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Phencyclidine Toxicity

  • Author: Patrick L West, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Apr 20, 2015
 

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.[1] PCP is often taken in conjunction with other co-ingestants, including ethanol and marijuana.

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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.[2] The half-life of PCP is estimated at 17.4 hours; however, half-lives of 1-4 days have been reported.[3] PCP is primarily metabolized in the liver.

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Epidemiology

Frequency

United States

The Drug Abuse Warning Network (DAWN) estimates that PCP-related emergency department (ED) visits increased more than 400% from 2005 to 2011 (from 14,825 to 75,538 visits). PCP-related ED visits doubled from 2009 to 2011. DAWN estimates from selected metropolitan areas show geographic variation in trends, with PCP-related ED visits increasing in some areas (New York City, Chicago) while remaining stable in others (Seattle, San Francisco, Phoenix).[4]

Of PCP-related ED visits in 2011, 72% involved PCP combined with other drugs; in about half, PCP was combined with illicit drugs (32% involved marijuana and 20% involved cocaine), and in about a quarter PCP was combined with pharmaceutical agents such as pain relievers (16%) and anti-anxiety and insomnia drugs (13%).

The 2013 National Survey on Drug Use and Health, polling persons 12 years of age and older, found a lifetime prevalence of 2.5% of the population trying PCP. In the past year, 90,000 people had tried PCP—a decrease from 172,000 in 2012. The number of persons who used PCP for the first time in the past year decreased from 123,000 in 2002 to 32,000 in 2013.[5]

The 2012 Monitoring the Future Survey of high school seniors showed 1.6% using PCP once in their lifetime (down from 2.13% in 2011), 0.9% had used PCP at least once in the last year, and 0.5% had used PCP at least once in the last 30 days.[6]

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 American Association of Poison Control Centers reported 16 major outcomes and two deaths from PCP in 2012.[7]

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

Chronic PCP toxicity results in cognitive deficits and mood disorders. Patients can develop speech impediments and also suffer from dysphoria, depression, anxiety, and psychosis.[8]

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Sex- and Age-related Demographics

DAWN estimates that in 2011, 69% of PCP-related ED visits were made by males. Approximately 45% were made by persons aged 25 to 34 years. Persons aged 18 to 24 years accounted for 19% of visits, as did those aged 35 to 44.[4]

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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)

Robert S Helman, MD Director, Premier Care of Great Neck Urgent Care Center

Disclosure: Nothing to disclose.

Nathanael J McKeown, DO Assistant Professor, Department of Emergency Medicine, Oregon Health and Science University School of Medicine; Medical Toxicologist, Oregon Poison Center; Attending Physician, Emergency Medicine, Portland Veteran Affairs Medical Center

Nathanael J McKeown, DO is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Fred Harchelroad, MD, FACMT, FAAEM, FACEP Attending Physician in Emergency Medicine, Excela Health System

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Lance W Kreplick, MD, FAAEM, MMM 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, FAAEM, MMM is a member of the following medical societies: American Academy of Emergency Medicine, American Association for Physician Leadership

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Nicole S Johnson, MD, and Mark A Silverberg, MD, to the development and writing of this article.

References
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