Phencyclidine (PCP) intoxication in children and adolescents

INTRODUCTION — An overview of phencyclidine (PCP) intoxication in children and adolescents will be reviewed here. The clinical manifestations and management of PCP intoxication in adults and ketamine poisoning are discussed separately.

●(See "Phencyclidine (PCP) intoxication in adults".)

●(See "Ketamine poisoning".)

BACKGROUND — PCP, ie, 1-(1-phenylcyclohexyl) piperidine hydrochloride, is a synthetic hallucinogen that has a variety of street names, including "angel dust," "dust," and "sherms" (table 1). These names, along with others, reflect its unpredictable and volatile effects. It was patented in the 1950s as a dissociative anesthetic agent called Sernyl but was later withdrawn from the market due to adverse effects, including severe agitation, confusion, hallucinations, and prolonged periods of decreased consciousness [1,2]. The recreational use of PCP gained popularity during the 1960s due to its hallucinogenic effects and ease of synthesis. In April of 1979, all legal manufacturing of PCP in the United States was terminated [3].

In the early 1970s, a laboratory investigation of PCP derivatives led to the discovery of ketamine. Ketamine is 5 to 10 percent as potent as PCP and is now used clinically to induce dissociative anesthesia. Ketamine is also abused as a recreational drug. (See "Ketamine poisoning".)

EPIDEMIOLOGY — According to the National Institute on Drug Abuse (NIDA) Monitoring the Future study, which tracks reported illicit drug use among high-school students, the recreational use of PCP in the prior year by United States high school seniors decreased from 7 percent in 1979 to 1.3 percent in 2013, the last year the study inquired about PCP use [4]. However, almost 100,000 children between 11 and 21 years of age in the United States report having used PCP at least once in the prior year and approximately 1500 annual emergency department visits for PCP intoxication occur in this age group [5]. Between 2005 through 2011, emergency department visits for PCP intoxication among those age 12 to 17 years increased 184 percent [6]. Deaths due to PCP intoxication are uncommon; most fatalities are due to traumatic injury rather than direct drug effects [7].

PCP intoxication in children under six years of age is rare and typically occurs as an inadvertent oral or inhalational exposure due to caregiver drug use [8].

PHARMACOLOGY AND CELLULAR TOXICOLOGY — PCP, or 1-(1-phenylcyclohexyl) piperidine hydrochloride, is an arylcyclohexylamine dissociative anesthetic with structural and pharmacologic properties similar to ketamine. It is synthesized from piperidine and cyclohexanone and is manufactured illegally in underground laboratories and distributed in varying dosage forms, strengths, and purities [9]. Drug users may be exposed inadvertently to PCP because it is used as an additive in lysergic acid diethylamide (LSD), marijuana, and methamphetamine [10].

Compared with ketamine, PCP is longer acting and more likely to cause seizures, confusion, and delirium. Synthetic derivatives of both PCP and ketamine, including dextromethorphan, are used as recreational drugs. (See "Ketamine poisoning", section on 'Clinical presentation'.)

PCP is available in white powder ("angel dust"), tablet ("peace pill"), crystal, and liquid ("whack") forms that can be ingested, inhaled, injected, or smoked. Young children can be exposed to PCP through secondhand smoke inhalation, PCP-impregnated cigarette butt ingestion, or inadvertent dermal exposure [8,11-13]. Adolescent use and pharmacologic effects are similar to adults. (See "Phencyclidine (PCP) intoxication in adults", section on 'Pharmacology and cellular toxicology' and "Phencyclidine (PCP) intoxication in adults", section on 'Kinetics'.)

PCP has three primary sites of action in the central nervous system [14]:

●The N-methyl-D-aspartate (NMDA) receptor complex – PCP has great affinity for NMDA receptor complexes in the hippocampus, neocortex, basal ganglia, and limbic system [15]. NMDA antagonism at these sites produces acute psychosis that mimics schizophrenia in humans and leads to excess excitatory neurotransmitters (eg, glutamate, glycine, aspartate) that can cause agitation and seizures. Animal studies also suggest that the developing brain is at greater risk for injury and cell death from excessive levels of these excitatory neurotransmitters [13].

●The neuronal dopamine, norepinephrine, and serotonin reuptake complex – PCP inhibits reuptake of dopamine, norepinephrine, and serotonin [16]. This action likely explains the adrenergic effects (eg, tachycardia, hypertension) and dopaminergic effects (eg, dystonia, choreoathetosis, anticholinergic findings) seen in children with PCP intoxication.

●The sigma receptor complex – PCP binding to the sigma receptor has been demonstrated and may also explain, in part, psychotic, anticholinergic, and movement abnormalities seen in human intoxication [17].

KINETICS — The kinetics of PCP in young infants and children has not been studied. The kinetics of PCP in adolescents is similar to adults and is discussed in detail separately. (See "Phencyclidine (PCP) intoxication in adults", section on 'Kinetics'.)

CLINICAL FEATURES OF OVERDOSE — PCP intoxication is a diagnosis that must be suspected clinically. PCP intoxication should be suspected in children with nystagmus, blank staring, strange behavior, altered mental status, agitation, choreoathetosis, seizures, acute psychosis, or a combination of these symptoms [8,12,18]. Duration of action is generally brief (four to eight hours).

History — The history of unexpected exposure or overdose in young children under six years of age is rarely available [12]. Caregivers typically note an abrupt onset of altered behavior consistent with neurobehavioral effects of PCP [8,11,12].

Older children and adolescents usually are exposed to PCP through recreational use, although passive or inadvertent exposure (eg, being unaware of PCP in a marijuana cigarette) may also occur. In many instances, the patient is unable to provide a history. Sometimes, friends or emergency medical services personnel may provide useful details. It can be helpful to know the street names for PCP, which include angel dust, embalming fluid, fry, wets, killer weed, peace pill, horse tranquilizer, and hog (table 1).

Physical examination — PCP intoxication produces a wide range of vital sign and neuropsychiatric findings.

General findings — Physical examination should begin with an assessment of the patient's airway, breathing, circulation, and mental status. Respiratory depression occurs more commonly in children with PCP intoxication than in adults. Apnea may immediately precede or follow generalized seizures [8,11]. These episodes usually are brief and self-limited, but some patients require mechanical ventilation. Patients may also exhibit irregular breathing, with alternating episodes of apnea and tachypnea [8,11].

Vital signs — Tachycardia and hypertension (both systolic and diastolic) are frequently seen. Hypertension is present in 30 percent of infants with PCP intoxication but is usually transient and asymptomatic. However, subarachnoid hemorrhage has been described [8]. Severe neuromuscular excitability can result in hyperthermia, while environmental exposure may cause hypothermia.

Eye findings — Horizontal, vertical, or rotatory nystagmus is found in the majority of children and adolescents with PCP intoxication (table 2). A stuporous blank stare is also often seen [8,11,12]. Classically, PCP has been listed as a cause of miosis. However, dilated pupils may also be seen. Rarely, oculogyric crisis may occur [19].

Neuropsychiatric findings — Infants and young children who are exposed to PCP may present with seizures, irritability, lethargy, coma, fluctuations in level of consciousness, choreoathetosis, dystonia, and ataxia [8,11,12]. In one review of PCP intoxication in 28 children younger than five years of age, choreoathetosis was present in more than 50 percent of cases [11]. Opisthotonos and hyperreflexia are less commonly seen [8,11,20].

Older children and adolescents may also present with lethargy, coma, agitation, seizures, and ataxia. However, a significant number may be alert with bizarre behavior.

Psychomotor agitation is commonly seen in older children and adolescents with PCP intoxication. Similar to adults, these patients may demonstrate violent and unpredictable behavior that is exacerbated by decreased pain perception, hallucinations, paranoid delusions, and delusions of superhuman strength. Patients require a cautious approach during initial treatment to ensure staff safety while addressing the child's medical needs. (See "Phencyclidine (PCP) intoxication in adults", section on 'Neuropsychiatric findings'.)

Additional categorization of psychiatric symptoms is derived from studies in adults (see "Phencyclidine (PCP) intoxication in adults", section on 'Neuropsychiatric findings'):

●Minor symptoms – Intermittent lethargy or stupor in combination with bizarre behavior, violence, agitation, or euphoria in patients who were otherwise alert and oriented

●Major symptoms – Psychosis with hallucinations, catatonia, coma, or acute brain syndrome (disorientation, confusion, lack of judgement, inappropriate affect, or memory loss)

Other findings — Diaphoresis may accompany other findings of adrenergic excess (eg, tachycardia, hypertension, agitation). Hypersalivation is also frequently seen.

Injuries occur commonly in patients with PCP intoxication because the drug produces a dissociative state with violent and unpredictable behavior. The evaluation of patients with suspected trauma is complicated by the anesthetic effects of PCP, which can mask serious injuries [21].

Complications — Fatalities in the setting of PCP intoxication are uncommon, and most are secondary to trauma. Other causes include hyperthermia, respiratory arrest, rhabdomyolysis with hyperkalemia, and intracranial hemorrhage.

Treating clinicians should be aware of the potential for multiple serious complications in children with PCP intoxication. These occur most often with large ingestions and may include:

●Rhabdomyolysis

●Seizures

●Hypoglycemia

●Prolonged comatose state

●Prolonged psychosis

Perinatal exposure — PCP crosses the placenta and can be detected in umbilical cord blood [22], amniotic fluid [23], breast milk [23], and neonatal urine [24,25]. Although microcephaly [25] and dysmorphic facial features have been reported [26], teratologic effects of PCP on the developing fetus are not well described. Newborns of mothers who used PCP during pregnancy present with jitteriness, sleep problems during the first year, and other neurobehavioral abnormalities [25,27,28]. Similar to adults, neonates may have sudden changes in the level of consciousness, with alternating periods of lethargy and irritability [24].

DIFFERENTIAL DIAGNOSIS — The clinical picture of PCP intoxication shares features common to many other intoxications and medical conditions, especially those that cause acute psychosis. The differential diagnosis and approach to acute psychosis in the emergency department are provided in the tables and algorithm (table 3 and table 4 and algorithm 1) and are discussed in detail separately. (See "Emergency department approach to acute-onset psychosis in children", section on 'Differential diagnosis' and "Emergency department approach to acute-onset psychosis in children", section on 'Approach'.)

Nystagmus is also a prominent physical finding in children with PCP intoxication. Other toxins that cause nystagmus are listed in the table (table 2).

Children without an apparent underlying medical or toxicologic etiology warrant evaluation for psychiatric causes of psychosis. (See "Psychosis in adults: Epidemiology, clinical manifestations, and diagnostic evaluation", section on 'Defining features'.)

ANCILLARY STUDIES — The diagnosis of PCP intoxication must be suspected clinically. Exposure to PCP is suggested by fluctuating levels of consciousness, psychotic features, nystagmus, and autonomic stimulation.

General studies — Ancillary studies are obtained to support the clinical diagnosis, evaluate for coingestants, and assess for the presence of rhabdomyolysis and its complications. We recommend the following studies in children and adolescents with altered mental status and suspected PCP intoxication:

●Rapid fingerstick blood glucose – Rapid assessment of blood glucose is essential in all patients with altered mental status. PCP intoxication is associated with hypoglycemia in adults due to excess energy demands. Infants and young children may be predisposed to hypoglycemia after PCP exposure to an even greater degree because of higher turnover of glucose per kilogram of body weight relative to adults.

●Serum creatine kinase – Creatine kinase elevation is commonly seen in patients with PCP intoxication and is an important indicator of rhabdomyolysis.

●Urine for myoglobin – Myoglobinuria supports the diagnosis of rhabdomyolysis.

●Liver enzymes – Elevations of aspartate transaminase (AST) and alanine transaminase (ALT) are seen in approximately one-half of PCP-intoxicated patients.

●Electrocardiogram (ECG) – Conduction abnormalities or arrhythmias may accompany hyperkalemia caused by rhabdomyolysis or may indicate the presence of other cardiotoxic agents.

●Serum acetaminophen (older children and adolescents with risk for intentional overdose) – Acetaminophen is a common coingestant in the adolescent age group.

●Serum salicylate level – Salicylate toxicity has some features (eg, hyperthermia, altered mental status) that are similar to PCP intoxication.

●Urine pregnancy test (postmenarchal females).

Further testing is performed based upon clinical assessment. As examples, blood urea nitrogen and serum creatinine are obtained if rhabdomyolysis or other potential causes of renal failure are suspected, while computed tomography of the head and evaluation of cerebrospinal fluid may be needed in the setting of a persistently altered mental status.

Testing for phencyclidine — Drug testing for PCP is not necessary in patients who admit to recreational use but may be helpful in patients with an undifferentiated psychosis and to identify inappropriate PCP exposure and initiate necessary social work assessment in victims of child abuse. (See "Emergency department approach to acute-onset psychosis in children", section on 'Ancillary studies' and "Physical child abuse: Diagnostic evaluation and management", section on 'Toxicology'.)

Qualitative testing of urine is more helpful than quantitative concentrations since serum levels do not correlate well with brain concentrations or clinical toxicity [18,29]. Confirmatory testing using gas chromatography with mass spectroscopy is performed on rare occasions when definitive drug identification is needed (eg, in cases of suspected child abuse).

The United States National Institute on Drug Abuse guidelines for federal workplace drug testing use a cutoff urine PCP concentration of 25 ng/mL. Urine toxicology screens may remain positive for several weeks. In one series of chronic users, urine screens remained positive for an average of 14 days [30]. Cerebrospinal fluid testing has been reported in two cases with concentrations one to four times the serum levels [31].

Multiple causes of false-positive urine tests have been reported, and the potential adverse medicolegal consequences of such results are profound. In one series, the rate of false-positive PCP screens greatly exceeded the rate of true-positive PCP screens [32]. Drugs capable of causing a false-positive urine test include ketamine [33], dextromethorphan [34,35], diphenhydramine [36], venlafaxine [37], lamotrigine [38], and tramadol [39]. When evaluating a positive qualitative test for PCP, the clinician should consider the clinical presentation and obtain confirmation with gas chromatography and mass spectrophotometry if clinical findings are inconsistent with PCP toxicity. Several PCP derivatives (eg, 3-methoxy-phencyclidine and 4-methoxy phencyclidine) have good cross-reactivity with the PCP screen, meaning the PCP immunoassay may be positive with these drugs, but the test tends to do poorly for other PCP derivatives (eg, methoxetamine or ketamine) [40].

MANAGEMENT — Recommendations for care of children and adolescents with PCP intoxication poisoning are derived from case series and reports, including observations in adults, and are driven by physical findings. The treatment of PCP toxicity is primarily supportive.

Airway, breathing, and circulation — Management of PCP intoxication begins with stabilization of airway, breathing, and circulation. Capillary glucose and pulse oximetry should be determined in patients presenting with altered mental status. A rectal temperature is imperative in agitated or seizing patients to assess for the presence of hyperthermia (rectal temperature >38.5°C [101°F]). Respiratory depression and apnea may occur abruptly in infants and young children necessitating rapid sequence intubation (RSI). We suggest avoiding succinylcholine when performing RSI in patients with known or suspected PCP intoxication who exhibit significant psychomotor agitation or hyperthermia because of the risk of exacerbating rhabdomyolysis-related hyperkalemia. Further acute interventions are based upon clinical findings as quantitative testing for PCP is generally unavailable and unhelpful. (See 'Treatment of complications' below.)

Tachycardia is common but rarely requires specific treatment in children and adolescents.

Agitated patients warrant careful evaluation for traumatic injuries once adequate sedation is achieved.

Sedation — Rapid control of psychomotor agitation is the cornerstone of successful management. Physical restraints may be necessary initially and several staff members are often needed to control patients agitated from PCP. Thereafter, chemical sedation is essential to control agitation, prevent or treat hyperthermia, perform a thorough physical examination, and obtain necessary studies.

Little evidence exists to guide the use of sedatives in the management of PCP intoxication. Based upon observational reports and broad clinical experience, we believe benzodiazepines (eg, lorazepam 0.1 mg/kg intravenously [IV], typical maximum single dose 4 mg; or diazepam 0.1 mg/kg IV, typical maximum single dose 10 mg) are the preferred agents for the initial treatment of PCP-induced agitation. Benzodiazepine dosing may be repeated every 8 to 10 minutes depending upon individual patient response.

Severe agitation — Early management of agitation or violent behavior is essential to prevent patient and staff injury. The emergency provider should exclude life-threatening hypoglycemia and hypoxia as contributing factors to agitation as soon as is safely possible. We treat severely agitated patients immediately with IV benzodiazepines (lorazepam 0.1 mg/kg IV, typical maximum single dose 4 mg; or diazepam 0.2 mg/kg IV, typical maximum single dose 10 mg). These doses can be repeated every 8 to 10 minutes based upon patient response. Although IV administration is preferred, intramuscular administration of midazolam (0.5 mg/kg, maximum single dose 10 mg) may be given in patients in whom IV access cannot be rapidly achieved.

Butyrophenones (eg, droperidol or haloperidol) are used as adjunctive therapy in adults with PCP intoxication when benzodiazepines do not adequately control symptoms and in adults with violent behavior due to other causes. (See "Phencyclidine (PCP) intoxication in adults", section on 'Sedation'.)

However, young children may be more susceptible to adverse effects of haloperidol (eg, dystonic reaction, seizures). In the United States, droperidol is also subject to a black box warning from the US Food and Drug Administration that recommends it only be used after a 12-lead electrocardiogram (ECG) is obtained and only if other treatments have failed. Furthermore, the warning states that droperidol should be used with extreme caution in patients who have risk factors for prolonged QT syndrome, are on medications that may prolong the QT interval, or have received IV benzodiazepines.

Thus, we suggest the following approach in children and adolescents with PCP-induced agitation not responsive to benzodiazepines:

●Butyrophenones should be avoided in infants and children under 12 years of age with PCP intoxication. If agitation is severe and risks life-threatening complications (eg, hyperthermia, rhabdomyolysis), then these patients should undergo RSI and muscle relaxation (ie, paralytic agent) (table 5).

●Haloperidol (initial dose 5 mg intramuscularly/IV) may be given to adolescents whose agitation is not controlled with IV benzodiazepines. Some clinicians prefer to avoid butyrophenones because they are purported to lower the seizure threshold and impair heat dissipation in hyperthermic patients. However, there are no high-quality studies in adolescents to support such claims. Furthermore, haloperidol may treat underlying psychotic symptoms that may, in part, be the source of agitation. Patients who receive haloperidol warrant a 12-lead ECG and cardiac monitoring. Adolescents whose agitation persists despite treatment with appropriate doses of benzodiazepines and haloperidol and whose agitation risks life-threatening complications (eg, hyperthermia, rhabdomyolysis) should undergo RSI and muscle relaxation (table 5).

●When RSI is performed for agitation, succinylcholine should be avoided if rhabdomyolysis-induced hyperkalemia is present or highly suspected. (See "Rapid sequence intubation in adults for emergency medicine and critical care" and "Rapid sequence intubation in adults for emergency medicine and critical care", section on 'Neuromuscular blocking agents' and "Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis", section on 'Succinylcholine'.)

●We suggest that droperidol not be used in children and adolescents with PCP intoxication.

Mild to moderate agitation — Patients with mild to moderate agitation should be placed in a quiet environment (darkened, quiet room). We suggest that these patients be given benzodiazepines (lorazepam 0.05 mg/kg IV, typical maximum single dose 2 mg; or diazepam 0.1 mg/kg IV, typical maximum single dose 5 mg). Oral benzodiazepines (eg, lorazepam 0.1 mg/kg, typical maximum single dose 2 mg) can be given instead of parenteral benzodiazepines to mildly agitated but cooperative patients.

Treatment of complications — The clinician should anticipate seizures, hyperthermia, rhabdomyolysis, hypertension, and dystonia in children and adolescents with PCP intoxication. Cardiac monitoring and frequent reexamination are essential in patients with any of these complications.

Seizures — Benzodiazepines (eg, lorazepam, initial dose 0.1 mg/kg, maximum single dose 4 mg, repeat in one to two minutes if seizures continue) are the first-line treatment for PCP-induced seizures. If seizures persist despite benzodiazepine administration, administer phenobarbital (20 mg/kg, maximum initial dose 1 g) or initiate an IV infusion of propofol. Respiratory depression requiring endotracheal intubation and ventilation is typical and should be anticipated (table 6). (See "Management of convulsive status epilepticus in children".)

Phenytoin or fosphenytoin is not effective for toxin-induced seizures and should be avoided.

Hyperthermia — Hyperthermia (rectal temperature >38.5°C [101°F]) may result from PCP-induced myotonic activity, seizures, rhabdomyolysis, or a combination of the three and should be managed aggressively with mechanical cooling measures.

Augmentation of evaporative cooling is considered the treatment modality of choice because it is effective, noninvasive, and easily performed. The naked patient is sprayed with a mist of lukewarm water while air is circulated with large fans. Shivering may be suppressed with IV benzodiazepines, such as diazepam (0.1 mg/kg, maximum single dose 5 mg IV) or lorazepam (0.05 to 0.1 mg/kg, maximum single dose 1 to 2 mg IV). Cold inspired oxygen, cold gastric lavage, cooling blankets, and cold IV fluids may be helpful adjuncts. (See "Heat stroke in children", section on 'Rapid cooling'.)

Some experts advocate that patients with marked hyperthermia (temperature >40ºC) might benefit from RSI followed by prolonged paralysis to stop heat generation from muscle activity (table 5). The clinician should avoid succinylcholine when performing RSI if hyperkalemia due to rhabdomyolysis is present or highly suspected. (See "Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis", section on 'Succinylcholine'.)

There is no role for antipyretic agents, such as acetaminophen or aspirin, in the management of drug-induced hyperthermia, since the underlying mechanism does not involve a change in the hypothalamic temperature set-point. Alcohol sponge baths should also be avoided because large amounts of the drug may be absorbed through dilated cutaneous vessels and produce toxicity.

Rhabdomyolysis — Hyperthermia, agitation, seizures, and muscle rigidity may lead to muscle cell breakdown (rhabdomyolysis) with significant risk for renal failure. Patients with rhabdomyolysis can present with the classic triad of pigmented granular casts in the urine, a red to brown color of the urine supernatant, and a marked elevation in the plasma level of creatine kinase, although rhabdomyolysis is not uncommon in patients whose urine is without visually discernable color change. Primary treatment goals consist of (see "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)"):

●Fluid repletion with normal saline infusion (20 to 40 mL/kg per hour up to 1 to 2 L per hour); the emergency provider should closely monitor urine output with the goal of maintaining a minimum urine flow of 4 mL/kg per hour (200 mL per hour in adults). Once diuresis is established with normal saline, alkalinization of the urine is commonly employed but efficacy is uncertain. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)", section on 'Bicarbonate in selected patients'.)

●Evaluation for significant electrolyte abnormalities (hyperkalemia, hyperphosphatemia, and hypocalcemia); management of hyperkalemia is of particular importance. Hypocalcemia is usually transient, and calcium administration should be avoided unless severe symptoms (eg, tetany) are present.

Hypertension — Hypertension is frequently transient, and many patients need no specific treatment. Benzodiazepine administration for agitation is often effective for elevated blood pressure. Because hypertension may primarily reflect alpha adrenergic effects due to decreased reuptake of norepinephrine, persistent, severe elevations of blood pressure may be treated with nitroprusside or phentolamine (0.1 mg/kg, maximum single dose 5 mg). Pure beta adrenergic blockers are contraindicated because they may cause unopposed accentuation of alpha adrenergic effects with exacerbation of hypertension. (See "Evaluation and treatment of hypertensive emergencies in adults", section on 'Sympathetic overactivity resulting in hypertensive emergencies'.)

Rarely, persistent hypertension in patients with depressed mental status or severe headache may indicate the presence of a subarachnoid hemorrhage with increased intracranial pressure. Such patients should undergo computed tomography of the head and treatment to reduce increased intracranial pressure while maintaining adequate cerebral perfusion pressure. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'General management'.)

Dystonic reaction — Diphenhydramine (1 to 2 mg/kg IV [preferred] or IM, maximum dose 50 mg) or benztropine (0.05 mg/kg IV, maximum single dose 2 mg in children over three years of age) typically provide rapid treatment of a dystonic reaction within minutes of administration. If possible, diphenhydramine should be administered after the urine sample is obtained for toxicologic screening if documentation of PCP intoxication is important because diphenhydramine may cause the specimen to test positive for PCP by immunoassay method [18]. (See "First-generation (typical) antipsychotic medication poisoning", section on 'Acute extrapyramidal syndromes'.)

Decontamination — Most patients survive PCP intoxication uneventfully with supportive care; decontamination is generally unnecessary in isolated ingestions. However, decontamination with activated charcoal (AC) may be useful if a massive ingestion of PCP or a potentially dangerous coingestant is present and treatment is started within one hour of ingestion. Patients who ingest large amounts of PCP to avoid police detection (body stuffers) or to transport drug for distribution (body packers) may sustain massive ingestions. Any potential benefit from AC must be weighed against the risk of aspiration, especially given the potential for altered mental status and seizures with severe PCP intoxication. AC is given in a dose of 1 g/kg (maximum 50 g). (See "Phencyclidine (PCP) intoxication in adults", section on 'Decontamination'.)

The greatest benefit occurs if AC is given within one hour. The efficacy of AC as a function of time from ingestion is discussed in detail separately. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Evidence of efficacy and adverse effects'.)

Patients who are exposed to PCP should not undergo gastric emptying by gastric lavage or by syrup of ipecac-induced emesis. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Syrup of Ipecac' and "Gastrointestinal decontamination of the poisoned patient", section on 'Gastric lavage'.)

Patients with PCP intoxication should also not undergo continuous nasogastric suction. Nasogastric suction is theoretically beneficial when performed soon after ingestion due to the high concentration of PCP in the stomach’s acidic environment. However, it has no proven benefit and may cause electrolyte abnormalities, aspiration, and unwanted difficulty in agitated patients.

Whole bowel irrigation is not routinely recommended although it may be used in patients who have ingested potentially lethal amounts of PCP, as may occur with body stuffers or body packers. (See "Internal concealment of drugs of abuse (body packing)".)

Elimination enhancement — We do not typically use multidose AC in patients with PCP intoxication. Although PCP undergoes enterohepatic circulation, its typical duration of action is short. Also, there is no evidence of clinical benefit in humans, and the potential for aspiration exists whenever AC is given.

Neither urine acidification nor charcoal hemoperfusion should be used in the treatment of PCP intoxication. Urinary acidification, in particular, is dangerous as it may worsen renal injury in patients with rhabdomyolysis [41].

Hemodialysis, which eliminates PCP only from the serum, is ineffective because of the large volume of distribution of the drug (6.2 L/kg).

Elimination enhancement following PCP intoxication is covered in more detail separately. (See "Phencyclidine (PCP) intoxication in adults", section on 'Enhanced elimination'.)

Antidote — The treatment of PCP intoxication is supportive; an effective antidote has not been developed. Anti-PCP Fab fragments have been studied in animals but are not available for use in humans. (See "Phencyclidine (PCP) intoxication in adults", section on 'Future considerations'.)

Child protection — Diagnosis of nonrecreational PCP exposure in an infant or young child should prompt involvement of an experienced child protection team (eg, social worker, nurse, subspecialist clinician), if available. In many parts of the world (including the United States, United Kingdom, and Australia), a mandatory report to appropriate government authorities is also required for cases of suspected abuse. (See "Child abuse: Social and medicolegal issues", section on 'Mandatory reporting'.)

DISPOSITION — Children and adolescents with mild recreational PCP intoxication typically improve rapidly to normal functioning within four to eight hours after exposure. Such patients may be discharged, provided that the effects of intoxication have resolved and the patient remains symptom-free during a brief (one to two hours) period of observation. Prior to discharge, these patients warrant assessment for drug abuse and possible referral to drug rehabilitation. In some adolescents, psychiatric evaluation or referral for concurrent mental illness may also be appropriate.

Infants and young children with mild PCP intoxication need a full assessment of the social circumstances that led to the exposure. Such an investigation often requires admission.

Any patient with significant complications (eg, rhabdomyolysis, coma, status epilepticus) or severe symptoms (eg, uncontrolled hypertension, hyperthermia) should be admitted to an intensive care setting. Patients with less severe but persistent symptoms should be admitted to an appropriate inpatient setting for further monitoring and treatment. Return to normal function may take weeks in patients with large ingestions. Severely intoxicated infants have been reported to need 48 hours to 4 days to recover [12].

As the PCP is eliminated and the intoxication level improves, some adolescent patients may develop psychosis, bizarre behavior, or depression (the so-called "emergence phenomenon") that may last from days to weeks and may require admission for psychiatric treatment, possibly including psychotropic medication [42]. Recovery from psychosis can take weeks to months [43]. Prolonged psychosis occurs more commonly in chronic abusers and is a poor prognostic sign. Withdrawal symptoms, such as depression, anxiety, irritability, restlessness, anergia, and disturbances of thought and sleep, have been described in chronic users after as little as one day of abstinence [42]. Chronic abusers may benefit from behavioral treatment for substance abuse.

ADDITIONAL RESOURCES

Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Treatment of acute poisoning caused by recreational drug or alcohol use".)

SUMMARY AND RECOMMENDATIONS

●Epidemiology – Phencyclidine (PCP) is a dissociative anesthetic that is abused by a significant number of adolescents. PCP exposure is rare in young infants and children and typically represents an inadvertent oral or inhalational exposure due to caregiver drug use. (See 'Epidemiology' above.)

●Clinical manifestations – PCP intoxication produces a wide range of vital sign and neuropsychiatric findings. In infants and young children, altered mental status (eg, lethargy, irritability), nystagmus, choreoathetosis, seizures, ataxia, and blank staring are common features. Abrupt respiratory depression with apnea may occur. In adolescents, nystagmus, psychomotor agitation, hallucinations, and violent behavior are prevalent. (See 'Clinical features of overdose' above.)

●Differential diagnosis – The clinical picture of PCP intoxication shares features common to many other intoxications and medical conditions, especially those that cause acute psychosis. The differential diagnosis and approach to acute psychosis in the emergency department is provided in the tables and algorithm (table 3 and table 4 and algorithm 1) and is discussed in detail separately. (See 'Differential diagnosis' above and "Emergency department approach to acute-onset psychosis in children", section on 'Differential diagnosis' and "Emergency department approach to acute-onset psychosis in children", section on 'Approach'.)

●Ancillary studies – Ancillary studies obtained to support the clinical diagnosis, evaluate for co-ingestants, and assess for the presence of rhabdomyolysis and its complications are discussed above. (See 'General studies' above.)

Quantitative drug levels have little role in the management of acute toxicity of known recreational drug users. Qualitative urine testing is appropriate when distinguishing acute psychosis due to drug toxicity from other types of psychosis and in situations where child abuse is suspected. Results may remain positive for weeks. Thus, a positive urine test may not indicate acute intoxication. (See 'Testing for phencyclidine' above and "Phencyclidine (PCP) intoxication in adults", section on 'Testing for PCP'.)

●Management – Treatment of PCP intoxication is primarily supportive. In addition to careful assessment and support of airway, breathing, and circulation, as needed, the clinician should anticipate and aggressively manage agitation, seizures, hyperthermia, rhabdomyolysis, hypertension, and dystonic reactions. (See 'Airway, breathing, and circulation' above and 'Sedation' above and 'Treatment of complications' above.)

Early management of agitation or violent behavior is essential to prevent patient and staff injury. Sedation should be administered as rapidly as possible. The emergency provider should exclude life-threatening hypoglycemia and hypoxia as contributing factors to agitation as soon as is safely possible. Our approach to sedation is as follows:

•Severe agitation – In a severely agitated child or adolescent, we suggest immediately administering an intravenous (IV) benzodiazepine (lorazepam 0.1 mg/kg IV, typical maximum single dose 4 mg; or diazepam 0.2 mg/kg IV, typical maximum single dose 10 mg) (Grade 2C). These doses can be repeated every 8 to 10 minutes based upon patient response. Although IV administration is preferred, intramuscular administration of midazolam (0.5 mg/kg, typical maximum single dose 10 mg) may be given in patients in whom IV access cannot be rapidly achieved. (See 'Severe agitation' above.)

•Severe agitation not responding to benzodiazepines – In an adolescent patient with severe agitation that threatens harm to themselves or others and is not controlled with parenteral benzodiazepines, we suggest administering parenteral haloperidol (initial dose 5 mg, IV or intramuscularly) (Grade 2C). An adolescent whose agitation persists despite treatment with appropriate doses of benzodiazepines and haloperidol and whose agitation risks life-threatening complications (eg, hyperthermia, rhabdomyolysis) should undergo rapid sequence intubation (RSI) and muscle relaxation (ie, paralytic agent) (table 5). (See 'Severe agitation' above.)

•Severe intoxication with risk for hyperthermia or rhabdomyolysis – In an infant or child under 12 years of age with severe PCP intoxication that risks life-threatening complications (eg, hyperthermia, rhabdomyolysis), we suggest performing RSI and muscle relaxation (ie, paralytic agent) (table 5) rather than administering haloperidol (Grade 2C). (See 'Severe agitation' above.)

•Mild or moderate intoxication – In a patient with mild or moderate PCP intoxication, we suggest administering a benzodiazepine (eg, lorazepam 0.05 mg/kg IV, typical maximum single dose 2 mg; or diazepam 0.1 mg/kg IV, typical maximum single dose 5 mg) (Grade 2C). The benzodiazepine may be repeated as needed. (See 'Mild to moderate agitation' above.)

●Role of gastrointestinal decontamination – Children and adolescents with PCP intoxication should not undergo gastric emptying (induced vomiting or gastric lavage) or continuous nasogastric suctioning. Children and adolescents with isolated PCP intoxication should also not receive activated charcoal (AC). However, patients with coingestants that bind to AC may benefit from its administration. (See 'Decontamination' above.)

●Child protection – Diagnosis of PCP exposure in an infant or young child should prompt involvement of an experienced child protection team (eg, social worker, nurse, subspecialist clinician), if available, and mandatory reporting, depending on the local legal requirements. Infants and young children with mild PCP intoxication need a full assessment of the social circumstances that allowed the exposure. Such an investigation often requires admission. (See 'Child protection' above and "Child abuse: Social and medicolegal issues", section on 'Mandatory reporting'.)

●Disposition – Patients of any age with persistent symptoms should be admitted to a monitored setting. Due to the relatively short duration of action, older children and adolescents with mild symptoms are candidates for a period of observation and discharge. Patients whose medical symptoms resolve but have persistent behavioral issues should receive psychiatric evaluation. (See 'Disposition' above.)