[Skip to Content]
[Skip to Content Landing]
Citations 0
January 14, 2004

Treatment of Sarin Exposure

Author Affiliations

Letters Section Editor: Stephen J. Lurie, MD, PhD, Senior Editor.

JAMA. 2004;291(2):181. doi:10.1001/jama.291.2.181-b

To the Editor: Dr Lee1 noted that "early endotracheal intubation and ventilatory support are critical . . . " in treating severely injured patients after sarin exposure. We disagree, however, with his assertion that succinylcholine should be avoided during rapid sequence intubation in these patients.

Death from sarin exposure is generally because of hypoxia from airway obstruction, weakness of the respiratory muscles, seizures, or respiratory failure.2 In patients with severe trauma, rapid sequence intubation with succinylcholine is the standard method of airway management. As Lee stated, sarin inhibits both acetylcholinesterase ("true" cholinesterase) and butyrylcholinesterase (pseudocholinesterase). Because succinylcholine is metabolized by butyrylcholinesterase, a patient exposed to sarin who receives succinylcholine would be expected to have prolonged neuromuscular blockade. This has been reported in patients who received succinylcholine after organophosphate insecticide poisoning.3 The duration of paralysis in most cases, however, was less than 4 hours. Similar prolongation of neuromuscular blockade has been reported for mivacurium, a nondepolarizing neuromuscular blocker (NMB) that is also metabolized by butyrylcholinesterase.4-6