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Nerve agents exposure victims

In June 1994 and again in May 1995 the Japanese cult group Aum Shinrikyo created much havoc when they released the deadly nerve agent sarin in two Japanese cities. In the first attack in Matsumoto, Japan, sarin vapor was released in a residential area where judges unfriendly to the cult resided. Seven people died as a consequence of this nerve agent exposure, and 500 people were injured. The 1995 attack occurred in the Tokyo subway system. Several coordinated releases of this potentially deadly vapor resulted in more than 5,000 visits to local emergency departments. Fortunately, the vast majority of exposed victims had few if any symptoms and there were only a handful of fatalities (Tucker, 2006 for further discussion, see chapter 19—Biological and Chemical Terrorism A Unique Threat). [Pg.484]

The only published study of the brain structural effects of nerve agent exposure in a human population focused on longterm changes induced in victims of the 1995 Tokyo subway sarin attack (Yamasue et al, 2007). In this event, which resulted in 12 deaths, approximately 5,500 victims were exposed to sarin, and essentially all patients exhibited typical symptoms of acute intoxication (Lee, 2003 Ohbu et al. [Pg.657]

Symptoms secondary to nerve agent exposure may be especially difficult to differentiate from stress-associated somatic symptoms. Disaster somatization reaction (DSD), an alternative nosological term to mass hysteria, psychogenic illness, worried well, vicarious victims and contagious fear, classifies the response in patients who interpret their anxiety symptoms as due to direct exposure or infection, or who develop symptoms similar to those identified with exposure or infection (25). [Pg.204]

The recognized need for respiratory support for the apneic victim of nerve agent exposure resulted in the development of a resuscitation device that could be attached to the M9 series of protective masks (Figure 2-49). [Pg.54]

Exposure to small amounts of nerve agents can produce several non-specific CNS effects. Victims of low-dose nerve agent exposures have complained of... [Pg.132]

Victims of certain chemical exposures will experience seizure activity. Patients must be protected from harm. Benzodiazepines are the mainstays in seizure treatment. Liberal doses are required titrate to effect. Termination of seizure activity may reflect onset of flaccid paralysis from the nerve agent rather than adequacy of anticonvulsant therapy. A bedside electroencephalograph (EEG) may be required to assess ongoing seizure activity. [Pg.514]

Whether there is sufficient time after an exposure to the CWA for a therapy to be beneficial is dependent on the initial dose. This will depend on the initial level of the agent released and how close a victim is to the point of release, or ground zero. If the dose is low, the risk of an acute life-threatening intoxication will likely not be an issue, but there is evidence that acute sublethal exposures to chemical nerve agent may be associated with long-term neurological sequelae (Hoffman et al., 2007 Yamasue et al, 2007). [Pg.892]


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See also in sourсe #XX -- [ Pg.41 , Pg.42 ]




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