Bioterrorism and Other Public Health Emergencies 

Pediatric Terrorism and Disaster Preparedness 

A Resource for Pediatricians 

Prepared for: 

Agency for Healthcare Research and Quality 

U.S. Department of Health and Human Services 

540 Gaither Road 

Rockville, MD 20850 

www.ahrq.gov

Purchase Order No. 05R000190 

Prepared by: 

American Academy of Pediatrics 

Elk Grove Village, IL 

Editors 

George L. Foltin, MD, FAAP, FACEP 

David J. Schonfeld, MD, FAAP 

Michael W. Shannon, MD, MPH, FAAP 

Section Editors 

Jane Knapp, MD, FAAP 

Marion J. Balsam, MD, FAAP 

Lorraine M. Giordano, MD, FACEP 

Julia McMillan, MD 

Frederick Henretig, MD, FACMT, FAAP 

David E. Jarrett, MD, FS, FACEP 

Arthur Cooper, MD, MS, FACS, FAAP, FCCM 

David Szydlo, MD, PhD 

David Markenson, MD, FAAP 

Irwin Redlener, MD, FAAP 

AHRQ Editor 

Mary L. Grady 

AHRQ Publication No. 06(07)-0056 

October 2006 
ii

Copyright Notice 

© 2006 by The American Academy of Pediatrics. All rights reserved except as and to the extent 

(but only to the extent) otherwise set forth below. 

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and Disaster Preparedness: A Resource for Pediatricians, when distributed by or through 

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The Resource may not be modified in any way by any user. The Resource and its contents may 

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The name and logo of AAP may only be used for purposes of reproduction of the Resource as 

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The AAP and AHRQ have made a good faith effort to take all reasonable measures to ensure that 

this product is accurate, up-to-date, and free of error in accord with clinical standards accepted at 

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unique circumstances that may apply in each situation they encounter. Neither AAP nor AHRQ 

are or shall be responsible for any adverse consequences arising from independent application by 

individual practitioners of the content of the Resource to particular patient circumstances 

encountered in their practices. 

Suggested citation 

American Academy of Pediatrics. Pediatric Terrorism and Disaster Preparedness: A Resource for 

Pediatricians. Foltin GL, Schonfeld DJ, Shannon MW, editors. AHRQ Publication No. 06(07)-

0056. Rockville, MD: Agency for Healthcare Research and Quality. October 2006. 
iii

Contents 

Chapter 1. Introduction......................................................................................................1 

Background......................................................................................................................................1 

Children Are Not Small Adults........................................................................................................5 

 Anatomic Differences ..........................................................................................................5 

 Physiologic Differences.......................................................................................................6 

 Immunologic Differences ....................................................................................................7 

 Developmental Differences .................................................................................................7 

 Psychological Differences ...................................................................................................8 

Overview of Practical Considerations for Children and Families During Disasters .......................9 

 Surge Capacity.....................................................................................................................9 

 Pediatric Readiness ..............................................................................................................9 

Summary........................................................................................................................................11 

Bibliography ..................................................................................................................................11 

Chapter 2. Systems Issues ............................................................................................15 

Types of Disasters..........................................................................................................................15 

 Natural Disasters................................................................................................................15 

 Manmade and Technological Disasters .............................................................................17 

Aftermath .......................................................................................................................................18 

Federal Response ...........................................................................................................................19 

 Centers for Disease Control and Prevention......................................................................19 

 Department of Homeland Security ....................................................................................19 

 Federal Response Plan .......................................................................................................20

 Department of Defense ......................................................................................................19 

 Summary............................................................................................................................21 

Bibliography ..................................................................................................................................22 

Chapter 3. Responding to a Disaster.......................................................................27 

Phases of Response........................................................................................................................27 

 Preparedness ......................................................................................................................27 

 Actual Resonse to the Event ..............................................................................................28 

 Mitigation...........................................................................................................................29 

 Recovery and Critique .......................................................................................................29

Regional Response.........................................................................................................................30 

 State and Federal................................................................................................................30 

 Emergency Medical Services.............................................................................................30 

 Hospitals ............................................................................................................................31 

 Incident Command Systems ..............................................................................................35 

 Regional Coordination of Hospital Response....................................................................36 

 Some Roles for the Pediatrician in Regional Hospital to Community Planning ...............37 

 Drills and Quality Assurance Activities ............................................................................38 

 Integration with Children’s Services .................................................................................39 

 JCAHO and Emergency Management...............................................................................40 
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 Appropriate Triage.............................................................................................................40 

Incident Management.....................................................................................................................41 

 Staging ...............................................................................................................................42 

 Triage Group......................................................................................................................42 

 Treatment/Decontamination ..............................................................................................42 

 Transportation....................................................................................................................43 

Bibliography ..................................................................................................................................43 

Chapter 4. Biological Terrorism..................................................................................47 

Background....................................................................................................................................47 

 History of Bioterrorism......................................................................................................47 

 Epidemiology of a Terrorist Attack ...................................................................................49 

Agents Categorized by System Predominantly Affected...............................................................50 

 Respiratory System ............................................................................................................50 

 Nervous System .................................................................................................................51 

 Gastrointestinal System .....................................................................................................52

 Dermatologic Manifestations.............................................................................................52 

Notifying Authorities.....................................................................................................................54 

 Health Department.............................................................................................................55 

 Hospital..............................................................................................................................55 

 Law Enforcement...............................................................................................................56 

 Laboratory Support and Submission of Specimens...........................................................56 

 Laboratory Response Network ..........................................................................................56 

Limiting Spread .............................................................................................................................56 

 Standard Precautions..........................................................................................................56 

 Transmission Precautions ..................................................................................................57 

Equipment and Supplies ................................................................................................................58 

Pediatric Practices..........................................................................................................................59 

Managing Patients: Treatment and Prevention..............................................................................60 

 Smallpox Vaccine ..............................................................................................................60 

 Anthrax Vaccine ................................................................................................................61 

Strategic National Stockpile ..........................................................................................................61 

Surge Capacity...............................................................................................................................62 

 Medications........................................................................................................................62 

 Isolation..............................................................................................................................62 

 Vaccination ........................................................................................................................63 

Information for Families................................................................................................................63 

Category A Agents.........................................................................................................................63 

 Anthrax ..............................................................................................................................63 

 Botulinum Toxin................................................................................................................66 

 Plague.................................................................................................................................69 

 Smallpox ............................................................................................................................71 

 Tularemia ...........................................................................................................................74 

 Viral Hemorrhagic Fevers..................................................................................................76 

Category B and C Agents ..............................................................................................................77 

 Ricin...................................................................................................................................77 
v

 Q Fever...............................................................................................................................78 

 Staphylococcal Enterotoxin B............................................................................................79 

Brucella..............................................................................................................................80 

Burkholderia mallei (Glanders) .........................................................................................80 

 Encephalitis Viruses and Yellow Fever Virus...................................................................81 

Clostridium perfringens.....................................................................................................83 

Bibliography ..................................................................................................................................84 

Chapter 5. Chemical Terrorism..................................................................................107 

Introduction..................................................................................................................................107 

 Specific Pediatric Vulnerabilities to Chemical Agents....................................................108 

 Chemical Injuries and Approach to the Unknown Chemical Attack...............................108 

 Initial Approach, Decontamination, and Triage ..............................................................109 

 Industrial Chemicals ........................................................................................................110 

 Community Preparedness ................................................................................................111 

Nerve Agents ...............................................................................................................................111 

 Background......................................................................................................................111 

 Toxicology and Clinical Manifestations..........................................................................112 

 Diagnostic Tests...............................................................................................................113 

 Treatment .........................................................................................................................114 

 Isolation and Control Measures .......................................................................................115 

Cyanide ........................................................................................................................................115 

 Toxicology .......................................................................................................................116 

 Clinical Presentation ........................................................................................................116 

 Treatment .........................................................................................................................117 

Vesicants......................................................................................................................................118 

 Characteristics..................................................................................................................119 

 Clinical Effects.................................................................................................................119 

 Treatment .........................................................................................................................120 

 Pediatric Considerations ..................................................................................................122 

Pulmonary Agents........................................................................................................................123 

 Chlorine and Phosgene ....................................................................................................123 

 Clinical Effects.................................................................................................................124 

 Treatment .........................................................................................................................125 

Riot Control Agents .....................................................................................................................126 

 Transmission and Pathogenesis .......................................................................................126 

 Clinical Manifestations ....................................................................................................126

 Diagnosis..........................................................................................................................127 

 Treatment and Control .....................................................................................................128 

Bibliography.... ...........................................................................................................................128 

Chapter 6. Radiological and Nuclear Terrorism...............................................143 

Radiological Threats: Scope and Implications ............................................................................143 

 Incident Management.......................................................................................................143 

 Nuclear Weapons.............................................................................................................144 

 Radiological Dispersal Devices (Dirty Bombs)...............................................................145 
vi

 Medical and Industrial Sources of Radiation...................................................................146 

 Nuclear Power Plants.......................................................................................................147

Historical Overview of Radiation Injury .....................................................................................147

 Hiroshima and Nagasaki, Japan 1945..............................................................................148 

 Mayak, Russia, former Soviet Union 1948-1990 ............................................................148 

 Marshall Islands 1954......................................................................................................149

 Three Mile Island, PA 1979.............................................................................................149 

 Chernobyl, Former Soviet Union 1986............................................................................149 

 Goiania, Brazil 1987 ........................................................................................................150 

Radiological Dispersal Devices (Dirty Bombs)...........................................................................150 

Other Radiation Uses and Injuries ...............................................................................................150 

Physical Principles of Ionizing Radiation....................................................................................151 

 Atomic Structure..............................................................................................................151 

 Stability and Radiation.....................................................................................................151 

 Radiation Interactions ......................................................................................................153 

 Radiation Damage and Protection ...................................................................................154 

 Radiation Units ................................................................................................................155 

 Radiation Background Exposure .....................................................................................156 

Radiation Biology and Dosimetry ...............................................................................................157 

 Radiation Biology ............................................................................................................157 

 Biodosimetry....................................................................................................................158 

 Biodosimetry and Radiological Terrorism.......................................................................161 

 Pediatric Issues.................................................................................................................161 

Medical Diagnosis: Acute Radiation Syndrome..........................................................................162 

 Pathophysiology...............................................................................................................162 

 Clinical Stages .................................................................................................................163 

 Syndromes........................................................................................................................164 

 Emergency Care...............................................................................................................165 

 Diagnostic Steps...............................................................................................................165 

 Overall Dose Assessment ................................................................................................167 

Medical Diagnosis: External Contamination...............................................................................167 

 Background......................................................................................................................167 

 Protection of Medical and Emergency Personnel............................................................168 

 Emergency Care...............................................................................................................168 

 Patient Evaluation ............................................................................................................168 

Medical Diagnosis: Internal Radionuclide Contamination..........................................................170 

 Background......................................................................................................................170 

 Internal Contamination ....................................................................................................170 

 Life Cycle of Internal Contamination..............................................................................172 

 Diagnosis..........................................................................................................................173 

Radiation Detection, Personal Protective Equipment, Personnel Monitoring, and 

Decontamination..........................................................................................................................175 

 Detection Using Radiation Survey Meters ......................................................................175 

 Dosimeters .......................................................................................................................177 

 Personal Protective Equipment........................................................................................178 

Monitoring of Personnel/Decontamination..................................................................................180 
vii

 Basic Principles................................................................................................................180 

 Decontamination Techniques...........................................................................................181 

Medical Treatment: General Issues Unique to Pediatrics............................................................182 

 Acute Susceptibility.........................................................................................................182 

 Long-Term Susceptibility ................................................................................................182 

 Psychological Vulnerability.............................................................................................183 

 Immediate Care................................................................................................................184 

Medical Treatment: Acute Radiation Syndrome .........................................................................184 

 Supportive Care ...............................................................................................................184 

 Neutropenia: Cytokine Therapy.......................................................................................185 

 Neutropenia: Antibiotic Therapy .....................................................................................186 

 Neutropenia: Viral and Fungal Infections........................................................................187 

 Neutropenia: Prophylactic Antimicrobials ......................................................................187 

 Thrombocytopenia and Anemia: Blood Products............................................................187 

 Bone Marrow Transplantation .........................................................................................187 

Medical Treatment: Internal Contamination................................................................................188 

 Radioactive Iodine: Potassium Iodide .............................................................................188 

 Radioactive Cesium and Thallium: Prussian Blue...........................................................190 

 Radioactive Plutonium, Americium, and Curium: DTPA Uranium:Bicarbonate ...........190 

 Other Radioactive Isotopes..............................................................................................191 

Surgical Issues .............................................................................................................................191 

 Local Radiation Injury: Cutaneous Radiation Syndrome ................................................191 

 Treatment and Management Issues..................................................................................193 

 Trauma and Radiation (Timing of Surgery) ....................................................................194 

 Management of the Patient with Embedded Radioactive Material and 

 Depleted Uranium............................................................................................................194 

Followup Care, Including Risk of Carcinogenesis ......................................................................195 

Environmental Issues Affecting Children After a Terrorist Incident Involving Radioactive 

Materials ......................................................................................................................................197 

 Type of Incident...............................................................................................................197 

 Environmental Exposure Pathways .................................................................................199 

 Short-Term Evacuation Versus Sheltering ......................................................................201 

 Long-Term Habitation Versus Abandonment .................................................................203 

 Rehabilitation/Abatement ................................................................................................203 

 Contamination of Crops, Water, Food Animals, and Milk Sources ................................203 

 Mortuary Affairs ..............................................................................................................204 

Bibliography ................................................................................................................................204 

Chapter 7. Blast Terrorism...........................................................................................237 

Introduction..................................................................................................................................237 

Explosives....................................................................................................................................237 

 Blast Fundamentals..........................................................................................................238 

 Blast Trauma....................................................................................................................239 

 Incendiary Weapons.........................................................................................................247

 Aviation Terrorism...........................................................................................................248 

Trauma Systems...........................................................................................................................248 
viii

 Trauma Hospitals.............................................................................................................248 

 Trauma Centers................................................................................................................248 

 Non-Trauma Centers........................................................................................................250 

Treatment .....................................................................................................................................250 

 Trauma .............................................................................................................................251 

 Burns................................................................................................................................251 

 Multiple Casualties ..........................................................................................................251 

 Mass Casualties................................................................................................................251 

Planning and Mitigation...............................................................................................................252 

 Planning ...........................................................................................................................252 

 Mitigation.........................................................................................................................253 

Bibliography ................................................................................................................................255 

Chapter 8. Mental Health Issues ...............................................................................265 

Mental Health and the Role of the Pediatrician...........................................................................265 

Trauma-Related Disorders...........................................................................................................265 

 Reaction to Disasters and Terrorism................................................................................266 

 Assessment and Treatment ..............................................................................................268 

Death Notification and Pediatric Bereavement............................................................................270 

 Considerations in Notifying Individuals About an Unexpected Death ...........................270 

 Explaining Death to Children ..........................................................................................275 

 Common Reactions Among Children Who Have Experienced a Personal Loss.............276 

 Indications of the Need for Referral ................................................................................277 

 Attendance of Children at Funerals and Memorial Services ...........................................278 

Therapies for Psychic Trauma .....................................................................................................278 

 Crisis Response................................................................................................................278 

 Crisis Response for Children and Families......................................................................279 

Medication ...................................................................................................................................280 

School Crisis Response................................................................................................................282 

Anniversary Reactions and Commemorative Activities..............................................................283 

 Anniversaries ...................................................................................................................283 

 Memorialization...............................................................................................................284 

 Planning a Memorial Activity..........................................................................................285 

 Supporting School Staff...................................................................................................286 

Impact on Health Care Providers.................................................................................................286 

 Make Psychological Contact............................................................................................287 

 Level of Coping ...............................................................................................................287 

 Explore Possible Solutions ..............................................................................................287 

 Take Action......................................................................................................................287 

 Followup ..........................................................................................................................287 

 Basic Objectives...............................................................................................................287 

 Benefits ............................................................................................................................288 

Risk Communication and Media Issues.......................................................................................288 

 Developing Goals and Key Messages..............................................................................288 

 Delivering Accurate and Timely Information..................................................................289 

Bibliography ................................................................................................................................290 
ix

Chapter 9. Integrating Terrorism and Disaster Preparedness into 

Your Pediatric Practice ..................................................................................................293 

Relevance for Office-Based Pediatricians ...................................................................................293 

 Internal Operations of the Practice: Office Readiness.....................................................293 

 External Operations: Communication and Coordination with Other Agencies...............296 

 Communicating Directly with Children and Families.....................................................298 

Relevance for Hospital-Based Pediatricians................................................................................299 

 Emergency Department Readiness ..................................................................................299 

 Inpatient Service Readiness .............................................................................................300 

 Hospital Infrastructure Needs ..........................................................................................300 

Bibliography ................................................................................................................................301 

Chapter 10. Working with Government Agencies...........................................303 

Introduction..................................................................................................................................303 

Community, Government, and Public Health Preparedness........................................................303 

 Community Response ......................................................................................................303 

 State Government.............................................................................................................304 

 Federal Government.........................................................................................................304

 Public Health Preparedness..............................................................................................305 

Advocating for Children and Families in Preparedness Planning ...............................................305 

Resources Available from Government Agencies.......................................................................306 

Chapter 11. Conclusion .................................................................................................309 

Systems Issues .............................................................................................................................309 

Regional, State, and Local Efforts ...............................................................................................309 

Vulnerable Populations................................................................................................................310 

 Separation of Children from Families..............................................................................310 

 Sheltering Families ..........................................................................................................310 

Providing Urgent Medical Care to Large Populations of Displaced Children ............................311 

 Setting up a Temporary Pediatric Clinic Lessons Learned..............................................311 

 Environment.....................................................................................................................312 

 Medical Needs .................................................................................................................312 

A Final Word ...............................................................................................................................312 

Acronyms...............................................................................................................................319 

Appendixes 

Appendix A. Learning Objectives ...............................................................................................323 

Appendix B. List of Contributors ................................................................................................333 
x

Figures and Tables

Figures

Figure 2.1 Federal Response Plan..................................................................................................24 

Figure 3.1 National Response Plan................................................................................................44 

Figure 4.1 Inhalational anthrax; chest radiograph taken 22 hours before death............................88 

Figure 4.2 Neurological signs, botulism, 6-week-old infant .........................................................89 

Figure 4.3 Cutaneous anthrax lesion with eschar on neck.............................................................90 

Figure 4.4 Physical distribution of smallpox lesions versus varicella lesions...............................91 

Figure 4.5 Small pox lesions..........................................................................................................92 

Figure 4. 6 Varicella lesions ..........................................................................................................93 

Figure 4.7 Expected smallpox vaccination site reaction (i.e., a “take”) in a 

 first-time vaccinate.............................................................................................................94 

Figure 4.8a Febrile rash illness algorithm for evaluating patients suspected of 

 having smallpox.................................................................................................................95 

Figure 4.8b Classification of risk Febrile rash illness algorithm...................................................96 

Figure 6.1 Probability of radiation casualties ..............................................................................216

Figure 6.2 Environmental exposure pathway ..............................................................................217 

Figure 6.3 Generic pediatric medical field card...........................................................................218 

Figure 6.4 Bone marrow irradiated to 3 Gy.................................................................................219 

Figure 6.5 Pattern of a series of blood counts graphed over time after 3 Gy of 

 whole-body exposure.......................................................................................................220 

Figure 6.6 Classic Andrews diagram...........................................................................................221 

Figure 6.7 Contamination versus exposure..................................................................................222 

Figure 6.8 Examples of radiation survey meters .........................................................................223 

Figure 6.9 Recommended procedures for monitoring personnel.................................................224 

Figure 6.10 Localized radiation effects .......................................................................................225 

Tables

Table 1.1 Types of disasters...........................................................................................................13 

Table 2.1 Types of disasters, hazards, or events that may require Federal assistance...................25 

Table 3.1 Training and competencies of prehospital emergency personnel..................................45 

Table 4.1 Early clinical signs and symptoms after exposure to selected 

 bioterrorist agents...............................................................................................................97 

Table 4.2 Infection control transmission precautions for Category A agents................................99 

Table 4.3 Diagnostic procedures, isolation precautions, treatment, and postexposure 

 prophylaxis for selected bioterrorist agents in children...................................................100 

Table 4.4a Diagnostic tests for anthrax........................................................................................103 

Table 4.4b Adjunctive diagnostic tests for anthrax .....................................................................103 

Table 4.5 Postexposure prophylaxis for anthrax..........................................................................104 

Table 4.6 Treatment recommendations for tularemia in children before 

 test results are known.......................................................................................................105 

Table 5.1 Pediatric vulnerabilities to chemical terrorism ............................................................132 

Table 5.2 Chemical weapons Summary of pediatric management considerations......................133 

Table 5.3 Representative classes of industrial chemicals Summary of pediatric 

 management considerations.............................................................................................135 
xi

Table 5.4 Nerve agent triage and dosing .....................................................................................137

Table 5.5 Clinical effects from sulfur mustard exposure.............................................................139 

Table 5.6 Riot control agents.......................................................................................................140 

Table 5.7 Medical treatment of riot control agent exposure........................................................141 

Table 6.1 Biological dosimetry assays and operational parameters ............................................226 

Table 6.2 Biodosimetry based on acute photon-equivalent exposures........................................227 

Table 6.3 Initial or prodromal phase, whole body irradiation from external radiation 

 or internal absorption (gamma radiation) ........................................................................228 

Table 6.4 Diagnostic steps in acute radiation syndrome..............................................................229 

Table 6.5 Timing to onset of vomiting (prodrome) .....................................................................230 

Table 6.6 Dose assessment summary...........................................................................................231

Table 6.7 Guidelines for bioassay sampling................................................................................232 

Table 6.8 Antibiotics for treatment of post-radiation neutropenia ..............................................233 

Table 6.9 Threshold radioactive exposures and recommended prophylactic single 

 doses of KI .......................................................................................................................234 

Table 6.10 Radionuclide specific therapies .................................................................................235 

Table 6.11 Reduction in exposure by sheltering..........................................................................236 

Table 7.1 Expected injuries at relative distances from detonation to open air ............................258 

Table 7.2 Spectrum of primary blast injury on body systems .....................................................259 

Table 7.3 Principles of Advanced Trauma Life Support ............................................................260 

Table 7.4 Principles of Advanced Burn Life Support .................................................................262 

Table 8.1 Concepts of death and implications of incomplete understanding for 

 adjustment to loss.............................................................................................................292 

Table 11.1 Environmental constraints to pediatric medical care after large-scale 

 natural disasters................................................................................................................313 

Table 11.2 Pediatric medical complaints after large-scale natural disasters: challenges 

 and adaptations based on post-hurricane responses.........................................................314 
Chapter 1. Introduction 

Background 

A disaster is a calamitous event that affects a large population and generally results in 

injury, death, and destruction of property. A disaster can also be thought of as any 

occurrence that taxes or overwhelms local response resources (e.g., law enforcement, 

transportation, shelters, etc.). Local resources can be overwhelmed by natural disasters or 

other events that result in multiple casualties such as earthquakes, fires, large motor 

vehicle crashes, or terrorist incidents. Because disasters vary, preparation should vary 

accordingly. Disasters caused by terrorism or accidents (e.g., a multiple car crash on an 

interstate highway) can occur without warning. In other types of disasters, such as 

hurricanes, there is usually some time for warning and preparation. Some disasters end 

quickly, while others can affect large populations over an extended period of time (e.g., a 

humanitarian disaster involving famine). Disasters can have physical, mental, and 

emotional effects on a large number of people without regard to age or other factors. This 

widespread negative impact is what makes terrorist attacks so effective. 

An understanding of the many types of disasters (Table 1.1) and the implications of each 

is essential for preparedness planning. In all cases, terrorism and disaster planning can be 

divided into three phases: 

1. The primary, or response, phase consists of actions and care taken during and 

immediately after the disaster. 

2. The secondary response, also called the recovery phase, is the period during 

which affected people work toward reestablishing normalcy. Emotional and 

mental health problems usually begin to emerge during this phase. 

3. The tertiary response, or the mitigation phase, consists of efforts to apply lessons 

learned to prevent future disasters or to lessen their impact. 

The lessons learned from past terrorist events and natural disasters should guide plans for 

future preparation and response. The first lesson is that natural disasters and terrorist 

events can and do occur in the United States. The second is that bombs, germs, toxic 

gases, and the forces of nature do not discriminate between children and adults. Despite 

our best efforts to shelter and protect them, children remain among the most vulnerable 

victims of terrorism and disasters. A third lesson is that disasters cannot always be 

predicted or prevented; they have the potential to affect anyone at any time. These 

lessons underscore the need for preparation by planning a comprehensive system of 

response that fully addresses and integrates the needs of everyone, including children. 

Several terrorist events in recent years have had profound consequences for children and 

families. When the Murrah Federal Building in Oklahoma City was bombed in 1995, 19 

children at the child care center inside the building were killed, and many more were 

injured. Hundreds of other children lost parents or relatives, and countless more suffered 

emotionally. Thousands of children lost parents in the terrorist attacks of 2001 at the 

World Trade Center and the Pentagon. 

1
There are many gaps in knowledge, especially with regard to children, regarding disaster 

preparation and planning. Historically, the unique characteristics and needs of children 

have not been adequately addressed in the planning process for response to terrorism. 

Why is this so? In the past, much of the terrorism response planning in the United States 

has centered on military preparedness, and therefore, plans have focused on the needs of 

adults. As we plan for response to terrorism, it is time to reassess education and planning 

for all disasters and to ensure that children and their families are included. Ensuring 

appropriate care for children during disasters cannot be accomplished by simply 

modifying current practices. Basic day-to-day issues that involve families have not been 

considered previously (e.g., incorporating schools and child care centers into disaster 

preparation and planning; also, planning for the likelihood that numerous children will 

become separated from their families) and should now be addressed. (See also Chapter 9, 

Integrating Terrorism and Disaster Preparedness into Your Pediatric Practice and Chapter 

11, Conclusion.) The likelihood of a disaster occurring while children are in school or at 

child care centers is high, and the site of the disaster could even be at the school or child 

care center. 

Incorporating the needs of children and families into terrorism and disaster planning 

requires multidisciplinary pediatric expertise at all phases. This Pediatric Terrorism and 

Disaster Preparedness resource presents information on including children and families 

at all levels of terrorism and disaster planning. A few of the many considerations include 

the following: 

• Writing and implementing child-specific protocols. 

• Planning for children who are separated from their parents and at schools and 

child care centers when disaster strikes. 

• Training providers to care for pediatric patients. 

• Developing equipment and medication dosage forms and delivery systems 

appropriate for children. 

• Providing education on the recognition and care of mental health needs of 

children in the aftermath of a disaster. 

• Planning for children with special health care needs. 

This resource is intended primarily to educate, inform, increase awareness among, and 

assist pediatricians in recognizing and fulfilling their important roles in disaster 

preparedness and response. Families and communities turn to pediatricians for 

anticipatory guidance on all issues involving children. Pediatricians can help families 

plan their response to disaster by referring them to available resources. The Family 

Readiness Kit has been developed by a coalition of the American Academy of Pediatrics 

(AAP), the American College of Emergency Physicians (ACEP), and 27 other State and 

national organizations to assist families in planning (see 

www.aap.org/family/frk/frkit.htm). 

Questions regarding immunization for infectious agents such as smallpox, antibiotic 

prophylaxis after exposure to infectious agents, coping with the effects of exposure to 

2
violence, and disaster preparedness in the home are common. Pediatricians should be 

ready to provide accurate answers. The AAP Web site includes information, created by 

the AAP Task Force on Terrorism, on disaster preparedness to meet the needs of children 

(www.aap.org/disaster), as well as links to many other sources of information. 

Pediatricians enjoy a high degree of public trust as expert sources of information and 

support on matters involving the health and well-being of children and families. 

Therefore, their roles in disaster preparedness and management are extremely important. 

For example, pediatricians act as first responders and care providers when the emergency 

medical system and emergency departments become rapidly overwhelmed in the 

recovery and mitigation phases of incidents of terrorism or disasters. Pediatricians, 

especially in instances of bioterrorism (such as the case of anthrax in an infant in New 

York City), could be the first to see victims and determine a diagnosis. This means that 

pediatricians should acquire further knowledge of infections and the effects of exposure 

to toxins that most likely they have never seen. Residency training in pediatrics has been 

limited on subjects such as biological and chemical terrorism, as well as nuclear 

exposure, and it should be broadened accordingly. Children’s hospitals, which serve 

many communities, should also generate and implement this information. 

The pediatric office could also be involved in the first response phase after a disaster. A 

good first step for the pediatrician is preparation of an office disaster plan that is 

periodically updated and practiced (see also Chapter 9, Integrating Terrorism and 

Disaster Preparedness into Your Pediatric Practice). As the office plan is prepared, 

pediatricians should consider other roles they might have in the community disaster 

response and familiarize themselves with liability and licensure issues. Working with an 

agreement with local/state government agencies to provide disaster services affords the 

best liability coverage and often allows reimbursement. For a discussion of their liability, 

pediatricians should review the AAP Policy Statement (reaffirmed in 2004) 

Pediatricians’ Liability During Disasters (see 

http://aappolicy.aappublications.org/cgi/content/full/pediatrics;106/6/1492). 

Recommendations include the following: 

• Familiarity with State statutes and protections afforded while providing 

emergency care during a disaster. 

• Familiarity with individual liability insurance coverage outside of the usual 

practice settings when providing urgent and routine care. 

• Working in concert with response agencies when providing disaster relief. 

Parents turn to pediatricians for help, guidance, support, treatment, and referral regarding 

mental health issues in the recovery and mitigation phases of disaster. A wide range of 

reactions can be expected, from anxiety to adjustment reactions and posttraumatic stress 

disorder (PTSD). The effects can be direct or indirect, affecting children who were not 

actually involved in the disaster. Parents will turn to pediatricians with many questions 

regarding how to explain the reasons for disaster, whether to let their children watch the 

events on television, and what to say about loved ones or acquaintances who have been 

3
injured or killed (see also Chapter 8, Mental Health Issues). Pediatricians should be able 

to recognize potential symptoms of adjustment reactions and PTSD and to give parents 

coping strategies and referrals. The role of pediatricians in the mental health care of 

children after terrorism and disasters is described in a recent article, “Psychosocial 

implications of disaster or terrorism on children: A guide for the pediatrician,” which is 

available at http://www.pediatrics.org/cgi/content/full/116/3/787. 

The pediatrician’s perspective is well-suited to assist in the community planning process. 

Pediatricians have an appreciation for children as part of families that comprise 

communities that become regions, States, and so on. This perspective is valuable, but 

pediatricians may have limited knowledge and skill in planning and response. 

Pediatricians should educate themselves, acknowledge their limitations, and/or obtain 

outside expert input. The role of the pediatrician has been comprehensively described and 

defined in the AAP Policy Statement The Pediatrician’s Role in Disaster Preparedness

prepared by the Committee on Pediatric Emergency Medicine 

(http://pediatrics.aappublications.org/cgi/content/full/99/1/130). 

Pediatricians are respected advocates for children. In this role, pediatricians should 

advocate for resources and products that currently do not exist for children, especially for 

children with special health care needs (including the chronically ill and technologically 

dependent). For example, children cannot always be decontaminated in adult 

decontamination units. Skin decontamination showers that are safe for adults may cause 

hypothermia in children unless warming equipment (e.g., heating lamps) is provided. 

Decontamination systems should be designed for use with children of all ages, for the 

child unaccompanied by a parent, for the nonambulatory child, and for the child with 

special health care needs. Little protective gear is available for children; when its use has 

been attempted, such as with gas masks, mishandling has led to fatalities from 

suffocation. 

Vaccines for anthrax and plague are not approved for use in children. The frequency of 

serious complications after administration of smallpox and yellow fever vaccines is 

higher in children than in adults; development and approval of safer vaccines are needed 

(see also Chapter 4, Biological Terrorism). Antidote kits for use after nerve agent 

exposure such as the Mark-1 kit (for adults) have only recently been developed for 

children (see Chapter 5, Chemical Terrorism). Common systems for determining drug 

dosages in children do not include dosages for antidotes. Recently, a liquid preparation of 

potassium iodide (65 mg/cc) has come on the market for use in preventing radiationinduced thyroid effects after radiation exposure (see also Chapter 6, Radiological and 

Nuclear Terrorism and the AAP Policy Statement on Radiation Disasters and Children at 

www.aap.org/policy/s040208.html). 

Planning and preparation for terrorism and disasters can be both daunting and 

challenging. For all, but especially for children, there are many recognized gaps in 

knowledge, resources, and professional education. This resource has been provided to 

increase pediatric expertise of those taking on the challenge of preparation and planning. 

This resource will be invaluable, not only for pediatricians, but also for other pediatric 

4
health care providers, public health professionals, health administrators, and 

policymakers who are committed to ensuring that planning for terrorism and disasters 

includes the special needs of children. 

Children Are Not Small Adults 

Many important differences distinguish children from adults and are the origin of the oftused truism “you can’t treat children as small adults.” Children have many unique 

anatomic, physiologic, immunologic, developmental, and psychological considerations 

that potentially affect their vulnerability to injury and response in a disaster. Failure to 

account for these differences in triage, diagnosis, and management of children is most 

often due to lack of knowledge or experience, or both. Experience has shown that such 

lack of knowledge and experience can result in grave errors, increasing the child’s risk of 

serious harm, and even death. 

Anatomic Differences 

An obvious difference between children and adults is size. Children are smaller than 

adults and vary in size depending on stage of growth and development. Their small size 

makes them more vulnerable to exposure and toxicity from agents that are heavier than 

air such as sarin gas and chlorine. These agents accumulate close to the ground in the 

breathing zone of infants, toddlers, and children. 

A child’s smaller mass means greater force applied per unit of body area. The energy 

imparted from flying objects, falls, or other blunt or blast trauma is transmitted to a body 

with less fat, less elastic connective tissue, and closer proximity of chest and abdominal 

organs. The result is a higher frequency of injury to multiple organs. 

A smaller body has smaller circulating blood volume (on average 80 mL/kg) and less 

fluid reserve. These differences have several important implications. Volumes of blood 

loss that would be easily handled by an adult can result in hemorrhagic shock in a child. 

Children are more vulnerable to the effects of agents such as staphylococcal enterotoxins 

or Vibrio cholerae that produce vomiting and diarrhea. Therefore, infections that might 

cause mild symptoms in adults could lead to hypovolemic dehydration and shock in 

infants, small children, and children with special health care needs. 

The child’s skeleton is more pliable than that of adults. It is incompletely calcified with 

active growth centers that are more susceptible to fracture. Orthopedic injuries with 

subtle symptoms and physical findings are easily missed in preverbal children. Internal 

organ damage can occur without overlying bony fracture. Serious cardiac or lung injuries 

without having incurred rib fractures are common. 

A child’s cervical spine is subject to distracting forces that are more likely to disrupt the 

upper cervical vertebra and ligaments. Numerous bony anatomic variations render the 

interpretation of radiographs potentially confusing. Additionally, children can have spinal 

cord injury without radiographic abnormality. 

5
Head injury is common in children. The head is a larger, heavier portion of a child’s body 

compared with the head of an adult. It accounts for a larger percentage of body surface 

area (BSA) than it does in adults, and it is a major source of heat loss. It is supported by a 

short neck that lacks well-developed musculature. The calvarium is thin and vulnerable to 

penetrating injury, thus allowing greater transmission of force to the growing brain of a 

child. The brain doubles in size in the first 6 months of life and achieves 80% of its adult 

size by age 2. During childhood, there is ongoing brain myelinization, synapse formation, 

dendritic arborization, and increasing neuronal plasticity and biochemical changes. Injury 

to the developing brain can affect or arrest these processes, resulting in permanent 

changes. 

The mediastinum is very mobile in children. Subsequently, a tension pneumothorax can 

quickly become life-threatening when the mediastinum is forced to the opposite side, 

compromising venous return and cardiac function. 

The thoracic cage of a child does not provide as much protection of upper abdominal 

organs as that of an adult. Hepatic or splenic injuries from blunt trauma can go 

unrecognized and result in significant blood loss leading to hypovolemic shock. 

The airway differs between children and adults. The tongue is relatively large compared 

with the oropharynx, which creates the potential for obstruction of a poorly controlled 

airway. The larynx is higher and more anterior in the neck, and the vocal cords are at a 

more anterocaudal angle. The epiglottis is omega-shaped and soft. The narrowest portion 

of the airway is the cricoid ring, not the vocal cords as in adults. Airway differences 

combine to make the child’s airway more difficult to maintain as well as to intubate. The 

short length of the trachea increases the risk of a right mainstem bronchus intubation. The 

lungs are smaller and subject to barotraumas, resulting in pneumothorax with 

inappropriate ventilation. 

The BSA to mass ratio is highest at birth and gradually diminishes as the child matures. 

The distribution of BSA also differs between children and adults. Children have a higher 

percentage of BSA devoted to the head relative to the lower extremities. This should be 

taken into account when determining the percentage of BSA involved in burn injuries and 

in treating or preventing hypothermia. 

The higher BSA to mass ratio also leads to more rapid absorption and systemic effects 

from toxins that are absorbed through thinner, less keratinized, highly permeable skin. 

Physiologic Differences 

Children differ physiologically in many ways from adults. They can compensate and 

maintain heart rate during the early phases of hypovolemic shock; this false impression of 

normalcy can lead to administration of too little fluid during resuscitation. This can be 

followed by a precipitous deterioration with little warning. 

Vital signs, including heart rate, respiratory rate, and blood pressure, vary with age. 

Caregivers should be able to quickly interpret whether a child’s vital signs are normal or 

6
abnormal for age. Temperature is an often forgotten but important vital sign in injured 

children. The child’s ability to control body temperature is affected not only by the BSA 

to mass ratio but also by thin skin and lack of substantial subcutaneous tissue. These 

factors increase evaporative heat loss and caloric expenditure. In fact, hypothermia is a 

significant risk factor for poor outcomes in many illnesses/injuries. Considerations of 

methods to maintain and restore normal body temperature are critical to the resuscitation 

of children. These can include thermal blankets, warmed resuscitation rooms, warmed 

intravenous fluids, and warmed inhaled gases. 

Children have a higher minute ventilation per kilogram of body weight than adults. This 

means that over the same period of time, they are exposed to relatively larger doses of 

aerosolized biological and chemical agents than are adults. The result is that children 

suffer the effects of these agents much more rapidly. Children are also more likely to 

absorb more of the substance from the lungs before it is cleared or diffused through 

ventilation. 

Fluid resuscitation, drug dosages, and equipment sizes are based on the child’s weight. 

Estimating the weight of a child can be difficult, particularly for health care workers with 

limited pediatric experience. An easy, quick method for determining a child’s weight is to 

use the Broselow–Hinkle Pediatric Resuscitation Measuring Tape®. This tool rapidly 

provides many common drug dosages and fluid resuscitation volumes. Health care 

providers should also make appropriate fluid choices for resuscitation. Children who 

receive large volumes of hypotonic fluid are at risk of hyponatremia and seizures. 

Limited glycogen stores and a higher relative metabolism in children than in adults puts 

children at a higher risk of hypoglycemia. Children compensate for cardiovascular and 

pulmonary problems with tachycardia and tachypnea (their ability to increase stroke 

volume and tidal volume is limited). 

Immunologic Differences 

Children have an immature immunologic system, which places them at higher risk of 

infection. Immunologically, children have less herd immunity from infections such as 

smallpox and a unique susceptibility to many infectious agents. For example, Venezuelan 

equine encephalitis is usually a brief, self-limiting infection in adults. In children, it can 

be severe, and life-threatening encephalitis develops in 4% of victims. Children 

immunized with the current smallpox vaccine are over-represented with serious side 

effects such as encephalitis. 

Developmental Differences 

Developmental differences between children and adults are also readily apparent. 

Children, especially infants and toddlers, might be unable to describe symptoms or 

localize pain. Children rely on parents or others caregivers for food, clothing, and shelter. 

Infants especially are vulnerable when their food sources are eliminated or contaminated. 

7
In situations of disaster, caregivers can be injured, killed, or simply not present. Children, 

especially infants and toddlers, are limited in their verbal ability to communicate their 

wants and needs. Children also have motor skills that are insufficient to escape from the 

site of an incident. Additionally, their cognitive development may limit their ability to 

figure out how to flee from danger or to follow directions from others, or even to 

recognize a threat. The developing brain has emotional instability with an inadequate 

ability to interact in stressful situations and an emotional state frequently dictated by that 

of their caregivers. A child’s reaction to danger or threat is influenced by their 

developmental stage, which means that responders should be familiar with ageappropriate interventions. 

Younger children are unable to take care of their needs for activities of daily living, so an 

adult caregiver must oversee them. Children with special needs often cannot perform 

some activities of daily living or medical interventions by themselves. Planning/response 

must allow for adult caregivers. 

Psychological Differences 

The psychological effects of disaster on children are neither uniform nor universal in 

nature (see Chapter 8, Mental Health Issues). Important factors in the psychological 

effect of a disaster on children include the nature of the disaster itself, the level of 

exposure to the disaster, the extent to which the children and those around them are 

personally affected, and individual characteristics of each child. In addition, children are 

unique because they are affected not only by their own reaction to the trauma of the event 

but also by their parent’s fears and distresses. Because children depend on adults for their 

emotional and psychological needs, any effects of trauma on adults can magnify the 

psychological impact on children. 

Children are still undergoing psychological development at the time of disaster. Their 

developmental stage characterizes their response and is responsible for the wide degree of 

variability in adjustment to traumatic events. This means that therapeutic interventions 

should be developmentally appropriate. 

The response of younger children is characterized by changes in mood and behavior and 

by anxiety. Younger children may exhibit regressive behaviors, increased temper 

tantrums, and symptoms of clinginess and difficulty with separation or sleep. Even 

infants whose lives have been disrupted by a disaster manifest symptoms of crying and 

irritability, separation anxiety, and a hyperactive startle response. 

School-age children may exhibit depression, anger, and despair. Their anxiety may be 

exacerbated by unrealistic fears for parents, families, and friends. They also may develop 

problems at school or somatization symptoms, typically with complaints of headache or 

abdominal pain. 

Adolescents differ from adults in their psychological response because they are in a 

period of development characterized by complex physical, psychological, and social 

transitions. They are especially vulnerable to the development of major psychiatric 

8
disorders such as depression. Of significant importance is the likelihood of engaging in 

risk-taking behaviors such as drug abuse or sexual relationships. Adolescents are also 

particularly vulnerable to impulsive behaviors including suicide. In addition, adolescents 

may try to hide their feelings or symptoms for fear of being perceived as abnormal. It is 

imperative that these symptoms not be minimized or overlooked because adjustment 

reactions left unrecognized and untreated can lead to lifelong behavioral and emotional 

problems. 

Overview of Practical Considerations for Children and 

Families During Disasters 

The anatomic, physiologic, immunologic, developmental, and emotional differences 

between children and adults give rise to many practical considerations for planning. 

Emergency medical services (EMS) agencies should consider adopting triage tools such 

as JumpSTART® (http://www.jumpstarttriage.com/) that use physiologic decision points 

adapted for ranges of pediatric normals and that consider apnea as a potentially 

salvageable respiratory emergency. The AAP has prepared a resource and course that 

provides training equipment guidelines for prehospital providers in the care of children, 

Pediatric Education for Prehospital Professionals (http://www.peppsite.com/). 

Surge Capacity 

Surge capacity is the ability of a hospital or other health care facility to expand quickly 

beyond normal services to meet an increased demand for medical care in the event of 

bioterrorism or other large-scale public health emergency. Converting a hospital or other 

health care facility from its current capacity to surge capacity is a daunting task. In 

addition to ensuring that essential supplies, staff, and services are available, planners also 

must ensure that facilities can accommodate the needs of vulnerable groups, such as 

children, the elderly, and the disabled. 

Pediatric Readiness 

Ambulances, clinics, and hospital emergency departments typically carry only limited 

quantities of pediatric equipment. Sufficient supplies and equipment should be readily 

available to treat large numbers of pediatric victims. Because equipment choices and drug 

dosages, including IV rates, depend on the child’s size, a quick, convenient system to 

guide appropriate choices should be in place. The system used should be comprehensive 

enough to include dosages for antidotes and other medications that may be relevant 

during a terrorist event. A surge in pediatric victims can quickly overwhelm hospital, 

regional, and even State pediatric capacity, so strategies should include solutions that 

involve hospital, regional, State, and Federal planning to manage such surges. Plans 

should also consider that pediatric victims will present as families when injured adults 

refuse to be separated from their children. 

The resuscitation of children can be further complicated by the technical difficulty of 

procedures such as intubation and intravenous access. Alternative methods for 

9
maintaining and securing the airway should be considered. When veins are small and/or 

constricted from shock or hypothermia, the equipment for alternative methods, such as 

intraosseous access, should be readily available. 

Planning should consider all potential aspects of a child’s life. Therefore, it should 

account for children who are at home, in school or child care, or in transit, as well as for 

children who cannot be reunited with their families. School disaster plans should 

coordinate with community plans and should also consider post-incident stress 

management during the recovery phase. Child care centers and community youth centers 

should have disaster plans that focus on ensuring safety, accessing and interacting with 

community emergency responders, notifying guardians, and reuniting families. 

Children are predisposed to illness and injury after a disaster for a variety of reasons. 

There can be lack of adult caretaker supervision, and the usual resources of school or 

child care may be unavailable. Environmental hazards can be increased from collapsed 

buildings or dangerous tools or from chemicals or availability of weapons. Increased 

stress on adults might lead to a higher risk of domestic violence or child abuse. Contagion 

present in the community, especially infections such as respiratory syncytial virus or 

influenza, may spread rapidly in group shelters. Contaminated food or water can lead to 

epidemic outbreaks of infectious diseases, resulting in gastroenteritis and dehydration. 

Changes in the environment can lead to heat-related illness or hypothermia. Use of 

alternative sources for heating or generators can lead to carbon monoxide exposure. 

Children with asthma may have acute exacerbations due to stress or environmental 

contaminants. Medications may be forgotten or the supply may be exhausted, resulting in 

exacerbations of chronic illnesses. Stress can produce a variety of symptoms in children 

including headaches, abdominal pain, chest pain, vomiting, diarrhea, constipation, 

changes in sleep, and changes in appetite. 

Many considerations in planning are prompted by the possibility of children in shelters. 

These include supplies and services such as diapers, infant formula, other childappropriate food, and games and other distractions for children. Staffing is an issue with 

regard to supervision. Shelters should be childproofed to promote safety for children as 

well as the elderly. Sick children should be isolated. Children should be protected from 

environmental hazards such as weapons, alcohol, and cigarette smoke. Children with 

special health care needs, especially those that depend on technology for survival, are 

particularly vulnerable and should be considered in shelter planning. Also, parents/single 

parents with sick children cannot be caregivers simultaneously for both a hospitalized 

child and non-hospitalized, sheltered children. 

Planning should also include pregnant women, the fetus, and the newly born. The stress 

of a disaster can contribute to premature labor and delivery. Infection acquired by the 

fetus in utero can lead to fetal death or to devastating consequences if the fetus survives. 

The risk of developing cancer is higher in children who have been exposed to radiation in 

utero. Radioactive iodine is transmitted to human breast milk and threatens infants who 

are breastfeeding. Cow’s milk can also be quickly contaminated if radioactive material 

settles onto grazing areas, threatening alternative sources of nutrition. 

10
Summary 

As demonstrated by past events, there is ample opportunity to improve preparedness for 

children involved in disasters (both man-made and natural). This Pediatric Terrorism and 

Disaster Preparedness resource contains information needed for pediatricians to be 

prepared for disasters at all phases of planning, response, recovery, and mitigation. The 

role of the pediatrician should not be minimized, underestimated, or overlooked in 

disaster planning and response. Pediatricians, based on their traditional roles in 

prevention, anticipatory guidance, and advocacy, can make a difference in 

comprehensive public health plans for disaster. 

Bibliography 

• American Academy of Pediatrics Task Force on Terrorism. Policy statement: how 

pediatricians can respond to the psychosocial implications of disasters. 

Pediatrics. 1999;103(2):521–523. Available at: 

http://aappolicy.aappublications.org/cgi/content/full/pediatrics;103/2/521. 

Accessed August 17, 2006. 

• American Academy of Pediatrics Committee on Environmental Health and 

Committee on Infectious Diseases. Chemical-biological terrorism and its impact 

on children. Pediatrics 2006 September; 118(3):1267-1278. Available at: 

http://pediatrics.aappublications.org/cgi/content/full/118/3/1267?submit.y=12&su

bmit.x=83&cga=118%2F3%2F1267&. Accessed September 6, 2006. 

• American Academy of Pediatrics Committee on Pediatric Emergency Medicine. 

Policy statement: the pediatrician’s role in disaster preparedness. 

Pediatrics.99(1)130-133. 

• American College of Surgeons Committee on Trauma. Pediatric Trauma in 

Advanced Trauma Life Support Manual, 6th ed. Chicago: American College of 

Surgeons; 1997. 353–375. 

• Cieslak TJ, Henretig FM. Bioterrorism. Pediatr Annals. 2003;32(3):1–12. 

• Hagan JF, Committee on Psychosocial Aspects of Child and Family Health, Task 

Force on Terrorism. Psychosocial implications of disaster or terrorism on 

children: a guide for the pediatrician. Pediatrics. 2005; 116:787-95. Available at: 

http://www.pediatrics.org/cgi/content/full/116/3/787. Accessed August 21, 2006. 

• Markenson D, Redlener I, eds. Pediatric Preparedness for Disasters and 

Terrorism: a National Consensus Conference; New York. New York: National 

Center for Disaster Preparedness, Columbia University; 2003. 

• Romig LE. Pediatric triage: a system to JumpSTART your triage of young 

patients at MCIs. JEMS. 2002;27(7):52–63. 

• Romig LE. Disaster Management. In APLS: The Pediatric Emergency Medicine 

Resource 4th ed. Gausche-Hill M, Fuchs S, Yamamoto L (eds). Sudbury MA: 

Jones and Bartlett; 2003. 542–567. 

• Schonfeld DJ. Almost one year later: looking back and looking ahead. J Dev 

Behav Pediatr. 2002;23(4):292–294. 

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• Schonfeld DJ. In times of crisis, what’s a pediatrician to do? Pediatrics. 

2002;110(1 Pt 1):165. 

• Schonfeld DJ. Supporting adolescents in times of national crisis: potential roles 

for adolescent health care providers. J Adolesc Health. 2002;30(5):302–307. 

12
Table 1.1 Types of disasters 

Natural Disasters 

 Hurricanes or cyclones Droughts 

 Tornadoes Wildfires 

 Mudslides Earthquakes 

 Tsunamis Infestations or disease epidemics 

 Ice or hail storms 

Technological Disasters 

 Hazardous materials 

releases or spills 

 Transportation crashes or 

derailments 

 Unintentional explosions 

or collapses 

 Power outages 

Terrorism, National or International Violence 

 Bombings or explosions Multiple or mass shootings 

 Chemical agent releases Cult-related violence 

 Biological agent releases Riots 

 Nuclear agent releases Arson 

Humanitarian Disasters, Complex Emergencies 

 War or violent political 

conflict 

 Genocidal acts 

 Famine Shelter, feeding, or medical care 

of displaced populations 

 Droughts 

Source: Courtesy of the American Academy of Pediatrics. From: Romig LE. Disaster Management. In 

APLS: The Pediatric Emergency Medicine Resource 4th ed, Gausche-Hill M, Fuchs S, Yamamoto L (eds). 

Sudbury MA: Jones and Bartlett, 2003. pp 542-567.

13
14
Chapter 2. Systems Issues 

Types of Disasters 

Disasters are sudden calamitous events that can result in great damage, loss, injury, and death. 

They can occur naturally, such as floods, earthquakes, hurricanes, tornados, tsunamis, or 

wildfires, or they can be caused by human error or intervention. The widespread injury and 

disruption associated with disasters can pose difficult problems for health care providers 

including triage of mass casualties, disruption of infrastructure (e.g., loss of power and fresh 

water), and the need to deal with the mental anguish associated with uncertainty and the loss of 

loved ones. 

The degree of injury, death, and damage caused by disasters is influenced by many factors, 

including population location and density, timing of the event, and community preparedness 

(e.g., emergency response infrastructure, local building codes, etc). Similarly, recovery after a 

disaster is influenced by resources (e.g., savings, insurance, and relief aid), preexisting 

conditions (e.g., season, local infrastructure, etc), experience, and access to information. In 

almost all cases, disasters are associated with mental and physical stress (both during and after 

the event) that can increase morbidity and mortality over and above that caused directly by the 

event itself. 

Natural Disasters 

Natural disasters usually occur suddenly and are often uncontrollable. However, they frequently 

cluster temporally or geographically, and therefore are somewhat predictable. In the United 

States and other developed countries, most natural disasters tend to cause extensive damage and 

social disruption with comparatively little loss of life. The most frequent types of natural 

disasters experienced in the United States are floods, earthquakes, hurricanes, tornados, and fires. 

Floods. The most common natural disaster is flood, which accounts for roughly 30% of disasters 

worldwide. Approximately 25–50 million Americans live or work in floodplains, and another 

110 million live in coastal areas. The frequency of flooding is increasing, due in part to 

increasing habitation in flood-prone areas and in part to deforestation and changing land-use 

patterns, which can increase the degree of flooding. 

Flash floods are especially hazardous and occur during sudden heavy rains, tidal surges, or when 

dams or levees give way. Most of the deaths during flash floods are caused by drowning, usually 

from people wading or driving through moving water. The hazards posed by rapidly moving 

water are often unrecognized. A gallon of water weighs 8 pounds; hundreds of gallons of rushing 

water represent thousands of pounds of force. As little as 2 feet of rushing water can carry a 

vehicle away, trapping the passengers. 

Except for flash flooding, floods generally are not directly associated with significant loss of life. 

However, flooding results in considerable destruction and disruption, and has the potential for 

widespread disease. Floodwaters frequently contain human or animal waste from sewage or 

agricultural systems that can lead to epidemics of infectious disease. Drinking water must be 

disinfected through boiling and/or chlorination, or an alternative clean water supply (e.g., bottled 

15
water) must be identified and made accessible. Water supplies and household surfaces can also 

become contaminated with petroleum products (e.g., fuel oil or kerosene), household chemicals, 

and molds. 

Contamination of floodwaters also poses a hazard to those participating in the clean up. Rubber 

boots and gloves should be worn, and open wounds and sores protected. Hands should be 

washed frequently, especially when handling food or food containers. Foods that may have been 

contaminated should be discarded. Eating utensils should be thoroughly washed with soap and 

hot water and disinfected with a solution of 1 cup bleach to 1 gallon water. All inside surfaces, 

especially those used for food preparation, should be similarly cleaned. Likewise, all child play 

areas need to be cleaned and disinfected, along with all toys, clothing, etc. Materials that cannot 

be readily disinfected should be discarded. 

Earthquakes. Earthquakes are a potential hazard throughout the continental United States, 

especially within the tectonically unstable areas of California, Idaho, Utah, and the Pacific 

Northwest. Only part of the destruction caused by earthquakes and their aftershocks occurs 

during the event. Subsequent events triggered by the quake, such as fires, tidal waves, and so on, 

can cause significant destruction. 

The force of an earthquake is measured on the Richter scale, which estimates the energy 

imparted by the quake or aftershock. Every increasing Richter unit represents an increase in 

energy by an order of magnitude. Richter units can be used as an estimate of earthquake 

probability/frequency, with an order of magnitude decrease in likelihood with every unit 

increase. For example, on average approximately 2 earthquakes of magnitude 8 are expected 

worldwide per year, 20 quakes of magnitude 7, and 200 quakes of magnitude 6. 

Although earthquakes cannot be prevented, much of the injury and damage they produce can. 

Improvements in emergency response and health infrastructure can speed up response time and 

lessen death and disability. Perhaps most importantly, structures built under improved building 

codes and with stronger construction materials can survive earthquakes with less damage. Also, 

as with all natural disasters, damage can be mitigated considerably through simple preventive 

measures, such as turning off utilities, securing appliances, and taping windows. 

Hurricanes and tornados. Hurricanes and tornados are similar weather events that differ in 

magnitude and location. Both involve rotating masses of air associated with severe weather. 

Tornados usually measure only a few hundred meters across and travel over only a few 

kilometers of land, while hurricanes can stretch over hundreds of kilometers. Both can have 

winds of up to 200 mph, but hurricanes are associated with much more energy and have much 

more potential for destruction. Tornados develop primarily over landmasses, especially those 

within the Midwestern and Southwestern United States, while hurricanes are associated with the 

coastal United States, primarily the East and Gulf coasts. 

Although hurricanes are associated with high winds, much of the destruction they cause is from 

the so-called “storm surge” and subsequent flooding. High winds and low pressure can cause 

water to pile up in coastal areas up to 14 meters above normal sea level. This can result in all the 

16
problems noted above for flooding, including the risk of drowning, electrocution, and disease 

associated with contaminated drinking water. 

Much of the risk associated with these severe weather events can be mitigated through advanced 

warning and preparation. This is especially true for tornados, because of their sudden onset. 

Redundant warning systems should be developed, and everyone should be encouraged to 

practice tornado drills. Special outreach efforts should be made to those with special needs or 

disabilities, including designation of a “buddy” who knows the individual’s needs and can ensure 

that they are prepared for an emergency. Each person/family should have a tornado shelter (e.g., 

cellar, basement, etc) that is equipped with an appropriate emergency kit. 

Most of the injury and death associated with hurricanes is through failure to heed warnings. 

Individuals may refuse to evacuate or seek shelter, may not properly secure their property, and 

may ignore guidelines on food and water safety and injury prevention. Therefore, effective risk 

communication is important both in preparation for the event and during cleanup and mitigation 

efforts. 

Tsunamis. Underwater earthquakes can result in the formation of gigantic waves that can cross 

thousands of miles of ocean at speeds up to 500 mph. These waves are often no taller than windgenerated waves, but they are much more dangerous. Tsunamis have long wavelengths up to 

several hundred miles, making them more like prolonged flood waves than normal surf. The 

waves slow as they reach shallow water, causing them to crest at heights up to 100 feet. When 

the waves break, they can destroy piers, buildings, and human life far inland. There is little 

warning as a tsunami wave front approaches the coast, allowing few life-saving preventive 

actions. Therefore, the best hope for protecting human life is prediction and advance warning 

through seismology, wave gauges, etc. 

Wildfires. Brush or forest fires can disrupt communities and cause substantial property damage, 

displacement, serious burns, and death. In addition, smoke from wildfires can result in irritation 

and respiratory difficulties, especially among those with preexisting medical conditions or 

impairment. As with other natural disasters, serious injury and death often result from failure to 

evacuate or otherwise heed warnings. Official agencies need to make provisions for those with 

disabilities to ensure that they are evacuated and that their special needs are addressed. 

Manmade and Technological Disasters 

Anthropogenic disasters are explosions, chemical releases, etc, directly associated with human 

action. They can be caused by accidents or deliberate malicious activities or when industrial 

facilities are disrupted by natural disasters. Examples of accidental anthropogenic disasters 

include the Bhopal chemical release and the Three-Mile Island nuclear accident. Intentional 

disasters include arson and terrorist attacks, such as the events of September 11, 2001. 

Anthropogenic disasters share many of the characteristics of natural ones but are typically less 

predictable. 

Accidental anthropogenic disasters. Accidental anthropogenic disasters include a broad range 

of incidents that vary with the nature of the industry involved. These include hazardous material 

releases of various types (e.g., caustic agents, asphyxiants, radioactive materials), fires, 

17
explosions, structural collapses, transportation failures, and many more. The medical and public 

health responses to such events depend on the incident and type of hazardous material involved. 

Although less predictable than natural disasters, accidental disasters are more preventable. Basic 

safety procedures and equipment, adequate training, and proper maintenance can go a long way 

toward preventing accidents. Emergency response training, safety drills and simulations, and 

medical training in appropriate responses to hazardous agents can greatly limit subsequent injury 

and death when accidents occur. 

Intentional anthropogenic disasters. Intentional manmade disasters are the least predictable, 

with no restrictions other than the limits of the imagination of a deviant mind. The nature of 

these disasters can vary from simple arson or sabotage, to release of chemical or biological 

agents, or even to detonation of a primitive nuclear device. These disasters are associated with 

most of the hazards described for accidental, and sometimes even natural, disasters. However, 

the malicious nature of the event and the fear associated with biological, chemical, and nuclear 

agents result in even greater stress and social disruption. 

Terrorists do not consider the age of victims, only the impact of their act on furthering a cause. 

Children have been and will be victims of terrorist acts. Schools, gyms, sporting events, concerts, 

amusement parks, shopping malls, or any other place where there are mass gatherings are all 

potential terrorist targets. Release of a product into the ventilation system of a local school or any 

of the other sites could result in rapid spread of an agent throughout a community. 

Aftermath 

Many deaths are possible in the aftermath of a disaster. Because considerable injury and 

destruction can be associated with any disaster, management after a disaster is critically 

important. The disruption caused by disasters can result in widespread disease from unhygienic 

conditions. Fuel leaks, live wires, and other hazards can cause injury or start fires. The physical 

and emotional stress associated with the event and cleanup can result in heart attacks, 

musculoskeletal injuries, mental illness, and other stress-related disorders. Displaced wildlife can 

hamper relief efforts and endanger workers. Injuries can also result from improper use of chain 

saws or other mechanical equipment involved in clean-up efforts. Children are especially prone 

to injury or poisoning through access to debris, chemicals, equipment, and other agents 

discovered while exploring in the aftermath of the disaster. 

When returning to a building or structure after a disaster, occupants need to check for structural 

damage, gas leaks, downed power lines, or other potentially hazardous situations. Sites should be 

inspected during daylight so that hazards are visible, and only battery-powered flashlights or 

lanterns should be used for auxiliary light, rather than candles, gas lanterns, or other open-flame 

devices. 

Immediately after a disaster, governments and community organizations will be called upon to 

provide safe (e.g., bottled) drinking water, as well as shelter, food, clothing, and medical care for 

displaced people. Victims will also look to these organizations for other services, including 

counseling and assistance with insurance claims and other sources of emergency funds. 

18
Federal Response 

The United States has established a robust emergency medical support infrastructure to respond 

to disasters at local, State, regional, and Federal government levels. Many response resources are 

deployable and can be relocated to accommodate varying disaster scenarios. Other response 

resources are integral to established health and medical systems in our country and provide 

health care to Americans and others on a daily basis. Populations with specific emergency 

medical needs in disasters—such as neonatal, pediatric, or adolescent populations—have limited 

support that is quickly available and specifically designed for to meet their urgent life-sustaining 

needs. 

Response resources dedicated to pediatric populations continue to be inadequate for most 

emergency medical response activities related to disasters, even though victims often include 

children. Many children were injured or killed during the attacks on the World Trade Center in 

New York City and the Federal Building in Oklahoma City, and countless more witnessed these 

events. These experiences highlight the need to include pediatric and other special populations in 

local, State, regional, and Federal disaster medical planning. Table 2.1 depicts the types of 

disasters that my require Federal assistance. 

 

Centers for Disease Control and Prevention 

The Department of Health and Human Services (DHHS) is the lead Federal agency for public 

health issues. The Centers for Disease Control and Prevention (CDC), one of 12 DHHS agencies, 

provides support to the Department in carrying out its mission. CDC priorities include disease 

prevention and control, environmental health, and health promotion and education activities. 

Within CDC, the Director’s Emergency Operations Center (DEOC) operates 24 hours a day, 7 

days a week to provide emergency consultation and assistance to clinicians, State and local 

health agencies, and citizens. The DEOC can be reached at 770-488-7100. The Clinician 

Information Line (877-554-4625) is available to clinicians 24 hours a day to provide guidance on 

the management of patients suspected of having bioterrorism-related illnesses and, when 

necessary, can refer pediatricians to agent-specific subject matter experts. 

Pediatricians can register to receive real-time CDC updates about preparing for (and possibly 

responding to) terrorism and other emergency events at 

http://www.bt.cdc.gov/clinregistry/index.asp. 

For more information about CDC’s organization and overall mission, see 

http://www.cdc.gov/aboutcdc.htm. 

Department of Homeland Security 

Within the last decade, because of the severity of manmade disasters and their devastating effects 

on life and safety, as well as the increased threat of terrorism, the Federal Government has 

positioned itself to respond promptly to any future terrorist events that may occur in the United 

States. A key step was creation of the Department of Homeland Security (DHS) in 2002. One of 

its missions is to minimize damage and assist in recovery from terrorist attacks that occur within 

the United Sates. 

19
State and local governments share the primary responsibility for protecting their citizens from 

disasters, and for helping them recover when a disaster strikes. In some cases, a mass disaster is 

beyond the capabilities of State and local governments to respond, and the Federal sector is 

called upon to provide assistance. 

The DHS now comprises 22 agencies, including the Federal Emergency Management Agency 

(FEMA). DHS is responsible for the comprehensive National Strategy for Homeland Security, 

which is focused on six key areas: 

• Intelligence and warning. 

• Border and transportation security. 

• Domestic counterterrorism; protecting critical infrastructure. 

• Defending against catastrophic threats. 

• Emergency preparedness and response. 

To learn more about DHS and its role in disaster preparedness and response, go to 

http://www.dhs.gov/dhspublic/theme_home2.jsp. 

Federal Response Plan 

The Federal Response Plan (FRP) was initially developed as the central document for the delivery 

of assistance to State and local governments in disasters or emergencies. It is a signed agreement 

among Federal departments and agencies that identifies actions that will be taken in the overall 

Federal response to disasters or emergencies. It is to be implemented in anticipation of an event 

that is likely to require Federal assistance and in response to an actual event requiring Federal 

disaster or emergency assistance. The FRP also may be implemented in response to a request made 

by a governor to the president for Federal assistance. 

Federal response operations are coordinated with State, local, and regional officials and include 

positioning of a Federal coordinating officer, and deployment of emergency response teams, 

regional support teams, and emergency support teams to operations centers near the incident site 

and at the regional and national operations centers. See Figure 2.1 for a graphic depicting the 

FRP or go to http://www.dhs.gov/dhspublic/interweb/assetlibrary/NRP_Brochure.pdf for more 

detailed information. 

Preserving lives and safety of victims are main priorities of disaster response. One component of 

the FRP, known as Emergency Support Function #8 (ESF #8), Health and Medical Services, is 

led by the Department of Health and Human Services (DHHS). This function is supported by 15 

Federal and non-Federal agencies and provides coordinated Federal assistance to augment State 

and local resources after a major disaster or during the development of an anticipated public 

health and/or medical emergency. Assistance is also provided when State, local, or tribal public 

health or medical assets are overwhelmed and Federal support has been requested through proper 

authorities or when pending disasters are expected to overwhelm State, local, or tribal resources. 

Federal support also can be provided when these public health resources are not able to address 

all public health needs. 

20
The scope of ESF #8 is broad and involves supplemental health and medical assistance to meet 

the needs of victims of a major disaster, emergency, or terrorist attack. In the FRP, this support is 

categorized in the following functional areas: 

• Assessment of health/medical needs. 

• Health surveillance. 

• Medical care personnel. 

• Health/medical equipment and supplies. 

• Patient movement/evacuation. 

• Patient care. 

• Safety and security of human drugs, biologics, medical devices, veterinary drugs, etc. 

• Blood and blood products. 

• Food safety and security. 

• Agriculture safety and security. 

• Worker health/safety. 

• All-hazard public health and medical consultation, technical assistance, and support 

• Behavioral health care. 

• Public health and medical information. 

• Vector control. 

• Potable water/wastewater and solid waste disposal. 

• Victim identification/mortuary services. 

• Protection of animal health. 

Federal resources that supplement regional, State, and local response are primarily from within 

DHHS and ESF #8 support agencies. However, other non-Federal sources such as major 

pharmaceutical suppliers, hospital supply vendors, the National Foundation for Mortuary Care, 

and certain international disaster response organizations and international health organizations 

also provide support. 

Department of Defense 

The Department of Defense (DOD) has many capabilities through which it can provide 

assistance to lead Federal agencies in response to a disaster. DOD medical and support 

capabilities include the following: 

• Triage and medical treatment. 

• Displaced populations support. 

• Hospital personnel augmentation. 

• Epidemiologic support. 

• Stress management. 

• Preventive medicine support. 

• Veterinary support. 

• Prophylaxis and immunization augmentation. 

• Mortuary affairs. 

• Medical logistics. 

• Transportation. 

21
• Communication. 

• Technical augmentation (e.g., modeling). 

• Surveying and monitoring the incident site. 

• Facility decontamination. 

For more information about DOD and its capabilities, go to http://www.defenselink.mil/. 

Summary 

Federal assistance has been used successfully for many years to respond to the emergent medical 

requirements of victims of natural disasters throughout the United States. Recent terrorist attacks 

within the United States have increased the Nation’s investment in homeland security through 

increased State, local, and regional health and medical resource development and acquisition in 

response to events involving weapons of mass destruction. Federal assistance is provided 

through the lead and supporting agencies designated within the NRP, including DoD. 

While Federal response assets are robust, timely management focused on the needs of at-risk 

groups is paramount to victim survival and positive medical outcome. Pediatric patients are 

among the populations gaining national attention regarding the need for appropriate medical 

support, including appropriate supplies and equipment, during a disaster. Historical data on 

disaster response, including the personal experiences of health care providers and victims, 

reinforce the medical requirements of pediatric populations. All sectors—Federal, State, 

regional, and local—must continue to be prepared to provide medical resources to a disaster, but 

these entities also must give attention to the needs of specific populations, including children. 

This is the best way to improve morbidity and mortality in response to mass casualty events. 

Bibliography 

• Centers for Disease Control and Prevention. About CDC. Available at: 

http://www.cdc.gov/aboutcdc.htm. Accessed August 17, 2006. 

• Centers for Disease Control and Prevention. Biological and chemical terrorism: strategic 

plan for preparedness and response. Recommendations of the CDC Strategic Work 

Group. MMWR. 2000;49(No. RR-4):1–14. 

• Centers for Disease Control and Prevention. PHIN’s Early Event Detection Component. 

Available at: http://www.cdc.gov/phincomponents/PHIN%20Brochure-

%20BioSense%20.ppt. Accessed August 17, 2006. 

• Centers for Disease Control and Prevention. CDC’s Disease Surveillance System Efforts: 

Testimony of Joseph M. Henderson, Director, Centers for Disease Control and 

Prevention, Before the Select Committee on Homeland Security, Subcommittee on 

Emergency Preparedness and Response, U.S. House of Representatives, September 24, 

2003. Available at: http://www.cdc.gov/washington/testimony/Bi924200355.htm. 

Accessed August 17, 2006. 

• Centers for Disease Control and Prevention. CDC Clinician Registry. Available at: 

http://www.bt.cdc.gov/clinregistry/index.asp. Accessed August 7, 2006. 

• Centers for Disease Control and Prevention. Epidemic Intelligence Service. Available at 

http://www.cdc.gov/eis/index.htm. Accessed August 17, 2006. 

22
• Centers for Disease Control and Prevention. Epidemic Intelligence Service. Available at: 

http://www.cdc.gov/eis/index.htm 

• Centers for Disease Control and Prevention. Laboratory Response Network. Available at: 

http://www.bt.cdc.gov/lrn/. Accessed August 17, 2006. 

• Centers for Disease Control and Prevention. CDC Clinician Registry for Terrorism and 

Emergency Response Updates and Training Opportunities.Available at: 

http://www.bt.cdc.gov/clinregistry/index.asp. Accessed August 17, 2006. 

• Centers for Disease Control and Prevention. Strategic National Stockpile. Available at: 

http://www.bt.cdc.gov/stockpile/index.asp. Accessed August 17, 2006. 

• Department of Homeland Security Home Page. Available at: 

http://www.dhs.gov/dhspublic/index.jsp. Accessed September 13, 2006. 

• Department of Homeland Security. National Response Plan. Available at: 

http://www.dhs.gov/interweb/assetlibrary/NRP_Brochure.pdf. Accessed July 7, 2006. 

• Homeland Security Act, Public Law 107-296, 6 U.S.C. 101 et seq. November 25, 2002. 

• Homeland Security Presidential Directive-1. Organization and Operation of Homeland 

Security Council. October 29, 2001. Available at: 

http://www.whitehouse.gov/news/releases/2001/10/20011030-1.html. Accessed August 

17, 2006. 

• Homeland Security Presidential Directive-2, Combating Terrorism Through Immigration 

Policies, October 29, 2001. Available at: 

http://www.whitehouse.gov/news/releases/2001/10/20011030-2.html. Accessed August 

17, 2006. 

• Hughes JM, Gerberding JL. Anthrax bioterrorism: lessons learned and future directions. 

Emerg Infect Dis. 2002;8(10):1013–14. 

• Hutwagner L, Thompson W, Seeman GM, et al. The bioterrorism preparedness and 

response Early Aberration Reporting System (EARS). J Urban Health. 

2003;S1;80(2):89–96. 

• Landesman LY. Public Health Management of Disasters: The Practice Guide. 

Washington, DC: American Public Health Association; 2001. 

• National Advisory Committee on Children and Terrorism. Recommendations to the 

Secretary. June 2003. Available at: http://www.bt.cdc.gov/children/recommend.asp. 

Accessed August 17, 2006. 

• National Archives and Records Administration. Public Health Security and Bioterrorism 

Preparedness and Response Act of 2002. Available at: 

http://frwebgate.access.gpo.gov/cgibin/getdoc.cgi?dbname=107_cong_public_laws&docid=f:publ188.107.pdf. Accessed 

August 17, 2006. 

• Perkins BA, Popovic T, Yeskey K. Public health in the time of bioterrorism. Emerg Infect 

Dis. 2002;8(10):1015–1018. 

• Public Health Security and Bioterrorism Preparedness and Response Act of 2002, Public 

Law 107-188, U.S.C. 247d and 300hh, June 12, 2002, Draft National Response Plan. 

February 25, 2004. Department of Homeland Security. Available at: 

http://www.fda.gov/oc/bioterrorism/PL107-188.html . Accessed August 17, 2006. 

• Robert T. Stafford Disaster Relief and Emergency Assistance Act, Public Law 93-288, 

Sections 5121-5206, et seq of Title 42 United States Code. 

23
Figure 2.1 Federal Response Plan 

EOC = Emergency Operations Center 

DHS = Department of Homeland Security 

ROC = Regional Operations Center 

24
Table 2.1 Types of disasters, hazards, or events that may require Federal assistance 

Type of event Examples 

Natural Flood, earthquake, hurricane, tornado, typhoon, landslide, tsunami, ice 

storm, drought, wildfire, epidemic, disease 

Accidental Chemical spill, transportation accident, industrial accident, radiological 

incident, nuclear incident, explosion, utility outage 

Civil/Political Public demonstration, protest, civil disturbance, strike, mass 

immigration 

Terrorist/Criminal Chemical attack, biological attack, radiological attack, nuclear attack, 

high-explosive attack, war 

Other Inauguration, State of the Union, Olympics, major sporting event, 

summit conference, cyber attack 

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26
27

Chapter 3. Responding to a Disaster 

Phases of Response 

There are four basic phases of response to a disaster. They are: 

1. Preparedness (including prevention and planning). 

2. Actual response to the event. 

3. Mitigation. 

4. Recovery (short- and long-term) and critique. 

Preparedness 

Although we usually cannot predict disasters, we can control them through prevention and 

planning efforts. Prevention through preparedness is probably the most important phase of 

response in emergency management. During the preparedness phase, governments, 

organizations, and individuals develop plans to save lives, minimize disaster damage, and 

enhance disaster response. Preparedness efforts include preparedness and evacuation planning; 

emergency exercises and training; warning systems; emergency communication systems; public 

information and education; and development of resource inventories, personnel contact lists, and 

mutual aid agreements. 

Physicians participate in preparedness and prevention in many different ways, including: 

immunization programs, dietary advice, health education, and safety precautions and planning. 

As participants in an emergency action plan, physicians need to help formulate ways of 

preventing incidents from occurring or limiting the consequences from an incident that has 

already occurred. Physicians need to know what will be expected of their hospital in the case of a 

potential infectious disease outbreak. They should also be prepared with the knowledge and 

resources needed to help identify the etiology of a problem and to provide timely treatment. 

In the case of acts of terrorism, law enforcement plays the lead role in prevention, although 

physicians are often called upon to lend their expertise in an effort to identify the impact that 

various scenarios would or could have on the health of the community. Part of prevention 

consists of participating in a pre-established medical surveillance network of communities that 

will alert public health and safety officials of suspicious trends. A communications network of 

pediatricians, school nurses, freestanding pediatric walk-in clinics, and pediatric emergency 

departments should be formed. 

Plans to share information within the Health Insurance Portability and Accountability Act 

(HIPAA) guidelines need to be developed and implemented so that patterns of illness can be 

tracked and investigated. An information-sharing network like this can provide invaluable data 

and assistance to public health and safety officials that will help them to make informed 

decisions about evacuations, quarantines, and any other planned responses to a biological or 

chemical incident. Law enforcement officials may also ask physicians to advise them on how 

best to educate and create awareness in school personnel and parent organizations without 

causing panic or mass hysteria. 
28

Medical staffs need to know what will be expected of them and their facilities in the event of a 

large-scale infectious disease outbreak. Because of their unique knowledge base, physicians, 

especially pediatricians, can be very valuable sources of information to law enforcement and 

public health policymakers in helping to identify and isolate the source of an outbreak and 

providing guidance on the need for isolation, quarantine, and treatment. 

Planning and prevention are closely related and work hand-in-hand. The people doing the 

planning cannot be strangers. It is important that they routinely and regularly meet and speak 

with each other to facilitate communication during a crisis. Communication is a key element for 

success. If managers cannot communicate successfully during routine circumstances, they cannot 

be expected to effectively communicate during times of crisis. 

Plans should be developed and then tested and refined, over and over again. For a plan to work 

efficiently and effectively during a crisis, it must be well rehearsed. Plans that have been tested 

on a regular basis enable the responders to know and understand their roles. During a crisis is not 

the time to find out that a vital component is missing or nonfunctional. 

 

Response plans must be shared with the people who will be doing the actual responding. Periodic 

in-service training should be conducted, including tabletop exercises with key players and fullscale field exercises. Pediatricians should be proactive in providing input regarding the unique 

needs of children during disasters and ensure that children’s issues are included in all 

preparedness activities. Lessons learned from either actual responses or from the exercises and 

discussions should be incorporated into existing plans and then tested and evaluated again. 

Planners need to ask themselves over and over again: “Are we ready?” Plans must be constantly 

changing and evolving to meet changing circumstances, and no matter how well prepared we 

think we may be, we can always be more prepared. Careful review and personal communication 

with all involved in both incident management and potential response can always identify more 

opportunities for improvement. Because disasters are dynamic events, plans must be flexible so 

that they can be adapted to an incident as it develops. People involved in the planning process 

should stay current regarding new trends, technologies, and intelligence information that become 

available. Planning done in a vacuum cannot be successful. 

Actual Response to the Event 

The next phase is the response to the actual event. Response activities provide emergency 

assistance for casualties, reduce the probability of secondary damage, and speed recovery. 

Response activities include activating public warning systems, notifying public authorities, 

mobilizing emergency personnel and equipment, providing emergency medical assistance, 

manning emergency operation centers, declaring disasters, evacuating the public, mobilizing 

security forces, providing search and rescue operations, and suspending laws on an emergency 

basis. 

Response to a mass casualty incident (MCI) begins at the scene by first responders. An integral 

role of the first responder is coordination with agencies able to recognize characteristics of MCI 

secondary to bombs or to biological, chemical, or radiological agents, such that ongoing risk is 

minimized. First responders collect casualties, triage survivors, institute treatment (including 
29

decontamination), and transport victims to emergency departments. In blast trauma, first 

responders should convey information to hospital personnel so that management of casualties 

can be facilitated. This information should include the sorts of injuries that are expected, initial 

estimates of the number of casualties, and any additional risks to personnel from toxic 

substances. Involvement of hazardous substances such as chemical or biological agents, fires, 

collapsed structures, or the possibility of a radiation dispersal device (dirty-bomb) should initiate 

specific response protocols. 

Incidents can be very dynamic, so personnel should be able to adapt plans to deal with the 

incident as needed. There should be an incident commander—a qualified, visible leader—who 

can take charge of the response and direct the responders. The incident commander must be able 

to think quickly, make rapid assessments, and switch direction as needed without holding a 

lengthy caucus. The incident commander should be surrounded by competent, knowledgeable, 

and trusted people. They will be called upon to provide complete and accurate information to the 

incident commander so that he or she has the tools needed to make rapid, informed decisions. 

The National Incident Management System (NIMS) provides the framework needed to 

successfully manage an incident. This is a standardized plan that allows for flexibility. The 

NIMS can be used by local, state, and federal authorities to use resources depending on the 

nature and the scope of the incident. The NIMS is available online at 

http://www.dhs.gov/interweb/assetlibrary/NIMS-90-web.pdf. 

Mitigation 

The next phase of response is mitigation, in which actions are taken to stop the incident from 

doing any further damage and to stabilize the situation. Although disasters cannot always be 

predicted, their consequences often can be controlled by preparation and planning. Mitigation 

activities are also important in the preparedness phase, where they can eliminate or reduce the 

probability of a disaster or reduce the impact of unavoidable disasters. The damage done can be 

limited or confined using the dynamics of the incident management plan. 

Mitigation preparedness measures include building codes, vulnerability analyses, tax incentives 

and disincentives, zoning and land use management, building-use regulations, safety codes, 

sharing of resources among States, preventive health care, and public education. Information 

resources, data, and services important in mitigation activities include: geographic information 

systems (GIS)-based risk assessment, claims history data, facility/resource identification, land 

use/zoning, building code information, and modeling/prediction tools for trend and risk analysis. 

Recovery and Critique 

The recovery phase evolves as steps are taken to mitigate the event. The objective of recovery is 

to return things to normal as quickly as possible, and recovery activities continue until all 

systems have been returned to normal or better. Depending on the scope of the incident, the 

recovery period can range from hours to years. Damage assessments are made, financial needs 

are identified, and timelines and plans are developed and implemented. 

Short- and long-term recovery measures include returning vital life-support systems to minimum 

operating standards; reconstruction; temporary housing; ongoing medical care; and public 
30

information, health and safety education, and counseling. One aspect of long-term recovery 

involves assessing the infrastructure, how it held up during the incident, what the cost of the 

response was, and how that cost can be recovered. Recovery efforts in economic support include 

paying out insurance/loans and grants to cover damage, providing disaster unemployment 

insurance, and performing economic impact studies. Information resources and services related 

to recovery include data collection related to rebuilding, claims processing, and documentation 

of lessons learned. 

During long-term recovery, participants also review and critique the response, evaluating how 

the overall plan worked in a real event, determining what needs to be done to update the plan and 

educate responders, and making changes necessary to improve the original response plan and 

prevent a recurrence. 

Regional Response 

State and Federal 

Communication and information sharing are key parts of successful incident management—both 

before and during an actual event. Although each area of the country handles emergency 

responses in somewhat different ways, all emergency response agencies use some form of an 

incident management system. Almost all use the NIMS with unified command. 

Regional physicians should review community emergency response plans, as well as the 

collaborative efforts between responders and planners designated by pertinent emergency 

response agencies. Local physicians should become familiar with the following: 

• The response agencies in their area. 

• Regional medical, operational, and administration protocols. 

• The various levels of training and the roles of all the different responders in a mass 

casualty incident, and how these change with the changing situation. For example, some 

responders may move victims only after they have been triaged by other more highly 

trained responders. In a different scenario, those same responders may actually move 

victims before triage because of unstable conditions (e.g., structural collapse, hazardous 

materials release). The dynamics of the incident dictate whether triage or transport is 

done first. 

• Whether the firefighters or police officers in their community are certified emergency 

medical technicians (EMTs) or paramedics. 

• The person who is in charge of an incident when there is a multi-agency response. 

• Where to go for information and to offer assistance during an actual emergency. 

• The regional and State emergency planning interface. Each state has its own unique 

emergency planning office and incident management system that ties in with the overall 

National Response Plan (see Figure 3.1). 

Emergency Medical Services 

The availability and capabilities of emergency medical services (EMS) in the United States have 

undergone explosive growth over the last 40 years. The Comprehensive Emergency Medical 

Services Systems Act of 1973 established the regional basis for coordination of emergency 
31

medical care throughout the United States. In addition, the National Highway Traffic Safety 

Administration (NHTSA) is charged with coordinating the development of national standard 

curricula for and education of EMTs. 

During the past 25 years, the scope and complexity of care rendered by prehospital EMS 

providers have expanded greatly. Four levels of prehospital emergency medical personnel are 

currently recognized, in order of increasing skill level with respect to the care of the trauma 

patient (Table 3.1). 

In recent years, the addition and expansion of initial and continuing education in prehospital 

pediatric trauma care (such as that provided by the Pediatric Emergencies for Prehospital 

Professionals [PEPP] course of the American Academy of Pediatrics), as well as the provision of 

expert pediatric medical direction, have greatly enhanced the capabilities of most regional EMS 

systems. In most regions, injured children can now receive emergency medical assistance 

comparable to that of injured adults. 

Hospitals 

In mass casualty incidents, including those involving release of biological or chemical agents, 

both children and adults are likely to be significantly affected. Children would probably be 

disproportionately affected by such an incident, so pediatricians should assist in planning 

coordinated responses for local hospitals that may have limited pediatric resources (see Chapter 

1). Health care facilities could also be a primary or secondary target. At the very least, facilities 

will be overwhelmed by a massive number of anxious and worried individuals. 

The problems associated with terrorist incidents differ from those usually faced by hospital 

disaster alert systems. In the typical scenario, most victims are triaged in the field and then 

carefully distributed among available resources, to avoid a single facility from being 

overwhelmed. In a terrorist attack, facilities will be particularly vulnerable to inundation with 

many victims who have not been appropriately triaged or transported by EMS. Arrivals without 

full notification could interfere with attempts to isolate contaminated victims and ensure 

protection of health care personnel. In addition, terrorist events will be further complicated by 

the issues of security and forensics. 

Hospital emergency department personnel become involved both before and after the arrival of 

victims. Activities prior to arrival include processing current patients in the emergency 

department to prepare for new arrivals, checking all equipment, activating additional personnel, 

assigning team leaders, and possibly assigning liaisons to government agencies. On arrival of 

patients, emergency department staff should ascertain (whenever possible) a victim’s location 

with respect to detonation, whether a victim was within an enclosed space or near a body of 

water, or whether the victim was crushed by debris. These data provide valuable information as 

to the degree of injury to expect in other victims. 

Triage is crucial, given the large number of minimally injured and ambulatory victims presenting 

to emergency departments after a terrorist incident. The importance of triage is highlighted by 

the Oklahoma City experience in April 1995. This explosion caused 759 casualties, of whom 167 

died, 83 were hospitalized, and 509 were treated as outpatients either in an emergency room or 
32

by private physicians. Approximately 85% of the 592 survivors sustained non-life-threatening 

soft-tissue injuries (including lacerations, abrasions, contusions, and puncture wounds), and 35% 

sustained musculoskeletal injuries (including fracture/dislocations and sprains). The 66 children 

who were injured in the Oklahoma City blast showed a similar pattern of soft-tissue and 

musculoskeletal injury. 

The first wave of patients from the Oklahoma City blast arrived either by ambulance or some 

other means of transportation within 15 to 30 minutes of the event. Medical systems were 

overloaded with minimally injured patients. As would be expected, hospitals closest to the attack 

were overwhelmed first. More seriously ill, non-ambulatory patients tended to arrive later 

because of the delay associated with field triage and transport via EMS. The experience after the 

World Trade Center attacks in 2001 was similar in that the vast majority of patients seen in 

emergency departments were ambulatory and were treated for minor soft-tissue injuries and 

released. However, hospital overload was mitigated somewhat due to the large number of 

fatalities, which decreased the number of survivors presenting for treatment. The main lesson to 

be learned from these experiences is that casualty profiles are event specific, but an effective 

triage system can better direct attention toward the critically ill. 

Regional coordination. The objective of risk assessment is to estimate the likelihood that an 

incident will have an impact on the hospital, as well as the size of that impact. Considerations in 

risk assessment include the following: 

• Attack has the potential to generate large number of causalities. 

• Effects may be immediate or delayed. 

• Response will require specialized equipment, procedures (decontamination), and 

medications, all adapted to pediatric needs. 

• Hospitals may be targets of secondary attacks to amplify effect. 

Situations with both high probability and the potential for high impact (e.g., an earthquake in 

California, or a tornado in the Midwest) should receive more attention in preparedness planning 

than either situations of low probability with the potential for high impact (e.g., industrial plant 

chemical leak) or situations of high probability and the potential for low impact (e.g., community 

outbreak of infectious gastroenteritis). 

Hazard vulnerability analysis (HVA) is an aspect of risk analysis that considers the hospital’s 

capabilities regarding the traditional elements of risk. This analysis allows a comparison between 

the potential risk factor (hazard) and the hospital’s ability to cope. The action plan resulting from 

this type of risk analysis should be directed toward those hazards against which the hospital is 

less able to cope (i.e., vulnerabilities). Areas of vulnerability may include attack on hospital 

information systems, inadequate ventilation systems (negative pressure, contained exhaust) for 

decontamination procedures in toxic exposures, hospital staff untrained in the proper use of 

personal protective equipment (PPE), and so on. 

The key benefit of HVA analysis is the ability to prioritize planning for the hospital in any given 

situation. The key to effective HVA is a good, frequently updated inventory of the resources and 

capabilities (within both the hospital and the community) that are available for dealing with a 

particular hazard-related emergency. 
33

Surge capacity. Most of our medical systems operate at near capacity in normal times. Pre-event 

planning and preparedness are essential to develop local capacity and expand health care 

resources to respond to increased needs. Surge capacity should be created on all levels, including 

the following: 

• Emergency department space. 

• Decontamination equipment. 

• Antitoxins and medications. 

• Hospital bed capacity. 

• Extra provider capacity. 

• Increased integration back into a community that can provide mental health services. 

In general, hospitals should plan to be self-sufficient for the first day or two after an incident. 

Most victims in the first 24 hours will be anxious or worried individuals who may or may not 

need decontamination before medical treatment. Assessment of hospital capacity for these 

victims is essential. Several teams in small areas can perform triage and rapid treatment. A 

system should be established to initially treat victims and then assign them to other facilities 

(away from the main site) for definitive treatment. There should also be followup to ensure that 

appropriate care is available at the other facilities. A system should also be established to rotate 

and supplement staff for the first 24–48 hours (or longer) until additional medical help can 

arrive. 

The following points should be considered in measurement and management of surge capacity: 

• Surge capacity expressed in terms of beds is not specific enough. Specific pediatric surge 

capacity that is somewhat intervention-specific is preferable. For example, there may be 

1,000 hospital beds available in a large community but only 10 pediatric intensive care 

unit beds. If these types of pediatric-specific resources are needed, the actual surge 

capacity is only 10 beds. 

• Non-disaster-related patients must be cared for in addition to disaster victims. Surge 

capacity and overall planning should accommodate both sets of patients. 

• Surge capacity and capabilities are determined by many factors (e.g., facilities, human 

resources, patients’ needs, legal and regulatory issues, policies, process design, supplies, 

equipment, etc.). Each factor should be systematically considered and optimized. A 

“bottleneck” in any factor can become the limiting condition. Poor management of these 

issues can affect outcomes more than the skill of the health professionals caring for 

individual patients. 

• Assumptions that pediatric patients will be cared for by adult health providers and 

facilities are not universally true or necessary in at least some situations. 

• Local contexts differ regarding inpatient capacity for high-acuity pediatric patients. In 

large urban areas, there are likely multiple pediatric hospitals within a short distance of 

each other. They can collaborate and probably handle patients from all but the largest of 

disasters. However, many communities have only one facility that may be a significant 

distance that is capable of handling high-acuity pediatric cases. These facilities often 

operate near or even above capacity many days each year. So, surge capacity and 

capability for pediatric but not adult disaster victims may be critically limited. 

Transporting pediatric patients to facilities outside of the region may be beneficial or 
34

even required (particularly if a pediatric facility is damaged or incapacitated). 

Pediatricians should educate and advocate regarding this type of planning. This is similar 

to the situation for high-end pediatric cardiac surgery, organ transplantation, and burn 

unit care for which pediatricians already refer to resources outside their region. 

• The frequent practice of making superheroic efforts at an overwhelmed hospital needs to 

be considered against the risk/benefit and outcomes of transferring patients to hospitals 

that are not overwhelmed. Generally, pediatric capability and capacity are available, but 

they may be at distant facilities. 

• Agencies other than hospitals may be needed to care for unaccompanied but otherwise 

medically stable children or for children with social but no serious physical medical 

issues. This will not occur unless pediatricians help the responsible agencies prepare in 

advance. 

Protection of personnel and levels of precaution. Hospital staff members are at high risk for 

secondary exposure from contaminated victims (e.g., skin, clothing, etc). The Occupational 

Safety and Health Administration (OSHA) provides protective standards for hospital response, 

including: 

• A written plan describing how contaminated patients will be managed. 

• An Incident Command System described for each type of hazard. 

• On-the-spot training and briefing for support personnel, such as physicians. 

• A plan for providing exposed employees with medical care and surveillance. 

• Training at a first-responder level for employees involved in decontamination operations, 

including training in hazard containment and prevention of spread. 

Biological agents are generally associated with a delay of hours to days in onset of illness. 

Therefore, illness may go unrecognized in the initial stages, which can result in widespread 

secondary exposure to others, including health care personnel and other patients. In this situation, 

containment of the exposing agents in negative-pressure environments is mandatory. In contrast, 

toxins derived from biological agents produce illness within hours of exposure. The patient 

exposed to a toxin does not usually pose a significant threat of secondary exposure to medical 

personnel, although decontamination may still be warranted (as in chemical exposure). 

PPE includes specifically designed barrier clothing (e.g., gown, boots, and gloves) to protect the 

skin and a mask to protect the respiratory tract. Clothing is designed to provide protection against 

liquids, vapors, dust, and particles. Respiratory masks fall into two categories: those that filter 

the ambient air to rid it of hazardous particles, and direct-line masks that provide pure air under 

pressure. 

Chemical weapons are intended to produce immediate discomfort, incapacitation, or death. 

Incapacitating chemical agents may be particularly toxic to small children. The mainstay of 

decontamination is rinsing with water, shedding exposed clothing, and in some instances, 

administering pharmacologic antidotes. 

The risks of contamination are usually recognized at the scene, so that personnel at the receiving 

hospital can be alerted. However, hospital personnel are at particular risk of contamination from 

exposure, due to the high number of anxious or worried victims who arrive at the hospital on 
35

their own without previous triage or information on risk factors from the incident scene. Health 

care personnel and any adjunct personnel in contact with victims or the hospital decontamination 

site should wear full PPE and self-contained breathing apparatus until the risk of exposure by 

secondary contamination is completely eliminated. Equipment used for universal precautions, 

such as surgical masks and latex gloves, are inadequate. Recognition of all agents involved in the 

exposure and determination of their toxic potential often take time and close coordination with 

the regional poison center, the fire department, and the CDC. Hospital personnel responsible for 

decontamination and protection should remember the possibility of more than one agent being 

used in an assault and also the possibility of terrorists using a “decoy” agent to mask and delay 

recognition of release of a more toxic or lethal agent. 

Radiological or nuclear agents are generally associated with a delay in onset of illness. As with 

biological agents, illness may go unrecognized in the early stages, so that the risk of 

contamination of hospital personnel by secondary exposure to radiation carried from the scene is 

significant. Contamination varies with the emission levels. 

PPE for radiological agents includes clothing barriers that prevent radioactive particles from 

reaching the skin. Any mask that will prevent dust from reaching the respiratory tract is 

protective. Gamma and neutron emitters penetrate clothing easily and require lead-type barriers. 

Lead aprons, such as those used for routine radiology, are not feasible for protection. Some 

exposure of hospital personnel may be unavoidable, and in these instances, the radiation 

exposure should be monitored and limited to safe doses. 

Potential problems with use of PPE include the following: 

• Bulky and cumbersome. 

o Impedes bending, kneeling to reach small children, infants. 

o Impedes nimble use of hands and fingers (needed for starting an IV line, intubating, 

drawing up medications, etc.). 

o May not be adapted to stethoscope use. 

• Poor ventilation and temperature control. 

o Profuse sweating, discomfort. 

o Potential fluid losses and dehydration. 

o Hyperthermia (for personnel working in warm environments [outside tents, hospital 

air conditioning system down], or working over-extended hours). 

• Unfamiliar “alien” appearance. 

o Frightens children. 

o Contributes to stress of the crisis. 

For additional information on PPE, see Chapters 5 and 6. 

Incident Command Systems 

Incident command systems (ICS) use a consistent organizational structure that includes 

individual positions for overall management of emergency situations. ICS systems are designed 

to facilitate interagency coordination (because each agency has organized their response on the 

same model). This is one of the system’s most important advantages. ICS can also expand and 

contract to meet the needs of the particular emergency situation at hand. 
36

ICS structure is hierarchical. For example, there will be one incident commander, three key 

assistants (safety officer, liaison officer, and public information officer), and four subordinate 

managers who report directly to the incident commander (operations, logistics, planning, and 

finance). Go to http://www.fema.gov/pdf/nims/nims_training_development.pdf for more 

information on developing an ICS. 

San Mateo County Emergency Services developed their Hospital Emergency Incident Command 

System (HEICS) in the 1990s to facilitate earthquake preparedness among California hospitals. 

This HEICS provides a useful example of a system that employs the concept of “unified 

command,” with establishment of an emergency operations center within the hospital, predesigned job action sheets, response activities, lines of communication, and reporting 

relationships. The HEICS structure is modeled on the ICS hierarchy. Key participants in the 

hospital ICS include the following: 

• Hospital chief executive officer. 

• Vice president of operations. 

• Medical director. 

• Emergency manager. 

• Community affairs director. 

• Critical care manager. 

• Emergency department manager 

• Hospital communications. 

• Facilities and engineering. 

For more information on the HEICS, see http://www.emsa.cahwnet.gov/dms2/heics3.htm. 

Regional Coordination of Hospital Response 

Emergency incidents also require hospitals to coordinate with community and medical 

stakeholders within the regional area. Coordination with community stakeholders includes 

liaison and planning with various local, State, and national agencies/organizations within the 

region: 

• Primary/prehospital/infrastructure Response: 

o EMS. 

o Fire. 

o Police, local environmental protection agency, sheriffs. 

o Military (local or regional). 

o Regional poison centers. 

o Local health department. 

• Community/citizen response: 

o Schools, public and private. 

o Day care units, public and private. 

o Service groups (Kiwanis, Rotary, Salvation Army, parent/teacher associations 

[PTAs], etc.). 

o Nonsecular groups (churches, synagogues). 
37

o Public recreation administrations (zoos, amusement parks, sports stadiums, museums, 

and the like). 

Regional coordination with medical stakeholders includes liaison and planning with various 

medical entities within the region: 

• Children’s hospital-based: 

o Pediatricians and pediatric subspecialists. 

o Pediatric nurse practitioners, physician assistants. 

o Administration. 

o Ancillary services (nursing, technicians, etc.). 

o Air/ground transport services. 

o Laboratory services. 

o Children’s services. 

o Support services (dietary, environmental). 

• Community-based private practitioners: 

o Pediatricians. 

o Family practice physicians. 

o Emergency medicine physicians. 

o Nurse practitioners. 

o Physician assistants. 

o Other types of physicians and health care providers. 

• Community/ regional hospitals: 

o Emergency department staff. 

o Hospitalists. 

o Surgeons. 

o Anesthesiologists. 

o Administration. 

Some Roles for the Pediatrician in Regional Hospital to Community 

Planning 

• Meet with hospital planners to ensure children’s needs are met, equipment is adequate, 

and contingency plans are in place. 

• Be present when hospitals work with prehospital groups on triage, stabilization, 

equipment, distribution, etc. 

• Help organize the response of community pediatricians to assist at the hospital and local 

secondary areas to redistribute care back to the community level. 

• Help coordinate the identification and movement of community pediatricians. Assure that 

local pediatricians have the appropriate identification needed to cross barriers, along with 

designated means of transportation to areas where care is needed. Local pediatricians 

should also be familiar with the regional disaster management plan, reporting 

requirements, and contingency plans for alternate forms of communication, as needed. 

• Plan for primary offices to initially use alternative areas, e.g., Disaster Medical 

Assistance Team (DMAT) field units, school gyms, etc. 

• Help develop education and assistance packets for family preparedness. 
38

• Provide community education so families are prepared with the basics, such as 

flashlights, alternative heating, lighting, water, food, and clothing. 

• Be familiar with protocols for the following: 

o Isolating and decontaminating victims. 

o Mobilizing additional staff. 

o Potentially using secondary-care sites (e.g., school auditoriums). 

o In-hospital care protecting existing patients, as well as medical and ancillary staff 

(e.g., cafeteria workers). 

o Use of reverse-ventilation isolation areas. 

o Use of decontamination showers with separate water collection systems. 

• Coordinate with the local educational system because children spend most of their time in 

school. Know plans for rapid evacuation and holding areas where triage and initial 

treatment of severely injured victims can begin. 

• Work with hospitals and schools to develop decision trees for the initial steps of 

decontamination, further triage, transport, and so forth. 

• Know designated sites for stockpiled antidotes, antibiotics, vaccines, and other drugs and 

routes for rapidly obtaining them from outside the hospital if necessary (e.g., CDC). 

• Help develop protocols for proper doses of vaccines and antidotes for use in children. 

• Coordinate with teams of health professionals dealing with post-event programs, 

including rehabilitation, posttraumatic stress syndrome (PTSS), and critical incident 

stress management for health care professionals. 

• Perform triage of pediatric victims, including those who arrive at the scene with EMS and 

those who arrive at the hospital without previous triage. 

• Help hospitals develop color-coded triage systems for adult and pediatric patients that 

arrive without previous triage. Systems should ensure that children are not separated from 

their caregiver(s) during the chaos (unless for valid medical reasons). 

• Help address long-term needs, such as counseling (e.g., for PTSS), rehabilitation, social 

support (e.g., orphaned children), triage systems, etc. 

• Work with local pediatricians to coordinate protocols for a variety of emergency 

processes and procedures, including disaster system management, procurement of PPE, 

setting up decontamination areas, hospital reporting, identification of sentinel cases, and 

post-incidence stress reduction. These protocols can be communicated by a variety of 

methods, including seminars for disaster management on the local level. These efforts 

should be coordinated with the hospitals and government agencies involved. 

Drills and Quality Assurance Activities 

It is essential to organize disaster drills in the hospital that are coordinated with community 

resources. These drills should include the following scenarios: 

• The incident is small and contained, with most patients triaged and transported by the 

EMS systems to designated facilities. 

• The facility is inundated with large numbers of anxious and worried individuals, both 

immediately and for a short time after the incident. 

Drills should include Disaster Life Support Teams performing their respective functions. 
39

The goal of disaster life support training is to standardize incident response across the Nation as 

a way of strengthening national public health. Basic disaster life support training provides a 

didactic review of all-hazard topics, including critical information on the role of the health care 

professional. Advanced disaster life support extends this training into incident-specific scenarios 

(e.g., decontamination of mass casualties) through didactic training and interactive sessions and 

drills. Drills for advanced disaster life support teams should include the following: 

• Human pediatric simulator scenarios including decontamination for biological, chemical, 

and nuclear hazards. 

• Essential clinical skills, performed in central and mini clinical areas. 

• Use and wear of PPE. 

• Implementation of the incident command center. 

Integration with Children’s Services 

The pediatrician’s strongest role can be in helping hospital disaster planning teams anticipate and 

manage pediatric victims who have been separated from their primary caregivers during a 

disaster. These children need immediate support until a definitive caregiver can be located. 

In the event that in-hospital support services are overwhelmed, other efforts will also be needed, 

including the following: 

• Alternative social support from the community. Community-based organizations can 

provide clothing, toys, and bedside sitter support and communicate with family members 

who may be out of town. 

• Psychological support services from the surrounding community that can be brought to 

the hospital. 

• Outreach support teams, using community members, pediatricians, and mental health 

providers. These teams can go into the communities, schools, daycare centers, churches, 

etc., to provide stress debriefing, triage for further mental health care, and long-term 

monitoring. 

In the event that community support and child-protective services are also overwhelmed, 

additional efforts will be needed, including the following: 

• Alternative plans need to be in place to cope with a large group of children needing 

immediate caretaker support (i.e., those who are orphaned or temporarily separated from 

caretakers because of decontamination or medical treatment needs). 

• Pediatricians can help families find alternative systems within their churches and 

neighborhood communities. 

• Pediatricians can create information cards of resources and supervise rehearsal scenarios. 

Pediatricians also can help communities plan to provide other support services for families and 

children: 

• Establish a plan with existing communication systems (e.g., television, radio) to provide 

ongoing information support. 

• Plan for non-medical family support centers to provide water, food, clothing, etc. 

• Plan for a system to notify next of kin (anticipation of this information system can be 

done by pediatricians). 
40

• Provide for crisis counseling. 

• Provide for legal services. 

• Provide for translation services. 

• Facilitate the implementation of State and Federal disaster relief programs. 

• Plan for temporary housing alternatives, immediate, short, and long term. 

• Conduct community memorial and grieving services. 

JCAHO and Emergency Management 

In January 2001, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) 

introduced new disaster preparedness standards, building on its prior position that health care 

organizations should be prepared for all types of emergencies. These standards represent an 

important evolution in the concept of managing emergencies. Health care organizations are 

expected to address the four specific phases of disaster management—preparedness, response, 

mitigation, and recovery—and conduct hazard vulnerability analysis. This “all-hazards” 

approach should result in a thorough review and risk analysis of credible hazards and serious 

threats to the facility and its surrounding community, as well as the subsequent development of 

plans to address the ramifications of all possible hazards. After plans are developed, the 

organization should implement and execute them by conducting training and drills. 

The new JCAHO Guidelines require hospitals to use formal emergency management processes 

as the foundation of their planning. These include the following: 

• Develop a hazard vulnerability analysis (risk assessment). 

• Assure the operational needs of the hospital facility and ample resources of critical 

services such as water, electricity, sewage services, and ventilation. 

• Integrate with local emergency response systems. 

• Identify alternative roles and responsibilities of personnel. 

• Establish a command structure, also known as an “incident command system.” 

• Perform ongoing monitoring of plan performance, including annual reevaluation. 

JCAHO has published an emergency planning guide for use by officials in small, rural, and 

suburban communities. The guide is available online at 

http://www.jointcommission.org/NR/rdonlyres/FE29E7D3-22AA-4DEB-94B2-

5E8D507F92D1/0/planning_guide.pdf.. 

 

Appropriate Triage 

Triage to the appropriate facility can be critical for a child. Therefore, the development and 

implementation of a mass casualty plan that considers the unique needs of children is imperative 

to avoid overloading one local facility (whenever possible). The community should have 

designated facilities for referral of critically injured pediatric patients. At the same time, each 

facility should be able to care for and at least initially stabilize both children and adults. Pediatric 

skills and equipment should be maintained at all facilities. 

Emergency departments and hospitals should have some mechanism to provide for the physical, 

as well as the medical needs of pediatric populations. These needs include shelter, clothing, food, 
41

supervision, and entertainment for pediatric victims, as well as protection from the media in the 

critical period immediately after a disaster. 

Incident Management 

The incident command system (ICS) is widely recognized and used in the field of emergency 

management to effectively manage resources and casualties during a disaster. The ICS is a 

unified management system that allows for expandability and accountability based on the 

magnitude and needs created by the specific incident. It is an organizational system of “best 

practices” for on-scene, all-hazard incident management. There are five major management 

functions: 

• Incident command. 

• Operations. 

• Planning. 

• Logistics. 

• Finance/administration. 

All have standardized position titles. The following nomenclature is used for organizational 

components and their supervisory personnel: 

• Incident commander. 

• Command staff officer. 

• General staff/section chief. 

• Division supervisor. 

• Group supervisor. 

• Branch director. 

• Task force leader. 

• Strike team leader. 

• Unit leader. 

In a unified command structure, there is one recognizable leader—the incident commander—

who has overall responsibility. Because the system is expandable, it allows for the use of many 

components that may be needed to manage the incident. Various component managers are 

granted the authority to manage their specific component, and they are held accountable for the 

performance of their area to the incident commander. 

This type of system is widely used in everyday business. For example, in the hospital setting, the 

incident commander could be compared with the chairperson of the medical board, and the group 

managers could be compared with the various chiefs of service. 

The National Incident Management System (NIMS) has been developed for use by all 

emergency response agencies in the country. NIMS is an updated more inclusive version of ICS. 

Its standardized framework, common terminology, and flexibility allow it to be used by Federal, 

State, and local agencies/authorities. 

ICS is modular and can be expanded to meet needs that arise during an incident. In a disaster, the 

triage, treatment, and transportation of casualties fall to the EMS Operations Branch. The 
42

incident command officer is most often a field officer of the local EMS agency. That officer is 

responsible for managing all medical resources needed to effectively handle the incident and for 

minimizing the impact on normal operations of the EMS system. Based on the scope of the 

incident, the divisions of smaller functional units are formed to manage the following: 

• Staging. 

• Triage. 

• Treatment/decontamination. 

• Transport. 

Staging 

The staging officer is responsible for setting up an area where incoming resources, including 

personnel, can gather and await an actual assignment. The staging group can be broken down 

further into smaller units of operation for specific incident needs. For example, incoming 

ambulances would be directed to a vehicle staging area; personnel not assigned to a specific unit 

or task would be sent to a personnel staging location; and needed equipment would be directed to 

a logistical staging location. These areas may be off site from the incident but easily accessible to 

it. This allows greater accountability of who is on the incident ground and monitoring of their 

respective functions and performance. 

Triage Group 

The triage group is tasked with prioritizing casualties based on pre-established medical protocol. 

Simple Triage and Rapid Transport (START) allows rescuers to assess and prioritize a victim 

with a 30-second, hands-on assessment. Immediate life-threatening conditions are rapidly 

identified and corrected with minimal intervention, and casualties are identified for immediate 

transport (e.g., airway problems are corrected with a tilt of the head, and the patient is marked 

“red” for immediate transport; intubation in the field would not be done during this initial 

assessment). For children, a variant known as JumpSTART pediatric mass casualty triage is used 

(see http://www.jumpstarttriage.com/). 

In incidents involving victims exposed to hazardous chemicals, a similar system of triage is used. 

Normal START procedures would be extremely difficult for rescuers in chemical protective 

clothing to use. In these cases, a form of triage based on observation of symptoms is used, and 

response to tactile stimulus determines the triage priority. 

Treatment/Decontamination 

The treatment group is tasked with providing a more definitive treatment regimen for incident 

victims. Casualties are removed from the incident ground to a safe, protected area so that 

treatment can be started, particularly if transport is to be delayed. Personnel in this group 

constantly monitor victims for changes in their condition and change their triage priority as 

needed. In large-scale incidents in which the patient load would cripple normal hospital 

resources, victims with minor injuries may be held in an off-site treatment area for an extended 

time. Physicians, nurses, and other ancillary staff may be assigned to staff this area. 
43

Victims that have been exposed to a chemical or biological agent should be decontaminated. 

Personnel assigned to this task should be trained hazardous materials technicians because they 

need to operate in chemical protective equipment. This may be as simple as a splash suit and 

gloves or as complex as a fully encapsulated suit and positive-pressure breathing apparatus, 

depending on what type of chemical or agent the victims were exposed to. 

Transportation

The transport group is tasked with the responsibility for transporting victims from the incident 

ground to field treatment centers, hospitals, or specialty referral centers (trauma, burn, replant, 

etc.). The group officer usually maintains listings of available hospital beds and medical 

evacuation and public transportation resources that may be needed to move victims. The 

transport group also performs the critical function of maintaining the log of destinations to which 

victims have been moved so that they may be tracked for public information and quality 

assurance reasons. 

Bibliography

• Comprehensive Emergency Medical Services Systems Act of 1973. Washington, DC: 

United States Congress, Senate Labor and Public Welfare Committee; 1973. 

• Department of Homeland Security. National Incident Management System. March 2004. 

Available at: http://www.dhs.gov/interweb/assetlibrary/NIMS-90-web.pdf. Accessed July 

10, 2006. 

• JumpSTART. Combined JumpSTART algorithm. Available at: 

http://www.jumpstarttriage.com/. Accessed August 17, 2006. 

• National Health Professionals Preparedness Consortium: Healthcare leadership and 

administrative decision-making in response to WMD incidents. Nobel Exercise Scenario 

Information, v.2.0. December 31, 2002. 

• President's Disaster Management Egov Initiative. Available at: 

http://www.whitehouse.gov/omb/egov/c-2-2-disaster.html. Accessed August 17, 2006. 

• San Mateo County Emergency Services. Hospital Emergency Incident Command System 

(HEICS) Update Project. January 1998. Available at: 

http://www.emsa.cahwnet.gov/dms2/heics3.htm. Accessed July 10, 2006. 

• U. S. Department of Justice, Office for Domestic Preparedness. Hospital Emergency 

Management—Concepts and Implications of WMD Terrorist Incidents. Washington, DC: 

U.S. Department of Justice; April 2002. 
44

Figure 3.1 National Response Plan 

DHS = Department of Homeland Security 

EOC = Emergency operations center 

ERT = Emergency response team 

ROC = Regional operations center 

Source: Courtesy U.S. Department of Defense 
45

Table 3.1 Training and competencies of prehospital emergency personnel 

Prehospital 

emergency 

personnel 

Hours of training 

(approximate) 

Medical procedures able to perform 

First responders 40 Basic airway support, including use of supplemental 

oxygen, airway adjuncts, and bag-mask ventilation 

Direct pressure bleeding control 

Cervical spine stabilization 

Cardiopulmonary resuscitation and automated external 

defibrillation 

Basic EMTs 120 All of the above, plus: 

Full spinal immobilization 

Splinting of extremities 

Management of open chest wounds and impaled sharp 

objects 

Emergency ambulance transport 

Advanced EMTs 300–400 All of the above, plus: 

Endotracheal intubation 

Intravenous fluid administration 

Paramedics 1000–1200 All of the above, plus: 

Needle cricothyroidotomy 

Needle decompression of tension pneumothorax 
46
Chapter 4. Biological Terrorism 

Background 

History of Bioterrorism 

Although recent world events have heightened awareness of bioterrorism and biowarfare, there 

are many historical accounts of both. During the middle ages, the Tartars are reported to have 

catapulted plague-infested cadavers into the walled city of Caffa. In the 15th century, Pizarro 

supplied the native people of South America with smallpox-contaminated clothing in an effort to 

gain control of land. During the Spanish-American war, the Spaniards are alleged to have 

supplied the American Indians with blankets infected with smallpox virus. Japanese researchers 

have admitted to feeding cultures of Clostridium botulinum to Chinese prisoners of war during 

the 1930s. During WWII, the Japanese again used bioterrorism against the Chinese when they 

dropped plague-infested fleas over China, causing outbreaks of plague. 

Two more recent bioterrorist events in U.S. history involved contamination of the food supply. 

In 1984, in The Dalles, OR, an outbreak of 751 cases of Salmonella typhimurium was linked to 

the intentional contamination of restaurant salad bars by members of the Rajneesh religious cult. 

In 1996, an outbreak of Shigella dysenteriae type 2 among laboratory workers at a large Texas 

medical center was traced to muffins and donuts anonymously left in the break room. Shigella 

isolates from infected victims matched those found in an uneaten muffin and in the laboratory’s 

stock strain. 

There are reports that the Japanese cult Aum Shinrikyo has attempted bioterrorist attacks across 

Tokyo using anthrax, sarin gas, and botulinum toxin. In 1994, this cult succeeded in sickening 

500 people and killing 7 with sarin gas. In 1995, again using sarin gas, Aum Shinrikyo injured 

3,800 people and killed 12 by releasing the gas in five subway stations around Tokyo. 

The anthrax attacks of October 2001, propagated through the U.S. Postal Service, led to 

infections in 22 people (11 cases of cutaneous anthrax and 11 cases of inhalational anthrax) and 

5 deaths. These attacks affected thousands of people around the world, including those who were 

presumed exposed and required antibiotic prophylaxis and/or vaccination; the numerous anxious 

and worried individuals who flooded hospital emergency rooms, physicians’ offices, and public 

health information hotlines; and the thousands of public health, medical, and law enforcement 

workers who investigated potential attacks. 

For a video about the history of bioterrorism, see 

http://www.bt.cdc.gov/training/historyofbt/index.asp. 

Bioterrorism research. Beginning in the 1920s, the Soviet biowarfare program reportedly 

conducted research on gas gangrene, tetanus, botulism, plague, and typhus. In the 1970s, this 

program was greatly expanded as the secret organization Biopreparat. At its height, this program 

involved 60,000 people working in more than 50 facilities across the former USSR. Plague, 

anthrax, smallpox, tularemia, brucellosis, glanders, Marburg virus, and Venezuelan equine 

encephalitis (VEE) virus were produced. Yersinia pestis, anthrax, and variola reportedly were 

47
prepared for use in intercontinental missiles. By WWII, the United States, the United Kingdom, 

Canada, Germany, Japan, and the USSR all had active biological weapons programs. 

The Iraqi bioterrorist program, initiated in 1974, has been of recent interest. Although much is 

still unknown about this program, the United Nations Special Commission has information from 

Iraq that this program studied the use of botulinum toxin, B. anthracis, influenza virus, aflatoxin, 

trichothecene mycotoxins, and ricin. During the Gulf War, Iraq reportedly prepared missiles and 

bombs that contained aflatoxin, botulinum toxin, and B. anthracis, although they were never 

used. 

Disarmament and legislation. In 1969, the United Kingdom and the USSR began to call for 

bioweapons disarmament. That same year, the U.S. offensive bioterrorist program was 

dismantled, although the biodefense program continued. In 1971, the U.S. Army Medical 

Research Institute of Infectious Diseases was opened to research biological protective measures, 

diagnostic procedures, and therapeutics. By 1973, the United States had destroyed its entire 

arsenal of bioterrorist agents. 

The Convention on the Prohibition of the Development, Production, and Stockpiling of 

Bacteriological (Biological) and Toxin Weapons and on Their Destruction, also called the 

Biological Weapons Convention (BWC), was opened for signature in 1972 and became effective 

in 1975. It was the first multilateral disarmament treaty banning an entire category of weapons. 

Although the BWC is an international agreement, there is no monitoring mechanism to ensure 

each party’s adherence. 

In 1979, a few years after the signing of BWC, there was a massive accidental release of 

aerosolized B. anthracis spores in Sverdlovsk, Russia; 79 people became ill and 69 died. The 

Soviets maintained that this outbreak was due to the ingestion of contaminated meat sold on the 

black market. However, President Yeltsin acknowledged in 1992 that in 1979 there had been an 

accidental release of an unspecified biological agent from a military facility. This is an important 

event in world history because it was the first major evidence that a nation was in direct violation 

of the BWC. 

In the United States in 1995, a member of a white supremacist group attempted to buy Y. pestis 

from an Ohio laboratory supply company and later attempted to purchase anthrax from a Nevada 

company. This resulted in the passage of the Antiterrorism and Effective Death Penalty Act of 

1996, commonly referred to as the “Select Agent Rule” (42 CFR Part 72.6, Fed Reg Oct. 24, 

1996). 

In June 2002, the Public Health Security and Bioterrorism Preparedness and Response Act of 

2002 was signed into law (PL 107-188). This Act updated the existing Select Agent Rule by 

requiring facilities to register if they possessed select agents. Previously, only facilities that 

wanted to transfer select agents needed to register with the Centers for Disease Control and 

Prevention (CDC). See also http://www.fda.gov/oc/bioterrorism/PL107-188.html. 

48
Epidemiology of a Terrorist Attack 

Biological terrorism is the deliberate use of any biological agent against people, animals, or 

agriculture to cause disease, death, destruction, or panic, for political or social gains. A 

bioterrorist agent may be a common organism, such as influenza or Salmonella, or a more exotic 

organism such as Ebola virus or variola virus. 

In June 1999, a panel of public health, infectious disease, military and civilian intelligence, and 

law enforcement experts was convened to determine which biological agents (microorganisms 

and toxins) posed the greatest potential for use in a bioterrorist attack, to be designated as 

“Category A” agents. These are the following: 

• Variola major (smallpox). 

• B. anthracis (anthrax). 

• Y. pestis (plague). 

• Francisella tularensis (tularemia). 

• Botulinum toxin (botulism). 

• Filoviruses and arena viruses (viral hemorrhagic fevers [VHF]). 

Category A agents would have the greatest adverse public health, medical, and social impact if 

used as a bioterrorist agent for the following reasons: 

• They are infectious and stable in aerosol form. 

• The world population is highly susceptible to the infections they cause. 

• They cause high morbidity and mortality. 

• Some can be transmitted from person to person (smallpox, plague, VHF). 

• The illnesses they cause can be difficult to diagnose and treat. 

• They have been previously developed for biowarfare. 

Although bioterrorist attacks ultimately could affect large numbers of people, disease in a single 

patient may be enough reason to investigate the possibility of biological terrorism. Although 

some bioterrorist events are subtle, a number of clues should heighten suspicion that a 

bioterrorist attack has occurred: 

• Disease caused by an uncommon organism (e.g., smallpox, anthrax, or VHF). 

• A less common presentation of infection with one of these organisms. For example, while 

a small number of cases of cutaneous anthrax occur naturally each year in the United 

States, cases of inhalational anthrax are highly unusual. 

• A disease identified in a geographic location where it is not usually found (e.g., anthrax 

in a non-rural area, or plague in the northeastern United States). 

• Unexpected seasonal distribution of disease (such as influenza in the summer). 

• Antiquated, genetically engineered, or unusual strains of infectious agents. 

• Multiple unusual or unexplained diseases in the same patient. 

• Disease in an atypical age group or population, such as anthrax in children or varicellalike rashes in adults. 

• Large numbers of cases of unexplained disease or death. 

49
• An unexplained increase in the incidence of an endemic disease that previously had a 

stable incidence rate. 

• An unusual condition striking a disparate population, such as respiratory illness in a large 

population. 

• A large number of people seeking medical care at a particular time (signaling they may 

have been present at a common site, timed with the release of an agent). 

• A large number of people presenting with similar illnesses, in noncontiguous regions 

(may be a sign that there have been simultaneous releases of an agent). 

• Animal illness or death that precedes, follows, or occurs simultaneously with human 

illness or death (may indicate release of an agent that affects both animals and people). 

However, because no list of clues can be all inclusive, all health care providers should be alert 

for the possibility that a patient’s condition may not be due to natural causes. When there is no 

other explanation for an outbreak of illness, it may be reasonable to investigate bioterrorism as a 

possible source. Common sources of exposure to an agent may include the following: 

• Food and water that has been deliberately contaminated. 

• Respiratory illness due to proximity to a ventilation source. 

• Absence of illness among those in geographic proximity but not directly exposed to the 

contaminated food, water, or air. 

Agents Categorized by System Predominantly Affected 

See also Table 4.1. 

Respiratory System 

Anthrax, plague, and tularemia are all caused by infections with Category A agents and may 

present as respiratory illnesses. 

Anthrax. The incubation period of inhalational anthrax is usually 1–6 days, although it can be 

longer. The initial symptoms are nonspecific and may resemble those of the common cold (lowgrade fever, nonproductive cough, fatigue, malaise, fussiness, poor feeding, sweats, and chest 

tightness or discomfort), although rhinorrhea is absent. During this phase, chest auscultation 

usually reveals no abnormalities, although vague rhonchi may be heard. The chest radiograph 

may reveal pathognomonic mediastinal widening, pleural effusion, and rarely, infiltrates (Figure 

4.1). The patient may seem to begin to recover and then become severely ill 1–5 days later. 

During this phase, sometimes called the “subsequent phase,” there is an abrupt onset of high 

fever and severe respiratory distress, including dyspnea, stridor, diaphoresis, and cyanosis. 

Despite ventilatory support and antibiotic therapy, shock and death (75% case fatality rate) often 

occur within 24 to 36 hours. Patients with inhalational anthrax are not contagious, so the only 

infection control measure necessary is standard precautions. 

Plague. Although natural plague can present in a number of forms (septicemic, bubonic, and 

pneumonic), aerosolization of Yersinia pestis causing pneumonic plague would be the most 

effective mode for a bioterrorist attack. The incubation period is short, about 2 to 4 days and is 

followed by fever, headache, malaise, cough, dyspnea, and cyanosis. The cough is productive 

50
and may be watery, purulent, or bloody. Chest radiographs often reveal bilateral infiltrates and 

lobar consolidation. Sometimes, gastrointestinal (GI) symptoms accompany pneumonic plague 

and include nausea, vomiting, diarrhea, and abdominal pain. The disease is rapidly progressive, 

often leading to disseminated intravascular coagulation, and 100% of patients die if untreated. 

Differential diagnoses include community-acquired pneumonias and hantavirus respiratory 

distress syndrome. The time from exposure to death may be as short as 2 days and is often 

between 2 and 6 days. Pneumonic plague is spread by respiratory droplet, so droplet precautions 

should be strictly enforced. 

Tularemia. The presentations of tularemia include glandular, oculoglandular, oropharyngeal, 

septicemic, typhoidal, and pneumonic forms. Similar to plague, the most effective bioterrorist 

release would be aerosolization, causing the pneumonic form, although the typhoidal form is 

possible. The incubation period is 1 to 14 days, and the initial illness is often influenza-like, 

beginning 3 to 5 days later. Clinical findings include sudden onset of fever (38–40°C), headache, 

malaise, coryza, sore throat, and chills and rigors. A dry, nonproductive cough may progress to 

bronchiolitis, pneumonitis, pleuritis, pleural effusions, and hilar lymphadenitis and may not be 

accompanied by objective signs of pneumonia (dyspnea, tachypnea, pleuritic pain, purulent 

sputum, or hemoptysis). The earliest findings on chest radiograph are peribronchial infiltrates 

that progress to bronchopneumonia. Only 25 to 50% of patients have radiological evidence of 

pneumonia in the disease’s early stages, and some patients show only minimal, discrete 

infiltrates. Other cases progress rapidly to respiratory failure and death. Mortality from tularemia 

pneumonia is 30% if untreated but drops to less than 10% with prompt antibiotic treatment. 

Nervous System 

Botulism is the category A disease most likely to present with CNS findings. The toxin from the 

C. botulinum bacteria is the most lethal toxin known for people, with an LD50 of 1 ng/kg, 

100,000 times more toxic than sarin gas. There are four forms of botulism: 

• Foodborne. 

• Wound. 

• Infant (the most common form, accounting for 72% of cases). 

• Inhalational (no natural occurrence). 

Botulinum toxin can be disseminated through contamination of food or water or via 

aerosolization and inhalation. When botulinum toxin is ingested, it may cause GI symptoms 

including abdominal cramping, nausea, vomiting, and diarrhea. Inhalational botulism does not 

cause a pneumonic process. 

Both ingestion and inhalation of the toxin lead to nervous system findings, i.e., an acute, afebrile, 

symmetrical, descending flaccid paralysis (Figure 4.2). The first signs may appear as quickly as 

2 to 72 hours; however, the rate of progression is dose dependent. In natural exposure, the 

symptoms may be insidious and unapparent for months. In a bioterrorist event, doses may be 

high, with prompt onset of symptoms. The first manifestation is a cranial nerve palsy, which may 

present as double or blurred vision, dysphagia, dysarthria, dysphonia, dry mouth, ptosis, gaze 

paralysis, enlarged or sluggishly reacting pupils, and nystagmus. Sensory changes do not occur. 

51
The paralysis eventually progresses to loss of head control, hypotonia, limb weakness, and 

respiratory muscle paralysis. Constipation often develops. Patients may appear comatose because 

of extreme weakness, but sensorium is intact. Deep tendon reflexes may be intact initially but 

eventually diminish. Without treatment, antitoxin, and ventilatory assistance, patients die of 

airway obstruction and inadequate ventilation due to respiratory muscle paralysis. Secondary 

respiratory infections due to aspiration pneumonia may also develop. 

Differential diagnoses for botulism include Guillain-Barré syndrome, myasthenia gravis, stroke, 

other ingestions/intoxications, tick paralysis, viral syndromes, and hypothyroidism. Bioterrorism 

should be considered when a botulism outbreak occurs within a common geographic area, yet no 

common source of ingestion can be identified. Botulism is not transmissible from person to 

person, so standard precautions are sufficient infection control measures. 

Gastrointestinal System 

A number of infections caused by Category A agents present primarily as syndromes other than 

GI, although they may be accompanied by some GI complaints. Those that present as respiratory 

syndromes after aerosol exposure (anthrax, plague, and tularemia) may also present with GI 

symptoms caused by respiratory distress, especially in children. It is not unusual for children 

with pneumonia and some degree of respiratory compromise and accessory respiratory muscle 

use to feed poorly and have nausea, vomiting, mild to moderate abdominal pain, and diarrhea. 

Botulism, in any of its forms, is primarily a nervous system illness manifested by paralysis. 

Paralysis may cause some GI manifestations such as poor feeding and constipation. 

GI anthrax can occur when food is purposefully contaminated with anthrax spores. The 

incubation period via this route ranges from a few hours to a week. Depending on where the 

spores are deposited and germinate, disease may affect the upper or lower GI system, causing 

acute inflammation and eschar formation, much like in cutaneous anthrax. Upper GI illness may 

result in an oral or esophageal ulcer, which may present with fever, drooling, dysphagia, regional 

lymphadenopathy, edema, and sepsis. Lower GI illness often affects the terminal ileum or 

cecum, and presents with fever, loss of appetite, vomiting, and malaise and progresses to 

vomiting, hematemesis, severe bloody diarrhea, an acute abdomen, or sepsis. Sometimes, 

massive ascites develops. This form of anthrax is not transmissible from person-to-person, and 

standard precautions suffice. 

Dermatologic Manifestations 

Almost all of the diseases caused by Category A agents (anthrax, smallpox, plague, tularemia, 

VHF) can cause skin lesions, although dermatologic findings may not be the primary finding in a 

bioterrorist attack using aerosol dispersion. 

Anthrax. Anthrax spores mixed with a fine powder substrate can be used as a weapon to cause 

respiratory and cutaneous disease. Cutaneous anthrax is the most common form of naturally 

occurring disease and accounts for 95% of cases. The incubation period is a few hours to 12 

days. A small pruritic papule, often mistaken for an insect bite, forms at the inoculation site and 

rapidly progresses to an ulcer (1–3 cm in diameter) over the course of 1–2 days and may be 

surrounded by small vesicles (1–3 mm). The organism may be isolated from the serosanguineous 

52
fluid in these vesicles. A painless, depressed eschar of dark necrotic tissue forms at the site, and 

toxin production causes surrounding edema (Figure 4.3). Adjacent lymph glands may become 

enlarged and painful. The eschar separates from the skin in 1 to 2 weeks, often leaving no scar. 

The mortality rate is 20% without treatment, although death is rare with prompt treatment. 

Smallpox. Rash is the key feature of smallpox, whether the disease is contracted via mechanical 

aerosolization or from person-to-person transmission. In ordinary-type smallpox, the most 

common form, exposure to the virus is followed by an asymptomatic incubation period of 7 to 17 

days (mean 12 to 14 days). The prodromal phase, lasting 2 to 4 days, begins with acute onset of 

high fever, malaise, head and body aches, and sometimes vomiting. The fever usually ranges 

from 101°F to 104°F, and patients are usually too ill to carry on their normal activities. The 

patient is not contagious during this period. 

The first sign of rash is an enanthema in the mouth that lasts less than 24 hours. These macules 

break down and shed large amounts of virus into the mouth and throat, making the patient highly 

contagious. A macular rash then develops on the face and forearms and spreads to the trunk and 

legs. When the rash begins, patients may defervesce and begin to feel better. Over 1 to 3 days, 

the lesions progress to papules, which within 1 to 2 days, progress to vesicles and then pustules. 

The pustules are painful and deep-seated, sometimes described as feeling like lentils or “BB” 

pellets under the skin. After about 8 to 9 days from onset of the rash, the lesions scab over and 

eventually separate from the skin. Once the scabs have separated (about 21 days from onset), the 

patient is no longer contagious, although extensive pitting scars may remain. The rash of 

smallpox may be confused with rashes of other conditions such as the vesicular pustular rashes 

(such as varicella), herpes zoster, monkeypox, herpes simplex, drug eruptions, and impetigo. The 

rash of smallpox may be distinguished from that of chickenpox by physical distribution of the 

lesions; smallpox lesions tend to concentrate on the face and extremities including the palms and 

soles, while varicella lesions concentrate on the face and trunk, usually sparing the palms and 

soles (Figure 4.4). Other distinguishing features of the smallpox rash are a monotonous 

appearance, with deep-seated lesions in the same stage of development. The pustules may be 

umbilicated (Figure 4.5). Varicella lesions are superficial, sometimes described as “dew drops on 

rose petals,” and appear in crops, resulting in lesions in different stages of development (Figure 

4.6). 

There are two clinical forms of smallpox. Variola major is the most severe and most common 

form of smallpox, with a more extensive rash and higher fever. There are four types of variola 

major smallpox: ordinary (accounting for 90% or more of cases), modified (mild and occurring 

in previously vaccinated individuals), flat (malignant), and hemorrhagic. Historically, 30% of 

patients with variola major smallpox die, usually during the second week of illness. Variola 

minor smallpox is a less common and less severe form of smallpox, with death rates historically 

of 1% or less. 

Two types of variola major smallpox are both rare and very severe. Malignant and hemorrhagic 

smallpox progress rapidly and are usually fatal, with death occurring about 5 to 6 days after the 

rash begins. In malignant smallpox, the rash appears as soft, velvety, confluent vesicles that do 

not progress to pustules or scabs. In hemorrhagic smallpox, the rash is petechial, with 

53
hemorrhages into the skin and mucous membranes. Patients with all types of smallpox require 

immediate isolation with precautions for airborne infection. 

The CDC has developed an “Acute, Generalized Vesicular or Pustular Rash Illness Protocol” to 

assist in the evaluation of patients for whom a diagnosis of smallpox is being considered. This 

algorithm classifies patients as at low, moderate, or high risk of smallpox, which in turn directs 

clinical laboratory testing. Before submitting laboratory specimens from patients suspected of 

having smallpox, consult your local and State health departments. 

For the algorithm and an accompanying worksheet, see 

http://www.bt.cdc.gov/agent/smallpox/diagnosis/evalposter.asp. 

For an interactive version of the algorithm, see

http://www.bt.cdc.gov/agent/smallpox/diagnosis/riskalgorithm/index.asp. 

For laboratory testing algorithms that complement the patient evaluation protocols, see

http://www.bt.cdc.gov/agent/smallpox/diagnosis/pdf/rashtestingprotocol.pdf. 

Tularemia. Although airborne Francisella tularensis would most likely cause pneumonic or 

typhoidal disease, ulceroglandular and oculoglandular forms may occur that have cutaneous 

manifestations. There is also a glandular form of the disease, which does not result in skin 

lesions. The rash of ulceroglandular tularemia begins with a papule at the inoculation site, 

accompanied by systemic symptoms (fever, chills, rigors, sore throat). The lesion forms a pustule 

that becomes a tender ulcer and may form an eschar. Regional lymph nodes become inflamed 

and fluctuant. The oculoglandular form of tularemia leads to conjunctival ulceration, blepharitis, 

chemosis, vasculitis, and regional lymphadenopathy. 

Viral hemorrhagic fevers. Viral hemorrhagic fevers (VHFs) are caused by a variety of 

organisms, with a variety of presentations, making clinical diagnosis difficult. After an 

incubation period of 2 to 21 days, a rash develops that may range from a subtle cutaneous 

flushing to a nonpruritic maculopapular rash, similar to that seen in measles. The condition 

progresses to a bleeding diathesis of petechiae, mucosal and conjunctival hemorrhages, 

hematuria, hematemesis, and melena. 

Notifying Authorities 

All public health and medical responses to events of bioterrorism begin at the local level. 

Pediatricians are front-line health care providers in every community and may become front-line 

responders in a bioterrorist attack. It is impossible to predict where a child or parent may first 

seek care for an illness caused by a bioterrorist agent, so primary-care pediatricians, as well as 

those working at secondary- and tertiary-care facilities, must be prepared to promptly diagnose 

and isolate a patient who has an illness potentially related to bioterrorism and to notify the proper 

authorities. 

Good infection control practices require that anyone, child or adult, who presents with a fever 

and rash be immediately placed in a private room with the door closed. This is standard practice 

because a number of highly contagious childhood infectious diseases present this same way 

(varicella, measles, rubeola, meningococcus), regardless of whether the illness is ultimately 

54
determined to be due to an agent of bioterrorism. Infection control precautions may also include 

the use of masks, gowns, gloves, and equipment for eye protection, depending on each situation. 

Once the initial history and physical examination have been completed, if a disease related to 

bioterrorism is suspected, the pediatrician must notify the proper authorities, including the 

infection-control practitioner (if one is available at the facility) and local public health 

authorities. Each local public health system is organized slightly differently, so pediatricians 

should become familiar with their own local public health agency and phone number for local 

reporting. 

Rapid reporting to authorities is essential. Each agency level has developed and continues to 

refine response plans to handle a bioterrorist event. Rapid activation of these plans provides the 

best opportunity to limit disease spread during an outbreak. Local authorities may initiate an 

immediate investigation or seek assistance from the State health department. 

For a list of State health department websites, see http://www.cdc.gov/other.htm#states. 

For a list of State epidemiologists, see 

http://www.cste.org/members/state_and_territorial_epi.asp. 

States report their investigations to and request epidemiologic assistance from the CDC. The 

CDC can provide public health consultation, epidemiologic support, and other technical 

assistance to State health departments. The CDC usually becomes involved in a State’s 

investigation at the request of the lead State epidemiologist or health officer. 

The CDC can be reached during all hours through the CDC Director’s Emergency Operation 

Center at 770-488-7100. 

Health Department 

Each State has a public health system, although the structure and reporting network varies from 

State to State. In some States, the State health department has authority over county and local 

health departments. In other States, county and local health departments function autonomously. 

State health departments facilitate consultations with specially designated laboratories that are 

capable of responding to public health emergencies (see the following section, Laboratory 

Response Network). State bioterrorism response plans will reflect these differences. All 

pediatricians and health care facilities should learn the structure of their local public health 

system and the point of contact for reporting illnesses suspected of being related to bioterrorism. 

Hospital 

Most hospitals have started to develop bioterrorist response plans that may be part of a larger 

hospital disaster plan. Hospitals play a very large role in the care of bioterrorist victims and 

anxious or worried parents and others. Optimally, hospitals should have been included in the 

response planning of local public health agencies. Office and hospital-based pediatricians can 

become better prepared to respond to a bioterrorist attack by becoming familiar with local 

hospital bioterrorist and disaster plans. In addition, pediatricians are uniquely qualified to ensure 

that the special needs of children (e.g., medical supplies and therapeutics specific for children) 

55
are addressed in local medical response plans. (See also Chapter 9. Integrating Terrorism and 

Disaster Preparedness into Your Pediatric Practice). 

 

Law Enforcement 

All suspected cases of bioterrorism are subject to criminal investigation. Public health authorities 

are responsible for notifying local and Federal law enforcement. In many jurisdictions, these 

relationships are already established and detailed in State and local public health bioterrorist 

response plans. 

Laboratory Support and Submission of Specimens 

Collecting the appropriate clinical laboratory specimens in a case of actual or suspected 

bioterrorist-related illness is critical for the medical care of the patient, as well as for public 

health and legal investigations. Specimen collection varies by the agent suspected and should be 

done in consultation with public health authorities. Local and State public health authorities can 

advise on specific specimen collection and shipping in each case and consult with the CDC as 

needed. For detailed information regarding specimen collection, packaging, and shipping, see 

http://www.bt.cdc.gov/labissues/index.asp. 

Laboratory Response Network 

The Laboratory Response Network (LRN) is a national network of local, State, and Federal 

public health, hospital-based, veterinary, agriculture, food, and environmental testing 

laboratories that provide laboratory diagnostic capability to respond to biological and chemical 

terrorism and to other public health emergencies. The CDC, along with the Association of Public 

Health Laboratories and the Federal Bureau of Investigation (FBI), created the LRN, which has 

been operational since 1999. There are more than 100 LRN laboratories across the United States, 

and the network continues to expand. Consultation with LRN facilities is facilitated through 

State health departments. For more information, see http://www.bt.cdc.gov/lrn/. 

Limiting Spread 

Rapidly detecting and isolating patients with an infectious illness related to bioterrorism is 

essential to prevent transmission in health care settings. If an infection related to bioterrorism is 

suspected, the patient should be placed on contact precautions and airborne infection isolation, in 

addition to standard precautions, until preliminary test results are available and the 

transmissibility of disease can be reevaluated. 

Agents of bioterrorism are generally not transmitted from person to person. The release of an 

agent is most likely from a point source. However, smallpox, VHFs, and pneumonic plague may 

be highly transmissible from person to person via respiratory droplet and, in some cases, by 

aerosol spread.

Standard Precautions 

All patients in a health care facility and all patients suspected of infection with a Category A 

bioterrorist agent (anthrax, botulinum toxin, plague, smallpox, tularemia, and VHFs) should be 

56
cared for using standard precautions. Formerly known as universal precautions, standard 

precautions are the minimal accepted level of precaution. Standard precautions prevent direct 

contact with blood, other body fluids, secretions, excretions, nonintact skin/rashes, and mucous 

membranes and should be observed during all aspects of patient care. 

Standard precautions include the following: 

• Gloves. Clean, nonsterile gloves should be worn when touching any of the above 

mentioned substances. Gloves should be removed immediately after contact with these 

fluids and hands should be washed between care of each patient. 

• Handwashing. Hands should be washed after contact with blood or body fluids, whether 

or not gloves have been worn. Plain or antimicrobial soap with warm water should be 

used according to facility policy. Alcohol-based hand rubs (≥60%) may also be used 

when soap and water are not readily available. 

• Masks/eye protection or face shields. Whenever procedures are performed that may cause 

splashes of blood or other body fluids, a mask and eye protection should be worn. These 

should be removed and discarded or cleaned between care of each patient. 

• Gowns. Whenever procedures are performed that may cause splashes of blood or other 

body fluids, a gown should be worn to protect the skin and clothing. The type of gown 

selected should be based on the amount of exposure anticipated for each patient care 

procedure. 

Transmission Precautions 

Effective infection control sometimes requires additional precautions beyond standard 

precautions. These are called transmission precautions and consist of the following: 

• Contact precautions. 

• Droplet precautions. 

• Airborne infection isolation. 

Transmission precautions are instituted based on the type of organism suspected (Table 4.2). 

Contact precautions. Contact precautions are used in addition to standard precautions when 

patients are suspected or known to be infected with agents transmitted by direct contact with the 

patient’s skin or by indirect contact with surfaces or patient-care items in the patient’s 

environment. 

• The patient should be placed in a private room. 

• Gloves should be worn when entering the room and at all times while in the room. Hands 

should be washed immediately after gloves are removed. After handwashing, care should 

be taken not to touch potentially contaminated surfaces or items. 

• Gowns (clean, nonsterile) should be worn when entering the patient’s room and removed 

immediately after leaving the patient’s room. After the gown is removed, care should be 

taken not to touch potentially contaminated surfaces or items. 

57
• The patient should be moved from the room only when necessary. When patients are 

moved, precautions must be maintained while they are in transport. 

• Equipment used for patient care should be dedicated for a single patient to avoid 

transmitting infection to other patients. If equipment must be shared, it must be cleaned 

and disinfected between patients. 

Droplet precautions. Droplet precautions are used in addition to standard precautions when 

patients are suspected or known to be infected with microorganisms transmitted by droplets 

>5μm in size that are generated when a patient coughs, sneezes, or talks. These particles, when 

expelled, may travel 3 feet before landing on a surface. 

• The patient should be placed in a private room or with patients who have only the same 

known illness. 

• Masks should be worn when entering the room or when working within 3 feet of the 

patient, according to facility policy. 

• The patient should be moved from the room only when necessary. When patients are 

moved, they should wear a mask to prevent dispersal of droplet particles. 

Airborne infection isolation. Formerly known as airborne precautions, airborne infection 

isolation is the highest level of precaution. It is used in addition to standard precautions when 

caring for patients suspected or known to be infected with microorganisms transmitted by nuclei 

of airborne droplets <5μm in size. When dispersed, these nuclei remain suspended in the air and 

can be dispersed over long distances and potentially throughout a health care facility. 

• The patient should be placed in a private, negative-air pressure room, with 6 to 12 air 

exchanges per hour. The room should be monitored for negative pressure and should 

have appropriate discharge of air to the outdoors or have high-efficiency filtration before 

the air is recirculated to other parts of the facility. The door should be closed at all times. 

• Only essential personnel should enter the room and should wear a PAPR or a fitted N95 

(or higher) respirator at all times. 

• Patients should be moved from the room only when necessary. When patients are moved, 

they should wear a mask to limit potential spread of particles. 

For additional information about infection control measures, see “Guideline for Isolation 

Precautions in Hospitals” at http://www.cdc.gov/ncidod/dhqp/gl_isolation.html and “Guideline 

for Environmental Infection Control in Health-Care Facilities, 2003: Recommendations of CDC 

and the Healthcare Infection Control Practices Advisory Committee” at 

http://www.cdc.gov/ncidod/dhqp/gl_environinfection.html.

Equipment and Supplies 

The equipment and supplies necessary to diagnose and treat a patient suspected of being infected 

with a bioterrorist agent vary by the level of care that will be provided at a particular facility. An 

office-based primary care pediatrician may need to be concerned only with short-term isolation 

and preliminary stabilization of a patient, which will require a relatively short list of supplies that 

usually are available in the well-stocked pediatric medical office. Hospital-based pediatricians 

58
may be providing longer term and more complex care to patients and should consult their 

hospital administration regarding the hospital’s bioterrorist response plan and the response plans 

of State and local health authorities. 

Response planning requires a detailed and integrated approach between public health and 

medical facility administrators. For guidance and helpful checklists, see “The Public Health 

Response to Biological and Chemical Terrorism: Interim Planning Guidance for State Public 

Health Officials, July 2001,” at 

http://www.bt.cdc.gov/Documents/Planning/PlanningGuidance.PDF, and “Bioterrorism 

Readiness Plan: A Template for Healthcare Facilities, April 1999,” at 

http://www.cdc.gov/ncidod/dhqp/pdf/bt/13apr99APIC-CDCBioterrorism.PDF. 

Pediatric Practices 

During a bioterrorist event, local pediatricians and their staffs should maximize their ability to 

keep the office running smoothly and to provide care. The first step is for every staff member to 

have a personal family emergency plan. Once staff members are assured that they and their 

family members are safe, they are better able to focus on their professional duties. 

Second, every office needs an emergency plan. This plan should include details for handling an 

emergency both in-office and in the community. Items that should be included in an in-office 

emergency plan include the following: 

• Isolation of the patient and family. 

• PPE for staff. 

• Contact information for local public health authorities. 

• Phone numbers for emergency patient transport. 

Items that should be included in a plan for an emergency in the community include the 

following: 

• Information sheets and telephone hotline numbers. 

• Telephone triage protocols. 

• Back-up staffing schedules. 

Depending on the situation, dedicated staff may be needed just to handle anxious or worried 

parents. (See also Chapter 9, Integrating Terrorism and Disaster Preparedness into Your Pediatric 

Practice, for further information on office emergency plans.) 

The community-based pediatrician should have the following items readily available to evaluate 

children suspected of having an illness related to bioterrorism: 

• An examining room with a door that closes, in which to isolate a patient and 

accompanying family members. 

• Surgical masks. 

• Clean, nonsterile gowns. 

59
• Clean, nonsterile disposable gloves. 

• Eye protection equipment (i.e., goggles, face shields). 

• The round-the-clock phone numbers of local and State public health authorities. 

Other laboratory supplies that might be required in the early evaluation of a patient should be 

available through public health authorities. Public health authorities will advise on the collection 

of specimens and on patient transport to locally designated emergency response facilities. 

Health care professionals can register to receive e-mail updates about bioterrorism and response 

planning at http://www.bt.cdc.gov/clinregistry/index.asp. 

Managing Patients: Treatment and Prevention 

Treatment consists of supportive care (e.g., fever management, fluid management, nutritional 

supplementation, ventilatory support, and emotional care) and medical treatment (antibiotics and 

antitoxins) specific to the bioterrorist organism implicated. 

 

The Department of Health and Human Services has stockpiled vaccine for potential use in an 

outbreak of smallpox and anthrax. Although these vaccines are not available to the public before 

a bioterrorist event, they could be made rapidly available to high-risk populations in the event of 

an attack. 

Smallpox Vaccine 

Smallpox vaccine contains live vaccinia virus, an orthopox virus that is related to smallpox virus 

but that does not cause smallpox. Currently, the United States has stockpiled two types of 

vaccine: 1) vaccine manufactured from calf lymph and produced in the 1960s (Wyeth and 

Aventis), and 2) a newly manufactured cell culture-derived vaccine (Acambis),which has 

completed phase III trials and is awaiting FDA decisions for next steps. 

The smallpox vaccine is administered using a bifurcated needle that results in multiple punctures 

to the superficial layers of the skin. For a video about smallpox vaccination administration, see 

http://www.bt.cdc.gov/agent/smallpox/vaccination/administration-video/index.asp. 

The vaccination site heals over the course of 3 weeks and leaves a small scar. In the 1960s 

through 1972 when smallpox vaccination was part of the routine childhood immunization 

schedule, children—especially girls—were often vaccinated in locations on the body where the 

scar was not visible. Because smallpox vaccine will be released only in response to a bioterrorist 

attack, it is recommended that the vaccine be administered only in the deltoid region of the arm, 

so that the vaccination site and scar can be seen easily and evaluated for both medical and public 

health purposes (Figure 4.7). 

If given before exposure, the smallpox vaccine is highly effective against smallpox (95–97%), 

and if given up to 4 days after exposure, it also can prevent or minimize the severity of disease. 

The lower age limit for vaccine administration for a child who has not been exposed is 1 year. 

There is no lower age limit for a child who has been exposed to smallpox. 

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The vaccine has a number of common side effects, as well as the risk of more serious adverse 

reactions. Although many children experience side effects commonly seen after other childhood 

vaccinations (e.g., fever, lymphadenopathy, fatigue, malaise, and fussiness), far fewer children 

experience vaccinia-specific adverse reactions such as generalized vaccinia, eczema vaccinatum, 

vaccinia necrosum, postvaccinal encephalitis, and fetal vaccinia. Fortunately, by screening for 

contraindications, these complications may be largely avoidable. 

For extensive information about smallpox vaccination, administration, screening for 

contraindications, adverse events, and treatment of adverse events, see 

http://www.bt.cdc.gov/agent/smallpox/vaccination/index.asp. 

Anthrax Vaccine 

Anthrax vaccine protects against invasive disease and is currently recommended only for highrisk populations: 

• Laboratory personnel working with anthrax. 

• People working with imported animal hides and furs in areas where standards are 

insufficient to prevent exposure to anthrax spores. 

• People who handle potentially infected animal products in high-incidence areas. 

• Military personnel deployed to areas with high risk for exposure to anthrax. 

The licensed AVA anthrax vaccine, manufactured by BioPort Corporation, Lansing, MI, is 

prepared from cell-free filtrate of Bacillus anthracis culture that contains no live or dead 

bacteria. The vaccine is administered in a series of six subcutaneous injections, given at 0, 2 

weeks, 4 weeks, 6 months, 12 months, and 18 months, followed by annual boosters. Mild local 

reactions are common in adults, occurring in approximately 30% of vaccinates. Systemic 

reactions are uncommon, occurring in <0.2% of vaccinates. 

The anthrax vaccine has not been tested in children and currently is not recommended for 

children younger than age18. However, the CDC is evaluating the safety and effectiveness of 

using anthrax vaccine after exposure in children. Prophylaxis for anthrax in children is currently 

based on antimicrobial treatment (e.g., ciprofloxacin, doxycycline, and amoxicillin). 

Strategic National Stockpile 

The Strategic National Stockpile (SNS) was established in 2003 and is jointly managed by the 

Department of Homeland Security (DHS) and the Department of Health and Human Services 

(DHHS). The SNS is a national repository of antibiotics, chemical antidotes, antitoxins, 

vaccines, life-support medications, and other medical and surgical items. SNS maintains a stock 

of supplies that are specific for the medical needs of children and has received guidance from the 

AAP, as well as from academic and public health experts in general pediatrics, pediatric 

infectious diseases, pediatric pharmacology, and pediatric critical care medicine. 

The SNS is designed to supplement and re-supply State and local public health agencies in the 

event of a national emergency anywhere and at any time in the United States or its territories. 

The SNS is prepared for immediate response by having push packs strategically positioned 

61
across the United States. Push packs provide medical supplies for an initial response to a broad 

range of emergencies and arrive on site within 12 hours of deployment. If additional supplies are 

required, they can be shipped within 24 to 36 hours through vendor-managed inventory. (See 

also Chapter 2, Systems Issues, Centers for Disease Control and Prevention and Federal 

Response Plan.) 

To receive SNS assets, the governor of the affected State should directly request deployment 

from the CDC or DHHS. Most likely there will already have been public health consultation 

between the State department of health and the CDC. Requests for consultation with the CDC or 

SNS deployment can be made through the CDC Director’s Emergency Operation Center at 770-

488-7100. For further details on the SNS, see http://www.bt.cdc.gov/stockpile/. 

Surge Capacity 

Medications 

Each State’s emergency response plan, which is coordinated with public health authorities, 

should involve some local stockpiling of critical antibiotics and emergency medical supplies. If 

needed, additional supplies are available through the SNS. Each State plan details the logistics 

for transporting shipments within the State to where they are needed. In addition, many local and 

State health departments have partnered with local health facilities to hold practice runs of largescale drug dispensing and vaccination clinics. 

Isolation 

Isolation needs will vary greatly depending on the type of attack. For those diseases that are not 

transmitted person to person (anthrax, tularemia, and botulism), isolation is not needed. The 

people exposed will be those at the geographic location where the organism or toxin was 

released. 

For diseases that are transmissible, such as smallpox, plague, and VHF, infection control 

measures include isolation. Depending on the number of cases, victims may be isolated within a 

hospital. If demand exceeds the capabilities of a traditional health care facility, supplemental 

isolation and medical care facilities may be needed (e.g., schools, college campuses, motels, 

churches, or unused hospitals). If patients do not require advanced medical care, home isolation 

may be sufficient. Home isolation was used successfully during the SARS and monkeypox 

outbreaks of 2003. 

As part of their bioterrorism response planning activities, public health agencies are identifying 

facilities that can be used to isolate patients during an outbreak. Related planning includes 

having an inventory of the isolation and negative-pressure rooms in a particular area, establishing 

back-up isolation facilities, establishing and training public health and medical response teams, 

and reviewing and updating State quarantine laws. For public health bioterrorism planning 

guidance documents, see http://www.bt.cdc.gov/. 

62
Vaccination 

Large-scale vaccination may be recommended in some outbreaks related to bioterrorism, namely 

smallpox. Vaccination may be offered to an affected community, county, State, or the entire 

Nation. Large-scale smallpox vaccination clinics are intended to supplement the concurrent 

“surveillance and containment” strategy, (also called “search and containment” and “ring 

vaccination”). Surveillance and containment requires that individuals who are ill with smallpox 

are quickly identified and isolated, followed by rapid identification and vaccination of their 

contacts within 4 days of exposure. 

For additional information about vaccination strategies to be used during a smallpox outbreak, 

see http://www.bt.cdc.gov/agent/smallpox/response-plan/index.asp. 

Large-scale vaccination clinics may offer vaccination to anyone who does not have medical 

contraindications to receiving the vaccine under emergency circumstances. The Advisory 

Committee on Immunization Practices (ACIP) is reviewing and refining the contraindications to 

smallpox vaccination after an event for people who have not been exposed. 

Information for Families 

During a bioterrorist attack, one of the most important and challenging roles for the local 

pediatrician is providing information to families with children. During the anthrax attacks of 

2001, public health and medical facilities were inundated with requests for information and 

medical evaluation. As a result, these same agencies have prepared communication messages and 

information sheets that can be shared with families before and during a crisis. Parents will want 

information that is age-appropriate for their children, as well as suggestions for ways to answer 

their children’s questions. Pediatricians may want to consider accessing some of these materials 

and having them available before an emergency occurs. 

A number of organizations have developed materials to help educate children and their families 

about emergencies and bioterrorism. More information can be obtained from the following 

organizations and their Web sites: 

• American Academy of Pediatrics 

http://www.aap.org/terrorism/resources/federal_resources.html

• The Department of Health and Human Services 

http://www.os.dhhs.gov/emergency/index.shtml

• The National Child Traumatic Stress Network 

http://www.nctsnet.org/nccts/nav.do?pid=ctr_aud_prnt

Category A Agents 

See also Table 4.3. 

Anthrax 

Bacillus anthracis, the etiologic agent of anthrax, is a gram-positive, anaerobic, spore-forming, 

bacterial rod. The three virulence factors of B. anthracis are edema toxin, lethal toxin and a 

capsular antigen. Human anthrax has three major clinical forms: 

63
• Cutaneous. 

• Inhalational. 

• Gastrointestinal. 

If untreated, anthrax in all forms can lead to septicemia and death. Anthrax generally is not 

contagious, but person-to-person transmission from cutaneous lesions has been reported rarely. 

For more information, see http://www.bt.cdc.gov/agent/anthrax/index.asp. 

Signs and symptoms. Symptoms usually occur within 2 weeks of exposure; however, the 

incubation period for inhalational anthrax may be as long as several months because of spore 

dormancy and delayed clearance from the lungs. 

Cutaneous anthrax. Cutaneous anthrax is the most common type of infection (>95%). It usually 

develops after skin contact with contaminated meat, wool, hides, or leather from infected 

animals. The incubation period ranges from 1 to 12 days. The skin infection begins as a small 

papule and progresses to a vesicle in 1 to 2 days, followed by a painless, necrotic ulcer with a 

black eschar, usually 1–3 cm in diameter (Figure 4.3). Patients may have fever, malaise, 

headache, and regional lymphadenopathy. 

Inhalational anthrax. Inhalational disease is the most lethal form of anthrax. The incubation time 

of inhalational anthrax in people is unclear, but it is reported to range from 1 to 7 days, possibly 

up to 60 days. Initial symptoms resemble common respiratory infections and include mild fever, 

muscle aches, and malaise. Some patients also complain of sore throat. These symptoms progress 

to nonproductive cough, pleuritic chest pain, shortness of breath, respiratory failure, and 

frequently, meningitis. Upper respiratory symptoms such as rhinorrhea are generally not seen 

with inhalational anthrax. 

Gastrointestinal anthrax. Gastrointestinal disease is the least common form of anthrax. It usually 

follows the consumption of raw or undercooked contaminated meat and has an incubation period 

of 1 to 7 days. Severe abdominal distress is followed by fever and signs of septicemia. The 

disease can take an oropharyngeal or abdominal form. Lesions at the base of the tongue, sore 

throat, dysphagia, fever, and regional lymphadenopathy usually characterize involvement of the 

oropharynx. Lower bowel inflammation usually causes nausea, loss of appetite, vomiting, and 

fever, followed by abdominal pain, hematemesis, and bloody diarrhea. 

Diagnosis. The clinical evaluation of patients suspected of having inhalational anthrax should 

include a chest radiograph and/or CT scan to evaluate for widened mediastinum and pleural 

effusion. (Figure 4.1). For chest radiographs, see 

http://phil.cdc.gov/PHIL_Images/02122002/00041/PHIL_1795_thumb.jpg and 

http://phil.cdc.gov/PHIL_Images/02122002/00042/PHIL_1796_thumb.jpg. 

Anthrax is not spread by person-to-person contact except in rare cases of transmission from 

cutaneous lesions. If the history does not reveal possible environmental exposure, anthrax is not 

a likely diagnosis. Depending on the clinical presentation, Gram stain and culture should be 

performed on specimens of blood, pleural fluid, CSF, and tissue biopsy or discharge from 

64
cutaneous lesions; however, previous treatment with antimicrobial agents can result in false 

negatives. Isolates can be definitely identified through the LRN in each State. Additional 

diagnostic tests, including immunohistochemistry, real-time PCR, time-resolved fluorescence,

and an enzyme immunoassay that measures IgG antibodies against B. anthracis protective 

antigen, are performed at the CDC and can be accessed through State health departments. 

Nasal swabs for detection of B. anthracis may assist in epidemiologic investigations but should 

not be relied on as a guide for prophylaxis or treatment of individual patients. Epidemiologic 

investigation in response to threats of exposure to B. anthracis may use nasal swabs of 

potentially exposed individuals as an adjunct to environmental sampling to determine the extent 

of exposure. See Table 4.4a and Table 4.4b. 

Treatment. A high index of clinical suspicion and rapid administration of effective antimicrobial 

therapy are essential for prompt diagnosis and effective treatment. No controlled trials have been 

performed in people to validate current treatment recommendations, and clinical experience is 

limited. For bioterrorism-associated cutaneous disease in adults or children, ciprofloxacin (500 

mg, PO, BID, or 10–15 mg/kg/day for children, PO, divided BID) or doxycycline (100 mg, PO, 

BID, or 5 mg/kg/day, PO, divided BID for children younger than 8 years of age) are 

recommended for initial treatment until antimicrobial susceptibility data are available. Because 

of the risk of concomitant inhalational exposure, consideration should be given to continuing an 

appropriate antimicrobial regimen for postexposure prophylaxis. 

Ciprofloxacin (400 mg, IV, every 8–12 hours) or doxycycline (200 mg, IV, every 8–12 hours) 

should be used initially as part of a multidrug regimen for treating inhalational anthrax, anthrax

meningitis, cutaneous anthrax with systemic signs, and GI anthrax until results of antimicrobial

susceptibility testing are known. Other agents with in vitro activity suggested for use in 

conjunction with ciprofloxacin or doxycycline include rifampin, vancomycin hydrochloride, 

imipenem, chloramphenicol, penicillin, ampicillin, clindamycin, and clarithromycin. 

Cephalosporins and trimethoprim-sulfamethoxazole should not be used. Treatment should 

continue for at least 60 days. Neither ciprofloxacin nor tetracycline is routinely used in children 

or pregnant women because of safety concerns. However, ciprofloxacin or tetracycline should be 

used for treatment of anthrax in children who have life-threatening infections until antimicrobial 

susceptibility patterns are known. 

About 20% of untreated cases of cutaneous anthrax result in death, but deaths are rare if patients 

receive appropriate antimicrobial therapy. The case fatality rate of inhalational anthrax is 

estimated to be 50% to 75%, even with early treatment. The case fatality rate of GI anthrax is 

estimated to be between 25% and 60%. The impact of antibiotic treatment on the case fatality 

rate of GI anthrax is unknown. 

Control measures. Standard precautions are recommended for hospitalized patients. 

Contaminated dressings and bed linens should be incinerated or steam sterilized to destroy 

spores. Autopsies performed on patients with systemic anthrax require special precautions. 

BioThrax (formerly known as Anthrax Vaccine Adsorbed [manufactured by BioPort Corp, 

Lansing, MI]) is the only vaccine licensed in the United States for prevention of anthrax in 

65
people. This vaccine is prepared from a cell-free culture filtrate. Immunization consists of six SC 

injections at 0, 2, and 4 weeks and at 6, 12, and 18 months, followed by annual boosters. The 

vaccine is currently recommended for people at risk of repeated exposures to B. anthracis spores, 

including select laboratory workers and military personnel. The vaccine is effective for 

preventing cutaneous anthrax in adults. Protection against inhalational anthrax has not been 

evaluated in people, but the vaccine has been effective in studies in nonhuman primates. Adverse 

events are mainly local injection site reactions; systemic symptoms, including fever, chills, 

muscle aches, and hypersensitivity are rare. No data on vaccine effectiveness or safety in 

children are available, and the vaccine is not licensed for use in children or pregnant women. 

Anthrax vaccine is not licensed for postexposure use in preventing anthrax. 

Based on the limited available data, the best means of preventing inhalational anthrax after 

exposure to B. anthracis spores is prolonged antimicrobial therapy in conjunction with a threedose regimen (at 0, 2, and 4 weeks) of anthrax immunization. However, because BioThrax is not 

licensed for postexposure prophylaxis or for use as a three-dose regimen or for use in children, it 

can be used only under an investigational new drug application as part of an emergency public 

health intervention. When no information is available about the antimicrobial susceptibility of 

the implicated strain of B. anthracis, initial postexposure prophylaxis for adults or children with 

ciprofloxacin or doxycycline is recommended. Although fluoroquinolones and tetracyclines are 

not recommended as first-choice drugs in children because of adverse effects, these concerns 

may be outweighed by the need for early treatment of pregnant women and children exposed to 

B. anthracis after a terrorist attack. As soon as susceptibility of the organism to penicillin has 

been confirmed, prophylactic therapy for children should be changed to oral amoxicillin, 80 

mg/kg/day, divided TID (not to exceed 500 mg, TID). Bacillus anthracis is not susceptible to 

cephalosporins and trimethoprim-sulfamethoxazole; therefore, these agents should not be used 

for prophylaxis (see Table 4.5). 

For more information, see http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5045a5.htm. 

Reporting. If a case of anthrax is suspected, immediately contact the local and State health 

departments and hospital infection control practitioner. If they are unavailable, contact the CDC 

at 770-488-7100. 

Botulinum Toxin 

For a quick fact sheet, see http://www.bioterrorism.slu.edu/botulism/quick/botulism01.pdf. 

For additional information, see http://jama.ama-assn.org/cgi/content/full/285/8/1059?. 

Disease. Botulism is a rare disease caused by ingestion of the anaerobic, spore-forming bacillus 

Clostridium botulinum. Botulism neurotoxins are the most potent toxins known. There are three 

forms of naturally occurring botulism: 

• Foodborne. 

• Wound. 

• Infant (intestinal). 

In addition, inhalational disease could occur if aerosolized botulinum toxin were used, such as in 

a bioterrorist incident. A thorough history may help determine the mode of infection. If no 

66
common food source is identified during an outbreak or cluster of cases, bioterrorism should be 

suspected. 

Signs and symptoms. The incubation period varies according to the type of botulism and the 

extent of exposure to the toxin: 

• Foodborne: 12-36 hours (range 6 hours to 10 days). 

• Wound: 7-8 days (range 4–18 days) after injury. 

• Infant: 18-36 hours after ingestion. 

• Inhalational: The true incubation period for aerosolized botulism is unknown. In the three 

known inhalational cases, onset was approximately 72 hours. In laboratory studies, 

monkeys developed disease 12–18 hours after exposure. 

Regardless of the means of exposure, botulinum toxin causes permanent nerve damage by 

irreversibly binding to nerve synapses and interfering with the release of acetylcholine. 

Botulinum toxin cannot cross the blood-brain barrier and does not affect the CNS. Sensory 

systems remain intact while the peripheral cholinergic synapses are damaged, resulting in flaccid 

paralysis in a patient who remains mentally alert and afebrile. 

The toxin first affects the muscles connected to the cranial nerves. Early symptoms of all forms 

of the disease include double or blurred vision, difficulty with speaking and swallowing, dry 

mouth, and fatigue. As the disease progresses, symmetrical muscle weakness develops, starting 

at the trunk and descending to the extremities; deep tendon reflexes generally remain intact. 

Without ventilatory support, death results when the toxin attacks the respiratory system, resulting 

in airway obstruction and respiratory paralysis. Recovery may occur if paralyzed muscles are 

reinnervated, but this process requires weeks to months of intensive supportive therapy. 

Foodborne. Infants may develop disease after ingestion of C. botulinum organisms and 

subsequent GI absorption of toxin. Among babies older than 6–12 months, disease results only 

from ingestion or inhalation of preformed toxin. Initial symptoms include vomiting, constipation, 

GI upset, and rarely diarrhea, followed by symptoms listed above. These GI symptoms are 

thought to be caused by other bacterial metabolites also present in the food and may not occur if 

purified botulinum toxin is intentionally placed in foods or aerosols. Respiratory support is 

required in 57% to 81% of patients. 

Wound. This form of the disease most closely resembles tetanus. Neurotoxins produced by the 

contaminating organisms in the affected wound disseminate throughout the body and destroy the 

nerve endings. Symptoms are similar to those of foodborne illness, except that there are no GI 

symptoms. 

Infants. The initial symptom is generally constipation, although lethargy, lack of appetite, 

drooling, and weakness also occur. Descending symmetrical paralysis follows, evidenced by 

bulbar palsies: poor head and muscle control; flat affect; ptosis; impaired gag, suck, and swallow 

reflexes; dilated or sluggish pupillary reaction; and a weak cry. Respiratory failure is common. 

Intubation is required in >80% of cases, and ventilatory support is necessary (see Figure 4.2). 

67
Diagnosis. A presumptive diagnosis can be made based on signs and symptoms. Laboratory 

confirmation is needed for definitive diagnosis. Obtaining a history that focuses on food intake 

and potential exposure to the organism is imperative. 

Signs and symptoms of botulism that help distinguish it from other causes of weakness include 

the following: 

• Disproportionate involvement of cranial nerves. 

• Involvement of facial muscles to a greater extent than more distal weakness. 

• The lack of sensory changes that usually accompany other disorders that result in flaccid 

paralysis. 

Confirmatory tests include detection of toxin through mouse bioassay using the following 

specimen(s): blood and feces (foodborne), blood and wound (wound), and feces (intestinal). 

Toxin can also be detected in gastric secretions, which might be the most useful specimen in a 

case of inhalational disease. For results of the bioassay to be accurate, all specimens should be 

refrigerated during storage, serum samples should be obtained before antitoxin treatment, and the 

laboratory should be notified if the patient has taken anticholinesterase medications. Definitive 

diagnosis may be made through monovalent and polyvalent diagnostic antitoxins available from 

the CDC and a limited number of public health departments. 

Treatment. Rapid diagnosis and initiation of treatment and supportive care provide the best 

opportunity for survival. Treatment should begin as soon as the diagnosis is suspected without 

waiting for laboratory confirmation. Antitoxin, available from the CDC by calling 770-488-7100, 

should be administered to all patients with known or suspected disease. Antitoxin cannot reverse 

the effects of toxin bound to nerve receptors, but it does prevent further progression of nerve 

damage. Because the antitoxin is derived from horse serum, serious complications (including 

anaphylaxis and serum sickness) can develop. Supportive care generally includes intensive care, 

tube feedings or total parenteral nutrition (TPN), and ventilator support (in 29% of foodborne 

cases and 80% of infant cases). 

Recommendations for safe and effective administration of antitoxin have changed over time; 

package insert materials should be reviewed before initiation. 

Foodborne and inhalational botulism. Trivalent equine botulinum antitoxin (types A, B, and E) 

and bivalent antitoxin (types A and B) are available from the CDC at 770-488-7100 or through 

State health departments for treatment of foodborne or wound botulism. Patients should be tested 

for hypersensitivity to equine sera before administration. Approximately 9% of treated people 

experience some degree of hypersensitivity to equine serum, but severe reactions are rare. 

Infant botulism. A 5-year, randomized, double-blind, placebo-controlled treatment trial of 

human-derived botulinum antitoxin (formally known as botulism immune globulin intravenous 

[BIGIV]) in infants with botulism showed a significant decrease in hospital days, mechanical 

ventilation, tube feedings, and cost associated with BIGIV administration ($70,000 less per 

case). The California Department of Health Services (24-hour telephone number, 510-540-2646) 

should be contacted to procure BIGIV. Treatment with BIGIV should begin as early in the illness 

as possible. BIGIV is available only for treatment of infant botulism. Approximately 9% of 

68
treated people experience some degree of hypersensitivity reaction to equine serum, but severe 

reactions are rare. 

Antimicrobial agentsshould be avoided in infant botulism because lysis of intraluminal C. 

botulinum could increase the amount of toxin available for absorption. Aminoglycosides can 

potentiate the paralytic effects of the toxin and should be avoided. 

Control. Standard precautions should be used in the care of hospitalized patients with botulism. 

Person-to-person transmission does not occur.

After exposure. Individuals known to be exposed or suspected of having been exposed to 

aerosolized botulinum toxin should be closely monitored and treated with antitoxin at the first 

sign of disease. Prophylactic equine antitoxin for asymptomatic people who have ingested a food 

known to contain botulinum toxin is not recommended. Because of the danger of 

hypersensitivity reactions, the decision to administer antitoxin requires careful consideration. 

Consultation about antitoxin use may be obtained from the State health department or the CDC. 

Elimination of recently ingested toxin may be facilitated by induction of vomiting, gastric 

lavage, rapid purgation, and high enemas. These measures should not be used in infant botulism. 

Enemas should not be administered to people with illness except to obtain a fecal specimen for 

diagnostic purposes. Exposed people should be observed closely. 

Decontamination. Clostridium botulinum is a hardy spore that is highly heat resistant, but 

botulism toxin in food is easily destroyed through the normal cooking process (heating >85o C 

for 5 minutes). Weather conditions and size of the aerosolized particles determine how long the 

toxin can remain airborne, but it is estimated that most toxin would be inactive within 2 days of 

aerosol release. If a warning is issued before a release, some protection can be achieved by 

covering the mouth with cloth or a mask; toxin may be absorbed through mucous membranes but 

cannot penetrate intact skin. After a known exposure, patients and their clothing should be 

washed with soap and water. Surfaces exposed to the initial release should be cleaned with a 

1:10 hypochlorite (bleach) solution. 

Reporting. If you suspect a case of botulism, immediately contact your hospital epidemiologist 

or infection control practitioner and local and State health departments. If local and State health 

departments are unavailable, contact the CDC at 770-488-7100. 

For further information and fact sheets, see http://www.bt.cdc.gov/agent/botulism/index.asp. 

Plague 

Plague is caused by Yersinia pestis, a pleomorphic, bipolar-staining, gram-negative 

coccobacillus. In nature, plague is a zoonotic infection of rodents, carnivores, and their fleas that 

are found in many areas of the world. Plague has been reported throughout the Western United 

States, but most human cases occur in New Mexico, Arizona, California, and Colorado as 

isolated cases or in small clusters. 

69
• Bubonic plague usually is transmitted by bites of infected rodent fleas and uncommonly 

by direct contact with tissues and fluids of infected rodents or other mammals, including 

domestic cats. 

• Septicemic plague occurs most often as a complication of bubonic plague but may result 

from direct contact with infectious materials or the bite of an infected flea. 

• Primary pneumonic plague is acquired by inhalation ofrespiratory droplets from a human 

or animal with respiratory plague or from exposure to laboratory aerosols. 

• Secondary pneumonic plague arises from hematogenous seeding of the lungs with Y.

pestis in patients with bubonic or septicemic plague.

The incubation period is 2–6 days for bubonic plague and 2–4 days for primary pneumonic 

plague.

Signs and symptoms. A bioterrorist incident involving plague would most likely occur through 

aerosolization and result in pneumonic involvement. The incubation period after flea-borne 

transmission is 2–8 days. Incubation after aerosolization would be expected to be shorter (1–3 

days). Clinical features of pneumonic plague include fever, cough with mucopurulent sputum 

(gram-negative rods may be seen on Gram stain), hemoptysis, and chest pain. A chest radiograph 

will show evidence of bronchopneumonia. 

Diagnosis. Plague is characterized by massive growth of Y. pestis in affected tissues, especially 

lymph nodes, spleen, and liver. The organism has a bipolar (safety-pin) appearance when viewed 

with Wayson or Gram stains. If plague organisms are suspected, the laboratory examining the 

specimens should be informed to minimize risks of transmission to laboratory personnel. 

Handling of specimens should be coordinated with local or State health departments and 

undertaken in Biosafety Level 2 or Level 3 laboratories. 

A positive fluorescent antibody test result for the presence of Y. pestis in direct smears or 

cultures of a bubo aspirate, sputum, CSF, or blood specimen provides presumptive evidence of Y. 

pestis infection. A single seropositive result by passive hemagglutination assay or enzyme 

immunoassay in an unimmunized patient who has not had plague previously also provides 

presumptive evidence of infection. Seroconversion and/or a four-fold difference in antibody titer

between two serum specimens obtained 1 to 3 months apart provides serologic confirmation. The 

diagnosis of plague usually is confirmed by culture of Y. pestis from blood, bubo aspirate, or 

another clinical specimen. PCR assay or immunohistochemical staining for rapid diagnosis of Y 

pestis is available in some reference or public health laboratories. Isolates suspected as Y. pestis

should be reported immediately to the State health department and submitted to the Division of 

Vector-Borne Infectious Diseases of the CDC. For additional information, see 

http://www.cdc.gov/ncidod/dvbid/plague/diagnosis.htm

http://www.bt.cdc.gov/Agent/Plague/ype_la_cp_121301.pdf. 

Treatment. Streptomycin sulfate (30 mg/kg/day, IM, divided BID-TID) is the treatment of 

choice for most children. Gentamicin sulfate in standard dosages for age given IM or IV is an 

equally effective alternative to streptomycin. Tetracycline, doxycycline, or chloramphenicol is 

also effective. Tetracycline or doxycycline should not be given to children younger than age 8 

unless the benefits of use outweigh the risks of dental staining. Chloramphenicol is the preferred 

70
treatment for plague meningitis. Antimicrobial treatment should be continued for 7–10 days or 

until several days after fever breaks. Drainage of abscessed buboes may be necessary; drainage 

material is infectious until effective antimicrobial therapy has been given. 

Control measures. In addition to standard precautions, droplet precautions are indicated for all 

patients with suspected plague until pneumonia is excluded and appropriate therapy has been 

started. Special air handling is not indicated. In patients with pneumonic plague, droplet 

precautions should be continued for 48 hours after appropriate treatment has been started. 

Postexposure prophylaxis should begin after confirmed or suspected exposure to Y. pestis and for 

postexposure management of health care workers and others who have had unprotected face-toface contact with symptomatic patients. In children, prophylactic treatment with doxycycline (5 

mg/kg/day, divided BID) or ciprofloxacin (20–30 mg/kg/day divided BID) is recommended and 

should be continued for 7 days after exposure or until exposure can be excluded. Household 

members and other people with intimate exposure to a patient with plague should report any 

fever or other illness to their physician. 

Currently, no vaccine for plague is commercially available in the United States. Information 

concerning the availability of plague vaccines is available from the Division of Vector-Borne 

Infectious Diseases of the CDC. 

Reporting. State public health authorities should be notified immediately of any suspected cases 

of plague in people. Initial suspicion of a bioterrorist event involving Y. pestis will likely involve 

identification of more than one case in a nonendemic area. If this occurs, immediately contact 

your local and State health departments and hospital infection control practitioner. If they are 

unavailable, contact the CDC at 770-488-7100. 

For additional information, see http://jama.ama-assn.org/cgi/content/short/283/17/2281. 

Smallpox 

Variola, the virus that causes smallpox, is a member of the Poxviridae family (genus

Orthopoxvirus). These DNA viruses are among the largest and most complex viruses known, and 

they differ from most other DNA viruses by multiplying in the cytoplasm. Monkeypox, vaccinia, 

and cowpox are other members of the genus and can cause zoonotic infection of people, but they 

usually do not spread from person to person. People are the only natural reservoir for variola 

virus. For additional information, see http://www.bt.cdc.gov/agent/smallpox/index.asp. 

In 1980, the World Health Organization (WHO) declared that smallpox (variola) had been 

successfully eradicated worldwide. The last naturally occurring case of smallpox occurred in 

Somalia in 1977, followed by two cases attributable to laboratory exposure in 1978. The United 

States discontinued routine childhood immunization against smallpox in 1971 and routine 

immunization of health care workers in 1976. The U.S. military continued to immunize military 

personnel until 1990. Since 1980, the vaccine has been recommended only for people working 

with nonvariola orthopoxviruses. Two WHO reference laboratories were authorized to maintain 

stocks of variola virus. There is increasing concern that the virus and the expertise to use it as a 

weapon of bioterrorism may have been misappropriated. 

71
Signs and symptoms. An individual infected with variola major develops a severe prodromal 

illness characterized by high fever (102°–104°F [38.9°–40.0°C]) and constitutional symptoms, 

including malaise, severe headache, backache, abdominal pain, and prostration, lasting 2–5 days. 

Infected children may have vomiting and seizures during this prodromal period. Most patients 

with smallpox tend to be severely ill and bedridden during the febrile prodrome. The prodromal 

period is followed by enanthemas that may not be noticed by the patient. This stage occurs <24 

hr before the onset of rash, which is usually the first recognized manifestation of infectiousness. 

With the onset of enanthemas, the patient becomes infectious and remains so until all skin crust 

lesions have separated. The rash, or exanthem, typically begins on the face and rapidly 

progresses to involve the forearms, trunk, and legs in a centrifugal distribution (greatest 

concentration of lesions on the face and distal extremities). Many patients have lesions on the 

palms and soles of their feet. With rash onset, fever decreases, but the patient does not fully 

defervesce. Lesions begin as maculas that progress to papules, then firm vesicles, and then deepseated, hard pustules described as “pearls of pus,” with each stage lasting 1–2 days. By day 6 or 

7 of the rash, lesions may begin to umbilicate or become confluent. Lesions increase in size for 

approximately 8–10 days, after which they begin to crust. Once all the lesions have separated, 3–

4 weeks after the onset of rash, the patient is no longer infectious. Infected people sustain 

significant scarring after the crusts have separated. Because of the relatively slow and steady 

evolution of the rash lesions, all lesions on any one part of the body are in the same stage of 

development (see Figure 4.5, smallpox lesions). 

 

Varicella (chickenpox) is the condition most likely to be mistaken for smallpox. Generally, 

children with varicella do not have a febrile prodrome; adults may have a brief, mild prodrome. 

Although the two diseases can be easily confused in the first few days of the rash, smallpox

lesions develop into pustules that are firm and deeply embedded in the dermis, whereas varicella 

lesions develop into superficial vesicles. Because varicella erupts in crops of lesions that evolve 

quickly, lesions on any one part of the body are in different stages of development (papules, 

vesicles, and crusts; see Figure 4.6, varicella lesions). The distribution of the rash in the two 

diseases differs. Varicella most commonly affects the face and trunk with relative sparing of the 

extremities, and lesions on the palms or soles are rare (see Figure 4.4, distribution of smallpox 

lesions vs. varicella lesions). 

In addition to the typical presentation of smallpox (≥90% of cases), there are two uncommon 

forms of variola major: 

• Hemorrhagic, characterized by hemorrhage into skin lesions and disseminated

intravascular coagulation. 

• Malignant or flat type, in which the skin lesions do not progress to the pustular stage but 

remain flat and soft. 

In the past, each variant occurred in approximately 5% of cases and was associated with a 95%–

100% mortality rate. Hemorrhagic smallpox rash commonly was confused with 

meningococcemia. Flat-type (velvety) smallpox occurred more commonly in children. By 

contrast, variola minor, or alastrim, was associated with fewer lesions, more rapid progression of 

rash, and a much lower mortality rate (approximately 1%) than variola major, or typical 

smallpox. 

72
Smallpox is spread most commonly in droplets from the oropharynx of infected individuals, 

although infrequent transmission from aerosol and direct contact with infected lesions, clothing, 

or bedding has been reported. Patients are not infectious during the incubation period or febrile 

prodrome but become infectious with the onset of mucosal lesions (enanthemas), which occur 

within hours of the rash. The first week of rash illness is regarded as the most infectious period, 

although patients remain infectious until all scabs have separated. Because most smallpox

patients are extremely ill and bedridden, spread generally is limited to household contacts, 

hospital workers, and other health care professionals. Secondary household attack rates for 

smallpox were considerably lower than for measles and similar to or lower than rates for 

varicella. The incubation period is 7–17 days (mean 12 days). 

Variola major in unimmunized people was associated with case fatality rates of approximately 

30% during epidemics of smallpox. The mortality rate was highest in children younger than 1 

year and adults older than 30. The potentialfor modern supportive therapy in improving outcome 

is not known. Death was most likely to occur during the second week of illness and was 

attributed to overwhelming viremia. Secondary bacterial infections occurred but were a less 

significant cause of mortality. 

For help in evaluating a rash illness suspicious of smallpox, see 

http://www.bt.cdc.gov/agent/smallpox/diagnosis/riskalgorithm/index.asp. 

Diagnosis. Variola virus can be detected in vesicular or pustular fluid by culture or by PCR 

assay. Electron microscopy can detect orthopoxvirus infection but cannot distinguish between 

viruses. Currently, variola diagnostic testing is conducted only at the CDC. Reports of patients 

classified by the CDC as at high risk of having smallpox will trigger a rapid response, with a 

team deployed to obtain specimens and advise on clinical management. 

Treatment. There is no effective antiviral therapy available to treat smallpox. Infected patients 

should receive supportive care. Cidofovir, currently licensed for cytomegalovirus retinitis, has 

been suggested as having a role in smallpox therapy, but data to support its use in smallpox are 

not available. The drug must be given IV and is associated with significant renal toxicity. 

Vaccinia immune globulin (VIG) is reserved for certain complications of immunization and has 

no role in treatment of smallpox. 

Control measures. If a patient is suspected of having smallpox, standard, contact, and airborne 

precautionsshould be implemented immediately, and the State and local health departments 

should be alerted at once. Hospital infection control personnel should be notified when the 

patient is admitted, and the patient should be placed in a private, airborne infection isolation 

room equipped with negative-pressure ventilation with high-efficiency particulate air filtration. 

Anyone entering the room must wear an N95 or higher-quality respirator, gloves, and gown, 

even if there is a history of recent successful immunization. If the patient is moved from the 

room, he or she should wear a mask and be covered with sheets or gowns to decrease the risk of 

fomite transmission. Rooms vacated by patients should be decontaminated using standard

hospital disinfectants, such as sodium hypochlorite or quaternary ammonia solutions. Laundry 

73
and waste should be discarded into biohazard bags and autoclaved, and bedding and clothing 

should be washed in hot water with laundry detergent followed by hot-air drying or incinerated. 

Vaccination. Postexposure immunization (within 3–4 days of exposure) provides some 

protection against disease and significant protection against a fatal outcome. Any person who has 

had significant exposure to a patient with confirmed smallpox during the infectious stage of 

illness should be immunized as soon after exposure as possible, but within 4 days of first 

exposure. Because infected individuals are not contagious until the rash (and/or enanthema) 

appears, individuals exposed only during the prodromal period are not at risk. 

Vaccinia immune globulin. Vaccinia immune globulin (VIG) prepared from plasma of 

immunized individuals was used in the past to prevent or modify smallpox when administered 

within 24 hours of a known exposure. Current supplies of VIG are used in the treatment of 

complications of smallpox immunization. The CDCis the only source of VIG in the United 

States. Supplies may be obtained by calling the CDC Smallpox Vaccine Adverse EventsClinical 

Information Line at 877-554-4625 for physicians in civilian medical facilities. 

Reporting. Cases of febrile rash illness for which smallpox is being considered in the 

differential diagnosis should be reported immediately to local or State health departments. After 

evaluation by the State or local health department, if smallpox laboratory diagnostic testing is 

considered necessary, the CDC Rash Illness Evaluation Team should be consulted at 770-488-

7100. Laboratory confirmation of smallpox is available only from the CDC. (See Figure 4.8, 

evaluating febrile rash illness in patients suspected of having smallpox [algorithm]). 

Tularemia 

Tularemia is caused by Francisella tularensis, a small, nonmotile, aerobic, gram-negative 

coccobacillus. Francisella tularensis is one of the most infectious pathogens known; inoculation 

with or inhalation of as few as 10 organisms can cause disease. It is found in diverse animal 

hosts and can be recovered from contaminated water, soil, and vegetation. Small mammals, 

including voles, mice, water rats, squirrels, rabbits, and hares, are natural reservoirs. They 

acquire infection through tick, fly, or mosquito bites and by contact with contaminated 

environments. Natural infection in people occurs through bites of infected arthropods; handling 

infectious animal tissues or fluids; direct contact with or ingestion of contaminated food, water 

or soil; or inhalation of infective aerosols. Person-to-person transmission does not occur. 

Aerosol release of F. tularensis as a bioterrorist event would be expected to cause primarily 

pleuropneumonitis, but some exposures might result in ocular tularemia, ulceroglandular or 

glandular disease, or oropharyngeal disease with cervical lymphadenitis. Release in a densely 

populated area would be expected to result in an abrupt onset of large numbers of people with 

acute, nonspecific febrile illness beginning 3–5 days later (incubation period is 1–14 days), with 

pleuropneumonitis developing in a significant proportion of cases during the ensuing days and 

weeks. 

Signs and symptoms. Francisella tularensis is a facultative intracellular bacterium that 

multiplies within macrophages. Major target organs are the lymph nodes, lungs and pleura, 

spleen, liver, and kidney. Bacteremia may be common in early stages. Initial tissue reaction is a 

74
focal, intensely suppurative necrosis that becomes granulomatous. After inhalational exposure, 

hemorrhagic inflammation of the airways develops and progresses to bronchopneumonia. 

Pleuritis with adhesions, and effusion and hilar lymphadenopathy are common. 

Illness begins with fever, headache, chills and rigors, generalized body aches, coryza, and sore 

throat. There may be a dry or slightly productive cough and substernal pain or tightness with or 

without objective signs of pneumonia. These findings are followed by sweats, fever, chills, 

progressive weakness, malaise, anorexia, and weight loss. These signs and symptoms would be 

similar to those caused by Q fever, but the progression of illness would be expected to be slower 

and the case-fatality rate lower than in inhalational plague or anthrax. 

Diagnosis. Francisella tularensis can be isolated from respiratory secretions and, sometimes, 

from blood in cases of inhalational infection. Gram stain, fluorescent antibody, or 

immunohistochemical stains (performed in designated reference laboratories in the National 

Public Health Laboratory Network) may demonstrate the organism in secretions, exudates, or 

biopsy specimens. If tularemia is suspected, the laboratory should be informed to minimize risks 

of transmission to laboratory personnel. Routine diagnostic procedures can be performed in 

Biosafety Level 2 conditions. Cultures in which F. tularensis is suspected should be examined in 

a biological safety cabinet. Manipulation of cultures and other procedures that might produce 

aerosols or droplets (e.g., grinding, centrifuging, vigorous shaking, animal studies) should be 

conducted under Biosafety Level 3 conditions. Bodies of patients who die of tularemia should be 

handled using standard precautions. Autopsy procedures likely to produce aerosols or droplets 

should be avoided. Clothing or linens contaminated with body fluids of patients with tularemia 

should be disinfected per standard hospital procedure. 

Treatment. In case of a bioterrorist event, antimicrobial susceptibility testing of isolates should 

be conducted quickly and treatment altered according to test results and clinical response. For 

treatment recommendations in children before test results are known, see Table 4.6. 

Control measures. Treatment with streptomycin, gentamicin, doxycycline, or ciprofloxacin 

started during the incubation period of tularemia and continued daily for 14 days can protect 

against symptomatic infection. Therefore, if an attack is discovered before individuals become 

ill, those who have been exposed should be treated prophylactically with oral doxycycline or 

ciprofloxacin for 14 days. If an attack is discovered only after individuals become ill, a fever 

watch should begin for those who potentially have been exposed. Treatment (as outlined above) 

should begin in those who develop an otherwise unexplained fever or flu-like illness within 14 

days of presumed exposure. 

Postexposure prophylactic treatment of those in close contact with tularemia patients is not 

recommended because person-to-person transmission is not known to occur. Standard 

precautions should be used in caring for hospitalized patients. 

Reporting. Initial suspicion of a bioterrorist event involving F. tularensis will likely involve 

identification of more than one case in a nonendemic area. If this happens, immediately contact 

the local and State health departments and hospital infection control practitioner. If they are 

unavailable, contact the CDC at 770-488-7100. 

75
For additional information, see http://www.bt.cdc.gov/agent/tularemia/facts.asp and 

http://www.bt.cdc.gov/agent/tularemia/faq.asp. 

Viral Hemorrhagic Fevers 

The term “viral hemorrhagic fevers (VHFs)” refers to a group of illnesses that are caused by 

several distinct families of viruses. In general, the term “viral hemorrhagic fever” is used to 

describe a severe multisystemic syndrome. Characteristically, the overall vascular system is 

damaged, and the body's ability to regulate itself is impaired. Although some types of 

hemorrhagic fever viruses cause relatively mild illnesses, many of these viruses cause severe, 

life-threatening disease. 

VHFs are caused by RNA viruses of four distinct families: 

• Arenaviruses (including Lassa fever). 

• Filoviruses (including Rift Valley fever and hantavirus). 

• Bunyaviruses (including Ebola and Marburg hemorrhagic fever). 

• Flaviviruses (including tick-borne encephalitis). 

In nature, the survival of these viruses depends on an animal or insect host called the natural 

reservoir. They are geographically restricted to the areas where their host species lives, and 

people are not the natural reservoir for any of these viruses. People may become infected when 

they come into contact with infected hosts, and in some cases, people can transmit the virus to 

one another. With a few exceptions, there is no cure or established drug treatment for VHFs. 

Signs and symptoms. Specific signs and symptoms vary by the type of VHF, but initial signs 

and symptoms often include marked fever, fatigue, dizziness, muscle aches, loss of strength, and 

exhaustion. Other signs and symptoms can include vomiting, diarrhea, abdominal pain, chest 

pain, cough, and pharyngitis. A maculopapular rash, predominantly on the trunk, develops in 

many patients about 5 days after the onset of symptoms. Patients with severe VHF often show 

signs of bleeding under the skin, in internal organs, or from body orifices like the mouth, eyes, or 

ears. However, although they may bleed from many sites around the body, patients rarely die 

because of blood loss. Severely ill patients may go into shock with nervous system malfunction, 

coma, delirium, and seizures. Some types of VHF are associated with renal failure. 

The incubation period is 4–21 days. The mortality rate varies depending on the specific virus 

involved. 

Diagnosis. Diagnosis of VHF introduced through bioterrorism is likely to be recognized only 

after a cluster of patients present with similar, severe illness. Clinical suspicion should prompt 

notification of infection control and State health officials. Serum for antibody testing and tissue 

samples should be sent through your State health department to the CDC. 

Treatment. In general, there is no specific treatment or established cure for VHFs. Treatment is 

supportive. Ribavirin has been effective in treating some individuals with Lassa fever or 

hemorrhagic fever with renal syndrome. Treatment with convalescent-phase plasma has been 

used with success in some patients with Argentinean hemorrhagic fever. 

76
Control measures. Some viruses that cause hemorrhagic fever—including Ebola, Marburg, 

Lassa fever, and Crimean-Congo hemorrhagic fever viruses—can spread from one person to 

another (once an initial person has become infected). This type of secondary transmission of the 

virus can occur directly through close contact with infected people or their blood or other body 

fluids. Contaminated syringes and needles have been involved in the spread of infection in 

outbreaks of Ebola hemorrhagic fever and Lassa fever. 

Both standard precautions and contact precautions should be used in caring for patients with 

suspected or confirmed VHF. A surgical mask and eye protection should also be worn by those 

coming within 3 feet of a patient with suspected or confirmed Lassa fever, Crimean-Congo 

hemorrhagic fever, or filovirus infections. Airborne isolation, including use of a HEPA-filtered 

respirator, should be used if patients with these conditions have prominent cough, vomiting, 

diarrhea, or hemorrhage. Decontamination should be performed using hypochlorite or phenolic 

disinfectants. 

There are no vaccines to protect against these diseases, except for yellow fever and Argentinean 

hemorrhagic fever. For more information about specific VHF illnesses and their management, 

see http://www.cdc.gov/ncidod/dvrd/spb/mnpages/vhfmanual/anx2.pdf. 

Reporting. These viruses are highly pathogenic and require handling in special laboratory 

facilities designed to contain them (Biosafety Level 4 facilities). If VHF is suspected, contact 

your State and local health departments immediately. If local and State health departments are 

unavailable, contact the CDC at 770-488-7100. 

Category B and C Agents 

Ricin 

Ricin is a potent cytotoxin that can be easily extracted from the beans of the castor plant (Ricinus 

communis). Castor beans are processed worldwide in production of castor oil, and ricin-rich 

waste mash is a by-product. Ricin can be prepared in liquid, crystalline, or powder form; as an 

agent of terrorism, it could be disseminated as an aerosol, injected, or used to contaminate food 

or water. Symptoms depend on the route of exposure: respiratory, enteral, or parenteral. 

Compared with other biological toxins (e.g., botulinum toxin), ricin has low toxicity, and large 

quantities would be required to affect large numbers of people. 

Signs and symptoms. Ricin inhibits cellular protein synthesis. Aerosol exposure results in fever, 

chest tightness, cough, dyspnea, nausea, and arthralgias after a delay of 4–8 hours. Death after 

aerosol exposure has not been reported in people, but animals develop necrosis and severe 

alveolar fluid collection. Ingestion of ricin causes necrosis of the GI epithelium with local 

necrosis of muscle and regional lymph nodes. Intravascular injection causes minimal pulmonary 

perivascular edema. 

Diagnosis. Ricin exposure should be suspected if a geographic cluster of individuals develop 

acute lung injury. Pulmonary edema develops 1–3 days after exposure (compared with about 12 

hours after Staphylococcus enterotoxin B exposure and about 6 hours after phosgene exposure). 

77
Ricin provokes a specific antibody response, and acute and convalescent sera should be obtained 

for antibody titer. Tissue can also be stained using immunohistochemical methods. 

Treatment. Treatment involves supportive care, including appropriate respiratory support and 

treatment for pulmonary edema if required. Enteral exposure should be treated by vigorous 

gastric lavage and use of cathartics. 

Control measures. Protective masks are effective in preventing exposure. No vaccine is 

available. 

Reporting. If ricin exposure is suspected, contact your State and local health departments. If 

they are unavailable, contact the CDC at 770-488-7100. 

Q Fever 

Q fever is caused by Coxiella burnetti, a rickettsial organism that causes usually asymptomatic 

infection in farm animals (cattle, sheep, goats). It can also infect dogs, cats, rodents, and some 

birds. Natural infection in people is rare. When it does occur, it usually is transmitted by 

aerosolized organisms from the tissues, fluids, or excreta of infected animals. Exposure through 

terrorism would likely involve aerosolization, and resulting disease would likely be similar to 

naturally occurring disease. 

Signs and symptoms. The incubation period is 9–39 days after exposure. Initial symptoms 

include sudden onset of fever, chills, headache, weakness, lethargy, anorexia, and profuse 

sweating. Approximately 50% of infected individuals have pneumonia. Liver function tests are 

often abnormal—a result of granulomatous hepatitis—but jaundice is rare. Neuropathies 

sometimes develop. Transmission to the fetus is common when pregnant women are infected. 

The infection becomes chronic in approximately 1% of infected individuals and can manifest as 

endocarditis or hepatitis. 

Diagnosis. Clinically, Q fever is not easily distinguished from other causes of flu-like symptoms 

and pneumonia. Coxiella can be isolated from blood cultures; however, if Q fever is suspected, 

blood cultures are not recommended because of the risk of exposure of laboratory personnel. 

PCR assays can identify the organism in tissue or environmental samples. Acute and 

convalescent sera should be submitted for antibody titers; antibody concentration may rise only 

after 2–3 weeks of illness. 

Treatment and prophylaxis. Most infections resolve without specific therapy. Treatment with 

doxycycline may hasten recovery in acute infection. Chronic infection may require prolonged or 

repeated treatment. Chloramphenicol and ciprofloxacin are alternate choices for children <8 

years of age and for pregnant women, respectively. The same antibiotics may be used for 

prophylaxis after known or suspected exposure. Prophylaxis should be delayed for 8–12 days 

after exposure and should be given for 5–7 days. Earlier prophylactic treatment may delay but 

not prevent disease. 

78
Control measures. Person-to-person transmission is not known to occur, although transmission 

from contaminated clothing has been reported. Soap and water or a 0.5% chlorine solution can 

be used for decontamination. 

Reporting. If Q fever is suspected, contact your local and State health departments. If they are 

unavailable, contact the CDC at 770-488-7100. 

Staphylococcal Enterotoxin B 

Staphylococcus enterotoxin B (SEB) is an exotoxin that acts on the intestine to produce a brisk 

cascade of pro-inflammatory cytokines, resulting in an intense inflammatory response. Food 

poisoning due to SEB results from ingestion of improperly handled food that contains 

enterotoxin. 

Signs and symptoms. Natural disease is generally localized to the GI tract. After a brief 

incubation period (30 minutes to 8 hours, usually 2–4 hours), the exposed individual experiences 

abrupt and sometimes violent onset of severe nausea, abdominal cramps, vomiting, and 

prostration, often accompanied by diarrhea. There may be an associated low-grade fever or 

subnormal temperature. Symptoms typically last 1–2 days. Inhalational exposure, as might be 

expected in an incident of bioterrorism, results in predominantly respiratory symptoms, including 

nonproductive cough, retrosternal chest pain, and dyspnea. GI symptoms may be seen as well if 

toxin is inadvertently swallowed. Fever (103°–106°F) is likely and may last up to 5 days with 

chills and prostration. There may be conjunctival injection, and fluid losses may lead to postural 

hypotension. Chest radiographs are likely to be normal, but overt pulmonary edema can occur. 

Diagnosis. Clinically, symptoms of staphylococcal enterotoxin ingestion can be distinguished 

from other causes of food poisoning except those due to Bacillus cereus. Illness due to 

Clostridium perfringens has a shorter incubation period and rarely is accompanied by vomiting. 

Foodborne Salmonella or Shigella infection usually is accompanied by fever. 

Symptoms of inhalation of SEB are similar to those caused by many other respiratory pathogens. 

However, the clinical condition of respiratory disease due to inhaled SEB would be expected to 

stabilize without specific therapy, unlike that caused by tularemia, anthrax, or pneumonic plague. 

The absence of infiltrates on chest radiographs should also help distinguish respiratory tract 

disease caused by SEB from that caused by other likely agents of bioterrorism. 

SEB antigen can be detected in urine, serum, or respiratory secretions. In addition, acute and 

convalescent serum samples should be submitted for antibody titer. 

Treatment. Supportive care should include close attention to hydration and oxygenation. 

Control measures. SEB is not absorbed through intact skin, and secondary aerosolization from 

affected patients is not hazardous. Environmental surfaces may be decontaminated using soap 

and water. Contaminated foodstuffs should be destroyed. 

Reporting. If disease due to SEB is suspected, contact your local and State health departments. 

If they are unavailable, contact the CDC at 770-488-7100. 

79
Brucella 

Brucella species that infect people include B. abortus, B. melitensis, B. suis, and rarely, B. canis. 

Brucella species are small, gram-negative coccobacilli. People contract disease naturally through 

direct contact with infected animals and their carcasses or secretions or by ingestion of 

unpasteurized milk or milk products. Brucella species, particularly B. melitensis and B. suis, are 

potential terrorist agents. Aerosolization also can result in human infection. 

Signs and symptoms. Most infected individuals become ill within 3–4 weeks of exposure, but 

the incubation period may vary from <1 week to several months. Clinical features after natural 

exposure are extremely variable and nonspecific. They include flu-like symptoms—i.e., fever, 

sweats, malaise, anorexia, headache, myalgia, and back pain. Disease in children is commonly 

mild and self-limited, but in adults the illness is more chronic. Physical findings may include 

lymphadenopathy, hepatosplenomegaly, and occasionally, arthritis. Serious complications 

include meningitis, endocarditis, and osteomyelitis. 

Diagnosis. Brucella can be recovered in culture from blood, bone marrow, or other tissues. 

Specimens should be incubated for a minimum of 4 weeks. Serum samples collected at least 2 

weeks apart can confirm the diagnosis with a four-fold rise in antibody titers. A polymerase 

chain reaction (PCR) test has been developed but is available only in reference laboratories. 

Treatment and prophylaxis. Oral doxycycline (2-4 mg/kg/day, max 200 mg/day, divided BID) 

should be administered for 4–6 weeks. For children younger than 8 years, trimethoprimsulfamethoxazole may be used (trimethoprim, 10 mg/kg/day, max 480 mg/day; sulfamethoxazole 

50 mg/kg/day, maximum 2.4 g/day) divided BID for 4–6 weeks. Rifampin (15–20 mg/kg/day, 

max 600–900 mg/day), divided BID, should be added to prevent relapse. For patients who have 

endocarditis, osteomyelitis, or meningitis, therapy is often extended for several months with 

streptomycin sulfate or gentamicin sulfate added to the above regimens. 

Prophylaxis after suspected exposure should be provided using doxycycline and rifampin. 

Control measures. Standard precautions provide adequate protection from spread of infection, 

except that contact precautions should be added for patients with draining wounds. 

Reporting. Reporting suspected Brucella infection, regardless of mechanism of exposure, is 

mandated throughout the United States. You should contact your local and State health 

departments. If they are unavailable, contact the CDC at 770-488-7100. 

Burkholderia mallei (Glanders) 

Glanders is caused by the gram-negative bacillus Burkholderia mallei. Most cases occur in 

horses, mules, or donkeys, but people may become infected through handling infected animals. 

There have been no naturally acquired cases of glanders in people in the United States in more 

than half a century; most human cases occur in Asia, the Middle East, or South America. It is 

believed that this organism was used during WWI and WWII as a weapon of terrorism to infect 

horses, mules, and people. Human cases diagnosed in the absence of animal cases should raise 

suspicion of terrorism. 

80
Signs and symptoms. The incubation period after exposure ranges from 1 to 14 days. Acute and 

chronic presentation is possible, but acute illness is most likely after a bioterrorist event. Disease 

may be localized (e.g., pneumonia) or disseminated (fulminant sepsis). Most commonly, 

symptoms include high fever, mucositis, and abscesses in multiple organs, predominantly the 

lungs, liver, and spleen. 

Symptoms and signs associated with acute septicemia include fever, rigors, headache, muscle 

pain, night sweats, pleuritic chest pain, jaundice, sensitivity to light, and diarrhea. Diffuse 

erythroderma may be accompanied by necrotizing lesions. Cervical adenopathy, tachycardia, and 

mild hepatomegaly or splenomegaly may be present. 

Acute localized disease may involve the lungs (after inhalation of particles or through 

hematogenous spread). In addition to the signs and symptoms associated with acute septicemia 

(above), miliary lesions and/or bilateral upper lobe infiltrates with or without consolidation or 

cavitation may be noted on chest radiograph. Mucous membrane involvement begins with nasal 

ulcers and nodules that secrete bloody discharge and often lead to sepsis. A papular and/or 

pustular rash, similar in appearance to the smallpox rash, may develop. Liver and spleen 

abscesses may be present. Septic shock usually follows. 

Diagnosis. Small bacilli may be seen on methylene blue or Wright stain of exudates. Both B. 

mallei and B. pseudomallei can be grown and identified from standard cultures. 

Treatment and prophylaxis. Without effective antibiotic therapy, mortality nears 100%. 

Localized disease may be treated successfully with oral therapy for 60-150 days, while systemic 

illness requires parenteral therapy. Definitive antibiotic therapy should be based on susceptibility 

testing. Presumptive therapy can be provided using amoxicillin/clavulanate (60 mg/kg/day, PO, 

divided TID), tetracycline (40 mg/kg/day, PO, divided TID), or trimethoprim-sulfamethoxazole 

(trimethoprim 4 mg/kg/day; sulfamethoxazole 20 mg/kg/day, PO, divided BID) for localized 

disease. 

The effectiveness of prophylactic, postexposure therapy is not known. Trimethoprimsulfamethoxazole may be tried. 

Control measures. Person-to-person transmission is unlikely after inhalational exposure as 

would be expected in disease due to terrorism. Transmission from direct contact between 

nonintact skin or mucous membranes and infected animal tissue is the usual means of natural 

infection. Standard precautions are adequate for most patients, while contact precautions should 

be added for patients with skin lesions. Environmental decontamination using 0.5% hypochlorite 

solution (bleach) is effective. 

Reporting. If glanders is suspected, contact your local and State health departments. If they are 

unavailable, contact the CDC at 770-488-7100. 

81
Encephalitis Viruses and Yellow Fever Virus 

Arboviruses (arthropod-borne viruses) are spread by mosquitoes, ticks, or sand flies and produce 

four principal clinical syndromes: 

• CNS infection (including encephalitis, aseptic meningitis, or myelitis). 

• Undifferentiated febrile illness, often with rash. 

• Acute polyarthropathy. 

• Acute hemorrhagic fever, usually accompanied by hepatitis. 

Infection with some arboviruses results in perinatal illness. Alpha viruses, including Eastern 

equine encephalitis (EEE) virus, Western equine encephalitis (WEE) virus, and Venezuelan 

equine encephalitis (VEE) virus, and yellow fever virus, a member of the Flavivirus genus, have 

been included in the CDC’s list of potential agents of bioterrorism. In nature, disease due to these 

viral agents is limited to the geographic areas in which their arthropod vectors live. 

Signs and symptoms. For many encephalitis viruses, asymptomatic infection is common. 

Clinical illness, when it occurs, ranges in severity from a self-limiting febrile illness with 

headache and vomiting to a syndrome of aseptic meningitis or acute encephalitis. EEE virus 

infection is typically a fulminant illness that leads to coma and death in one-third of cases and to 

serious neurologic sequelae in another third. The clinical severity of WEE virus infection is 

intermediate, with a case fatality rate of 5%; neurologic impairment is common in infants. VEE 

virus infection produces acute systemic febrile illness, with encephalitis developing in a small 

percentage (4% in children; <1% in adults). The incubation period for EEE and WEE 

encephalitis viruses is 2–10 days, while that for VEE virus infection is 1–4 days. 

Yellow fever virus infection evolves through three periods from a nonspecific febrile illness 

(with headache, malaise, weakness, nausea, and vomiting) through a brief period of remission, to 

a hemorrhagic fever with GI tract bleeding and hematemesis, jaundice, hemorrhage, 

cardiovascular instability, albuminuria, oliguria, and myocarditis. The incubation period is 3–6 

days, and 50% of cases are fatal. 

Diagnosis. Diagnosis is made by serologic testing of cerebrospinal fluid (CSF) or serum or by 

viral isolation. Detection of virus-specific IgM antibody in CSF is confirmatory, and its presence 

in a serum sample is presumptive evidence of recent infection in a patient with acute CNS 

infection. Greater than four-fold change in serum antibody titer in paired serum samples obtained 

2–4 weeks apart is confirmatory. A single increased antibody titer defines a case as presumptive. 

During the acute phase of yellow fever and VEE virus infection, virus can be isolated from blood 

and, in Venezuelan encephalitis, from the throat. 

Treatment. Active clinical monitoring and supportive therapy may be life saving. 

Control measures. Respiratory precautions are recommended when caring for patients with 

VEE virus infection. Patients with yellow fever may have active virus circulating in the blood, so 

they should be kept away from potential vector mosquitoes that could feed on them and 

subsequently transmit infection to others. Standard precautions are recommended for patients 

with EEE and WEE virus infection. A live-attenuated yellow fever vaccine is available and is 

82
currently used for individuals traveling to countries where yellow fever is endemic (some parts 

of South America and Africa). The vaccine is currently available in the United States only at 

approved vaccination centers. 

Reporting. If viral encephalitis or yellow fever is suspected, contact your local and State health 

departments. If they are unavailable, contact the CDC at 770-488-7100. 

Clostridium perfringens 

Food poisoning may be caused by a heat-labile toxin produced in vivo by C. perfringens type A; 

type C causes enteritis necroticans. Spores of C. perfringens may survive cooking. Spores 

germinate and multiply during slow cooling and storage at temperatures of 20°–60°C (68°–

140°F). Once ingested, an enterotoxin produced by the organisms in the lower intestine is 

responsible for symptoms. Beef, poultry, gravies, and dried or precooked foods are common 

sources. Infection usually is acquired when food is prepared in large quantities and kept warm 

for prolonged periods (e.g., at banquets or institutions or from food provided by caterers or 

restaurants). 

Signs and symptoms. Onset of watery diarrhea and moderate to severe, crampy, midepigastric 

pain is sudden. Vomiting and fever are uncommon. Symptoms usually resolve in 24 hours. The 

incubation period is usually 8–12 hours. 

Diagnosis. The short incubation, short duration, and absence of fever in most patients 

differentiates C. perfringens foodborne disease from shigellosis and salmonellosis. The 

infrequency of vomiting and longer incubation period contrast with the clinical features of 

foodborne disease associated with heavy metals, Staphylococcus aureus enterotoxins, and fish 

and shellfish toxins. Diarrheal disease caused by Bacillus cereus enterotoxin may be 

indistinguishable from that caused by C. perfringens. Enteritis necroticans is a cause of severe 

illness and death attributable to C. perfringens food poisoning among children in Papua, New 

Guinea (where it is also known as pigbel). 

Because the fecal flora of healthy people commonly includes C. perfringens, counts of 106

/gram 

of feces obtained within 48 hours of onset of illness are required to support the diagnosis. The 

diagnosis can be suggested by detection of C. perfringens enterotoxin in feces by commercially 

available kits. To confirm C. perfringens as the cause, the concentration of organisms should be 

at least 105

/gram in the epidemiologically implicated source of infection (food). Although C. 

perfringens is an anaerobe, special transport conditions are unnecessary because the spores are 

durable. Fecal samples, rather than rectal swab specimens, should be obtained. 

Treatment. Oral rehydration or, occasionally, IV fluid and electrolyte replacement may be 

indicated to prevent or treat dehydration. Antimicrobial agents are not indicated. 

Control measures. Clostridium perfringens food poisoning is not transmissible from person to 

person. 

Reporting. If C. perfringens food poisoning is suspected, contact your local and State health 

departments. If they are unavailable, contact the CDC at 770-488-7100. 

83
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87
Figure 4.1. Chest radiograph taken 22 hours before death 

Note: Film shows widened mediastinum due to inhalation anthrax. 

Source: Centers for Disease Control and Prevention. Available at http://www.bt.cdc.gov/agent/anthrax/. 

88
Figure 4.2. Neurological signs, botulism, 6-week-old infant 

Source: Centers for Disease Control and Prevention. Available at http://www.bt.cdc.gov/bioterrorism/. 

89
Figure 4.3. Cutaneous anthrax lesion with eschar on neck 

Source: Centers for Disease Control and Prevention. Available at http://www.bt.cdc.gov/bioterrorism/. 

 

90
Figure 4.4. Physical distribution of smallpox lesions versus varicella lesions 

Note: The smallpox lesions are concentrated on the face and extremities, including the palms and soles. In contrast, 

the varicella lesions are concentrated on the face and trunk 

Source: Centers for Disease Control and Prevention. Available at http://www.bt.cdc.gov/agent/smallpox/. 

91
Figure 4.5. Smallpox lesions 

Note: The lesions are in the same stage of development, deep-seated, and umbilicated, and they appear to be firm. 

Source. World Health Organization. Available at: 

http://www.who.int/emc/diseases/smallpox/Africanseries/pages/WHO-Spx-Dx-Africa48-MedRes.htm. 

 

92
Figure 4.6. Varicella lesions 

Note: The lesions are in varied stages of development, more superficial than those of smallpox, and irregular in 

shape. 

Source: Centers for Disease Control and Prevention. Available at http://www.bt.cdc.gov/agent/smallpox/. 

93
Figure 4.7. Expected smallpox vaccination site reaction (i.e., a “take”) in a first-time 

vaccinate 

 

Note: Figure demonstrates the progression from papule (day 4) to pustule (days 7-14) to scab (day 21). 

Source: Centers for Disease Control and Prevention. Available at http://www.bt.cdc.gov/agent/smallpox/. 

94
Figure 4.8a. Febrile rash illness algorithm for evaluating patients suspected of having 

smallpox 

Varicella Testing

Optional

History and Exam

Highly Suggestive

 of Varicella

Test for VZV

and Other Conditions

as Indicated

Diagnosis

Uncertain

Low Risk for Smallpox

(see criteria below)

Non-Smallpox

Diagnosis Confirmed

Report Results to Infx Control

Cannot R/O Smallpox

Contact Local/State Health Dept

No Diagnosis Made

Ensure Adequacy of Specimen

ID or Derm Consultant

Re-Evaluates Patient

ID and/or Derm Consultation

VZV +/- Other Lab Testing

as indicated

Moderate Risk of Smallpox

(see criteria below)

NOT Smallpox

Further Testing

SMALLPOX

Testing at CDC

Smallpox Response Team

Collects Specimens and

Advises on Management

ID and/or Derm Consultation

Alert Infx Control &

Local and State Health Depts

High Risk for Smallpox

(see criteria below)

Institute Airborne & Contact Precautions

Alert Infection Control on Admission

Patient with

Acute, Generalized

Vesicular or Pustular Rash Illness

95
Figure 4.8b. Classification of risk – Febrile rash illness algorithm 

• High risk (All three major criteria)

– Febrile prodrome (1–4 days pre-rash, >101° F), and

– Classic smallpox lesions, and

– Same stage of development 

• Moderate risk 

– Febrile prodrome, and

– 1 other major or ≥4 minor criteria 

• Low Risk 

– No fever or

– Febrile prodrome and <4 minor criteria 

Minor Criteria 

• Greatest concentration of lesions on face and distal extremities 

• Lesions first appeared on oral mucosa/palate, face, forearms 

• Patient appears toxic or moribund 

• Lesions evolve slowly from macules to papules to pustules over days 

• Lesions on palms and soles 

Source: CDC. Emergency Preparedness and Response. Poster: Evaluating patients for smallpox. 

Note: Full protocol available at http://www.bt.cdc.gov/agent/smallpox/diagnosis/evalposter.asp. 

96
Table 4.1. Early clinical signs and symptoms after exposure to selected bioterrorist 

agents 

Clinical signs and symptoms* Agent or disease 

Respiratory 

Influenza-like illness ± atypical pneumonia Tularemia 

Brucellosis 

Q fever 

Venezuelan equine encephalomyelitis 

Eastern equine encephalomyelitis 

Western equine encephalomyelitis 

Influenza-like illness with cough and 

respiratory distress 

Inhalational anthrax 

Pneumonic plague 

Inhalational tularemia 

Ricin 

Aerosol exposure to Staphylococcal 

enterotoxin B 

Hantavirus 

Exudative pharyngitis and cervical 

lymphadenopathy 

Oropharyngeal tularemia 

Neurologic 

Flaccid paralysis Botulism 

Encephalitis Venezuelan equine encephalomyelitis 

Eastern equine encephalomyelitis 

Western equine encephalomyelitis 

Meningitis Inhalational anthrax 

Septicemic and pneumonic plague 

Venezuelan equine encephalomyelitis 

Eastern equine encephalomyelitis 

Western equine encephalomyelitis 

Gastrointestinal 

Diarrhea Salmonella species 

Shigella dysenteriae 

Escherichia coli O157:H7 

Vibrio cholerae 

Cryptosporidium parvum 

Vomiting, abdominal pain, bloody diarrhea, 

hematemesis 

GI anthrax 

Dermatologic 

Vesicular rash† associated with fever, 

headache, malaise 

Smallpox 

Painless ulceration progressing to black eschar Cutaneous anthrax 

Ulcer plus painful regional lymphadenopathy 

and influenza-like illness 

Ulceroglandular tularemia 

Petechiae† with fever, myalgia, prostration Viral hemorrhagic fever 

97
Table 4.1. Early clinical signs and symptoms after exposure to selected 

bioterrorist agents, continued 

Cardiovascular 

Shock after respiratory distress Inhalational anthrax 

Ricin 

Viral hemorrhagic fever 

Hematologic 

Thrombocytopenia Brucellosis 

Viral hemorrhagic fever 

Hantavirus 

Neutropenia Viral hemorrhagic fever 

Venezuelan equine encephalomyelitis 

Eastern equine encephalomyelitis 

Western equine encephalomyelitis 

Hemorrhage Viral hemorrhagic fever 

Disseminated vascular coagulation Viral hemorrhagic fever 

Renal 

Hemolytic-uremic syndrome, thrombotic 

thrombocytopenic purpura 

Escherichia coli O157:H7 and other 

shiga toxin-producing E. coli

Shigella dysenteriae

Oliguria, renal failure Viral hemorrhagic fever 

Hantavirus 

Other 

Painful lymphadenopathy Bubonic plague 

Purulent conjunctivitis with preauricular or 

cervical lymphadenopathy 

Oculoglandular tularemia 

* Based on route of exposure; likely to make someone seek medical attention; other manifestations 

 (e.g., fever, headache, vomiting, diarrhea) possible and common early on in many illnesses. 

†

 Rashes of diseases that cause petechiae or vesicular skin lesions may start as macular or papular lesions. 

98
99

Table 4.2. Infection control transmission precautions for Category A agents 

Agent Transmission Infection control Special features 

Anthrax Contact (cutaneous form) Standard 

Plague Contact (bubonic form) 

Droplet (pneumonic form) 

Standard, droplet Masks 

Tularemia No Standard 

Botulism No Standard 

Smallpox Droplet and aerosol Standard, airborne 

infection isolation 

Fitted N-95 

Negative-pressure 

room 

Viral 

hemorrhagic 

fevers 

Contact and droplet Standard, contact, 

droplet 

Masks 
Table 4.3. Diagnostic procedures, isolation precautions, treatment, and postexposure prophylaxis for 

agents in children 

Agent Incubation 

period 

Diagnostic 

specimens and 

procedures 

Isolation 

precautions 

Treatment Postexposure 

prophylaxis1

Alphaviruses (VEE, EEE, and WEE) 

2–10 days CSF for viral 

isolation, antibody detection in CSF and acute and convalescent serum 

Standard; respiratory precautions for WEE virus 

Supportive Protection from 

mosquito vectors 

Anthrax 1–60 days Gram stain of buffy 

coat, CSF, pleural fluid, swab of skin lesion; culture of blood, CSF, pleural fluid, skin biopsy 

Standard; contact for skin lesions 

Ciprofloxacin2 or 

doxycycline3; 

combine with one or two additional antimicrobial agents for inhalational, GI, or oropharyngeal disease4

Ciprofloxacin2, 

doxycycline3, or 

amoxicillin5; 

anthrax vaccine 

Aainoinvacima

Botulism Foodborne: 

2 hr–8 days Inhalational: 24–72 hr 

Toxin detection from serum, feces, enema fluid, gastric fluid, vomitus, or suspected food samples; culture of feces or gastric sections; nerve conduction testing 

Standard Supportive care; 

mechanical ventilation and parenteral nutrition may be required; equine botulism antitoxin given as soon as possible (CDC)6

Tswpdr

Brucellosis 5–60 days Culture of blood or 

bone marrow; acute and convalescent serum for antibody testing 

Standard; contact for draining skin lesions 

Doxycycline3 and 

rifampin; if younger than 8 yr old, use TMP-SMX 

Doxycycline3 and 

rifampin 

Tsw

100 

100
Table 4.3. Diagnostic procedures, isolation precautions, treatment, and postexposure prophylaxis for s

agents in children, continued Plague 2–4 days Culture or 

fluorescent antibody staining of blood, sputum, lymph node aspirate 

Droplet Streptomycin 

sulfate or gentamicin sulfate; doxycycline3 or 

tetracycline3

Doxycycline3; 

tetracycline3

Tacm

Q fever 10–40 days Acute and 

convalescent serum samples 

Standard Doxycycline3 or 

tetracycline3

Doxycycline3 or 

tetracycline3

Cao

Smallpox 7–19 days Culture of 

pharyngeal swab of skin lesions 

Airborne, contact 

Supportive care Vaccine if 

administered within 4 days 

Staphylococcal enterotoxin B 

3–12 hr Serum, urine, and 

respiratory secretions for toxin; acute and convalescent serum for antibodies 

Standard Supportive care None available 

Ricin 4–8 hr Serum and/or 

respiratory secretions for enzyme immunoassay 

Standard Supportive care; 

gastric lavage and cathartics if toxin is ingested 

Protective mask 

Viral hemorrhagic fevers 

6–17 days Culture and/or 

antigen detection of blood and other body tissues7; 

serum for acute and convalescent antibody detection 

Standard, droplet, and contact precautions8

Ribavarin IV for Lassa fever; plasma from convalescent patients for Argentinean hemorrhagic fever; supportive care 

101
102

Table 4.3. Diagnostic procedures, isolation precautions, treatment, and postexposure prophylaxis f

bioterrorist agents in children, continued

1 Prophylaxis should be administered only after consultation with public health officials and only in situations in which exposure i

duration of prophylaxis has not been determined for most agents. 

2 If susceptibility is unknown or indicates resistance to other agents. Ciprofloxacin is not licensed by the FDA for use in people yo

indicated for potentially serious or life-threatening infections. 

3 Tetracyclines, including doxycycline, are not approved by the FDA for this indication and are usually contraindicated for childre

treatment is warranted for selected serious infections. 

4 Treatment should be administered parenterally initially but may be changed to oral therapy for cutaneous infection without disse5 Amoxicillin may be used as prophylaxis only if the organism is known to be susceptible. 6 Botulism antitoxin must be obtained from the CDC Drug Service, 404-639-3670 (weekdays, 8 am to 4:30 pm) or 404-639-2888 

holidays). 

7 Isolation should be attempted only under Biosafety Level-4 conditions. 8 Because of the risk of nosocomial transmission, the State health department and the CDC should be contacted for specific advice 

diagnosis of suspected cases. 
Table 4.4a. Diagnostic tests for anthrax 

Anthrax type Diagnostic tests 

Cutaneous Vesicular fluid and blood culture (anaerobic and aerobic) 

Inhalational Blood culture, CSF, chest radiograph, CT scan 

Gastrointestinal Blood culture 

Table 4.4b. Adjunctive diagnostic tests for anthrax 

Test Comments 

CBC WBC may be normal or slightly increased. 

Increased neutrophils or band forms common. 

Leukopenia or lymphocytosis does not support diagnosis of anthrax. 

Chest 

radiograph 

Frequently abnormal in inhalational anthrax; may show signs of mediastinal 

widening, paratracheal or hilar fullness, pleural effusions, pulmonary 

infiltrates (uni- or multilobar), and mediastinal lymphandenopathy; changes 

may be subtle and better defined on chest CT. 

Nasal swab May assist in epidemiologic investigations but should not be relied on as a 

guide for prophylaxis or treatment of individual patients. 

103
Table 4.5. Postexposure prophylaxis for anthrax 

Patient Prophylactic treatment 

Adults (including pregnant women and 

immunocompromised people) 

Ciprofloxacin 500 mg, PO, BID × 60 days or

Doxycycline 100 mg, PO, BID × 60 days 

Children Ciprofloxacin 10–5 mg/kg, PO, BID × 60 days 

(total daily dose not to exceed 1000 mg) or

Doxycycline at: 

>8 yr and >45 kg: 100 mg, PO, BID × 60 days 

>8 yr and <45 kg: 2.2 mg/kg, PO, BID × 60 days 

8 yr or younger: 2.2 mg/kg, PO, BID ×60 days 

104
Table 4.6. Treatment recommendations for tularemia in children before test results 

are known 

Drug Dosage

Preferred choices

Streptomycin 15 mg/kg, IM, BID × 10 days (should not exceed 2 gram/day) 

Gentamicin 2.5 mg/kg, IM or IV, TID × 10 days (not an FDA-approved use) 

Alternative choices

Doxycycline* If weight ≥45 kg, 100 mg, IV × 14–21 days 

If weight <45 kg, give 2.2 mg/kg, IV, BID × 14–21 days 

Chloramphenicol* 15 mg/kg, IV, 4 times daily × 14–21 days (not an FDA-approved use)

Ciprofloxacin* 15 mg/kg, IV, BID × 10 days (should not exceed 1 gram/day) 

* Treatment with doxycycline, chloramphenicol, or ciprofloxacin given IM or IV can be switched to oral 

administration when clinically indicated. 

105
106
 107

Chapter 5. Chemical Terrorism 

Introduction 

Chemical terrorism is the intentional use of toxic chemicals to inflict mass casualties and 

mayhem on an unsuspecting civilian population, including children. Such an incident 

could potentially overwhelm the capacity of regional emergency medical services and 

pose extraordinary medical management challenges to pediatricians. However, careful 

community planning, robust research and development (by academic, private, and 

governmental collaborative efforts), and rigorous medical education could mitigate such 

a catastrophe. 

The risk of chemical terrorism is more tangible since the events of September 11, 2001, 

and the subsequent intentional spread of anthrax through the U.S. mail. However, the 

specter of purposeful toxic exposures predates the September 11 attack. The 20th century 

witnessed Iraqi military attacks with nerve agents on civilian villages in Iran in the 1980s, 

the release of the nerve agent sarin in the Tokyo subway system in 1995, a chlorine bomb 

scare at Disneyland in 1995, and the finding of ricin in U.S. Senate office buildings in 

2004. 

Chemical terrorism often refers to the use of military chemical weapons that have been 

illicitly obtained or manufactured de novo. However, additional concerns might include 

the intentional explosion of an industrial chemical factory, a tanker car, or a transport 

truck in proximity to a civilian residential community, school, or worksite. These events 

underscore the need for all pediatricians to expand their working knowledge of the 

approach to mass casualty incidents involving traditional military chemical weapons and 

other toxic chemicals that might be used as “weapons of opportunity.” 

The medical consequences and epidemiology of a chemical terrorist attack mimic more 

conventional disasters but also reflect some distinct differences. Such an incident 

combines elements of both a traditional mass disaster (e.g., an earthquake) and a 

hazardous materials incident. Potential differences of a chemical terrorist attack 

compared with a “routine” hazardous materials incident include the following: 

• Intent to cause mass casualties. 

• Great toxicity of substances. 

• Delayed initial identification of substance. 

• Greater risk to first responders. 

• Overwhelming numbers of patients. 

• Many anxious individuals. 

• Mass hysteria, panic. 

• Discovery of dispersal device. 

Casualties occur almost immediately, and the attack would likely be recognized rapidly. 

First responders are EMS, police, fire, and paramedic personnel. Decontamination and 

initial care of small children on-scene pose enormous management issues for personnel 

wearing bulky personal protective gear. In addition, many children who have been 
 108

exposed but not critically injured will be taken by parents to hospitals and pediatricians’ 

offices without prior on-scene decontamination—thus posing similar challenges for and 

possibly personal risk to pediatric care providers themselves. 

Specific Pediatric Vulnerabilities to Chemical Agents 

Children have inherent physiologic, developmental, and psychological differences from 

adults that may enhance susceptibility and worsen prognosis after a chemical agent 

exposure (see also Chapter 1, Children Are Not Small Adults). Briefly, such physiologic 

differences include higher minute ventilation, increased skin permeability, relatively 

larger body surface area, less intravascular volume reserve in defense of hypovolemic 

shock, and shorter stature (which places children nearer to the greatest gas vapor density 

at ground level). Children who are pre-ambulatory or pre-verbal and those who have 

special needs are less able to evade danger or seek attention effectively. A chaotic 

atmosphere compounded by rescuers wearing unfamiliar garb may frighten children of all 

ages and potentially increase the posttraumatic response to stress. Those providing care 

for children are faced with additional complexities posed by developmental, age, and 

weight considerations beyond the general scope of the already enormous challenge. 

Pediatric vulnerabilities become particularly significant when weapons of mass 

destruction are involved. A chemical agent will most likely be dispersed via an aerosol 

route or in combination with traditional warfare. Chemical exposures warrant expedient 

and thorough decontamination to limit continued primary and secondary exposures. 

Children’s relatively large body surface area plays a key role in degree of contamination 

and in their ability to maintain thermal homeostasis after decontamination. Table 5.1 

summarizes pediatric-specific vulnerabilities to chemical agents. 

Chemical Injuries and Approach to the Unknown Chemical 

Attack 

A listing of many of the most notable chemical agents of concern has been compiled by 

the CDC (see http://www.bt.cdc.gov/agent/agentlistchem.asp). Toxic effects from 

chemical agents usually follow dermal or inhalational exposure and may develop via 

injury to the skin, eyes, and respiratory epithelium, as well as via systemic absorption. 

The intensity and route of exposure to chemical agents affect both the rapidity of onset 

(seconds to hours) and the severity of symptoms. For example, a mild exposure to sarin 

vapor results in lacrimation, rhinorrhea, miosis, and slightly blurry vision; an intense 

exposure leads to seizures, apnea, and rapid death within minutes. 

Clinical syndromes and management after exposure to various chemical agents (nerve 

agents, vesicants, pulmonary agents, cyanide, and riot-control agents) are summarized in 

Table 5.2 and detailed in the following sections. For in-depth discussions of general 

principles of supportive care for victims of chemical warfare agents, see Osterhoudt, et al, 

2005, and Erickson, 2004. 

Understanding the epidemiology of acute mass exposure to a toxin is helpful in 

recognizing a covert chemical attack with unknown agents. Mass exposure to a toxin will 
 109

likely manifest as an acute onset of illness (within seconds to minutes or within hours in 

the case of some of the vesicants and pulmonary agents). In more severe chemical 

incidents, numbers of people may collapse or die within minutes of exposure. 

Chemical weapons can be categorized based on the predominant symptoms they cause: 

• Neurologic (nerve agents or cyanide). 

• Respiratory (phosgene or chlorine, high-dose riot-control agents, or sulfur 

mustard with a delay of several hours from time of exposure). 

• Mucocutaneous syndromes (vesicants). 

For additional advice on more definitive diagnosis and management strategies, contact 

public health authorities or the regional poison control center (1-800-222-1222). 

The initial decision that will need to be made immediately will likely be the distinction of 

cyanide from nerve agent attack because the antidotal therapies are quite different. In 

both cases, large numbers of victims may suddenly collapse, have seizures, or go into a 

coma, and many deaths occur rapidly. Nerve agent casualties are likely to be cyanotic and 

have miotic pupils with altered vision, copious oral and nasal secretions, and acute 

bronchospasm and bronchorrhea. 

The initial protection of everyone in a community exposed to a hazardous chemical 

requires safe evacuation or local sheltering. Circumstances may vary considerably, but it 

is expected that local and Federal authorities will decide and quickly advise on 

evacuation or local sheltering and broadcast their advice quickly and widely in the public 

media. 

For the CDC guidelines for evacuation, see 

http://www.bt.cdc.gov/planning/evacuationfacts.asp. 

For the CDC guidelines for sheltering in place in a chemical emergency, see

http://www.bt.cdc.gov/planning/shelteringfacts.asp.

Initial Approach, Decontamination, and Triage 

The general treatment of contaminated victims begins with extrication, triage, 

resuscitation as needed, and decontamination performed by rescue workers or health care 

providers wearing appropriate personal protective equipment (PPE). Ideally, 

decontamination would be done at the scene to avoid the considerable challenges posed 

by the arrival of contaminated patients, including children, at health care facilities. 

However, in a large-scale terrorist incident, it is far more likely that some victims will 

arrive at hospitals or other health care facilities without having been previously 

decontaminated. In this context, significantly contaminated victims should be 

decontaminated before they are allowed into the emergency department (ED). Even if 

decontamination has been done in the field, hospitals are likely to repeat decontamination 

procedures to protect the facility from contamination (which would result in closure or 

having to go “off line”); this would also address the possibility of cross-contamination 

moving from the scene. Decontamination to limit secondary exposures is especially 

important in exposures to nerve agents and vesicants. 
 110

Appropriate PPE for ED staff involved in patient decontamination is an important 

consideration. The amount of chemical agent believed to contaminate patients who arrive 

at the ED after a chemical terrorist attack would essentially consist of that on their skin 

and clothing (i.e., far lower concentration of chemicals than rescue workers would face at 

the scene of exposure). Most authorities believe that ED staff wearing level C PPE would 

be adequately protected. Level C PPE consists of a non-encapsulated, chemically 

resistant body suit, gloves, boots, and a PAPR mask containing a cartridge with both an 

organic-vapor filter for chemical gases and vapors and a HEPA filter to trap aerosols of 

biological and chemical agents. Such PPE is much less cumbersome to work in than level 

A or B outfits (which use self-contained breathing apparatus) and is also less expensive. 

Cardiopulmonary and airway support, including endotracheal intubation, and emergent 

intramuscular antidotal therapy are provided as necessary and appropriate for the specific 

exposure. Contaminated clothing should be removed as soon as possible. The 

contamination hazard is reduced by as much as 80-90% simply by removing clothing. 

This is accompanied or immediately followed by more definitive decontamination. For 

vapor-exposed victims, decontamination may be accomplished primarily by clothing 

removal and washing of hair. In contrast, for victims with liquid dermal exposure, more 

thorough decontamination is required. Their skin and clothing pose considerable risk to 

ED personnel. Clothing should be carefully removed and disposed of in double bags. 

Victims with ocular exposure require eye irrigation with copious amounts of saline or 

water. Skin and hair should be washed thoroughly, but gently, with soap and tepid water. 

In the past, some authorities had recommended 0.5% sodium hypochlorite (dilute bleach) 

for skin decontamination of nerve agents and vesicants. However, this may be a skin 

irritant, thus increasing permeability to the agent. In addition, its use is time-consuming 

and has not been proven superior to washing with copious soap and water or water alone. 

Furthermore, there is little experience with this approach in infants and young children. A 

difficult question that remains is whether EMS and ED staff wearing bulky PPE will be 

able to provide significant advanced life support to small children before 

decontamination. 

Ambulatory, asymptomatic victims may be able to be discharged from the scene, while 

those with minimal symptoms may be directed toward local shelters (e.g., American Red 

Cross stations, local schools, or other sites designated by local or State health 

departments) after decontamination for medical observation. These shelters may also 

serve as sites for reuniting children with their families, keeping track of all victims, and 

communicating with law enforcement agencies. 

Industrial Chemicals 

The potential of a terrorist attack on industrial sources of hazardous chemicals (e.g., 

factories, railroad and vehicular tank cars, or storage depots) expands the list of potential 

“chemical weapons” considerably. In general, many of the relevant industrial chemicals 

might be expected to induce respiratory effects analogous to those of chlorine or 

phosgene (see the section on pulmonary agents later in this chapter) or dermatologic 

injury from irritant or caustic properties, as well as more systemic effects in severe 
 111

exposures (Table 5.3). For an in-depth discussion of principles in managing such toxic 

injuries, see Osterhoudt, et al., 2005, and Erickson, 2004. 

Community Preparedness 

In the aftermath of September 11, 2001, many agencies are collaborating to ensure 

coordinated care of pediatric victims (see Chapter 2, Systems Issues). All pediatricians 

are encouraged to participate in disaster management training. The need to stock 

appropriate antidotes, practice decontamination strategies, and learn the use of PPE is 

apparent. Although perhaps not every practicing pediatrician needs to be competent in all 

aspects of disaster response, all in the community should work together to optimize the 

overall capacity for providing disaster care to chemically exposed children. 

Successful planning and response to events involving chemical terrorism require strong 

collaboration and integrated functioning of many agencies and facilities, both 

governmental and nongovernmental, including local treatment facilities, local and State 

health departments, and Federal agencies (CDC, FEMA, FBI, etc.). 

Nerve Agents 

Nerve agents are organophosphorous compounds similar to the organophosphate 

insecticides used in agriculture or industry but far more toxic. Four compounds are 

currently regarded as nerve agents: tabun, sarin, soman, and VX (“Venom X”). All of 

these agents are hazardous by ingestion, inhalation, or cutaneous absorption, the latter 

being particularly true for VX. The toxic effects of nerve agent vapors depend on the 

concentration of the agent inhaled and on the time exposed to the agent. The toxicity of 

nerve agent liquid depends on the time exposed and the bodily site of exposure. Nerve 

agents exist as liquids at standard temperatures and pressures. In gaseous form, they are 

denser than air and vary in volatility, with some (e.g., VX) being more persistent than 

others (e.g., sarin). 

Background 

The Iran-Iraq War of the 1980s reportedly resulted in more than 100,000 casualties from 

chemical weapons. Iranian sources reported that the number of casualties caused by nerve 

agents was far greater than the number of casualties caused by mustard agent. Many 

nerve agent casualties that were only mildly to moderately affected were not counted. 

A chemical warfare campaign by the Iraqi military on Kurdish civilians in the late 1980s 

caused thousands of deaths. The exact agents are not definitively known, but Iraq is 

known to have stockpiled tabun, sarin, and VX. 

A Japanese religious cult that manufactured sarin deployed it in 1994 in attacks on a 

residential neighborhood of Matsumoto and again in 1995, in the Tokyo subway. 

Immediate mortality was low, but thousands of individuals arrived at emergency rooms. 

The lack of a decontamination process resulted in significant morbidity to health care 

personnel. The sarin was released by a relatively primitive method (punctured plastic 
 112

bags allowing sarin vapor to escape); many experts believe a more sophisticated delivery 

system might have resulted in far higher mortality. 

Nerve agent exposures in the United States have been individual cases associated with 

industrial exposures. 

Toxicology and Clinical Manifestations 

Nerve agents inhibit the action of acetylcholinesterase at cholinergic neural synapses, 

where acetylcholine then accumulates markedly. The resulting cholinergic syndrome is 

classically divided into central, nicotinic (neuromuscular junction and sympathetic 

ganglia), and muscarinic (smooth muscle and exocrine gland) effects. 

Clinical manifestations vary with the type of exposure. Symptoms after a vapor exposure 

appear suddenly with a full range of clinical effects, or there may be a partial expression 

of the syndrome. Symptoms after a liquid exposure may start with local sweating and 

then progress. 

Central nervous system effects. Effects on the CNS include headache, seizures, coma, 

respiratory arrest, confusion, slurred speech, and respiratory depression. Although the 

seizures probably begin due to excess cholinergic stimulation, other effects (e.g., 

excitatory glutamate receptor stimulation and antagonism of inhibitory gammaaminobutyric acid [GABA] receptors) may also play a role. Little experience with nerve 

agents is available to distinguish clinical effects in children from those in adults, although 

two cases of antichlolinesterase pesticide poisonings in children suggest a 

disproportionate degree of depressed sensorium and muscle weakness. Thus, children 

may manifest primarily central and/or neuromuscular effects after nerve agent exposure.

Autonomic nervous system effects. These include both nicotinic and muscarinic 

findings. Nicotinic effects on sympathetic activity can result in the following: 

• Tachycardia. 

• Hypertension. 

• Metabolic aberrations (e.g., hyperglycemia, hypokalemia, and metabolic 

acidosis). 

Muscarinic effects involve multiple systems: 

• Ocular (miosis, eye pain, visual blurring, lacrimation). 

• Respiratory (watery rhinorrhea, increased bronchial secretions and bronchospasm 

causing cough, wheezing, dyspnea, and cyanosis). 

• Cardiovascular (bradycardia, hypotension, atrioventricular block). 

• Dermal (flushing, sweating). 

• Gastrointestinal (salivation, nausea, vomiting, diarrhea progressing to fecal 

incontinence, abdominal cramps). 

• Urinary (frequency, urgency, incontinence). 
 113

Neuromuscular effects. At the neuromuscular junction, initial stimulation of cholinergic 

synaptic transmission is followed by paralysis. Thus, nicotinic effects include muscle 

fasciculations and twitching, followed by weakness progressing to flaccid paralysis and 

respiratory failure. 

The clinical syndrome of organophosphate toxicity is summarized by various 

mnemonics, including “bag the puddles,”1

 “sludge” syndrome, and “dumbbels.” 

B = bronchoconstriction, bronchorrhea 

A = apnea 

G = graying/dimming of vision 

P = pupillary constriction (miosis) 

U = urination 

D = diarrhea 

D = diaphoresis 

L = lacrimation 

E = emesis 

S = salivation, seizures 

S = salivation, seizures 

L = lacrimation 

U = urination 

D = diarrhea 

G = graying/dimming of vision 

E = emesis 

D = diarrhea 

U = urination 

M = miosis 

B = bronchoconstriction 

B = bronchorrhea 

E = emesis 

L = lacrimation 

S = salivation 

Diagnostic Tests 

The diagnosis of nerve agent toxicity is primarily based on clinical recognition and 

response to antidotal therapy. Measurements of acetylcholinesterase in plasma or red 

blood cells (RBCs) may confirm organophosphate poisoning, but correlation between 

cholinesterase levels and clinical toxicity is poor in some contexts; also, these analyses 

are rarely available on an emergent basis. RBC cholinesterase levels may help in 

monitoring recovery or in forensic investigations. In symptomatic patients, treatment is 

 

1

 Adapted from Rotenberg JS, Newmark J. Nerve agent attacks on children: diagnosis and management. 

Pediatrics 2003; 112:648-58. 
 114

indicated without waiting for cholinesterase levels, while in exposed asymptomatic 

patients, antidotal therapy is not needed, even if cholinesterase is depressed. 

Treatment 

If recognized early, this is a treatable and reversible syndrome. Triage, resuscitation, and 

decontamination should begin at the scene and at accepting health care facilities (see 

Chapter 1). Individuals exposed to liquid should be observed for at least 18 hours. 

Treatment focuses on airway and ventilatory support; aggressive use of antidotes, 

particularly atropine and pralidoxime (2-PAM); prompt control of seizures; and 

decontamination as necessary. Antidotal therapy is titrated according to clinical severity 

(Table 5.4). 

Atropine, in relatively large doses, is used for its antimuscarinic effects, and pralidoxime 

chloride serves to reactivate acetylcholinesterase and thus enhance neuromuscular 

function. Atropine counters bronchospasm and increased bronchial secretions; 

bradycardia; GI effects of nausea, vomiting, diarrhea, and cramps; and may lessen seizure 

activity. Severely affected nerve agent casualties in the military have received 20-200 mg 

of atropine. Atropine should be administered until respiratory status improves, because 

tachycardia is not an absolute end-point for atropinization. Atropine cannot reverse 

neuromuscular symptoms, and paralysis may persist without pralidoxime. 

Pralidoxime cleaves the organophosphate away from the cholinesterase, thus regenerating 

the intact enzyme if aging has not occurred. This effect is noted most at the 

neuromuscular junction, with improved muscle strength. Prompt use of pralidoxime is 

recommended in all serious cases. 

Both atropine and pralidoxime should be administered IV in severe cases (intraosseous 

access is likely equivalent to IV). However, animal studies suggest that hypoxia should 

be corrected, if possible, before IV atropine use, to prevent arrhythmias; otherwise IM 

use might be preferable initially. Atropine has also been administered by the endotracheal 

or inhalational route in some contexts, and such use might have a beneficial effect. 

Experience with organophosphate pesticide poisoning in children suggests that 

continuous IV infusion of pralidoxime may be optimal. Nevertheless, the IM route is 

acceptable if IV access is not readily available. This may be of considerable relevance in 

a mass casualty incident involving children. In fact, most EMS programs in the United 

States now stock military IM auto-injector kits of atropine and 2-PAM. Similar kits with 

pediatric doses are currently not available in the United States. However, pediatric autoinjectors of atropine in 0.25 mg, 0.5 mg, and 1.0 mg sizes have recently been approved 

by the FDA. In dire circumstances, the adult 2-PAM auto-injector (600 mg) might be 

used in children older than 2–3 years or weighing more than 13 kg. 

Seizures are primarily controlled with benzodiazepines. Diazepam is principally used by 

the U.S. military, but other benzodiazepines may be equally efficacious (e.g., midazolam 

or lorazepam). Midazolam is believed optimal for IM administration in the treatment of 

status epilepticus in general and so may be especially useful in nerve agent toxicity in 
 115

children. Finally, routine administration of anticonvulsant doses of benzodiazepines has 

been recommended in severe cases even without observed convulsive activity because 

animal studies have indicated some amelioration of subsequent seizures and morphologic 

brain damage with such use. 

Supportive care is critical to patient outcome and includes the following: 

• Protect airway/relieve bronchospasm/pulmonary toilet. 

o 100% oxygen, bronchodilators, nasogastric tubes. 

• Monitor for cardiac arrhythmias. 

• Treat complicating injuries and infections. 

o Wounds and foreign bodies may be contaminated. 

o Treat skin lesions. 

• Provide fluids, electrolytes, and nutrition. 

o Nursing mothers should discard breast milk. 

• Prevent hypothermia. 

• Provide eye care. 

o Consider ophthalmic analgesics for ocular pain. 

o Consider topical mydriatics for miosis (atropine given systemically may not 

reverse miosis). 

• Consider EEG and brain imaging for victims who do not promptly regain 

consciousness. 

Isolation and Control Measures 

Isolation is required only for potentially exposed victims before they are definitively 

decontaminated. Health care workers should wear PPE to treat victims before 

decontamination is complete. 

Cyanide 

Cyanide has long been used for sinister purposes, including as an agent of murder, 

suicide, chemical warfare, and judicial execution. In addition, it may pose an 

occupational hazard, and it has been ingested (usually in a precursor form) by children. 

Its efficacy as an agent of chemical terrorism is considered somewhat limited by its 

volatility in open air and relatively low lethality compared with nerve agents. However, if 

cyanide were released in a crowded, closed room, the effects could be devastating. This 

was more than amply illustrated by its notoriety as the chemical weapon used by the 

Nazis in the concentration camp gas chambers. More than 900 people ingested potassium 

cyanide salt in the 1978 Jonestown mass suicide incident. Chemical warfare agents 

involving cyanide include the liquids hydrocyanic acid (HCN, the form used by the 

Nazis, as “Zyclon B”) and cyanogen chloride (deployed during World War I), which 

rapidly vaporize after detonation. Cyanogen chloride may cause some initial eye, nose, 

throat, and airway irritation, but otherwise its effects are the same as those of hydrocyanic 

acid and result from systemic cyanide toxicity. 
 116

Toxicology 

Cyanide has a strong affinity for the ferric iron (Fe3+) of the heme ring and thus inhibits 

many heme-containing enzymes. Its primary effect in acute toxicity is inhibition of 

cytochrome a3, thereby interfering with normal mitochondrial oxidative metabolism in 

the electron transport chain, causing cellular anoxia and lactic acidosis. It may also 

interfere with other important enzymes, including succinic acid dehydrogenase and 

superoxide dismutase, which may underlie some of its chronic toxicity. In addition, 

cyanide is believed to be a direct neurotoxin contributing to an excitatory injury in the 

brain, probably mediated by glutamate stimulation of N-methyl D-aspartate receptors. 

The primary human enzyme, rhodanese, detoxifies cyanide by combining it with a sulfate 

moiety such as thiosulfate to form the relatively nontoxic thiocyanate ion, which is then 

excreted by the kidneys. Therefore, exposure to a potentially lethal dose of cyanide that 

occurs slowly though continually over time may be tolerated, making it relatively unique 

among the agents of chemical terrorism. 

Clinical Presentation 

Clinical manifestations of cyanide toxicity vary considerably depending on dose, route of 

exposure, and acuteness of exposure but in general reflect the effects of cellular anoxia 

on organ systems. Thus, the most metabolically active tissues, the brain and heart, tend to 

be the most affected. With exposure to low concentrations of vapor, early findings 

include tachypnea and hyperpnea, tachycardia, flushing, dizziness, headache, diaphoresis, 

nausea, and vomiting. As exposure continues, symptoms may progress to those 

associated with exposures to high concentrations of vapor. The latter include rapid onset 

(within 15 seconds) of tachypnea and hyperpnea, followed by seizures (30 seconds), 

coma and apnea (2-4 minutes), and cardiac arrest (4-8 minutes). “Classical” signs of 

cyanide poisoning include severe dyspnea without cyanosis—or even with cherry-red 

skin (due to lack of peripheral oxygen use)—and a bitter almond odor to breath and body 

fluids. However, some patients do develop cyanosis (likely secondary to shock), and only 

about half the population is genetically capable of detecting the cyanide-induced bitter 

almond odor. Laboratory abnormalities in cyanide poisoning include metabolic acidosis 

with a high anion gap and increased serum lactate and an abnormally high mixed venous 

oxygen saturation (also due to decreased use of peripheral oxygen). Blood cyanide levels 

can be determined but not usually on an emergent basis. 

In an aerosol attack using recognized military chemical weapons, if people are 

convulsing or dying within minutes of exposure, the weapon is likely to be either cyanide 

or a nerve agent. Although the symptoms of exposure to cyanide and nerve agents may be 

hard to distinguish, when there are high concentrations of cyanide, seizures begin within 

seconds and death within minutes, generally with little cyanosis or other findings. The 

course for lethal nerve agent toxicity is characteristically somewhat longer and 

accompanied by copious nasal secretions, miotic pupils, muscle fasciculations, and 

cyanosis before death. 
 117

Treatment 

Management of cyanide poisoning begins with removing the victim from the

contaminated environment to fresh air. Dermal decontamination is rarely necessary 

because these agents are so volatile but in case of contact with liquid agent, wet clothing 

should be removed and underlying skin washed. Ingested cyanide may be partially bound 

by activated charcoal. 

Basic supportive intensive care is critical, including providing 100% oxygen, mechanical 

ventilation as needed, and circulatory support with crystalloid and vasopressors; 

correcting metabolic acidosis with IV sodium bicarbonate; and controlling seizures with 

benzodiazepines. Symptomatic patients, especially those who have lost consciousness or 

have other severe manifestations, may benefit further from antidotal therapy, which is a 

multistep process. 

First, a methemoglobin-forming agent is administered, typically inhaled amyl nitrite or 

IV sodium nitrite because methemoglobin has a high affinity for cyanide and 

disassociates it from cytochrome oxidase. However, nitrite administration can be 

hazardous because it may cause hypotension, and overproduction of methemoglobin may 

compromise oxygen-carrying capacity. Thus, nitrite is probably not indicated for mild 

symptoms or if the diagnosis of cyanide poisoning is uncertain. Furthermore, people with 

cyanide poisoning who may have concomitant hypoxic insult (e.g., most victims of 

smoke inhalation) probably are not good candidates for nitrite therapy. Optimal nitrite 

dosing, especially when given parenterally, depends on body weight and hemoglobin 

concentration, which is of particular importance in pediatric patients, who have a broad 

range of hemoglobin concentrations. In the pre-hospital setting, or whenever IV access is 

not possible, amyl nitrite may be used to begin nitrite therapy. Amyl nitrite is provided in 

glass pearls, which are used by crushing the pearl and then either allowing spontaneous 

inhalation or introducing the vapor into a ventilation circuit, for 30 seconds of each 

minute. As soon as IV access is established, sodium nitrite may be given. The 

recommended pediatric dosage, assuming a hemoglobin concentration of 12 g/dL, is 0.33 

mL (of the standard 3% solution)/kg, given slowly IV over 5-10 minutes (with a 

maximal, or adult, dose of 10 mL). Dosing may be adjusted for patients with significant 

anemia, although this would not likely be known in emergent treatment of a poisoned 

child in critical condition. 

The second step is providing a sulfur donor, typically sodium thiosulfate, which is used 

as substrate by the rhodanese enzyme for conversion to thiocyanate. Thiosulfate 

treatment itself is believed efficacious and relatively benign, and thus it may be used 

alone empirically in cases in which the diagnosis is uncertain. (This approach has also 

been recommended, for example, in the management of the situation described above of 

cyanide toxicity complicating smoke inhalation, with likely concomitant lung injury and 

carbon monoxide poisoning). The recommended pediatric dosage of thiosulfate is 1.65 

mL (of the standard 25% solution)/kg, IV (with a maximal, or adult, dose of 50 mL). 

Each agent may be given a second time at up to half the original dose as needed, or in the 

case of thiosulfate, even a full dose would be unlikely to pose inherent toxicity. Both 
 118

these medications are packaged together in commercially available “cyanide antidote 

kits,” along with amyl nitrite pearls. Additionally, most hospital pharmacies stock 25% 

sodium thiosulfate solution in vials containing sufficient volume (50 mL) to treat even 

adult patients. This has been used routinely in the preparation of nitroprusside infusions, 

premixed with thiosulfate, so as to obviate nitroprusside-induced cyanide toxicity. 

Several alternative therapies and experimental antidotes have been used in Europe (cobalt 

salts, hydroxocobalamin) or are in clinical trials (aldehydes, aminophenol derivatives) or 

animal studies (dihydroxyacetone, alpha-ketoglutarate). Hydroxocobalamin, in particular, 

has been cited as a potentially quite useful antidote in civilian terrorism scenarios because 

of its relative safety compared with nitrites. However, it currently is not commercially 

available in the United States in a pharmacologically appropriate concentration for 

antidotal efficacy. 

Vesicants 

The term “vesicant” is commonly applied to chemical agents that cause blistering of the 

skin. Direct contact with these agents can also result in damage to the eyes and 

respiratory system. Systemic absorption may affect the GI, hematologic, and central 

nervous systems as well. 

The four compounds historically included in this category—sulfur mustard, the nitrogen 

mustards, lewisite, and phosgene oxime—were all manufactured initially as potential 

chemical warfare agents. Phosgene oxime is technically not a true vesicant because the 

skin lesions it causes are urticarial as opposed to vesicular. The nitrogen mustards, 

although first synthesized in the 1930s for anticipated battlefield use, were found to be 

less effective for chemical warfare than the already existing sulfur mustard. Subsequent 

development for of nitrogen mustards for weapons use was therefore largely abandoned. 

However, one form of nitrogen mustard, HN2, became a highly used and effective 

chemotherapeutic agent. Lewisite was first synthesized during the latter part of World 

War I, but other than reports of its use by Japan against China between 1937 and 1944, it 

is not known to have ever been used on the battlefield. An antidote, British antilewisite 

(BAL, or dimercaprol), can minimize its effects if given promptly. Because so little is 

known about the toxicity and mechanisms of action of phosgene oxime and lewisite, and 

because anticipated medical management issues of these agents are somewhat similar, the 

following section focuses on the clinical effects and management issues regarding sulfur 

mustard exposure—historically the most frequently used and available of this class of 

chemical agent. 

Sulfur mustard has been the most widely used of all chemical warfare agents over the last 

century. Approximately 80% of chemical casualties in World War I were due to sulfur 

mustard, and its use has been verified in multiple military conflicts since then. In 

addition, Iraq used sulfur mustard on numerous occasions during its war against Iran 

from 1980 to1988 and as a weapon of terror against thousands of Kurdish civilians, 

including children, by using aerially dispersed mustard bombs in 1988. 
 119

Sulfur mustard is stockpiled both in the United States and in several other countries as 

well. It is not difficult to manufacture, making it even more favorable for use by 

terrorists. In addition to its accessibility and ease of production, several other factors 

enhance its suitability as a terrorist or warfare agent. Although mortality associated with 

sulfur mustard is considerably lower than that caused by other chemical weapons such as 

nerve agents, sulfur mustard exposure results in significant and prolonged morbidity that 

may potentially overwhelm health care resources. The risk of direct contamination either 

from patient contact or from the agent’s persistence in the environment may force health 

care providers to wear bulky protective gear, which makes it difficult to administer care, 

particularly to children. Although tissue damage occurs within minutes of exposure, 

clinical symptoms are delayed for hours, potentially rendering the victim ignorant of 

exposure until the opportunity for effective decontamination has passed. Lastly, unlike 

the case for lewisite, there is no known antidote for sulfur mustard exposure. 

Characteristics 

Sulfur mustard is an alkylating agent that is highly toxic to rapidly reproducing and 

poorly differentiated cells. Under normal environmental conditions, it is an oily liquid 

that varies in color from yellow to brown, depending on amounts and types of impurities. 

Its odor has been described as similar to garlic or to mustard itself. In warmer climates, 

mustard vapor is a particular concern due to its low volatility, while at lower 

temperatures (<14°C or 58°F); it becomes a solid and may persist in the environment for 

an extended time. On contact with tissue surfaces, mustard vapor or liquid is rapidly 

absorbed and exerts its cellular damage within minutes. Both vapor and liquid readily 

penetrate most clothing, although rubber overgarments may be protective for several 

hours. 

Clinical Effects 

After exposure to sulfur mustard, skin findings do not appear for 2–48 hours, depending 

on the mode of exposure, the sensitivity of the individual, and the environmental 

conditions (Table 5.5). The most common early sign in exposed areas is erythema 

resembling sunburn, which may coincide or even be preceded by significant pruritus. If 

the exposure is mild, this may be the only skin manifestation. More typically, yellowish 

blisters begin to form over the next 24 hours. Penetration of the agent is enhanced by thin 

skin, warmth, and surface moisture, rendering areas such as the groin, axillae, and neck 

particularly susceptible. Once they appear, the vesicles frequently coalesce to form 

bullae. Although largely painless, these fragile bullae commonly rupture, resulting in 

painful ulcers that may take weeks or months to heal. The fluid from the blisters does not 

contain free mustard and is therefore not hazardous. If skin exposure has been severe, 

these earlier stages of developing lesions may be bypassed altogether with the direct 

appearance—albeit delayed—of skin sloughing similar to that seen in a full-thickness 

thermal burn. 

Although skin findings may be dramatic, the organ most sensitive to mustard exposure is 

the eye, with mild symptoms occurring at concentrations 10-fold lower than those needed 

to produce effects on the skin. Like the skin findings, ocular symptoms are also delayed, 
 120

usually for 4–6 hours. The first symptoms are usually pain and irritation, followed 

progressively by photophobia, worsening conjunctivitis, corneal ulceration, and 

perforation of the globe with severe exposures. Although visual impairment is common, 

it is usually transient and simply reflects eye closure from intense pain and reflex 

blepharospasm as opposed to true damage to the optic nerve. Severe lid edema caused by 

inflammation of soft tissue around the eyes is also common. 

With inhalation of mustard vapor, both the proximal and distal respiratory tract may be 

affected. Proximal involvement usually manifests after several hours and consists of 

rhinorrhea, hoarseness, a dry and painful cough with expectoration, and eventually a 

characteristic toneless voice due to vocal cord damage. With more significant inhalational 

exposures, necrosis of the airway mucosa can lead to a sterile tracheobronchitis with the 

necrotic epithelium forming pseudomembranes that may obstruct the airway. Bacterial 

superinfection may develop as well, usually days later, facilitated by a weakened immune 

response. Respiratory failure can be the end result of either early mechanical obstruction 

from laryngospasm or pseudomembrane formation or later by overwhelming bacterial 

infection enhanced by the denuded respiratory mucosa and necrotic tissue. Early onset of 

dyspnea, along with other signs of impaired peripheral gas exchange, such as hypoxia, is 

a sign of severe inhalational exposure and indicates a poor prognosis. 

All cellular elements of the bone marrow can be affected by sulfur mustard due to its 

DNA alkylating effects, which impair replication in rapidly dividing stem cells. 

Megakaryocytes and granulocyte precursors are more susceptible than those of the 

erythropoietic system, and therefore the presence of anemia along with leukopenia 

indicates significant exposure and a poorer outcome. During the first few days after 

exposure, there may be a reactive leukocytosis that may or may not progress to 

leukopenia, depending on the level of exposure. 

Gastrointestinal symptoms can develop from the general cholinergic activity of sulfur 

mustard, resulting in nausea and vomiting that occurs after several hours and is rarely 

severe. Direct injury to the GI mucosa from ingestion of mustard either directly or from 

contaminated food or water can lead to a later onset of more severe vomiting, diarrhea, 

abdominal pain, and prostration. 

Although historically a large percentage of battlefield victims have reported CNS 

findings such as lethargy, headaches, malaise, and depression, the role of the mustard 

agent itself in development of symptoms, as opposed to that of other environmental 

stressors, is unclear. Clinicians should be aware that, regardless of their etiology, these 

symptoms are a frequent presentation. In addition, absorption of high doses of sulfur 

mustard can result in CNS hyperexcitability, convulsions, abnormal muscular activity, 

and coma. 

Treatment 

The most effective treatment is decontamination, because once sulfur mustard penetrates 

tissues, its effects are irreversible. Unfortunately, sulfur mustard is rapidly absorbed on 

contact, usually exerting damage within 3–10 minutes of exposure. Effectiveness of 
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decontamination is therefore extremely time dependent. Self-decontamination may be the 

quickest method and should include removing clothing and physically eliminating any 

mustard residue on the skin. 

Anyone providing aid to an exposed person should take proper precautions including 

ocular, respiratory, and skin protection, ideally with a chemical protection overgarment, 

rubber boots, and gloves. Exposed individuals should be washed with soap and warm 

water, or just rinsed with water, as soon as possible. The use of bleach is not 

recommended in children because it can cause liquefactive epithelial damage to their thin 

skin, which may in fact promote further penetration of the agent. 

Other methods of physical removal, particularly if the mustard is predominately in solid 

form, include scraping or plucking the agent from the skin, as well as using adsorptive 

agents such as earth, powdered soap, or flour, followed by rinsing with water. 

Regardless of decontamination method, the most important aspect is speed. While ideally 

all victims should be decontaminated before entering a medical treatment facility, if 

exposed individual arrive via personal transportation or on foot, they may first need to be 

taken to a separate area for decontamination. Even if delayed, decontamination should be 

done to protect others from exposure, to avoid further absorption, and to prevent spread 

to other areas of the body. 

After decontamination and basic life-support issues and other life-threatening 

concomitant injuries have been addressed, it is important to remain aware of the latency 

of most symptoms of vesicant exposure. Even if no symptoms are seen at presentation, 

exposed patients should be observed for at least 8 hours before being discharged. Because 

of the lack of a specific antidote, the remainder of therapy is supportive. 

Skin lesions are treated similarly to those of burn victims. However, fluid losses tend to 

be less. For this reason, traditional formulas for fluid replacement in burn victims often 

overestimate losses in vesicant-exposed patients. Erythema and symptoms such as 

pruritus should be treated with topical and systemic analgesia and antipruritics, as well as 

soothing lotions such as calamine. Small vesicles (<2 cm) should be left intact, but larger 

vesicles and bullae should be incised and treated with frequent irrigation and topical 

antibiotics such as silver sulfadiazine. Widespread and severe partial or full-thickness 

involvement should be managed in a burn unit if possible. 

Eye treatment should center on removing the agent and on preventing scarring and 

infection. After irrigation of the eye with copious amounts of water, cyclopegic agents 

should be applied for comfort and to prevent formation of synechiae. Topical antibiotics 

should then be applied directly along with lubricating ointments such as petroleum jelly 

to the eyelids to prevent adhesions and subsequent scarring. 

Mild respiratory symptoms involving the upper airway can be treated with cough 

suppressants, throat lozenges, and cool mist vapor. More severe lower respiratory 

involvement generally requires ventilation with positive end-expiratory pressure. The 
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patient should be intubated promptly if there are any signs of laryngeal spasm or edema. 

Direct bronschoscopy may be necessary for removal of obstructive pseudomembranes. 

The need for prolonged intubation (>5–10 days) is a sign of significant proximal airway 

damage and suggests a poor prognosis. The temptation to use systemic antibiotics during 

the first 3–4 days despite the not uncommon findings of fever, leukocytosis, and cough 

should be avoided to prevent the growth of resistant organisms. However, if these signs 

and symptoms persist beyond this period and there is radiographic evidence of 

consolidation, systemic antibiotics may then be indicated. 

For severe GI effects, in addition to fluid replacement, antiemetics or anticholinergics 

may be helpful. In the rare case of vesicant ingestion, gastric lavage may be useful if 

performed within 30 minutes; vomiting should never be induced. 

If anemia from bone marrow involvement is severe, blood transfusions may be of benefit. 

Other therapies, such as administration of hematopoietic growth factors and bone marrow 

transplantation, although used successfully in animal studies, have never been used in 

people exposed to vesicants. 

Pediatric Considerations 

The unique susceptibilities of children (see Chapter 1, Children Are Not Small Adults) 

emphasize the need to consider a number of practical treatment issues after vesicant 

exposure. The first consideration is the time from exposure to onset of skin 

manifestations, which is shorter in children than in adults. As a result, children may be 

overrepresented in the initial index cases in a mass civilian exposure. Because a child’s 

skin is more delicate, the caustic effects of decontamination agents (such as bleach) on an 

already damaged skin surface are potentially much greater; consequently, these agents 

should probably be avoided altogether in children. Soap and water used for washing and 

rinsing should be warmed if possible to prevent the greater likelihood of hypothermia in 

children. In addition, low water pressure (60 psi preferred; if not available, <100 psi) 

should be used if possible to minimize potential further penetration of the agent into the 

thinner skin of the child. 

Because mustard vapor is denser than air, it tends to settle close to the ground, which has 

obvious ramifications for small children. In addition to more common facial and eye 

involvement, pulmonary involvement can also be more extensive, ostensibly from the 

lower breathing zones and increased respiratory rates of children. Therefore, intubation 

may be needed earlier, and more aggressive ventilatory management may be necessary in 

the vapor-exposed child who has lower respiratory tract symptoms. 

Fluid replacement may also need to be more aggressive in children because of the greater 

potential for dehydration secondary to their lower volume reserve. Pain management is 

another important consideration, particularly in the very young child who is preverbal. 
 123

Pulmonary Agents 

Toxic industrial chemicals used as terrorist weapons are a potentially significant threat to 

civilian populations. The Chemical Weapons Convention, a disarmament and 

nonproliferation treaty with 145 signatory countries, identifies 33 chemical and chemical 

precursors that can be used as weapons. Although some of the chemicals are well-known 

weapons (e.g., sarin, VX, sulfur mustard), others are more familiar as common industrial 

chemicals such as chlorine, phosgene, and others. In the United States today, millions of 

tons of these chemicals are manufactured yearly for the production of dyes, textiles, 

medicines, insecticides, solvents, paints, and plastics. 

The potential terrorist threat posed by industrial chemicals is well known. A January 

2002 report to Congress by the Central Intelligence Agency reports that terrorist groups 

“have expressed interest in many other toxic industrial chemicals—most of which are 

relatively easy to acquire and handle—and traditional chemical agents, including chlorine 

and phosgene.” Although of clear interest to terrorist groups, traditional nerve agents 

require a greater degree of technical sophistication to manufacture and deliver as 

weapons. 

Chlorine and Phosgene 

As chemical weapons, chlorine and phosgene are commonly known as “pulmonary,” 

“inhalational,” or “choking” agents. These terms are ambiguous to the point of confusion, 

and it is better to conceptualize these compounds along a spectrum. Type I agents act 

primarily on the central, or tracheobronchial, components of the respiratory tract; Type II 

agents act primarily on the peripheral, or gas-exchange, regions (i.e., the respiratory 

bronchioles, alveolar ducts, and alveoli). Type I agents are typically water soluble and 

chemically reactive and attack the respiratory epithelium of the bronchi and larger 

bronchioles. The resultant pathologic effects are necrosis and denudation with or without 

the formation of pseudomembranes; the resultant clinical effects are mucosal irritation, 

with prominent components of noise (coughing, sneezing, hoarseness, inspiratory stridor, 

and wheezing). Type II agents cause noncardiogenic pulmonary edema initially 

manifested clinically by dyspnea without accompanying signs of either radiologic or 

laboratory anomalies. 

Few agents are pure Type I or Type II agents, and high doses of either kind of agent can 

affect both central and peripheral compartments. For example, chlorine, which is 

intermediate in both aqueous solubility and chemical reactivity, typically produces a mix 

of both central and peripheral effects. Phosgene, however, has few Type I effects except 

at moderately high doses. Sulfur mustard has poor aqueous solubility, but once dissolved, 

it cyclizes to form such a powerfully reactive cyclic ethylene sulfonium oxide that it acts 

in the airways primarily as a Type I agent at low to moderate doses. Used as weapons of 

mass destruction, agents such as hydrogen cyanide and hydrogen sulfide would most 

likely be released as vapors or gases and, in that respect, would be “inhalational” agents. 

However, in contrast to Type I and Type II agents—the major pathologic and clinical 

effects of which are local on respiratory epithelium or alveolar septae—cyanides are 

widely distributed via the blood throughout the body and therefore merit a separate 
 124

classification as Type III (systemically distributed) agents. Finally, some agents such as 

sulfur mustard exhibit both local (in this case, initially Type I) and systemic (Type III) 

effects, although the systemic effects of mustard (which may include bone-marrow 

depression and resulting pancytopenia) become clinically significant only after a delay. 

Although not stockpiled in the United States for military purposes, chlorine, phosgene, 

and hydrogen cyanide are common components in industrial manufacturing. Primarily 

liquids, they are easily vaporized, allowing for widespread gaseous dispersion. 

Clinical Effects 

The significant morbidity from pulmonary agents is caused by pulmonary edema. With 

chlorine, edema may appear within 2–4 hours or even sooner with more significant 

exposures. Radiologic signs lag behind clinical symptoms: pulmonary interstitial fluid 

must be increased 5- to 6-fold to produce Kerley B lines on a chest radiograph. 

Pulmonary edema may be exceptionally profuse; in a study from the 1940s, pulmonary 

sequestration of plasma-derived fluid could reach volumes of up to 1 L/hr. This problem 

may be exceptionally profound in children, who have less fluid reserve and are at 

increased risk of rapid dehydration or frank shock with the pulmonary edema. 

Additionally, because children have a faster respiratory rate, there is exposure to a 

relatively higher toxic dose. 

Chlorine. Chlorine is a greenish yellow gas that is denser than air and, therefore, settles 

closer to the ground and low-lying areas. This may have significant consequences for 

small children and infants, who would be exposed to higher concentrations of the vapor 

and thus receive higher inhaled doses of the agent. Chlorine has a strong, pungent odor 

that most people associate with swimming pools. Because the odor threshold (at 0.08 

ppm) is less than the toxicity threshold, the odor may warn individuals that exposure is 

occurring. 

The initial complaints in chlorine exposure may be either intense irritation or the 

sensation of suffocation, or both; the suffocating feeling is what led to its characterization 

as a “choking” agent. Low-level exposures to chlorine result in mucosal irritation of the 

eyes, nose, and upper airways. Higher doses lead to respiratory symptoms that progress 

from choking and coughing to hoarseness, aphonia, and stridor—classically Type I 

effects. Dyspnea after chlorine exposures indicates damage to the peripheral 

compartment (Type II insult) and incipient pulmonary edema. 

Phosgene. Like chlorine, phosgene is also heavier than air, thus posing an increased risk 

for children who are exposed. Phosgene itself is colorless, but associated condensation of 

atmospheric water produces a dense white cloud that settles low to the ground. It has the 

characteristic odor of newly mown hay. However, the odor threshold for phosgene (at 1.5 

ppm) is higher than the toxicity threshold, and unlike the case with chlorine, detection of 

the odor would be inadequate and too late to serve as a warning against toxic exposure. 

Phosgene is primarily associated with the development of pulmonary edema. However, 

because in low to moderate doses it does not cause the mucosal irritation associated with 
 125

Type I agents, the significance of the exposure may be underestimated. Exposure to 

progressively higher doses produces mild cough, sneezing, and other effects on the 

central compartment. Dyspnea is seldom present initially except when doses have been 

massive; instead, there is a clinically asymptomatic, or latent, period usually of several 

hours and inversely correlated with dose. Dyspnea and associated clinical deterioration 

have in several instances been triggered by slight to moderate exertion. 

Treatment 

Decontamination. Decontamination consists primarily of removing the victim from the 

source of the pulmonary agent to fresh air. For first responders such as paramedics and 

fire-rescue workers, PPE with self-contained breathing apparatus is required; however, 

because the gases are volatile, cross-contamination is unlikely. Victims of chlorine 

exposure may require copious water irrigation of the skin, eyes, and mucosal membranes 

to prevent continued irritation and injury. 

Management. Management is primarily supportive; there are no antidotes or specific 

postexposure treatments for inhalational agents. Victims should be observed and 

monitored for both central (Type I) and peripheral (Type II) acute effects, including 

development of pulmonary edema. Most deaths are due to respiratory failure and usually 

occur within the first 24 hours. Because of the delay in onset of pulmonary edema, 

prolonged observation of victims of phosgene and chlorine attacks is warranted. 

Treatment of central, or Type I, damage involves administering warm, moist air and 

supplemental oxygen, and treating bronchospasm either produced de novo by the toxicant 

in normal airways or resulting from toxicant-induced exacerbation of airway 

hyperresponsiveness in individuals with underlying pathology such as asthma or reactive 

airways. Aggressive bronchodilator therapy with beta-agonists is appropriate. The value 

of corticosteroids is less clear, but they may be efficacious in victims with severe 

bronchospasm or a history of asthma. Nebulized lidocaine (4% topical solution) has been 

recommended to provide analgesia and reduce coughing. The possibility of laryngospasm 

should always be anticipated and the necessity and timing of intubation carefully 

assessed. Associated central damage from inhaled particles of smoke in situations 

involving fire should also be considered. Pseudomembrane formation may lead to airway 

obstruction and may require bronchoscopic identification and removal of 

pseudomembranous debris. Necrotic debris from central damage provides an excellent 

culture medium for secondary bacterial colonization and infection, and bacterial 

superinfections are commonly seen 3–5 days after exposure. Early aggressive antibiotic 

therapy directed against culture-identified organisms is imperative. Prophylactic 

antibiotics are of no value. 

Treatment of peripheral (Type II) damage from pulmonary agents includes adequate 

oxygenation, establishment of effective intra-alveolar pressure gradients using positive 

end-expiratory pressure (for example, in conscious patients, with continuous positive 

airway pressure, or CPAP), and careful attention to fluid balance. In cases of florid 

pulmonary edema, using a central line to monitor hemodynamics in critically ill children 

may be necessary. The length of the latent period in a dyspneic patient can provide 
 126

clinically valuable information about the intensity of exposure; patients who develop 

breathing difficulty within the first 4 hours after exposure may face a grave prognosis, 

and even patients with mild dyspnea, because of the timing of the dyspnea, may be 

candidates for urgent or priority evacuation. All patients at risk of pulmonary edema 

induced by pulmonary agents should be maintained on strict bed rest to avoid 

cardiopulmonary decompensation associated with exertion. 

Riot Control Agents 

Modern riot control agents comprise a heterogeneous group of chemical compounds that 

have been used widely around the world since the 1950s (Table 5.6). These agents have 

the ability to incapacitate at low aerosol concentrations and have a high safety ratio (ratio 

of lethal dose to effective dose). However, prolonged exposure or release in enclosed 

areas can intensify the physical effects of these agents. CS (2-chlorobenzylidene), CN (1-

chloroacetophenone, Mace®), and pepper spray (Oleoresin capsicum) are commercially 

available to the public in the United States. 

Transmission and Pathogenesis 

Mode of transmission varies by agent. Common means include spraying a solution, 

release of pressurized canisters, explosive dispersion (smoke “grenades”), and burning. 

Explosive modes of transmission may cause traumatic injuries in addition to the 

incapacitating effects. CS is very flammable and poses a fire hazard. Most agents 

disperse soon after release, although persistent forms of CS exist. Riot control agents may 

contaminate clothing, buildings, and furniture and may cause ongoing symptoms in 

continued or repeat exposure. 

When dispersed, riot control agents are chemical irritants of the skin and mucous 

membranes of the eyes, nose, mouth, airways, and GI tract. CS and CN incapacitate 

through direct chemical irritation, acting like chemical thorns. Due to its low vapor 

pressure, CR (dibenzoxazepine) has limited effects on the respiratory tract. In addition to 

direct irritation, pepper spray also induces local release of the neurotransmitter 

substance P in peripheral afferent sensory nerves. This mechanism causes pain, capillary 

leakage, and vasodilation. 

Clinical Manifestations 

Riot control agents have specific effects on the eyes, nose, mouth, and airway, with 

variation in intensity depending on mode of exposure and agent used. Symptoms occur 

quickly after exposure and typically resolve in 1–2 hours once the victim has been 

removed from the agent. On contact, these agents induce eye burning, eye pain, tearing, 

conjunctival infection, blepharospasm, periorbital edema, and photophobia. Exposures at 

close range, particularly to exploding CS and CN grenades or canisters, may cause 

serious damage to the eye including corneal edema, conjunctival laceration, hyphema, 

vitreous hemorrhage, and secondary glaucoma. Permanent effects such as cataracts and 

traumatic optic neuropathy may also be seen. 
 127

After dispersal of riot control agents, nasal burning and pain, copious rhinorrhea, and 

persistent sneezing begin along with oral irritation and salivation. Pulmonary effects 

include chest tightness and burning, bronchorrhea, bronchospasm, and coughing. 

Gagging, retching, and vomiting frequently accompany mucosal and airway irritation. 

Exposed skin stings and may progress to erythema, vesiculation, and bullae depending on 

the conditions of exposure; prolonged exposure, high ambient temperature, and humidity 

favor worsening skin effects. These manifestations may occur hours to days after 

exposure to CS. Skin exposed to CR may become painful in water for up to 2 days after 

exposure. CN and CS can cause allergic contact dermatitis in people who are repeatedly 

exposed. 

Severe clinical effects from riot control agents are uncommon. Intense exposure to CS, 

CN, and pepper spray has caused laryngospasm, pneumonitis, bronchospasm, and 

noncardiogenic pulmonary edema. Often, the agent was released in an enclosed space, or 

the victim was not able to leave the vicinity of the agent. Individuals with asthma are 

predisposed to serious pulmonary symptoms. Experience with a 4-week-old infant who 

was unintentionally exposed to pepper spray at close range suggests that severe lung 

injury from Oleoresin capsicum is reversible in young children, provided that intensive 

medical support is provided. Deaths caused by pulmonary effects have occurred after CN 

exposure in victims who had previously normal lung function. Pepper spray was 

implicated in the death of one asthmatic prisoner in custody. Prolonged reactive airway 

disease has also been described after CS exposure in a previously healthy person with no 

prior history of atopy. In general, riot control agents are incapacitating but rarely lethal, 

especially relative to other deployable chemical agents such as the nerve agents, 

vesicants, and pulmonary agents. 

Diagnosis 

Some physical characteristics of the compounds can assist in detection when riot control 

agents are used. The most common agents (CS, CN, and pepper spray) are deployed in 

identifiable canisters. CS and pepper spray have a pungent pepper odor. CN has a flowery 

apple odor. Pepper spray frequently contains fluorescein dye that becomes readily 

apparent on exposed skin under a Wood’s lamp. No environmental monitoring systems 

currently exist for riot control agents. 

Differentiation of clinical effects caused by riot control agents from those of other 

chemicals can be a challenge during early management. Tearing, salivation, 

bronchorrhea, bronchospasm, and vomiting suggest the cholinergic effects of nerve agent 

exposure. Intense exposure to riot control agents with pneumonitis and pulmonary edema 

mimic symptoms of exposure to pulmonary agents, such as chlorine and phosgene. The 

potential for delayed skin effects, including vesiculation and bullae, with riot control 

agents makes them similar to vesicants such as sulfur mustard. However, symptoms 

rapidly resolve once contact with the agent ceases. Lack of progression to more severe 

symptoms such as bone marrow failure, paralysis, and seizures, combined with negative 

results from field detection systems and the physical characteristics mentioned above 

make identification of riot control agent release ultimately possible. 
 128

Treatment and Control 

Decontamination requires that all victims be moved to a well-ventilated, uncontaminated 

space and have their outer clothing removed. Clothing should be double bagged to 

prevent secondary exposure. Medical treatment of riot control agent exposure focuses on 

ending contact, assessing for serious pulmonary effects, and addressing ongoing eye and 

skin irritation (Table 5.7). 

In most instances, clinical signs and symptoms resolve over 30–60 minutes, and specific 

medical treatment is not needed. Pulmonary effects may be delayed. Victims who exhibit 

prolonged dyspnea or have other objective lung findings should be admitted to a medical 

facility for ongoing monitoring and treatment. 

All first responders should wear PPE including, but not limited to, a full-face gas mask, 

properly rated outer clothing, gloves, and boots. Field incident command should identify 

a hot zone, decontamination area, and cold zone. Ideally, decontamination should begin 

in the field and be complete before entry into a medical facility. 

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• Sidell FR. What to do in case of an unthinkable chemical warfare attack or 

accident. Postgrad Med 1990;88:70–84. 

Vesicants 

• Andreassi L. Chemical warfare and the skin. Int J Dermatol. 1991;30. 

• Armada M, Mendelson M. Chemical terrorism update: vesicants. Emerg Med.

2002:34(9):51–57. 

• Barranco VP. Mustard gas and the dermatologist. Int J Dermatol. 1991;30;684–

686. 

• Briggs SM, Brinsfield KH. Advanced Disaster Medical Response. Manual for 

Providers. Boston, MA: Harvard Medical International Trauma and Disaster 

Institute, 2003. 

• Hu H, Cook-Deegan R, Shukri A. The use of chemical weapons: conducting an 

investigation using survey epidemiology. JAMA. 1989;262;640–643. 

• Marshall E. Chemical genocide in Iraq? Science. 1988;241:1752. 

• Momeni A, Arminjavaheri M. Skin manifestations of mustard gas in a group of 

14 children and teenagers: a clinical study. Int J Dermatol. 1994;33:184–187. 

• Momeni A, Enshaeih S, Meghdadi M, et al. Skin manifestations of mustard gas. 

Arch Dermatol. 1992;128:775–780. 

• Safarinejad MR, Moosavi SA, Montazeri B. Ocular injuries caused by mustard 

gas. Diagnosis, treatment, and medical defense. Military Med. 2001;166;67–70. 

• Sidwell FR, Takafuji ET, Franz DR, eds. Textbook of Military Medicine Part 1: 

Medical Aspects of Chemical and Biological Warfare. Washington DC: Office of 

the Surgeon General, Walter Reed Army Medical Center; 1997. 

• Smith WJ, Dunn MA. Medical defense against blistering chemical warfare agents. 

Arch Dermatol. 1991;127:1207–1213. 

• U.S. Army Medical Research Institute of Chemical Defense. Medical 

Management of Chemical Casualties, 3rd ed. Aberdeen Proving Ground, MD: US 

Army Medical Research Institute of Chemical Defense; 2000. 

Pulmonary Agents 

• Bunting H. Clinical Findings in Acute Chlorine Poisoning. In: Respiratory Tract. 

Vol 2. In: Fasciculus on Chemical Warfare Medicine. Washington, DC: 

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51–60. 

• Central Intelligence Agency. Unclassified Report to Congress on the Acquisition 

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Conventional Munitions, 1 January through 30 June 2001. Washington, DC 

Central Intelligence Agency: Available at: 

https://www.cia.gov/cia/reports/721_reports/jan_jun2001.htm. Accessed August 

18, 2006. 
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Response to Incidents of Biological and Chemical Terrorism. In: Fleisher GR, 

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Reed Army Medical Center; 1997. 

Riot Control Agents 

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failure treated with extracorporeal membrane oxygenation. Pediatrics.

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exposure. Amer J Dis Child. 1972;123:245–247. 

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Medical Center; 1997. 450–476. 

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2002;52:595–600. 

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 132

Table 5.1. Pediatric vulnerabilities to chemical terrorism

Realm Potential vulnerability Potential response 

Increased respiratory exposure (higher 

minute ventilation, live “closer to the 

ground) 

Early warning, sheltering* (gas 

masks not advised because of 

risk of poor fit, suffocation) 

Increased dermal exposure (thinner, more 

permeable skin; larger body surface 

area/mass ratio) 

Protective clothing, early 

decontamination1

Increased risk of dehydration, shock with 

illness-induced vomiting, diarrhea 

(decreased fluid reserves, larger body 

surface area/mass ratio) 

Recognition, aggressive fluid 

therapy 

Increased risk of hypothermia during 

decontamination (larger body surface 

area/mass ratio) 

Warm water decontamination 

Physiologic 

More fulminant disease; (possible) 

physiologic detoxification immaturity; more 

permeable blood-brain barrier 

Pediatric-specific research for 

early diagnosis and treatment 

of chemical weapons victims1

Developmental Less ability to escape attack site, take 

appropriate evasive actions (developmental 

immaturity, normal dependence on adult 

caregivers who might be injured or dead) 

? 

Less coping skill of children who suffer 

injury or witness parental, sibling death 

(psychological immaturity) 

Child psychiatry involvement, 

research for preventing 

pediatric post-traumatic stress 

disorder1

Psychological 

Greater anxiety over reported incidents, 

hoaxes, media coverage, etc 

Pediatric counseling of parents 

and children†

Less capacity to cope with influx of critical 

pediatric patients 

Community and regional 

planning with significant 

pediatric input 

Loss of routine hospital transfer protocols 

EMS 

Limited ability to expand pediatric hospital 

bed capacity through NDMS 

* Plausible, but unproved or unstudied, and/or not intuitively obvious 

†

 For AAP and AACAP resources for parents and pediatricians, see 

http://www.aap.org/advocacy/releases/disastercomm.htm and 

http://www.aacap.org/publications/factsfam/disaster.htm. 

Source: Adapted from Henretig FM, Cieslak TJ, Eitzen EM Jr. Biological and chemical terrorism. 

J Pediatr 141:311–326, © 2002, with permission from Elsevier. 
 

133

Table 5.2. Chemical weapons – Summary of pediatric management considerations 

Agent Toxicity Clinical findings Onset Decontamination* Manag

Nerve Agents Tabun Sarin Soman VX 

Anticholinesterase: muscarinic, nicotinic, and CNS effects 

Vapor: miosis, rhinorrhea, dyspnea Liquid: diaphoresis, 

vomiting Both: coma, paralysis, seizures, apnea 

Vapor:seconds Liquid:minuteshours 

Vapor: fresh air, remove clothes, wash hair Liquid: remove clothes, copious washing of skin and hair with soap and water, ocular irrigation 

ABCs Atropine: 0.05 mg/kg IVmax 5 mg), repeat q2–5 secretions, bronchospasm Pralidoxime: 25 mg/kg IIM), may repeat within 3again every hour for 1 or persistent weakness, high Diazepam: 0.3 mg/kg (mlorazepam: 0.1 mg/kg IVmidazolam: 0.2 mg/kg (mseizures or severe exposu

Vesicants Mustard Alkylation Hours Symptomatic care Lewisite Arsenical 

Skin erythema, vesicles, ocular inflammation, respiratory tract inflammation 

Immediate pain 

Wash skin with soap and water, ocular irrigation (major impact only if done within min of exposure) 

Possibly BAL 3 mg/kg Ieffects in severe cases 

Pulmonary Agents Chlorine Phosgene 

Liberate HCL, alkylation 

Eyes, nose, throat irritation (especially chlorine); bronchospasm, pulmonary edema (especially phosgene) 

Minutes: eyes, nose, throat irritation; bronchospasm Hours: pulmonary edema 

Fresh air, wash skin with water 

Symptomatic care 
 

134

Table 5.2. Chemical weapons – Summary of pediatric management considerations, continued Cyanide Cyanide Cytochrome 

oxidase inhibition: cellular anoxia, lactic acidosis 

Tachypnea, coma, seizures, apnea 

Seconds Fresh air, wash skin 

with soap and water 

ABCs, 100% oxygen Sodium bicarbonate prn Sodium nitrite (3%):  Dosage (mL/kg) Est 0.27  0.33  0.39 Sodium thiosulfate (25%mL) 

Riot Control Agents CS CN (eg, Mace®) 

Capsaicin (pepper spray) 

Neuropeptide substance P release; alkylation 

Ocular pain, tearing, blepharospasm; nose and throat irritation; pulmonary failure (rare) 

Seconds Fresh air, ocular 

irrigation 

Topical ophthalmics, sym

* Should be performed by health care providers garbed in adequate personal protective equipment, especially if victims hav

exposure to nerve agents or vesicants. For emergency department staff, adequate PPE consists of a non-encapsulated, che

suit, boots, and gloves with a full-face air purifier mask/hood. 

† Intraosseous route likely equivalent to intravenous. ‡ Atropine via endotracheal tube or inhalation, or aerosolized ipratropium of possible benefit. 

Note: ABCs = airway, breathing, and circulatory support; BAL= British anti-lewisite; Hgb= hemoglobin concentration; prn Adapted from Henretig FM, Cieslak TJ, Eitzen EM Jr. Biological and chemical terrorism. J Pediatr 141:311-326 © 2002, 

Elsevier. 
 

135

Table 5.3 Representative classes of industrial chemicals – Summary of pediatric management cons

Agent Clinical findings Onset Decontamination Mana

Strong acids/bases Eye: caustic injury 

Skin: chemical burns GI: chemical burns of mouth, 

larynx, esophagus, stomach 

Rapid Eye, skin: immediate 

copious water irrigation GI: defer, immediate emergency department referral 

Supportive care, early significant ingestion; acontroversial, should bPoison Control Center

Respiratory tract irritants (e.g., ammonia, HCl and HF gases) 

EENT and respiratory tract irritation with cough, chest pain, dyspnea, wheeze (possible pulmonary edema in severe cases) 

Rapid Move to fresh air Supportive respiratory 

calcium gluconate soluPoison Control Center

Fentanyl and other opioids 

CNS and respiratory depression, miosis 

Rapid Move to fresh air (for 

aerosol exposure), consider AC for ingestion, consult Poison Control Center 

Supportive care, nalox

Cellular asphyxiants (e.g., phosphine, sodium azide) 

Cough, dyspnea, headache, dizziness, vomiting, tachycardia, hypotension, severe metabolic acidosis; may progress to coma, seizures, death; may have delayed onset pulmonary edema with phosphine 

Rapid (except pulmonary edema with phosphine) 

Move to fresh air (consider AC for ingested sodium azide—caution with vomitus, which may emit toxic hydrazoic acid fumes; consult Poison Control Center) 

Airway, breathing, and 100% oxygen 

Arsine Severe hemolysis 2–4 hr Move to fresh air Supportive care, enhan

alkalinization, consult 

* Contact Poison Control Center at 1-800-222-1222. Note: EENT = eye, ear, nose, and throat; HCl = hydrogen chloride; HF = hydrogen fluoride; AC = activated charcoal (1g

nasogastric). 

108
 

136

Table 5.3. Representative classes of industrial chemicals – Summary of pediatric management considAdapted from: Henretig FM, Cieslak TJ, Madsen JM, Eitzen EM Jr, Fleisher GF. The emergency department response to inand chemical terrorism. In: Fleisher GF, Ludwig S, Henretig FM (eds). Textbook of Pediatric Emergency Medicine, 5th ed. 

Wilkins, Philadelphia, in press, 2005. 
 

137

Table 5.4. Nerve agent triage and dosing 

Symptoms Triage level: 

disposition 

Anticholinergics Oxime-pralidoxime 

chloride (2-PAM) Benz

Asymptomatic Delayed: 

observe 

None None 

Miosis, mild rhinnorhea 

Delayed: admit or observe 

None None 

Miosis and any other symptom 

Immediate: admit 

Atropine 0.05 mg/kg IV, IM, IO, to max 4 mg; repeat as needed q 5–10 min until pulmonary resistance improves or secretions resolve; correct hypoxia before IV use; increased risk of ventricular fibrillation Alternatives: Consider scopolamine for nervous system and peripheral effects; glycopyrrolate for peripheral effects only 

2-PAM 25–50 mg/kg IV, IM, to max 1,800 mg; repeat q 1 hr prn; watch for muscle rigidity, laryngospasm, tachycardia, hypertension 

If neurologic syprogression: Midazolam 0.15–0.2 mg/kgnecessary or stless likely to caDiazepam IV, pLorazepam IV at 0.05–0.1 variable) If IV or IM is nmidazolam givintranasal at 0.2 prn or lorazepa
 

138

Table 5.4. Nerve agent triage and dosing, continued  Apnea, convulsions, cardiopulmonary arrest 

Immediate: admit, intensive-care status 

Atropine 0.05–0.10 mg/kg IV, IM, IO Repeat q 5–10 min as above (no max) Endotracheal tube: increase dose 2–3 times, mix with 3–5 mL normal saline and introduce via suction catheter, flush 3–5 mL normal saline 

2-PAM 25–50 mg/kg IV, IM, as above 

Midazolam, as Diazepam 30 days to 5 yr IV, max 5 mg/d≥5 yr old: 0.05mg/dose Repeat q 15-30 Lorazepam IV, 

 Autoinjector Atropine 2 mg for ≥40 kg 

1 mg for ≥20 kg 0.5 mg for ≥10 kg (0.05 mg/kg/dose) 

2-PAM 600 mg for ≥12 kg 

(50 mg/kg/dose) 

Diazepam 10 mg for ≥30 

(0.3 mg/kg/dos

*Monitor respiratory status and blood pressure. Note: Remember airway, breathing, circulation, decontamination/drugs. Consider oxygen, bronchodilators, nasogastric tu

mydriatics, temperature control. If prolonged impairment of consciousness, EEG (to rule out nonconvulsive status epilepticAdapted from Rotenberg JS, Newmark J. Pediatrics 2003; 112:648-58. 
 

139

Table 5.5. Clinical effects from sulfur mustard exposure 

 Eyes Skin Respiratory tract Bone 

marrow 

GI tract 

Minimal Tearing, burning, 

mild conjunctivitis, photophobia 

Erythema Rhinorrhea, 

hoarseness, hacking cough 

Reactive leukocytosis 

Nausea, vomiting Apa

depranxi

Moderate Severe 

conjunctivitis with blepharospasm, lid edema, pain, miosis 

Blisters Severe cough, 

expectoration, aphoria 

Leukopenia (often preceded by leukocytosis) 

As above As a

Severe Corneal edema, 

severe pain, ocular perforation 

Deep burning with fullthickness skin loss 

Dyspnea, pulmonary edema, asphyxia, bronchopneumonia 

Severe leukopenia, aplastic anemia 

Later nausea, vomiting (possible bloody), diarrhea 

Agihypexciabnomusactiv
 140

Table 5.6. Riot control agents 

Chemical name Abbreviated/common 

designation 

Uses 

2-Chlorobenzylidene CS Military, law enforcement, 

personal protection 

1-Chloroacetophenone CN (Mace®) Military, law enforcement, 

personal protection 

Dibenzoxazepine CR Military 

Oleoresin capsicum Pepper spray Military, law enforcement, 

personal protection 

Diphenylaminearsine DM Military (rare) 

Bromobenzylcyanide CA Military (rare) 
 141

Table 5.7. Medical treatment of riot control agent exposure 

Affected 

organ/symptoms 

Treatment 

Lungs

Dyspnea Oxygen 

Bronchospasm Albuterol 0.5% inhaled: 

 <15 kg: 2.5 mg (0.5 mL in 2 mL normal saline) 

 >15 kg: 5.0 mg (1.0 mL in 2 mL normal saline) 

Ipratropium bromide inhaled*: >2 yr: 500 μg (1 vial) 

Bronchorrhea Atropine, IV or IM: 0.02 mg/kg/dose (min 0.1 mg) 

Glycopyrrolate, IV or IM: 0.004 mg/kg/dose (max 0.1 mg) 

Eyes

Decontamination Remove and discard contacts 

Copious irrigation with normal saline 

If CS powder present, blow out of eyes using fan, avoiding 

contamination of space downwind 

Pain Topical anesthetic (tetracaine 1%, proparacaine 1%)†: 1 drop to each 

eye (apply before irrigation) 

Skin

Decontamination Copious irrigation with soap and water (may transiently increase 

symptoms) 

Do not use bleach (hypochlorite)‡

Pruritus Oral antihistamines (H1 receptor blockers): 

 Diphenhydramine 5 mg/kg/day divided into 4 doses or

 Hydroxyzine 2 mg/kg/day divided into 4 doses or 

 Equivalent medication 

Erythema, dermatitis Topical steroid preparation, apply sparingly BID to affected area 

 Mild potency on face and genitalia (e.g., hydrocortisone 1% 

cream) 

 Moderate to high potency on remainder of body (e.g., 

hydrocortisone 2% ointment, fluocinolone acetonide 0.025% 

ointment) 

Ensure proper decontamination 

Vesicles, bullae Burn dressings with topical antibiotic (silver sulfadiazine 1%) 

* For severe bronchospasm. Do not give ipratropium bromide to patients with peanut allergy. 

†

 Do not give to patients with allergy to local anesthetics. 

‡ Bleach may increase riot agent skin exposure and exacerbate erythema, vesiculation, and blistering. 
 142
143

Chapter 6. Radiological and Nuclear Terrorism 

Radiological Threats: Scope and Implications 

Nuclear and radiological weapons pose a significant terrorist threat. In the past, terrorists 

have attacked discrete locations with explosive materials that are not inherently toxic. 

However, the tactics and technological sophistication of terrorists are continually 

evolving. The September 2001 terrorist attacks demonstrated sophistication and planning 

not previously encountered. Future attacks with radiological devices are a real possibility 

that is outside the experience of most local emergency and health officials. Radiological 

terrorism could include detonation of one or more nuclear weapons, deployment of a 

radiation-producing device or other isotopic weapon (e.g., “dirty bomb”), or simply 

placement of a radioactive source (e.g., nuclear waste material) in a public location. The 

probability and nature of injuries depends on the type of disaster involved (see Figure 

6.1).

Such materials are sought by a variety of terrorist or criminal organizations and have 

been successfully seized by law enforcement personnel on many occasions. The 

increasing sophistication and inventiveness exhibited by transnational crime syndicates, 

drug cartels, anarchists, paramilitary warlords/insurgents and other groups challenge 

traditional law enforcement approaches. The danger posed by these various illicit 

organizations blurs the lines between international and domestic threats, as well as 

between criminal and military threats. 

Incident Management 

The National Council on Radiation Protection and Measurements (NCRP) suggests that 

attacks with radioactive materials can result in an area of contamination that is much 

larger than the immediate scene. Such “weaponized” hazardous materials are not readily 

amenable to local cleanup and require a paradigm shift in incident management. 

However, incident management will be difficult until the required and appropriate 

monitoring equipment is available, along with well-trained technical personnel. Incident 

response and the forensic investigation are also likely to be complicated by public fear 

and hysteria, need for personal protective equipment, potential contamination of 

evidence, and pressure for prompt cleanup and long-term site remediation. Consequently, 

police, fire, and EMS departments are training and equipping themselves to respond 

appropriately. State and Federal agencies are planning for how they will to coordinate 

transport and management of contaminated evidence for rapid diagnostic and forensic 

analysis, while still preserving safety and the evidentiary chain of custody. 

There are several key public health and safety considerations in managing radiological 

incidents. These include the potential for both immediate and long-term health effects, 

depending on the specific radionuclide(s) and method of dispersal involved. Other 

concerns include protection of first responders (including forensic investigators) as well 

as the general public, casualty triage, decontamination, treatment, and management of 

emotional distress and fear associated with possible exposure to radiation. Key decision 

points include evacuation versus sheltering in place and potential restrictions on food and 
144

water consumption. Initial response capabilities will be limited unless appropriate 

expertise, specialized equipment, and supplies are readily available. 

Nuclear Weapons 

The so-called “dirty bomb” disperses radioactive material and is relatively simple to 

deploy. A nuclear weapon would be much more difficult to deploy. Nevertheless, the 

potential for detonation of a nuclear weapon in a major city cannot be dismissed. A crude 

nuclear weapon constructed outside of a national program would likely be limited to a 

yield <10 kilotons (10,000 tons) of TNT equivalent. Theft or provision of a stockpile 

weapon from a nuclear nation could provide a more efficient and higher yield device. 

The destructive action of nuclear weapons is mainly due to blast and heat, as in 

conventional explosives. However, there are several important differences between 

nuclear and conventional explosions: 

• Nuclear explosions are hundreds to millions of times more powerful than 

conventional explosions. 

• The temperatures attained by nuclear weapons are much higher (tens of millions 

of degrees versus a few thousand), causing much more of the explosive energy to 

be emitted as light and heat (thermal radiation). This can result in skin burns and 

fires at considerable distances from the detonation. 

• Nuclear detonations release tremendous amounts of initial radiation. 

• The various substances remaining after a nuclear explosion are radioactive and 

may emit radiation for an extended period of time (i.e., residual radioactivity). 

Medical providers should be prepared to adequately treat injuries complicated by ionizing 

radiation exposure and radioactive contamination. Medical facilities in the immediate 

area will be nearly unusable due to heavy physical damage. Medical facilities in the 

adjacent areas will be severely compromised by downed power and phone lines; probable 

loss of all city utilities; and damage to electronics, communications, and HVAC control 

induced by the electromagnetic pulse produced by a nuclear blast. Patients who need 

more than basic medical care will require transport to functioning medical facilities well 

outside the immediate area of destruction. 

Radiation from a nuclear detonation. A nuclear detonation produces four kinds of 

ionizing radiation: neutron, gamma, beta, and alpha (see section on Radiation Physics 

later in this chapter). Neutron and gamma radiation are emitted immediately at 

detonation, in a ratio that decreases with increasing weapon yield and distance from 

ground zero. The residual radiation is composed largely of alpha particles, beta particles, 

and gamma rays. This residual radiation comes from fission products, unfissioned 

residual nuclear material, and ground-zero materials made radioactive by neutrons from 

the initial radiation (i.e., neutron-activation). 

For most weapons, blast and thermal injuries will outnumber radiation injuries. The types 

of injuries associated with the initial detonation vary with yield, distance from ground 

zero, time of day, and other factors. For weapons <10 kilotons (KT), most injuries 

requiring medical attention are caused by blast and ionizing radiation within a km or so 
145

from ground zero. For weapons larger than 10 KT, thermal radiation is the primary cause 

of injury, as this extends over a greater distance than blast or radiation effects. Flashblindness and retinal burns may occur out to 20 km during daytime and 50 km at night. 

Fallout. Fallout is defined as radioactive material from a nuclear detonation that returns 

to the ground after the explosion. A detonation close to ground level (i.e., surface burst) 

will result in large quantities of earth and/or water being thermally vaporized and drawn 

up into a radioactive cloud. Much of this material may be blasted into the atmosphere and 

subsequently return to earth as fallout. This material becomes radioactive from either 

neutron activation or from condensing together with various radioactive isotopes. In 

highly contaminated areas, fallout can cause potentially lethal external radiation 

exposure, as well as provide a serious internal hazard from the inhalation or ingestion of 

radioactive materials, such as milk (see Figure 6.2). 

A surface burst over the ground produces particles that range in size from submicron to 

several millimeters in diameter. The finer particles rise into the stratosphere and may be 

dispersed as worldwide fallout. The larger particles settle to earth within 24 hours as local 

radioactive fallout. The heaviest fallout usually occurs in the first 4 hours. In contrast, 

bursts over water are characterized by lighter and smaller particles, producing a smaller 

volume of fallout that extends over a larger area. These particles consist mostly of sea 

salts and water, which may produce a “cloud seeding” effect that results in areas of high 

local fallout as radioactive materials are washed out of the air. 

The primary method of fallout protection is initial sheltering, with rapid evacuation from 

the contaminated area until the risk has been eliminated through decay and/or 

remediation. In general, it is very difficult to accurately predict the rate of radioactive 

decay for fallout. Thus, relevant decisions should be based on actual radiological survey 

data. The 7:10 rule can be used to estimate residual radiation decay after all fallout is on 

the ground and the dose rate is beginning to measurably decrease. 

Radiological Dispersal Devices (Dirty Bombs)

A radiological dispersal device (RDD) is designed to spread radioactive material through 

detonation of conventional explosives or other (non-nuclear) means. These “dirty bombs” 

blast radioactive material into the area around the explosion, exposing people and 

buildings. The purpose of a dirty bomb is to frighten people and make buildings or land 

unusable for a long period of time. 

An RDD is a weapon of “mass disruption” more than a weapon of mass destruction. 

However, an RDD can produce external contamination, an exposure hazard, and a risk of 

internal contamination (via inhalation, ingestion, or wounds) if basic safety and hygiene 

precautions are not followed. An RDD also may pose a radiation injury risk in the event 

that a strong source (e.g., Cs-137 or Co-60) is kept relatively concentrated. In this 

situation, the RDD acts as a high-intensity sealed gamma source. 

The principal use of an RDD is to cause fear and to disrupt infrastructure. Use of an RDD 

also tends to generate panic and social and economic disruption from the physical and 
146

psychological impacts of the attack. The severity of the psychological effects depends in 

part on the type of RDD material and the method of deployment. Mass psychosomatic 

symptoms resulting from an unrealistic fear of the effects of radioactive material could 

place unnecessary strain on the medical system, through medical screening of large 

numbers of anxious individuals. This would add to the chaos of identifying truly exposed 

cases, also mixed in among the existing cases of gastrointestinal, dermatologic, and 

respiratory illness that are prevalent in any population at baseline. 

In the event an RDD is deployed, everything possible should be done to contain panic. It 

is very important to reassure the public that all necessary steps are being taken to 

safeguard their health and well being. This allows appropriate authorities to methodically 

contain and manage the incident in an atmosphere free of public interference. Public 

perception that appropriate treatment is not being provided, particularly for children and 

other vulnerable individuals, could markedly increase the psychological impact of the 

event. Medical authorities also need to manage the flow of casualties through proper 

layout and use of casualty reception stations, decontamination areas, and patient 

assessment and triage procedures. 

Medical and Industrial Sources of Radiation

Radioactive materials used in medical or industrial settings can produce irradiation or 

contamination from accidental or intentional misuse. Irradiation and contamination are 

significantly different problems—a person can be irradiated from a distance without 

being contaminated by radioactive material. Radiological contamination is an issue 

because of the close proximity of the radionuclide to tissue, whether the contamination 

lies against the skin (external) or is inside the body (internal). 

Powerful industrial radiography sealed sources used in the nondestructive testing of oil 

and water pipelines have caused severe exposures. Their bright stainless steel casings are 

eye-catching when the sources are accidentally left behind, and they have been stolen 

when positive control of the source was lost. They are a potential terrorist weapon and 

could present a serious localized radiation threat. 

Another important medical/industrial source is Cs-137, which is an important decay 

product resulting from the fission of uranium and plutonium fuels. This isotope is used in 

both industrial sealed-gamma sources as well as medical therapeutic sealed sources. 

Cesium (Cs) is an alkaline metal that is metabolized much like potassium and excreted 

through the kidneys. It has a radioactive half-life of 30 years but a biological half-time in 

adults ranging from 68 to 165 days (average 109 days). The biological half-time is 

shorter in children, ranging from 12 days in infants to 57 days in older children. It is also 

shorter in women (84 ± 27days) than in men. 

An example of the potential danger from an uncontrolled Cs-137 source occurred in 

1987. An abandoned radiotherapy sealed source containing 1400 Curies (Ci) of Cs-137 

powder was opened by looters in Goiania, Brazil. About 250 people were subsequently 

exposed. The victims included children who rubbed the glowing powder on their bodies 

and, in at least one case, ingested it. Resulting radiation doses were as high as 10 Sv 
147

(1000 rem), resulting in four fatalities from acute radiation sickness (ARS). In this case, 

the Cs-137 had the exposures characteristic of both a sealed source (producing ARS) and 

an RDD causing both external and internal contamination. An estimated 120,000 

concerned people had to be screened for possible contamination, with incident 

management costs in the millions of dollars. 

Nuclear Power Plants

The United States has 104 nuclear reactors licensed to provide electric power, as well as 

36 reactors licensed for other uses. The U.S. Nuclear Regulatory Commission (NRC) has 

stringent physical protection requirements against sabotage, which cover both plant 

design and security protection features. Unlike the design of some foreign reactors, 

designs for power reactors operating in the United States incorporate a layered system of 

physical shields and walls, including a potentially pressurized containment vessel. 

Consequently, there have been relatively few mishaps involving American-designed 

power reactors. 

The primary down-wind hazard from destruction or sabotage of a nuclear reactor is the 

venting of radioactive iodine gas. Power reactors cannot detonate like a nuclear bomb, 

because reactor fuel does not contain the highly enriched uranium needed for detonation. 

The only significant U.S. catastrophic reactor failure occurred in March 1979, at the 

Three Mile Island (TMI) nuclear power facility in Pennsylvania. At that time, one of the 

TMI reactors experienced overheating and a meltdown of a portion of its fuel rods. This 

event resulted in a small release of radioactive gas to the environment, primarily Iodine131. The radiation produced negligible doses to people residing near the plant (estimated 

maximum dose of 0.001 Sievert [Sv] [100 mrem]), which is equivalent to a routine chest 

radiograph). There has been no evidence to date of public injury resulting from the small 

amount of nuclear material that was vented as a result of this incident. 

Pediatricians may be asked about the safety of consuming milk after a reactor accident. 

Iodine-131 fallout on vegetation has an effective half-life of about 5 days (combination of 

radioactive decay half-life [8 days] and vegetation half-life). An infant consuming 1 L of 

milk per day contaminated with 1 microCurie (μCi)/L would receive a total cumulative 

dose to the thyroid of about 16 rem. Therefore, locally produced milk, fruit, and 

vegetables should be declared fit for consumption only after clearance by appropriatelytrained health inspectors. Emergency reference doses of 0.25 μCi/L peak level in milk 

and 1.5 μCi/m2

 on pasture can be used to guide consumption (exposure) 

countermeasures. (See Medical Treatment section later in this chapter for information on 

radioactive iodine and thyroid issues.) 

Historical Overview of Radiation Injury 

Radiation in the form of “x-rays” was discovered in 1895 by the German physicist 

Wilhelm Roentgen. Radioactivity in ore was discovered by Antoine Henri Becquerel in 

1898. Within a few years of discovery, ionizing radiation was used for a wide variety of 

medical diagnostic and treatment purposes. Radiation was found to be an extremely 
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useful modality for medical imaging and an effective means for treating a variety of 

conditions from acne to malignancies. However, some of the side effects of radiation 

became known within a few years. Some early radiologists developed radiation skin 

injury and leukemia from their exposure to ionizing radiation. 

Since 1940, there have been over 300 significant radiation accidents in the United States 

alone. These include both medical and industrial errors, as well as accidents involving the 

production and storage of nuclear weapons. Some of the most significant worldwide 

events associated with radiation injury are described below. 

Hiroshima and Nagasaki, Japan — 1945

The atomic bomb blasts over Hiroshima and Nagasaki in 1945 during World War II 

resulted in massive firestorms that obliterated much of the city. They also provided 

information on the medical effects of uncontrolled ionizing radiation over a wide dose 

range among those casualties who initially survived the blast and firestorm. The bomb 

detonated over Hiroshima was equivalent to 15,000 tons (15 KT) of TNT, while the 

Nagasaki weapon was equivalent to 22 KT of TNT. 

It has been estimated that 50% of those exposed to a 2.7–3.1 Gray (Gy) bone marrow 

dose died within 60 days from their radiation exposure, as little medical assistance was 

available. Radioactive fallout was very limited, because both of the detonations were 

airbursts, in which the actual fireball does not reach the ground. The estimates of 

maximum dose due to fallout are 1–3 centigray (cGy) in Hiroshima and 20–40 cGy in 

Nagasaki. 

The principal effects of radiation in unborn infants in Hiroshima and Nagasaki were 

small head size (microcephaly) and mental retardation. Of the 1,600 children exposed 

before birth who were followed, 30 were found to have severe mental retardation. Those 

with severe mental retardation were noted to have received radiation exposure between 8 

weeks and 25 weeks gestation. The most sensitive time of the gestational period was 

found to be 8–15 weeks after conception. 

Ionizing radiation is a relatively weak carcinogen. Among 86,000 atomic-bomb survivors 

at Hiroshima and Nagasaki followed from 1950 to 1990, there were 7,578 deaths from 

solid cancer (versus 7,244 expected) and 249 deaths from leukemia (versus 162 

expected), representing 421 additional deaths from cancer. The minimum elapsed time 

between radiation exposure and clinical disease was 2–3 years for leukemia, 3–4 years 

for bone cancer, 4–5 years for thyroid cancer, and 10 years for other solid tumors. 

Mayak, Russia, Former Soviet Union — 1948-1990

The Mayak Production Association (Mayak) is an industrial complex in the Southern 

Urals of Russia, where the former Soviet Union produced tons of plutonium for nuclear 

weapons. Between 1948 and 1956, radioactive waste was poured directly into the Techa 

River, which was the source of drinking water for many villages. It is reported that 

124,000 people were exposed to medium and high levels of radiation. In 1957, one of the 
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cooling systems at Mayak exploded, and more than half the amount of radioactive waste 

released at Chernobyl went into the atmosphere. Another incident occurred after a 

reservoir for waste storage evaporated during a dry hot summer. Windstorms then carried 

600,000 curies of radioactive dust over 2,700 square kilometers. According to one source, 

the radiation accidents and radioactive discharge at Mayak killed thousands and made 

many more ill. The implications for children who were living in this area are enormous, 

although health data for this population are not readily available. 

Marshall Islands — 1954

Fallout played a large role in the Marshall Islands after a 1954 nuclear weapons test on 

Bikini Island caused fallout on nearby islands, resulting in significant health effects in 

children. Acute effects included skin injuries from beta radiation (so-called “beta burns”), 

especially of the feet. The most heavily exposed were the 64 people of Rongelap Island, 

who were exposed to 190 cGy of external radiation plus 1000–5000 cGy to the thyroid 

from radioactive iodine. Of 32 individuals who were younger than 20 years old when 

exposed to the radioactive fallout, 4 developed thyroid cancer and 1 developed leukemia. 

Two individuals who were younger than 1 year old at exposure developed myxedema and 

short stature. 

Three Mile Island, PA — 1979

On March 28, 1979, a nuclear power plant at Three Mile Island (TMI), PA, had a near 

meltdown (overheating of the fuel rods and a release of radioactive material). The 

accident produced negligible doses among people living nearby, with a maximum dose of 

0.001 Sievert (Sv) (100 mrem) to the community. Immediate administration of potassium 

iodide (KI) was recommended for those living near TMI, but this drug was not available. 

There were no biological effects from the exposure, although significant psychological 

sequelae occurred. 

Chernobyl, Ukraine, Former Soviet Union — 1986 

In April 1986, a power plant in Chernobyl (aka Chornobyl), Ukraine, had a mishap that 

produced a meltdown and hydrogen gas explosion within the reactor core. The area 

around the reactor was heavily contaminated with plutonium, cesium, and radioactive 

iodine because there was no containment vessel designed into the facility. An estimated 

120 million curies (Ci) of radioactive material was released, contaminating more than 

21,000 square kilometers of land. The greatest areas of fallout occurred in Ukraine, 

Belarus, and the Russian Federation. Approximately 135,000 people were permanently 

evacuated. 

Almost 17 million people, including 2.5 million children younger than age 5, were 

exposed to excess radiation. The first delayed health effects were noted 4 years after 

exposure, with a sharp increase in the occurrence of thyroid cancers in children and 

adolescents, especially among those younger than 4 years at the time of the accident. As 

of 2002, there were more than 2,000 excess cases of childhood thyroid cancer in the 
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exposed population. A large area remains uninhabitable because of environmental 

contamination that exceeds the legally allowable limits. 

Goiania, Brazil — 1987

An abandoned radiation therapy facility in Goiania, Brazil, was looted on September 13, 

1987. The looters took a canister containing 1,400 Ci of radioactive Cs-137, which was 

subsequently opened and distributed to a junkyard owner and several families. Children 

played with the material, rubbing it on their bodies so that they glowed in the dark. 

As word of this event spread, thousands of people became anxious about their possible 

exposure. A stadium was used to screen self-referred potential casualties. Approximately 

112,000 people were evaluated, and 249 individuals were found to have either external or 

internal exposure. Radiation doses were determined to be as high as 10 Sievert (1,000 

rem) using cytogenetic techniques (see Radiation Biology and Dosimetry later in this 

chapter). Twenty individuals needed hospitalization, and four died of acute radiation 

sickness. Victims developed radiation-associated illnesses that ranged from significant 

skin irradiation injury to acute radiation sickness and long-term health problems. 

Treatment for victims with significant exposure included Prussian Blue, which binds 

cesium and helps eliminate it from the body, and granulocyte macrophage colony 

stimulating factor (GM-CSF), which stimulates white blood cell production for victims 

with radiation-induced neutropenia. Mitigation efforts required the removal of 6,000 tons 

of dirt, furniture, clothing, and other materials. 

Radiological Dispersal Devices (Dirty Bombs) 

Terrorists are clearly interested in obtaining RDDs, although a dirty bomb has not yet 

been exploded. Some incidents involving RDDs are described below. 

• November 1995: Chechen rebels in Moscow, Russia, informed a Russian 

television station that they had buried a cache of radiological materials in a park. 

Authorities found a partially buried source of cesium. 

• March 1998, Greensboro, NC: 19 tubes of Cs-137 were stolen from a hospital. 

• December 1998, Argun, Chechnya: A container filled with radioactive material 

was found attached to an explosive mine near a railway line. 

• June 2002, Chicago, IL: An American citizen was arrested on suspicion of 

planning to build and detonate a dirty bomb in an American city. 

• January 2003, Herat, Afghanistan: British intelligence agents reported that Al 

Qaeda had succeeded in constructing a small dirty bomb. 

Other Radiation Uses and Injuries 

Prior to the 1960s, ionizing radiation was deemed nearly innocuous and was often 

believed to be beneficial. Individual exposures to low-level radiation commonly occurred 

from cosmetics, luminous paints, medical and dental x-ray machines, and gadgets for 

fitting shoes in retail stores. Fluoroscopy was widely used, as in the routine monthly wellbaby visits of at least one large pediatric practice, and to shrink the thymus gland in other 
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pediatric practices. This put infants at risk of thyroid cancer years later. Radium-224 was 

given intravenously to treat tuberculosis of the bone, resulting in an excess incidence of 

bone malignancies. Thorotrast® was also used as an intravenous radiographic contrast 

medium in Europe, Japan, and the United States, producing excess malignancies of the 

liver, bile ducts, spleen, brain, and bone in all age groups. Children and adults were also 

subjected to radiation exposure as part of experimental research in people that would not 

have met today’s ethical standards. 

In 1956, the U.S. National Academy of Sciences—National Research Council and the 

U.K. Medical Research Council published similar conclusions about the potential hazards 

and the late effects of radiation. Since that time, the uses of ionizing radiation have come 

under increasing scrutiny and regulation. 

Physical Principles of Ionizing Radiation 

Atomic Structure 

Atoms have two distinct parts that are made up of three main particles. Protons and 

neutrons are found in the nucleus, which is the tiny, dense center that contains almost the 

entire mass of the atom. Electrons surround the nucleus, moving in paths called orbitals. 

Protons. Protons have a mass of about 1.7 × 10-27 kg, which is assigned the value of 1 

atomic mass unit (AMU). Protons carry an electrical charge, which is assigned a value of 

+1. The density of an atom is determined by the number of protons in the nucleus. For 

example, uranium has 92 protons, making it much denser than hydrogen, which has only 

one proton. 

Neutrons. Neutrons also have a mass of about 1 AMU, differing from the proton by 

<0.14%. Unlike the proton, the neutron has no charge. While the number of protons 

determines the density/identity of an atom, the number of neutrons can vary. Atoms with 

the same number of protons but different numbers or neutrons are called isotopes of each 

other. For example, 235U and 237U are two different isotopes of uranium. 

Electrons. The mass of an electron is about 1/1800th of an AMU, or about 9 × 10-31 kg. 

The electron charge is –1. In a neutral atom, the number of electrons and protons match, 

with their charges canceling each other out. An ion is an atom that has either gained or 

lost electrons and hence carries a net negative or positive charge, respectively. 

Stability and Radiation 

Several factors can influence the stability of an element, leading to the potential for 

radioactivity. An electron or nucleus can become excited by radiation, causing it to 

become unstable and to give up energy in the form of photons. For example, technetium99m (99mTc) is an unstable (i.e., metastable) form of technetium that is used in medical 

settings. When 99mTc goes from an excited state to a non-excited state, it gives off a 

photon and becomes 99Tc. 
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The ratio of protons to neutrons in the nucleus is also important to stability. The lighter 

elements are usually stable, with a ratio of about 1:1. As elements get heavier, the ratio 

reaches about 2:3, increasing the chances of instability. Whenever the ratio shifts from a 

stable configuration to an unstable one (for whatever reason), the nucleus attempts to 

regain stability by emitting radiation. 

When an unstable atom emits radiation, it is said to decay. The half-life of a radionuclide 

is the average amount of time that it takes for half of the atoms in a sample to decay. 

Half-lives can vary from fractions of a second to millions of years. When an atom decays, 

it does not necessarily become stable. Rather, it is quite common for decay to be a series 

process, in which a given atom might decay dozens of times in different ways before 

becoming stable. Radon gas is a common example of this, with a very long decay chain. 

Radioactive decay can be associated with several different types of radiation. 

Photons (x-rays and gamma rays). Photons are (nearly) massless “bundles” of energy. 

The energy determines the wavelength, which can be classified into various categories for 

convenience. Radio waves, visible light, ultraviolet light, x-rays, and gamma rays are all 

photons of various energies. X-rays and gamma rays differ only in their origin. An 

electron losing energy yields an x-ray photon, while loss of energy from a nucleus 

exciting produces a gamma photon. X-rays and gamma rays with the same energy are 

otherwise identical. 

Gamma or x-rays are often released to remove residual energy that remains after other 

forms of decay (e.g., alpha or beta particles). For example, 60Co, a common industrial 

and medical radionuclide, decays by beta emission, while simultaneously giving off two 

powerful gamma rays during its transformation into the stable element 60Ni. 

Beta particles (electrons). One of the ways that an unstable nucleus can adjust its 

proton:neutron ratio is to emit an electron, effectively transforming a neutron into a 

proton and an electron. This electron is then ejected from the nucleus as a “beta particle,” 

which in all respects is identical to any other electron. Beta particles can cause damage to 

tissue directly or through secondary processes. 

Bremstrahlung. When an electron decelerates (or turns), it loses energy in the form of 

photons, which is a process called “bremstrahlung.” The quicker the deceleration, the 

greater the energy imparted to the photons. Electron paths tend to curve near heavy 

nuclei, so that electrons lose energy when interacting with dense matter. This is one of 

the reasons that lightweight materials are preferred as protection against beta radiation. 

For example, in old televisions, leaded glass was used for the picture tube. When the 

electrons from the electron guns hit the back of the screen, they produced bremstrahlung 

that were roughly equivalent to weak x-rays. Newer televisions are designed to produce 

minimal bremstrahlung. 

Positrons. Some nuclei (e.g., 12N or 124I) emit an anti-electron or positron, converting a 

proton to a neutron. The ejected positron is identical to an electron but has a +1 charge 

rather than a –1 charge. Because it is an anti-particle to an electron, the two will 

annihilate when they interact. The annihilation completely converts both particles to 
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energy, releasing two photons of exactly 0.511 MeV. Positron emission and the detection 

of the annihilation photons form the basis of positron emission tomography (PET), a 

fairly common medical imaging procedure. 

Alpha particles. Alpha particles are stable helium nuclei (two protons and two neutrons) 

ejected mainly (but not exclusively) by heavy nuclei during adjustment of improper 

proton:neutron ratios. The two protons and two neutrons are emitted, often with 

considerable energy, and the particle has a +2 charge. Alpha particles are the most 

massive and highly charged of the common types of radiation. Both of these properties 

make them potentially very damaging but also very easy to shield. 

Neutrons. Neutrons are rarely emitted as decay products. Rather, they are more 

commonly emitted as by-products of nuclear fission or fusion. As neutrons have no 

charge, they are able to interact readily with the nucleus of an atom, possibly being 

absorbed into it. This affects the proton:neutron ratio and can lead to the atom becoming 

radioactive or otherwise unstable. 

Radiation Interactions 

Radioactive particles can interact in many ways, leading to potentially hazardous 

processes and by-products. 

Electron excitation. The simplest way for a radiation particle (including a photon) to 

interact with a target atom is for it to impart some energy to the electrons of the atom. If 

enough energy is imparted, the electron will be knocked out, and an ion will be formed. If 

the energy is not sufficient to form an ion, the electron will merely be excited, giving 

back this extra energy in the form of a photon. This photon can be in the form of visible 

light (e.g., the phosphors in a television) or as a more hazardous x-ray. 

Ionization. The primary radiation effect of medical concern is ionization, in which an 

electron is completely removed from an atom. Ionization can directly or indirectly break 

chemical bonds, leading to tissue damage. Furthermore, if an electron is removed from 

the inner shell of an atom, the cascade of electrons dropping to fill the gap may produce a 

series of x-rays, which can carry the damage beyond the original track of the incident 

particle. Similarly, if the electron that was removed has sufficient energy, it may induce 

its own ionization events, again carrying the effects away from the original track. These 

follow-on events are called secondary radiation. 

Nuclear excitation. If an incident particle interacts with the nucleus of an atom, several 

outcomes are possible. Nuclear fission or fusion is possible, although the simplest 

outcome is excitation. As noted above, when a nucleus goes from an excited to an 

unexcited state, it will usually emit a photon in the form of a gamma ray.

Nuclear fission. When certain heavy nuclei become unstable with respect to their 

proton:neutron ratio, they can undergo a splitting process termed fission. Typically, this 

process is induced by the absorption of a neutron into the nucleus of the target atom. The 

nucleus then breaks into two or more fission fragments, including lighter elements, 

subatomic particles, and energy. 
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The subatomic particles that can be released during fission include more neutrons, which 

can in turn induce new fissions if the conditions are appropriate. This latter process is 

called a chain reaction and is the heart of nuclear reactors and weapons. Uranium, 

thorium, and plutonium have isotopes that can undergo fission. A large number of 

different possible fission fragments can be created, and many of them are themselves 

unstable and hence radioactive. Some of the most common and hazardous byproducts of 

fission include 131I, 137Cs, and 90Sr. 

Activation. Neutrons lack a charge and can therefore readily reach the nucleus of an 

atom. If the neutron is absorbed by the nucleus, the new nucleus may have an unstable 

proton:neutron ratio as well as excess energy. This new configuration may or may not be 

stable. If it is not stable, it will eventually decay. In other words, the new nucleus may be 

radioactive. This process of creating a new radioactive radionuclide is called activation 

and is mainly associated with nuclear reactors and nuclear detonations. 

Secondary radiation. The radiation “particle” that initially enters a volume/space is 

considered primary radiation. Any electrons or photons (or anything else) liberated with 

enough energy to produce new ionizations are considered secondary radiation. Secondary 

radiation does not necessarily travel in the same direction as the primary energy, leading 

to secondary damage in new spaces. Furthermore, the secondary radiation is not 

necessarily of the same type as the primary radiation, leading to different types of effects. 

For example, a neutron will liberate electrons and numerous gamma and x-rays as it 

decelerates. Very high energy radiation (e.g., cosmic radiation) travels quickly through a 

given space (e.g., human tissue), producing only a small number of interactions. 

However, each of these interactions can transfer large amounts of energy as secondary 

radiation, which can then distribute throughout the given space. 

Radiation Damage and Protection 

Linear energy transfer (LET). As a radiation “particle” passes through matter, it loses 

energy through the various mechanisms discussed above. The rate at which it loses that 

energy is the LET, which is measured in energy per unit distance (e.g., MeV per micron). 

A particle with high LET transfers energy very quickly, slowing down rapidly and 

depositing energy on a dense “track” in the target volume. A particle with low LET 

interacts much less often and slows down only gradually. For example, photons are low 

LET radiation because they have no mass or charge, while alpha particles are high-LET 

radiation due their large mass and +2 charge. Beta particles and neutrons are 

intermediate, with neutrons having the higher LET of the two. 

Penetration and radiation shielding. The more rapidly a given radiation particle loses 

energy (high LET), the more quickly and easily it is stopped. Therefore, the LET and the 

degree to which a particle is considered penetrating are inversely related—i.e., the higher 

the LET, the less penetrating the particle. For example, an alpha particle deposits very 

large amounts of energy in a very short distance, which can result in considerable damage 

to living cells. However, alpha particles cannot penetrate even the thickness of a piece of 

paper or the dead layer of skin on your body. Therefore, alpha particles generally do not 
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need to be shielded, although the alpha-emitting materials should be prevented from 

entering the airways (e.g., with filtering masks) to protect delicate lung tissue. On the 

other hand, high-energy gamma rays need to be shielded with very thick lead or concrete 

because they interact so little and penetrate so deeply. As noted earlier, lightweight 

materials such as Plexiglas® or aluminum are preferred as shielding for beta particles to 

reduce bremstrahlung. 

Radiation Units 

The measurement of radiation required the creation of new units to describe various 

aspects that were new to science. The major units used to describe radiation and its 

effects are discussed below. This discussion will include both the older American 

nomenclature and the newer nomenclature under the System International (SI), because 

both are still widely used. 

Radioactivity; curie/becquerel. The units used to describe radioactivity are the curie 

and the becquerel (SI). Activity represents the number of radioactive decays that take 

place in 1 second. One curie (Ci) is the number of decays that occur in 1 gram of pure 

radium-226 in 1 second (i.e., 3.7 × 1010 disintegrations/second). The becquerel (Bq) is 

one disintegration per second, so that there are 3.7 × 1010 Bq per Ci. 

The specific activity (activity per unit of mass) varies from radionuclide to radionuclide, 

so that the same weight of different materials does not necessary have the same level of 

radioactivity. For example, 1 curie of 226Ra weighs about 1 gram, as noted above, while 

1 Ci of 232Th weighs just under 10 million grams (ten metric tons). 

Exposure; roentgen. Formally, the roentgen (R) is a unit of electrical charge liberated by 

photons per kilogram of air. This unit is specific to x- and gamma rays and cannot be 

applied to any other form of radiation or to any other medium. It does not have an SI 

equivalent. 

Absorbed dose; Rad/Gray. “Absorbed dose” is the amount of energy absorbed per unit 

of mass, which applies to any type of radiation in any type of matter. The Rad (radiation 

absorbed dose) is defined as 100 erg per gram. The SI equivalent is the Gray (Gy), 

defined as 1 joule per kilogram. One Gy is equivalent to approximately 100 Rad. Often 

the unit of centiGray (cGy) is used because it is equal to 1 Rad. 

Effective dose. Absorbed dose is a very useful concept, but it does not account for the 

different biological effects of different types of radiation on different types of tissues. 

Two artificial weighting factors are used to represent the impact of these differences in 

“effective dose.” 

Relative biological effectiveness. This weighting factor accounts for how strongly a given 

radiation interacts with the particular mix of elements that makes up the human body. 

This factor does not account for shielding and is partially dependent on energy. Note that 

this weighting factor seems to match up reasonably well with the discussion of LET. For 
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example, alpha particles and certain neutrons have the greatest effectiveness, while 

photons and beta particles have the lowest effectiveness (see Table 6.1). 

Tissue weighting factors. Different tissues in the human body have differing sensitivities 

to radiation. Nerve tissue, for example, is fairly insensitive to radiation, while the lining 

of the GI tract is very sensitive. These weighting factors apply only to cancer risk and 

cannot be correctly applied to other risks. The sum of all the weighting factors is one. A 

whole body exposure receives a weighting factor of one, while a partial body exposure 

would receive the appropriate fraction. 

Dose equivalent. The dose equivalent is the product of absorbed dose and the various 

weighting factors in units of energy per unit mass. The traditional American unit is the 

REM, which stands for roentgen equivalent man. The REM is defined as 100 ergs per 

gram, just like the Rad. The SI equivalent is the Sievert (Sv), which is defined as 1 joule 

per kilogram and is equal to 100 REM. The absorbed dose and the dose equivalent are 

not the same. The former is a measurable physical quantity, while the latter is the product 

of consensus weighting factors with a special focus on biological effects. 

Radiation Background Exposure 

Americans typically receive about 360 millirem of background radiation per year. Of this, 

approximately 295 millirem is considered natural (cosmic rays, radon, etc.), and the other 

65 millirem is considered manmade (x-rays, etc). The main sources of radiation exposure 

are discussed below. 

Natural exposures. There are four sources of natural exposure: radon, cosmic radiation, 

internal radiation, and terrestrial exposure. 

Radon. Radon gas is a natural by-product of the decay of uranium and thorium in rocks 

and soil. Remember that decay can occur in chains of radionuclides. Radon is part of a 

long chain. Because it is a gas, it “percolates” up through the soil and into the 

atmosphere. If it happens to come up under a building, it can become trapped and 

accumulate in the basement or first floor, leading to sometimes appreciable radiation 

doses to the occupants. Radon decays eight times before becoming stable, and many of 

the decays produce very high-energy alpha particles. Because radon is a gas, it can enter 

the lungs where there is no dead layer of skin to block the alpha particles. Radon and its 

daughter products account for about 200 millirem of exposure per person per year. 

Cosmic radiation. Cosmic radiation, as the name implies, originates from space, either 

from the sun or from extra-solar sources like supernovae and quasars. Much cosmic 

radiation is of exceedingly high energy and does not interact at all with the human body. 

Much more is blocked either by the solar atmosphere or by the earth’s atmosphere. The 

annual cosmic radiation dose at sea level is about 27 millirem, while people living or 

working at higher elevations (e.g., airline pilots) receive more. 

Internal radiation. A number of materials are present in food, water, etc., that expose us 

to small doses of radiation. Most commonly considered is 40K, a common, naturally 
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radioactive isotope of potassium. Bananas and some nuts contain elevated levels of 

radioactivity from this radionuclide. The total dose due to naturally occurring radioactive 

material incorporated into the body is about 39 millirem per year. 

Terrestrial exposure. The earth itself contains a number of radioactive elements. Uranium 

and potassium have already been mentioned. The annual dose from external radiation by 

rocks and soils is about 28 millirem. 

Manmade exposures. Manmade exposures may occur through medical procedures, 

consumer products, and/or fallout/nuclear power fallout and waste. 

Medical. By far the largest manmade exposure is from medical procedures, such as 

radiology, radiation therapy, and so forth. For example, the ubiquitous chest x-ray 

exposes a patient to about 8 millirem. The average annual dose from all medical 

procedures is about 53 millirem. 

Consumer products. A variety of small radiation doses come from consumer products. 

Cathode ray tubes, radium dials, airport x-rays, etc., all contribute to the 10 millirem 

annual dose. 

Fallout and nuclear power. Combined, fallout from weapons testing and waste from the 

nuclear power industry produce an annual dose of <1 millirem. 

Radiation Biology and Dosimetry 

Radiation Biology 

Ionizing radiation interacts with biological systems through discrete energy deposition 

events referred to as spurs, blobs, and tracks. This can occur by direct interaction with 

cellular and tissue component targets or through the indirect production of free radicals 

(e.g., hydroxyl radicals, etc.) or other harmful molecules. Radiation-induced damage to 

DNA and the cellular capacity to repair DNA/chromosome damage have a major 

influence on the deleterious cellular effects. Additional cellular-specific parameters (e.g., 

oxygen tension, cell-cycle distribution, proliferative status or rate of cell division, extent 

of cell differentiation, etc.) and radiation-specific parameters (dose, type of radiation, 

dose rate, etc.) can modulate the degree of cellular and tissue injury. 

The consequences of radiation exposure to cells and tissues are highly variable, including 

both acute effects (e.g., delay in cell division, cell death) and late effects (e.g., cataracts, 

mutagenesis, carcinogenesis, etc.). Tissues vary in sensitivity to radiation; various tissues 

in order of most to least sensitive are lymphoid, gastrointestinal, reproductive, dermal, 

bone marrow, and nervous system. The response to radiation of self-renewing tissues is 

dynamic and influenced by tissue-specific transit times. Transit time includes both the 

time course for stem-cell differentiation and for the lifespan of mature, functioning cells. 
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Biodosimetry 

Effective medical management for suspected radiation overexposure necessitates the 

recording of dynamic medical data and the measurement of level of injury using 

appropriate radiation bioassays. Biodosimetric assays can provide diagnostic information 

to the attending physician, as well as an estimate of the dose for personnel radiation 

protection records. Radiation biodosimetry usually encompasses multiple parameters, 

including the following: 

• Radioactivity measurements and monitoring of the exposed individual. 

• Observation and recording of prodromal signs/symptoms and erythema. 

• Complete blood counts with WBC differential. 

• Chromosome-aberration cytogenetic bioassay, using the “gold standard” dicentric 

assay for dose assessment. 

• Bioassay sampling (if appropriate) to determine radioactivity contamination. 

• Other available approaches. 

The biological response to an absorbed dose of ionizing radiation should be assessed to 

predict the medical consequences. Physical dosimeters (e.g., film badges) may 

misrepresent the actual radiation dose and may not be available in a radiological accident 

or terrorism incident. Multiparameter dose assessments represent the current approach on 

which to base medical treatment and management decisions. Radiation syndromes are 

generally characterized into three phases: prodromal, manifest, and latent. The early or 

prodromal signs and symptoms will be emphasized later in this chapter. 

Medical recording. Radiation-induced signs, symptoms, and erythema should be 

recorded during the course of medical management for radiation casualties to help triage 

patients and to guide medical management of casualties. Default standard mechanisms 

and procedures include recording of medical data by the respective medical responders 

and health care providers. 

Additional medical guidance available to first responders and health care providers 

includes the following: 

• International Atomic Energy Agency’s (IAEA) Generic Procedures for Medical 

Response during Nuclear and Radiological Emergency (http://wwwpub.iaea.org/MTCD/publications/PDF/EPR-MEDICAL-2005_web.pdf). 

• Armed Forces Radiobiology Research Institute’s (AFRRI) radiation casualty 

management software application (i.e., Biodosimetry Assessment Tool or BAT), 

which was developed for radiation casualty management. It is distributed to 

authorized users who have access to the AFRRI Web site. 

The BAT software application equips health care providers with diagnostic information 

(e.g., clinical signs and symptoms, physical dosimetry, etc.) relevant to the management 

of radiation casualties. Designed primarily for prompt use after a radiation incident, the 

program facilitates the collection, integration, and archiving of data obtained from 

exposed individuals. Data collected in templates are compared with established radiation 

dose responses obtained from the literature to provide multiparameter dose assessments. 
159

An integrated, interactive human body map permits convenient documentation of the 

location of a personnel dosimeter (if worn by the individual at the time of exposure), 

radiation-induced erythema, and radioactivity detected by an appropriate radiation 

detection device. 

Radioactivity counting and bioassay. In the case of suspected internal radioactive 

contamination, the following processes are typically performed concurrently: 

• Decontamination to minimize the local radiation dose to the potential wound site. 

• Removal and collection of metallic (or other) fragments for isotope identification. 

• Biological sample collection for determination of committed dose. 

Monitoring/sampling of wounds (i.e., wound swabs or wound cleansing wipes), body 

orifices (i.e., nasal swabs, oral swabs), and skin surfaces (i.e., wipes) should be 

performed for confirmation of internal contamination. Although not strictly considered 

biological samples, metal fragments, bandages/dressings, and clothing should be retained 

for isotope identification. 

Biological specimens should also be collected to determine possible internal radionuclide 

deposition. Urinalysis and fecal sample analysis are the primary in vitro methods for 

determining internal dose. Urine is generally a high priority for bioassay, and therefore, 

“spot” urine as well as 24-hour urine specimens should be collected from accident 

victims. 

In the special case of an improvised nuclear device or any event involving nuclear 

fission, there is also a need to collect whole blood specimens for biodosimetry. The blood 

specimens should be labeled, packaged, and shipped to the network of radionuclide 

bioassay laboratories for neutron activation analysis to estimate individual neutron doses 

for the casualties. 

Prodromal signs, symptoms, and erythema. The pattern of biological responses 

associated with acute radiation sickness (ARS) can provide initial diagnostic indices and 

help with triage of potentially exposed individuals. The early clinical responses 

associated with the radiation prodromal phase include the following: 

• Nausea. 

• Vomiting. 

• Headache. 

• Fever. 

• Tachycardia. 

• Fatigue. 

• Weakness. 

• Abdominal pain. 

• Parotid pain. 

• Erythema. 

For the dose-dependent signs and symptoms associated with the prodromal phase of 

whole-body exposure to photon-equivalent radiation, see Table 6.2. An increase in the 
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exposure dose is associated with a parallel increase in both the constellation of prodromal 

signs and symptoms and the percentage of exposed individuals affected. For example, 

only 50% of individuals exposed to 2-Gy acute photon radiation will exhibit emesis. 

Radiation doses above 2 Gy will result in a progressive increase in the percentage of 

individuals who vomit and also express the broad range of prodromal symptoms. 

Hematology. Radiation exposure produces a predictable pattern of changes in bloodforming tissues. A crude estimate of absorbed dose can be obtained by serial 

measurement of peripheral lymphocyte blood counts. Therefore, a CBC with WBC 

differential should be obtained immediately after exposure, three times a day for the next 

2–3 days, and then twice a day for the next 3–6 days. Lymphocyte cell counts and 

lymphocyte depletion kinetics can be used to estimate exposures between 1 and 10 Gy 

photon equivalent dose range. This biodosimeter is useful only for a few days (<10) after 

exposure because of the transient nature of radiation-induced lymphocyte depletion. 

Cytogenetic bioassay. The analysis of chromosomal aberrations, particularly the 

incidence of chromosomes with two centromeres (dicentrics) in peripheral blood 

lymphocyte cultures, is widely used to assess dose after exposure to radiation. Human T 

lymphocytes have a long half-life, and a small proportion survive for decades. The 

frequency of dicentrics after exposure to radiation remains fairly stable for up to a few 

weeks. After acute partial-body exposure, the irradiated lymphocytes rapidly mix with 

unirradiated blood, reaching equilibrium within 24 hours. 

Blood for cytogenetic bioassay should generally be collected within 24 hours of the 

irradiation incident. Peripheral blood (10 mL) from the exposed person is collected in a 

lithium-heparin collection tube, although an EDTA tube can be substituted if necessary. 

The blood must be transported immediately to a cytogenetic laboratory that is familiar 

with biodosimetry according to internationally accepted guidelines. During transport, the 

sample should be chilled with cold packs sufficient to keep the sample cool (4o

C) but not 

frozen. The blood lymphocytes are then isolated and stimulated to grow in culture. Cell 

proliferation is arrested in the first metaphase, and metaphase spreads are observed under 

a microscope. The observed level of dicentrics can then be used to estimate dose by 

comparison with an established dose-response curve. 

High-dose partial-body radiation exposures represent a common clinical scenario after 

accidents. Differences of 10% in absorbed dose can produce clearly observable variations 

in biological response. Hematological recovery in heavily irradiated areas of the body 

will be possible if a sufficient number of stem cells survive in unirradiated or mildly 

irradiated portions of the hematopoietic system. Knowledge of the heterogeneity of the 

absorbed dose is particularly important in making appropriate medical treatment 

decisions for patients exhibiting radiation-induced bone marrow syndrome. Cytokine 

therapy will stimulate proliferation of spared stem cells, but in cases of whole-body stemcell sterility, bone-marrow transplant or alternative therapeutic measures may become 

necessary. In high-dose partial-body exposure scenarios, chromosome damage measured 

in peripheral blood lymphocytes helps determine the absorbed dose. 
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Biodosimetry and Radiological Terrorism 

Effective medical management of radiation casualties after a terrorist incident requires a 

coordinated and adequate biodosimetric assessment for individuals suspected of 

exposure. A Medical Field Card (Figure 6.3) should be kept with the patient and used to 

record early signs and symptoms. This is consistent with an all-hazard approach for 

medical first responders and health care providers. Emphasis should be placed on 

recording the characteristic early signs and symptoms of radiation exposure (Table 6.3). 

Table 6.2 illustrates several of the quantitative multiparameter biodosimetry indices 

(stratified by 100 cGy dose windows from 1 to 10 Gy) that could be used for early 

diagnosis and triage of suspect radiation casualties. 

There are two important issues to consider when collecting appropriate specimens for 

radioactivity counting and bioassay in a mass casualty situation. 

1. A vigorous screening process should be implemented at an assessment center(s). 

This helps determine the most likely candidates for bioassay of internal 

contamination by external counting, using hand-held or portal radiation detectors. 

Effective screening assures that appropriate victims are assayed, while avoiding 

the default decision of assaying everyone. The latter could overwhelm the limited 

resources available for performing the analyses. 

2. Specimens must be shipped to confirmed qualified laboratories. It is imperative to 

have established laboratory standards for bioassay procedures for assessment of 

internal radionuclide deposition, as well as a robust certification process for the 

laboratory network that will be conducting the analyses. The Department of 

Energy (DOE) performs bioassay and dosimetry at a number of sites and also has 

a program (DOE Laboratory Accreditation Program) to certify these laboratories. 

The above laboratories will probably be different from those providing blood cell counts 

and cytogenetic biodosimetry. During the first 3 days of a mass radiological casualty 

situation, each potentially exposed person should have a minimum of five CBCs with 

WBC differentials. To adequately address this requirement, additional assistance (i.e., 

deployable hematology laboratory capacity) will likely be required to supplement local 

medical resources. 

Cytogenetic confirmation (lymphocyte dicentric assay) of clinical triage has been 

proposed to help deal with mass radiological casualties or when there is an urgent need 

for rapid results. Confirmation of clinical triage can generally be accomplished using a 

simplified assay that scores only 20–50 metaphase spreads per subject, as compared with 

a typical analysis of 500–1,000 spreads. However, additional scoring is recommended 

after the initial results are communicated to the physician to resolve potential conflicts in 

dose assessment and to assist physicians considering marrow-stem-cell transfusions to 

mitigate bone marrow ablation caused by high doses. 

Pediatric Issues 

Compared with adults, children have a significantly higher risk of developing cancer 

from radiation exposure. For this reason, pediatricians should be prepared for any special 
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medical needs supporting biodosimetry assessments. There is limited knowledge in the 

available literature about biological dosimetry in pediatric populations. Current models to 

determine committed dose based on internal contamination are generally based on adult 

population parameters. However, the procedures applied to the general population are 

probably applicable to children in most cases. Special containers are required for 

collecting radioactivity counting and bioassay samples from infants and children (e.g., 

pediatric urine collection device). 

With today’s microtechnology, as little as 1 mL of blood can be collected for blood cell 

counts and cytogenetic biodosimetry in children, given their smaller blood volume and 

concerns about blood loss. The kinetic lymphocyte depletion method is preferred over 

single blood lymphocyte counts of dose assessment, given that normal lymphocyte counts 

in children decrease with advancing age. 

The cytogenetic bioassay (dicentrics in metaphase spreads) can also be used in pediatric 

populations, although normal values may need to be adjusted. The consensus background 

frequency of dicentrics is 1 in 1000 metaphase spreads for the healthy adult population. 

Children generally show a lower frequency of dicentrics, and older adults (older than 60 

years) a slightly higher frequency, compared with the normal adult background. There is 

one report in the literature that children younger than 1 year of age may be relatively 

more radiosensitive. This study found that dicentric yields after in vitro irradiation of 

blood from children are higher than in blood from adults exposed to similar radiation 

levels. 

Medical Diagnosis: Acute Radiation Syndrome 

Acute radiation syndrome (ARS) can occur from radiation exposures during peacetime or 

as a result of war or terrorism. A case of ARS can be caused by an accident with a 

military or civilian radioactive source or as a complication of medical treatment. A 

radiation dispersal device (RDD) would probably not result in exposures high enough to 

cause ARS, although it is possible. This section describes ARS as it has occurred since 

the 1940s and as it may occur in the future. 

Acute radiation syndrome is also termed acute radiation sickness or radiation toxicity. It 

is an acute illness that presents as a combination of clinical signs and symptoms. These 

generally occur in stages during the hours to weeks after acute exposure to a high dose of 

penetrating radiation (e.g., ≥0.7 Gy). This syndrome generally occurs after irradiation of 

the whole body (or most of the body), although the signs and symptoms evolve as injury 

to various tissues and organs is expressed. ARS follows a predictable course after a high 

or potentially fatal dose of penetrating radiation (e.g., gamma, neutron, or high energy xrays). ARS is usually associated with prompt exposure or exposure within minutes at a 

high dose rate, although fractionated doses can also induce ARS. 

Pathophysiology 

High doses of ionizing radiation cause depletion of stem cell lines and microvascular 

injury, which lead to the clinical features of ARS. The most radiosensitive cells are 
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primitive/progenitor cells and other rapidly dividing cells, while slower growing and 

more mature cells are generally radio-resistant. The most radiosensitive mammalian cells, 

in decreasing order, include the following: 

• Spermatogonia. 

• Lymphocytes and oocytes. 

• Erythroblasts. 

• Other hematopoietic tissue. 

• Small-intestine crypt cells. 

• Hair follicles. 

All of these cells contain rapidly dividing cell lines. Clinicians are familiar with the 

effects of radiotherapy and chemotherapy on these tissues, as sterility, bone marrow 

damage, diarrhea, and hair loss all involve radiosensitive stem cell lines. With survivable 

radiation doses, some stem cells survive, and their cell lines regenerate. Microvascular 

injury can result in dramatic systemic symptoms and in permanent and irreversible 

damage such as local radiation injury. 

Clinically detectable effects first appear at doses >0.2 Gy (≥20 cGy or 20 rad). These 

effects include decreased sperm count, chromosome abnormalities, and mild bone 

marrow depression. Whole-body radiation doses >0.7 Gy can cause clinical illness. The 

lethal dose 50 (LD50) for penetrating radiation is approximately 3.5 Gy for untreated 

patients and 5 Gy for those receiving full medical treatment. The LD50 is the dose of 

radiation that will kill half the exposed population. 

Clinical Stages 

All health effects from radiation exposure tend to follow a similar clinical pattern that can 

be divided into a series of time-dependent stages: prodrome, latent period, and manifest 

illness. At higher radiation doses, these stages are associated with shorter time of onset, 

more severe signs and symptoms, and decreased survival. However, there is individual 

variation, and symptoms may not occur in all patients. 

Prodrome. The initial stage of prodromal symptoms (prodrome) begins within the first 

few hours to 2 days after exposure. Symptoms include nausea and vomiting, with 

subsequent malaise, fatigue, and weakness. This is a nonspecific clinical response to 

acute radiation exposure caused by the cell membrane and free-radical effects of radiation 

energy, as mediator chemicals such as histamine, interleukins, and cytokines are released. 

Latent period. On recovery from the prodrome, there is usually a latent period during 

which most symptoms subside, although fatigue and weakness may remain. 

Manifest illness. This is the full disease picture that develops from the clinical signs and 

symptoms associated with damage to major organ systems (e.g., blood-forming elements, 

intestine, cardiovascular, CNS). The molecular cause of disease is DNA damage. Death is 

usually caused by sepsis. 
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Syndromes 

ARS is not a single syndrome but rather a series of sub-syndromes, each of which 

evolves over time. The first syndrome involves the hematopoietic system, usually from 

doses as low as 0.7 Gy. The GI system is affected next, followed by the cardiovascular 

system and the CNS. These sub-syndromes are progressive and additive with increasing 

dose, as each organ system is damaged in turn. The cardiovascular and CNS subsyndromes are usually discussed together because both are rapidly lethal, caused by 

microvascular injury, and without effective treatment. 

Hematopoietic sub-syndrome. The hematopoietic system is affected at doses >0.7 Gy. 

Although the dose range has been stated as 1–5 Gy, the hematopoietic system actually 

begins to show damage at doses below 1 Gy, and damage continues at all higher doses. 

The stem cells of all bone marrow cell lines are affected, so that all production of all 

blood cells is reduced or stopped. The clinical severity increases with dose, with 

ancytopenia occurring above about 2 Gy. 

The prodrome begins 3–26 hours after doses of 1 to 5 Gy, lasting 48 hours or less. The 

latent period is mostly asymptomatic, except for possible mild weakness, fatigue, and 

anorexia that lasts 3–4 weeks. Hair loss (which requires about 3 Gy) and weight loss 

appear at about day 14. The manifest illness phase sets in at 3–5 weeks, sooner at higher 

doses. Bone marrow atrophy with pancytopenia (Figure 6.4) can lead to hemorrhage and 

infection, similar to that which occurs in chemotherapy patients. 

Uncomplicated cases can survive with treatment, which includes bone marrow 

resuscitation and prevention of infections and hemorrhage. Marrow irradiated to 3 Gy 

shows depletion of cells, which are replaced with fat. Many remaining cells undergo 

pyknotic death or look grossly abnormal, containing large, bizarre nuclei.

Typical changes in the peripheral blood profile occurs as early as 24 hours after 

irradiation. Figure 6.5 shows the pattern of blood counts over time after 3 Gy of 

exposure. Lymphocyte levels fall immediately on day 1. At about 4 weeks, cell counts 

are at their lowest. The depleted white cells and platelets predispose to hemorrhage and 

overwhelming infection. Treatment is aimed at protecting patients from infection and 

restoring blood-forming elements. 

Gastrointestinal sub-syndrome. This sub-syndrome is also termed radiation enteropathy 

and is seen occasionally in the setting of radiation oncology or among victims of a highdose regional abdominal exposure. Major injury of the GI tract is clinically evident at 

absorbed, whole-body doses of >5 Gy. The prognosis is grave at doses >6 Gy. Doses >8 

Gy are generally lethal. 

The prodrome begins abruptly in 1–4 hours (usually 1–2 hours), can last >48 hours, and 

can be severe. The latent period is 5–7 days, with symptoms of malaise and weakness 

severe enough to be disabling. The clinical course can be stormy during the manifest 

illness phase, with complete paralytic ileus as the mucosa breaks down. This is marked 

by abdominal distention, vomiting, diarrhea, and GI collapse. The damaged mucosa 
165

permits bacterial translocation and sepsis, which is the usual cause of death. If patients 

survive long enough, hematopoietic syndrome will develop concurrently. 

Cardiovascular and CNS sub-syndromes. The radiation dose affecting the 

cardiovascular system and the CNS begins at >20 Gy, with the full syndrome occurring 

above 50 Gy. Such extremely high doses have been rare, such as during nuclear fuel 

handling accidents, in which victims were near a critical mass that suddenly formed 

(“criticality event”). The key pathological insult is acute microvascular injury with 

increased endothelial membrane permeability, especially in the brain, leading to cerebral 

edema and its subsequent clinical effects. The prodrome begins in as little as 5–10 

minutes, with rapid onset of uncontrollable nausea, explosive vomiting and diarrhea, and 

CNS signs that include epileptic seizures and altered mental status. The brief latent period 

lasts several hours to 2 days. During the latent period, victims have generally been lucid, 

even euphoric, with a clear sensorium. However, orthostatic hypotension and weakness 

are often present. The manifest illness phase is marked by rapidly deteriorating CNS 

status and reduced consciousness, with or without epileptic seizures and a measurable 

increase in intracranial pressure. Watery diarrhea, respiratory distress, and uncontrollable 

swings in systemic blood pressure are also common during manifest illness. Coma and 

death from cerebral edema occur in 2–3 days. 

Miscellaneous sub-syndromes. Other radiation-induced clinical sub-syndromes can be 

observed in special cases or severe exposures. These include radiation pneumonitis, as 

well as cutaneous and local injuries. Pulmonary effects often play a major role in patients 

who sustain lethal-dose exposures of >5 Gy, then survive for several weeks with 

hematopoietic and GI sub-syndromes. With high radiation skin doses, there is acute skin 

injury, often termed a radiation burn. This is the result of high doses limited to the skin, 

usually from poorly penetrating radiation (e.g., beta particles) or whole-body irradiation 

doses >6 Gy. Radiation burns are also a common complication of radiation therapy. 

Acute local injury can result from external radiation exposures in which parts of the body 

are shielded. For example, local injury can occur after exposure to a collimated radiation 

beam or to a highly radioactive material (e.g., radiotherapy or industrial source) placed in 

close proximity to tissue. 

Emergency Care 

In an ARS patient, life-threatening medical complications should be addressed first (as in 

any life-threatening emergency). The other aspects of ARS can be treated after the patient 

has been stabilized. Airway/breathing/circulation (ABCs) of BLS, ACLS, should be 

addressed, along with other required emergency resuscitation. After the patient has been 

stabilized, the need for external decontamination can be addressed. 

Diagnostic Steps

The first diagnostic step is to assess the dose of radiation exposure, which may not be 

obvious. A dose assessment involves collection and analysis of the medical data 

discussed in this section, as well as consultation with health physicists and subject matter 

experts. Clinicians and health physicists calculate or determine an initial estimate of dose, 
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which is revised over time as more clinical and dosimetric data become available (Table 

6.4). 

Rapid diagnosis. The initial diagnosis provides an initial determination of dose that 

guides early treatment. Diagnostic steps can begin in an emergency department, in any 

acute-care setting, or even at a field hospital. The best and quickest diagnostic indicators 

are: 

• The time to onset of vomiting (prodrome). 

• The speed of lymphocyte depletion (serial lymphocyte counts). 

The time to onset of vomiting provides an estimate of the prodrome and suggests a dose 

range. The clinician should then observe the onset and duration of the subsequent latency. 

These various times combine to provide an estimate of dose, which suggests a treatment 

plan (Table 6.5). For example, prodromal symptoms of vomiting that began 1–2 hours 

after exposure, with duration of approximately 24 hours, suggests radiation exposure in 

the range of 3–5 Gy (Table 6.6). 

The most useful early laboratory test is the CBC, including an absolute WBC count. 

WBC counts should be performed every 6-8 hours during the first day after exposure and 

at least daily thereafter for the next week. Lymphocyte counts are the best rapid gauge of 

dose. The classic Andrews diagram for lymphocyte depletion curves (Figure 6.6) was 

published in 1965 and is still useful. Lymphocyte counts drop quickly with high radiation 

doses. A drop of 50% or more in 24 hours indicates a severe radiation injury. 

Later diagnostic data. Later diagnostic data help to refine both the estimate of dose and 

the treatment plan. Data that should be gathered over time include physical dosimetry, 

biodosimetry, and clinical physical findings. These data should be recorded for all 

patients, regardless of symptoms or estimated level of exposure. Such group data may be 

crucial to clinical evaluation of individuals within the group. These data can also provide 

a pattern of illness for the group, which can lead to changes in the estimate of dose or 

even the diagnosis.

Physical dosimetry. The dose assessment method most familiar to medical personnel is 

physical dosimetry. This can be used for victims who wore a personal dosimeter (e.g., a 

film badge), thermoluminescent device (TLD), or pocket ionization chamber. However, it 

is unlikely that civilians—or even most police, firefighters, and military personnel—will 

have worn dosimeters. It is also important to remember that dosimeters can be damaged 

during the radiation event, rendering them unreliable. Therefore, clinicians should request 

dosimetric data from emergency response agencies or military units with trained 

technicians. Such specialized personnel may be able to estimate dose using radiation 

detection, indication and computation (RADIAC) equipment and isotope counters. 

Biodosimetry. Biodosimetry can provide a good estimate of dose but requires specialized 

testing. This is performed at a few national centers, including AFRRI in Bethesda, MD, 

and the Radiation Emergency Action Center Training Site (REAC-TS) in Oak Ridge, TN. 
167

To assess radiation dose, a researcher counts the radiation-induced chromosomal 

abnormalities in peripheral blood lymphocytes. The classic method is a standard genetic 

karyotype, which takes about 3 days but offers a good dose estimate. This approach 

counts the aberrations on a chromosome smear, especially aberrations involving two or 

more centromeres (dicentrics). The number of chromosomal abnormalities correlates 

directly with radiation dose (see Appendix E of the AFRRI Handbook, available at 

www.afrri.usuhs.mil). 

Radiation-induced skin injury. Skin changes after radiation exposure offer a rough 

estimate of minimum dose, given that skin changes do not develop below about 3 Gy. 

Radiation-induced skin injury takes 10–14 days to appear and may resemble a skin burn. 

“Burns” that appear earlier may not be from radiation but rather from thermal or chemical 

exposure associated with the event. The severity of the burn increases with increasing 

dose. 

Overall Dose Assessment 

All of the above signs, symptoms, and tests can be used to provide an estimate of dose 

(Table 6.6). Dose assessment is an ongoing process that should include the techniques 

described above, as well as others recommended by experts. Close attention to dosimetric 

clues will eventually lead to a reasonably accurate estimate of dose. As the saying goes 

among health physicists, “Eventually the patient will tell you the dose.” 

Medical Diagnosis: External Contamination 

Background

External contamination with radionuclides can occur in the same settings and situations 

that cause internal contamination. Any person who simply passes through a contaminated 

area without appropriate personal protective equipment (PPE), as well as any person who 

is injured in a contaminated area, will become externally contaminated. Civilians, 

emergency responders, and military personnel can encounter radionuclides both in 

peacetime and while waging the war on terrorism. Accidents in medical, industrial, 

institutional, military, and nuclear research and nuclear power settings can cause external 

contamination, as could an RDD (e.g., dirty bomb) or nuclear detonation. The largest 

amount of fallout is on the surface of the ground, so children and crawling infants are 

particularly prone to pick up this material on their bare skin. 

Contaminated materials present as solid particulate matter or liquids that are on the 

ground or exposed surfaces. Health physicists have described these contaminants as 

“radioactive dirt” that can be washed off skin and hair. Radionuclides can be deposited 

on the skin and into body orifices during the immediate event or afterward through 

contact with contaminated surfaces or liquids. Liquids that contain radioactive materials 

can readily penetrate body orifices and non-protective clothing, allowing contamination 

of other external areas or internal contamination by absorption or ingestion. However, up 

to 95% of contamination is on the outer clothing and shoes. The body surfaces most 

likely to be contaminated include the hands, face, lower legs, and oral and nasal cavities. 
168

Most radioactive contaminants will be alpha- and beta-particle emitters. Alpha particles 

do not penetrate the skin but can be a significant source of internal contamination. Beta 

emitters can cause full-thickness skin damage and subsequent scarring (so-called 

“radiation burns”) when decontamination is delayed or performed improperly. Any 

radionuclide that emits a high level of gamma radiation can cause whole-body irradiation 

and ARS in a contaminated victim. 

Protection of Medical and Emergency Personnel 

Assessment and care of externally contaminated patients pose little to no risk to 

emergency or medical personnel. Proper technique and correct PPE allow medical 

personnel to treat radiation patients without fear of medical consequences to either 

themselves or the patient. First responders and hospital emergency department personnel 

may assume that care of such patients is dangerous, but history suggests otherwise. There 

has never been a major exposure among U.S. medical personnel treating radiation 

victims, with all measured secondary exposures being 14 mRem (0.14 mSv) or less. This 

dose of radiation is well within occupational standards. High-energy isotopes that pose an 

immediate medical threat can be detected at safe distances using radiation survey 

instruments (e.g., RADIACs). 

Emergency Care 

As with all other patients who present for emergency care, life-threatening complications 

should be addressed first. External contamination with radioactive agents is unlikely to 

cause acute injury, so emergency resuscitation and treatment of injuries come first. This 

is in contrast to external contamination with chemical agents, in which rapid 

decontamination may be more important. Emergency treatment should not be delayed out 

of fear of secondary contamination of health care providers because a living patient is 

unlikely to be a direct threat to health care personnel. The patient has already received a 

radiation dose several orders of magnitude higher than any caregiver, given that the 

patient is in direct contact with the contaminants for the longest time. 

Decontamination can begin during emergency care but only after the patient is stable. 

Simply removing contaminated clothing will significantly reduce the subsequent 

exposure. For a decontamination technique, see the section on medical treatment later in 

this chapter. 

Patient Evaluation 

Recommended steps for patient evaluation are as follows: 

1. Address life-threatening conditions and significant injuries. 

Note: External contamination has no early signs or symptoms. 

2. Disrobe the patient and provide a clean gown and foot covers. 

3. Obtain a history; this is crucial. 

What happened during the event? 

Where was the casualty? 

What has been done since the event that would change patient contamination 
169

status? 

4. Conduct an initial survey with RADIACs. 

5. Collect samples – external swabs/swipes (orifices, wounds, “hot” areas). 

6. Begin external decontamination. 

History. Diagnosis of external contamination is usually revealed by medical history. A 

history of some exposure event, together with suspicion of contamination, should lead 

medical personnel to check the patient with detection instruments. External 

contamination would probably be asymptomatic at this time, unless the presenting 

complaint is a skin lesion occurring a considerable time after the incident. 

Initial survey and samples. External monitoring and sample collection should begin at 

the accident scene if possible. This use of monitoring equipment to search for 

radioactivity is termed a radiological survey. This readily detects external contamination 

and guides decontamination efforts. First responders can be quickly taught basic survey 

techniques from health physicists, who are experienced users of survey equipment. 

The initial survey involves passing a RADIAC slowly over the entire body, using both 

alpha- and beta-gamma detectors. The RADIAC should be moved slowly from head-totoe and side to side, at a rate of about 2–3 cm/sec, and the number of counts/minute 

should be recorded frequently. At any site that has a high count (i.e., “hot”), a smear 

sample should be collected, or the area should be “swiped” using gauze or filter paper. 

These samples should be saved individually in suitable specimen containers for later 

laboratory analysis (see also the section on medical treatment later in this chapter). 

Evaluation of wounds and orifices. Wounds and orifices should also be surveyed to see 

if decontamination of these sites is indicated. All wounds should be surveyed with 

RADIAC, because wounds are more likely to be contaminated than intact skin. A 

“swipe” sample should be collected from any wound with a high count. Wounds should 

be uncovered and exudates removed/collected before the survey, because dressings and 

exudates can block alpha particles and low-energy beta particles. Wounds should be dried 

by application of absorbent material, rather than by rubbing with gauze, which can force 

contaminants into the tissue. 

Contaminants can be naturally cleared from the mouth and nose within about an hour. 

Therefore, nasal and oral swabs must be collected in the first hour. These should be 

collected at the accident scene if possible but certainly before the patient is washed or 

showered. Both nostrils should be swabbed and activity on the swab measured with the 

RADIAC. The swabs should be saved. Contamination of only one nostril means that the 

patient has touched his nose with contaminated hands, or that there is unilateral nasal 

obstruction. Samples of saliva, sputum, and vomitus should also be collected if available. 

After each decontamination, all the above RADIAC surveys should be repeated, taking 

additional samples if there is residual radioactivity. Each sample should be labeled with 

the patient’s identification, the sample site, and the date and time of sample collection. 
170

Medical Diagnosis: Internal Radionuclide Contamination 

Background 

Worldwide, there have been hundreds of recorded accidents with significant radioactive 

contamination, but only the accidents that occurred at Chernobyl, Ukraine, and Goiania, 

Brazil, resulted in significant numbers of children who required internal and external 

decontamination (see historical overview earlier in this chapter). Radionuclides are 

widely used in research, medicine, nuclear power, and industry, so further incidents of 

external and internal contamination will certainly occur. Exposure to radionuclides can 

occur in peacetime and as a result of a terrorist event such as use of a radiological 

dispersal device (RDD). Both military and civilian populations are potential targets. 

Medical management requires knowledge of the physical and chemical characteristics of 

radionuclides, as well as the indications and methods for their removal from the body. 

Patient management must be a team effort that includes physicians, other health care 

professionals, and health physicists. Patients can be contaminated by any one of the 

hundreds of radioisotopes in common use, although only a limited number are medically 

significant. The medical effects from these different exposures vary. Reference materials, 

such as the National Council on Radiation Protection and Measurements (NCRP) Report 

No. 65, health physics texts, and standard operating procedures, can be used to guide 

patient management. 

Internal Contamination 

Internal contamination occurs when radioactive material enters the bodies of unprotected 

people through inhalation, ingestion, or wound contamination. Health physicists have 

defined internal contamination as “unwanted radioactive material present in the body.” 

Contamination and exposure are not the same. Patients can have external exposure to 

radiation, external contamination by radioactive material, internal contamination with 

radionuclides, or any combination thereof (Figure 6.7). 

Medical effects. ARS has occurred after contamination with high-energy isotopes (e.g., 

Cs-137). However, internal contamination is usually asymptomatic initially, with no 

acute medical effects. The main medical concerns are chronic radiation injury of target 

organs, such as lung or bone, and long-term stochastic effects, such as malignancy. 

Causes. The greatest public concern currently centers around terrorism involving 

radioactive materials. However, medical errors made during medical diagnosis and 

treatment historically have been the most common cause of significant internal 

contamination. Industrial accidents are the second most common cause. Institutional and 

military use of a great number and variety of isotopes has also led to contamination 

events. 

The “dirty bomb.” The most likely terrorist use of radioactive materials would be an 

RDD, variously referred to as a contaminated conventional explosive or “dirty bomb.” 

Such a weapon can contain any liquid or particulate radioisotope. There is no nuclear 

detonation. Rather, the radioactive material is actually most hazardous before the 
171

explosion, when it is concentrated in one place. The goal of terrorists is to add a 

radionuclide to an existing bomb (e.g., truck bomb) to create an RDD that can 

contaminate both victims and the surrounding terrain. 

First responders can take several steps to avoid injury from a suspected RDD explosion. 

RADIAC devices can be used to detect radioactivity at a distance, confirming the RDD. 

First responders should don protective gear before entering the site and setting up a safe 

perimeter. A health physicist or a nuclear-biological-chemical team can then analyze 

samples using specialized laboratory equipment to determine the specific radionuclide. 

Isotopes of interest. Internal contamination and casualties are most likely to occur from 

common radionuclides linked to improper disposal of radioactive sources or damage to a 

medical or commercial facility. Commonly used radioisotopes include high-energy 

gamma emitters, such as cesium (Cs)-137, cobalt (Co)-60, and iridium (Ir)-192. These 

materials are used in industrial and research applications, medical and commercial 

irradiation, tracer units, thickness gauges, and calibration devices. Standard nuclear fuels, 

such as uranium and plutonium (Pu) isotopes, are also relatively common. Radioactive 

iodines (e.g., I-131), Cs-137, and strontium (Sr)-90 are the most medically important 

fission products associated with rupture of a reactor core or radioactive fallout from 

nuclear weapon detonations. 

Pathophysiology. Radionuclides, their non-radioactive (stable) counterparts, toxins, and 

chemicals are all governed by the same principles of toxicology. The same 

pharmacokinetics also apply, as all toxic agents must be absorbed, distributed, and 

expressed (through toxicological effects on target organs). Factors that determine the 

amount of internal hazard are the amount of radionuclide, the energy and type of 

radiation, the length of time in the body, the inherent chemical toxicity, and the critical 

organ(s) affected. The greatest potential for radiological injury is from large amounts of 

very energetic, long-lived radioisotopes that can affect certain critical (target) organs. 

Biological half-time. Biological half-time (biological half-life) is defined as the time 

required for half of a substance to be removed from the body. This number comprises 

both the physical half-life and the metabolic clearance of a radioisotope. A treatment plan 

can be developed by combining information on half-life and the amount of nuclide 

exposure. This requires knowledge of the exposure and access to reference texts or 

experts, because every isotope and chemical formulation has a different half-time. For 

example, salts of Cs-137 have a half-time of 68–109 days, while tritium (H-3), Pu-239, 

and soluble uranium salts have biological half-times of 8–12 days, 100 years, and 15 

days, respectively. 

The critical organ. The critical organ is defined as the bodily location where an isotope 

exerts its primary effect. A radioisotope is chemically identical to a stable isotope of the 

same element. Both are metabolized according to their chemistry, so that the critical 

organ is determined by the chemical properties of the isotope. 
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Radionuclides that distribute to the whole-body include sodium (Na)-24, Cs-137 (which 

mimics potassium) and tritium (which is incorporated into water). Bone is the critical 

organ for radioactive minerals that the body uses as calcium. Similarly, radioactive 

iodides (e.g., I-131) are rapidly concentrated in the thyroid gland. Ultimately, these toxins 

will be eliminated through the body’s normal excretory mechanisms. 

Life Cycle of Internal Contamination

The life cycle of a radioisotope consists of its several stages of transit through the body: 

• Intake. 

• Uptake. 

• Deposition. 

• Elimination. 

Intake. Radioactive materials can enter the body through inhalation, ingestion, and skin 

penetration. 

Inhalation pathway. Inhalation is the most efficient route of absorption for most toxins, 

including radionuclides in insoluble particulate aerosols. Large particles are deposited 

only in the upper airways, from which the mucociliary system clears insoluble particles. 

The “respirable fraction” is 1–5 microns in size, which is the size associated with 

efficient deposition in the terminal bronchioles and alveoli. The most hazardous 

biowarfare agents (e.g., anthrax spores) and industrial dusts (e.g., silica) are in this size 

range. 

Insoluble radioactive particles continue to irradiate surrounding tissues until cleared from 

the respiratory tract. Soluble isotopes are absorbed quickly and completely from the 

entire respiratory tract. Insoluble particles are cleared from the upper bronchi within 1 

hour, before much injury occurs. The clearance time from the alveoli can be 100 to 1,500 

days or more for some compounds. Radioisotopes deposited within alveoli are cleared to 

regional lymph nodes, where they may remain or be transported systemically. Alpha 

radiation is the most damaging to alveolar tissue, causing fibrosis and scarring to a 

spherical volume of tissue around the particle, in addition to any local inflammatory 

response to the foreign particles. 

Ingestion pathway. Swallowed radioactive material enters the digestive tract and is 

handled like any other ingested material. This is true for material originating from 

contaminated food or water, as well as for material cleared from the respiratory tract. As 

with inhalation, absorption from the GI tract depends on the isotope chemistry, including 

solubility. Most radionuclides are insoluble, with GI absorption <10%. These materials 

stay in the GI tract without becoming a systemic hazard. The clearance time for the GI 

lumen is 1–5 days. As a rule, insoluble alpha-particle emitters do not cause significant 

injury, because the exposure time within the critical organ is relatively short. 

However, soluble radionuclides and strong gamma emitters—which have occasionally 

been ingested—become a whole-body hazard and are capable of causing ARS. Soluble 

radionuclides are absorbed and metabolized according to their chemistry. 
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Skin pathway. Although intact skin is generally a barrier to most radionuclides, skin 

absorption can be important. Most skin absorption occurs through wounds or by passive 

diffusion. Examples of the latter include tritium-water and radioactive iodine, which can 

pass readily through skin. Skin permeability rates depend on relative solubility in both 

lipids and water. Infants are particularly at risk because of their thin epithelium and large 

surface area to mass ratio. Injuries such as trauma, burns, and chemical exposures also 

increase skin permeability. Abrasions and partial thickness burns create large denuded 

skin surfaces, which greatly increases absorption. Clinicians must evaluate all wounds for 

the presence of radioactivity, and thoroughly clean, debride, or excise all contaminants. 

Uptake and deposition. Uptake can occur by simple deposition, diffusion, or metabolic 

processes. Many soluble nuclides are metabolic analogs of body chemicals, so the body 

incorporates them like normal building blocks. The critical organs for these soluble 

nuclides are identical to storage sites for their metabolic analogs (e.g., radium, calcium, 

and bone). Once a soluble radionuclide is absorbed, it may distribute to the whole body. 

The liver, kidney, adipose tissue, and bone have higher capacities for binding chemicals, 

including radionuclides, due to their high protein and lipid content. 

Excretion. Insoluble radionuclides pass through the GI tract unchanged. At least some of 

the absorbed nuclide is eventually excreted, either in its original state or as metabolites. 

The main route of excretion is via urine, particularly for water-soluble compounds. Lipidsoluble compounds are excreted via the bile into the intestine. There is much individual 

variability in elimination. 

Diagnosis

Clinicians may need to evaluate patients who are both contaminated and injured. 

Furthermore, patients with internal contamination will almost certainly be externally 

contaminated at the time of exposure. Initial management and diagnosis should be 

performed simultaneously if possible. Any life- or limb-threatening medical or surgical 

emergencies should be addressed first. Initial emergency care is the same as for cases 

unrelated to radiation injury, because contamination causes no acute medical effects. 

Assessment and treatment of internal contamination must wait until the patient is 

medically stable and external decontamination has been completed. 

Initial evaluation. The initial evaluation begins at the same time as emergency treatment 

and consists of the following: 

1. Address life-threatening conditions/injuries – the ABCs. 

2. Evaluate and control initial contamination. 

3. Assess potential for internal deposition and treat as indicated. 

4. Patient history is crucial. Patient (or someone else) states what happened. 

5. No sign or symptoms.

6. Perform initial survey (RADIAC) and collect nasal swabs (reflect lung 

deposition). 

History. Patients exposed to radiation are usually asymptomatic at the time of 

presentation. However, history is still the biggest component of initial diagnosis of 
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contamination. Typically, the patient or someone else provides the important information 

that an exposure occurred. To quote the experts, “How does a physician become aware 

that his patient(s) may have an external exposure to radioactive material? Usually, 

someone tells her.” 

After a radiological attack, the history provides the best initial indicator of the likelihood 

of internal exposure. The history should include the exposure setting (e.g., enclosed 

space, open air in fallout field, etc.) and the protection status of the patient (e.g., wearing 

a mask). The patient or a fellow worker may know which isotope was used, or this may 

need to be determined by a health physicist in the laboratory. 

Initial patient survey and nasal swabs. The initial external survey of the body can be 

performed using standard RADIACs with both beta-gamma and alpha probes. Nasal 

swabs collected before decontamination can help diagnose, but cannot exclude, a 

significant inhalation injury (because the nares are self-cleaning). These swabs should be 

collected early, in the first hour and before the patient is washed off or showered, but 

decontamination should not be delayed just to obtain nasal samples. 

Each nostril should be swabbed separately, and the radioactivity on each swab measured 

using a RADIAC. The swabs should be saved. Activity measured by a RADIAC on a 

nasal swab reflects lung deposition. Health physicists can calculate the lung burden of the 

contaminant using standard equations and extrapolation curves. If both nostrils are “hot,” 

the patient probably inhaled contamination. If only one nostril is hot, the patient either 

has touched his nose with a contaminated finger (suggesting no lung contamination), or 

there is unilateral nasal obstruction. 

Measuring internal contamination. The laboratory tests most familiar to medical 

personnel (e.g., CBC and chemistry panels) are not helpful in diagnosing internal 

contamination. Instead, internal contamination is measured either directly with RADIACs 

or indirectly using samples of body fluids and excreta. 

Direct measurement. Machines such as RADIACs and larger stationary units such as 

whole-body counters directly measure radioactivity of the body. The operator sweeps the 

RADIAC slowly over the body, maintaining a constant distance above the skin. A wholebody counter is a large fixed device, associated with a heavily shielded walk-in or liedown chamber. This is the most reliable diagnostic instrument, although availability is 

limited. 

Indirect measurement. Body fluids (obtained by swabs), tissue samples, and excreta can 

be directly examined for radioactivity and for the specific radioactive isotopes involved. 

A health physicist can then estimate the patient’s “body burden” using extrapolation 

curves. 

Nasal swabs should be obtained as soon as possible after contamination, as noted above. 

These are sent with the patient to the medical facility. Medical or health physics 
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personnel should also take a wipe sample from the surface of wounds or skin wherever 

hot spots are noted via RADIAC. 

The level of radioactivity in urine and feces can also be used to estimate internal 

contamination. Initial radioactivity in urine and feces should be quantified with a baseline 

sample, followed by multiple postexposure urine and fecal samples. A thorough 

evaluation of serial samples is the only sure method of confirming contamination and 

quantifying body burden, which are key components of successful treatment. 

Bioassay methods vary according to each nuclide. Published methods can be found in 

health physics texts and standard guidance documents (e.g., NCRP Report No. 65). Table 

6.7 summarizes the sampling regimens for some important radionuclides. Biodosimetric 

approaches are useful for insoluble nuclides that are either ingested or inhaled, because 

inhaled particles will be swallowed and passed through the GI tract into feces. 

Tritium exposure can be measured with a single voided urine sample. For uranium, a 

baseline 24-hour urine sample should be collected as soon as possible after the exposure. 

This establishes the pre-existing excretion of uranium commonly distributed in soil. This 

initial urine sample is then followed by another 24-hour sample to measure new 

contamination and an additional 24-hour sample 7–10 days later. Insoluble plutonium 

may not appear in the urine until 2–3 weeks after ingestion, so both urine and fecal 

bioassays are needed to identify this radionuclide. 

Radiation Detection, Personal Protective Equipment, 

Personnel Monitoring, and Decontamination 

Detection Using Radiation Survey Meters

Various instruments are available for detecting and measuring radiation, which cannot be 

detected by human senses. These instruments (Figure 6.8) use the energy of the radiation 

to create an electrical “pulse,” which can then be measured and used to determine 

information about the radiation field. These various Radioactivity, Detection, Indication, 

and Computation meters are generally referred to by the acronym RADIAC.

Radiation detectors can be configured in several different ways. Some have an internal 

probe, while others have an external probe connected by a wire. The intended use of the 

meter is the most important factor in determining what configuration to use. If the meter 

will be used only for large area surveys, an internal probe works fine. If the meter will be 

used to determine the dose rate from a point source or to detect contamination, then an 

external probe will most likely be used. 

Things to check before using a RADIAC: 

• Check to see if the meter is in calibration. Most calibrations are good for 1 year, 

but always refer to the sticker on the meter, which indicates when calibration is 

due. 

• Inspect for physical damage (broken meter face, frayed cables, etc.). 
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• Check the batteries (most RADIACs are battery powered). This is normally done 

by either pushing a button labeled BAT(T), or turning the switch to BAT and 

watching the meter. If it moves to within the designated area, it is satisfactory. On 

the newer digital meters, a self-diagnostic may run as soon as the meter is 

switched on, and the battery level will be displayed. 

• In all cases, follow the procedures approved at your facility for use of these 

instruments. 

There are two main classes of RADIAC instruments used to detect and survey for 

ionizing radiation: gas-filled and scintillation detectors. 

Gas-filled detectors. The first and oldest type of RADIAC is the gas-filled detector. 

These are constructed by filling an electrically conductive chamber with an inert gas. The 

system contains two electrodes, one through the center of the chamber and the chamber 

itself, which also functions as an electrode. When a voltage is applied to the system, the 

center wire becomes positively charged (anode) and the outer (chamber) electrode takes 

on a negative charge (cathode). The fill gas, usually a noble gas such as argon, helium, or 

neon, is ionized by the radiation that strikes and penetrates into the chamber. This 

produces a pair of ions (a positive base ion and a free electron), which are attracted to the 

electrode of the opposite charge. The free electrons that are collected along the anode 

then create an electrical impulse. The electrical impulse (or current) is measured and 

converted to a meter reading, generally in counts/min or mR/hour. 

As the amount of voltage applied to the tube increases, the attractive forces of the anode 

and cathode get stronger and the production of secondary ionizations increases. 

Secondary ionizations are those not caused by the incident radiation, but by 

multiplication within the inert gas (gas amplification). There are six distinct regions 

corresponding to the amount of voltage applied. 

Detectors are described according to the radiation regions they detect. The regions most 

commonly used for detection are the Ion Chamber Region, the Proportional Region, and 

the Geiger-Mueller Region. 

• Ion chambers operate at low voltages, which do not produce any gas 

multiplication. The applied voltage is just enough that the ions migrate to their 

opposite poles; without secondary ionization, they travel through the gas. This 

means that only the primary ions created by the initial radiation event are 

collected, so that one radiation interaction produces one count. The ion chamber is 

very good for exposure measurements but not for detection. It is therefore used 

mainly as a dosimeter (see below). 

• Proportional counters rely on gas multiplication to amplify the charge created by 

the original ionization in the gas. The pulses they produce are therefore 

considerably larger than those from ion chambers used under the same conditions. 

This allows proportional counters to be used when the number of ion pairs is too 

low for effective detection by an ion chamber. Proportional counters are widely 

used in detection of low energy x-rays and neutrons. Because the current signal in 

a proportional counter is “proportional” to the energy of the radiation, these 

counters can also be used for spectroscopy of low energy x-rays. 
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• Geiger-Mueller or G-M counters operate at a significantly higher voltage than 

either ion chambers or proportional counters. They produce a large signal due to 

the “avalanche effect,” in which one initial event can cause millions of subsequent 

secondary ionizations. Due to this effect, the signal is not proportional to energy, 

and the G-M detector cannot discriminate between different types and energies of 

radiation. Additionally, at high radiation levels, G-M counters will experience 

dead time, in which an ionization event is lost because it occurs too quickly after 

the preceding event. At high count rates, these dead time losses can become 

severe, requiring a correction to ensure accurate measurements. The G-M 

instrument is very good for detection but not so good for measurement of 

exposure. That is to say, it can accurately confirm contamination on a patient, but 

it cannot quantify it accurately. The probe is held approximately 0.5 inches off the 

surface and moved at a rate of 1–2 inches/second. 

Scintillation detectors. The other common type of detector is the scintillation detector, 

which uses a liquid or a solid phosphor crystal. When radiation strikes the crystal, the 

energy of the incident radiation is expended to produce ionization and excitation. The ion 

that was formed eventually recombines, or the excitation decays, both of which result in 

the production of light. On average, the number of light photons emitted is proportional 

to the amount of energy originally deposited. A photomultiplier tube is then used to 

convert the scintillation photons (light) into an electrical pulse, which is counted or 

otherwise analyzed electronically. Some common scintillators use zinc sulfate, sodium 

iodide, or plastics. To detect alpha particles, scintillation detectors must be held 1/16th–

1/8th of an inch from the surface being monitored because of the short range of alpha 

radiation. 

The so-called multi-function RADIACs represent a modern innovation in radiation 

monitoring. These instruments use one readout unit, which can be connected to various 

probes so that most types of radiation and contamination can be detected. Most of these 

units use what is called a “smart box,” which can detect the type of probe being used. 

These “smart” units automatically show the correct units for the monitor being used and 

calibrate themselves accordingly. Many of these units come with everything in one case, 

eliminating the need to carry many separate detectors. 

Dosimeters 

Dosimeters are a special type of instrument used to determine the total dose of radiation 

that a person receives. The simplest dosimeters are made of film (like camera or x-ray 

film), tiny wafers of plastic, or other specially formulated materials that respond to 

radiation in ways that can be assessed and matched to a particular radiation dose. Simple 

dosimeters require special processing to determine dose but are very reliable and 

accurate. 

Slightly more complex are pocket ion chambers, which use the ionization caused by 

radiation to move a very tiny fiber that tracks the dose. Pocket chambers are inexpensive 

and can be read directly, but they are not very accurate and have to be protected from 

bumps that might cause the needle to move. 
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The standard dosimeter for most radiation workers, including medical personnel, is some 

form of thermoluminescent device (TLD). These use some type of crystal, such as 

lithium fluoride (LiF), calcium sulfate (CaSO4), or calcium fluoride (CaF) as the detector 

element. These dosimeters are usually read by placing them in a machine that heats the 

crystal and reads its light output, which is proportional to the radiation dose received. An 

advantage of some TLDs is that one dosimeter can be used for beta, gamma, x-ray, and 

neutron radiation. Another advantage of the LiF dosimeters is that they are relatively 

resistant to “fade” (i.e., the loss of dose over time) and are sensitive down to 1 mrem 

(new LiF-Cu version). 

Finally, electronic dosimeters have become popular. Most are about the size of a personal 

pager. These are more costly than pocket chambers but are much more reliable, accurate, 

and rugged. They also have a variety of features (e.g., alarms, digital readouts, dose rate 

readout, etc.) that can make them attractive to many first responders. 

Personal Protective Equipment 

This discussion describes many aspects of personal protective equipment (PPE), 

including the following: 

• The need for PPE. 

• The type of PPE needed for radiation contamination. 

• How PPE for radioactive isotopes is different from PPE for chemical or biological 

exposure. 

• Temporary PPE in an emergency. 

• Disposal of PPE. 

• Department of Energy Guidance on PPE. 

Need for PPE. Radioactive isotopes in the form of dust particles can harm a victim via 

external or internal contamination. Radioactive contamination can be carried by air 

currents in the form of fallout, which may travel great distances or settle on surfaces 

locally, depending on climactic conditions. In war-torn countries, children can potentially 

be contaminated externally by radioactive particles on the skin or clothing or by playing 

on vehicles that have been destroyed by depleted uranium munitions. Terrorist attacks 

with RDD (dirty bombs) can also generate considerable risk of contamination. PPE can 

protect a health care provider from contamination when dealing with casualties from such 

events. 

In internal contamination, radioactive material enters the body via inhalation, ingestion, 

or wound penetration. A small amount of radioactive material could also enter the body 

through the mucus membranes of the eyes. 

Type of PPE needed for radiation contamination. Personal protective equipment refers 

to three types of equipment: 

• Respiratory protection. 
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• Protective clothing— Disposable clothing, such as Tyvek® coveralls or something 

similar, is probably the least expensive option if an organization must purchase a 

large number. 

• Monitoring equipment. 

The goal of PPE is to prevent an individual from becoming contaminated and to prevent 

the spread of contamination from an already contaminated person. PPE does not shield 

the wearer from penetrating radiation, such as photons. 

First responders. PPE should provide protection to the skin, respiratory and digestive 

orifices, and the eyes. Boots are part of the PPE needed to prevent contamination of 

footwear with radioactive material. The PPE should be sturdy enough to avoid tearing in 

emergency situations. If the PPE is not airtight, tape may be placed where the PPE suit 

contacts gloves and boots to avoid radioactive material from getting inside the suit. A 

variety of PPE is available commercially. The National Institute for Occupational Safety 

and Health (NIOSH) provides information and a statement of certification for respirators 

at http://www.cdc.gov/niosh/npptl/. 

Hospital personnel. Radioactive fallout in the air should not be present inside a medical 

facility. Therefore, medical personnel working inside a facility do not need to wear as 

much PPE as first responders. Medical personnel who are decontaminating patients or 

providing emergency care to patients who have not yet been decontaminated should wear 

PPE similar to that worn in the operating room (e.g., head cover, face mask, scrubs or 

gown, and shoe covers). Wearing double gloves is recommended, in case the outer glove 

tears or breaks. 

Differences in PPE for radioactive isotopes and chemical or biological exposure.

First responders should wear PPE appropriate for “all hazards,” because the type of 

hazard may not be initially known. However, radioactive material is easier to identify 

than chemical or biological material, because it can be readily identified with a RADIAC. 

If the hazard is identified as solely radiological, then first responders can reduce their 

level of protection to that necessary for radioactive material (e.g., self-contained 

breathing apparatus is not usually needed). Waterproof PPE is appropriate if the 

contaminant is wet. Otherwise, cotton or Tyvek® coveralls would be adequate. 

Temporary PPE in an emergency. A person without PPE in a radioactive environment 

should take immediate emergency precautions, including the following: 

• Cover nose and mouth with a handkerchief. 

• Try to cover exposed skin. 

• Move away from the event. 

• Take shelter as soon as possible. 

Adults should direct children to do the same and lead the children to a safe area. 

Disposal of PPE. PPE may have radioactive contamination after an event. All such PPE 

should be collected in one area, placed in plastic bags (preferably red or yellow), and 
180

labeled as radioactive material. A health physicist can later evaluate the material for the 

presence and amount of radioactivity and then advise if the PPE can be washed without 

radiation precautions, should be disposed of, or should be stored in a special manner. 

DOE guidance. The Department of Energy Web site “Radiation Emergency Assistance 

Center/Training Site (REAC/TS)” at http://orise.orau.gov/reacts/rad-incidentresponse.htm provides guidance on proper use and disposal of PPE. Key information is 

summarized below. 

• The purpose of PPE is to keep bare skin and personal clothing free of 

contaminants. Members of the radiological emergency response team should dress 

in surgical clothing (scrub suit, gown, mask, cap, eye protection, and gloves) and 

use waterproof shoe covers. A waterproof apron can also be worn by any member 

of the team using liquids for decontamination purposes. All open seams and cuffs 

should be taped using masking or adhesive tape. Fold-over tabs at the end of each 

taped area will aid in removal. 

• Two pairs of surgical gloves should be worn. The first pair of gloves should be 

under the arm cuff and secured by tape. The second pair of gloves should be 

easily removable and replaced if they become contaminated. 

• A radiation dosimeter should be assigned to each team member and attached to 

the outside of the surgical gown at the neck where it can be easily removed and 

read. If available, a film badge or other type of dosimeter can also be worn under 

the surgical gown. 

• The above PPE effectively stops alpha and some beta particles but not gamma 

rays. Lead aprons, such as those used in x-ray departments, are not recommended, 

because they do not stop most gamma rays and give a false sense of security. 

Monitoring of Personnel/Decontamination

The DOE Web site “Radiation Emergency Assistance Center/Training Site (REAC/TS)” 

at http://orise.orau.gov/reacts/rad-incident-response.htm also presents guidance on 

recommended procedures for monitoring of personnel (Figure 6.9). 

The various aspects of decontamination include the following: 

• Basic principles. 

• How clean is clean? 

• Techniques. 

• Ambulatory versus non-ambulatory. 

• Wet versus dry. 

Basic Principles 

The primary objective of skin decontamination is to prevent internal contamination 

through secondary ingestion or inhalation. The secondary objective is to minimize the 

radiation dose to the skin. Each potentially exposed person should be monitored. 

Contamination levels should be recorded in the appropriate location on a form containing 

an anatomical figure. 
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Decontamination priorities are as follows: 

• Do not impede life-saving medical care. 

• Decontaminate wounds first, then cover with waterproof bandage. 

• Decontaminate areas where risk of internal contamination is high (i.e., the face). 

• Decontaminate areas of greatest contamination. 

• If multiple personnel are contaminated, decontaminate personnel first who may be 

most valuable in combating the casualty. 

Simply removing clothing may eliminate up to 95% of contamination. 

Treatment of life-threatening injuries always takes precedence over decontamination. No 

U.S. health care worker has ever suffered a radiation injury from caring for a 

contaminated patient. 

How clean is clean? An individual is generally considered “clean” if all areas of the body 

are below 100 counts/minute above background. 

Decontamination Techniques

For a conscious patient, the first step is an interview. Ask for a description of the 

contamination event (to determine likelihood of internal contamination), extent of skin 

contamination, and number of other people affected. The next step is decontamination of 

eyes, ears, nose, skin, and injury site, which should be performed (or supervised) by 

medical personnel familiar with decontaminating these body areas. 

A number of techniques have proved quite effective for decontamination of radioactive 

material. The least invasive, or least potentially damaging, technique should be done first 

before moving to more aggressive techniques. The need for decontamination must be 

balanced with potential injury to the skin caused by aggressive decontamination methods. 

The individual should be monitored after each decontamination attempt. 

Dry particulates. For a dry particulate or dust, the “tape-press method” has proven to be 

effective. In this procedure, an adhesive tape (e.g., masking tape) is pressed onto the 

contaminated area to lift off the contaminant. Strongly adhesive tape (e.g., duct tape) 

should not be used, because it may damage skin. The tape-press method should not be 

used on hairy areas or fragile tissue, such as eyelids. 

Washing. Washing a contaminated area with soap and water for 1–3 minutes is very 

effective. The goal of this type of decontamination is to float the contaminants off the 

skin and rinse them away. This can be done in a basin for small areas of contamination, 

or in the shower if large portions of the body are contaminated. If plain soap and water 

are ineffective, then a mild abrasive soap (such as Lava® or Soft Scrub®) may be used. If 

only a small area of skin is contaminated, waterless hand cleaner may be used instead of 

soap and water. 

During washing, care must be exercised not to splash contaminated wash solution around 

the area. A washcloth or soft surgical scrub brush may be used to help remove 
182

contamination. The water should be lukewarm, and care must be taken not to damage the 

skin. If erythema becomes evident, decontamination should be stopped to prevent driving 

contaminants into the skin. 

If washing is not effective, the site should be wrapped or covered with a bandage to allow 

removal through sweating and skin sloughing. Both the contamination site and the 

bandaging material should be monitored after 6–9 hours to determine effectiveness of this 

technique. 

Wounds. Irrigation with sterile water or saline has proven to be effective for wound 

decontamination. If the wound is a mild burn or abrasion, gentle washing with soap and 

water may be effective. All contamination does not have to be removed, because the 

residual remaining on the surface will normally be incorporated into, and sloughed off 

with, the scab. For contamination remaining in a puncture wound, simple wet 

debridement may be used following standard surgical procedures. However, before any 

surgical procedure, careful consideration should be given to the risks/benefits of the 

procedure. 

Medical Treatment: General Issues Unique to Pediatrics 

Acute Susceptibility 

The clinical manifestations of radiation injury in children are generally similar to those in 

adults. However, there are a number of characteristics that render the pediatric patient 

uniquely sensitive to the effects of radiation exposure (see also Chapter 1, Children Are 

Not Small Adults). 

Children have a greater body surface area to weight ratio than adults and skin that is more 

permeable and less keratinized, which renders them more vulnerable to both thermal and 

radiation burns. The inability of young children to shield their eyes also makes them 

more susceptible to ocular injury from blast, radiation, and thermal effects. This latter 

problem is compounded by the increased sensitivity of a child’s lens to radiation damage. 

Children have a higher baseline respiratory rate than adults and also exist in a lower 

breathing zone, which makes them more vulnerable to both generalized inhalation 

exposure and particulate exposure from radioactive fallout. Children also have a lower 

intravascular volume reserve, rendering them more susceptible to dehydration from the 

GI losses encountered in acute radiation syndrome (ARS). 

Infants and young children are also more likely to engage in pica of radioactively 

contaminated materials in their environment. In addition, radioiodine, a common 

byproduct of nuclear reactor activity, is efficiently transmitted through both human breast 

milk and cow’s milk, which are staples of the childhood diet. 

Long-Term Susceptibility 

The well-documented long-term effects of radiation exposure to the fetus and child are 

potentially of even greater concern for the more broadly exposed pediatric population. 
183

These effects can occur anywhere from months to years after initial exposure. The 

collective experience from the events in Hiroshima and Nagasaki, the Marshall Islands, 

and most recently Chernobyl, clearly show that children are more susceptible to 

developing many more long-term consequences of radiation exposure than adults over 

the same latent period. The most well-studied of these outcomes is the increased 

incidence of thyroid cancer in children after the Chernobyl accident in Belarus, Ukraine, 

and the Russian Federation. These thyroid cancers began within 4 years of exposure and 

continue to the present. Thyroid cancer incidence was dramatically increased almost 

exclusively in those younger than 20 years of age at the time of exposure, underscoring 

the unique susceptibility of the pediatric thyroid gland to radiation-induced malignant 

transformation. 

The incidence of leukemia from Hiroshima and Nagasaki was twice as high in children as 

in adult survivors. This increased incidence began within 2 years, peaked at 6 years, and 

then regressed to baseline after 25 years. There was a particularly high incidence of 

chronic myelocytic leukemia and acute myelocytic leukemia, which are cancers not 

typically seen in non-irradiated pediatric populations. 

In addition to thyroid and hematologic malignancies, the incidence of breast cancer in 

female Japanese survivors of the atomic bomb was increased among those who were 10 

to 19 years of age at the time of exposure compared with those older than age 20. The 

minimum period of latency appeared to be 10 years after exposure. There was also a 

surprisingly higher incidence of subsequent breast cancer in girls who were younger than 

age 10 at the time of exposure, indicating increased sensitivity even in prepubertal girls 

with little breast tissue. 

A number of effects have also been documented from fetal exposure to radiation 

throughout gestation, such as children born to female survivors in Nagasaki and 

Hiroshima. These effects include a higher incidence of mental retardation, microcephaly, 

and postnatal growth retardation, particularly with exposures in the first trimester. Fetal 

exposure after the first trimester was associated with a significantly greater risk of 

development of leukemia and thyroid cancer. 

Psychological Vulnerability 

Children involved in a radiation-related incident will be particularly vulnerable to 

psychological trauma, as in any disaster or terrorist event. Depending on the child’s stage 

of development, this increased vulnerability can manifest as generalized fear and anxiety, 

developmentally regressive behavior, sleep and appetite problems, altered play, school 

problems, or greater dependence on caregivers. This latter problem may be exacerbated 

by physical separation from parents in the chaos of the event. Repetitive television and 

news broadcasts relating to the event may even traumatize children in areas remote from 

the actual disaster, convincing them that they are also at risk. 

Children also experience stress by witnessing the reactions of their parents. In one survey 

of adults exposed to the Chernobyl accident, the group displaying the highest level of 

psychological distress were mothers with children younger than 18 years of age. This 
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finding has relevance to children, because a direct correlation exists between a parent’s 

response to a disaster and the response of the child. 

Any treatment plan regarding children exposed to radiation should take these unique 

vulnerabilities and parental reactions into consideration. Although many of the 

psychological reactions of children involved in a radiation-related incident are to be 

widely expected as an initial response, severe reactions or those persisting beyond several 

weeks may prompt the need for involvement by pediatric mental health professionals. 

See also Chapter 8, Mental Health. 

Immediate Care 

The first priority during the care of anyone exposed to radiation is to treat life-threatening 

injuries before addressing radiation exposure and contamination. In general, evolving 

injuries such as burns, lacerations, and fractures need to be stabilized before 

decontamination and subsequent transport to facilities where radiation-specific injuries 

are managed. In most instances, radiation levels will not be known, and survey 

instruments may not be available. Contamination risks to medical responders will be 

minimal in most cases, unlike situations involving biological and chemical exposures. 

However, simple precautions such as wearing gloves and wrapping victims in sheets or 

blankets to reduce the spread of contamination should be done before transport. 

Medical Treatment: Acute Radiation Syndrome 

Treatment of acute radiation syndrome (ARS) includes both general supportive care and 

specific actions and medications. No one is known to have survived whole body doses of 

radiation exceeding about 8 Gy. Therefore, those receiving doses of greater than 8 Gy can 

be considered expectant, although they may survive for a few months with extensive 

medical care. ARS is usually caused by direct radiation exposure, not internal 

contamination.

Supportive Care

Supportive therapy is a key factor in minimizing morbidity and mortality with significant 

whole body exposure, regardless of the type of radiation. A baseline history should be 

obtained before or shortly after supportive therapy is initiated. The history should include 

information regarding the source of radiation, the duration of exposure, the interval 

between exposure and presentation, and the physical property of the radioactive 

compounds (e.g., solid, liquid, particulate). The review of systems and physical 

examination should be as complete as possible, particularly focused on those organ 

systems that show early signs of damage, such as the skin and the hematopoietic, GI, and 

neurovascular systems. 

The first step is to make sure the victim has been medically stabilized and 

decontaminated, and that appropriate samples have been obtained for biological 

dosimetry. Next, the first symptoms likely to occur during the prodromal phase, such as 

nausea, vomiting, and diarrhea, should be addressed. Treatment of these early 
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manifestations of ARS may range from minimal intervention to the use of parenteral 

fluids and antiemetic agents. Antiemetic agents include ondansetron or granisetron at 

dosages commonly used to prevent nausea and vomiting during chemotherapy. For 

children 4–18 years of age, ondansetron is usually given at 0.15 mg/kg tid, and 

granisetron at 10 μg/kg/day. However, antiemetics may be contraindicated initially, 

particularly if catharsis is deemed necessary for internal decontamination. 

During the first day, the focus should be not only on treating acute symptoms, but also on 

systematically recording them as a way of estimating the dose involved. When combined 

with other biodosimetric indices, the time to onset of clinical symptoms is particularly 

useful in determining prognosis and the extent of supportive care that may be needed 

much later in the clinical course. 

Nutrition. Maintenance of adequate nutrition is important to counter the catabolic effects 

of radiation and to allow healing and recovery. Oral feeding is preferred if possible to 

maintain functioning of the intestinal mucosa and reduce risk of infection from parenteral 

feeding. Parenteral feeding may be necessary if the patient is not able to tolerate oral 

feedings or if fluid loss is profound due to diarrhea. 

Hematopoietic syndrome. The main focus of supportive therapy in patients with 

survivable exposures between 1 and 8 Gy centers around the hematopoietic system. 

Hematopoietic syndrome may not become clinically apparent until after a latent period of 

2–4 weeks. A key feature of this syndrome is neutropenia. 

Established or suspected infection after exposure to radiation is usually characterized by 

neutropenia and fever. In general, such patients can be managed the same as other febrile 

neutropenic patients. However, important differences between the two conditions exist. 

Most individuals exposed to irradiation are otherwise healthy. They also generally are 

exposed to total body irradiation without the shielding that is used in therapeutic 

exposure to irradiation. Patients with neutropenia after radiation are also susceptible to 

irradiation damage to other tissues (e.g., lungs, CNS, etc.), which may require therapeutic 

interventions not needed in other types of neutropenic patients. Furthermore, irradiated 

individuals may respond to antimicrobial therapy in unpredictable ways, as has been 

shown in experimental studies in which metronidazole and pefloxacin therapies were 

detrimental to irradiated laboratory animals. 

Neutropenia: Cytokine Therapy 

Hematopoietic growth factors, such as granulocyte colony stimulating factor (G-CSF) 

and granulocyte macrophage colony stimulating factor (GM-CSF), are not FDA approved 

for the management of radiation-induced marrow aplasia. However, these growth factors 

have been used in the aftermath of a number of radiation accidents (e.g., Chernobyl and 

Goiania) in an effort to lessen the severity and duration of neutropenia and thereby reduce 

the risk of infection. The experience with these few clinical cases, along with even more 

convincing data from controlled studies in animals, suggest that early cytokine therapy 

can significantly enhance survival. Benefit is maximal if treatment begins within the first 

24–72 hours after radiation exposure. In the absence of significant complicating injuries, 
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cytokine therapy is recommended for radiation doses ≥3Gy in adults, and >2Gy in 

children. Practical limitations, such as limited availability and supply of cytokines, need 

to be considered when determining the level of exposure that indicates this treatment. 

None of these cytokines is approved for the specific indication of radiation-induced 

illness. The long-acting form of G-CSF (pegfilgrastim) is FDA approved as a one-dose 

therapy for the management of chemotherapy-induced neutropenia in adults and 

adolescents weighing more than 45 kg. It is not approved for younger children and 

infants. The other two FDA-approved cytokines are G-CSF (filgrastim) and GM-CSF 

(sargramostim). These are administered daily until the absolute neutrophil count reaches 

>1,000. Dosages for adults and children are 5 μg/kg/day for G-CSF and 250 μg/m2

/day 

for GM-CSF. 

Neutropenia: Antibiotic Therapy 

Each institution or agency should follow established guidelines to develop a standardized 

plan for the management of febrile, neutropenic patients. Antimicrobials should be used 

mainly in radiation victims who develop fever and neutropenia. An empirical regimen of 

antibiotics should be selected, based on the degree of neutropenia and on the pattern of 

bacterial susceptibility and nosocomial infections in the particular area and institution 

(Table 6.8). Broad-spectrum empirical therapy (see below for choices) with high doses of 

one or more antibiotics should be initiated at the onset of fever. The antimicrobial 

spectrum should include efficacy against gram-negative aerobic organisms, which 

account for more than 75% of the isolates causing sepsis. Aerobic and facultative grampositive bacteria (mostly alpha-hemolytic streptococci) cause sepsis in about 25% of 

victims, so coverage for these organisms may also be necessary, especially in institutions 

where infection from these organisms is prevalent. Antimicrobials that decrease the 

number of strict anaerobes in the gut (e.g., metronidazole) generally should not be given, 

because they may promote systemic infection and death from aerobic or facultative 

anaerobic bacteria. 

If infection is confirmed by cultures, the empirical regimen may require adjustment to 

provide appropriate coverage for the specific isolate(s). After the patient becomes 

afebrile, the initial regimen should be continued for a minimum of an additional 7 days. 

Therapy may need to be continued for at least 21–28 days or until the risk of infection has 

declined because of recovery of the immune system. A mass casualty situation may mandate 

the use of oral antimicrobials. 

The initial antibiotic regimen should be modified when microbiological culture shows 

specific bacteria that are resistant to the initial antimicrobials. Modification, if needed, 

should also be considered after a thorough evaluation of the history, physical examination 

findings, laboratory data, chest radiographs, and epidemiologic information. If resistant 

gram-positive infection is evident, vancomycin should be added. If diarrhea is present, 

fecal cultures should be examined for enteropathogens (e.g., Salmonella, Shigella, 

Campylobacter, and Yersinia). 
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Neutropenia: Viral and Fungal Infections 

Antifungal coverage with amphotericin B is indicated for certain situations, including: 

• Clinical evidence of infection in patients who remain persistently febrile for 7 

days or more on antimicrobial therapy. 

• A new instance of fever on or after day 7 of antimicrobial therapy. 

Oral and pharyngeal mucositis and esophagitis suggest Herpes simplex infection or 

candidiasis. Either empirical antiviral therapy, antifungal therapy, or both, should be 

considered in this situation. 

Neutropenia: Prophylactic Antimicrobials 

Prophylactic antimicrobials should also be considered in any individuals exposed to 

doses >2 Gy, when the absolute neutrophil count is <0.5 × 109

 cells/L. Whenever 

possible, exposure dose should be estimated by biological dosimetry and detailed history 

of exposure. 

Thrombocytopenia and Anemia: Blood Products 

Platelets are the blood products most commonly needed for treatment of radiationinduced marrow aplasia, because they have a shorter lifespan than red blood cells and 

will likely regenerate later (i.e., marrow transplant is not necessary). Prophylactic 

transfusions have traditionally been recommended when platelet counts are <20 × 109

cells/L, although a level of 10 × 109 cells/L in the absence of overt bleeding may be 

adequate unless surgery is planned. A platelet count >75 × 109 cells/L is desirable before 

surgery. 

Red blood cell transfusions are used to maintain a hemoglobin of 80–100 g/L, which 

provides a sufficient reserve in case of severe bleeding. Limited experience with 

granulocyte transfusions has not revealed any significant clinical benefit, so it cannot be 

recommended at this time. All blood products should be leukoreduced and irradiated to 

25 Gy to prevent the risk of cytomegalovirus infection and transfusion-associated graft 

versus host disease, respectively. 

Bone Marrow Transplantation 

The use of bone marrow transplantation in victims of radiation exposure dates back to the 

1950s and on up to the 1999 radiation accident in Tokaimura, Japan. Despite the 

theoretical benefit of stem cell transplantation, the cumulative experience in these clinical 

situations (e.g., Chernobyl and Goiania) have not demonstrated any clear lifesaving 

benefit. However, it is difficult to interpret the results from these events because of the 

lack of precision with which the radiation exposure was known in most patients and the 

heterogeneity of comorbid conditions. 

From a theoretical standpoint, comprehensive supportive therapy alone can save many 

patients with exposures <8 Gy, while death from complications of gastrointestinal 

syndrome is virtually inevitable in those with exposures >10 Gy. Therefore, the decision 
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to pursue stem cell transplantation will need to be carefully considered for a narrow 

subset of patients with exposures between 8 and 10 Gy and no other significant 

comorbidity. The limitations of stem cell transplantation include potential complications 

(e.g., graft-versus-host disease), potential for morbidity associated with other organ 

toxicity, and a limited pool of suitable donors. In the rare instance in which a syngeneic 

donor (i.e., a twin sibling) or previously harvested stem cells are available, stem cell 

transplantation may be considered for those with exposures of 4–10 Gy. This 

recommendation applies to both adults and children. 

Medical Treatment: Internal Contamination 

External decontamination should be performed before treatment of internal 

contamination, which depends on the chemical nature of the radioisotope, its physical 

quantity, and the nature of radioactivity. A risk/benefit decision must be made. For small 

amounts of radioactive material or those with a short half-life, treatment may be 

unnecessary. Medical providers need to consult health physicists or medical physicists for 

information about the nature and amount of internal contamination. The National Council 

on Radiation Protection and Measurements Report No. 65 Management of Persons 

Accidentally Contaminated with Radionuclides is a valuable reference. 

Treatment of internal contamination reduces the absorbed radiation dose and the risk of 

future biological effects. Administration of diluting and blocking agents enhances 

elimination rates of radionuclides. Treatment with mobilizing or chelating agents should 

be initiated as soon as practical when the probable exposure is judged to be significant. 

Gastric lavage and emetics can be used to empty the stomach promptly and completely 

after the ingestion of poisonous materials. Purgatives, laxatives, and enemas can reduce 

the time that radioactive materials are present in the colon. 

Radioactive Iodine: Potassium Iodide 

Thyroid uptake of radioactive iodine can be reduced if potassium iodide (KI) is taken 

before or shortly after exposure. The main exposure routes for radioiodine are through 

inhalation and through ingestion of contaminated food, milk, or water. In 1986 during the 

Chernobyl nuclear reactor disaster, large populations in the proximity of Chernobyl— 

most notably in Belarus, northern Ukraine, and the Russian Federation—were not 

initially aware of the danger and were not evacuated, sheltered, or treated with KI. Since 

1990, the incidence of thyroid cancer in children has increased significantly. To date, the 

largest public health action involving the use of KI involved the distribution of 18 million 

doses to children and adults in Poland after the Chernobyl accident. KI was distributed to 

90% of the children younger than 16 years and to about 25% of the adults in Poland from 

the 4th day to the 7th day after the beginning of the release of radioactivity from the 

Chernobyl power plant. Although no significant increase in thyroid cancer has been noted 

in KI-treated populations in Poland, there are several factors that may have contributed to 

this difference. The dose of radioactive iodine to the Polish population may have been 

less than that to the population closer to Chernobyl. Also, the children in the Chernobyl 

area may have been more iodine-deficient than the children in Poland and therefore more 

susceptible to uptake of the radioactive iodine from Chernobyl. 
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The main reason for targeting pregnant women and children specifically for KI 

prophylaxis is that the smaller thyroid gland of the fetus and child concentrates 

proportionately more radioactive iodine than that of an adult, resulting in the welldocumented increased risk of thyroid cancer in this age group. Despite the fact that the 

fetal thyroid is not functional until approximately 12 weeks gestation, KI administration 

is still recommended during the first trimester for maternal protection. 

Although the potential side effects of stable iodine administration are well-described, 

during the Chernobyl experience, virtually no major side effects were seen in the 10 

million children to whom it was administered. Moderate effects observed in Poland 

included transient hypothyroidism in 12 neonates and otherwise occasional 

gastrointestinal symptoms and rash in others. In the adult population of 7 million who 

received KI, only two severe reactions were noted, both in individuals with an already 

known allergy to iodine. The incidence and severity of these side effects would be 

expected to be greater with repeated dosing, but there are minimal data available 

regarding the true risk associated with repeated KI administration. 

The indication for using KI to block uptake of radioactive iodine by the thyroid depends 

on the predicted thyroid dose and the age of the patient (Table 6.9). KI dosages are also 

age-dependent. If KI is administered, timing of the dose is of major importance. If given 

before or within 1 hour of the exposure, >90% blockage of uptake can be expected. After 

4–5 hours, there is 50% blockage. After 12 hours, the effect is minimal. Because of the 

short time period for effective administration, supplies of KI need to be already in place 

in areas at highest risk of exposure, such as around nuclear power plants from which high 

levels of radioiodine might be released. 

Because of the expected increased risk of side effects with repeated dosing, particularly 

in pregnant women and neonates, the decision to repeat KI administration because of 

ongoing unavoidable exposure needs to be made at a broader public health level, 

carefully considering the risk-benefit ratio. Regardless of how many doses are given, the 

thyroid function of the newborn should be monitored through a TSH level 2–4 weeks 

after administration, and thyroid hormone should be given to those found to be 

hypothyroid. Because of the risk for transmission to the child from breast milk, nursing 

should be interrupted until public health authorities recommend resumption. 

KI is stockpiled as tablets for logistical reasons, but it may be difficult for very young 

children to take the medication in this form. When dissolved in water, KI is very salty; 

however, a variety of liquids such as raspberry syrup, low-fat chocolate milk, orange 

juice, or flat soda such as cola make the taste more acceptable. Although KI pills are 

available over-the-counter, KI is also available in prescription form as potassium iodide 

oral solution, USP (saturated) (SSKI) containing 1,000 mg/mL. SSKI has such a high 

concentration of KI that accurate dose titration for children would be complicated by 

dilution calculations. For detailed instructions for home preparation, see 

http://www.fda.gov/cder/drugprepare/kiprep.htm. 
190

Radioactive Cesium and Thallium: Prussian Blue 

Ferric hexacyanoferrate, also known as Prussian blue, is a prescription medication 

approved by the FDA for the treatment of internal contamination with cesium or thallium. 

Prussian blue is taken orally, is not absorbed by the gastrointestinal tract, and serves as an 

ion exchanger during the enterohepatic cycling of these isotopes. During the Goiania 

incident, 249 individuals were exposed to cesium-137 from an abandoned medical 

radiotherapy device. Forty-six of these individuals were treated with Prussian blue, 

including 13 children who received daily doses up to 3 g/day in 3 divided doses. Prussian 

blue treatment reduced the whole-body effective half-life of Cs-137 by 46% in 

adolescents and by 43% in children 4–12 years of age. 

Dosage and administration of Prussian blue: 

• Adults and adolescents: 3 g, PO, tid. 

• Children (2–12 yr): 1 g, PO, tid. 

• Dosing in infants and neonates has not been established. 

Treatment should start as soon as possible after contamination is suspected and continue 

for a minimum of 30 days. 

Prussian blue is manufactured as a 500-mg gelatin capsule and is available directly from 

the manufacturer, Heyl, in Germany. Supplies are also maintained by the U.S. Strategic 

National Stockpile and are available from the Radiation Emergency Action 

Center/Training Site (REAC/TS), Oak Ridge, TN. Significant side effects are rare and 

consist mainly of mild to moderate constipation. 

Radioactive Plutonium, Americium, and Curium: DTPA 

Uranium: Bicarbonate

Diethylenetriaminepentaacetate (DTPA) is a powerful chelating agent effective in 

removing some heavy metal isotopes. In 2004, the FDA approved calcium-DTPA and 

zinc-DTPA for treatment of individuals with known or suspected internal contamination 

with plutonium, americium, or curium to increase the rates of elimination. These 

chelators, however, should not be used to decorporate for uranium because of potential 

renal toxicity. Instead, for uranium, urine alkalinization with bicarbonate should be done 

in an effort to promote excretion (Table 6.10). 

Dosage and administration of DTPA. There are two salts of DTPA, Ca-DTPA and ZnDTPA. In general, treatment should be started with Ca-DTPA on the first day and then 

changed to Zn-DTPA on the second day. This is because Ca-DTPA is more effective than 

Zn-DTPA on the first day, while being no more effective than Zn-DTPA later on. It does, 

however, have increased risks of causing metabolic abnormalities. It is supplied as 1 g in 

5 mL of diluent, and is currently available from the U.S. Strategic National Stockpile and 

from the Radiation Emergency Action Center/Training Site (REAC/TS), Oak Ridge, TN, 

and directly from the manufacturer in Germany. 
191

No significant side effects from its usage have been reported, although cases of nausea, 

vomiting, diarrhea, chills, fever, pruritus, and muscle cramps have been noted in the first 

24 hours after administration when given repeatedly and with short intervals allowed for 

recovery. 

Adults and adolescents. The initial dose of Ca-DTPA is 1 g IV. On day 2, start ZnDTPA at 1 g as daily maintenance dose. Pregnant women should begin and continue with 

Zn-DTPA. Nursing mothers should not breastfeed if they are suspected of having internal 

radionuclide contamination. 

Children younger than 12 years of age. The initial dose of Ca-DTPA is 14 mg/kg IV. 

On day 2, start Zn-DTPA at 14 mg/kg as daily maintenance dose. 

Other Radioactive Isotopes 

Because every element has one or more radioactive isotopes, there are hundreds of 

different radioactive isotopes. Each radioactive isotope behaves chemically the same as 

the non-radioactive isotope of the same element. Treatment of internal radioisotope 

contamination depends on the specific chemical properties of each isotope. The main 

radioactive isotopes that have caused internal contamination in people are described 

above. Detailed information about the diagnosis and treatment of these and other 

radioactive isotopes is available in the National Council on Radiation Protection Report 

No.65 and also by calling REAC/TS or the Armed Forces Radiobiology Research 

Institute (AFRRI). 

Surgical Issues 

Local Radiation Injury: Cutaneous Radiation Syndrome (CRS) 

A complication of external contamination or of close contact with a radioactive source is 

the effect of local radiation on tissues and organ systems (see Figure 6.10). This scenario 

along with partial body exposure has occurred more often than incidents involving whole 

body irradiation in past radiation mishaps. Local radiation injury will also alter the 

clinical course of patients suffering from acute radiation syndrome (ARS). In fact, 

significant morbidity and mortality in these cases may result from local injury rather than 

from ARS itself. The damage to tissues results in the release of endogenous toxins into 

the circulatory system, resulting in high body temperatures, metabolic disorders and 

neurological complications. 

The basic pathophysiology involves the response of the various cell types of the skin and 

organs that are exposed to radiation. That response is a function of the relative 

radioresponsiveness of the tissues involved. Individual cell types respond differently 

based on the amount of radiation delivered. The individual cellular response to radiation 

is also a function of its lineage, its level of development or maturity, and the stage during 

cell division when it is irradiated. Cell lineage is important because some cells are more 

radiosensitive (e.g., erythroblasts) than others (e.g., muscle cells). The developmental 

stage during which a cell is irradiated also is an important determinant of cellular 
192

response. Precursor/stem cells are more sensitive than fully developed, mature cells. 

Similarly, cells that are actively replicating (going through mitosis) are also more 

responsive. 

After receiving a radiation dose, a progressive, chronic, and complex inflammatory 

process begins. The clinical course is a function of the following: 

• Type of radiation. 

• Inherent energy of the source. 

• Dose and the dose rate. 

• Length of exposure. 

• Tissue involved. 

• How the energy is distributed within that tissue. 

• Size and area of the body involved in the exposure. 

Although only a small superficial area may initially appear to be affected, because of the 

amount of energy involved, deeper tissues and organ systems may also be affected. 

Depending on the individual cells involved, onset of clinical symptoms will be variable. 

Perhaps the most pertinent rule of thumb in these types of injuries is that there is no 

pathognomonic sign or symptom of radiation injury. There is not always a specific linear 

relationship between the dose of radiation that a tissue receives and the subsequent 

somatic manifestations that result. Skin damage evolves over time according to the local 

dose with the tissue furthest from the direct local injury being the slowest to display 

damage. The extent of tissue damage or involvement is inversely proportional to the 

square of the distance from the source of radiation. There is no definite correlation 

between specific symptoms and cell types. 

CRS has been divided into five time-related stages: prodromal erythematous, 

manifestational, subacute, chronic, and late. 

Prodromal erythematous stage. This stage may last minutes to hours after exposure to 

doses >5–6 Gy. The time to onset, intensity, and duration are used to predict prognosis. 

The early erythema is likely due to release of vasoactive amines and secondary 

vasodilation. A clinically asymptomatic latent period may follow. At this stage, high-dose 

and low-dose casualties cannot be distinguished. If additional symptoms (e.g., nausea, 

vomiting, CNS changes) develop along with relevant patient history, then further 

assumptions or conclusions will be possible. 

Manifestational stage. After a latency period of 7–21 days, clinical signs develop that 

range from bright erythemas with a burning sensation to painful blisters and ulcers. These 

changes are due to injury to blood vessels and underlying connective tissue and death of 

skin stem cells. From 8 to 12 Gy, there is dry desquamation, and from 15 to 20 Gy, moist 

desquamation ensues. Moist desquamation occurs less commonly in children undergoing 

radiation therapy than in adults. This is probably because of the ability of the epithelium 

to recover more quickly in children than in adults. More changes are also observed in 

fair-skinned individuals and at the more radiosensitive areas of the body such as the 
193

axilla, groin, and skin folds. Radiation sensitivity in other areas of the body decreases in 

the following order: 

• Inner neck. 

• Antecubital, popliteal, flexor surface of extremities. 

• Chest. 

• Abdomen., 

• Face. 

• Back. 

Least sensitive areas are the nape of the neck, scalp, palms, and soles. Dry desquamation 

usually leads to complete recovery. However, recovery from moist desquamation 

depends on the extent of injury. 

Subacute stage. The subacute stage is characterized by initiation of progressive dermal 

and subcutaneous fibrosis leading to a second ulcerative phase and cutaneous ischemia in 

affected areas. 

Chronic stage. Onset is usually from 16 weeks to 2 years after initial irradiation with 

epidermal atrophy and erosions associated with dermal and subcutaneous fibrosis being 

the main clinical manifestations. Concomitant inflammation tends to progress indefinitely 

with no endpoint. As such, long-term evaluation and management may be required. 

Late stage. This occurs 10–30 years after irradiation in the exposed field with 

development of “spontaneous” angiomas, keratoses, ulcers, and squamous and basal cell 

carcinomas. 

Treatment and Management Issues 

There are no specific protocols published to guide treatment. However, treatment of past 

victims provides a valuable point of reference for treating future victims. The clinical 

situation helps guide whether the treatment approach should be conservative or surgical, 

based on the following guidelines: 

• Radiation ulcer and localized necrosis without signs of regeneration is the primary 

and most often encountered indication for surgical intervention, as well as severe 

pain. The more rapid the progression of the pathologic process, the more severe 

the injury is, and the earlier the intervention should be performed. 

• Resection of injured and dead tissue must be accomplished to permit an effective 

engraftment. Erythematous tissue surrounding frank ulcers is likely to ulcerate if 

traumatized. 

• Antihistamines and topical antipruritic agents may be used for the relief of 

symptoms. Antihistamines may also prevent or weaken the subsequent 

inflammatory process. 

• Use of high-dose systemic glucocorticoids, combined with topical class III or IV 

steroids, should be considered. 

• Potential opportunistic pathogens (i.e., bacteria, fungi, and viruses) should be 

treated. 
194

• Necrotic areas should be carefully debrided. 

• Treatment of radiation fibrosis with pentoxifylline (to improve blood flow) and 

vitamin E should be considered. 

• There is no standard treatment for radiation fibrosis. Consensus has been to 

attempt to treat patients who have a subacute onset of radiation injury with 

corticosteroids if they have symptoms. Other agents include pentoxifylline, 

vitamin E, colchicines, penicillamine, interferon-gamma, and pirfenidone. 

Trauma and Radiation (Timing of Surgery) 

The overall morbidity and mortality of trauma patients is exacerbated when there has 

been acute exposure to ionizing radiation or contamination with radioactive materials. 

Trauma can be in the form of lacerations, puncture wounds, abrasions, gunshot wounds, 

blunt force injuries, crush injuries, and burn injuries (see also Chapter 7, Blast 

Terrorism). 

The initial step in the management of victims with combined injuries, i.e., radiation and 

trauma, should be the immediate stabilization of the most life-threatening injury as well 

as addressing airway, breathing, and circulation problems. After stabilization, radiation 

injury can be assessed and further managed. The fundamental concept to appreciate is 

that radiation injuries are not acutely life threatening. 

Thermal burn injuries may be complicated by the fact that the wounds may become 

contaminated with radioactive particles that need to be removed. Tissue that is irradiated 

may not respond in the normal physiological manner afterward. This may affect surgical 

success. Animal studies have indicated that performing initial surgery within 36–48 hours 

is optimal. Surgery beyond that time puts the patient at risk of life-threatening sepsis due 

to profound neutropenia with the acute radiation syndrome. 

Management of the Patient with Embedded Radioactive Material 

and Depleted Uranium 

Radioactive material embedded in wounds should be removed if possible. Otherwise, a 

victim is at risk of both infection and local radiation injury. Surgeons should never touch 

the radioactive particles (even with a gloved hand) due to the high probability of direct 

permanent damage to the fingers. Particles should be touched only with forceps. 

Depleted uranium (DU) munitions may be encountered because they are a critical 

component of U.S. weaponry. DU has <50% of the radioactivity found in natural 

uranium. DU is not a radiation risk, but it is a heavy metal risk. Prime concern is its effect 

on the kidneys as a heavy metal if it is absorbed. However, DU has also been 

demonstrated to have potential tumorigenic effects in animal studies. Therefore, DU 

fragments should be removed from wounds if possible, the victim should be kept 

hydrated, and renal function should be monitored. Sodium bicarbonate helps bind DU 

and reduce renal toxicity. DU may also be absorbed via inhalation from a DU fire or 

ingestion. 
195

Followup Care, Including Risk of Carcinogenesis 

Children are particularly susceptible to the transforming effects of ionizing radiation. 

This is true for children exposed to radioactive fallout, release of radioactive materials 

from nuclear power plants, and external beam radiation therapy for medical conditions. 

External beam radiation therapy, used for example in the treatment of Hodgkin’s disease 

or CNS tumors, is associated with an increased risk of second malignancies, particularly 

solid tumors arising in the radiation field. In contrast, children exposed to high levels of 

radioactive fallout from nuclear weapons at Hiroshima, Nagasaki, or the Marshall Islands 

testing site have increased risks of leukemia, benign and malignant thyroid neoplasms, 

and breast cancer (as young women). Those exposed to lower levels of radiation or 

possibly a more limited number of isotopes, such as from the Chernobyl nuclear accident, 

have an increased risk of thyroid neoplasms. 

Thyroid nodules and cancers are one of the most frequent late complications of ionizing 

radiation. Although generally uncommon in children, they are very frequent 10–20 years 

after radiation exposure. Four of the 39 children (10%) exposed after the Bravo nuclear 

test in the Marshall Islands developed thyroid cancer, and the incidence of thyroid 

cancers increased by 193-fold in areas contaminated by the Chernobyl nuclear accident. 

In contrast, only 1 of 39 children (2.5%) developed leukemia after the Marshall Islands 

nuclear test (compared with 10% incidence of thyroid cancer), and the incidence of 

leukemia did not increase after the Chernobyl nuclear accident (compared with 193-fold 

increase in the incidence of thyroid cancer). From these data, it is clear that children are 

very susceptible to radiation-induced thyroid neoplasia. Indeed, children were found to be 

10-fold more likely than adults to develop thyroid neoplasms after exposure to similar 

doses of ionizing radiation. It is also clear that thyroid neoplasms are a more common late 

effect from radiation exposure than are leukemias. 

Although there may be quantitative differences in the risk of thyroid neoplasia after both 

of these accidents (Marshall Islands Bravo test and the Chernobyl accident), this could 

relate to differences in the types of radionuclides released or the doses absorbed. Exact 

quantification of the doses to which these children were exposed has been difficult to 

determine because many ingested contaminated milk, which would be a leading source. 

Quantification of the level of contamination and the quantity of milk consumed has 

proved difficult. Current studies are underway to better define the individual levels of 

exposure. 

These data underscore the particular susceptibility of the thyroid that arises from unique 

genetic changes known as recombinant ret proto-oncogene in papillary thyroid cancer 

(ret/PTC) rearrangements. These rearrangements can be induced by ionizing radiation 

and are sufficient to cause thyroid cancer in experimental animals. Once induced, 

ret/PTC gene rearrangements generate a chimeric gene that places the tyrosine kinase 

portion of the ret proto-oncogene under the control of different gene promoters, leading 

to increased and uncontrolled ret tyrosine kinase activity. 

Stable iodine prophylaxis can reduce the risks of thyroid cancer after nuclear disasters or 

accidents but has no effect against external beam radiation therapy because the latter does 
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not involve radioactive iodine. The World Health Organization and the U.S. Food and 

Drug Administration recommend stable iodine prophylaxis for exposed populations 

stratified according to age. Thyroid function tests should be monitored in infants to allow 

early recognition and treatment of hypothyroidism. 

In general, radiation-induced thyroid cancers appear to be more aggressive than 

“spontaneous” thyroid cancers and are frequently multifocal. Exposed children should be 

monitored by serial ultrasound examinations, and suspicious lesions should be removed 

by total thyroidectomy to eliminate other microscopic foci of disease. 

Most children who develop thyroid cancer present with a thyroid nodule. Malignancy 

must be considered in any child with a thyroid nodule because the risk of malignant 

disease is much higher in children (30–50%) than in adults (10–14%), and it is even 

higher after radiation exposure. Routine serum thyroid function tests are not helpful in 

making a diagnosis of malignant disease because they are usually normal even in the 

presence of malignancy. 

Suspicious lesions can be evaluated by ultrasound, which may reveal features highly 

suggestive of malignancy (such as microcalcifications, heterogeneous echo-density, and 

central blood flow), in addition to identifying other unsuspected lesions that may also 

require surgical removal. Radionuclide scans generally cannot distinguish benign from 

malignant disease and should not be routinely ordered for this purpose. Determination of 

serum calcitonin levels should be reserved for patients with a family history suggestive of 

multiple endocrine neoplasia (MEN) because medullary thyroid carcinoma, which is the 

form associated with MEN and elevated serum calcitonin, is not induced by radiation 

exposure. Also, there is some risk of false-positive calcitonin levels in patients with any 

thyroid nodule. Fine needle aspiration cytology is the best single test to distinguish 

benign from malignant disease but may have a higher false-negative rate in children than 

in adults unless combined with clinical risk assessment. Due to the high risk of malignant 

disease, some have recommended removing all thyroid nodules from children, especially 

those with a history of radiation exposure. Thyroid hormone has been prescribed to 

reduce the size of benign nodules. Only a few respond, but those that increase in size 

must be removed. 

A logical sequence to evaluate a thyroid nodule would involve ultrasound to define the 

architectural features and the presence of other unsuspected disease, fine needle 

aspiration to determine benign or malignant cytology, and then removal if the overall 

clinical picture is suspicious of malignant disease. Most centers do not rely entirely on 

the results of a single test such as a fine needle aspirate but would remove the entire 

thyroid gland due to the increased risk of developing another malignant lesion in any 

remaining thyroid tissue that was exposed to radiation. 

Thyroid cancer is most frequently treated in children with total thyroidectomy, cervical 

lymph node dissection, and radioactive iodine ablation (RIA). This approach has induced 

remission in 70% of children but with a significant risk of disease recurrence (19%) and 

complications (5–25%). Disease-specific mortality is low (1–2%), but this could be 
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artificial because followup in almost all studies has been brief. After surgery and RIA, 

thyroid hormone is prescribed to suppress thyrotropin (thyroid stimulating hormone 

[TSH]) without inducing hyperthyroidism. Routine surveillance for recurrence has 

generally included 131iodine whole body scans and serum thyroglobulin (Tg) levels 

performed after thyroid hormone withdrawal. After total thyroidectomy and RIA, 

undetectable serum Tg when the patient is off thyroid hormone is predictive of complete 

remission, whereas Tg levels >10 ng/mL off thyroid hormone suppression or TSHstimulated Tg levels >2 ng/mL indicate residual disease. Despite favorable survival, 

recurrence is three times as likely in children as in adults. 

Due to the increased incidence of leukemia in children exposed to high doses of 

radiation, close followup with regular physical examinations and complete blood counts 

is warranted. The incidence of breast cancer is also increased in young women who had 

been either pubertal or lactating at the time of exposure to the Hiroshima device. Cancers 

began to appear as early as ages 25 to 30 years, which was earlier than in sibling controls. 

For that reason, regular breast examinations should be emphasized, and abnormalities 

should be evaluated with a high level of suspicion. Enrollment in a high-risk breast clinic 

may be indicated. The latency period (i.e., the time interval between irradiation and 

appearance of a malignancy) is shortest for leukemia (5–7 years) but can extend to 45 

years or more for solid tumors. 

Environmental Issues Affecting Children After a 

Terrorist Incident Involving Radioactive Materials 

The environmental damage from a terrorist incident involving radiation has many 

potential consequences for children. These effects can be minimized by a better 

understanding of the types of incidents that involve radioactive material and the 

environmental exposure pathways involved. Response planning involves actions that may 

be taken to minimize exposure both immediately after and during recovery from a 

terrorist incident. 

Type of Incident 

The environmental damage and effects on children differ significantly depending on the 

type of terrorist incident. More specifically, whether the incident involves a/an: 

• Radiological dispersal device (RDD, or “dirty bomb”). 

• Improvised nuclear device (IND). 

• Attack on a nuclear power plant. 

Radiation dispersal device. An RDD is any device that causes the spread of radioactive 

material across an area, typically to contaminate people and buildings in an urban 

environment. RDDs can also be used to contaminate water, livestock, fish, and food 

crops. The radioactive material acts as a toxic chemical that is harmful or fatal. RDDs use 

an explosive device to scatter the radioactive material over a general but fairly confined 

area. Simple RDDs spread radioactive material without the use of explosives, typically by 

the covert placement of radioactive material in a high traffic area. The radioactive 
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material is then spread when it is disturbed, e.g., by people walking through material 

spread on the ground or spread on the wheels of vehicles that drive over the material. 

Sources1

 of radioactive material for construction of an RDD include medical facilities, 

military, industrial and waste storage facilities, the black market, and orphaned sources. 

The vast majority of sources contain only one radioactive element, such as cesium-137, 

strontium-90, cobalt-60, or iridium-192.2

 Cesium chloride is of particular concern 

because of the fine powder form in which it is normally used. However, any nuclear 

material, including nuclear power plant fuel rods (uranium-235) or spent fuel rods 

(contains a mixture of radioactive components), could be used for dispersal. 

The health effects of RDD weapons can vary sharply. The time required to accumulate 

significant doses of radiation can vary. Harmful effects often require either inhalation or 

ingestion. Although exposure does not require actual contact with radioactive material, 

health effects are further reduced as the radioactive material spreads. In most cases, it is 

extremely unlikely that an RDD can spread enough radioactive material to the air and 

ground to pose an immediate health hazard to people near the event. 

Improvised nuclear device. INDs (improvised nuclear devices) use fissile material, 

either uranium or plutonium, and produce a nuclear yield. The fission process produces 

tremendous, potentially catastrophic damage from an initial intense radiation, intense 

heat, and blast effects over a large area. A plume of radioactive fallout is usually 

produced, composed of large quantities of a variety of radioactive products. Although 

fallout is carried by atmospheric conditions and potentially may circle the earth, the 

heaviest dispersal pattern—and the area of greatest concern for health effects—is the area 

close to the blast zone. Health effects from an IND include injuries from the blast and 

heat effects, as well as acute radiation syndrome symptoms from the high doses of 

radiation released from the nuclear weapons explosion. Depending on the population 

density, an IND is capable of killing tens to hundreds of thousands of people. 

Attack on a nuclear power plant. A terrorist attack at a nuclear power plant could 

release radioactive material into the environment. Nuclear power plants produce energy 

through the controlled release of energy from a critical mass of nuclear material by the 

fission process. Many safety and security features have been designed into U.S. reactors. 

For example, U.S. reactors use containment structures designed to contain release of 

 

1

 Medical facilities contain high activity irradiators, teletherapy machines and brachytherapy sources, as 

well as radionuclides which are vulnerable to malevolent use. Military and industrial sources include: 

radioisotopic thermoelectric generators (RTGs), high activity irradiators, gamma radiography equipment, 

high activity gauges and well logging equipment, used in drilling or oil, gas and water exploration. 

Vulnerability to theft or malevolent intent, including sale on the black market, of these sources is increased 

by factors such as bankruptcy, abandonment, long-term storage, transport, or change in expert personnel. 

An orphan source is defined by the International Atomic Energy Agency (IAEA) as a radioactive source 

that poses sufficient radiological hazard to warrant regulatory control but which is not under regulatory 

control because it has never been so or because it has been abandoned, lost, misplaced, stolen, or otherwise 

transferred without proper authorization. See International Atomic Energy Agency, IAEA-TECDOC-1388, 

dated February 2004. 

2

 Each radioactive element has its own decay scheme by which it becomes a stable element. Most sources 

have short decay schemes, with few radioactive intermediates. 
199

radioactive material in an accident. The most serious U.S. nuclear power plant accident 

occurred at Three Mile Island Unit 2 (TMI) in 1979. The accident at TMI was the worst 

case scenario of a nuclear power plant accident, namely, a loss of coolant, resulting in the 

partial meltdown of the reactor core and release of radioactive material into the 

atmosphere. Although the reactor core at TMI was damaged by excessive heat, the 

mishap resulted in only very small releases of radioactivity into the surrounding 

environment. Environmental samples of air, water, milk, vegetation, soil, and foodstuffs 

at TMI showed that most of the radiation was contained, and that those isotopes released 

had no physical or health effects on individuals or the environment. 

More extensive releases at TMI did not occur primarily because of the containment 

structure. Containment structures have been included in U.S. reactor designs since the 

early stages of commercial power plants. They are meant to prevent the release of 

radioactive material to the area surrounding the power plant if an accident occurs. In 

contrast, in the reactor accident at Chernobyl in 1986, which was the costliest industrial 

and environmental accident ever, there was no containment structure. The reactor core at 

Chernobyl continued to release radioactive material—mainly xenon-133, iodine-131, 

and, to a lesser extent, cesium-137, strontium-90, and plutonium-239—into the 

atmosphere for 2 weeks after the accident occurred due to graphite fires that could not be 

extinguished. 

Environmental Exposure Pathways 

There are three main routes of exposure by which the health of people are affected by 

radioactive material: 

• Inhalation of radioactive material (e.g., breathing the plume). 

• Ingestion of radioactive material (e.g., through food contamination). 

• External exposure (e.g., from ground contamination). 

Figure 6.2 illustrates one way in which children could be harmed by radiation in the 

aftermath of a terrorist attack involving radioactive material. In this example, I-131 is 

used because it is the isotope for which there is the most evidence of its environmental 

exposure pathway—namely, the grass-cow-milk pathway—and because it is one of the 

few isotopes for which there is a specific radioprotective agent. However, the likelihood 

of an RDD using I-131 is extremely low because of its short half-life (a few weeks). I131 will be released if there is a nuclear yield after an attack using an IND, and it may be 

released after a terrorist attack on a nuclear power plant if the attack results in an 

environmental release of radioactive material. 

In contrast, strontium-90, which also follows the grass-cow-milk pathway, is of lesser 

concern because it does not become airborne as easily as the iodines and thus is less 

likely to travel as far as the radioiodines. However, strontium-90 has a much longer halflife (30 years), and although there is less concern, it will last for decades. 

In contrast to radioiodine, most radioisotopes do not have a stable isotopic form that is 

biologically important and for which the radioactive form can cause biological damage 

via normal metabolic pathways. The element of each isotope has different biological, 
200

chemical, and physical properties that would result in different health effects. Most of the 

effects of the radiation from radioiodine are on the thyroid. Radioiodine is also one of the 

few radioisotopes for which there is a targeted organ and specific method of prevention 

and treatment, namely, administration of stable potassium iodide. 

The Chernobyl nuclear power plant accident in 1986 provides the best documented 

example of a massive radionuclide release in which large numbers of people across a 

broad geographical area were exposed to radionuclides released into the atmosphere. 

Chernobyl also most closely mimics the worst-case scenario of a successful terrorist 

attack on a nuclear power plant. At Chernobyl, radioiodine was released from a graphite 

and nuclear fuel fire that burned for 2 weeks after the initial core meltdown. 

The medical effects on children from an environmental radioiodine release have been 

extensively studied. The U.S. Food and Drug Administration did a comprehensive review 

of the data relating radioiodine exposure to thyroid cancer risk after the Chernobyl 

reactor accident in 1998. Hundreds of thousands of measurements were made from some 

of the millions of people exposed in the most heavily contaminated regions of the former 

Soviet Union: Belarus, Ukraine, and the Russian Federation. 

Thyroid radiation exposures after Chernobyl were virtually all internal, either through 

ingestion or inhalation of radioiodines. Starting 4 years after the accident, thyroid cancer 

increases of 30- to 100-fold were observed (compared with pre-Chernobyl rates), with 

estimated doses of <30 cGy (30 rads) to the thyroid. Consistent with the short half-life of 

iodine-131, children born more than 9 months after the accident have not shown an 

incidence of thyroid cancer above the levels seen prior to the Chernobyl accident. The 

FDA concluded from the Chernobyl data that there is a significant increase in the risk of 

childhood thyroid cancer at exposures of ≥5 cGy (5 rads) or greater. In contrast, there 

was no perceived increase in thyroid cancer in adults from the exposure to radioiodine 

during the accident. 

Stable KI protects the thyroid by preventing the uptake of radioactive iodine. Stable KI 

was distributed throughout Poland after the Chernobyl accident to more than 10.5 million 

children younger than 16 years of age. Although there is no evidence on the degree of 

protection provided by the KI distribution throughout Poland compared with other 

regions around Chernobyl, the widespread distribution does provide valuable data on the 

safety and tolerability of KI in the general population. Twelve of 3,214 neonates treated 

with KI in Poland after Chernobyl showed a transient hypothyroidism. The FDA

concluded that the benefits of KI treatment are especially important to children and 

neonates to reduce the risk of thyroid cancer and outweigh the risks of transient 

hypothyroidism. In contrast, the recommendation for adults older than 40 years is to 

administer stable KI only in the case of a projected dose of radiation to the thyroid greater 

than 500 cGy (rads), 100 times the exposure level for children. 

Other measures may be taken to reduce exposures. For example, bans on the sale of milk 

products from contaminated areas prevent internal contamination during the first few 

weeks after an emergency where radioiodines are released. Due to the short half-life of I-
201

131, canned milk or other milk products that can be stored for a few months will not have 

any residual radioactive iodine and may be consumed. 

Short-Term Evacuation Versus Sheltering 

Decisions and actions to prevent radiation exposure must “do more good than harm.” In 

other words, the benefit to health effects from dose reduction by using protective actions 

should more than offset the socioeconomic disadvantages of the protective actions. 

Evacuation is an effective countermeasure to the presence of radiation and may prevent 

exposure to children. The decision to evacuate should take into account the potential 

disruption and actual risk. Area evacuations can result in increased risk of exposure if a 

plume already exists or if evacuation is to a location with a higher risk of exposure. Also, 

casualties can result from the evacuation process, and negative psychological effects can 

occur. Ideally, the evacuation would begin before the passage of any radioactive material 

carried in a dispersal cloud. Evacuation is almost always indicated if the projected 

average effective dose is likely to be >0.5 Sv (50 rem) within a day. 

Variables affecting the pattern of radioactive material distribution include the time of day 

and year, the elapsed time since the accident, the size of the accident, and meteorological 

data to include wind patterns. Again, when deciding whether to evacuate or shelter in 

place, it is not recommended that predetermined levels alone be used for the decision. 

Basing the decision on these levels alone might lead to socioeconomic, physical, and 

psychological hardships that outweigh the benefits of lower exposure. For example, 

during the TMI accident, the Governor of Pennsylvania recommended that those 

members of society most vulnerable to radiation—namely, pregnant women and preschool-age children within a 5-mile radius of the plant—leave the area. Studies done 

more than 10 years after the TMI accident found that many residents still showed 

psychological symptoms of stress. Most vulnerable to stress were the mothers of young 

children and those who had been evacuated. Symptoms included somatic complaints, 

anxiety, and depression, posttraumatic stress disorder symptoms and physiological 

symptoms, hypertension, and higher levels of norepinephrine, epinephrine, and cortisol. 

Persistent fears and anxiety were found that centered on the fact that the residents had 

been living close (within 5 miles) to the source of such potentially catastrophic danger 

years earlier. 

The evacuation after the Chernobyl accident was poorly planned and chaotic. The 45,000 

residents of Pripyat, the city closest to the power plant, were evacuated during a 3-hour 

period 36 hours after the accident occurred and were not allowed to return to their homes. 

Ninety thousand more people were evacuated over the next few days, clearing a 30-km 

zone around the power plant. Thousands of farm animals were slaughtered because there 

was no longer anyone to tend to them. The evacuees often were relocated to areas that 

were openly unreceptive and even hostile to them. Preliminary reports suggest that 

women pregnant at the time of the accident were more likely to have stress symptoms 

than others evacuated during the accident. Children evacuated to Kiev were more likely 

to report frequent headaches, chronic illness, and poorer overall health. 
202

Additional factors must be considered when deciding whether to advise evacuation or 

sheltering in place in response to a radiological terrorist incident. Earlier 

recommendations by the EPA for evacuation were written for a nuclear power plant 

accident in which the release of radioactive material would occur hours after the initial 

accident, allowing the population to be evacuated in a plume-free environment. However, 

a terrorist attack is more likely to release a plume within minutes rather than hours of the 

initiation of the event. Therefore, sheltering is likely to be more protective in response to 

a radiological terrorist event. Sheltering should be performed whenever it is more 

protective than evacuation. 

Sheltering in place for protection from radioactive fallout is also an effective 

countermeasure with little negative impact for short periods of time (hours) and may be 

done in a fallout shelter, an underground area, or in the middle of a large building. Any 

roofed structure would be of some benefit and would protect people from alpha and beta 

radiation, because the structure would keep radioactive particles from falling on the skin 

and further reduce the chance of inhalation. The degree of protection from gamma 

radiation increases with the type of material used in constructing the shelter, from wood, 

to masonry, to metal, metal being the most effective. Glass is not very effective in 

preventing the penetration of gamma radiation, and windows should be avoided because 

of the risk of lacerations from broken glass due to pressure changes or other 

consequences of the accident. Sheltering generally reduce exposures to external and 

internal contamination by 5 to 10 times. Sheltering is almost always justified if it will 

prevent exposures of 0.050 Sv (5 rem). At exposures <0.005 Sv (500 mrem), sheltering is 

not warranted. Sheltering provides protection from the falling radioactive material by 

absorbing the radiation (shielding) and keeping the radiation outside of the shelter 

(distance) while the radioactive material decays (time). 

Table 6.11 shows the shielding factors from gamma radiation in a radioactive cloud 

plume. After the plume has passed and local authorities have announced that it is 

permissible or advisable to leave indoor protection, there will still be some radioactive 

material spread by the plume that is contaminating tree leaves, automobiles, and outdoor 

playground areas. Care should be taken to ensure that when children go outside they are 

in an area that has not been contaminated. Also, after leaving the shelter, it may still be 

necessary to relocate the population surrounding the region if the levels of contamination 

cannot be reduced quickly. It is also important to remember that family pets are not 

allowed in government shelters. Families should make plans and arrangements for the 

family pets ahead of time to keep them safe during the crisis. 

Water and food may be scarce. They should be used prudently, but severe rationing of 

water should not be imposed, especially for children because they are more susceptible to 

dehydration than adults. 

Parents should check with school officials to determine the school’s plans for an 

emergency and discuss with their children what procedures will be followed to reunite 

children with parents and caregivers. It may not be possible to reach children away from 
203

home immediately after the incident. A prearranged plan of where the children should go, 

if not in school, should be discussed and agreed on ahead of time. 

Long-Term Habitation Versus Abandonment 

The decision whether to remain long-term in an area or to abandon the area will depend 

on the levels of radiation remaining, the decay properties of the material, and the ability 

to physically remove the contaminated material. The decision should be reached in 

coordination with qualified health physicists because of complicating factors. 

Rehabilitation/Abatement 

Response organizations (local, State, and Federal) will need to prepare a site remediation 

plan. The clean-up process is lengthy and depends on the type of contamination and the 

site contaminated. There are temporary measures to fix radioactive material in place that 

will stop the spread of contamination. For example, flour and water mixtures, road oil, 

and water can be used to wet ground surfaces and prevent resuspension of the radioactive 

material. 

Rehabilitation of contaminated areas, equipment, and facilities depends on the physical 

removal of contaminated particles. Usually, this will be done by trained personnel. It is 

important to determine whether or not water sources have been contaminated. 

Hard surfaces are easier to rehabilitate than porous ones. Walls will generally be less 

contaminated than top and ground surfaces. Washing clothes and blankets in home 

washing machines can remove most contamination. It may not be possible to remove all 

contaminated material, however. Some articles can no longer be safely used (e.g., toys 

that have been left outside). 

Contamination of Crops, Water, Food Animals, and Milk Sources 

RDDs can also be used to contaminate livestock, fish, and food crops. However, huge 

quantities of radioactive material would be required to effectively contaminate food or 

water, and most radioactive material is not soluble in water. The U.S. Food and Drug 

Administration has guidance for accidental radioactive contamination of human food and 

animal feed. 

Water may also be contaminated as an aftereffect of an explosion involving an RDD or 

IND. The safety of water sources should be evaluated after the attack. Water filtration in 

the home can reduce levels of radiation by removing many of the radioactive particles, 

but boiling or chlorination is not beneficial. Until the water supply has been determined 

to be safe, only bottled water should be used for drinking and cooking. 

Water of questionable quality can be used for cleaning contaminated skin. This is because 

radiation exposure follows the principles of time, distance, and shielding. Radioactive 

material left on the skin will cause a higher level of exposure to an individual than 

exposure to water or the exposure from washing with contaminated water. Cleaning and 
204

washing the hands and face are especially important to prevent internal contamination 

when eating and drinking. 

Women who are breastfeeding should be especially concerned about the products they 

are ingesting. Fruit may be eaten if thoroughly washed or after the skin has been 

removed. Many types of fallout can become more concentrated in breast milk. For 

example, commercial milk can become contaminated with radioactive fallout if the milk 

was produced by cows grazing in the contaminated area. Contamination is further 

concentrated in human breast milk. Commercial formula reconstituted with bottled water 

is a safe alternative to breastfeeding until the mother’s milk is demonstrated to be safe. 

Bottled water and canned food products or foodstuffs imported from noncontaminated 

areas or produced before the radiological incident occurred should be free of radioactive 

contamination. 

Pets may bring radioactive material into the house on the bottoms of their paws and 

should be kept indoors. Wiping or washing the pet’s paws can be helpful to reduce the 

spread of contamination into the house. 

Mortuary Affairs 

The body retains radioactive materials after death. The body itself provides adequate 

shielding for alpha and beta-emitters. For gamma emitters (e.g., cesium-137), which are 

more penetrating radiation sources, radiation levels will be emitted by a contaminated 

corpse. Cremation should be avoided to prevent the radioactive material from vaporizing 

and becoming airborne. Guidance should be sought from local health physicists or city or 

State radiation safety experts or health departments. Concerns about burying the victims 

of radiation accidents have, in the past, raised fears in a community; specifically, the 

radiation accident in Goiania, Brazil, in 1987, and this possibility will need to be 

considered. 

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216

Figure 6.1. Probability of radiation casualties

Source: Armed Forces Radiobiology Research Institute. 
217

Figure 6.2. Environmental exposure pathway 

Note: Radioactive particles produced from a terrorist event travel to pastures as fallout. If 

the fallout contains radioactive iodine, some of it eaten by the cow would be passed into 

the cow’s milk. Consumption of contaminated fresh milk must be controlled during the 

first few weeks of an emergency. However, products made with contaminated milk, e.g., 

cheeses and canned milk, which can be stored for several months, may then be consumed 

safely. 

Source: Armed Forces Radiobiology Research Institute. 
218

Figure 6.3. Generic pediatric medical field card 

1. LAST NAME, FIRST NAME 

 

AGE 

 

 MALE 

 FEMALE 

PATIENT ID 

 

ESTIMATED WEIGHT 

 

RELIGION 

 

2. ADDRESS 

 

PARENT/GUARDIAN’S NAME 

 

NATIONALITY 

 

 

 NON-COMBATANT INJURY DISEASE PSYCH 

 AIRWAY 

 HEAD 

 WOUND 

 NECK/BACK INJURY 

 BURN 

 AMPUTATION 

 STRESS 

 OTHER (SPECIFY) 

3. INJURY 

 FRONT BACK 

 

 

4. LEVEL OF CONSCIOUSNESS 

 ALERT PAIN RESPONSE 

 VERBAL RESPONSE UNRESPONSIVE 

5. PULSE 

 

TIME 

 

6. TOURNIQUET 

 NO YES 

TIME 

 

7. MORPHINE 

 NO YES 

DOSE 

 

TIME 

 

8. IV 

 

TIME 

 

9. TREATMENT/OBSERVATIONS/CURRENT MEDICATION/ALLERGIES/NBC (ANTIDOTE) 

 

10. DISPOSITION 

 

 RELEASED 

 EVACUATED 

 DECEASED 

TIME 

 

11. PROVIDER/UNIT DATE/DATE (YYMMDD) 

12. REASSESSMENT 

DATE (YYMMDD) TIME OF ARRIVAL 

TIME 

BP/PS 

PULSE/POULS 

RESP/RESP 

13. CLINICAL COMMENTS/DIAGNOSIS 

 

DATE/TIME 

 

14. ORDERS/ANTIBIOTICS (SPECIFY)/TETANUS/IV FLUIDS 

 

15. PROVIDER DATE (YYMMDD) 

16. DISPOSITION RELEASED TO PARENT/GUARDIAN 

 EVACUATED 

 DECEASED 

TIME 

 

17. RELIGIOUS SERVICES BAPTISM 

 ANOINTING 

 CONFESSION 

 PRAYER 

 COMMUNION 

 OTHER 

CUSTODIAL ADULT AT DISPOSITION 

Source: Armed Forces Radiobiology Research Institute. 
219

Figure 6.4. Bone marrow irradiated to 3 Gy

Source: Armed Forces Radiobiology Research Institute. 
220

Figure 6.5. Pattern of a series of blood counts graphed over time after 3 Gy of 

whole-body exposure 

Note: Typical changes in the peripheral blood profile will occur as early as 24 hours after irradiation, with 

lymphocytes falling immediately on day 1. At about 4 weeks, cell lines bottom out. Without white cells, 

overwhelming infection occurs, and without platelets, hemorrhage is expected. 

Source: Armed Forces Radiobiology Research Institute. 
221

Figure 6.6. Classic Andrews diagram (1965) 

Note: Lymphocytes drop quickly with high radiation doses; a drop of 50% or more in 24 hours indicates a 

severe radiation injury. 

Source: Armed Forces Radiobiology Research Institute. 
222

Figure 6.7. Contamination versus exposure

Note: Contamination and exposure are not the same. Patients can have external exposure to radiation, 

external contamination by radioactive material, internal contamination with radionuclides, or any 

combination thereof. 

S = Source of radiation. 

Source: Armed Forces Radiobiology Research Institute. 
223

Figure 6.8. Examples of radiation survey meters
224

Figure 6.9. Recommended procedures for monitoring personnel 

1. Have the person stand on a clean 

pad. 

2. Instruct the person to stand straight, 

feet 

spread slightly, arms extended with palms 

up 

and fingers straight out. 

3. Monitor both hands and arms; then 

repeat with hands and arms turned over.

4.Starting at the top of the head, cover the 

entire body, monitoring carefully the 

forehead, 

nose, mouth, neckline, torso, knees, and 

ankles.

ankles.

5. Have the person turn around, and repeat 

the survey on the back of the body.

6. Monitor the soles of the feet. 

Source: Courtesy Oak Ridge Associated Universities’ REAC/T Center. 

© 2000, Oak Ridge Associated Universities 

Contract acknowledgement Notice to Users
225

Figure 6.10. Localized radiation effects 

35

• Skin - No visible injuries < 100 rem

– Main erythema, epilation >500 rem

– Moist desquamation >1,800 rem

– Ulceration/Necrosis >2,400 rem

• Cataracts

– Acute exposure >200 rem

– Chronic exposure >600 rem

• Permanent Sterility

– Female >250 rem

– Male >350 rem

Localized Radiation Effects - Organ System 

Threshold Effects

Source: Health Physics Society. From “Emergency Department Management of Radiation Casualties,” a 

presentation for hospital staff trainees. Available for download at 

http://hps.org/hsc/documents/emergency.ppt. 
226

Table 6.1. Biological dosimetry assays and operational parameters 

Class of 

biomarker 

Assay Time window Operating dose 

window (Gy, 

acute photonequivalent) 

Prodromal 

signs and 

symptoms 

Onset of vomiting <12 hr 2–20 

Hematological Depletion of peripheral 

blood lymphocytes 

<1.5 wk 2–8 

Cytological Lymphocyte-metaphase 

spread dicentric 

Lympho cyte-premature 

chromosome condensation 

<several months* 

<several months* 

0.2–5 

0.2–20 

* Generally, blood is sampled 24 hours after radiation exposure for cytological chromosome aberration 

analysis of dose. 
227

Table 6.2. Biodosimetry based on acute photon-equivalent exposures 

Dose 

estimate

Time to onset 

of vomiting

Absolute lymphocyte count 

(× 109

/L)b (day)

Lymphocyte 

depletion 

ratec

Number of 

dicentricsd

Gy %a Time 

(hr)

0.5 1 2 4 6 8 Rate 

constant

Per 50 

cells

Per 1000 

cells

0 — — 2.45 2.45 2.45 2.45 2.45 2.45 — 0.05-0.1 1-2 

1 19 2.30 2.16 1.90 1.48 1.15 0.89 0.126 4 88 

2 35 4.63 2.16 1.90 1.48 0.89 0.54 0.33 0.252 12 234 

3 54 2.62 2.03 1.68 1.15 0.54 0.25 0.12 0.378 22 439 

4 72 1.74 1.90 1.48 0.89 0.33 0.12 0.044 0.504 35 703 

5 86 1.27 1.79 1.31 0.69 0.20 0.06 0.020 0.63 51 1024 

6 94 0.99 1.68 1.15 0.54 0.12 0.03 0.006 0.756 

7 98 0.79 1.58 1.01 0.42 0.072 0.012 0.002 0.881 

8 99 0.66 1.48 0.89 0.33 0.044 0.006 <0.001 1.01 

9 100 0.56 1.39 0.79 0.25 0.030 0.003 <0.001 1.13 

10 100 0.48 1.31 0.70 0.20 0.020 0.001 <0.001 1.26 

Note: Depicted above are the three most useful elements of biodosimetry. The first column illustrates the 

percent of people who vomit, based on dose received and time to onset. The middle section reveals the time 

frame in which a patient develops lymphopenia. Two lymphocyte samples drawn at different times can 

then be used to predict a rate constant, which is then used to estimate exposure dose. The final column 

represents the current “gold standard,” which requires several days before the result is known. We 

recommend initiating colony-stimulating factor if either onset of vomiting or lymphocyte depletion kinetics 

suggests an exposure for which treatment is recommended, which can then be discontinued if necessary 

when data from chromosome dicentrics are known. a Cumulative percentage of victims with vomiting. b Normal range 1.4–3.5 × 109

/L. c The lymphocyte depletion rate is based on the model Lt = 2.45 × 109

/L × e-k(D)t, in which Lt equals the 

lymphocyte count (× 109

/L), 2.45 × 109/L equals a constant representing the consensus mean lymphocyte 

count in the general population, k equals the lymphocyte depletion rate constant for a specific acute 

photon dose, and t equals the time after exposure (days). d Number of dicentric chromosomes in human peripheral blood lymphocytes. 

Acknowledgments: The authors thank W.E. Jackson for assistance in preparation of this table. Special 

thanks go to Mark Behme for expert graphical assistance. This work was supported in part by the Armed 

Forces Radiobiology Research Institute, work number AFRRI-04-3. 
228

Table 6.3. Initial or prodromal phase, whole body irradiation from external 

radiation or internal absorption (gamma radiation) 

Subclinical range (cGy 

[rad]) 

Sublethal range(cGy 

[rad]) 

Lethal range(cGy 

[rad]) 

0–100 100–200 200–600 600–800 800–3000 >3000

Vomiting 

(onset and 

percentage)

None 3–6 hr 

5%–50%

2–4 hr 

50%–100%

1–2 hr 

75%–100%

<1 hr 

90%–100%

<1 hr 

100%

Nausea 

duration

<24 hr <24 hr <48 hr <48 hr <48 hr

Diarrhea 

(severity, 

onset, and 

percentage)

 Moderate 

3–8 hr 

<10%

Severe 

1–3 hr 

>10%

Severe 

<3 hr 

>10%

Very 

severe 

<1 hr 

100%

Lymphocyte 

count (× 

106

/L)*

Unaffected Minimally 

decreased 

within normal 

range

2000–1000 

at 24 hr

1000–800 at 

24 hr

<1000 at 24 

hr

Decreases 

with 

hours

Headache, 

(severity, 

onset, and 

percentage) 

 Slight Mild to 

moderate 

4–24 hr 

<50% 

Severe 

3–4 hr 

<80% 

Severe 

<4 hr 

>80% 

CNS 

function 

No 

impairment 

No impairment Routine task 

performance; 

cognitive 

impairment 

for 6–20 hr 

Simple and 

routine task 

performance; 

cognitive 

impairment 

for >24 hr 

Progressive 

incapacitation 

Body 

temperature 

(severity, 

onset, and 

percentage) 

 Normal Increased 

and fever 

<3 hr 

10%–100% 

High fever 

<1 hr 

100% 

Source: Adapted from other resources (Armed Forces Radiobiology Research Institute, 2003; International 

Atomic Energy Agency. Diagnosis and Treatment of Radiation Injuries. Safety Reports, Series 2. IAEA, 

Vienna, Austria; 1998); used with permission. 

*Normal range 1400–3500 × 106

/L 
229

Table 6.4. Diagnostic steps in 

acute radiation sickness 

Rapid diagnosis 

Prodrome: nausea, vomiting 

Lymphocyte counts – best

Later 

Physical dosimetry 

Biodosimetry 

Skin changes 
230

Table 6.5. Timing to onset of vomiting (prodrome) 

Dose (Gy) Onset (hr) Duration (hr) Latency 

0.5–2 Absent or 6–24 <24 Absent to 3+ wk 

2–3 2–6 12 to <24 2–3 wk 

3–5 1–2 24 1–2.5 wk 

>5 Minutes to 1 48 2–4 days 
231

Table 6.6. Dose assessment summary 

Signs and symptoms Radiation dose (Gy) 

Chromosome abnormalities 0.20 

Lymphocytes reduced 1 

Nausea/vomiting at 3 hr 2–3 

Skin: erythema (1 day), 

epilation (14 days) 

3–5 
232

Table 6.7. Guidelines for bioassay sampling 

Suspected 

radioactive 

material 

Feces: begin 

sample after 

exposure 

Urine: begin sample 

after exposure 

Sample quantity 

Plutonium 24 hr 24 hr then 2 wk 24 hr total 

Uranium 24 hr 24 hr then 7–10 days 24 hr total 

Tritium N/A 12 hr 1 voiding 
233

Table 6.8. Antibiotics for treatment of post-radiation neutropenia 

Antimicrobial Dosage and 

route

Comments and spectrum of activity

First-choice antimicrobials (listed in order of potential efficacy) 

Cefepime 150 mg/kg divided 

q 8 h, IV or IM 

Not available in oral form. 

Activity against gram-positive organisms, except Enterococcus spp. 

Activity against gram-negative organisms, including 

Pseudomonas aeruginosa and certain Enterobacteriaceae that 

generally are resistant to most third-generation 

cephalosporins.

Ceftazidime 100–300 mg/kg/day 

divided q 8 h 

May need to add amoxicillin* or vancomycin† 

Not available in oral form. 

Activity against gram-negative organisms, including 

Pseudomonas aeruginosa and certain Enterobacteriaceae that 

generally are resistant to most third-generation 

cephalosporins.

Ceftriaxone 50–75 mg/kg/day, 

IV or IM, once a 

day 

Not available in oral form. 

Activity against gram-positive organisms, except Enterococcus spp. 

Second-choice 

Gentamicin 3–7.5 mg/kg/day 

divided q 8–24 h, 

IV or IM

May need to add amoxicillin* or vancomycin† 

Not available in oral form. 

Amikacin 15–22.5 

mg/kg/day 

divided q 8 h, IV 

or IM

May need to add amoxicillin* or vancomycin† 

Not available in oral form. 

Third-choice 

Ciprofloxacin 20-30 mg/kg/day 

divided q 12 h, 

PO, IV, or IM

May need to add amoxicillin* or vancomycin† 

Effective against gram-negative organisms and atypical 

bacteria. 

Also effective against Pseudomonas species but poor 

coverage against gram-positive organisms (including 

Staphylococcus aureus and nonhemolytic streptococci).

Levofloxacin 10 mg /kg/day, 

PO, IV, or IM

May need to add amoxicillin* or vancomycin† 

Effective against gram-negative organisms and atypical 

bacteria. 

More gram-positive coverage than ciprofloxacin.

Gatifloxacin 10 mg/kg/day, 

PO or IV 

Expanded spectrum against both gram-negative and grampositive organisms. 

Can be administered as single agent.

* Dosage: 25–50 mg/kg/day divided q 8 h, PO 

† Dosage: 40–60 mg/kg/day divided q 6–8 h, IV 
234

Table 6.9. Threshold radioactive exposures and recommended prophylactic 

single doses of KI 

Predicted thyroid 

exposure (Gy) KI dose (mg) 

No. of 130-mg 

tablets 

No. of 65-mg 

tablets 

Adults 

>40 yr old ≥5 130 1 2 

Adults 

18–40 yr ≥0.1 130 1 2 

Pregnant or 

lactating women ≥0.05 130 1 2 

Adolescents 12–

18 yr old ≥0.05 130 1 2 

Children 

3–12 yr old ≥0.05 >65 1⁄2 1 

Children 

1 mo to 3 yr old ≥0.05 32 1⁄4 1⁄2 

Neonates 

birth to 1 mo old ≥0.05 16 1/8 1⁄4 

Adapted from U.S. Department of Health and Human Services, FDA, Center for Drug Evaluation and 

Research. Potassium Iodide as a Thyroid Blocking Agent in Radiation Emergencies. Available at 

http://www.fda.gov/cder/guidance/4825fnl.htm. 
235

Table 6.10. Radionuclide specific therapies 

Radionuclide Therapy Mechanism of action 

Iodine KI Blocks thyroid deposition 

Cesium/Rubidium/Thallium Prussian blue Blocks GI absorption and prevents 

recycling 

Plutonium and transuranics 

(Americium, Californium, 

Lanthanum, Curium) 

DTPA Acts as chelating agent 

Uranium Bicarbonate Alkalinizes urine, decreases 

chances of acute tubular necrosis 

Tritium Forced fluids, diuretics Dilutes isotope 

Strontium Oral aluminum phosphate 

or barium sulfate 

Blocks GI absorption 

Radium Magnesium sulfate lavage Prevents absorption 

Phosphorus Stomach lavage, aluminum 

hydroxide, oral phosphates

Prevents absorption, blocks 

cellular deposition 

Cobalt Gastric lavage, purgatives; 

penicillamine if severe 

Prevents absorption, acts as 

chelating agent 

Source: National Council on Radiation Protection and Measurements. Management of Persons Accidentally 

Contaminated with Radionuclides. Report Number 65, 1979. Bethesda, MD. Reprinted with permission. 
236

Table 6.11. Reduction in exposure by sheltering 

Material – structure or location Relative shielding strength 

Outside No reduction in exposure 

Vehicle No reduction in exposure 

Wooden frame house Slight reduction in exposure 

Basement of wooden house Almost 50% reduction in exposure 

Masonry home Almost 50% reduction in exposure 

Basement of masonry house >50% reduction in exposure 

Large office or industrial building 

(inner areas, away from windows) 

80% reduction in exposure 

Source: Adapted from Management of Terrorist Events Involving Radioactive Material, Report 138, Table 

8.5, p. 109. Bethesda, MD: National Council on Radiation Protection and Measurements; October 2001. 

Used with permission. 
237

Chapter 7. Blast Terrorism 

Introduction 

In the short time between January and September 2003, explosive devices were involved 

in 73 of 189 terrorist events that occurred worldwide. A 1997 report by the Department of 

Justice found an abundance of evidence suggesting that given intent, the knowledge 

required to build bombs is readily available in print and on the Internet. The report cited 

at least 50 publications in the Library of Congress; several texts intended for military 

training, agricultural, and engineering use; 48 different underground pamphlets and 

publications; and countless sources on the World Wide Web. Bomb data from the FBI 

indicate that from 1987 to 1997, bombing incidents increased approximately 2.5 times, 

peaking in 1994 with 3,163 domestic bombing incidents. Of those incidents, 66% 

involved explosive devices, and the remaining 24% involved incendiary devices. More 

recent bomb data indicate that the number of domestic bombing incidents has decreased 

since 1994, with 1,797 incidents in 1999. In most incidents, low-explosive fillers were 

used. High-explosive ammonium nitrate mixtures, however, were used during the first 

World Trade Center bombing and the Oklahoma City bombing, highlighting the 

tremendous destructive power of a significant amount of a high explosive. 

The raw materials for explosive devices are regularly found in areas of farming or mining 

activities. Due to the public accessibility of explosives materials and bomb-building 

knowledge, a domestic terrorist attack would probably take the form of a conventional 

explosive munitions attack. This chapter introduces the spectrum of injuries caused 

during an explosion and the differences between blast trauma and conventional trauma. 

Both blast trauma and conventional trauma have aspects of blunt, penetrating, burn, 

crush, and inhalational injuries. However, victims of a blast may suffer all of these 

injuries simultaneously, with additional injury caused by the blast wave itself, i.e., 

primary blast injury. Primary blast injuries are lethal, unique, and often subtle. Although 

the vast majority of blast injury victims suffer from conventional injuries, lack of 

knowledge about primary blast injuries and failure to recognize a blast’s effect on certain 

organs can result in additional morbidity and mortality. 

Explosives 

Explosives are solid, liquid, or gaseous substances that, when detonated, transform 

rapidly into more stable products in the form of heat, gas, and energy. Explosives are 

frequently used in military, demolition, and industrial applications and are categorized as 

low explosives or high explosives. Low explosives are considered propellants and are 

used chiefly in small arms and munitions. Two examples are smokeless powder or black 

powder. High explosives have a greater potential for destruction due to their higher 

burning rate and therefore higher shattering effect. Notable examples of high explosives 

are TNT (trinitrotoluene), dynamite, RDX, C-4, ammonium nitrate, ammonium-nitrate 

fuel oil, HMX, and PETN. Due to their relative stability, these compounds require 

another explosive (e.g., a primer or detonator) to initiate a charge. 
238

Blast Fundamentals 

Understanding how an explosion causes tissue damage and injures victims requires some 

knowledge of the physics occurring during an explosion. Detonation of an explosive 

device causes rapid chemical conversion of an explosive material with the release of 

high-pressure gases and energy. These high-pressure gases expand supersonically, 

moving air particles, called the blast wind, and propagating in all directions in the form of 

a shock wave. The blast wind lasts milliseconds, and its strength varies with the strength 

of the explosive device detonated. Wind velocity can vary from 40 mph from the 

generation of 1 psi (pound per square inch) to 1,500 mph from a 100 psi detonation. As it 

expands, this shock wave causes compression of the ambient atmosphere and an 

instantaneous rise in atmospheric pressure above baseline, known as overpressure. The

leading edge of the expanding blast wave is termed the blast front. As the wave of 

overpressure passes through, it subjects tissues in its path to enormous forces called blastloading forces (measured in psi). The amount of force capable of perforating a tympanic 

membrane is 5 psi, and that considered to be lethal in 50% of exposures is 80 psi. 

Pressure measurements of the blast wave recorded in one place reveal the pressure-time 

relationship of the waveform. Key observations include the following: 

• Atmospheric pressure rises almost instantaneously to a peak overpressure as the 

wave passes through. 

• Atmospheric pressure remains supra-atmospheric for some period of time and 

then decays to dip below the atmospheric pressure baseline, heralding the 

negative pressure phase. 

Over time, atmospheric pressure returns to baseline. Due to the expansion of gases, a 

state of relative vacuum is created at the detonation site. This causes the gas flow to 

reverse during the negative phase—in contrast to the outward air flow occurring during 

the positive phase. All of the tissue injuries described by the blast wave have been due to 

overpressure. However, the pathophysiologic effects of underpressure are still under 

investigation, there has been some suggestion that underpressure itself can cause injury. 

Many believe that the harmful effects on the body caused by a blast result from the 

pressure differentials exerted on tissues by the expanding wave. However, because the 

peak overpressure decays exponentially, a victim must be relatively close to the 

detonation for the blast wave itself to induce tissue injury. Several factors, including the 

following, affect the degree of blast pressure loaded to objects: 

• The distance between the object and the detonation. 

• The orientation of the object to the incident wave. 

• The degree of reflected waves to which the object is subjected. 

This latter point is the reason that, given equal peak overpressures, victims found in 

corners or in underwater blasts suffer greater injury. In both situations, the victim is 

subject to the incident wave in addition to multiple reflected waves. 

The three physical properties that cause tissue damage during a blast are the spalling 

effect, implosion, and inertia. 
239

Spalling effect. When a blast wave travels through tissue of homogenous density, it 

causes the tissue to vibrate. However, when a wave passes through air-filled tissue such 

as the lungs, intestinal lumen, or the middle ear, it travels from areas of higher density to 

the air-filled areas of lower density. The result is tension at the surface interface, and 

particles are thrown or spalled into the less dense medium. This causes micro- and 

macro-tears in the tissue wall, resulting in hemorrhage, edema, and the loss of structural 

integrity. 

Implosion. In implosion, the blast wave is thought to cause compression of tissues (or 

organs), resulting in recoil and expansion of the tissue (or organ) as the wave exits. This 

causes structural damage to solid tissues principally at the areas of attachment, e.g., at the 

hila for solid organs. 

Inertia. Blasts result in a wind with the ability to accelerate people and large stationary 

objects. Acceleration and deceleration causes multiple types of injuries, in particular 

blunt injuries. Experimental data have suggested that inertia may act at the level of 

tissues themselves. In the lungs, due to differing densities, bronchovascular elements 

would be expected to accelerate at different rates than delicate alveolar tissue, resulting in 

shearing at these sites. 

Blast Trauma 

Many mechanisms of injury are involved in blast injuries. 

• Primary blast injury refers to tissue damage by the blast wave itself, specifically 

in areas with tissue-gas interfaces such as the lungs, the intestines, and the 

tympanic membrane. 

• Secondary injury refers to penetrating or blunt injury that results from the 

acceleration of shrapnel or debris. Terrorists often add metallic fragments such as 

nails to devices to maximize the potential for penetrating injuries. Secondary 

injury is the most common type of injury seen, because it does not require the 

victim to be near the point of detonation. 

• Tertiary injuries result from acceleration-deceleration forces imposed as the blast 

wind propels the victim. As the body is tumbled on a rigid surface, it suffers from 

blunt injury, in particular closed head injury, as well as penetrating injuries as it is 

accelerated over sharp debris. 

• A fourth mechanism includes flash and flame burns, inhalational injury, and crush 

injuries incurred from fires and structural collapse. 

Secondary and tertiary injury overlap significantly, and both are more common than 

primary blast injury. However, primary blast injuries are the most severe. 

The effects of the blast wave on structural elements and on human tissues combine to 

cause complex combinations of injuries in blast victims; injuries are variable within one 

event. The principal factor that determines severity of injury is the distance of the victim 

from the site of detonation (Table 7.1). Injuries also vary due to the victim’s position with 
240

respect to incident waves and the degree of reflected shock waves to which the victim is 

exposed. 

Primary blast injury. Primary blast injuries (PBI) are injuries caused specifically by 

exposure of the body to the blast wave. Pulmonary barotrauma, air embolization, and 

intestinal perforation are the unique principal causes of death after a blast. Although most 

injuries in an explosion are secondary, tertiary, and miscellaneous (crush, burn, 

inhalational), a person close enough to a detonation would be subjected to the effects of 

the blast on a microscopic level. 

Urban bomb blasts tend to have the following characteristics: 

• Most victims sustain minor injuries. 

• Most injuries affect the head, neck, and extremities. 

• Torso injuries are uncommon yet lethal. 

• Primary blast injuries are uncommon because victims tend to die before arriving 

at the hospital. 

However, because all bomb blast incidents are different, the types of injuries seen are 

variable. A blast that occurs in an enclosed space, such as a bus, is associated with more 

severe injuries and a higher incidence of primary blast injuries. The number of casualties 

would be expected to be less than in an equipotent detonation in open space. Mortality is 

also higher when a blast occurs in an enclosed space, because the shock wave is 

contained and reaches a higher overpressure and a longer positive phase. However, 

containment of the wave does not affect the generation of propelled debris. Therefore, 

secondary and tertiary injuries, including amputations from large objects, are the same 

whether the blast occurs in an enclosed space or open air. 

The spectrum of PBI reflects involvement of the gas-containing organs and the 

pathophysiologic effects of these organs on other systems (Table 7.2). As in conventional 

trauma, all victims should be managed with careful attention to the airway, breathing, and 

circulation; however, in certain patients, complications may arise with respect to positivepressure ventilation and fluid resuscitation management. 

Blast lung injury and air embolization. The anatomic structure of the lung makes it 

susceptible to the effects of blast barotrauma. Alveolar spaces are engulfed by delicate 

capillaries in a way that maximizes the surface area available for gas exchange. 

Pathophysiology. The pathophysiology induced by the blast involves the spalling of 

particles across the tissue-gas interface (alveolus) with the generation of micro-tears. This 

fills the air space with blood, edema, and tissue particles, impairing gas exchange. The 

most common lesion of the airway is the stripped-epithelium lesion, in which the 

bronchial epithelium and mucociliary apparatus are stripped from the basal lamina, 

resulting in ulcerations of the submucosa and impaired clearing of secretions. Structural 

tears occur through interfaces of blood vessels and air spaces, creating direct openings 

where air bubbles could escape into the circulation. 
241

Clinical findings and diagnosis. Clinically, blast lung injury is evidenced by various 

degrees of the following: 

• Hemoptysis. 

• Hypoxia. 

• Hemothorax. 

• Dyspnea. 

• Tachypnea. 

• Chest pain. 

• Cough. 

• Wheezing. 

• Rales/crackles. 

• Decreased breath sounds. 

• Pneumothorax. 

• Hypopharyngeal hemorrhage. 

• Subcutaneous crepitus. 

• Tracheal deviation. 

Clinical findings range from contusion and ecchymosis to massive hemoptysis, severe 

ventilation/perfusion mismatch, and air leak, leading rapidly to death. Most blast lung 

injury develops early in the course of treatment, within 1–2 hours. Signs and symptoms 

may progress within 24–48 hours to respiratory failure or acute respiratory distress 

syndrome (ARDS), or both. Respiratory failure is often due to secondary additive effects 

such as shock, organ failure, or inhalation of smoke and toxic substances. 

The most important diagnostic test for blast lung injury is a chest radiograph. However, 

in stable patients, CT scans provide important additional information. Pulmonary 

hemorrhage is the most consistent microscopic finding in blast lung injury, and most 

survivors of a blast will have infiltrates on a chest radiograph. 

Treatment and complications. Blast lung injury is not universally fatal, given aggressive 

and timely management. Initial management involves maximizing oxygenation and 

minimizing additional barotrauma. Most important is maintaining a patent airway, free of 

blood and secretions. Victims should be placed on oxygen to prevent hypoxia. Control of 

massive hemoptysis involves tracheal intubation and, whenever possible, selective 

ventilation of the contralateral lung. The source of bleeding in massive hemoptysis may 

be from one or both lungs and is often difficult to determine. Having a high index of 

suspicion for pneumothorax or tension pneumothorax cannot be overstated. The risk is so 

great that prophylactic tube thoracostomy has been suggested. 

The development of systemic air embolization from injured lung tissue is a grave 

complication. The greater the degree of lung injury, the higher the risk of emboli 

formation. Although the actual incidence is unknown and is probably underrecognized, 

air embolization in blast injury is speculated to be the main cause of death within the first 

hour after a blast. Air emboli in the vascular system carry a high mortality rate because 

the air bubbles can potentially cause occlusion of the coronary arteries (myocardial 

ischemia), cerebral vessels (stroke), or cardiac outflow tracts (shock). They cause 
242

additional morbidity in the nature of blindness (occlusion of retinal arteries) and ischemia 

of end organs. The ultimate clinical result depends on the site of embolization. Signs and 

symptoms that suggest arterial air embolization include the following: 

• Air bubbles in retinal vessels. 

• Blindness. 

• Chest pain. 

• Arrhythmia. 

• Myocardial ischemia. 

• Focal neurologic signs. 

• Seizures. 

• Loss of consciousness. 

• Vertigo. 

• Livedo reticularis. 

• Tongue blanching. 

Air emboli pose a challenge in emergency management of blast victims. Air emboli are 

not only difficult to diagnose, but also have a clinical presentation similar to that of other 

more familiar clinical entities. For example, myocardial ischemia, which is usually easily 

recognized, is most likely to be secondary to coronary vessel embolization (versus the 

traditional mechanisms of ischemia) in victims with blast lung injury. Management of 

these patients should focus on halting the passage of air. However, in patients exhibiting 

a change in their mental status, more common traumatic causes (e.g., intracranial 

hemorrhage from blunt head injury) should be addressed first, before focusing on 

embolization. 

Air emboli can be confirmed by direct visualization of air bubbles or disrupted air 

passages via echocardiography, transcranial Doppler, CT scan, or bronchoscopy. 

Unfortunately, there are no data on the sensitivity of these techniques in detecting emboli 

in blast victims. Transesophageal echocardiography can detect gas bubbles as small as 

2 μm, but its availability is limited. Sudden circulatory or neurologic collapse, especially 

if PPV has been started, combined with a high index of suspicion, is enough to make the 

diagnosis of air embolization until proved otherwise. Other suggestive clinical findings 

include possible evidence of bubbles in retinal vessels, aspiration of air from arterial 

lines, or marbling of the skin or tongue. 

In conventional penetrating and blunt lung injuries, management of massive air 

embolization involves thoracotomy on the affected side to stop the passage of air. Based 

on this experience, management of air embolization in blast lung injury has also been 

primarily surgical. However, in blast lung injury, identifying the source of emboli may be 

difficult, since both lungs or multiple sites may be involved. Temporarily placing patients 

in specific positions to trap air bubbles anatomically (to prevent them from entering the 

circulation) has been suggested. However, there is no single maneuver that prevents air 

from entering both the arterial and venous circulation simultaneously. Despite the lack of 

data, placing the patient in a modified left decubitus position (more toward prone) or 

prone position is thought to be the most anatomically logical alternative. These positions 

place the coronary ostia in the lowest position in the body and the left atrium in the 
243

highest position. Because of the practical limitations of having patients in these positions, 

placing the patient with the injured lung down, or in the dependent position, to minimize 

embolization by increasing venous pressures on that side, has also been suggested. 

Hyperbaric oxygen therapy has been successfully used to treat cerebral air emboli from 

diving decompression injuries by actually causing bubble volume to decrease. Again, 

recommendations for management of blast-induced air embolization are largely based on 

conventional trauma experience. Stopping the passage of air bubbles into the circulation 

is paramount; however, doing so by surgically clamping the hilum when the injury is not 

clearly unilateral may not be necessary. Knowledge of lung isolation techniques is 

important for patient management. 

Positive-pressure ventilation (PPV) is a last resort for blast victims; it is reserved for 

cases of severe respiratory failure or massive hemoptysis, or for patients requiring 

emergency surgery for other reasons. Cardiovascular, respiratory, or neurologic collapse 

within minutes of PPV being instituted has been reported. In addition, PPV is thought to 

contribute to the generation of air emboli due to the high airway pressures it causes, and 

it has been implicated in the later reopening of fistulas. 

In the spontaneously breathing patient, pulmonary venous pressures are higher than 

airway pressure, which prevents the passage of emboli into the venous system. During 

PPV or when pulmonary vascular pressures are low (e.g., with hypovolemia), airway 

pressures are higher, and the gradient is reversed, facilitating the passage of air and debris 

into the vascular system. Techniques based on experience in ventilating patients with 

pulmonary contusion and ARDS have been proposed for ventilating victims of blast lung 

injury who must be intubated. These techniques include low peak inspiratory pressures 

(<35–40 cm H2O), low tidal volumes, high peak end-expiratory pressures, permissive 

hypercapnea, high-frequency jet ventilation, pressure-controlled inverse-ratio ventilation, 

and nitric oxide inhalation. As a last heroic attempt, extracorporeal membrane 

oxygenation has been suggested. 

Gastrointestinal blast injury. After lung injury, GI injury is the second most lethal 

injury after a blast. Abdominal injuries secondary to open-air blasts are less common than 

blast lung injury; however, they are much more common in underwater blasts. 

Pathophysiology. The pathophysiology of GI injury is similar to that of blast lung injury, 

and abdominal injuries are a significant cause of delayed mortality. As the wave impacts 

the abdominal cavity, it compresses and distorts the internal tissues, resulting in 

hemorrhage and/or rupture of solid organs. As the blast wave passes through tissues with 

a gas interface, it causes spalling of particles into the intestinal lumen. The terminal ileum 

and colon are predisposed to injury because they contain the greatest amount of air, while 

the small intestine is relatively spared. The resultant wall tears, intramural hematomas, 

and hemorrhage may predispose the intestine to perforation. In severe blasts, the direct 

force of the wave itself may also cause perforation, although it is unknown whether the 

perforation is immediate or delayed. 
244

Clinical findings and diagnosis. The signs and symptoms of GI injury may be nonspecific 

and change over time. They include the following: 

• Lack of bowel sounds. 

• Hematochezia. 

• Hypotension. 

• Involuntary guarding. 

• Rebound tenderness. 

• Abdominal pain. 

• Nausea and vomiting. 

• Orthostasis or syncope. 

• Testicular pain. 

• Tenesmus. 

Evaluation of the abdomen begins with a physical examination, standard trauma 

screening laboratory tests, and a high index of suspicion for injury. Making the diagnosis 

of perforation in an area of trauma is challenging for many reasons. First, the findings can 

be subtle and masked by other, more critical injuries. Second, the patient may be 

unconscious, making the value of serial examinations limited. Third, diagnostic 

examinations, although useful for detecting hemorrhage, may be misleading or 

insensitive in the early stages of perforation. 

Management. The goals of management are to identify and control internal bleeding and 

to identify and repair any perforated viscus. In stable patients in whom injury is 

suspected, the abdominal radiograph has largely been replaced by CT scan, 

ultrasonography, and diagnostic peritoneal lavage. CT scan provides useful information 

regarding intra-abdominal hemorrhage, organ injury, free intraperitoneal air, and 

intramural hematoma; however, it has a low sensitivity for identifying a hollow viscus 

perforation. In hemodynamically stable patients with blast lung injury too severe to be 

surgical candidates, exploratory abdominal procedures may be delayed. In these patients, 

broad-spectrum antibiotics are recommended pending confirmation of an intact bowel. 

Exploratory laparotomy may be necessary in hemodynamically unstable patients in 

whom internal bleeding is suspected. Because surgical outcomes in blast victims are 

poor, surgery, like intubation, is a last resort and should be weighed against the risk 

associated with missing a perforation. 

Blast auditory injury. The auditory system is the system most frequently injured during 

a blast. Auditory injury is more common than lung or GI injury because the overpressure 

necessary to perforate tympanic membranes (5 psi) is well below that expected to cause 

lung or GI injury. Hearing loss either with or without a ruptured tympanic membrane is 

quite common. It can be debilitating and make communication with the victim difficult. 

Although some sensorineural hearing deficits improve over the first few hours, deficits 

are permanent in approximately 30% of victims. 

Pathophysiology. Normally, sound pressure waves are transmitted from the tympanic 

membrane through the ossicular bones in the middle ear, where they are converted into 

mechanical vibrations. These mechanical vibrations, through the involvement of 
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perilymph in the membranous labyrinth, are converted again into nerve impulses at the 

organ of Corti in the cochlea. The blast wave overwhelms this intricate and delicate 

system and is then amplified down the conductive and sensory neural pathways. The 

result can be injury to any of part of the auditory system, including perforation of the 

tympanic membrane, disruption of the ossicular chain, or damage to the organ of Corti. 

In addition to the damage caused by amplification of the shock wave within the auditory 

system, the instantaneous rise in overpressure inflicts additional damage. The ability to 

equilibrate middle ear pressure via the eustachian tube is overwhelmed. The resulting 

expansion of the cavity and distortion of tissue causes additional mechanical injury. 

Tympanic membrane rupture. Tympanic membrane rupture from most causes heals 

spontaneously, with 10% of the eardrum expected to heal per month. Spontaneous 

healing has been observed in perforations involving <80% of the membrane. 

Complications include failure to heal (10-20%), infection, and cholesteatoma formation. 

Despite the long-held belief that tympanic membrane perforation is a marker for delayed 

onset of pulmonary and GI blast injuries, this does not appear to be the case based on 

outcomes of 142 survivors of suicide bombings. Of the survivors who had perforated 

tympanic membranes, none developed delayed presentations of other primary blast 

injuries. Those with pulmonary blast injury were acutely ill early in their course, and 

none had a delay in presentation of respiratory symptoms. Notably, 18% of those with 

blast lung injury did not have perforated tympanic membranes. Therefore, isolated 

tympanic membrane rupture does not seem to be a marker for delayed onset of other 

primary blast injuries. Regardless, due to the paucity of data, and in particular the lack of 

pediatric data, it would seem prudent to delay the implementation of official clinical 

guidelines regarding the management of pediatric victims of auditory blast injury. 

Evaluation and management should be done on a case-by-case basis. 

Ossicular chain and cochlear injury. Ossicular bones attach to the tympanic membrane 

and transmit its vibrations to the cochlea, where the vibrations are converted into neural 

impulses via tiny hair cells. The overpressure can cause distortion and fracture of the 

ossicular bones, but this is rare, and blasts causing inner-ear damage, yet sparing the 

ossicular bones have been reported. The relative resilience of the ossicular bones is not 

shared with the cochlea at the organ of Corti. This delicate system is overwhelmed by the 

amplification of waves, causing loss of structural integrity with damage of the inner and 

outer hair cells. The result is the development of conductive and/or sensorineural hearing 

loss. 

Clinical findings. Victims may be initially unaware of acoustic injury or may complain of 

tinnitus, hearing loss, or ear pain. The spectrum of clinical findings in auditory blast 

injury includes the following: 

• Tinnitus. 

• Otalgia. 

• Tympanic perforation. 

• Ossicular chain disruption. 
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• Ossicular chain fracture. 

• Labyrinthine fistula. 

• Perilymphatic fistula. 

• Loss of hair cell integrity. 

• Conductive hearing loss. 

• Sensory hearing loss. 

• Basilar membrane rupture. 

Management. In general, emergency management of auditory injuries involves clearing 

the ear canal of debris, minimizing exposure to loud noises or water, and taking 

precautions against infection. Otolaryngology followup for a complete evaluation and to 

watch for future complications (e.g., cholesteatoma formation) is recommended. 

Prophylactic use of antibiotics is not recommended. 

Cardiovascular effects. The heart and blood vessels can be directly or indirectly injured 

by a blast wave. Cardiac involvement during a blast usually manifests as coronary vessel 

embolization and ischemia. Blood vessels within certain organs have a propensity for 

injury and may contribute to the generation of microthrombi, which results in 

disseminated intravascular coagulation. Cardiac blast injury that manifests as hemorrhage 

in the epicardium, myocardium, or papillary muscles is quite rare. 

Hypotension in blast victims often has multiple causes. It can involve blood loss from 

major musculoskeletal or abdominal injury or from a blast-related, vagally mediated 

reflex. This reflex, which is seen immediately after a significant blast exposure, causes 

hypotension without vasoconstriction and bradycardia. It is the most common effect on 

the cardiovascular system by the blast wave itself. The hypotension can be profound and 

self-limiting, and there may be no external signs of injury. 

Traditionally, aggressive volume replacement to support circulation is required in trauma 

victims with cardiovascular collapse. However, excessive volume replacement is 

detrimental to patients with lung injury. Research in animals has suggested that fluid 

replacement actually impairs cardiovascular performance in the setting of a blast. 

However, inadequate pulmonary vascular pressure has been suggested to promote the 

passage of air into the pulmonary venous system. Therefore, administration of fluids in 

increments of 5 mL/kg, titrated to clinical response, has been recommended. Either too 

much or too little fluid can be harmful, and the judicious use of fluids to maintain 

euvolemia is probably the best approach. As in all trauma patients, colloids should be 

used to replace massive hemorrhage, improve oxygenation, and minimize oncotic fluid 

shifts. Monitoring of central venous pressure and/or pulmonary pressures is a useful 

adjunct to fluid management. 

Sentinel injuries. Sentinel injuries are subtle injuries that can increase the risk of having 

or developing serious blast injury. These patients should be monitored closely, no matter 

how clinically well they appear. Sentinel injuries include the following: 

• Traumatic amputations. 

• Hypopharyngeal contusion. 
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• Hemoptysis. 

• Subcutaneous emphysema. 

• Hearing loss. 

• Ruptured tympanic membrane. 

Traumatic amputations frequently result from a blast. However, they are rarely found 

among survivors because the overpressure needed to cause such injury more often than 

not causes death at the scene. The mechanism for traumatic amputations has been 

hypothesized to be a combination of the blast wave itself, the effect of propelled 

fragments on tissues, and the added force of the blast wind. 

Incendiary Weapons 

Incendiary devices are fire-bombs used to cause maximal fire damage to flammable 

objects including people, buildings, and equipment. The massive fire caused by these 

devices effectively and easily causes mass panic, and the relative ease of obtaining 

materials to fabricate some devices makes them a potential vehicle for terrorist attacks. 

Incendiary devices range from simple Molotov cocktails, which are gasoline-filled bottles 

ignited with a rag, to military bombs that contain flammable materials such as napalm. 

Modern incendiary devices are complex bombs with flammable substances (e.g., 

kerosene) that can be ignited by either a fuse or a primary explosive. 

Napalm was originally made by mixing an aluminum soap of naphthalene and palmitate 

with gasoline. The result was a sticky flammable substance that, in contrast to liquid 

flammables, would stick to the intended target and burn longer. Napalm was later 

modified to contain mixtures of benzene, gasoline, and polystyrene. Napalm stores were 

eventually destroyed; however, incendiary devices containing napalm have allegedly 

been used in the 1990s in northern Iraq and Croatia. Incendiary devices containing 

mixtures of kerosene still have military applications. 

The principal incendiary agents are thermite, magnesium, white phosphorus, and 

hydrocarbons. Based on FBI data for 1999, most of the devices involved in incendiary 

bombing incidents (223 actual bombings and 114 attempts) in the United States used 

gasoline as the flammable agent. 

Emergency management of victims of incendiary devices involves identifying and 

treating the following: 

• Severe burns (second- and third-degree). 

• Respiratory compromise. 

• Carbon monoxide poisoning. 

• Dehydration. 

These burn victims should be managed as any other burn victim, with special attention to 

identifying blast injuries and removing the incendiary agent from the skin. Carbon 

monoxide poisoning is of particular concern in napalm exposure, because carbon 
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monoxide is a byproduct of napalm combustion. Due to the radiant heat emitted from the 

combustion of these materials, prolonged exposure may lead to severe dehydration. 

Aviation Terrorism 

The Aviation and Transportation Security Act, signed into law on November 19, 2002, 

instituted several measures with the goal of making flying safer, including the following: 

• Creating the Transportation Security Administration (TSA). 

• Screening of all baggage for explosive materials. 

• Fortifying of cockpit doors. 

• Increasing the number of sky marshals aboard planes. 

• Training flight crews on management of hijacking incidents. 

According to TSA data, 100% of baggage is now screened (compared with 5% prior to 

September 11, 2001). By August 2003, the TSA had intercepted 2.4 million knives, 

nearly 1,500 firearms, and more than 51,000 box cutters. 

Trauma Systems 

The medical response to blast terrorism is built on the foundation of the regional trauma 

system. About 98% of all terrorist events worldwide involve physical trauma, and 

approximately 75% of all terrorist events are due to blast trauma. Therefore, regional 

emergency management, public safety, and public health agencies should include not 

only regional child health care experts, but also regional pediatric trauma professionals in 

planning for mass casualty events that could affect children. Blast terrorism, like all other 

mass casualty events, needs to be directed with an Incident Command Structure (see 

Chapter 2, Systems Issues). 

Trauma Hospitals 

Most trauma hospitals are full-service general hospitals that provide the highest level of 

health care service in their communities. However, modern trauma system design does 

not rely solely on such hospitals but integrates all health facilities within the region to the 

level of their resources and capabilities. Thus, the complete trauma system should consist 

of an integrated network of health care facilities within a region, designed for safe and 

rapid transport of injured patients to the health care facilities that best meet their medical 

needs. As of April 2002, 35 States had formally designated or certified trauma centers, 

while the remaining States had at least one verified trauma center, which is the key 

element recognized as essential to trauma systems. Many stand-alone pediatric hospitals 

also serve as “pediatric trauma centers.” 

Trauma Centers 

Trauma centers are general hospitals that are committed, both institutionally and 

financially, to priority care of injured patients. Emergency medicine physicians and 

emergency trauma surgeons are the primary care providers within the context of the 

trauma center, and they provide appropriate information and followup to each patient’s 

usual primary health care provider. Emergency medicine physicians begin evaluation and 
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management and immediately involve emergency trauma surgeons whenever injuries 

meet any of the following criteria: 

• Are multiple or severe. 

• Require support of a full trauma team, based on previously established trauma 

triage criteria or scores. 

• Would benefit from trauma consultation with an emergency trauma surgeon 

Trauma centers should have the following attributes: 

• Designated as such by emergency medical and public health authorities within the 

region, based on self categorization according to established standards. 

• Followed by on-site peer verification by impartial trauma experts. 

• Subject to ongoing review of performance and participation in the regional trauma 

system. 

All trauma centers have key organizational characteristics in common: 

• All trauma services should be led by a properly qualified and credentialed 

emergency trauma surgeon who has education, expertise, and experience in 

trauma care. 

• This emergency trauma surgeon, together with a trauma nurse program manager 

and trauma registrar, should maintain active programs of continuing education 

and performance improvement for all members of the trauma service. 

• Trauma care should be provided by properly qualified and credentialed physician 

specialists in general or pediatric emergency medicine, general or pediatric 

trauma surgery, anesthesiology, radiology, pathology, and the three core surgical 

subspecialties (critical care, neurologic surgery, and orthopedic surgery). 

• This physician team should work in collaboration with properly qualified and 

credentialed nursing personnel. 

• Appropriate physical resources should include properly equipped emergency 

departments, operating suites, intensive and acute-care units, imaging capabilities, 

laboratory facilities, and blood bank. 

• The in-house trauma team should be available immediately, 24 hours per day, 7 

days per week. 

• Appropriate and culturally competent mental health, social work, pastoral care, 

injury prevention programs, and ideally, professional education and trauma 

research programs should be in place to serve both patients and the community. 

Level One Trauma Centers. Level One Trauma Centers offer comprehensive care of 

seriously injured patients that includes specialists and services for resuscitation, recovery, 

and rehabilitation. They usually are located in full-service general or university hospitals 

or, in the case of children, in full-service children’s hospitals in which comprehensive 

care of the trauma patient is part of the institutional mission. The key issue is 

comprehensive, readily available, and consistent care of injured patients by all needed 

specialists and services. 

Level Two Trauma Centers. Level Two Trauma Centers provide most specialists and 

services that are available in Level One Trauma Centers, but typically they are located in 
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full-service general hospitals that do not support medical or nursing educational programs 

(e.g., residency training) or trauma research. Patient care remains exemplary, and 

community outreach activities are a key part of the hospital’s mission. Most Level Two 

Trauma Centers are located in large urban areas that are served by an academic medical 

center but with a sufficiently large population to require a second full-service trauma 

center, or they are in mid-sized urban areas that are not served by an academic medical 

center. In the latter situation, the Level Two Trauma Center acts as the regional trauma 

center, serving as the tertiary referral center for Level Three and Four Trauma Centers, as 

well as for non-trauma centers and other facilities within the region. 

Level Three Trauma Centers. Level Three Trauma Centers provide most trauma care in 

the United States. They typically are located in community hospitals that serve small 

urban or large suburban areas. Key specialists and services are available, suitable for 

managing patients with injuries of a single system and few comorbidities. However, 

medical and surgical subspecialist coverage may be limited, and patients with multiple or 

severe injuries, with complex comorbidities, or who are very young or very old are 

usually transferred to a nearby Level One or Level Two Trauma Center after initial 

stabilization. Most Level Three Trauma Centers play an integral role in the regional 

trauma system and collaborate with a Level One or Level Two Trauma Center within the 

region. Again, patient care is exemplary, within the resources of the hospital and the 

community. Community outreach is essential, particularly in terms of support for the 

typically volunteer local emergency medical service agencies that serve the area. 

Non-Trauma Centers 

All facilities that receive emergency patients, including hospitals and free-standing 

diagnostic and treatment clinics, should have the capabilities for resuscitating and 

stabilizing injured patients of all ages. Therefore, protocols should be in place for 

sustentative trauma care (including education of medical and nursing staff in early care of 

injured patients) and for identification of patients in need of transfer to hospitals capable 

of providing definitive trauma care (which should be known to all urgent care personnel 

through prior development of formal transfer agreements). All such facilities should be: 

• Considered part of the regional trauma system. 

• Prepared to provide, within their communities, anticipatory guidance related to 

injuries that is consistent with programs advocated by regional experts in injury 

prevention. 

• Participants in regional programs for performance improvement of community 

trauma care, with special emphasis on the outcomes of patients transferred to 

local trauma centers. 

Treatment 

Treatment of blast trauma involves full integration of the regional EMS system and the 

regional trauma system, in accordance with plans developed in collaboration with 

regional public safety and emergency management agencies. Although most blast trauma 

is caused by explosive or incendiary agents, the possibility of other weapons of mass 

destruction (WMD), such as biological, chemical, or nuclear weapons, should always be 
251

considered (see Chapter 4, Biological Terrorism; Chapter 5, Chemical Terrorism; and 

Chapter 6, Radiological and Nuclear Terrorism). 

Trauma 

The treatment of victims of major trauma, including blast trauma, follows wellestablished protocols. The American College of Surgeons Committee on Trauma has 

developed and disseminated such protocols through its support of the Advanced Trauma 

Life Support® for Doctors Course (see Table 7.3). The Emergency Nurses Association 

and the Society of Trauma Nurses have undertaken like responsibilities for nurses 

through the Trauma Nursing Core Course and the Advanced Trauma Care for Nurses

Course. All three courses focus on a practical approach to the initial care and 

management of the injured patient, assuming no special knowledge of trauma care, 

including the steps to be taken during the “golden hour” of trauma care—the critical first 

hour after injury has occurred. 

Burns 

Major burns and major trauma are often seen together in victims with injuries caused by 

explosive or incendiary devices. The treatment of victims of major burns also follows 

well-established protocols. Specific education on the initial resuscitation of these victims 

is included in both the Advanced Trauma Life Support® for Doctors course (American 

College of Surgeons Committee on Trauma) and the Advanced Burn Life Support course 

(American Burn Association) (see Table 7.3, Table 7.4). 

Multiple Casualties 

The strict definition of a multiple casualty incident is an incident involving more than one 

casualty that overwhelms the capacity of emergency medical providers at the scene. In 

general, this happens when a local EMS system must care for five or more victims who 

have the same illness or injury at the same place and time. Because local hospital 

emergency departments may also be overwhelmed by such events, EMS systems usually 

attempt to transport multiple victims to several hospitals in the vicinity of the event when 

feasible. In such circumstances, attempts are usually made to transport members of the 

same family to the same hospital, particularly if ill or injured children are involved. 

However, the availability of specialized pediatric health care resources, such as children’s 

hospitals, may justify preferential transport of pediatric victims of multiple casualty 

incidents to these facilities. 

Mass Casualties 

The strict definition of a mass casualty event is an event involving large numbers of 

casualties, generally 20 or more, that overwhelms and disrupts the resources and 

capabilities of the entire regional trauma and EMS systems to provide immediate care for 

all ill or injured victims. This situation develops when the need for ambulances, hospitals, 

or both exceeds the emergency resources of the regional health care system. The 

definition further implies the following: 
252

• The need to activate regional disaster plans that mobilize all available ancillary 

resources to assist with providing emergency medical care. This includes using 

the surge capability of both the regional EMS system to deploy extra ambulances 

(via mutual aid agreements) and of the regional hospital system to maximize the 

number of victims who can be cared for by opening spare beds, discharging stable 

patients, canceling elective procedures, and conscripting off-duty staff. 

• The need to prioritize care such that those at greatest risk of loss of life or limb 

are treated first (unless they are unlikely to survive). The most widely used 

pediatric resource is JumpSTART, modified by Romig 

(www.jumpstarttriage.com) from the Simple Triage and Rapid Treatment 

(START) triage system used for adults. 

Planning and Mitigation 

The approach to planning for the possibility of blast injury after a terrorist attack should 

combine knowledge of the epidemiology of blast injury with awareness of the resources 

available to the regional trauma system. The Federal Government has adopted a similar 

approach for routine trauma system planning that allies the regional public health system 

with the regional health care system to form regional partnerships for the purpose of 

developing and implementing comprehensive injury control strategies at the community 

level. 

Medical disaster planning should fully integrate regional public health agencies, regional 

health care organizations, EMS, emergency departments, and trauma centers before a 

disaster occurs. Public health officials and trauma care professionals should collaborate to 

evaluate, and redesign if needed, each system component for optimal performance. 

Current regional trauma system design maintains an artificial separation between the preevent, event, and post-event phases of injury control. The comprehensive public health 

approach to regional trauma system design integrates all phases of injury control into a 

single system. Regional injury control systems that have adopted such an approach (e.g., 

San Diego County, CA) have seen steady improvement in the quality of their injury 

prevention programs and the outcomes of their trauma patient care. 

Public health reasons to apply this approach to blast terrorism include the documented 

lack of public health preparedness of most regions for terrorist attacks, despite excellent 

resources that describe the necessary elements for treatment of victims. 

Planning 

The enormous variability in the following characteristics hinders comparative analysis, 

and hence accurate prediction, of needs and resources for victims of blast terrorism: 

• Type, quality, quantity, force, and delivery (human, bicycle, motorcycle, car, 

truck, plane) of explosive. 

• Environment (closed space vs. open air). 

• Time (day vs. night). 

• Distance (proximate vs. distant). 
253

• Circumstances (weather conditions, hazardous materials, etc.). 

• Protection (clothes, barriers, etc.). 

• Sequelae (structural collapse, structural fire, etc.). 

• Victims (ages, number, density). 

In general, small, frequent blasts in open air usually result in less serious injury than 

large, single blasts in closed spaces, which historically have resulted in life-threatening 

injury. 

Regional trauma system planning should also consider the special needs of children who 

are injured due to blast terrorism and the special resources needed to care for them. 

Children and young adults are at higher risk of serious injury than adults for several 

reasons (see Children Are Not Small Adults in Chapter 1). Specific to blast trauma is that 

while blast tolerances in children are poorly defined, there is good reason to believe that 

children may absorb more blast energy per unit body mass than adults after blast trauma. 

This predisposes children to morbidity and mortality rates higher than those of adults as 

compressive shock waves passing through the body are compacted into a smaller total 

body mass. 

Mitigation 

Because most blast terrorism in recent years has involved children, with the notable 

exceptions of the terrorist airliner attacks on the World Trade Center in New York and 

the Pentagon in Washington on September 11, 2001, significant personal experience has 

been gained with pediatric disaster and emergency preparedness and management by 

child health professionals. Reports in the literature (summarized below) point out the 

woeful state of emergency preparedness for disasters that involve children. They also 

describe the common problems in pediatric disaster planning and management such that 

pediatric professionals involved in disaster planning will be knowledgeable about these 

problems and thus can seek to anticipate and thereby avoid them in future disasters. 

In the Avianca jetliner crash in New York in January 1990, 22 of 25 (80%) children 

survived versus 70 of 132 (50%) adults, despite the fact that pediatric patients were 

inadequately treated and transported (State, regional, and county disaster plans did not 

address pediatrics). Only three children died, and only seven survivors sustained highrisk injuries. The spectrum of injuries resulting from this event were as follows: 

• A 3-month-old boy with intracranial bleeding and aortic rupture (died). 

• A 5-year-old boy with massive hemothorax (died). 

• A 7-year-old boy with severe traumatic brain injury (died). 

• Six children with traumatic brain injury. 

• Five children with hypotensive shock. 

• Three children with femur fractures with either hypotensive shock or traumatic 

brain injury. 

Triage and transport of pediatric patients: 

• Of seven children with a pediatric trauma score (PTS) <8, only one was taken to a 

Level I Pediatric Center. 
254

• Of five high-risk children (greater risk of death) initially taken to a Level III 

Pediatric Center, only two were subsequently transported to a higher level 

Pediatric Center. 

• Two high-risk patients and one low-risk patient (low risk of death) were 

transported by helicopter. 

After the bomb blast that destroyed the Alfred P. Murrah Federal Building in Oklahoma 

City, OK, in April 1995, there were 816 casualties, including 66 children. Of these, 19 

children died, and 47 survived. Of the 20 children in the day care center who were seated 

by windows, 16 died and 4 survived. The spectrum of injuries resulting from this event 

was as follows: 

Of the 35 children who died— 

• 90% had skull fractures, most with skull capping. 

• Associated injuries: 37% trunk, 31% amputations, 47% arm fractures, 26% leg 

fractures, 21% burns, 100% soft-tissue injuries. 

Of the children who survived— 

• 15% required hospitalization. 

• Documented injuries: two open depressed skull fractures with partially extruded 

brain, two closed head injuries, three arm fractures, one leg fracture, one arterial 

injury, one splenic injury, five tympanic membrane perforations, four burns (one 

burn >40% total BSA). 

No children were injured in the terrorist airliner attack on the Pentagon on September 11, 

2001, because the Pentagon daycare center was located on the opposite side of the 

building from the location of attack. However, as a result of the attack, issues were raised 

about children’s hospital disaster preparedness. Immediately after the disaster, the 

hospital disaster plan was invoked, resulting in the discharge of more than 50 patients and 

the cessation of all nonurgent activities. Although hospital staff had conducted disaster 

drills in preparation for Y2K, hospital leaders continued to question their actual state of 

readiness. Emergency preparations were complicated by the fact that all of their news 

came not from official sources, but from local television, leaving hospital leaders unsure 

about what to expect. 

These experiences highlight a number of vitally important issues regarding blast 

terrorism mitigation in children. 

• After a blast, injuries in children are to be expected with most children injured in 

closed or confined spaces, which greatly increases the magnitude of forces of 

injury. 

• As with blast injuries in adults, most children will either die at the scene or sustain 

minor injuries. Only a small number of children in the “penumbra” of the blast 

wind who sustain major injuries will survive to require hospital care, but typically 

they will not begin to arrive at the trauma center until 30–60 minutes after the 

blast event. 

• Most surviving children with major injuries will require early surgery and 

subsequent care in a pediatric critical care unit, followed by lengthy 

hospitalization and rehabilitation, both physical and psychological. 
255

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• Stein M, Hirshberg A. Medical consequences of terrorism. Surg Clin No Am. 

1999;79(6):1537–1552. 

• Stuhmiller JH, Phillips YY, Richmond DR. The physics and mechanisms of 

primary blast injuries. In: Bellamy RF, Zajtchuk R (eds). Conventional Warfare: 

Ballistics, Blasts, and Burn Injuries. Washington, DC: Office of the Surgeon 

General of the U.S. Army; 1991:241–270. 

• Uretsky G, Coter S. The use of continuous positive airway pressure in blast injury 

of the chest. Crit Care Med. 1980;8:486–489. 

• U.S. Department of Justice. 1997 Report on the Availability of Bomb Making 

Information. U.S. Department of Justice. April 1997. 

• Virginia Department of Emergency Management. VDEM Terrorism Toolkit. 

Weapons of mass destruction—explosives. Available at 

http://www.vaemergency.com/threats/terrorism/toolkit/wmd.cfm. Accessed 

August 24, 2006. 

• Wightman JM, Gladish SL. Explosions and blast injuries. Annals Emerg Med. 

2001;37(6):664–678. 

• Wikoff RP, Lerner MR, Mantor PC, et al. Fluid resuscitation is detrimental in a 

blast injury model. J Trauma. 1999;46(1):204. 
257

Trauma Systems and Planning/Mitigation 

• American Burn Association. Advanced Burn Life Support Course. Available at: 

http://www.ameriburn.org/ABLS/ABLSNow.htm. Accessed August 24, 2006. 

• Briggs SM, Brinsfield KH, eds. Advanced Disaster Medical Response. Boston: 

Harvard Medical International, Inc., 2003. 

• Committee on Trauma and Committee on Shock, Division of Medical Sciences, 

National Research Council, National Academy of Sciences. Accidental Death and 

Disability: The Neglected Disease of Modern Society. Washington: National 

Academy of Sciences, 1966. 

• Committee on Trauma, American College of Surgeons. Advanced Trauma Life 

Support® for Doctors 1997 Student Course Manual. Chicago: American College 

of Surgeons, 1997. 

• Committee on Trauma, American College of Surgeons. Resources for Optimal 

Care of the Injured Patient 1999. Chicago: American College of Surgeons, 

1999. 

• Cooper G, Dawson D, Kaufmann C, Esposito T, Cooper A, et al. Trauma 

Systems Planning and Evaluation: A Model Approach to a Major Public Health 

Problem. Washington: National Highway Traffic Safety Administration, 2004. 

• Dieckmann R, Brownstein D, Gausche-Hill M, eds. Pediatric Emergencies for 

Prehospital Professionals. Sudbury: Jones and Bartlett Publishers, 2000. 

• Farmer JC, Jimenez EJ, Talmor DS, et al, eds. Fundamentals of Disaster 

Management. Des Plaines: Society of Critical Care Medicine, 2003. 

• Freishtat RJ, Wright JL, Holbrook PR. Issues in children’s hospital disaster 

preparedness. Clin Ped Emerg Med 2002;3:224-230. 

• Goldfrank LR, ed. Public Health. Washington: Institute of Medicine, National 

Academy of Sciences, 2001. 

• MacKenzie EJ, Hoyt DB, Sacra JC, et al. National inventory of hospital trauma 

centers. JAMA 2003;289:1515–1522. 

• Quintana DA, Jordan JB, Tuggle DW, et al. The spectrum of pediatric injuries 

after a bomb blast. J Pediatr Surg 1997;32:307–311. 

• Society of Trauma Nurses. Advanced Trauma Care for Nurses Course. Available 

at: http://www.traumanursesoc.org/education.html. 

• Trauma Nursing Core Course. Emergency Nurses Association. 

• van Amerongen RH, Fine JS, Tunik MG, et al. The Avianca plane crash: 

emergency medical system response to pediatric survivors of the disaster. 

Pediatrics 1993;92:105–110. 

• West JG, Trunkey DD, Lim RC. Systems of trauma care: a study of two 

counties. Arch Surg 1979;114:455–460. 
258

Table 7.1. Expected injuries at relative distances from detonation in open air 

Injury Closest Farthest 

Body disruption ● 

Burn/inhalation ●

Toxic inhalation ● ● 

Amputation ● ● ● 

Primary blast injury, 

lung and bowel 

● ● ● ● 

Tertiary mechanism ● ● ● ● ● 

Primary blast injury, 

ear 

● ● ● ● ● ● 

Secondary mechanism ● ● ● ● ● ● ●
259

Table 7.2 Spectrum of primary blast injury on body systems 

System Injuries 

Respiratory 

 Pulmonary contusion 

 Pulmonary hemorrhage

 Respiratory failure

 Stripped-epithelium lesion

 Alveolo-venous fistula

 Bronchopleural fistula

 Pneumothorax

 Traumatic emphysema

 Air embolism

 Acute respiratory distress syndrome

GI 

 GI hemorrhage 

 GI perforation 

 Spleen or liver hemorrhage or rupture 

 Retroperitoneal hemorrhage 

 Tunica albuginea (testis) hemorrhage 

Auditory 

 Tympanic membrane rupture 

 Ossicular chain disruption 

 Cochlear nerve injury 

 Labyrinthine fistula 

 Perilymphatic fistula 

Circulatory 

 Coronary embolism 

 Myocardial contusion 

 Thrombosis/disseminated intravascular 

coagulation 

CNS 

 Cerebral air embolism 

 Retinal artery embolism 

Source: Sharpnack DD, Johnson AJ, Phillips Y. The Pathology of Primary Blast Injury. In: Bellamy RF, 

Zajtchuk R, eds. Conventional Warfare: Ballistics, Blasts, and Burn Injuries. Washington, DC: Office of 

the Surgeon General of the U.S. Army; 1991: 271-294. 
260

Table 7.3 Principles of Advanced Trauma Life Support®

Primary Survey and Resuscitation 

Airway/cervical spine Open: jaw thrust/spinal stabilization 

Clear: suction/remove particulate matter 

Support: oropharyngeal/nasopharyngeal airway 

Establish: orotracheal/nasotracheal intubation1

Maintain: primary/secondary confirmation2

Bypass: needle/surgical cricothyroidotomy 

Breathing/chest wall Ventilation: chest rise/air entry/effort/rate 

 Oxygenation: central color/pulse oximetry 

Support: distress – NRB/failure – BVM3

 Chest wall: ensure integrity/expand lungs 

 Tension pneumothorax: needle, chest tube4

 Open pneumothorax: occlude, chest tube 

 Massive hemothorax: volume, chest tube 

Circulation/external 

bleeding 

Stop bleeding: direct pressure, avoid clamps 

Shock evaluation: pulse, skin CRT, LOC5

 Blood pressure: avoid over/undercorrection 

 Infant/child: low normal = 70 + (age × 2) mmHg 

 Adolescent: low normal = 90 mmHg 

 Volume resuscitation: Ringer’s lactate → packed cells 

 Infant/child: 20 mL/kg RL, repeat x 1-2 → 10 mL/PRBC 

 Adolescent: 1–2l, repeat 1–2 × → 1–2 U PRBC 

Disability/mental 

status 

Pupils: symmetry, reaction 

 LOC: GCS 

 Track and trend as a vital sign 

 Significant change = 2 points 

 Intubate for coma = GCS ≤8 

 Motor: strength, symmetry 

 Abnormality or deterioration: call neurosurgeon 

 Mild TBI (GCS 14–15): observe, consider CT for history of LOC 

 Moderate TBI (GCS 9–13): admit, obtain CT, repeat CT 12–24 hr 

 Severe TBI (GCS 3–8): intubate, ventilate, obtain CT, repeat CT 

12–24 hr 

Exposure and 

environment 

Remove clothing 

 Logroll: requires four people 

 Screening examination: front and back 

 Avoid hypothermia: keep patient warm 

Adjuncts 

Foley catheter unless contraindicated6

Gastric tube unless contraindicated7 
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Table 7.3 Principles of Advanced Trauma Life Support®, continued

Secondary Survey and Reevaluation 

 History and physical: SAMPLE history, complete examination 

Imaging studies: plain radiographs8, special studies9

1 RSI technique: etomidate then succinylcholine 2 Primary: chest rise, air entry; secondary: exhaled CO2 detector, esophageal detector device; watch for 

DOPE: Dislodgement, Obstruction, Pneumothorax, Equipment failure 3 NRB: nonrebreather mask; BVM: bag valve mask 4 Do not wait for confirmatory chest x-ray. 5 CRT = capillary refill time, LOC = level of consciousness; consider obstructive and neurogenic as well 

as hypovolemic shock: exclude tension pneumothorax, cardiac tamponade, spinal shock 6 Meatal blood, scrotal hematoma, high riding prostate 7 CSF oto/rhinorrhea, basilar skull fracture, midface instability 8

 Chest, pelvis, lateral cervical spine; others as indicated 

9

 FAST, CT as indicated 

Source: Adapted with permission from the American College of Surgeons Committee on Trauma, 

Advanced Trauma Life Support® for Doctors Student Course Manual. 
262

Table 7.4 Principles of Advanced Burn Life Support®

Primary Survey 

Airway Rapid upper airway closure may occur following inhalation injury and 

require early intubation 

Breathing Circumferential full thickness burns of the trunk may impair 

ventilation and require escharotomy 

Circulation Circulation in a limb with full thickness burns may be impaired and 

require escharotomy 

Disability Consider carbon monoxide poisoning if the patient is not initially alert 

and oriented 

Exposure and 

environment 

Remove all jewelry to avoid constriction of digits 

Adjuncts 

Foley catheter Needed to titrate fluid replacement against urine output 

Gastric tube Needed to decompress stomach due to burn ileus 

Resuscitation 

Stop the burning 

process 

Fluid resuscitation Parkland formula: 3–4 mL Ringer’s lactate × body weight in kg × 

total BSA burned; administer half the amount during the first 8 hr after 

injury, half over the next 16 hr 

Modification for pediatric patients: Add maintenance fluid to 

Parkland formula for children and infants; 100 mL/kg for first 10 kg + 

50 mL/kg for next 10 kg + 20 mL/kg for each additional kg 

Secondary Survey 

History and physical

Obtain as much 

information as 

possible regarding the 

circumstances of 

injury 

Flame 

How did the burn occur? 

Did the burn occur outside or inside? 

Did the clothes catch on fire? 

How long did it take to extinguish the flames? 

How were the flames extinguished? 

Was gasoline or another fuel involved? 

Was there an explosion? 

Was there a house fire? 

Was the patient found in a smoke-filled room? 

How did the patient escape? 

If the patient jumped out a window, from what floor? 

Were others killed at the scene? 

Was there a motor vehicle crash? 

How badly was the car damaged? 

Was there a car fire? 

Are there other injuries? 

Are the purported circumstances of the injury consistent with the 

burn characteristics? 
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Scald 

How did the burn occur? 

What was the temperature of the liquid? 

What was the liquid? 

How much liquid was involved? 

What was the temperature setting of the water heater? 

Was the patient wearing clothes? 

How quickly were the patient’s clothes removed? 

Was the burned area cooled? 

Who was with the patient when the burn took place? 

How quickly was care sought? 

Where did the burn occur? 

Are the purported circumstances of the injury consistent with the 

burn characteristics? 

Chemical 

What was the agent? 

How did the exposure occur? 

What was the duration of contact? 

What decontamination occurred? 

Was there an explosion? 

Electrical 

What kind of electricity was involved? 

What was the duration of contact? 

Did the patient fall? 

What was the estimated voltage? 

Was there loss of consciousness? 

Was cardiopulmonary resuscitation administered at the scene? 

Determine the severity 

of the burn 

Extent of burn

Rule of nines for adolescents 

Lund-Browder chart for children and infants (Table 6.5) 

Depth of burn 

Adjuncts 

Imaging and 

laboratory studies 

Carboxyhemoglobin 

Reevaluation 

Continued assessment of ventilatory effort 

Continued assessment of extremity perfusion 

Pain management 

Psychosocial assessment 

Burn Wound Care 

Thermal burns Cover the area with a clean, dry sheet 

Ice applications are appropriate only in small burns 

Chemical burns Flush the chemical agent from the body surface with copious amounts 

of water 

Powdered chemicals should be brushed from the skin prior to flushing 

the involved area 
264

Remove all contaminated clothing 

Chemical eye injuries require continuous irrigation until otherwise 

instructed by an expert 

Electrical burns Continuous cardiac monitoring may be necessary during the first 24 hr 

after injury 

Maintain urine output at twice normal target volumes if myoglobinuria 

Burn Center Referral 

Partial thickness burns >10% total BSA 

Burns that involve face, hands, feet, genitalia, perineum, or major joints 

Full-thickness burns 

Chemical burns 

Electrical burns, including lightning injury 

Inhalation injury 

Burn injury in patients with significant comorbidities; concomitant trauma; or who require 

special social, emotional, or rehabilitative intervention 

Burned children in hospitals without qualified personnel or equipment for care of children 

 Note: The principles of Advanced Burn Life Support are identical to the principles of Advanced Trauma 

Life Support® (Table 7.3), with additional caveats pertinent to Advanced Burn Life Support. 

Source: Courtesy American Burn Association. Used with permission. 

 

 Note: The principles of Advanced Burn Life Support are identical to the principles of Advanced Trauma 

Life Support® (Table 7.3), with additional caveats pertinent to Advanced Burn Life Support. 

Source: Courtesy American Burn Association. Used with permission. 
265

Chapter 8. Mental Health Issues 

Mental Health and the Role of the Pediatrician 

Schools and pediatricians have generally become the de facto mental health providers for 

children. Children are most likely to receive treatment from primary care physicians for 

symptoms associated with mental disorders, and most psychotropic drug prescriptions for 

children and adolescents are prescribed by primary care physicians. In a disaster or 

terrorist event, the need for mental health services will be far greater and the resources 

even less adequate. Pediatricians and other health professionals that care for children will 

play many critical roles in identifying and addressing the mental health needs of children 

and families in a disaster or terrorist event. 

For many, if not most, children affected by a critical event, pediatricians and other health 

care providers for children will be the first responders. Therefore, pediatricians need to be 

able to identify psychological symptoms, perform timely and effective triage of mental 

health complaints, initiate brief supportive interventions, and make appropriate referrals 

when necessary. Many children (and their parents) with emotional reactions to a disaster 

(manmade or otherwise) will not identify their problems as psychological in nature. 

Pediatricians will have to be vigilant for somatization and help children, and their 

families, recognize and address the underlying psychological cause of these physical 

complaints. Because children’s adjustment depends to a great extent on their parents’ 

own ability to cope with the situation, pediatricians should also attempt to identify 

parents who are having difficulties adjusting to the event and encourage them to seek 

support for themselves. Pediatricians can also help families identify and access 

appropriate supportive or counseling services, and they can help support families who are 

reluctant to seek mental health services because of misunderstandings related to the 

nature of the treatment or associated stigma. 

Trauma-Related Disorders 

Children are not immune to the emotional and behavioral consequences of disasters and 

terrorism. Their reactions depend on their own inherent characteristics and experiences 

and their developmental level, family and social influences, and the nature and magnitude 

of the event and their exposure to it. 

Exposure to disasters and terrorism can be direct, interpersonal, or indirect. Children who 

are physically present during an incident are directly exposed. Interpersonal exposure 

occurs when relatives or close associates are directly affected. Indirect exposure occurs 

through secondary negative consequences of an event such as chaos and disruption in 

daily activities. Children who are far away from an incident may be remotely affected 

with fear and generalized distress as they perceive the societal impact of these 

experiences. 

Exposure to media coverage may play a role in the child’s reaction to an event. Studies 

have documented an association between viewing television coverage of terrorist 
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incidents and posttraumatic stress reactions, but these associations do not establish a 

causal relationship. Aroused children may be drawn to the information provided by the 

media, and it is possible that other factors are responsible for the link between exposure 

to media coverage and these emotional states. 

Reaction to Disasters and Terrorism 

Children may develop psychiatric symptoms and disorders—including posttraumatic 

stress disorder (PTSD), anxiety, depression, and behavioral problems—after exposure to 

disasters or terrorist incidents. Grief in these situations can be compounded by the 

traumatic circumstances associated with the loss. 

Risk factors for adjustment difficulties. The following factors are associated with an 

increased risk of posttraumatic symptoms and other adjustment difficulties: 

• Children or others close to them are direct victims, especially if injury is involved 

(or the death of significant others). 

• Children directly witness the event, especially if there was exposure to horrific 

scenes (indirect exposure through the media to these scenes is also associated with 

increased risk). 

• Children perceive during the event that their life is in jeopardy (even if the 

perception is inaccurate). 

• Event results in separation from parents or other caregivers. 

• Event results in loss of personal property or other disruption in regular 

environment. 

• Children have a history of prior traumatic experiences. 

• Children have a history of prior psychopathology. 

• Parents have difficulty coping with the aftermath of the event. 

• Family lacks a supportive communication style. 

• Community lacks the resources to support children after the event. 

Posttraumatic stress disorder. The essential feature of PTSD is the development of 

characteristic symptoms after exposure to a traumatic event that arouse intense fear, 

helplessness, or horror or that lead to disorganized or agitated behavior. Signs and 

symptoms are categorized into three clusters: 

1. Persistent intrusive re-experiencing (one symptom required for diagnosis). 

• Unwanted memories, images, thoughts, or perceptions of the experience 

including repetitive play with themes of the trauma. 

• Bad dreams and nightmares. 

• Acting or feeling like the event is recurring, including flashbacks or reenactment of the experience. 

• Feeling intense distress when reminded of the experience. 

• Physiological reactivity to reminders. 

2. New onset and persistent avoidance and numbing (three symptoms required for 

diagnosis). 

• Avoiding thoughts, feelings, or conversations associated with the experience. 

• Avoiding activities, places, or people that arouse memories of the experience. 
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• Amnesia for important parts of the experience. 

• Loss of interest or involvement in usual activities. 

• Feeling distant and isolated. 

• Decreased range of emotions. 

• Sense of foreshortened future. 

 3. New onset persistent hyperarousal (two symptoms required for diagnosis). 

• Sleep difficulties. 

• Irritability and angry outbursts, 

• Difficulty concentrating. 

• Hypervigilance. 

• Exaggerated startle response. 

The symptoms must last for more than 1 month and must cause clinically significant 

distress or impaired functioning. Because of developmental influences, symptoms in 

young children may not correspond exactly to those in adults. 

Other conditions. Other conditions, especially anxiety and affective disorders, are 

common after crisis events and may occur independently or together with PTSD. These 

conditions may precede, follow, or develop at the same time as PTSD. Establishing the 

temporal relationship in onset of disorders may aid in treatment. For example, PTSD 

stems from the primary traumatic event, while depression may result secondarily from 

persistent severe PTSD symptoms, intervening stresses, or unresolved grief. Fear and 

avoidance of situations reminiscent of the trauma may persist for years. 

Behavioral reactions. Signs of trauma may be evident in children’s behavior, mood, and 

interactions with others. Traumatized children may adopt behavior more appropriate of 

younger children. Although they may not share their concerns and they may be especially 

compliant in the aftermath of an incident, compliant behavior does not mean the child is 

unaffected. Withdrawal is a cause for concern as it may represent a symptom of PTSD, 

and it potentially distances the child from adults who could provide support and 

assistance. Girls are more likely to express anxiety and sadness; boys tend to exhibit 

more behavior problems. 

The child’s reaction will reflect his or her developmental level. Infants may experience 

sleep and feeding problems, irritability, and failure to achieve developmental milestones. 

Problems in preschool children include separation anxiety, dependence, clinging, 

irritability, misbehavior, sleep disturbance, and withdrawal. Problems in school-aged 

children include irritability, somatic complaints, withdrawal, misbehavior, and change in 

academic performance. Problems in adolescents include anxiety, irritability, isolation and 

withdrawal, guilt, anger and hate, and preoccupation with death. 

Grief and traumatic grief. Although grief is not a mental disorder, it may require 

professional attention, especially if it is complicated by depression or PTSD. Traumatic 

deaths are of particular concern in disasters because of the implications for assessment, 

which should include an evaluation of the circumstances of the death and the child’s 

exposure, and for treatment, which should address trauma symptoms as well as grief. In 
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some ways, any death may be perceived by survivors as subjectively traumatic; however, 

five factors have been described that are likely to be present in death circumstances that 

are considered “traumatic deaths”: 

• Sudden, unanticipated deaths. 

• Deaths involving violence, mutilation, and destruction. 

• Deaths that are perceived as random or preventable, or both. 

• Multiple deaths. 

• Deaths witnessed by the survivor that are associated with a significant threat to 

personal survival or a massive or shocking confrontation with the death and 

mutilation. 

Deaths that occur in the context of a disaster or terrorist situation often meet these criteria 

and pose an increased risk of traumatic grief. Referral to a pediatric mental health 

professional is often indicated in these situations. 

Assessment and Treatment 

Assessment and treatment of children after a disaster will vary, depending on the 

characteristics of the disaster and the child’s exposure, the setting, and the length of time 

since the event. 

Early interventions. In the acute-impact and early post-impact phases, supportive 

interventions should ensure the child’s safety and protection from additional harm, 

address immediate physical needs, provide reassurance, minimize exposure to traumatic 

aspects of the event, validate experiences and feelings, and restore routine. Children 

benefit from accurate information, but it should be age-appropriate and measured. If 

possible, pediatric mental health professionals can help other health professionals and 

family members with the process of death notification. Reuniting family members is a 

priority. 

Assessment and screening. Assessment should include a history of the child’s exposure 

and reactions. When children or their close family members have been directly exposed, 

the children may require more comprehensive assessment. Children with less direct 

exposure may also need attention. Children and their parents should be educated about 

trauma reactions and coping, and they may welcome opportunities to ask questions and 

correct misperceptions. Children may not spontaneously describe their feelings, and 

adults may underestimate trauma in children. Therefore, it is essential to ask children 

directly about their experiences. Observation and the use of projective techniques, such as 

play and the use of art, aid in assessment and are useful in treatment as well. 

Screening to identify children at risk and those needing referral can be conducted with 

symptom rating scales (such as the UCLA PTSD Reaction Index), which typically 

measure the type and degree of exposure, subjective reactions, personal consequences, 

PTSD symptoms, and other related symptoms such as fear and depression, grief, and 

functioning. Group interviews, conducted in classrooms or other small clusters, may also 

be used to assess the need for more comprehensive individual evaluation and to begin the 

process of healing after large-scale or mass casualty events. 
269

Treatment. Treatment should be guided by the child’s exposure and reactions. Directly 

traumatized and bereaved children should be seen individually, but groups are useful for 

identifying children in need of more comprehensive evaluation and treatment. Cognitive 

behavioral therapy and educational information provide structure and support and may be 

used in individual or group sessions after disasters. 

Group sessions are ideal for providing age-appropriate explanations of acute and longer 

term reactions, reactions to traumatic reminders, secondary effects, anniversaries, and 

coping. Some children are uncomfortable sharing in a group, and group discussions may 

traumatize the children again through re-exposure to their own experiences or through 

exposure to the experiences of others. Groups vary with respect to structure and may 

include play, art, and other projective techniques. Parallel parent groups provide a means 

to address parental reactions and concerns and to discuss effective management. These 

groups also provide an opportunity to teach parents how to parent their traumatized child. 

The family has a major role in the child's adjustment to trauma, and parents should be 

included in treatment. Often, more than one family member will be traumatized, although 

specific aspects of exposure may differ among family members. Helping parents resolve 

their own emotional distress can increase their perceptiveness and responsiveness to their 

children. Parents may also benefit from psychoeducation about symptoms, how to 

manage symptoms effectively, and ways to decrease traumatic reminders and secondary 

stresses. 

Medication is rarely indicated in children after disasters but might be used for those with 

severe reactions. Consultation with a child psychiatrist is recommended when medication 

is being considered. When used, medication should be coupled with psychotherapeutic 

interventions such as play therapy or cognitive behavioral approaches. Specific 

symptoms determine whether to use a drug, which drug to use, and how long to use it. 

Comorbid conditions should be considered in selecting an agent. Selective serotonin 

reuptake inhibitors may be effective in treating childhood PTSD and comorbid anxiety 

and depression (see also the section on medication, later in this chapter). 

School-based interventions. Schools are an excellent setting to deliver mental health 

services to children and families after a disaster. They provide access to children, 

encourage normalcy, and minimize stigma. PTSD and associated symptoms are likely to 

emerge in the school setting. For example, intrusive thoughts and difficulty concentrating 

may interfere with academic performance and social adaptation. Therefore, school 

consultation about the consequences of trauma and the recovery process may be 

indicated. School-based interventions, which can include curricular materials and 

activities, should be appropriate for the setting and should not supplant efforts to identify 

and refer children in need of more intensive individual evaluation and treatment. 

Long-term and staged interventions. Long-term interventions may be necessary, 

especially for children with direct or interpersonal exposure and for those with enduring 

symptoms, pre-existing or comorbid conditions, prior or subsequent trauma, or family 
270

problems. New issues related to trauma may emerge as children mature. Thus, 

developmentally appropriate staged interventions, which anticipate and address the 

course of recovery, should be considered during developmental transitions and at marker 

events such as anniversaries. 

Death Notification and Pediatric Bereavement 

Considerations in Notifying Individuals About an Unexpected 

Death 

At the time of a disaster or terrorist attack, it is very unlikely that pediatric health care 

providers will have the time and resources to deliver death notification in an optimal 

manner. Nonetheless, sensitivity to the issues discussed here can help minimize the shortand long-term impact on survivors. 

• Verify the identity of the deceased and identify the next of kin. 

• Establish contact as soon as possible. Do not delay contact waiting for a time 

thought to be more convenient for the survivors (e.g., if the death occurs in the 

middle of the night, do not wait until the following morning). 

• Contact the next of kin. Phone calls can be used to contact next of kin, but death 

notification is preferably done in person. Alternatively, someone (e.g., police) can 

be sent to the home of the next of kin to ask them to come to the hospital for 

notification purposes. 

• Minimize the likelihood that you will be compelled to notify the family members 

of the death over the phone. If you contact the survivor(s) by phone to request 

they come to the hospital, try to contact the family before the death has been 

declared (i.e., during resuscitation) or have someone else who has not been 

directly involved in the care call on your behalf. Someone not directly involved in 

the care could make a statement such as: “I know that your husband was seriously 

hurt in the bombing, but I don’t have any further information. If you come to the 

hospital now, someone who has been taking care of your husband will be 

available to talk with you when you arrive.” If family members demand 

information on the phone, the caller can state: “I would prefer to talk with you 

about this in person when you arrive at the hospital.” 

• Consider inviting additional family members or friends to accompany the next of 

kin to the hospital for notification. If a child has died, it is best to notify both 

parents at the same time. When any family member has died, survivors may 

benefit from being told with at least one other family member or friend present. 

Family members and friends can provide support to the next of kin and help 

notify other relatives and friends (instead of the entire burden being placed on one 

survivor). 
271

• Before notifying the family, briefly review the basic facts, including the name of 

the deceased, the relationship to individual(s) that will be notified, the basic 

circumstances of injury and death, and the nature of medical care provided. For 

example, the individual was in a building when a bomb detonated and was found 

under rubble; CPR was done until arrival in the emergency department, where 

after an attempt at resuscitation, he was pronounced dead. Identify who else will 

participate in the notification, and consider planning in advance how to initiate the 

conversation. 

• When the family arrives at the hospital (or site where death notification will be 

occurring), have them escorted to a private location if possible. Try to inform 

them in as private a site as possible; if there is no opportunity for a private room, 

make every reasonable effort to maximize privacy (e.g., use a curtain or notify the 

family while standing behind the building instead of in front). Do not inform 

family members in view of the media; anticipate the presence of media and try to 

offer survivors the opportunity to maintain their privacy as much as possible 

immediately after notification. 

• If possible, have the notification conducted by a physician who was involved in 

the care, especially if he or she knows the family or had some direct involvement. 

Comments such as “I was with your husband when he first arrived at the hospital. 

He was not conscious at the time and therefore was not feeling any pain” can be 

very helpful to families. Inform the patient’s primary care provider whenever 

possible. 

• Consider involving at least one other professional on the health care team, such as 

a social worker, chaplain, nurse, etc. If more than one family member is receiving 

the notification, conducting the notification with another professional is especially 

helpful; however, one staff person should be in charge of the discussion. Try to 

include at least two staff people for notification, even when notification is 

conducted in the field, but limit the number of staff to those directly involved. It 

can be overwhelming for a family member to be notified by a large team. 

• Introduce yourself and any other member(s) of the health care team who are 

participating by name and title and offer to shake hands. 

• Offer seating to the survivors. Sit close to them and face them so that eye-to-eye 

contact can be easily maintained. 

• Refer to the deceased by name and/or relationship to the survivor (e.g., “Mr. 

Smith” or “your husband”). Avoid referring to the person as “the deceased” or 

“the victim.” 

• If children are included, involve professionals with training and experience in 

working with children in the notification process. Notification of the death of a 

family member is preferably provided to children by family members (such as the 
272

surviving parent), rather than by professionals unknown to the child. However, 

parents may wish for professionals to be present when children are told to provide 

support and to help answer questions. 

• Remember that informing survivors of a death is a process, not an act. Pacing of 

the discussion is important. Do not start by stating that the individual is dead 

because survivors are unlikely to hear any further information. 

• Start by asking the family what they have already been told or know. Then 

provide a brief description of the circumstances of the injury and the relief efforts. 

This information helps the survivors understand the context of the death; not 

knowing what happened introduces a discontinuity in the history that impairs 

adjustment. After giving brief background information, it is useful to give a 

“warning notice” and then proceed fairly quickly to stating that the individual 

died. Ideally, the family will be present during the resuscitation efforts, and 

medical staff can provide the background information when the resuscitation 

begins and return to deliver updates that may serve as a “warning notice.” For 

example, “The team has given several medications to try to get your husband’s 

heart starting again, but so far there has not been any response.” 

• An example of a notification initiated after a death might be: “There was an 

explosion 2 hours ago that we believe was caused by a bomb in the building 

where your husband works. The explosion started a fire that spread rapidly. 

Firefighters arrived on the scene within several minutes, but the exits were 

blocked and flames spread quickly. Many individuals were unable to get out of 

the building before they were overwhelmed by smoke. I am sorry to say that your 

husband did not get out of the building in time. We believe he died as a result of 

the smoke from the fire. His body was recovered by a firefighter, and we 

identified him by the wallet that we found in his pocket. We found your phone 

number in the wallet. I am very sorry to have to be telling you this news.” 

• After notifying the survivor(s) of the death, pause to allow both the information to 

be processed and emotions to be expressed. Do not try to fill the silence, even 

though it may seem awkward. Listen more than you speak. Silence is often better 

than anything you can say. Stay with the family members as they are reacting to 

the news, even if they are not talking. 

• Use clear and simple language. Avoid euphemisms such as terminated, expired, or 

passed away. State that the individual died or is dead. 

• Don’t provide unnecessary graphic details. Begin by providing basic information 

and allow the individual to ask questions for more details. 

• Don’t lie or speculate. If you do not know the answer to a question, say so. Try to 

get the answer if possible. 
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• Be conscious of nonverbal communication and cues, both those of the family as 

well as your own. 

• Be aware of and sensitive to cultural differences. If you do not know how a 

particular culture deals with a death, it is fine to ask the family. Be particularly 

attentive to difficulty speaking or understanding English. If there is any doubt 

whether the family members are fluent in English, make sure to have a 

professional translator present unless you are fluent in the family’s preferred 

language. Using family and friends as unofficial translators often leads to 

inadequate translation in the general medical setting. Such reliance on family and 

friends as translators for death notification is particularly burdensome to them and 

should be avoided. 

• Consider the use of limited physical contact (e.g., placing a hand on the family 

member’s shoulder or providing a shoulder to cry on). Monitor the individual’s 

body language and if at all in doubt whether such contact would be well received, 

ask first. 

• Realize that the individual may initially appear to be in shock or denial. Expect 

additional reactions, such as sadness, anger, guilt, or blame. Acknowledge 

emotions and allow them to be expressed without judgment. 

• Do not ignore or dismiss suicidal or homicidal statements or threats. Investigate 

any such statements (often this will be facilitated by the involvement of mental 

health professionals) and if concerns persist, take appropriate action. 

• Just before and during the notification process, try to assess if the survivors have 

any physical (e.g., severe heart disease) or psychological (e.g., major depression) 

risk factors, and assess their status after notification has been completed. 

• If possible, write down your name and contact information in case the family 

wants further information at a later time. If the situation is not appropriate for 

providing your name and contact information, then consider how the family may 

be able to obtain additional information in the future (even months later). For 

example: “I work as a volunteer for the Red Cross. Here is my name and the 

contact information for the Red Cross Chapter. If later you wish more information 

about what happened to your husband, you can call them at this number and they 

should be able to look at the records.” Survivors may not be ready to think of or 

ask questions and may later regret not asking for critical information. 

• Do not try to “cheer-up” survivors by making statements such as “I know it hurts 

very much right now, but I know you will feel better within a short period of 

time.” Instead, allow them their grief. Do not encourage them to be strong or to 

cover up their emotions by saying “You need to be strong for your children; you 

don’t want them to see you crying, do you?” 
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• Feel free to express your own feelings and to demonstrate empathy, but do not 

state you know exactly how family members feel. Comments such as “I realize 

this must be extremely difficult for you” or “I can only begin to imagine how 

painful this must be to hear” can demonstrate empathy. Avoid statements such as 

“I know exactly what you are going through” (you can’t know this) or “You must 

be angry” (let the individual express his or her own feelings; don’t tell the person 

how to feel) or “Both my parents died when I was your age” (don’t compete with 

the survivor for sympathy). Provide whatever reassuring information you may be 

able to, such as “It appears your husband died immediately after the explosion. It 

is unlikely he was even aware of what happened and did not suffer before he 

died.” However, do not use such information as an attempt to cheer up family 

members (e.g., “You should be happy, many people suffered painful burns or 

were trapped under rubble for an hour before they died. At least your husband 

didn’t experience that.”) 

• Feel free to demonstrate that you are upset as well—it is fine to cry or become 

tearful. If you feel, though, that you are likely to become overwhelmed (e.g., 

sobbing or hysterical), then try to identify someone else to do the notification. 

• After you have provided the information to the family and allowed adequate time 

for them to process the information, you may wish to ask questions to verify 

comprehension. 

• Offer the family the opportunity to view the body of the deceased and to spend 

some time with their loved one. Before allowing the family to view the body, the 

health care team should prepare it for viewing by others. A member of the health 

care team should escort the family to the viewing and remain present, at least 

initially.1

 

• Help families figure out what to do next. Offer to help them notify additional 

family members or close friends. Tell them what needs to be done regarding the 

disposition of the body. Check to see if they have a means to get home safely (if 

they have driven to the notification, they may not feel able to drive back safely), 

and inquire if they have someone they can be with when they return home. 

• Help survivors identify potential sources of support within the community (e.g., 

member of the clergy, their pediatrician, family members, or close friends). 

• Take care of yourself. Death notification can be very stressful to health care 

providers. Health care providers need to explore and come to understand their 

own reactions to patient death and associated emotions, which may include 

 1 For further information about preparation of the body for viewing, as well as additional 

recommendations about the death notification process, see Leash RM. Death Notification: A Practical 

Guide to the Process. Hinesburg, VT: Upper Access, 1994.
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sadness, anger, guilt, or a sense of responsibility. It is important to provide 

informal support and debriefing to professionals who provide death notification, 

especially if related to tragic deaths or when multiple deaths are involved (as 

would be anticipated in a major disaster or terrorist event). 

Explaining Death to Children 

Children’s understanding of death may be very different from that of adults. Children 

have had far less personal experience of loss and have accumulated less information 

about death. They can also have difficulty understanding what they have seen and what 

they are told unless the basic concepts related to death are explained to them. Adults will 

need to provide especially young children with both the basic facts about what happens to 

people after they die, as well as the concepts that help them to explain those facts. For 

example, young children may be told that after people have died, their body is buried in a 

cemetery or turned to ashes that can then be buried or scattered. Children can be very 

distressed by these facts unless they are helped to understand the concept that at the time 

of death, all life functions end completely and permanently—the body can no longer 

move, and the person is no longer able to feel pain. That is why it is okay to bury or 

cremate the body. 

Children need to understand four concepts about death to comprehend what death means 

and to adjust to a personal loss: irreversibility, finality, inevitability, and causality (Table 

8.1). Most children will develop an understanding of these concepts between ages 5 and 

7, but this varies widely among children of the same age or developmental level, based in 

part on their experience and what others have taught them. When faced with a personal 

loss, some children 2 years old or younger may demonstrate at least some comprehension 

of these concepts. Adults should not underestimate the ability of young children to 

understand what death means if it is explained to them properly. Therefore, it is best to 

ask children what they understand about death, instead of assuming a level of 

comprehension based on their age. As children explain what they already understand, it 

will be possible to identify their misunderstandings and misinformation and to correct 

them accordingly. 

When providing explanations to children, use simple and direct terms. Be sure to use the 

words “dead” or “died” instead of euphemisms that children may find confusing. If 

young children are told that the person who died is in “eternal sleep,” they may expect 

the deceased to later awaken and be afraid to go to sleep themselves. This description 

does little to help children understand death and may cause more confusion and distress. 

Religious explanations can be shared with children of any age, but adults should 

appreciate that religious explanations are generally very abstract and therefore difficult 

for young children to comprehend. It is best to present both the facts about what happens 

to the physical body after death, as well as the religious beliefs that are held by the 

family. 

Even when children are given appropriate explanations, they still may misinterpret what 

they have been told. For example, some children who have been told that the body is 

placed in a casket worry about where the head has been placed. After explanations have 
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been given to children, it is helpful to ask them to review what they now understand 

about the death. 

Common Reactions Among Children Who Have Experienced a 

Personal Loss 

Like adults, children may be reluctant to talk about a death. They may at first be shocked 

by the news or fail to understand its implications. Young children have difficulty 

sustaining strong emotions, so they may appear upset for a brief period of time and then 

return to play. They may also use play or other creative activities, such as artwork or 

writing, to both express and work through their feelings associated with a loss. By 

observing play and the products of children’s creative activities, we may find some clues 

as to what is bothering them, but it is important not to jump to conclusions about the 

meaning or relevance of what is observed. 

Soon after notification, children often ask questions about the deceased and the meaning 

it has for them personally. These questions may cause surviving family members distress 

because they often are particularly poignant. Children pick up readily on the cues from 

others in their family that adults are made uncomfortable by these inquiries. They may 

conclude that such questions are unwelcome, inappropriate, or even represent 

misbehavior and stop asking. The silence that results is not an indication that children do 

not understand what has happened or have already coped. Rather, it may be a sign that 

they are trying to protect their parents who appear overwhelmed or that they do not feel 

comfortable asking questions or expressing their emotions, leaving them to deal with 

both alone. Therefore, it is important for adults to explicitly invite children to share their 

questions and feelings. Often it is helpful for an adult who is familiar with child 

development and who knows the child personally to provide an additional outlet for 

discussion. The child’s pediatrician or a social worker from the child’s school, for 

example, may be in a good position to start such a conversation. 

Older children and adolescents may initially decline the assistance of adults because they 

are more accustomed to turning to peers for support and to address issues of concern. It is 

important to extend an open invitation to these young people to talk with you when they 

have questions or want to talk about the situation and to help them identify other adults in 

their lives they can turn to for support and assistance (e.g., a chaplain, coach, or teacher). 

Even in the setting of a natural disaster or terrorist event, children may still wonder if 

they were in some way responsible for the death. After a traumatic death, such guilt 

feelings may increase posttraumatic symptoms and complicate the grieving process. 

Young children in particular have a very limited understanding of why things occur and 

tend to be self-centered. As a result, they often use magical thinking to explain situations 

that they do not understand. This may result in extreme feelings of personal responsibility 

for a death that has occurred, even in situations when there is absolutely no logical reason 

why the child should feel responsible. 

Often such feelings of guilt are irrational. “If only I hadn’t gone to school that day, my 

dad would never have gone to the office and wouldn’t have been killed by the bomb,” “I 
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was mean to my father yesterday and that’s probably why he died,” etc. Understandably, 

children are often reluctant to share their guilt feelings with adults; adults may not 

anticipate these feelings (or be burdened with their own guilt feelings). It may be helpful 

to reassure children of their complete lack of responsibility, even if they do not express 

feelings of guilt, and there is no logical reason why you might anticipate they would feel 

guilty. 

At the time of a traumatic loss, children often think first about their own needs. Parents 

should be warned that this self-centeredness is not a sign that children are selfish; more 

likely, it is a sign that they are under considerable stress and in need of more support and 

assistance. 

Children often regress in response to the stress of a personal loss. Children who had been 

successfully toilet-trained may now begin to wet their bed; children who had not had 

difficulty attending daycare may now begin to show separation problems; children who 

had good social skills may now argue more or have difficulty getting along with peers. 

Children and adolescents may also develop somatic complaints, such as headaches, 

stomach aches, or generalized fatigue. 

A disaster or terrorist event may uncover children’s concerns about another loss or 

personal crisis that has not been fully resolved. Children may react strongly to the death 

of someone that they did not know well or perhaps did not know at all. Or, children may 

be more preoccupied with their own personal crises than they are affected by the death of 

someone in their family or community. 

Indications of the Need for Referral 

Not every child who has experienced the death of a family member or friend requires 

professional counseling, and in the setting of a major disaster or terrorist event, such 

resources are unlikely to be available. It generally is helpful though for children who 

have experienced the death of a family member or friend to speak with someone outside 

of the immediate family who understands child development and can attend to the child’s 

needs (without being burdened with his or her own grief), such as their pediatrician or a 

school counselor or social worker. When a community disaster or crisis has occurred, it is 

important to help establish access to supportive services within community sites, such as 

schools, to provide services to larger numbers of children. 

Significant stigma continues to be associated with receiving mental health services, and 

this stigma remains even in the setting of a major crisis event. Parents and other 

caregivers need to understand that even though bereavement is a normative experience, it 

still can be profoundly difficult. People, including children, can be helped through 

supportive services and, when indicated, group or individual counseling. 

Children who have extreme reactions (e.g., anxiety, posttraumatic symptoms, depression, 

or thoughts of suicide), atypical reactions (e.g., appearing happy or disinterested), or 

prolonged reactions (e.g., prolonged sleep problems or somatization) should be evaluated 

by their pediatrician and likely referred to a mental health professional experienced in the 
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management of pediatric bereavement. Children should be referred who are having 

difficulty returning to their normal daily routines several weeks after the death or are 

demonstrating the new onset or worsening of problems interacting with peers. Children 

who are experiencing traumatic grief may require treatment of posttraumatic 

symptomatology before they are able to continue with normal grieving. 

Soon after a death has occurred, many children may find comfort in returning to school, 

spending time with their friends, and taking part in the same activities that they did before 

the death. Allowances and adjustments should be made for a time (such as extra help with 

homework because of difficulty concentrating and learning) so that they can return to 

their day-to-day life as soon as possible. Some children may resist returning to school or 

resuming their regular daily activities. They may be fearful to leave other family 

members, worrying that they may die in their absence or that grieving family members 

may need their support. These children require reassurance of the safety and well-being 

of surviving family members and encouragement to return to school. Other grieving 

family members, especially parents or guardians, should receive the support and 

assistance they need, so that the children do not feel it is their responsibility.

Attendance of Children at Funerals and Memorial Services 

Children can be told in simple terms what to expect at a funeral or memorial service. If an 

open casket or gravesite ceremony is planned, children should be told and given 

explanations about what this involves. Children can be invited to participate to their level 

of comfort but should not be forced or coerced to attend. They should be encouraged to 

ask questions, which should be answered simply and honestly but without unnecessary 

details. At the ceremony, children should be accompanied by an adult they know and like 

(who is not personally grieving to the same extent as close family members) who can 

monitor the child’s reactions, answer questions, and step out of the ceremony with the 

child if the child appears distressed or indicates a desire to leave. Even if children play 

quietly in the lobby of a funeral home, they may still have a sense of having participated 

in the ritual. Children who are not allowed to attend the funeral or memorial service often 

feel angry and hurt and lose out on the benefits of religious, family, and community 

support. They also may create fantasies about what occurs during funerals that are 

actually more frightening than the reality. It is also helpful if children can perform a small 

task at the funeral, such as handing out Mass cards at the entrance of the funeral home or 

selecting flowers to be placed near the coffin. Such tasks should be predominantly 

symbolic, of the child’s choosing, and not overwhelming for the child. 

Therapies for Psychic Trauma 

Crisis Response 

Mass violence presents unique issues that differ from other episodes of interpersonal, 

community, and other forms of violence. Responding to those individuals who are 

directly affected by the event is not enough—a multilevel strategy is required and should 

include victims and witnesses, individuals with whom they are associated, and the 

broader community. Although crisis response providers do not have to perform all of 
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these roles, they should work closely and collaborate with a number of individuals and 

agencies to ensure that the psychological impact of mass violence is addressed. 

The first and foremost response to mass events is both directed and performed by the 

government and its agents. These are usually under the auspices of law enforcement, fire 

personnel, and/or emergency medical services, which are typically managed by an 

Incident Command System (ICS). Mental health early responders should have preexisting relationships with the ICS to perform their duties effectively. In most States and 

other jurisdictions, ICS staff members meet regularly to ensure efficient operation when 

needed. During episodes of mass violence, mental health providers need to be part of the 

ICS staff whenever possible. The pre-existing relationship with emergency response 

commanders permits more expeditious access to affected individuals and for the 

community’s psychological needs to be considered consonant with emergency responses. 

In addition, when mental health providers are members of the ICS, access to and 

allocation of resources for mental health crisis responders in situations of mass violence 

improves. Situating providers in the most useful locations, ensuring the flow of needed 

information and communications, and preventing well-intended, but inexperienced and 

unlinked clinicians from arriving en masse in an attempt to provide services are essential 

to lessen the general confusion and chaos that accompany disasters. 

A useful way of defining and understanding a traumatic response is that the affected 

individual experiences the loss of both internal and external control. Therefore, 

maximizing organization and structure is a necessary prerequisite in providing mental 

health crisis response and early intervention. Mental health crisis models are best 

equipped to achieve this organization and structure when they are firmly rooted in the 

ICS. 

Crisis Response for Children and Families 

Unfortunately, there is no clear empirical evidence for the effectiveness of any crisis 

response intervention. In fact, the frequently used and previously heralded Critical 

Incident Stress Debriefing or Management (CISD or CISM) strategies have not 

demonstrated effectiveness, and in some studies they have proved detrimental. Indeed, it 

has been recommended that compulsory debriefing of victims of trauma should cease. 

However, it is possible that an alternative method of early crisis intervention may be 

helpful for assisting people who may be recently traumatized. The following 

recommendations and guidelines for early intervention strategies are based on evidence 

from research on the risk factors for PTSD as well as some intervention research. Thus, 

they provide an empirical foundation for appropriate and useful approaches to assist 

potentially traumatized individuals. 

Currently, there is no evidence that global intervention for all trauma survivors serves a 

function in preventing subsequent psychopathology. However, there is consensus that 

providing comfort, information, and support and meeting the immediate practical and 

emotional needs of affected individuals can help people cope with a highly stressful 

event. This intervention should be conceptualized as supportive and noninterventional but 
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definitely not as a therapy or treatment. This suggestion recognizes that most people do 

not develop PTSD and other posttraumatic symptoms immediately. Instead, they usually 

will experience transient stress reactions that will abate with time. The goal of early 

intervention is to create a supportive (but not intrusive) relationship that will result in the 

exposed individual being open to followup, further assessment, and referral to treatment 

when necessary. Inherent in this early intervention is the recognition that interpretation or 

directive interventions are not to be provided. 

After assuring that basic necessities are available and are not a pressing concern, the 

basic principles of intervention should be followed. These principles should ensure that 

no harm is being done in the intervention process and hopefully prevent or reduce 

symptomatology and impairment. 

• Interventions should be grounded in the basic principles of child development, 

and providers should be experienced in working with children of different ages 

and levels of development. 

• Mental health providers should have collaborative relationships with community 

providers to ensure access and community support for children and families. 

• Children and families should be assessed for risk factors and symptoms, and 

interventions should be crafted to address the findings. 

• An essential objective is to improve parental attention and family cohesion 

through assessment, psychoeducation, and treatment, when necessary, to parents 

and primary caregivers. 

• Providers should make concerted efforts to prevent social disruption and 

displacement. 

• Providers should identify, assess, and attempt to ameliorate or remove children 

and families from the continued threat of danger. 

• Providers should have continued contact and monitor children for symptoms or 

impairment. 

Handouts or flyers that describe trauma, what to expect, and where to get help should be 

made available. Individuals should be given an array of intervention options that may 

best meet their needs. The goal is not to maximize emotional processing of horrific 

events, as in exposure therapy, but rather to respond to the acute need that arises in many 

to share their experience, while at the same time respecting those who do not wish to 

discuss what happened. 

Medication 

There is not yet clear evidence to support the use of pharmacotherapy in the treatment of 

posttraumatic symptoms in children, and no randomized controlled trial has been 

completed. The first line of treatment for posttraumatic symptoms in children is traumafocused cognitive behavioral treatments (CBT), which includes such interventions as 

graded desensitization and other CBT. 

So, why consider the use of psychopharmacology for children with posttraumatic 

symptoms? 
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• Lack of availability of trauma-focused psychotherapy (CBT). In many areas of the 

country, these therapies are not available for children and although nondirective 

therapies can be helpful for children with posttraumatic symptoms, they do not 

appear to directly treat the symptoms. 

• Some children do not respond to trauma-focused psychotherapies. As in all 

situations, first-line treatments do not always work, and other interventions are 

required. 

• Randomized controlled trials have demonstrated the efficacy of medications in 

adults with posttraumatic symptoms. Although the analogy between medication 

effectiveness in adults and children is frequently made, extreme care is indicated. 

Metabolic and neurodevelopmental factors have great influence on dosage and 

frequency of medications and responses in children. Some medications that are 

effective in adults are not effective in children, and furthermore, they may have 

different or more dangerous side effects. 

Considering the use of medications for children with early posttraumatic symptoms 

prompts certain considerations: 

• Is a trauma-focused therapy available, and if so, has the child completed a trial 

without responding? 

• What specific symptoms are being targeted? 

• Different psychotropic medications are better for different symptoms (see below). 

• What is the child’s level of distress (symptomatic and functional)? In nearly 60% 

of cases, early posttraumatic symptoms are transient and resolve without 

treatment. So the question is whether the current amount of distress and functional 

impairment warrants a medication trial. 

• Are other family members symptomatic? 

• Ascertaining the level of untreated symptomatology of other family members, 

especially parents, is essential, because posttraumatic symptoms—especially 

anxiety and hypervigilance—are highly transferable to the child. So, treating the 

child may have no impact on symptoms if they originated with the parent. 

• What is the developmental or neuromaturational level of the child? 

Again, psychotropics are much more difficult to use in younger children and may have an 

increased propensity to cause side effects. 

Neurotransmitters implicated in PTSD symptoms include the following: 

• Adrenergics (norepinephrine, epinephrine). 

• Dopamine. 

• Serotonin (5-HT). 

• Endogenous opioids. 

Symptoms that appear to be directly related to dysregulation in the adrenergic system 

include increased heart rate, blood pressure, and anxiety, as well as hyperarousal 

symptoms such as nightmares, poor sleep, hypervigilance, and panic attacks. 
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Blocking norepinephrine and epinephrine may treat these symptoms. The first choices, 

especially for sleep difficulties, are the α2-blockers clonidine and guafacine. These agents 

are especially good at improving sleep and decreasing nightmares acutely and may 

improve other hyperarousal symptoms such as impulsivity and hypervigilance. 

Symptoms associated with dysregulation of the dopaminergic system include anxiety, 

hypervigilance, aggressive impulsivity, flashbacks, and paranoia. Studies of risperidone 

indicate that it may be useful for this constellation of symptoms. 

There is clear evidence of dysregulation of the serotonergic system in individuals with 

posttraumatic symptoms. Deficit of 5-HT is associated with depression, thoughts of 

suicide, aggression, impulsivity, anxiety, and obsessive thoughts. This suggests that 

increasing 5-HT availability may treat these symptoms, and studies in adults have found 

selective serotonin reuptake inhibitors (SSRIs) to be the only class of drugs to decrease 

all three PTSD symptom clusters. However, with acute posttraumatic symptoms, 6–8 

weeks may be needed for effect, so it is better used as a first-line therapy for children 

who meet the criteria for PTSD. At present, the SSRIs of choice are fluoxetine and 

citalopram. 

Although benzodiazepines would seem an obvious choice for acute posttraumatic 

symptoms, their use is controversial. In two randomized controlled trials of 

benzodiazepine use for this purpose, one demonstrated moderate positive effects, while 

the other showed increased likelihood of the individual developing PTSD. 

School Crisis Response 

Most children benefit from receiving supportive services in the aftermath of a disaster or 

terrorist attack. Pediatricians can play a vital role in advocating for, consulting for, and 

actively participating in school crisis response teams to ensure that such supportive 

services can be provided to children within schools and other community sites. 

School administrators, teachers, and other school staff will be affected by the same crisis 

event that is affecting their students. During such times, organizing and implementing an 

effective crisis response can be difficult or even impossible. Therefore, it is imperative 

that schools begin planning for potential crisis events before they occur, both to avert 

disasters whenever possible and to decrease the negative impact on students and staff 

when disasters cannot be prevented. 

The school crisis response plan should include generic protocols for the following: 

• Notification of team members, school staff, students, and parents of a crisis event. 

• Delivery of psychoeducational services and brief crisis-oriented counseling, such 

as through support rooms or short-term support groups. 

• Memorialization and commemoration (see guidelines at 

http://www.csee.net/pageview.aspx?id=55). 

• Followup. 
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The structure provided by a preexisting plan can be very comforting in times of crisis and 

helps to ensure that key issues are considered, appropriate steps are taken, and necessary 

resources are in place. 

In addition, the crisis response plan should include guidelines on the following: 

• Crisis team membership. 

• Roles of crisis team members. 

• Protocols for delivery of crisis intervention services. 

• Specific guidelines for responding to unique situations, such as large-scale natural 

disasters or a terrorist attack. 

• Physical safety and security. 

• Rapid dissemination of accurate and appropriate information. 

• Attention to the emotional impact of the events and the crisis response. 

All areas should be addressed concurrently and in a coordinated fashion. 

Delivery of supportive services to children during a crisis can be demanding work for 

school staff and community mental health providers working within the schools. Plans 

should also include mechanisms to ensure that supportive services for staff are included 

as a key component of a crisis response. 

Anniversary Reactions and Commemorative Activities

As the anniversaries of stressful, critical, or traumatic events approach, many children 

and adults still have significant reactions. Throughout the year, reminders of the original 

crisis may add to children’s sense of further danger and emotional distress. Those 

reminders of the events may also increase the reactions of peers, parents, teachers, and 

other adults. 

Remember: 

• Memorial activities can further the process of healing and learning. 

• The planning process is as important as the memorial activities themselves. 

• Doctors, teachers, parents, and children all benefit from the planning process. 

• Symptoms and reactions vary from child to child. 

• There is no one “best way” to acknowledge an anniversary. 

• Helping children deal with a difficult event is hard work; pediatricians need to 

take care of themselves and their staff as well. 

Anniversaries 

At the time of the anniversary, children frequently experience a recurrence of some of the 

feelings associated with a loss or tragedy. These reactions vary widely, and they can be 

seen in both children and adults. Some children may not be interested in revisiting the 

events. For these children, it may be more appropriate that they are occupied with the 

typical concerns of childhood. 
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It is important to find ways within the school to recognize the anniversary of such an 

important event without imposing personal emotions or expectations on either students or 

staff. 

Some children directly affected by the traumatic event may appear to be “back to normal” 

but may still be feeling sad, scared, anxious, or angry. Children do not always 

demonstrate their feelings directly, and we should pay special attention to signs of 

concern or distress. Children who are known to have histories or ongoing exposure to 

trauma or loss, even if they are not directly related to the traumatic event, may be 

especially vulnerable in the days and weeks surrounding the anniversary. 

Heightened media coverage and publicity of memorial events may increase reactions in 

children. Parents should monitor and supervise their watching of television and, 

especially for younger children, consider limiting the amount of television exposure. 

Some signs of distress to look for include the sudden appearance of or noticeable change 

in the following: 

• Depressed or irritable mood. 

• Oppositional and defiant attitude. 

• Attention-getting or other behavioral problems. 

• Difficulties getting along with classmates and peer group. 

• Social isolation or withdrawal. 

• Deterioration in academic performance. 

• Physical complaints. 

• Changes in appetite. 

• Sleep disturbances. 

The extent and nature of potential difficulties may be related to many factors, including 

the following: 

• Age and developmental level. 

• Personal history (e.g., prior trauma, loss, or emotional difficulties). 

• Support from peers, parents, and school staff. 

Memorialization 

Memorialization is any activity designed to formally mark the anniversary or memory of 

a significant event. Memorial events can help children express and cope with their 

feelings that might otherwise seem overwhelming to deal with alone. By actively 

planning and participating in a memorial event, children can exercise some control over 

how they will remember the disturbing event. 

Children may have needs similar to those of adults in times of crisis, but they often meet 

those needs in very different ways. It is important to find out from the children what they 

would like to remember and what they think would be the best way to acknowledge the 

anniversary. Children need to be part of the planning process for memorial events. A 

memorial planned by adults for children is likely to be more helpful to the adults and not 
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necessarily meet the children’s needs. The planning of a memorial activity can be more 

therapeutic than participating in the activity itself. 

Remember also that different groups of children and adults will have different needs and 

wishes at the time of the anniversary. Memorial activities do not need to be formal or 

elaborate. It is best to take cues from children, considering their age and developmental 

level, when planning memorial activities. Discussion allows children to explore how they 

are feeling and to think about what might help them feel better. 

Some children may wish to acknowledge the anniversary in a personally meaningful way 

(e.g., drawing a picture, writing a poem or essay) but resist a group activity centered 

around the anniversary. Some children may prefer not to mark the anniversary with any 

formal or even informal activity. It is important to remember that those children who are 

grieving their own personal losses may resent or feel frustrated if the memorial event 

focuses only on the heroic efforts of rescue workers. 

Planning a Memorial Activity 

Memorial activities can be planned at various levels, including individual consultation 

with the pediatrician, with family members, in small student groups, or in larger 

community or school-wide committees. Children should be involved in the planning 

process, but it is equally important for adults to provide guidance, structure, and support. 

• Consider the children’s ages and developmental levels when planning activities. 

• Some children may wish to involve other friends or family members in the planning 

process. 

• Coordinate the planned events with the family and the school. 

• Not all children will want to be involved in the planning process, and participation 

should be voluntary. 

• Don’t feel pressured to plan the “perfect event.” Any memorial event or activity, big 

or small, may be a helpful means for children to understand and mark an anniversary. 

• Activities within a school or individual classroom may affect other students and staff 

within the school as well as children’s families at home. Therefore, other families 

should be informed about plans for memorial events within a school. 

• Other adults will benefit from additional support and guidance on how to mark an 

anniversary in a sensitive manner. 

• Awareness of school activities and plans often can help to initiate discussions at 

home, where children may be most comfortable talking about critical events and 

anniversaries. 

• Parents should be invited to share any concerns related to the anniversary or relevant 

family experiences with the pediatrician, teachers, and school staff. Pediatricians, 

teachers, and school personnel should keep the lines of communication open with 

parents throughout the planning process. Parents should be encouraged to continue to 

discuss the planned activities with their children at home. 

• Open discussion communicates to children that adults are available for further 

discussion and support. 
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• Look for signs of distress in students, such as agitation, acting out, or other 

unexpected behaviors, and help teachers, parents, and school personnel to be aware of 

them. 

In some instances, families may not wish to have their children participate in memorial 

activities. Remember that many children and their families choose not to disclose 

personal losses, and their privacy should be respected. 

Supporting School Staff 

Some adults may find it difficult to discuss traumatic events, especially if dealing with 

their own losses. Adults should seek out support from other adults and colleagues when 

needed. This is difficult work for everyone, and it is important for staff to think about 

what their own feelings are in relation to the events. Providing an opportunity for staff to 

talk about their own reactions may be useful to them personally and may better prepare 

them to meet the children’s needs. 

Remember that children look to adults for guidance and support during difficult times. 

We need to think about how our own reactions may impact children. Children’s questions 

may sometimes take us off guard and make us confront issues we would rather not think 

about. 

Having a plan to address these concerns in advance will help make the task easier. If the 

task seems too difficult, staff should share the responsibility with a colleague or invite 

someone else to help with the planning and process of memorialization. 

Impact on Health Care Providers 

Very often, first responders and other adult service providers show signs of stress and 

emotional disruption after responding to situations involving disasters, including 

terrorism, that result in trauma. Typically, programs such as Critical Incident Stress 

Debriefing or Management (CISD or CISM) are effectively used with first responders. 

Fire departments and emergency medical teams have incorporated these strategies into 

the response programs to critical incidents. A short but specialized training is needed for 

an individual to apply this model, which basically walks the responder through a guided 

exploration of their experience in responding to a critical situation. 

Pediatricians may be approached by a colleague, a fellow worker, or any health care 

provider in distress. The following basic, common sense rules can help: 

• Make psychological contact. 

• Assess the individual’s level of coping. 

• Explore possibilities for getting further help. 

• Assist in taking action. 

• Followup. 
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Make Psychological Contact 

Tune in—empathetic listening is a precondition for any helping activity: 

• Invite the person to talk. 

• Listen for what happened (facts). 

• Listen for the person’s reaction to the events (feelings). 

• Maintain a calm, controlled manner. 

Level of Coping 

Examine the dimensions of the problem. Ask questions that focus on three areas: 

• Immediate situation. What were the events leading up to the current difficulties in 

coping? 

• Present. What life situations may increase or decrease the level of stress (family, 

work, children, etc.)? Have the person tell the story. 

• Immediate future. What are the likely future difficulties? What coping strategies 

have been attempted? 

Explore Possible Solutions 

Take a step-by-step approach; ask first about what has already been tried, then try to get 

the individual to generate alternatives, and finally, add other possible solutions. Some 

people may need coaching to even consider the idea that a possible solution exists. 

Examine obstacles to implementation and address these issues before a plan is 

implemented. Part of the solution may include helping the individual to establish a 

supportive social network. Finally, it may be appropriate to suggest that the individual 

seek professional help for emotional difficulties. 

Take Action 

The objective is very limited, i.e., no more than taking the best next step given the 

situation. Help the individual implement the agreed upon immediate solutions(s) aimed at 

dealing with the immediate need(s). 

Followup 

The last component involves establishing a way to provide the support the individual 

needs to ensure that the necessary steps are taken toward a satisfactory resolution of the 

situation. 

Basic Objectives 

• Help caregiving adults recognize the immediate emotional, cognitive, and 

behavioral impact of overwhelming events on themselves, typically through 

psychoeducational approaches. 
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• Engage the responder or care provider for purposes of followup assessments and 

identification of service needs across multiple domains, including home, clinical, 

work, and community settings that involve individuals, families, and groups. 

Benefits 

One of the primary ways to reduce stress for first responders and other service providers 

is through “psychoeducational programs,” especially training that emphasizes skills in the 

following: 

• Coping with people. Stress reduction also occurs through increased confidence 

and abilities to have an impact on and help other people rather than just oneself 

(e.g., microcounseling, “psychological first aid,” human relations training, 

assertiveness training). 

• Interpersonal awareness. Stress reduction also occurs through increased 

understanding and awareness of your own and other people’s cognitive and 

emotional reactions to traumatic events. 

These programs significantly decrease the following: 

• Depression. 

• Anxiety. 

• Psychological strain. 

• Physical strain. 

• Emotional exhaustion. 

• Vocational strain. 

• Interpersonal strain. 

Additionally, these programs decrease anger and improve relationship adjustment. 

Risk Communication and Media Issues 

Information should be communicated to the public in timely, accurate ways that do not 

heighten concern and fear. Communicating effectively during a crisis requires the 

following: 

• Planning. 

• Preparation. 

• An understanding of communications protocols, messaging, and the media. 

• The ability to manage the flow of information. 

Each element is a challenge that can be met effectively, to the benefit of those receiving 

messages in times of crisis. 

Developing Goals and Key Messages 

People often fail to communicate effectively due to a lack of clear communications goals 

and key messages to support them. Setting such goals and identifying support messages 

are tasks that should be accomplished before issuing any public comment and are 

especially important in a crisis. 
289

A communications goal of “educating the public on the complexities of bioterrorism and 

preparing them for any eventuality” is not realistic. Informing the public of the problem 

and specific dangers, providing guidance on appropriate responses, and easing concerns 

are achievable goals. Messages in support of these goals should also be direct and speak 

effectively to the audience. 

A risk message is a written, verbal, or visual statement containing information about risk 

that may or may not include advice about behaviors to reduce risk. A formal risk message 

is a structured written, audio, or visual package developed with the express purpose of 

presenting information about risk. Risk messages may aim to ease public concern or 

provide guidance on how to respond. 

Messages to ease public concern. Examples of messages to ease public concern are: 

• The risk is low. 

• The illness is treatable. 

• It is not easily contracted. 

• Symptoms are easily recognized. 

Messages on how to respond. Examples of messages that give guidance on how to 

respond include: 

• Take these precautions. 

• If possibly exposed, contact a physician. 

• If symptomatic, contact a physician. 

• Note possible symptoms in others. 

If the goal is to ease concern and the message in support of that goal is “the risk to the 

public is low,” that message should be clearly stated at the outset and returned to as often 

as possible. 

• Raise points often enough that the audience leaves with a clear understanding of 

the message you wanted them to hear. 

• Take opportunities to begin or end statements with a reiteration of your message. 

• Don’t be so repetitious with a single message that you appear to be trying to 

convince people of something that isn’t true. 

• Don’t repeat messages word-for-word every time you answer a question. 

Exercise some control over the conversation you are having, be it an interview, press 

conference, or questions from an audience. Don’t allow the conversation to be led down 

paths that are not pertinent to the goals or message—no matter how persistent the 

questioner might be in pursuing a line of inquiry. 

Delivering Accurate and Timely Information

In a risk-communication situation, there is constant tension between providing accurate 

information and providing information quickly. Both demands pose challenges. To wait 

for all information to be complete and verified before releasing it to the public can create 
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an information vacuum that will almost certainly be filled with rumor and speculation. To 

release information that has not been confirmed and turns out to be inaccurate, however, 

runs the risk of misleading the public and undermining your credibility as a 

spokesperson. 

• Goals and messages should be simple, straightforward, and realistic. 

• Information should be delivered with brevity, clarity, and effectiveness. 

Most importantly, always provide statistics and key information to the media in written 

form. In presenting information, always know how the information was gathered and how 

any conclusions were reached.2

Bibliography 

Trauma-Related Disorders 

• American Psychiatric Association. Diagnostic and Statistical Manual of Mental 

Disorders-IV-TR (4th ed). Washington, DC: American Psychiatric Association; 

2000. 

• Bolton D, O’Ryan D, Udwin, et al. The long-term psychological effects of a 

disaster experienced in adolescence: II: General psychopathology. J Child 

Psychol Psychiatry. 2000;41(4):513–523. 

• Cohen JA, Bernet W, Dunne JE, et al. Practice parameters for the assessment and 

treatment of children and adolescents with posttraumatic stress disorder. J Am 

Acad Child Adolesc Psychiatry. 1998;37(Suppl 10):4S–26S. 

• Eth S, Pynoos RS. Developmental perspective on psychic trauma in childhood. In 

Figley CR (ed), Trauma and Its Wake. New York: Brunner/Mazel;1985:36–52. 

• Goenjian AK, Pynoos RS, Steinberg AM, et al. Psychiatric comorbidity in 

children after the 1988 earthquake in Armenia. J Am Acad Child Adolesc 

Psychiatry. 1995;34(9):1174–1184. 

• Pfefferbaum B, Nixon SJ, Krug RS, et al. Clinical needs assessment of middle 

and high school students following the 1995 Oklahoma City bombing. Am J 

Psychiatry. 1999;156(7):1069–1074. 

• Rando T. Treatment of Complicated Mourning. Champaign, IL: Research Press, 

1993. 

• Schuster MA, Stein BD, Jaycox LH, et al. A national survey of stress reactions 

after the September 11, 2001, terrorist attacks. N Engl J Med. 

2001;345(20):1507–1512. 

• Steinberg AM, Brymer M, Decker K, et al. The UCLA PTSD Reaction Index. 

Curr Psychiatry Rep. 2004;6:96–100.

Crisis Response 

• Leash RM. Death Notification: A Practical Guide to the Process. Hinesburg, VT: 

Upper Access; 1994. 

 

2

 From Communicating in a Crisis: Risk Communication Guidelines for Public Officials. Rockville, MD: 

Substance Abuse and Mental Health Services Administration; 2002. 
291

• Schonfeld D. Crisis intervention for bereavement support: A model of 

intervention in the children’s school. Clin Pediatr. 1989; 28(1):27-33. 

• Schonfeld D. Almost one year later: looking back and looking ahead. J Dev 

Behav Ped. 2002;23(4):1–3. 

• Schonfeld D. School-based crisis intervention services for adolescents: Position 

paper of the Committees on Adolescence and School Health, Connecticut Chapter 

of the American Academy of Pediatrics. Pediatrics. 1993;91(3):656–657. 

• Schonfeld D, Kline M, and Members of the Crisis Intervention Committee. 

School-based crisis intervention: an organizational model. Crisis Intervention and 

Time-Limited Treatment. 1994;1(2):155–166. 

• Schonfeld D, Lichtenstein R, Pruett MK, et al. How to Prepare for and Respond 

to a Crisis (2nd ed). Alexandria, VA: Association for Supervision and Curriculum 

Development; 2002. 

• Substance Abuse and Mental Health Services Administration. National Child 

Traumatic Stress Network. Available at: http://www.nctsnet.org Accessed 

September 18, 2006. 

 

Risk Communication and Media Issues 

• Substance Abuse and Mental Health Services Administration. Communicating in 

a Crisis: Risk Communication Guidelines for Public Officials. Rockville, MD: 

2002. SAMHSA Publication No. SMA02-3461. 
292

Table 8.1 Concepts of death and implications of incomplete understanding for 

adjustment to loss 

Concept Example of incomplete 

understanding 

Implication 

Irreversibility

Death is seen as a 

permanent phenomenon 

from which there is no 

recovery or return. 

Child expects the 

deceased to return, as if 

from a trip. 

Failure to comprehend this 

concept prevents child from 

taking the first step in the 

mourning process, that of 

appreciating the permanence 

of the loss and the need to 

adjust ties to the deceased. 

Finality (Nonfunctionality)

Death is seen as a state in 

which all life functions 

cease completely. 

Child worries about a 

buried relative being in 

pain or trying to dig 

himself or herself out of 

the grave; child wishes to 

bury food with the 

deceased. 

Can lead to preoccupation 

with physical suffering of the 

deceased and may impair 

readjustment; serves as the 

basis for many horror stories 

and films directed at children 

and youth (e.g., zombies, 

vampires, and other “living 

dead”). 

Inevitability (Universality)

Death is seen as a natural 

phenomenon that no living 

being can escape 

indefinitely. 

Child views significant 

individuals (i.e., self, 

parents) as immortal. 

If child does not view death as 

inevitable, he or she is likely 

to view death as a punishment 

(either for actions or thoughts 

of the child or the deceased), 

leading to excessive guilt and 

shame. 

Causality

A realistic understanding of 

the causes of death is 

developed. 

Child who relies on 

magical thinking is apt to 

assume responsibility for 

death of a loved one by 

assuming bad thoughts or 

unrelated actions were 

causative. 

Tends to lead to excessive 

guilt that is difficult for child 

to resolve. 

Adapted from Schonfeld D. Crisis intervention for bereavement support: a model of intervention in the 

children’s school. Clin Pediatr 1989;28(1):27-33. Reprinted with permission of Sage Publications, Inc. 
293

 Chapter 9. Integrating Terrorism and Disaster 

Preparedness into Your Pediatric Practice 

Relevance for Office-Based Pediatricians 

Emergency preparedness should be exercised at all organizational levels, and office-based 

physicians (either in the hospital or free-standing practice) should understand the role of their 

specific office in the general system response to disasters. Integrating the office’s response to 

disaster within the overall Federal, State, regional, and community response is essential. 

Office-based policies and procedures ideally should be specific to the location of the practice 

and its characteristics and be consistent with the policies of affiliate institutions and public 

and governmental agencies. 

Preparedness for disaster by office-based physicians can be subdivided into two broad 

categories: 

• Internal operations of the practice. 

• External operations related to communication and coordination with other agencies, 

institutions, and the community. 

Internal Operations of the Practice: Office Readiness 

Framework for disaster preparedness. A child-oriented, comprehensive, emergency care 

system maintains the concept of systematic intervention in response to disasters while 

viewing the needs of the child in the context of family and community. This framework is 

particularly suited to the office-based physician, who attends to the whole child. Pediatric 

health care professionals bring knowledge about responses and needs of children involved in 

disasters and should work across public systems to render effective medical, educational, and 

community interventions. The objective is to ensure that the biological and psychological 

needs of children are addressed before, during, and after trauma. 

Basic office readiness. There are several aspects to basic office readiness. They involve 

facilities, equipment and supplies, and records. 

Facilities. In the face of a natural or manmade disaster, two modes of mitigating the results 

have been termed “hard” or “soft.” Soft mitigation refers to emergency preparedness or 

emergency response as discussed throughout this chapter. Hard mitigation refers to 

engineering efforts in the built environment to withstand destruction. These include building 

standards for structures to withstand destruction from earthquakes, hurricanes, floods, fires, 

technological hazards, etc., and on-site permanent emergency systems such as fire 

suppression systems, uninterruptible power supplies, and standby generators. 

Office-based physicians should be aware of the particular vulnerabilities of free-standing 

practice buildings based on geographic location, and their practices should comply with strict 

building code regulations and be equipped with emergency system back-ups. In the event of 

structural damage to the practice, there should be a plan for its relocation (e.g., by making 
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arrangements to share facilities with another practice). Considerations in such planning 

include the following: 

• Partner with a practice that is unlikely to have incurred the same damage due to 

geographic location and clearly work out the operations of the practices ahead of time 

with respect to volume of patients, sharing of staff and resources, etc. 

• Contact vendors for a change in delivery address, notify laboratories of relocation, 

and select alternative vendors and laboratories (in case the usual vendors have also 

been affected). 

• Ensure that all staff members are apprised of the plans. 

• Develop specific evacuation plans and conduct periodic in-service and practice drills. 

• Periodically review the location of fire extinguishers, first aid, and emergency 

equipment. 

Equipment and supplies. Offices should have emergency kits assembled that contain water, a 

substantial first-aid kit (including thermometer, blood pressure cuff, and stethoscope), radios, 

flashlights, batteries, heavy-duty gloves, food, sanitation supplies, and medical reference 

books and cards. Emergency supplies should be located both on-site and off-site. Lack of 

refrigeration for medications and vaccines is a likely scenario in a disaster. Back-up 

generators are important in case of outages. Back-up communication systems such as cellular 

phones, direct telephone lines that are not part of the regular telephone system, two-way 

radios, beepers, and ham radios should be considered. Practices located within hospitals 

should comply with JCAHO requirements. 

Records. The Health Insurance Portability and Accountability Act (HIPAA) mandates that 

copies of records be stored off-site (some experts recommend at least 50 miles away) in case 

of catastrophe. This includes copies of patient charts and other vital records, even if most 

records are stored electronically. In addition to patient charts, other records that should be 

stored off-site include the following: 

• Contact lists. 

• Chain of command list. 

• Pertinent contact information for government and emergency agencies. 

• Copies of insurance policies. 

• Loan applications. 

• Real estate leases. 

• Other materials relevant to the practice operations. 

A number of Web sites that provide computer data storage capability are currently available. 

The choice of vendors should be researched carefully, and the various options for secure 

access (e.g., wireless) should be explored. Free-standing practices need to consider all 

contingencies. Practices located within larger hospital institutions need to be aware of the 

provisions made by the larger institution. 

Communication system. Having a communication system in place for the office—including 

the chain of command, a listing of contact information for all staff members, and the 

delineation of staff responsibilities—is vital to office readiness in the event of a manmade or 

terrorist disaster. 
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Chain of command. A chain of command in case of emergency situations is routine in 

hospital settings. However, office-based physicians also need to consider this organizational 

step, which includes the following: 

• Deciding a hierarchy (or who will be in charge) and their responsibilities vis-à-vis 

patient records. 

• Informing staff members about recovery plans. 

• Informing patients about new location and hours. 

• Listing other important contacts. 

Reviewing the nature of the catastrophe that may close or affect the practice should 

incorporate ways to contact employees and patients and take into account the possibility that 

phone lines will be inaccessible. 

Contact list. A confidential contact list of all physicians, nurses, and other staff that includes 

home numbers, cellular phones, and alternative phone numbers should be kept by individuals 

designated in the chain of command. The contact list should also include back-up providers. 

Importantly, this confidential list should be kept in multiple places (e.g., the practice, outside 

location, and/or with the designated individuals). Practices may need to consider keeping a 

list of technologically dependent children who, during a disaster or emergency situation, may 

need specific planning (e.g., availability of back-up generators) and instructions about where 

to go in case equipment fails. 

Staff responsibilities. Staff should be made aware that they have a professional responsibility 

to discuss their availability in case of disasters. This would include calling in to check where 

their services are needed and the feasibility of responding based on previously discussed 

office-readiness plans. Discussion with staff of their multiple responsibilities for their own 

families, work, and the community will help to alleviate concerns and anticipate problem 

areas. Staff should prepare a “Family Emergency Plan” so that they will be assured that the 

needs of their own families will be addressed while they are performing critical health care 

duties. The roles of the physician, nurse, and support staff should be briefly outlined. For 

example, everyone should know who will contact the police or fire department, who will aid 

in evacuation, who will reschedule patients, etc. Periodic exercises or drills can help to 

ensure that each staff member knows his or her role in the event of a disaster. Practices may 

choose to hire a consultant to advise staff members in the development of their plans. Again, 

individual practice efforts should be coordinated with more regional efforts as described 

below. 

Infectious disease identification and control; chemical and radiological injuries and 

exposures. The office-based physician may be the first contact for an individual who is the 

victim of a biological agent and may be called on to treat or answer questions with regard to 

chemical and radiation exposure. Pediatricians should understand the following:

• The classification and qualities of possible biological agents. 

• The natural history and management of biological, chemical, and radiological injuries 

and exposures. 

• Chemical agents that may be used and their properties. 
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• Types of radiological terrorism. 

• Decontamination procedures, especially those specific to children. 

• Availability of antidotes and other therapeutics. 

The procedure and numbers for alerting the proper authorities (e.g., Department of Health, 

CDC, etc.) should be detailed in the practice policies and procedures and chain of command 

protocol. 

Triage, screening, and prioritization. Although office-based physicians may feel that they 

have no role to play in disaster planning or management, emergency pediatricians may need 

to draw on community pediatricians to provide the best possible management of children. 

Office-based physicians may be asked to help hospital-based pediatricians to determine 

which pediatric patients can be discharged or transferred to another hospital. In addition, 

office-based physicians will need to triage their own patients who show up at the practice to 

determine whether they need to go to the hospital or can be safely managed without 

emergency care. Office-based pediatricians also play a critical role in screening for 

psychological distress of the child and family (see also Chapter 8, Mental Health Issues). 

Increasingly, risk assessment involves screening protocols applied at the school or 

community level to detect psychological needs of the population after a disaster. Leadership 

from the office-based physician can be instrumental in guiding these processes in a coherent 

and rational way. 

Practice readiness and staff development. Staff development programs that provide 

accurate, reliable, and timely information on disaster preparedness for the office practice are 

essential. These programs can be organized by the practice, or the practice may choose to 

participate in programs developed by affiliate institutions specific to the needs of officebased physicians. 

Insurance. Adequate business insurance is stressed in office readiness in the face of disaster. 

This may include the following: 

• Determining how much revenue the practice can afford to lose, preferably slightly 

overestimating the necessary coverage. 

• The details of the insurance policy (e.g., does it cover acts of terrorism, floods, etc.). 

• Overall cost and possible liens against the business. 

Keep in mind that building code requirements are essential in determining if insurance 

coverage applies. Reading and re-reading the policy is critical to upgrade coverage based on 

evolving or changing potential threats. 

External Operations: Communication and Coordination with Other 

Agencies 

Communication systems. The office-based physician should determine how the practice 

will link and coordinate efforts with affiliate hospitals, schools, daycare centers, local 

response teams, the local department of health, and city, State, regional and Federal efforts. 
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The chain of command established by the practice should identify the points(s) of contact 

within the organizational structure for communication with the various larger agencies. 

Ideally, a list of all the relevant relationships should be developed in advance with contact 

numbers listed: 

• Local and regional hospitals. 

• Local emergency management agency. 

• State and city departments of health. 

• State and city police. 

• State office of mental health. 

• City fire department. 

• City department of sanitation. 

• Utility services. 

• Medical equipment/supply resources. 

• Pharmacies. 

• Shelters. 

• Poison Control Center (1-800-222-1222). 

• Centers for Disease Control and Prevention (1-800-311-3435). 

• American Red Cross (Disaster Assistance Info: 1-866-GET-INFO [1-866-438-4636]). 

• Occupational Safety and Health Administration (OSHA). 

The city Office of Emergency Management (OEM) can serve as a conduit for coordination of 

the various local agencies, including other Federal and State agencies. Practices can take 

advantage of already established relationships (e.g., with school-based health centers, 

daycare centers, hospitals). Communication before, during, and after a disaster would allow 

the efforts of the larger community to be coordinated with knowledge of the available 

resources at the practice level. Realistic scenarios can be investigated as part of community 

disaster drills. 

Community as a resource. Community resources can mitigate the adverse effects of 

disasters. Successful programs include extensive training provided by fire, police, mental 

health, and emergency services personnel. The office-based physician can be integrated into 

this larger community response and should participate in drills and exercises. Three examples 

of such community programs include citizen disaster preparedness programs, the Citizen 

Emergency Response Training (CERT) programs, and the Collaborating Agencies 

Responding to Disasters (CARD) programs. 

Citizen disaster preparedness programs. These include basic preparedness (e.g., a course to 

assist individuals in preparing their homes), neighborhood response teams (e.g., choosing a 

block captain, setting up a response area, establishing teams to address such things as search 

and rescue, safety and utilities, damage assessment), and advance training to augment public 

safety and response. 

Citizen Emergency Response Training (CERT) programs. The CERT programs (established 

in Los Angeles, CA in 1985) provide citizen training through the fire department. 
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Collaborating Agencies Responding to Disasters (CARD) programs. The CARD programs 

(established in 1994 after the Northridge earthquake in Los Angeles) were originally 

organized to provide services for vulnerable and underserved populations (e.g., homeless 

individuals, veterans, at-risk youth, people with special needs). This group of agencies has 

extended its services to develop disaster preparedness plans. This kind of program has the 

advantage of linking culturally sensitive community services and preparedness, thereby 

addressing ongoing issues such as homelessness, cardiopulmonary resuscitation (CPR) 

training, and maintaining a set structure and mission. The clusters of service teams provide 

support services such as transportation, counseling, shelter and housing, health services, and 

commodities. Conceivably, this structure could accommodate a pediatric focus in 

collaboration with community-based pediatric health care professionals. 

Policies and procedures. Office-based physicians should be aware of the emergency 

numbers and protocols of their local department of health. These policies should be included 

in the overall office practice manual for easy reference. If practices are affiliated with a 

hospital, also being aware of those policies and procedures will facilitate collaboration. When 

they exist, current best practices can be adopted with respect to emergency response plans 

and to physician and nurse training for disasters. 

Communicating Directly with Children and Families 

The pediatrician plays a central role in disaster and terrorism preparedness with families and 

children. Families view pediatricians as their expert resource, and most expect pediatricians 

to be knowledgeable in areas of concern. Providing expert guidance entails both educating 

families in anticipation of events and responding to questions during and after actual events. 

In many areas of the country, the threat of natural disasters is ongoing, and guiding and 

educating families on home disaster preparedness can be done in the pediatrician’s office or 

as a community focus. Family preparedness may include training in cardiopulmonary 

resuscitation, rendezvous points, lists of emergency telephone numbers, and an out-of-thearea friend or relative whom all family members can contact after the event to report their 

whereabouts and condition. Home preparedness (such as installing storm shutters or 

earthquake-proofing the home) should be covered. Parents should maintain emergency 

supplies of food, water, and medicine; a first-aid kit; and clothing. Family members should 

know the safest place in the home, make special provisions, know community resources, and 

have a plan to reunite. Medications for chronic illness and resources for children who depend 

on technological means for survival should be included in the plan (see also the AAP Family 

Readiness Kit at www.aap.org/family/frk/frkit/htm). 

Answering questions during events. During any event, children and families will receive 

good and bad information from a multitude of sources, including friends, media, and public 

officials. The problems caused by panic, overreaction, and overwhelming the emergency 

health care system with anxious families cannot be overstated. A well-educated and available 

pediatrician who can appropriately respond to numerous and varied questions can be of great 

service. 
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Advice for families of children with special health care needs. Pediatricians should 

provide guidance to families of children with special health care needs. This may include the 

following: 

• Notifying utility companies to provide emergency support during a disaster. 

• Maintaining a supply of medications and equipment in case availability is disrupted 

during a disaster. 

• Knowing how to obtain additional medications and equipment during times of a 

disaster. 

• Training family members to assume the role of in-home health care providers who 

may not be available during a disaster. 

• Keeping an up-to-date emergency information form to provide health care workers 

with the child’s medical information in case the regular care provider is unavailable. 

• Knowing back-up hospitals/providers in the region in case primary 

hospital/specialists/providers become unusable or are unavailable. 

• Providing advice on power of attorney, living wills, advance directives, and other 

important legal tasks/documents. 

Relevance for Hospital-Based Pediatricians 

In mass casualty incidents, including those involving chemical and biological agents, 

casualties among children and adults could be significant. Because children are likely to 

become victims in many disaster events, pediatricians should assist in preparedness planning 

to ensure coordinated responses of local hospitals that may in fact each have limited pediatric 

resources. In addition, health care facilities could be a primary or secondary target 

themselves. Also, facilities may be overwhelmed by massive numbers of anxious individuals 

and families. Pediatricians working in or supporting hospitals can play a vital role in ensuring 

the enhanced care of the pediatric disaster victim by participating in all levels of disaster 

preparedness planning. 

Emergency Department Readiness 

The hospital disaster alert system is designed to triage victims in the field and carefully 

distribute them among available resources to keep a single facility from being overwhelmed. 

However, in many crisis situations, facilities are vulnerable to inundation with patients who 

arrive in large numbers without EMS transport and pre-entry triage. Pediatricians working in 

or supporting hospitals should interact with the planning committee to ensure adequate 

training and preparation of supplies and treatment areas in the emergency department. 

Pediatricians working in hospitals can be key facilitators between emergency department 

services, critical care services, and regular inpatient services. Coordination with the local 

community should involve primary/prehospital/infrastructure response (with liaison planning 

to State and Federal agencies) and community/citizen response. Considerations should be 

made as usual referral patterns may not typically include accepting pediatric patients. 

Primary/prehospital/infrastructure response includes the following: 

• EMS. 

• Fire. 
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• Police, Environmental Protection Agency (EPA), sheriff. 

• Military (local or regional). 

• Regional poison centers. 

• Local health department. 

Community/citizen response involves the following: 

• Schools, public and private. 

• Daycare centers, public and private. 

• Service groups (Kiwanis, Rotary, Salvation Army, parent/teacher associations 

(PTAs), etc.). 

• Nonsecular groups (churches, synagogues). 

• Public recreation administrations (zoos, amusement parks, sports stadiums, museums, 

etc.). 

Inpatient Service Readiness 

Anticipating surge capacity for inpatient care is vital in preparedness planning and perhaps is 

the greatest contribution of pediatricians working in hospitals. Areas that should be 

considered include the following: 

• Increasing the number of inpatient beds within a community (e.g., by using several 

strategies such as converting cafeterias and meeting spaces into ward capacity or 

making arrangements with other community hospitals). Local hotels, school 

gymnasiums, etc., may be converted into low-acuity medical facilities with some 

planning. 

• Contingency plans for acquiring or maintaining essential services, such as water, 

electricity, portable oxygen, garbage/trash removal, etc. 

• Planning for stockpiling or readily acquiring medical supplies such as vaccines, 

antitoxins, and antibiotics (in dosages, formulations, etc., appropriate for pediatric 

patients). In addition, pediatric-specific supplies and equipment in a full range of 

sizes to accommodate pediatric patients should be available. 

• Networking community resources to organize volunteers to become proxy caretakers 

for orphaned children. 

Hospital Infrastructure Needs 

Crisis drills. Hospital and community-wide drills are essential to preparedness planning. 

They need to be done on both a wide scale and with a narrow focus. Drills should include not 

only the initial triage and decontamination, but also the 48-72 hours after impact to measure 

readiness with all provider and support services that will be needed. Specific drills should be 

planned and practiced for evacuation in response to fire or other disasters. 

Infection control plans. Infection control plans closely parallel quarantine procedures in the 

community and on a public health basis. The in-hospital level involves quarantine or 

isolation and control measures to limit spread of infection to staff and other patients. 
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Quarantine procedures. Quarantine procedures should be a well-established means of 

limiting the spread of infection. Quarantine may become an active part of inpatient needs in a 

given hazard-related disaster. Children who become ill may require isolation to prevent 

spread of disease to other patients and health care providers. The exact nature and severity of 

quarantine will depend on the specific hazard involved. Close coordination with the public 

health service, CDC, and local poison centers is essential in both the planning and execution 

stage. 

Staff training. Staff training should include the following: 

• Training in use of protective gear. 

• Orientation to all aspects of the plan from the disaster site to the emergency 

department to hospital floors, as well as to rehabilitation and rebuilding in the 

community. 

• Staff preparedness for notification, transportation to treatment sites, self preparedness 

(emergency packages of personal items), strategies for coping with family demands, 

psychological demands, and plans for personal health and hygiene. 

• Support for families of health care workers so that the health care workers are 

available to provide services. 

• Mechanism for tracking resources. 

• Media/public communication issues. 

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2002;18(1):33–35. 

• Caffo E, Belaise C. Psychological aspects of traumatic injury in children and 

adolescents. Child Adolesc Psychiatric Clin No Am. 2003;12:493–535. 

• Chemtob CM, Nakashima JP, Hamada RS. Psychosocial interventions for 

postdisaster trauma symptoms in elementary school children. Arch Pediatr Adolesc 

Med. 2002;156:211–216. 

• Cowan ML, Cloutier MG. Medical simulation for disaster casualty management 

training. J Trauma. 1988;28(1Suppl):S178–S182. 

• Flowers LK, Mothershead JL, Blackwell TH. Bioterrorism preparedness: II. the 

community and emergency medical services systems. Emerg Med Clin No Am. 

2002;20(2):457–476. 

• Harner A. Will you be ready when your patients need you the most? Disaster 

planning for the medical practice. MGMA Connexion, Nov/Dec 2001: 40–41. 

• Hazinski FM, Markenson D, Neish S, et al. Response to cardiac arrest and selected 

life-threatening medical emergencies: the medical emergency response plan for 

schools. A statement for healthcare providers, policymakers, school administrators, 

and community leaders. American Heart Association, Emergency Cardiovascular 

Care Committee. Policy Statement, Pediatrics. 2004;113(1):155–168. 

• Laor M, Wolmer L, Spriman S, Wiener Z. Facing war, terrorism, and disaster: toward 

a child-oriented comprehensive emergency care system. Child Adolesc Psychiatric 

Clin No Am. 2003(12);343–361. 
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• Leonard RB. Role of pediatricians in disasters and mass casualty incidents. Ped 

Emerg Care. 1988;4(1):41–44. 

• Lichterman JD. A “community as resource” strategy for disaster response. Public 

Health Rep. 2000;115(2–3):262–265. 

• Mattox, K. The World Trade Center attack disaster preparedness: health care is ready, 

but is the bureaucracy? Crit Care 2001;5:323:325. 

• Perry RW, Lindell MK. Preparedness for emergency response: guidelines for the 

emergency planning process. Disasters. 2003;27(4):336–350. 

• Redlener I, Markenson D. Disaster and terrorism preparedness: what pediatricians 

need to know. Adv Ped. 2003;50:1–37. 

• Rose MA, Larrimore KL. Knowledge and awareness concerning chemical and 

biological terrorism: continuing education implications. J Cont Ed Nursing. 

2002;33(6):253–258. 

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to a medical disaster. Aust Fam Physician. 1999;28(Suppl 1):S10–S14. 

• Veenema GT. Chemical and biological terrorism preparedness for staff development 

specialists. J Nurses Staff Devel. 2003;19(5):215–222. 
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Chapter 10. Working with Government Agencies 

Introduction 

The challenge of dealing with the threat of terrorism in the United States is daunting not 

only for disaster planners, but also for our medical system and health professionals of all 

types, including pediatricians. All possible forms of terrorism should be considered, 

including chemical, biological, explosive, radiological, and nuclear events. Pediatricians 

need to be able to answer concerns of patients and families, recognize signs of possible 

exposure to a weapon of terror, understand first-line response to such attacks, and 

sufficiently participate in disaster planning to ensure that the unique needs of children are 

satisfactorily addressed in the overall process. 

Community, Government, and Public Health 

Preparedness 

Emergency preparedness is important at many levels—personal, family, community, 

regional, State, and Federal—with the State and Federal Governments having pivotal 

roles. The Federal Government provides significant funding for disaster preparedness and 

response and to a large extent establishes the framework that is then followed by States, 

regions, and communities. In disaster response, the funding and planning tends to be top 

down, while the response and use of resources tends to be from the bottom up. In other 

words, as resources are exhausted at the local level, assistance is requested from the next 

level, such as the State, which then requests Federal assistance. 

Volunteer organizations, such as the Red Cross and Salvation Army, also have key roles 

in disaster response. Recent concepts of disaster and aftermath response and planning 

include the involvement of neighborhoods and families and have begun to include needs 

at the individual level. A successful response to a disaster requires the interaction of 

personnel and resources from multiple agencies in an organized and coordinated manner 

according to a well-formulated plan. While this planning has increased in recent times, 

the attention to the unique needs of children and the inclusion of pediatric expertise in the 

planning phases is still insufficient and deserves much more attention. 

Community Response 

Local governments are the first line of defense in emergencies and are primarily 

responsible for managing the response to most disasters. The primary responsibility for 

the protection of citizens belongs to such local elected officials as mayors, city councils, 

and boards of commissioners. When a local government receives a warning that an 

emergency could be imminent, its first priorities are to warn citizens and to take whatever 

actions are needed to minimize damage and protect life and property. If necessary, an 

evacuation may be ordered. The emergency operations plan is at the center of 

comprehensive emergency planning. This plan spells out the scope of activities required 

for community response. It should be a living document that accurately describes what 

the community can realistically do. Historically, these documents usually do not address 
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pediatric considerations and in only the rarest of cases have pediatricians been part of the 

planning process. 

State Government 

All States have laws that describe the responsibilities of the State government in 

emergencies and disasters. These laws provide governors and State agencies with the 

authority to plan for and carry out the necessary actions to respond to and recover from 

emergencies. State emergency management legislation describes the duties and powers of 

the governor, whose authority includes the power to declare a state of emergency and to 

decide when to terminate this declaration. 

Performing and maintaining the provisions of emergency management legislation is 

generally the responsibility of the State emergency management offices (some 

municipalities also have offices of emergency management). These offices are organized 

in a number of ways and have different names. Emergency managers are responsible for 

preparing for emergencies and for coordinating the activation and use of resources 

controlled by the State government when they are needed to help local governments 

respond to and recover from emergencies and disasters. In its coordinating role, the State 

emergency management office is involved in virtually all serious emergencies, terrorist 

events, and natural or manmade disasters. 

Using procedures specified in the State emergency operations plan, the State emergency 

management organization coordinates deployment of personnel and resources to the 

affected areas. Again, pediatric concerns are rarely considered. The emergency 

operations plans of many States do not include child-specific guidelines. Pediatricians 

need to be involved in the State emergency planning committees to ensure that pediatric 

considerations are included in State plans and become part of the plans of each State 

agency and part of funding for disaster and terrorism preparation. This pediatrician 

involvement can be accomplished through both grassroots efforts and involvement in 

local chapters. 

Federal Government 

The authority for Federal involvement in disasters is based on provisions of the Stafford 

Act.1 This Act establishes the presidential declaration process for major disasters and 

emergencies, provides for the implementation of disaster assistance, and sets forth the 

various disaster assistance programs. FEMA’s role is to coordinate the delivery of 

Federal assistance by managing its own programs and by coordinating disaster assistance 

from other Federal departments and agencies. FEMA coordinates these activities using 

the interagency Federal response system, also called the Federal Response Plan (FRP). 

The FRP describes the basic mechanisms and structures by which the Federal 

Government mobilizes resources and conducts activities to augment State and local 

response efforts. To facilitate the provision of Federal assistance, the FRP uses a 

functional approach to group the types of Federal assistance that a State is most likely to 

 

1

 Robert T. Stafford Disaster Relief and Emergency Assistance Act, Public Law 93-288, Sections 5121-

5206, et seq of Title 42 United States Code. 
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need under the 12 Emergency Services Functions (ESFs). Each ESF is headed by a 

primary agency that has authorities, resources, and capabilities in the particular functional 

area. Other agencies have been designated as support agencies for one or more ESFs 

based on their resources and capabilities to support the functional area. The FRP is also 

important in that most States use it as a base for the structure and some content of their 

emergency operations plans. In turn, local emergency operations plans are based on the 

State plans. (See Chapter 2, Systems Issues, for more information.) 

One of the major functions physicians will be involved with and should become familiar 

with is Emergency Services Function Number 8 (ESF #8), the Health and Medical 

Services Function. ESF #8 provides assistance to supplement State and local resources 

for public health and medical care needs during a disaster. In a federally declared 

disaster, the U.S. Public Health Service (USPHS), a component of the U.S. Department 

of Health and Human Services (DHHS), forms a Crisis Action Team and activates the 

National Disaster Medical System (NDMS) as needed to provide health and medical care 

assistance. A Disaster Medical Assistance Team (DMAT) is a deployable unit of 35 

physicians, nurses, technicians, equipment, and supplies for austere medical care. A 

Management Support Unit (MSU) manages field health and medical resources of 

deployed DMATs. A Disaster Mortuary Assistance Team (DMORT) provides a 

temporary morgue facility, victim identification, processing, preparation, and disposal of 

remains. A Metro Medical Strike Team (MMST) provides assistance in the medical 

treatment/management of chemical, biological, or radiological incidents resulting from 

deliberate or accidental acts. In some cities, there are Metropolitan Medical Response 

Teams that provide additional medical response capability. The parent agency of all of 

these groups is the United States USPHS, with assistance from the Department of 

Homeland Security (DHS). 

Public Health Preparedness 

On a larger scale, we should also recognize the need for public health preparedness. This 

requires the existence of a strong public health system. To allow for rapid and efficient 

response, we need both central organization as specified by Federal planning and State 

implementation and decentralization of some resources, such as diagnostic capabilities. 

It is important for pediatricians to understand the importance of public health and their 

relationship to departments of health. This includes their role in public health, reporting 

requirements and mechanisms, and mechanisms for receiving and soliciting information 

from departments of health. 

Advocating for Children and Families in Preparedness 

Planning 

To ensure that children are included in government and community planning and 

preparedness activities, informed and motivated pediatricians should advocate for 

children at all levels. This advocacy can take several forms. Grassroots advocacy can 

include efforts to ensure legislation and funding to support an emphasis on children in 

disaster planning at every level. Pediatricians can also serve as expert advisors to local, 
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State, and Federal agencies and committees. Often, this activity can be through 

involvement in professional organizations such as the American Academy of Pediatrics, 

its chapters, and special committees and task forces. 

Pediatricians as the experts in the care of children should: 

• Advocate for inclusion of the needs of children in all Federal, State, and local 

disaster planning. 

• Advocate for research on the pediatric aspects of biological, chemical, and 

radiological terrorism, including mechanisms, pathophysiology, and treatments. 

This includes the availability of appropriate medications and antidotes. 

• Work with DMATs to ensure that they are equipped and trained for the care of 

children. 

• Assist in developing a hospital disaster plan that provides for the proper care of 

children. 

• Provide on-site emergency and primary health care at emergency shelters. 

• Be involved in emergency medical services (EMS), e.g., develop proficiency in 

cardiopulmonary resuscitation and first aid, train first responders in pediatric 

assessment, assist in development of prehospital pediatric protocols, help 

establish protocols for consent to treat and identification of minors, and ensure the 

availability of pediatric resources. 

At the local and community level, pediatricians should: 

• Work with local police, fire, and EMS departments to ensure that their plans and 

equipment address the needs of children. 

• Be involved with local and community emergency preparedness task forces and 

committees. 

• Work with schools, child care centers, and other locations where children spend 

their time to ensure that they have adequate emergency plans. 

Similarly, at the State level, pediatricians should: 

• Ensure that State emergency management, department of health, and EMS 

advisory committees have pediatric expertise as part of their membership. 

• Advocate for all State disaster and terrorism education and funding to require 

inclusion of provisions for children. 

Resources Available from Government Agencies 

A number of State and Federal Government agencies have information, tools, electronic 

media, and other materials to assist physicians, including pediatricians, and other health 

care providers in disaster planning, preparedness, and response. Many of these resources 

can be found in the bibliographies that follow chapters in this report. 

Another Federal agency, the Agency for Healthcare Research and Quality (AHRQ), has 

provided support for research on bioterrorism preparedness and response and the 

development of materials to improve the Nation’s capacity to respond to bioterrorism and 

other disasters. AHRQ’s multimillion dollar investment in bioterrorism research 
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recognizes that community clinicians—including pediatricians—have a vital role to play 

in disaster planning, preparedness, and response at the Federal, State, and local levels. 

Hospitals, health care systems, professional organizations, and other groups also have 

essential roles in the public health infrastructure and need evidence-based information 

and tools to help them respond appropriately in the event of a disaster. 

To inform and assist these groups in meeting the health care needs of the U.S. population 

in the face of bioterrorist threats and other disasters, AHRQ-supported research has 

focused on the following: 

• Emergency preparedness of hospitals and health care systems for bioterrorism and 

other rare public health events. 

• Technologies and methods to improve the linkages between the personal health care 

system, emergency response networks, and public health agencies. 

• Training and information needed to prepare community clinicians to recognize the 

manifestations of bioterrorist agents and manage patients appropriately. 

AHRQ contracted with the American Academy of Pediatrics to develop this report to 

ensure that the needs of children are an integral part of disaster planning and 

preparedness activities. 

AHRQ has developed a number of other reports, tools, and other materials that focus on 

disaster planning, preparedness, and response. They are available online at the Agency’s 

Web site (http://www.ahrq.gov/browse/bioterbr.htm), and in many cases, print copies are 

available from the AHRQ Publications Clearinghouse. Information about print 

availability is also online at the above Web site. 
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Chapter 11. Conclusion 

This report has presented detailed information to assist pediatricians—both those based in the 

community and those based in hospitals and other health care systems—in becoming active 

participants in disaster planning, preparedness, and response. Additional sources of information 

and many other valuable resources are provided in the bibliographies that follow each chapter. In 

addition, valuable lessons can be drawn from several disasters, both manmade and natural, that 

have occurred in the United States. 

 

The hurricanes in the Gulf Coast and their aftermath serve as a reminder that nature is capable of 

destruction greater than that of most terrorist attacks. An important lesson regarding the 

organization and focus of disaster response is to include natural as well as manmade events in 

planning and preparedness efforts. Consideration also should be given to the organizational and 

logistical issues involved in evacuating a major city. 

Systems Issues 

Activities pertaining to disaster planning, preparedness, and response take place at all levels, 

including Federal, State, regional, and local, and everyone has a role to play. For example, at the 

Federal level, the Centers for Disease Control and Prevention (CDC) has provided excellent 

information on the impact of hurricanes and on methods to help mitigate the impact and facilitate 

management immediately after the event (see http://www.bt.cdc.gov/disasters/hurricanes/). 

Much of this information can be applied to both natural disasters and terrorism. The Web site 

includes information on family readiness, evacuation, power loss, recovery (including keeping 

food and water safe, preventing injury, monitoring infections, etc.), animal and insect hazards, 

environmental issues, clean-up safety, returning home, and mental health issues. 

Regional, State, and Local Efforts 

Valuable lessons have been learned from our experiences with Hurricane Katrina and its 

aftermath. A large part of the problem was insufficient coordination and planning at all levels. 

The situation was exacerbated by the need for evacuation of large numbers of people and their 

long-term displacement from their homes and schools. 

Future planning and preparedness efforts in major U.S. cities should recognize the potential for 

severe and long-term consequences. In disasters, State and Federal aid is always going to take 

some time to arrive. Local and regional authorities, as well as individual families, should have an 

effective plan in place that includes efforts to be undertaken before other outside assistance can 

arrive. This should include an effective evacuation plan that covers quickly setting up emergency 

shelters, providing food and managing water sanitation for large numbers of people, and 

providing affected individuals—including children who may or may not have chronic illnesses 

and other special needs—with medical and mental health care. 
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Vulnerable Populations 

In a disaster, the most vulnerable are going to suffer the most and need the most assistance. 

Clearly, vulnerable populations include the poor, the infirm, individuals with mental illness, the 

elderly, and children. Hospitalized patients, people in nursing homes, and incarcerated 

individuals are at special risk in a natural or manmade disaster. 

Hospitalized children, particularly premature infants and those in neonatal intensive care units, 

are particularly vulnerable. Their lives may depend on the ability of hospitals to maintain critical 

emergency power and life support equipment until transfer to other regional specialty facilities 

can be arranged. 

These situations highlight the need for including large numbers of technologically dependent 

patients, many of whom require highly specialized regionalized care, in planning efforts to 

mitigate the impact of a disaster. 

Separation of Children from Families 

Hurricane Katrina also highlighted the need to plan for the likelihood of numerous children being 

separated from their parents or other caregivers. The National Center for Missing and Exploited 

Children has a hotline (1-800-843-5678) and Web link (http://www.missingkids.com/) to report 

missing children, missing adults, and found children. The Red Cross also has a hotline (1-866-

GET-INFO) and Web link (http://www.redcross.org) to help separated family members find each 

other. As of March 2006, the National Center reported that all children separated from families 

as a result of Hurricane Katrina have been reunited with their families. 

This issue should receive more attention in preparedness and mitigation plans. Pre-disaster 

identification of children (e.g., name tags, other forms of ID, etc.), especially for those who are 

not verbal, or who cannot give their own name, a parent’s name, or other critical information, 

should be considered. Neonates and their mothers are purposefully given matching ID bracelets 

in hospitals immediately after delivery so the identity of the maternal-child pair is never in doubt. 

Similar identification of parent-child pairs at the time of separation (e.g., during rescue or 

evacuation) could greatly aid in the identification of the child and more accurately track and 

reunite children separated from their parents. 

Sheltering Families 

The immediate first response to a disaster the magnitude of Hurricane Katrina includes the 

mobilization and evacuation of a large region. Subsequently, those displaced from their homes, 

schools, and neighborhoods will require basic necessities, including a place to stay, water, food, 

clothing, health and mental health care, etc. 

The unique needs of children in shelter situations include the need for special foods (e.g., 

formula), clothing and sanitation (e.g., diapers), and sleeping accommodations (e.g., cribs). 

Efforts to distract, entertain, comfort, and even separate families with crying newborns and 

toddlers will help calm other evacuees in the shelter who find these sounds discomforting. 
311

Planning for special medical needs and for mental health care that focuses on children’s unique 

developmental stages is also critical.

The immediate issues of emergency sheltering, providing food and water, and other necessities 

do not take into account the problem of returning some semblance of stability and normalcy to 

children and families. These significant issues will likely create severe mental health issues for 

an extended period of time for many of these displaced children. 

Providing Urgent Medical Care to Large Populations of 

Displaced Children 

Following Hurricane Katrina, a Mobile Pediatric Emergency Response Team (MPERT) staffed a 

temporary pediatric clinic near the displaced population. As Houston, TX, became the new home 

for 300,000 people, a percentage of evacuated children needed medical triage, evaluation, and 

management. They otherwise would have been likely to seek care at local emergency 

departments, many of which were already at surge capacity. To prevent severe overcrowding in 

these local emergency departments, a large children’s hospital expended the resources necessary 

to care for these displaced children near the site of their temporary shelter. 

A temporary pediatric clinic provided a high level of care for the evacuated children. The clinic 

cared for approximately 2,000 patients. Notably, not a single child died, and less than 50 

required EMS transport to area hospitals. Other cites—e.g., Dallas, Birmingham, Ft. Worth, and 

Baton Rouge—also set up temporary clinics. 

Setting up a Temporary Pediatric Clinic—Lessons Learned 

In every large metropolitan area that received evacuees, temporary pediatric clinics evolved. 

These temporary clinics matched caregivers who were comfortable with and accustomed to 

providing care to children with incoming newborns, children, and adolescents with medical 

needs. Equally important, children were removed from adult waiting lines, allowing moe 

effective care to be given to that population as well. 

• Physicians and nurses who are trained and experienced in the emergency care of children 

should always be included, even at the most basic level, when planning for and 

responding to a disaster. 

• Access to local tertiary pediatric care resources should be arranged for in advance, and 

the tertiary care provider supplying those resources should be involved in the planning 

discussions. 

• While volunteerism is essential in the event of a mass casualty, guaranteed staffing of the 

MPERTS should be a priority. 

• The medical director of the MPERTS should be knowledgeable in pre-hospital medicine 

and associated or familiar with the local EMS system. 

• The appropriate allocation of physician and nursing resources is vitally important to 

patient flow: 

o Physicians trained and experienced in pediatric emergency management should be 

placed at main triage and as charge physicians at the pediatric arena clinic. 

o A good charge nurse will either make or break patient flow. 
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• MPERTS should be able to mobilize rapidly. 

• Cooperation with regional disaster command is essential. 

• Choosing the appropriate venue for the staging of the disaster response is critical: 

o Providing enough room upfront to create a scaled-down version of an emergency 

department, including an area for observation and isolation, is critical. 

• Mental health care and social services should be made available to the evacuated 

population as early as possible. 

• A centrally located functional communication device (e.g., phone, cell phone, radio) is 

crucial to successful implementation; it provides access to additional essential staff and 

services quickly, on an ongoing basis. 

• There should be a planned exit strategy: 

o The clinic should not be allowed to outlive its resources. 

o Once the cost of running the clinic outweighs the cost of referring those patients 

to the emergency department, the clinic should close its doors. 

Environment 

Many of the environmental problems that occur after a natural or manmade disaster are typical 

and predictable. These problems include temperature extremes; lack of clean water, food, and 

electricity; and environmental hazards not usually present before the event. See Table 11.1 for 

some of the more common environmental conditions and hazards that are likely to be present 

following a disaster. 

Medical Needs 

The medical needs of children and families are also predictable and consistent because they 

closely match the needs of the affected children and communities before the disaster. See Table 

11.2 for common pediatric medical issues, challenges, and adaptations that can be expected after 

a disaster. 

A Final Word 

Timely response and appropriate medical management are essential to minimizing injuries and 

maximizing survival when a disaster occurs. Being prepared ahead of time is the key to timely 

and appropriate medical care. Children and other vulnerable populations have special needs that 

must be considered in the course of planning for a mass casualty event. 

 

Pediatricians can play a very important and unique role in advocating for the needs of children 

and families who seldom receive enough attention in disaster planning. Response resources 

dedicated to pediatric populations remain unavailable or extremely limited for most emergency 

medical response activities related to disasters, even though victims often include children. To 

address this shortcoming, it is vitally important that pediatricians and other representatives of 

special populations take part in local, State, regional, and Federal disaster planning to ensure 

appropriate care for the most vulnerable populations. 
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Table 11.1 Environmental constraints to pediatric medical care after large-scale 

natural disasters 

Physical constraint Consequences/examples 

Temperature/exposure Heat 

Cold 

Overexposure to the sun 

Dehydration 

Lack of clean water Dehydration 

Poor hygiene 

Inability to comply with wound care instructions 

Potential for GI complications 

Lack of food Inadequate nutrition 

Inappropriate diet 

Potential for GI complications 

Lack of electricity Inability to use non-battery-powered medical devices such as 

nebulizers, pumps, ventilators 

Inability to maintain medications at appropriate temperatures 

Difficulty maintaining safe thermal environment 

Inadequate light/ventilation as a safety hazard 

Difficulty receiving critical information about medical care 

and available medical and non-medical assistance 

Hazardous environments Chemicals 

Physical hazards (e.g., nails, tree limbs, debris, roofs, 

unregulated traffic intersections) 

Tools (e.g., chainsaws) 

Weapons 

Animals or insects 

Allergens/plants (e.g., poison ivy) 
314

Table 11.2 Pediatric medical complaints after large-scale natural disasters: challenges and adaptations post-hurricane responses 

Challenges Adaptations to Usual Care Dec

Pulmonary 

• Bronchospasm is common in those 

with and without histories of asthma. 

• Children with bad/labile asthma 

present early due to stress, environmental triggers, lack of medication. 

• Stable asthmatics start showing up 

as triggers increase or medication runs out. 

• Children with bronchospasm due to 

respiratory infection start to present after the first 3–5 days. 

• October storms correspond to high 

allergy season and a slight peak in RSV incidence. 

• Winter storms may occur during 

RSV outbreaks.

• Need adequate supplies to treat patients. • Premixed beta agonists for nebulizers (infant and child 

dosing). 

• Nebulizer capability with and without oxygen. • Pediatric nebulizer masks and pipes. • Oral and parenteral steroids. • Peak flow monitoring helpful but not essential. • Outpatient treatment: • Allow use of facility’s electricity for families giving 

their own nebulization. 

• Using MDIs with spacer chambers more frequently. • Be liberal with steroids. • Counsel regarding allergen exposure.

• Lower thresh

based on avaiongoing haza

• Consider reco

temporarily rthe area to he

• Temper decis

consideration resources and members.
315

Table 11.2 Pediatric medical complaints after large-scale natural disasters: challenges and adaptations post-hurricane responses, continued

Challenges Adaptations to usual care 

Gastrointestinal 

• Close living quarters may lead to 

transmission of GI viral illnesses, 

• Limited water and facilities for 

washing; limited diaper/hygiene supplies. 

• Inadequate sanitation in field 

kitchens/food distribution points. 

• Norovirus precautions go beyond 

soap and water or alcohol. 

• Erratic availability of potable water 

and oral rehydration solutions. 

• MREs have high sodium/high 

calorie content.

• Ask about sheltering situation. Give specific infection 

control instructions (written if possible). 

• Health care sites can act as distribution points for hygiene 

items such as alcohol solution, diaper wipes, diapers, soap, garbage (biohazard?) bags/gloves, bleach. 

• Maintain contact with public health officials. • Ask about diet specifics, including origin of drinking water 

and food storage conditions. 

• Warn families of need to increase fluid intake if eating 

MREs. 

• Consider unusual electrolyte abnormalities in clinically 

dehydrated children. 

• Distribute oral rehydration solutions. • Focus on oral rehydration protocols unless staff and IV 

fluids are in adequate supply. 

• Limit use of antiemetics and antidiarrheals in children. • Minimize infant formula-switching. • Use fecal volume replacement techniques in cases of 

diarrhea. 

• Admiss

include shelter 

• Lower 

if adequmanage

• If in do

recheck
316

Table 11.2 Pediatric medical complaints after large-scale natural disasters: challenges and adaptations post-hurricane responses, continued

Challenges Adaptations to usual care 

Infectious Diseases 

• Infections will mostly follow 

existing community patterns. 

• “Third world” epidemics have 

not occurred in the US. 

• Isolation/segregation of 

infected people is difficult in the post-storm environment. 

• Children need different 

preparations of antibiotics, some requiring controlled environmental conditions. 

• Pharmacies and drug supplies 

may be limited and may focus on adult medications. 

• Skin infections are common; 

good hygiene is not. 

• Penetrating injuries to the foot 

are common; Pseudomonas must be suspected. 

• Community-acquired MRSA is 

an increasing problem. 

• Animal control may be 

problematic; may need to vaccinate patients against rabies. 

• Contact local public health or hospital officials for intelligence regarding 

existing infection patterns and sensitivities. 

• Cooperate with public health officials in monitoring efforts. 

• Assist in informing shelter staffs of infection patterns seen and what to 

look for. 

• Assist public health personnel with projects needed to protect exposed 

high-risk groups, such as giving VZIG to exposed immunocompromised victims or tetanus boosters to those who need them. 

• Educate patients and families about infection control issues, especially if 

they are shelter residents. 

• Prescribe antibiotics judiciously; use the simplest appropriate form for 

the shortest practical course. 

• Use alternative medication formulations (chewable tabs, crushed tabs) 

and those that do not require refrigeration. 

• Obtain and distribute information about pharmacies in operation. • Inform local pharmacies about prescribing privileges for federal 

responders. 

• Consider distribution of starter doses of medications. • Distribute hygiene and wound care supplies, insect repellant, and topical 

or oral medications for itching/inflammation. 

• Plan follow-up for penetrating and contaminated injuries (especially 

nails into feet). 

• Consider using ciprofloxacin for children with penetrating wounds into 

feet. 

• May use first-generation cephalosporins for most skin infections. 

• Consider adding TMP-SMX or clindamycin if community-acquired 

MRSA is suspected. 

• Communicate with local public health authorities about rabies exposure. 

Recognize that most children will not need a tetanus booster. 

• C

emmaow

• M

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• C

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317

Challenges Adaptations to usual care De

Trauma 

• The post-storm environment is 

hazardous! 

• Children may not have adequate 

supervision or may be asked to perform inappropriate tasks. 

• Children are risk-takers. 

• Minor skin and musculoskeletal 

injuries are common. 

• Penetrating injuries by contaminated 

objects are common. 

• Skin foreign bodies are common. • Major trauma is not common. • Increased chance of: 

o Carbon monoxide exposure 

o Hydrocarbon and bleach 

ingestion/aspiration 

o Ingestion of medications 

o Drowning 

o Traffic incidents due to 

unregulated intersections 

• Intentional injury 

• Carefully document mechanisms of injury. • Be prepared to stabilize a badly injured child while 

arranging for transfer. 

• Identify local pediatric trauma and burn care 

resources. 

• Have access to poison control resources. • If lacking x-ray capabilities, splint the injured 

extremity on any child with bony tenderness, regardless of lack of deformity. 

• Emphasize elevation and splinting of an injured 

extremity for control of pain and swelling; ice may not be a viable option. 

• Provide the best possible initial wound care in an 

environment as comfortable for the patient as possible. 

• Consider delayed/no closure for contaminated wounds 

or possible retained foreign bodies. 

• Consider self-absorbing sutures for children with lip, 

finger or toe lacerations. 

• Use skin glue only if wound is clean and can be kept 

dry. 

• Don’t forget pain management! 

• Follow-up ca

issue; patientanother faciliwith follow-u

• Make some a

unusual circualert for potendangerous fam

• Depending on 

resources, cosedation/anala consideratiostressful proc
318

Challenges Adaptations to usual care Dec

Psychosocial 

• Families may have difficulty coping 

with their child’s illness or injury. 

• Delays in seeking care may be more 

common than in ordinary circumstances. 

• Families may not have had primary 

care resources before the disaster. 

• Compliance with treatment 

recommendations may be difficult for many reasons. 

• Stress may lead to higher risk for 

domestic and child abuse. 

• Pediatric mental health goes beyond 

PTSD. 

• Children with mental health issues 

may present with acute or prolonged nonspecific physical symptoms. 

• Parents are often not well informed 

about children’s reactions to catastrophic stress. 

• Assume family members do not get your message the 

first time. 

• Write down instructions for the family. • Always ask, “Is there anything else we can help you 

with?” 

• Address children directly; let them know what they 

have to say is important and that they have a role in feeling better. 

• Encourage children to express their feelings. • Make the visit as pleasant as possible for the child. • Explore alternatives with the family to help ensure 

compliance with treatment recommendations. 

• Avoid judgmental attitudes. • Identify local resources for family psychosocial 

support. 

• Use available mental health resources. 

• Recognize ris

intentional nelocal reportinprocedures. 

• Try to keep fa

together. 

• Remember th

will reflect wthe rest of the 

• Be willing to 

therapeutic cohelp increase abilities withopatient care. 

Notes: MDI = metered-dose inhaler 

MRE = Meal, Ready-to-Eat MRSA = methcillin-resistant Staphylococcus aureus 

RSV = respiratory syncytial virus VZIG = Varicella zoster immunoglobulin 
319

Acronyms 

AAP American Academy of Pediatrics 

ACEP American College of Emergency Physicians 

ACIP Advisory Committee on Immunization Practices 

AFRRI Armed Forces Radiobiology Research Institute 

AHRQ Agency for Healthcare Research and Quality 

AMU Atomic mass unit 

ARDS Acute respiratory distress syndrome 

ARS Acute radiation sickness/syndrome 

BAL British antilewisite (dimercaprol) 

BAT Biodosimetry assessment tool 

BIGIV Botulism immune globulin intravenous 

BSA Body surface area 

BWC Biological Weapons Convention 

CARD Collaborating Agencies Responding to Disasters 

CBT Cognitive behavioral treatment 

CDC Centers for Disease Control and Prevention 

CERT Citizen Emergency Response Training 

cGy centiGray 

CISD/CISM Critical incident stress debriefing/management 

CNS Central nervous system 

CPAP Continuous positive airway pressure 

CPR Cardiopulmonary resuscitation 

CR Dibenzoxazepine 

CRS Cutaneous radiation syndrome 

CS 2-chlorobenzylidene 

CSF Cerebrospinal fluid 

DEOC Director’s Emergency Operations Center (CDC) 

DHHS Department of Health and Human Services 

DHS Department of Homeland Security 

DMAT Disaster Medical Assistance Team 

DMORT Disaster Mortuary Assistance Team 

DOD Department of Defense 

DOE Department of Energy 

DTPA Diethylenetriaminepentaacetate 

DU Depleted uranium 

ED Emergency department 

EEE Eastern equine encephalitis 

EMDR Eye movement desensitization and reprocessing 

EMS Emergency medical services 

EMT Emergency medical technician 

EPA Environmental Protection Agency 

ESF #8 Emergency services function #8 

FBI Federal Bureau of Investigation 

FEMA Federal Emergency Management Agency 
320

FRP Federal Response Plan 

G-CSF Granulocyte colony stimulating factor 

GI Gastrointestinal 

GIS Geographic information systems 

G-M Geiger-Mueller 

GM-CSF Granulocyte macrophage colony stimulating factor 

Gy Gray 

HEICS Hospital emergency incident command system 

HIPAA Health Insurance Portability and Accountability Act 

HVA Hazard vulnerability analysis 

HVAC Heating, ventilation, air conditioning 

IAEA International Atomic Energy Agency 

ICS Incident command system 

IND Improvised nuclear device 

JCAHO Joint Commission on Accreditation of Healthcare Organizations 

KT Kiloton 

LET Linear energy transfer 

LRN Laboratory Response Network 

MCI Mass casualty incident 

MEN Multiple endocrine neoplasia 

MMST Metro Medical Strike Team 

MPERT Mobile Pediatric Emergency Response Team 

MSU Management Support Unit 

NCRP National Council on Radiation Protection and Measurements 

NDMS National Disaster Medical System 

NHTSA National Highway Transportation Safety Administration 

NIMS National Incident Management System 

NIOSH National Institute for Occupational Safety and Health 

NRC Nuclear Regulatory Commission 

OEM Office of Emergency Management 

OSHA Occupational Safety and Health Administration 

PBI Primary blast injury 

PCR Polymerase chain reaction 

PEPP Pediatric Emergencies for Prehospital Professionals 

PPE Personal protective equipment 

PPV Positive-pressure ventilation 

PSI Pound(s) per square inch 

PTA Parent/teacher association 

PTS Pediatric trauma score 

PTSD/S Posttraumatic stress disorder/syndrome 

Rad Radiation absorbed dose 

RADIAC Radiation detection, indication, and computation 

RBC Red blood cell 

RDD Radiological dispersal device 

REAC-TS Radiation Emergency Action Center Training Site 

REM Roentgen equivalent man 
321

RIA Radioactive iodine ablation 

RTG Radioisotopic thermoelectric generators 

SCIWORA Spinal cord injury without radiographic abnormality 

SEB Staphylococcus enterotoxin B 

SI System International 

SNS Strategic National Stockpile 

SSRI Selective serotonin reuptake inhibitor 

START Simple Triage and Rapid Transport 

Sv Sievert 

TLD Thermoluminescent device 

TMI Three Mile Island 

TNT Trinitrotoluene 

TPN Total parenteral nutrition 

TSA Transportation Security Administration 

TSH Thyroid stimulating hormone 

USPHS United States Public Health Service 

VEE Venezuelan equine encephalitis 

VHF Viral hemorrhagic fever 

VIG Vaccinia immune globulin 

WEE Western equine encephalitis 

WHO World Health Organization 

WMD Weapons of mass destruction 
322
323

Appendix A. Pediatric Terrorism and Disaster 

Preparedness: Learning Objectives 

Chapter 1. Introduction 

Goal: To prepare pediatricians to participate in pediatric disaster planning, 

taking into consideration the differences between children and adults.

Learning Objectives: 

At the end of this chapter, the reader will be able to: 

1. Describe the phases of terrorism and disaster planning. 

2. Access the major Web sites available for further information on disaster 

preparedness to meet the needs of children. 

3. Work in concert with response agencies when providing disaster relief. 

4. Advocate for resources and products that currently do not exist for children, 

especially for children with special health care needs. 

5. Identify children’s anatomic, physiologic, immunologic, developmental, and 

psychological considerations that are different from adults and potentially could 

affect children’s vulnerability to injury and response in a disaster. 

6. Participate in community planning efforts that consider all potential aspects of a 

child’s life. 

7. Prepare for disasters at all phases of planning, response, recovery, and mitigation. 

Chapter 2. Systems Issues 

Goal: To prepare pediatricians to participate in pediatric disaster planning, 

by ensuring their familiarity with the U.S. disaster response system 

infrastructure. 

Learning Objectives: 

At the end of this chapter, the reader will be able to: 

1. List the five major types of natural disasters. 

2. Define and describe anthropogenic disasters. 

3. Identify the lead federal agencies involved in planning, preparedness, emergency 

medical services (EMS), and other disaster response. 

4. Access the Clinician Information Line run by the Centers for Disease Control 

Director’s Emergency Operations Center. 
324

Chapter 3. Responding to a Disaster 

Goal: To prepare pediatricians to respond to a disaster.

At the end of this chapter, the reader will be able to: 

1. Identify and describe the four phases of response to a disaster or act of terrorism 

(preparedness, actual response to the event, mitigation, and recovery). 

2. Describe the function of the National Incident Management System and how it 

could be used as part of local emergency response plans. 

3. Determine who would be in charge of an incident when there is a multi-agency 

response. 

4. Describe the various types of EMS personnel and their function. 

5. Identify problems that may be encountered by hospitals when dealing with a 

disaster or act of terrorism, including issues related to regional coordination, surge 

capacity, protection of personnel, and levels of precaution. 

6. Describe potential problems with using personal protective equipment (PPE). 

7. Describe the structure and function of an Incident Command System, including a 

Hospital Emergency Incident Command System, and its key participants. 

8. Describe how hospitals coordinate their response to a disaster with other 

community and medical entities. 

9. Provide a number of examples of the roles pediatricians may play in regional 

hospital to community planning. 

10. Participate in the organization, implementation, and quality assurance activities 

related to disaster drills. 

11. Assist in integrating children’s services into disaster life support drills. 

12. Refer children and families to existing support services in their communities. 

13. Explain the new Joint Commission on Accreditation of Healthcare Organizations 

(JCAHO) disaster preparedness standards. 

14. Explain the importance of appropriate triage. 

15. Describe the major management functions of the Incident Command System 

(incident command, operations, planning, logistics, finance/administration). 

16. Recognize the standardized position titles used for ICS supervisory personnel. 

17. Describe the roles of smaller ICS functional units (staging, triage, 

treatment/decontamination, transport). 

Chapter 4. Biological Terrorism 

Goal: To prepare pediatricians to recognize signs and symptoms, diagnose, 

treat, perform infection control measures, and report biological terrorism 

agents and events. 

Learning Objectives: 

At the end of this chapter, the reader will be able to: 
325

1. List which biological agents (microorganisms and toxins) pose the greatest 

potential for use in a bioterrorist attack, designated as “Category A” agents. 

2. Explain the reasons why Category A agents have the greatest adverse public 

health, medical, and social impact if used as bioterrorist agents. 

3. Recognize a wide number of clues that should heighten suspicion that a 

bioterrorist attack has occurred. 

4. Describe how biological agents affect and manifest themselves in pediatric 

respiratory, nervous, gastrointestinal, and dermatologic systems. 

5. Promptly diagnose and isolate a patient who has an illness potentially related to 

bioterrorism and notify the proper authorities. 

6. Access and properly use PPE. 

7. Describe the structure of his or her local public health system and the point of 

contact for reporting illnesses suspected of being related to bioterrorism. 

8. Rapidly detect and isolate patients with an infectious illness related to 

bioterrorism to prevent transmission in health care settings. 

9. Care for patients using standard precaution, contact precautions, droplet 

precautions, and airborne infection isolation techniques. 

10. Access the major Web sites available for further information on isolation and 

environmental control guidelines. 

11. Stock and use equipment and supplies necessary to diagnose and treat a patient 

suspected of being infected with a bioterrorist agent according to the level of care 

that will be provided at a particular facility or pediatrician’s office. 

12. Create an emergency plan and train office staff to follow it. 

13. Rapidly treat high-risk populations via administration of smallpox or anthrax 

vaccines. 

14. Access the Strategic National Stockpile managed by the Department of Homeland 

Security and the Department of Health and Human Services. 

15. Plan for surge capacity strains on existing pediatric resources. 

16. Provide families with the information they need to plan and prepare for a disaster. 

17. Provide clinical evaluation of patients suspected of being infected by Category A 

agents including all forms of anthrax, botulinum toxin, plague, smallpox, 

tularemia, and viral hemorrhagic fevers; as well as Category B and C Agents, 

including Ricin, Q Fever, Staphylococcus enterotoxin B, Brucella, Burkholderia 

mallei (Glanders), encephalitis viruses and yellow fever virus, and Clostridium 

perfringens.

Chapter 5. Chemical Terrorism 

Goal: To prepare pediatricians to recognize signs and symptoms, diagnose, 

treat, perform infection control measures, and report chemical terrorism 

agents and events. 

Learning Objectives: 

At the end of this chapter, the reader will be able to: 
326

1. Define chemical terrorism. 

2. Explain how careful community planning, robust research and development (by 

academic, private, and governmental collaborative efforts), and rigorous medical 

education could mitigate a chemical terrorism catastrophe. 

3. Explain why pediatricians need to understand the approach to mass casualty 

incidents involving traditional military chemical weapons and other toxic 

chemicals that might be used as “weapons of opportunity.” 

4. Explain the similarities and differences between a chemical terrorist attack and a 

more conventional chemical disaster in terms of the epidemiology and medical 

consequences associated with each. 

5. Create a management plan for decontamination and initial care of small children 

by personnel wearing bulky PPE. 

6. Recognize the risks and challenges to pediatric care providers posed by contact 

with many exposed children who are not critically injured but have been taken by 

parents to hospitals and pediatricians’ offices without prior on-scene 

decontamination. 

7. Describe how children have inherent physiologic, developmental, and 

psychological differences from adults that may enhance susceptibility and worsen 

prognosis after a chemical agent exposure. 

8. Recognize the epidemiology of acute mass exposure to a toxin as an aid in 

recognizing a covert chemical attack with unknown agents. 

9. Formulate an approach for managing chemical injuries sustained by children from 

an unknown chemical agent. 

10. Describe clinical syndromes and management after exposure to various chemical 

agents (nerve agents, vesicants, pulmonary agents, cyanide, and riot-control 

agents). 

11. Categorize chemical weapons based on the predominant symptoms they cause: 

neurologic (nerve agents or cyanide); respiratory (phosgene or chlorine, high-dose 

riot-control agents, or sulfur mustard with a delay of several hours from time of 

exposure); and mucocutaneous syndromes (vesicants). 

12. Access and alert the CDC, local public health authorities, and/or regional poison 

control center. 

13. Differentiate between cyanide and nerve agent attacks. 

14. Plan for the initial protection of everyone in a community exposed to a hazardous 

chemical using CDC Guidelines for Evacuation and for Sheltering in Place in a 

Chemical Emergency. 

15. Discuss treatment of contaminated victims via extrication, triage, resuscitation as 

needed, and decontamination performed by rescue workers or health care 

providers wearing appropriate PPE. 

16. Provide cardiopulmonary and airway support, including endotracheal intubation, 

and emergent intramuscular antidotal therapy as necessary and appropriate for the 

specific exposure. 

17. Prepare to treat potential victims of a terrorist attack involving industrial sources 

of hazardous chemicals. 

18. Participate in disaster management training, including stocking appropriate 

antidotes, practicing decontamination strategies, and learning the use of PPE. 
327

19. Identify chemical terrorism toxins such as nerve agents (tabun, sarin, soman, and 

VX (“Venom X”) and their delivery systems, toxicology and clinical 

manifestations, central and autonomic systems effects, neuromuscular effects, 

diagnostic tests, treatment, isolation, and control measures. 

20. Describe comprehensive plans to address terrorist threats to infection control (for 

biological agents), epidemiology, public affairs, and administration of health care 

facilities. 

21. Explain the lethality of cyanide, its toxicology, clinical presentation, and 

treatment. 

22. List the agents known as vesicants (sulfur mustard, the nitrogen mustards, 

lewisite, and phosgene oxime) and their characteristics, clinical effects, treatment, 

and special pediatric considerations. 

23. Describe pulmonary agents (chlorine and phosgene) and their characteristics, 

clinical effects, treatment, including decontamination and management. 

24. Identify riot control agents (CS [2-chlorobenzylidene], CN [1-

chloroacetophenone, Mace®], and pepper spray [Oleoresin capsicum]), their 

transmission and pathogenesis, clinical manifestations, diagnosis, treatment, and 

control. 

Chapter 6. Radiological and Nuclear Terrorism 

Goal: To prepare pediatricians to recognize the signs and symptoms 

associated with radiologic and nuclear exposure and to diagnose, treat, and 

report nuclear and radiologic terrorism events and agents. 

Learning Objectives: 

At the end of this chapter, the reader will be able to: 

1. List sources of radioactivity and the terrorism threats they pose. 

2. Describe the scope, implications, and incident management of radiological 

threats. 

3. Differentiate between nuclear and conventional explosions. 

4. Explain the process of radiation from nuclear detonation and fallout. 

5. Describe the purpose and effects of radiological dispersal devices (“dirty 

bombs”). 

6. Describe medical and industrial sources of radiation. 

7. Define the potential hazards of destruction or sabotage of a nuclear power plant. 

8. Recount the historical overview of radiation injury. 

9. Explain the physical principles of ionizing radiation. 

10. Describe radiation interactions including electron excitation, ionization, nuclear 

excitation, nuclear fission, activation, and secondary radiation. 

11. Provide information to patients concerning the safety of consuming milk after a 

reactor accident. 

12. List natural and man-made types of radiation exposure. 
328

13. Record radiation-induced signs, symptoms, and erythema during the course of 

medical management for radiation casualties to help triage and guide medical 

management of casualties. 

14. Recognize the pattern of biological responses associated with acute radiation 

sickness (ARS). 

15. Describe the pathophysiology and effects of radio- and chemotherapy including 

bone marrow damage, diarrhea, and hair loss. 

16. Explain the time-dependent clinical stages of radiation exposure (prodrome, latent 

period and manifest illness). 

17. List the diagnostic steps to assess a dose of radiation exposure. 

18. Medically diagnose external radiological contamination. 

19. Assess and care for externally contaminated patients. 

20. Properly use PPE to eliminate personal risk while caring for victims of radiation 

exposure. 

21. Explain the mechanisms of internal contamination when radioactive material 

enters the bodies of unprotected people through inhalation, ingestion, or wound 

contamination. 

22. Differentiate between public concern about terrorism involving radioactive 

materials and medical errors during diagnosis that have been the most common 

cause of significant internal contamination. 

23. Describe the three pathways through which radioactive material can enter the 

body (inhalation, ingestion and skin penetration). 

24. List the various instruments available for detecting and measuring radiation. 

25. Discuss the need for PPE, type needed for radiation contamination, disposal of 

PPE, and Department of Energy Guidance on PPE. 

26. Differentiate between PPE for radioactive isotopes and chemical or biological 

exposures. 

27. Describe emergency precautions when PPE is not available in a radioactive 

environment. 

28. Explain the basic principles of decontamination and priorities. 

29. Explain the characteristics that render pediatric patients uniquely sensitive to the 

effects of radiation exposure. 

30. Explain the well-documented long-term effects of radiation exposure to the fetus 

and child. 

31. Recount the psychological vulnerability of children involved in a radiation related 

incident. 

32. Treat acute pediatric radiation syndrome both supportively and with specific 

actions and medications. 

33. Prioritize external decontamination before treatment of internal decontamination. 

34. Use potassium iodide (KI) to reduce thyroid uptake of radioactive iodine. 

35. Keep available and use a table of threshold radioactive exposures and 

recommended prophylactic single doses of KI. 

36. Treat internal contamination with appropriate chelating agents. 

37. Prioritize steps in the treatment of victims of combined injuries, that is, 

stabilization of life threatening injuries prior to radiation injuries. 

38. Manage the patient with embedded radioactive material and depleted uranium. 
329

39. Provide followup care, being mindful of the risk of carcinogenesis. 

40. Describe environmental issues affecting children after a terrorist incident 

involving radioactive materials. 

41. Make knowledgeable decisions and actions to prevent radiation exposure related 

to short-term evacuation versus sheltering. 

42. Access the FDA guidance for accidental radioactive contamination of human food 

and animal feed. 

Chapter 7. Blast Terrorism 

Goal: To prepare pediatricians to recognize signs and symptoms, diagnose, 

treat, and report blast terrorism events and agents. 

Learning Objectives: 

At the end of this chapter, the reader will be able to: 

1. Explain the four primary mechanisms involved in blast injuries. 

2. List the three primary causes of death after a blast. 

3. Describe four characteristic results of urban bomb blasts. 

4. Explain how the anatomic structure of the lung makes it susceptible to the effects 

of blast barotraumas. 

5. List typical clinical findings in blast lung injuries. 

6. Treat blast lung injury and resulting complications. 

7. List the signs and symptoms that suggest arterial air embolization. 

8. Treat arterial air emboli. 

9. List the clinical findings in GI injury from a blast. 

10. Manage gastrointestinal blast injuries by controlling internal bleeding and 

identifying and repairing any perforated viscus. 

11. Describe the clinical findings in blast auditory injuries. 

12. Explain the cardiovascular effects of a blast wave. 

13. Recognize sentinel injuries (subtle injuries that can increase the risk of developing 

serious blast injury). 

14. Provide emergency management of victims of incendiary devices. 

15. Describe a trauma center. 

16. Describe the key organizational characteristics common among all trauma centers. 

17. Delineate the services provided by the three levels of trauma centers. 

18. Access the Advanced Trauma Life Support® for Doctors Course protocols. 

19. Access the Advanced Burn Life Support® Course protocols. 

20. Define a mass casualty event. 

21. Participate in planning for and mitigation of an attack involving blast terrorism. 

22. Recognize the need for proper triage and transport of pediatric patients to an 

appropriate trauma center. 
330

Chapter 8. Mental Health Issues 

Goal: To prepare pediatricians to address the mental health needs of 

children and families in a disaster or terrorist event. 

Learning Objectives: 

At the end of this chapter, the reader will be able to: 

1. Recognize pediatric psychiatric symptoms and disorders, including posttraumatic 

stress disorder (PTSD), anxiety, depression, and behavioral problems, after 

exposure to disasters or terrorist incidents. 

2. List the risk factors that are associated with an increased risk of posttraumatic 

symptoms. 

3. Describe three characteristic symptoms that are essential features of PTSD after 

exposure to a traumatic event. 

4. List five factors that are likely to be present in death circumstances that are 

considered “traumatic deaths.” 

5. Assess, screen and treat (or refer for treatment), children who are at risk for 

mental health problems after exposure to a traumatic event. 

6. Follow procedures for notification about an unexpected death with sensitivity to 

key issues that will minimize the short- and long-term impact on survivors. 

7. Explain death to children in a manner they can understand. 

8. Recognize common reactions that children may have in response to a personal 

loss. 

9. Identify children who have extreme reactions, atypical reactions, or prolonged 

reactions that require referral to a mental health professional experienced in the 

management of pediatric bereavement. 

10. Explain the controversy that surrounds the use of psychopharmacology in children 

with PTSD. 

11. Advocate for, consult with, and actively participate in school crisis response 

teams. 

12. Prepare families to cope with anniversary reactions and commemorative activities 

of a traumatic event. 

13. Recognize the emotional impact experienced by school staff, first responders, and 

other health care professionals following a disaster. 

14. Communicate effectively during a crisis. 

Chapter 9. Integrating Terrorism and Disaster 

Preparedness into Your Pediatric Practice 

Goal: To assist general pediatricians in integrating the information in this 

resource into their office- or hospital-based practices. 
331

Learning Objectives: 

At the end of this chapter, the reader will be able to: 

1. Explain their role in the general system response to disasters. 

2. Create a disaster-preparedness framework for a general practice pediatric office. 

3. Describe the components for basic internal office readiness (facilities, equipment, 

records, communication system, chain of command, contact list, staff 

responsibilities, triage, screening, prioritization, practice readiness, staff 

development, and insurance). 

4. Determine how the practice will link and coordinate efforts with affiliate 

hospitals, schools, daycare centers, local response teams, the local department of 

health, and city, State, and Federal efforts. 

5. Develop a list of contact numbers for all existing agencies that are components in 

the external disaster management system. 

6. Establish relationships with the local or regional Office of Emergency 

Management and strengthen already established relationships with 

organizations/institutions in the community. 

7. Integrate into the larger community response effort. 

8. Participate in disaster drills and exercises. 

9. Describe disaster protocols of local departments of health. 

10. Communicate directly with children and families about disaster and terrorism 

preparedness. 

11. Answer the questions of children and families during events. 

12. Provide advice for families of children with special health care needs. 

13. Participate in creating contingency plans to increase hospital surge capacity. 

14. Help to produce contingency plans for acquiring and maintaining essential 

services (water, electricity, oxygen, garbage disposal). 

15. Plan for stockpiling medical supplies. 

16. Participate in a network of community resources that will be able to organize 

volunteers to become proxy caretakers for orphaned children. 

17. Participate in planning hospital infrastructure needs for children (disaster drills 

involving children, infection control plans, quarantine procedures, staff training). 

Chapter 10. Working with Government Agencies to 

Enhance Preparedness 

Goal: To assist pediatricians working with government agencies to enhance 

preparedness for meeting children’s needs. 

Learning Objectives: 

At the end of this chapter, the reader will be able to: 

1. Describe the role of various government agencies in disaster preparedness and 

response. 
332

2. Work with community, State, and Federal Government entities in disaster 

preparedness for children. 

3. Explain the importance of the pediatrician’s role in determining public health 

preparedness. 

4. Advocate for children and families in preparedness planning. 

Chapter 11. Conclusion 

Goal: To assist pediatricians in understanding the consequences of a recent 

major disaster and applying the lessons learned to current planning and 

preparedness efforts. 

Learning Objectives: 

At the end of this chapter, the reader will be able to: 

1. Describe the problems that emerged following Hurricane Katrina and how these 

experiences can inform future planning efforts. 

2. Ensure that preparedness plans include provisions for identification and care of 

displaced children who have been separated from their families. 

3. Understand the needs of children and families in sheltering situations. 

4. Recognize the importance of and maintain up-to-date professional and personal 

contact information for themselves and their families and staff members. 

5. Participate and assist in coordination of disaster relief efforts, both locally and 

farther away, depending on areas of greatest need. 
333

Appendix B. List of Contributors1

Lead Editors 

George L. Foltin, MD, FAAP, FACEP 

Director, Center for Pediatric Emergency Medicine 

Director, Division of Pediatric Emergency Medicine 

Associate Professor of Pediatrics and Emergency Medicine 

New York University School of Medicine 

Bellevue Hospital Center, New York, NY 

System Issues; Blast Trauma; Integrating Preparedness Into Your Practice 

Working With Government Agencies and Advocacy 

Conclusion/Lessons Learned—First Impressions 

David J. Schonfeld, MD, FAAP 

Thelma and Jack Rubinstein Professor of Pediatrics 

Director, Division of Developmental and Behavioral Pediatrics 

Cincinnati Children's Hospital Medical Center, Cincinnati, OH 

Professor Adjunct of Pediatrics 

Yale University School of Medicine, New Haven, CT 

Children Are Not Small Adults; Mental Health Issues

Michael W. Shannon, MD, MPH, FAAP 

Chief and CHB Chair 

Division of Emergency Medicine 

Director, The Center for Biopreparedness 

Children’s Hospital Boston 

Professor of Pediatrics 

Harvard Medical School, Boston, MA 

Biological Terrorism; Chemical Terrorism; Nuclear and Radiological Terrorism 

Children Are Not Small Adults 

Section Editor and Contributor 

Jane Knapp, MD, FAAP 

Co-Director, Center for Childhood Safety 

Professor of Pediatrics 

Clinical Scholar in Pediatric Emergency Medicine 

Children’s Mercy Hospital 

University of Missouri-Kansas City School of Medicine, Kansas City, MO 

 

1 Note: For all contributors who are affiliated with the U.S. Army, the views, opinions and assertions 

contained in this resource are those of the authors and should not be construed as official Department of 

the Army policy. 
334

Systems Issues 

Section Editors 

Marion J. Balsam, MD, FAAP 

Executive Secretary of the Federal Advisory Committee 

Research Partnerships Program Director for the National Children’s Study 

National Institute of Child Health and Human Development 

National Institutes of Health, Bethesda, MD 

Lorraine M. Giordano, MD, FACEP 

Medical Director 

NYC Office of Emergency Management, New York, NY 

Program Director 

Medical Oversight and Quality Assurance 

NYC Health & Hospitals Corporation, New York, NY 

Contributors 

Steven Baldwin, MD, FAAP 

Associate Professor of Pediatrics and Emergency Medicine 

Children’s Hospital of the University of Alabama, Birmingham, AL 

Marie Diglio, EMT-P 

Executive Director, Operations 

Regional Emergency Medical Services Council, New York, NY 

Jessica C. Foltin, MD

Director, Pediatric Emergency and Transport Services 

Associate Professor of Pediatrics and Emergency Medicine 

New York University School of Medicine 

New York University Medical Center, New York, NY 

Katherine Gnauck, MD 

Division of Pediatric Emergency Medicine 

Department of Emergency Medicine 

University of New Mexico Health Science Center 

Albuquerque, NM 

Robert Iannarelli 

Chief (retired) 

NYC Fire Department, New York, NY 

Francesca C. Music 

Director, Homeland Security and National Medical Contingency Planning 

Office of the Assistant Secretary of Defense for Health Affairs 

Force Health Protection & Readiness 

Office of the Assistant Secretary of Defense for Homeland Defense 

Department of Defense, Washington, DC 
335

James Tsung, MD, FAAP 

Attending Physician 

Division of Pediatric Emergency Medicine 

Departments of Pediatrics and Emergency Medicine 

Bellevue Hospital Center and New York University Medical Center 

Assistant Professor of Pediatrics and Emergency Medicine 

New York University School of Medicine 

Biological Terrorism 

Section Editor 

Julia McMillan, MD 

Vice Chair for Pediatric Education 

Professor of Pediatrics 

Residency Program Director 

Department of Pediatrics 

Johns Hopkins University School of Medicine, Baltimore, MD 

Editor-in-Chief, Contemporary Pediatrics

Contributors 

Joanne Cono, MD, ScM, FAAP 

Assistant Associate Director for Science 

Coordinating Office of Terrorism Preparedness and Emergency Response 

Medical Epidemiologist, Bioterrorism Preparedness and Response Program 

National Center for Infectious Diseases 

Centers for Disease Control and Prevention, Atlanta, GA 

Hanoch A. Patt, MD 

Fellow in Pediatric Cardiology 

Department of Pediatrics 

Baylor College of Medicine, Texas Children's Hospital, Houston, TX 

Chemical Terrorism 

Section Editor 

Frederick Henretig, MD, FACMT, FAAP 

Emergency Medicine Attending Physician 

Director, Section of Clinical Toxicology 

Senior Toxicologist and Associate Medical Director, Poison Control Center 

Children’s Hospital of Philadelphia 

University of Pennsylvania Medical Center, Philadelphia, PA 

Contributors 

Thomas R. Burklow, MD 

Lieutenant Colonel, Medical Corps, United States Army 

Chief, Department of Pediatrics 

Walter Reed Army Medical Center, Washington, DC 

Uniformed Services University of the Health Sciences, Bethesda, MD 
336

James M. Madsen, MD, MPH 

Colonel, Medical Corps, United States Army 

Former Deputy Director, National Capital Consortium Residency in Occupational and Environmental 

Medicine 

Former Assistant Professor of Preventive Medicine and Biometrics, of Military and Emergency Medicine, 

of Pathology, and of Emerging Infectious Diseases 

Uniformed Services University of the Health Sciences, Bethesda, MD 

Michele McKee, MD 

Department of Pediatrics and Toxicology 

University of Pennsylvania Medical Center, Philadelphia, PA 

Joshua S. Rotenberg, MD, MS, FAAP 

Major, Medical Corps, United States Army 

Founding member of The Working Group on Chemical and Biological Terrorism

Departments of Child and Adolescent Neurology and Pediatrics 

Walter Reed Army Medical Center, Washington, DC 

Uniformed Services University of the Health Sciences, Bethesda, MD 

James F. Wiley II, MD 

Associate Professor of Pediatrics and Emergency Medicine/Traumatology 

Head, Division of Pediatric Emergency Medicine 

University of Connecticut School of Medicine 

Medical Consultant, Connecticut Regional Poison Control Center 

Connecticut Children’s Medical Center, Hartford, CT 

Clifton E. Yu, MD 

Lieutenant Colonel, Medical Corps, United States Army 

Assistant Professor of Pediatrics 

Director, National Capital Consortium Residency in Pediatrics 

Uniformed Services University of the Health Sciences, Bethesda, MD 

Nuclear and Radiological Terrorism 

Section Editor 

David E. Jarrett, MD, FS, FACEP

Colonel, Medical Corps, United States Army 

Director, Armed Forces Radiobiology Research Institute 

US Army Medical Research Institute of Infectious Diseases, Bethesda, MD 

Contributors 

William F. Blakely, PhD 

Head of Radiation Biology 

Biological Dosimetry Team Leader 

Armed Forces Radiobiology Research Institute, Bethesda, MD 

Adjunct Assistant Professor of Preventive Medicine/Biometrics 

Adjunct Assistant Professor of Environmental and Occupational Health 

Uniformed Services University of the Health Sciences, Bethesda, MD 
337

Gerald S. Braley, PhD 

Major, United States Air Force 

Science Advisor, Office of Emergency Response 

National Nuclear Security Administration, Department of Energy, Germantown, MD 

Itzhak Brook, MD 

Professor of Pediatrics 

Georgetown University School of Medicine, Washington DC 

Curtis Cummings, MD, MPH 

Associate Professor of Environmental and Occupational Health 

Drexel University School of Public Health, Philadelphia, PA 

William E. Dickerson, MD 

Colonel, Medical Corps, United States Air Force 

Director of Military Medical Operations 

Staff Radiological Oncologist 

Armed Forces Radiobiology Research Institute, Bethesda, MD 

Gary Francis, MD, PhD 

Professor of Pediatrics and Pediatric Endocrinology 

Director of Pediatric Endocrinology Fellowship Program 

Uniformed Services University of Health Sciences, Bethesda, MD 

Sarah K. Kirtland, MS 

Commander, United States Navy 

Deputy Director of Military Medical Operations 

Armed Forces Radiobiology Research Institute, Bethesda, MD 

Philip L. Liotta, PhD 

Former Chief Health Physicist, Former Chairman 

Radiation Sciences Department 

Armed Forces Radiobiology Research Institute 

Robert W. Miller, MD, DrPH 

Pediatric Epidemiologist, Clinical Epidemiology Branch 

National Cancer Institute, Bethesda, MD 

Pataje Prasanna, PhD 

Radiation Biologist 

Armed Forces Radiobiology Research Institute, Bethesda, MD 

Richard Sedlak, MD, MPH 

Colonel, United States Army 

Director, Military Medical Operation 

Armed Forces Radiobiology Research Institute, Bethesda, MD 
338

Horace Tsu, MD 

Lieutenant Colonel, Medical Corps, United States Air Force 

Former Deputy Head, Military Medical Operations 

Armed Forces Radiobiology Research Institute, Bethesda, MD 

Clifton E. Yu, MD 

Lieutenant Colonel, Medical Corps, United States Army 

Assistant Professor of Pediatrics 

Director, National Capital Consortium Residency in Pediatrics 

Uniformed Services University of the Health Sciences, Bethesda, MD 

Acknowledgments 

Donna Solyan 

Head of Illustration and Editing Section 

Armed Forces Radiobiology Research Institute, Bethesda, MD 

Nimae Angwafo, MD, AFRRI 

LCDR Charles R. Woodruff, AFRRI 

Jamie Waselenko, MD, AFRRI 

Blast Trauma 

Section Editor 

Arthur Cooper, MD, MS, FACS, FAAP, FCCM 

Director of Trauma and Pediatric Surgical Services 

Columbia University Affiliation 

Harlem Hospital Center, New York, NY 

Contributors 

Julie Quintero, MD 

Attending Physician 

Assistant Professor of Pediatrics and Emergency Medicine 

Robert Wood Johnson University Hospital, New Brunswick, NJ 

Former Fellow in Pediatric Emergency Medicine 

Bellevue Hospital Center, New York, NY 

Acknowledgments 

Sherlita Amler, MD 

Yaron Bar-Dayan, MD 

Susan M. Briggs, MD 

Lt. Gen. Paul K. Carlton, Jr., MC, USAF (Ret) 

T. Forcht Dagi, MD 

Timothy E. Davis, MD, MPH 

Yoel Donchin, MD 

Zvi Feigenberg, MD 

Eric R. Frykberg, MD 

Pinchas Halpern, MD 

Richard D. Hunt, MD 

Catherine Y. Lee, MPH 
339

Kobi Peleg, PhD 

Michael Stein, MD 

John A. Weigelt, MD 

Mental Health Issues 

Section Editor 

David Szydlo, MD, PhD 

Education and Curriculum Development Director 

National Center for Children Exposed to Violence 

Associate Research Scientist, Child Study Center 

Yale University School of Medicine, New Haven, CT 

Currently Director, Centro de Estudios Psicoanaliticos A.C., Mexico 

Contributors 

Steven Berkowitz, MD, FAAOS, FACS, CIME 

Medical Director 

National Center for Children Exposed to Violence, Child Study Center 

Yale University School of Medicine, New Haven, CT 

Associate Director, Connecticut Trauma Response Program, New Haven, CT 

Russell T. Jones, PhD 

Terrorism Disaster Branch 

National Center for Child Traumatic Stress, Blacksburg, VA 

Professor of Clinical Psychology 

Virginia Tech University, Blacksburg, VA 

Betty Pfefferbaum MD, JD 

Director and Professor of Psychiatry and Behavioral Sciences 

Department of Psychiatry and Behavioral Sciences 

University of Oklahoma Health Sciences Center, Oklahoma City, OK 

Acknowledgment 

Steven Marans, PhD 

Director, National Center for Children Exposed to Violence, Child Study Center 

Harris Associate Professor of Child Psychoanalysis 

Associate Professor of Psychiatry 

Yale University School of Medicine, New Haven, CT 

Integrating Preparedness into Your Pediatric Practice 

Section Editors 

David Markenson, MD, FAAP 

Director, Center for Disaster Medicine 

School of Public Health, New York Medical College 

Chief, Pediatric Emergency Medicine 

Maria Fareri Children's Hospital 

Westchester Medical Center, New York, NY 
340

Irwin Redlener, MD, FAAP 

President and Co-Founder 

Children’s Health Fund, New York, NY 

Director, National Center for Disaster Preparedness 

Associate Dean for Public Health Advocacy and Preparedness 

Mailman School of Public Health 

Columbia University, New York, NY 

Contributor 

Danielle Laraque, MD, FAAP 

Debra and Leon Black Professor of Pediatrics 

Chief, Division of General Pediatrics 

Mount Sinai School of Medicine 

Mount Sinai Medical Center, New York, NY 

Working with Government Agencies and Advocacy 

Section Editors and Contributors 

David Markenson, MD, FAAP 

Irwin Redlener, MD, FAAP 

Conclusion and Lessons Learned 

Section Editor 

George L. Foltin, MD, FAAP, FACEP 

Contributors 

Steven Baldwin, MD, FAAP 

Dan Kavanaugh, MSW 

Director, Emergency Medical Services for Children Program 

Health Resources Services Administration 

Maternal & Child Health Bureau, Rockville, MD 

Errol McRae, RN, MN 

Executive Director, Louisiana Chapter–ACEP 

Baton Rouge, LA 

Gretchen Mahan 

AAP Chapter Executive Director 

Mississippi Chapter–AAP, Jackson, MS 

Keith E. Parker, RN 

Director, Bureau of Emergency Medical Services 

Mississippi Department of Health, Jackson, MS 

William D. Payne, MD, FAAP 

President, Mississippi Chapter–AAP, Jackson, MS 
341

Lou E. Romig MD, FAAP, FACEP 

Children’s Hospital Medical Director 

Pediatric Emergency Medicine, Miami, FL 

FL-5 Disaster Medical Assistance Team, FEMA/Department of Homeland Security 

David J. Schonfeld, MD, FAAP 

Michael Shannon, MD, MPH 

Paul E. Sirbaugh, DO, FAAP 

Director, Prehospital Medicine 

Texas Children’s Hospital 

Assistant Professor of Pediatrics 

Baylor College of Medicine, Houston, TX 

Linda Hill Southward, PhD, ACSW 

Research Professor 

Coordinator, Family and Children Research Unit 

Social Science Research Center 

Mississippi State University, Mississippi State, MS 

Michael Tunik, MD, FAAP 

Associate Professor of Pediatrics and Emergency Medicine 

NYU School of Medicine 

Research Director, Center for Pediatric Emergency Medicine 

Bellevue Hospital Center, New York, NY 

Other Contributors 

Deborah Levine, MD 

Clinical Assistant Professor of Pediatrics and Emergency Medicine 

New York University School of Medicine 

Bellevue Hospital Center, New York, NY 

Virginia M. Ferrante, MA 

Medical Illustrator 

Ferrante Medical Media, Darien, CT 

Reviewers 

Errol Alden, MD, FAAP 

Executive Director, American Academy of Pediatrics 

Steven Baldwin, MD, FAAP 

Jay Berkelhammer, MD, FAAP 

President Elect, American Academy of Pediatrics 

Carol Berkowitz, MD, FAAP 

Immediate Past President, American Academy of Pediatrics 
342

Carden Johnston, MD, FAAP, FACEP, FRCP 

Former President, American Academy of Pediatrics 

Emeritus Professor of Pediatrics 

Children’s Hospital of the University of Alabama, Birmingham, AL 

Kathryn Nichol, MD, FAAP 

Board of Directors, American Academy of Pediatrics 

Eileen Ouellette, JD, MD, FAAP 

President, American Academy of Pediatrics 

Committee on Pediatric Emergency Medicine 

Steven E. Krug, MD, FAAP 

Committee Chairman, 2004-2008 

Children’s Memorial Hospital, Chicago 

Thomas Bojko, MD, MS, FAAP 

Robert Wood Johnson Medical School 

Margaret A. Dolan, MD, FAAP 

Karen S. Frush MD, FAAP 

Duke University Medical Center 

Joan E. Shook, MD, MBA 

Baylor College of Medicine 

Robert E. Sapien, MD, FAAP 

University of New Mexico Health Sciences Center 

Kathy Shaw, MD, MSCE, FAAP 

The Children’s Hospital of Philadelphia 

Paul Sirbaugh DO, FAAP 

Texas Children's Hospital 

Loren Yamamoto, MD, MPH, MBA 

University of Hawaii Hospital 

Liaisons 

American College of Emergency Physicians 

Sharon Mace, MD, FAAP, FACEP 

American College of Surgeons 

David W. Tuggle, MD, FAAP 

EMSC National Resource Center 

Jane Ball, RN, DrPH 

Susan Eads Role, JD, MSLS 
343

Maternal & Child Health Bureau 

Dan Kavanaugh, MSW 

National Association of EMS Physicians 

Kathleen Brown, MD, FAAP 

American Academy of Family Physicians 

Kim Bullock, MD 

American Academy of Pediatrics 

Project Manager 

Mary McGowan, MA 

Staff 

Michael Glasstetter, JD 

Graham Newson, MA 

Cindy Pellegrini 

Susan Tellez