Risk Factors, Clinical Features, Diagnosis, and Management of Organophosphorus Poisoning

Pathophysiology of Organophosphorus Poisoning: Mechanism of Toxicity and Cholinergic Crisis

Organophosphorus poisoning occurs due to excessive exposure to organophosphate compounds, commonly used in pesticides and chemical warfare agents. The toxic effects result from the inhibition of acetylcholinesterase, leading to an accumulation of acetylcholine at synapses, causing a cholinergic crisis.

Risk Factors

• Occupational exposure (agricultural workers, pesticide handlers)
• Accidental ingestion or inhalation
• Intentional self-poisoning (suicidal attempts)

Clinical Features

The hallmark of organophosphorus toxicity is excessive cholinergic stimulation, leading to muscarinic, nicotinic, and central nervous system effects.

Muscarinic Effects

• Salivation, lacrimation, urination, defecation
• Bronchospasm and respiratory distress
• Bradycardia and hypotension

Nicotinic Effects

• Muscle fasciculations and weakness
• Hypertension and tachycardia

CNS Effects

• Confusion, seizures, and coma

Diagnosis

Diagnosis is based on clinical presentation, exposure history, and laboratory tests measuring plasma cholinesterase activity.

Management

Emergency treatment aims to reduce toxin exposure and support vital functions.

• Decontamination: Remove contaminated clothing and wash affected skin.
• Antidotes: Administer atropine to counteract muscarinic effects and pralidoxime to restore cholinesterase function.
• Supportive Care: Respiratory support with oxygen and mechanical ventilation if needed.