Nerve agents intravenous

Nerve Agent Antidote Kit (NAAK or MARK I) consists of an atropine auto-injector (2 mg), a pralidoxime chloride auto-injector (2-Pam-Cl, 600 mg), the plastic clip joining the two injectors, and a foam case. The kit serve as a countermeasure to nerve agents, including tabun (GA), sarin (GB), soman (GD), GF, and VX. Military personnel can receive three MARK I for self/buddy aid. Possible side effects of atropine and/or 2-PAM-C1 are deemed insignificant in a nerve agent casualty. Intravenous atropine and 2-PAM-C1 can also be made available. The MARK I kit is manufactured by Survival Technology, Inc., Rockville, Maryland. 

Drugs For mild or moderate nerve agent contamination in an adult, the standard first dose for atropine is 2 to 4 mg IM, (intramuscular) and for 2-PAM Cl is 15 mg/kg (lg) IV (intravenous) slowly for an adult victim with severe symptoms, a first dose would be atropine at 6 mg IM (intramuscular), and for 2-PAM Cl the dose should be 15 mg/kg(lg) IV (intravenous) slowly. There are different recommended doses for Infants, Children, Adolescent, and Elderly/Frail. 

The human intravenous bolus dose of oximes in nerve agent treatment ranges between 250 and 500 mg ". Side effects of oxime treatment in humans were monitored in 750 volunteers, and the main adverse effects reported were changes in blood pressure, pulse rate, dizziness, nausea and blurred vision . Oral administration of oximes produces gastrointestinal distress. ... 

Van der Schans, M.J., Lander, B.J., Van der Wiel, H., Langenberg, J.P., Benschop, H.P. (2003). Toxicokinetics of nerve agent ( )-VX in anesthetized and atropinized hairless guinea pigs and marmosets after intravenous and percutaneous administration. Toxicol. Appl. Pharmacol. 191 48-62. 

The immediate treatment for nerve agent intoxication is intravenous injection of 2 mg atropine sulfate (intramuscular injection should be considered if the patient is hypoxic and ventilation cannot be initiated, as there is a risk of ventricular fibrillation). This should be followed by additional injections of atropine at 10-15 min intervals, continuing until bradycardia has been reversed (e.g., until the heart rate is at 90 beats per minute). If breathing has stopped, a mechanical respirator should be used to ventilate the patient. Mouth-to-mouth resuscitation should not be attempted. If possible, oxygen or oxygen-enriched air should be used for ventilation. If possible, cardiac activity should be monitored. 

Given that early responders may not know for certainty which nerve agent was responsible, patients suffering from nerve agent symptoms should receive pralidoxime immediately, in conjunction with atropine. The adult dose of pralidoxime (see Tables 3.3 and 3.4) is l-2g (15-25mg kg ) intramuscularly (18) or 1 g (15mg kg ) intravenously in lOOmL of saline over 15-30min. Intravenous administration, if possible, is preferable (3). After an hour, if paralysis persists, patients should receive a second dose (21). Severely iU adult patients may benefit from an intravenous 2g pralidoxime bolus followed by a maintenance infusion of 7.5mg kg h ... 

In mass casualty situations, intravenous antidotes may not be available. In that case, the intramuscular administration is acceptable. Most Emergency Medical Systems in the United States now stock military Autoinjector units containing atropine and pralidoxime, although kits with pediatric doses may not be available. However, in critical situations, children older than 2 or 3 years of age weighing at least 13 kg might benefit from 2 mg of atropine and 600 mg pralidoxime administered intramuscularly with auto-injectors (7). Experience with the accidental atropine auto-injection in 240 Israeli children unexposed to nerve agents revealed that... 

During the clinical usage of oxime for the treatment of poisonings with nerve agent or OPI, we must be fully aware of the possible occurrence of oxime-induced side effects. The rapid intravenous injection of pralidoxime can produce drowsiness, headache, disturbance of vision, nausea, dizziness, tachycardia and... 

Toxicokinetics of the nerve agent (+/-)-VX in anesthetized and atropinized hairless guinea pigs and marmosets after intravenous and percutaneous administration. Toxicol Appl Pharmacol, 191, 48-62. 

In symptomatic patients, intravenous access should be established and blood should be taken for measurement of erythrocyte cholinesterase activity to confirm the diagnosis. If the characteristic features of nerve agent poisoning are present, however, antidotal treatment should not be delayed until the result is available. 

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. 

Where nerve agent-induced convulsions are present, the standard intravenous dosage regime for diazepam for the treatment of convulsions is used ... 

Figure 10. Relationship between vapour pressure and the relative percutaneous toxicity (expressed as the ratio of the percutaneous LD50 to the intravenous LD50) of four nerve agents (VX, GF, GD and GB indicated by solid circles). A notable exception to this relationship is GA (indicated with a solid triangle) which may undergo dermal metabolism prior to systemic absorption...

The inhibition of AChE activity in nerve tissues of animals at different times after exposure to low-dose nerve agents are depicted in Table 3.3. In most studies, subcutaneous, intravenous, inhalation, and oral routes of exposure were used. AChE activity in whole brain, spinal cord, and brain regions such as cerebral cortex, corpus striatum, meduUa, and cerebellum was significantly decreased in rats, " " mice, and hens, ° hours, days, and weeks after low-dose exposure to nerve agents such as soman, sarin, and tabun. 

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