Bioterrorism and Weapons of Mass Destruction

A small amount of cyanide exposure can quickly lead to an array of symptoms, some of which include (CDC, 2024f; Williams et al., 2023):

• Chest pain and/or palpitations
• Dyspnea or wheezing
• Tachycardia or bradycardia
• Tachypnea or bradypnea
• Headache, weakness, and/or dizziness
• Nausea and/or vomiting
• Cyanosis
• Metabolic acidosis
• Serious adverse effects: Serious adverse effects often occur with higher levels of exposure and include hypertension or hypotension, seizures, coma, or death.

If cyanide exposure occurs, patients should be placed immediately on 100% supplemental oxygen. Some patients will require mechanical ventilatory support. Injections of sodium thiosulfate (two vials of 12.5 grams [G]/50 milliliter [mL], sodium nitrate (2 ampules of 300 milligrams [mg]/10 mL), and hydroxocobalamin (5 G) are administered. Additionally, ampules of the inhalant amyl nitrite are administered for treatment. Patients are closely monitored for hemodynamic stability, and blood levels are drawn for monitoring and development of further complications (Williams et al., 2023).

Healthcare clinicians should carefully remove the individual's clothing and bag it in the proper plastic bag (in some cases, only double plastic bagging is available). Then, place the bag in the designated disposal area (it cannot be discarded in regular trash) and call the local authorities for disposal pickup. When possible, do not attempt to remove clothing over the person’s head, as this can worsen exposure and cause respiratory and skin symptoms to become more severe. Blot any liquid from the patient’s body with dry towels or cloths. The most effective method for removing liquid cyanide from the skin is to shower or wash the affected area thoroughly. If possible, gently wash the person’s body with lukewarm water and mild soap for about 90 seconds, starting with the face, hair, and hands. Do not scrub the individual’s skin and avoid areas like the eyes, nose, and mouth. Once washed, rinse with water for about 30 seconds (CDC, 2024f).

Mustard gas has a prolonged symptom onset, where signs and symptoms do not appear immediately and can take up to 24 hours. The signs and symptoms of this blistering agent depend on the area of the body affected, and can include (CDC, 2024h; Williams et al., 2023):

• Skin itching, pain, redness, and blisters
• Weakness
• Diarrhea
• Nausea and/or vomiting
• Eye tearing, pain, swelling, and/or blindness
• Cough, difficulty breathing, wheezing, and/or dyspnea
• Increased susceptibility to infections
• Reduced blood cell production
• Reduced platelet formation
• Serious adverse effects: Serious adverse effects are more likely when exposed to large amounts of mustard gas. Adverse effects like convulsions, pulmonary edema, insomnia, permanent blindness, respiratory failure, and death may occur.

Lewisite is another blistering agent that was produced during World War I but was never used. This liquid blistering agent, in its purest form, has an oily and colorless appearance. When in an impure liquid form, it ranges in color from amber to black. Some individuals report that Lewisite smells like geraniums. Lewisite contains arsenic, which makes it highly poisonous. Symptoms develop within minutes of exposure (CDC, 2024g). Lewisite exposure can cause a constellation of symptoms, such as (CDC, 2024g; Williams et al., 2023):

• Eye tearing, pain, and/or swelling
• Cough, bloody nose, wheezing, and/or dyspnea
• Diarrhea
• Nausea and/or vomiting
• Serious adverse effects: Again, there is an increased likelihood of serious adverse effects with a larger exposure to Lewisite. Adverse effects such as hypotension and “Lewisite shock” are possible.

If exposed to blistering agents, it is imperative to remove clothing, blot any visible liquid, and gently wash the body with mild soap and water. Healthcare clinicians should follow institutional protocols and clothing disposal procedures. Unfortunately, mustard gas has no antidote or cure, so supportive treatment is indicated. For patients exposed to Lewisite, the antidote called British anti-lewisite is available, which should be administered immediately. After antidote administration, supportive care is given (CDC, 2024b; CDC, 2024g; Williams et al., 2023).

Blistering agents can cause long-term health effects. For sulfur mustard, long-term effects like second and third-degree burns, skin scarring, and skin cancer are highly likely. Temporary or permanent blindness is possible, as well as recurrent eye infections. In addition, long-term respiratory complications like chronic respiratory diseases, infections, and cancers are possible (CDC, 2024h). Lewisite can still result in skin scarring and burns, but it is less likely when compared to sulfur mustard. Other long-term complications, like permanent blindness and respiratory diseases, may develop after exposure (CDC, 2024g).

Chlorine gas exposure is primarily a respiratory irritant, but can also contribute to the development of other symptoms, like (CDC, 2024b; Morim & Guldner, 2023):

• Burning of the eyes, throat, and/or lungs
• Skin blistering and redness
• Eye tearing, burning, or blurry vision
• Cough
• Chest tightness
• Shortness of breath
• Nausea and/or vomiting
• Frostbite (with liquid chlorine exposure)
• Severe adverse effects: More severe effects may develop, such as pulmonary edema, acute lung injury, and acute respiratory distress syndrome (ARDS).

Similar to chlorine, phosgene is a respiratory chemical agent that comes in both liquid and gaseous forms. It is also known as CG, is colorless to pale yellow in color, and smells like freshly mown hay or green corn (CDC, 2024i). Signs and symptoms of phosgene exposure may not show up until about 48 hours after exposure and include (CDC, 2024i; Williams et al., 2023):

• Cough
• Chest tightness
• Nausea and/or vomiting
• Burning of the eyes, throat, and/or lungs
• Skin irritation, redness, and pain
• Frostbite (with liquid exposure)
• Severe adverse effects: Severe adverse effects, such as heart and respiratory failure, pulmonary edema, hypotension, and dyspnea, typically appear 48 hours after exposure.

If exposure to pulmonary agents occurs, it is important to get away from the area where the exposure occurred (find an area of fresh air). Most pulmonary agent gases are heavier than air, so do not crawl when attempting to get away from the area, since it exponentially increases the risk of exposure. Again, clothing is removed and properly disposed of, and the skin is blotted with a towel and gently washed. Treatment for chlorine and phosgene gas exposure is supportive since there is no known antidote or cure. Supportive care measures should include the administration of supplemental oxygen (via nasal cannula or mechanical ventilation in more severe cases) and managing secretions by suctioning. If chlorine liquid is ingested, do not induce vomiting (CDC, 2024b; CDC, 2024i; Williams et al., 2023). Treatment for other pulmonary agents, such as nitrogen oxides, is also supportive. If patients are exposed to nitrogen oxides and develop pulmonary edema, administration of high-dose steroids, intubation, and mechanical ventilation is warranted. The positive end-expiratory pressure (PEEP) should be maintained at a partial pressure of oxygen of at least 60 millimeters of mercury (mmHg)(Williams et al., 2023).

Chemical pulmonary agents can cause long-term health effects. Fortunately, most patients who experience short-term exposure to chlorine will return to normal lung function within two weeks and make a complete recovery. However, in some cases, long-term pulmonary diseases may develop, like reactive airway dysfunction syndrome (RADS) (CDC, 2024b). Individuals exposed to phosgene are also likely to recover completely, but may have chronic respiratory problems like bronchitis, emphysema, and RADS (CDC, 2024i).

Once exposure occurs, symptoms can develop within a few minutes to hours (CDC, 2024l; Williams et al., 2023):

• Blurry vision or watery eyes
• Cough
• Chest tightness
• Drooling
• Increased urination
• Pinpoint pupils
• Hypotension or hypertension
• Bradycardia or tachycardia
• Severe adverse effects: Convulsions, loss of consciousness, respiratory failure or arrest, and paralysis.

Sarin, also known as “GB,” is another colorless, tasteless, odorless chemical nerve agent. Individuals exposed to this nerve agent can develop (CDC, 2024k; Williams et al., 2023):

• Blurry vision or watery eyes
• Cough
• Diarrhea
• Nausea and/or vomiting
• Drooling and/or excessive sweating
• Increased urination
• Pinpoint pupils
• Hypotension or hypertension
• Bradycardia or tachycardia
• Severe adverse effects: Convulsions, seizures, paralysis, coma, loss of consciousness, and the potential for cardiac or respiratory arrest leading to death.

These lists are not exhaustive of the signs and symptoms that may develop from nerve agent exposure.

As with most other chemical agents, healthcare professionals should remove the individual from the area where exposure occurred, carefully remove the person’s clothing, and blot areas of liquid exposure with dry cloths. When available, the patient should then be gently washed with mild soap and water.

The management and treatment for patients exposed to all types of nerve agents are similar. The healthcare clinician, first responder, or first receiver should administer atropine every 5-10 minutes until secretions begin to dry. Three injections (roughly 600 mg) of 2-PAM CL are also given within a few minutes. These medications are given as soon as possible to reduce the possibility of severe health effects. Additionally, clinicians provide supportive care measures like life-saving procedures, hemodynamic stability, supplemental oxygen, and monitoring (CDC, 2024l; CDC, 2024k; Williams et al., 2023).

Although most people recover with no lasting effects from nerve agent exposure, some may develop long-term health issues. Examples of long-term health effects are paralysis, nerve pain, muscle weakness, and neuropathy. Individuals who are exposed to higher doses of nerve agents are unlikely to survive (CDC, 2024l; CDC, 2024k).

Incapacitating agents differ from riot control agents based on their intended effects. Incapacitating agents are intended to produce systemic effects, whereas riot control agents produce localized reactions or irritation. Signs and symptoms of incapacitating agents are (Williams et al., 2023):

• Dry mouth
• Runny nose
• Dyspnea
• Dizziness and/or confusion
• Tachycardia
• Hypertension 

Riot control agents can produce irritative symptoms, including excessive eye tearing or burning, skin burns and rash, and mouth and nose burning, as well as difficulty swallowing. Nausea and vomiting, coughing, and chest tightness are also possible. Lasting exposure to incapacitating agents can cause more severe adverse effects, such as blindness, glaucoma, and chemical burns to the respiratory tract, leading to respiratory failure and, ultimately, death (CDC, 2024j).

Patients exposed to incapacitating agents should flush their eyes, mouth, and skin as much as possible to remove the biohazard. Furthermore, supportive care measures are instituted. Many individuals require supplemental oxygen to prevent the worsening of chemical burns, as well as bronchodilators and steroids to open the airways. Skin burns are treated according to burn management protocols, which entail gently washing the affected areas and applying bandages (CDC, 2024j; Williams et al., 2023).

Smallpox, also known as the variola major virus, is a highly contagious virus that was eradicated in the 1980s but still exists in small research laboratories today. Once exposed to the virus, individuals develop symptoms within 12 to 14 days, including (Rathish et al., 2023; Reed-Schrader et al., 2023):

• High-grade fever
• Malaise
• Headache
• Myalgias
• Other flu-like symptoms

The lesions of smallpox develop about one to two days after symptom onset. Initially, the lesions appear toward the center of the body and then spread outward to the face, extremities, and palms of the hands and soles of the feet. Furthermore, initial skin lesions are flat and red (macular) but then develop into painful, fluid-filled pustules over the next several days. Those infected with smallpox are considered contagious during the week in which their rash appears. Once the blisters start to heal and scabs separate, the person is no longer contagious (Rathish et al., 2023; Reed-Schrader et al., 2023).

The diagnosis of smallpox is based on the patient’s clinical presentation. However, healthcare providers may order laboratory tests and collect specimens, which are then sent to a specialized processing facility to confirm the diagnosis. Specialized lab tests may include polymerase chain reaction (PCR) for the variola virus, electron microscopy, or a viral culture (not routinely ordered). Laboratory testing is not generally recommended for people with known exposure to smallpox. However, if smallpox is suspected, and exposure is unknown, then PCR testing is recommended.

Since smallpox is highly contagious, healthcare clinicians should immediately institute isolation precautions. Placing patients in a negative-pressure room without any other patients is necessary to reduce transmission and outbreaks. Healthcare clinicians should wear proper PPE when entering the patient's room or providing care. Proper PPE entails both contact and airborne precautions, so providers must wear an N95 mask, goggles, gloves, and a gown. In addition, proper channels, such as the public health department and/or the CDC, are notified of the potential smallpox case. They can help determine if testing is recommended. If smallpox is suspected and viral testing is recommended according to the guidelines (typically following an unknown exposure), then PCR testing is warranted. The laboratory test to confirm smallpox can only be performed in specialized labs, such as the CDC or an approved Biosafety Level 4 lab. These authorities may also help with contact tracing and monitor close contacts of the infected patient for signs and symptoms. There is no cure for smallpox, so treatment is supportive care (fluid replacement and antibiotics for secondary skin infections, if necessary). Antiviral medications have not been proven to be an effective treatment, so they are not typically prescribed. Although the U.S. Food and Drug Administration (FDA) has approved two medications, Tecovirimat and Brincidofovir, for use, they are not routinely prescribed due to the lack of human studies and well-proven efficacy. Vaccination against smallpox is the best method of prevention and can lessen the severity of symptoms if a person becomes infected. Routine vaccination against smallpox is not available since the virus was claimed to be eradicated; however, some military personnel and first responders may receive the vaccine due to their increased likelihood of exposure (CDC, 2024d; Rathish et al., 2023; Reed-Schrader et al., 2023).

The group of viral hemorrhagic fevers encompasses viruses such as Ebola, Hantavirus, Dengue, and Marburg, among others, which can lead to severe bleeding and fever. From the group, Ebola and Marburg are the deadliest, with a mortality rate ranging from 50% to 90% (Reed-Schrader et al., 2023). Symptom onset depends on the type of virus. Individuals infected with Ebola and Marburg virus typically develop symptoms within 2 to 21 days of exposure, whereas those infected with Machupo virus develop symptoms within 3 to 16 days. People who are infected will develop signs and symptoms, such as (CDC, 2025e; Williams et al., 2023):

• Fever
• Fatigue
• Chills
• Myalgias
• Other flu-like symptoms
• Nausea and/or vomiting
• Petechiae
• Bleeding from orifices
• Hypoglycemia (common with Ebola)
• Severe adverse effects: As viral hemorrhagic fevers progress, patients develop hypotension, multiple organ failure, and hypovolemic shock from bleeding (loss of blood volume) and cardiovascular collapse, which eventually result in death.

Patients with viral hemorrhagic fevers should be placed in strict isolation and PPE precautions. Those infected individuals are placed in a single-patient room, and strict airborne precautions are implemented. If entering the patient’s room with suspected viral hemorrhagic fever, clinicians should wear a disposable fluid-resistant gown or coveralls, a full-face shield, a facemask (N95 or PAPR), and two pairs of single-use gloves with extended cuffs. If the patient has confirmed viral hemorrhagic fever or exhibits signs of bleeding, diarrhea, or vomiting, then additional PPE is worn, including mid-calf boot covers and a torso apron (CDC, 2025e).

There is no cure for any type of viral hemorrhagic fever, so treatment is focused on supportive care measures (Williams et al., 2023). Many antiviral medications are not FDA-approved or are only readily available in countries with a high risk of infections and outbreaks. However, for the treatment of Ebola, two monoclonal antibody medications are FDA-approved: Ebanga and Inmazeb. These medications can be requested by contacting the CDC's viral pathogens department. Patients become dehydrated due to blood and fluid loss, so intravenous (IV) fluids are carefully administered to prevent fluid overload. Supplemental oxygen is provided, and additional measures and medications are implemented for hemodynamic monitoring and stability (CDC, 2025e).

The signs and symptoms of individuals infected with fungi vary from person to person. Depending on the extent of exposure, patients can develop infections, ranging from mild skin infections to pneumonia. Histoplasmosis, caused by Histoplasma capsulatum, contributes to symptoms like:

• Cough
• Chills
• Fatigue
• Fever
• Chest pain or tightness
• Myalgias and/or arthralgias

Coccidioides immitis causes coccidiomycosis, which is also known as valley fever. Patients infected with Coccidioides immitis often do not have symptoms. However, if symptoms occur, they are similar to those of histoplasmosis. Patients with coccidioidomycosis are more likely to develop lung nodules, hemoptysis, and weight loss (Oliveira et al., 2023).

Healthcare professionals should abide by respiratory and standard PPE precautions when caring for patients with fungal infections. Depending on the extent and type of the individual’s illness, wearing an N95 (for airborne precautions) or a surgical mask (for droplet precautions) is warranted. Care measures, such as administering supplemental oxygen, IV fluids, and patient monitoring, are taken. Antifungal medications are prescribed for treatment. Blood work and cultures may be drawn to determine the exact pathogen and its susceptibility to fungal medications. Typical treatments include systemic azoles (e.g., fluconazole), echinocandins (e.g., micafungin), and antimetabolites (e.g., flucytosine) or polyene therapy (Oliveira et al., 2023).

Ricin is a toxic biological agent derived from the seeds of the castor bean or oil plant. This plant is a common household plant, making it difficult to limit the production of this toxin. Ricin is available in three forms: injection, oral, and inhalation. Inhalation is the deadliest form, and even small amounts can be fatal (Williams et al., 2023).

Castor Bean Plant

• Cough
• Diarrhea
• Nausea and/or vomiting

• Abdominal pain 
• Fever
• Weakness
• Hypotension
• Seizures
• Severe adverse effects: If inhaled or ingested, airway symptoms like edema, hemorrhage, and necrosis lead to necrotizing pneumonia and tracheobronchitis. Eventually, shock occurs and results in death (Reed-Schrader et al., 2023; Williams et al., 2023).

If confirmed or suspected ingestion occurs, gastric charcoal lavage should be immediately initiated. If skin or respiratory exposure occurs, immediately remove clothing and wash the body with mild soap and water. Shock from ricin poisoning can be difficult to distinguish from sepsis, as many of their signs and symptoms overlap. Additional treatment measures are supportive, like administering supplemental oxygen, IV fluids, and medications to control blood pressure (vasopressors to aid with hypotension) and prevent seizures (Reed-Schrader et al., 2023; Williams et al., 2023).

Abrin is another toxic biological agent that is roughly 30 times more deadly than ricin. It is derived from the seeds of the rosary pea and inhibits the ribosome protein pathway. Abrin can be ingested or inhaled, causing symptoms to appear within 8-24 hours of exposure, and ultimately, death within 36 to 72 hours. If exposed or ingested, the signs and symptoms are (Williams et al., 2023):

• Eye irritation, redness, and tearing
• Cough and/or chest tightness
• Sweating
• Nausea and/or vomiting
• Abdominal cramping/pain and/or diarrhea
• Blood in the urine (hematuria)
• Severe adverse effects: A small amount of abrin exposure via mist can result in retinal hemorrhage, blindness, and systemic toxicity. Gastrointestinal bleeding, cyanosis, and respiratory failure may also occur.

The management and treatment of poisoning from abrin are similar to those of ricin poisoning. If ingested, administration of activated charcoal and gastric lavage is indicated. In the event of eye exposure, thoroughly flushing the eyes with water or saline can help remove the toxin. Since abrin poisoning has no known cure, treatment involves implementing supportive care measures, such as administering supplemental oxygen, IV fluids, and medications to maintain hemodynamic stability, as indicated. Additionally, airway management and mechanical ventilation may be necessary measures (Williams et al., 2023).

Anthrax is a type of gram-positive bacterium (Bacillus anthracis) found in the soil that is transmitted through the handling of animal products. Since it creates spores, anthrax is easily absorbed through the skin. It is one of the most dangerous biological agents that is readily absorbed through inhalation. Thus, many federal employees are vaccinated against anthrax. However, the vaccination takes three doses (injections) to become effective. If exposed, individuals can develop symptoms within 1-7 days, such as (Reed-Schrader et al., 2023; Williams et al., 2023):

• Skin symptoms: Itchy papular or macular rash, ulcerations, or eschar
• Edema and/or lymph node swelling
• Nausea and/or vomiting (sometimes bloody vomit)
• Abdominal pain (can lead to a perforated bowel)
• Cough
• Difficulty breathing
• Fever
• Severe adverse effects: Severe effects like hemorrhagic mediastinitis (bleeding and inflammation of the mediastinum space), hemodynamic instability, and respiratory failure are likely.

If left untreated, the fatality rate of anthrax exposure is greater than 20%, and less than 1% if treated (Williams et al., 2023).

Fortunately, anthrax is not readily transmitted from one individual to another, so standard and contact precautions are used when caring for patients who have been exposed. The diagnosis of anthrax exposure is confirmed through bloodwork, which measures the presence of antibodies or anthrax toxin in the bloodstream. It can also be confirmed by collecting a swab from a skin lesion, respiratory secretions, or a cerebrospinal fluid sample. If anthrax inhalation occurs, a chest X-ray or computed tomography (CT) scan of the lungs may show mediastinal widening with or without a pleural effusion (CDC, 2025b).

If anthrax exposure is suspected, prompt treatment is recommended. Healthcare providers should not wait for bloodwork and other test results to return. Administration of IV antibiotics is the mainstay of treatment, and patients may be converted to oral antibiotics once stabilized. Antibiotics that are FDA-approved and effective against anthrax include doxycycline, ciprofloxacin, and penicillin. In some cases, erythromycin and vancomycin may be given, though the FDA does not approve these (CDC, 2025b; Williams et al., 2023). Additionally, anthrax is a reportable disease, where healthcare clinicians must report suspected or confirmed cases to state or federal authorities (CDC, 2025b).

Post-exposure prophylaxis (PEP), which prevents anthrax from developing in individuals without symptoms who are exposed, involves taking either ciprofloxacin or doxycycline, both antibiotics. Since anthrax can lie dormant in the body for up to 60 days, a 60-day PEP course of either of these antibiotics is prescribed. Again, anthrax vaccination (administered in three doses) is recommended for federal employees aged 18 to 65 who are at a higher risk of exposure (CDC, 2025b).

Botulism is a deadly neurotoxin produced by the bacteria Clostridium botulinum. Exposure typically occurs through ingestion of contaminated food; however, it can also develop if a wound becomes infected. Symptoms develop within several hours to days after exposure, including (CDC, 2024c; Reed-Schrader et al., 2023; Williams et al., 2023):

• Double or blurred vision
• Drooping eyelids (ptosis)
• Difficulty with speech and swallowing (dysphagia)
• Muscle weakness, often starting in the face
• Severe adverse effects: Botulism is deadly, where individuals have descending muscle weakness and paralysis, ultimately leading to respiratory failure.

Unfortunately, botulism is frequently misdiagnosed because it resembles other diseases that also contribute to muscle weakness and paralysis, such as stroke, Guillain-Barré syndrome, myasthenia gravis, and Miller-Fisher syndrome. A key way to differentiate botulism from these other diseases is that botulism typically presents as symmetric flaccid paralysis, beginning in the cranial nerves of the face, and also affects both motor and autonomic nerve pathways (CDC, 2024c).

If botulism is suspected, healthcare clinicians must immediately notify state or federal authorities and the CDC. Usually, the local health department will have a clinician with expertise to confirm the diagnosis clinically and order the antitoxin for treatment. There are two forms of antitoxin: Botulism Antitoxin Heptavalent (for adults) and BabyBIG (for infant botulism). This medication neutralizes botulism in the bloodstream and prevents progressive worsening of paralysis. However, it does not immediately reverse the damage that has already been done. Treatment with antitoxin is initiated before botulism is confirmed via laboratory testing of stool, blood, or wound (CDC, 2024c).

Patients with botulism require intensive care treatment, including supportive measures such as supplemental oxygen and medications to maintain hemodynamic stability. Intensive monitoring of respiratory compromise is warranted, as patients can develop respiratory paralysis. If this occurs, mechanical ventilatory support is necessary. Additionally, monitoring for potential complications, including urinary tract infections, pressure injuries, and deep vein thromboses, is also indicated, as botulism can rapidly progress in these areas as well. Wound debridement alongside the administration of antibiotics is necessary for patients with wound botulism.

Patients with botulism take several months to recover, especially if they require mechanical ventilation. Nerve tissue takes several months to regenerate, and intense physical, occupational, and speech therapy is needed, as well as psychological support (CDC, 2024c).

Tularemia, also known as rabbit fever, is caused by the bacterium Francisella tularensis. It is an illness commonly found and spread through infected ticks, flies, contaminated water or dust, and other infected animals. If infected, individuals develop classic symptoms like (Reed-Schrader et al., 2023; Williams et al., 2023):

• Fever
• Cough
• Chest pain and/or tightness
• Adenopathy
• Severe adverse effects: Tularemia can develop into pneumonia and a systemic infection.

Tularemia is often mistaken for other febrile illnesses since many of its symptoms overlap. If tularemia is suspected, blood cultures and tests help confirm the diagnosis. The cornerstone of treatment is IV streptomycin for 10 to 21 days, although gentamicin may be given as an alternative. Supportive patient care measures are also implemented. Fortunately, most patients recover from tularemia (Reed-Schrader et al., 2023; Williams et al., 2023).

The plague, also known as the bubonic plague, is caused by the bacterium Yersinia pestis. It is a highly contagious illness transmitted through an insect bite to the skin by an infected rat flea. This disease has the potential for aerosolization, causing pneumonic plague. Once infected, rapid symptoms develop (Reed-Schrader et al., 2023; Williams et al., 2023):

• Fever and/or chills
• Malaise
• Myalgias
• Cough with blood-tinged sputum
• Enlarged lymph nodes (buboes)
• Severe adverse effects: Hypotension and pulmonary complications like pneumonia and pulmonary edema can quickly evolve. Other complications include sepsis, meningitis, and organ failure.

Healthcare professionals should implement isolation and droplet precautions for patients suspected of or with confirmed plague. Treatment involves supportive care measures and antibiotic administration. Appropriate IV antibiotics for treatment include streptomycin, gentamycin, ciprofloxacin, and doxycycline. If patients develop meningitis, chloramphenicol is also administered. For individuals exposed to the plague but without symptoms, PEP coverage entails either ciprofloxacin or doxycycline (Reed-Schrader et al., 2023; Williams et al., 2023).

Q fever is caused by the bacterium Coxiella burnetii, which is commonly found in animals such as dogs, cats, sheep, cows, and goats, and is spread through contact with their feces, urine, or other secretions. This bacterium can survive in a wide temperature range and for up to 60 days on surfaces. Once exposure occurs, symptoms take about 2-3 weeks to develop, and include (Reed-Schrader et al., 2023; Williams et al., 2023):

• Fever and/or chills
• Malaise
• Myalgias and/or arthralgias
• Nausea, vomiting, or diarrhea
• Severe adverse effects: Pneumonia, ARDS, endocarditis, and granulomatosis hepatitis can occur with Q fever. Some patients develop chronic Q fever, which can last for several years.

Infected patients are managed with supportive care measures as well as antibiotics. Doxycycline is the preferred treatment, but alternatives include clarithromycin, ciprofloxacin, and rifampin. For patients who develop chronic Q fever, long-term treatment regimens, such as doxycycline and a quinolone or hydroxychloroquine, are indicated (Williams et al., 2023).

Cholera is a bacterial infection caused by the bacterium Vibrio cholerae, which can live in the water supply. Thus, water supply and water treatment facilities pose a threat from biological agent attacks. Cholera causes a dangerous diarrheal infection, and sometimes, accompanying symptoms are nausea and vomiting. Due to the extent of the diarrhea and vomiting, dehydration is one of the most common complications of this illness (Williams et al., 2023).

Patients with cholera are treated with supportive care measures. Since dehydration is common with this illness, administering IV fluids and electrolytes for rehydration therapy is indicated. Oral rehydration salts are another form of therapy, where patients drink prepackaged powders containing salts and minerals that are mixed with water. In addition, patients are educated to avoid consuming drinks that have a high sugar content since they will worsen symptoms. In some cases, antibiotics are administered to shorten the course of the illness. Fortunately, most patients survive cholera if fluid replacement therapy is initiated early on (Williams et al., 2023).

Melioidosis is a bacterial infection caused by the gram-negative bacterium Burkholderia pseudomallei, which is often found in the water and soil. This bacterium has the potential to be used as a biological weapon. The incubation period for this illness ranges from 1-21 days (acute infection) but can also last for many years (chronic). Thus, it is also referred to as the “Vietnam time bomb.” The patient mortality rate ranges from 10% to 80% for uncomplicated cases to those who develop sepsis, respectively. Four types of infection can develop, including pulmonary, localized, blood-borne, and disseminated. Acute symptoms range from fever and cough with pleuritic chest pain to bone or joint pain. Abscesses can develop within the abdomen, affecting organs like the liver, spleen, or prostate. People with chronic melioidosis will have symptoms for two months or more and have chronic skin infections, lung nodules, and pneumonia (Williams et al., 2023).

Since patients with melioidosis can develop abscesses, ultrasound and CT imaging should be performed, especially for patients with abdominal or vague symptoms. On CT, melioidosis abscesses have a characteristic “Swiss cheese” or “honeycomb” pattern. For patients who develop septic arthritis or abscesses of the prostate or parotid glands, surgical drainage is warranted. Additional treatment of this illness involves administering IV ceftazidime over the course of 10 to 14 days. Other antibiotic alternatives are imipenem, meropenem, and cefoperazone-sulbactam. In some cases, IV amoxicillin-clavulanate may be administered, but only if the previous antibiotics are not available. After initial treatment, antibiotic maintenance therapy is recommended for 12 to 20 weeks. Maintenance therapy includes coadministration of co-trimoxazole and doxycycline (Williams et al., 2023).

Since the food chain or system is vulnerable to contamination and serves as a natural vehicle for microbes, foodborne bacteria can be utilized as a biological weapon to target populations. Common bacteria that can contaminate food are Salmonella, Shigella, and Escherichia coli (E. coli). If a person consumes food contaminated with bacteria, they may develop signs and symptoms like the following (Williams et al., 2023):

• Diarrhea
• Nausea and/or vomiting
• Abdominal bloating and cramping

Dehydration often results from fluid loss. Treatment for individuals infected with any type of food-borne bacterium involves rehydration with fluids and other supportive care measures. Antibiotics are typically reserved for patients with severe cases of foodborne illnesses.

One of the most common illnesses that can develop from radioactive material exposure is acute radiation syndrome. This syndrome occurs when an individual’s entire body or a large portion of their body is exposed to a high amount of external radiation (greater than 0.7 Gy or 70 rads) over a very short period of time. A common source of this is nuclear devices, atomic bombs, and, in some cases, unintentional exposures to sterilization irradiators. Examples of people who developed acute radiation syndrome throughout history are those affected by the Hiroshima and Nagasaki bombs and the Chernobyl Nuclear Power Plant event (CDC, 2024a).

Acute radiation syndrome is classified into three main types:

1. Bone marrow syndrome: This syndrome is also sometimes called hematopoietic syndrome, where radiation exposure causes bone marrow cells to die. Symptoms like fever, lack of appetite, and malaise are common with hemopoietic syndrome. Since blood cells are destroyed, the patient’s blood cell counts will drop. Subsequently, infection and hemorrhage result, often leading to death due to multisystem organ failure. Low doses of radiation at about 0.3 Gy can cause symptoms, but usually, full-blown bone marrow syndrome develops anywhere ranging from 0.7 to 10 Gy.
2. Gastrointestinal syndrome: Symptoms of gastrointestinal syndrome can develop at around 6 Gy, but full-blown gastrointestinal syndrome occurs when exposed to 10 Gy or more. Patients who develop this radiation gastrointestinal syndrome will also have bone marrow syndrome, destroying gastrointestinal and bone marrow cells and tissues. Symptoms of gastrointestinal syndrome are severe bloody diarrhea, weight loss, nausea, and vomiting. Complications like infection, dehydration, electrolyte imbalances, and hemorrhage often result in death within about two weeks.
3. Cardiovascular and central nervous system syndrome: This syndrome is also called cerebrovascular syndrome of ARS. Individuals exposed to very high amounts of radiation (50 Gy or more) will develop cardiovascular and nervous system symptoms. Lower doses, at about 20 Gy, can also lead to these syndromes. Patients will have convulsions, watery diarrhea, and loss of consciousness or fall into a coma. Destruction of cardiovascular and nervous system cells and tissues leads to complications like shock, increased intracranial pressure, edema, meningitis, and vasculitis. Typically, patients with these syndromes will die within three days. Those exposed to greater than 100 Gray will die within a few hours (CDC, 2024a; Williams et al., 2023).

There are four stages of acute radiation syndrome, which include:

1. Prodromal stage (prodrome): Also called the N-V-D stage, it is the first stage, which happens within minutes or days of radiation exposure. The three classic symptoms of the prodromal stage are nausea, vomiting, and diarrhea; hence the name N-V-D. Other symptoms, like anorexia and abdominal cramping, are common. The prodromal stage can last several days, but sometimes occurs for minutes or episodes. The earlier an individual develops prodromal symptoms, the higher the likelihood of a poor health prognosis.
2. Latent stage (clinical latency): This is the second stage of acute radiation syndrome, where patients may feel and look healthy. The latent stage can last anywhere from a few hours to several weeks.
3. Manifest illness stage (clinical manifestations): This is the third stage of acute radiation syndrome, where patients develop specific symptoms related to the exposure amount and acute radiation syndrome classification (hematopoietic, gastrointestinal, and cerebrovascular). The manifest illness stage can last from a few hours to several months.
4. Recovery or death: Patients in this last stage will either begin to recover from acute radiation syndrome within several weeks to up to two years. Unfortunately, patients who do not begin to recover will die. Patients with cerebrovascular syndrome are not expected to recover (CDC, 2024a; Williams et al., 2023).

Treatment of acute radiation syndrome involves a team of healthcare professionals simultaneously working together to provide prompt assessment and patient care. If radiation exposure is suspected or confirmed by the patient or another individual, the healthcare team provides triage measures like:

• Start by assessing the patient’s ABCDEs (airway, breathing, circulation, disability, and exposure) and providing proper care measures in a stepwise fashion. First, ensure the patient’s airway is stable. If stable, then move to assessing their breathing, and then once breathing is stable, move to circulation, and so on and so forth (ABC assessment). Health clinicians should also initiate appropriate physiologic monitoring (e.g., blood pressure, blood gases, electrolytes, and urine output).
• Healthcare providers should address any major traumatic burns or respiratory injuries immediately.
• In addition to trauma-related labs, clinicians collect blood samples for:
  • Complete blood count (CBC) to assess blood counts, with particular attention to the patient’s lymphocyte count. If the patient was exposed to radiation within the last 12 hours, repeat CBCs are taken every 2-3 hours, two to three times over eight hours, to look for signs of lymphocyte count decline.
  • Human leukocyte antigen (HLA typing) for possible blood transfusion. This is always collected before any transfusion and at intervals after transfusion.
  • Perform external decontamination if contamination is suspected (CDC, 2024a; Williams et al., 2023).

Acute radiation syndrome is challenging to diagnose because it presents with nonspecific signs and symptoms. After initial triage, other diagnostic tools can help with the diagnosis of acute radiation syndrome. Again, depending on the radiation dose, the prodromal phase may be delayed for several hours or days. However, the patient may appear healthy despite significant exposure, meaning they may already be in the latent phase upon evaluation. Therefore, it is important to monitor the patient’s blood counts by following these parameters closely:

• If the patient’s radiation exposure exceeded 0.05 Gy or five rads, 3-4 CBCs are performed within the first 8-12 hours. Monitoring the blood count trends helps provide an early estimate of the patient’s radiation exposure dose.
• If initial blood samples are not taken, radiation dose estimation is still possible using CBC trends over the next several days. Ideally, a radiation dosimetrist should perform this analysis, so they should be consulted immediately. Radiation dosimetrists work alongside healthcare providers to help assess the patient’s level of possible radiation exposure and develop a treatment plan.
• For patients with a known or suspected exposure to a high radiation dose, several CBC studies are taken. These are drawn every 2-3 hours during the first eight hours and then repeated every 4-6 hours over the next 48 hours.
• If no radiation exposure is suspected, patients are always observed for clinical signs and symptoms (e.g., nausea, vomiting, bleeding, hair loss, and declining or low white blood cell and platelet count). Consultation with a radiology specialist or dosimetrist should always be performed before excluding the possibility of acute radiation syndrome (CDC, 2024a; Williams et al., 2023).

After the initial patient triage and bloodwork is drawn, initial additional patient care measures include:

• Treat vomiting as needed by administering antiemetics.
• Repeat bloodwork as indicated and ordered by the healthcare provider or radiation dosimetrist.
• Additional orders to consider are prophylactic treatment measures, tissue and blood type, and crossmatch. Monitoring trends in the patient’s absolute lymphocyte counts is of utmost importance. The radiation dosimetrist typically monitors these trends, who uses the Andrews Lymphocyte Nomogram to determine the severity of radiation injury.

Andrews Lymphocyte Nomogram

• A chromosome aberration cytogenetic bioassay test is the best method to assess the amount of radiation exposure.
• Nurses and other health clinicians must monitor and document all clinical symptoms carefully, especially if patients develop symptoms like nausea, vomiting, diarrhea, weight loss, fever, and any skin changes (itching, redness, blistering). Taking and documenting photographs of the patient’s skin can be helpful. Additionally, clinicians should record the exact time of symptom onset for accurate assessment and staging.
• The patient should be placed on neutropenic precautions and transferred to a burn intensive care unit. Neutropenic precautions are necessary since the patient’s blood count will drop, which significantly increases their risk of infection.
• The nurse or healthcare provider should call the Radiation Emergency Assistance Center/Training Site (REAC/TS) for consultation with radiation exposure experts and to report it to the Radiation Accident Registry System (CDC, 2024a; Williams et al., 2023).

Other care measures include:

• Gastric lavage with charcoal and fluids to reduce the absorption of radioactive agents.
• Administer radioactive iodine mixed with potassium iodide to reduce the thyroid uptake of the radioactive materials.
• Penicillamine helps to reduce tissue uptake of radioactive metals and increase their excretion from the body.
• Stem cell transplants and platelet transfusions may be necessary, especially if the patient’s platelet count becomes low.
• Antibiotics, cytokines, fluids, and electrolytes may also be administered.
• For patients whose neutrophil count drops to less than 500 cells/cubic millimeter (mm3), prophylactic antibiotics, antivirals, and antifungals may be ordered as well.
• Hematopoietic growth factor, such as filgrastim, is given to patients with hematopoietic syndrome to stimulate the production of new blood cells.
• For cesium exposure, ferric hexacyanoferrate helps reduce gastrointestinal absorption. 
• For americium, plutonium, and curium exposure, agents like Ca-DTPA and Zn-DPTA (calcium- or zinc-diethylenetriamine pentaacetate) may be administered (CDC, 2024a; Williams et al., 2023).

For patients with any form of acute radiation syndrome, psychological support is warranted and is a critical component of the overall management of patients with acute radiation syndrome. The physical effects of radiation exposure, along with the fear and uncertainty surrounding their prognosis, can lead to significant emotional and psychological distress. Acute radiation syndrome can lead to increased anxiety, depression, panic, post-traumatic stress symptoms, as well as feelings of isolation or hopelessness (CDC, 2024a).

Acute radiation exposure to the skin can result in a cutaneous radiation injury (CRI). These types of injuries are common in individuals with a small area of exposure, especially if the radiation comes from beta or X-rays. However, more severe symptoms can also develop, as described above. In CRI, radiation results in the basal layer of the skin becoming damaged, causing symptoms like skin redness, itching, swelling, hair follicle damage, and desquamation (dry or moist shedding of the skin). Over time, the skin may blister, ulcerate, and redden, but eventually will heal. People with CRI who are exposed to higher radiation doses may have more permanent skin changes, like hair loss, atrophy, skin pigmentation changes, necrosis, and damaged sweat and sebaceous glands (CDC, 2024a; CDC, 2024e).

The timeline of stages for patients with CRIs resembles that of acute radiation syndrome, and includes:

• Prodromal stage: This stage happens within hours of exposure and lasts anywhere from one to two days. The patient’s skin will itch and develop the first wave of erythema (reddened skin).
• Latent stage: One to two days after the initial exposure, the patient's skin will appear healthy without any obvious injury. Interestingly, the skin on the patient’s neck, face, and cheeks has a shorter latency period than other areas of the body, like the palms of the hands and soles of the feet.
• Manifest illness stage: Next, the second or main wave of erythema occurs, lasting anywhere from a few days to weeks after the initial exposure. Edema, desquamation, ulcers, or skin necrosis may develop, and the skin’s pigment will increase.
• Erythema (third wave): A third wave or erythema occurs up to 10 days after the initial exposure. The patient’s skin may appear blue with readily observed areas of ulcers, necrotic tissue, and atrophy. Patients often report increasing pain in this stage.
• Late effects: Late effects happen months to years after radiation exposure, especially for patients exposed to about 10 Gy of radiation. Lasting effects, like skin necrosis, deformity, and complications to the surrounding blood vessels, tissues, and lymphatic system, are common (CDC, 2024e).

CRIs are also classified into grades I through IV:

1. Grade I: Grade I CRIs happen if a patient is exposed to 2 Gy or 200 rads of skin radiation. Some patients may have a prodromal stage within days of exposure, while others may not have this stage at all. They may experience 2-5 weeks of the latent stage, and then clinical manifestations develop, lasting 20 to 30 days. Dry skin desquamation typically occurs around six weeks post-exposure. A third wave of erythema does not develop in patients with grade I CRIs. Patients are expected to recover and completely heal within 3-6 months. Some patients may experience late effects, like skin atrophy and decades later skin cancer, while others have none.
2. Grade II: If a patient is exposed to 15 Gy or 1500 rads of radiation to the skin, this is classified as a grade II CRI. Patients will likely experience an immediate heat sensation lasting one to two days and the prodromal stage within about 6-24 hours of exposure. The latent stage typically occurs one to three weeks after initial exposure. As patients transition to the manifest illness stage, they will have skin redness, edema, a heat sensation, and increased pigmentation (skin will turn brown). At about 5-6 weeks postexposure, subcutaneous tissue edema develops, and the skin blisters with moist desquamation. Next, at about 10-16 weeks postexposure, patients develop the third wave of erythema accompanied by increasing pain and injury to the blood vessels. Skin ulcers and necrosis may develop as well. The recovery stage depends on the extent of the CRI, and patients may experience more cycles of erythema. Late effects, such as skin atrophy, ulcers, and telangiectasia (widened blood vessels on the skin, also called “spider veins”), are likely. Again, patients have an increased likelihood of skin cancer developing, even years after radiation exposure.
3. Grade III: Grade III exposures typically happen when patients are exposed to greater than 40 Gy or 4000 rads of radiation. Patients will likely experience an immediate pain and/or tingling sensation, which typically lasts one to two days, and the prodromal stage typically occurs within about 4-24 hours of exposure. The latent stage happens within 2 weeks of exposure, but some patients do not experience latency at all. As patients transition to the manifest illness stage (one to two weeks postexposure), they will have skin redness, blisters, edema, a heat sensation, and the possibility of increased pigmentation. Skin erosions, ulcerations, and severe pain follow these symptoms. Next, anywhere from 10-16 weeks after exposure, the third wave of erythema occurs. Patients’ signs and symptoms are edema, new skin ulcers, increasing pain, and necrosis. During the recovery stage, skin ulcers are very difficult to treat and heal, often requiring months to years to heal completely. The late effects of grade III CRIs are skin atrophy, depigmentation, and deformity. Blood vessels can become occluded, lymph tissues destroyed, and connective tissue fibrosed and sclerosed, causing more complications. Last, telangiectasia and skin cancer are possibilities.
4. Grade IV: Grade IV CRIs develop when patients are exposed to greater than 550 Gy or 55,000 rads of cutaneous radiation. The prodromal stage develops within minutes to hours of radiation exposure, and patients will experience immediate tingling and/or pain along with swelling in the affected site(s). Patients with grade IV CRIs will not have a latent stage. Clinical manifestations, such as skin blisters, usually occur within 1-4 days of exposure. Signs of tissue ischemia, like the skin turning white, then transitioning to dark blue or black, and increased pain, are possible in more severe CRIs. The patient's tissue becomes necrotic due to the lack of blood flow to the tissues. Since there is severe necrosis of the skin, patients will not experience a third wave of erythema. For patients with grade IV CRIs, recovery is possible. However, they may require several skin grafts, plastic surgeries, and possible amputation. Patients will also need long-term wound care, pain management, and psychological support (CDC, 2024e).

Treatment of CRIs is similar to that of thermal burns and acute radiation syndrome. Healthcare clinicians and providers must know the typical stages and grades of CRIs to manage and treat patients properly. Regardless of the provider's experience, consultation with a radiation specialist via the REAC/TS is necessary. Patients who do have symptoms do not require emergency care but will need close follow-up over many weeks. For patients presenting with radiation exposure and additional traumatic injuries, care measures like wound closure, covering the burns, fracture reduction, surgical stabilization, and other definitive treatments are provided within the first 48 hours post-injury. After this window, clinicians should delay surgical procedures until hematopoietic recovery is evident. The nurse or another healthcare professional should obtain a baseline CBC with differential, which is repeated at several intervals for trends. Additional treatment measures are outlined by the stage below:

• Prodromal stage: Initial treatment entails administering antihistamines and topical anti-pruritic medications since skin itching can be intense and, if scratched, can quickly introduce bacteria. Anti-inflammatory and sedative medications can also provide some relief to the affected area(s).
• Latent stage: During this stage, anti-inflammatories and sedatives are continued to provide relief. Over time, proteolysis inhibitors may be prescribed to aid with wound healing.
• Manifestation illness stage: During this stage, antibiotics or other prophylactic medications are given to prevent or treat secondary skin infections caused by bacteria, fungi, or other organisms. Repeat wound and skin culture swabs guide what medications may be needed to monitor for and treat infections. The application of topical corticosteroids, vitamin E, and antibiotic ointments aids in healing. Medications used to stimulate the blood supply are given at 3-4 weeks of this stage. Blisters should not be punctured unless under sterile conditions. If punctured, the covering skin should not be removed. Necrotic tissue may need tissue and wound debridement. Since patients will have increasing pain, which is difficult to manage, additional pain medications are ordered and administered.
• Late effects: Healing from CRIs takes several weeks to months to years. Treatment of late effects includes pain management, medications to stimulate tissue vascularization, and reconstructive or plastic surgeries. Close attention and care to the patient’s psychological well-being is also paramount (CDC, 2024e).

Lung blast injuries are one of the most common primary blast injuries that can result in patient mortality for those who survive the initial explosion. Pulmonary contusions are the most common lung injury, whereas “blast lung” is the most severe. Blast lung is often a fatal injury caused by the over-pressurization wave from a high-explosive blast, injuring the lung parenchyma. Symptoms are typically present during the initial medical evaluation but can be delayed, emerging up to 48 hours post-blast. Patients with lung blast injuries are also more likely to have additional injuries, like skull fractures, burns covering more than 10% of their bodies, and penetrating head and torso injuries.

Patients with lung blast injuries may present with symptoms such as dyspnea, chest pain, and a cough with bloody sputum. Pulmonary damage may range from scattered petechiae to extensive confluent hemorrhaging. Patients with the more severe injury of blast lung will often present with the classic triad of symptoms, including bradycardia, hypotension, and apnea.

Lung imaging via chest X-ray should be performed for anyone with primary blast injury. A hallmark sign of blast lung is the "butterfly" pattern seen on chest X-ray. For initial treatment, patients are placed on high-flow supplemental oxygen to aid with hypoxemia via a non-rebreather, continuous positive airway pressure (CPAP) device, or endotracheal (ET) tube. Patients with mild hypoxemia will need the least invasive form of supplemental oxygen delivery, whereas patients with severe hemoptysis or airway compromise will require intubation. However, providers should consider that positive pressure devices increase the likelihood of air embolism or alveolar rupture. Administration of IV fluids is also warranted for patients with lung blast injuries, but is used with caution to prevent volume overload.

For patients with a hemothorax or pneumothorax, a chest tube is placed to decompress the lung cavity. If blast lung is suspected, sometimes a prophylactic chest tube is placed to relieve lung pressure, especially for patients who may need general anesthesia or air transport. Health clinicians should monitor the patient for signs of air embolism, such as claudication, stroke, and myocardial infarction. If an air embolism is suspected, high-flow oxygen is administered, and the patient should be immediately placed in either the left lateral, prone, or semi-left lateral position. In addition, providers should transfer the patient to a facility that offers hyperbaric oxygen therapy. After the patient is initially stabilized, immediate transport to the appropriate facility via mass casualty protocols is necessary (CDC, 2012; Jorolemon et al., 2023).

The gastrointestinal tract is particularly susceptible to primary blast injuries, especially structures that are gas-filled, like the colon. However, solid organs can also be affected, resulting in injuries such as contusions and lacerations. Blast belly is a common term used for abdominal blast injuries causing abdominal hemorrhage or perforation (Jorolemon et al., 2023). Common primary blast injuries include immediate bowel perforation, hemorrhages, solid organ lacerations, and mesenteric shear injuries. Penetrating and blunt traumatic abdominal injuries are common with secondary and tertiary blast injuries, whereas crushing abdominal injuries are common with quaternary blast injuries. Children are more susceptible to abdominal blast injuries since their abdominal walls are smaller, more pliable, and thinner compared to adults.

Furthermore, children’s organs (i.e., liver and spleen) are proportionately larger when compared to adults, making these organs more vulnerable to injury. Interestingly, abdominal injuries are more severe with underwater blasts since the explosion radius is three times larger than that of an above-water explosion. This is primarily due to the fact that underwater waves propagate faster and lose less energy with distance when compared to blast waves traveling through the air.

Patients may present with a wide array of symptoms, ranging from abdominal, testicular, or rectal pain to nausea, vomiting, and hematemesis. Additional signs and symptoms are abdominal guarding, distention, tenderness, fever, and absent bowel sounds. Complications, like hypovolemia, hemorrhage, ischemia, and air embolism, can also develop quickly, so clinicians should remain diligent and thorough with their initial and ongoing assessment (CDC, 2012). Patients with intestinal perforation may present with delayed symptoms, up to 48 hours after the injury (Jorolemon et al., 2023).

For any patient suspected of an abdominal injury, prompt assessment and diagnostic evaluation are necessary. Initial assessment of patients with abdominal blast injuries entails following the ABC assessment and placing the patient on NPO (nothing by mouth or nil per os) status. If the patient is not receiving treatment at a trauma center, they should be stabilized and immediately transferred to a trauma facility. If the patient has any objects penetrating the abdomen, then these should not be removed. Instead, penetrating objects are removed in the operating room setting due to the increased risk of patient hemorrhage. Tests such as initial laboratory studies (e.g., CBC, complete metabolic panel [CMP], clotting factors) and radiological tests to detect free air, hemorrhaging, contusions, abscesses, and lacerations along the gastrointestinal tract are ordered. Serial abdominal exams, blood work, and imaging are also recommended to monitor the patient’s condition closely. Antibiotics and tetanus vaccination may also be administered to prevent or treat infection (CDC, 2012).

Blast injuries affecting the auditory system or ears are very common but can be easily missed. The severity of acoustic damage often depends on the position of the ear relative to the blast wave. Tympanic membrane perforation or rupture is the most frequent middle ear injury (Jorolemon et al., 2023; Pennardt, 2021).

Signs of ear trauma are typically evident during the initial assessment. Injury should be suspected in anyone with hearing loss, tinnitus, ear pain (otalgia), vertigo, bleeding from the external ear canal, a ruptured tympanic membrane, or mucopurulent discharge (otorrhea). These signs and symptoms will vary based on the portion of the ear affected, whether the tympanic membrane, or external, middle, or inner ear structures. All individuals exposed to a blast should undergo an otologic examination and audiometric testing as soon as possible. However, this is always performed after initial patient triage, assessment, and other life-saving measures are completed. Clinical presentation and initial treatment for each of these structures include:

• Tympanic membrane: The pressure from the explosive blast creates an increase in atmospheric pressure on the external auditory canal, resulting in overstretching and displacing the tympanic membrane. Symptoms like hearing loss, ear pain, and bloody discharge from the ear may be present. Otoscopy may reveal a laceration to one or both tympanic membranes and can appear smooth, punched out, or with ragged edges. Perforations can be partial or complete, affecting one or both ears. Most tympanic membrane ruptures spontaneously heal; however, consultation with an otolaryngologist (also referred to as an ENT or ear, nose, and throat specialist) is needed since complications, like ossicle disruption, cholesteatoma formation, and perilymphatic fistulae development, are likely. Unfortunately, around one-third of patients with a perforated tympanic membrane will have permanent hearing loss (CDC, 2012; Pennardt, 2021).
• External ear: Injuries to the external ear are typically caused by secondary blast injuries from flying debris from the explosion. Foreign bodies may need to be removed from the external ear tissue, and wounds are irrigated, cleansed, and closed with sutures or via another primary method of closure. Serious injury to the ear’s cartilage, like degloving of the ear’s cartilage (skin and cartilage being torn away from the underlying tissues), requires immediate medical attention. Degloving of the ear’s cartilage requires cleansing of the area and primary closure. The underlying cartilage should not be left exposed, so consultation with an otolaryngologist or plastic surgeon is recommended for cartilage repair and wound closure.
• Middle ear: Blast injuries affecting the middle ear primarily disrupt the small bones involved in the ossicular chain of this region (i.e., malleus, incus, and stapes). Cholesteatoma (a growth inside the middle ear and mastoid cavity) may develop. Since this type of lesion can expand and erode the surrounding tissues and supporting structures (e.g., temporal bone, base of the skull, and other middle ear structures), consultation with an otolaryngologist is warranted. Resulting complications of middle ear trauma are also important to monitor and include conductive and sensorineural hearing loss, cranial nerve palsy, and vestibular disturbances. Complications affecting the patient’s central nervous system are possible, such as meningitis or brain abscess, resulting in an increased risk of patient mortality.
• Inner ear: Blast injuries to the inner ear involve destruction to the ear’s auditory and vestibular components. Most of the patient’s symptoms, like hearing loss or threshold changes, are temporary and resolve within a few hours. However, for some patients, symptoms may take several weeks to subside. Again, treatment of inner ear injuries requires consultation and follow-up with a specialist. Initial baseline audiometry testing should be performed for patients with blast injuries, and serial interval audiometric testing is completed to monitor the patient’s recovery of their hearing deficit (CDC, 2012; Jorolemon et al., 2023).

It is vital to note that if a patient develops vestibular symptoms with any type of ear blast injury, referral to a neurologist is recommended for continued follow-up. In some cases, physical therapy for vestibular rehabilitation is helpful (Pennardt, 2021).

Blast injuries can cause damage to the eye, potentially rupturing the globe of the eye. Symptoms like eye pain, swelling, bleeding, blurred or reduced vision, or blindness may be present. There may also be swelling around the eye’s orbit, lacerations, or ecchymosis (Jorolemon et al., 2023). Other individuals may experience eye irritation or foreign body sensation, conjunctival hemorrhage, eye tearing, or have normal vision with minimal symptoms. Examples of minor eye injuries are conjunctivitis, superficial foreign bodies, and corneal abrasions, whereas more serious eye injuries are open globe injuries, including those that penetrate or perforate the cornea or sclera. Eyelid lacerations or orbital injuries also fall into the category of eye blast injuries. Serious non-penetrating eye injuries like hyphema, vitreous hemorrhage, retinal detachment, traumatic cataracts, and optic nerve injuries are possible as well.

During initial patient assessment, it should be assumed that the injury affects the globe of the eye. The clinician should not apply pressure to the eye or place an eye patch or bandage over the patient’s eye since it can cause further injury. An initial visual acuity exam should be performed for each eye, along with testing for light perception, hand motion, and counting fingers. If the patient cannot open their eyelids to complete the exam or if there is significant swelling, do not force their eyes open. The clinician should look for subtle signs of globe rupture or intraocular foreign bodies, like a misshapen pupil, conjunctival hemorrhage, and pigmented or gel-like tissue outside of the globe. If a patient has an eye blast injury of any type or is suspected of having one, immediate consultation with an ophthalmologist is necessary.

The ophthalmologist or emergency room provider may order diagnostic imaging to determine the extent of eye injury after an initial examination. A CT of the orbits can help identify foreign bodies. An MRI should not be initially ordered, as there may be metallic objects in the eye that could cause further injury if this test were performed. However, if it is confirmed that no metallic objects are present, then an MRI can be used to detect non-metallic foreign bodies in the eye, like wood or plastic.

An eye specialist removes any foreign bodies in the eye, as this requires a specialized technique and precision. For healthcare facilities that lack specialized ophthalmic operating room capabilities, patients should be transferred to another facility as soon as possible that offers this service. Other treatment measures to consider are administering a tetanus vaccine and administering IV broad-spectrum antibiotics (CDC, 2012).

Primary blast waves can lead to a concussion or traumatic brain injury (TBI), even without any direct impact on the head, which is sometimes referred to as blast brain. A blast brain is an injury to the parenchyma of the brain (the brain’s functional tissue, like the neurons and glial cells). It is essential to consider how close the individual was to the blast, particularly if they are experiencing symptoms. For patients with symptoms like headache, fatigue, amnesia, difficulty concentrating, lethargy, depression, anxiety, or insomnia, a blast brain injury should be considered (Jorolemon et al., 2023).

Since TBIs are possible, the following focuses on the management and treatment of this type of injury. If a patient presents with symptoms consistent with a TBI, the clinician should immediately conduct a comprehensive neurological examination. During the exam, close attention to the patient’s motor and sensory function, coordination and balance, mental status, mood and behavior, hearing, speech, and other cranial nerve tests is essential. The Glasgow Coma Scale can also be used to assess a patient’s eye opening, verbal response, and motor response. Clinicians should also quickly follow the ABC assessment to help stabilize the patient’s airway, breathing, and circulation, if necessary. Immediate consultation with a neurologist is warranted. If the patient is not located at a trauma center, then they should be stabilized and transferred as soon as possible.

Diagnostic imaging to assess the extent of the brain injury may include a CT or MRI of the brain. A brain CT shows brain structures and can be used to evaluate injuries like skull fractures, brain swelling, bleeding, or bruising. An MRI is more sensitive than a CT. However, an MRI is initially contraindicated until it can be determined that the patient has no metal in their body or metal objects from the blast.

Patients with a mild TBI may not require intervention. Their treatment may consist of bed rest and medications for symptom relief with close monitoring. Other medications, such as anticonvulsants to prevent or treat seizures, anticoagulants to reduce the likelihood of blood clots, diuretics to reduce intracranial pressure, and stimulants to increase alertness, may be ordered as well.

Patients with severe TBIs should be urgently stabilized to protect their vital organ function. They may require supplemental oxygen, airway management devices, and medications for hemodynamic stability. Devices to monitor the patient’s brain blood flow, intracranial pressure, brain temperature, and oxygen supply may be used. Some patients require emergency brain surgery to remove brain tissue or debris, repair skull fractures, or relieve intracranial pressure. Patients with severe TBIs require intense care from a multidisciplinary team and are admitted to the intensive care unit for close monitoring. Monitoring the patient’s neurological status and potential complications, such as infection, deep vein thrombosis, or increased intracranial pressure, is crucial (National Institute of Neurological Disorders and Stroke, 2025).

Blast from explosions can also cause injury to the extremities, with the most extreme being traumatic amputation. Primary blast injuries from the blast wind or wave can result in traumatic amputation through the bony shaft of a limb. Materials that become airborne during the explosion cause secondary blast injuries (penetrating trauma). Initial management includes consultation with an orthopedic surgeon since wound contamination requiring debridement and open fractures are possible. Contaminated wounds are irrigated with sterile saline and soaked with iodophor sponges and then dressed with bandages. The initial wound dressing is not removed until the patient undergoes surgery in an operating room for wound debridement. It is important to note that all open fractures are considered contaminated wounds. Assessing the affected extremity’s vascular, muscular, and neurological function is also essential.

Diagnostic radiographs or CT imaging of the extremity may be ordered to determine the extent of the injury or if foreign bodies are present. After initial evaluation and care measures are performed, fractures may be splinted to provide stability. Patients with extensive injuries (wound contamination or open fractures) will need surgery to debride wounds and stabilize the fractures. Patients with vascular injuries may need vascular grafts.

After initial operative management, patients with wound debridement may be on low-pressure pulsatile lavage to irrigate the wound and a vacuum wound dressing. Wound debridement is repeated every 24 to 72 hours until a stable soft tissue bed is obtained. Patients necessitating bony stabilization are placed on external fixation with secondary conversion to a plate or intramedullary fixation. Nurses and other healthcare clinicians must closely monitor the patient’s affected extremity(s), especially for complications such as compartment syndrome. Patients also need tetanus immunization (if indicated) and early antibiotic treatment to prevent wound infections (CDC, 2012).

Crush injuries and syndrome are a type of quaternary blast injury, resulting in tissue injury, organ dysfunction, and metabolic disturbances. The most common area of the body affected by crush injuries is the lower extremities, followed by the upper extremities and the trunk. Patients with crush injuries presenting with systemic symptoms or manifestations have developed crush syndrome (CDC, 2012). Crush syndrome is the consequence of muscle injury, resulting in rhabdomyolysis and then subsequently acute kidney injury (Haines & Doucet, 2023). Reperfusion syndrome is a condition that develops if the pressure is suddenly released from the affected area, which results in acute hypovolemia, metabolic disturbances, renal failure, and sometimes lethal cardiac arrhythmias (CDC, 2012).

Initial scene management of patients with crush injuries involves a primary assessment of the ABCs and implementation of supportive measures to maintain the patient's airway, breathing, and circulation. Before hospital transfer, patients with crush injuries should receive IV fluids without potassium before releasing the crushed extremity. If IV fluid administration is not possible, then a tourniquet may be applied. However, the use of a tourniquet should be reserved for controlling bleeding and used as a last resort (CDC, 2012; Haines & Doucet, 2023). Once the patient arrives at the hospital, IV fluids are administered to prevent hypotension and renal failure. Medications like sodium bicarbonate, calcium gluconate, insulin, and others may be given to prevent or treat metabolic abnormalities. Patients are closely monitored for changes in their cardiac rhythm (CDC, 2012). A metabolic panel and arterial blood gases are obtained, as well as urine myoglobin and creatine kinase to detect if the patient has developed rhabdomyolysis. Diagnostic imaging may also be necessary (e.g., X-rays, CT scans). Additional crush injury management and treatment depend on the area and extent of injury. Consultation and coordination of care from a multidisciplinary team is necessary, with specialties including, but not limited to, vascular, emergency, renal, orthopedic, and other relevant specialists (Haines & Doucet, 2023).