Nerve agent exposure
This section summarises recognition, pathophysiology, immediate ED management and disposition of patients exposed to nerve agents (organophosphorus chemical warfare agents). Practical priorities are clinician and departmental safety, decontamination, airway and respiratory support, antidote therapy and rapid escalation to critical care.
UK national guidance underpins these recommendations; contact the National Poisons Information Service (NPIS/TOXBASE) and local CBRN/UKHSA incident teams for agent‑specific or novel‑agent advice (CBRN handbook; RCEM; Resuscitation Council UK).
Why nerve agents matter (clinical overview)
Nerve agents irreversibly inhibit acetylcholinesterase, causing accumulation of acetylcholine at muscarinic, nicotinic and central receptors. The classical result is a cholinergic toxidrome with life‑threatening bronchorrhoea, bronchospasm, respiratory muscle weakness/paralysis, seizures and coma.
Some agents are volatile (rapid inhalational onset); others are persistent liquids (dermal contamination, delayed deterioration). Rapid recognition and early supportive and antidotal therapy are essential to prevent respiratory arrest and death.
Common agents and practical differences
- G agents (e.g., GA Tabun, GB Sarin, GD Soman): generally more volatile with rapid inhalational effects; some (e.g., soman) cause very rapid “ageing” of AChE, reducing oxime benefit.
- V agents (e.g., VX, VE, VG, VM): highly toxic, persistent low‑vapour liquids that adhere to skin and clothing and can cause delayed percutaneous poisoning; contaminated clothing/areas remain hazardous.
Key point: volatile agents typically cause early respiratory and ocular presentations; persistent agents typically cause dermal exposure with...