Biomedical Engineering Reference
In-Depth Information
receptors at motor end plates. Nicotinic receptors
are also found at the presynaptic symapthomimetic
synapses in the spinal cord. Stimulation at these
sites leads to dilated pupils, tachycardia and hyper-
tension. Nerve agent effects at central nervous
system synapses cause coma and seizures. One
series described a preponderance of central and
sympathomimetic effects in children under 2
years of age after organophosphate poisoning
[30]. Although the spectrum of physical find-
ings after nerve agent exposure in children will
be similar to adults, pediatric patients are likely
to be sicker due to increased dose and greater
vulnerability to the toxic effects of nerve agents
(see above).
Atropine, pralidoxime, and benzodiazepines
counteract the effects of nerve agents. Atropine
provides drying of secretions with reversal of
bronchorrhea serving as the endpoint for treat-
ment. Atropine may also provide protection against
seizures. Pralidoxime, when given in a timely
manner, prevents irreversible binding of the
nerve agent to acetylcholinesterase and prevents
paralysis. Benzodiazepines also treat seizures and
provide improved outcomes in animal exposure
studies. In the USA, atropine is the only antidote
packaged as an autoinjector specifically for chil-
dren (Atropen™). This autoinjector kit does not
contain pralidoxime. Table 10.3 provides weight-
based dosing recommendations for hospital treat-
ment of nerve agent exposure [31].
Children represent a major challenge in deliver-
ing effective field treatment in the USA due to
no availability of a comprehensive pediatric nerve
agent kit. Currently, expert opinion recommends
the Mark I kit as the preferred treatment for chil-
dren down to the age of 3 years as follows [32]:
used based on weight in situations where Mark I
administration to children is specifically prohib-
ited by regulations or legislation: Under 7 kg,
0.25mg autoinjector; 7-18 kg, 0.5mg autoinjector;
18-40 kg, 1mg. autoinjector [31].
10.3.10 Vesicants
This category consists of the alkylating mustard
agents, especially sulfur mustard and the chem-
ical arsenical agent, lewisite. These agents cause
irritation and chemical burns of the eyes, skin,
and respiratory tract. Higher exposures lead to
bone marrow inhibition and gastrointestinal tract
injury. Developed during World War I, lewisite
was never used extensively and has not been
stockpiled to a very large degree. In contrast,
sulfur mustard exists in large amounts and was
recently used by Saddam Hussein against Iranian
troops and Kurds in the past two decades. Pedi-
atric exposure data from these events indicate
that children may develop clinical effects rapidly
after mustard exposure and have more extensive
skin lesions [28]. Mustards have no antidote. The
most important treatment is rapid decontamination
within minutes of exposure. Severe exposures to
lewisite may benefit by therapy with British anti-
lewisite (BAL, Table 10.3).
10.3.11 Pulmonary Agents
Chlorine and phosgene comprise the commonly
weaponized pulmonary agents. They also are
prime chemical weapons of opportunity given
their ubiquitous use in industrial chemical produc-
tion. Irritation of the eyes, nose, and throat are
common, especially with chlorine. Bronchospasm
and pulmonary edema follow serious exposure.
Pulmonary edema may occur 2-4 hours after chlo-
rine exposure and anywhere from 6 to 24 hours
after phosgene exposure. Treatment is supportive
and does not differ from adults. Children are more
vulnerable to the effects of these agents as previ-
ously discussed in section 10.2 [29].
1. 3-7 years or 13-25 kg : 1 Mark I autoinjector
(2mg Atropine/ 600mg Pralidoxime)
2. 8-14 years or 26-50 kg : 2 Mark I autoinjectors
(4mg Atropine/1200mg Pralidoxime)
3. Over 14 years or >51 kg : 3 Mark I autoinject-
ors (6mg Atropine/1800mg Pralidoxime)
10.3.12 Cyanide
Cyanide, the notorious poison used in the Nazi
gas chambers, causes cellular anoxia and death
Children under 3 years require weight-based
dosing as per Table 10.3. The AtroPen™ may be
