Organophosphate Poisoning and Treatment
Organophosphate (OP) compounds, commonly used as insecticides (e.g., malathion, parathion) and nerve agents (e.g., sarin), cause poisoning by inhibiting acetylcholinesterase, an enzyme responsible for breaking down acetylcholine (ACh) in synapses. The resultant accumulation of ACh at muscarinic and nicotinic receptors leads to overstimulation of the parasympathetic nervous system, neuromuscular junctions, and central nervous system, causing a cholinergic crisis.
Mechanism of Toxicity
- Organophosphates irreversibly inhibit acetylcholinesterase by phosphorylating the enzyme, resulting in increased ACh levels and overstimulation of cholinergic receptors.
- Symptoms of OP poisoning are categorized into muscarinic, nicotinic, and central nervous system effects:
Muscarinic Effects ("SLUDGE" Syndrome)
- Salivation
- Lacrimation (tearing)
- Urination
- Diarrhea
- Gastrointestinal distress
- Emesis (vomiting)
Additional muscarinic symptoms include bradycardia, bronchoconstriction, and miosis (constricted pupils).
Nicotinic Effects
- Muscle weakness, fasciculations, and paralysis
- Respiratory muscle paralysis, which can lead to death if untreated
Central Nervous System Effects
- Anxiety, confusion, seizures, and coma
Diagnosis
Diagnosis is based on history of exposure, clinical presentation, and, in some cases, laboratory confirmation of decreased plasma cholinesterase activity.
Treatment
1. Decontamination
- Remove contaminated clothing and wash skin with soap and water.
- Take precautions to protect healthcare personnel from exposure.
2. Supportive Care
- Maintain airway, breathing, and circulation.
- Administer oxygen and provide mechanical ventilation if necessary due to respiratory muscle paralysis.
3. Antidotes
- Atropine (muscarinic antagonist): Blocks the effects of ACh at muscarinic receptors, alleviating symptoms such as bradycardia, salivation, and bronchoconstriction.
- Dose: Administered intravenously, starting with 1–2 mg, repeated every 5–10 minutes until respiratory secretions dry up and heart rate stabilizes.
- Pralidoxime (2-PAM): Reverses the binding of OPs to acetylcholinesterase if administered early, before "aging" (when OP-enzyme binding becomes irreversible).
- Dose: Given as an intravenous bolus or infusion, typically 1–2 grams in adults.
- Primarily effective for nicotinic symptoms, improving muscle strength and reversing respiratory paralysis.
4. Benzodiazepines
- Diazepam or lorazepam may be used for seizure control and to reduce agitation.
Additional Treatment Measures
- Glycopyrrolate: An anticholinergic that does not cross the blood-brain barrier and may be used instead of atropine to minimize central side effects.
- Activated Charcoal: If ingestion occurred within 1–2 hours, activated charcoal may help limit absorption.
Monitoring and Prognosis
Continuous monitoring of vital signs, oxygen saturation, and cardiac rhythm is essential. Patients should be observed for at least 72 hours, as symptoms can recur due to redistribution of OPs from body fat or delayed clearance.
Importance of Early Intervention: Prompt treatment can prevent life-threatening complications like respiratory paralysis and seizures, reducing morbidity and mortality associated with OP poisoning.
