Lesson 18, Volume 16—Chemical Terrorism

By James A. Geiling, MD, FCCP

Objectives

1. Review the history of chemical warfare agents.
2. Examine the pathophysiology of chemical agents.
3. Review detection, protection, and decontamination challenges related to chemical agents.
4. Using a plausible case scenario, review the possible presentation and diagnostic challenges providers may face in a terrorist event employing chemical agents.
5. Outline the presentation and management of a likely chemical warfare agent.

Key words

agent; chemical; history; management; presentation; terrorism

Abbreviations

Ach = acetylcholine; AChE = acetylcholinesterase; EMS = emergency medical services; HAZMAT = hazardous material; ICAD = Individual Chemical Agent Detector; 2-PAMCl = pralidoxime chloride

"If supposedly civilized nations confined their warfare to attacks on the enemy's troops, the matter of defense against warfare chemicals would be a purely military problem, and therefore beyond the scope of this study. But such is far from the case. In these days of total warfare, the civilians, including women and children, are subject to attack at all times."—Colonel Edgar Erskine Hume, Medical Corps, US Army, 1943¹

Why should biological or chemical agents concern pulmonary and critical care physicians? The events of September 11, 2001, and the anthrax cases that followed demonstrate that acts of terrorism, to include those of chemical or biological agents, have come to the forefront of our daily lives. Current governmental reports predict repeated events over time. Only through intensive education and training can physicians adequately prepare to meet the medical challenges imposed by chemical, biological, radiologic, nuclear, and explosive weapons of terror. Much work lies ahead, for > 70% of hospitals may not be prepared to handle such incidents² and only 20% have any plans for managing biological or chemical incidents.³

This review presents a plausible terrorist case scenario as a mechanism to explore the realm of chemical agents, including a review of their history, the biochemical and physiologic effects of the most common chemical warfare agents, detection of their presence, protection from their effects, and management of the casualties who succumb to them.

Biological and chemical weapons have developed into weapons of choice for terrorists because of a variety of characteristics of the agents.⁴ Most important is they can be found in stores everywhere and are available at low cost. Simple components in small amounts can be turned into biological or chemical weapons with minimal education and training; the directions oftentimes are published on the Internet. Once produced, they are usually odorless, colorless, and tasteless, making detection difficult. When they are employed, they do not destroy the target's infrastructure like an explosive device, so the terrorist can deploy the weapon with maximum impact on people. In addition, these agents (particularly biological weapons) often have a latency period.

Knowledgeable experts often have worked for governments involved in developing or employing these weapons around the world. Many of these specialists, now without their government's employment, may be employed by terrorist networks or nations seeking to develop such weapons. These persons often include physicians; four out of five physicians who become involved in terrorist activities engage in biological and chemical terrorism.⁴ Government-sponsored programs normally have extensive supplies of agents, documented procedures, and experimental results to support their efforts. Finally, the notoriety of these agents attracts intensive media attention, often supporting the terrorist's motives in seeking such attention.

Historically, chemical weapons studies are rare in peacetime except for military research efforts. Operation Desert Storm and the sarin gas release in Tokyo reintroduced the chemical weapons concept into the mainstream of society's consciousness. Future terrorist activities will eventually include the use of chemical weapons because "…trained chemists would have no difficulty producing such chemical agents."⁵

Historical Review

First reports of the use of chemical agents date to 1000 BC, when the Chinese used arsenical smokes. During the Peloponnesian War in 423 BC, the allies of Sparta overtook an Athenian fort with smoke. In the 7th century AD, the Greeks used "Greek fire" floating on water for naval operations. In the 15th and 16th centuries, Venetians used poison-filled mortar shells and poison chests to taint wells, crops, and animals.

The horrors of chemical agents have been recognized by societies for many years. In 1812, the British rejected the use of burning sulfur-laden ships prior to marine landings in France; in 1854, they again opposed the use of cyanide to break the siege of Sebastopol in the Crimean War. Attempts to formalize a ban on these agents were attempted in 1874 at the Brussels Convention and again in 1899 and 1907 at the Hague Convention. However, the resolutions were weak and poorly worded, prompting little adherence by world powers.

The use of chemical weapons in wartime came to the forefront of the world's attention in the afternoon of April 15, 1915, when the German army released 150 tons of chlorine gas from 6,000 cylinders near Ypres, Belgium. Approximately 800 deaths occurred as a consequence of this event, but more importantly, 15,000 Allied troops retreated, in large part because of the psychological terror of the weapon.

The next major use on the battlefield occurred again near Ypres, Belgium on July 12, 1917, when German artillery shells delivered sulfur mustard. This release caused approximately 20,000 casualties, with < 5% of them dying of their injuries. A nonvolatile substance, the mustard posed new problems for the victims, including a latency period before effects appeared, persistence of the agent, and the need for both men and horses to be protected by overgarments.⁶

The horrors and psychological trauma imposed by these chemical agents in World War I resulted in the 1925 Geneva Protocol's ban on chemical weapons. This treaty, which was ratified by all of the major world powers except the United States and Japan, implied no first use of chemical or biological weapons, but did not prohibit their possession.

The disdain for their use did not last long. In 1935, the Italian dictator Benito Mussolini ordered the use of nitrogen mustard in an attempt to end the Italian-Ethiopian War early. The Italians dropped bombs filled with mustard and sprayed it from the air. They also employed it in powder form as a "dusty agent," a form devised for use against the barefoot Ethiopians.⁷ Finally, immediately before World War II in 1937, the Japanese reportedly used tear gas and other smokes and chemicals during their invasion of China. They eventually escalated the use of chemicals through the use of mustard and lewisite in 1939.⁵

The nerve agents appeared in the 1930s when the German industrial chemist, Dr. Gerhard Schrader began work on the development of stronger insecticides, the first two being tabun (GA) and sarin (GB). These agents and others were stockpiled by the German army in World War II but never used. Many theories abound as to why the Germans never employed them, but most likely it relates to Adolf Hitler's experience as a mustard casualty in World War I and his fear of nerve agent retaliation by the United States. One chemical agent release did occur, in 1943 in Bari Harbor, Italy. German aircraft bombed the American ship John Harvey, which was loaded with 2,000 100-lb mustard bombs. Those who swam in mustard-laden water had a 14% fatality rate.⁶

More recently, from 1963 to 1967 during the Yemen War, Egyptian troops used mustard against royalist troops in North Yemen. During the Vietnam War, the United States extensively used defoliants and riot-control agents. In 1975 after the war, the United States finally ratified the Geneva Treaty, but noted that the treaty did not apply to the defoliants and riot-control agents they had recently used in Vietnam. During the late 1970s and early 1980s, chemical agents may have been used against Hmong tribesmen in central Laos, and the Soviet Union may have employed them during its war in Afghanistan.⁷

During the Iran-Iraq War in the 1980s, Iraq used mustard, tabun (GA), and eventually sarin (GB) against Iran. After Desert Storm, inspections in Iraq confirmed nerve agents and mustard at Al Muthanna, 80 km northwest of Baghdad. Reports also surfaced during the late 1980s of possible cyanide use against the Kurds in northern Iraq.

Finally, the most publicized use of chemical agents for terrorism occurred in Tokyo in the mid-1990s, when on two occasions the Aum Shinrikyo Japanese religious cult released sarin gas. The first release came in June 27, 1994, in the city of Matsumoto and resulted in 600 persons being exposed, of whom 58 were admitted to the hospital and 7 died.⁸ The more famous and larger event took place in Tokyo on March 20, 1995, when the cult released sarin gas in the subway, resulting in the deaths of 11 commuters and the medical evaluation of 5,000 persons.⁹

Agent Weaponization and Physical Characteristics

Although they are relatively easy to make in the laboratory, use of many of the known biological and chemical agents as terrorists' weapons can be difficult. Many factors affect the dispersion and effectiveness of the agents. Agents may require a narrow range of atmospheric or meteorologic conditions in order to remain physiologically active, such as the requirement for an inversion to maintain a chemical agent's persistence. Additionally, weaponization of the agent can induce other challenges, such as hot gases from an explosion that limit the agent's effectiveness. Some agents work directly against their target, whereas others, particularly bioweapons, may be more effective using a vector for dissemination. Some agents are best released at a point source, whereas other may require line dissemination as from a vehicle such as an airplane. Finally, residue effects from persistent agents can affect how terrorists use the agents and the overall time course of effects.

Chemical agents can be divided into broad classifications based on their mechanisms of action and physiologic effects. The most common categories include: (1) pulmonary agents; (2) cyanide; (3) vesicants; (4) nerve agents; (5) incapacitating agents; and (6) riot control agents.

The pulmonary agents include phosgene (CG) [carbonyl chloride] and diphosgene (DP) [trichloromethyl chloroformate]. A review of their characteristics can be found in Table 1. Hydrogen cyanide (AC) and cyanogen chloride (CK) have in the past been known as "blood agents." A summary of these agents is found in Table 2. The most common vesicant used in warfare has been mustard (HD) [bis(2-chloroethyl)sulfide] (Table 3). Other vesicants available include lewisite (L) [2-chlorovinyldichloroarsine] (Table 4) or a mustard-lewisite mixture (HL).

The agents with the greatest reputation for terror are the nerve agents. These include the volatile agents tabun (GA) [ethyl N,N-dimethyl-phosphoramidocyanidate], sarin (GB) [isopropyl methylphosphonofluoridate], soman (GD) [1,2,2-trimethylpropyl methylphosphonofluoridate], and GF (cyclohexyl-methylphosphonofluoridate). VX, or O-ethyl-S-[2-(diisopropylamino)ethyl] methylphosphonothiolate, is a persistent nerve agent of low volatility. Summary information on these agents is in Table 5.

Finally, both terrorists and law-abiding government agencies can use nonlethal agents that have been developed. They include the incapacitating agents BZ (QNB) [3-quinuclidinyl benzilate] (Table 6) and riot-control agents or tear gas, of which there are two versions–CN [2-chloro-1-phenylethanone], or Mace (Mace Security International, Inc; Bennington, VT), and CS [2-chlorobenzalmalononitrile] (Table 7).

Detection

Unfortunately, unless the use of chemical agents is suspected, patients or animals who are exposed serve as "canaries in the coal mine." The best methods for "detecting" a release are to prevent it from occurring in the first place, or to prepare for such an event should it occur. Intelligence activities may assist law enforcement agencies in monitoring and preparing for such a release, thereby aiding the medical community in planning for such a disaster. However, this only occurs if medical planners seek out such information and become involved in community preparedness.

Detection equipment does exist in two basic formats, point and standoff detection. The most common point detection can take the form of Chemical Agent Detection Paper or a hand-held electronic Chemical Agent Monitor (CAM). This device uses ion mobility spectrometry and can detect mustard and nerve agent. Other devices include a Chemical Agent Detector Kit capable of detecting nerve, blister, and cyanide agents, and an Automatic Chemical Agent Alarm that can sense nerve agent vapors and inhalable aerosols. Standoff detection is possible with devices such as a Remote Sensing Chemical Agent Alarm (RSCAAL), which, through the use of optical remote sensing, can detect nerve and blister agents at 1.5 km. This capability is best in open terrain. Finally, specialty vehicles such as the Fox NBC Mobile Detector or Recon Vehicle can enter a potentially contaminated environment to determine the presence of most chemical agents.

Personal Protection

The most effective personal protection is avoidance of the agent. Although an obvious concept, medical providers often put themselves in danger in an effort to reach and treat persons who have been harmed or injured. Unfortunately, entering the "hot zone," whether it is a contaminated environment or an unsecured, unsafe area, may jeopardize the personal safety of medical providers. If they become injured, the rescue effort deteriorates because of the need to care for an additional casualty, and the operation has lost a valuable health-care worker. For the most part, only experienced prehospital providers should perform rescue efforts and treatment in a hot zone.

Masks provide the standard protection against chemical agents and can be extremely effective alone against volatile agents. The standard issue M17A2 or variant serves the US military well and has been adapted for many civilian agencies. Other masks include air-purifying respirators, full-face respirators, Quick Masks (Survivair; Santa Ana, CA), powered air-purifying respirators, and the self-contained breathing apparatus. Many other gas masks have appeared on the market in response to recent terrorist events. These may include expired or malfunctioning former military equipment or uncertified masks that may result in further injury to the provider if used in a contaminated environment.

Protective clothing in the military includes the battle dress overgarment containing activated charcoal, with rubber gloves and boots. Many varieties of this clothing are available; the most common ones used for short-duration exposure are disposable Tyvek® (DuPont; Wilmington, DE) suits.

Decontamination

Decontamination of personnel and equipment poses great challenges in a chemical agent release. Once contaminated, the condition of victims may continue to deteriorate depending on the persistence of the agent. In addition, health-care workers subjected to agent off-gassing or direct contact may themselves become victims. This potential hazard requires well-planned coordination not only with prehospital emergency personnel, but also with security agencies in order to manage those victims who arrive via their own means to seek care.¹⁰ Lastly, equipment contamination can become a major challenge in the overall scene management, as vehicles, litters, mechanical equipment, etc, that become contaminated pose additional threats to rescue and health-care personnel if they are taken to "clean" areas without proper and thorough decontamination.

Personnel decontamination involves one of three methods: physical removal of the agent, chemical deactivation, or, perhaps in the future, biological deactivation. The equipment required may be individual and portable, or large and power driven. Physical removal most commonly takes place by removing clothing and simply flushing with water, but may also include the use of adsorbent materials such as Fuller's Earth, flour, or other resins. Chemical methods include simple soap and water. Additional benefit may occur through oxidation with chlorine compounds (normally household bleach), such as 0.5% hypochlorite for personnel and 5.0% hypochlorite for equipment.

Other decontamination issues that must be considered in the management of a site include weather factors, principally wind direction and temperature. The water and hypochlorite or bleach source, as well as runoff and waste disposal, must be planned. Decontamination planning must also involve the management of associated injuries, particularly from an explosion. Finally, the need to conduct mass decontamination exposes the notion of the public health consequences of a chemical terrorist event.¹¹

Case Scenario

Setting

On September 11, 2001, terrorists hijacked four aircraft. Three were flown into the World Trade Center towers and the Pentagon, and one crashed in Pennsylvania, killing approximately 3,000 people. The prime suspects for the event remain Osama bin Laden and the al Qaeda terrorist group. As a consequence, civilian security and military force protection dramatically increased across the United States, and US forces were deployed to the Middle East and Central Asia to support Operation Enduring Freedom. As a result of the September 11 events, the increased costs associated with fighting terrorism, and many other factors, economic downturn and instability continue worldwide. Initial US citizen unity and support begin to erode as security measures increase and personal economic security deteriorates.

Federal Bureau of Investigation sources report increased activity from ultraright militias in the United States, some of which may be cooperating with terrorist networks. Their antigovernment sentiment stems in part from the loss of some individual freedoms imposed by antiterrorist legislation and because of ongoing US support of Israel. The national psyche remains on edge, with cases of anthrax appearing as a result of dissemination through the mail and the source remaining unknown.

Scene

Facing a bleak holiday buying season, local stores and malls drastically cut prices to attract buyers. On the Friday after Thanksgiving, shoppers flock to a local outlet mall to take advantage of many sales. The weather is clear, winds are light and variable, and the temperature ranges from 28 to 45°F. At 12:15 PM, your colleagues in the emergency department begin to hear via emergency medical services (EMS) radio traffic that there is a mass emergency at the mall. Initial reports describe a scene near the food court where many people are unconscious or seizing. Many people outside the mall are lying on the ground, seizing, vomiting, or generally feeling ill. Initial estimates report more than 800 automobiles in the parking lot. EMS vehicles dispatched to the scene report mass hysteria, a large traffic snarl leaving the area, and frantic people heading for the ambulances. EMS personnel that arrive at the food court report themselves becoming weak, having difficulty seeing, and feeling nauseous.

Discussion

The acute onset of this event with obvious casualties most likely signals a chemical agent or hazardous material (HAZMAT) release in the area of the food court. However, many clues (see Table 8) may signal a chemical weapon (or biological weapon for completeness).

Mass casualty incidents or those involving HAZMATs will require excess hospital capabilities and therefore involve the hospital's administration and leadership. When there are numerous casualties and mass care, particularly if they involve a suspected chemical or biological weapon, public health agencies must be involved in the interest of public welfare. While often unrecognized, an additional source of medical information may come from local veterinary agencies and personnel. Command and control of local disasters or terrorist events begins with the mayor and local resources, including law enforcement agencies; their employment at the hospital itself may become necessary for the safety of health-care workers and patients. Local officials normally remain in charge of the event, depending on the resources required. However, the nature of a suspected terrorist event often requires state or federal government assets. Organizations that may appear include the state Emergency Management Agency, the Federal Bureau of Investigation, the Federal Emergency Management Agency, and other agencies.

Poststudy questions 1 to 5 relate to the case scenario presented here.

Nerve Agents

Background

Nerve agents are normally liquids, with "G" agents being more volatile than "V" agents; sarin (GB) is the most volatile. They can be dispersed from missiles, rockets, bombs, artillery shells, spray tanks, land mines, canisters, or other munitions.

Nerve agents act as organophosphorous cholinesterase inhibitors, inhibiting plasma butyrylcholinesterase, RBC acetylcholinesterase, and acetylcholinesterase at tissue cholinergic receptor sites. After an acute exposure, the RBC enzyme activity best reflects enzyme activity in tissue, whereas the plasma enzyme activity more accurately reflects tissue activity during recovery. Nerve agents bind to acetylcholinesterase (AChE) and prevent hydrolysis of acetylcholine (ACh). The clinical effects, therefore, occur from an excess of ACh. Attachment of the agents to AChE is permanent, its activity returning only with new enzyme synthesis or RBC turnover (1%/d).⁶

Excess ACh affects both muscarinic and nicotinic sites. Muscarinic sites that become involved include postganglionic parasympathetic fibers, glands, pulmonary and GI smooth muscles, and organs targeted by CNS efferent nerves, such as the heart via the vagus nerve. Nicotinic sites include autonomic ganglia and skeletal muscle.

Clinical Effects

Nerve agents possess chemical similarities and properties to organophosphate insecticide poisons, and hence have a similar clinical presentation. The symptom complex can be summarized by the "SLUDGE" toxidrome: increased salivation, lacrimation, urination, diarrhea, gastric distress, and emesis.¹²

The principal effect on the eyes is miosis as a consequence of direct contact with vapor. This rarely occurs with skin contact alone unless the exposure level is high. Symptoms begin within seconds to minutes and can be associated with sharp or dull pain (which may induce nausea or vomiting), dim and blurred vision, and conjunctival injection. Significant lacrimation also typically occurs.

Rhinorrhea may be the first respiratory sign and symptom, the significance being dose dependent. Also depending upon the dose and duration of exposure, bronchorrhea and bronchoconstriction develop. Skeletal muscle weakness further impairs breathing. CNS-mediated apnea may also occur.

Vagal input may decrease heart rate, although normally patients are tachycardic from a fight-or-flight mechanism or hypoxia. Blood pressure remains near normal until a terminal decline.

Increased salivary gland secretion and other evidence of GI glandular hypersecretion occur with exposure. Consequently, victims often experience nausea, vomiting, and diarrhea.

Localized sweating can occur at the site of exposure, but generalized sweating only presents with a large vapor or skin exposure. Skeletal muscles develop fasciculations and twitching initially, but later become weak and eventually flaccid.

Effects on the CNS vary with exposure. Small doses result in variable and nonspecific findings, such as an inability to concentrate, insomnia, bad dreams, irritability, impaired judgment, and depression. Large exposure may lead to a loss of consciousness, seizure activity, and apnea. Psychological and behavioral changes include anxiety, tenseness, fatigue, forgetfulness, irritability, and mild confusion. Complete disorientation and hallucinations do not occur.

Initial effects can be seen within seconds to minutes, and the rapidity and severity are dependent upon the dose. High-dose vapor exposure can lead to loss of consciousness and seizures within 1 min, whereas low-dose skin contact can present with GI complaints as long as 18 h after exposure. Very few other illnesses mimic nerve agent exposure, although low-dose sporadic cases may be initially be diagnosed as an upper respiratory illness, allergic syndrome, or gastroenteritis.

Laboratory findings include inhibition of red cell AChE activity, which may assist in establishing the diagnosis of early or confusing cases. Red cell AChE activity is more sensitive than plasma AChE activity in the presence of a nerve agent. Although helpful in establishing or confirming the diagnosis, inhibition of enzyme activity does not correlate with symptom severity. Other common laboratory abnormalities include hypoxia and respiratory acidosis as a consequence of the respiratory signs described above.

Medical Management

Decontamination remains the mainstay of initial patient management in an attempt to mitigate agent effect and prevent contamination of other patients, equipment, and health-care workers. Patients require ventilatory support because of increased airway resistance (50 to 70 cm H₂O) and airway secretions. This support requirement may last for 30 min to 3 h in severe cases, even if treated.

Fortunately, atropine is an effective antidote for nerve agents. Atropine acts as a cholinergic blocking agent (ie, anticholinergic); its actions are most effective at muscarinic sites. If 2 mg of atropine is administered to an unexposed person, the results include mydriasis, decreased secretions and sweating, mild sedation, decreased GI motility, and tachycardia (a potential problem in unexposed persons who self-administer atropine based upon a perceived exposure). The recommended dosing in nerve agent treatment is 2 mg every 3 to 5 min titrated to secretions. In severe cases, 10 to 20 mg of atropine have been used in the first hour after exposure. Many of the eye symptoms can be relieved with topical homatropine or atropine.

Pralidoxime chloride (2-PAMCl) is another effective antidote for nerve agent casualties. 2-PAMCl is an oxime that attaches to the nerve agent and breaks the agent-enzyme bond. Its actions are most effective at nicotinic sites, thereby improving muscle strength; it does not decrease secretions. Unfortunately, aging decreases its effectiveness, ie, the longer the time interval between exposure to the agent and administration of 2-PAMCl, the less useful it becomes. For example, the aging period for Soman (GD) is 2 min, whereas that interval for sarin (GB) is 3 to 4 h. The dose is 15 to 25 mg/kg or approximately 1 g IV piggyback every 20 to 30 min.

Atropine and 2-PAMCl are often combined into an injector kit or system. The MARK I kit (Meridian Medical Technologies, Inc; Columbia, MD) used by the US military, which increasingly is becoming available on the civilian market, includes an AtroPen Auto-Injector (Meridian Medical Technologies, Inc) containing 2 mg of atropine and a ComboPen Auto-Injector (Meridian Medical Technologies, Inc) containing 600 mg of 2-PAMCl (8.9 mg/kg in a 70-kg person). In the US Army, each soldier normally is issued three kits. Military doctrine recommends that individuals exposed to nerve agent self-administer one MARK I kit if they are experiencing the effects of a nerve agent. If they remain symptomatic, they are instructed to seek "buddy aid" to determine if additional injections are necessary.

Diazepam remains the anticonvulsant drug of choice, based primarily on its history and demonstrated effectiveness. In the US military, diazepam is issued as a 10-mg autoinjector under guidance from the unit's commander and staff physician. Soldiers are trained to administer one autoinjector to their buddy after three MARK I kits have been used. Unit medical personnel carry additional diazepam.

There are several specific treatment caveats:

1. Titrate treatment to secretions, dyspnea, or retching and vomiting.
2. Miosis does not typically respond to atropine.
3. Treat eye pain/headache with topical atropine/homatropine.
4. Supportive care becomes the standard once the patient has been stabilized.
5. Fasciculations can persist after restoration of consciousness, ventilation, and even ambulation.

See Table 9 for a summary of recommendations.¹³

Pretreatment with pyridostigmine bromide was used in Operation Desert Storm and potentially could be used for high-threat civilian events. The dose is 30 mg q8h and will require public health or senior-level leadership decisions to implement. Pyridostigmine bromide binds to AChE through carbamylation and thereby blocks the nerve agent from attaching to AChE. This effectively increases the median lethal dose several-fold for soman (GD). Decarbamylation occurs after 4 h, whereupon the AChE becomes fully functional.

Summary

As with many activities in medicine, conducting casualty management through the use of a checklist ensures that all aspects are thoroughly addressed. The 10 steps in the management of casualties of chemical terrorism are as follows:

1. Maintain an index of suspicion.
2. Protect yourself.
3. Assess the patient.
4. Decontaminate as appropriate.
5. Establish a diagnosis.
6. Render prompt treatment.
7. Practice good HAZMAT protection.
8. Alert the proper authorities.
9. Assist in the epidemiologic/criminal investigation.
10. Maintain proficiency and educate health-care personnel about chemical agents.⁴

Many parts of the world have faced the threat and experienced the consequences of chemical terrorism. That menace has, unfortunately, now moved throughout the world. Education, planning, equipment purchases, and training must occur in order for hospitals and physicians in most institutions to prepare for such horrific events. Preparation has usually involved emergency department personnel, those with the greatest understanding of and interaction with the prehospital environment and disaster planning. Large chemical terrorist events or even commercial HAZMAT incidents, however, may result in 25% of admitted casualties requiring mechanical ventilation and critical care.¹⁴

Critical care physicians traditionally practice within the confines of the ICU. Moving outside the unit to assist with mass casualty incident triage, codes, or preoperative consultation, particularly in concert with the evolving hospitalist function, will necessarily involve intensivists in supporting a hospital's response to a terrorist event. This expansion in roles and responsibilities requires that an understanding of disaster management, including the consequent management of chemical, biological, radiologic, nuclear, and explosive events, be part of the critical care physician's education and training.¹⁵ The Centers for Disease Control and Prevention have embarked on an ambitious program to develop a public health distance-learning system in order to assist in such an educational process.¹⁶ These and other efforts, as well as integration of such education into physician-training programs,¹⁷ will yield a cadre of physicians well prepared to face the medical challenges posed by modern terrorist threats.

Additional sources of information are listed after the references.

ACKNOWLEDGMENTS: The author would like to thank COL Tom Fitzpatrick, Chief of Critical Care Medicine, Walter Reed Army Medical Center and the Chemical Casualty Care Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground for their support and assistance in this endeavor.

References

1. Hume, EE. Victories of army medicine. Philadelphia: J.B. Lippincott Company, 1943; 10-11.
2. Treat KN, Williams JM, Furbee PM, et al. Hospital preparedness for weapons of mass destruction incidents: an initial assessment. Ann Emerg Med 2001; 38:562–565
3. Wetter DC, Daniell WE, Treser CD. Hospital preparedness for victims of chemical or biological terrorism. Am J Public Health 2001; 19:710–716
4. Cieslak T. Biological warfare and terrorism: medical issues and response. US Army Medical Research Institute of Infectious Disease Satellite Broadcast, 2000
5. Stern J. The ultimate terrorist. Cambridge, MA: Harvard Press, 1999; 50
6. US Army Medical Research Institute of Chemical Defense (USAMRICD). Medical management of chemical casualties handbook. Aberdeen Proving Ground, MD: USAMRICD, 2000
7. Smart JK. History of chemical and biological warfare: an American perspective. In: Sidell FR, Takafuji ET, Franz DR, eds. Medical aspects of chemical and biological warfare. The textbook of military medicine. Washington, DC: Office of the Surgeon General, Department of the Army, 1997; 9–86. Available at http://chemdef.apgea.army.mil/textbook/contents.asp. Accessed July 23, 2002
8. Okudera H, Morita H, Iwashita T, et al. Unexpected nerve gas exposure in the city of Matsumoto: report of rescue activity in the first sarin gas terrorism. Am J Emerg Med 1997; 15:527–528
9. Okumura T, Takasu N, Ishimatsu S, et al. Report on 640 victims of the Tokyo subway sarin attack. Ann Emerg Med 1996; 28:129–135
10. Burgess JL, Kirk M, Borron SW, et al. Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34:205–212
11. Brennan RJ, Waeckerle JF, Sharp TW, et al. Chemical warfare agents: emergency medical and emergency public health issues. Ann Emerg Med 1999; 34:191–204
12. Heck JJ, Geiling JA, Bennett BL, et al. Chemical weapons: history, identification, and management. Critical Decisions in Emergency Medicine 1999; 13(12):1–8
13. Sidell FR. Nerve agents. Sidell FR, Takafuji ET, Franz DR, eds. Medical aspects of chemical and biological warfare. The textbook of military medicine. Washington, DC: Office of the Surgeon General, Department of the Army, 1997; 129–179. Available at http://chemdef.apgea.army.mil/textbook/contents.asp. Accessed July 23, 2002
14. Tur-Kaspa I, Lev EI, Hendler I, et al. Preparing hospitals for toxicological mass casualties events. Crit Care Med 1999; 27:1004–1008
15. Kvetan V. Critical care medicine, terrorism and disasters: are we ready? Crit Care Med 1999; 27:873–874
16. The Centers for Disease Control and Prevention. Biological and chemical terrorism: strategic plan for preparedness and response: recommendations of the CDC Strategic Working Group. MMWR Morb Mortal Wkly Rep 2000; 49(RR-4)
17. Pesik N, Keim M, Sampson TR. Do US emergency medicine residency programs provide adequate training for bioterrorism? Ann Emerg Med 1999; 34:173–176

Additional Sources of Information

Reference Websites

1. Nuclear Biological Chemical Links. http://www.nbc-links.com/
2. Biological and Chemical Warfare and Terrorism Training. http://www.biomedtraining.org
3. Homeland Defense. http://hld.sbccom.army.mil/
4. Medical Nuclear Biological Chemical Online. http://www.nbc-med.org/
5. US Army Medical Research Institute of Infectious Disease. http://www.usamriid.army.mil/
6. Weapons of Mass Destruction First Responders. http://wmdfirstresponders.com/
7. National Disaster Medical Center. http://ndms.dhhs.gov/
8. Occupational Safety and Health Administration. http://www.osha.gov/

Reference Texts

1. Institute of Medicine. Chemical and biological terrorism: research and development to improve civilian medical response. Washington, DC: National Academy Press, 1999
2. Mansicalco PM, Christen HT. Understanding terrorism and managing the consequences. Upper Saddle River, NJ: Prentice Hall, 2002

US Army Medical Research Institute of Chemical Defense

Address: Commander, U.S. Army Medical Research Institute of Chemical Defense, ATTN: MCMR-UV-ZM, 3100 Ricketts Point Rd, Aberdeen Proving Ground, MD 21010-5400

For specific information or questions, contact the Chemical Casualty Care Division; telephone: (410) 436-2230, (410) 436-3393, or toll-free (888) 556-0286; website: http://ccc.apgea.army.mil; e-mail: ccc@apg.amedd.army.mil

Copyright ©2003 American College of Chest Physicians