A patient comes to the casualty with organophosphate poisoning. He was started on atropine infusion and pralidoxime. After 2 hours, the patient had a sudden rise in temperature. What is the likely cause of fever?

Explanation

## Correct Answer: D. Atropine toxicity Atropine toxicity causes fever through **anticholinergic overdose syndrome**. Atropine blocks muscarinic receptors, including those on sweat glands, leading to **anhidrosis** (inability to sweat). In organophosphate poisoning management, atropine is titrated to drying of bronchial secretions—but excessive dosing or rapid infusion causes systemic anticholinergic effects. Loss of sweating impairs thermoregulation, causing uncontrolled heat retention and fever. This is a classic sign of atropine toxicity, appearing within hours of high-dose administration. The fever is typically accompanied by other anticholinergic signs: dry mouth, dilated pupils, tachycardia, urinary retention, and CNS effects (agitation, confusion). In Indian toxicology practice, atropine-induced fever in organophosphate cases is a recognized complication requiring dose reduction or cessation. The sudden rise at 2 hours fits the timeline of cumulative atropine effect during infusion. ## Why the other options are wrong **A. Due to organophosphate poisoning** — Organophosphate poisoning itself causes **cholinergic crisis** (excessive salivation, bronchospasm, bradycardia, miosis), not fever. Fever is not a direct manifestation of organophosphate toxicity. The fever appears *after* atropine initiation, not at presentation, making it iatrogenic rather than toxin-related. This is a temporal misdirection trap. **B. A side effect of pralidoxime** — Pralidoxime (2-PAM) is an **oxime that reactivates acetylcholinesterase**. Its side effects include headache, dizziness, blurred vision, and rarely muscle weakness—but NOT fever. Pralidoxime does not interfere with thermoregulation. This option distracts by pairing it with atropine as a co-administered drug, but pralidoxime's mechanism is enzymatic reactivation, not anticholinergic. **C. Idiopathic** — Calling fever 'idiopathic' in a patient on high-dose atropine infusion is premature and clinically unsafe. The temporal relationship (fever after atropine initiation) and the known anticholinergic mechanism of atropine make this a **preventable, iatrogenic complication**, not an unexplained phenomenon. This option rewards diagnostic laziness. ## High-Yield Facts - **Atropine toxicity** causes fever via **anhidrosis** (loss of sweating due to muscarinic blockade on sweat glands). - **Anticholinergic syndrome** triad: dry mouth, dilated pupils, fever—remember 'hot as a hare, dry as a bone, red as a beet, mad as a hatter'. - **Atropine dosing** in organophosphate poisoning is titrated to drying of bronchial secretions; overdose causes systemic toxicity including fever within 1–3 hours. - **Pralidoxime** reactivates acetylcholinesterase and does NOT cause fever; it is safe to continue while reducing atropine. - **Organophosphate poisoning** presents with cholinergic crisis (SLUDGE: salivation, lacrimation, urination, defecation, GI upset, emesis), not fever. ## Mnemonics **Anticholinergic Toxicity (Atropine OD)** **DRY as a bone, HOT as a hare, RED as a beet, MAD as a hatter** — Dry mouth/skin (anhidrosis), Fever (loss of sweating), Flushed skin, CNS agitation. Use this when any anticholinergic drug (atropine, antihistamines, TCAs) causes fever. **Organophosphate Management: Atropine vs Pralidoxime** **Atropine = Symptomatic (blocks excess ACh effects), Pralidoxime = Curative (reactivates enzyme)**. Atropine has toxicity risk at high doses; pralidoxime does not cause fever. Remember: atropine is titrated, pralidoxime is not. ## NBE Trap NBE pairs atropine and pralidoxime as co-administered drugs to lure students into blaming pralidoxime for fever, or into assuming fever is part of organophosphate toxicity itself. The key discriminator is **timing**: fever appears *after* atropine infusion, and **mechanism**: only atropine blocks sweat glands. ## Clinical Pearl In Indian emergency departments, atropine-induced fever in organophosphate cases is a red flag to **reduce atropine infusion rate or switch to bolus dosing**. Fever + anhidrosis + tachycardia in a patient on atropine infusion = stop and reassess; do not escalate atropine further. This distinction saves lives in rural toxicology settings where atropine is often over-administered. _Reference: KD Tripathi Ch. 4 (Anticholinergic Drugs & Toxicity); Harrison Ch. 475 (Poisoning & Drug Overdose)_