Recreational drugs are substances used for nonmedical purposes to enhance one’s personal experience or enjoyment. A wide range of substances are available and this chapter focuses on well-known drugs including phencyclidine, ketamine, and cocaine as well as newer “designer drugs” including synthetic marijuana and cathinone products. Other recreational drugs that are often abused in the pediatric population but are beyond the scope of this chapter include solvents, hallucinogenic mushrooms, lysergic acid diethylamide (LSD), ecstasy, and dextromethorphan.

Phencyclidine (PCP) first came to the market as a surgical anesthetic and sedative in the 1950s as Sernyl by Parke Davis Pharmaceutical Company. However, it was removed from the market due to adverse side effects such as hallucinations. In the late 1960s, PCP made its return to commercial use as a veterinary tranquilizer. It was first reported as an illicit drug used for recreational purposes in San Francisco, where it was called the “Peace Pill.” The Controlled Substance Analogue Enforcement Act of 1986 made PCP and its derivatives illegal. The drug has various street names such as “angel dust,” “hog,” “horse tranquilizer,” “crystal joint,” and “illy.”¹ Marijuana cigarettes (“joints”) can be dipped in a liquid form of PCP colloquially known as “wet,” “embalming fluid,” or “formaldehyde.”^2,3

Ketamine is a legal analogue of PCP used in humans for sedation and anesthesia. Ketamine is also a drug of abuse. Adolescents often use it at raves and nightclubs for the hallucinatory, out-of-body experiences it provides. It has various street names such as “Special K,” “K,” “KitKat,” and “Vitamin K.” It has a relatively short duration of action of 15 to 45 minutes, and is one-tenth as potent as PCP. Because of its abuse potential, ketamine is in the Controlled Substance Act of 1999. There have been reports of a newer designer drugs and ketamine analogues, such as methoxetamine. It is likely that additional ketamine and PCP analogues will be developed as further “legal” highs are sought.⁴

PHARMACOLOGY AND PATHOPHYSIOLOGY

Phencyclidine is classically categorized as a dissociative anesthetic because when anesthetized, the patient is conscious yet experiences a feeling of dissociation from themselves—the “out-of-body” experience. After ingestion, PCP absorption occurs in the upper intestine. The drug has an enterogastric circulation; it is secreted by the stomach and then absorbed in the small intestine. Because the drug recirculates in this way, it produces cyclical effects.⁵ It interacts at many receptor sites, but its primary mechanism of action is N-methyl-d-aspartic acid (NMDA)-type glutamate receptor antagonism.

The therapeutic doses of ketamine for endotracheal intubation and procedural sedation are 1 to 2 mg/kg IV over 1 minute and 1 mg/kg IV, respectively. The onset of action is rapid; the dissociative state is achieved within seconds.⁶

CLINICAL FINDINGS

The clinical presentation in the emergency department (ED) after PCP use depends on the dose, route of administration, concomitant drug use, and the patient’s susceptibility to the drug. Typically, abnormal vital signs and psychomotor abnormalities are present. Mild hypertension, tachycardia, and hyperthermia can all be present. Respiratory drive is not compromised and hypoventilation is rare unless extremely high doses are used, or with concomitant ingestion of a sedative. Laryngeal and pharyngeal reflex hyperactivity in children has been documented.⁷ Horizontal, vertical, and rotary nystagmus can be present with PCP toxicity. Pupils may be miotic or mydriatic, but react to light. A fluctuating level of consciousness is typical of PCP intoxication. Patients may exhibit remarkable strength, and completely disregard lacerations, fractures, or other traumatic injuries.⁸

Ketamine has a similar clinical presentation, and is commonly used as a dissociative anesthetic for procedural sedation. Ketamine allows for the respiratory drive to remain intact, and hypoventilation is uncommon.⁹ Depression of cough reflex can occur, and this coupled with ketamine’s potential to increase secretions has been reported to obstruct the airway. Rare cases of respiratory depression and apnea have been associated with rapid infusion. Infusing ketamine over 1 to 2 minutes decreases this risk.¹⁰ Laryngospasm is a rare complication with dissociative dosing for sedation, with an incidence of ~0.3%.⁶

DIAGNOSIS AND LABORATORY STUDIES

Phencyclidine toxicity is diagnosed clinically. Diagnostic testing is required only in cases where child abuse or foul play is suspected. Qualitative tests are available as a part of the urine toxicology screen. In an acute PCP exposure, urinary metabolites are present for 8 days.¹¹ Useful laboratory studies include blood urea nitrogen and creatinine to assess renal function and creatine phosphokinase, and myoglobin to screen for rhabdomyolysis. The white blood cell count is frequently elevated. Blood glucose should be obtained to exclude hypoglycemia.⁵

Ketamine may cross-react with PCP on urine immunoassay.¹¹ Other drugs that can cause a false positive result are dextromethorphan, diphenhydramine, doxylamine, ibuprofen, imipramine, meperidine, mesoridazine, metamizol, methyphenidate, thioridazine, tramadol, and venlafaxine.^11–13

MANAGEMENT

Management of the patient’s airway, circulation, and thermoregulation are of utmost importance. Potential airway threats caused by PCP or ketamine toxicity include increased salivation, increased tracheobronchial tree secretions, and laryngospasm. Emergence reactions and agitation have been reported and can be treated with benzodiazepines. Vomiting is a common reaction in early adolescents in doses associated with dissociation.¹⁴

The risks of activated charcoal are usually greater than the potential benefits because of the risk of aspiration in an agitated or somnolent patient.

Urinary acidification to enhance renal elimination is not recommended. The benefit of the minor increase in renal clearance of PCP from ion trapping of the weak base is far outweighed by the potential harm created by systemic acidemia. Adequate hydration, supportive care, and symptomatic treatment are the mainstays of therapy.¹⁵

DISPOSITION

Monitoring in the ED or the intensive care unit (ICU) is appropriate for the patient experiencing adverse reactions to PCP or ketamine until the signs and symptoms resolve. Supportive care is the recommended therapy. Patients with recreational exposures should be discharged with follow-up that includes referral for drug counseling.

Cocaine abuse and toxicity continue to be pervasive problems.¹⁶ Adolescents and adults predominantly use cocaine as a recreational drug. Children suffer toxicity when exposed to cocaine being used by others.¹⁷ Seizures have been reported in children who accidentally ingest cocaine and in infants exposed via breast milk.^18,19 Toxicity has occurred in toddlers who inhaled cocaine being “freebased” by nearby adults.¹⁷ Cocaine, multiple-drug ingestions, and tricyclic antidepressants are among the most prominent causes of cardiac arrest for patients younger than 40 years.²⁰

According to data obtained by the Drug Abuse Warning Network (DAWN) in 2011, there were a total of 2.5 million ED visits related to drug abuse or misuse. Of these, 505,224 involved cocaine. In children aged 12 to 17, there were 5904 ED visits.²¹ In one study, 2.4% of children in a group of inner city preschoolers tested positive for the cocaine metabolite benzoylecgonine in their urine.²²

PHARMACOLOGY AND PATHOPHYSIOLOGY

Cocaine is benzoylmethylecgonine, a naturally occurring local anesthetic. It is derived from the plant Erythroxylum coca and is rapidly absorbed from mucous membranes, lung tissue, and the gastrointestinal tract. It is a sympathomimetic that blocks fast sodium channels. The primary target organs are the central nervous system (CNS), cardiovascular system, lungs, gastrointestinal tract, skin, and thermoregulatory center.

CLINICAL FINDINGS

Clinically, cocaine causes CNS stimulation that can result in agitation, hallucinations, abnormal movements, and convulsions.¹⁹ Paradoxically, children may present with lethargy. Both ischemic and hemorrhagic strokes have been reported.²³