Phencyclidine (PCP) is a dissociative anesthetic and noncompetitive NMDA receptor antagonist that produces dose-dependent effects ranging from euphoria and dissociation at low doses to coma, seizures, and death at high doses. [1] It is commonly smoked, snorted, taken orally, or injected, and is known by street names including "angel dust," "hog," and "crystal". [2] The hallmark clinical triad is nystagmus (especially vertical), hypertension, and behavioral disturbance. [2-3]
1. History
- Route of exposure: smoked (most common), oral, intranasal, IV — onset is particularly rapid with smoking, snorting, or IV use [1]
- Timing of ingestion and amount if known; effects may last several days with fluctuating levels of consciousness [2]
- Symptom characterization: euphoria, dissociation, numbness, confusion, hallucinations, paranoia, violent behavior [1]
- Progression: low dose → confusion, ataxia, nystagmus; moderate dose → catatonic-like state with eyes open; high dose → seizures, coma, severe hypertension [2]
- Co-ingestions: PCP is frequently sold in mixtures with other drugs (marijuana laced with PCP is common) [2]
- Important negatives: no pain complaints (analgesia is prominent), no awareness of injuries sustained
2. Alarm Features
- Hyperthermia >106°F — may occur hours after use and is life-threatening [2]
- Seizures or status epilepticus [3-4]
- Coma with respiratory depression or apnea (2.8% of cases) [3]
- Severe hypertension — risk of hypertensive encephalopathy or intracerebral hemorrhage [2]
- Rhabdomyolysis — occurred in 2.2–2.5% of cases in large series, with 40% of those developing acute renal failure [5-6]
- Cardiac arrest — reported in 0.3% of cases [3]
- Extreme violence or self-injurious behavior with risk of traumatic injuries (16% of cases) [5]
3. Medications
- Benzodiazepines (diazepam, midazolam, lorazepam): First-line for agitation, seizures, and muscle rigidity. Diazepam is the most classically cited agent. [7-9]
- Antipsychotics: Haloperidol (5 mg IM) has shown improvement in schizophreniform symptoms (delusions, hallucinations). Droperidol or olanzapine may be considered for severe acute behavioral disturbance. [10-11]
- Avoid: Phenothiazines were historically cautioned against due to anticholinergic properties and potential to lower seizure threshold; diazepam is preferred over phenothiazines for sedation. [9]
- Urinary acidification (ammonium chloride, ascorbic acid) was historically recommended to enhance PCP excretion, but this practice is now generally avoided due to risk of worsening rhabdomyolysis-associated renal injury and metabolic acidosis. [2]
- Avoid physical restraints when possible — prolonged restraint may exacerbate hyperthermia and agitation. [12]
4. Diet
- NPO if altered mental status or risk of aspiration (aspiration pneumonia occurred in 1% of cases) [5]
- Aggressive IV hydration is critical, especially if rhabdomyolysis is suspected [6][13]
- No specific dietary triggers or long-term dietary management applicable
5. Review of Systems
- Neurologic: Confusion, hallucinations, numbness, ataxia, dysarthria, seizures, hyperacusis [1]
- Psychiatric: Paranoia, delusions, violent ideation, euphoria, emotional withdrawal [1]
- Musculoskeletal: Muscle rigidity, dystonic reactions, involuntary movements [3]
- Cardiovascular: Chest pain, palpitations (hypertension, tachycardia) [3]
- Genitourinary: Urinary retention (uncommon, <5%) [3]
- Respiratory: Bronchospasm (uncommon), apnea in severe cases [3]
- Autonomic: Diaphoresis, hypersalivation [3]
6. Collateral History and Family History
- Collateral from friends, EMS, or bystanders is critical — patients are often unable to provide reliable history
- Confirm substance used: PCP is frequently misrepresented as THC or other drugs [2]
- Prior episodes of PCP use — recurrent use is common (48% of confirmed cases in one series had prior ED visits for PCP intoxication) [14]
- Psychiatric history: PCP can precipitate prolonged psychotic episodes, especially in those with pre-existing thought disorders or prepsychotic personalities [15]
- Family history of psychiatric illness may increase vulnerability to PCP-induced psychosis
7. Risk Factors
- Polysubstance use — PCP is often combined with marijuana, cocaine, or other drugs [2]
- Pre-existing psychiatric disorders (schizophrenia, bipolar disorder) — increased risk of prolonged psychosis [15-16]
- Young age — most commonly used by adolescents and young adults
- Urban settings with higher availability
- Prior PCP use — tolerance develops to effects, leading to dose escalation [15]
- Chronic use associated with long-lasting cognitive impairments in memory and attention [17]
8. Differential Diagnosis
- Sympathomimetic toxicity (amphetamines, cocaine, cathinones): Similar agitation, hypertension, tachycardia, and hyperthermia, but typically lacks nystagmus and the dissociative/catatonic features [1][12]
- Anticholinergic toxicity: Mydriasis (vs. miosis in PCP), dry skin, urinary retention, absent bowel sounds — PCP causes hypersalivation and diaphoresis [1]
- Serotonin syndrome: Hyperreflexia, clonus, myoclonus — distinct from the lead-pipe rigidity of PCP [18]
- Neuroleptic malignant syndrome: Lead-pipe rigidity and hyperthermia, but occurs in context of antipsychotic use [18]
- Acute psychosis / schizophrenia: PCP-induced psychosis closely mimics schizophrenia with both positive and negative symptoms [16]
- Hypoglycemia, hyponatremia, CNS infection, seizure disorder [1]
- Key distinguishing feature: Vertical nystagmus is highly suggestive of PCP — it is the only drug of abuse that characteristically causes this finding [2]
9. Past Medical History
- Prior PCP or substance use episodes
- Psychiatric history (schizophrenia, psychotic disorders) — PCP exacerbates pre-existing thought disorders [15]
- Seizure disorder — PCP lowers seizure threshold
- Renal disease — increased vulnerability to rhabdomyolysis-induced renal failure [6]
- History of traumatic injuries from prior intoxication episodes
10. Physical Exam
- Vital signs: Hypertension and tachycardia (57% had hypertension in a 1,000-case series), fever (may be delayed), tachypnea [3][14]
- Eyes: Nystagmus (vertical or horizontal, present in 57–85% of cases) — the single most important exam finding; miotic pupils [3][7][14]
- Neurologic: Ataxia, dysarthria, muscle rigidity, generalized or localized dystonias, catalepsy, athetosis, increased deep tendon reflexes, diminished pain response [3][7]
- Mental status: Ranges from alert and oriented (46%) to catatonic stare with eyes open to deep coma [2-3]
- Skin: Diaphoresis; assess for traumatic injuries (16% of cases) [5]
- Oral: Hypersalivation [3]
- Catatonic-like state: Blank stare, unresponsive, eyes remain open even in coma — characteristic of moderate-dose PCP [2]
11. Lab Studies
- Urine drug screen: PCP is detectable in urine for up to 8 days or longer at high doses. Note: urine PCP levels do not correlate with clinical severity [1][3]
- CK (creatine phosphokinase): Elevated in rhabdomyolysis — screen all PCP-intoxicated patients [13-14]
- BMP: Assess for renal failure (BUN/Cr), hyperuricemia, hyperphosphatemia, hypocalcemia (seen with rhabdomyolysis and renal failure) [6]
- Glucose: Hypoglycemia is common [3]
- LFTs: SGOT/SGPT elevations reported [3]
- Uric acid: Marked hyperuricemia in rhabdomyolysis cases [6]
- Urinalysis: Myoglobinuria [13]
- Lactate, VBG/ABG: Assess for metabolic acidosis
- Coagulation studies: If concern for DIC in severe cases
- Comprehensive tox screen: Rule out co-ingestions (alcohol, opioids, stimulants) [14]
12. Imaging
- CT head (non-contrast): Indicated if severe hypertension with concern for intracerebral hemorrhage, focal neurologic deficits, or prolonged altered mental status [2]
- Chest X-ray: If concern for aspiration pneumonia (1% incidence) or respiratory compromise [5]
- Imaging is generally not routinely necessary in straightforward mild-to-moderate PCP intoxication
- Consider trauma imaging based on mechanism (patients frequently sustain injuries due to violent behavior and analgesia)
13. Special Tests
- Urine drug immunoassay for PCP — widely available on standard ED tox panels; confirmatory testing via GC-MS if needed
- Bedside glucose — hypoglycemia is common and must be excluded early [3]
- Point-of-care ultrasound: Assess for bladder distension (urinary retention), cardiac function if hemodynamically unstable
- Rectal temperature: Core temperature measurement essential if hyperthermia suspected
14. ECG
- Obtain ECG in all moderate-to-severe cases
- Sinus tachycardia is the most common finding
- Monitor for QTc prolongation if antipsychotics are administered [19]
- Cardiac arrest (VF, VT, PEA) reported in 0.3% of cases [3]
- No pathognomonic ECG pattern for PCP toxicity, but ECG helps exclude other causes of altered mental status and guides antipsychotic safety
15. Assessment
PCP intoxication can be stratified into three stages of severity: [20]
- Mild (Stage 1): Alert or mildly confused, nystagmus, ataxia, bizarre behavior, agitation, euphoria — primarily psychiatric manifestations. Most common presentation (32.5% alert and oriented with minor behavioral changes) [5][20]
- Moderate (Stage 2): Stupor to coma with intact deep pain responses, catatonic-like state with eyes open, muscle rigidity [2][20]
- Severe (Stage 3): Deep coma without response to pain, seizures, severe hypertension, hyperthermia, respiratory depression, rhabdomyolysis [5][20]
Major clinical patterns described in a 1,000-case series: acute brain syndrome (24.8%), toxic psychosis (16.6%), catatonic syndrome (11.7%), and coma (10.6%). [5] Complications include rhabdomyolysis with renal failure, aspiration pneumonia, traumatic injuries, and rarely pulmonary embolism and death. [5]
16. Treatment Plan
Initial stabilization
- ABCs — secure airway if GCS ≤8 or apneic; have suction ready for hypersalivation
- Minimize stimulation — place in quiet, dark room; reduce verbal and physical stimulation [7-8]
- IV access, continuous monitoring, core temperature
Agitation/seizures
- Benzodiazepines first-line: Diazepam 5–10 mg IV/IM, or midazolam 5–10 mg IM; repeat as needed [7-9]
- For refractory agitation with psychotic features: Haloperidol 5 mg IM or droperidol 5–10 mg IM [10-11]
- Avoid combination antipsychotic + benzodiazepine if possible due to increased adverse effects without clear added efficacy [11]
- Ketamine (2–5 mg/kg IM) reserved for extremely dangerous, refractory agitation [11][19]
Hypertension
Hyperthermia
- Aggressive external cooling (ice packs, evaporative cooling, cold IV fluids)
- Benzodiazepines to reduce muscle activity
- Consider paralysis and intubation for refractory hyperthermia >106°F
Rhabdomyolysis
- Aggressive IV crystalloid resuscitation (target urine output 200–300 mL/hr) [6][13]
- Monitor CK, electrolytes, renal function serially
- Avoid urinary acidification — historically recommended for PCP excretion but contraindicated in rhabdomyolysis [2][13]
Decontamination
17. Disposition
Admit (ICU or monitored bed) if
- Coma or severe altered mental status [5]
- Seizures or status epilepticus
- Severe hypertension requiring IV antihypertensives
- Hyperthermia
- Rhabdomyolysis (CK >5,000 or rising, renal impairment) [6]
- Respiratory depression or need for intubation
- Cardiac arrest or significant dysrhythmia [3]
Observation (ED or clinical decision unit)
- Moderate intoxication with improving mental status
- Mild agitation controlled with benzodiazepines
- Observe for minimum 6–8 hours given prolonged and fluctuating effects [2]
Discharge if
- Mild intoxication with return to baseline mental status
- Normal vital signs, ambulating safely
- No evidence of rhabdomyolysis (normal CK) or end-organ injury
- Reliable follow-up and safe disposition plan
- Psychiatric clearance if psychotic symptoms have resolved
18. Follow Up / Return Precautions
- Return immediately for: recurrent confusion, fever, dark/brown urine (myoglobinuria), seizures, chest pain, inability to urinate, worsening agitation or psychosis
- PCP effects may fluctuate and recur over days due to prolonged elimination (half-life ~8 days) [1-2]
- Psychiatric follow-up is essential — PCP can precipitate prolonged psychotic episodes lasting weeks, particularly in vulnerable individuals [1][15]
- Substance use counseling and referral to addiction services
- Expected course: most mild cases resolve within hours; moderate-to-severe cases may take days for full resolution [8]
- Counsel on dangers of re-exposure and polysubstance use
References
1. Diagnostic and Statistical Manual of Mental Disorders. — Dilip V. Jeste, Jeffrey A. Lieberman, David Fassler, et al American Psychiatric Association (2022). 2022.
2. Role of the Primary Care Physician in Problems of Substance Abuse. — Weaver MF, Jarvis MA, Schnoll SH. Archives of Internal Medicine. 1999.
3. Acute Phencyclidine Intoxication: Incidence of Clinical Findings in 1,000 Cases. — McCarron MM, Schulze BW, Thompson GA, Conder MC, Goetz WA. Annals of Emergency Medicine. 1981.
4. Phencyclidine Poisoning. — Tong TG, Benowitz NL, Becker CE, Forni PJ, Boerner U. The Journal of the American Medical Association. 1975.
5. Acute Phencyclidine Intoxication: Clinical Patterns, Complications, and Treatment. — McCarron MM, Schulze BW, Thompson GA, Conder MC, Goetz WA. Annals of Emergency Medicine. 1981.
6. Rhabdomyolysis With and Without Acute Renal Failure in Patients With Phencyclidine Intoxication. — Akmal M, Valdin JR, McCarron MM, Massry SG. American Journal of Nephrology. 1981.
7. Phencyclidine. Nine Cases of Poisoning. — Liden CB, Lovejoy FH, Costello CE. The Journal of the American Medical Association. 1975.
8. Clinical Pharmacology of Phencyclidine Toxicity. — Showalter CV, Thornton WE. The American Journal of Psychiatry. 1977.
9. Management of Hallucinogen Abuse. — Haddad LM. American Family Physician. 1976.
10. Physostigmine and Haloperidol Treatment of Acute Phencyclidine Intoxication. — Castellani S, Giannini AJ, Adams PM. The American Journal of Psychiatry. 1982.
11. What Is the Best Approach for Parenteral Sedation to Manage Severe Acute Behavioral Disturbance in the Emergency Department?. — Isoardi KZ, Cole JB, Hoffman RS, Isbister GK. Clinical Toxicology. 2026.
12. 2023 American Heart Association Focused Update on the Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. — Lavonas EJ, Akpunonu PD, Arens AM, et al. Circulation. 2023.
13. Phencyclidine-Associated Acute Rhabdomyolysis. — Cogen FC, Rigg G, Simmons JL, Domino EF. Annals of Internal Medicine. 1978.
14. Phencyclidine Intoxication: Clinical Experience in 27 Cases Confirmed by Urine Assay. — Barton CH, Sterling ML, Vaziri ND. Annals of Emergency Medicine. 1981.
15. Phencyclidine (PCP): Some Human Studies. — Pradhan SN. Neuroscience and Biobehavioral Reviews. 1984.
16. Recent Advances in the Phencyclidine Model of Schizophrenia. — Javitt DC, Zukin SR. The American Journal of Psychiatry. 1991.
17. Opposing short‐ and long‐term effects on muscarinic M1/4 receptor binding following chronic phencyclidine treatment. — Newell KA, Zavitsanou K, Huang XF. Journal of Neuroscience Research. 2007.
18. Neuroleptic Malignant Syndrome. — Wijdicks EFM, Ropper AH. The New England Journal of Medicine. 2024.
19. Safety and Efficacy of Pharmacologic Agents Used for Rapid Tranquilization of Emergency Department Patients With Acute Agitation or Excited Delirium. — Kim HK, Leonard JB, Corwell BN, Connors NJ. Expert Opinion on Drug Safety. 2021.
20. Diagnosis and Management of Phencyclidine Intoxication. — Milhorn HT. American Family Physician. 1991.