Soman symptoms

PHY +SCO 2x LD50 Soman HI-6 + AS + DZP After first symptoms appeared... 

Post-intoxication symptoms The symptomatology after 2x LD50 soman followed by a post-intoxication therapy of animals pretreated with PYR was comparable with no pretreatment (see Fig. 1). Pretreatment with PHY+SCO improved the signs compared with PYR This was mainly found on severe symptoms. On the other hand, animals pretreated with PHY+PC did not show any worse symptoms as was found in the other groups. In some cases the post-intoxication therapy was not necessary because no symptoms were present. 

Post-intoxication incapacitation The post-intoxication incapacitation was measured immediately after most symptoms disappeared, 24 hours, and one week after the intoxication. However, one day after soman intoxication no animals from the PYR group were available. Since the un-pretreated animals all died very shortly after soman no post-intoxication incapacitation was tested in these animals. The shuttle-box performance declined after soman intoxication with approximately 60% in all animals pretreated with PHY and SCO or PC. This decrease of performance was significant in the groups treated with a post-intoxication therapy (not... 

Figure 1. Mean (SEM) severity of symptoms after soman followed by a post-intoxication therapy on indication. The occurrence of symptoms is expressed as a percentage of observations. The number of animals in which the symptoms were observed is indicated above the bars.

Symptoms Soman exposure results in pupil constriction, blurred and dimmed vision, pain in the eyeballs chest tightness, difficulty in breathing sweating, salivation, increased bronchial secretions, bradycardia, hypotension, vomiting and diarrhea, bronchoconstric-tion, and urinary and fecal incontinence. 

Hassel, B. (2006). Nicotinic mechanisms contribute to soman-induced symptoms and lethality. Neurotoxicology 27 501-7. 

There have been descriptions of the acute toxic effects in humans that follow high-dose exposure (>LD5o) to the nerve agents soman (Lekov et al., 1966 Sidell, 1974), sarin (Sidell, 1974 Inoue, 1995 Nakajima et al., 1998), and VX (Nozaki et al., 1995). The same cluster of behavioral symptoms that are reported following lower doses (anxiety, psychomotor depression, intellectual impairment, and sleep disturbances) dominate the clinical picture in the immediate period following resolution of the acute toxic signs of intoxication and then slowly fade with time, sometimes taking months to fiiUy resolve. 

Efficacy of the combined usage of two or more ChR depends upon OPC type. The prophylactic usage of atropine, HI-6 and toxogonine is indicated in animals poisoned with tabun at the same time, symptoms of soman intoxication are eliminated without use of toxogonine [78],... 

Convulsions are among the most severe symptoms of intoxication with high toxic OPC. The reduction of central convulsive syndrome exerts positive effect on both the course of OPC intoxication and the delayed consequences. For this, antidotic formulas are supplemented with anticonvulsants of different chemical structures (diazepam, clonazepam, phenazepam, etc ). Anticonvulsants facilitate normalization of metabolism of biogenic amines and CNS uptake of glucose, whose consumption grows up steeply in poisonings with soman [92]. 

About 50% of 34 subjects (22 male and 12 female laboratory workers) detected the odor of soman in concentrations of 3.3-7.0 mg m-3 and described it as sweet, fruity or nutty (Dutreau etal., 1950). About 65% of the subjects had mild nasal and airway symptoms from the agent. 

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