Pediatrics
Toxic Elements and Poisoning
Pediatric poisoning for MBBS: lead chelation, kerosene, organophosphorus, paracetamol and free radicals, mapped to NMC codes PE14.1 to PE14.5.
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Toxic Elements and Poisoning
Pediatric poisoning for MBBS: lead chelation, kerosene, organophosphorus, paracetamol and free radicals, mapped to NMC codes PE14.1 to PE14.5.
This chapter covers common childhood poisonings including lead, kerosene, organophosphorus and paracetamol, along with the biology of free radicals and oxidative stress. It emphasises specific antidotes, chelation rules and the do-not-do points such as no emesis in kerosene ingestion.
High-yield: Toxic Elements and Poisoning
- In lead poisoning, oral DMSA (succimer) 10 milligrams per kilogram per dose is used for blood lead levels of 45 to 69 micrograms per decilitre.
- Lead encephalopathy or a blood lead level of 70 micrograms per decilitre or more needs BAL plus calcium disodium EDTA, with BAL given first.
- BAL must precede calcium disodium EDTA by about 4 hours to prevent redistribution of lead into the brain.
- Source removal is a non-negotiable part of lead poisoning management regardless of the blood lead level.
- In kerosene ingestion, do not induce vomiting and do not give activated charcoal, because the danger is aspiration pneumonitis, not gut absorption.
- Kerosene ingestion is managed with supportive care and oxygen, as the lung is the target organ.
- Organophosphorus poisoning produces muscarinic features remembered as DUMBELS: diarrhoea, urination, miosis, bradycardia/bronchorrhoea, emesis, lacrimation and salivation.
- The atropine end-point in organophosphorus poisoning is drying of secretions, not tachycardia or pupil dilation.
- Pralidoxime 25 to 50 milligrams per kilogram is given early in organophosphorus poisoning before the enzyme ages.
- Intermediate syndrome 24 to 96 hours after organophosphorus poisoning can cause sudden respiratory arrest after apparent recovery.
- In paracetamol poisoning the N-acetylcysteine loading dose is 150 milligrams per kilogram intravenously over 60 minutes.
- The treatment decision in paracetamol poisoning is based on the nomogram for a single timed ingestion, not on symptoms.
- Paracetamol Phase I is deceptively well and Phase III at 72 to 96 hours is when liver failure becomes apparent.
- Free radicals have an unpaired electron making them highly reactive, and the hydroxyl radical is the most biologically damaging, generated by the iron-catalysed Fenton reaction.
Poison-specific antidotes and rules
- **Lead:** DMSA for BLL 45 to 69; BAL then CaNa2EDTA for BLL >= 70 or encephalopathy.
- **Kerosene:** No emesis, no charcoal; supportive care and oxygen; lung is the target.
- **Organophosphorus:** Atropine to dry secretions plus early pralidoxime; watch for intermediate syndrome.
- **Paracetamol:** N-acetylcysteine 150 mg/kg loading; treat by nomogram, not symptoms.
NMC competencies in this chapter
- **PE14.1:** Lead poisoning: risk factors, clinical features, diagnosis and management
- **PE14.2:** Kerosene ingestion: risk factors, clinical features, diagnosis and management
- **PE14.3:** Organophosphorus poisoning: risk factors, clinical features, diagnosis and management
- **PE14.4:** Paracetamol poisoning: risk factors, clinical features, diagnosis and management
- **PE14.5:** Free radicals, oxidant stress and their role in disease
Frequently Asked Questions
How is severe lead poisoning treated?
Blood lead levels of 45 to 69 micrograms per decilitre are treated with oral DMSA 10 milligrams per kilogram per dose, while encephalopathy or a level of 70 or more needs BAL followed by calcium disodium EDTA, with BAL given first and source removal in every case.
Why is emesis avoided in kerosene ingestion?
In kerosene ingestion, vomiting and activated charcoal are avoided because the main danger is aspiration causing chemical pneumonitis rather than gastrointestinal absorption. Management is supportive care with oxygen.
What is the atropine end-point in organophosphorus poisoning?
The end-point of atropinisation is drying of secretions, meaning clear chest and dry mouth, rather than tachycardia or pupil dilation. Pralidoxime should be given early before the enzyme ages, and intermediate syndrome can cause late respiratory arrest.
How is paracetamol poisoning managed?
N-acetylcysteine is given with a loading dose of 150 milligrams per kilogram intravenously over 60 minutes, and the treatment decision is guided by the paracetamol nomogram for a single timed ingestion rather than by symptoms, since Phase I is deceptively well.
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