Significant advancements in the prevention and treatment of pediatric poisonings have evolved during the past few decades. Child-resistant packaging, ingestion safety education, organized poison control centers, and the emergence of medical toxicology as a discrete discipline have contributed to the decrease in childhood poisonings and deaths annually.1 No longer are poisonings treated by protocol. New antidotes and therapies have been developed, and many long-standing therapies are being critically reviewed.
Despite this, there were more than 1.5 million poison exposures in children reported to the Toxic Exposure Surveillance System in 1998, continuing to make ingestions a major health care problem.2 Therefore, the pediatrician is often faced with the need to determine the likelihood of toxicity and to initiate appropriate interventions. In addition to the hundreds of pharmaceuticals available, there are an increasing number of illicit and designer drugs available, as well as an increase in the use of herbal medications. Thus, the field of medical toxicology continues to become more complex, making these decisions even more challenging for the pediatrician.
The American Association of Poison Control Centers Toxic Exposure Surveillance System2 captured an estimated 95.3% of all human exposures that precipitated poison center contacts in the United States for 1998. Of the more than 2.2 million exposures reported, approximately 1.5 million were in children (0 to 18 years old). Of the 56 pediatric deaths, 35 occurred in 13 to 18 year olds, 23 by suicide and 10 with drugs of abuse (Table 1). Of the calls to poison centers, approximately 21% were referred to health care facilities for further treatment, with 69.5% of these individuals being younger than 19 years. Among these, 57.3% were treated and released, 12.8% were admitted for critical care, and 7% were admitted for noncritical care.
The most frequent poison exposures for children younger than 6 years were readily available substances that were not highly toxic, including cosmetics and personal care products, cleaning substances, arts and crafts supplies, plants, cough and cold preparations, and insecticides (Figure). Pharmaceuticals were involved in 66% of the pediatric fatalities, including antidepressants, analgesics, stimulants and street drugs, anticonvulsants, and cardiovascular drugs. However, nonpharmaceuticals such as hydrocarbons, fumes and gases, heavy metals, and other chemicals were the cause of 34% of the fatalities (Table 2). Prehospital cardiac arrest, respiratory arrest, or both occurred among 43% of the pediatric fatalities.
APPROACH TO THE PATIENT WITH A POSSIBLE POISONING
As in all pediatric emergencies, the ABCs (airway, breathing, and circulation) are the first priority. The maintenance of an airway, ventilation, oxygenation, fluid status, and appropriate cardiovascular support has contributed more toward survival from an ingestion or poisoning than have antidotes. Because most patients will not require intervention with antidotes, it becomes a challenge to determine what, if any, intervention should be undertaken. Most young children are closely watched such that the time interval between ingestion and discovery is usually short. Also, most young children have access to only single substances and, with exploration, will not usually take a substantial quantity of a "bad-tasting" medication. However, there are many substances for which a single pill or swallow can have significant toxicity, especially for the 20-lb toddler.3 These include camphor, chloroquine, hydroxychloroquine, Imipramine, desipramine, quinine, methyl salicylate, theophylline, thioridazine, and chlorpromazine.4 Therefore, the following information needs to be obtained in the history: a list of available toxins (remembering that over-the-counter medications and nonpharmaceuticals such as plants and cleaning agents can pose significant toxicity); the maximum amount available; the minimal amount per kilogram that can produce symptoms; the nature, severity, and timing of potential symptoms; and the potential to alter the course with decontamination or specific antidotes.
Figure. Substances most frequently involved in poison exposures in children younger than 6 years. (Data from Litovitz et al.2)
Reasons for Poison Exposures and Ages Among 56 Pediatric Deaths In 1998*
The adolescent poses a more difficult dilemma. The ingestion is often a suicide attempt, and often involves multiple substances or is a result of drugs of abuse. For these reasons, the time between ingestion and discovery is often prolonged and the correct substances and amounts are often concealed. Therefore, it may be helpful to approach these patients by using "toxidromes," groups of related signs and symptoms that are seen after ingestion of certain classes of drugs (Table 3). The best-defined ones include sympathomimetic, cholinergic, anticholinergic, and opiate-sedative-ethanol syndromes.5
Substances Causing Pediatric Deaths4
Smelling the patienf s breath can yield some clues to certain ingestions, as noted in Table 4.6 Analysis of the urine can also be helpful. Calcium oxalate crystals are pathognomonic for ethylene glycol poisoning. Positive results of a ferric chloride test for phenylpyruvic acid usually indicate phenothiazine or salicylate overdoses. Urine color can also give clues. Orange to red-orange hue can be seen with rifampin, deferoxamine, mercury, phenazopyridine, or chronic lead poisoning. Pink urine can be seen with overdoses of cephalosporins or ampidllin. Brown urine can signal chloroquine or carbon tetrachloride toxicity. Green to blue urine can be seen with amitriptyline poisoning. Examination of the skin to determine whether it is dry or diaphoretic can also give clues to certain classes of drugs such as anticholinergic and cholinergic agents, respectively. In addition, the skin (including hidden areas such as the groin, neck, supraclavicular areas, dorsum of feet, and tongue) should be closely examined for needle tracts.
Once the risk has been determined, most children can be discharged home after a brief period of observation without monitoring or decontamination. Patients should be admitted to the hospital if they have signs or symptoms of significant toxicity or if the possibility of significant delayed symptoms is present. The risk assessment, the need for monitoring, and the potential for decompensation requiring intensive intervention should detennine whether the child should be admitted to the ward, a monitored bed, or an intensive care unit. A poisoning severity score for grading acute poisonings has been developed by the International Programme on Chemical Safety and the European Commission.7 This score grades severity as (0) none, (1) minor, (2) moderate, (3) severe, or (4) fatal poisoning. Unfortunately, the score was not intended to be prognostic, does not take into account anticipated signs or symptoms, and does not factor in the type or amount of toxin ingested. Therefore, there is no well-devised scoring system that can be employed to determine the need for specific supportive therapies.
For the small number of poisoned children who are unstable on presentation, the ABCs should be instituted. Oxygen should be administered and oxygen saturation monitored by pulse oximetry. Special attention should be given to protective airway reflexes because many poisons may cause emesis. Therefore, elective intubation may be indicated at a slightly lower threshold than might be tolerated in other patients with central nervous system depression. In addition, intravenous access should be obtained in patients with signs and symptoms of cardiopulmonary compromise, in those who might have acute deterioration in respirations, heart rate, rhythm, perfusion, or blood pressure, or in those at risk for seizures or significant central nervous system depression. Hypoperfusion or hypotension usually responds to intravenous isotonic fluids. More aggressive treatment, including adding inotropes such as epinephrine or dopamine, may be needed for those patients who are unresponsive to repeat fluid boluses. Evaluation and correction of electrolyte abnormalities and acid-base balance may be needed to further improve cardiac output. Some poisonings, especially tricyclic antidepressants, can trigger significant dysrhythmias.
Rapid assessment of level of consciousness can be performed using the Glasgow Coma Scale or the AVPU scale (ie, alert, response to verbal stimuli, response to pain, or unresponsive). If rapid bedside glucose testing is not available, men a trial dose of 0.5 to 1.0 g/kg of glucose as a 10% to 25% solution should be administered. Of note, toxininduced or drug-induced hypoglycemia does not always present as seizures or coma, but can be seen as alterations in behavior, speech, or focal neurologic findings. Hypoglycemia is often seen following ethanol, oral hypoglycemic, beta-blocker, or salicylate ingestions, as well as with insulin injections. In an unresponsive patient, naloxone can not only improve symptomatology, but can also help determine the etiology in unknown poisonings. Many dose recommendations are based on weight (0.01 to 0.1 mg /kg). However, many sources now recommend a unified dose beyond the newborn period of 1 to 2 mg based on the concept of total load of narcotics and the number of opioid receptors. In patients with strong suspicion for opioid intoxication, 0.3 mg/ kg up to 10 mg may be required to see a response, especially with higher doses of opiates, propoxyphene, pentazocine, and illicit fentanyl derivatives. In adults, 100 mg of thiamine given intravenously or intramuscularly is recommended prior to dextrose administration in alcoholic patients with altered mental status to prevent Wernicke's encephalopathy. However, this practice is generally not warranted in pediatric patients.
Odors That Suggest the Diagnosis
Optimal Timing for Quantitative Toxicology Tests
LABORATORY EVALUATION: MUDPlLES AND COINS
Most poisonings can be managed appropriately without extensive laboratory studies. The "tox screens" that are often reflexively ordered are rarely helpful. There are many drugs and toxins that are not detected by most drug screens. Those that are potentially missed include bromide, carbon monoxide, chloral hydrate, Clonidine, cyanide, organophosphates, and tetrahydrozoline, which can lead to coma, and beta-blockers, calcium-channel blockers, Clonidine, colchicine, digitalis, and iron, which cause hypotension or bradycardia.8 The delay before results are available does not help with acute management decisions. Drug screens that include blood and urine can be of benefit in detecting an occasional medication, such as acetaminophen, especially in the adolescent who has ingested multiple medications as an intentional overdose. In addition, the results of drug screens may be helpful with medicolegal issues. If a toxicology screen is to be performed, it should include urine and serum. Table 5 shows the recommended time between ingestion and sampling of serum to help with quantitative toxin measurements.9
Serum chemistries and osmolarity are of more help than toxicology screening in a patient with altered mental status and suspected, yet unknown, ingestion. Causes of metabolic acidosis with a high anion gap [Na - (Cl + HCO3); normal = 12 mEq/L ± 2 mEq/L] can be remembered using the mnemonic MUDPILES: methanol, uremia, diabetic ketoacidosis, paraldehyde and phenforrnin, isoniazid and iron, Zactic acidosis, ethanol and ethylene glycol, and salicylates. An osmolar gap of greater than 10 mOsm/kg H2O determined as the difference between the measured and the calculated serum osmolarity may suggest intoxication with an alcohol-like ethanol, isopropanol, methanol, or ethylene glycol. Osmolarity is calculated using the following formula: 2 Na + BUN /2.8 + glucose/ 18.
Additional studies that may be helpful include obtaining an electrocardiogram, especially to look for conduction delays (prolonged QT interval) or dysrhythmias associated with ingestion of tricyclic antidepressants. Plain radiographs can be helpful to evaluate for radiopaque pills or to look for toxin-associated evidence of aspiration or pulmonary edema. Drugs or toxins that are likely to be visible on plain radiographs can be remembered by the mnemonic COINS: chloral hydrate and cocaine packets, opiate packets, iron and other heavy metals such as lead, arsenic, and mercury, neuroleptics, and sustained-release or enteric-coated tablets.6
SKIN AND EYE DECONTAMINATION
In patients with topical exposures such as insecticides and pesticides, all clothing should be removed and the skin thoroughly washed with soap and water. Health care providers should wear gloves and gowns to protect themselves from dermal contamination. Ocular exposures to acids and alkali can be devastating. Therefore, the eyes should be copiously irrigated with normal saline solutions.
GASTROINTESTINAL DECONTAMINATION: RECOMMENDATIONS HAVE CHANGED
Attempts to "get the poison out" remain one of the main topics of discussion in the management of toxic exposures. The safety and efficacy of different modes of decontamination are still controversial. In 1997, the American Board of Applied Toxicology and the Canadian Association of Control Centers endorsed position statements regarding ipecac syrup, gastric lavage, singledose activated charcoal, cathartics, and whole bowel irrigation.10 In preparing these position statements, all relevant scientific literature was reviewed by recognized experts, with well-conducted clinical and experimental studies given precedence over anecdotal case reports.
Syrup of ipecac was once recommended for all households with young children. The American Association of Poison Control Centers now reports that ipecac administration rates decreased from 15% in 1985 to 1.2% in 1998.2 According to the position statement, syrup of ipecac should not be routinely recommended because experimental studies have shown the amount of toxin removed to be highly variable, with diminution of removal over time. In addition, there is no evidence from clinical studies that ipecac administration in emergency departments improved outcome, and it could delay the administration or reduce the effectiveness of activated charcoal, oral antidotes, and whole bowel irrigation. Ipecac should not be administered to a child with actual or impending alteration in mental status or to a child who has ingested a hydrocarbon or corrosive substance.
The position statement continues that gastric lavage should also not be routinely employed. As with ipecac, experimental studies found the amount of toxin removed to be highly variable and to diminish over time. There is no definite evidence that it improves outcome, and it may cause significant morbidity. Therefore, gastric lavage should be considered only if the patient has ingested a potentially life-threatening amount of poison and lavage can be performed within 60 minutes of the ingestion. Even then, controlled studies have not confirmed a benefit. Gastric lavage is contraindicated in nonintubated patients who have lost their protective airway reflexes and in patients with hydrocarbon or corrosive ingestions. If gastric lavage is to be performed, the patient should be placed in the left lateral, head down position. A large-bore 36 to 40 French catheter should be used for adolescents and young adults, and a 24 to 48 French catheter for children. Lavage should be performed using 10 cc /kg of warm 0.9% saline in children or up to 200 to 300 mL in the adolescent or young adult. Lavage should be continued until the recovered solution is clear.
Agents Not Adsorbed by Activated Charcoal
Regarding the use of single-dose activated charcoal, the position statement relates that it should not be routinely administered to all poisoned patients, but can be considered if a patient has ingested a potentially toxic amount of a poison that is known to be adsorbed by charcoal (Table 6) and the charcoal can be given within an hour of ingestion. There are insufficient data to support or exclude its use after 1 hour of ingestion. There is no evidence that activated charcoal improves clinical outcome. Activated charcoal is contraindicated in a patient without an intact or protected airway or if the gastrointestinal tract is not anatomically intact. If activated charcoal is to be used, the recommended dose is 1 g/ kg in children up to 1 year old, 25 to 50 g in children 1 to 12 years old, and 25 to 100 g in adolescents and young adults. Few adverse effects have been reported from single-dose activated charcoal.
The position statement indicates that the administration of a cathartic alone has no role in the treatment of poisoned patients and therefore is not recommended as a means of gut decontamination. No clinical studies have been published that determine whether a cathartic, with or without charcoal, reduces the bioavailability of a toxin or improves outcome. Therefore, based on available data, the position statement does not endorse the routine use of a cathartic combined with activated charcoal. If a cathartic is used, it should be limited to a single dose to minimize adverse effects of dehydration, hypernatremia, or hypermagnesemia. If a cathartic is to be added to activated charcoal, the recommended dose for sorbitol is 1 to 2 g /kg (1-2 mL/kg of 70% solution for young adults, and 4.3 mL/kg of 35% solution for children older than 1 year). The recommended dose for magnesium citrate is 250 mL of 10% solution for young adults or 4 mL/kg for a child.
According to the position statement, whole bowel irrigation with polyethylene glycol electrolyte (PEG-ES) is not recommended for routine use. Although there are some volunteer studies that showed substantial decreases of 67% to 73% in bioavailability of ingested drugs,11 no controlled clinical trials have been performed. Therefore, based on the volunteer studies, whole bowel irrigation may be considered for potentially toxic ingestions of sustained-release or entericcoated drugs. Whole bowel irrigation has been used for potential toxic ingestions of iron, lead, zinc, and packets of illicit drugs. However, according to the position statement, there are insufficient data to support or exclude its use. Whole bowel irrigation is contraindicated in patients with bowel obstruction, perforation, or ileus, and in patients with hemodynamic instability or compromised unprotected airways. A single dose of activated charcoal administered prior to whole bowel irrigation does not appear to alter the binding capabilities of the charcoal or decrease the osmotic properties of the irrigation solution. However, the binding capacity of the charcoal is decreased if administered during whole bowel irrigation.
Whole bowel irrigation is typically administered via a small-bore (12 French) nasogastric tube placed into the stomach, because patients cannot drink the PEG-ES at the required rate. The rate of administration of PEG-ES is 500 mL/h in children 9 months to 6 years old, 1,000 mL/h in children 7 to 12 years old, and 1,500 to 2,000 mL/h in adolescents and young adults. If emesis occurs, it is usually as a consequence of the ingested toxin, not from the PEG-ES. A nonsedating antiemetic such as metoclopramide has been used, with the additional advantage of promoting gastric emptying. Because PEG-ES is not absorbed, there is no need to monitor the patient's fluid or electrolyte status during the procedure except for reasons related to the ingestion itself. Whole bowel irrigation should be continued until the liquid stool is clear, which usually takes several hours.
Because most patients present for care long after most toxin has been absorbed, gastrointestinal decontamination is not of benefit. If the patient does present with a potentially toxic ingestion within 1 hour of exposure, then consideration should be given for a single dose of activated charcoal. The exception to this is with sustained-released pharmaceuticals because they are designed to release medication during several hours and can be present in the bowel for hours. As a result, activated charcoal, whole bowel irrigation, or both might still be of benefit later than 1 hour after ingestion.
The elimination of some toxins may be enhanced with diuresis, dialysis, hemoperfusion, and multi-dosing of activated charcoal. Because all of these techniques have some risks associated with them, they should be considered only if the ingestion is life-threatening or if a significant benefit for specific toxins is likely.
Forced diuresis may be helpful with toxins that are primarily renally excreted. Enhanced diuresis achieved simply with increased fluid administration has been of limited benefit. Osmotic diuresis with mannitol may be more likely to prevent reabsorption of the specific toxin. Clearance of long-acting barbiturates and salicylates can be further enhanced by alkalinization of the urine because excretion is favored with the drug in the ionized form. For drugs that are weak acids, alkalinization of the urine can be effective. Similarly, acidification of the urine can help clear weak bases, but this is rarely done because of the significant side effects of systemic acidosis. The patient should be hemodynamically stable, have normal renal function, have no evidence of cerebral or pulmonary edema, and have ingested a significant or life-threatening amount of a drug that is renally excreted. The goal of alkalinization is to achieve a urine pH of 7.5 or greater by administering intravenous sodium bicarbonate. In addition to the clinical monitoring of cardiopulmonary and neurologic status, electrolytes and osmolality should also be closely observed.
According to the position statement about multiple-dose activated charcoal from the American Academy of Clinical Toxicology and the European Association of Poisons Centres and Clinical Toxicologists,12 although many studies in animals and volunteers have demonstrated that multipledose activated charcoal increases elimination of some drugs, no controlled studies have shown this to reduce morbidity or mortality. Therefore, multiple-dose activated charcoal is not recommended except with life-threatening ingestions of carbamazepine, dapsone, phenobarbital, quinine, or theophylline. Other volunteer studies have suggested enhanced elimination of medications such as amitriptyline, dextropropoxyphene, digitoxin, digoxin, disopyramide, nadolol, phenylbutazone, phenytoin, piroxicam, salicylates, and Sotalol, but the position statement maintains that there are inconclusive data to support or exclude multiple dosing of activated charcoal for these. Multiple doses should be administered only if the patient has an intact or protected airway and no evidence of intestinal obstruction. The addition of concurrent cathartics is not recommended.
Dialysis and hemoperfusion is recommended for select potentially fatal ingestions (Table 7) or when renal failure exists.13 Hemodialysis is the most effective means of dialysis, yet it requires highly technical skills and intensive care monitoring. In addition, hemodialysis requires anticoagulation and has significant potential for hemodynamic compromise, especially in the patient who has already been poisoned. A toxin must have a molecular weight of less than 500 d, be water soluble, and not be bound to plasma proteins to be effectively hemodialyzed.
Toxins That Can Have Enhanced Elimination by Extracorporeal Techniques
Hemoperfusion is the process of passing blood through an extracorporeal circuit and a cartridge containing an adsorbent, with the decontaminated blood returned to the patient. It has the advantage over hemodialysis in that it can enhance clearance of toxins that are adsorbed by activated charcoal and can also clear toxins that are protein bound. Again, this technique has risks similar to those of hemodialysis, with additional risk for thrombocytopenia, leukopenia, and hypocalcemia, and therefore should be used only with life-threatening ingestions.
As stated earlier, supportive care is the mainstay for most ingestions. There are few ingestions for which a specific antidote is necessary or beneficial. A few new notable antidotes are available: fomepizole for ethylene glycol and methanol poisonings, octreotide for sulfonylurea poisoning, and flumazenil for benzodiazepines.
Ethylene glycol and methanol are not toxic themselves. Rather, it is their metabolites that are harmful. Both are metabolized by alcohol dehydrogenase and then aldehyde dehydrogenase to the toxic metabolites glycoaldehyde, glycolic and oxalic acids (ethylene glycol), and formaldehyde and formic acid (methanol). The traditional treatment for methanol and ethylene glycol poisoning has been ethanol infusion to block the generation of these toxic metabolites and hemodialysis for removal of the parent alcohol. This therapy has the disadvantages of further altering the patient's mental status and causing hypoglycemia and the potential adverse effects of hemodialysis.
Fomepizole, also called 4-methylpyrazole or 4MP, is a competitive inhibitor of alcohol dehydrogenase. It can be given orally or intravenously, with intravenously the preferred route in the United States. As opposed to ethanol infusions, fomepizole has few side effects. These include headache, nausea, and dizziness. In addition, it has a longer half-life than ethanol, and does not require a continuous infusion. Unfortunately, it is expensive, but the overall hospital expense compared with conventional therapy might be less because fomepizole may obviate the need for hemodialysis and intensive care monitoring if the patient does not have a significant metabolic acidosis or renal dysfunction. The loading dose is 15 mg/ kg followed by 10 mg/ kg every 12 hours for 4 doses and then 15 mg /kg every 12 hours thereafter. It induces its own metabolism via the cytochrome P450 oxidase system, decreasing its level within 48 hours. All doses are given intravenously during 30 minutes. The end point is a serum concentration of ethylene glycol or methanol less than 20 mg/dL. Because fomepizole is removed by hemodialysis, the dosing frequency should be increased to every 4 hours when hemodialysis is used.14
Octreotide, a long-acting somatostatin analogue, is a promising antidote for the treatment of sulfonylurea poisoning. The more commonly prescribed sulfonylureas are glyburide, acetohexamide, and chlorpropamide. Sulfonylureas stimulate the secretion of insulin, producing significant hypoglycemia. Of the 4,581 exposures reported to poison control centers in 1998, 623 had moderate adverse outcomes and 96 had major adverse outcomes, with an additional 10 deaths.2 Young children who have ingested only 1 or 2 tablets should be referred to an emergency department for further evaluation. Most patients can be treated with glucose supplementation. However, 2 recent case series reported a total of 278 patients in whom intravenous dextrose supplementation alone was not sufficient therapy.15 Glucagon has been recommended with mixed experience. Although glucagon has potent stimulatory effects on gluconeogenesis and glycogenolysis, it does not inhibit insulin release and may actually stimulate further insulin production. Likewise, glucocorticoids have not produced a predictable response. Diazoxide is an inhibitor of insulin secretion, but carries the risk of hypotension, tachycardia, nausea, vomiting, and dizziness.
Octreotide has been successfully used for neonatal hyperinsulinemia. It reduces insulin secretion, but does not appear to eliminate secretion completely, returning it to near basal rates. In a simulated overdose study, Boyle et al. found octreotide to be superior to glucose alone or diazoxide in maintaining eugly cernia.16 Optimal dosing for octreotide has not been established. It can be given subcutaneously or intravenously. The current recommendation is 1 ^g /kg subcutaneously every 12 hours, with more frequent redosing if necessary. In severe refractory cases, a constant infusion of 15 ng/kg/min, titrated to effect, has been used. There are few transient minor adverse effects of octreotide. These include local discomfort at the injection site, nausea, headache, diarrhea, and abdominal discomfort.15
Flumazenil is a highly selective competitive antagonist of the central benzodiazepine receptors. It has the potential for rapid reversal of benzodiazepine overdose-induced coma and respiratory depression. Flumazenil has been used as both a diagnostic aid and a potential substitute for endotracheal intubation, and has been described as part of the "coma cocktail" to be administered to patients who present with suspected druginduced or toxin-induced coma. This practice is no longer recommended. Flumazenil alone is not associated with adverse hemodynamic effects. However, seizures can be precipitated in patients with underlying seizure disorders or in those who have co-ingested tricyclic antidepressants. In addition, arrhythmias can occur in patients who have ingested chloral hydrate.17 Because of these serious side effects, and often the lack of an accurate history regarding an underlying seizure disorder or other potential medications, supportive care alone, including intubation and mechanical ventilation, is usually employed. If flumazenil is given, the recommended dose is 0.01 to 0.02 mg /kg. If there is no response, repeated increased doses are titrated to a total maximum of 1 mg. The onset of action occurs in 1 to 2 minutes. The effect may last 1 to 5 hours, which may be shorter than the effects of the benzodiazepine. Therefore, if repeated doses are needed, a continuous infusion can be started.
Common Poisonous Houseplants
POISONOUS PLANTS AND HERBAL TOXICITY
Plant ingestions among children are common, making up 5% to 10% of calls to poison information centers. It is difficult to compile a complete list of hazardous plants for several reasons. Many have both edible and toxic parts, such as the potato, tomato, rhubarb, and asparagus. In addition, it may be difficult for the non-botanist to correctly identify plants, as they are often known by many different names, with many common names describing different plants depending on the region of the country. Poisonous Plants of the United States and Canada is the preferred text of poison centers in North America.18
It is difficult to determine how much of a toxic plant is needed to cause poisoning. Unless the child is under constant observation, it is difficult to determine how much a child has ingested. Furthermore, not all berries, leaves, or roots of the same classification contain the same amount of toxin. For most plants, a single berry or bite of a leaf smaller than a half dollar is considered to be mildly toxic, making it generally safe to observe that child at home. More significant ingestions should be evaluated for possible removal and an additional single dose of activated charcoal. Table 8 provides a list of common houseplants that contain toxins. These should be avoided in homes with young children.19
The increasing interest in herbs, herbal medications, and performance-enhancing products poses further problems because there are no regulations to control their distribution and sale. The Dietary Supplement Health and Education Act of 1994 exempts "dietary supplements" from drug regulations if they do not claim to diagnose, mitigate, treat, cure, or prevent disease.20 Many dietary supplements are excluded from the definition of food additives and may not be labeled, or, if they are, common names are often used to identify the herbs. Also, because they require no prescription and are often purchased in "health" food stores, most individuals believe them to be safe and healthy.
DRUGS OF ABUSE
Poisonings caused by drugs of abuse are common among adolescents: 19.6% of pediatric deaths from poisonings in 1998 were caused by intentional abuse of drugs.2 Adolescents or préadolescents who willingly abuse drugs for their mind-altering effects are most typical. However, neonates exposed to toxins in utero may present with intoxication or withdrawal, and infants or toddlers may accidentally ingest drugs that are left in accessible places or be victims of chemical child abuse if intentionally given drugs by their caretakers.
The preadolescent or adolescent often presents after an accidental overdose, a suicide attempt, or because of bizarre behavior. He or she may also present after trauma, such as a motor vehicle accident. It is difficult to obtain an accurate history of what was ingested because the patient may not be mentally able to correctly report or because he or she withholds the information, fearing legal consequences. In addition, drugs may often be reported by their street names, and many street drugs may be "laced" with substances unknown to the patient. Typical drug screens may not identify many of these substances, especially inhalants, which are increasing in popularity.
Management is generally supportive. In assessing these patients, it is important to include a temperature because many of these drugs can cause hyperpyrexia. Physical or chemical restraint with short-acting benzodiazepines may be required to prevent the patient from harming himself or herself or others. Gastrointestinal decontamination should be considered, especially if multiple drugs are involved. However, because there may be many routes of exposure and the patient rarely presents within 1 hour of the exposure, gastrointestinal decontamination is often not appropriate.
Inhalant abuse, where gas or vapor is intentionally breathed in to get high, is commonly known as "huffing," "sniffing," or "bagging." In many cases, inhalants are the first mood-altering substances used by children. Patients with acute abuse can often present with symptoms of asthma, allergies, sinusitis, or hay fever. Chronic abuse can result in multi-organ system disease that may mimic many other disorders. The children may experience memory loss, emotional instability, cognitive impairment, slurred speech, and loss of the sense of smell. Often their breath or clothing may have a chemical smell. A 1998 "Monitoring the Future" study surveyed 50,000 teenagers nationwide and found that approximately onefifth of eighth graders have used inhalants. Lifetime use of inhalants was 18.3% among 10th graders and 15.2% among 12th graders.21
The more commonly abused inhalants are gasoline, Freon, butane, propane, spray paint, toluene, and correction fluid. In one study that reviewed 165 cases of inhalant abuse reported to a regional poison center, spray paint and gasoline accounted for 61% of all cases, with gasoline alone accounting for 83% of exposures in the 18 children younger than 9 years. There was 1 death, and an additional 15 patients had life-threatening symptoms.22 Table 9 lists the harmful chemicals that are found in some common inhalants. Inhalants can cause serious central nervous system damage and sudden death. They may sensitize the heart to epinephrine, such that ventricular fibrillation and sudden death can occur. This "sudden sniffing death syndrome" can occur on the first or fiftieth time someone uses an inhalant and is responsible for more than half of the deaths related to inhalant abuse. In addition, the process of "bagging," where the compound is placed into a large bag and the drug user places his or her head in the bag, can lead to asphyxia.
The Internet currently provides easy access to illicit information about recreational drug use. Not only can many of the new designer drugs be purchased via the Internet, but many "recipes" and inexpensive kits are available to manufacture these drugs in the average kitchen. In addition, information is available on how to "safely" get high from many over-the-counter preparations such as dextromethorphan and diphenhydramine hydrochloride.
Ecstasy, or 3,4 methylenedioxymethamphetamine (MDMA), is a designer drug that has gained popularity and notoriety at dance halls known as "raves" in the United Kingdom and now on many college campuses in the United States. MDMA is a selective serotoninergic neurotoxin. MDMA has an undeserved reputation for safety and long duration of action. It is appealing to many young people because it is believed to enhance empathy and closeness to others. Shortterm adverse effects include sweating, tachycardia, fatigue, and muscle spasm, including jaw clinching. More serious adverse effects are fluid and electrolyte depletion, along with central nervous system, renal, hepatic, and muscular dysfunction. Heat stroke is the most serious adverse effect and has caused many deaths. Alcohol is generally avoided at these raves because it may blunt the high. To escape, many of the adverse effects, rave dancers are encouraged to drink frequently and copiously and to consume "power drinks" and salty foods.23
Herbal ecstasy is a Chinese herb called Ephedra sinica (Ma Huang) that contains ephedrine and caffeine (kola nuts). It is used by body builders and dieters to increase metabolism, promote weight loss, and build greater muscle mass. Because of its availability in health food stores, herbal ecstasy is often substituted for MDMA.24 Ephedra can cause vasoconstriction, leading to intracerebral hemorrhage, seizures, myocardial infarcts, and sudden death. Management of acute intoxication of MDMA includes rapid rehydration and core cooling. Rhabdomyolysis may occur, requiring alkalinization of the urine and forced diuresis, hydration, and electrolyte replacement. Cardiac arrhythmias can also occur.
Gamma hydroxybutyrate (GHB) is a structural analog of GABA commonly referred to as liquid ecstasy. It was developed as a general anesthetic and used for the treatment of narcolepsy. It has a dose-related depressant effect on the central nervous system. Because of its ability to stimulate growth hormone release, aiding in fat reduction and muscle growth, it became a popular product obtained from health food stores by body builders. In the past decade, it has been used recreationally for its alcohol-like, hangover-free effects and, because of its prosexual effects, has been one of the predatory drugs used in date rapes. GHB is no longer available in health food stores, but recipes and kits to manufacture the drug at home are available, especially via the Internet. Sleep aids containing gamma butyrolacetone, marketed under various brand names, and 1,4 butanediol are metabolized to GHB. Gamma butyrolactone is also found in some acetone-free nail polish removers and in cyanoacrylate glue. GHB in toxic doses can cause sedation, nausea and vomiting, seizures and myoclonus, and fatal respiratory depression and coma.25
Harmful Chemicals Found In Common Inhalants
Poisonings represent one of the most common medical emergencies in children and further account for a large portion of emergency department visits. Early recognition and management can save lives. Initial management should involve the traditional ABCs of airway securement and cardiorespiratory support. Subsequent management can then focus on identification of a specific toxin and consideration for decontamination, with determination of the extent of intoxication deciding the patient's ultimate disposition.
1. Bond GR. The poisoned child: evolving concepts in care. Emerg Med Clin North Am. 1995;13:343-355.
2. Litovitz TL, Klein-Schwartz W, Caravati EM, Youniss J, Crouch B, Lee S. 1998 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am ] Emerg Med. 1999;17:435-487.
3. Koren G. Medications which can kill a toddler with a tablet or teaspoon. Clin Toxicol. 1993;31:407-413.
4. Emery D, Singer JI. Highly toxic ingestions for toddlers: when a pill can kill. Pediatric Emergency Medicine Reports. 1998;3:111-122.
5. Conway EE. Overdose. In: Friedman SB, Fisher M, Schonberg SK, Alderman EM. Comprehensive Adolescent Health Care. St. Louis, MO: Mosby; 1998:664-667.
6. Erickson TB. Dealing with the unknown overdose. Emergency Medicine. 1996;28:74-88.
7. Persson HE, Sjöberg GK, Haines JA, et al. Poisoning severity score: grading of acute poisoning. Clin Toxicol. 1998;36:205-213.
8. Wiley JF. Difficult diagnoses in toxicology: poisons not detected by the comprehensive drug screen. Pediatr Clin North Am. 1991;38:725-737.
9. Weisman RS, Howland MA, Flomenbaum NE. The toxicology laboratory. In: Goldfrank LR, Flomenbaum NE, Weisman RS, Howland MA, eds. Toxicologic Emergencies. Stamford, CT: Appleton & Lange; 1990:39-48.
10. Krenzelok E, Vale A. Position statements on gut decontamination: American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35:695-762.
11. Tenenbein M. Recent advancements in pediatric toxicology. Pediatr Clin North Am. 1999;46:1179-1188.
12. Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning: American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1999;37:731-751.
13. Goldfarb DS, Pond SM. Principles and techniques applied to enhance elimination of toxins. In: Goldfrank LR, Flomenbaum NE, Lewin NA, Weisman RS, Howland MA, eds. Toxicologic Emergencies. Stamford, CT: Appleton & Lange; 1998:53-62.
14. Barceloux DG, Krenzelok EP, Olson K, et al. American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol Poisoning. Clin Toxicol. 1999;37:537-560.
15. Spiller HA. Management of sulfonylurea ingestions. Pediatr Emerg Care. 1999;15:227-230.
16. Boyle PJ, Justice K, Kreatz AJ, Nagy RJ, Schade DS. Octreotide reverses hyperinsulinemia and prevents hypoglycemia induced by sulfonylurea overdoses. J Clin Endoainol Metab. 1993;76:752-756.
17. Weinbroum AA, Flaishon R, Sorkine P, Szold O, Rudick KV. A risk-benefit assessment of flumazenil in the management of benzodiazepine overdose. Drug Saf. 1997;17:181-196.
18. Kingsbury JH. Poisonous Plants of the United States and Canada. Englewood Cliffs, NJ: Prentice-Hall; 1964.
19. Lawrence RA. Poisonous plants: when they are a threat to children. Pediatr Rev. 1997;18:162-168.
20. Angeli M, Kassirer JP. Alternative medicine: the risks of untested and unregulated remedies. JV Engl J Med. 1998; 339:12.
21. Bykowski M. Don't miss inhalant abuse diagnosis. Pediatric News. 1999-33:37.
22. Spiller HA, Krenzelok EP. Epidemiology of inhalant abuse reported to two regional poison centers. Clin Toxicol. 1997;35:167-173.
23. Schwartz RH, Miller NS. MDMA (ecstasy) and the rave: a review. Pediatrics. 1997;100:705-708.
24. Brown ER, Jarvie DR, Simpson O. Use of drugs at "raves." Scott Med J. 1995;40:168-171.
25. Adverse events associated with ingestion of gamma-butyrolactone in Minnesota, New Mexico, and Texas, 1998-1999. MMWR. 1999;48:137-140.
Reasons for Poison Exposures and Ages Among 56 Pediatric Deaths In 1998*
Substances Causing Pediatric Deaths4
Odors That Suggest the Diagnosis
Optimal Timing for Quantitative Toxicology Tests
Agents Not Adsorbed by Activated Charcoal
Toxins That Can Have Enhanced Elimination by Extracorporeal Techniques
Common Poisonous Houseplants
Harmful Chemicals Found In Common Inhalants