Pharmacology of Spice
Synthetic cannabinoids began emerging in 1965 in an effort to capture the cannabinimetic activity of tetrahydrocannabinol (THC), with three well-known synthetic cannabinoid medications evolving from the research: dronabinol (Marinol), a synthetically pure THC used for pain and as an antiemetic; nabilone (Cesamet), a synthetic cannabinoid used for treatment of anorexia and nausea; and rimonabant (Acomplia), a selective CB1 receptor antagonist that was used to treat obesity but has been withdrawn because of severe adverse effects (UNODC, 2011). Synthetic cannabinoids bind to one of the cannabinoid receptors (i.e., CB1 or CB2). CB1 is found in the central nervous system (CNS) and is responsible for the physiological and psychotropic effects of cannabis or THC, whereas CB2 is found in the CNS and the cells of the immune system, particularly the leukocytes (Johnson et al., 2011; UNODC, 2011). Four major currently identified synthetic cannabinoid groups may be found in Spice, based on their chemical structure. The JWH group of compounds has a greater affinity to the cannabinoid receptors than does THC, with JWH-018 having four times the affinity for the CB1 receptor and 10 times the affinity for the CB2 receptor than does THC (Loeffler et al., 2012). The CP group of cannabinoid receptor agonists has greater affinity for CB1 and is 28 times more potent than THC (Loeffler et al., 2012). The HU compounds bind to the CB1 and the CB2 receptors and are 100 to 800 times more potent than THC (Loeffler et al., 2012). The fourth group, the benzoylindoles, are the most recent compounds to be found in Spice and have not been investigated to understand their pharmacology (Loeffler et al., 2012; UNODC, 2011). The U.S. Drug Enforcement Administration (DEA) has placed JWH-018, JWH-073, HU-210, and CP 47 and 497 as Schedule I under the Controlled Substances Act (U.S. Department of Justice [DOJ] DEA, 2012a).
Spice is usually smoked via a joint or water pipe, and quick absorption of synthetic cannabinoids occurs via the lungs, with onset of action occurring within minutes (UNODC, 2011). The synthetic compounds are lipophilic and thus are distributed into the brain and fat tissues. The active ingredients in Spice appear to be metabolized in the liver and excreted in the urine and feces (UNODC, 2011). Synthetic cannabinoids may not be detected on a routine urine drug test (Loeffler et al., 2012).
Spice users report effects similar to marijuana: elevated mood, relaxation, and altered perception (NIDA, 2012b). Onset of impaired cognition and changes in perception and mood occur within 10 minutes of inhaling (Johnson et al., 2011). Other symptoms include scleral injection, tachycardia, xerostomia, and increased appetite, and symptoms last up to 6 hours (Johnson et al., 2011). Uncomfortable symptoms of nausea and vomiting may occur (the severity of which may clinically differentiate Spice from marijuana use).
From January 1, 2012, to October 31, 2012, 4,710 calls were placed to poison centers in the United States about exposures to synthetic marijuana, mostly because patients were exhibiting symptoms that may be life-threatening (AAPCC, 2012). Poison centers report symptoms that include severe agitation and anxiety, muscle spasms, seizures and tremors, intense hallucinations and psychotic episodes, and suicidal thoughts and actions (AAPCC, 2012). Severe tachycardia and hypertension have been reported, as well as fever, hyperglycemia, hypokalemia, chest pain, and acidosis (Loeffler et al., 2012). In a 6-month period in 2012, six cases of acute kidney failure were identified in patients (all male, with a median age of 18 years) residing in Oregon and Southwest Washington who had smoked Spice (Oregon Public Health Division [OPHD], 2012a). All six had onset of symptoms within hours of smoking "Spice" and presented with severe nausea, vomiting, back pain, and hypertension, with creatinine elevation to greater than 8 mg/dl in less than 24 hours (OPHD, 2012a). A published case series of 10 cases of patients ages 21 to 25 years who were admitted to an inpatient psychiatric ward with psychosis after using synthetic cannabinoids found that the psychotic symptoms lasted 5 to 8 days in seven of the patients, and three patients continued to have psychotic symptoms 5 months after initial presentation (Hurst, Loeffler, & McLay, 2011). These case study findings suggest that synthetic cannabinoids may trigger acute psychosis, worsen chronic psychotic disorders, and possibly trigger chronic primary psychotic disorders in predisposed patients (Loeffler et al., 2012). Providers should suspect Spice intoxication in any patient without a known psychiatric history who presents with bizarre behavior, especially anxiety, agitation, and psychosis (Jerry, Collins, & Streem, 2012).
Once synthetic cannabinoid toxicity is suspected, treatment is aimed at the presenting symptoms (Table 1). Benzodiazepine (lorazepam) is most commonly used to treat both agitation and seizures (Jerry et al., 2012). Routine laboratory tests include a complete blood cell count, complete metabolic panel, serial cardiac enzymes if chest pain is present, and urine toxicology (Jerry et al., 2012). If the patient is having severe muscle spasms or ongoing seizure activity, creatine phosphokinase (CPK) and myoglobin levels also may need to be a consideration in the face of potential rhabdomyolysis. If the patient is seizing or suspected of having a seizure, an electroencephalogram is indicated. Jerry and colleagues (2012) recommend judicious use of antipsychotic agents because they may lower the seizure threshold. A psychiatric consultation is warranted if the patient is psychotic and difficult to manage, because the patient may need inpatient treatment.
Salvia (Salvia divinorum) is an herb and a member of the mint family. It is grown in Mexico and Central and South America (Ahern & Greenberg, 2011), is a naturally occurring hallucinogen, and has been used by Mazatec shamans in Mexico for religious and medicinal purposes (Salomone, 2011). The MTF survey added a question in 2010 to assess salvia use in the past 12 months, with 5.9% of 12th graders reporting use in the past 12 months in the 2011 survey (Johnston et al., 2012). Adolescents abuse salvia for its hallucinogenic effects. Salvia is available for purchase via the Internet and currently is not restricted under the Controlled Substances Act (U.S. DOJ DEA, 2012b).
Pharmacology of Salvia
Salvia divinorum's active ingredient, Salvinorin A, selectively activates the kappa opioid receptors in the brain, leading to hallucinations and dysphoria (U.S. DOJ DEA, 2012b).
Salvia may be chewed or smoked (NIDA, 2011). When the leaf is chewed and the leaf mass held in the buccal space, absorption occurs and effects begin to appear in 5 to 10 minutes. The dried leaves may be smoked, with effects within 30 seconds that last for 30 minutes (U.S. DOJ DEA, 2012b). Little is known about the metabolism, distribution, or excretion of salvia.
Patients who chew or smoke salvia experience short-term hallucinations or "psychomimetic" experiences similar to psychosis (NIDA, 2011). Effects of salvia include visual perceptions of psychedelic bright lights, vivid colors and shapes, and body or object distortions (Oether, Behrman, & Ketcham, 2010; U.S. DOJ DEA, 2012b). Users also describe dysphoria or mood swings, uncontrolled laughter, overlapping realities, altered perception of self, and hallucinations (NIDA, 2011; U.S. DOJ DEA, 2012b). Users are at risk of self-harm if they attempt to drive while using salvia (Ahern & Greenberg, 2011). Adverse effects of salvia include incoordination, dizziness, and slurred speech.
The effects of salvia are generally short, with most of the effects wearing off in 30 minutes to 3 hours. Patients should be put in a quiet environment if they are hallucinating or have delirium. Vital signs and neurologic status is monitored and benzodiazepines are administered if the patient becomes combative (Oether et al., 2010).
Ecstasy is the street name for the synthetic drug 3,4-Methylenedioxymethamphetamine (MDMA). MDMA was first synthesized in Germany by Merck and Company in 1912, and before it became a Schedule I drug, it was used by some therapists to increase self-awareness (Hahn, 2011). MDMA is considered a party or "rave" drug and is used by adolescents and young adults, and it is also popular among gay and bisexual men (NIDA, 2006).
MDMA is often illegally manufactured in the Netherlands, Belgium, and Canada and smuggled into the United States (U.S. DOJ DEA, 2011). Tablets often are engraved with symbols or logos that indicate certain "brands" and are sold for $20 to $25 per tablet. It is not uncommon for Ecstasy tablets to also contain ketamine, methamphetamine, caffeine, ephedrine, and other substances (Hahn, 2011; U.S. DOJ DEA, 2011). Users also often use other drugs with MDMA such as alcohol or marijuana.
Pharmacology of MDMA
MDMA is structurally similar to the stimulant methamphetamine and the hallucinogen mescaline (Hahn, 2011; U.S. DOJ DEA, 2011). Similar to other amphetamines, MDMA causes a release of the neurotransmitters dopamine, norepinephrine, and serotonin from storage. Compared with other amphetamines, MDMA causes greater serotonin release, which is most likely the reason MDMA users report elevated mood (Hahn, 2011; NIDA, 2006). Tolerance to MDMA occurs, and users often take repeated doses, known as "stacking," to maintain the drug's effects.
MDMA may be taken in tablet, powder, or liquid form. After oral intake of MDMA, onset of effects occurs in 30 to 60 minutes, with a peak effect at 90 minutes (Hahn, 2011). The effects of MDMA last 3 to 6 hours (NIDA, 2006). MDMA is metabolized by the liver by CYP 2D6, and poor metabolism may be implicated in fatalities associated with MDMA use (Hahn, 2011). MDMA inhibits its own metabolism, leading to increased levels with repeated use in a short time. MDMA is renally excreted and has a half-life of 12 to 34 hours.
MDMA has significant short-term adverse effects on the body and long-term adverse effects on the brain that may last for years after use. Ecstasy or MDMA users report euphoria and increased sensitivity to touch, increased energy, increased sensual arousal, emotional warmth, and the need to be touched (U.S. DOJ DEA, 2011; NIDA, 2011). Acute effects of MDMA begin 30 minutes after oral intake, and adverse effects include anxiety, tachycardia, and elevated blood pressure (Hahn, 2011). In an hour the sympathomimetic effects of MDMA subside and the user experiences relaxation and euphoria. Users report a post-use period of lethargy, anorexia, and dysphoria for 24 to 48 hours that may be severe (Hahn, 2011; National Institute on Drug Abuse, 2011, National Institute on Drug Abuse, 2006).
The short-term adverse effects of MDMA on the body can affect multiple body systems. Serotonin syndrome may occur from the massive serotonin release caused by MDMA, with symptoms of hyperthermia, changes in level of consciousness, autonomic instability, and altered muscle tone or rigidity (Hahn, 2011). The sympathetic effects of MDMA include tachycardia, hypertension, and hyperthermia, which may lead to dysrhythmias including ventricular fibrillation and asystole (Hahn, 2011). The prolonged dancing associated with "raves" or club use predisposes the user to dehydration, hyperthermia, and hyponatremia because of excessive sweating. Hyperthermia from MDMA also may lead to rhabdomyolysis and acute renal failure (Hahn, 2011). MDMA may stimulate syndrome of inappropriate antidiuretic hormone from vasopressin release. MDMA also may cause hepatotoxicity, ranging from elevated liver enzymes to fulminant liver failure (Hahn, 2011). As with any amphetamine, MDMA may cause stroke from cerebral infarct or hemorrhage.
MDMA has long-term adverse effects on the brain that may last for years after use. MDMA can damage the serotonin receptors, leading to decreased serotonin nerve terminals and transporters (NIDA, 2006; U.S. DOJ DEA, 2011). Recovery of normal serotonin function after use may take weeks or months. Long-term effects seen in MDMA users include poor performance on cognitive and memory tasks and depression for weeks and months after use (NIDA, 2011).
Treatment for MDMA toxicity should begin as soon as toxicity is suspected, and the patient should be transported to the emergency department (ED). If the patient has mild symptoms and is hemodynamically stable, treatment is symptomatic. Symptoms of moderate-to-severe toxicity require intensive, prompt intervention to decrease mortality. Prehospital care includes administration of oxygen and intravenous fluids, with serial neurologic checks (Hahn, 2011). In the ED, patients will need constant monitoring for dysrhythmias, seizures, hyperthermia, and hyponatremia/syndrome of inappropriate antidiuretic hormone. Electrolytes, glucose level, and renal and liver function are monitored via laboratory values. Interventions include administration of intravenous fluids and glucose as indicated. Hyperthermia may be life-threatening and requires aggressive treatment to cool the core temperature, including undressing the patient, using fans, placing ice packs in the groin and axilla, and performing iced gastric lavage (Hahn, 2011). Chilled intravenous fluids and iced bladder lavage may also be used. Urine output is monitored, with rhabdomyolysis suspected if urinalysis is positive for blood on dip but negative for red blood cells on microscopic examination. Serum myoglobin levels and creatine kinase are monitored to evaluate for rhabdomyolysis, with frequency of monitoring determined by patient status (Hahn, 2011). Female patients should have pregnancy ruled out. Seizures or muscle spasms are treated with benzodiazepines. Supplies for emergent airway management should be readily available. Severe toxicity usually requires admission to the intensive care unit for close monitoring. Long-term care includes referral to drug addiction treatment because MDMA may be addictive for some users.
Bath salts are synthetic stimulants that contain mephedrone and/or methylenedioxypyrovalerone (MDPV) and have had a surge in use since first appearing in the United States in 2009 (Loeffler et al., 2012). Bath salts are labeled "not intended for human consumption" and may be purchased via the Internet. As of October 2011, the Drug Enforcement Administration, in an emergency ruling due to public safety, has determined that the three common stimulants used in bath salts, mephedrone, MDPV, and Methylone, are Schedule I drugs for a year to allow further study to determine permanent status (U.S. Department of Justice Drug Enforcement Administration, n.d., U.S. Department of Justice Drug Enforcement Administration, n.d.). Bath salts are difficult to regulate because of emerging synthetic stimulants.
Pharmacology of Synthetic Cathinones
The synthetic cathinones are structurally similar to amphetamines. Mephedrone is derived from phenethylamine and is thought to work as a monoamine reuptake inhibitor, inducing the presynaptic release of monamines (Jerry et al., 2012). The effect of mephedrone is to increase dopamine, norepinephrine, and serotonin levels in the synapse, leading to a stimulant effect and euphoria (Jerry et al., 2012; Loeffler et al., 2012). MDVP is a synthetic analog of pyrovalerone that has been used to treat chronic fatigue. MDVP acts as a dopamine and norepinephrine inhibitor, with little effect on serotonin, leading to stimulation and euphoria. Tolerance to both substances occurs (Loeffler et al., 2012).
Synthetic stimulants or bath salts are usually snorted but may be injected or used rectally. Mephedrone has an onset of action 10 to 20 minutes after snorting or ingestion, with a peak effect in 45 minutes to 1 hour and a duration of action of 60 to 120 minutes (Loeffler et al., 2012). MDPV has an onset of action 1 hour after ingestion, with a peak at 90 minutes and duration of stimulant action lasting 2.5 to 3.5 hours (Loeffler et al., 2012). Metabolism and elimination of synthetic cathinones is not known. Standard urine drugs screens do not detect synthetic cathinones.
Bath salts are stimulants and cause intense stimulation, alertness, and euphoria (Loeffler et al., 2012). Adverse effects of synthetic stimulants include agitation, insomnia, irritability, anxiety, paranoia, memory impairment, tremors and seizures (U.S. Department of Justice Drug Enforcement Administration, n.d., U.S. Department of Justice Drug Enforcement Administration, n.d.; Loeffler et al., 2012). Poison centers have received reports of hallucinations and paranoia, as well as tachycardia and hypertension (Jerry et al., 2012). Deaths have been reported (Jerry et al., 2012). Mephedrone use has been associated with altered renal function, acidosis, elevated creatine kinase, leukocytosis, myocarditis, and dysrhythmias (Jerry et al., 2012; Loeffler et al., 2012).
Treatment of synthetic stimulant toxicity is based on the presenting symptoms and is similar to the treatment of synthetic marijuana or Spice toxicity. Agitation and seizures are treated with benzodiazepines (lorazepam), with an electroencephalogram indicated if seizure is suspected or observed (Jerry et al., 2012). Antipsychotic agents in synthetic cathinone intoxication have been shown to increase risk of seizure activity and should be used with great caution. Routine laboratory tests include a complete blood cell count, metabolic panel, and urine toxicology screen for other possible substances ingested.
Dextromethorphan, also known as DXM or by the street names of "poor man's PCP" or "Skittles," is an OTC cough suppressant approved by the FDA in 1958, with first accounts of abuse reported more than 30 years ago (Banken & Foster, 2008). The MTF survey added the question, "How often have you taken cough or cold medicines to get high?" to its questionnaire in 2006 and reported in the 2011 survey that 3% of 8th graders, 6% of 10th graders, and 5% of 12th graders used cough or cold medicines to get high in the past 12 months (Johnston et al., 2012). Information on how to get high on dextromethorphan is available on the Internet, including sites labeled, "So you want to try DXM? A Beginner's Guide to DXM," which gives dosing for different levels or "plateaus" of intoxication, as well as suggestions for which dextromethorphan products are "recommended" for getting high (The Third Plateau, 1998). "Purple Drank," which is favored by some teens and preteens and consists of DXM and codeine cough preparations mixed with soda and Skittles, also has various recipes available on the Internet. DXM powder sold over the Internet is a source of dextromethorphan for abuse. DXM also is distributed in illicitly manufactured tablets that contain only dextromethorphan or are mixed with other illicit drugs such as Ecstasy or methamphetamine.
Pharmacology of Dextromethorphan
Dextromethorphan (d-3-methoxy-N-methyl-morphine), the d-isomer of the codeine analogue levorphanol, acts centrally in the cough center in the medulla to elevate the threshold for coughing. Dextromethorphan does not bind to the opioid receptors; it inhibits the N-methyl-d-aspartate (NMDA) receptor, which is why it gives a dissociative experience similar to PCP and ketamine (Anderson, 2007). Dextromethorphan also inhibits the reuptake of serotonin. When dextromethorphan is used at recommended doses of 10 to 30 mg taken every 6 to 8 hours, the user may experience drowsiness or dizziness, nausea, and gastrointestinal upset. Internet sources (including the U.S. DOJ DEA) indicate different doses or plateaus of dextromethorphan effects, as described in Table 2 (U.S. Department of Justice Drug Enforcement Administration, n.d., U.S. Department of Justice Drug Enforcement Administration, n.d.; Third Plateau, 1998). When doses of DMX get above 120 mg (2 mg/kg of body weight), the user experiences symptoms similar to phencyclidine (PCP), lysergic acid diethylamide (LSD), and ketamine (Banken & Foster, 2008). To confuse evaluation, dextromethorphan may cause a false-positive phencyclidine (PCP) assay (Anderson, 2007).
OTC dextromethorphan often is found in a combination cough and cold medication in combination with an analgesic (acetaminophen), decongestant (phenylephrine or pseudoephedrine), an antihistamine (chlorpheniramine or diphenhydramine), or alcohol. Toxic effects of other ingredients also must be evaluated when one is faced with an adolescent who has taken dextromethorphan to get high.
Dextromethorphan is well absorbed from the gastrointestinal tract, with onset of CNS effects within 20 minutes. Dextromethorphan is extensively metabolized in the liver by CYP 2D6 into the active metabolite dextrorphan and excreted in the urine, mostly as metabolites. Approximately 5% to 10% of White persons of European ancestry and Mexican Americans are deficient in CYP 2D6 and are poor metabolizers; they are unable to convert dextromethorphan to dextrophan, leading to toxicity (Casner, 2005; Zhou, 2009). Extensive 2D6 metabolizers may experience more euphoria associated with higher levels of dextrorphan (Anderson, 2007).
The way an intoxicated adolescent presents depends on the amount of dextromethorphan ingested, as described inTable 2. At lower doses (100 mg to 200 mg), the user reports mild stimulation effects, whereas at higher doses (greater than 500 mg), users may report out-of-body experiences (U.S. Department of Justice Drug Enforcement Administration, n.d., U.S. Department of Justice Drug Enforcement Administration, n.d.). In addition to the sensations users report as the drug dosage increases, users also may experience the unpleasant adverse effects of nystagmus, dilated pupils, body itching, rash, ataxia, sweating, hot/cold flashes, fever, hypertension, shallow respiration, urinary retention, diarrhea, opisthotonos (a spasm where the head and heels are bent back and the torso is bent forward), tachycardia, hyperthermia, toxic psychosis, and coma (Banken & Foster, 2008). Chronic ingestion of dextromethorphan may cause a withdrawal syndrome when it is discontinued.
Users may experience adverse effects from consuming large amounts of dextromethorphan combined with other medications found in cough and cold medications. Dextromethorphan and guaifenesin (Robitussin DM) will cause nausea and vomiting when consumed in amounts required to alter perception, or approximately 120 ml of syrup. Dextromethorphan combined with the antihistamine chlorpheniramine (Coricidin HBP Cough & Cold, Dimetapp Long Acting Cough Plus Cold, and Robitussin Cough & Cold Long-Acting) at high doses can lead to anticholinergic toxicity. Symptoms seen with anticholinergic toxicity include warm, dry, flushed skin, mydriasis, tachycardia, and delirium (Schwartz, 2005). Acetaminophen toxicity occurs when users take products such as Nyquil or Coricidin HBP Maximum Strength Flu, and thus careful attention to which product the adolescent took is critical to preserve liver function; acetaminophen levels should be included in toxicology screens routinely. Selective serotonin reuptake inhibitors also inhibit CYP 2D6, and if an adolescent combines selective serotonin reuptake inhibitors with dextromethorphan, they may experience serotonin syndrome; likewise if they combine MDMA (Ecstasy) with dextromethorphan (Anderson, 2007).
A consensus agreement was published in 2007 by a committee from the AAPCC establishing guidelines for out-of-hospital treatment for dextromethorphan ingestions (Chyka et al., 2007). If it is determined that an adolescent has consumed more than 5 to 7.5 mg per kg of body weight of dextromethorphan, they should be referred to an ED for evaluation if they exhibit more than mild symptoms; if 7.5 mg per kg has been ingested, ED care is mandated to evaluate and treat adverse effects (Chyka et al., 2007). Activated charcoal can be administered in the ED if it has been less than an hour since ingestion. If the patient is sedated or in a coma after dextromethorphan ingestion, naloxone can be administered (Chyka et al., 2007), although relatively high doses often are required to achieve effect.
2C-E or 4-ethyl-2,5-dimethoxyphenethylamine, also known as "Europa," is a relatively new psychoactive substance specifically designed as a hallucinogen by Alexander Shulgin (Erowid.org, 2009; Sacks, Ray, Williams, & Opatowsky, 2012). 2C-E is a psychedelic drug that produces visual and mental distortions similar to LSD or methamphetamine and has gained popularity because of easy access via the Internet (OPHD, 2012b; Sacks et al., 2012). It is thought that 2C-E binds to the 5-HT2A serotonin receptor. The onset of action is 20 to 90 minutes after ingestion, and the duration of action of a single dose is 8 to 12 hours.
Little is known about the toxic effects of 2C-E other than case reports to poison centers of users with poor outcomes. A case report of fatal toxic leukoencephalopahy has been reported in a 2C-E user (Sacks et al., 2012). In Oregon, two unrelated users had acute onset of cyanosis after ingesting a product labeled "2C-E" they had purchased from a Chinese Web site. Upon evaluation in the ED, methemoglobinemia developed in both patients, with methemoglobin levels peaking at 79.6% and 74.4% (normal level, 1% to 3%) (OPHD, 2012b). The FDA tested the substance and found it was aniline, an industrial solvent that is known to cause methemoglobinemia (OPHD, 2012b). The U.S. DOJ DEA has labeled 2C-E a Schedule I drug.
Recent headlines have warned of deaths from energy drinks Monster and 5 Hour Energy (DeNoon, 2012; Meier, 2012). DAWN has reported a large increase in ED visits associated with ingesting energy drinks, often in combination with alcohol (DAWN, 2011). Energy drinks are classified as supplements by the FDA and thus have less regulation than foods or drugs.
Pharmacology of Energy Drinks
Energy drinks usually contain caffeine, with amounts ranging from 80 mg to 500 mg per serving, plus B vitamins, taurine, ginseng, gingko biloba, guarana (a plant that contains concentrated caffeine), and other herbal supplements (DAWN, 2011; Wolk, Ganetsky, & Babu, 2012). Caffeine is a methylxanthine in the same drug class as theophylline. It is a central nervous stimulant that is used to increase alertness and is used by shift workers to stay awake.
Caffeine is rapidly absorbed and crosses the blood-brain barrier when ingested orally, with a peak onset of 30 to 60 minutes (Buck, 2008). Caffeine is metabolized into active methylxanthine metabolites, including 3% to 10% into theophylline (Buck, 2008). Caffeine metabolites are excreted in the urine.
Caffeine intoxication can cause seizures, tachydysrhythmias, and death, but less is known about the toxic effects of other energy drink ingredients (Wolk et al., 2012). Additionally, adolescents often combine alcohol and energy drinks, with the caffeine possibly masking the intoxicating effects of the alcohol, leading to increased ingestion of both (DAWN, 2011).
Adolescents who present with caffeine intoxication with or without alcohol will require supportive care in the ED to treat the stimulant effects of the caffeine. If presenting within 1 hour of ingestion, charcoal can be administered to decrease absorption (Wolk et al., 2012). Nausea and vomiting can be treated with ondansetron. Benzodiazepines are used to treat central nervous excitation or seizures and tachycardia (Wolk et al., 2012). Hemodialysis may be necessary if the serum concentration of caffeine is greater than 90 μg/ml and the patient is experiencing dysrhythmias or seizures (Wolk et al., 2012).
Hand Sanitizer/Purell Shots
A number of reports have been made of adolescents presenting to EDs in California intoxicated from ingesting hand sanitizer (Nordqvist, 2012). Hand sanitizers contain 60% ethyl alcohol, and some adolescents are drinking the liquid straight, known as "Purell Shots," to get drunk. Salt may be used to separate the ethyl alcohol from the glycerin in the gel, with the glycerin forming a thick viscous gel that separates from the alcohol and can be strained with a cheesecloth. Instructions for separation are easily obtained from the Internet (eHow, 2012). Adolescents present with alcohol intoxication or poisoning, which can be fatal. The medical literature contains little information regarding the overall incidence of hand sanitizer intoxication, yet it is seen fairly commonly around the United States by emergency physicians and toxicologists.
J Pediatr Health Care. 2013;27(2):135-144. © 2013 Mosby, Inc.