eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Phencyclidine: Treatment & Medication

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

Treatment

Prehospital Care

  • Evaluate and stabilize the patient's airway, breathing, and circulation (ABCs) including cervical spine immobilization if traumatic injury is suspected.
  • Physical restraints may be required to prevent self-injury and to protect the medical staff. These patients should be monitored closely due to several death reports of PCP-intoxicated patients while being physically restrained.
  • Chemical restraints may also be used. Establish intravenous access and administer benzodiazepines for patients with severe agitation. Intramuscular benzodiazepines are an alternative if intravenous access is unobtainable.

Emergency Department Care

  • After addressing and stabilizing the ABCs, treatment of PCP intoxication starts with initial supportive measures (IV, O2, cardiac monitor). ECG may be indicated to assess for dysrhythmias.
  • Obtain a fingerstick to rule out hypoglycemia.
  • Place patients in a dark, quiet room under continuous observation to minimize environmental stimuli.
  • Consider activated charcoal for oral ingestions and co-ingestions. Multiple doses of charcoal may be beneficial in the case of large overdose. Only one dose of sorbitol should be given, usually with the initial dose. Clinicians should be aware that inappropriate administration of activated charcoal can convert relatively benign exposure (eg, mild PCP intoxication) into a very serious condition (eg, aspiration pneumonia).
  • Extreme violent psychotic behavior requires sedation with parenteral benzodiazepines. Seizures should be treated with benzodiazepines.
  • Haldol (haloperidol) should be reserved for patients with mild, predominately psychotic symptoms, with normal vital signs. 
  • Butyrophenones (haloperidol, droperidol) and phenothiazines (eg, chlorpromazine) should be avoided in moderate and severe intoxications because they can lower seizure threshold, cause dystonic reactions, induce hypotension, and worsen anticholinergic symptoms, including hyperthermia.
  • Hyperthermia may be treated by conventional cooling methods.
  • Rhabdomyolysis is treated with intravenous hydration, urine alkalinization, and osmotic/diuretic agents. Possible caveat: There is a theoretical, but clinically unproven, concept of increased PCP reabsorption secondary to the urine alkalinization.
  • For hypertensive emergencies, try to control agitation first with parenteral benzodiazepines. For persistent hypertension, intravenous nitroprusside is the agent of choice. Because of the theoretical concept of unopposed alpha effect (worsening of hypertension) and the availability of other antihypertensive agents (eg, calcium-channel blockers, intravenous nitroglycerin), pure beta-blockade should be avoided. Even labetalol, which has both alpha- (weak) and beta-blocking abilities, can be given only after alpha-blockade with phentolamine is achieved.
  • New research is focused on the development of antibodies to neutralize the toxic effects of PCP.
  • Acute PCP toxicity can usually be managed conservatively with an observation period of a few hours. More serious ingestions may require admission to an intensive care unit for days to weeks.

Consultations

Consult with a board-certified medical toxicologist or a local poison control center for further recommendations.

Medication

The goals of pharmacotherapy are to relieve the toxic effects of PCP, reduce morbidity, and prevent complications.

GI decontaminant

These agents prevent further absorption of adsorbable toxins from the GI tract. They are most beneficial if administered within 1-2 h of ingestion.


Activated charcoal (Liqui-Char)

Because PCP undergoes enterohepatic recirculation, may be indicted if clinically feasible. Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.

Adult

1 g/kg PO/NG (30-100 g usual dose) typically as a mixture with 70% sorbitol or similar cathartic; may administer 0.5 g/kg PO/NG as repeat dose if desired

Pediatric

<2 years: 1 g/kg PO/NG (15-30 g usual dose); may administer 0.5 g/kg PO/NG as repeat dose prn; coadministration with cathartic not recommended
>2 years: Administer as in adults

May inactivate syrup of ipecac if used concomitantly; effectiveness of other medications decrease with coadministration; do not mix charcoal with sherbet, milk, or ice cream (decreases absorptive properties of activated charcoal)

Documented hypersensitivity; poisoning or overdose of mineral acids and alkalies; unprotected airway with absent gag reflex

Pregnancy
Precautions

Protect airway to reduce risk of aspiration; not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before administration; after emesis with ipecac, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black; if comatose, administer via nasogastric tube

Benzodiazepines

Indications include agitation, violent behavior, psychosis, seizures, and muscular rigidity.


Diazepam (Valium)

Enhances GABA transmission. Appears to act on part of the limbic system, the thalamus and hypothalamus, to induce a calming effect. Rapidly distributes to other body fat stores. Twenty minutes after initial IV infusion, serum concentration drops to 20% of Cmax.
Individualize dosage and increase cautiously to avoid adverse effects.

Adult

5-10 mg IV; repeat q5-10min prn; IM/PR may be used if IV not available

Pediatric

30 days to 5 years: 0.2-0.5 mg IV (slowly) q2-5min prn; not to exceed 5 mg
>5 years: 1 mg IV (slowly) q2-5min prn; not to exceed 10 mg

Phenothiazines, barbiturates, alcohols, and MAO inhibitors increase CNS toxicity when administered concurrently

Documented hypersensitivity; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity); monitor for respiratory depression and propylene glycol toxicity with high or repeated doses


Lorazepam (Ativan)

Short-acting anxiolytic with relatively long half-life.
Increases transmission of GABA, a major inhibitory neurotransmitter in the brain.
May be used IV and is well absorbed after IM injection. Onset of action occurs within min of an injection, and effects peak 15-20 min after injection. Duration of action is 6-8 h. No active metabolites exist.

Adult

1-4 mg IV/IM; may repeat q15min prn; not to exceed 8 mg
Status epilepticus: 0.05-0.1 mg/kg IV over 2-5 min; may repeat in 10-15 min prn; not to exceed 8 mg/dose

Pediatric

0.05-0.1 mg/kg IV slowly over 2-5 min, maximum 4 mg/dose

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAO inhibitors

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease; monitor for respiratory depression and/or propylene glycol toxicity with high or repeated doses


Midazolam (Versed)

Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.

Adult

0.01-0.05 mg/kg (usually 0.5-4 mg, not to exceed 10 mg) IV slowly over several min; may repeat q10-15min prn

Pediatric

<32 weeks: 0.5 mcg/kg/min IV infusion
>32 weeks: 1 mcg/kg/min IV infusion
Children: 0.05-0.2 mg/kg IV over 2-3 min, followed by 1-2 mcg/kg/min continuous infusion
Status epilepticus (refractory to standard therapy), >2 months and children: 0.15 mg/kg followed by continuous infusion of 1 mcg/kg/min, titrate upward q5min prn

Sedative effects of midazolam may be antagonized by theophyllines; narcotics and erythromycin may accentuate sedative effects of midazolam due to decreased clearance

Documented hypersensitivity; preexisting hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, pulmonary disease, renal impairment, and hepatic failure; monitor for respiratory depression with high or repeated doses

Antihypertensives

These agents are used for blood pressure control in hypertensive crises to minimize end-organ damage.


Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing the heart rate.

Adult

Begin infusion at 0.3-0.5 mcg/kg/min IV and use increments of 0.5 mcg/kg/min; titrate to desired effect; average dose is 1-6 mcg/kg/min
Infusion rates >10 mcg/kg/min may lead to cyanide toxicity

Pediatric

Administer as in adults

Effects are additive when administered with other hypotensive agents

Documented hypersensitivity; subaortic stenosis; decreased cerebral perfusion; arteriovenous shunt or coarctation of aorta (eg, compensatory hypertension); atrial fibrillation or flutter

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity at high infusion rates and when used in combination with a diuretic; sodium nitroprusside has ability to lower blood pressure and thus should be used only in patients with mean arterial pressures >70 mm Hg

Neuroleptics

These agents are used for acute psychosis when no contraindications are present.


Haloperidol (Haldol)

Butyrophenone noted for high potency and low potential for causing orthostasis. Downside is high potential for EPS and dystonia. Lowers seizure threshold and worsens anticholinergic symptoms, including hyperthermia. Should be reserved only for mild PCP intoxications with predominantly psychotic features and normal vital signs.
Parenteral dosage form may be admixed with 2 mg lorazepam for better anxiolytic effects.

Adult

0.5-5 mg IV (unlabeled use), may be repeated q30min
2-5 mg IM q1-8h; not to exceed 100 mg/d

Pediatric

<3 years: Not established
3-12 years: 0.5 mg IV/IM
>12 years: Administer as in adults

May increase tricyclic antidepressant serum concentrations and hypotensive action of antihypertensive agents; phenobarbital or carbamazepine may decrease effects of haloperidol; haloperidol coadministration with anticholinergics may increase intraocular pressure; encephalopathylike syndrome associated with concurrent administration of lithium and haloperidol

Documented hypersensitivity; narrow-angle glaucoma; bone marrow suppression; severe cardiac or liver disease; severe hypotension; hyperthermia; seizures

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Severe neurotoxicity manifesting as rigidity or inability to walk or talk may occur in patients with thyrotoxicosis also receiving antipsychotics; if IV/IM, watch for hypotension; caution in those with CNS depression, subcortical brain damage, or cardiac disease; if history of seizures, benefits must outweigh risks; significant increase in body temperature may indicate intolerance to antipsychotics (discontinue if this occurs)

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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