Further Reading
Although this material is provided as a convenient initial reference, readers are strongly recommended to refer to the resources listed at the end of this chapter for more detailed information, particularly the website for radiation-associated injury, which is updated periodically.
Biological Warfare Agents
- 1.
Bacteria
- a.
Anthrax: Bacillus anthracis is a gram-positive, spore-forming bacteria that can cause cutaneous, gastrointestinal (GI), or pulmonary symptoms, depending on route of infection. Weaponized anthrax is delivered via aerosol for inhalation of the spores; the following information is for pulmonary anthrax.
- i.
Signs and symptoms: incubation period is 1 to 6 days, followed by an initial phase (1–5 days) of nonspecific symptoms such as low-grade fever, malaise, fatigue, nonproductive cough, and mild chest discomfort. This may be followed by 1 to 3 days of apparent improvement before an abrupt onset of high fever and severe respiratory distress with dyspnea, diaphoresis, stridor, and cyanosis. Shock and death ensue within 24 to 36 hours after onset of severe symptoms.
- ii.
Diagnosis: physical findings are nonspecific. A widened mediastinum may be seen on chest x-ray (CXR) (or chest computed tomography [CT] if CXR is negative and exposure is strongly suspected). Detectable by gram stain (gram-positive rods) and blood culture. Nasal swab, sputum, and induced sputum will reveal pathogen. Blood and cerebrospinal fluid (CSF) will be used for culture, polymerase chain reaction (PCR), and antibody studies.
- iii.
Treatment: although effectiveness may be limited after symptoms have developed, high-dose antibiotic treatment with penicillin, ciprofloxacin, or doxycycline should be undertaken. Supportive therapy may be necessary. Anthrax Vaccine Adsorbed is available under investigational new drug (IND) for postexposure use in conjunction with above drug therapy.
- iv.
Prophylaxis: doxycycline, ciprofloxacin levofloxacin, and penicillin G may be considered for preexposure prophylaxis. For postexposure prophylaxis, consider 60 days of ciprofloxacin or doxycycline plus a three-dose series of anthrax vaccine.
- v.
Isolation/decontamination: standard precautions for healthcare workers. After an invasive procedure or autopsy, instruments and affected area should be disinfected with sporicidal agent such as 5% sodium hypochlorite. Autoclaving, steam sterilizing, or burning is required for complete eradication of spores. Decontamination of patients using water and soap is sufficient (collecting the effluent to prevent spreading of the displaced spores).
- i.
- b.
Cholera ( Vibrio cholera )
- i.
Signs and symptoms: incubation period is 4 hours to 5 days (usually 2–3 days). Asymptomatic to severe with sudden onset. Vomiting, headache, intestinal cramping with little or no fever, followed rapidly by painless, voluminous diarrhea. Fluid losses may exceed 5 to 10 L/d. Without treatment, death may result from severe dehydration, hypovolemia, and shock.
- ii.
Diagnosis: clinical. “Rice water” diarrhea and dehydration. Microscopic examination of stool reveals few/no red or white cells. Organisms can be visualized with darkfield or phase contrast microscopy, or by observation of darting motile vibrio under direct microscopy.
- iii.
Treatment: fluid and electrolyte replacement. Antibiotics (tetracycline, ciprofloxacin, or erythromycin) may shorten the duration of diarrhea and reduce the shedding of the organism.
- iv.
Prophylaxis: a licensed, killed vaccine is available but provides only about 50% protection which lasts no longer than 6 months. Vaccine is given at 0 and 4 weeks, with boosters every 6 months.
- v.
Isolation/decontamination: standard precautions for healthcare workers. Bactericidal solutions such as hypochlorite may be used to decontaminate areas.
- i.
- c.
Pneumonic plague ( Yersinia pestis )
- i.
Signs and symptoms: pneumonic plague usually requires 1 to 6 days of incubation before acutely presenting with high fever, chills, headache, malaise, myalgias, cough, and tachypnea within 24 hours, eventually producing bloody sputum (hemoptysis). The pneumonia progresses rapidly to dyspnea, stridor, and cyanosis. Death from respiratory failure, circulatory collapse, and a bleeding diathesis. Bubonic plague incubates for 2 to 10 days and may present with malaise, high fever, and tender lymph nodes (buboes); may progress spontaneously to the septicemic form, with spread to the central nervous system (CNS), lungs, and so on.
- ii.
Diagnosis: presumptive diagnosis can be made by gram, Wright, Wright-Giemsa or Wayson stain of lymph node aspirates, sputum, or CSF. Plague bacilli may also be cultured on standard media.
- iii.
Treatment: early administration of antibiotics is necessary. Supportive therapy is required.
- iv.
Postexposure prophylaxis: doxycycline or ciprofloxacin for 7 days.
- v.
Isolation/decontamination: standard precaution for healthcare workers for those exposed to bubonic plague, and droplet precautions are mandatory for pneumonic plague (for at least 48 hours of therapy antibiotics). Heat, disinfectants (2%–5% hypochlorite) and exposure to sunlight inactivates the bacteria.
- i.
- d.
Tularemia ( Francisella tularensis )
- i.
Signs and symptoms: after an incubation period of 3 to 6 days (up to 21 days), ulceroglandular tularemia presents with a local ulcer and regional lymphadenopathy and a sudden fever, chills, headache, and malaise. Typhoidal tularemia presents with a nonspecific febrile syndrome consisting of abrupt onset of fever, headache, malaise, myalgias, substernal discomfort, prostration, weight loss, and a nonproductive cough.
- ii.
Diagnosis: clinical. Physical findings are usually nonspecific. CXR may reveal a pneumonic process, mediastinal lymphadenopathy, or pleural effusion. Routine culture is possible but difficult. The diagnosis can be established retrospectively via serology.
- iii.
Treatment: administration of antibiotics (streptomycin or gentamicin) with early treatment is effective.
- iv.
Postexposure prophylaxis: a 2-week course of tetracycline, ciprofloxacin, or doxycycline is effective when given after exposure.
- v.
Isolation/decontamination: standard precautions for healthcare workers. Organisms can be inactivated by exposure to 55°C for 10 minutes or with standard disinfectants. Control of ticks, mosquitoes, deer flies, and lice is important in disrupting transmission.
- i.
- e.
Q fever ( Coxiella burnetii )
- i.
Signs and symptoms: after an incubation period (7–21 days, or up to 41 days), abrupt onset of high fever, fatigue, severe headache, chills, myalgias, dry cough, nausea, and pleuritic chest pain. Patients are usually not critically ill, and the illness lasts from 2 days to 2 weeks.
- ii.
Diagnosis: Q fever is not a clinically distinct illness and may resemble a viral illness or other types of atypical pneumonia. The diagnosis is confirmed serologically.
- iii.
Treatment: Q fever is generally a self-limited illness without treatment. Tetracycline or doxycycline are the treatments of choice and are given orally for 14 to 21 days. Q fever endocarditis is much more difficult to treat but is fortunately quite rare.
- iv.
Postexposure prophylaxis: treatment with doxycycline or tetracycline for 7 days during the incubation period (start 8–12 days postexposure) may delay but not prevent the onset of symptoms.
- v.
Isolation/decontamination: standard precautions for healthcare workers. Patient decontamination may be accomplished with soap and water or after a 30-minute contact time with 5% microchem plus (quaternary ammonium compound) or 70% ethyl alcohol.
- i.
- f.
Brucellosis ( Brucella spp.)
- i.
Signs and symptoms: incubation period 5 to 60 days (usually 1–2 months). Nonspecific findings include irregular fever, headache, profound weakness and fatigue, chills, diaphoresis, arthralgias, myalgias, depression, and mental status changes. May see osteoarticular changes (i.e., sacroiliitis, vertebral osteomyelitis). Rarely fatal.
- ii.
Diagnosis: blood cultures require a prolonged time for growth, and bone marrow cultures may be of higher yield. Confirmation requires phage-typing, oxidative metabolism, or genotyping procedures. Enzyme-linked immunosorbent assays (ELISAs), followed by Western blotting are used.
- iii.
Treatment: doxycycline and rifampin (or streptomycin or gentamycin) for at least 6 weeks. For complicated disease (i.e., endocarditis, meningoencephalitis), treat with rifampin, a tetracycline, and an aminoglycoside.
- iv.
Prophylaxis: no approved vaccine. Avoid consumption of unpasteurized milk and cheese.
- v.
Isolation/decontamination: standard precautions for healthcare workers. Environmental decontamination can be accomplished with a 0.5% hypochlorite solution.
- i.
- g.
Inhalational glanders ( Burkholderia mallei )
- i.
Signs and symptoms: incubation ranges from 10 to 14 days after inhalation of causative organism. Fever, rigors, diaphoresis, sweats, myalgia, headache, pleuritic chest pain, cervical adenopathy, splenomegaly, and generalized papular/pustular eruptions may occur. Almost uniformly fatal without treatment.
- ii.
Diagnosis: methylene blue stain of exudates may reveal scant small bacilli. CXR may show miliary lesions, small multiple lung abscesses, or bronchopneumonia. B. mallei can be cultured from infected secretions using meat nutrients.
- iii.
Treatment: ciprofloxacin, doxycycline, and rifampin have in vitro efficacy. Extrapolating from guidelines for melioidosis, a combination of trimethoprim-sulfamethoxazole (TMP-SMX) + ceftazidime ± gentamicin might be appropriate. The intravenous (IV) therapy will be continued for a minimum of 10 to 14 days before maintenance oral therapy is initiated for weeks to months.
- iv.
Prophylaxis: no approved vaccine. Postexposure prophylaxis may be tried with TMP-SMX.
- v.
Isolation/decontamination: standard precautions for healthcare workers. Environmental decontamination may be achieved with 0.5% hypochlorite solution.
- i.
- a.
- 2.
Viruses
- a.
Smallpox
- i.
Signs and symptoms: after an incubation period of 7 to 19 days (average 12 days): begins acutely with malaise, fever, rigors, vomiting, headache, and backache. Two to three days later lesions appear in the oropharynx, followed by (or concomitantly with) a rash on the face, then forearms and legs, then trunk, and subsequently hands and feet. The lesions will quickly progress from macules to papules, and eventually to pustular vesicles. They are more abundant on the extremities and face and develop synchronously.
- ii.
Diagnosis: electron and light microscopy are not capable of discriminating variola from vaccinia, monkeypox, or cowpox. PCR may be more useful. Samples should be sent to international reference laboratories such as Centers for Disease Control and Prevention (CDC), the World Health Organization (WHO), or other reference laboratories such as the French Armed Forces Biomedical Research Institute (IRBA) in France.
- iii.
Treatment: no effective specific chemotherapy. Supportive care should be given.
- iv.
Prophylaxis: immediate vaccination or revaccination should be undertaken for all exposed personnel. Vaccinia immune globulin (VIG) is of value in postexposure prophylaxis of smallpox when given within the first week following exposure.
- v.
Isolation/decontamination: droplet and airborne precautions for a minimum of 16 to 17 days following exposure for all contacts (3–6 feet of person). Patients should be considered infectious until all scabs separate.
- i.
- b.
Venezuelan equine encephalitis (VEE)
- i.
Signs and symptoms: following a 1 to 6 -day incubation period, sudden onset of illness with generalized malaise, spiking fevers, rigors, severe headache, photophobia, and myalgias (prominent in the thighs and lower back). Nausea, vomiting, cough, sore throat, and diarrhea may follow. Full recovery takes 1 to 2 weeks.
- ii.
Diagnosis: clinical—physical findings are nonspecific. Complete blood count (CBC) often demonstrates a striking leukopenia and lymphopenia. Virus isolation may be achieved from serum and in some cases from throat swab specimens. Both neutralizing or immunoglobulin (Ig)G antibody in paired sera or VEE-specific IgM present in a single serum sample indicate recent infection.
- iii.
Treatment: supportive only.
- iv.
Isolation/decontamination: standard precautions for healthcare workers. Control mosquito vectors and vaccinate horses in the vicinity.
- i.
- c.
Viral hemorrhagic fevers (VHFs)
- i.
Signs and symptoms: febrile illnesses often complicated by easy bleeding, petechiae, hypotension/shock, flushing of the face and chest, and edema. Malaise, myalgias, headache, vomiting, and diarrhea may occur as well.
- ii.
Diagnosis: specific virologic techniques or PCR are required.
- iii.
Treatment: intensive supportive care may be required. Antiviral therapy with ribavirin may be useful in several of these infections. Convalescent plasma may be effective for Argentine hemorrhagic fever.
- iv.
Prophylaxis: the only licensed VHF vaccine is for yellow fever. Prophylactic ribavirin may be effective for Lassa fever, Rift Valley fever, Crimean-Congo hemorrhagic fever (CCHF); not recommended for pulmonary virus hantavirus hemorrhagic fever with renal syndrome (HFRS).
- v.
Isolation/decontamination: contact preparations for healthcare workers. Decontamination is accomplished with hypochlorite or phenolic disinfectants. Isolation measures and barrier nursing procedures are indicated.
- i.
- a.
- 3.
Biological toxins
- a.
Botulinum
- i.
Signs and symptoms: after 12 to 36 hours (range 2 hours to 8 days after inhalation): ptosis, generalized weakness, dizziness, dry mouth and throat, blurred vision and diplopia, dysarthria, and dysphagia, followed by symmetrical descending flaccid paralysis and development of respiratory failure.
- ii.
Diagnosis: clinical. No routine laboratory findings.
- iii.
Treatment: intubation and ventilatory assistance for respiratory failure—anticipate possible need for tracheostomy. Administration of heptavalent botulinum antitoxin (IND product) may prevent or decrease progression to respiratory failure and hasten recovery.
- iv.
Isolation/decontamination: standard precautions for healthcare workers. Toxin is not dermally active, and secondary aerosols are not a hazard from patients. Soap and water suffice for patient decontamination.
- i.
- b.
Staphylococcal enterotoxin B
- i.
Signs and symptoms: from 2 to 12 hours (range 1.5–24 hours) after aerosol exposure, sudden onset of nonspecific flu-like symptoms: fever, chills, headache, myalgia, and nonproductive cough. Later symptoms depend on the route of exposure. Inhalation: some patients may develop shortness of breath and retrosternal chest pain, dyspnea (may progress to pulmonary edema). upper respiratory tract infection (URTI) symptoms (rhinorrhea, sinus congestion, pharyngitis) are observed in approximately one-third of the cases. Fever may last 2 to 5 days, and cough may persist for up to 4 weeks. Ingestion: patients may also present with nausea, vomiting, and diarrhea if they swallow toxin. Presumably, higher exposure can lead to septic shock and death.
- ii.
Diagnosis: clinical. Patients present with a febrile respiratory syndrome without CXR abnormalities. If performed with 24 hours postinhalation, nasal swabs and induced respiratory secretions will be used for different toxin assays (PCR, Ag ELISA, electrochemiluminiscent tests). Leukocytosis is common.
- iii.
Treatment: limited to supportive care, including ventilatory support with meticulous fluid management.
- iv.
Prophylaxis: use of protective mask. No vaccine available.
- v.
Isolation/decontamination: standard precautions for healthcare workers. Soap and water should suffice to remove potential contamination. Destroy any food that may have been contaminated.
- i.
- c.
Ricin
- i.
Signs and symptoms: 4 to 8 hours after exposure weakness, fever, chest tightness, cough, dyspnea, nausea, and/or diaphoresis with sublethal doses in humans. Higher inhaled doses would lead to labored breathing within 18 to 24 hours, and then to pulmonary edema, followed by severe respiratory distress and death from hypoxemia in 36 to 48 hours. After 1 to 2 hours following ingestion, the clinical presentation is different: severe nausea, vomiting, abdominal cramps, followed by diarrhea, vascular collapse shock, and possibly death at higher doses. Organ necrosis starting with the GI tract is observed.
- ii.
Diagnosis: aside from clinical suspicion, serum ELISA is available for acute and convalescent sera. Nasal swabs and induced respiratory secretions would be used for toxin assays (PCR, Ag ELISA) within 24 hours of aerosol exposure.
- iii.
Treatment: management is supportive, directed primarily toward pulmonary edema. Gastric decontamination measures should be used if ingested (vigorous gastric lavage, cathartics such as magnesium citrate).
- iv.
Prophylaxis: no vaccine or prophylactic antitoxin available. Use of protective mask is currently the best protection against inhalation.
- v.
Isolation/decontamination: standard precautions for healthcare workers. Secondary aerosols should generally not be a danger to healthcare providers. Weak hypochlorite solutions (0.1% sodium hypochlorite) and/or soap and water can decontaminate skin surfaces.
- i.
- d.
T-2 mycotoxins
- i.
Signs and symptoms: exposure causes skin pain, pruritis, redness, vesicles, necrosis and sloughing of epidermis. Nose and throat pain, nasal discharge, itching and sneezing, cough, dyspnea, wheezing, chest pain, and hemoptysis may follow inhalation. Ingestion or eye contact leads to local symptoms as well. Severe poisoning results in prostration, weakness, dizziness, ataxia and loss of coordination, collapse, shock, and death.
- ii.
Diagnosis: should be suspected if an aerosol attack occurs in the form of “yellow rain” with droplets of yellow fluid contaminating clothes and the environment. Confirmation requires testing of blood, tissue, and environmental samples.
- iii.
Treatment: no specific antidote. Superactivated charcoal should be given orally if the toxin is swallowed.
- iv.
Prophylaxis: protective mask and clothing during an attack.
- v.
Isolation/decontamination: standard precautions for healthcare workers. Outer clothing should be removed and exposed skin should be decontaminated with soap and water (even 4–6 hours after exposure), although a quicker decontamination (<1 hour) may prevent toxicity entirely. Eye exposure should be treated with copious saline irrigation. Once decontamination is complete, isolation is not required. Environmental decontamination requires use of hypochlorite solution under alkaline conditions such as 1% sodium hypochlorite and 0.1 M NaOH with 1-hour contact time. Secondary aerosols are not a hazard.
- i.
- a.
Chemical Warfare Agents
- 1.
Nerve agents (GA, GB, GD, GF, VX)
- a.
Mechanism of action: inhibiting acetylcholinesterase, leading to excess acetylcholine in synapses and other parts of the body.
- b.
Symptoms and signs
- i.
Vapor: small exposure leads to miosis, rhinorrhea, mild difficulty breathing. large exposure leads to sudden loss of consciousness, convulsions, apnea, flaccid paralysis, copious secretions, and miosis.
- ii.
Liquid on skin: small to moderate exposure leads to localized sweating, nausea, vomiting, feeling of weakness with a delay of minutes-hours. Large exposure, as with vapor exposure, results in sudden loss of consciousness, apnea, flaccid paralysis, copious secretions.
- i.
- c.
Decontamination: Fuller’s earth (decontamination mitt), followed by soapy water used with a sponge/towel (0.5% hypochlorite solution does not have a clear benefit) or Reactive Skin Decontamination Lotion (RSDL) sponge, large amounts of water if nothing else (efficacy of the latter depends on the agent considered: sarin is fully soluble in water, whereas VX has limited solubility).
- d.
Immediate management: atropine sulfate and pralidoxime chloride (or other salts). Add diazepam (or other benzodiazepine) if severe poisoning with signs of CNS involvement (e.g., seizures); intubation and ventilation with aggressive pulmonary toilet for respiratory distress.
- a.
- 2.
Vesicants
- a.
Mustard (HD, H)
- i.
Signs and symptoms: asymptomatic latent period up to several hours, followed by skin erythema and blisters, eye irritation with conjunctivitis and corneal opacity, respiratory embarrassment, GI effects, and bone marrow suppression.
- ii.
Decontamination: Fuller’s earth (decontamination mitt), followed by soapy water used with a sponge/towel (0.5% hypochlorite solution does not have a clear benefit) or RSDL sponge, large amounts of water if nothing else.
- iii.
Immediate management: decontaminate, symptomatic treatment.
- i.
- b.
Lewisite (L)
- i.
Signs and symptoms: immediate pain or irritation of skin and mucous membranes. Skin and eye lesions, and airway damage similar to that seen with mustard gas exposure develop later.
- ii.
Decontamination: hypochlorite, large amounts of water.
- iii.
Management: immediate decontamination, symptomatic management of lesions as with mustard agents—giving bronchoalveolar lavage (BAL) will decrease systemic effects but beware of the adverse effects (including for person allergic to peanuts).
- i.
- c.
Phosgene oxime (CX)
- i.
Signs and symptoms: immediate burning and irritation followed by wheal-like skin lesions and eye and airway damage.
- ii.
Decontamination: large amounts of water.
- iii.
Management: immediate decontamination, symptomatic treatment.
- i.
- d.
Cyanide (AC, CK)
- i.
Signs and symptoms: few—if very high exposure, may see seizures, respiratory and cardiac arrest.
- ii.
Decontamination: skin decontamination usually not necessary because highly volatile, but wet, contaminated clothing should be removed and underlying skin decontaminated with water or other standard decontaminants.
- iii.
Management: antidote = IV sodium nitrite and sodium thiosulfate or IV hydroxocobalamine; supportive oxygen and acidosis correction helpful.
- i.
- a.
- 3.
Pulmonary agents (CG)
- a.
Signs and symptoms: eye, airway irritation, dyspnea, chest tightness, and delayed pulmonary edema.
- b.
Decontamination: vapor → fresh air; liquid (rare situation)→ copious water irrigation.
- c.
Management: termination of exposure, ABC’s, rest and observation, oxygen ± positive pressure ventilation, other supportive care.
- a.
- 4.
Riot control agents (CS, CN, pepper spray)
- a.
Signs and symptoms: burning and pain on exposed mucous membranes and skin, eye pain and tearing, burning in the nostrils, respiratory discomfort, paresthesia in exposed skin.
- b.
Decontamination: flush eyes thoroughly with water or isotonic solution such as normal saline. Flush skin with copious amounts of water, alkaline soap and water, or a mildly alkaline solution (sodium bicarbonate or sodium carbonate). Generally, decontamination is not needed if the wind is brisk. Hypochlorite may exacerbate the skin lesions induced by CS and should not be used.
- c.
Management: usually none is necessary as effects are self-limiting.
- a.
Nuclear Weapons
- 1.
Nomenclature and introduction to ionizing radiation
- a.
Charged particles: alpha-particles (essentially ionized helium nuclei with a charge of 2+), beta-particles (essentially liberated electrons), and positrons (positively charged electrons).
- b.
Uncharged, indirectly ionizing x-rays (electromagnetic radiation), gamma-rays (electromagnetic radiation), and neutrons.
- c.
Units of radiation measurement
- i.
Measures of activity: Curie (1 Ci = 1 g of Ra-226), Becquerel (1 Bq = 1 disintegration/s).
- ii.
Measures of exposure: Roentgen (number of ion-pairs produced in a volume of air, defined only for x-rays, gamma-rays).
- iii.
Measures of absorbed: rad—radiation absorbed dose (energy deposited by any ionizing radiation per unit mass of any absorber: 1 rad = 100 erg/g ∼100 mosquito pushups); gray is the SI unit (1 Gy = 1 J/kg = 100 cGy = 100 rad). LD 50/60 = 3.5–4 Gy for average person.
- i.
- a.
- 2.
Determinants of biological effects
- a.
Density of tissue: high-density tissue (muscle) is affected more severely than low-density tissue (lung). Also, for particulate radiation, damage is proportionate to charge and size; for both photon and particulate radiation, damage is inversely proportionate to energy (higher energy means less time spent passing through tissue).
- b.
Type of radiation
Must “weigh” relative effects of different types of radiation. For example, one Gy of alpha absorbed is much more damaging than one Gy of gamma-radiation absorbed.
- i.
W R x-rays, gamma-rays, beta-particles.
- ii.
Neutrons: continuous function of neutron energy #peak at 20 at about 1 Mev, for low and high energy under 5.
- iii.
Alpha 20.
- i.
- c.
Measurements of dose equivalents
- i.
Rad equivalent mean (rem): measure of relative effectiveness of radiation in causing biological damage: DE(rem) = Dose (rad) × W R .
- ii.
The sievert (Sv): SI unit of dose equivalent: 1 Sv = 1 J/kg (if W R = 1), 1 Sv = 100 rem.
- iii.
Sources of energy.
- ■
If weight is 2 neutrons and 2 protons, their mass is greater than the weight of a helium nucleus; this discrepancy is termed the “mass defect” and is converted into the binding energy of a nucleus.
- ■
In a typical U 235 fission, the neutrons perpetuate a chain reaction which liberates additional neutrons as well as gamma- and beta-radiation.
- ■
In both fission and fusion, the end mass is less. Fusion liberates three times as much energy as fission.
- ■
Bremsstrahlung (“braking radiation”): in a nuclear explosion, x-ray photons ionize the surrounding air, forming the surface or “radiation front” of the fireball.
- ■
- i.
- a.
- 3.
Physical effects of nuclear weapons
- a.
Of the energy released from a standard fission weapon: 50% is dissipated as mechanical blast, 35% as thermal energy, 5% as initial radiation, and 10% as residual radiation with several hundred different nuclides/isotopes formed along with x-rays.
- b.
The blast results in an initial compression, followed by a suction phase. At blast strengths of 1 psi, windows are shattered; at 5 psi, brick houses are destroyed and tympanic membranes burst; 15 psi causes lung damage; and 50 psi is lethal to the average person 50% of the time. Additionally, wind effects can lead to deceleration injuries (injury threshold 5 mph, LD 50 = 55 mph) and missile injuries.
- c.
Thermal injuries can cause conventional body burns and ophthalmic trauma in the form of retinal burns and flash blindness.
- d.
If have some degree of warning, effects can be reduced with some postural changes. Once a blast occurs, lie head toward ground zero if wearing helmet, feet toward ground zero if not wearing helmet. Any clothing or protective barriers can be beneficial.
- e.
Nuclear fallout: early fallout arrives within the first day and is concerning for whole-body exposure from gamma-radiation, external burns from beta-radiation, and internal exposure from ingested/inhaled alpha-particles (0.01–1-cm diameter particles). During the first weeks, I 131 is a great concern. Delayed fallout arrives after the first day, with smaller particles, and can be a global concern. Primary risk is from ingestion of long-lived fission products such as Sr 90/89 and Cs 137 , with half-lives of 30 years or more. Generally, rate of decay falls logarithmically; after every 7 hours, there is one-tenth of the activity as before.
- a.
- 4.
Biological effects of radiation
- a.
Ionizing radiation damages through ionization and excitation, which either directly ionizes molecules or generates free radicals that do the same.
- b.
Radiation can overwhelmingly damage DNA, damage cell membranes, and cause other effects; lethal effects are primarily in the nucleus/DNA molecule (cytoplasm can withstand much higher doses of radiation than nucleus); at very high doses, lethal effects quickly occurr from neurovascular damage secondary to edema.
- c.
Modifiers of effects
- i.
Total dose: more is worse.
- ii.
Dose rate/fractionation: if spread dose over time, greater survivability.
- iii.
Chemical modifiers: oxygen potentiates effects; anoxia/antioxidants are radioprotective.
- iv.
Cell type: actively dividing cells more vulnerable, quiescent stem cells more resistant, and those with large volume of nucleic acids are most vulnerable. Also, those cells in mitosis are at increased vulnerability.
- v.
Route of exposure: open wound, inhalation, ingestion all determine what tissues are affected, as well as the “critical organ” (the tissue or organ where radionuclide is ultimately deposited—i.e., iodine becomes concentrated in the thyroid).
- ■
In utero, radiation can cause growth retardation (esp. 3–20 weeks gestation), microcephaly, mental retardation, skeletal abnormalities, and ocular anomalies (esp. 6–11 weeks). After exposure, males initially fertile, but 35 cGy leads to 8 to 20 months of sterility; 6 Gy leads to permanent sterility. In females, do see immediate sterility, and as little as 350 cGy leads to 60% infertility.
- ■
Somatic effects include aplastic anemia, cataracts (threshold is 1.5–3 Gy for single exposure, cardiovascular, cancer.
Leukemia (especially in children), thyroid (malignant and nonmalignant) increased rate after Nagasaki/Hiroshima. Breast cancer seen after A-bomb survivors (gamma, neutrons) and fluoroscopy patients. Bone cancer noted in radium dial painters (alpha). Lung cancer seen in uranium miners (alpha).
Recommended dose limits: occupational = 20 mSv per year; public 1 mSv in year.
- ■
- i.
- a.
- 5.
Acute radiation syndrome
- a.
More than 0.12 Gy whole body → sperm decreases to nadir by day 45; 0.20 Gy, whole body → detectable increase in chromosomal aberrations; 0.20 to 0.50 Gy, whole body → detectable bone marrow depression with lymphocytopenia.
- b.
LD 50/60 for whole-body irradiation without treatment is 3.5 to 4 Gy without treatment, increasing to 5 to 6 with supportive care (abx, transfusion) and 6 to 8 with early CSF administration.
Worsened by coexisting trauma, nutritional deficits, infection, or chronic disease. Improved by radioprotectants (anoxia, vitamins A/E/C), partial body exposure, poorly penetrating radiation, fractionation, good medical support.
- c.
Sensitivity: hematopoietic > GI > CV > CNS.
- d.
Stages of acute radiation syndrome: prodrome, latent, manifest illness, recovery.
- e.
Hematopoietic syndrome: dose range 1 to 6 Gy, affects dividing stem cells and progenitors for all marrow cell lines.
- i.
Prodromal period: N/V, anorexia, possible diarrhea.
- ii.
Latent period: asymptomatic except mild weakness for about 3 weeks.
- iii.
Overt clinical period: bone marrow atrophy, hemorrhage, and infection, onset at 3 to 4 weeks. Lymphocytes show first drop in 1 to 3 days, then slowly stabilize. Neutrophils may actually increase in the first day or so, then gradually decrease to nadir within 30 to 40 days. Thrombocytes begin to decrease at 15 days, reaching minimal levels by 30 to 40 days.
- i.
- f.
Gastrointestinal syndrome: dose range over 6 Gy, affects GI stem cells.
- i.
Prodromal period: severe N/V, occasionally watery diarrhea and cramps, onset within hours after exposure.
- ii.
Latent period: asymptomatic for 5 to 7 days.
- iii.
Overt clinical period: return of severe diarrhea (progression to bloody), vomiting, fever, may develop into shock and death.
- ■
Can see malabsorption, paralytic ileus, dehydration, ARF with CV collapse, GI bleeding, anemia, and sepsis.
- ■
- i.
- g.
Cardiovascular and CNS syndrome: more than 15 Gy, affects circulatory endothelium.
- i.
Prodromal period: burning sensation within minutes of exposure, N/V develop within 30 minutes, with loss of balance and confusion with prostration eventually developing.
- ii.
Latent period: apparent improvement for several hours.
- iii.
Overt clinical period: within 5 to 6 hours, watery diarrhea, respiratory distress, and gross CNS signs.
- i.
- h.
Summary of acute radiation syndrome
# Gy
Performance Loss
Injury
Survival
Hematologic Syndrome
1
Motivational loss
Marrow
probable
2
Fatigue, weakness
Marrow
probable
3
Anorexia
Marrow
likely
4
Nausea/vomiting
Severe marrow
possible
5
Diarrhea
Severe marrow
LD 50 w/ tx
Gastrointestinal Syndrome
6
↑ Reaction time
Mod intestinal
death 2–3 weeks
7
“”
“”
“”
8
Hypotension
“”
“”
9
“”
“”
“”
10
“”
Severe intestinal
death 1–2 weeks
15
Early transient incapacitation
“”
“”
CV/CNS
15
“”
“”
Death 5–12 days
20
Loss of consciousness
Neurovascular
“”
25
“”
“”
“”
30
“”
“”
Death 2–5 days 
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- a.
