PCP has acid and alkaloid forms. Both are odorless, nonvolatile, sold as “angel dust,” and may be ingested or injected intravenously. PCP acid is a white crystalline substance sold as or incorporated into tablets. It deteriorates when heated and is not suitable for smoking. PCP alkaloid is a grayish–white amorphous powder smoked after incorporation into marijuana (e.g., “super grass,” “super weed”) or tobacco (e.g., “clickers,” “primos”) cigarettes. More often, the alkaloid is dissolved in a liquid hydrocarbon and applied to the wrapper of a tobacco cigarette. The ether-like or formaldehyde odor surrounding some patients who have used PCP is the smell of the volatile hydrocarbon used to dissolve PCP alkaloid.

Several analogs of PCP are occasionally used as street drugs (Table 142.3). Their pharmacologic actions are similar to those of PCP and cannot be distinguished clinically. In addition, street PCP samples may be contaminated with 1-piperidinocyclohexane-carbonitrile, a precursor of PCP that is more potent than PCP and capable of generating cyanide [1], although the clinical significance of this is unknown.

PCP has multiple mechanisms of action (Table 142.4), which helps to explain the varied signs and symptoms associated with PCP intoxication. It is well absorbed from the gastrointestinal (GI) and respiratory tracts. PCP is a weak base (pK_a 8.5), has a volume of distribution 6.2 L per kg, and is extensively protein-bound (65%) [2]. PCP concentrates in the brain, lungs, adipose tissue, and liver. The average serum half-life in controlled studies is 17 hours [2]. PCP is metabolized by the liver and excreted predominantly as inactive compounds [2,3,4,5]. Small amounts of PCP are excreted in perspiration, saliva, and gastric juice. PCP has been detected in umbilical and infant blood, amniotic fluid, and breast milk [6,7].

Drinking PCP, injecting intravenous PCP, or swallowing the remnants of a PCP-soaked cigarette has resulted in severe
intoxication within 1 hour. Clinical experience with PCP intoxication is derived from case reports [8,9,10,11,12,13,14,15] and small clinical series [16,17,18,19,20]. The hallmarks of PCP intoxication are nystagmus and hypertension. Nystagmus may be horizontal, vertical, or rotary. Patients may have systolic or diastolic hypertension. Hypertension usually resolves within 4 hours, but a significant number of patients may remain hypertensive for more than 24 hours.

Tachycardia is common, but heart rates more than 120 per minute are unusual. Hypothermia (< 36.7°C), hyperthermia (> 38.9°C), respiratory compromise, tachypnea, hypotension, and cardiac arrest are reported, but are uncommon.

Patients may present with delirium or normal sensorium. Lethargy, stupor, and unconsciousness are uncommon presentations. The most common behavioral effects are violent and agitated behavior, which may result in severe penetrating or blunt trauma. Patients may exhibit bizarre behavior such as driving less than 10 mph on the freeway, “playing bumper cars” on the freeway, sleeping on top of cars that are blocking traffic, lying down in a busy street, and wandering or acting wildly in public. Only 20% of PCP users report hallucinations or delusions. The visual hallucinations are typically concrete and realistic (e.g., blue fish). Patients may appear mute or may stare blankly.

The most common neuromuscular finding is rigidity of all extremities. It is often associated with jerky or thrashing movements, tremors, or twitching. Other musculoskeletal disturbances include oculogyric crisis, trismus, facial grimacing, circumoral muscle twitching, lip smacking or chewing movements, torticollis, tongue spasms, opisthotonos, and catalepsy. Patients may exhibit self-limited slow, writhing movements of the extremities or body. Athetosis and muscle stiffness may appear simultaneously. Intermittent athetoid movements may last for more than 10 hours. Rhabdomyolysis may occur, even in calm-appearing patients. Grand mal seizures and status epilepticus are uncommon.

The major autonomic effects are profuse diaphoresis, copious oral or pulmonary secretions, and urinary retention. Bronchospasm has been reported in patients who smoked or sniffed PCP. Pupillary size is usually normal, but miosis or mydriasis may be evident.

Clinically, acute PCP intoxication can be divided into major and minor clinical syndromes [20]. Major syndromes, representing moderate-to-severe PCP intoxication, are delirium, toxic psychosis, catatonic syndrome, and coma. They may include any of the effects previously discussed. Minor syndromes are lethargy or stupor, bizarre behavior, violent behavior, agitation, and euphoria. They represent mild PCP intoxication, and complications are rare.

Delirium is the most common presentation of PCP intoxication. Patients may be found wandering in traffic or appear intoxicated with ethanol. Patients exhibit signs and symptoms such as slurred, bizarre, or repetitive speech; ataxia; disorientation; confusion; poor judgment; inappropriate affect; amnesia of recent events; bizarre behavior; agitation; and violence. The duration of this syndrome often lasts for a few hours and rarely lasts more than 3 days, but has been reported to persist for 1 to 3 weeks.

Patients presenting with toxic psychosis often have a history of chronic PCP use (e.g., smoking) during the week before admission. This psychosis is characterized primarily by hallucinations, delusions, and paranoid ideation. Hallucinations may be auditory or visual, or both, and may involve seeing brilliantly colored objects, but objects are not distorted and there are no kaleidoscopic effects. Patients may be preoccupied with religious thoughts or have religious delusions. It is common for patients to have pressured speech, scream, or make animal sounds. Signs and symptoms persist for a median of 3 days (range, 1 to 30 days).

The catatonic syndrome manifests primarily as a combination of signs: posturing, catalepsy, rigidity, mutism, staring, negativism, nudism, impulsiveness, agitation, violence, and stupor. Stereotypies, mannerisms, grimacing, and verbigeration may also be present. Patients are typically mute, staring blankly, motionless, stiff, standing with extremities or head in bizarre positions, and unresponsive to noxious stimuli. Catatonic syndrome usually does not persist for more than 24 hours (range, 2 to 6 days), and most patients recover within 4 to 6 hours. The majority of patients emerging from catatonic syndrome are agitated or combative for several hours; the other patients emerge with delirium, lethargy, psychosis, bizarre behavior, or normal sensorium.

Patients with delirium and violent or bizarre behavior may subsequently lapse into coma. Coma may also occur abruptly and may last up to 6 days. Patients emerging from coma may exhibit delirium, catatonic syndrome, toxic psychosis, stupor, agitation, violence, bizarre behavior, or normal sensorium. The duration of the emergent phenomenon is variable.