Toxic exposures in the pediatrie population are encountered routinely by the general pediatrician as well as the pediatrie emergency physician. Lack of clinical research and rapidly changing treatment recommendations have allowed unrealistic impressions of these childhood poisonings to propagate. The American Association of Poison Control Centers (AAPCC) Toxic Exposure Surveillance System (TESS) reported more than 1,582,000 exposures in children in 2003 ;! and this underestimates the actual incidence of exposures in this population.
In these cases, medical histories frequently are unknown, and the substances involved often are unfamiliar. As technology has improved, an excess of laboratory and diagnostic studies have become available to aid in the identification of potential toxins. Which studies are necessary and when to order advanced testing can be confusing even to the seasoned physician. The treatment of toxic exposures, specifically decontamination methods, has changed dramatically during the past 2 decades, and these decisions continue to be highly controversial today.
Although pediatrie toxic exposures are extremely common, morbidity and mortality associated with these exposures are exceedingly uncommon. Of the 1.5 million exposures in people younger than 20, only 0.18% (2,778) were categorized as causing a major effect, and just 0.007% (106) resulted in to death.1 As Figure 1 (see page 938) illustrates, the overwhelming majority of toxic exposures cause minimal to no effect. Ingestion was the primary route of exposure to toxic substances (76.9%), and deaths associated with toxic exposure were associated predominately with ingestions (71.9%) as well.1
With this in mind, this article focuses on the evaluation and diagnosis of acute toxic ingestions in children. Chronic ingestions and occupational exposures are not discussed. This article provides a realistic guide to the evaluation and treatment of pediatrie toxic ingestions by simplifying the controversial topics and providing a basic approach to care.
The challenge to the clinician is deciding which ingestions are potentially high risk and which are inconsequential. The clinician must triage patients based on risk of toxicity. This process of toxic triage allows the clinician to assess which decontamination and treatment regimens potentially are beneficial and which are unnecessary. A focused medical history, a physical examination, and a few selected tests allow the clinician to find the potentially dangerous ingestion in the haystack of nontoxic exposures and rapidly initiate the decontamination and treatment interventions that are most likely to be of benefit (Figure 2, see page 939).
Occasionally, aggressive interventions need to be performed before the complete history, physical examination, and diagnostic tests are completed. The initial priority in any sick patient, regardless of the cause, should focus on a primary survey, including an evaluation of the patient's airway, breathing, and circulation (ABCs). Once life-saving measures have been initiated, a more detailed evaluation as outlined in this article can be performed. This article does not discuss the initial stabilization of the severely ill patient, as it is assumed throughout that necessary life-saving interventions have been performed.
History has been described as unreliable in the toxic ingestion patient,2 and many authors appropriately advise caution when interpreting histories obtained from suicidal patients or others with the potential for secondary gain or perceived risk of arrest.3'4 The history is not limited to information volunteered by the patient, however. Critically evaluating the patient's age, obtaining information from other sources, and probing for specific details of the event are essential aspects of obtaining a thorough history.
Age is an important detail that can help the clinician develop appropriate toxic triage. Serious poisoning is a rare problem in infancy. Before children are able to ambulate or crawl, they rarely are able to obtain dangerous medications and poisons, more commonly acquiring less toxic substances in their immediate grasp, such as cosmetics and soaps. Infants and nonmobile babies with profound symptoms should prompt consideration of child abuse or, possibly, sudden infant death syndrome.
In 2003, children younger than 6 were involved in 52% of all toxic exposures.1 Of these, 0.06% (732) led to a major effect, and 0.003% (34) died. As these data illustrate, the majority of exposures in this age-group cause minimal to no toxicity. History should focus on medications the child has access to (both over-the-counter and prescription) and potential household toxins. Special attention should be paid to those toxins associated with deadly exposures in the last few years, including analgesics (eg, acetaminophen, salicylates, opioids), hydrocarbons, caustic agents, carbon monoxide, and antidepressants.1'5'6
Unlike the younger age groups, fatalities in those ages 13 to 19 predominately are associated with intentional events, such as suicide and abuse. The history should, therefore, include specific questioning about suicidal intentions and illicit or recreational drug use. Because there may be secondary gain issues, obtaining information from other sources is especially important in this populatioa The most common classes of substances involved in fatalities in this age group have been analgesics, stimulants and street drugs, antidepressants, cardiovascular agents, and sedatives/hypnotics/antipsychotics.1
A thorough history for the potential toxic exposure includes information provided by witnesses, family members, friends, and emergency medical services personnel. Inquiring about the environment in which the patient was found, circumstances preceding and surrounding the incident, pill bottles or containers nearby, smells or unusual materials in the home, occupation of those in the family, and the presence of a suicide note all may provide information helpful for treatment.
Quantifying the exact amount of agent ingested by the patient is usually difficult. The worst possible scenario should be assumed when calculating quantity of toxin potentially ingested. This worst-case setting should be used for initial toxic triage decisions. As more information becomes available, toxic triage can be re-evaluated and treatment decisions modified.
A thorough physical examination is the second key component of toxic triage. History may help determine which agents were ingested, but more important, physical examination findings can determine which agents are likely to be causing the toxic symptoms. A critical evaluation of both will determine if these symptoms are likely to lead to morbidity.
Although all toxins take time to be absorbed and distributed throughout the body, clinicians should maintain a healthy suspicion for toxins known to cause minimal initial symptoms but profound delayed toxicity and symptoms. Commonly encountered toxins with delayed presentations are outlined in Sidebar 1 (see page 938). Many of the laboratory and ancillary studies performed in the poisoned patient are directed towards identifying these delayed or silent poisons.
Figure 2. Integrating information from the medical history, physical examination, and laboratory evaluation yields an estimation of the risk of morbidity and mortality. This process has been termed "toxic triage. "The risk estimation is used to guide decontamination and treatment decisions. Aggressive interventions should be reserved for those at higher risk of morbidity or mortality.
Delayed symptoms aside, a patient's presenting symptoms can affect toxic triage significantly. A critical evaluation of vital signs combined with a thorough physical examination can narrow an initially wide differential diagnosis, direct initial treatment interventions, and focus diagnostic evaluations. Other reviews provide extensive lists of drugs that cause specific vital sign abnormalities that are not included in this article.7'8 A general understanding of the common mechanisms leading to these abnormalities may be more helpful than extensive lists to direct toxic triage.
Changes in vital signs frequently are affected by the complex interactions of hormones, cellular messengers, and neurotransmitters on specific receptors in the brain and at endorgans. A basic understanding of this receptorology can allow the clinician to hone toxic triage and focus treatment strategies. A summary of important receptor interactions is provided in Table 1 (see page 941).
Some clinicians prefer to group physical findings into categories that are common to specific groups of drugs or toxins. These symptom groups have been described as toxic syndromes or toxidromes. It is important to remember that toxidromes describe a classic presentation, but depending on the amount of toxin ingested, other toxin or medication actions, competing effects from co-ingestants, and patient comorbidities, patients can present with a spectrum of symptoms that may be difficult to categorize.
Some important toxidromes and their effect on specific organ systems are outlined in Table 2 (see page 942-943). Space limitations preclude a thorough discussion of the pathophysiology related to these toxidromes, but further detail can be found in other reviews.9
Nontoxic conditions produce vital sign abnormalities that can resemble toxic ingestions, frequently through similar mechanisms. A high index of suspicion for nontoxic etiologies is an essential component of toxic triage. A directed lab exam can help to exclude these nontoxic etiologies.
As technology has advanced, a dizzying number of tests have become available to measure and identify potential toxins. Which tests to order and how many tests are necessary can be difficult to determine and is dependant on the reliability of historical facts, the patient's symptoms, vital signs, and physical examination findings. Devising a standard laboratory set for the broad spectrum of patients from asymptomatic to emergently ill can be difficult.
Initial studies should be focused towards finding the dangerous and potential life-threatening toxins (the safety net set; Sidebar 2, see page 943). Hypoglycemia can present with nearly any neurological deficit, and blood glucose should be performed on every patient with altered mental status. Electrolytes with BUN/ creatinine enable the clinician to probe for an anión gap acidosis, check electrolyte status, and evaluate renal function. The electrocardiogram screens not only for dysrhythmias but also for early signs of cardiotoxins, such as a wide QRS or QT interval. Serum acetaminophen should be ordered on nearly all poisoning patients to ensure this common killer is not overlooked. A urine pregnancy test should be performed in all women of childbearing age being investigated for a potential toxic ingestion.
More detailed studies are used to investigate specific concerns based on the toxic triage evaluation (the probing set; Sidebar 2). Urinalysis may reveal telltale signs of poisonings such as crystals or myoglobinuria. If rhabdomyolysis is considered, creatinine phosphokinase should be ordered and serial levels followed. An arterial blood gas can determine acid-base status, and co-oximetry will aid in the diagnosis of carbon monoxide poisoning and methemoglobinemia. Serum osmolality may be a helpful tool when considering toxic alcohol ingestion, but proper interpretation is critical. Urine drug screens are discussed in detail below. Comprehensive drug screens and specific drug levels can positively identify and quantify particular toxins, but the results may not be available in time to affect initial interventions. Other specific tests not mentioned in this article may be necessary in some situations.
All tests have limitations. Physicians frequently order toxicologie tests without understanding the limitations or the implications of a positive or negative result. The urine drug screen is probably the most common example of this mistake. The urine drug screen is a selected group of immunoassay tests that generally were developed for workplace or drug screening programs. By design, they are meant to detect the parent drug or its metabolites up to days after use. Therefore, a positive urine drug screen does not necessarily confirm the patient's symptoms are due to that agent, as it may have been used days previously.
Furthermore, many immunoassays are poorly sensitive and specific, leading to frequent false positives and false negatives. Thus, the urine drug screen rarely influences acute interventions except in some specific situations. Urine drug testing is discussed in more detail in the article by Ahrendt and Miller (see page 956).
Not long ago, many physicians treated all poisonings in a similar manner, with aggressive decontamination and standard antidote regimens. Today, evidence indicates decontamination is unlikely to benefit most patients. Deciding which patients will benefit remains a highly controversial topic.
Rece ptero logy
Decontamination should be individualized based on the toxic triage risk assessment for each patient. Consideration of the known historical information, potential danger of the toxins ingested, and symptoms of the patient all should be considered when deciding how aggressively to pursue methods of decontamination.
Another important aspect of choosing decontamination methods is an understanding of the evidence (or lack thereof) showing potential benefit as well as the possibility of risk. During the past 2 decades, much has been learned regarding the potential benefit of decontamination, and general recommendations have changed dramatically.
Syrup of Ipecac
Syrup of ipecac (SOI) is a derivative of the ipecacuanha plant (CephaUs ipecacuanha). The active alkaloids, emetine and cephaeline, lead to vomiting by acting both centrally at the chemoreceptor trigger zone and locally by stimulating the gastric mucosa.10'11 SOI recovers possibly significant amounts of simulated toxin if given within minutes of the ingestion.12'16 Unfortunately, this benefit diminishes rapidly with time,10'13 and there is no clinical evidence that SOI improves patient outcomes, even after early administration.17·19 The time to vomiting and duration of emetic effect after SOI is variable.12'13'15'16'20'21
SOI treatment is limited or contraindicated in patients who might develop a compromised airway or who have ingested corrosive substances or hydrocarbons. It also carries the potential complications of lethargy, drowsiness, and prolonged vomiting that could delay other therapies. These cumulative data led the American Academy of Clinical Toxicology (AACT) and the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) to issue a position statement regarding SOI. An excerpt from this position statement reads: "(SOI) should not be administered routinely in the management of poisoned patients. ... its routine administration in the emergency department should be abandoned."10 This position statement appears to be in line with routine practice. In 2003, only 0.4% of exposures reported to the AAPCC were treated with ipecac.1 This probably has declined further following the release of a similar policy statement by the American Academy of Pediatrics (AAP).22
SOI use in the home is also losing popularity. In 1989, the AAP published the recommendation to keep a 1 -ounce bottle of SOI in the home,22 although the efficacy and effectiveness of this recommendation had been questioned.23-24 Since that time, literature revealing frequency of inappropriate SOI use,25 lack of efficacy when administered in the home,26 guidelines from the AAPCC,27 and the position statement from AACT/ EAPCCT10 led the AAP to revise its previous recommendation. An excerpt from the new AAP recommendation includes: "After reviewing the evidence, the AAP believes ipecac should no longer be used routinely as a home treatment strategy, [and] that existing ipecac in the home should be disposed of safely ..."22
Gastric lavage has been used for nearly 200 years28 as an empirically helpful method of removing toxins from the stomach. Gastric lavage involves passing a large-bore orogastric tube into the stomach, followed by sequential administration and aspiration of liquid in the hope of removing toxins present in the stomach. As with SOI, the efficacy of gastric lavage has been questioned. Similar to the literature in SOI, gastric lavage has been shown to recover substantial amounts of simulated toxin from the stomach,15'16 but the amount diminishes with time.12'29 Kulig et al.19 found some benefit to performing lavage within the first hour after ingestion in a subset of patients defined as moderately or severely intoxicated, but studies with similar design have been contradictory.17
Gastric lavage is contraindicated in a number of incidences, including inappropriately protected airways, ingestion of corrosive substances or hydrocarbons, and patients at risk of gastrointestinal perforation or hemorrhage. Reported complications include aspiration, respiratory insufficiency, mechanical injury or perforation, and electrolyte imbalance.28'30 Gastric lavage remains controversial because relatively few clinical studies have been performed. A position statement by the AACT/EAPCCT states: "[Gastric lavage] should not be employed routinely in the management of poisoned patients ... There is no evidence that its use improves clinical outcome and it may cause significant morbidity. [Gastric lavage] should not be considered unless a patient has ingested a potentially life-threatening amount of a poison and the procedure can be undertaken within 60 minutes of ingestion. Even then, clinical benefit has not been confirmed in controlled studies."30 These last statements appropriately restrict the procedure to a small subset of patients who present to the emergency department quickly after ingestion. Further limiting this subset to those with potentially life-threatening outcomes narrows the number of patients that could potentially benefit from gastric lavage to a very small number indeed.
The United States physician population appears to understand, because the use of gastric lavage has decreased during the past few years.1'5'6 Because performing the procedure inadequately is likely to increase complications and decrease potential benefit, gastric lavage should only be performed by staff experienced with its proper execution.
Activated charcoal is made by superheating highly carbonaceous materials with activating agents, such as steam or carbon dioxide, to form a substance with a huge surface area and, in turn, a high adsorptive capacity.31'32 Activated charcoal potentially can decrease the absorption of a wide variety of toxins and is ineffective for only a small number of specific agents. Sidebar 3 lists those agents that are unlikely to respond to activated charcoal administration.
Numerous studies have concluded that gastric emptying with lavage or SOI is no more efficacious than activated charcoal alone,17'18'33 supporting the use of activated charcoal as the sole intervention for the overwhelming majority of ingestions that require decontamination. Like other forms of gastric decontamination, the benefit of activated charcoal is dependant on how quickly it can be administered after toxin ingestion. Even with its high adsorption rates, there is little evidence showing clinical improvement after activated charcoal.
The AACT/EAPCCT position statement for single-dose activated charcoal summarizes: "Activated charcoal should not be routinely administered in the management of poisoned patients ... the effectiveness of activated charcoal decreases with time, the greatest benefit is within 1 hour of ingestion ... there are insufficient data to support or exclude its use after 1 hour of ingestion. There is no evidence that the administration of activated charcoal improves clinical outcome."32 However, most agree the indirect evidence is convincing enough to warrant the use of activated charcoal if toxic triage estimates make decontamination necessary.34
The optimal dose of activated charcoal is dependant on many variables, including substances ingested, time of ingestion, and patient characteristics. Based on results of in vitro studies, a charcoal-to-drug ratio of 10:1 is a reasonable goal for most ingestions, with a 1 g/kg recommendation for unquantified ingestions.34'35 Activated charcoal should be used only in patients with adequately protected airways.
Cathartics, most commonly sorbitol, are occasionally used in combination with activated charcoal. Unfortunately, experimental data are conflicting regarding this combination, and improved outcomes have not been demonstrated.36 The AACT/EAPCCT recommend against using cathartics with or without activated charcoal: 'The administration of cathartic alone has no role in the management of the poisoned patient"; "the routine use of a cathartic in combination with (activated charcoal) is not endorsed."36
Multiple doses of activated charcoal (MDAC) have been promoted as possibly beneficial in the treatment of poisonings with drugs with prolonged half-lives and small volumes of distribution. The theory involves interrupting the enterohepatic and enteroenteric recirculation of drugs and pulling drug into the gut lumen following its concentration grathent. Although MDAC has been shown to increase the elimination of a number drugs,37 clinical benefit has never been proven.38 The AACT/EAPCCT position statement summarizes; "(MDAC) should be considered only if a patient has ingested a life-threatening amount of carbamazepine, dapsone, phénobarbital, quinine or theophylline ... no controlled studies have demonstrated clinical benefit."37
MDAC can lead to constipation and bowel obstruction. Its use is contraindicated in the presence of decreased peristalsis or obstruction.
Whole Bowel Irrigation
The technique of whole bowel irrigation (WBI) initially was used for preoperative bowel cleansing,39 but concerns about fluid and electrolyte shifts precluded its use in toxic ingestions. The advent of osmotically balanced polyethylene glycol electrolyte solutions (PEG ES) alleviated these concerns, and toxícologists became interested in the idea of pushing toxins through the gut and out of the body before they are absorbed. This process involves administering large volumes of PEG ES, preferably through a nasogastric or feeding tube.
Selected Antidotes and Methods of Enhancing Toxin Elimination
Few clinical trials have been performed, so the bulk of the information relating to WBI comes from volunteer studies, animal studies, and case reports.40 Although benefit has not been proven, there is theoretical benefit after large ingestions of heavy metals, sustained-release or enteric-coated tablets, and illegal drug packets. The AACT/ EAPCCT position statement is understandably vague: 'There is no conclusive evidence that WBI improves outcome in the poisoned patient."40
The best dose of PEG ES in WBI has not been studied, but most recommend a goal of 1,500 to 2,000 mL per hour in adults, 1,000 mL per hour in children ages 6 to 12, and 500 mL per hour in children ages 9 months to 6 years.41 WBI is contraindicated in patients with unprotected airways, hemodynamic instability, intractable vomiting, GI hemorrhage, ileus, perforation, or obstruction.40
The majority of pediatrie toxic ingestions cause little or no morbidity, and the only treatment required is supportive care. To get to this point, good toxic triage involving a detailed history, physical examination, and directed laboratory evaluation should be performed to exclude deadly and delayed toxins. Lowrisk patients can be discharged to the care of sensible parents. Some may need to be observed to ensure delayed toxicity does not occur as drugs are absorbed or metabolized. Noninvasive decontamination procedures (primarily activated charcoal) may be appropriate in some of these cases. High-risk patients and those exhibiting prolonged or dangerous symptoms need admission for treatment and extended observation. Aggressive decontamination procedures may be considered in this small subgroup of patìents, and serial laboratory studies are likely to be necessary.
As the risk of toxicity increases, the invasiveness of monitoring and level of supportive care should increase in kind. Low-risk patients may require no monitoring, while high-risk patients require intravenous access, frequent or continuous vital sign checks, cardiac monitoring, and possibly invasive monitoring methods (eg, arterial line, central pressure monitoring). In symptomatic patients, diligent attention to ABCs and aggressive interventions to preserve stable vital signs are necessary.
Antidotal therapy is the "glamorous" side of toxicology, where people foresee single interventions producing immediate, dramatic reversals of toxicity. Unfortunately, the response usually is not that dramatic. Antidotes are available only for a limited number of toxins and are used rarely in everyday practice. With the exception of N-acetylcysteine and naloxone, few antidotes are used routinely in the treatment of poisoned patients.
Antidotal therapy is, however, a vital aspect of treatment for some specific toxins that complements the continual reassessment of toxic triage, appropriate use of decontamination, and meticulous supportive care provided in all poisonings. Table 3 (see page 944) gives a list of antidotes with which the general physician should be familiar. Although not strictly antidotes, common methods used to enhance the elimination of toxins also are listed. Unless the clinician is familiar with the use, indications, side effects, and contraindications of the antidote, an AAPCC-certified poison control center should be contacted when considering its use.4:W4
Poison prevention efforts can have a great effect on the incidence of pediatrie poisonings. Laws requiring childresistant packaging, the cooperation of manufacturers to decrease the concentrations of alkali in cleaning products, warning labels, public education efforts, and poison control center involvement all most likely have contributed to decreasing the morbidity associated with pediatrie toxic ingestions.41'45'46
While improvements have been made, the bulk of pédiatrie ingestions are still easily preventable.1'47 Creative packaging efforts, such as the United Kingdom's experience with paracetamol blister-packs,48 improving public health education, enhancing clinician awareness, better collaboration among agencies to synergize efforts while avoiding duplication, and increasing funding for research are all easy targets for improvement
A universal poison control center telephone number in the US, 1-800-2221222, routes all calls to a local poison control center. Clinicians can help by distributing this number, as well as the AAP poison prevention and treatment brochures, available online at http:// www. aap.org/healthtopics/safety. cfm.
Pediatrie toxic ingestions are treated commonly by pediatricians and emergency physicians. Significant injury after these ingestions is infrequent, but identifying the dangerous ingestion is sometimes a difficult task. By performing a detailed history, focused physical examination, and directed laboratory evaluation, an estimation of risk can be developed. This article introduced the term "toxic triage" to describe this process. The toxic triage estimation allows the clinician to make thoughtful decontamination and treatment decisions. Familiarity with the literature supporting or refuting each decontamination method allows educated decisions to be made. Supportive care is an integral part of treatment for all poisonings, from asymptomatic to life-threatening. Most antidotes are used rarely in clinical practice, but familiarity with common antidotes benefits those patients with specific hazardous ingestions. Prevention efforts have the potential to decrease the incidence of pediatrie poisonings. The universal poison control center number provided should be distributed and posted in homes, clinics, and emergency departments.
1. Watson WA, Lìtovìtz TL, Kleìn-Schwartz W, et al. 2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med, 2004; 22(5): 335-404.
2. Wright N. An assessment of the unreliability of the history given by self-poisoned patients. CKn Toxicol. 1980; 16(3): 38 1-384.
3. HackJB,HoffmanRS. General management of poisoned patients, hi: Tìntìnallì JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 5th ed. New York, NY: McGraw-Hill; 2000: 1057-1062.
4. Kulig K. Toxicologie problems: general management principles, hi: Rosen P, Barkin R, Danzi DF, et al. Emergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby; 1998:1244-1249.
5. Litovitz TL, Klein-Schwartz W, Rodgers GC Jr, et al. 2001 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2002;20(5):391-452.
6. Watson WA, Litovitz TL, Rodgers GC Jr, et al. 2002 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2003; 2 1(5): 353-421.
7. Goldfrank LR, Flomenbaum NE, Lewin NA, et al. Vital signs and toxic syndromes. In: Goldfrank, LR, Flomenbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologie Emergencies. 7th ed. New York, NY: McGraw-Hìll; 2002:255-260.
8. Krenzelok EP, Leìkin JB. Approach to the poisoned patient. Dis Mon. 1996;42(9): 509-607.
9. Oison KR, Pentel PR, Kelley MT. Physical assessment and differential diagnosis of the poisoned patient. MedToxicol. 1987;2(1):52-81.
10. Krenzelok EP, McGuigan M, Lheur P. Position statement: ipecac syrup. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol CUn Toxicol. 1997;35(7):699-709.
11. Chomchai CG. Ipecac syrup, hi: Olson KR, ed. Poisoning & Drug Overdose. 4th ed. New York, NY: Lange Medical Books/McGrawHiU; 2004:228-229.
12. Tenenbein M, Cohen S, Sitar DS. Efficacy of ipecac -induced emesis, orogastric lavage, and activated charcoal for acute drug overdose. Ann Emerg Med. 1987; 16(8): 838-841.
13. Saincher A, Sitar DS, Tenenbein M. Efficacy of ipecac during the first hour after drug ingestion in human volunteers. J Toxicol Clin Toxicol. 1997;35(6):609-615.
14. Neuvonen PJ, Vartiainen M, Tokola O. Comparison of activated charcoal and ipecac syrup in prevention of drug absorption. Eur J Clin Pharmacol, 1983;24(4):557-652.
15. Young WF Jr, Bìvìns HG. Evaluation of gastric emptying using radìonuclìdes: gastric lavage versus ipecac -induced emesis. Ann EmergMed, 1993;22(9): 1423-1427.
16. Auerbach PS, Osterloh J, Braun O, et al. Efficacy of gastric emptying: gastric lavage versus emesis induced with ipecac. Ann Emerg Med. 1986;15(6):692-698.
17. Pond SM, Lewis-Driver DJ, Williams GM, Green AC, Stevenson NW. Gastric emptying in acute overdose: a prospective randomised controlled trial. Med JAust. 1995; 163(7): 345-349.
18. Merigian KS, Woodard M, Hedges JR, et al. Prospective evaluation of gastric emptying in the self-poisoned patient. Am J Emerg Med. 1990;8(6):479483.
19. Kulig K, Bar-Or D, Cannili SV, Rosen P, Rumack BH. Management of acutely poisoned patients without gastric emptying. Ann Emerg Med. 1985;14(6):562-567.
20. Curtis RA, Barone J, Gìacona N. Efficacy of ipecac and activated charcoal/cathartic. Prevention of salicylate absorption in a simulated overdose. Arch Intern Med. 1984; 144(l):48-52.
21. McNamara RM, Aaron CK, Gemborys M, Davidheiser S. Efficacy of charcoal cathartic versus ipecac in reducing serum acetaminophen in a simulated overdose. Ann Emerg Med. 1989;18(9):934-938.
22. Poison treatment in the home. American Academy of Pediatrics Committee on Injury, Violence, and Poison Prevention. Pediatrics. 2003;112(5):1182-1185.
23. Dershewitz RA, Niederman LG. Ipecac at home - a health hazard? Clin Toxicol. 1981; 18(8):969-972.
24. Garrettson LK. Ipecac home use: we need hope replaced with data. J Toxicol Clin Toxicol. 1991;29(4):515-519.
25. Chafee-Bahamon C, Lacouture PG, Lovejoy FH Jr. Risk assessment of ipecac in the home. Pediatrics. 1985;75(6):1105-1109.
26. Bond GR. Home syrup of ipecac use does not reduce emergency department use or improve outcome. Pediatrics. 2003;112(5):1061-1064.
27. Manoguerra AS, Cobaugh DJ; Guidelines for the Management of Poisonings Consensus Panel. Guideline on the Use of Ipecac Syrup in the Out-of-Hospital Management of Ingested Poisons. American Association of Poison Control Centers. 2004. Available at: http://www.aapcc.org/Finalized PMGdlns/Ipecac%20Guideline% 20-% 20 final%20for%20JTCT.pdf. Accessed November 9, 2005.
28. Tucker JR. Indications for, techniques of, complications of, and efficacy of gastric lavage in the treatment of the poisoned child. Curr Opin Pediatr. 2000;12(2):163-165.
29. Comstock EG, Faulkner TP, Boisaubin EV, Oslon DA, Comstock BS. Studies on the efficacy of gastric lavage as practiced in a large metropolitan hospital. Clin Toxicol. 1981; 18(5):58 1-597.
30. Vale JA. Position statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35(7):711-719.
31. Rowland MA. Antidotes in depth: activated charcoal. In: Goldfrank, LR, Flomenbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologie Emergencies. 7th ed. New York, NY: McGraw-Hill; 2002:469474.
32. ChykaPA, Seger D. Position statement: singledose activated charcoal. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997; 35(7):721-741.
33. Komberg AE, Dolgin J. Pediatrie ingestions: charcoal alone versus ipecac and charcoal. Ann Emerg Med. 1991;20(6):648-651.
34. Smilkstein MJ. Techniques used to prevent gastrointestinal absorption of toxic compounds. In: Goldfrank, LR, Flomenbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologie Emergencies. 7th ed. New York, NY: McGraw-Hill; 2002:44-57.
35. Keamey TE. Charcoal, activated. In: Olson KR, ed. Poisoning & Drug Overdose. 4th ed. New York, NY: Lange Medical Books/McGraw-Hill; 2004:427-428.
36. Position paper cathartics. J Toxicol Clin Toxicol. 2004;42(3): 243-253.
37. 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(6):731-751.
38. Bradberry SM, VaIeJA. Multiple-dose activated charcoal: a review of relevant clinical studies. J Toxicol CUn Toxicol. 1995;33(5):40M16. 39. Perrone J, Hoffman RS, Goldfrank LR. Special considerations in gastrointestinal decontamination. Emerg Med Clin North Am. 1994;12(2):285-299.
40. Position paper whole bowel irrigation. J Toxicol Clin Toxicol. 2004;42(6): 843-854.
41. Mannenbach M. An update on pediatrie toxicology. Pediatrie Emergency Medicine Reports. 2004 Aug:93-104.
42. Erdman AR. Hydroxycobalamin. In: Olson KR, ed. Poisoning & Drug Overdose. 4th ed. New York, NY: Lange Medical Books/MeGraw-Hill; 2004:453-454.
43. Yuan TH, Kerns WP 2nd, Tomaszewski CA, Ford MD, Kline JA. Insulin-glucose as adjunctive therapy for severe calcium channel antagonist poisoning. J Toxicol Clin Toxicol. 1999;37(4):463474.
44. Megarbane B, Karyo S, Baud FJ. The role of insulin and glucose (hyperinsulinaemia/euglycaemia) therapy in acute calcium channel antagonist and beta-blocker poisoning. ToxicolRev. 2004;23(4):215-222.
45. Lovejoy FHJr, Robertson WO, Woolf AD. Poison centers, poison prevention, and the pediatrician. Pediatrics. 1994;94(2Pt l):220-224.
46. Miller TR, Lestina DC. Costs of poisoning in the United States and savings from poison control centers: a benefit-cost analysis. Ann EmergMed. 1997; 29(2): 239-245.
47. Hoecker JL, Dougherty CH, Loney L, Mìddelkamp JN. Pediatrie ingestions and poison control. Mo Med. 1976;73(11):619-621. 48. Turvill JL, Burroughs AK, Moore KP. Change in occurrence of paracetamol overdose in UK after introduction of blister packs. Lancet. 2000;355(9220): 2048-2049.
Selected Antidotes and Methods of Enhancing Toxin Elimination