Chapter 105 Principles of Toxin Assessment and Screening
Despite significant progress in preventive measures, poisonings in children and adolescents continue to be common occurrences. More than 51% of almost 2.5 million poison center calls in the United States in 2007 involved children younger than 6 years of age.1 Although many of these exposures are medically trivial, poisonings account for an important number of all pediatric hospital visits and hospitalizations. Not all children are equally at risk for serious poisoning. The incidence of poisoning is highest among children 1 to 3 years of age. Boys slightly outnumber girls as victims of unintentional exposures. Children with developmental delays and/or pica, as occurs with autistic spectrum disorders, have an increased risk for self-poisoning. A second peak of serious poisonings occurs in adolescence, when a suicide attempt by poisoning (with females disproportionately overrepresented) or a misadventure involving substance abuse becomes the common circumstance underlying a poisoning episode. Adolescents with anorexia nervosa or psychiatric conditions such as clinical depression are especially vulnerable to self-poisoning.
Common Agents Involved
The most common agents involved in preschooler poisonings are medications, such as analgesics, cough and cold preparations, and dermatological preparations; household products, such as cleaning agents, soaps, and detergents; and plants. Table 105-1 lists those agents responsible for the majority of calls to poison control centers. The agents most frequently involved in serious pediatric poisonings (those requiring intensive care) are prescription medications (tricyclic antidepressants, anticonvulsants, digitalis, and opiates), alcohol, and hydrocarbon-based household products. Lead poisoning and carbon monoxide poisoning related to house fires are less recognized, but frequent causes of poisoning hospitalization in childhood. International adoptees and children immigrating to the United States may have been exposed to lead, arsenic, or other toxins in a polluted environment in their home countries or by their family’s use of poorly regulated remedies. Clinicians should ask caretakers about the types and doses of any medications, herbs, vitamins, diet supplements, or ethnic remedies being used to treat the child’s other health problems. Such therapies may be interacting with the toxins responsible for the poisoning or otherwise contributing to the child’s toxicity.
Toxic Agent | Number of Poison Center Calls | Percent (%) Total |
---|---|---|
Total | 1,234,137 | 100% |
Percentages are based on the total number of exposures in children <6 years (1,169,478) rather than the number of substances.
Modified from Bronstein AC, Spyker DA, Cantilena LR Jr, et al: 2007 annual report of the American Association of Poison Control Centers’ national poison data system (NPDS): 25th annual report, Clin Toxicol (Phila) 46(10):927, 2008.
Resources for the Clinician
In making the diagnosis of an unknown poisoning, the physician must rely on observation, history-taking abilities, and clinical skills. Laboratory analyses and radiographic findings are sometimes helpful. References such as Drug Information (available annually from the American Hospital Formulary Service [AHFS], American Society of Hospital Pharmacists Bethesda, Md.) and the Poisindex computer database (Micromedex Cooperation, Greenwood Village, Colo.) can be helpful in identifying drugs and their actions and precautions. The regional poison control center (telephone: 800-222-1222) can provide helpful consultative services by toxicologists. Such services may include:
General Assessment of the Poisoned Patient
History
An accurate history is vitally important in the diagnosis of unknown poisoning. Surprisingly, the physician in the intensive care unit (ICU) may be the first health professional who can sit with parents and carefully review the possible circumstances of the exposure. Poisonings may occur by various routes including ingestion, inhalation, ocular exposure, dermal exposure, mucous membrane involvement, or parenteral exposure. Once the child’s condition has been stabilized, the pediatrician should query the family about the incident, with particular attention to the environmental, patient, and toxic agent factors as outlined in Table 105-2. In acute, unintentional exposures in young children, the time of exposure and toxin involved frequently are accurately known. The importance of obtaining the precise ingredients in the suspected toxic agents cannot be overemphasized. Parents should bring the product containers or medication labels. For estimations of liquid toxins, the average swallow of a young child is approximately 5 to 10 mL while that of the older child and adolescent is 10 to 15 mL. The clinician must appreciate the fact that parents frequently minimize the child’s exposure to a toxin in an attempt to deny the threat of injury or to assuage their guilt that such an episode occurred. Therefore it is prudent to assume the worst possible scenario in calculating the maximum dose of a drug or household product a child could have swallowed in a poisoning and to treat the patient accordingly. Calculation of the dose the child might have received is sometimes helpful, using the maximum number of missing tablets or amount of liquid, the concentration of the drug or chemical, and the child’s weight.
Environment | Patient | Toxin |
---|---|---|
The latency between the time of ingestion and the onset of symptoms is important. The tempo of progression of symptoms and signs also may help the clinician gauge the severity of the intoxication and the urgency with which intervention is necessary. However there are some exceptions to this rule. Patients poisoned by some toxins, such as paraquat and the Amanita mushroom toxin, classically have a relatively asymptomatic period of 12 hours or more but then manifest life-threatening pulmonary or hepatic toxicity, respectively.2,3 Some drugs, such as sulfonylurea hypoglycemics and valproic acid, can also have similar latency periods prior to the onset of severe toxicity.4,5 Adolescent poisonings are confounded by the intentionality of the episode and the frequent unreliability of the adolescent’s history. Adolescents in distress may be evasive, misleading, or otherwise uncommunicative. Their ability to remember or provide a coherent account of what happened may be distorted by the effects of the drugs taken. The clinician cannot assume that the time of exposure, the dose, or even the toxic agents themselves are accurately recounted.
Physical Examination
The physical examination is crucial for assessment of the patient’s medical stability and for identification of the unknown poison. Specific changes in vital signs and symptoms are associated with likely toxins or groups of toxins. Such characteristic clinical patterns of illness are sometimes termed toxidromes. Table 105-3 lists some of the more common toxidromes important in pediatric poisoning. Families are using herbs and diet supplements with increasing frequency to treat their children’s illnesses or simply to promote their general well-being. However, serious poisonings in which herbs and dietary supplements are implicated are appearing in the medical literature.6 Table 105-4 lists some examples of toxicities associated with particular herbal remedies.
Signs and Symptoms | Agent |
---|---|
Dilated pupils, tachycardia, tachypnea, warm moist skin, flushing, increased sweating, agitation | Sympathomimetic syndrome |
Miosis, salivation, diarrhea, bronchorrhea, lacrimation, seizures, respiratory failure, bradycardia | Organophosphate insecticides |
Fever, tachypnea, hyperpnea, lethargy, metabolic acidosis | Salicylates |
Seizures, metabolic acidosis, history of tuberculosis, hyperglycemia | Isoniazid |
Dry mouth and skin, flushed appearance, dilated pupils, fever, ileus, urinary retention, disorientation | Anticholinergic syndrome |
Oculogyric crises, dystonia, opisthotonus | Phenothiazines |
Severe metabolic acidosis, sluggish pupils, hyperemic retina, blurred vision | Methanol |
Hypoglycemia, lethargy, ataxia, seizures, characteristic breath odor | Ethanol |
Lethargy or coma, metabolic acidosis, active urinary sediment, crystalluria | Ethylene glycol |
Headache, flulike symptoms, lethargy, dizziness, coma | Carbon monoxide |
Pinpoint pupils, coma, respiratory depression | Opiate |
Hyperthermia, neuromuscular rigidity, autonomic dysfunction, agitation, delirium | Serotonin syndrome |
Metabolic acidosis, prolonged QRS interval, coma, seizures, dilated pupils, dysrhythmias | Tricyclic antidepressants |
Protracted vomiting, tremors, tachycardia, anxiety, seizures, hypotension | Theophylline |
Feeling of impending doom, sudden coma, metabolic acidosis, hypotension, bitter almond odor | Cyanide |
Rotatory nystagmus, delirium; “4 C’s”: combative, catatonia, convulsions, coma | Phencyclidine |
Herbal Product | Toxic Chemicals | Toxic Effects |
---|---|---|
Aconite (Aconitum spp.) | Aconitine alkaloids | Nausea, vomiting, paresthesias, weakness, hypotension, asystole, arrhythmias, bradycardia |
Chamomile (Matricaria chamomilla, Anthemis nobilis) | Allergens | Anaphylaxis, contact dermatitis |
Chapparal (Larrea divaricata, Larrea tridentata) | Nordihydroguaiaretic acid | Nausea, vomiting, lethargy, hepatitis |
Cinnamon oil (Cinnamomum spp.) | Cinnamaldehyde | Dermatitis, abuse syndrome |
Coltsfoot (Tussilago farfara) | Pyrrolizidines | HVOD |
Comfrey (Symphytum officinale) | Pyrrolizidines | HVOD |
Crotalaria spp. | Pyrrolizidines | HVOD |
Echinacea (Echinacea angustifolia, Compositae spp.) | Polysaccharides | Asthma, atopy, angioedema, anaphylaxis, urticaria |
Eucalyptus (Eucalyptus globulus) | 1,8-cineole | Drowsiness, ataxia, nausea, vomiting, seizures, coma, respiratory failure |
Garlic (Allium sativum) | Allicin | Dermatitis, chemical burns, oxidizing agent |
Germander (Teucrium chamaedrys) | Hepatotoxicity | |
Ginseng (Panax ginseng) | Ginsenoside | Ginseng abuse, diarrhea, anxiety, insomnia, hypertension |
Glycerated asafetida | Oxidants | Methemoglobinemia |
Grousel (Senecio longilobus) | Pyrrolizidines | HVOD |
Heliotrope, turnsole (Crotalaria fulva, Heliotropium, Cynoglossum officinale) | Pyrrolizidines | HVOD |
Jin bu huan (Stephania spp., Corydalis spp.) | L-Tetrahydropalmitine | Hepatitis, lethargy, coma |
Kava-kava (Piper methysticum) | Kawain, methysticin | Hepatic failure, “kavaism” neurotoxicity |
Kelp | Iodine | Thyroid dysfunction |
Laetrile | Cyanide | Coma, seizures, death |
Licorice (Glycyrrhiza glabra) | Glycyrrhetic acid | Hypertension, cardiac arrhythmias, hypokalemia |
Ma huang (Ephedra sinica) | Ephedrine | Cardiac arrhythmias, seizures, stroke, hypertension |
Monkshood (Aconitum napellus, A. columbianum) | Aconite | Cardiac arrhythmias, weakness, coma, shock, paresthesias, vomiting, seizures |
Nutmeg (Myristica fragrans) | Myristicin, eugenol | Hallucinations, emesis, headache |
Nux vomica | Strychnine | Seizures, abdominal pain, respiratory arrest |
Pennyroyal (Mentha pulegium or Hedeoma spp.) | Pulegone | Centrilobular liver necrosis, fetotoxicity, seizures, shock |
Ragwort (golden) (Senecio aureus, Echium) | Pyrrolizidines | HVOD |
Wormwood (Artemisia spp.) | Thujone | Seizures, dementia, tremors, headache |
HVOD, Hepatic veno-occlusive disease.
Modified from Committee on Injuries & Poison Prevention: Children’s environmental health, ed 2, Elk Grove Village, IL, 2003, American Academy of Pediatrics.
Table 105-5 lists examples of drugs and toxic agents associated with specific effects on the cardiovascular system. Drugs with cardiotoxic effects, especially those with membrane stabilizing activity, are among those most commonly associated with life-threatening toxicity. In one 10-year retrospective study, 15 out of 17 poisoned patients requiring extracorporeal life support measures for refractory shock or prolonged cardiac arrest had overdosed on cardiotoxic agents.7 Toxins may cause hypertension or hypotension by direct effects on vascular smooth muscle, neurogenic effects on autonomic nervous centers governing vascular innervation, direct effects on the heart, or renal effects. Specific agents associated with hypertension include adrenergic stimulants, such as amphetamines, cocaine, phencyclidine, phenylpropanolamine, ephedrine, and phenylephrine. Although the hypertension caused by sympathomimetics frequently lasts only a few hours, it may be associated with acute encephalopathy and/or intracranial hemorrhage.
Sign | Agents |
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