taken the drug.

Physical Examination

In a study by McCarron et al that evaluated 1,000 patients presenting with acute phencyclidine (PCP) intoxication, clinical effects ranged from lethargy and coma to extreme agitation and psychosis.[15]

Common physical examination findings include the following:

  • Nystagmus (horizontal, vertical, or rotary) - Rotary often considered a hallmark of PCP 
  • Intoxication (57-89%)
  • Hypertension (57%)
  • Acute brain syndrome involving confusion, amnesia, disorientation, and violence (37%)
  • Agitation and violent behavior (35%)
  • Tachycardia (30%)
  • Bizarre behavior including public nudity (29%)
  • Hallucinations and delusions (19%)
  • Miosis - Often reported with a blank stare

Rare findings, usually only seen with high doses, include the following:

  • Seizures (3.1%)
  • Dystonia
  • Ataxia
  • Apnea (often seen with co-ingestants)
  • Catatonia
  • Coma - PCP coma usually presents with nystagmus and the absence of respiratory depression. Unlike opioid-induced coma, it does not improve with naloxone.
  • Hypertensive crisis
  • Myocardial infarction (non-Q wave, cardiac enzyme leak)
  • Intracranial and subarachnoid hemorrhage

Other manifestations include the following:

  • Hyperthermia, hyperreflexia, and muscle rigidity have been reported.
  • Rhabdomyolysis with or without acute kidney injury may also occur.


Diagnostic Considerations

The acute toxicity of phencyclidine (PCP) is often misdiagnosed because of its similarity to schizophrenic episodes. In fact, PCP-induced psychosis may respond to antipsychotics, which may further confound the diagnosis. Other problems to be considered in the differential diagnosis of PCP toxicity include the following:

  • Lysergic acid diethylamide (LSD) toxicity
  • Plant poisoning, mescaline
  • Malignant hyperthermia
  • Serotonin syndrome

Differential Diagnoses



Laboratory Studies

The diagnosis of phencyclidine (PCP) intoxication is a difficult one to make without a history of drug use from the patient. It should be considered in patients with bizarre behavior, hypertension, and nystagmus, or coma unresponsive to naloxone in a substance abuse case.

Exposure to PCP can be confirmed by qualitative urine toxicology screening. Serum screening for PCP is not useful clinically because the test is not readily available. In addition, quantitative serum PCP levels do not correlate with the clin.

A fingerstick glucose test should be performed in all patients with altered mental status, as hypoglycemia can cause symptoms consistent with PCP intoxication. In addition, McCarron et al found that 20% of patients with acute PCP intoxication were hypoglycemic on presentation.[15]

No laboratory tests are specific for PCP intoxication but, in addition to hypoglycemia, elevations in WBC count and BUN and creatinine levels may be seen. Serum creatine phosphokinase and urine myoglobin levels should also be measured to rule out rhabdomyolysis, especially in the patients with severe agitation.

Consider an arterial blood gas (ABG) measurement to assess for hypoxemia and metabolic acidosis in unresponsive patients.

Urine pregnancy tests are indicated for female patients of childbearing age.

Do not rely on the urine toxicology screen to diagnose acute PCP intoxication. Long-term PCP users can have positive test results for weeks after their last use. In addition, false-positive results for PCP have also been reported with many agents, including diphenhydramine (Benadryl) and dextromethorphan, agents in over-the-counter allergy and cough formulations that can produce clinical effects similar to PCP when taken in high doses.[16, 17] Other reported confounders include methadone, ibuprofen, chlorpromazine, and venlafaxine.[18] Consult the laboratory for a list of confounders. If contaminants are a concern, a gas chromatography–mass spectroscopy (GC-MS) confirmatory test can be ordered.

Imaging Studies

No imaging studies are necessary for the evaluation of acute PCP intoxication. Consider a CT scan of the head to rule out an intracranial cause for altered mental status. Consider specific imaging to evaluate traumatic injuries associated with PCP intoxication.


For patients who are unable to protect their airway or have evidence of respiratory compromise, endotracheal intubation and mechanical ventilation may be needed.

Consider lumbar puncture in patients with altered mental status and fever in whom the diagnosis is unclear.



Prehospital Care

Evaluate and stabilize the patient's airway, breathing, and circulation (ABCs) and provide cervical spine immobilization if traumatic injury is suspected.

Physical restraints may be required to prevent self-injury and to protect the medical staff. These patients should be monitored closely due to several reports of death in PCP-intoxicated patients who were being physically restrained.

Chemical restraints may also be used. Establish intravenous access and administer benzodiazepines for patients with severe agitation. Intramuscular benzodiazepines are an alternative if intravenous access is unobtainable.

Emergency Department Care

After addressing and stabilizing the ABCs, treatment of PCP intoxication starts with initial supportive measures (intravenous fluid, supplemental oxygen, cardiac monitoring). An electrocardiogram may be indicated to assess for dysrhythmias. Obtain a fingerstick to rule out hypoglycemia. Place patients in a dark, quiet room under continuous observation to minimize environmental stimuli.

Consider activated charcoal for oral ingestions and co-ingestions. Multiple doses of charcoal may be beneficial in the case of large overdose. Only one dose of sorbitol should be given, usually with the initial dose. Clinicians should be aware that administration of activated charcoal to a patient with an unprotected airway can convert relatively benign exposure (eg, mild PCP intoxication) into a very serious condition (eg, aspiration pneumonia).

Patients exhibiting extremely violent psychotic behavior require sedation with parenteral benzodiazepines. Seizures should be treated with benzodiazepines. Haloperidol should be reserved for patients with mild, predominantly psychotic, symptoms and normal vital signs. Butyrophenones (haloperidol, droperidol) and phenothiazines (eg, chlorpromazine) should be avoided in moderate and severe intoxications because they can lower seizure threshold, cause dystonic reactions, induce hypotension, and worsen anticholinergic smanifestations, including hyperthermia.

Hyperthermia may be treated by conventional cooling methods.

Rhabdomyolysis is treated with intravenous hydration, urine alkalinization, and osmotic/diuretic agents. A possible caveat is the theoretical, but clinically unproven, concept of increased PCP reabsorption secondary to the urine alkalinization.

For hypertensive emergencies, try to control agitation first with parenteral benzodiazepines. For persistent hypertension, intravenous nitroprusside is the agent of choice. Because of the theoretical concept of unopposed alpha effect (worsening of hypertension) and the availability of other antihypertensive agents (eg, calcium-channel blockers, intravenous nitroglycerin), pure beta-blockade should be avoided. Even labetalol, which has both alpha- (weak) and beta-blocking abilities, can be given only after alpha-blockade with phentolamine is achieved.

Acute PCP toxicity can usually be managed conservatively with an observation period of a few hours. More serious ingestions may require admission to an intensive care unit for days to weeks.

Any patient with evidence of unrelenting agitation, hypertensive crisis, hyperthermia, seizures, respiratory depression, rhabdomyolysis, or severe traumatic injuries should be admitted to the hospital, and possibly to an intensive care setting if indicated.

Consider a psychiatric evaluation for substance abuse counseling and/or suicidal ideations. Consider referral to a drug rehabilitation program. Repeated use of PCP can result in addiction, and abrupt discontinuation of the drug can produce withdrawal symptoms, including craving, confusion, and depression.


Consult with a board-certified medical toxicologist or a local poison control center for further recommendations.



Medication Summary

The goals of pharmacotherapy are to relieve the toxic effects of phencyclidine (PCP), reduce morbidity, and prevent complications.

GI decontaminant

Class Summary

These agents prevent further absorption of adsorbable toxins from the GI tract. They are most beneficial if administered within 1-2 h of ingestion.

Activated charcoal (Liqui-Char)

May be indicated in patients with PCP toxicity, if clinically feasible, because PCP undergoes enterohepatic recirculation. The network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.


Class Summary

Indications include agitation, violent behavior, psychosis, seizures, and muscular rigidity.

Diazepam (Valium)

Enhances GABA transmission. Appears to act on part of the limbic system, the thalamus and hypothalamus, to induce a calming effect. Rapidly distributes to other body fat stores. Twenty minutes after initial IV infusion, serum concentration drops to 20% of Cmax.

Individualize dosage and increase cautiously to avoid adverse effects.

Lorazepam (Ativan)

Short-acting anxiolytic with relatively long half-life.

Increases transmission of GABA, a major inhibitory neurotransmitter in the brain.

May be used IV and is well absorbed after IM injection. Onset of action occurs within min of an injection, and effects peak 15-20 min after injection. Duration of action is 6-8 h. No active metabolites exist.

Midazolam (Versed)

Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.


Class Summary

These agents are used for blood pressure control in hypertensive crises to minimize end-organ damage.

Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing the heart rate.


Class Summary

These agents are used for acute psychosis when no contraindications are present.

Haloperidol (Haldol)

Butyrophenone noted for high potency and low potential for causing orthostasis. Downside is high potential for EPS and dystonia. Lowers seizure threshold and worsens anticholinergic symptoms, including hyperthermia. Should be reserved only for mild PCP intoxications with predominantly psychotic features and normal vital signs.

Parenteral dosage form may be admixed with 2 mg lorazepam for better anxiolytic effects.