A 28-year-old woman is brought to the emergency department 2 hours after ingesting an unknown quantity of organophosphate pesticide (commonly used in Indian agriculture). She presents with profuse salivation, pinpoint pupils, muscle fasciculations, and severe bronchospasm. Her respiratory rate is 32/min and SpO₂ is 88% on room air. Which of the following is the most appropriate immediate management?

Explanation

## Organophosphate Poisoning: Acute Management **Key Point:** Organophosphates irreversibly inhibit acetylcholinesterase, causing accumulation of acetylcholine and a cholinergic crisis. The triad of management is: airway control, atropine, and pralidoxime. ### Pathophysiology Organophosphates phosphorylate the anionic site of acetylcholinesterase. Excess acetylcholine at nicotinic and muscarinic receptors causes: - **Muscarinic effects:** salivation, lacrimation, urination, defecation, miosis, bronchospasm, bradycardia - **Nicotinic effects:** muscle fasciculations, paralysis, weakness ### Management Algorithm ```mermaid flowchart TD A[Organophosphate exposure]:::outcome --> B[Secure airway, give O₂]:::action B --> C[Atropine 2-5 mg IV]:::action C --> D{Signs of atropinization?}:::decision D -->|No| E[Repeat atropine q5-10 min]:::action D -->|Yes| F[Start pralidoxime 1 g IV]:::action F --> G[Repeat pralidoxime q4-6h if needed]:::action G --> H[Supportive care + monitoring]:::action ``` ### Atropine: First-Line Agent **High-Yield:** Atropine is a **muscarinic antagonist** — it blocks excess acetylcholine at muscarinic receptors, relieving salivation, bronchospasm, and bradycardia. It does NOT reverse nicotinic effects (fasciculations, paralysis). - **Dose:** 2–5 mg IV bolus, repeated every 5–10 minutes - **Endpoint:** Dry mouth, dilated pupils, increased heart rate (signs of atropinization) - **Why first?** Atropine acts immediately; it is life-saving for bronchospasm and airway secretions ### Pralidoxime (2-PAM): Oxime Reactivator **Clinical Pearl:** Pralidoxime reactivates acetylcholinesterase by removing the phosphate group from the enzyme — but only if given *before* "aging" (irreversible bond formation). Aging occurs within hours; hence early administration is critical. - **Dose:** 1 g IV bolus, then 0.5 g IV every 4–6 hours - **Mechanism:** Nucleophilic attack on the phosphorus–enzyme bond - **Limitation:** Does NOT cross the blood–brain barrier; ineffective for CNS effects - **Timing:** Give after atropine; pralidoxime alone is insufficient ### Why This Patient Needs Both | Agent | Muscarinic | Nicotinic | CNS | Timing | |-------|-----------|-----------|-----|--------| | **Atropine** | ✓ | ✗ | ✗ | Immediate | | **Pralidoxime** | ✓ | ✓ | ✗ | Early (before aging) | This patient has severe bronchospasm and respiratory compromise — atropine is **immediately life-saving**. Pralidoxime is then given to address both muscarinic and nicotinic effects and prevent aging. **Mnemonic:** **SLUDGE** = Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis (muscarinic signs treated by atropine). [cite:KD Tripathi 8e Ch 12]