Accidental Organophosphate Poisoning in a Toddler: A Case Report

While accidental poisoning is fairly common in children, the data are sparse when organophosphate (OP) is considered the culprit toxin. Only case reports of such patients from the Southeast Asian Region have been documented, despite it contributing largely to the global burden of organophosphorus poisoning in the adult population. This can be attributed to difficulty in diagnosing children because of varied presentations in the pediatric population and unreliable or unavailable exposure history. We present a case of a 19-month-old toddler who presented to the ED with OP poisoning, which proved to be a diagnostic and management challenge because of more common differentials and the unavailability of a clear history.


Introduction
Organophosphates (OPs) are widely used insecticides worldwide and are one of the leading causes of death because of poisoning in developing nations, especially in South Asia [1].An estimated 150,000 deaths worldwide are attributed to pesticide poisoning each year, according to the World Health Organization.India accounts for 70,000 of these deaths annually or around 47% of all deaths globally [1,2].
Since pharmacological intervention is required to break the spontaneous reversible link between the OP and cholinesterase, these chemicals function as irreversible cholinesterase inhibitors.Cholinergic toxidrome is the result of excessive activation of both muscarinic and nicotinic acetylcholine receptors, which is brought upon by the buildup of acetylcholine and an increase in synaptic acetylcholine levels caused by this inhibition [3,4].
Although accidental poisoning is fairly common in children, data are variable as per geographical locations when OP is considered as the culprit toxin.The US has reported only 550 cases in patients less than 12 years in 2020 [5].Only a few cases of such patients from the Southeast Asian region have been reported [6,7].This can be attributed to difficulty in diagnosing children because of varied presentations in the pediatric population and unreliable or unavailable exposure history.Hence, we would like to present a case of accidental OP poisoning in a 19-month-old toddler who presented to the ED of a tertiary care hospital in India.

Case Presentation
A 19-month-old previously healthy male child was brought into the ED with complaints of cough and cold for two days and difficulty in breathing for the preceding 12 hours.The primary assessment revealed a rectal temperature of 100.3 F, a heart rate of 190/min, respiratory rate of 40/min, and oxygen saturation (SpO 2 ) of 85% on room air with severe respiratory distress and labored breathing.He had pinpoint pupils and profuse bronchial secretions.His Glasgow Coma Scale (GCS) score was nine on arrival at the ED.Respiratory examination revealed bilateral conducted sounds.Emergency airway management was done.This comprised immediate oropharyngeal suction, endotracheal intubation, and assisted ventilation.The patient was also started on IV fluids and antibiotics.
Routine investigations were sent urgently, including blood gas analysis, chest X-ray, a complete hemogram, renal function test, and liver function test.
Because of excessive bronchial secretions and pinpoint pupils, serum cholinesterase level was sent, which was reduced to 1,842 u/L (normal: 3,930-11,500 u/L).A working diagnosis of OP poisoning was established.Further and directed questioning from the parents revealed suspected exposure to an OP compound insecticide from toys (the toys were kept out in the open in the fields where pesticides were sprayed regularly).Dermal decontamination of the patient was done immediately (by removal of all the clothes and The patient was first given an injection of atropine 0.05 mg/kg bolus; however, because of increasing tachycardia, three further doses were given 20 minutes apart.A loading dose of injection pralidoxime (PAM) was given at a dose of 25 mg/kg over one hour and was repeated at 12-hour intervals with two more doses.Serum cholinesterase level was repeated after 24 hours of loading dose showed improvement (Figure 1).

FIGURE 1: A line graph demonstrating pseudocholinesterase levels over time
The patient gradually improved with supportive management in the ICU over the next six days.He was weaned off ventilatory support on the sixth day of admission.However, during the ICU stay, the patient developed ventilator-associated pneumonia for which IV antibiotics were initiated and continued.
He was discharged after 19 days of hospital stay with no residual sequelae (both pulmonary and neurological).The patient was followed up after a month, and during that visit, he showed no delayed signs of neurological deficits.

Discussion
An exposure history and the telltale symptoms of a cholinergic overdose are the primary factors used to diagnose OP poisoning.However, a history of exposure may not be evident sometimes, especially in pediatric cases as we saw in our case [6].It was only after directed history-taking that, a possible source of insecticide exposure was identified.The severity of intoxication can be related to the type of receptor activity that dominates the clinical presentation.At lower doses of OPs, muscarinic symptoms usually predominate.At higher doses, nicotinic and central muscarinic activity may become prominent.Thus, tachycardia and hypertension can be important signs of severe poisoning as was seen in our case and the presence of these features should not delay therapy or confuse the clinician who traditionally expects the patient to have bradycardia [7,8].The characteristic complex of symptoms (lacrimation, salivation, urination, and diarrhea) is an unreliable indicator of OP poisoning in the pediatric population, making it more challenging to diagnose correctly at the time of presentation.In a study, of the 20 patients, Zwiener and Ginsburg found that only four had an accurate diagnosis [6].The differential diagnoses include bronchiolitis, bronchopneumonia, head trauma, opiate overdosage, and diabetic ketoacidosis.Bronchiolitis and bronchopneumonia are more common in the age group of our patient, and, because of the unavailability of exposure history, the clinician may not be able to make an accurate and prompt diagnosis [6].