Biological weapons of mass destruction and emergency preparedness
Part 1

Since the terrorist acts of Sept. 11, 2001, there have been many changes in our lives. From the federal government to our local communities, many efforts have been made to prevent additional attacks and to be prepared if another attack occurs. Hospitals and health care agencies provide a critical part of these preparedness efforts and as providers are expected to be prepared for victims of these attacks, whether they suffer from a traumatic injury or are infected with an exotic disease. Of these, no type of terrorist incident has the potential to generate more fear than a covert attack with a biological weapon. But no terrorist action could be hampered more by the vigilance of informed health care professionals.

Health care providers, particularly nurses, must increase their knowledge of the effects a biological attack would have on a population. With this knowledge, providers could bethe first to notice an increase of consistent symptoms resulting from a covert attack. With rapid recognition and diagnosis, treatment can begin early and save many lives. Some hospitals, clinics, and physicians’ offices are connecting to regional web-based surveillance tools that will allow for even faster recognition of health syndromes that could be related to a biological attack. All health care professionals need to be armed with current knowledge. Additionally, each health care facility must have plans in place to provide isolation and personal protective equipment to ensure the safety of both their staff and facility from contamination and possible secondary infections from a contagious agent.¹

Biological weapons include bacteria, viruses, and biological toxins. Of the possible biological agents, the most likely or most hazardous include the bacteria Bacillus anthracis (anthrax) and Yersinia pestis (plague), the variola virus (smallpox), and the biological toxin botulisum (Clostridium botulinum). Both the U.S. and Soviet Union participated in weaponizing these and other agents after World War II. In 1972, many countries, including the U.S. and the Soviet Union, signed an agreement at the Biological Weapons Convention prohibiting the development, production, and stockpiling of bacteriological (biological) and toxic weapons. Despite this, many countries continued their research and development. Today, several of those, including state-sponsored terrorist organizations hostile to the U.S., are suspected of proliferating biological weapons for their use.² Biological weapons are not new. In 1346, the Tatar army hurled the corpses of soldiers who had died of the plague over the Kaffa City walls, infecting residents who were defending the city. Some of those who left Kaffa may have started the Black Death pandemic that spread throughout Europe. Russian troops used this same tactic against Sweden in 1710.²Biological warfare also occurred during the French and Indian War of 1754 to 1767 when an Englishman, Sir Jeffery Amherst, gave smallpox-laden blankets to Native Americans who were loyal to the French. The Native Americans sustained epidemic casualties as a result.²

With the possibility that such agents could be used again, heightened vigilance of health care providers is necessary. Early recognition of these illnesses could trigger earlier diagnosis and allow preventive measures that could save many lives. Caregivers need to learn the early signs and symptoms and the modes of transmission of biological agents, not only for the well-being of their patients, but also for themselves. The health of nurses who work on the front line of acute health care could be at risk. For example, those working in physicians’ offices, clinics, and EDs could be at risk of secondary infection from pathogens, such as plague and smallpox. And in the event of an attack, nursing challenges would not end with acute care. Large numbers of patients would require intensive care for weeks or even months. Entire wings of hospitals or clinics would be subject to quarantined isolation. Only education can reduce the risk.

Anthrax After suffering through several years of anthrax letter hoaxes, real anthrax letters were mailed in 2001 to media and political offices. As a result, 22 people were infected with the bacteria. Inhalation exposure caused infection for 11 of the 22 victims, and at least the first nine were caused by exposure to anthrax found in letters.³ Although there has not been a repeated attack since then, the next episode may be right around the corner. The perpetrator of the 2001 attack has never been found, and it remains uncertain whether it was an act of domestic or international terrorism. Bacillus anthracis is a spore-forming bacterium that causes a rapidly progressing infection. Once the infection is established, the victim is said to have anthrax. B. anthracis derives its name from the Greek word for coal (anthrakis) because of the black, coal-like skin lesions it creates.⁴ Anthrax can develop from inhalation, ingestion, or exposure of nonintact skin to the bacterium. The spores are hardy and can remain viable for more than 40 years.⁵ At least 17 countries have developed an anthrax weapon program.⁴ In 1970, the World Health Organization (WHO) concluded that the release of 50 kg of aerosolized anthrax upwind of a population of 5 million could lead to an estimated 250,000 casualties and 100,000 deaths,6 substantiating the perceived threat from Bacillus anthracis. Because of the efficiency and durability of its spore, the bacterium’s use as a biological weapon has brought great concern to the U.S. military and, more recently, the public. The Japanese Aum Shinriko religious sect spent millions of dollars developing an anthrax weapon and on at least eight occasions released anthrax or botulism. Because of the difficulty encountered in the dispersion, the sect members failed to produce any infection and eventually concentrated their efforts on Sarin, a nerve agent. Sarin was used with only moderate success as a lethal agent in both Matsumoto and Tokyo.⁴ The largest incident involving inhalation anthrax occurred in 1979 in Sverdlovsk, USSR, when a military biological facility accidentally released spores into the air from a faulty laboratory ventilation system. The Soviet Ministry of Health stated that the deaths were due to contaminated meat, but in the summer of 1992, President Boris Yeltsin acknowledged that the deaths were due to an accidental release from a military microbiology facility, Compound 19. In total, 77 people developed anthrax, and 66 died.⁷Although the majority of inhalation anthrax cases from Sverdlovsk developed between four and 14 days, cases continued to emerge up to 43 days after the release.⁴ Some argue that secondary aerosolization may be responsible for those infections that developed beyond seven days after the primary aerosolization.⁴

Cutaneous, ingested, pulmonary anthrax Cutaneous anthrax infection occurs when bacteria enter through cuts or breaks in the skin and cause a localized infection. In two to six days, the infection results in itching followed by papular lesions that turn vesicular and into depressed black scabs. At this point, a Gram stain and culture of vesicular fluid can confirm the diagnosis. Anthrax occurs most frequently on the head, hands, and arms of people who work with infected cows, sheep, or horses. Recent cutaneous infections have resulted from handling letters that contained anthrax spores and then touching open skin. Skin infections not promptly treated can progress into sepsis and have a mortality of 5% to 20%.⁷Because cutaneous anthrax does not progress as rapidly as the pulmonary or gastrointestinal infection, it is usually not fatal if treatment is started before the onset of septicemia. Ingested bacteria can also cause infection. Nonintentional infections are usually associated with the ingestion of meat from infected animals. Incubation is from one to seven days after ingestion. The bacteria invades the mucosa of the mesenteric region and infects the lymph nodes, resulting in nausea, vomiting, bloody diarrhea, abdominal pain, sepsis, and ascities. The fatality rate is 50%.⁵ since it progresses to toxemia and sepsis. The only recorded case of ingested anthrax in the U.S. took place in May 2000, when an infected cow was butchered and eaten by a farm family. The infection was discovered early and treated successfully.⁸ The most dangerous form is pulmonary anthrax, also known as wool sorter’s or rag picker disease because livestock workers have inhaled spores and developed pulmonary infections from sorting hides of infected animals. The last naturally occurring case of pulmonary anthrax in the U.S. took place in 1978.⁹ An inhalation of 8,000 to 50,000 spores is needed to establish an infection.² B. anthracis spores are only 3 to 5 microns in size, allowing easy implantation in fine bronchioles and alveoli. Once spores are inhaled, pulmonary macrophages carry them to the mediastinal lymph nodes, causing hemorrhaging and edema that can be seen on a chest X-ray as a symmetrically widened mediastinal area. Although blood cultures may be negative, the sputum is usually positive at this point. In the first phase of pulmonary anthrax, victims experience flu-like symptoms, followed by a significant improvement or even apparent recovery that may stop them from seeking medical care.²Aggressive treatment with antibiotics during the initial flu phase can be successful. However, because many health care providers are unfamiliar with the disease, many patients receive supportive treatment then are discharged, subsequently dying. Providers who see unusually large numbers of normally healthy patients presenting with similar flulike symptoms should be suspicious of an intentional attack and alert local public health officials. There is no magic number that will trigger an investigation, but the astute recognition of an unusual chest X-ray combined with other consistent symptoms should be highly suspicious. Early detection is the key to saving lives.¹⁰

The second phase of pulmonary anthrax develops suddenly with severe respiratory symptoms, hypotension, and shock. The patient may have a fever and profuse sweating. Stridor and crepitant rales may also be present. Blood cultures will be positive, and bacteria may be visible on a Gram-stain smear. Specimens thought to be B. anthracis should be confirmed through a state public health lab and the Centers for Disease Control and Prevention (CDC).⁵ This phase generally lasts less than 24 hours, with mortality approaching 100% even with aggressive antibiotic therapy.⁸ Health care providers must be alert for patients who present with symptoms consistent with early anthrax,11 obtain appropriate diagnostic tests (e.g., blood cultures and chest radiograph),12 and report suspicious illnesses to local or state public health authorities. Infected patients are generally no danger to health care workers. Anthrax is not contagious, and there are no known cases of person-to-person transmission. Only standard precautions for blood and body fluids should be taken. Unless a patient has had an intentional contamination with large amounts of visible spores, decontamination beyond carefully removing clothing and washing hands and other exposed skin with soap and water is not needed. Contaminated clothing should be placed in a bag for disinfecting or disposal.¹³ Prophylaxis is accomplished in two ways. First, there is a licensed vaccine that consists of a series of six doses — one given initially and others at two and four weeks, then at 6, 12, and 18 months, followed by annual boosters. At least three doses are needed for prophylaxis before exposure and should be followed by an additional three doses. The vaccine is now offered to all military personnel and civilians who are at risk of exposure. The vaccine is not routinely available to members of the public unless they are thought to be in high-risk environments. The vaccine is not recommended for pregnant women or people with depressed immune systems. Thirty percent of men and 60% of women who have the vaccine experience mild local reactions, but serious events occur at one per 200,000 doses.¹⁴

A second means of prophylaxis is with antibiotics, much like the treatment of an active infection. Because laboratories have produced penicillin- and tetracycline-resistant forms of the bacteria, initial postexposure prophylaxis with oral fluoroquinolones, such as ciprofloxacin (Cipro), or doxycycline over four weeks is recommended. If available, the vaccine may also be initiated. Although diagnosis and treatment may begin at the hospital, patients undergoing prophylaxis will be sent home to continue an antibiotic regimen, especially if a large-scale exposure has taken place. Treatment for inhalation anthrax may continue for up to 60 days because inhaled spores can remain latent for extended periods.¹⁰

Bubonic and pneumonic plague The plague has a colorful history. In A.D. 541, the first great plague began in Egypt, spreading across North Africa, Europe, and Central and Southern Asia. During a period of four years, 50% to 60% of the population died. The second plague pandemic began in 1346 and spread throughout the Middle East, killing one-third of the European population and more than 13 million in China, where it earned the name Black Death.¹⁵
A childhood nursery rhyme encapsulates the ravages of the plague: “Ring around the rosie” (describing the red ring around the infected lymph node), “pocket full of posies” (the smell of death was so overwhelming that people carried pockets full of fragrant flowers to hold under their noses), “ashes, ashes, we all fall down” (“ashes” are related to burning the bodies and “falling” to victims dying). According to some texts, another lasting impression of the disease survives in a saying used even today. Because the number of deaths from the pneumonic plague overwhelmed the ability of priests to give last rights, they gave other church members the power to issue last rights by saying, “God bless you” after the victims coughed or sneezed.¹⁶

Although much has been done to improve the living conditions that contributed to plague outbreaks, about 13 cases occur annually in the U.S., most in New Mexico, Arizona, California, and Colorado.⁵ These occurrences are usually not related to living conditions but to flea bites from infected rodents commonly found in the Western states. The animals most commonly found to carry the bacteria include rock squirrels, ground squirrels, prairie dogs, wood rats, chipmunks, and their fleas.¹⁷ In these geographic locations, the disease is endemic in the rodent population and is passed from generation to generation through flea vectors. In recent years, most of the cases of primary pneumonic plague in the U.S. have been acquired through an exposure to domestic cats with pneumonic plague, and exposure has become an occupational hazard for veterinarians in the Western U.S.⁸ Health care workers should be highly suspicious of cases of plague outside these geographical areas, specifically if pneumonic plague is the first presentation. Terrorists could pose a serious threat by using the bacteria in an attack. Local and state public health authorities should be notified immediately if a case of plague is suspected.⁸

During the 1950s and 1960s, the U.S. developed the bacterium Yersinia pestis as a biological weapon. The Soviet Union reportedly had more than 10 institutions and thousands of scientists working to develop plague-based weapons.²These weapons were based on the spread of aerosolized bacteria upwind from the targeted population. Japan even investigated using infected fleas dropped in areas of enemy troops as a way of spreading the plague. In 1970, WHO assessed a worst-case scenario of a dissemination of 50 kg of Y. pestis in an aerosol cloud over a city of 5 million. The agency estimated the results to be 150,000 cases of pneumonic plague, with 36,000 deaths.⁶

Exposure to Y. pestis can cause three forms of the plague: bubonic, septicemic, and pneumonic. Bubonic plague is usually a flea-borne disease transmitted from an infected rodent. Direct contact of open skin with infected tissue or fluids can also cause a bubonic form of the disease.⁵ The bacteria migrates to the lymph nodes, where an infection is established typically between two to eight days after exposure.¹⁵ Because infected fleas usually bite the legs of a victim, inguinal lymph nodes are most often affected (90%).⁷As the infection develops, the lymph nodes become painful, swollen, and hot to the touch before ulcerating. If left untreated, septicemic infection results in fever, chills, prostration, abdominal pain, shock, and bleeding into the skin and other organs. The death rate is 50% to 60%.⁷In some cases, septicemia can spread the infection to the lungs, causing the pneumonic form of the disease.

Pneumonic plague causes fever, chills, cough and difficulty breathing; rapid shock; and death. Talking, coughing, or sneezing spreads the disease in heavy droplets from person to person. The incubation period is one to four days,7 depending on the dose of inhaled bacteria. Pneumonic disease is characterized by overwhelming pneumonia, fever, bloody sputum, chills, and cough. The death rate is more than 50% and approaches 100% if treatment is not instituted within 24 hours of the onset of symptoms. Culturing or Gram staining lymph-node needle aspirate, sputum, or cerebrospinal fluid samples makes the diagnosis.⁵ Additionally, a complete blood count, urinalysis, and arterial blood gases (ABGs) should be obtained.
Test results that may indicate pneumonic plague are:

• A markedly elevated white blood count to levels of 20,000 or greater and a shift to the left. In late septic shock, the WBC count may be low.
• Gross hematuria, RBC casts, and proteinuria found on urinalysis.
• ABG evidence of hypoxia or acidosis.¹⁸
  Y. pestis is a nonmotile, Gram-negative bacillus that shows bipolar (looks like a safety pin) staining with Wright, Giemsa, or Wayson stain.¹⁵

Patients diagnosed with bubonic plague and a cough or those with pneumonic plague must be placed on droplet precaution in a private room or cohorted with similarly diagnosed patients.^{15, 19}
Decontamination of these patients is not necessary, but caregivers in close contact with them must wear protective equipment, including masks and eye protection; to limit droplet production, patients should wear masks also. Patients are considered contagious until after 48 hours of antibiotic therapy.⁶ Antibiotic treatment for those exposed to the disease should continue for seven to 10 days. Streptomycin, tetracycline, chloramphenicol, gentamycin, and quinolone antibiotics are all effective.¹⁵

An attack involving infected mass casualties will rapidly deplete the pharmaceutical stocks in most hospitals. As a result, many area public health and state health agencies provide additional local stockpiles of antibiotics for treating mass casualties related to an intentional attack. The Center for Disease Control and Prevention also maintains a stockpile program called the Strategic National Stockpile. There are currently 13 SNSs in the United States, placed in different secret locations for rapid deployment anywhere in the country. They contain antibiotics and other materials to treat mass casualties from terrorist attacks. Typically, the initial stockpiles, called a “push pack,” contain the following antibiotics:²⁰

• More than 200,000 patient days of fluoroquinolone prophylaxis.
• More than 2,000,000 patient days of doxycycline prophylaxis.
• More than 20,000 patient days of pediatric fluoroquinolone prophylaxis.
• More than 40,000 patient days of therapeutic treatment.

The push pack can be followed by a “vendor managed inventory” that is more specific for the needs of the incident. In the case of a biological attack, the VMI may contain vaccines, additional antibiotics, or extra personal protective equipment.²⁰
The occurrence of either of these diseases requires a report to be filed with local public health agencies, and the CDC subsequently investigates all cases of inhalational anthrax. The CDC maintains the Health Alert Network, an around-the-clock Internet-based network of information about evidence-based practices and procedures for health care preparedness and response. When the CDC is informed about a possible biological attack, the Health Alert Network can be used to alert public health agencies in all 50 states to heighten their awareness to the threat. The network is also used for education and information sharing. In addition, The CDC uses Epi-X to alert public health officials across jurisdictions. Epi-X is a secure, Web-based communication system to enhance bioterrorism preparedness efforts by facilitating the sharing of preliminary information about disease outbreaks. The security of this system allows public officials to share information without generating fear among the public.²¹

Unfortunately, anthrax and plague are but two of four major biological agents that bioterrorists may use. The next module will discuss smallpox and botulism, as well as measures of emergency preparedness that may counter these threats.

Part 2

Almost daily, some type of terrorist activity is taking place in the world. Because of terrorist activity here in the United States, preparedness activities have reached beyond federal, state, and county agencies into our everyday lives. Nursing is one of the professions that has been affected the most dramatically with these preparedness efforts. Remember the obscure diseases like anthrax and plague that as a student nurse you never thought you’d see beyond a textbook? Chances are greater than ever that you might need to be adept at recognizing their symptoms. And you may have to confront other diseases that could emerge through the acts of terrorists. For example, what do you remember about botulism and smallpox? The following sections will discuss botulism and smallpox and the nurse’s role in emergency preparedness in the event of an attack.

Botulism

Botulinus toxin, produced by Clostridium botulinum, is the most toxic substance known. A single gram of crystalline toxin evenly dispersed for inhalation over a population could kill more than 1 million people.²² Research found that only 0.001 mcg/kg of body weight was a lethal dose for 50% of a test animal population. To put this in perspective, botulinus toxin is about 100,000 times more toxic than the military nerve agent Sarin, which was used in the terrorist attack in a Tokyo subway.²³

During the Cold War, the Soviet Union extensively researched botulinus toxin as a biological weapon because of its extreme toxicity. In 1991, Iraq admitted to a United Nations inspection team its research in the use of botulinus toxin as a biological weapon. Four years later, it was discovered that Iraq had also filled and deployed more than 100 munitions containing the toxin. Here in the U.S., a religious extremist group, the Bhagwan Shree Rajneesh, gained recognition by cultivating Salmonella bacteria to contaminate restaurant salad bars and affect the outcome of a local election. Although the attempt to influence the election was unsuccessful, 751 people became ill and 45 were hospitalized. Authorities later found that the group intended to develop C. botulinum for other malicious purposes.²³

C. botulinum is a spore-forming bacillus that produces seven types of toxin. These toxins, types A through G, create similar effects through three presentations of botulism — food-borne, wound, and intestinal.²⁴ Naturally occurring cases are rare, and usually improperly prepared or canned food cause disease.²⁵ Once colonized in the body, the bacterium systemically releases the botulinus toxin, resulting in signs and symptoms that ranging from visual difficulty to flaccid paralysis.²⁴ To prevent botulism, all food must be heated to more than 240 degrees F or boiled for 10 minutes to destroy both bacterium and toxin.²³,26 Botulism is somewhat rare, but has occurred. The largest outbreak in the United States happened in 1977 when 59 people were identified and treated after eating poorly preserved jalapeño peppers.²³

Botulinus toxins enzymatically block acetylcholine release at the terminal end of presynaptic motor neurons,22 halting the conduction of stimulus across the synaptic junction in cholinergic autonomic sites. The interruption of neurotransmissions results in descending flaccid paralysis of motor and autonomic nerves, causing double or blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness.²⁷ The early signs and symptoms include marked fatigue, weakness, and vertigo. These are followed by blurred vision, dry mouth, and difficulty swallowing and speaking. The early prominent signs can be easily remembered as the “4Ds” — diplopia, dysarthria, dysphonia, and dysphagia.²² The initial signs and symptoms are easily confused with Guillain-Barre syndrome or myasthenia gravis, and paralysis of the respiratory muscles can progress to respiratory failure. Definitive treatment may include fluids, nutritional support, and mechanical ventilation lasting from weeks to months.²² The presentation of this toxin-related clinical syndrome is known as “botulism.”

The onset of signs and symptoms is generally quicker after ingestion of the bacterium than after inhalation exposure. Depending on the dose, the onset of symptoms from ingestion can be two hours to 10 days, averaging 12 hours to 36 hours.²⁶,28 Inhalation symptoms generally occur between 24 hours and 36 hours. Although symptoms progress to respiratory failure slower than with food-borne exposure,28 one reported case resulted in respiratory failure in only 24 hours after the onset of symptoms.

Diagnosing this illness is difficult because symptoms can mimic many other diseases. Generally, patients will not have a fever, and cerebrospinal fluid will be normal. Paralysis is symmetrical, and there are no changes in mental status. The standard test for the toxin is to use serum or fecal specimens in a mouse bioassay. This test is time-consuming, and clinicians should not wait for definitive results from the bioassay to begin treatment. Instead, the decision to treat should be based on history and clinical findings. Therapy consists of passive immunization with an antitoxin and supportive care.²²

If botulism is suspected or diagnosed, it must be reported to the local public health department. To obtain the botulism antitoxin, the Centers for Disease Control and Prevention (CDC) must be contacted. Antitoxin administration is indicated as soon as possible after clinical diagnosis has been made. Severe cases of botulism require additional supportive treatment that may include the use of ventilators over a period of weeks or months.²⁹ Many communities have prepared for possible large-scale attacks by increasing the availability of ventilators for mass casualties. In addition, the CDC has available large quantities of ventilators through Strategic National Stockpiles.³⁰

Although the CDC has an antitoxin, it might not be used during a mass casualty event related to botulism exposure because up to 9% of those treated experience hypersensitivity.²² Any use of the antitoxin requires prior testing for an allergic response. This licensed antitoxin contains neutralizing antibodies against botulinus toxin types A, B, and E, the most common causes of human botulism. Only experimental antitoxins are available for the other toxin types.²² A vaccine has also been developed, but it is not available to the public unless an identified occupational risk is established. This vaccine is associated with many adverse effects, including some serious ones, such as anaphylaxis in as much as 2% of the population. To be effective, the vaccine must be given before exposure. After the initial dose, the vaccine is given at two and 12 weeks.²² Antibodies produced after the third dose slowly diminish, necessitating an annual booster.

People with botulism do not require decontamination and present no risk to health care workers. Botulism is not contagious and has never been reported to cause a person-to-person infection. There is no reason to isolate these patients; universal precautions are sufficient. Patients who survive the illness may have shortness of breath and fatigue for years, and complete recovery occurs only after all affected nerve endings are regenerated.²³

Smallpox

Exposure to variola virus causes the disease known as smallpox. Although the World Health Organization declared smallpox eradicated from the world population in 1980, fear remains that a state-sponsored terrorist group could use it as a biological weapon.²⁹ The high fatality rate and easy transmissibility of the variola virus makes smallpox the most serious terrorist threat from a biological weapon. And the virus still exists in laboratories in at least two locations: the CDC in Atlanta and at Vector in Novosibirsk in the former Soviet Union. Specimens may also exist in other locations, including North Korea, which may have acquired it from the Soviet Union.²²

Smallpox received its name at the end of the 15th century in England. Its original name, small pokes (poke means sac), distinguished it from syphilis, which was then called great pokes. Before vaccinations were available, almost everyone contracted the disease, but an aggressive vaccination program dramatically reduced the incidence of smallpox by the 1970s.³¹ The last naturally contracted case of smallpox occurred in October 1977 when Ali Maow Maalin, a hospital cook in Somalia, broke out with the world’s final case of variola, which resulted in the vaccination of 57,000 people and control of a possible outbreak. Ali survived the disease. In 1978, a British medical photographer, Janet Parker, died after an accidental exposure at the University of Birmingham in England.²⁴ Her mother and father contracted the disease from her. Her father died of a heart attack early in the disease process, and her mother subsequently recovered from smallpox and became the last person on earth to publicly have the disease.³¹ There have been no subsequent cases. It has been reported that when several World Health Organization doctors told Ali Maow Maalin about the deaths in the Parker family, he wept, stating, “I’ll no longer be the last case of smallpox!”³²

Variola occurs in at least two principal forms: variola minor, which has a fatality rate of about 1%, and the more serious variola major. Both variola major and minor progress in a similar fashion, with variola minor having lesser signs and lasting for a shorter period of time.³¹

The incubation period after exposure is about 12 days. Symptoms begin with malaise, fever, rigors, vomiting, headache, and backache, with some patients developing delirium. Lesions in the mouth and throat appear early in the illness and release large amounts of virus into the saliva. This earliest period of infectivity occurs before any outward signs are noted. The smallpox rash appears several days after the other symptoms and progresses from macules to papules, which then become pustular vesicles. The progression of variola vesicles differs from varicella (chickenpox) in that they begin primarily on the face and extremities and in only small numbers on the trunk. This is the opposite of varicella, which usually begins on the trunk.²³ The illness remains contagious until all scabs separate, after about three weeks.

Although at least 90% of the cases follow the pattern described above, there are two other variations of the disease that present very differently: hemorrhagic and malignant. The hemorrhagic form of smallpox is always fatal. The illness begins with a shorter onset and rapidly progresses into severe prostration, high fever, and head, back, and abdominal pain. The skin produces an erythema followed by petechiae and frank hemorrhages on both the skin and mucous membranes. Death occurs within about five to six days. The malignant form of the disease is frequently fatal. The onset of symptoms is similar to the hemorrhagic form, but the confluent lesions develop slowly and never progress to the pustular stage. The lesions remain soft and flattened. If the patient survives, the lesions gradually disappear without forming a scab.³¹

Suspicion of the illness is based on the clinical presentation. Either electron microscopy used on a culture or Gispen’s modified silver stain then viewed under a microscope can yield clues to a microbiologist, but none that conclusively differentiate among variola or other orthopoxviruses, such as those causing monkeypox or cowpox. Suspected cases of variola must be reported immediately to local public health authorities. Because smallpox no longer naturally occurs, even one case will stimulate a national response from the CDC and experts from the Department of Homeland Security and other national law enforcement authorities. To isolate any outbreak, a strict quarantine with respiratory isolation of all people in direct contact with the index case will probably be implemented for at least 17 days.²³

Smallpox spreads directly from person to person through droplets and airborne virus during coughing, sneezing, or talking. It is more contagious during the pre-eruptive period. About 30% of those exposed through close contact will develop the disease, and 30% of those will die five to seven days after the onset of symptoms.²⁴ Health care providers must protect themselves from all body fluids, and extensive efforts to protect from respiratory exposure should be taken using N95 respirator masks, which are designed specifically for use in health care settings. Care should be taken when handling bed linen because contaminated clothing and linen can also spread the virus.³¹ All bed linen should be autoclaved or incinerated. Because of variola’s infectivity, the challenges of finding large isolation areas to provide care to numerous contagious patients may be overwhelming to hospitals and clinics. There is no drug available to directly treat smallpox, so care is supportive.²²

Late in 2002, the federal government released a plan to once again vaccinate the American public. The plan consisted of three phases. During Phase I, smallpox health care responders were vaccinated. These included hospital and health department personnel who would respond to care for patients infected with smallpox. These responders would also become the vaccinators to limit or stop an outbreak. Phase 2 provided vaccinations to emergency medical services personnel, firefighters, and law enforcement officers who would be the first responders to an outbreak. Phase 3 was for members of the public who requested the vaccine. Phase 3 was never initiated because of the possible side effects of the vaccine. These vaccines were all voluntary.³³

States initially expected that they would administer 450,000 doses to health workers during Phase 1. Though the CDC shipped almost 300,000 doses, fewer than 40,000 were given. The same situation took place during Phase 2. The low number of volunteers was related to the contraindications and general fear of receiving the vaccine.³⁴ The smallpox vaccine was not recommended for people who were immunocompromised. This included anyone on steroids, receiving chemotherapy, pregnant or expecting to become pregnant, or who has had an organ transplant. The vaccine was also not recommended for anyone who lived with a person in any of these categories. Additionally, individuals who had various heart conditions were not recommended to receive the vaccine. These included three or more of the following factors: high blood pressure, high cholesterol, diabetes, a first-degree relative with a heart condition before the age of 50, and/or a cigarette smoker.³⁵

It was determined that any person who had previously had a smallpox vaccine, no matter how many year prior, would have many fewer incidents of reactions.³⁶ Currently, research continues into developing a new and safer vaccine to protect the American public.
Even one case of smallpox would be considered an outbreak and treated as an act of terrorism. If an outbreak occurs in the U.S., the CDC plans to institute ring vaccinations. Simply stated, ring vaccinations are an effort to vaccinate every person who was in contact with a confirmed case of smallpox. When feasible, double ring vaccinations will be instituted to stop an outbreak. Double ring vaccinations include vaccinating all contacts of the contacts to a confirmed case of smallpox. This can include hundreds of thousands of people surrounding just one confirmed case.³⁷

If health care providers suspect that any patient has been infected with either botulism or smallpox, they must immediately call their local public health agency. Both botulism and smallpox are reportable diseases requiring immediate action within the community. If bioterrorism is suspected, the CDC immediately becomes involved, and a federal response will follow. Nurses as frontline health care providers must be able to recognize signs and symptoms of these diseases and know what needs to be done to protect themselves and others if the disease is contagious.

Unlike the immediate effects of bombings or chemical incidents, the effects of a clandestine use of a biological agent could progress over hours, days, and weeks, rapidly becoming a public health emergency capable of causing mass anxiety and even panic. To remain safe and offer the best care, providers must understand the implications and clinical issues resulting from the intentional heinous use of a biological agent.

The CDC, recognizing that local health care providers cannot do it all, has developed nine Strategic National Stockpiles to counter large chemical or biological attacks. These stockpiles are strategically located around the country to be mobilized during a terrorist disaster. When brought to a community, they provide large supplies of antibiotics, chemical antidotes, and other medical supplies to help in the health care management of mass casualties. It would take less than 12 hours for a stockpile to arrive in any region of the U.S., but the community must manage the logistical dispersal of medication and supplies.³⁸ If plans don’t already exist for dispersal and personnel and transportation resources haven’t already been identified, the stockpile’s use will be limited during the disaster. Health care providers must take immediate, active steps to ensure that the plans and needed resources for the dispersal of this stockpile have been addressed and identified in their community or region.³⁸

Preparedness efforts for terrorism are widespread and include many disciplines. Most hospitals have extensive plans for dealing with mass casualties related to trauma. Accreditation agencies require hospitals to practice these plans at least annually to ensure proficiency during a disaster. However, acts of terrorism have consequences for health care organizations that differ from the typical mass casualties of trauma. In these cases, contaminated or contagious mass causalities as well as larger numbers of psychologically injured victims will confront already taxed health care systems. The Joint Commission on Accreditation of Healthcare Organizations (JCAHO) recognizes that this type of preparedness is different and recently issued a 24-page advisory emphasizing the need for a new level of preparedness. The level at which hospitals prepare for terrorism and mass emergencies will be a key part of JCAHO’s quality-rating process, and deficient organizations may risk losing accreditation. Hospitals and other health care providers must react with education for the clinical staff, better and more comprehensive plans, effective personal protective equipment, and unprecedented coordination among local, state, and federal agencies.³⁹

Health care employees need assurances that they will be protected first if public health representatives determine that vaccinations or post-exposure prophylaxis is needed. Without these assurances, a health care agency runs the risk that staff will leave or refuse to come to work. Health care agencies should increase their stock of pharmaceuticals so that assurances made to employees can be carried out if a biological attack takes place. Planning for terrorism must extend beyond traditional boundaries to involve cooperation among competing health care organizations so that ideas, best practices, and resources can be assessed and consistently used.³⁹

Emergency preparedness efforts are under way in many acute health care facilities. These efforts should include moving triage outside of the hospital during a disaster to lessen the possibility of contaminating waiting rooms and emergency departments. Hospitals and clinics are increasing decontamination capabilities for mass casualties of biological or chemical attacks. Plans for satellite treatment facilities to reduce the burden and risk of overwhelming hospitals and clinics are being discussed and developed in most urban communities. Hospitals and clinics are developing disaster plans that complement each other and draw on each other’s resources. These health care disaster plans are working more urgently with other local resources, such as emergency medical services, law enforcement, and fire departments. An act of terrorism is not just a concern of hospitals, but of communities, states, and the nation.³⁹

Recently, we’ve witnessed horrible acts of violence around that world that have caused thousands of deaths and injuries to innocent people. We watched as suicide bombers have created death and fear throughout the world. We’ve seen our own troops in foreign counties attacked as they act as peacekeepers for other counties. And in the fallout of these terrible events, health care providers have been diligently preparing for events such as these to occur in the United States. Both JCAHO and OSHA have developed guidelines for training and preparedness for health care providers dealing with mass casualties from terrorist incidents.^{39, 40}

The intentional outbreaks of anthrax in New York; Washington, DC; and Boca Raton, Fla., brought hundreds of worried well into local emergency rooms wondering whether their flu symptoms were related to a hidden intentional exposure to anthrax.⁴¹ The outbreak of severe acute respiratory syndrome (SARS) that occurred in 2003 caused serious concern for the American public. Although this was a naturally occurring event, it became an eye-opening experience that demonstrated how our ability to rapidly travel the world could contribute to an uncontrolled spread of a contagious disease.

The biological agents that terrorists could use have the capability to generate casualties in the thousands. Anthrax, plague, botulism, and smallpox are all examples of these. Probably the biggest challenge in the health care environment is to find room to care for large numbers of infected patients and to do so safely. To make matters worse, hospitals across the nation are suffering with emergency department overcrowding.⁴² Additionally, there has been a loss of 38,000 hospital beds (4.4%) nationwide since 1996. This includes a 20% decrease of ICU capacity from 1995 to 2001.⁴³

Planning for mass casualties goes beyond separate health care facilities. Planning must occur on community, regional, and state levels. Planning for patient surge must be scaled and flexible to allow for the care of large numbers of patients on any given day. Help has come from several departments of the federal government in the form of grant funding.⁴⁴ The Health Resources and Services Administration, a division of the U.S. Department of Health and Human Services, has been one of the most active in offering funds for hospitals to prepare through planning and training and to purchase equipment needed to treat mass casualties.⁴⁴

But the buck stops here. Health care providers represent the last stop for victims needing medical care from acts of terrorism. We must take on that challenge and continue to prepare for the worst while providing the best care available.

Chemical Weapons and Emergency Preparedness

Today, the thought of using a toxic chemical against a civilian population is considered barbaric, but many countries, including the United States once had chemical weapons programs. For many countries the chemical weapons programs began even before WWI and reached its intensity in the 1960s. These programs produced human toxic chemicals with the intent to both kill and incapacitate enemy soldiers.¹

Not until the last 10 years has there been significant concern about the use of these military chemical against civilian populations.² It should be noted that in 1993 most counties that had developed chemical weapons signed an agreement to destroy current stockpiles and stop future production. Both the United States and Russia signed the agreement. At the time Russia had approximately 40,000 tons of chemical weapons, followed by the United States with 31,000 tons. Both are in the process of destroying the weapons.³ Because much scientific study and practical application has gone into the use of chemicals as a weapon, there is speculation that terrorist groups could tap into this expertise to manufacture and disseminate toxic chemicals against civilians.

In March 1988, Saddam Hussein attacked the Kurds in Iraq using a chemical cocktail of mustard gas and various nerve agents. An estimated 5,000 Kurds died in the attack. Half of those living in the region of the attack have respiratory complications and on an average day, there are no normal births, mostly miscarriages. Those that survive have significant birth defects and mental retardation.⁴
Then in March 1995, a terrorist group, the Aum Shinrikyo, released sarin nerve agent into a Tokyo Subway station and perpetrated the largest non-wartime chemical attack on record against a civilian population. The attack resulted in more than 5,000 injuries, 12 deaths and 1,000 victims were hospitalized. This act of terrorism stimulated many of the efforts in this country to prepare for a chemical attack against our civilian population.¹

The chemical agents that could be used as a terrorist weapon fall under four major categories: neurotoxins, cyanides, respiratory irritants, and vesicants. These chemicals are both military and industrial based. Although American industries use and produce many toxic chemicals, most are not manufactured to intentionally cause harm to humans. In contrast, military anti-personnel chemicals are produced to both injure and kill.⁵ 

Neurotoxins (nerve agents)

Neurotoxins are organophosphate-based chemicals commonly common agents selected for use in wartime activities.² These agents are very effective because they can enter through virtually any route and cause severe incapacitation and death.  Neurotoxins have been formulated to be extremely toxic to the intended target, but break down rapidly so that invading troops can inhabit the area within days after an attack. There are similar compounds used in industry, such as organophosphate insecticides; some of these possess extremely toxic qualities and could be used in place of military nerve agents. 

Several commercially available organophosphate insecticides such as Parathion and tetraethylpyrophosphate (TEPP) are extremely toxic and may be easier to acquire than military-based nerve agents.2 These insecticides trigger the same nervous system stimulation as a military nerve agent. Although these commercially available insecticides are very toxic, they do not have the extreme toxicity found in the military agents.³

Military nerve agents

Tabun (GA), sarin (GB), soman (GD), and VX (V-Agent) are the most widely known military neurotoxins. These agents are organophosphate compounds that can be sprayed in the air as a vaporizing mist or can be spread as a liquid that vaporizes through evaporation.³  G agents, developed in Germany during WWII, are volatile and evaporate slightly faster than water. This makes them very dangerous as an inhalation hazard. Although none of these agents are easy to make, tabun (GA) and sarin (GB) are easier to synthesized and therefore, may be more readily available. Soman is not easily formulated and is the most deadly of the G agents because of its ability to cause irreversible damage even with rapid use of antidotes.^3,2 VX (V for venom) is not as volatile as G agent, evaporating only as rapid as motor oil. This makes VX primarily a skin absorption hazard. For VX to become a respiratory hazard, it must be mechanically aerosolized or heated to increase volatility.  Because of the viscosity of this agent, it will last longer on objects in the environment, causing injury or death days later.^3,2

The military nerve agents are odorless, so they can be used without easy detection.  Terrorists, on the other hand, may not care so much about the odor generated by the chemical and may produce them without the additional synthesis needed to remove the odor. Typically, G agents produced without the removal of the aroma will have a fruity smell while VX will have a sulfur smell.³

 Physiology of neurotoxins poisoning

In the synaptic junctions using acetylcholine as the neurotransmitter, the enzyme acetylcholinesterase functions to remove acetylcholine once a nerve impulse is transmitted across the junction.4 These nerve pathways are primarily located in the parasympathetic nervous system, but are also found in the central and somatic system.  Nerve agents work by binding with the enzyme acetylcholinesterase, allowing acetylcholine to remain in the junction and over stimulate nerve pathways by sending continuous nerve impulses across the synapse. The bond between the nerve agent and acetylcholinesterase ages over time and eventually becomes a permanent bond that cannot be broken, even with the use of an antidote. Signs and symptoms of the over stimulation include excessive salivation, urination, diarrhea, excessive mucus production, muscle fasciculation, constricted pupils, and seizures. The acronym DUMBELS (diarrhea, urination, meiosis, bronchospasm, emesis, lacrimation, and salivation) abbreviates the most prevalent signs and symptoms.⁶ 

Physical properties and routes of entry

Neurotoxins are found in a liquid form and evaporate slowly having a viscosity ranging from water-like to motor oil thickness. The most volatile of the group is sarin, which can evaporate slightly faster than water.3 These agents can enter through all routes, but inhalation causes the most rapid effects. Because an enemy cannot guarantee that inhalation will occur, some nerve agents have thickeners, ensuring that the agents will remain on objects for long periods of time and, thus, be transmitted to the victim hours or days later. Once on the victim, the agent is absorbed through the skin, causing systemic poisoning. 

An exposure to vapors usually generates mild to severe symptoms that occur within seconds to minutes. Mild symptoms include those defined in the acronym DUMBELS. Severe symptoms include all of the mild symptoms, with the addition of loss of consciousness, seizures, and apnea. ² When there is a liquid exposure, the onset of symptoms is slower, ranging from five minutes to 18 hours, and is generally localized to the area of exposure during the onset of symptoms. As the poisoning become more systemic, effects will spread throughout the body. ⁷

Decontamination

Decontamination is necessary for people exposed to neurotoxins. Victims’ clothing and skin can have enough chemical to cause harm to nurses trying to care for them. Those providing decontamination to victims must wear appropriate chemical personal protective equipment (PPE) including proper respiratory protection.  Water has the ability to decontaminate nerve agents through a process of hydrolysis.1 The process works well, but when thickening substances are added to the nerve agents, they are not easily soluble, and hydrolysis occurs slowly.  The addition of soap to water will make the decontamination process more efficient by breaking down oil-based materials.1 Hospital personnel participating in mass casualty decontamination efforts or those wearing chemical protective PPE to triage or treat patients must be trained under OSHA standards. 

Chemically contaminated patients can present a secondary contamination hazard to health care providers. Appropriate PPE for chemically contaminated patients including airway protection may be necessary. Information about PPE is available from the American Hospital Association, the local emergency planning committee,  or local fire department.

Treatment

The first treatment is to provide an open airway and support ventilation.  Because patients are hypersecreting, the airways frequently become blocked and must be suctioned to ensure airway patency. If treatment is being provided in a health care setting, the first priority should be establishing a patent airway and starting oxygen before providing an antidote.⁸ 

Antidotes for nerve agent poisoning include atropine IM or IV, followed by pralidoxime chloride (protopam chloride, 2-PAM chloride).  Atropine is administered rapidly in high doses under close cardiac and vital sign monitoring.9 Atropine blocks the release of acetylcholine in the synaptic junction and limits the need for acetylcholinesterase.  Atropinization must be maintained until all the absorbed organophosphate has been metabolized and the body again produces sufficient quantities of acetylcholinesterase.  The treatment could last from days to weeks, necessitating the use of huge quantities of atropine. The normal dosage is  2-6 mg every five minutes until the mucous membranes dry.⁹ The military provides an antidote kit for troops who are in danger of an attack with a nerve agent. The kit, called a Mark I, contains two auto injectors. One of the auto injectors contains 2 mg of atropine and the other 600 mg of pralidoxime for self-injection into intramuscular tissue. Many EMS agencies and even some hospitals in the U.S. have purchased these kits for treating mass casualties related to nerve agent poisoning.³

Pralidoxime is used as the second part of the nerve agent antidote. Pralidoxime has three desirable effects: frees and reactivates (breaks the bond) acetylcholinesterase; detoxifies the nerve agent; and has anticholinergic (atropine-like) effects. Pralidoxime’s ability to break the nerve agent/acetylcholinesterase bond lessens over time, so the faster this drug can be administered, the better the outcome.10
Valium should be considered any time that somatic system toxicity (seizures) is noted. If significant inhalation of a nerve agent occurred, it may be necessary to use Valium even before muscular involvement is witnessed.⁹ 

Cyanides (blood agents)

Terrorists can easily obtain and use cyanides and cyanide compounds to cause mass casualties in civilian populations. Not only have cyanides been used by militaries as anti-personnel chemical weapons, but these chemicals are common in industry. Cyanide is used in industry for heat treating and plating, fumigation, mineral extraction, dyeing, printing, photography, agriculture, and the manufacture of plastics, paper, and textiles. It is a chemical asphyxiant causing cellular suffocation. It is found as a gas, solid, or liquid. 

Military blood agents

Military cyanide compounds consist of two chemicals, hydrogen cyanide (military call this chemical AC) and cyanogen chloride (military CK). These agents are identical to their civilian counterparts used in industry. For this reason, terrorist may choose these agents to inflict harm.  Hydrogen cyanide is a liquid at less than 79 degrees, but vaporizes quickly.  Cyanide gas is lighter than air, so when it is released, it rises and dissipates rapidly.  For this reason, AC does not remain in surrounding areas. CK, is a liquid at less than 55 degrees F,  so it becomes a gas much quicker. CK gas is twice as heavy as air and therefore has a tendency to linger in low-lying areas and inflict harm for longer periods of time.¹¹

Physiology of cyanide poisoning

Cyanide has the odor of bitter almonds.  The ability to detect this odor is a sex-linked recessive trait of only 60% to 80% of the population. The remaining population cannot detect the odor due to a sensory deficit that is greater in men than women by a ratio of 3-1.⁹
These agents work by inhibiting the ability of cells to use oxygen. Following an exposure, the cyanide ion enters the cells, binding with the mitochondrial enzyme cytochrome oxidase. This enzyme, in its original form, is necessary for electron transport needed for cellular respiration (the use of oxygen to convert glucose to energy). By binding to cytochrome oxidase, these ions cause a paralysis of the cells’ ability to carry out aerobic metabolism. The process eventually causes the cells to function under anaerobic metabolism. This anaerobic state ultimately causes decreased cellular energy production, metabolic acidosis, cellular suffocation, and death. The half-life of cyanide in the body is only about an hour, but during an exposure, death takes place well before the body starts to detoxify or excrete the chemical.¹¹ 

Physical properties , routes of entry Cyanide is one of the most rapidly acting poisons. It most often gains access to the body through inhalation but can be ingested or absorbed through the skin and mucous membranes. Cyanide causes death within minutes to hours, depending on its concentration and route of entry as well as the exposure time and activity level of the victim.7 
Patients present with a wide variety of symptoms because cyanide poisoning affects virtually all of the cells in the body.  The most sensitive target organ is the central nervous system where the urgent need for oxygen is first sensed. Early effects can include headache, restlessness, dizziness, vertigo, agitation, and confusion. Later signs are seizures and coma.¹¹ 

Decontamination

Generally decontamination is not needed if a victim is only exposed to cyanide gas or vapor. The removal of a patient’s clothing is usually enough to remove any chemical hazard. If a victim is exposed to a liquid or solid, a soap and water wash is recommended.

Treatment

Treatment consists of establishing a patent airway then, as quickly as possible, begin advanced treatment using a cyanide antidote kit. The kit contains amyl nitrite, sodium nitrite, and sodium thiosulfate. ⁷
The first step in the use of the cyanide antidote kit is to break a perle (similar to an ammonia capsule) of amyl nitrite.  Allow the patient to inhale the amyl nitrite for 15 to 30 seconds of every minute while an IV is established.⁹ Once an IV is established, slowly administer 300mg (10ml) of sodium nitrite IVP over 10 minutes. Both of these nitrites are vasodilators and can cause a decrease in blood pressure that can usually be corrected with positioning and fluids.⁹

Last, infuse 50ml of a 25% solution of sodium thiosulfate, IV, over at least 10 minutes. Sodium thiosulfate acts as a clean-up agent by changing the remaining cyanide into a relatively harmless substance that is renally eliminated.⁹ 

The nitrites (amyl nitrite and sodium nitrite) convert hemoglobin into methemoglobin. Essentially, these chemicals change the iron ion in the hemoglobin from Fe++ (ferrous iron) into Fe+++ (ferric iron) converting hemoglobin into methemoglobin. Methemoglobin will not carry oxygen but has an affinity for (wants to bond with) the cyanide ion. Methemoglobin competes with cytochrome oxidase for the cyanide ion, actually attracting the cyanide away from the cytochrome oxidase. The cyanide antidote kit will convert about 20% of the hemoglobin into methemoglobin. This frees the cytochrome oxidase to participate again in aerobic cellular metabolism. Providing oxygen at a 100% concentration is necessary to reduce hypoxia related to the decreased hemoglobin.⁹ 

Respirator irritants (choking irritants)
Strong respiratory irritants have a long history of use by military forces. Even today, chlorine (CL) and phosgene (CG) remain in military arsenals around the world. When discussing terrorism, we cannot discount the possible use of these agents.¹

Many communities use chlorine gas in its pure form for chlorinating drinking water. It’s also used as an anti-mold and fungicide agent. Compounds containing chlorine are even used for chlorinating home swimming pools and cleaning toilets and showers. There is no doubt that this chemical is easily available to produce single exposures or mass casualty events. 

Phosgene, although not as common as chlorine, is found in industry and used for organic synthesis during the production of polyurethane, insecticides, and dyes.It is also a by-product of burning Freon, which has lead to many injuries among firefighters.^1,9

Military choking agents

Chlorine and Phosgene are typically stored as liquids but rapidly become gases once released into the atmosphere. Their expansion ratios allow them to be transported in smaller containers, and, once released the fill a large area.¹

These agents were used on the battlefield to incapacitate an enemy force so that it could be overtaken by advancing troops.  This strategy worked well, because both of these gases dispersed rapidly into the environment, leaving no contaminated objects behind to cause injury. 

Once exposed, victims are overcome with severe, uncontrollable coughing, gagging, and tightness in the chest.¹²  Bronchospasms and laryngeal spasms are common, causing apnea and unconsciousness. Other injuries include tissue sloughing, localized edema, and pulmonary edema, all contributing to obstruction of the airways. Because chlorine is water soluble, injury begins in the upper airways where the chemical combines with the water-based mucous lining the airways. 
Phosgene is not easily soluble in water and therefore directly attacks the alveoli, where tissue destruction at this level can be severe. The breakdown of these cells allows fluid from the bloodstream to advance into the airways, a condition called noncardiogenic pulmonary edema. This form of pulmonary edema is very difficulty to treat.  When the injury is not fatal, many times the victim is left with destroyed lung tissue and a lifetime of respiratory disease ranging from chronic obstructed pulmonary disease to chronic pneumonia.¹³

Physiology of respiratory irritant injury
Injuries to the upper respiratory areas are usually a result of exposure to water-soluble chemicals that readily dissolve into the moisture-coated airways. In the case of chlorine, this results in the production of hydrochloric acid and chemical burns at the site. Laryngeal edema and laryngeal spasms should be expected and treated aggressively. ^7,9   Injuries to the lower regions of the respiratory tract usually result when the chemical inhaled is not water-soluble, is in a high concentration, or is inhaled over an extended period of time. This deeper injury causes swelling of the finer bronchioles, sloughing of damaged tissue, and damage to the alveoli. Cilia that may be damaged are unable to rid the fine bronchioles of the sloughed cells and increased mucous production caused by the damaged airways.  The lower airways obstruction caused by this exposure adds to the complexity of the injury and increases the chance of death. ^7,9
Noncardiogenic pulmonary edema is the result of a chemical irritant reaching the alveoli and causing damage. The damage interferes with the alveoli’s natural ability to keep fluids out of the alveolar space, which results in fluids filling injured alveoli and fine bronchioles, eventually advancing into the upper airways. If the exposure causes severe alveolar damage, the end result will be death.⁷

Physical properties, routes of entryBoth chlorine and phosgene are heavier than air and are able to seek out low-lying areas and persist for long periods of time.  Although these chemicals are considered respiratory hazards, chlorine has additional effects on both mucous membranes and moist skin. Exposed patients will present with burning eyes, nose, and possibly burning skin in areas that are moist (under arms and groin areas).¹⁰

Decontamination

Chlorine will combine with any moisture on the skin and form a solution of hydrochloric acid causing skin burns. Decontamination consists of removing clothing and rinsing/washing with soap and water. ⁶

Treatment

The treatment for respiratory irritant is twofold. Initial treatment is to open the airways to allow the free movement of air into the alveoli. The second part of the treatment is to reduce the fluid in the alveoli to allow gas exchange with the blood.  Getting oxygen to the alveoli is vitally important. ⁸  In upper respiratory injury, oxygen must pass through narrowed passageways to gain access to the lower system. Bronchodilators like albuterol given in an updraft will provide some dilation of the airways. Brethine (terbutaline sulfate) and epinephrine given subcutaneously may also assist in making the bronchioles larger to allow for the passage of air and oxygen. However, care must be taken with any of these drugs as their side effects, high blood pressure and rapid heart rate, will be with hypoxia.⁹

When lower airway injury results, the outcome is usually pulmonary edema (PE).   Reducing pulmonary pressure with the use of Lasix, Morphine, or Nitroglycerine may produce a positive effect but will usually not stop the progression of chemically induced PE. Because the alveolar tissue is injured causing the infusion of fluid from the bloodstream. Definitive treatment will involve positive pressure ventilation using a volume-cycled ventilator.  This will serve to both reduce the infusion of fluid from the blood stream and assist oxygen exchange in alveoli that have been injured from the chemical exposure. ⁷

Vesicants (blister agents)

Vesicants were originally developed by the military to be used both as area contaminants to severely injure exposed skin and as a respiratory and eye irritant when vaporized. Many chemicals in industry are capable of causing skin irritation, but none to the degree that military blister agents can.¹

Military blister agents

Three types of blister agents are primarily used by the military.  These agents include mustard (H), phosgene oxime (CX), and lewisite (L). These agents are all liquids that vaporize slowly. Skin and eye exposure is the most common effect that results from direct contact with the liquid.¹

Physiology of blister agent exposure

These agents are capable of causing extreme pain and large blisters on contact. If the vapors are inhaled, the lung tissue will form large obstructing blisters. Once the blisters break, a large open wound results that allows the establishment of infections that can eventually cause death. 

After blister agents gain access into the body, the chemical cycles in the extracellular fluid forming an extremely reactive substance binding with both intracellular and extracellular enzymes and proteins causing extensive tissue damage. Once exposed, a victim may manifest a latent period when no symptoms are present. Two to 24 hours later, the reaction appears with the formation of blisters on the skin and necrosis of the mucosa of the airways with progressive involvement of the airway musculature, and severe irritation to the eyes including swelling in the cornea and related tissues that leads to permanent scarring. Injuries from blister agents are considered radiomimetic in nature as these agents have the ability to alter DNA, similar to radiation poisoning.¹⁴

Lewisite acts similarly to mustard but has additional effects that are systemic.  Symptoms beyond the blistering effects may include pulmonary edema, diarrhea, vomiting, weakness, and low blood pressure. The irritation lewisite causes to the eyes is devastating. If a victim is not decontaminated within one minute, damage will probably be permanent.¹

Physical properties and routes of entry

Mustard has a freezing point of 57 F,  so it solidifies at temperatures less than this. For this reason it does not readily vaporize unless it is heated to above 100 F and, therefore, is not a significant respiratory hazard. Lewisite and phosgene oxime vaporize more readily than mustard, making them more of a respiratory hazard. All of the blister agent vapors are heavier than air, allowing them to stay near the ground and not dissipate quickly.^5,9

Decontamination

Decontamination for all blister agents must be immediate and involve the removal of all contaminated clothing. Caution must be exercised in removing victims’ clothing as secondary contamination could take place. Clothing must be handled using chemical protective gloves and other appropriate PPE.⁵ The decontamination solution of choice is soap and water.

Each vesicant harms tissues on contact.  Mustard differs from the other agents, as it does not produce symptoms for several hours, leaving the victim without a clue that an exposure has taken place. Both phosgene oxime and Lewisite cause irritation almost immediately, which alerts the victim to the exposure and allows earlier decontamination. ⁸

Treatment

Treatment after exposure to blister agents is mostly supportive. The skin damage is similar to that seen in thermal burns and could be as simple as treating a sun burn to total management of a severely ill person with burns and the challenges of controlling fluid and electrolyte balance.  Burns to the eyes are treated with ophthalmic ointment and topical antibiotics.  Respiratory involvement may require intubation and ventilation utilizing PEEP or CPAP to maintain oxygenation. ³

Health care issues

Although there have been no significant acts of terrorism using chemicals in the U.S., state and local governments are busy preparing for chemical terrorism. Fire and  police departments have training programs that teach emergency responders how to respond safely if chemicals are involved in an incident.⁵ The military has shared its experience with training centers and has helped develop programs to teach health care providers how to treat casualties of chemical exposures. 

Special chemical protective equipment has been developed for hospitals’ use if mass casualties arrive and are contaminated with hazardous chemicals. Nurses, especially those working in emergency rooms, must know how to both protect themselves from contaminated patient and know how to treat those exposured.⁵ If an act of terrorism involving chemicals occurs, the FBI will respond and will be the lead agency in charge of the incident. The Environmental Protection Agency will have oversight of environmental clean-up and the Department of Homeland Security will coordinate overall federal actions. Health departments will stay in contact throughout the nation using the Health Alert Network (HAN), one of the means of communicating information about the event. The HAN is an Internet-based communication program that can be used to alert other areas of the county about an attack and share experiences in dealing with the event. 

When mass casualties involving a chemical exposure occur, supplies and equipment needed to treat the victims can be rapidly depleted. When a shortage of supplies and equipment is predicted, local emergency management can be contacted for help. Local emergency management can contact the state (governor’s office) and request the Strategic National Stockpile. Once requested, the SNS will be in a community within 12 hours and provide large quantities of antidotes and equipment to supply hospitals that are treat mass casualty victims.¹⁵ 

Managing Radiation Incidents

We know that terrorists will use any means to gain attention, cause harm, and disrupt the lives of the American people. Radiation emergencies are one of the least understood and emphasized segments of health provider education and therefore one of the most frightening.¹ You can’t see, smell, or touch radiation.² Most health workers feel unprepared to deal with radiological incidents. We know that a mass casualty (MASCAL) incident resulting from radiation is likely to generate large numbers of frightened people, or “worried well,” who may or may not require decontamination.^3,4

Radiation 101

Radiation is energy that can be characterized as waves or particles trying to become stable. Radioactive materials contain energized atoms that are unstable and release energy. This energy may damage certain critical cellular structures, causing a cell to malfunction or die and may also interact with water molecules in the body to create unstable, hyperoxide molecules causing further damage. (See the sidebar for characteristics of ionizing radiation.)

Every year, people worldwide are exposed to naturally occurring background radiation from the sun, outer space, and radioactive materials in the soil. The average U.S. resident receives a background radiation dose from all sources of about 100 millirems.⁶ Man-made sources of radiation include some industrial measurement devices and radiotherapeutics used for medical diagnoses and treatment. Sources of radioactive materials include nuclear power plants, nuclear waste processors, university research centers, medical radiotherapy clinics, and even industrial complexes.¹

The Gray (Gy) is a unit of measure for absorbed dose and reflects the amount of energy deposited into a mass of tissue (1 Gy = 100 rads). The U.S. annual occupational exposure allowed by the Department of Energy for those who work with and around radioactive materials is 0.05 Gy [1] (or 15,000 millirems).⁶

Weapons of mass destruction

There are four general scenarios you consider when classifying radiological weapons of mass destruction (WMD).⁷ The four scenarios are examined here in order of least likely to occur to more likely to occur.

Nuclear bombs or improvised nuclear devices (IND), also known as suitcase nukes, require high-grade radioactive fissionable materials and the scientific and technical sophistication to assemble the components for detonation. Nuclear devices create a tremendous blast, extreme heat, and a significant dose of radiation to those in close proximity (two miles for an IND and more than 50 miles for a 1 kiloton nuclear bomb).^1,8 The purchase and transportation of fissionable materials are highly regulated in most countries, which significantly limits their availability. This type of an event is extremely unlikely.

In the history of the nuclear power industry, industrial accidents involving nuclear power plants have been rare. Nuclear plants have a number of redundant safety systems to take a plant off-line as well as well-exercised emergency plans involving local authorities (police, fire, and EMS). Their physical structures have been bolstered to prevent accidental releases, even from a terrorist attack.

There have been a few reports of hidden or “silent” sources, defined as a radioactive source that is lost or abandoned, or intentionally placed in areas to expose people. By placing a source on mass transportation, such as under a subway seat, or in a large movie theater, a large numbers of casualties could occur over time..
Finally, radiological dispersion devices, or dirty bombs, combine an ordinary explosive with a radioactive material. Although there has been no documented use to date, it is believed that a dirty bomb could be constructed with radiologic materials found in common use. Materials such as Cesium 137 and Cobalt 60, frequently found in medical teletherapy, and Iridium 192, found in industrial instrumentation, can be purchased legitimately or illegitimately, or stolen.^1,2

While it is unlikely that a dirty bomb would cause large numbers of actual radiation casualties, detonation of one would likely result in panic and economic disruption.²

How radiation affects the body

Exposure occurs when all or part of the body is exposed to penetrating radiation. We subject patients to exposures every day when we perform a CT scan or an X-ray. The radiation is either absorbed or passes completely through. Once removed from the source, the patient is not radioactive and can be treated like any other patient.^5,7,9

Contamination is radioactive material where it does not belong. It can be a solid, liquid, or gas or even dust particles that float through the air and eventually settle on the ground or some other surface. External contamination is radioactive material on the outside of the body, usually on the skin or on clothing. It can be easily removed by removing clothing and washing the skin with soap and water. Internal contamination involves the deposition of radioactive material inside the body through inhalation, ingestion, or penetrating wounds.^5,7
Incorporation is the uptake of radioactive materials by body cells, tissues, and target organs such as bone, the liver, the thyroid, or the kidney, causing chemical changes at the cellular level. Incorporation cannot take place unless contamination occurs.⁵ Cells that replicate rapidly, such as spermatocytes, blood elements, and intestinal crypt cells are very sensitive. Lymph tissue and bone marrow are the most radiation-sensitive tissues. The most radiation sensitive organs are the skin, intestines, kidneys, and gonads.^6,9

Radiation can affect the body in a number of ways, and harmful health consequences may not be seen for many years.⁷ Effects depend on the amount of radiation absorbed by the body (the dose), the type of radiation, the route of exposures, and the length of time a person is exposed. Effects can be mild such as reddening of the skin or serious such as cancer and even death.¹⁰ Special populations that are more radiation-sensitive include those under 12 years and pregnant women because of their rapidly growing tissues, those over the age of 60 because of declining immune systems and co-morbidities, and those with pre-existing conditions that may result in immunosuppression, blood loss, or infectious complications. The human embryo and fetus are particularly sensitive to ionizing radiation, and the health consequences of exposure can be severe, even at radiation doses too low to immediately affect the mother. Consequences can include growth retardation, malformations, impaired brain function, and cancer. At higher doses, the health effects depend on dose and the stage of gestation.^9,11

Nursing considerations

The Joint Commission on Accreditation of Healthcare Organizations requires facilities it accredits to have and exercise emergency plans for radiologic incidents that use the Incident Command System (ICS).⁹ Plans should involve hospital radiation experts such as the radiation safety officer, health physicists, and medical physicists. These experts can help hospital staff document the presence of radioactive materials, activity levels, and accident details; collect samples that document contamination; assist in decontamination procedures; conduct and document dose calculations; and dispose of radioactive wastes.

Other federal guidelines exist. For example, the Occupational Safety and Health Administration recently published mass casualty guidelines addressing protection for first receivers during releases of chemicals, radiological particles, and biological agents (overt releases) that produce victims who may need decontamination before medical care is administered.¹²

Protecting yourself

First and foremost, remember that no health care provider has ever received a significant radiation exposure by treating a contaminated patient.^5,9   Protection involves limiting your radiation exposure, the use of personal protective clothing, and contamination control. You can reduce your exposure through time, distance, and shielding. Limit time near a radiation source, increase your distance from the source, and use shielding between you and the radiation source.⁷

Protective clothing in a radiation emergency is similar to that used in universal precautions and includes gowns, caps, masks, splash shields, and waterproof boots.^5,7,9 All open seams and cuffs should be taped using masking or adhesive tape. Two pairs of gloves should be worn. The first pair, preferably colored, should be worn under the arm cuff of the outer gown and secured by tape. The second pair of gloves should be easily removable and replaced if they become contaminated. The outer gloves should preferably be white to clearly show if the outer glove has been removed and not replaced. A radiation dosimeter should be assigned to each team member and attached to the outside of the surgical gown at the neck, where it can be easily removed and monitored by a radiation safety officer. Waterproof aprons can be worn when using liquids for decontamination.^5,7

The Nuclear Regulatory Commission limits the exposure of pregnant workers to 5 mGY for the entire pregnancy.⁹ Therefore, during a radiation emergency pregnant hospital workers should be reassigned to areas where exposure is unlikely.

Remember, unlike most hazardous materials, radioactive material can be easily detected, even in small quantities, with the use of a simple and readily available survey meter, such as a Geiger counter.⁷ The purpose of donning extra clothes mentioned above is to give yourself a layer of clothing to keep your own clothes and body from becoming contaminated.

Organizing for an incident

Detailed response procedures are beyond the scope of this article; however, the website of the  Radiation Emergency Assistance Center/Training Site (REAC/TS) at the Oak Ridge Associated Universities (www.orau.gov/reacts/) has demonstrations of using protective clothing, prepping a treatment area, removing contaminated clothing, surveying for contamination, and decontamination procedures for wounds and intact skin. See the end of this article for more information.

If your hospital receives advance notification, you should implement your hospital’s radiation emergency plan. Your primary goal should be to provide patient care while limiting the spread of contamination. Preparation is great if you have the time, but if you have an unstable patient who arrives, the priority is to stabilize the patient.
Select a treatment area near an outside entrance. Remove any equipment that will not be needed and assemble any additional required items. This will include a survey meter (Geiger counter), extra 4x4s, ABD pads, small and large sample bags, surgical drapes, tape, and irrigation solution. You will also need a number of large, plastic-lined waste containers. The treatment beds should be covered with several layers of waterproof sheets that can be removed as you decontaminate the area.

Check your survey meter to obtain and record a background reading. This reading will be used to compare readings with the patient. The goal for removing contamination is to get as close to the background level as possible. The average background reading is 20 to 60 counts per minute.⁵

REAC/TS  gives the following guidelines:⁵

General:

• If in doubt, assume contamination.
• Avoid contact with contaminants.
• Do not eat, drink, or smoke in areas where radioactive materials are located.
• Wear protective clothing.

When providing emergency care:

• Set up a controlled area large enough to hold anticipated number of victims.
• Prevent tracking of contaminants by covering floor areas with paper if your hospital plan calls for it. Some hospitals with nonporous floors like linoleum have made the decision not to cover them.
• Monitor and restrict access to the controlled area through the use of security personnel.
• Use a buffer zone or secondary control line for added security.
• Use a radiation meter and assess anyone or anything leaving the controlled area to prevent further contamination, taking special care with hands, feet, and face. People exhibiting radiological contamination must remain in their controlled area until they can be sufficiently decontaminated or wrapped in sheets if their medical condition requires their emergent movement to another section of the hospital.
• Use strict isolation precautions, including double bagging of all wastes and protective clothing.
• Control waste by using large, plastic-lined containers for clothing, linens, dressings, etc.
• Control ventilation to prevent airborne contamination.
• Survey hands and clothing with radiation meters at frequent intervals. Change instruments, outer gloves, drapes, etc., when they become contaminated or when preparing to touch “clean” areas.
• Use waterproof materials to limit the spread of contaminated liquids, for example, waterproof surgical drapes.
  

Triage

The goal of triage is to evaluate and sort victims for priority in treatment to do the greatest good for the most people.⁹ In many radiological events, the vast majority of people involved will be exposed to very low doses of radiation (if they are exposed at all). In these cases there will be no immediate effects, with a potential for delayed effects depending on the dose received. Remember that if the patient has only been exposed and does not have radioactive material on their person, then there is no need to take any unusual precautions.⁵ They can be cared for like any other emergency case.

People who are uninjured or minimally injured and stable should be evaluated at the scene. Removal of clothing and washing the skin with warm soap and water is 95% effective in removing contamination.¹
Some people may be exposed to doses large enough to cause immediate effects. The onset of nausea, vomiting, fatigue, and anorexia within hours usually indicates a significant and lethal radiation dose.^7,9

Most patients in the immediate vicinity of a dirty bomb will present with symptoms of blast or burn (chemical or thermal) injury in addition to radiation exposure.⁹ Patients who have combined injury will have increased morbidity compared to patients who received the same dose of radiation without trauma.

Assessment and treatment of serious medical problems is the No. 1 priority.^5,7 Never delay critical interventions because you are concerned about contamination. Patients with life-threatening presentations such as a compromised airway or severe hemorrhage should receive enough immediate treatment to preserve life and to stabilize them. While the health team conducts the standard ABC’s of triage, the radiation safety officer will quickly survey the patient. A quick survey tells you if you are dealing with a contaminated patient or not.

Once stabilized, patients should have all their clothes removed for a more definitive survey. Care should be taken not to spread the contamination around. Clothing should be cut off, not ripped, from head to foot (away from the airway) and rolled outward so that the outer surface that is most likely more contaminated is rolled away from the patient. Before log rolling the patient, you should change your gloves because you have touched the patient’s outer garments and are likely contaminated. Sheets and clothing should be double bagged, labeled, and removed from the treatment room to prevent them from causing inaccurate survey readings.

Decontamination involves removing external contamination and is conducted first in open wounds, then in or near body orifices, and finally on intact skin.⁵ Open wounds are a direct pathway for internal contamination and should be decontaminated as soon as medical priorities permit. Decontamination of intact skin can be delayed because most radioactive materials are not readily absorbed through intact skin in the first hour after contact.

Decontamination is accomplished by simple irrigation or gentle washing with soap and water starting at the outside of the area and circling inward. First washes have the greatest chance of removing large amounts of contaminated material. Do not scratch or abrade intact skin while trying to get it clean or you risk internal contamination. Care must be taken not to spread contamination through splashes or water spills. Field dressings and embedded particles should be removed using tongs to maintain as much distance between a possible source and your fingers as you can. Decontamination should continue until efforts are no longer giving you lower survey readings. Decontaminated wounds should be bandaged with sterile waterproof dressings.⁵

The dose received is determined by dosimeter readings; biological changes are determined by lab tests, accident reconstruction models, and other methods.^9,13 Dose can be estimated by observing the onset of signs and symptoms, especially vomiting, and observation of lymphocyte depletion.^1,7<