Sarin respiratory effects

Unfortunately, there are no data on the long-term effects of nerve agent poisoning in children, and the effects must be extrapolated from what has been discovered in the adult population (Rotenberg and Newmark, 2003). Surveillance studies performed on victims of the sarin attacks in Japan revealed a wide range of sequelae, such as continued respiratory problems, vision disturbances, headache, and fatigue. Neuropsychiatric problems were also reported as a delayed effect. 

Worek, F., Kirchner, T., Szinicz, L. (1995). Effect of atropine and bispyridinium oximes on respiratory and circulatory function in guinea-pigs poisoned by sarin. Toxicology 95 123-33. 

Stewart, W. C. (1959). The effects of sarin and atropine on the respiratory center and neuromuscular junctions of the rat. Canadian Journal of Biochemistry and Physiology, 37, 651-660. 

Miosis may also occur as a systemic feature, although more usually it follows direct exposure. This explains why, for example, modest dermal exposure may produce systemic features but not miosis. Abdominal pain, nausea and vomiting, involuntary micturition and defecation, muscle weakness and fasciculation, tremor, restlessness, ataxia and convulsions may follow dermal exposure, inhalation or ingestion of a nerve agent. Bradycardia, tachycardia and hypertension may occur, dependent on whether muscarinic or nicotinic effects predominate. If exposure is substantial, death may occur from respiratory failure within minutes, whereas mild or moderately exposed individuals usually recover completely, although EEG abnormalities have been reported in those severely exposed to sarin in Japan (Murata etal., 1997 Sekijima et al., 1997). 

There are only a few reports in the open literature on the effect of oximes in nerve agent-exposed humans. Pralidoxime chloride was very effective in reactivating erythrocyte AChE in individuals exposed to sublethal intravenous or oral VX while this oxime was substantially less effective in humans exposed to IV sarin (Sidell and Groff, 1974). Accidental sarin exposure by inhalation resulted in an initial progressive deterioration (coma, apnea) of the patient despite atropine and 2-PAM treatmentand substantial recovery of erythrocyte AChE activity (Sidell, 1974). It took several hours until the patient s condition improved. Sidell also reported an accidental oral soman exposure. A lethal dose of diluted soman splashed into and around the mouth of an individual, resulting in coma, bronchoconstriction and respiratory depression, which was successfully treated with repeated atropine injections. 2-PAM (2 g IV) had no effect on inhibited erythrocyte AChE. 

American name given to a series of organophos-phorus compounds containing a basic nitrogen side chain. Low-volatility nerve agents, active via the skin. Effects as per sarin classic anticholinesterase effects miosis, increased secretions, bradycardia, respiratory paralysis, death. 1 drop on skin can be fatal. See VX. 

The direct injection of sarin into the pons and medulla of the rabbit produces tachypnoea, bradycardia, hypotension and respiratory arrest which are reversed by the intravenous administration of atropine [73]. Respiratory arrest also is produced when sarin is injected into the lateral reticular nuclei of the rabbit and bradycardia occurs following its introduction into the ventrolateral reticular formation, an effect which may be reversed by both atropine and vagotomy [73], This suggests these to be the target sites in the brain of the rabbit at which cholinesterase inhibition results in respiratory arrest and bradycardia. 

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