You are moonlighting in a rural emergency room when a father rushes his 3-year-old daughter into the waiting area. You quickly determine that the child had been playing with her chihuahua at a relative’s farm where they were spraying for insects in a field. While at the farm she developed abdominal cramping, cough, drooling, and tearing. While in route the child seems to be having increased respiratory difficulty, and the dad notes she soiled and urinated upon herself.
What is the most likely diagnosis?
How is the diagnosis made?
What is the best therapy?
ANSWERS TO CASE 11: Organophosphate Poisoning
Summary: A 3-year-old, previously healthy child who, while playing where spraying for insects was ongoing, develops salivation, lacrimation, respiratory distress, and gastrointestinal (GI) symptoms.
• Most likely diagnosis: Organophosphate poisoning.
• Making the diagnosis:High index of suspicion so therapy is not delayed; confirmation via decreased serum pseudocholinesterase and erythrocyte cholinesterase levels.
• Best therapy: Decontamination of the child, supportive care, administration of atropine or pralidoxime.
1. Understand the signs, symptoms, and treatment of organophosphate poisoning.
2. Be familiar with the treatment options of various commonly ingested agents.
This child is demonstrating evidence of organophosphate poisoning, the leading cause of nonpharmaceutical ingestion fatality in children. She was exposed during the spraying for insects in a field, and is at risk for ongoing absorption of toxin until decontamination of her clothing is achieved.
Note:For some children exposed to a toxic substance, parents are able to provide a container of the toxic agent. For others either the container is not available or the symptoms are not obviously related to a toxic exposure. In all cases a thorough history and physical examination, along with a high index of suspicion in younger children, is required to ensure the diagnosis of accidental toxic exposure.
NICOTINIC SYMPTOMS:Cardiac (hypertension, tachycardia, arrhythmia); muscle (fasciculations, weakness, tremors); respiratory failure due to diaphragm paralysis; hypertension.
MUSCARINIC SYMPTOMS: Gastrointestinal (emesis, urinary and fecal incontinence); respiratory (bronchorrhea, bronchospasm); cardiac (hypotension, bradycardia); tearing and drooling; miosis.
Millions of children are poisoned each year with about 90% of exposures occurring in the home. About half of all accidental poisonings occur in children younger than 5 years of age. Children aged from about 6 to 12 years are much less likely to be exposed, and those with toxic exposures beyond 12 years of age often do so intentionally. Death due to accidental poisonings has become unusual since a variety of measures have been implemented, including poison prevention as part of all well-child visits, development of regional poison control centers, child-resistant packaging, and improved medical management.
Organophosphate poisoning can occur across skin or mucous membranes, by inhalation, or by ingestion. Commonly found in such pesticides as parathion, malathion, and diazinon, organophosphates bind irreversibly to cholinesterase of neurons and erythrocytes, as well as to liver pseudocholinesterase. The common finding is failure to terminate the effects of acetylcholine at the receptor sites.
Signs and symptoms of cholinergic excess are often remembered with the mnemonic “dumb bells,” which includes:
In addition to these muscarinic and nicotinic effects, central effects including obtundation, seizures, and apnea are also seen.
Confirmation of the exposure can be confirmed by finding decreased serum pseudocholinesterase and erythrocyte cholinesterase levels, but the correlation of these levels to the magnitude of exposure or the symptoms observed is poor. Thus, a high index of suspicion must be maintained to quickly and accurately diagnose organo-phosphate exposure.
Treatment of the patient exposed to organophosphate consists of rapid decontamination by removing all clothing and washing of all skin surfaces. For ingestions, gastric lavage or activated charcoal may be attempted, but the organophosphate compounds are rapidly absorbed and the benefits somewhat limited. The ABCs of medicine apply: preserve the Airway (intubation may be required); maintain Breathing (excessive secretions may require frequent suctioning); and ensure appropriate Circulation.
Two specific therapies to counter the effects of organophosphate poisonings include atropine and pralidoxime. Atropine works by antagonizing the muscarinic receptor; large, repeated, and sometimes continuous doses may be required. Often the amount and number of atropine doses required correlates to the degree of exposure, and may assist in the prediction of course duration. Pralidoxime is a cholinesterase-reactivating oxime, often used for patients with significant muscle weakness, especially if mechanical ventilation is required owing to muscle failure.
Careful attention to a child’s environment can help prevent countless instances of toxic ingestion. Counseling parents to “poison proof” their home is a first step toward prevention. Written and video materials are readily available through the American Academy of Pediatrics, local and state health departments, and poison control centers. All families are taught to become familiar with the national network of poison control centers, reached toll-free at 1-800-222-1222.
11.1 Students attending a school built in 1951 are at risk for which of the following?
C. Dichlorodiphenyltrichloroethane (DDT)
E. Polychlorinated biphenyls (PCBs)
11.2 An 8-year-old, mentally delayed child ingests the contents of a mercury thermometer. Which of the following symptoms are most likely to be seen?
A. Ataxia, dysarthria, and paresthesias
B. Chest pain and dyspnea
C. Gingivostomatitis, tremor, and neuropsychiatric disturbances
D. No symptoms
E. Pulmonary fibrosis
11.3 A 4-year-old child is found with a bottle of insecticide that contains arsenic. Which of the following symptoms is most likely to occur?
A. Bradycardia with third-degree heart block
C. Hemorrhagic gastroenteritis with third spacing of fluids
11.4 Exposure to environmental toxins can occur in a number of ways. Which of the following is the most likely mechanism of exposure?
A. Asbestos exposure from hazardous arts and crafts materials
B. Exposure of a child to beryllium from the child’s parents’ clothing
C. Iron intoxication from vehicular emissions
D. Lead toxicity from ingesting pieces of a pencil
E. Transplacental exposure to benzene
11.1 B. Between 1947 and 1973 asbestos was commonly sprayed on school ceilings as a fire retardant. Deterioration results in release of microscopic fibers into the air. Drop ceilings or placement of barriers usually is sufficient protection against this carcinogen.
11.2 D. The child in the question is unlikely to develop symptoms (the quantity of mercury is small); a larger acute elemental ingestion might result in a variety of gastrointestinal (GI) complaints. If the elemental mercury were in vapor form, GI complaints would be seen, along with fever, chills, headaches, visual changes, cough, chest pain, and possibly pneumonitis and pulmonary edema. Exposure to inorganic mercury salts (pesticides, disinfectants, explosives, dry batteries) can cause gastroesophageal burns, nausea, vomiting, abdominal pain, hematemesis, hematochezia, cardiovascular collapse, or death. Ataxia, dysarthria, and paresthesias are seen in methyl mercury intoxication (contaminated fish exposure). Gingivostomatitis, tremor, and neuropsychiatric disturbances are seen with chronic inorganic mercury intoxication; indeed, the term “mad as a hatter” originates from the occupational hazard of workers’ exposure in the early industrial period to mercury-containing vapors during the process of felt hat making.
11.3 C. Acute arsenic ingestions can cause nausea, vomiting, abdominal pain, and diarrhea. The third spacing and hemorrhage in the gut can lead to hypovolemic shock. Cardiac symptoms include ventricular tachycardia (QT prolongation) and congestive heart failure (CHF). These patients can develop seizures, cerebral edema, encephalopathy, and coma. Early on, patients develop loss of deep tendon reflexes, paralysis, painful dysesthesias, and respiratory failure similar to Guillain-Barré syndrome. Fever, anemia, alopecia, hepatitis, and renal failure also can be seen.
11.4 B. Fat-soluble compounds can be transmitted transplacentally (but benzene would be unusual). Parents’ work clothes can transmit potentially hazardous compounds. Arts and crafts supplies likely do not contain asbestos. Vehicular emissions are responsible for a number of pollutants including lead prior to lead-free gasoline, many of which are carcinogens, but iron intoxication would be unusual. Pencil “lead” is actually graphite (carbon) and not elemental lead.
Organophosphate poisoning is the leading cause of nonpharmacologic ingestion fatality in the United States.
The mnemonic “dumb bells” outlines the signs and symptoms of cholinergic excess.
Therapy for organophosphate toxicity includes supportive care and use of either atropine or pralidoxime.
Feng S-Y, Goto CS, Baker MD. Toxic ingestions and exposures. In: Rudolph CD, Rudolph AM, Lister G, First LR, Gershon AA, eds. Rudolph’s Pediatrics. 22nd ed. New York, NY: McGraw-Hill; 2011:455-469.
Fortenberry JD, Mariscalco MM. General principles of poisoning management. In: McMillan JA, Feigin RD, DeAngelis CD, Jones MD, eds. Oski’s Pediatrics: Principles and Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:747-754.
O’Donnell KA, Ewald MB. Poisonings. In: Kleigman RM, Stanton BF, St. Geme JW, Schor NF, Behrman RE, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: WB Saunders; 2011:250-270.
Rumack BH, Dart RC. Poisoning. In: Hay WW, Levin MJ, Sondheimer JM, Deterding RR. Current Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011:321-347.