01Approach to the Critical Patient/attcp51

Immediate stabilization

›Airway threats

›GCS <= 8 or apnea — immediate RSI

›Have suction at bedside for hypersalivation

›Video laryngoscopy preferred for agitated intubation

›Respiratory depression with PCP coma

›Supplemental oxygen titrated to SpO2 >= 94%

›Bag-valve-mask if apneic prior to intubation

›Aspiration risk from hypersalivation and altered consciousness

›Lateral decubitus positioning if not immobilized

›Continuous suction availability

›Circulation and hemodynamic threats

›Severe hypertension (SBP > 180 mmHg or end-organ signs)

›Benzodiazepines first-line for hypertension via sedation

›If refractory, IV antihypertensives (nicardipine or nitroprusside)

›Hyperthermia >= 40 C

›Life-threatening — initiate aggressive cooling immediately

›Ice packs to groin, axillae, neck

›Evaporative cooling and cold IV fluids

›Rhabdomyolysis shock

›Aggressive IV crystalloid resuscitation

›Target urine output 200-300 mL/hr

›Behavioral and safety threat

›Extreme agitation or violence (16% of cases sustain traumatic injuries)

›Chemical sedation preferred over prolonged physical restraint

›Prolonged restraint exacerbates hyperthermia and agitation

›Minimize external stimulation — quiet, dark environment

02History/hx43

Exposure details

›Route of ingestion

›Smoked (most common) — rapid onset within minutes

›Intranasal — rapid onset

›Oral — delayed onset, longer duration

›Intravenous — rapid onset, higher severity risk

›Timing and quantity

›Time since last use — effects may last several days with fluctuating consciousness

›Estimated amount if known

›Chronicity of use — tolerance develops with repeated use

›Co-ingestions

›PCP frequently laced into marijuana without user knowledge

›Polysubstance combinations with cocaine, alcohol, opioids common

›Collateral from EMS or bystanders essential — patient history often unreliable

Symptom characterization

›Classic symptom sequence by dose

›Low dose — euphoria, dissociation, numbness, confusion, ataxia, nystagmus

›Moderate dose — catatonic-like state with eyes open, stupor

›High dose — seizures, coma, severe hypertension, hyperthermia, respiratory depression

›Psychiatric symptoms

›Paranoia and violent ideation

›Delusions and hallucinations (both positive and negative symptoms)

›Hyperacusis — extreme sensitivity to sound

›Neurologic and musculoskeletal symptoms

›Dysarthria and ataxia

›Muscle rigidity and dystonic reactions

›Numbness and diminished pain response — major safety concern for hidden injuries

03Physical Exam/exam45

Vital signs

›Cardiovascular vitals

›Hypertension — present in 57% of a 1,000-case series

›Tachycardia — frequent accompanying finding

›Blood pressure target in severe hypertension: SBP < 180 mmHg

›Temperature

›Fever may be absent initially but delayed hyperthermia is life-threatening

›Core temperature measurement required (rectal thermometry)

›Respiratory rate and oxygen saturation

›Tachypnea with agitation

›Apnea or respiratory depression in severe coma

Neurological exam

›Eye findings (most important examination)

›Nystagmus — present in 57-85% of cases

›Vertical nystagmus highly specific for PCP — only drug of abuse with this finding

›Horizontal nystagmus also seen

›Pupil size — variable, often miotic

›Level of consciousness

›Ranges from alert and oriented (46% of cases) to catatonic stare to deep coma

›Catatonic-like state: blank stare, unresponsive, eyes remain open even in coma

›Fluctuating consciousness is characteristic — may appear awake but unresponsive

›Motor and cerebellar exam

›Ataxia and dysarthria

›Muscle rigidity — lead-pipe type

›Dystonias — generalized or focal

›Increased deep tendon reflexes

›Catalepsy and athetosis

›Pain response

04Differential Diagnosis/ddx41

Life-threatening mimics

›Sympathomimetic toxicity

›Amphetamines, cocaine, cathinones (bath salts)

›Similar agitation, hypertension, tachycardia, hyperthermia

›Key difference: typically lacks nystagmus and dissociative/catatonic features

›ICD-10 T43.6 for amphetamine toxicity

›Excited delirium syndrome

›Extreme agitation, hyperthermia, superhuman strength

›May coexist with PCP toxicity

›Management overlaps — sedation and cooling

›Intracerebral hemorrhage

›Severe hypertension with focal neurologic deficits or coma

›CT head required when focal signs present or severe HTN

›ICD-10 I61.9

Toxicologic mimics

›Anticholinergic toxicity

›Mydriasis (versus miosis in PCP)

›Dry skin (versus diaphoresis in PCP)

›Urinary retention, absent bowel sounds

›No nystagmus

›Serotonin syndrome

›Hyperreflexia, clonus, myoclonus

›Distinct from lead-pipe rigidity of PCP

›Clonus most distinguishing feature

›ICD-10 T43.205

›Neuroleptic malignant syndrome

›Lead-pipe rigidity and hyperthermia

›Context of antipsychotic use distinguishes

05Laboratory Tests/lt39

Core toxicology and metabolic labs

›Urine drug screen

›PCP immunoassay — widely available on standard ED toxicology panel

›Detectable for up to 8 days or longer with heavy use

›Urine PCP level does not correlate with clinical severity

›Confirmatory GC-MS if immunoassay result affects clinical decisions

›Comprehensive toxicology panel

›Rule out co-ingestions (alcohol, opioids, stimulants, salicylates)

›Acetaminophen level in all undifferentiated overdose presentations

›Bedside glucose

›Hypoglycemia is common in PCP intoxication — exclude first

›Point-of-care testing within first 5 minutes

Rhabdomyolysis and renal labs

›Creatine kinase (CK)

›Screen all PCP-intoxicated patients

›Rhabdomyolysis in 2.2-2.5% of PCP cases

›40% of rhabdomyolysis cases develop acute renal failure

›CK > 5,000 U/L indicates significant muscle injury

›Serial CK every 6-8 hours if elevated

›Basic metabolic panel

›Creatinine and BUN — renal function assessment

›Hyperuricemia — marked elevation in rhabdomyolysis

›Hyperphosphatemia and hypocalcemia with rhabdomyolysis

›Urinalysis

›Myoglobinuria — tea-colored or brown urine

›Dipstick positive for blood without RBCs on microscopy suggests myoglobinuria

Inflammatory and organ function labs

›Complete blood count

06Diagnostic Tests/dt61

Scoring Systems

›PCP severity staging (clinical stratification)

›Stage 1 — mild toxicity

›Alert or mildly confused

›Nystagmus, ataxia, bizarre behavior, agitation, euphoria

›32.5% of cases in large series presented with minor behavioral changes

›Stage 2 — moderate toxicity

›Stupor to coma with intact deep pain responses

›Catatonic-like state with eyes open

›Muscle rigidity

›Stage 3 — severe toxicity

›Deep coma without response to pain

›Seizures, severe hypertension, hyperthermia

›Respiratory depression and rhabdomyolysis

›Clinical syndromes from 1,000-case series (McCarron 1981)

›Acute brain syndrome — 24.8%

›Toxic psychosis — 16.6%

›Catatonic syndrome — 11.7%

›Coma — 10.6%

›Richmond Agitation-Sedation Scale (RASS)

›Useful for titrating sedation in agitated patients

›Target RASS -1 to 0 for controlled sedation

MRI

›Brain MRI role in PCP toxicity

›Not routinely indicated in acute PCP intoxication

›CT head preferred for acute emergencies (faster, more available)

›Instability and agitation make MRI acquisition unsafe

›Indications for deferred MRI

07Disposition/dispo29

ICU admission

›ICU-level indications

›Coma (GCS < 9) or severe altered mental status

›Intubated or at risk of airway compromise

›Seizures or refractory status epilepticus

›Severe hypertension requiring IV antihypertensives

›SBP > 180 mmHg or end-organ damage

›Hyperthermia requiring active cooling

›Rhabdomyolysis with CK > 5,000 or rising, with renal impairment

›Respiratory depression or mechanical ventilation

›Cardiac arrest or significant dysrhythmia (0.3% of cases)

Monitored bed admission

›Step-down or monitored ward indications

›Moderate toxicity with improving but not yet baseline mental status

›Mild agitation controlled with benzodiazepines but ongoing monitoring needed

›Rhabdomyolysis with normal renal function — serial CK monitoring

›Observation minimum 6-8 hours given prolonged and fluctuating effects

›Patients with underlying psychiatric illness at risk for prolonged psychosis

Discharge criteria

›Safe discharge requirements

›Return to baseline mental status

›Alert, oriented, and ambulating safely

›Normal vital signs for at least 2-4 hours

›No hypertension, tachycardia, or fever

›No evidence of rhabdomyolysis

›Normal CK or declining trending CK with normal creatinine

›No significant traumatic injuries requiring admission

›Psychiatric clearance if psychotic symptoms have resolved

08Treatment/t93

Immediate interventions

›Stimulation minimization

›Quiet, dark environment to reduce agitation

›Sensory stimulation worsens behavioral dysregulation

›Staff to speak calmly and minimize unnecessary interactions

›NPO if altered mental status or aspiration risk

›IV access and monitoring

›Two large-bore peripheral IVs

›Continuous cardiac monitoring and pulse oximetry

›Core temperature monitoring

›Activated charcoal

›Consider if oral ingestion within 1-2 hours and airway is protected

›Not routinely recommended

›Gastric lavage no longer recommended

Sedation for agitation

›Benzodiazepines — first-line for agitation and behavioral dyscontrol

›Diazepam IV

›5-10 mg IV every 5-10 minutes as needed

›Most classically cited agent for PCP agitation

›Preferred over phenothiazines — lower seizure threshold risk with phenothiazines

›Midazolam IM

›5-10 mg IM for rapid intramuscular route when IV unavailable

›Onset 5-10 minutes IM

›Repeat dosing every 5-10 minutes as needed

›Lorazepam IV or IM

›2-4 mg IV or IM

›Alternative when diazepam or midazolam unavailable

›Antipsychotics — adjunct for psychotic features

›Haloperidol IM

›5 mg IM for schizophreniform symptoms (delusions, hallucinations)

›Improvement demonstrated in controlled trial (Castellani 1982)

›Monitor QTc if repeated dosing

›Droperidol IM

›5-10 mg IM for severe acute behavioral disturbance

›Rapid onset — 10-20 minutes

›Olanzapine IM

›10 mg IM for agitation with psychotic features

›Avoid combination with benzodiazepines — respiratory depression risk

›Ketamine — reserved for extreme refractory agitation

›2-5 mg/kg IM for dangerously refractory cases

›Note: both PCP and ketamine are NMDA antagonists — monitor closely

›Use only when benzodiazepines and antipsychotics have failed

Seizure management

›Benzodiazepines first-line

›Lorazepam IV 2-4 mg IV, repeat every 5-10 minutes

›Diazepam IV 5-10 mg IV, repeat as needed

›Midazolam IM 5-10 mg IM if IV access not available

›Refractory seizures

›Phenobarbital IV 15-20 mg/kg IV at 50-75 mg/min

›If benzodiazepines fail

›Respiratory monitoring required

›Intubation and propofol infusion for status epilepticus

›Propofol 1-2 mg/kg IV induction, 50-200 mcg/kg/min infusion

›Avoid phenytoin

›Not effective for toxin-induced seizures

›May exacerbate cardiac toxicity

Hypertension management

›Benzodiazepines often sufficient

›Sedation reduces agitation-driven sympathetic hypertension

›First-line before adding dedicated antihypertensives

›Nicardipine IV for refractory hypertension

›5 mg/hr IV infusion

›Titrate by 2.5 mg/hr every 5-15 minutes

›Maximum 15 mg/hr

›Sodium nitroprusside IV for hypertensive emergency

›0.3-0.5 mcg/kg/min IV infusion

›Titrate to target SBP < 160 mmHg

›Thiocyanate toxicity with prolonged use > 72 hours

›Avoid beta-blockers in isolation

›Risk of unopposed alpha stimulation and paradoxical hypertension

Hyperthermia management

›Aggressive external cooling

›Ice packs to groin, axillae, and neck

›Evaporative cooling — wet towels with fanning

›Cold IV saline boluses

›Target temperature < 38.5 C

›Pharmacologic adjuncts

›Benzodiazepines to reduce muscle activity and heat generation

›Avoid antipyretics (acetaminophen, NSAIDs) — not effective for drug-induced hyperthermia

›Refractory hyperthermia > 40 C

›Neuromuscular blockade and intubation

›Vecuronium 0.1 mg/kg IV or rocuronium 1 mg/kg IV

›Continuous sedation with propofol or midazolam infusion

Rhabdomyolysis management

›IV crystalloid resuscitation

›Normal saline or lactated Ringer's

›Target urine output 200-300 mL/hr

›Initial bolus 1-2 L over 30-60 minutes if hemodynamically stable

›Ongoing infusion rate guided by urine output and hemodynamics

›Serial monitoring

›CK every 6-8 hours until trending down

›Creatinine, electrolytes, urine output

›Urinary alkalinization — controversial, not routinely recommended

›Sodium bicarbonate to urine pH > 6.5 may reduce myoglobin precipitation

›Risk of worsening hypocalcemia — monitor calcium

›Urinary acidification — contraindicated

›Historically used to enhance PCP excretion

›Contraindicated — worsens rhabdomyolysis renal injury and metabolic acidosis

›Do not use ammonium chloride or ascorbic acid

09Special Populations/sp60

Pregnancy

›Maternal considerations

›PCP crosses the placenta readily

›Fetal NMDA receptor blockade

›Neonatal withdrawal syndrome reported

›PCP concentrated in fetal brain and tissues

›Neurodevelopmental risk with prenatal exposure

›Higher risk of premature labor with severe agitation or hyperthermia

›Management modifications

›Benzodiazepines can be used for agitation and seizures

›Short-term use preferred

›Diazepam and lorazepam are pregnancy category D — risk-benefit must favor treatment

›Aggressive cooling for hyperthermia

›Maternal hyperthermia is teratogenic and can cause fetal distress

›Fetal monitoring if viable gestation (>= 24 weeks)

›Continuous fetal heart rate monitoring in severe cases

›Obstetric consultation for all pregnant patients

›Antipsychotic use in pregnancy

›Haloperidol has limited safety data — use only if essential for severe psychosis

›Avoid droperidol in first trimester

›QTc monitoring if antipsychotics administered

Geriatric

›Altered pharmacokinetics

›Reduced hepatic clearance prolongs PCP half-life

›Already long half-life (approximately 8 days) further extended

›Effects may persist longer than expected

›Reduced protein binding increases free drug concentration

›Reduced renal clearance increases rhabdomyolysis risk

10Background/b64

Epidemiology

›Prevalence and trends

›PCP use peaked in 1970s-1980s in United States

›Persistent use in urban settings, particularly among young Black males historically

›PCP presenting to EDs increasingly seen in combination with other substances

›Most common in adolescents and young adults aged 15-35 years

›ED burden data

›48% of confirmed PCP cases in one series had prior ED visits for PCP intoxication

›Major clinical patterns from 1,000-case series (McCarron 1981)

›Acute brain syndrome 24.8%

›Toxic psychosis 16.6%

›Catatonic syndrome 11.7%

›Coma 10.6%

›Vital sign abnormalities: hypertension in 57% of cases; nystagmus in 57-85%

›Complications and mortality

›Rhabdomyolysis in 2.2-2.5% with 40% developing acute renal failure

›Traumatic injuries in 16% due to violent behavior and analgesia

›Aspiration pneumonia in 1%

›Cardiac arrest in 0.3%

›Coma with respiratory depression in 2.8%

›ICD-10 T41.291A — Poisoning by other general anesthetics, initial encounter

Pathophysiology

›Primary mechanism — NMDA receptor antagonism

›Noncompetitive antagonist at NMDA glutamate receptors

›Blocks the ion channel of the NMDA receptor complex

›Glutamate is primary excitatory neurotransmitter in CNS

›NMDA blockade produces dissociation

›Altered perception of external environment

›Analgesia from disrupted pain signal integration

›Relevance to schizophrenia model

›PCP reproduces positive and negative symptoms of schizophrenia

›NMDA hypofunction hypothesis of schizophrenia pathogenesis

›Secondary mechanisms

›Dopamine reuptake inhibition — contributes to psychosis and agitation

›Sigma receptor agonism — dissociative effects

›Muscarinic receptor antagonism — contributes to tachycardia

›Sympathomimetic effects — norepinephrine and dopamine release cause hypertension and tachycardia

›Pharmacokinetics

›Half-life approximately 8 days — prolonged and fluctuating effects

›Highly lipophilic — large volume of distribution

›Hepatic metabolism with urinary excretion

›Enterohepatic recirculation — explains fluctuating consciousness

›Sequestration in acidic gastric contents — rationale for historical acidification (now abandoned)

Therapeutic Considerations

›Benzodiazepine-first strategy

›Diazepam historically preferred as it addresses multiple PCP effects simultaneously

›Agitation and behavioral dyscontrol

›Seizure prevention and treatment

›Muscle relaxation reducing rhabdomyolysis risk

›Indirect antihypertensive effect via sedation

›Phenothiazines avoided — lower seizure threshold and anticholinergic side effects

›Chlorpromazine specifically contraindicated by some toxicologists

›Antipsychotic use considerations

›Haloperidol has demonstrated benefit for schizophreniform PCP symptoms

›1982 controlled trial (Castellani) showed improvement vs physostigmine

›Reasonable adjunct when benzodiazepines alone insufficient for psychosis

›Butyrophenones (haloperidol, droperidol) preferred over phenothiazines

›Monitor QTc with any antipsychotic use

›Urinary acidification — historically advocated, now contraindicated

›Ion trapping in acidic urine increases PCP ionization and excretion

›Ammonium chloride and ascorbic acid were used

›Abandoned due to risk of worsening rhabdomyolysis renal injury

›Metabolic acidosis worsening is additional contraindication

›Stimulation reduction as therapy

›Quiet dark environment is a documented therapeutic intervention

›Reduces sensory-driven agitation and hyperthermia generation

›Physical restraints avoided when possible — exacerbate hyperthermia

11Patient Discharge Instructions/pdi29

copy discharge instructions

›What happened in the emergency department

›Treated for phencyclidine (PCP) intoxication

›Blood and urine tests performed to check kidney function and muscle breakdown

›IV fluids given to protect kidneys if muscle breakdown was detected

›Home care instructions

›Rest and avoid strenuous activity for 48-72 hours

›Drink plenty of fluids — water or electrolyte drinks

›Do not drink alcohol or use any recreational substances

›Do not drive or operate machinery until fully recovered

›Avoid environments where PCP or other drugs are used

›Warning signs — return to emergency department immediately

›Confusion or unusual behavior returning

›Dark, brown, or tea-colored urine (could indicate kidney damage)

›Inability to urinate

›Muscle pain, weakness, or swelling

›Seizure or convulsion

›Fever higher than 38.5 C

›Severe headache or neck stiffness

›Chest pain or palpitations

›Worsening agitation or seeing or hearing things that are not there

›Important information about PCP

›PCP effects can last several days — mood and thinking may remain affected

›PCP can trigger prolonged mental health symptoms lasting weeks

›PCP is often present in other drugs without your knowledge (marijuana, other pills)

›Follow-up appointments

›Repeat blood tests in 48-72 hours if kidney or muscle issues were found

›Mental health follow-up appointment arranged before discharge

12References/r18

Guidelines and key sources

›Landmark clinical studies

›McCarron MM et al. Acute Phencyclidine Intoxication: Incidence of Clinical Findings in 1,000 Cases. Annals of Emergency Medicine 1981; PMID 7224271

›McCarron MM et al. Acute Phencyclidine Intoxication: Clinical Patterns, Complications, and Treatment. Annals of Emergency Medicine 1981; PMID 7235337

›Castellani S, Giannini AJ, Adams PM. Physostigmine and Haloperidol Treatment of Acute Phencyclidine Intoxication. Am J Psychiatry 1982; PMID 7065301

›Akmal M et al. Rhabdomyolysis With and Without Acute Renal Failure in Patients With Phencyclidine Intoxication. Am J Nephrology 1981; PMID 7349047

›Key references

›Tong TG et al. Phencyclidine Poisoning. JAMA 1975; PMID 1242170

›Barton CH et al. Phencyclidine Intoxication: Clinical Experience in 27 Cases Confirmed by Urine Assay. Ann Emerg Med 1981; PMID 7224272

›Showalter CV, Thornton WE. Clinical Pharmacology of Phencyclidine Toxicity. Am J Psychiatry 1977; PMID 910974

›Cogen FC et al. Phencyclidine-Associated Acute Rhabdomyolysis. Ann Intern Med 1978; PMID 626451

›Society guidelines and updates

›Lavonas EJ et al. 2023 AHA Focused Update on Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning. Circulation 2023

›Isoardi KZ et al. Best Approach for Parenteral Sedation to Manage Severe Acute Behavioral Disturbance in the ED. Clinical Toxicology 2026; PMID 41355751

›Kim HK et al. Safety and Efficacy of Pharmacologic Agents for Rapid Tranquilization of ED Patients With Acute Agitation. Expert Opinion Drug Safety 2021; PMID 33327811

›Coding reference

›ICD-10 T41.291A — Poisoning by other general anesthetics, initial encounter

›ICD-10 F16.10 — Hallucinogen abuse, uncomplicated (PCP classified under hallucinogens)

›SNOMED CT — Phencyclidine poisoning (disorder)

Evidence & Review

Evidence & Review