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<p><strong>You Are Here:</strong> <span class="crumb_link"><a href="/" class="crumb_link">AHRQ Archive Home</a> > <a href="/prep/" class="crumb_link">Public Health Preparedness Archive</a> > <a href="." class="crumb_link">Pediatric Terrorism and Disaster Preparedness</a> > Chapter 5</span></p>
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<td height="30px"><span class="title"><a name="h1" id="h1"></a>Pediatric Terrorism and Disaster Preparedness </span></td>
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<td><div id="centerContent"><p><strong>Public Health Emergency Preparedness</strong></p> <div class="headnote">
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<p>This resource was part of AHRQ's Public Health Emergency Preparedness program, which was discontinued on June 30, 2011, in a realignment of Federal efforts.</p>
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<p>Please go to <a href="https://www.ahrq.gov/">www.ahrq.gov</a> for current information.</p></div>
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<h2>Chapter 5. Chemical Terrorism</h2>
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<h3><a name="Introduction" id="Introduction"></a>Introduction</h3>
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<p>Chemical terrorism is the intentional use of toxic chemicals to inflict mass
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casualties and mayhem on an unsuspecting civilian population, including children.
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Such an incident could potentially overwhelm the capacity of regional emergency
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medical services and pose extraordinary medical management challenges to pediatricians.
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However, careful community planning, robust research and development (by academic,
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private, and governmental collaborative efforts), and rigorous medical education
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could mitigate such a catastrophe.</p>
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<p>The risk of chemical terrorism is more tangible since the events of September
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11, 2001, and the subsequent intentional spread of anthrax through the U.S.
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mail. However, the specter of purposeful toxic exposures predates the September
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11 attack. The 20th century witnessed Iraqi military attacks with nerve agents
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on civilian villages in Iran in the 1980s, the release of the nerve agent sarin
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in the Tokyo subway system in 1995, a chlorine bomb scare at Disneyland in
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1995, and the finding of ricin in U.S. Senate office buildings in 2004.</p>
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<p>Chemical terrorism often refers to the use of military chemical weapons that
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have been illicitly obtained or manufactured <em>de novo</em>. However, additional
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concerns might include the intentional explosion of an industrial chemical
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factory, a tanker car, or a transport truck in proximity to a civilian residential
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community, school, or worksite. These events underscore the need for all pediatricians
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to expand their working knowledge of the approach to mass casualty incidents
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involving traditional military chemical weapons and other toxic chemicals that
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might be used as "weapons of opportunity."</p>
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<p>The medical consequences and epidemiology of a chemical terrorist attack mimic
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more conventional disasters but also reflect some distinct differences. Such
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an incident combines elements of both a traditional mass disaster (e.g., an
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earthquake) and a hazardous materials incident. Potential differences of a
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chemical terrorist attack compared with a "routine" hazardous
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materials incident include the following:</p>
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<ul>
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<li>Intent to cause mass casualties.</li>
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<li>Great toxicity of substances.</li>
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<li>Delayed initial identification of substance.</li>
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<li>Greater risk to first responders.</li>
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<li>Overwhelming numbers of patients.</li>
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<li>Many anxious individuals.</li>
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<li>Mass hysteria, panic.</li>
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<li>Discovery of dispersal device.</li>
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</ul>
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<p>Casualties occur almost immediately, and the attack would likely be recognized
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rapidly. First responders are emergency medical services (EMS), police, fire, and paramedic personnel.
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Decontamination and initial care of small children on-scene pose enormous management
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issues for personnel wearing bulky personal protective gear. In addition, many
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children who have been exposed but not critically injured will be taken by
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parents to hospitals and pediatricians' offices without prior on-scene
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decontamination—thus posing similar challenges for and possibly personal
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risk to pediatric care providers themselves.</p>
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<h4><a name="Vulnerabilities" id="Vulnerabilities"></a>Specific Pediatric Vulnerabilities to Chemical Agents</h4>
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<p>Children have inherent physiologic, developmental, and psychological differences
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from adults that may enhance susceptibility and worsen prognosis after a chemical
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agent exposure (also read the Chapter
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1 section, <a href="pedchap1.htm#Children">Children Are Not Small Adults</a>). Briefly,
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such physiologic differences include higher minute ventilation, increased skin
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permeability, relatively larger body surface area, less intravascular volume
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reserve in defense of hypovolemic shock, and shorter stature (which places
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children nearer to the greatest gas vapor density at ground level). Children
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who are pre-ambulatory or pre-verbal and those who have special needs are less
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able to evade danger or seek attention effectively. A chaotic atmosphere compounded
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by rescuers wearing unfamiliar garb may frighten children of all ages and potentially
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increase the posttraumatic response to stress. Those providing care for children
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are faced with additional complexities posed by developmental, age, and weight
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considerations beyond the general scope of the already enormous challenge.</p>
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<p><a name="Tab5.1" id="Tab5.1"></a>Pediatric vulnerabilities become particularly significant when weapons of
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mass destruction are involved. A chemical agent will most likely be dispersed
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via an aerosol route or in combination with traditional warfare. Chemical exposures
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warrant expedient and thorough decontamination to limit continued primary and
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secondary exposures. Children's relatively large body surface area plays
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a key role in degree of contamination and in their ability to maintain thermal
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homeostasis after decontamination. <a href="pedtab5_1.htm">Table
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5.1</a> summarizes pediatric-specific
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vulnerabilities to chemical agents.</p>
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<h4><a name="Injuries" id="Injuries"></a>Chemical Injuries and Approach to the Unknown Chemical Attack</h4>
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<p>A listing of many of the most notable chemical agents of concern has been
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compiled by the Centers for Disease Control and Prevention (CDC). Go to <a href="http://www.bt.cdc.gov/agent/agentlistchem.asp">http://www.bt.cdc.gov/agent/agentlistchem.asp</a>.
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Toxic effects from chemical agents usually follow dermal or inhalational exposure
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and may develop via injury to the skin, eyes, and respiratory epithelium, as
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well as via systemic absorption. The intensity and route of exposure to chemical
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agents affect both the rapidity of onset (seconds to hours) and the severity
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of symptoms. For example, a mild exposure to sarin vapor results in lacrimation,
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rhinorrhea, miosis, and slightly blurry vision; an intense exposure leads to
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seizures, apnea, and rapid death within minutes.</p>
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<p><a name="Tab5.2" id="Tab5.2"></a>Clinical syndromes and management after exposure to various chemical agents
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(nerve agents, vesicants, pulmonary agents, cyanide, and riot-control agents)
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are summarized in <a href="pedtab5_2.htm">Table 5.2</a> and detailed in the following sections.
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For in-depth discussions of general principles of supportive care for victims
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of chemical warfare agents, go to: Osterhoudt, et al, 2005, and Erickson, 2004.</p>
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<p>Understanding the epidemiology of acute mass exposure to a toxin is helpful
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in recognizing a covert chemical attack with unknown agents. Mass exposure
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to a toxin will likely manifest as an acute onset of illness (within seconds
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to minutes or within hours in the case of some of the vesicants and pulmonary
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agents). In more severe chemical incidents, numbers of people may collapse
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or die within minutes of exposure.</p>
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<p>Chemical weapons can be categorized based on the predominant symptoms they
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cause:</p>
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<ul>
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<li>Neurologic (nerve agents or cyanide).</li>
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<li>Respiratory (phosgene or chlorine, high-dose riot-control agents, or sulfur
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mustard with a delay of several hours from time of exposure).</li>
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<li>Mucocutaneous syndromes (vesicants).</li>
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</ul>
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<p>For additional advice on more definitive diagnosis and management strategies,
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contact public health authorities or the regional poison control center (1-800-222-1222).</p>
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<p>The initial decision that will need to be made immediately will likely be
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the distinction of cyanide from nerve agent attack because the antidotal therapies
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are quite different. In both cases, large numbers of victims may suddenly collapse,
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have seizures, or go into a coma, and many deaths occur rapidly. Nerve agent
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casualties are likely to be cyanotic and have miotic pupils with altered vision,
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copious oral and nasal secretions, and acute bronchospasm and bronchorrhea.</p>
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<p>The initial protection of everyone in a community exposed to a hazardous chemical
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requires safe evacuation or local sheltering. Circumstances may vary considerably,
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but it is expected that local and Federal authorities will decide and quickly
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advise on evacuation or local sheltering and broadcast their advice quickly
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and widely in the public media.</p>
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<p>For the CDC guidelines for evacuation, go to: <a href="http://www.bt.cdc.gov/planning/evacuationfacts.asp">http://www.bt.cdc.gov/planning/evacuationfacts.asp</a>.</p>
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<p> For the CDC guidelines for sheltering in place in a chemical emergency, go
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to: <a href="http://www.bt.cdc.gov/planning/shelteringfacts.asp">http://www.bt.cdc.gov/planning/shelteringfacts.asp</a>.</p>
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<h4><a name="Approach" id="Approach"></a>Initial Approach, Decontamination, and Triage</h4>
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<p>The general treatment of contaminated victims begins with extrication, triage,
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resuscitation as needed, and decontamination performed by rescue workers or
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health care providers wearing appropriate personal protective equipment (PPE).
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Ideally, decontamination would be done at the scene to avoid the considerable
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challenges posed by the arrival of contaminated patients, including children,
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at health care facilities. However, in a large-scale terrorist incident, it
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is far more likely that some victims will arrive at hospitals or other health
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care facilities without having been previously decontaminated. In this context,
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significantly contaminated victims should be decontaminated before they are
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allowed into the emergency department (ED). Even if decontamination has been
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done in the field, hospitals are likely to repeat decontamination procedures
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to protect the facility from contamination (which would result in closure or
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having to go "off line"); this would also address the possibility
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of cross-contamination moving from the scene. Decontamination to limit secondary
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exposures is especially important in exposures to nerve agents and vesicants.</p>
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<p>Appropriate PPE for ED staff involved in patient decontamination is an important
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consideration. The amount of chemical agent believed to contaminate patients
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who arrive at the ED after a chemical terrorist attack would essentially consist
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of that on their skin and clothing (i.e., far lower concentration of chemicals
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than rescue workers would face at the scene of exposure). Most authorities
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believe that ED staff wearing level C PPE would be adequately protected. Level
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C PPE consists of a non-encapsulated, chemically resistant body suit, gloves,
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boots, and a powered purifying air respirator (PAPR) mask containing a cartridge with both an organic-vapor filter
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for chemical gases and vapors and a high efficiency particulate air (HEPA) filter to trap aerosols of biological
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and chemical agents. Such PPE is much less cumbersome to work in than level
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A or B outfits (which use self-contained breathing apparatus) and is also less
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expensive.</p>
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<p>Cardiopulmonary and airway support, including endotracheal intubation, and
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emergent intramuscular antidotal therapy are provided as necessary and appropriate
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for the specific exposure. Contaminated clothing should be removed as soon
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as possible. The contamination hazard is reduced by as much as 80-90% simply
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by removing clothing. This is accompanied or immediately followed by
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more definitive decontamination. For vapor-exposed victims, decontamination
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may be accomplished primarily by clothing removal and washing of hair. In contrast,
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for victims with liquid dermal exposure, more thorough decontamination is required.
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Their skin and clothing pose considerable risk to ED personnel. Clothing should
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be carefully removed and disposed of in double bags. Victims with ocular
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exposure require eye irrigation with copious amounts of saline or water. Skin
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and hair should be washed thoroughly, but gently, with soap and tepid water.
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In the past, some authorities had recommended 0.5% sodium hypochlorite (dilute
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bleach) for skin decontamination of nerve agents and vesicants. However, this
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may be a skin irritant, thus increasing permeability to the agent. In addition,
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its use is time-consuming and has not been proven superior to washing with
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copious soap and water or water alone. Furthermore, there is little experience
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with this approach in infants and young children. A difficult question that
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remains is whether EMS and ED staff wearing bulky PPE will be able to provide
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significant advanced life support to small children before decontamination. </p>
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<p>Ambulatory, asymptomatic victims may be able to be discharged from the scene,
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while those with minimal symptoms may be directed toward local shelters (e.g.,
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American Red Cross stations, local schools, or other sites designated by local
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or State health departments) after decontamination for medical observation.
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These shelters may also serve as sites for reuniting children with their families,
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keeping track of all victims, and communicating with law enforcement agencies.</p>
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<h4><a name="Industrial" id="Industrial"></a>Industrial Chemicals</h4><a id="Tab5.3" name="Tab5.3"></a>
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<p>The potential of a terrorist attack on industrial sources of hazardous chemicals
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(e.g., factories, railroad and vehicular tank cars, or storage depots) expands
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the list of potential "chemical weapons" considerably. In
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general, many of the relevant industrial chemicals might be expected to induce
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respiratory effects analogous to those of chlorine or phosgene (read the <a href="pedchap5b.htm#Pulmonary">section
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on pulmonary agents</a> later in this chapter) or dermatologic injury from irritant
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or caustic properties, as well as more systemic effects in severe exposures
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(<a href="pedtab5_3.htm">Table 5.3</a>). For an in-depth
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discussion of principles in managing such toxic injuries, see Osterhoudt, et
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al., 2005, and Erickson, 2004.</p>
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<h4><a name="Preparedness" id="Preparedness"></a>Community Preparedness</h4>
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<p>In the aftermath of September 11, 2001, many agencies are collaborating to
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ensure coordinated care of pediatric victims (<a href="pedchap2.htm">Chapter
|
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2, Systems Issues</a>).
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All pediatricians are encouraged to participate in disaster management training.
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The need to stock appropriate antidotes, practice decontamination strategies,
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and learn the use of PPE is apparent. Although perhaps not every practicing
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pediatrician needs to be competent in all aspects of disaster response, all
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in the community should work together to optimize the overall capacity for
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providing disaster care to chemically exposed children.</p>
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<p>Successful planning and response to events involving chemical terrorism require
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strong collaboration and integrated functioning of many agencies and facilities,
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both governmental and nongovernmental, including local treatment facilities,
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local and State health departments, and Federal agencies (CDC, FEMA, FBI, etc.).</p>
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<p class="size2"><a href="index.html#Contents">Return to Contents</a> </p>
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<h3><a name="Nerve" id="Nerve"></a>Nerve Agents</h3>
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<p>Nerve agents are organophosphorous compounds similar to the organophosphate
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insecticides used in agriculture or industry but far more toxic. Four compounds
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are currently regarded as nerve agents: tabun, sarin, soman, and VX ("Venom
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X"). All of these agents are hazardous by ingestion, inhalation, or cutaneous
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absorption, the latter being particularly true for VX. The toxic effects of
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nerve agent vapors depend on the concentration of the agent inhaled and on
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the time exposed to the agent. The toxicity of nerve agent liquid depends on
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the time exposed and the bodily site of exposure. Nerve agents exist as liquids
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at standard temperatures and pressures. In gaseous form, they are denser than
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air and vary in volatility, with some (e.g., VX) being more persistent than
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others (e.g., sarin).</p>
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<h4><a name="Background" id="Background"></a>Background</h4>
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<p>The Iran-Iraq War of the 1980s reportedly resulted in more than 100,000 casualties
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from chemical weapons. Iranian sources reported that the number of casualties
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caused by nerve agents was far greater than the number of casualties caused
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by mustard agent. Many nerve agent casualties that were only mildly to moderately
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affected were not counted.</p>
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<p>A chemical warfare campaign by the Iraqi military on Kurdish civilians in
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the late 1980s caused thousands of deaths. The exact agents are not definitively
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known, but Iraq is known to have stockpiled tabun, sarin, and VX.</p>
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<p>A Japanese religious cult that manufactured sarin deployed it in 1994 in attacks
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on a residential neighborhood of Matsumoto and again in 1995, in the Tokyo
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subway. Immediate mortality was low, but thousands of individuals arrived at
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emergency rooms. The lack of a decontamination process resulted in significant
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morbidity to health care personnel. The sarin was released by a relatively
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primitive method (punctured plastic bags allowing sarin vapor to escape); many
|
|
experts believe a more sophisticated delivery system might have resulted in
|
|
far higher mortality. </p>
|
|
<p>Nerve agent exposures in the United States have been individual cases associated
|
|
with industrial exposures.</p>
|
|
<h4><a name="Toxicology" id="Toxicology"></a>Toxicology and Clinical Manifestations</h4>
|
|
<p>Nerve agents inhibit the action of acetylcholinesterase at cholinergic neural
|
|
synapses, where acetylcholine then accumulates markedly. The resulting cholinergic
|
|
syndrome is classically divided into central, nicotinic (neuromuscular junction
|
|
and sympathetic ganglia), and muscarinic (smooth muscle and exocrine gland)
|
|
effects.</p>
|
|
<p>Clinical manifestations vary with the type of exposure. Symptoms after a vapor
|
|
exposure appear suddenly with a full range of clinical effects, or there may
|
|
be a partial expression of the syndrome. Symptoms after a liquid exposure may
|
|
start with local sweating and then progress.</p>
|
|
<p><strong>Central nervous system (CNS) effects.</strong> Effects on the CNS include headache, seizures,
|
|
coma, respiratory arrest, confusion, slurred speech, and respiratory depression.
|
|
Although the seizures probably begin due to excess cholinergic stimulation,
|
|
other effects (e.g., excitatory glutamate receptor stimulation and antagonism
|
|
of inhibitory gamma-aminobutyric acid [GABA] receptors) may also play a role.
|
|
Little experience with nerve agents is available to distinguish clinical effects
|
|
in children from those in adults, although two cases of antichlolinesterase
|
|
pesticide poisonings in children suggest a disproportionate degree of depressed
|
|
sensorium and muscle weakness. Thus, children may manifest primarily central
|
|
and/or neuromuscular effects after nerve agent exposure.</p>
|
|
<p><strong>Autonomic nervous system effects. </strong> These include both nicotinic and muscarinic findings. Nicotinic effects on sympathetic
|
|
activity can result in the following:</p>
|
|
<ul>
|
|
<li>Tachycardia.</li>
|
|
<li>Hypertension.</li>
|
|
<li>Metabolic aberrations (e.g., hyperglycemia, hypokalemia, and metabolic
|
|
acidosis).</li>
|
|
</ul>
|
|
<p>Muscarinic effects involve multiple systems:</p>
|
|
<ul>
|
|
<li>Ocular (miosis, eye pain, visual blurring, lacrimation).</li>
|
|
<li>Respiratory (watery rhinorrhea, increased bronchial secretions and bronchospasm
|
|
causing cough, wheezing, dyspnea, and cyanosis).</li>
|
|
<li>Cardiovascular (bradycardia, hypotension, atrioventricular block).</li>
|
|
<li>Dermal (flushing, sweating).</li>
|
|
<li>Gastrointestinal (salivation, nausea, vomiting, diarrhea progressing to
|
|
fecal incontinence, abdominal cramps).</li>
|
|
<li>Urinary (frequency, urgency, incontinence).</li>
|
|
</ul>
|
|
<p><strong>Neuromuscular effects. </strong> At the neuromuscular junction, initial stimulation of cholinergic synaptic
|
|
transmission is followed by paralysis. Thus, nicotinic effects include muscle
|
|
fasciculations and twitching, followed by weakness progressing to flaccid
|
|
paralysis and respiratory failure.</p>
|
|
<p>The clinical syndrome of organophosphate toxicity is summarized
|
|
by various mnemonics, including "bag the puddles,"<sup><a href="#ftn1">1</a></sup> "sludge" syndrome,
|
|
and "dumbbels."</p>
|
|
<p><strong>B</strong> = bronchoconstriction, bronchorrhea<br />
|
|
<strong>A</strong> = apnea<br />
|
|
<strong>G</strong> = graying/dimming of vision<br />
|
|
<strong>P</strong> = pupillary constriction (miosis)<br />
|
|
<strong>U</strong> = urination<br />
|
|
<strong>D</strong> = diarrhea<br />
|
|
<strong>D</strong> = diaphoresis<br />
|
|
<strong>L</strong> = lacrimation<br />
|
|
<strong>E</strong> = emesis<br />
|
|
<strong>S</strong> = salivation, seizures</p>
|
|
<p align="left"><strong>S</strong> = salivation, seizures<br />
|
|
<strong>L</strong> = lacrimation<br />
|
|
<strong>U</strong> = urination<br />
|
|
<strong>D</strong> = diarrhea<br />
|
|
<strong>G</strong> = graying/dimming of vision<br />
|
|
<strong>E</strong> = emesis</p>
|
|
<p align="left"><strong>D</strong> = diarrhea<br />
|
|
<strong>U</strong> = urination<br />
|
|
<strong>M</strong> = miosis<br />
|
|
<strong>B</strong> = bronchoconstriction<br />
|
|
<strong>B</strong> = bronchorrhea<br />
|
|
<strong>E</strong> = emesis<br />
|
|
<strong>L</strong> = lacrimation<br />
|
|
<strong>S</strong> = salivation</p>
|
|
<h4><a name="Diagnostic" id="Diagnostic"></a>Diagnostic Tests</h4>
|
|
<p>The diagnosis of nerve agent toxicity is primarily based on clinical recognition
|
|
and response to antidotal therapy. Measurements of acetylcholinesterase in
|
|
plasma or red blood cells (RBCs) may confirm organophosphate poisoning, but
|
|
correlation between cholinesterase levels and clinical toxicity is poor in
|
|
some contexts; also, these analyses are rarely available on an emergent basis.
|
|
RBC cholinesterase levels may help in monitoring recovery or in forensic investigations.
|
|
In symptomatic patients, treatment is indicated without waiting for cholinesterase
|
|
levels, while in exposed asymptomatic patients, antidotal therapy is not needed,
|
|
even if cholinesterase is depressed.</p>
|
|
<h4><a name="Treatment" id="Treatment"></a>Treatment</h4>
|
|
<p>If recognized early, this is a treatable and reversible syndrome. Triage,
|
|
resuscitation, and decontamination should begin at the scene and at accepting
|
|
health care facilities (go to <a href="pedchap1.htm">Chapter
|
|
1</a>). Individuals exposed to liquid should
|
|
be observed for at least 18 hours.</p><a id="Tab5.4" name="Tab5.4"></a>
|
|
<p>Treatment focuses on airway and ventilatory support; aggressive use of antidotes,
|
|
particularly atropine and pralidoxime (2-PAM); prompt control of seizures;
|
|
and decontamination as necessary. Antidotal therapy is titrated according to
|
|
clinical severity (<a href="pedtab5_4.htm">Table 5.4</a>).</p>
|
|
<p>Atropine, in relatively large doses, is used for its antimuscarinic effects,
|
|
and pralidoxime chloride serves to reactivate acetylcholinesterase and thus
|
|
enhance neuromuscular function. Atropine counters bronchospasm and increased
|
|
bronchial secretions; bradycardia; gastrointestinal (GI) effects of nausea, vomiting, diarrhea,
|
|
and cramps; and may lessen seizure activity. Severely affected nerve agent
|
|
casualties in the military have received 20-200 mg of atropine. Atropine should
|
|
be administered until respiratory status improves, because tachycardia is not
|
|
an absolute end-point for atropinization. Atropine cannot reverse neuromuscular
|
|
symptoms, and paralysis may persist without pralidoxime.</p>
|
|
<p>Pralidoxime cleaves the organophosphate away from the cholinesterase, thus
|
|
regenerating the intact enzyme if aging has not occurred. This effect is noted
|
|
most at the neuromuscular junction, with improved muscle strength. Prompt use
|
|
of pralidoxime is recommended in all serious cases.</p>
|
|
<p>Both atropine and pralidoxime should be administered intravenously (IV) in severe cases (intraosseous
|
|
access is likely equivalent to IV). However, animal studies suggest that hypoxia
|
|
should be corrected, if possible, before IV atropine use, to prevent arrhythmias;
|
|
otherwise intramuscular (IM) use might be preferable initially. Atropine has also been administered
|
|
by the endotracheal or inhalational route in some contexts, and such use might
|
|
have a beneficial effect. Experience with organophosphate pesticide poisoning
|
|
in children suggests that continuous IV infusion of pralidoxime may be optimal.
|
|
Nevertheless, the IM route is acceptable if IV access is not readily available.
|
|
This may be of considerable relevance in a mass casualty incident involving
|
|
children. In fact, most EMS programs in the United States now stock military
|
|
IM auto-injector kits of atropine and 2-PAM. Similar kits with pediatric doses
|
|
are currently not available in the United States. However, pediatric auto-injectors
|
|
of atropine in 0.25 mg, 0.5 mg, and 1.0 mg sizes have recently been approved
|
|
by the Food and Drug Administration (FDA). In dire circumstances, the adult 2-PAM auto-injector (600 mg) might
|
|
be used in children older than 2-3 years or weighing more than 13 kg.</p>
|
|
<p>Seizures are primarily controlled with benzodiazepines. Diazepam is principally
|
|
used by the U.S. military, but other benzodiazepines may be equally efficacious
|
|
(e.g., midazolam or lorazepam). Midazolam is believed optimal for IM administration
|
|
in the treatment of status epilepticus in general and so may be especially
|
|
useful in nerve agent toxicity in children. Finally, routine administration
|
|
of anticonvulsant doses of benzodiazepines has been recommended in severe cases
|
|
even without observed convulsive activity because animal studies have indicated
|
|
some amelioration of subsequent seizures and morphologic brain damage with
|
|
such use.</p>
|
|
<p>Supportive care is critical to patient outcome and includes the following:</p>
|
|
<ul>
|
|
<li>Protect airway/relieve bronchospasm/pulmonary toilet.<ul>
|
|
<li>100% oxygen, bronchodilators, nasogastric tubes.</li>
|
|
</ul></li>
|
|
<li>Monitor for cardiac arrhythmias.</li>
|
|
<li>Treat complicating injuries and infections.<ul>
|
|
<li>Wounds and foreign bodies may be contaminated.</li>
|
|
<li>Treat skin lesions.</li>
|
|
</ul></li>
|
|
<li>Provide fluids, electrolytes, and nutrition.<ul>
|
|
<li>Nursing mothers should discard breast milk.</li>
|
|
</ul></li>
|
|
<li>Prevent hypothermia.</li>
|
|
<li>Provide eye care.<ul>
|
|
<li>Consider ophthalmic analgesics for ocular pain.</li>
|
|
<li>Consider topical mydriatics for miosis (atropine given systemically
|
|
may not reverse miosis).</li>
|
|
</ul></li>
|
|
<li>Consider electroencephalogram (EEG) and brain imaging for victims who do not promptly regain consciousness. </li>
|
|
</ul>
|
|
<h4><a name="Isolation" id="Isolation"></a>Isolation and Control Measures</h4>
|
|
<p>Isolation is required only for potentially exposed victims before they are
|
|
definitively decontaminated. Health care workers should wear PPE to treat victims
|
|
before decontamination is complete.</p>
|
|
<p class="size2"><a href="index.html#Contents">Return to Contents</a> </p>
|
|
<h3><a name="Cyanide" id="Cyanide"></a>Cyanide</h3>
|
|
<p>Cyanide has long been used for sinister purposes, including as an agent of
|
|
murder, suicide, chemical warfare, and judicial execution. In addition, it
|
|
may pose an occupational hazard, and it has been ingested (usually in a precursor
|
|
form) by children. Its efficacy as an agent of chemical terrorism is considered
|
|
somewhat limited by its volatility in open air and relatively low lethality
|
|
compared with nerve agents. However, if cyanide were released in a crowded,
|
|
closed room, the effects could be devastating. This was more than amply illustrated
|
|
by its notoriety as the chemical weapon used by the Nazis in the concentration
|
|
camp gas chambers. More than 900 people ingested potassium cyanide salt in
|
|
the 1978 Jonestown mass suicide incident. Chemical warfare agents involving
|
|
cyanide include the liquids hydrocyanic acid (HCN, the form used by the Nazis,
|
|
as "Zyclon B") and cyanogen chloride (deployed during World War
|
|
I), which rapidly vaporize after detonation. Cyanogen chloride may cause some
|
|
initial eye, nose, throat, and airway irritation, but otherwise its effects
|
|
are the same as those of hydrocyanic acid and result from systemic cyanide
|
|
toxicity.</p>
|
|
<h4><a name="CyanToxicology" id="CyanToxicology"></a>Toxicology</h4>
|
|
<p>Cyanide has a strong affinity for the ferric iron (Fe3+) of the heme ring
|
|
and thus inhibits many heme-containing enzymes. Its primary effect in acute
|
|
toxicity is inhibition of cytochrome <em>a</em>3, thereby interfering with
|
|
normal mitochondrial oxidative metabolism in the electron transport chain,
|
|
causing cellular anoxia and lactic acidosis. It may also interfere with other
|
|
important enzymes, including succinic acid dehydrogenase and superoxide dismutase,
|
|
which may underlie some of its chronic toxicity. In addition, cyanide is believed
|
|
to be a direct neurotoxin contributing to an excitatory injury in the brain,
|
|
probably mediated by glutamate stimulation of N-methyl D-aspartate receptors.
|
|
The primary human enzyme, rhodanese, detoxifies cyanide by combining it with
|
|
a sulfate moiety such as thiosulfate to form the relatively nontoxic thiocyanate
|
|
ion, which is then excreted by the kidneys. Therefore, exposure to a potentially
|
|
lethal dose of cyanide that occurs slowly though continually over time may
|
|
be tolerated, making it relatively unique among the agents of chemical terrorism.</p>
|
|
<h4><a name="Presentation" id="Presentation"></a>Clinical Presentation</h4>
|
|
<p>Clinical manifestations of cyanide toxicity vary considerably depending on
|
|
dose, route of exposure, and acuteness of exposure but in general reflect the
|
|
effects of cellular anoxia on organ systems. Thus, the most metabolically active
|
|
tissues, the brain and heart, tend to be the most affected. With exposure to
|
|
low concentrations of vapor, early findings include tachypnea and hyperpnea,
|
|
tachycardia, flushing, dizziness, headache, diaphoresis, nausea, and vomiting.
|
|
As exposure continues, symptoms may progress to those associated with exposures
|
|
to high concentrations of vapor. The latter include rapid onset (within 15
|
|
seconds) of tachypnea and hyperpnea, followed by seizures (30 seconds), coma
|
|
and apnea (2-4 minutes), and cardiac arrest (4-8 minutes). "Classical" signs
|
|
of cyanide poisoning include severe dyspnea without cyanosis—or even
|
|
with cherry-red skin (due to lack of peripheral oxygen use)—and a bitter
|
|
almond odor to breath and body fluids. However, some patients do develop cyanosis
|
|
(likely secondary to shock), and only about half the population is genetically
|
|
capable of detecting the cyanide-induced bitter almond odor. Laboratory abnormalities
|
|
in cyanide poisoning include metabolic acidosis with a high anion gap and increased
|
|
serum lactate and an abnormally high mixed venous oxygen saturation (also due
|
|
to decreased use of peripheral oxygen). Blood cyanide levels can be determined
|
|
but not usually on an emergent basis.</p>
|
|
<p>In an aerosol attack using recognized military chemical weapons, if people
|
|
are convulsing or dying within minutes of exposure, the weapon is likely to
|
|
be either cyanide or a nerve agent. Although the symptoms of exposure to cyanide
|
|
and nerve agents may be hard to distinguish, when there are high concentrations
|
|
of cyanide, seizures begin within seconds and death within minutes, generally
|
|
with little cyanosis or other findings. The course for lethal nerve agent toxicity
|
|
is characteristically somewhat longer and accompanied by copious nasal secretions,
|
|
miotic pupils, muscle fasciculations, and cyanosis before death.</p>
|
|
<h4><a name="CyanTreatment" id="CyanTreatment"></a>Treatment</h4>
|
|
<p>Management of cyanide poisoning begins with removing the victim from the contaminated
|
|
environment to fresh air. Dermal decontamination is rarely necessary because
|
|
these agents are so volatile but in case of contact with liquid agent, wet
|
|
clothing should be removed and underlying skin washed. Ingested cyanide may
|
|
be partially bound by activated charcoal.</p>
|
|
<p>Basic supportive intensive care is critical, including providing 100% oxygen,
|
|
mechanical ventilation as needed, and circulatory support with crystalloid
|
|
and vasopressors; correcting metabolic acidosis with IV sodium bicarbonate;
|
|
and controlling seizures with benzodiazepines. Symptomatic patients, especially
|
|
those who have lost consciousness or have other severe manifestations, may
|
|
benefit further from antidotal therapy, which is a multistep process.</p>
|
|
<p>First, a methemoglobin-forming agent is administered, typically inhaled amyl
|
|
nitrite or IV sodium nitrite because methemoglobin has a high affinity for
|
|
cyanide and disassociates it from cytochrome oxidase. However, nitrite administration
|
|
can be hazardous because it may cause hypotension, and overproduction of methemoglobin
|
|
may compromise oxygen-carrying capacity. Thus, nitrite is probably not indicated
|
|
for mild symptoms or if the diagnosis of cyanide poisoning is uncertain. Furthermore,
|
|
people with cyanide poisoning who may have concomitant hypoxic insult (e.g.,
|
|
most victims of smoke inhalation) probably are not good candidates for nitrite
|
|
therapy. Optimal nitrite dosing, especially when given parenterally, depends
|
|
on body weight and hemoglobin concentration, which is of particular importance
|
|
in pediatric patients, who have a broad range of hemoglobin concentrations.
|
|
In the pre-hospital setting, or whenever IV access is not possible, amyl nitrite
|
|
may be used to begin nitrite therapy. Amyl nitrite is provided in glass pearls,
|
|
which are used by crushing the pearl and then either allowing spontaneous inhalation
|
|
or introducing the vapor into a ventilation circuit, for 30 seconds of each
|
|
minute. As soon as IV access is established, sodium nitrite may be given. The
|
|
recommended pediatric dosage, assuming a hemoglobin concentration of 12 g/dL,
|
|
is 0.33 mL (of the standard 3% solution)/kg, given slowly IV over 5-10 minutes
|
|
(with a maximal, or adult, dose of 10 mL). Dosing may be adjusted for patients
|
|
with significant anemia, although this would not likely be known in emergent
|
|
treatment of a poisoned child in critical condition.</p>
|
|
<p>The second step is providing a sulfur donor, typically sodium thiosulfate,
|
|
which is used as substrate by the rhodanese enzyme for conversion to thiocyanate.
|
|
Thiosulfate treatment itself is believed efficacious and relatively benign,
|
|
and thus it may be used alone empirically in cases in which the diagnosis is
|
|
uncertain. (This approach has also been recommended, for example, in the management
|
|
of the situation described above of cyanide toxicity complicating smoke inhalation,
|
|
with likely concomitant lung injury and carbon monoxide poisoning). The recommended
|
|
pediatric dosage of thiosulfate is 1.65 mL (of the standard 25% solution)/kg,
|
|
IV (with a maximal, or adult, dose of 50 mL).</p>
|
|
<p>Each agent may be given a second time at up to half the original dose as needed,
|
|
or in the case of thiosulfate, even a full dose would be unlikely to pose inherent
|
|
toxicity. Both these medications are packaged together in commercially available "cyanide
|
|
antidote kits," along with amyl nitrite pearls. Additionally, most hospital
|
|
pharmacies stock 25% sodium thiosulfate solution in vials containing sufficient
|
|
volume (50 mL) to treat even adult patients. This has been used routinely in
|
|
the preparation of nitroprusside infusions, premixed with thiosulfate, so as
|
|
to obviate nitroprusside-induced cyanide toxicity.</p>
|
|
<p>Several alternative therapies and experimental antidotes have been used in
|
|
Europe (cobalt salts, hydroxocobalamin) or are in clinical trials (aldehydes,
|
|
aminophenol derivatives) or animal studies (dihydroxyacetone, alpha-ketoglutarate).
|
|
Hydroxocobalamin, in particular, has been cited as a potentially quite useful
|
|
antidote in civilian terrorism scenarios because of its relative safety compared
|
|
with nitrites. However, it currently is not commercially available in the United
|
|
States in a pharmacologically appropriate concentration for antidotal efficacy.</p>
|
|
<hr />
|
|
<p class="size2"><a name="ftn1" id="ftn1"></a><sup>1</sup> Adapted from
|
|
Rotenberg JS, Newmark J. Nerve agent attacks on children: diagnosis and
|
|
management. <em>Pediatrics</em> 2003; 112:648-58. </p>
|
|
<hr />
|
|
<p class="size2"><a href="index.html#Contents">Return to Contents</a><br />
|
|
<a href="pedchap5b.htm">Proceed to Next Section</a></p>
|
|
<p> </p>
|
|
<div class="footnote">
|
|
<p> The information on this page is archived and provided for reference purposes only.</p></div>
|
|
<p> </p>
|
|
|
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|
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