Miosis nerve agent exposure

Anticholinesterase effects of nerve agent exposure can be characterized as muscarinic, nicotinic, or CNS. Muscarinic effects occur in the parasympathetic system and, depending on the amount absorbed, can be expressed as conjunctival congestion, miosis, ciliary spasm, nasal discharge, increased bronchial secretion, bronchoconstriction, anorexia, emesis, abdominal cramps, sweating, diarrhea, salivation, bradycardia, and hypotension. Nicotinic effects are those that... 

Even though the lethal nerve agent exposure level for animals may be higher than that for humans, it is still possible that animals eould exhibit other nonlethal effects sooner and more notieeably than humans. Rabbits develop 90% miosis at a lower inhaled eoneentration of cyclohexyl sarin when compared to humans (2.71 mg.min/m versus 13.85 mg.min/m ) (NRC, 2003). 

Miosis, pain, dim vision, and nausea can be relieved by topical atropine in the eye. Pretreatment with carbamates may protect the cholinesterase enzymes before nerve agent exposure. 

Miosis, pain, dim vision, and nausea can be relieved by topical atropine in the eye. Pretreatment with carbamates may protect the cholinesterase enzymes before nerve agent exposure. It is available in 30 mg tablets and the tablets should be administered every 8h. When used prior to exposure, it should be followed by atropine and pralidoxime chloride after exposure. 

It is important to realize that miosis is caused by contraction of the papillary muscles and that these muscles lack traditional capillaries. In reality, these eye muscles are isolated from the rest of the bloodstream. The nutritional needs of these muscles are supplied by the humors of the eye, not blood vessels, and the effect on them by liquid nerve agent not directly applied to the eyes would be dose and time dependent. Small doses of systemically absorbed liquid nerve agent would probably not cause the pupils to constrict medium doses might, and large doses probably would, cause miosis. In any case, the effect would take a period of time to develop and therefore, with nonocular systemically absorbed liquid nerve agent exposure, absence of miosis should not rule out nerve agent exposure. 

With liquid nerve agent exposure, moderate intoxication will yield Gl symptoms of nausea, vomiting, abdominal pain and cramps from increased peristalsis, increased Gl secretions and involuntary defecation, etc. If the only sign of Gl symptoms is nausea, one should consider the possibility that this effect could also be due to vapor nerve agent exposure precipitating miosis in the eyes. It is well documented that the development of miosis can cause nausea. 

It is generally considered that systemic effects in humans followtiig acute nerve agent exposures arc likely when RBC ChE is inhibited by 75-80% (c.g., lo 20-25% of normal activity levels) (Sidell, 1992). Nevertheless, it is well known that local sign.s and symptoms of the eye and nose in humans and animals (c.g.. miosis and rhinoirhea) can occur in the absence of any measurable change from ba.seline ChE or CarbE activity in the blood (Harvey. 1952 Craig and Woodson, 1959 Sidell. 1992 see also Tables 2 and 3). 

Rhinorrhea is common after both local and systemic nerve agent exposure. It may occur soon after exposure to a small amount of vapor and sometimes precedes miosis and dim vision, or it may occur in the absence of miosis. Even a relatively small exposure to vapor may cause severe rhinorrhea. One exposed worker compared the nasal secretions to the flow from a leaking faucet, and another said that they were much worse than those produced by a cold or hay fever (personal observation). 

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