Pesticides are widely used chemicals in agriculture and household environments. Due to their availability, pesticide poisoning is a significant clinical issue, particularly in developing countries. The major pesticide groups involved in poisoning include organophosphorus compounds, carbamates, organochlorines, and pyrethroids. Understanding their mechanisms, clinical features, and management is essential for effective toxicology practice.
1. Organophosphorus Compounds (OPCs)
Organophosphorus compounds are potent insecticides commonly involved in acute poisoning. They are highly lipid-soluble and absorbed rapidly through inhalation, ingestion, and the skin.
Mechanism of Toxicity
OPCs inhibit acetylcholinesterase, leading to accumulation of acetylcholine at synapses and continuous stimulation of muscarinic, nicotinic, and central nervous system receptors. The enzyme becomes phosphorylated and may undergo “aging,” resulting in irreversible inhibition.
Clinical Features
Symptoms appear within minutes to hours depending on compound type and route of exposure.
Muscarinic Effects
- Salivation, lacrimation, urination, diarrhoea, vomiting
- Bronchorrhoea, bronchospasm
- Miosis, bradycardia, hypotension
Nicotinic Effects
- Muscle weakness and fasciculations
- Tachycardia and hypertension
- Respiratory muscle paralysis
CNS Effects
- Drowsiness, confusion, agitation
- Seizures
- Coma and respiratory failure in severe poisoning
Delayed Effects
- Intermediate Syndrome: muscle weakness, respiratory paralysis occurring 1–4 days after exposure.
- Delayed Neuropathy: distal limb weakness and paresthesias appearing after 1–4 weeks.
Management
- Airway support and oxygenation
- Atropine for muscarinic symptoms
- Pralidoxime (oxime therapy) to reactivate acetylcholinesterase
- Benzodiazepines for seizures
- Ventilatory support if respiratory failure develops
2. Carbamates
Carbamate insecticides act similarly to organophosphorus compounds but bind reversibly to acetylcholinesterase.
Mechanism
They carbamylate acetylcholinesterase, causing transient inhibition. However, unlike OPCs, they do not undergo aging, and spontaneous enzyme recovery occurs more rapidly.
Clinical Features
Symptoms resemble organophosphate poisoning but tend to be shorter in duration and less severe.
- Increased salivation and sweating
- Miosis
- Muscle weakness
- Nausea, vomiting, diarrhoea
Management
- Supportive care and airway protection
- Atropine is effective for muscarinic symptoms
- Oximes are generally not required and may not provide clear benefit
3. Organochlorines
Organochlorines, such as DDT, are highly persistent environmental pollutants. Their toxicity is primarily neurological.
Mechanism
They interfere with sodium channel inactivation, leading to repetitive neuronal firing and CNS stimulation.
Clinical Features
- Tremors and twitching
- Convulsions
- Hyperexcitability
- Nausea, vomiting
Management
- Control of seizures with benzodiazepines
- Activated charcoal for recent ingestion
- Avoid epinephrine due to arrhythmia risk
- Supportive airway and cardiac care
4. Pyrethroids
Pyrethroids are synthetic analogues of pyrethrins and are widely used because of their safety profile. However, poisoning can occur with high exposures.
Mechanism
Pyrethroids prolong sodium channel opening, causing repetitive neuronal firing. Type II pyrethroids also affect GABA receptors.
Clinical Features
- Paresthesias (common with dermal exposure)
- Tremors, twitching, and incoordination
- Seizures in severe cases
- Nausea and vomiting
Management
- Supportive care and decontamination
- Control seizures with benzodiazepines
- Dermal washing for skin exposure
Detailed Notes:
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