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Toxicity, Phencyclidine

Author: Patrick L West, MD, Clinical Instructor, Medical Toxicology Fellow, Department of Emergency Medicine, Oregon Health and Sciences University; Staff Physician, Department of Emergency Medicine, Portland Veterans Affairs Medical Center
Coauthor(s): Nathanael J McKeown, DO, Assistant Professor, Oregon Health and Science University; Medical Toxicologist, Oregon Poison Center; Attending Physician, Emergency Medicine, Portland Veteran Affairs Medical Center, Oregon Health and Science University
Contributor Information and Disclosures

Updated: Jan 21, 2009

Introduction

Background

Phencyclidine (PCP) was originally developed for use as a general anesthetic for surgery under the trade name Sernyl in the 1950s. Its use was discontinued in humans in 1965 because it often produced postanesthetic delirium with psychotic features, dysphoria, and occasionally extreme agitation. PCP under the name Sernylan was used as a veterinary anesthetic until 1978, after which time it became illegal to use altogether. 

In the 1960s, people began illegally manufacturing phencyclidine in laboratories, and, by the late 1970s, it became a popular street drug. Common street names include angel dust, peace pill, crystal joint, hog, rocket fuel, KJ, elephant tranquilizer, supergrass, boat, tic-tac, zoom, wet, embalming fluid, and wack. PCP is a white crystalline powder that is available in liquid, tablet, or powder forms. It can be snorted, ingested orally, or injected intravenously. It also can be smoked as a "joint" or "wet" when sprinkled on cigarettes or applied to mint or marijuana leaves. PCP is often taken in conjunction with other co-ingestants, including ethanol and marijuana.

Pathophysiology

PCP, also known as 1-(1-phenylcyclohexyl-piperidine), is classified as a dissociative anesthetic. PCP acts mainly in the CNS, producing both stimulation and depression. Its sympathomimetic effects are thought to be due to weak reuptake inhibition of norepinephrine and dopamine. PCP also exerts some cholinergic and anticholinergic effects and has some other actions at nicotinic and opioid receptors.

The dissociative properties of PCP are believed to be due to its actions as a glutamate antagonist at the N -methyl-D-aspartate (NMDA) receptors. NMDA antagonists have been known to produce behavioral effects similar to those observed in schizophrenia, and they are used to induce an animal model of schizophrenia for research. PCP also affects the actions of dopamine, which may cause the psychomotor effects seen with PCP.

Clinical effects occur within minutes and usually last several hours. These symptoms may last up to 48 hours in the event of significant overdose. However, even more prolonged effects may be seen in chronic users either from enterohepatic recirculation or from delayed release of PCP from lipid stores. Because PCP is fat soluble, it accumulates in adipose tissue and the brain. Recurrent and fluctuating symptoms occur as PCP is remobilized from lipid stores, which can occur days, weeks, or months after the initial use.1 The half-life of PCP is estimated at 17.4 hours; however, half-lives of 1-4 days have been reported.2 PCP is primarily metabolized in the liver.

Frequency

United States

  • The 2006 National Survey on Drug Use and Health, polling adults older than 12 years, found  a lifetime prevalence of 2.7% of the population trying PCP. In the last year, 0.1% (an estimated 187,000 people) had tried it, and in the last month, 30,000 had used PCP.3  
  • The 2007 Monitoring the Future Survey of high school seniors showed 2.1% using PCP once in their lifetime (down from 2.2% in 2006), 0.9% had used PCP at least once in the last year (up from 0.7% in 2006), and 0.5% (up from 0.4% in 2006) had used PCP at least once in the last 30 days.4
  • The 2007 Monitoring the Future Survey also showed 21% of high school seniors felt PCP was "very easy" or "fairly easy" to obtain (down from 23.1% in 2006 and down from the high of 31% in the early 1990s).
  • However, in their 2006 report, the American Association of Poison Control Centers only reported a total of 303 individual exposures to PCP and 208 hospital visits for PCP.5

Mortality/Morbidity

Doses of 20 mg or more of PCP may cause prolonged coma, seizures, and even death. One death has been reported from an ingestion of 150-200 mg in an acute overdose. The AAPCC reported one death and 19 major outcomes from PCP in 2006.5  

Morbidity and mortality are usually associated with rhabdomyolysis, renal failure, hypertensive crises, accidental trauma, and self-destructive behavior.

Race

According to the Drug Abuse Warning Network (DAWN) report of 2004, of all PCP-related ED visits in 2002, 43% of abusers were black, 30% were white, and 12% were Hispanic.6

Sex

Nationally, patients presenting to the ED for PCP intoxication are more likely to be male (64%) than female (36%).

Age

According to a national survey in 2006, 2.7% of the population aged 12 years and older reported using PCP at least once.

Clinical

History

Because of the numerous routes of administration, variations in dosage, and possibility of co-ingestants, PCP produces a wide variety of physical and behavioral effects. Most commonly, witnesses may report agitation, bizarre actions, or violent behavior. Users of PCP often appear to be having a psychotic episode and may or may not report to the physician that they have taken the drug.

Physical

Based on a study by McCarron et al in which 1,000 patients presenting with acute phencyclidine intoxication were evaluated, clinical effects ranged from lethargy and coma to extreme agitation and psychosis.7
 
Common physical examination findings include the following:

  • Nystagmus (horizontal, vertical, or rotary) - Often considered a hallmark of PCP intoxication (57-89%)
  • Hypertension (57%)
  • Acute brain syndrome involving confusion, amnesia, disorientation, and violence (37%)
  • Agitation and violent behavior (35%)
  • Tachycardia (30%)
  • Bizarre behavior including public nudity (29%)
  • Hallucinations and delusions (19%)
  • Miosis - Often reported with a blank stare
  • Rare findings - Usually only seen with high doses
    • Seizures (3.1%)
    • Dystonia
    • Ataxia
    • Apnea (often seen with co-ingestants)
    • Catatonia
    • Coma - PCP coma usually presents with nystagmus and the absence of respiratory depression. Unlike opioid-induced coma, it does not improve with naloxone.
    • Hypertensive crisis
    • Myocardial infarction (non-Q wave, cardiac enzyme leak)
    • Intracranial and subarachnoid hemorrhage
  • Other manifestations include the following:
    • Hyperthermia, hyperreflexia, and muscle rigidity have been reported.
    • Rhabdomyolysis with or without acute renal failure may also occur.

More on Toxicity, Phencyclidine

Overview: Toxicity, Phencyclidine
Differential Diagnoses & Workup: Toxicity, Phencyclidine
Treatment & Medication: Toxicity, Phencyclidine
Follow-up: Toxicity, Phencyclidine
References

References

  1. Marx JA, Hockberger RS, Walls RM. Phencyclidine. In: Rosen's Emergency Medicine Concepts and Clinical Practice. 5th ed. St Louis: Mosby Inc; 2002:2146-8.

  2. Poisindex Editorial Staff. Phencyclidine (Acute Toxicity). In: Klasco RK, ed. POISINDEX System. Thomson Micromedex: Greenwood Village, CO; 2005.

  3. OAS Home of Alcohol, Tobacco, and Drug Abuse Statistics. 2006 National Survey on Drug Use and Health (NSDUH). [Full Text].

  4. National Institute on Drug Abuse. 2007 Monitoring the Future (MTF) Survey, funded by the National Institute on Drug Abuse, National Institutes of Health, DHHS, and conducted by the University of Michigan's Institute for Social Research. [Full Text].

  5. Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol (Phila). Dec 2007;45(8):815-917. [Medline].

  6. Drug Abuse Warning Network. Trends in PCP-Related Emergency Department Visits. January 2004. The Drug Abuse Warning Network Report. Available at www.dawninfo.samhsa.gov.

  7. McCarron MM, Schulze BW, Thompson GA, Conder MC, Goetz WA. Acute phencyclidine intoxication: clinical patterns, complications, and treatment. Ann Emerg Med. Jun 1981;10(6):290-7. [Medline].

  8. Babu K, Boyer E, et al. Emerging drugs of abuse. Clin Pediatr Emerg Med. Jun 2005;6(2):81-4.

  9. Bryson P. Phencyclidine. In: Comprehensive Review in Toxicology for Emergency Clinicians. 3rd ed. Taylor & Francis; 1996:509-16.

  10. Budai B, Iskandar H. Dextromethorphan can produce false positive phencyclidine testing with HPLC. Am J Emerg Med. Jan 2002;20(1):61-2. [Medline].

  11. Goldfrank LR, et al. Phencyclidine and Ketamine. In: Goldfrank's Toxicologic Emergencies. 7th ed. New York: McGraw-Hill; 2002:chap 69.

  12. Greydanus DE, Patel DR. Substance abuse in adolescents: a complex conundrum for the clinician. Pediatr Clin North Am. Oct 2003;50(5):1179-223. [Medline].

  13. Haroz R, Greenberg MI. Emerging drugs of abuse. Med Clin North Am. Nov 2005;89(6):1259-76. [Medline].

  14. Leshner A. Hallucinogens and Dissociative Drugs Including LSD, PCP, Ketamine, Dextromethorphan. National Institute on Drug Abuse Research Report Series. Mar 2001;NIH Pub. No. 01-4209.

  15. Marchei E, Pellegrini M, Pichini S, Martin I, Garcia-Algar O, Vall O. Are false-positive phencyclidine immunoassay instant-view multi-test results caused by overdose concentrations of Ibuprofen, metamizol, and dextromethorphan?. Ther Drug Monit. Oct 2007;29(5):671-3. [Medline].

  16. Mokhlesi B, Leikin JB, Murray P, Corbridge TC. Adult toxicology in critical care: Part II: specific poisonings. Chest. Mar 2003;123(3):897-922. [Medline].

  17. Morocco AP, Osterhoudt KC. Getting "wet" from recreational use of embalming fluid. Pediatr Case Rev. Apr 2003;3(2):111-3. [Medline].

  18. Morris BJ, Cochran SM, Pratt JA. PCP: from pharmacology to modelling schizophrenia. Curr Opin Pharmacol. Feb 2005;5(1):101-6. [Medline].

  19. Rimsza ME, Moses KS. Substance abuse on the college campus. Pediatr Clin North Am. Feb 2005;52(1):307-19, xii. [Medline].

  20. Sena S, Kazimia S, et al. False positive phencyclidine results caused by venlafaxine. Am J Psychiatry. Feb 2007;164(2):349.

  21. Wills B, Erickson T. Drug- and toxin-associated seizures. Med Clin North Am. Nov 2005;89(6):1297-321. [Medline].

Further Reading

Keywords

phencyclidine toxicity, PCP, PCP overdose, phencyclidine overdose, angel dust, peace pill, crystal joint, supergrass, wack, rocket fuel, KJ, illy, elephant tranquilizer, embalming fluid

Contributor Information and Disclosures

Author

Patrick L West, MD, Clinical Instructor, Medical Toxicology Fellow, Department of Emergency Medicine, Oregon Health and Sciences University; Staff Physician, Department of Emergency Medicine, Portland Veterans Affairs Medical Center
Disclosure: Nothing to disclose.

Coauthor(s)

Nathanael J McKeown, DO, Assistant Professor, Oregon Health and Science University; Medical Toxicologist, Oregon Poison Center; Attending Physician, Emergency Medicine, Portland Veteran Affairs Medical Center, Oregon Health and Science University
Nathanael J McKeown, DO is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Lance W Kreplick, MD, MMM, FAAEM, FACEP, Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC
Lance W Kreplick, MD, MMM, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physician Executives
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Fred Harchelroad, MD, FACMT, Chair, Department of Emergency Medicine, Director of Medical Toxicology, Department of Emergency Medicine, Associate Professor, Allegheny General Hospital
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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