Wide World of Kids

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
iii
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
iv
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
v
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
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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
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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
viii
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
ix
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
x
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
xi
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 radiation-
induced 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 oft-
used 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 age-
appropriate 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 child-
appropriate 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.
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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                    Transportation crashes or
releases or spills                     derailments
Unintentional explosions               Power outages
or collapses
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               Genocidal acts
conflict
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 wind-
generated 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.
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• 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/cgi-
bin/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.
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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                  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.
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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 full-
scale 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
28
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
29
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
30
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
31
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.
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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
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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
34
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.
35
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, pre-
designed 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).
36
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.
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•   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.
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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).
39
•    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,
40
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
41
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.
42
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.
43
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
44
Table 3.1    Training and competencies of prehospital emergency personnel
Prehospital      Hours of training          Medical procedures able to perform
emergency         (approximate)
personnel
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
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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.
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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 varicella-
like rashes in adults.
•   Large numbers of cases of unexplained disease or death.
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•   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 (low-
grade 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
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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.
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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
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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)
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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.
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•   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
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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.
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•   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 high-
risk 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
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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 large-
scale 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/.
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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:
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•   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
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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
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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 three-
dose 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).
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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
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treated people experience some degree of hypersensitivity reaction to equine serum, but severe
reactions are rare.
Antimicrobial agents should 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.
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•   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 of respiratory 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
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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-to-
face 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.
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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 deep-
seated, 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.
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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 potential for 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
precautions should 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
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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 CDC is the only source of VIG in the United
States. Supplies may be obtained by calling the CDC Smallpox Vaccine Adverse Events Clinical
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.
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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.
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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).
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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.
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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.
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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, trimethoprim-
sulfamethoxazole 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. Trimethoprim-
sulfamethoxazole 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
Bibliography
• Arnon SS, Schechter R, Inglesby TV, et al. Botulinum toxin as a biological weapon: medical
and public health management. JAMA. 2001;285:1059–1070.
• Borio L, Inglesby T, Peters CJ, Schmaljohn, et al. Hemorrhagic fever viruses as biological
weapons: medical and public health management. JAMA. 2002:287:2391–2405.
• Centers for Disease Control and Prevention. Acute, Generalized Vesicular or Pustular Rash
Illness Protocol. An Algorithm for Evaluating Patients for Smallpox. Available at:
http://www.bt.cdc.gov/agent/smallpox/diagnosis/evalposter.asp. Accessed July 12, 2006.
• Centers for Disease Control and Prevention. Anthrax. Available at:
http://www.bt.cdc.gov/agent/anthrax/index.asp. Accessed July 13, 2006.
• Centers for Disease Control and Prevention. Bioterrorism Readiness Plan: A Template for
Healthcare Facilities. April 1999. Available at:
http://www.cdc.gov/ncidod/dhqp/pdf/bt/13apr99APIC-CDCBioterrorism.PDF. Accessed July
12, 2006.
• Centers for Disease Control and Prevention. Emergency Preparedness and Response. Agents,
Diseases, & Other Threats. Available at: http://www.bt.cdc.gov/. Accessed July 13, 2006.
• Centers for Disease Control and Prevention. Emergency Preparedness and Response.
Botulism. Available at: http://www.bt.cdc.gov/agent/botulism/index.asp. Accessed July 19,
2006.
• Centers for Disease Control and Prevention. Emergency Preparedness and Response.
Clinician Registry for Terrorism and Emergency Response Updates and Training
Opportunities. Available at: http://www.bt.cdc.gov/clinregistry/index.asp.
Accessed July 12, 2006.
• Centers for Disease Control and Prevention. Emergency Preparedness and Response.
Evaluate a Rash Illness Suspicious for Smallpox. Available at:
http://www.bt.cdc.gov/agent/smallpox/diagnosis/riskalgorithm/index.asp. Accessed July 12,
2006.
• Centers for Disease Control and Prevention. Emergency Preparedness and Response.
Frequently Asked Questions (FAQ) About Tularemia. Available at:
http://www.bt.cdc.gov/agent/tularemia/faq.asp.
Accessed August 17, 2006.
• Centers for Disease Control and Prevention. Emergency Preparedness and Response. Key
Facts About Tularemia. Available at: http://www.bt.cdc.gov/agent/tularemia/facts.asp.
Accessed July 19, 2006.
• Centers for Disease Control and Prevention. Emergency Preparedness and Response.
Laboratory Information. Available at: http://www.bt.cdc.gov/labissues/index.asp. Accessed
July 12, 2006.
• Centers for Disease Control and Prevention. Emergency Preparedness and Response.
Smallpox Diagnosis and Evaluation. Available at:
http://www.cdc.gov/ncidod/dvbid/plague/diagnosis.htm.
Accessed July 19, 2006.
• Centers for Disease Control and Prevention. Guideline for Environmental Infection Control
in Health-Care Facilities, 2003. Available at:
http://www.cdc.gov/ncidod/dhqp/gl_environinfection.html.
84
Accessed July 12, 2006.
• Centers for Disease Control and Prevention. Guideline for Isolation Precautions in Hospitals.
Available at: http://www.cdc.gov/ncidod/dhqp/gl_isolation.html. Accessed July 12, 2006.
• Centers for Disease Control and Prevention. The History of Bioterrorism (Video). Available
at: http://www.bt.cdc.gov/training/historyofbt/index.asp. Accessed August 17, 2006.
• Centers for Disease Control and Prevention. Laboratory Response Network. Available at:
http://www.bt.cdc.gov/lrn/. Accessed July 12, 2006.
• Centers for Disease Control and Prevention. Laboratory Response to Suspicious Substances.
Available at: http://www.bt.cdc.gov/labissues/substanceresponse.asp. Accessed August 7,
2006.
• Centers for Disease Control and Prevention. Notice to readers: Update: interim
recommendations for antimicrobial prophylaxis for children and breastfeeding mothers and
treatment of children with anthrax. MMWR. 2001; 40(45):1014-1016.
• Centers for Disease Control and Prevention. Plague Diagnosis. Available at:
http://www.cdc.gov/ncidod/dvbid/plague/diagnosis.htm. Accessed July 19, 2006.
• Centers for Disease Control and Prevention. Programs in Brief: Select Agent Program.
Available at: http://www.cdc.gov/programs/php07.htm. Accessed August 17, 2006.
• Centers for Disease Control and Prevention. The Public Health Response to Biological and
Chemical Terrorism. Interim Planning Guidance for State Public Health Officials, July 2001.
Available at: http://www.bt.cdc.gov/Documents/Planning/PlanningGuidance.PDF. Accessed
July 12, 2006.
• Centers for Disease Control and Prevention. Recognition of illness associated with the
intentional release of a biologic agent. MMWR. 2001; 50(41):893-897.
• Centers for Disease Control and Prevention. Smallpox Response Plan and Guidelines
(version 3.0). Available at: http://www.bt.cdc.gov/agent/smallpox/response-plan/index.asp.
Accessed July 13, 2006.
• Centers for Disease Control and Prevention. Smallpox Vaccination. Information for Health
Professionals. Available at: http://www.bt.cdc.gov/agent/smallpox/vaccination/index.asp.
Accessed August 17,
2006.
• Centers for Disease Control and Prevention. Smallpox Vaccine Administration Video.
Available at: http://www.bt.cdc.gov/agent/smallpox/vaccination/administration-
video/index.asp. Accessed July 12, 2006.
• Centers for Disease Control and Prevention. Specimen Shipping and Packing. Available at:
http://www.cdc.gov/ncidod/srp/specimens/shipping-packing.html. Accessed August 7, 2006.
• Centers for Disease Control and Prevention. State and Local Health Department Web Sites.
Available at: http://www.cdc.gov/other.htm#states.
Accessed July 12, 2006.
• Centers for Disease Control and Prevention. Strategic National Stockpile. Available at:
http://www.bt.cdc.gov/stockpile/. Accessed July 13, 2006.
• Centers for Disease Control and Prevention. Use of anthrax vaccine in the United States.
MMWR. 2000; 49(RR-15):1-20.
• Centers for Disease Control and Prevention. Vaccinia (smallpox) vaccine. Recommendations
of the Advisory Committee on Immunization Practices (ACIP), 2001. MMWR. 2001; 50(RR-
10):1-25.
85
• Centers for Disease Control and Prevention. Special features of VHFs. Available at:
http://www.cdc.gov/ncidod/dvrd/spb/mnpages/vhfmanual/anx2.pdf. Accessed July 19, 2006.
• Cono J, Casey CD, Bell DM. Smallpox vaccination and adverse events: Guidance for
clinicians. MMWR. 2003; 52(RR-04):1-28.
• Council of State and Territorial Epidemiologists. Current State and Territorial
Epidemiologists. Available at: http://www.cste.org/members/state_and_territorial_epi.asp.
Accessed July 12, 2006.
• Davis CJ. Nuclear blindness: an overview of the biological weapons programs of the former
Soviet Union and Iraq. Emerg Infect Dis. 1997;278(5):351–356.
• Dennis DT, Inglesby TV, Henderson DA, et al. Tularemia as a biological weapon: medical
and public health management. JAMA. 2001;285:2763-2773.
• Franz DR, Jahrling PB, Friedlander AM, et al. Clinical recognition and management of
patients exposed to biological warfare agents. JAMA. 1997:278; 399–411.
• Fritz SB, Singer AM, Revan VB, et al. Bioterrorism: relevance to allergy and immunology
in clinical practice. J Allergy Clin Immunol. 2002;109(2):214–228.
• Garner JS, Hospital Infection Control Practices Advisory Committee. Guideline for isolation
precautions in hospitals. Infect Control Hosp Epidemiol. 1996;17:53–80, and Am J Infect
Control. 1996;24:24–52.
• Henderson DA, Inglesby TV, Bartlett JG, et al. Smallpox as a biological weapon: medical
and public health management. JAMA. 1999;281:2127–2137.
• Inglesby TV, Henderson DA, Bartlett JG, et al. Anthrax as a biological weapon: medical and
public health management. JAMA. 1999;281:1735–1745.
• Inglesby TV, Dennis DT, Henderson DA, et al. Plague as a biological weapon: medical and
public health management. JAMA. 2000;283:2281–2290.
• Kadlec RP, Zelicoff AP, Vrtis AM. Biologic weapons control: prospects and implications
for the future. JAMA. 1997;288:351–356.
• Kolavic SA, Kimura A, Simons SL, et al. An outbreak of Shigella dysenteriae Type 2
among laboratory workers due to intentional food contamination. JAMA.
1997;278:396–398.
• McGovern TW, Christopher GW, Eitzen EM. Cutaneous manifestations of biological
warfare and related threat agents. Arch Derm. 1 999;135(3):311–322.
• Meffert, JJ. Biological warfare from a dermatologic perspective. Curr Allergy Asthma Rep.
2003; 3:304–310.
• National Child Traumatic Stress Network. Resources for Parents and Caregivers. Available
at: http://www.nctsnet.org/nccts/nav.do?pid=ctr_aud_prnt. Accessed July 13, 2006.
• Noah DL, Huebner KD, Darling RG, et al. The history and threat of biological warfare and
terrorism. Emerg Med Clin No Am. 2002;20:255–271.
• Olson KB. Aum Shinrikyo: once and future threat? Emerg Infect Dis.
1999;5(4):513–516.
• Patt HA, Feign RD. Diagnosis and management of suspected cases of bioterrorism: a
pediatric perspective. Pediatrics. 2002;109(4);685–692.
• Public Health Security and Bioterrorism Preparedness and Response Act of 2002.
Washington, DC: U.S. Congress; 2002. Available at:
http://www.fda.gov/oc/bioterrorism/PL107-188.html.
Accessed August 17, 2006.
86
• Roffey R, Tegnell A, Elg HF. Biological warfare in a historical perspective. Clin Microbiol
Infect. 2002;8:450–454.
• Rotz LD, Khan AS, Lillibridge SR. Public health assessment of potential biological
terrorism agents. Emerg Infect Dis [serial online] 2002 Feb;8(2). Available at:
http://www.cdc.gov/ncidod/eid/vol8no2/01-0164.htm. Accessed August 17, 2006.
• Török TJ, Tauxe RV, Wise RP, et al. A large community outbreak of salmonellosis caused
by intentional contamination of restaurant salad bars. JAMA.
1997;278:389–395.
• Treadwell TA, Koo D, Kurer K, et al. Epidemiologic clues to bioterrorism. Pub Health Rep.
2003; 18:92–98.
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
Patient with
Acute, Generalized
Vesicular or Pustular Rash Illness
Institute Airborne & Contact Precautions
Alert Infection Control on Admission
Low Risk for Smallpox                                       Moderate Risk of Smallpox                             High Risk for Smallpox
(see criteria below)                                           (see criteria below)                               (see criteria below)
History and Exam                        Diagnosis                          ID and/or Derm Consultation                        ID and/or Derm Consultation
Highly Suggestive                       Uncertain                            VZV +/- Other Lab Testing                             Alert Infx Control &
of Varicella                                                                    as indicated                               Local and State Health Depts
Varicella Testing                      Test for VZV             Non-Smallpox                       No Diagnosis Made            Smallpox Response Team
Optional                      and Other Conditions     Diagnosis Confirmed              Ensure Adequacy of Specimen         Collects Specimens and
as Indicated     Report Results to Infx Control           ID or Derm Consultant           Advises on Management
Re-Evaluates Patient
Cannot R/O Smallpox                 Testing at CDC
Contact Local/State Health Dept
NOT Smallpox         SMALLPOX
Further Testing
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             Inhalational anthrax
respiratory distress                              Pneumonic plague
Inhalational tularemia
Ricin
Aerosol exposure to Staphylococcal
enterotoxin B
Hantavirus
Exudative pharyngitis and cervical                Oropharyngeal tularemia
lymphadenopathy
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,        GI anthrax
hematemesis
Dermatologic
Vesicular rash† associated with fever,            Smallpox
headache, malaise
Painless ulceration progressing to black eschar   Cutaneous anthrax
Ulcer plus painful regional lymphadenopathy       Ulceroglandular tularemia
and influenza-like illness
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                        Escherichia coli O157:H7 and other
thrombocytopenic purpura                                     shiga toxin-producing E. coli
Shigella dysenteriae
Oliguria, renal failure                                      Viral hemorrhagic fever
Hantavirus
Other
Painful lymphadenopathy                                      Bubonic plague
Purulent conjunctivitis with preauricular or                 Oculoglandular tularemia
cervical lymphadenopathy
*   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
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)     Standard, droplet    Masks
Droplet (pneumonic form)
Tularemia      No                         Standard
Botulism       No                         Standard
Smallpox       Droplet and aerosol        Standard, airborne   Fitted N-95
infection isolation  Negative-pressure
room
Viral          Contact and droplet        Standard, contact,   Masks
hemorrhagic                               droplet
fevers
99
Table 4.3. Diagnostic procedures, isolation precautions, treatment, and postexposure prophylaxis for selected bioterrorist
agents in children
Agent                                                                 Incubation                                                                                                                                                                                                                                                                                                                                                                                                     Diagnostic                                                                                                                                 Isolation                                                                                                                                                                                                                                                                       Treatment                                                                                Postexposure                                                                                                                                                                                                                                                                                                                                                                          Comments
prophylaxis1
period                                                                                                                                                                                                                                                                                                                                                                                specimens and                                                                                                                                            precautions
procedures
Supportive                                                                                                                                                                                                                                                                    Protection from
Standard;
Alphaviruses                                                     2–10 days                                                                         CSF for viral
mosquito vectors
respiratory
(VEE, EEE, and                                                                                                                                                                                                                    isolation, antibody
precautions for
WEE)                                                                                                                                                                                                                                   detection in CSF
WEE virus
and acute and
convalescent serum
Ciprofloxacin2 or                                                                                                                                                                                                                                                                                                   Ciprofloxacin2,
Standard;
Anthrax                                                                                         1–60 days                                                                                                                                                                                                                                                                                                                                                                                        Gram stain of buffy                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Additional antimicrobial
doxycycline3;                                                                                                                                                                                                                                                                                 doxycycline3, or
contact for skin
coat, CSF, pleural                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               agents to be used for
amoxicillin5;
lesions
fluid, swab of skin                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             combine with one                                                                                                                                                                                                                                                                                                                                                                                                                    inhalational, GI, or
lesion; culture of                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           or two additional                                                                                                                                                                                                                                                                                                                                                                                                                       oropharyngeal disease
anthrax vaccine
blood, CSF, pleural                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         antimicrobial                                                                                                                                                                                                                                                                                                                                                                                                                               include rifampin,
fluid, skin biopsy                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    agents for                                                                                                                                                                                                                                                                                                                                                                                                                                      vancomycin, penicillin,
inhalational, GI, or                                                                                                                                                                                                                                                                                                                                                                                                                                         ampicillin,
oropharyngeal                                                                                                                                                                                                                                                                                                                                                                                                                                       chloramphenicol,
disease4                                                                                                                                                                                                                                                                                                                                                                                                                                                             imipenem, clindamycin,
and clarithromycin
Standard                                                 Supportive care;
Botulism                                                                      Foodborne:                                                                                                                                                                                                                                                  Toxin detection                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Type-specific antitoxin
mechanical
2 hr–8 days                                                                                                                                                                                                                                                                                                             from serum, feces,                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       should be administered
ventilation and
enema fluid, gastric                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         when possible; antitoxin
Inhalational:
parenteral nutrition
fluid, vomitus, or                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               prevents additional nerve
24–72 hr
may be required;
suspected food                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          damage but does not
equine botulism
samples; culture of                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          reverse existing paralysis
antitoxin given as
feces or gastric
soon as possible
sections; nerve
(CDC)6
conduction testing
Doxycycline3 and                                                                                                                                                                                                                                                                                  Doxycycline3 and
Brucellosis                                                 5–60 days                                          Culture of blood or                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Standard;                                                                                                                                                                                                                                                                                                                                                                                                                     TMP-SMX may
bone marrow; acute                                                                                                                                                                                                                                                                                                                          contact for                                                                                                                                                       rifampin; if                                                                                                                                                                                                                     rifampin                     substitute for rifampin
and convalescent                                                                                                                                                                                                                                                                                                                     draining skin                                                                                                                                                      younger than 8 yr                                                                                                                                                                                                                                                        with doxycycline
serum for antibody                                                                                                                                                                                                                                                                                                                lesions                                                                                                                                                                old, use TMP-SMX
testing
100
100
Table 4.3. Diagnostic procedures, isolation precautions, treatment, and postexposure prophylaxis for selected bioterrorist
agents in children, continued
Doxycycline3;
Plague           2–4 days      Culture or            Droplet        Streptomycin                           TMP-SMX is an
tetracycline3
fluorescent                          sulfate or                             alternative;
antibody staining of                 gentamicin sulfate;                    chloramphenicol for
doxycycline3 or
blood, sputum,                                                              meningitis
tetracycline3
lymph node
aspirate
Doxycycline3 or        Doxycycline3 or
Q fever          10–40 days    Acute and             Standard                                              Chloramphenicol is an
tetracycline3          tetracycline3
convalescent serum                                                          alternative for treatment
samples                                                                     or prophylaxis
Smallpox         7–19 days     Culture of            Airborne,      Supportive care        Vaccine if
pharyngeal swab of    contact                               administered
skin lesions                                                within 4 days
Standard       Supportive care        None available
Staphylococcal   3–12 hr       Serum, urine, and
enterotoxin B                  respiratory
secretions for toxin;
acute and
convalescent serum
for antibodies
Ricin            4–8 hr        Serum and/or          Standard       Supportive care;       Protective mask
respiratory                          gastric lavage and
secretions for                       cathartics if toxin is
enzyme                               ingested
immunoassay
Standard,
Viral            6–17 days     Culture and/or                       Ribavarin IV for
droplet, and
hemorrhagic                    antigen detection of                 Lassa fever; plasma
contact
fevers                         blood and other                      from convalescent
body tissues7;        precautions8   patients for
Argentinean
serum for acute and
hemorrhagic fever;
convalescent
supportive care
antibody detection
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Table 4.3. Diagnostic procedures, isolation precautions, treatment, and postexposure prophylaxis for selected
bioterrorist agents in children, continued
1
Prophylaxis should be administered only after consultation with public health officials and only in situations in which exposure is highly likely. The
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 younger than 18 yr but is
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 children younger than 8 yr, but
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 dissemination.
5
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 (weekends, nights,
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 about management and
diagnosis of suspected cases.
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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            Frequently abnormal in inhalational anthrax; may show signs of mediastinal
radiograph       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.
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Table 4.5. Postexposure prophylaxis for anthrax
Patient                                             Prophylactic treatment
Adults (including pregnant women and Ciprofloxacin 500 mg, PO, BID × 60 days or
immunocompromised people)            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
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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                   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
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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
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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.
109
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
110
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
111
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 gamma-
aminobutyric 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).
112
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.
113
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 auto-
injectors 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
114
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.
115
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.
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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
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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.
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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,
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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.
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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
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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
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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
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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.
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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.
127
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.
Bibliography
Introduction
•    American Academy of Pediatrics: Chemical and biological terrorism and its
impact on children; a subject review. Pediatrics. 2000;105:662–70.
•    Brennan RJ, Waeckerle JF, Sharp T, et al. Chemical warfare agents: emergency
medical and emergency public health issues. Ann Emerg Med. 1999;34:191–204.
•    Centers for Disease Control and Prevention. Emergency Preparedness and
Response. Chemical Agents. Available at:
www.bt.cdc.gov/agent/agentlistchem.asp. Accessed July 20, 2006.
•    Erickson TB. Toxicology: ingestions and smoke inhalation. In: Gausche-Hill M,
Fuchs S, Yamamoto L (eds). APLS The Pediatric Emergency Medicine Resource,
4th ed. American Academy of Pediatrics and American College of Emergency
Medicine. Subury, MA: Jones and Bartlett; 2004. p. 234–267.
•    Henretig FM, Cieslak TJ, Madsen JM, et al. The emergency department response
to incidents of biological and chemical terrorism. In: Fleisher GF, Ludwig S,
Henretig FM, ed. Textbook of Pediatric Emergency Medicine, 5th ed.
Philadelphia: Lippincott Williams & Wilkins; 2005.
•    Henretig FM. Biological and chemical terrorism defense: a view from the “front
lines” of public health. Am J Public Health. 2001;91:718–720.
•    Henretig FM, Cieslak TJ, Eitzen EM Jr. Biological and chemical terrorism. J
Pediatr. 2002;141:311–326.
•    Henretig FM, McKee MR. Preparedness for acts of nuclear, biological and
chemical terrorism. In: Gausche-Hill M, Fuchs S, Yamamoto L (eds). APLS The
Pediatric Emergency Medicine Resource, 4th ed. American Academy of
Pediatrics and American College of Emergency Medicine. Sudbury MA: Jones
and Bartlett; 2004. p. 568–591.
128
•  Kales SN, Christiani DC. Acute chemical emergencies. N Engl J Med.
2004;350:800–808.
•  Macintyre AG, Christopher GW, Eitzen E Jr, et al. Weapons of mass destruction
events with contaminated casualties: effective planning for health care facilities.
JAMA. 2000;283:242–249.
•  Okumura T, Takasu N, Ishimatasu S, et al. Report on 640 victims of the Tokyo
subway sarin attack. Ann Emerg Med. 1996;28: p.129–135.
•  Osterhoudt KC, Ewald, MB, Shannon M, Henretig FM. Toxicologic emergencies.
In: Fleisher GF, Ludwig S, Henretig FM (eds). Textbook of Pediatric Emergency
Medicine, 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2005.
•  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; 1999.
Nerve Agents
•  Amitai Y, Almog S, Singer R, et al. Atropine poisoning in children during the
Persian Gulf crisis. A national survey in Israel. JAMA. 1992;268:630–632.
•  Holstege CP, Kirk M, Sidell FR. Chemical warfare: nerve agent poisoning. Crit
Care Clin 1997;13:923–942.
•  Lee EC. Clinical manifestations of sarin nerve gas exposure. JAMA. 2003;
290:659–662.
•  McDonough JH Jr, Shih TM. Neuropharmacological mechanisms of nerve agent-
induced seizure and neuropathology. Neurosci Behav Rev. 1997;15:559–579.
•  Okumura T, Takasu N, Ishimatsu S, et al. Report on 640 victims of the Tokyo
subway sarin attack. Ann Emerg Med. 1996;28:129–135.
•  Rotenberg JS, Newmark J. Nerve agent attacks on children: diagnosis and
management. Pediatrics. 2003; 112:648–658.
•  Sidell FR, Borak J. Chemical warfare agents: II. nerve agents. Ann Emerg Med.
1992;21:865–871.
•  Sofer S, Tal A, Shahak E. Carbamate and organophosphate poisoning in early
childhood. Pediatr Emerg Care. 1989;5:222–225.
•  US Army Medical Research Institute of Chemical Defense. Medical Management
of Chemical Casualties-Handbook. Aberdeen Proving Grounds, MD: US Army
Medical Research Institute of Chemical Defense; 1999.
Cyanide
•  Berlin CM. The treatment of cyanide poisoning in children. Pediatrics.
1970;46:793–796.
•  Beasley DMG, Glass WI. Cyanide poisoning: pathophysiology and treatment
recommendations. Occup Med. 1998;48:427–431.
•  Sauer SW, Keim ME. Hydroxocobalamin: improved public health readiness for
cyanide disasters. Ann Emerg Med. 2001;37;635–641.
•  Kerns W II, Isom G, Kirk MA. Cyanide and Hydrogen Sulfide. In: Goldfrank LR,
Flomenbaum NE, Lewin NA, Howland MA, Hoffman RS, Nelson LS (eds):
129
Goldfrank’s Toxicologic Emergencies, 7th ed. Norwalk, CT: Appleton & Lange;
2002. p.1498–1510.
•  Rotenberg JS. Cyanide as a weapon of terror. Pediatr Annals 2003;32:236–240.
•  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:
Committee on Treatment of Gas Casualties, National Research Council; 1945:
51–60.
•  Central Intelligence Agency. Unclassified Report to Congress on the Acquisition
of Technology Relating to Weapons of Mass Destruction and Advanced
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.
130
•  Gray EA, Love JW, Arnold JL. CBRNE—Lung-damaging Agents, Phosgene. In:
eMedicine: Emergency Medicine (Textbook Online). St. Petersburg, FL:
WebMD; June 13, 2006.
•  Grimaldi JV and Gugliotta G. Chemical plants are feared as targets: views differ
on ways to avert catastrophe. The Washington Post. December 16, 2001:A1.
•  Henretig FM, Cieslak TJ, Madsen JM, et al. The Emergency Department
Response to Incidents of Biological and Chemical Terrorism. In: Fleisher GR,
Ludwig S, Henretig FM, eds. Textbook of Pediatric Emergency Medicine, 5th ed.
Philadelphia: Lippincott Williams and Wilkins, 2005.
•  Noltkamper D, O’Malley GF. CBRNE—Lung-damaging Agents, Chlorine. In:
eMedicine: Emergency Medicine. (Textbook Online). St. Petersburg, FL:
WebMD.
•  Organization for the Prohibition of Chemical Weapons. Chemical Weapons
Convention. Available at: http://www.opcw.org/html/glance/index.html.
•  Sidell FR and Franz DR. Overview: Defense Against the Effects of Chemical and
Biological Warfare Agents. In: Sidell 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.
•  Urbanetti JS. Toxic Inhalational Agents. In: Sidell 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.
Riot Control Agents
•  Billmire DF, Robinson NB, Panitch HB, et al. Pepper-spray induced respiratory
failure treated with extracorporeal membrane oxygenation. Pediatrics.
1996;98:961–963.
•  Park S, Glammons ST. Toxic effects of tear gas on an infant following prolonged
exposure. Amer J Dis Child. 1972;123:245–247.
•  Sidell FR. Riot Control Agents. In: Sidell FR, Takafuji ET, Franz DR, eds.
Textbook of Military Medicine: Medical Aspects of Chemical and Biological
Warfare. Washington DC: Office of the Surgeon General, Walter Reed Army
Medical Center; 1997. 450–476.
•  Smith J, Greaves I. The use of chemical incapacitant sprays: a review. J Trauma.
2002;52:595–600.
•  Weir E. The health impact of crowd-control agents. CMAJ. 2001;164:1889–1890.
131
Table 5.1.       Pediatric vulnerabilities to chemical terrorism
Realm                    Potential vulnerability                     Potential response
Physiologic        Increased respiratory exposure (higher          Early warning, sheltering* (gas
minute ventilation, live “closer to the         masks not advised because of
ground)                                         risk of poor fit, suffocation)
Increased dermal exposure (thinner, more        Protective clothing, early
decontamination1
permeable skin; larger body surface
area/mass ratio)
Increased risk of dehydration, shock with       Recognition, aggressive fluid
illness-induced vomiting, diarrhea              therapy
(decreased fluid reserves, larger body
surface area/mass ratio)
Increased risk of hypothermia during            Warm water decontamination
decontamination (larger body surface
area/mass ratio)
More fulminant disease; (possible)              Pediatric-specific research for
physiologic detoxification immaturity; more     early diagnosis and treatment
of chemical weapons victims1
permeable blood-brain barrier
Developmental      Less ability to escape attack site, take        ?
appropriate evasive actions (developmental
immaturity, normal dependence on adult
caregivers who might be injured or dead)
Psychological      Less coping skill of children who suffer        Child psychiatry involvement,
injury or witness parental, sibling death       research for preventing
(psychological immaturity)                      pediatric post-traumatic stress
disorder1
Greater anxiety over reported incidents,        Pediatric counseling of parents
and children†
hoaxes, media coverage, etc
EMS                Less capacity to cope with influx of critical   Community and regional
pediatric patients                              planning with significant
pediatric input
Loss of routine hospital transfer protocols
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.
132
Table 5.2.    Chemical weapons – Summary of pediatric management considerations
Decontamination*                        Management
Agent        Toxicity        Clinical findings       Onset
Nerve Agents
ABCs
Vapor: fresh air,
Vapor: miosis,
Anticholinesteras                      Vapor:
Tabun
Atropine: 0.05 mg/kg IV†, IM‡ (min 0.1 mg,
remove clothes, wash
rhinorrhea, dyspnea  seconds
e: muscarinic,
Sarin
hair
Liquid: diaphoresis,
nicotinic, and                                                                  max 5 mg), repeat q2–5 min prn for marked
Liquid:
Soman
Liquid: remove
vomiting             minutes-
CNS effects                                                                     secretions, bronchospasm
VX
clothes, copious
Both: coma,          hours                                    Pralidoxime: 25 mg/kg IV, IM (max 1 g IV; 2 g
washing of skin and
paralysis, seizures,                                          IM), may repeat within 30–60 min prn, then
hair with soap and
apnea                                                         again every hour for 1 or 2 doses prn for
water, ocular irrigation persistent weakness, high atropine requirement
Diazepam: 0.3 mg/kg (max 10 mg) IV;
lorazepam: 0.1 mg/kg IV, IM (max 4 mg);
midazolam: 0.2 mg/kg (max 10 mg) IM prn for
seizures or severe exposure
Vesicants
Mustard    Alkylation                             Hours                                    Symptomatic care
Skin erythema,                       Wash skin with soap
vesicles, ocular                     and water, ocular
Lewisite   Arsenical                              Immediate                                Possibly BAL 3 mg/kg IM q4–6hr for systemic
inflammation,                        irrigation (major
pain                                     effects in severe cases
respiratory tract                    impact only if done
inflammation                         within min of
exposure)
Pulmonary Agents
Fresh air, wash skin  Symptomatic care
Minutes: eyes,
Chlorine   Liberate HCL,     Eyes, nose, throat
with water
nose, throat
Phosgene   alkylation        irritation
irritation;
(especially
bronchospasm
chlorine);
Hours:
bronchospasm,
pulmonary
pulmonary edema
edema
(especially
phosgene)
133
Table 5.2.        Chemical weapons – Summary of pediatric management considerations, continued
Cyanide
Cyanide        Cytochrome          Tachypnea, coma,        Seconds        Fresh air, wash skin  ABCs, 100% oxygen
oxidase             seizures, apnea                        with soap and water   Sodium bicarbonate prn for metabolic acidosis
inhibition:                                                                      Sodium nitrite (3%):
cellular anoxia,                                                                     Dosage (mL/kg) Estimated Hgb (g/dL)
lactic acidosis                                                                         0.27               10
0.33               12 (est. for avg. child)
0.39               14 (max 10 mL)
Sodium thiosulfate (25%): 1.65 mL/kg (max 50
mL)
Riot Control Agents
Seconds        Fresh air, ocular     Topical ophthalmics, symptomatic care
Ocular pain,
Neuropeptide
CS
irrigation
tearing,
substance P
CN (eg,
Mace®)                             blepharospasm;
release;
nose and throat
Capsaicin alkylation
irritation;
(pepper
pulmonary failure
spray)
(rare)
* Should be performed by health care providers garbed in adequate personal protective equipment, especially if victims have had significant
exposure to nerve agents or vesicants. For emergency department staff, adequate PPE consists of a non-encapsulated, chemically resistant body
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 = as needed
Adapted from Henretig FM, Cieslak TJ, Eitzen EM Jr. Biological and chemical terrorism. J Pediatr 141:311-326 © 2002, with permission from
Elsevier.
134
Table 5.3                                                                                                                                                                                                                                    Representative classes of industrial chemicals – Summary of pediatric management considerations
Agent                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Clinical findings                                                                 Onset                                                                                                                                                                                                                                                                                                                                                                          Decontamination                                                                                                                                                                                                                                                                                                            Management
Supportive care, early endoscopy for
Rapid                                                                  Eye, skin: immediate
Strong acids/bases                                                                                                                                                                                                                                                                                                                 Eye: caustic injury
significant ingestion; antibiotics and steroids
copious water irrigation
Skin: chemical burns
controversial, should be individualized, consult
GI: defer, immediate
GI: chemical burns of mouth,
Poison Control Center*
emergency department
larynx, esophagus, stomach
referral
Rapid                                                                                                                                                                                                                                                                                                                                                                                                                  Move to fresh air                                                                                                                                                                                                                                                                                                                            Supportive respiratory care (consider nebulized
Respiratory tract                                                                                                                                                                                                                                                                                                                                                                                                EENT and respiratory tract
calcium gluconate solution for HF, consult
irritants (e.g.,                                                                                                                                                                                                                                                                                                                                                                                                          irritation with cough, chest
Poison Control Center)
ammonia, HCl and                                                                                                                                                                                                                                                                                                                                                                                                                      pain, dyspnea, wheeze
HF gases)                                                                                                                                                                                                                                                                                                                                                                                                                                  (possible pulmonary edema in
severe cases)
Supportive care, naloxone (0.01-0.1 mg/kg)
Fentanyl and other                                                                                                                                                                                                                                                                                                                                                                                                                                                          CNS and respiratory                                                                                                                                                                                                                                                   Rapid                                                                                                                                                       Move to fresh air (for
opioids                                                                                                                                                                                                                                                                                                                                                                                                                                                                      depression, miosis                                                                                                                                                                                                                                                                                                                                                                                                                   aerosol exposure),
consider AC for
ingestion, consult Poison
Control Center
Airway, breathing, and circulatory support;
Move to fresh air
Rapid
Cellular asphyxiants                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Cough, dyspnea, headache,
100% oxygen
(consider AC for
(except
(e.g., phosphine,                                                                                                                                                                                                                                                                                                                                                                                                                                                                            dizziness, vomiting,
ingested sodium azide—
pulmonary
sodium azide)                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   tachycardia, hypotension,
caution with vomitus,
edema with
severe metabolic acidosis;
which may emit toxic
phosphine)
may progress to coma,
hydrazoic acid fumes;
seizures, death; may have
consult Poison Control
delayed onset pulmonary
Center)
edema with phosphine
Arsine                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Severe hemolysis                                                                  2–4 hr                                                                                                                                                                                                                                                                                                                                                                         Move to fresh air                                                                                                                                                                                                                                                                                                          Supportive care, enhance urine flow, consider
alkalinization, consult Poison Control Center
* Contact Poison Control Center at 1-800-222-1222.
Note: EENT = eye, ear, nose, a