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Phencyclidine (PCP) abuse: A close-up look at a growing problem

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  • Phencyclidine (PCP) abuse A close-up look at a growing problem

    S. Ovid Isaacs, M.S., D.M.D.,* Paul Martin, D.D.S.,** and James A. Washington, Jr., D.D.S.,*** New York, N.Y.

    DIVISION OF ORAL AND MAXILLOFACIAL SURGERY, HARLEM HOSPITAL CENTER

    PCP or angel dust is a dissociative anesthetic agent with notoriety as an abuse substance. Numerous members of many subcultures are frequent users of this drug. It is well known in Californias psychedelia, along the East Coast, and in the middle- and working-class suburbs of the Midwest. It is important that practitioners become acquainted with the drug and its effects. Persons intoxicated with PCP have murdered their own children and have even jumped out of high-rise apartment buildings. States of florid psychosis lasting for days can follow a brief encounter with PCP. Inadvertent administration of narcotics and barbiturates to patients with acute PCP intoxication can lead to a crisis that could prove to be fatal. (ORAL SURG. ORAL MED. ORAL PATHOL. 61:126-129, 1986)

    P hencyclidine (PCP), or angel dust, was origi- nally developed in the late 1950s as an analgesic and anesthetic agent. During clinical trials, however, it was found to have severe adverse effects, including symptoms resembling manic-depressive psychosis and schizophrenia, and the drug was never approved for use in human patients.,* Approval was later given for the use of PCP in veterinary medicine, but as of April, 1979, all legal manufacture of the drug stopped. Today it is classified as a Class II controlled substance. Despite the adverse effects of the drug and cessation of its legal manufacture, PCP is a very popular recreational drug, ranking number 2 in the streets today, after marijuana, because of its illicit production.

    It is essential for oral surgeons and other dental practitioners to become familiar with PCP and its multifaceted effects and management in emergen- cies. Practitioners who have not yet encountered a PCP emergency in their offices or institutions prob- ably will before long.

    HISTORY OF THE DRUG

    Phencyclidine is the general name for 1-( 1 -phenyl- cyclohexyl)piperidine hydrochloride. It is highly lip- id soluble and is a weak base with a pKa between 8.6 and 9.4. Thirty or more derivatives of PCP have

    *Formerly Chief Resident, Oral and Maxillofacial Surgery. **Attending Oral and Maxillofacial Surgeon. ***Director, Oral and Maxillofacial Surgery.

    126

    appeared on the streets in the last 5 years. Two of these analogues-N-ethyl- 1-phenylcyclohexamine (PCE) and l-[-(2 thiencyl) cyclophexyl] piperidine (TCP)-have been found to be more behaviorally active than the parent compound.3 PCP and its analogues are usually tolerated in street doses of 0.02 to 0.05 mg/kg by smoking or 1.5 to 3.5 mg/kg by ingestion. In many instances, however, the deceived and uninformed user may consume more and end up with PCP intoxication, which could be fatal.4v5

    PCP is very easy to synthesize and can be abused in many modes. The most common are smoking (mixed with low-grade marijuana or oregano), snort- ing (mixed with cocaine), oral ingestion (mixed with peanut butter), and, to a lesser extent, intravenous injection. The drug is sold on the street under different names: angel dust, dust, T, tic tat, KJ, crystals, goon, soma, crystal joints, hog, mist, and scuffle. Every practitioner should become familiar with the various names for PCP.

    PHARMACOLOGIC AND CUNICAL EFFECTS

    In general, PCP is not well classified as either a central nervous system stimulant (upper) or depressant (downer), and its direct mechanism of action is not well understood. However, it is known to inhibit presynaptic uptake of norepinephrine, dopa- mine, and serotonin. Furthermore, it may compete with acetylcholine at postsynaptic sites.6 Some work- ers have also shown that PCP has the capacity to inhibit total brain protein synthesis.

    The effects of PCP usually begin within 1 hour of

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    Phenylcyclidine abuse 127

    use if the drug is ingested and within 1 minute if it is smoked, with the drug metabolizing in the liver by hydroxylation? The high lasts for 4 to 6 hours, and it takes 24 to 48 hours before the abuser feels normal again. The earliest clinical sign observed in the PCP abuser is hypertension. The pressor effects of PCP have been well documented in both human beings and animals.9 In addition, several investigators have reported on PCP-induced hypertensive crises which have resulted in death..

    Ross and Wongi2 reported that many persons under the influence of PCP show loss of memory. This loss of memory has been attributed to the inhibition of brain protein synthesis. It has been suggested that phencyclidine might produce organic brain disorder associated with long-term neuropsy- chological damage. In addition, a review of the literature has shown that chronic use of PCP has resulted in psychological and physiologic depen- dence. It is clear that as the amount of PCP usage increases, and if there is simultaneous use of other drugs (particularly barbituates), severe toxic symp- toms become likely. These include coma, seizures, and respiratory arrest. Numerous PCP users have experienced a disorganized state after 2 or 3 days of normality following a good high. Most research- ers are of the opinion that this delay is due to the continued presence of the drug in the central nervous system as a result of gastroenteric recirculation and lipid storage of the material. Thus, a high index of suspicion is justified when a patient gives a history of chronic PCP abuse and recent use. This person should, indeed, be considered a high-risk patient.

    Intoxication can occur from either large or low doses of PCP. Typically, in low-dose intoxication some patients may appear awake while others may appear agitated or, in some instances, asymptomatic. However, vertical or horizontal nystagmus (and in some instances both forms) is common, with the pupils being of normal size. Nystagmus is specifical- ly diagnostic for PCP intoxication. In most instances intoxication usually results from oral or parenteral use of the drug rather than from smoking it. McCar- ron and associatesI have described the major and minor clinical patterns of acute PCP intoxication and give the incidence of their findings. Among the major patterns noted were acute brain syndrome (ABS), toxic psychosis, catatonic syndrome, coma, and aspi- ration pneumonia, whereas the minor patterns included lethargy, euphoria, stupor, and violence.

    DENTAL CONSIDERATIONS

    Parenteral administration of narcotics and barbi- turates is very common in dental offices and clinics

    Table I. Treatment of phencyclidine intoxication in adults

    When no antidote is available: PRIMARY TREATMENT: OBSERVATION AND SUPPORTIVE CARE

    1. Control status epilepticus (Note: IV phenobarbital noi recommended A. Diazepam IV-5 to 10 mg (usual maximum dose 30

    mg); watch for apnea B. Neuromuscular blockage for refractory cases-treat

    in ICU with assisted ventilation 2. If respiratory rate is less than 1 Z/minute-rule out possi-

    ble associated narcotic overdose A. Naloxone IVA.4 mg stat; may repeat dose if

    response in respiratory rate is inadequate B. Ventilate patient

    3. Control violence or agitation-may need restraints to protect patient and others; quiet room desirable A. Comatose patients: Diazepam IV 5 to IO mg; watch

    far apnea B. Conscious patients: Haloperidol IM 5 to IO mg

    (maximum dose usually 30 mg in first half-hour) 4. Counteract possible hypoglycemia

    A. Comatose and catatonic patients: Start IV and give 50 ml 50% dextrose/water

    B. Conscious patients: Give glass of sweetened cranberry juice as soon as patient will accept it

    5. Hypertension with diastolic pressure over 115 mm Hg A. Control violence or agitation first; further treatment

    may not be necessary; monitor vital signs B. If BP still elevated, consider low-dose diazoxide IV C. Alternate method for conscious patients with pulse

    less than 120/minute, respirations less than 30, minute, and no seizures: Chlorpromazine 25 mg IM initially instead of haloperidol

    6. Remove drug if possible A. Comatose patients:

    I. Endotracheal intubation, then gastric lavage with Ewald tube

    2. Insert NC tube and connect to continuous suction to remove any PCP secreted in gastric acid

    B. Conscious patients: Lavage or induced emesis not recommended unless there is a strong history of PCP ingestion within 4 hours or a multiple overdose is suspected

    7. Localized dystonic reactions (from PCP, haloperidol, or chlorpromazine) Conscious patients: Diphenhydramine 50 mg IV (Norer Do not treat this reaction in comatose patients)

    8. Hyperthermia: Stat cooling measures and aspirin rectal suppository

    9. Bronchospasm: Aminophylline 250 mg by IV piggyback over 20 minutes

    Keep under observation until all symptoms except nystag- mus have resolved; Patients with major PCP syndromes may have to be admitted

    today. For this reason, patients who are potential candidates for sedation or general anesthesia must be evaluated diligently to avoid problems.

    In many PCP abusers there is a 48-hour delayed

  • 128 Zsaacs, Martin, and Washington Oral Surg. February, 1986

    disorganized state after use of the drug. Therefore, the administration of narcotics or barbiturates espe- cially ultra-short-acting barbiturates, should be avoided in these patients. This prevents the supra- additive pharmacologic effects and toxicity that can result in seizures, respiratory distress, or coma in the PCP patient.

    A large number of dentists administer multiple drug combinations in their everyday practice, and giving these to a PCP-loaded patient could be disas- trous to both d