Day # 165: Phencyclidine (PCP) Use Disorder
- Marcus Hunt
- Aug 16
- 5 min read
Today we will discuss phencyclidine (PCP). In this post, we’ll cover the history, neurobiology, epidemiology, clinical presentation, and evidence-based treatment strategies for PCP use disorder.
Today's Content Level: Intermediate
Phencyclidine = PCP = street name is “angel dust."
PCP is a dissociative anesthetic, which is a class of anesthetic agents that produce analgesia and amnesia by functionally disconnecting the thalamocortical and limbic systems, disrupting sensory perception and integration. Users experience a unique trance-like state with reduced awareness of the environment and self in addition to analgesia, amnesia, and sedation.
First synthesized in the 1950s as an intravenous anesthetic. Pulled due to severe reactions — agitation, hallucinations, and delirium.
Recreational use took off in the 1960s–70s. It’s now a Schedule II substance. Though less common than other substances of abuse, it is often seen in emergency psychiatry.
Structurally related to ketamine but more potent. Sold as powder, liquid, pill, or added to marijuana joints or cigarettes ("wet" or "sherm sticks").
Mechanism of action: NMDA receptor antagonist → glutamate blockade. Also hits dopamine, norepinephrine, and sigma receptors → unpredictable CNS effects (CNS stimulant vs depressant effects depending on the dose).
Diagnostic Criteria 3
Diagnostic criteria for all substance use disorders are the same, characterized by a ≥ 12-month period of problematic substance use that leads to impairment or distress and requires ≥2 additional criteria. See Day #160: Introduction to Substance Use Disorders for complete diagnostic criteria and severity specifiers.
Genetics, environmental influences, and mental health comorbidities contribute to vulnerability.
Prevalence and Age: ~0.2% annual average prevalence, in the 18–25 age range, the prevalence is higher—around 0.6%. ~2.5% of the population in the U.S. reports having ever used PCP.
Gender: Men have higher rates than women.
Genetics and Biology: Limited specific data, but likely similar heritability to other substance use disorders (~40–60%).
Risk factors: overlap with polysubstance use (especially cannabis, stimulants, and hallucinogens), early cannabis use, high association with psychotic disorders, areas with high unemployment and poverty, most common in urban areas, exposure to community violence, and peer/social influences.
History:
General SUD: Obtain a detailed history (onset, frequency, quantity, last use, forms and routes), prior treatment attempts, periods of sobriety, withdrawal symptoms, impact on daily functioning, social history with triggers, legal obligations, and co-occurring psychiatric or medical conditions. Ask about prescription misuse and illicit use. Ask about injection drug use, overdose history, co-use of other substances. Assess for other safety concerns related to use, including IV/IN use, sharing paraphernalia, needle licking, exchanging sex for drugs, body packing/stuffing, or impaired driving.
PCP specific: Listen for history of sleep deprivation, paranoia, aggression/violence, or impulsivity. Intoxication may mimic acute psychosis, delirium, stimulant intoxication, or catatonia. The primary psychoactive effects of PCP last a few hours, but it takes over 8 days to be fully eliminated from the body. In some cases, hallucinogenic effects can persist for weeks, resembling prolonged psychotic episodes similar to schizophrenia. Long-term use may result in cognitive impairments and speech difficulties lasting several months. Users often unknowingly consume PCP, as it may be laced in marijuana.
Physical Exam:
Classic triad: agitation + nystagmus (esp. rotary) + muscle rigidity.
Vital signs: hypertension, tachycardia, hyperthermia.
Neuro: ataxia, slurred speech, vertical or rotary nystagmus. Rotary nystagmus is strongly suggestive for PCP intoxication.
"Super strength" and decreased pain response. The so-called "super strength" is not truly increased muscular power, but related to decreased pain and fatigue cues that would normally limit exertion in combination with the stimulant-like heightened arousal that causes agitation, paranoia and aggression.
Labs/Diagnostics:
Urine drug screen: positive for ~4-7 days. Cross-reactivity can produce false positives (e.g., dextromethorphan, diphenhydramine, tramadol, ketamine, venlafaxine & desvenlafaxine, meperidine, ibuprofen & naproxen [less common with modern assays]). Confirm with gas chromatography–mass spectrometry (GC-MS) if unsure.
Check renal function, electrolytes, and temperature.
CPK (rhabdo risk) and AST are often elevated.
Cardiac: ECG + troponins for chest pain or arrhythmia risk.
Intoxication 8
Symptoms:
Low dose: euphoria, numbness, distorted perceptions, emotional detachment, synesthesia (one sensory stimulation evokes another).
High dose: severe agitation, muscle rigidity, delusions, hallucinations (tactile, visual), disorganized thinking, memory impairment, paranoia, combativeness.
Medical emergencies: seizures, rhabdomyolysis, coma, hyperthermia, delirium, intracranial hemorrhage, cardiac arrest, respiratory problems, neurological toxicity (e.g., dystonia, dyskinesias, catalepsy), death.
Treatment:
Supportive care + calm environment. Minimize sensory stimulation.
Monitor vital signs and temperature. Cool them down if hyperthermic. External cooling measures — ice packs to groin/axillae, cooling blankets, mist and fan, chilled IV fluids if severe. Hyperthermia in PCP intoxication is not due to hypothalamic set-point change, so acetaminophen or NSAIDs don’t help.
Always check CK, renal function, and electrolytes given risk of rhabdomyolysis and AKI.
Benzodiazepines: first-line for agitation, anxiety, muscle spasms, and seizures.
Antipsychotics: may be used to control severe agitation or psychotic symptoms but use cautiously — may lower seizure threshold or worsen dystonia/rigidity.
Restraints if necessary, but use with caution — can provoke further agitation or injury. The combination of agitation, psychosis, analgesia, and violent behavior can make physical restraint dangerous both for staff and for the patient (risk of rhabdomyolysis, hyperthermia, and asphyxiation). Supportive care and benzodiazepines are preferred.
Withdrawal
Unlike most other substance use disorders, PCP does not have a classic withdrawal syndrome.
Some may experience: cravings, dysphoria, anhedonia, depression, irritability, or sleep disturbances.
Psychotic symptoms may linger for days or weeks post-use.
“Flashbacks” may occur, described as recurrence of intoxication symptoms due to release of the drug from body fat stores.
Treatment of PCP Use Disorder
•Effective treatment requires a combination of medical, psychological, and social interventions. A multi-disciplinary team—often including psychiatrists, primary care providers, therapists, social workers, and peer support specialists collaborates to address all aspects of the disorder.
Determine the Appropriate Treatment Setting: Choosing the right level of care depends on substance use severity, comorbid conditions, and prior treatment history. See Day 60: Intro to SUD for a description of each level of care.
Psychosocial Interventions:
Individual and/or group therapy should be part of every SUD treatment approach. See Day 60: Intro to SUD for a discussion of interventions that include behavioral therapies, peer support & 12-step programs, and family support resources.
Off-Label Medication Adjuncts:
There is no approved medication for PCP use disorder outside of the acute intoxication window. No medication has sufficient evidence for off-label use at this time.
Address psychiatric comorbidities, especially psychotic and mood disorders.
Conclusion
Think PCP in young, agitated, violent patients with rotary nystagmus.
Treat with benzos, fluids, cooling, and quiet environment.
Don’t over-rely on UDS — false positives are common.
No classic withdrawal, but mood and psychotic symptoms can linger.
Behavioral therapy is the cornerstone of long-term management.
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