Academe Learn
CBME Curriculum Preview

Page 14 of 14

PE14.1-3 | Childhood Poisoning — PBL Case

CLINICAL SETTING

The emergency department of a 200-bed district hospital in a semi-urban area of Andhra Pradesh. It is a busy Saturday afternoon in late October — harvest season, when pesticide use (and accidental poisoning) peaks. The department has one paediatric resident on duty and access to a basic laboratory and pharmacy. The nearest tertiary paediatric centre is 90 km away. A 3-year-old girl, Amrutha, is rushed in by her distraught grandmother. There is a faint chemical odour around the child.

Trigger 1: The Rushed Arrival

Amrutha, a 3-year-old weighing 14 kg, is carried in unresponsive by her grandmother who is crying and incoherent. The grandmother eventually explains: Amrutha was found 45 minutes ago near the agricultural shed on the family farm, clutching a plastic bottle of 'crop spray' — the bottle was open and partially emptied. The grandmother wiped the child's mouth but does not know how much she swallowed. The child has been becoming progressively drowsier during the journey. There is no past medical history. She is not on any medications. On initial observation: Amrutha is drowsy (GCS 10/15), has bilateral pinpoint pupils, profuse secretions drooling from the mouth, audible wheeze, and a rhythmic twitching of both hands.

DISCUSSION POINTS

  • What clinical syndrome does this presentation represent? List the features and classify them as muscarinic, nicotinic, or CNS effects.
  • What is the most likely causative agent? What clues from the setting and clinical features support this?
  • What are the three most important immediate actions in the first 2 minutes of this child's arrival?
Click to reveal Trigger 2: The First Antidote Decision (discuss previous trigger first!)

Trigger 2: The First Antidote Decision

A quick primary survey reveals: Airway — secretions and wheeze; Breathing — RR 36/min, SpO2 81% on room air; Circulation — HR 48/min, BP 80/60 mmHg, CRT 3 seconds; Disability — GCS 10. The ward nurse asks: 'Doctor, should we use the suction machine or try to give activated charcoal?' The pharmacist confirms atropine and pralidoxime are available. The grandmother remembers the bottle had a green-and-yellow label and says 'it's the chlorpyrifos spray all the farmers use.' A visiting medical student from the city says, 'We should do gastric lavage before starting antidotes — isn't that the protocol?'

DISCUSSION POINTS

  • Is gastric lavage or activated charcoal indicated here? What is the evidence and reasoning for or against each? Who is correct — the student or the current guideline?
  • Which antidote should be given FIRST and why? Calculate the correct dose of atropine for Amrutha (14 kg). What clinical endpoint tells you she has received enough?
  • Calculate the pralidoxime dose for Amrutha. What is the maximum effective time window for PAM given that exposure was approximately 45 minutes ago? How do you explain this window to the nurse?
Click to reveal Trigger 3: Deterioration and Difficult Decisions (discuss previous trigger first!)

Trigger 3: Deterioration and Difficult Decisions

Amrutha receives atropine 0.7 mg IV (0.05 mg/kg) and her secretions begin to decrease within 10 minutes. Her SpO2 improves to 93% with high-flow oxygen. Pralidoxime infusion is started. However, 90 minutes later, despite adequate atropinisation (dry secretions, HR 100), Amrutha's respiratory rate begins to climb again (RR 42/min), her SpO2 drops to 89%, and she can no longer generate a strong cough. The nurse reports her breath sounds are now clear. A second-year resident takes over and says: 'Increase the atropine dose — her secretions must be coming back.' The on-call consultant (available by phone) suggests possible respiratory muscle paralysis.

DISCUSSION POINTS

  • Why is the child deteriorating despite adequate atropinisation with dry secretions? What receptor mechanism explains this and why does atropine not help here?
  • Reconcile the apparent contradiction: clear breath sounds (no secretions/wheeze) but worsening respiratory failure. What does this tell you about the mechanism?
  • What is the appropriate management for this type of respiratory failure? What monitoring should be in place if intubation is considered? What precaution must be taken regarding muscle-relaxant choice at intubation?
Click to reveal Trigger 4: Recovery, Counselling, and Prevention (discuss previous trigger first!)

Trigger 4: Recovery, Counselling, and Prevention

After 5 days in the paediatric ICU on mechanical ventilation (with continued atropine + PAM for the first 36 hours), Amrutha is extubated and makes a complete recovery. She is transferred to the ward on day 7. The family is gathered — her parents (farmers), the grandmother, and a younger sibling aged 14 months. The ward consultant asks the residents to conduct the discharge counselling. Back in the town, the village health worker mentions that this is the third pesticide ingestion in children from this village in the last 6 months. The health worker asks: 'Doctor, what can we do at the village level to stop this from happening again?'

DISCUSSION POINTS

  • Design the discharge counselling for Amrutha's family: What specific instructions will you give about pesticide storage? What warning signs should prompt immediate return to hospital? How will you ensure the 14-month-old sibling is also protected?
  • What community-level interventions would you recommend to the village health worker to reduce childhood pesticide poisoning in this region? Consider WHO Hazard Classification labelling, legislation, and the National Poison Information Centre.
  • The family asks: 'Could her brain or liver be permanently damaged?' What are the known long-term sequelae of severe OP poisoning in children and what follow-up is indicated?

Group Task Assignments

Group 1: Collaborative Task

Group 2: Collaborative Task

Group 3: Collaborative Task

Learning Issues

Research these questions and bring your findings to the discussion.

  1. [PE14.1] What are the risk factors, clinical features, and management of kerosene ingestion in children, and why is GI decontamination contraindicated?
  2. [PE14.2] What are the clinical features of organophosphorus poisoning across muscarinic, nicotinic, and CNS receptor pathways, and what is the evidence-based antidote regimen (dosing, sequencing, endpoints, and time windows)?
  3. [PE14.3] What are the risk factors, clinical features, and management of paracetamol poisoning, including the Rumack-Matthew nomogram, toxic dose threshold, and N-acetylcysteine protocol?