PCP Toxicity

Updated: Jan 23, 2021
Author: Stephan Brenner, MD, MPH; Chief Editor: Stephen L Thornton, MD 


Practice Essentials

Phenylcyclohexyl piperidine (PCP), also known as phencyclidine, was originally discovered in 1926; however, PCP was not introduced as a dissociative general anesthetic until the 1950s. Because of severe adverse effects, such as postoperative psychoses and dysphoria, its clinical use in humans was discontinued in 1965, although it remained widely used in veterinary medicine. Ketamine, a dissociative anesthetic commonly used in pediatrics, and MK-801/Dizocilpine, a potent N-methyl-D-aspartate (NMDA) receptor antagonist commonly used for research purposes, are structural analogues of PCP that possess varying degrees of adverse clinical effects.

PCP was first introduced as a street drug in the late 1960s; despite gaining a reputation as a drug that could cause unpleasant side effects, its use grew to epidemic proportions during the 1970s for its mind-altering effects. Many PCP users state that they have feelings of strength, power, and invulnerability while intoxicated with PCP. Some also report a numbing effect that may lead to anger, rage, selective amnesia of unpleasant memories, and acute psychoses. In 1978, PCP was transferred from Schedule III to Schedule II under the Federal Controlled Substance Act.

2-(2-chlorophenyl)-2-(methylamino)-cyclohexanone (Ketamine) is a tranquilizer, analgesic, and dissociative anesthetic commonly used in pediatrics and surgery for procedural sedations, as well as in veterinary medicine. It was developed by Parke-Davis in 1962 to replace PCP. The drug was initially introduced as a battlefield anesthetic for American soldiers during the Vietnam War and is still widely used in humans. Its beneficial effect is the “dissociation” of brain stem functions from higher brain areas, which alters the sensation of pain and other stimuli during medical procedures, and produces amnesia to the event. In addition, patients receiving ketamine maintain spontaneous breathing and relatively stable cardiovascular functions.

Since 1965, the recreational use of ketamine has increased and it became very popular during the 1990s among young adults at dance clubs and raves in combination with other so-called “club drugs” (eg, gamma-hydroxybutyric acid, lysergic acid diethylamide [LSD], ecstasy). Because of its increased illicit use in the United States, ketamine was placed in Schedule III as a non-narcotic controlled substance in 1999.[1, 2]

Drug forms

Because PCP is inexpensive and relatively easy to manufacture, it is often misrepresented as other hallucinogenic substances, such as LSD, tetrahydrocannabinol (THC), mescaline, psilocybin, cocaine, and amphetamine. PCP is distributed in widely varying purities and forms (eg, powder, liquid, tablets, leaf mixtures, rock crystal) (see image below).[3]

Phenylcyclohexyl piperidine (PCP), also known as p Phenylcyclohexyl piperidine (PCP), also known as phencyclidine, in tablet form. Image courtesy of the US Drug Enforcement Administration.

Many drug users are unknowingly exposed to PCP because it is often used as an adulterant in marijuana, LSD, and methamphetamine to save on production costs of those other drugs. PCP can be taken in pill form, snorted as a powder, smoked, or injected intravenously or subcutaneously. In certain forms, PCP can inadvertently be absorbed by means of contact with the skin.

PCP that is sold on the street is known by names such as angel dust, ozone, wack, rocket fuel, dust, elephant tranquilizer, hog, ethyl-phenylcyclohexylamine (PCE), thienyl-cyclohexylpiperidine (TCP), porker, zoot, embalming fluid, love boat, crystal, horse tranquilizer, tic-tac, peace pill, sherms, purple rain, zombie, worm, live ones, little ones, and boat. When PCP is added to marijuana, the combination is sometimes sold as crystal super grass, killer joints, super weed, killer weed, krystal joint (KJ), and green leaves. When PCP is dusted on marijuana or mint leaves and soaked in embalming fluid, the combination is known as illy, wet, hydro, or fry. The various street names for PCP reflect its unpredictable and volatile effects.

Ketamine sold on the street is known by terms such as super acid, “K”, “special k,” vitamin K, cat Valium, cat tranquilizer, horse tranquilizer, ket, kit-kat, vetamine, K wire, KFC, keezy, kenny, ketanest, kenfitamine, ketaset, ketalar, kez, kitty, kustard, regretamine, wibble, forgetamine, triple K, and wonky. Ketamine is odorless and tasteless and is available as a clear liquid, or a white/near-white crystalline powder. The liquid form is injected, mixed into drinks, or added to materials that can be smoked as with PCP. The powdered form is mostly snorted, compressed into pills, or used for intravenous or intramuscular injection when dissolved. Because of the induction of amnesia the drug has reportedly been used in sexual assaults referred to as “drug rape” or “date rape."[1]


Because PCP is relatively inexpensive to synthesize, it is an attractive drug for dealers. Its recipe can be found easily on the Internet, and it can be manufactured illegally in crude, underground laboratories. Most nonpharmaceutical PCP in the United States is manufactured in the Southern California area. Because of its continued use in veterinary medicine, pharmaceutical-grade formulations can be obtained through diversion.

Ketamine, unlike PCP, is relatively difficult to manufacture. For this reason, most illicit ketamine comes from diversion of pharmaceutical products destined for human or veterinary applications. According to reports from the US Drug Enforcement Administration (DEA), the major source of illegal ketamine in the United States is diverted from pharmacies in Mexico.


PCP is a 3-ringed molecule that is structurally similar to ketamine. However, PCP differs from ketamine in that it is longer acting, is more likely to cause seizures, and tends to cause more emergent confusion and delirium.

PCP is a noncompetitive antagonist at the glutamate NMDA receptor and binds to sites located in the cortex and limbic structures of the brain. This mechanism is believed to be responsible for most of the dissociative effects of PCP. PCP has been shown to effect biogenic amine (eg, dopamine, norepinephrine, serotonin) release and reuptake in a dose-dependent manner. These actions may account for the sympathomimetic effects after PCP ingestion. In addition, PCP may indirectly modulate cholinergic and GABAergic outflow in the CNS.

Ketamine’s molecular structure and mechanism of action are similar to those of PCP. It acts as a noncompetitive antagonist on the NMDA receptor. The drug's secondary interactions with muscarinic, nicotinic, and cholinergic receptors inhibit the neuronal uptake of norepinephrine, dopamine, and serotonin. At high doses, ketamine binds to mu and sigma opioid receptors, which are thought to be responsible for the loss of consciousness under controlled anesthesia.[2]


PCP is a weak base with a pKa of 8.6-9.4. In its nonionized or free base form, PCP is lipid soluble and easily diffuses across membranes. However, in an acidic environment, such as the stomach, PCP forms an ionized salt and becomes functionally trapped, preventing it from freely diffusing across the gastric mucosa. PCP that is absorbed from the alkaline duodenum can be secreted into the acidic stomach, creating a gastroenteric circulation. This phenomenon may explain the prolonged and wavering course of PCP intoxication.

PCP has a large volume of distribution (6.2 L/kg). Although the initial dose is distributed quickly in the brain, it is redistributed to other lipid-containing organs and can remobilize for hours, days, or possibly even weeks.[4] After entering the brain and reaching the acidic environment of the CSF, PCP becomes ionized. This ion trapping can produce levels of PCP in the CSF that are 6-9 times higher than those in plasma. PCP is predominantly metabolized in the liver to form glucuronide metabolites that are then excreted in the urine. A small amount of PCP is excreted unchanged in the urine.

Ketamine acts similarly to, but is less potent than PCP. The drug is highly bioavailable after intravenous or intramuscular injection with a volume of distribution of about 3-5 L/kg. Oral doses are less well absorbed and undergo extensive first-pass metabolism in the liver. The elimination phase lasts 45-60 minutes but can be as long as 4-6 hours in combination with other cerebral depressants. The half-life of ketamine is 10-15 minutes; however, 24-48 hours may be required before the user returns completely to baseline. Similar to PCP, ketamine is redistributed from the CNS and undergoes hepatic transformation by the cytochrome P450 system into its active metabolite norketamine. Norketamine has about one third of the anesthetic potency of ketamine with a half-life of 2.5 hours. Ketamine metabolites are mainly excreted in the urine.[2]


Epidemiologic data indicate that PCP abuse is not widespread and that its abuse is not prevalent in adolescents. The National Institute on Drug Abuse (NIDA) Monitoring the Future Study revealed that the overall use of PCP by high-school seniors has decreased since 1979, when 7% of seniors used PCP.[5] In 2018,1.1% of high-school seniors used PCP at least once during the year before the study.[6] PCP has retained the lowest lifetime prevalence and highest noncontinuation rates among high-school seniors compared with other hallucinogenic drugs (eg, LSD, ecstasy).

The 2019 Annual Report of the American Association of Poison Control Centers' National Poison Data System reported 130 single exposures of PCP, with 19 major outcomes and 1 death. In addition, 137 single exposures to ketamine with 19 major outcomes and 1 deaths were also reported. Of note, in children and adolescents age 19 and younger, 24 cases of PCP exposure and 29 cases of ketamine were reported.[7]

The Drug Abuse Warning Network (DAWN) estimated the number of PCP-related ED visits increased more than 400% between 2005 and 2011 (from 14,825 to 75,538 visits); between 2009 and 2011, the number of visits doubled (from 36,719 to 75,538). During that time, the largest increase in PCP-related ED visits was seen in patients 25 to 34 years old (from 5,556 to 34,329 visits). In 2011, 69% of patients making PCP-related ED visits were males, and 45% were 25 to 34 years old. Other illicit drugs, such as marijuana, cocaine, and heroin, were involved in 48% of PCP-related ED visits in 2011.[8]

The 2016 National Survey on Drug Use and Health (NSDUH) reported 18,000 individuals 12-17 years old used PCP in the past 12 months. An additional 15,000 18-25 year olds and 11,000 25-34 year olds reported usage during the same 12 month period.[9]   

The use of ketamine among high-school seniors has declined in recent years, and the 2006 prevalence in this group was 1.4%. Ketamine use tends to be more frequent among high-school seniors of lower socioeconomic status. From 1994-1999, ketamine-associated ED visits increased from 19 per year to 400 per year but have remained relatively unchanged since that point. Approximately 80% of ketamine-related ED visits involved consumption of multiple drugs in addition to ketamine, mostly other “club drugs,” or in combination with alcohol, marijuana, cocaine, and heroine. Ketamine use was found to be highest among males younger than 26 years.[5]

The 2014 National Survey on Drug Use and Health comparison of 12 month ketamine use during 2006-2014 and found that usage spiked in 2011 with 336,000 users and has steadily declined with 247,000 users in 2014. Male users outnumbered female users by approximately 2 to 1.[10]

According to the NIDA, in 2014, 1.5% of 12th graders reported using ketamine in the past year. This represented a significant decrease from the peak year of 2002, in which 2.6% reported past-year use.


The usual street dose of PCP is 1-6 mg and results in mild intoxication. Larger ingestions (6-10 mg) can cause toxic psychoses and signs of sympathetic hyperactivity, including hypertension, rigidity, hyperthermia, tachycardia, and seizure. Very large doses (≥ 200 mg) can result in death. Deaths from the direct effects of PCP intoxication are related to hyperthermia, renal failure, DIC, or rhabdomyolysis.

The major cause of death with PCP intoxication is behavioral disturbances that lead to self-destructive behaviors and impaired judgment, including self-inflicted injuries, injuries resulting from exceptional physical exertion, or injuries sustained from resisting physical restraints. Deaths from the direct effects of PCP intoxication are related to hyperthermia, renal failure, disseminated intravascular coagulation (DIC), and rhabdomyolysis. In a study of 1000 patients with phencyclidine intoxication, rhabdomyolysis occurred in 25 patients and 10 patients developed acute renal failure.[11, 12]

Despite reports of increased recreational use, only a few fatalities are attributed to ketamine poisoning alone or in combination with other drugs. Deaths related to ketamine abuse are mainly caused indirectly and related to falls, traffic injuries, drowning, and burns due to impaired perception, muscle weakness and ataxia. However, death through choking on vomit has been reported.[13]

Patient Education

For excellent patient education resources, see eMedicineHealth's patient education articles Club Drugs and Substance Abuse.





The dissociative effects of phenylcyclohexyl piperidine (PCP), also known as phencyclidine, cause patients to have disorganized thought processes, including delirium, amnesia, paranoia, and dysphoria. Therefore, obtaining a reliable history may not be possible. In addition, because PCP is frequently an adulterant, patients are unlikely to know that they have ingested PCP. The patient's friends and family should be questioned, if possible, to gain a greater understanding of the situation.


Diagnosis of PCP intoxication is generally made clinically. PCP exposure is suggested by the patient's fluctuating behavior, nystagmus, motor disturbances, and autonomic stimulation.

The presentation of patients with PCP intoxication widely varies from inebriated and calm to agitated and, in some cases, extremely violent. An important diagnostic clue is nystagmus (lateral, horizontal, or rotatory). A large case series demonstrated nystagmus in 57% of patients with PCP intoxication, although smaller studies have found an incidence of 85% or higher.[14] Many CNS depressants can produce nystagmus when taken in high doses; however, the patient is generally sedated when nystagmus is observed. In PCP exposure, the patient may have nystagmus when he or she is awake and agitated. Additional autonomic effects at low doses (less than 5 mg) include hypertension, tachycardia, tachypnea with shallow breathing, salivation, flushing, and diaphoresis.

Central and peripheral nervous system effects include generalized numbness of extremities, loss of muscular coordination, and mental status can vary from stimulation and euphoria to depression and coma, which occurs in a dose-related manner. At high doses (10 mg or more) blood pressure, heart rate and respirations may fall. This is often accompanied by nausea, vomiting, blurred vision, drooling, ataxia and dizziness.

Patients may demonstrate bizarre posturing or facial expressions. Motor disturbances include the following dystonic reactions:

  • Opisthotonos

  • Torticollis

  • Tortipelvis

  • Facial grimacing

  • Myoclonic movements

  • Tremor

  • Hyperactivity

  • Athetosis

  • Stereotypies

  • Catalepsy

Psychobehavioral features of PCP intoxication often mimic symptoms of schizophrenia and can include delusions, hallucinations, acute anxiety, paranoia, disorganized thinking, violence, and a sensation of distance from one’s environment.[15] Elevation of anxious symptoms is frequently experienced. Long-term abuse of PCP may produce memory loss, speech difficulties, depression, and weight loss. Addiction to and withdrawal from PCP can occur after chronic use and manifest as craving and compulsive PCP-seeking behavior.[16]

During acute presentations in the emergency department, PCP abusers may become violent or suicidal and should be seen as a danger to themselves and/or others. High doses of PCP can cause seizures, coma, hyperthermia and death (frequently related to unintentional injury or suicide while intoxicated). Coma is often related to substances like alcohol or benzodiazepines that can enhance the sedative effects of PCP.[17]

The evaluation of PCP-intoxicated patients with actual or suspected trauma may be challenging because of the dissociative anesthetic effects that can mask signs and symptoms (eg, abdominal pain or those associated with hidden injuries). Like ketamine, PCP is thought to prevent the integration of sensory input to create meaningful responses. Because of the analgesic effects of PCP and lack of normal pain response, PCP-intoxicated patients have sometimes been described as having extraordinary strength. PCP-intoxicated patients have broken handcuffs and fractured bones in the process.

Children may inhale PCP fumes in their environments, or they may ingest or have topical exposure to PCP in their surroundings. Most parents who accompany their children for treatment of PCP exposure deny the possibility of their child's drug intoxication. Children exposed to PCP typically have symptoms similar to those of adults and can exhibit diminished response to tactile and verbal stimuli, bizarre behavior, ataxia, nystagmus, expressionless stare, dystonic posturing, irritability, poor feeding, seizures, and possibly miosis and hypertension.[18]

Incidences of hallmark findings in 1000 patients with PCP intoxication are as follows:[11]

  • Nystagmus - 57.4%

  • Hypertension - 57%

Incidences of sensorium findings in 1000 patients with PCP intoxication are as follows:

  • Alert and oriented - 45.9%

  • Acute brain syndrome - 36.9%

  • Unconsciousness - 10.6%

  • Lethargy, stupor, or both - 6.6%

Incidences of behavioral findings in 1000 patients with PCP intoxication are as follows:

  • Violence - 35.4%

  • Agitation - 34%

  • Bizarreness - 28.8%

  • Hallucinations, delusions, or both - 18.5%

  • Muteness and stare - 11.7%

  • Nudism - 3.3%

  • None - 3.5%

Incidences of motor findings in 1000 patients with PCP intoxication are as follows:

  • Generalized rigidity - 5.2%

  • Grand mal seizures - 3.1%

  • Localized dystonias - 2.4%

  • Facial grimacing - 1.7%

  • Athetosis - 1.3%

Incidences of cholinergic findings in 1000 patients with PCP intoxication are as follows:

  • Diaphoresis - 3.9%

  • Bronchospasm - 2.1%

  • Pupils smaller than 1 mm - 2.1%

  • Hypersalivation - 1.7%

  • Bronchorrhea - 0.6%

Incidences of anticholinergic findings in 1000 patients with PCP intoxication are as follows:

  • Pupils larger than 4 mm - 6.2%

  • Urinary retention - 2.4%

Incidences of abnormal vital signs in 1000 patients with PCP intoxication are as follows:

  • Tachycardia - 30%

  • Hypothermia - 6.4%

  • Apnea - 2.8%

  • Hyperthermia - 2.6%

  • Cardiac arrest - 0.3%

  • Hypotension - 1.6%


Ketamine produces physical effects similar to PCP; however, symptoms are often of shorter duration. The hallmark of ketamine is its dissociative effect. Ketamine-provoked sensations are dose-related and range from a pleasant feeling of floating in a colorful “wonder world” (“K-land”) to the terrifying feeling of complete sensory detachment similar to a near-death or out of body experiences (“K-hole”).[19]

Other symptoms that can occur with ketamine intoxication include the following:[1]

  • Increased intracranial and intraocular pressures, decreased seizure threshold, dizziness

  • Neuromuscular disturbances, including muscle rigidity, slurred speech, blank stare, loss of coordination, numbness, polyneuropathy, diplopia, and nystagmus

  • Effects on the autonomic nervous system at low doses (eg, bronchodilation, hypersalivation, hyperthermia, elevated blood pressure and heart rate); respiratory and cardiac arrest (at high doses)

  • Psychobehavioral symptoms (eg, sense of invulnerability/exaggerated strength, aggressive/violent behavior, hallucinations, delirium, amnesia, depression, long-term memory loss, cognitive deficits); tolerance and dependence (with chronic use)





Laboratory Studies

In general, routine laboratory workup in patients who present with toxicity involving phenylcyclohexyl piperidine (PCP), also known as phencyclidine, should be focused on the following:

  • Renal function

  • Fluid balance

  • Electrolyte abnormalities

  • Hypoglycemia

  • Lactic acidosis

  • Serum creatine phosphokinase (CPK) level

  • Urine myoglobin level

Quantitative laboratory analysis is generally not very helpful because serum and urine levels do not reflect the drug's vast lipid storage, nor does the precise serum concentration correlate with the clinical effect. Results of toxicologic urine screening may remain positive for several weeks because of PCP's large volume of distribution.

Qualitative plasma or urine levels may help establishing the diagnosis but should be interpreted with care. Urine screening for PCP should be part of the diagnostic workup in children and infants presenting with acute dystonic reactions.[20]

Ketamine levels, as well as norketamine levels, can be determined in urine; however, these specific tests are generally not readily available and are not clinically useful. PCP may cross-react with ketamine assays.

Diphenhydramine and dextromethorphan (which are also frequently abused N-methyl-D-aspartate [NMDA] receptor antagonists) can produce false-positive urine drug screens for PCP because of their similar chemical structures.

Other useful tests to determine the presence of rhabdomyolysis, renal dysfunction, and hypoglycemia include measurements of electrolytes, glucose, BUN, creatinine, and total creatine kinase levels, as well as a urinalysis (myoglobin). An arterial blood gas (ABG measurement may be indicated to assess the occurrence of metabolic acidosis and hypoxemia. A urine pregnancy test is indicated in female patients of childbearing age.



Medical Care

Medical management of intoxication with phenylcyclohexyl piperidine (PCP), also known as phencyclidine, is primarily supportive and encompasses treatment of agitated behavior, seizures, and hyperthermia. Therefore, close monitoring of vital signs including temperature is required. If delirium is severe and compromises patient or staff safety, deep sedation with endotracheal intubation may be necessary.

The American Academy of Child and Adolescent Psychiatry (AACAP) has established a practice parameter guideline for the assessment and treatment of children and adolescents with substance use disorders.[21]

Patients with recent oral use of PCP are candidates for GI decontamination. Activated charcoal (1 g/kg) may be administered and repeated every 4 hours for several doses in most symptomatic patients. Activated charcoal adsorbs PCP and increases its nonrenal clearance.[22] Because mental status can abruptly change, ipecac syrup and GI lavage are not recommended for GI decontamination.

Because PCP is a weak base, treatment in the past included acidification of the patient's urine to increase the drug's urinary excretion. This therapy is no longer recommended because severely intoxicated patients are at risk for acidosis and rhabdomyolysis and because the acidification of urine promotes the precipitation of myoglobin within the renal parenchyma. Furthermore, urinary acidification has never been proven to decrease morbidity or mortality. Because of its large volume of distribution, PCP is not effectively removed with hemodialysis or hemoperfusion.

Patients intoxicated with PCP have been known to demonstrate violent behavior, and they can often present a danger to the clinical staff. The most important approach to management of agitated behavior is the implementation of safe physical restraints and chemical sedation. Benzodiazepines are usually effective in managing aggressive behavior.

Anxiety and agitation can be managed by decreasing external stimuli such as noise, light, and touch. Benzodiazepines are the first means in anxiety treatment, and large doses may be required in severely agitated patients. Benzodiazepines also reduce the occurrence of vivid dreams.

Phenothiazines and butyrophenones should be avoided because they may cause significant hypotension, worsen hyperthermia, exacerbate any anticholinergic effect, may induce dysrhythmias, lower the seizure threshold, and cause dystonic reactions. Acute dystonic reactions can be controlled with diphenhydramine.

Seizure activity is seen in approximately 3% of patients presenting with PCP intoxication. Seizures should be treated with benzodiazepines, followed by barbiturates, propofol, or both.

In some patients severe hypertension with end-organ effects may persist even after the use of benzodiazepines. Phentolamine or nitroprusside are the agents of choice in such cases in order to achieve adequate blood pressure control.

Management of hyperthermia should include aggressive mechanical cooling. In profoundly hyperthermic (> 40.5°C) patients, rapid sequence induction with endotracheal intubation and paralysis should be considered if no response to more conservative measures is noted.

Rhabdomyolysis requires adequate hydration with normal saline in order to maintain a urine output of 2-3 mL/kg/h, as well as close monitoring of creatine phosphokinase (CPK) levels.

Admit the patient who has ingested phenylcyclohexyl piperidine (PCP), also known as phencyclidine, to an ICU if evidence of hyperthermia, seizure activity, or rhabdomyolysis is present.


A medical toxicologist or the staff at a regional poison control center may provide additional information about PCP intoxication and about current patient care recommendations.

Long-Term Monitoring

Refer the patient for drug rehabilitation.

Because of its long-lasting side effect of inducing or unmasking psychopathologic symptoms, continued outpatient therapy including prolonged use of tranquilizers may be necessary for patients after PCP intoxication.[23]



Medication Summary

No proven antidotes for phenylcyclohexyl piperidine (PCP), also known as phencyclidine, toxicity are known. Pharmacologic therapy facilitates supportive care and seizure control with special attention to respiratory and cardiac function.

Sedative/hypnotic and anticonvulsant agents

Class Summary

Benzodiazepines are first-line agents for controlling seizures in patients with PCP toxicity. Barbiturates, propofol, or both provide a useful adjunct in the treatment of seizures or treatment of status epilepticus unresponsive to benzodiazepines. All of these agents are helpful in sedating patients with extreme agitation.

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Although seizures may be promptly controlled, seizure activity resumes in a significant proportion of patients, presumably because of the short duration of action with an initial dose of IV diazepam. Rapidly distributes to other body fat stores. Twenty minutes after initial IV infusion, serum concentration drops to 20% of Cmax.

Lorazepam (Ativan)

By increasing the action of GABA, (major inhibitory neurotransmitter in the brain), may depress all levels of CNS, including limbic and reticular formation

Pentobarbital (Nembutal)

Short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties; can produce all levels of CNS mood alteration.

Propofol (Diprivan)

Phenolic compound that is a sedative hypnotic agent used for induction and maintenance of anesthesia or sedation. Has also been shown to have anticonvulsant properties.

Decontamination agents

Class Summary

Consider activated charcoal decontamination in patients with oral PCP overdose who present within 4 hours of ingestion.

Activated charcoal (Actidose-Aqua, Liqui-Char)

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.


Class Summary

These are used for treatment for acute ketamine-induced dystonia.

Diphenhydramine (Benadryl)

First-generation antihistamine with anticholinergic effects that binds to H1 receptors in the CNS and the body.

Competitively blocks histamine from binding to H1 receptors. Has significant antimuscarinic activity and penetrates CNS, which causes pronounced tendency to induce sedation. Approximately half of those treated with conventional doses experience some degree of somnolence. A small percentage of children paradoxically respond to diphenhydramine with agitation.

DOC for initial treatment of acute dystonia or akathisia not caused by antihistamines. Use diazepam for treatment of acute dystonia secondary to antihistamines.

Antihypertensive agents

Class Summary

Recommended treatment agents for PCP-induced malignant hypertension with end-organ damage, if blood pressure control continues to be inadequate after agitation treatment.

Nitroprusside (Nitropress)

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

Phentolamine (OraVerse, Regitine)

Alpha-1 and alpha-2 adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension that results from catecholamine effects on the alpha receptors.