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PHTLS_ Prehospital Trauma Life Support 8TH

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PHTLS_ Prehospital Trauma Life Support 8TH

PHTLS_ Prehospital Trauma Life Support 8TH

518 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

BOMB THREAT STAND-OFF CHART ~ I

Threat Description Explosives Outdoor
Capacity1 (TNT Evacuation
Improvised Explosive Device (IED) Distance3
Equivalent)
I Pipe Bomb 1200 FT
5 LBS

&CL Suicide Bomber 20 LBS 1700 FT
Bri efc ase/ S u itc a s e 50 LBS 1850 FT

Ca r 500 LBS 1500 FT

SUVNan 1,000 LBS 2400 FT
4,000 LBS 3800 FT
Small Moving Van/ 10,000 LBS 5100 FT
Delivery Truck 60,000 LBS 9300 FT
Moving Van/
Water Truck

Semi-Trailer

1. These capacities are based on the maximum weight of explosive material that could reasonably fit in a container of similar size.
2. Personnel in buildings are provided a high degree of p rotection from death or serious injury; however, glass breakage and building debris may
still cause some inj uries. Unstrengthened buildings can be expected to sustain damage that approximates five percent of their replacement cost.
3. If personnel cannot enter a building to seek shelter they must evacuate to the minimum distance recommended by Outdoor Evacuation
Distance.These distance 1s governed by the greater hazard of fragmentation distance, glass breakage or threshold for ear d rum rupture.

Figure 20-6 Explosives Safe Distance Stand-off Chart.

Source: Courtesy of U.S. Department of Homeland Security.

(2) rapid comp ression of and subsequent re-expansion of gas- cause cerebral or cardiac embolic complications. Damage to the
filled structures, and (3) reflection of the wave at the tissue-gas bowel may include petechiae or hematomas of the bowel wall
interface. Depending on the proximity of the victim to the explo- or even perforation of the bowel. Tympanic membrane rupture
sion, as well as shielding from or augmentation to the shock or disruption of the middle ear ossicles also may occur. Loss of
wave ifthe explosion occurs in a closed space, a victim may suf- hearing is common after an explosion and may be temporary or
fer primary blast injury. p er ma nent.

Shear waves are transverse waves with a lower velocity Evidence of primary blast injury to the lung (or blast lung
and longer duration that cause asynchronous movement of tis- injury) is found more often in patients who die minutes after
sues. The degree of damage depends on the extent to which the explosion from associated injuries than those who survive;
the asynchronous motions overcome inherent tissue elasticity, however, pulmonary primary blast injury has been noted with
resulting in tearing of tissue and possible disruption of attach- greater frequency among surviving victims of confined-space
ments. However, muscle, bone, and solid-organ injury are much explosions.21-23 Primary blast injury has also been associated
more likely to result from the tertiary and quaternary effects of with other severe injuries and is indicative of increased mortality
the explosion than from the shock wave alone. 19•20 risk in survivors of the initial event. After an open-air explosion
in Beirut , only 0.6% of survivors had evidence of primary blast
Primary blast injury occurs in gas-filled organs such as the injury, and 11% of those died.13 In a confined-space explosion in
lung, bowel, and middle ear. The injury to the tissue occurs at Jerusalem, 38%ofsurvivors had evidence of primary blast injury,
the gas-fluid interface, presumably from a rapid compression with a similar mortality rate of approximately g<>,.-6.24 Similarly,
of the gas in the organ, causing violent collapse of that organ, two of the three bombs that were detonated in the London sub-
followed by an equally rapid and violent expansion, resulting way system exploded in wide tunnels, resulting in six and seven
in tissue injury. Damage to the lung manifests as pulmonary fatalities, respectively. The third device det onated in the subway
contusions, or possibly hemopneumothoraces, resulting in system was exploded in a narrow tunnel, causing 26 fatalities.
hypoxemia if the patient does not immediately succumb to the This difference in mortality between open- and closed-space
injuries (Figure 20-8). The alveolar-capillary interface can also bombings results from the reflection of the blast wave back onto
become disrupted, resulting in arterial gas emboli, which may

CHAPTER 20 Explosions and Weapons of Mass Destruction 519

Primary Direct blast effects (over- and • Contact of blast • Tympanic membrane
underpressurization) shockwave w ith body rupture

• Stress and shear waves • Blast lung
occurring in tissues • Eye injuries
• Concussion
• Waves reinforced/reflected
at tissue density interfaces

• Impact with gas-filled
organs (lungs, ears, etc.),
which are at particular risk

Secondary Projectiles propelled by Ballistic wounds produced • Penetrating injuries
explosion by: • Traumatic amputations
• Lacerations
• Primary fragments (pieces • Concussion
of exploding weapon)

• Secondary fragments
(environmental fragments
[e.g., glass])

Tertiary Propulsion of body onto • Whole-body translocation • Blunt injuries
hard surface or object, or • Crush injuries caused by • Crush syndrome
propulsion of objects onto • Compartment syndrome
individuals structural damage and • Concussion
building collapse

Quaternary Heat and/or combustion • Burns and toxidromes • Burns
fumes from fuel and metals • Inhalation injury
• Asphyxiation
• Septic syndromes from
soil and environmental
contamination

Qui nary Additives such as radiation Contamination of tissue • Variety of health effects,

or chemicals (e.g., dirty from: depending on agent

bombs) • Bacteria, radiation, or

chemical agents

• Allogeneic bone fragments

~~~ ~~~

Source: Data from Department of Defense Diredive: Medical Research for Prevention, Mitigation, and Treatment of Blast Injuries. Number 6025.21 E. http://www.dtic.miV

whs/diredives/corres/pdf/602521p.pdf. Accessed April 19, 2014

the victims rather than the dispersal of the blast wave into the rupture 50% of exposed tympanic membranes (approximately
surrounding area. 5 psi) can briefly generate blast winds of 145 miles per hour
(233 lan per hour). Blast winds associated with an overpres-
Secondary Blast Injury sure resulting in significant primary blast injury may exceed
831 miles per hour (1,337 lan per hour).18 Although brief in
Secondary blast injury is caused by flying debris and bomb duration, these blast winds can propel debris with great force
fragments. Secondary blast injury (fragment [fragmentation] and for great distances, causing both penetrating and blunt
injury or secondary injury) is the most common category of trauma.
injury in terrorist bombings and low explosions. These pro-
jectiles may be components of the bomb itself, as in military Tertiary Blast Injury
weapons designed to fragment, or may be parts of improvised
bombs augmented with nails, screws, and bolts. Secondary Tertiary blast injury is caused by the blast wind throwing the
blast injury is also caused by debris that is carried by the blast victim's body, resulting in tumbling and collision with station-
wind. The force required to create enough overpressure to ary objects. This can result in the whole spectrum of injuries

5 2 0 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Figure 20-8

Current patterns in worldwide terrorist activity have and consider ot her hazards t hat may have resulted as a
increased the potential for casualties related to explosions, consequence of the primary explosion. Patient assessment
yet few civilian prehospital care providers in the United and management steps are as follow s:
States have experience treating patients w ith explosion- • Initial triage, trauma resuscitation, and t ransport of
related injuries. Blast lung injury (BU) presents unique
triage, diagnostic, and management challenges and is a patients should follow standard protocols for multiple
direct consequence of the blast wave from high-explosive injured patients or mass casualties, including assessment
detonations upon the body. Persons in enclosed space and t reatment of the ABCDEs (airway, breathing,
explosions or those in close proximity to the explosion are circulation, disability, and expose/environment) and
at a higher risk. BLI is a clinical diagnosis characterized by immediate control of exsanguinating hemorrhage.
respiratory difficulty and hypoxia. BU can occur, although • Note t he patient's location and the surrounding
rarely, without obvious external injury to the chest. environment. Explosions in a confined space result in a
higher incidence of primary blast injury, including lung
Clinical Presentation injury.
• Symptoms may include dyspnea, hemoptysis, cough, and • All patients with suspected or confirmed BU should
receive supplemental high-flow oxygen sufficient to
chest pain . prevent hypoxemia.
• Signs may include tachypnea, hypoxia, cyanosis, apnea, • Impending airway compromise requires immediate
intervention.
wheezing, decreased breath sounds, and hemodynamic • If vent ilatory failure is imminent or occurs, patients
instability. should be intubated; however, prehospital care providers
• Victims with greater than 10% body surface area burns, must realize that mechanical ventilation and positive
skull fractures, and penetrating torso or head injuries may pressure may increase the risk of alveolar rupture,
be more likely to have BU. pneumothorax, and air embolism in BU patients.
• Hemothoraces or pneumothoraces may occur. • High-flow oxygen should be administered if air embolism
• Due to tearing of the pulmonary and vascular t ree, air is suspected, and the patient should be placed in a prone,
may enter the arterial ci rculation (air embo/1) and result semileft lateral, or left lateral position.
in embolic events involving the central nervous system, • Clinical evidence of or suspicion for a hemothorax
retinal arteries, or coronary arteries. or pneumothorax warrants close observation . Chest
• Clinical evidence of BU is typically present at t he time of decompression should be performed for patients
initial evaluation; however, it has been reported to occur clinically presenting with a tension pneumothorax. Close
over the course of 24 to 48 hours after an explosion. observation is warranted for any patient with suspicion of
• Other injuries are often present. BU who is transported by air.
• Fluids should be administered judiciously, as
Prehospital Management Considerations overzealous fluid administration in the patient w ith BU
Wh ile scene safety is always a major consideration for may result in volume overload and the worsen ing of
prehospital care providers, incidents such as these often pulmonary status.
requ ire emergency responders of all types to enter • Patients with BU should be transported rapidly to
the scene before it can be declared completely secure. the nearest, appropriate facility, in accordance w ith
Prehospital care providers must remain aware of their community response plans for mass-casualty events.
surroundings, be observant for possible additional devices,

Source: Data from Centers for Disease Control and Prevention, Atlanta.

associated with blunt trauma and even penetrating trauma, such trauma from structural collapse, septic syndromes from soil, and
as an impalement. environmental contamination.

Quaternary and Quinary Effects The increasing threat of radiation-, chemical-, or biologic-
enhanced explosives (i.e., "dirty bombs") has given rise to a fifth
Following the blast itself, quaternary effects may be seen.17 (quinary) category of effects, which includes injuries caused by
These injuries include burns and toxicities from fuel, metals, radiation, chemicals, or biologic agents and projectiles such as
bone fragments of a suicide bomber.25•26

CHAPTER 20 Explosions and Weapons of Mass Destruction 521

Injury Patterns Evaluation and Management

The prehospital care provider will be confronted with a combi- The general evaluation and management of trauma victims are
nation of familiar penetrating, blunt, and thermal ir\jwies and applicable to the casualty from a WMD and are addressed in
possibly survivors with primary blast ir\jury.27 The numbers and other chapters. Unique to this patient population, however, is
types of ir\jury will depend on multiple factors, including explo- the possibility of primary blast injury. Primary blast injuries
sion magnitude, composition, environment, and location and might increase the likelihood that prehospital care providers
number of potential victims at risk. will encounter patients with hemoptysis and pulmonary contu-
sions, pneumothorax or tension pneumothorax, or even arte-
Various mortality rates have been associated with different rial gas embolism. Among survivors of primary blast ir\jury,
types of bombing. One study that examined terrorist bombings clinical manifestations may be present immediately31•32 or may
showed that 1 of 4 victims died immediately after structural- have a delayed onset of 24 to 48 hours.33 Intrapulmonary hem-
collapse bombings, 1 of 12 died immediately in closed-space orrhage and focal alveolar edema result in frothy bloody secre-
bombings, and 1 of 25 died immediately after open-space bomb- tions and lead to ventilation-perfusion mismatch, increased
ings.15·28 Additional studies have found that mortality is higher intrapulmonary shunting, and decreased compliance. Hypoxia
when an explosion occurs in an enclosed space.29•30 Soft-tissue results, with increased work of breathing, pathophysiologi-
ir\jwies, orthopedic trauma, and traumatic brain ir\jury are pre- cally similar to pulmonary contusions induced by other mecha-
dominant among survivors (Figure 20-9). nisms ofnonpenetrating thoracic trauma.34 The presence of rib
fractures should increase suspicion of tertiary or quaternary
For example, of592 survivors ofthe Oklahoma City bomb- injury to the thorax.
ing, 85% had soft-tissue injuries (lacerations, puncture wounds,
abrasions, contusions), 25% had sprains, 14% had head inju- Primary blast ir\jwies are not immediately apparent, and,
ries, 10% had fractures/dislocations, 10% had ocular injuries (9 therefore, care at the scene should include (1) monitoring for
with ruptured globes), and 2% had burns.10 The most common frothy secretions and respiratory distress, (2) sequential oxygen
location for soft-tissue injury was the extremities (74%), fol- saturation (Sp02) measurements, and (3) provision of oxygen.
lowed by head and neck (48%), face (45%), and chest (35%). Decreased Sp02 is a "red flag" for early blast lung ir\jury even
Eighteen survivors had severe soft-tissue injwies, including before symptoms begin. Fluid administration must be carefully
carotid artery and jugular vein lacerations, facial and popliteal managed, with care taken to avoid fluid overload.1
artery lacerations, and severed nerves, tendons, and ligaments.
Seventeen survivors had serious internal organ injury, includ- The likelihood of multi.system trauma is increased in bomb
ing partial bowel transection, lacerated kidney, spleen, and victims.35 The management principles for these patients are sim-
liver, pneumothorax, and pulmonary contusion. Of patients ilar to those for trauma from other mechanisms.
with fractures, 37% had multiple fractures. Of those diagnosed
with a head injury, 44% required admission to the hospital.3° Transport Considerations

Figure 20-9 Patients requiring transport must be brought to an appropriate
medical treatment facility for further evaluation and manage-
• Most wounds are noncritical soft-tissue or skeletal ment. These patients will often require the services of a desig-
injuries. nated trauma center. Prehospital care providers should be aware
of the epidemiology of patient transport after an explosives
• Head injury predominates among casualties who die event. Patient arrival at hospitals is usually bimodal, with ambu-
(50%-70%). latory patients arriving first and more critically ill patients arriv-
ing later by ambulance.
• Most head injury survivors (98.5%) have noncritical
injuries. This bimodal patient transport was demonstrated in the
Oklahoma City bombing. Patients began to arrive in the EDs
• Head injuries are disproportionate to exposed total 5 to 30 minutes after the bombing, with patients more seriously
body surface area. ir\jured taking longer to arrive. Also, the geographically closest
hospitals in Oklahoma City received the majority of victims,
• Most casualties with blast lung injury die immediately. as seen with other disasters. Nearby hospitals that are over-
• Survivors have a low incidence of abdominal and whelmed by the first wave of patients may experience some
difficulty managing the critically ill patients that arrive in the
chest wounds, burns, traumatic amputations, and second wave. In Oklahoma City, the aggregate peak arrival rate
blast lung injury, although specific mortalities are of patients to EDs was 220 per hour at 60 to 90 minutes; 64%
high (10%-40%). of patients visited EDs within a 1.5-mile radius of the event.
Prehospital care providers should consider this latter fact when
Source: Data from Frykberg ER, Tepas JJ Ill: Terrorist bombings: lessons learned determining the destination of patients transported by ambu-
from Belfast to Beirut, Ann Surg 208:569, 1988. lance from the bomb scene.1

5 2 2 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Incendiary Agents Chemical Agents

Incendiary agents are typically encountered in the military and Many scenarios could expose the prehospital care provider to
are used to burn equipment, vehicles, and structures. The three chemical agents, including an industrial complex accident, a
incendiaries most often recognized are thermite, magnesium, spilled tanker truck or railway car, unearthed military ordnance,
and white phosphorus. All three are highly flammable com- or a terrorist attack (Figure 20-10). The 1984 Union Carbide
pounds that burn at extremely high temperatures. industrial accident in Bhopal, India, and the sarin gas attack in
Tokyo in 1995 are examples of such incidents.

Thermite Physical Properties of Chemical
Agents
Thermite is powdered aluminum and iron oxide that burns furi-
ously at 3,600°F (l,982°C) and scatters molten iron.36 Its primary The physical properties of a substance are affected by its chemi-
mechanism of injury is partial-thickness or full-thickness burns. cal structure, the environmental temperature, and ambient pres-
The primary and secondary assessments are performed with sure. These factors will determine whether a substance exists
intervention directed at treating burns. Thermite wounds can be as a solid, liquid, or gas. Understanding the physical state of a
irrigated with copious amounts of water and any residual parti- chemical agent is important for the prehospital care provider
cles or material subsequently removed. because it gives clues as to the likely route of exposure and the
potential for transmission and contamination.
Magnesium
A solid is in a state of matter that has a fixed volume and
Magnesium is also a metal in powdered or solid form that burns shape; a powder is an example of a solid. When heated to its
furiously hot. In addition to its ability to cause partial-thickness melting point, solids become liquids. Liquids that are heated to
or full-thickness burns, magnesium can react with tissue fluid their boiling point become a gas. Solid particles and liquid parti-
and cause alkali burns. The same chemical reaction produces cles can become suspended in the air, similar to a dust particle
hydrogen gas, which can cause the wound to bubble or can result or a liquid mist. This is considered an aerosol. A vapor is sim-
in subcutaneous emphysema. Inhalation of magnesium dust can ply a solid or liquid that is in a gaseous state, but technically
produce respiratory symptoms, including cough, tachypnea, would be expected to be found as a solid or liquid at standard
hypoxia, wheeze, pneumonitis, and airway burns. Residual mag- temperature and pressure, defined as 32°F (0°C) and normal
nesium particles in a wound will react with water, so irrigation atmospheric pressure (1 atmosphere, 14.7 psi). Some solids and
is discouraged until the wounds can be debrided and the partic- liquids can, therefore, emit vapors at room temperature. The
ulates removed. If irrigation is required for other reasons, such process of solids emitting vapors, bypassing the liquid state, is
as decontamination of another suspected material, care should
be taken to ensure flushing or removal of magnesium particles Figure 20-10
from the wound.36

White Phosphorus • Cyanides (blood agents or asphyxiants)
• Hydrogen cyanide, cyanogen ch loride
White phosphorus (WP) is a solid that spontaneously ignites
when exposed to air, causing a yellow flame and white smoke. • Nerve agents
WP that comes in contact with skin can quickly result in • Tabun (GA), sarin (GB), soman (GD), cyclosarin
partial-thickness or full-thickness burns. WP can become (GF), VX
embedded in the skin, propelled by the blast of WP munitions.
The substance will continue to burn in the skin if exposed to • Lung toxicants (choking or pulmonary agents)
air. Prehospital care providers can decrease the likelihood of • Chlorine, phosgene, diphosgene, ammonia
combustion in the skin by immersing the affected areas in water
or applying saline-soaked dressings to the area. Oily or greasy • Vesicants (blistering agents)
dressings are avoided in these patients because WP is lipid sol-
uble, and application of these dressings may increase the like- • Mustard, lewisite
lihood of systemic absorption and toxicity. Copper sulfate has • Incapacitating agents
historically been used to neutralize WP and facilitate its removal
because the reaction results in a black compound, which is eas- • BZ (3-quinuclidinyl benzilate)
ier to identify in the skin. Copper sulfate has fallen out of favor, • Lacrimating agents (riot control agents)
however, because of complications from its use--specifically,
intravascular hemolysis (breakdown or rupture of red blood • CN, CS (tear gas agents), Oleoresin Capsicum
cells within blood vessels).37 (OC or pepper spray)

• Vomiting agents
• Adamsite

CHAPTER 20 Explosions and Weapons of Mass Destruction 5 2 3

called sublimation. The likelihood that solids or liquids vaporize Once the victim has been properly decontaminated, the pre-
into a gaseous form at room temperature is defined as the vola- hospital care provider will likely encounter patients with signs
tility of the substance. Highly volatile substances easily convert and symptoms of exposure to a hazardous substance that has
into a gas at room temperature. not yet been specifically identified. Victims of chemical agents
can manifest signs and symptoms of exposure that affect:
These physical properties have implications for primary
and secondary contamination and possible routes of exposure. • The respiratory system, affecting oxygenation and
Primary contamination is defined as exposure to the chemi- ventilation
cal agent at its point of release. For example, primary contam-
ination occurs, by definition, in the hot zone. Gases, vapors, • The mucous membranes, causing eye and upper airway
liquids, solids, and aerosols can all play a role in primary iajury
contamination.
• The nervous system, resulting in seizures or coma
Secondary contamination is defined as exposure to a • The gastrointestinal (GI) tract, causing vomiting or
chemical agent after it has been carried away from the point
of origin, whether by a victim, an emergency responder, or a diarrhea
piece of contaminated equipment or debris. Secondary con- • The skin, causing burning and blistering
tamination generally occurs in the warm zone, although it may
happen at more remote locations if the exposed victim is able It is important to evaluate the presenting signs and symp-
to self-evacuate. Solids and liquids (and sometimes aerosols) toms and whether they are improving or progressing. Patients
generally contribute to secondary contamination. Gases and with worsening clinical :findings likely had incomplete cleansing
vapors do not typically play a role in secondary contamination ofthe contaminant and should undergo repeat decontamination
because they cause iajury by inhalation of the substance and to assure complete removal.
do not deposit on skin. However, vapors can become trapped
in clothing and then off-gas to potentially expose others to the Patients will require a primary assessment to determine
hazard. what lifesaving intervention may be immediately required. A sec-
ondary assessment may then assist in the identification ofsymp-
Volatility plays a significant role in the risk of secondary tom constellations that might indicate the nature of the chemical
contamination. More volatile substances are considered "less agent and suggest a specific antidote. This constellation of clini-
persistent,n meaning that because they vaporize, the likelihood cal signs and symptoms suggesting exposure to a certain class of
of long-lasting physical contamination is unlikely. These chemi- chemical or toxin is called a toxidrome.39
cal agents will readily disperse and be carried away by the wind.
Less volatile substances are considered "more persistent." These The irritant gas toxidrome will include mucous membrane
substances do not vaporize, or do so at a very slow rate, thereby burning and inflammation, coughing, and difficulty breath-
remaining on exposed surfaces for a long time, increasing the ing. Agents responsible might include chlorine, phosgene, or
risk of secondary contamination. For example, the nerve agent ammonia.
sarin is a nonpersistent agent, whereas the nerve agent VX is a
persistent agent.38 The asphyxiant toxidrome is caused by cellular oxygen
deprivation. This can result from inadequate oxygen availability,
Personal Protective Equipment as in an oxygen-poor atmosphere; inadequate oxygen delivery to
the cells, as in carbon monoxide poisoning; or inability to utilize
PPE is selected based on the threat of exposure to the chemical oxygen at the cellular level, as in cyanide poisoning. Signs and
agent. Level A is appropriate for emergency responders entering symptoms include shortness ofbreath, chestpain, dysrhythmias,
the hot zone. syncope, seizures, coma, and death.

Evaluation and Management The cholinergic toxidrome is characterized by rhinorrhea,
respiratory secretions, difficulty breathing, nausea, vomiting,
After ensuring the safety of the scene, the prehospital care pro- diarrhea, profuse sweating, pinpoint pupils and possible altered
vider will first confirm that victims are undergoing decontami- mental status, seizures, and coma. Pesticides and nerve agents
nation. Patients with likely skin exposure to the liquid form of a can cause these cholinergic signs and symptoms.4o,41
chemical will require decontamination with water. If available,
soap may be used as well, but showering with copious amounts Most often, prehospital care providers will initiate
of water will generally suffice. Exposure to a gas only does not supportive therapy without knowing the specific chemical cause
mandate decontamination by shower, but does mandate removal of the iajury. If the offending agent is properly identified, or if
from any ongoing exposure as well as removal of any clothing its identity is suggested by the toxidrome or clinical presenta-
that may have trapped residual vapors, which can subsequently tion, therapy specific to the agent may be delivered. Cyanide and
off-gas and pose a hazard to care providers in the field or in the nerve agent victims are examples of patients who can benefit
hospital. from agent-specific antidote therapy.

Transport Considerations

Contaminated patients should not be transported until they
have been decontaminated. Transporting contaminated patients

5 2 4 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

results in cross-contamination of the transporting vehicle and The organs most affected are the central nervous system
personnel, thus taking them out of service until they have been (CNS) and the heart. Symptoms of mild cyanide poisoning
decontaminated. This leads to compromise ofthe response capa- include headache, dizziness, drowsiness, nausea, vomiting, and
bility of the ambulance service and may prolong the scene time mucosal irritation. Severe cyanide poisoning includes alteration
and management of ill or iajured patients. This same concern of consciousness, dysrhythmias, hypotension, seizures, and
about not transporting contaminated patients applies to air- death. Death can occur within a few minutes after inhalation of
medical services as well. high levels of cyanide gas.

Patients must be brought to an appropriate medical Management
treatment facility for further evaluation and management.
Transporting to the optimal facility is particularly important Supportive therapy is important, including high-con centration
because some chemical toxic effects may not become apparent oxygen delivery, correction of hypotension with fluids or vaso-
for 8 to 24 hours. Communities may identify preferred hospitals pressors, and management of seizures. Cyanide antidote kits
for the managem ent of ch emical casualties. These facilities may are available for patients with known or suspected cyanide
be more capable of managing these patients by virtue ofspecial- poisoning. The traditional cyanide antidote treatment involved
ized training or availability of critical care services and specific treatment with two medications, a nitrite followed by thiosul-
antidotes. Considerations similar to those previously noted for fate. The administration of inhaled amyl nitrite, or preferably
explosive incidents regarding transport epidemiology also apply intravenous (IV) sodium nitrite, creates methemoglobin (itself
to these patients. a poison that in high enough con centrations can kill) , which
binds cyanide in the bloodstream, making it less available to
Nearby EDs may become overwh elmed by ambulatory, poison the patient's cellular respiration. The nitrite is followed
self-evacuated, self-transported patients. Of the 640 patients by IV administration of sodium thiosulfate to assist th e body
presenting to one hospital in Tokyo after the sarin incident, in the conversion of cyanide t o harmless thiocyanate, which is
541 arrived without EMS assistance.42 Hospitals closest to excreted by the kidneys.
the event will likely receive the largest number of ambulatory
patients. These factors should be considered in determining the In late 2006, the U.S. Food and Drug Administration (FDA)
destination of patients transported via ambulance. approved the use of hydroxocobalamin for treatment of cyanide
poisoning. This medication has been used in Europe for over
Selected Specific Chemical Agents a decade for cyanide therapy. Hydroxocobalamin given intra-
venously binds with cyanide to form cyanocobalamin (vitamin
Cyanides B12), which is nontoxic. Hydroxocobalamin has become the pre-
ferred antidote for cyanide poisoning because it is easy to use, it
Most commonly, prehospital care providers might encounter involves a single medication administration instead of two, and
cyanides when responding to a fire in which certain plastics are it does not create an intermediate chemical that is itself a poison.
burning or in certain industrial complexes, where it is found in
large quantities and used in chemical syntheses, electroplating, Nerve Agents
mineral extraction, dyeing, printing, photography, and agricul-
ture, and in the manufacture of paper, textiles, and plastics. Nerve agents were originally developed as insecticides, but
However, cyanide has been inventoried in military stockpiles once their effects on humans were recognized, numerous dif-
and some terrorist websites have provided the instructions for ferent types were developed in the early to mid-1900s. These
making a cyanide dispersal device. deadly ch emicals can be found in the military stockpiles of
many nations. The most recent known use in a military conflict
Hydrogen cyanide is a highly volatile liquid and, thus, will was in the Syrian civil war in 2013. Nerve agents have also been
most often be en countered as a vapor or gas. Therefore, it has produced and used by terrorist organizations, the most notori-
greater potential for mass casualties in a confined space with ous releases occurring in Matsumoto, Japan, in 1994 and in the
poor ventilation than if released outdoors. Although a smell of Tokyo, Japan, subway system in 1995. Commonly available pesti-
bitter almonds h as been associated with this agent, this is not a cides (e.g., malathion, carbaryl [Sevin)) and common therapeutic
reliable indicator of hydrogen cyanide exposure. It is estimated drugs (e.g., physostigmine, pyridostigmine) share properties
that as much as 400Ai to 500Ai of the general population is incapable with nerve agents, causing similar clinical effects.
of detecting the odor of cyanide.
Nerve agents are usually liquids at room temperature. Sarin
Cyanide's mechanism of action is arrest of metabolism or is the most volatile of the group. VX is the least volatile and
respiration at the cellular level, quickly resulting in cell death. is found as an oily liquid. The main routes of intoxication are
Cyanide binds in the mitochondria of cells, preventing oxygen through inhalation of the vapor (usually the volatile or nonper-
usage in cellular metabolism. Victims of cyanide poisoning actu- sistent agents) and absorption through the skin (usually VX).
ally are able to inhale and absorb oxygen into the blood, but are Nerve agents can iajure or kill at very low doses. A single, small
unable to use it at the cellular level. Thus, patients who are venti- drop the size of a pinhead of VX, the most potent n erve agent
lating will present with eviden ce of acyanotic hypoxia.

CHAPTER 20 Explosions and Weapons of Mass Destruction 5 2 5

developed, placed on the skin could kill a victim. Because nerve patient complains of blurry or dim vision), shortness of breath,
agents are liquids, they pose a risk for secondary contamination excessive salivation and sweating, nausea, vomiting, abdominal
from cont.act with contaminated clothes, skin, and other objects. cramps, involuntary urination and defecation, muscle fascicula-
tions, confusion, seizures, flaccid paralysis, coma, respiratory
The mechanism of action of nerve agents is inhibition of the failure, and death.
enzyme acetylcholinesterase. This enzyme is necessary to inhibit
the action of acetylcholine. Acetylcholine is a neurotransmitter Management
that stimulat.es cholinergic receptors. These receptors are found
in smooth muscles, skeletal muscles, the CNS, and most exocrine Management of nerve agent poisoning includes decontamina-
(secretory) glands. Some ofthese cholinergic receptors are t.ermed tion (Figure 20-12), a primary assessment, administration of
muscarinic sites (because experimentally they are stimulated by antidotes, and supportive therapy. Ventilation and oxygenation
muscarine), mostly found in smooth muscles and glands. Others of the patient may be difficult because of bronchoconstriction
are termed nicotinic sites (because experimentally they are stimu- and copious secretions. The patient will likely require frequent
lat.ed by nicotine), mostly found in skeletal muscle. The mnemonic suctioning. These symptoms improve after the antidote is admin-
DUMBELS (diarrhea, urination, miosis, bradycardia, bronchor- istered. The three therapeutic drugs for the management of
rhea, bronchospasm, emesis, lacrimation, salivation, sweating) nerve agent poisoning are atropine, pralidoxime chloride, and
represents the constellation of symptoms associat.ed with the diazepam.
muscarinic effects ofnerve agent toxicity. The mnemonic MTWHF
(mydriasis [rarely seen], tachycardia, weakness, hypert.ension, Atropine is an anticholinergic drug that reverses most of
hyperglycemia, fasciculations) represents the const.ellation of the muscarinic effects of the nerve agent but has little effect
symptoms associat.ed with stimulation of nicotinic receptors on the nicotinic sit.es. Atropine is indicated for exposed victims
(Figure 20-11). The CNS effects, a result of both muscarinic and with pulmonary complaints. Miosis alone is not an indication for
nicotinic receptors, include confusion, convulsions, and coma atropine, and furthermore, atropine will not correct the ocular
abnormalities. Atropine is given according to local system proto-
The clinical effects depend on the dose and route of nerve cols. It is titrat,ed until the patient's ability to breathe or ventilate
agent exposure (inhalation or dermal) and whether the musca- is improved or there is drying of pulmonary secretions. In mod-
rinic or nicotinic effects predominate. Small amounts of vapor erat,e to severe exposures, it is not unusual to st.art with an initial
exposure primarily cause irritation to eyes, nose, and airways. dose of 4 to 6 milligrams (mg) and give as much as 10 to 20 mg of
Large amounts ofvapor exposure can quickly lead to loss of con- atropine over a few hours.
sciousness, seizures, apnea, and muscularflaccidity. Miosis (con-
strictedpupils) is the most sensitive marker ofexposure to vapor. Pralidoxime chloride (2-PAM chloride) is an oxime.
Symptoms of dermal exposure also vary according to dose and Pralidoxime works by uncoupling the bond between the nerve
time of onset. Small doses may not result in symptoms for up to agent and acetylcholinesterase, thereby reactivating the enzyme
18 hours. Fasciculations of the underlying muscles and localized and helping to reduce the effects of the nerve agent, primarily
sweating at the site of the skin exposure may occur, followed on nicotinic receptors. The oxime therapy needs to be initiated
by GI symptoms, nausea, vomiting, and diarrhea. Large dermal within minutes to a few hours of the exposure to be effective,
doses will result in onset of symptoms in minutes, with effects depending on the nerve agent released; otherwise, the bond
similar to a large vapor exposure. between acetylcholinesterase and the nerve agent will become
permanent ("aging"), delaying recovery of the patient.
Clinical symptoms of the nerve agents include rhinorrhea
(runny nose), chest tightness, miosis (pupil is pinpoint, and

Figure 20-11

The mnemonic DUMBELS (diarrhea, urination,
miosis, bradycardia, bronchorrhea, bronchospasm,
emesis, lacrimation, salivation, sweating) represents
the constellation of symptoms associated with the
muscarinic effects of nerve agent toxicity. The mnemonic
M1WHF(mydriasis [rarely seen], t achycardia, w eakness,
hypertension, hyperglycemia, fasciculations) represents
the constellation of symptoms associated with
stimulation of nicotinic receptors.

Figure 20-12 Decontamination from nerve agents.

Source:© Jones and Bartlett Learning. Photographed by Glen E. Ellman.

526 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Diazepam (Valium) is a benzodiazepine and anticonvulsant. Lung Toxicants
If patients develop seizures after significant exposure, benzodi-
azepine therapy is initiated to manage the seizures and help to Lung toxicants, including chlorine, phosgene, ammonia, sulfur
reduce the brain injury and other life-threatening effects associ- dioxide, and nitrogen dioxide, are present in numerous indus-
ated with status epilepticus. Diazepam given intramuscularly has trial manufacturing applications. Phosgene has been stockpiled
erratic absorption; therefore, the preferred route forpatients who for military applications and was the most lethal chemical war-
are actively seizing is intravenous if access is available. In addi- fare agent used in World War I.
tion, diazepam administration is recommended for all patients
with signs of severe nerve agent poisoning, whether or not they Lung toxicants that are chemical pulmonary agents may be
have begun to seize. There are no data in either humans or ani- gases, vapors, aerosolized liquids, or solids. The properties of the
mals for rectal administration of diazepam.43 Lorazepam (Ativan) agent influence its ability to cause injury. For example, aerosol-
has been studied in animal models and found to be less effec- izedparticles of2 micrometers (µm) or smaller readily access the
tive than diazepam.43 Midazolam (Versed), on the other hand, has alveoli of the lung, causing injury there, whereas larger particles
been shown to be effective in animal models and, in the future, are filtered out before reaching the alveoli. Water solubility of an
may become the first-line medication for nerve agent-induced agent also affects the injury pattern. Ammonia and sulfur diox-
seizures.44 ide, which are highly water soluble, cause irritation and injury
to the eyes, mucous membranes, and upper airways. Phosgene
All three of these medications are available and packaged and nitrogen oxides, which have low water solubility, tend to
as autoinjectors. Atropine and pralidoxime come packaged cause less immediate irritation and injury to the eyes, mucous
together in a single autoinjector called DuoDote (Figure 20-13). membranes, and upper airways, thus providing little warning to
The dose of atropine is 2. 1 mg, and the dose of pralidoxime is the victim and allowing for prolonged exposure to these agents.
600 mg. This autoinjector is intended for rapid intramuscular Prolonged exposure makes it more likely that the alveoli will be
injection in the event of a nerve agent exposure. Total dosage injured, resulting not only in upper-airway injury, but also in alve-
is determined by protocol and titration of these drugs to effect. olar collapse and noncardiogenic pulmonary edema. Moderately
In the past, the atropine and pralidoxime were supplied in indi- water-soluble agents, such as chlorine, can cause both upper air-
vidual autoinjectors marketed as the Mark-1 kit. These kits have way and alveolar irritation.
largely been supplanted by the single autoinjector containing
both antidotes. Diazepam for seizures is also available as an The mechanisms of injury vary among the lung toxicants.
autoinjector. Ammonia, for example, combines with the water in the mucous
membranes to form a strong base, ammonium hydroxide.
Chlorine and phosgene, when combined with water, produce
hydrochloric acid, causing injury to the tissues. Lung toxicants
are not systemically absorbed but compromise the victim by
damaging components of the pulmonary system, from the upper
airway to the alveoli.

The agents with high water solubility cause burning of the
eyes, nose, and mouth. Tearing, rhinorrhea, coughing, dyspnea,
and respiratory distress secondary to glottic irritation or laryn-
gospasm are possible. Bronchospasm can result in coughing,
wheezing, and dyspnea. Agents with low watersolubility, causing
injury to the alveoli, can immediately injure the alveolar epithe-
lium in the case of a large exposure, leading to death from acute
respiratory failure, or, with less massive exposure, can result in
a delayed onset (24 to 48 hours) of respiratory distress, second-
ary to development of mild noncardiogenic pulmonary edema
to fulrninant acute respiratory distress syndrome, depending on
the dose.

Figure 20-13 DuoDote. Management

Source: Courtesy of pfizer, Inc. Management of lung toxicants includes removal of the patient
from the offending agent, decontamination with copious irri-
gation (if solid, liquid, or aerosol exposure, especially for
ammonia), primary assessment, and supportive therapy, which
will likely require interventions to maximize ventilation and
oxygenation. Eye irritation can be managed with copious irri-
gation using normal saline. Contact lenses should be removed.
Expect to manage profuse airway secretions, which will

CHAPTER 20 Explosions and Weapons of Mass Destruction 527

require suctioning. Bronchospasm may respond to inhaled and respiratory tract. Unlike mustard, lewisite does not cause
beta-adrenergic agonists. Hypoxia will require correction with bone marrow suppression. Also unique to this agent is "lewisite
high-flow oxygen and possibly intubation with positive-pres- shock," the result of intravascular volume depletion secondary
sure ventilation . Prehospital care providers need to be pre- to capillary leak.
pared to encounter difficult airway management secondary
to copious secretions, inflammation of glottic structures, and As with sulfur mustard, prehospital management of these
laryngeal spasm. All victims exposed to phosgene should be exposed patients involves decontamination,primaryassessment,
transported for evaluation because of the likelihood of delayed and supportive care. British anti-lewisite is an antidote available
symptoms. for the in-hospital treatment of lewisite-exposed patients. It is
administered intravenously for patients with hypovolemic shock
Vesicant Agents or pulmonary symptoms. Applied topically, British anti-lewisite
ointment has been reported to prevent mucous membrane and
The vesicants include sulfur mustard, nitrogen mustards, and skin injury.
lewisite. These agents have been stockpiled for military oper-
ations by many countries. Sulfur mustard was first introduced Bialagic Agents
to the battlefield in World War I. It was reportedly used by
Iraq against its Kurdish population and also in its conflict Biologic agents in the form of contagious disease exposure
with Iran in 1980. It is relatively easy and inexpensive to represent a threat to prehospital care providers on a daily basis
manufacture. (Figure 20-14). Proper infection control procedures must be in
place to prevent the contraction or transmission of tuberculo-
Sulfur mustard is an oily, clear to yellow-brown liquid that sis, influenza, human immunodeficiency virus (HIV), methicillin-
can be aerosolized by a bomb blast or a sprayer. Its volatility is resistant staphylococci (MRSA), SARS, meningococcus, and a
low, allowing it to persist on surfaces for a week or more. This myriad of other organisms.
persistence allows for easy secondary contamination. The agent
is absorbed through the skin and mucous membranes, resulting Preparing for bioterrorist events increases the complexity
in direct cellular damage within 3 to 5 minutes of the exposure, of EMS system preparation. An intentional terrorist act might
althoughclinical symptoms and signs may take 1to 12 hours (usu- include delivery of a biologic agent with the potential to cause
ally 4 to 6 hours) after exposure to develop. The delayed onset disease or illness, such as aerosolized spores, aerosolized live
of symptoms often makes it difficult for the victim to recognize organisms, or an aerosolized biologic toxin. Patients with patho-
that the exposure occurred and, therefore, increases the poten- gens not typically seen by prehospital care providers, such as
tial for secondary contamination. Warm, moist skin increases
the likelihood of skin absorption, making the groin and axillary Figure 20-14
regions particularly susceptible. The eyes, skin, and upper air-
ways can develop a range offindings, from erythema and edema • Bacterial agents
to vesicle development to full-thickness necrosis. Upper airway • Anthrax
involvement can result in cough and bronchospasm. High-dose • Brucellosis
exposures can result in nausea and vomiting, as well as bone • Glanders
marrow suppression. • Plague
• Q fever
Management for sulfur mustard involves decontamina- • Tularemia
tion using soap and water, primary assessment, and supportive
therapy; no antidote exists for the effects of mustard agents. In • Viral agents
fact, it is important to note that because the cellular damage • Smallpox
from sulfur mustard occurs within several minutes of the expo- • Venezuelan equine encephalitis
sure, decontamination will not change the clinical course of the • Viral hemorrhagic fevers
exposed patient. It is primarily intended to prevent inadvertent
cross-contamination. Eyes and skin should be decontaminated • Biologic toxins
with copious amounts of water as soon as exposure is recog- • Botulinum
nized to minimize further absorption of the agent and prevent • Ricin
secondary contamination. The fluid in resulting vesicles and • Staphylococcal enterotoxin B
blisters is not a source of secondary contamination. Pulmonary • T-2 mycotoxins
bronchoconstriction may benefit from nebulized beta-agonists.
Skin wounds should be treated as burns, with regard to local
wound care.

Lewisite has a similar constellation of symptoms, but
the onset of action is much quicker than with sulfur mustard,
resulting in immediate pain and irritation to the eyes, skin,

5 2 8 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

plague, anthrax, and smallpox, might be encountered, requiring patient in this scenario is not necessary because the exposure
appropriate PPE and precautions. Familiar infection control occurred several days in the past.
procedures will be effective in the safe management of these
potentially contagious patients. If the prehospital care provider All prehospital care providers should be familiar with PPE
is responding to an overt release event, appropriate precautions for infection-control purposes. Different types of PPE are rec-
regarding decontamination ofvictims and PPE are required, sim- ommended, depending on the potential for transmission and the
ilar to other hazardous materials events. likely route of transmission. Transmission-based PPE is used
in addition to the standard precautions, which are used in the
Concentrated Biohazard Agent Versus care of all patients. These include contact, droplet, and aerosol
Infected Patient precautions.

Prehospital care providers can experience bioterrorism Contact Precautions
in two ways. The first scenario involves the overt release
of a material t hat is either identified as, or thought to be, a This level ofprotection is recommended to reduce the likelihood
biologic agent. The anthrax hoaxes of 1998 and 1999 and the of transmission of microorganisms by direct or indirect contact.
anthrax letters of 2001 are good examples. Prehospital care Contact precautions include the use of gloves and a gown.
providers responded on countless occasions to individuals
covered in "white powder" or suspected anthrax. In this situa- Commonly encountered organisms that require contact
tion, the prehospital care provider will encounter an environ- precautions include viral conjunctivitis, MRSA, scabies, and
ment or a patient contaminated with a suspicious substance. herpes simplex or zoster virus. Organisms that require strict
EMS systems may be summoned to suspicious activity, such contact precautions that might be encountered as a result of
as a device delivering an unknown aerosol agent. The nature bioterrorism include bubonic plague or the viral hemorrhagic
of the threat at these events is usually unknown and precau- fevers, such as Marburg or Ebola, as long as the patient does not
tions for personal safety should always be paramount. These have pulmonary symptoms or profuse vomiting and diarrhea, in
incidents must be respected and treated as a WMD incident which case airborne precautions should also be taken.
until proven otherwise. If the suspicious substance is in fact a
con centrated aerosol of an infectious organism or toxin, PPE Figure 20-15
appropriate for the biologic agent and decontamination are
required. The type of PPE used will vary based on the level of
precautions required (e.g., standard preca utions and
In this situation, prehospital care providers will be caring contact, droplet, or airborne infection isolation).
for victims contaminated with suspected biologic agent on their
skin or clothing. Any person, patient, or prehospital care pro- 1. Gown
vider coming in direct physical contact with a suspected biologic • Fully cover torso from neck to knees, arms to
agent should remove all exposed articles of clothing and per- end of wrists, and wrap around the back.
form a thorough washing of exposed skin with soap and water.45 • Fasten in back of neck and waist.
Clinically significant re-aerosolization of material from victims'
skin or clothing is unlikely, and the risk to the prehospital care 2. Mask or respirator
provider is negligible.46 However, as a matter of routine prac- • Secure ties or elastic bands at middle of head
tice, potentially contaminated clothing normally removed by and neck.
pulling the item over the face and head should instead be cut • Fit flexible band to nose bridge.
off to minimize any risk of inadvertent inhalation of contami- • Fit snug to face and below chin.
nant. Decontamination may then proceed using water or soap • FiVcheck respirator.
and water. Consultation with appropriate public health and law
enforcement officials will then determine the need for antibiotic 3. Goggles or face shield
prophylaxis. • Place over face and eyes and adjust to fit.

The second scenario involves a response to a patient who 4. Gloves
is a victim of a remote, covert bioterrorist event. Perhaps the • Extend to cover wrist of isolation gown.
patient inhaled anthrax spores after a covert attack at work
and now, several days later, is manifesting signs of pulmonary Use safe work practices to protect yourself and limit
anthrax. Perhaps a terrorist has inoculated himself or herself the spread of contamination:
with smallpox, and you are summoned to assist the victim with
a suspicious rash. In these cases, personal and public safety can • Keep hands away from face.
be ensured by knowledge ofproper infection control procedures • Limit surfaces touched.
and the proper donning and removal of PPE appropriate for the • Change gloves when torn or heavily contaminated.
biohazard (Figures 20-15 and 20-16). Decontamination of the • Perform hand hygiene.

Source: From Centers for Disease Control and Prevention, Atlanta.

CHAPTER 20 Explosions and Weapons of Mass Destruction 5 2 9

Figure 20-16 in air, no additional respiratory protection or air filtration is
required.
Except for the respirator, remove PPE at the doorway
or in an anteroom of the involved room. Remove the Typically encountered organisms in this category
respirator after leaving the contaminated room and include influenza, Mycoplasma pneumoniae, and invasive
closing the door. Haemophilus irifluenzae or Neisseria meningitidis, caus-
ing sepsis or meningitis. Pneumonic plague is an example
1. Gloves of a possible agent encountered as a result of a bioterrorist
• The outside of the glove is contaminated! event.
- Grasp outside of glove with opposite gloved
hand; peel off. Aerosol Precautions
- Hold removed glove in gloved hand.
- Slide fingers of ungloved hand under This level ofprotection is recommended to reduce the likelihood
remaining glove at wrist. of transmission of microorganisms by the airborne route. Some
- Peel glove off over first glove. organisms can become suspended in the air attached to small
- Discard gloves in waste container. droplet nuclei (less than 5 µm) or attached to dust particles. In
this case, microorganisms can become widely dispersed by air
2. Goggles currents immediately around the source or more distant from
• The outside of the goggles or face shield is the source, depending on environmental conditions. To avoid
contaminated! such dispersion, these patients are kept in negative-pressure iso-
- To remove, handle by headband or ear pieces. lation rooms in a hospital in which the exhaust ventilation can
- Place in designated receptacle for reprocessing be filtered.
or in waste container.
Aerosol precautions include gloves, gown, eye protec-
3. Gown tion, and a fit-tested high-efficiency particulate air (HEPA)
• The gown front and sleeves are contaminated! filter mask, such as the N-95 (Figure 20-17). Examples of
- Unfasten gown ties. illnesses typically encountered that would require aerosol
- Pull away from neck and shoulders, touching precautions include tuberculosis, measles, chickenpox, and
inside of gown only. SARS. Smallpox and viral hemorrhagic fever with pulmonary
- Turn gown inside out. symptoms are examples that could possibly be related to a
- Fold or roll into a bundle and discard. bioterrorist event.

4. Mask or respirator Selected Agents
• The front of the mask/respirator is contaminated-
do not touch! Anthrax
- Grasp bottom, then top ties or elastics, and
remove. Anthrax is a disease caused by the bacterium Bacillus
- Discard in waste container. anthracis. B. anthracis is a spore-forming bacterium and,
thus, can exist as a vegetative cell or as a spore. The vegeta-
Once PPE is removed, wash the hands. tive cell lives well in a host organism but cannot survive long

Source: From Centers for Disease Control and Prevention, Atlanta. Figure 20-17

Droplet Precautions Note that many illnesses associated w ith biologic events
require no additional protection beyond standard
This level of protection is recommended to reduce the like- precautions, provided there is no risk of exposure
lihood of transmission of microorganisms that are known to to a concentrated agent. Examples include patients
be transmitted by large droplet nuclei (greater than 5 µm) with inhalational anthrax or a biologic toxin such
expelled by an infected person in the course of talking, sneez- as botulinum. However, in most cases, the specific
ing, or coughing or during routine procedures, such as suction- biologic agent will likely not be identified for several
ing. These droplets infect by landing on the exposed mucous days. Although some agents, such as anthrax, are not
membranes of the eyes, nose, and mouth. Because the droplets spread from person to person, prehospital care providers
are large, they do not remain suspended in air, and therefore, must assume the worst-that the biologic agent is
contact must be in close proximity, usually defined as 3 feet contagious-and use all available precautions, including
(0.9 meter) or less. Droplet precautions include the contact aerosol precautions.
precautions of gloves and gown and add eye protection and a
surgical mask. Because the droplets do not remain suspended

5 3 0 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

outside the body, unlike the spore, which can be viable in the provide supportive therapy and transport ill patients to facilities
environment for decades. in which critical care services are available.

The disease is naturally occurring, contracted most often by Management
persons in contactwith infected animals oranthrax-contaminated
animal products resulting in the cutaneous form of the disease. Prophylaxis with antibiotics is required only for individuals who
The spores have been weaponized and are known to be invento- have been exposed to spores. Local public health officials will
ried in several nations' military stockpiles. The accidental release determine the appropriate antibiotic and length of prophylactic
of aerosolized anthrax spores from a Soviet military facility at treatment. The latest recommendations suggest 60 days of ther-
Sverdlovsk in 1979 resulted in approximately 79 cases of pul- apy with oral doxycycline or a quinolone antibiotic.
monary anthrax with 68 reported deaths. Letters contaminated
with anthrax spores were sent through the U.S. Postal Service in An anthrax vaccine does exist, and an immunization pro-
2001 to prominent legislators and media outlets. Although only gram for U.S. military forces was instituted in 1998. The cur-
22 cases (11 pulmonary, 11 cutaneous) and 5 deaths resulted, rent regimen requires a series of six initial shots and annual
thousands of people required prophylaxis with antibiotics. An boosters. It is currently recommended only for military per-
efficient release of 220 pounds (100 kilograms [kg]) of anthrax sonnel and for laboratory and industrial workers at high
spores over Washington, DC, is reported to be capable ofcausing risk for exposure to spores. The CDC has purchased tens of
130,000 to 3 million deaths.47 thousands of doses of the anthrax vaccine for the Strategic
National Stockpile that would be made available to emergency
Routes of exposure to anthrax include the respiratory tract, responders in the event of an anthrax incident with risk of
the GI tract, and breaks in the skin. Exposure to anthrax through exposure.
the respiratory tract leads to inhalational or pulmonary anthrax.
Exposure through the GI tract causes gastrointestinal anthrax, Plague
and skin infection causes cutaneous anthrax.
Plague is a disease caused by the bacterium Yersini a pestis. It is
Gastrointestinal anthrax is rare and would result from naturally occurring, found in fleas and rodents. If an infected flea
ingesting food substances contaminated with spores. Patients bites a human, the person can develop bubonic plague. If this
would have nonspecific symptoms of nausea, vomiting, malaise, local infection goes untreated, the patient can become systemi-
bloody diarrhea, and acute abdomen; mortality is approximately cally ill, resulting in septicemia and death. A number of patients
500A>. Cutaneous anthrax follows deposition of spores or organ- may proceed to develop pulmonary symptoms (pneumonic
isms into a break in the skin. This results in a papule, which plague). Plague was responsible for the Black Death of 1346,
subsequently ulcerates and causes a dry, black eschar with local which killed 20 to 30 million people in Europe, approximately
edema. If not treated with antibiotics, mortality approaches 20%; one-third of its population at that time. Y. pestis has been weap-
with antibiotics, mortality is less than 1%. onized for military stockpiles with techniques developed to aero-
solize the organism directly, bypassing the animal vector. The
For maximal effectiveness in a terrorist attack, anthrax World Health Organization reports that in a worst-case scenario,
would likely be disseminated in its spore form. Anthrax spores 110 pounds (50 kg) of Y. pestis, released as an aerosol over a city
are approximately 1 to 5 µm in size, which allows the spores to of 5 million, would result in 150,000 cases of pneumonic plague
be suspended in air as an aerosol. Aerosolized spores can be and 36,000 deaths.51
inhaled into the lungs and deposited in the alveoli. They are then
consumed by macrophages and carried to the mediastinal lymph Naturally occurring plague, resulting from the bite of an
nodes, where they germinate, manufacture toxins, and cause infected flea, will cause symptoms in 2 to 8 days, with onset
acute hemorrhagic mediastinitis (bleeding into the lymph of fever, chills, weakness, and acutely swollen lymph nodes
nodes in the middle of the chest cavity) and often death. The (buboes) in the neck, groin, or axilla. Untreated patients
onset of symptoms after inhalation of spores varies, with most can deteriorate to systemic illness and death. 1\velve per-
victims developing symptoms within 1 to 7 days, although there cent have been described as developing pneumonic plague,
may be a latencyperiod as long as 60 days. Symptoms initially are with complaints of chest pain, dyspnea, cough, and hemop-
nonspecific, including fever, chills, dyspnea, cough, chest pain, tysis, and these patients can also succumb from systemic
headache, and vomiting. After a few days, symptoms improve, illness.
followed by a rapidly deteriorating course of fever, dyspnea, dia-
phoresis, shock, and death.45•48•49 Before the 2001 anthrax attacks, Plague occurring from terrorist deployment of a weapon
mortality from inhalational anthrax was thought to be 900,6, but would likely result from aerosolized organisms, and thus, it
recent experience suggests that with early antibiotic therapy and would clinically present as the pneumonic form of the disease.
critical care services, mortality may be less than 500;6.50 Inhalation of Y. pestis aerosol will result in symptoms in 1 to
6 days. Patients will present with fever, cough, and dyspnea,
Inhalational anthrax is not contagious and does not pose a with bloody or watery sputum. They may also develop nausea,
risk to the prehospital care provider. Only exposure to aerosol- vomiting, diarrhea, and abdominal pain. Buboes are not typically
ized spores poses a risk ofinfectivity. Caring for patients known present. Without antibiotics, death occurs in 2 to 6 days after
to be infected with inhalational anthrax requires only standard development of respiratory symptoms.52
precautions; however, if the specific agent is unknown, aerosol
precautions are warranted. The prehospital care provider will

CHAPTER 20 Explosions and Weapons of Mass Destruction 531

Currently, no vaccine is available to protect from pneumonic presentation distinguishes smallpox from varicella, or chicken-
plague. Treatment of the disease includes antimicrobial and sup- pox (Figure 20-19), which begins on and is more dense on the
portive therapy, often requiring critical care services. Antibiotic trunk (centripetal) and has lesions at various stages of develop-
regimens are also recommended for individuals with unpro- ment (new lesions appear with older, crusted lesions) (Figure
tected close exposure to patients with known pneumonic plague. 20-20). Mortality from naturally occurring smallpox was approx-
imately 300Ai. Little is known about the natural course of the dis-
Patients with plague represent a communicable disease ease in immunocompromised patients, such as those with HIV.
risk. Ifpatients present with only cutaneous signs and symptoms
(bubonic plague), contact precautions are adequate to protect Smallpox is a contagious disease that is primarily spread
the prehospital care provider. Ifpatients present with pulmonary by droplet nuclei projected from the oropharynx of infected
signs of plague (pneumonic plague), a more likely scenario after patients and by direct contact. Contaminated clothing and bed
a terrorist attack, prehospital care providers will be required to linens can also spread the virus. Patients are contagious begin-
wear PPE suitable for respiratory droplet protection. Droplet ning slightly before the onset of the rash, although this might not
precautions include a surgical mask, eye protection, gloves, and always be obvious if the rash is subtle in the oropharynx. When
a gown. Responders to the scene of an overt Y. pestis aerosol managing a patient with smallpox, prehospital care providers
delivery, which would not likely be a recognized event, would must wear PPE appropriate for contact and aerosol precautions.
require level A PPE suitable for a hazardous environment if This includes N-95 mask, eye protection, goggles, and gown.
entering the hot zone or warm zone. Ideally, persons managing patients with smallpox will have been
immunized.54
Management

Plague victims are treated in the field with supportive ther- Day 3 of rash Day 5 of rash Day 7 of rash
apy. Communication with the receiving facility is vital before
arrival to ensure that the pneumonic plague patient can be
properly isolated in the ED and that staff are prepared with the
appropriate PPE. Asking the patient to wear a surgical mask,
if tolerated, may also decrease the likelihood of secondary
transmission.

Decontamination of the vehicle and equipment is similar to
that required after transport of any patient with communicable
disease. Contact surfaces should be wiped down with disinfec-
tant approved by the Environmental Protection Agency (EPA) or
1:1,000 diluted bleach solution. There is no evidence to suggest
that Y. pestis poses a long-term environmental threat after dis-
solution of the primary aerosol.52 The organism is sensitive to
heat and sunlight and does not last long outside the living host.
Y. pestis does not form spores.

Smallpox On any part of the body, all lesions are in the
same stage of development.
Smallpox is also known as varioi,a major and varioi,a minor,
depending on the severity of the illness. This naturally occurring Most patients Umbilicated Confluent
viral disease was eradicated in 1977 but still exists in at least two
laboratories-Russia's Institute ofVirus Preparations and the CDC. have lesions lesions lesions
It was alleged that the Soviet government began a program in 1980 on the palms
to produce large quantities ofsmallpox virus for use in bombs and or soles
missiles, as well as to develop more virulent strains of the virus for
military purposes. There is concern that smallpox virus may have Figure 20-18 Smallpox.
changed hands after the dissolution of the Soviet Union.53
Source: Courtesy Cent ers for Disease Control and Prevent ion, At lanta.
The smallpox virus infects its victim by entering the mucous
membranes of the oropharynx or respiratory mucosa. After
a 12- to 14-day incubation period, the patient develops fever,
malaise, headache, and backache. The patient then develops a
maculopapular rash that starts on the oral mucosa and quickly
progresses to a generalized skin rash with characteristic round,
tense vesicles and pustules. The rash tends to affect the head
and extremities more densely than the trunk (centrifugal), with
the stage of the lesions appearing uniform (Figure 20-18). This

5 3 2 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Figure 20-19

Chickenpox (varicella) is the most likely condition to be Healthy child Healthy adult Bacterial super-
confused with smallpox. Characteristics of chickenpox with varicella with varicella infection of
include the following : lesions
• There is no prodrome or mild prodrome. Note centripetal Day 3 of rash
• Lesions are superficial vesicles: "dewdrop on a rose distribution of Lesions are in
rash different stages
petal." of development
• Lesions appear in crops; on any one part of the body,

there are lesions in different stages (papules, vesicles,
crust s).
• Distribution is centripetal, with the greatest
concentration of lesions on the trunk, and the fewest
lesions on distal extremities. Lesions may involve the face/
scalp; occasionally, the entire body is equally affected.
• First lesions appear on the face or trunk.
• Patients are rarely toxic or moribund.
• Lesions evolve rapidly, from macules to papules to
vesicles to crusts (less than 24 hours).
• Palms and soles are rarely involved.
• Patient lacks a reliable history of varicella or varicella
vaccination.
• Of these patients, 50% to 80% recall an exposure to
chickenpox or shingles 10 to 21 days before rash onset.

Source: Courtesy Centers for Disease Control and Prevention, Atlanta.

The smallpox vaccination program in the United States was Healthy adult Healthy adult Pregnant
stopped in 1972. The residual immunity provided by this vacci- with varicella with varicella woman with
nation program is unknown, and it is suggested that individuals varicella
whose last immunization was 40 years ago will likely now be
susceptible to contracting smallpox.53 Vaccination for the small- Figure 20-20 Chickenpox.
pox virus is available to certain U.S. Department of Defense and
State Department members. It was also made available under a Source: Courtesy Centers for Disease Control and Prevention, Atlanta.
Department of Health and Human Services program to develop
public health Smallpox Response Teams. It is currently available precautions can be taken to prevent transmission of the virus.
to the general public only for participants in clinical trials. In The identification of a patient with smallpox would be consid-
case of a public health emergency, the United States has stock- ered a public health emergency of enormous significance.
piles of vaccine that can be released for mass immunization of
the public. Vaccination within 4 days of the exposure has been Proper removal of PPE without breach in infection control
shown to offer some protection against contracting the illness procedures is important for the safety ofthe prehospital care pro-
and substantial protection against a fatal outcome.53 vider. All contaminated disposable medical waste must be prop-
erly bagged, labeled, and disposed of as other regulated medical
Management waste. Reusable medical equipment must be cleaned after use
according to standard protocol, either by autoclaving or by sub-
Prehospital care providers will provide supportive care to man- jecting the equipment to high-level disinfection. Environmental
age a patient with smallpox. The recommended PPE must be surfaces need to be cleaned by an approved EPA-registered
worn at all times, and it is imperative that there is no breach detergent-disinfectant. Air decontamination or fumigation of the
in infection-control procedures. Hospitals with the appropriate emergency vehicle is not required.55
isolation facilities and properly trained staff should be identi-
fied in the community. The receiving facility must be contacted Botulinum Toxin
to inform the staff of the intention to transport the confirmed
or suspected case of smallpox to their facility so that proper Botulinum toxin is produced by the bacterium Clostridium
botulinum and is the most poisonous substance known. It is

CHAPTER 20 Explosions and Weapons of Mass Destruction 5 3 3

15,000 times more toxic titan tile nerve agent VX and 100,000 it is not a contagious disease. Botulism aerosols degrade read-
times more toxic titan sarin.56 Botulinum toxin has been weap- ily in tile environment, and it is anticipated tltat after delivery
onized for military use by the United States, the former Soviet in a terrorist incident, substantial inactivation will occur after
Union, Iraq, and probably Iran, Syria, and Nortlt Korea.57 The 2 days. Responders to an overt aerosol dissemination event
Aum Shinrikyo cult, responsible for tile Tokyo subway sarin would require level A PPE suitable for a hazardous environment
attack, attempted to deliver an aerosol of botulinum toxin witlt- ifworking in tile hot zone or warm zone.
out success in 1995. Despite tile reported difficulty of concen-
trating and stabilizing tile toxin for dissemination, it is estimated Because tile aerosol can persist for approximately 2 days
that a terrorist point-source delivery of botulinum aerosol could under average weatlter conditions, victims who have been
incapacitate or kill 100'6 of persons downwind 0.3 mile (0.5 km). exposed to botulinum aerosol require decontamination by clotlt-
The toxin could also be introduced into tile food supply in an ing removal and washing with soap and water. Equipment can
attempt to poison large numbers of people. be decontaminated using a 0.1% hypochlorite bleach solution.58
Patients will not require isolation after arrival at tile hospital,
Three forms of botulism exist naturally. Wound botulism but critical care services may be needed for patients requiring
occurs when toxins are absorbed from a dirty wound, often witlt mechanical ventilation.
devitalized tissue, in which C. botulinum is present. Food-borne
botulism occurs whenimproperlyprepared orhome-cannedfoods Radiologic Disasters
allow tile bacteriato grow and produce toxin, which is ingested by
tile victim. I ntestinal botulism occurs when toxin is produced and Since tile terrorist attacks of September 11, 2001, new con-
absorbed witltin tile GI tract. In addition to tltese tltree naturally sideration has been given to the likelihood of EMS systems
occurring forms, a man-made form of botulism, called inhala- needing t o manage a radiologic emergency. Historically, plan-
tional botulism, is a result ofaerosolized botulinum toxin. ning has focused on civil-defense preparation for a strategic
exchange of military nuclear weapons or the rare occurrence
Regardless of the route, botulinum toxin is carried to the of a nuclear power plant accident. Currently, however, tltere
neuromuscular junction where it binds irreversibly, prevent- is increasing awareness of the possibility that terrorists could
ing normal release of the neurotransmitter acetylcholine and deploy an improvised nuclear detonation device, or perhaps
causing a descending flaccid paralysis. Onset of symptoms more likely a radiologic dispersal device, that uses conven-
is several hours to a few days. All patients will present with tional explosives to disseminate radioactive material into the
diplopia (double vision) and multiple cranial nerve deficits, environment.
causing difficulty with sight, speech, and swallowing. The
extent and rapidity of the descending paralysis depend on Although radiologic accidents are rare, tltere have been
the dose of the toxin. Patients become fatigued, lose the abil- 243 radiation accidents since 1944 in the United States, with
ity to control the muscles of the head and neck, may lose 1,342 casualties that met criteria for significant exposure.
their gag reflex, or may progress to paralysis of the mus- Worldwide, 403 accidents have occurred, witlt 133,617 vic-
cles of respiration and develop respiratory failure, requiring tims, 2,965 with significant exposure, and 120 fatalities. The
intubation and months of mechanical ventilation. Untreated Chernobyl disaster of 1986 was responsible for 116,500 to
patients usually die of mechanical upper airway obstruction 125,000 exposed casualties and close to 50 deaths as of 2005,
or inadequate ventilation. The classic triad of botulinum although it is estimated that the total number of deaths could
toxicity is (1) descending symmetric flaccid paralysis with reach as many as 4,000 as additional cancer victims suc-
cranial nerve deficits, (2) lack of fever, and (3) a clear sen- cumb.59·60 The Fukushima nuclear power plant in Japan was
sorium. After weeks to months, patients may recover as new seriously damaged after a nearby earthquake and tsunami in
axon buds develop to innervate the denervated muscles. 2011, resulting in the destruction of several reactors and the
release of radiation into the environment. It will take years
Management and even decades before the health impact of this incident
on the surrounding population and environment can be fully
Care for tilepatient witlt botulism is supportive, witlt administra- evaluated.
tion of antitoxin in tile hospital. Early use of antitoxin will mini-
mize further deterioration but cannot reverse existing paralysis. Radiation disasters have tile potential to generate fear
This antitoxin is available from tile CDC. and confusion in botlt victims and emergency responders.
Familiarization with tile hazard and management principles will
Prehospital care providers caring for victims of botulism help to ensure an appropriate response and help to reduce panic
would need to be vigilant about airway compromise and and disorder (Figure 20-21).
inadequate ventilation. Patients may not be able to manage tlteir
secretions or maintain a patent airway. Because of diaphragm Exposure to ionizing radiation and radioactive con-
paralysis, patients may not be able to generate an adequate tidal tamination may result from several different scenarios: (1)
volume. This may be exacerbated by having tile patientina supine detonation of a nuclear weapon, whether high grade or an
or semi-recumbent position. Patients experiencing respiratory improvised low-yield device; (2) detonation of a "dirty bomb"
difficulty should be intubated and adequately ventilated. or radiation dispersion device, in which there is no nuclear
detonation, but rather conventional explosives are deto-
Standard precautions are adequate for the management of nated to disperse a radionuclide (radioactive material); (3)
patients experiencing tile effects of botulinum toxicity because

5 3 4 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Figure 20-21

1. Assess the scene for safety. minimum, standard precautions, including protective
2. All patients should be medically stabilized from clothing, gloves, and a mask.
6. Patients who develop nausea, vomiting, or skin
their traumatic injuries before radiation injuries are erythema within 4 hours of exposure have likely
considered. Patients are then evaluated for their received a high external radiation exposure.
external radiation exposure and contamination. 7. Radioactive contamination in wounds should be treated
3. An external source of radiation, if great enough, can as dirt and irrigated as soon as possible. Avoid handling
cause tissue injury, but it does not make the patient any metallic foreign body.
radioactive. Patients with even lethal exposures to 8. Potassium iodide (Kl) is only of value if there has been
external radiation are not a threat to prehospital care a release of radioactive iodine. Kl is not a general
providers. radiation antidote.
4. Patients can become contaminated with radioactive 9. The concept of time/distance/shielding is key in
material deposited on their skin or clothing. More than the prevention of untoward effects from radiation
90% of surface contamination can be removed by exposure. Radiation exposure is minimized by
removal of clothing. The remainder can be washed off decreasing t ime in the affected area, increasing distance
with soap and water. from a radiation source, and using metal or concrete
5. Prehospital care providers should protect themselves shielding.
from radioactive contamination by observing, at a

Source: Modified from Department of Homeland Security Working Group on Radiological Dispersion Device Preparedness/Medical Preparedness and Response Subgroup,
2004, http://www1.va.gov/emshg/docs/Radiologic_Medical_Countermeasures_OS 1403.pdf.

sabotage or accident at a nuclear reactor site; and (4) mishan- to manage the injuries caused by the conventional explosive.
dled nuclear waste. RDDs could cause confusion and panic in the public and among
emergency responders concerned about radioactivity, hindering
Medical Effects of Radiation efforts to assist victims.
Catastrophes
Ionizing radiation causes injury to cells by interacting
The injuries and risks associated with a radiologic catastrophe with atoms and depositing energy. This interaction results in
would be multifactorial. In the case of a nuclear detonation, ionization, which can either damage the cell nucleus directly,
casualties would be produced by the explosion, resulting in pri- causing cell death or malfunction, or indirectly, damaging cell
mary, secondary, and tertiary blast injuries, thermal injury, and components by interacting with water in the body and resulting
structural collapse. Victims may be further subjected to radiation in toxic molecules. Acute exposure to large doses of penetrating
injury from irradiation, in which radiation passes through the ionizing radiation (irradiation with gamma rays and neutrons) in
body causing damage but does not result in contamination (simi- a short time can result in acute radiation illness. Types of ioniz-
lar to getting an x-ray); from external radioactive contamination, ing radiation include alpha particles, beta particles, gamma rays,
which can be deposited on skin and clothing from fallout; orfrom and neutrons.
internal radiation through radioactive particulate contamination,
which victims may inhale, ingest, or have deposited in wounds. Alpha particles are relatively large and cannot penetrate
even a few layers ofskin. Intact skin or a uniform offers adequate
Accidents at nuclear reactors could generate large doses protection from external contamination emitting alpha particles.
of ionizing radiation, without a nuclear detonation, especially Ionizing radiation from alpha particles is a concern only if it is
under circumstances in which the reactor reaches a point of internalized in the body by inhaling or ingesting alpha-particle
"criticality." Explosions, fire, and gas release could also result in emitters. When internalized, alpha-particle radiation can cause
radioactive gas or particulate matter, which could expose emer- significant local cellular injury to adjacent cells.
gency responders to the risk of exposure to contamination with
radioactive particles. Beta particles are small charged particles that can pene-
trate more deeply than alpha particles and can affect deeper
Radiation dispersion devices (RDDs) typically would not layers of the skin with the ability to injure the base of the skin,
deliver enough radiation to cause immediate injury. However, causing a beta burn. Beta-particle radiation is found most fre-
RDDs would complicate management for prehospital care pro- quently in nuclear fallout. Beta particles also result in local radi-
viders by distributing radioactive particulates that could con- ation injury.
taminate victims and emergency responders and make it difficult
Gamma rays are similar to x-rays and can easily penetrate
tissue. Gamma rays are emitted with a nuclear detonation and
with fallout. They could also be emitted from some radionuclides

CHAPTER 20 Explosions and Weapons of Mass Destruction 5 3 5

Figure 20-22

Diagnosis • Marrow suppression (neut ropenia, lymphopenia, and
Be alert to the following : th rom bocytopenia)
1. The acute radiation syndrome follows a predictable
• Epilation (hair loss)
pattern after substantial exposure or catastrophic
events (Figure 20-23). Understanding Exposure
2. Individuals may become ill from contaminated Exposure may be known and recognized or clandestine and
sources in the community and may be identified over may occur by the following means:
much longer periods based on specific syndromes 1. Large recognized exposures, such as a nuclear bomb or
(Figure 20-24).
3. Specific syndromes of concern, especially with a 2- to damage to a nuclear power station
3-week prior history of nausea and vomiting, are: 2. Small radiation source emitting continuous gamma
• Thermal burnlike skin effects without documented
radiation, producing group or individual chronic
thermal exposure intermittent exposures (e.g., radiologic sources from
• Immunologic dysfunction with secondary infections medical treatment devices, environmental water or
• Tendency to bleed (epistaxis, gingival bleeding, food pollution)
3. Internal radiation from absorbed, inhaled, or ingested
petechiae) radioactive material (internal contamination)

Source: Modified from Department of Veterans Affairs pocket guide produced by Employee Education System for Office of Public Health and Environmental Hazards.
This information is not meant to be complete, but to be a quick guide; please consult other references and expert opinion.

that might be present in an RDD. Gamma radiation can result in receiving greater than 2 Gy will become ill and require hospital-
what is termed whole-body exposure. Whole-body exposure can ization; at greater than 6 Gy, mortality becomes high. At doses
result in acute and chronic radiation illnesses (Figures 20-22, greater than 30 Gy, neurologic signs are manifest, and death is
20-23, and 20-24). most likely.19

Neutrons can penetrate tissue easily, with 20 times the Acute radiation syndrome generally follows a defined
destructive energy of gamma rays, disrupting the atomic struc- progression that first manifests in a prodromal phase charac-
ture of cells. Neutrons are released during a nuclear detonation terized by malaise, nausea, and vomiting. This is followed by a
but are not a fallout risk. Neutrons also contribute to whole- latent phase, in which the patient is essentially asymptomatic.
body radiation exposure and can result in acute radiation illness. The length of the latent phase depends on the total absorbed
Neutrons can convert stable metals into radioactive isotopes. dose ofradiation. The greater the dose ofradiation, the shorter
This ability has significance in patients with metal hardware or the latent phase. The latent phase is followed by the subse-
those in possession of metal objects at the time of exposure. quent illness phase, manifested by the organ system that has
been injured. Damage to the bone marrow occurs with total
Whole-body exposure is measured in terms of t he gray doses of 0.7 to 4.0 Gy and results in decreasing levels of white
(Gy). The rad (radiation absorbed dose) was a familiar dose blood cells and decreased immunity to infection over several
unit that was replaced by the gray; 1 Gy equals 100 rad. The days to weeks. Decreased platelets can result in easy bruising
rem (radiation equivalent-man) describes the dose in rad and bleeding. Decreased red blood cells will result in anemia.
multiplied by a "quality factor," which takes into account the At 6 to 8 Gy, the GI tract will also be affected, resulting in diar-
intrinsic special deposition pattern of different types of radi- rhea, volume loss, and hematochezia (bloody stools). Above
ation. The rem has been replaced with the sievert (Sv); 1 Sv 30 Gy, the patient will manifest symptoms of the neurovascu-
equals 100 rem. lar syndrome, experiencing the prodromal phase of nausea
and vomiting, a short latent phase lasting only a few hours,
Radiation affects rapidly dividing cells most readily, result- followed by a rapid deterioration of mental status, coma, and
ing in injury to the bone marrow and GI tract where high cell death, sometimes accompanied by hemodynamic instability.
turnover rates occur. Higher doses can affect the CNS directly. Doses this high can occur after a nuclear detonation, but the
The dose of whole-body exposure determines the medical conse- victim will most likely have been killed by injuries associated
quences of the exposure. Patients receiving up to 1 Gy of whole- with the blast. Victims could also be exposed to these high
body irradiation would typically not exhibit signs of injury. At doses at a nuclear power facility where no blast has occurred,
1 to 2 Gy, less than half of patients will develop nausea and vom- but a reactor core has reached criticality. 19
iting, many will subsequently develop leukopenia (decreased
white blood cell count), and deaths will be minimal. Mostvictims

5 3 6 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Nausea, None 5-50% 50-100% 75-100% 90-100% 100%
vomiting
3-6 hr 2-4 hr 1-2 hr < 1 hr N/A
Time of onset
< 24 hr < 24 hr < 48 hr 48 hr N/A
Duration
Lymphocyte Unaffect ed Minimally < 1000 at < 500 at 24 hr Decreases Decreases
No impairment decreased 24 hr
count w ithin hours w ithin hours

CNS function No impairment Routine task Si m ple, Rapid incapacitation; May have
performance routine task a lucid interval of several hours
performance
Cognitive
impairment Cogn itive
for 6-20 hr impairment
for> 24 hr

Signs/symptoms None Moderate Severe leukopenia, purpura, Diarrhea, fever, Convulsions,
leukopenia hemorrhage, pneumonia, hair electrolyte ataxia,
loss after 300 rad disturbance t remor,
lethargy

Time of onset > 2 wk 2 d to 4 wk 2 d to 4 wk 1-3 d 1-3 d

Critical period None 4-6 wk; greatest potent ial for 2-14 d 1-46 hr
effective medical intervent ion

Organ system None Hematopoietic; respiratory GI tract CNS
(mucosal) systems MucosaI

systems

Hospitalization 0% < 5% 90% 100% 100% 100 %
duration 45-60 d 60-90 d 100+ d Weeks to Days to weeks

months

Mortality None Minimal Low with High Very high; significant neurologic
aggressive symptoms indicate lethal dose
t herapy

CNS, central nervous system; d, day(s); hr, hour(s); N/A, not available; w k, w eek(s).

Source: Modified from Armed Forces Radiobiology Research Institute: Medical management of radiological casualties, Bethesda, MD, 2003.

Not all radiation accidents or terrorist events will result in cancer. The acute effects ofRDD detonation, besides the effects of
high-dose radiation exposure. Low-dose radiation exposure, as the detonation ofthe conventional explosive, will likely be psycho-
would most likely occur after an RDD detonation, probably would logical, including stress reactions, fear, acute depression, and psy-
not produce acute irtjury secondary to radiation. Dependent on chosomatic complaints, which would significantly strain the EMS
dose, the patient may have an increased future risk of developing agencies and medical infrastructure.

CHAPTER 20 Explosions and Weapons of Mass Destruction 5 3 7

Figure 20-24 •• .. . .. .. . .

1234

Headache Anorexia Partial-thickness and Lymphopenia
Fatigue Nausea full-thickness skin damage Neutropenia
Weakness Vomiting Thrombocytopenia
Diarrhea Epilation (hair loss) Pu rpura
Ulceration Opportunistic infections

Source: Modified from Armed Forces Radiobiology Institute, Medical management of radiological casualt ies, Bethesda, MD, 2003.

Patients can become contaminated with material that offer some protection from inhaled particulates. A standard
emits alpha, beta, and even gamma radiation, but the most splash-resistant suit will protect against particulates that emit
common contaminants will emit alpha and beta radiation. alpha radiation and will offer some protection from beta radi-
Only gamma radiation contributes to whole-body irradiation, ation, but will provide no protection from gamma radiation
as previously described. Alpha and beta radiation have lim- or neutrons. This type of barrier protection will assist in the
ited ability to penetrate, but still can cause local tissue injury. decontamination of particulate matter from an individual, but
Patients can easily be decontaminated by clothing removal it does not protect against the risks of acute radiation illness
and washing with water or soap and water. It is impossi- when the person is exposed to high-energy sources of external
ble for a patient to be so contaminated as to be a radiologic radiation.
hazard to prehospital care providers caring for the individ-
ual, so management of traumatic life-threatening injury is None of the typical PPE carried by prehospital care pro-
an immediate priority and should not be delayed pending viders protects from a high-energy point source of radiation.
d e c on t amination. 19 This type of radiation is encountered during the first minute of
a nuclear detonation, in a critical reactor core, or with a high-
As described, radioactive particles can be inhaled, energy radiation source such as cesium-137, which may be dis-
ingested, or absorbed through the skin or contaminated persed in an RDD. The best protection from these sources is
wounds. This type of exposure to radiation will not result in decreased time of exposure, increased distance from the source,
acute effects of radiation exposure but can result in delayed and shielding. Some new materials that may offer some protec-
effects. Any victims or emergency responders who operate in tion from low-level gamma radiation for emergency responder
an area at risk for airborne radioactive particles without the PPE are under investigation.
benefit of respiratory protection would require subsequent
evaluation to identify internal contamination, which could Unlike insufficient PPE worn to protect against chem-
require medical intervention to dilute or block the effects of ical agents, the inhalation, ingestion, or skin absorption
the inhaled radionuclide. of radiation-emitting gas or particulate will not immedi-
ately incapacitate a prehospital care provider or victim. All
Personal Protective Equipment prehospital care providers who operated in an environment
potentially contaminated with radioactive material would
Prehospital care providers would be operating in an environ- have to undergo a radiation survey to determine if internal
ment with risk ofexposure to ionizing radiation after a radiologic contamination had occurred and undergo active management
disaster. The radiation risk would depend greatly on the type of if warrant ed.
radiologic event.
Dose rate meters or alarms should be worn if available.
The PPE available to prehospital care providers for use Standards exist for acceptable doses of ionizing radiation in
in chemical and biologic hazards will offer some protec- the occupational environment under normal and emergency
tion from radioactive particulate contamination. However, conditions.20 Dose rates of ionizing radiation can be measured
it will not provide protection from high-energy radiation to prevent emergency responders from putting themselves
sources, such as a damaged reactor or nuclear blast at at risk for acute radiation illness or an unacceptably higher inci-
ground zero. dence ofcancer. The incident commander should be approached
for guidance on radiation-exposure readings and limits.
Radioactivity can be present in gases, aerosols, sol-
ids, or liquids. If radioactive gases are present, SCBA will Assessment and Management
offer the highest protection. If aerosols are present, an APR
may be adequate to prevent internal contamination caused Patients who have been injured in a radiologic catastrophe
by inhalation of contaminated particles. An N-95 mask will should receive primary and secondary assessments as dictated

5 3 8 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

by the mechanism of injury. Prehospital care providers can Figure 20-25
expect to evaluate patients who have sustained blast injury
and thermal injury in the case of a nuclear detonation, or Treatment Considerations
from the conventional high explosive detonation of an RDD • If trauma is present, treat.
(Figure 20-25). Priority should be given to management of trau- • If external radioactive contaminants are present,
matic injuries with the radiologic aspects of the case receiving
secondary consideration. Decontamination of the victim is rec- decontaminate (after treatment of life-threatening
ommended to eliminate radioactive particulate contamination problems).
but should not delay the care of patients requiring immediate • If radioiodine (e.g., reactor accident) is present,
intervention for their traumatic injuries. If the patient does not consider giving prophylactic potassium iodide (Lugol's
show signs ofserious injury requiring immediate intervention, the solution) within fi rst 24 hours only (ineffective later).
patient can be decontaminated first. • See http://www.afrri.usuhs.mil or http://www.orau
.gov/reacts/guidance.h t m .
If radioiodine is present in the environment, as might be
encountered in a nuclear reactor, following a spent fuel rod acci- Decontaminat ion Considerations
dent, or following detonation of a nuclear device, then giving • Exposure without contamination requires no
potassium iodide to emergency responders and victims may
help prevent accumulation of radioiodine in the thyroid, where decon tamination .
it can increase the likelihood of cancer. Other bwcking and • Exposure with contamination requires standard
decorporation therapy may be recommended by the hospital or
federal assistance agencies when more information about the (universal) precautions, removal of patient clothing,
catastrophe is available. Blocking therapy is designed to inter- and decontamination with water.
fere with the effects of the radiologic agent, whereas decorpora- • Internal contamination will be determined at the
tion treatment is targeted at removing the agent from the body hospital.
using medications that combine with the agent and allow for its • Treating contaminated patients before
elimination. decontamination may contaminate the facility; plan for
decontamination before arrival.
Transport Considerations
• For a patient with a life-threatening condition, treat,
Patients should be transported to the nearest appropriate medi-
cal center that is capable of managing trauma and radiation inju- then decontaminate.
ries. All hospitals are required to have a plan for management • For a patient with a non-life-threaten ing condition,
of a radiologic emergency, but communities may have identified
institutions that have decontamination facilities, are capable decontaminate, then treat.
of managing trauma, and have staff trained to deal effectively
with possible external or internal radioactive contamination, as Source: Modified from Armed Forces Radiobiology Institute: Medical
well as the complications of whole-body exposure to ionizing management of radiological casualties, Bethesda, MD, 2003.
radiation.

• Weapons of mass destruction manufactured by terrorist regimes pose a significant threat to civilized society.
• Prehospital care providers may also come in contact with explosions and with chemical and radiologic

material as the result ofindustrial mishaps.
• The safety of prehospital care providers is paramount. They should possess a working lmowledge of levels

of personal protective equipment and the fundamentals of decontamination.
• Explosive agents have predominated in recent terrorist attacks. High explosives produce primary blast

injuries in survivors who are in close proximity to the blast, and secondary injuries result from flying debris.
• Chemical agents may not only injure the skin and pulmonary system but may also result in systemic illness,

manifesting as a specific toxidrome that yields clues to the agent. Antidotes are used for some of these
agents.
• Biologic agents can be highly virulent bacteria or viruses, or toxins produced by living organisms. The types
of protective precautions used by providers vary with the specific agents.
• Several types of radiation exist. Exposure to these agents may result in acute radiation illness, which is
typically a function ofthe type of radiation and the length of exposure.

CHAPTER 20 Explosions and Weapons of Mass Destruction 5 3 9

It is a warm summer evening and you are dispatched to the scene of a reported explosion outside of a popular cafe. You know that
this cafe is usually quite busy and that it typically has patrons both inside and outside on the patio. Dispatch tells you that at this point
the number of victims is unknow n but t hat they have received multiple emergency calls. Ot her public safety agencies have also been
dispatched to the location.

Upon arrival at the location, you note that you are the first prehospital care provider on scene. No incident command has yet been
established. Dozens of people are running about the scene. Many are screaming for you to assist victims who are obviously bleeding.
Other victims are lying on the ground.
• What w ill you do first?
• What are your priorities as you determine your course of action?
• How w ill you care for so many people?

As always, the first priority is safety. Assess the scene. Look for evidence of a secondary device that may pose a t hreat to emergency
responders. Are there other hazards? Look for hanging debris, downed or exposed power lines, or hazardous materials spills. Carefully
observe the crowd for evidence of a toxidrome. Is there an unusually high proportion of respiratory difficulty? A re victims vomiting and
seizing? Is there evidence of agent dispersal in addition t o the explosive blast? Don PPE appropriate for the incident.

Communicate with your chain of command and use the incident command system (ICS). As the first emergency responder to the
scene, the communications center will be relying on you for information. Describe pertinent details of the scene, observed hazards,
numbers of victims, and likely number of resources required to manage the scene and victims. Based on your observations, the commu-
nications center and t he on-duty supervisor can apprise other units and agencies of your sit uat ion and dispatch the necessary resources.
A predef ined disaster response plan may be activated.

Once the personal safety of all emergency responders has been ensured and information has been communicated, prepare to serve
as the incident commander until relieved by another competent authority.

As soon as is feasible, approach the victims with t he intention of triaging t hem for treatment and transport using the START algo-
rithm. Without engaging in the medical management of victims initially, sort t he victims into immediate, urgent, delayed, and expectant
categories. Remember, blast victims may not be able to hear directions or questions from emergency responders. As ot her assistance
arrives, direct personnel to assume roles of the ICS unt il supervisory personnel arrive to assume command and control functions.

References 6. Hall JR Jr. Deaths due to unintentional injury from explosions.
Quincy, MA: National Fire Protection Association, Fire Analysis and
1. Hogan DE, Waeckerle JF, Dire DJ, et al. Emergency department Research Division; 2008.
impact of the Oklahoma City terrorist bombing. Ann Emerg Med.
1999;34:160. 7. Mohtadi H, Murshid A A global chronology of incidents ofchemical,

2. Kennedy K, Aghababian R, Gans L, et al. Triage: techniques biological, radioactive and nuclear attacks: 1950-2005. http://www
and applications in decision making. Ann Emerg Med. .ncfpd.umn.edu/Ncfpd/assets/File/pdf/GlobalChron.pdf. Accessed
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12. National Counterterrorism Center. 2006 Report on Terrorist 35. Peleg K, Limor A, Stein M, et al. Gunshot and explosion iajuries:
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13. Frykberg ER, Tepas JJ, Alexander RH. The 1983 Beirut Airport 36. Tappan J. Magnesium and thermite poisoning. http://emedicine
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37. Irizarry L. White phosphorus exposure. http://emedicine.medscape
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and biological warfare, TMM series, Part 1, Warfare, weaponry and
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39. Walter FG, ed. Advanced HAZMAT Life Support. 2nd ed. Tucson,
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40. U.S. Army, Medical Research Institute of Chemical Defense. Medical
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logical and chemical weapons of warfare and terrorism. Am J Med
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42. Okumura T, Takasu N, lshimatsu S, et al. Report on 640 victims of
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57. Amon SS, Schechter R, Inglesby TV, et al. Botulinum toxin as a scale of the accident. http://www.who.int/mediacentre/news/
biological weapon. Medical and public health management. JAMA. releases/2005/pr38/en/index.htrnl. Accessed January 10, 2014.
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Suggested Reading
58. Amon SS, Schechter R, Inglesby TV, et al. Botulinum toxin as a
biological weapon: medical and public health management. JAMA. Centers for Disease Control and Prevention Emergency Preparedness
2001;285(8) :1059. and Response Site: http://www.bt.cdc.gov/

59. Hogan DE, Kellison T. Nuclear terrorism. Am J M ed Sci. U.S. Army Medical Research Institute of lnfectious Diseases: http://www
2002;323(6) :341. .usamriid.army.mil/

60. World Health Organization, International Atomic Energy Agency, U.S. Army Public Health Command: http://phc.amedd.army.mil/home/
United Nations Development Programme. Chernobyl: the true

At the completion of this chapter, the reader will be able to do the following:

• Explain why heatstroke is considered an emergent • Identify the differences in the management
life-threatening condition. of mild hypothermia from t hat of severe
hypothermia.
• Identify the similarities and differences between
heatstroke and exercise-associated hyponatremia. • List the signs of mild, moderate, and severe
frostbite and discuss how to prevent its
• Describe the two most effective and rap id cooling progression.
procedures for heatstroke.
• Explain reasons for actively w arming hypot hermic
• List the five factors that place prehospital care patients in cardiopulmonary arrest.
providers at risk for heat illness.

• Discuss the fluid hydration guidelines and how
they can be applied to prevent dehydration in
warm or cold environments.

CHAPTER 21 Environmental Trauma I: Heat and Cold 5 4 3

It is a hot summer afternoon wit h temperatures reaching 102°F (38.9°C). Over the past 30 days, it has been very humid, with tempera-
tures reaching over 100°F (37.8°C) daily. The ambient temperature has resulted in many heat-related injuries that have required emer-
gency medical services (EMS) personnel to transport numerous patients to the emergency departments (EDs) of the inner city.

At 1700 hours, your ambulance unit responds to a dispatch for an unresponsive male patient in a vehicle. As your ambulance unit
arrives on scene, you observe a 76-year-old man who appears to be unconscious in a vehicle parked outside a department store. Your
rapid assessment of t he patient's airway, breathing, and circulation (ABCs) and level of consciousness reveals that the patient is verbal,
but he is saying th ings that are illogical and irrational.

• What are t he potential causes for this patient's decreased level of consciousness?
• What hallmark signs support a heat-related diagnosis?
• How would you emergently manage th is patient at the scene and en route to t he ED?

-1'/•~ Introduction incidents each year. By the end of this century, that number is
This chapter focuses on recognizing and treat- expected t o increase to an average of 4,500 per year due to cli-
ing exposure to both hot and cold tempera- mate change. The year 2012 was documented as the warmest
tures. The most significant morbidity and mortality in the United year in recorded history according to the U.S. National Oceanic
States from all environmental traumas are caused by thermal and Atmospheric Administration. More deaths were caused by
trauma1·5 heat stress than by hurricanes, lightning, tornadoes, floods, and
earthquakes combined. Of the 8,015 deaths previously men-
Environmental extremes of heat and cold have a common tioned, 3,829 (48%) were related to high ambient temperatures
outcome of injuries and potential death that can affect many and includes an average of about 182 heat-related deaths per
individuals during the peak summer and winter months. It is month during the four warmest months (May through August).
critical to know that mortality increases significantly when a The greatest percentage of deaths (1,891, or 45%) occurred in
traumatized patient presents in the hospital with either hypo- those who are 65 years of age and older.
thermia (core body temperature less than 96.8°F [36°C]) or
hyperthermia (core body temperature greater than 100.4°F Furthermore, morbidity and mortality can be extremely
[38°C])6 (Figure 21-1). Individuals who are especially suscepti- high when periodic seasonal heat waves occur (more than 3 con-
ble to both highs and lows of temperature are very young per- secutive days of air temperatures 90°F [32.2°C] or higher). The
sons, the elderly population, people living in urban areas and Centers for Disease Control and Prevention reported a total of
in poverty, individuals who take specific medications, patients 3,442 deaths (1999 to 2003) resulting from exposure to extreme
with chronic illnesses, and persons with alcoholism.u,7-10 The heat (annual mean of688). In 2,239 (65%) of the deaths recorded,
majority of emergency medical services (EMS) responses in the the underlying cause was exposure to excessive heat, whereas
United States for heat and cold injuries are for patients with in the remaining 1,203 (35%), hyperthermia was recorded as a
hyperthermia or hypothermia in an urban setting. However, contributing factor. Males accounted for 66% of deaths and out-
expanding interest in recreational and high-risk adventure activ- numbered deaths among females in all age groups. Of the 3,401
ities in the wilderness backcountry during periods of environ- decedents for whom age information was available, 228 (7%)
mental extremes places more individuals at risk for heat-related were aged less than 15 years; 1,810 (53%) were aged 15 to 64
and cold-related injuries and fatalities.11•14 years; and 1,363 (40%) were aged 65 years and older.3

Epidemiology In July of 1995, a record heat wave occurred during a
17-day period in Chicago, Illinois.15•16 The Chicago Medical
Heat-Related Illness Examiner's office reported 1,177 heat-related deaths during
this short period. These cases included deaths in which heat
During a20-yearperiod (1979 to 1999) in the United States, 8,015 was determined to be the underlying (primary) cause of death
heat-related deaths from all causes were recorded.2 Currently, an and in which cardiovascular disease was listed as the cause of
average of 1,300people in the United States die from heat-related death and heat as a contributing factor (secondary). Compared
with the same period in 1994, this was an 84% increase in heat-
related deaths. Of these 1,177 cases, heat was the primary cause
of death in 465 (39.5%).16

544 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Figure 21-1 adjusted for age, death from hypothermia occurred approximately
2.5 times more often in men than in women. The incidence of
Fahrenheit Centigrade hypothermia-related deaths progressively increases with age and
is three times higher in males than in females after age 15 years.
110 43.3 From 1999 through 2011, the CDC reports an average of 1.301
deaths were reportedfrom exposure to cold weather inthe United
109 42.8 States; of these deaths, 6'l°Ai were males and 51%were older than
65 years of age.8 Major contributing factors for accidental hypo-
108 42.2 thermia are urban poverty, socioeconomic conditions, alcohol
intake, malnutrition, and age (very young and senior citizens).4•8
107 41.7
While hypothermia is typically associated with cool or
106 4 1.1 colder weather, it may occur in conditions that one would ordi-
narily not consider cold, but that allow the body's temperature
105 40.6 to fall below 96°F (35.6°C). For example, the elderly and infants
may develop hypothermia in sununertime if the air conditioning
104 40.0 in their home is too cold for their limited adaptive mechanisms.
Swimmers and surfers can become hypothermic in the sununer
103 39.4 when exposed to water that is cooler than body temperature.
Hypothermia is not just a cold weather disease.
102 38.9
Anatomy
101 38.3
The Skin
100 37.8
The skin, the largest organ of the body, interfaces with the exter-
99 37.2 nal environment and serves as a layer of protection. It prevents
the invasion of microorganisms, maintains fluid balance, and reg-
98.6 37.0 ulates temperature. Skin is composed of three tissue layers: the
epidermis, dermis, and subcutaneous tissue (Figure 21-2). The
98 36.7 outermost layer, the epidermis, is made up entirely of epithelial
cells, with no blood vessels. Underlying the epidermis is the
97 36.1 thicker dermis. The dermis is 20 to 30 times thicker than the
epidermis. It is made up of a framework of connective tissues
96 35.6 that contain blood vessels, blood products, nerves, sebaceous

95 35.0

94 34.4

93 33.9

92 33.3

91 32.8

90 32.2

88 31.1 ..6=---- Hair ~

86 30.0

Pore

84 28.9 - Germinal layer of
epidermis

82 27.8 --.,-1-~1---'-"f-- Sebaceous gland

p:,.,E--!"-----'-- Erector pillae

80 26.7 --;-tt-:r:.!._~:::::=7=..,__ muscle
Nerve (sensory)

Note: To convert from °F to 0 0 ( = (°F - 32) x 5/9
(:
Sweat gland
To convert from °C to °F: °F= (0 ( x 9/5) + 32 _, ,_._,.,,___ _ _ _ _ Hair follicle

--9--- --== ---='--- Blood vessel

=:::-,;-:~~~~::::::~ .=::;;;;;..;;;;;..=::::;::;;: - Subcutaneous fat

Cold-Related Illness SUBCUTANEOUS TISSUE

Mild to severe cold weather conditions cause an average of 689 Figure 21-2 The skin is composed of three tissue layers-epidermis,
deaths per year in the United States. Almost one-half of these dermis, and subcutaneous layer-and associated muscle. Some layers
deaths occurred in persons 65 years of age and older.4 When contain structures such as glands, hair follicles, blood vessels, and
nerves. All these structures are interrelated to the maintenance, loss,
and gain of body temperature.

CHAPTER 21 Environmental Trauma I: Heat and Cold 5 4 5

glands, and sweat glands. The innermost layer, the subcutane- core and from skeletal muscle contraction. The heat generated
ous layer, is a combination of elastic and fibrous tissue as well is transferred throughout the body by blood in the circulatory
as fatty deposits. Below this layer is skeletal muscle. The skin, system. Heat transfer and its dissipation from the body by the
nerves, blood vessels, and other underlying anatomic structures cardiopulmonary system are important in the assessment and
have major roles in regulating body temperature. management of heat illness, as discussed later in the chapter.

Physiology Shivering increases the metabolic rate by increasing mus-
cle tension, which leads to repeated bouts of muscular contrac-
Thermoregulation and Temperature tion and relaxation. There are some individual differences, but
Balance typically shivering starts when the core temperature drops to
between 94°F and 97°F (34.4°C to 36.1°C) and continues until the
Humans are considered homeotherms, or warm-blooded ani- core temperature is 88°F (31.1°C).15 With maximal shivering, heat
mals. A key feature of homeotherms is that they are able to regu- production is increased by five to six times the resting levei.1s,19
late their own internal body temperature independent of varying
environmental temperatures. The physiologic thermoregulation systems that control heat
production and heat loss responses are well documented.11,19,20
The human body is essentially divided into a warmer, inner Two principles in thermoregulation are key to understanding
core and an outer shell. The brain and the thoracic and abdom- how the body regulates core temperature: thermal gradient
inal organs are included in the inner core, and the skin and sub- and thermal equilibrium. A thermal gradient is the difference
cutaneous layer make up the outer shell. The outer shell plays in temperature (high vs. low temperature) between two objects.
a critical role in the regulation of the body's core temperature. Thermal equilibrium is the state at which two objects in contact
The core temperature is regulated through a balance ofheat-pro- with one another are at the same temperature; it is achieved by
duction and heat-dissipation mechanisms. The temperature of the transfer ofheat from a warmer object to a colder object until
the skin's surface and the "thickness" of the outer shell depend the objects are the same temperature.
on the environmental temperature. The outer shell becomes
"thicker" in colder temperatures and "thinner" in warmer tem- When body temperature rises, the normal physiologic
peratures based on the shunting of blood away from or to the response is to increase skin blood flow and to begin sweating.
skin, respectively. This outer shell or tissue insulation, as induced The majority of body heat is transferred to the environment at
by vasoconstriction, has been estimated to offer about the same the skin surface by conduction, convection, radiation, and evap-
level of protection as wearing a light business suit. oration. Because heat is transferred from greater temperature to
lower temperature, the human body can gain heat by radiation
Metabolic heat production will vary based on activity levels. and conduction during hot weather conditions.
Independent of the variation of external temperature, the body
normally functions within a narrow temperature range, known Methods to maintain and dissipate body heat are important
as steady-state metabolism, of about 1°F on either side of concepts for prehospital care providers. They must understand
98.6°F (37°C ± 0.6°C). Normal body temperature is maintained how both heat and cold are transferred to and from the body so
in a narrow range by homeostatic mechanisms regulated in the that they can effectively manage a patient who has hyperther-
hypothalamus, which is located in the brain. The hypothalamus mia or hypothermia (Figure 21-3). The methods of heat and cold
is known as the thermoregulatory center and functions as the transfer are described as follows:
body's thermostat to control neurologic and hormonal regulation
of body temperature. As noted in preceding chapters, trauma to • Radiation is the loss or gain of heat in the form of elec-
the brain can disrupt the hypothalamus, which in turn causes an tromagnetic energy; it is the transfer of energy from a
imbalance in the regulation ofthe body temperature. warm object to a cooler one. A patient with heat illness
can acquire additional body heat from the hot ground
Humans have two systems to regulate body temperature: or directly from the sun. These sources of heat will
behavioral regulation and physiologic thermoregulation. increase body temperature and impede interventions
Behavioral regulation is governed by the individual's thermal to cool the patient until the prehospital care provider
sensation and comfort, and the distinguishing feature is the con- eliminates these sources of radiant heat when assess-
scious effort to reduce thermal discomfort (e.g., adding clothing, ing and treating the patient.
seeking shelter in cold environments). The processing of sen-
sory feedback to the brain of thermal information in behavioral • Conduction is the transfer of heat between two objects
regulation is not well understood, but the feedback of thermal in direct contact with each other, such as a patient lying
sensation and comfort responds more quickly than physiologic on a frozen lawn after a fall. A patient will generally
responses to changes in environmental temperature. 17 lose heat faster when lying on the cold ground than
when exposed to cold air. Therefore, prehospital care
Heat Production and Thermal Balance providers need to lift the patient off the ground in cold
temperatures rather than merely covering the patient
Basal metabolic rate is the heat produced primarily as a with a blanket.
by-product of metabolism, mostly from the large organs of the
• Convection is the transfer ofheat from a solid object to
a medium that moves across that solid object, such as
air or water over the body. The movement of cool air or

5 4 6 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

because they are regulated by the body to control core
temperature.5

Solar Sky thermal Increases (hyperthermia) and decreases (hypothermia) in
radiation radiation body temperature beyond the steady-state range (98.6°F ± 1°F
[37°C ± 0.6°C]) can result from different internal and external
Evaporation Air temperature causes, and return to steady-state temperature can occur with-
(respiration) Air humidity out complications.20 Hyperthermia occurs primarily in one of
three ways:
Convection
• As a normal response to sustained exercise, in which
the heat produced elevates core temperature and is the
stimulus for heat-dissipating responses (e.g., sweating,
increased blood fl.ow in skin)

• When the sum of heat production and heat gained from
the environment is greater than the body's heat dissipa-
tion capability

• From a fever

Reflected solar Unlike the first two ways, fever usually occurs in response
radiation to inflammation because of a change in the thermoregulatory
set point (body temperature setting) of the brain, and the body
responds by elevating body temperature to a higher value (100°F
to 106°F [37.8°C to 41.1°C]). Heat production increases only tem-
porarily to achieve a new thermoregulatory set point tempera-
ture in an attempt to make the environment less hospitable for
the invading infection.20

radiation

Figure 21-3 How humans exchange thermal energy with the Homeostasis
environment.
All of these anatomic structures and physiologic systems are
water across the warmer skin provides for the contin- interacting so that the body functions properly when exposed
uous elimination of heat from the body. The body will to temperature changes. The body is in a constant state of neu-
lose heat 25 times faster in water than in air of the same rologic feedback from peripheral and internal regions to the
temperature. A patient with wet clothing will lose body thermoregulatory center and other regions in the brain-all in an
heat rapidly in mild to cold temperatures, so prehospi- effort to maintain constant, stable internal conditions, or homeo-
tal careproviders should remove wet clothing and keep stasis, in the body. However, at times, this does not occur. For
a patient dry to maintain body heat. When prehospital example, when an imbalance occurs in the cardiovascular and
care providers effectively manage a patient with heat thermoregulatory adjustments to eliminate excessive body heat,
illness, they use the principle of convective heat loss one outcome is the loss of excessive body fluid through sweat-
by moistening and fanning the patient to dissipate body ing, which causes acute dehydration and may lead to signs and
heat quickly. symptoms of heat illness.
• Evaporation of sweat from a liquid to a vapor is an
extremely effective method of heat loss from the Risk Factors in Heat
body, depending on the relative humidity or moisture Illness
in the air. A basal level of both water and accompa-
nying heat loss from exhaled air, skin, and mucous Many studies on humans have demonstrated large individual
membranes is called insensible loss and is caused differences in their tolerance to hot environments.21 These
by evaporation. This insensible loss is normally about differences can be partially explained by both physical char-
10% of basal heat production, but when the body acteristics and medical conditions that are associated with
temperature rises, this process becomes more active an increased risk for heat illness (Figure 21-4). It is import-
(sensible), and sweat is produced. Evaporative heat ant to realize that any situation in which heat production
loss increases in cool, dry, and windy conditions (e.g., exceeds the body's ability to dissipate heat may result in heat
deserts). Collectively, convection and evaporation are injury.
more important than other methods of heat transfer

CHAPTER 21 Environmental Trauma I: Heat and Cold 547

Figure 21-4

Conditions • Decrease thirst
• Cardiovascular disease • Haloperidol
• Dehydration • Angiotensin-converting enzyme (ACE) inhibitors
• Autonomic neuropathies (nerve dysfunction involving the
• Decrease sweating
sympathetic, parasympathetic, or both systems) • Antihistamines
• Parkinsonism • Anticholinergics
• Dystonias (abnormal, involuntary muscle movements or • Phenothiazines
• Glutethimide
contractions) • Beta blockers
• Skin disorders: psoriasis, sunburn, burns
• Endocrine disorders (hyperthyroidism, • Increase water loss
• Diuretics
pheoch romocytoma) • Ethanol
• Fever • Nicotine
• Delirium tremens (alcohol withdrawal)
• Psychosis Behavior
• Neonates, elderly persons • Injudicious exertion (e.g., excessive exercise in hot
• History of heatstroke
• Obesity conditions)
• Low fitness • Inappropriate clothing
• Poor acclimatization
Toxins/Drugs • Poor fluid intake
• Increase heat production • Poor supervision
• High motivation (e.g., working too hard in hot
• Thyroid hormone
• Cyclic antidepressants conditions)
• Hallucinogens (e.g., LSD) • Athletic profile
• Cocaine • Military recruit profile
• Amphetamines

Source: This article was published in Emerg Med Clin North Am 10(2), Tek D, Olshaker JS: Heat illness, p. 299, Copyright Elsevier 1992.

Key risk factors that contribute to the onset of heat illness reduce tolerance to heat exposure. Physical fitness provides a
are alcohol consumption, medications, dehydration, higher body cardiovascular reserve to maintain cardiac output as needed to
mass index, obesity, inadequate diet, improper clothing, low fit- sustain thermoregulation. Individuals who are overweight have
ness, sleep loss, extremes of age, cardiovascular disease, skin a normal response to heat exposure-vasodilation of skin blood
injuries, previous heat-relatedillness, sickle cell trait, cysticfibro- vessels and increased sweating; however, the combination of
sis, sunburn, viral illness, and exercise during the hottest hours low fitness, lack of heat acclimatization, and higher body mass
of day.22•23 Transient conditions include those affecting individ- index increases the energy cost of movement, placing them at
uals who travel from cooler climates and are not heat-acclima- greater risk for heat illness.
tized to wanner climates on arrival. Other transient factors that
place individuals at risk for heat illness are common illnesses, Age
including colds and other conditions that cause fever, vomiting,
and diarrhea, along with poor dietary and fluid intake.24•25 Thermoregulatory capacity and tolerance to heat diminish with
age, particularly in those individuals 65 years or older. These indi-
Factors considered to be chronic conditions that place indi- viduals can improve their heat tolerance by maintaining a low
viduals at greater risk for heat illness are fitness level, body size, body weight and obtaining an improved level of physical fitness.
age, medical condition, and medication use.
Special consideration must be given for infants and young
Fitness and Body Mass Index children since their body surface area makes up a much greater
proportion of their overall weight compared to an adult, caus-
Low levels of physical fitness caused by genetic factors or a ing them to face a much greater risk of heat-related illness.
sedentary lifestyle with inadequate daily physical activity will Furthermore, infants have an immature thermoregulatory

5 4 8 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

capacity that cannot adequately maintain body temperature during physical activity, as seen with profuse sweating in ath-
when exposed to high heat. letes. Generally, these individuals consume no fluid or low vol-
umes of fluid during daily activities, not replacing the depleted
Gender body water. Children (younger than 15 years) and persons older
than 65 years are particularly susceptible to dehydration.
A long-held belief was that women are less tolerant of heat than
men are. Although wide variation was reported previously, these Body water is lost daily through sweat, tears, urine, and
differences resulted from women who were less physically fit stool. Normally, drinking fluids and eating foods that contain
and had less exposure to heat compared with men in conditions water replace body water. When a person becomes sick with
that would induce full heat acclimatization. More recent studies fever, diarrhea, or vomiting, or an individual is exposed to heat,
have controlled for differences in physicalfitness and heat accli- dehydration occurs. Occasionally, drugs that deplete body fluids
matization between men and women and indicate that women and electrolytes, such as diuretics, can cause dehydration.
demonstrate equal work tolerance in heat and, in some studies,
are more tolerant ofheat than men are. During heat exposure, body water is primarily lost as
sweat. Individuals can sweat 0.8 to 1.4 liters per hour (liters/
Medical Conditions hour), and it has been reported that some elite athletes who are
heat-acclimatized can sweat up to 3.7 liters/hour during compe-
Underlying medical conditions such as diabetes mellitus, thy- tition in hot environments.26 The keys to avoiding the onset of
roid disorders, and renal disease can increase the risk for heat heat illness are to maintain a body fluid balance and to minimize
intolerance and heat illness. Cardiovascular disease and circu- dehydration during daily activities, particularly during any phys-
latory problems that increase cutaneous blood fl.ow and circula- ical activity in moderate to high heat exposure. Individuals nor-
tory demand are aggravated by heat exposure. In these extreme mally do not perceive thirst until a deficit ofapproximately 2% of
environmental conditions, heart disease and pulmonary diseases body weight has resulted from sweating.27 Thirst provides a poor
may be the presenting signs and symptoms aggravated by high indicator of body water needs during rest or physical activity.
ambient temperatures. A mild form of heat illness seen in indi-
viduals is "prickly heat rash," which has been shown to cause With mild to moderate levels of acute dehydration (2% to
reduced heat tolerance. 6% body weight), individuals experience fatigue, headache,
decreased heat tolerance, and cognitive deterioration, along
Medications with reductions in strength and aerobic physical capacity.28•29
People will consistently underconsume fluids and remain
The use of specific prescription or over-the-counter medica- dehydrated at approximately 1% to 2% of body weight without
tions can place individuals at a greater risk for heat illness (see some form of fluid hydration guidelines to direct them regard-
Figure 21-4). Certain medications can increase metabolic heat ing the amount of fluids to consume per hour when exposed to
production, suppress body cooling, reduce cardiac reserve, and mild or high heat exposure. The underconsumption of fluid to
alter renal electrolyte and fluid balance. Sedative and narcotic restore normal water balance is currently known as voluntary
drugs will affect mental status and can affect logical reasoning dehydration.23
and judgment, suppressing decision-making ability, when the
individual is exposed to heat. When individuals are encouraged to drink fluids frequently
during heat exposure, the rate at which fluids can be replaced by
Dehydration mouth is limited by the rate of gastric emptying and the rate of
fluid absorption in the small intestine.30 Fluids empty from the
Body water is the largest component of the human body, repre- stomach to the small intestine, where absorption occurs into the
senting 45% to 700Al of body weight. For example, a 165-pound bloodstream, at a maximal rate of approximately 1 to 1.2 liters/
(75-kilogram [kg]) man contains approximately 45 liters of hour.29 Furthermore, gastric emptying rates are decreased
water, representing 600Ai of body weight. Excessive changes in approximately 20% to 25% when sweat-induced weight loss
the normal body water balance (euhydration) resulting from causes dehydration of 5% of total body weight (e.g., 5% of a
either overconsumption of water (hyperhydration) or fluid loss 200-pound male= 10-pound weight loss).31
(causing acute dehydration) alter homeostasis, producing spe-
cific signs and symptoms. Acute dehydration can be a serious The important message is that once dehydration occurs,
outcome of both heat and cold exposure, but it is also seen as a it becomes more challenging to rehydrate the individual ade-
dangerous side effect of diarrhea, vomiting, and fever. quately with oral fluids. In addition, rapid oral administration
of fluids may lead to nausea and vomiting, further exacerbating
Dehydration is a common :finding in many cases of heat ill- the dehydration problem. The key to minimizing dehydration
ness occurring over many days, as seen in geriatric patients, or during heat exposure is to begin consuming oral fluids before
heat exposure and to maintain fluid intake frequently during and
after heat exposure. The goal of oral hydration throughout daily
activity is to prevent excessive dehydration (less than 2% body
weight loss) and excessive changes in electrolytes (e.g., sodium,
potassium, and chloride).32

CHAPTER 21 Environmental Trauma I: Heat and Cold 549

Signs and Symptoms of Dehydration seen on the skin in areas of restrictive clothing and heavy
sweating (Figure 21-6). This condition is caused by inflamma-
The following are the most common signs and symptoms of tion of the sweat glands that blocks the sweat ducts. As a result,
dehydration in infants, children, and adults, although each indi- affected areas cannot sweat, putting individuals at increased
vidual may experience symptoms differently: risk of heat illness, depending on the amount of skin surface
involved.
• Less frequent urination and dark color urine
• Thirst Management
• Dryskin
• Fatigue Treatment begins by cooling and drying the affected area(s) and
• Light-h eadedness by preventing further conditions that cause sweat in these areas.
• Headache For example, get the patient out of the heat and humidity and
• Dizziness into a cooler, dryer environment.
• Confusion
• Dry mouth and mucous membranes Heat Edema
• Increased heart rate and breathing
Heat edema is a mild, dependent edema in the hands, feet, and
In infants and children, additional symptoms may include ankles seen during early stages of heat acclimatization when
the following: plasma volume is expanding to compensate for the increased
need for thermoregulatory blood flow. This form of edema does
• Dry mouth and tongue not indicate excessive fluid intake or cardiac, renal, or hepatic
disease. In the absence of other diseases, this condition is of no
• No tears when crying clinical significance and is self-limited. Heat edema is observed
more often in females.
• No wet diapers for more than 3 hours
Management
• Sunken abdomen, eyes, or cheeks
Treatment consists of loosening any constricting clothes,
• High fever removing any tight or constricting jewelry, and elevating the
legs. Diuretics are not indicated and may increase risk of heat
• Listlessness illness.

• Irritability

• Skin that does not flatten when pinched and released
(skin tenting)

Injuries Caused by HeatTetany

Heat Heat tetany is a rare and self-limited condition that may occur
in patients acutely exposed to short, intense heat conditions.
Heat-related disorders can range from minor to severe in patients The hyperventilation that results from these conditions is
with heat illness.23•33 It is important to note that prehospital care considered to be the principle cause of the symptoms that
providers may or may not see a progression of signs and symp- develop, including numbness and tingling; spasm of the
toms, starting with minor syndromes (e.g., heat rash or muscle hands, fingers, and toes (carpopedal spasm); and muscle
cramps) and advancing to major heat-related illness (e.g., classic spasms.
heatstroke). In the majority of heat exposures, the patient is able
to dissipate core body heat adequately and maintain core tem- Management
perature within the normal range. However, when heat-related
conditions result in a call for EMS assistance, the minor heat- Treatment consists of removal from the source of heat and
related conditions may be apparent to the prehospital care pro- controlling hyperventilation. Dehydration is not a common
vider during patient assessment, along with signs and symptoms occurrence with these short heat exposures. Heat tetany may
of a major heat illness (Figure 21-5). be seen along with signs and symptoms of heat exhaustion and
heatstroke.
Minor Heat-Related Disorders

The minor heat-related disorders include heat rash, heat edema, Muscle (Heat) Cramps
heat tetany, muscle (heat) cramps, and heat syncope. These
are not life-threatening problems but require assessment and Muscle cramps are manifested by short-term, painful muscle con-
treatment. tractions frequently seen in the calf (gastrocnemius) muscles,
but also in the voluntary muscles of the abdomen and extrem-
Heat Rash ities, and are commonly observed following prolonged physical
activity, often in warm to hot temperatures. These cramps occur
Heat rash, also known as "prickly heat" and miliaria rubra, is in individuals during exercise that produces profuse sweating or
a red, pruritic (itchy), papular (raised bumps) rash normally during the exercise-recovery period. Smooth muscle, cardiac,

5 5 0 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Figure 21-5 • Cause/Problem ...- Signs/Symptoms Treatment

Disorder Failure to replace sodium Painful muscle cramps, Move to cool place; massage/
Muscle (heat} cramps chloride (salt, or NaCl) usually in legs or stretch muscle; encourage
lost through sweating; abdomen drinking sport drinks or
Dehydration electrolyte and muscle drinks with NaCl (e.g.,
problems tomato juice). Transport
Heat exhaustion those with signs or
Failure to replace sweat loss Thirst, nausea, excessive symptoms listed below.
Heatstroke with fluids fatigue, headache,
hypovolemia, decreased Replace sweat loss with
Exercise-associated thermoregulation; lightly salted fluids;
hyponatremia (also reduces physical and rest in cool place until
referred to as water mental capacity body weight and water
intoxication) losses are restored. In some
Excessive heat strain with Low urine output, patients, IV rehydration is
inadequate water intake; tachycardia, weakness, necessary.
cardiovascular problems unstable gait, extreme
with venous pooling, fatigue, wet clammy Remove from heat source and
decreased cardiac filling skin, headache, place in cooler location;
time, reduced cardiac dizziness, nausea, cool body with water and
output; untreated, may collapse fanning; encourage drinking
progress to heatstroke lightly salty fluids (e.g.,
sport drinks); administer
High core temperatures Mental status changes; intravenous (IV) 0.9%
> 105°F(40.6°C); irrational behavior NaCl or lactated Ringer's
cellular disruption; or delirium; possible solution.
dysfunction of multiple shivering; tachycardia
organ systems common; initially, then bradycardia Emergency: Apply rapid,
neurologic disorder with late; hypotension; rapid immediate cooling by water
thermoregulatory center and shallow breathing; immersion, or wet patient
failure dry or wet, hot skin; or wrap in cool wet sheets
loss of consciousness; and fan vigorously. Continue
seizures and coma until core temperature is
< 102°F (38.9°C). Treat for
Low plasma sodium Nausea, vomiting, malaise, shock if necessary once core
concentration; typically dizziness, ataxia, temperature is lowered.
seen in individuals during headache, altered Immediately transport to
prolonged activity in hot mental status, polyuria, emergency department.
environments; drinking pulmonary edema, signs
water(> 4 liters/hour) that of intracranial pressure, Restrict water intake;
exceeds sweat rate; failure seizures, coma; core give salty foods/saline.
to replace sodium loss in temperature < 102°F Unresponsive patients
sweat (38.9°C); mimics signs of receive "ABC" standard
heat illness care, 15 liters/minute
oxygen by nonrebreathing
I mask. If available, provide
IV hypertonic saline 100-
ml bolus of 3% hypertonic
saline, which can be repeated
twice at 10-minute intervals.
Transport immediately
with alert patient in sitting
position or left-lateral

position if unresponsive. -

CHAPTER 21 Environmental Trauma I: Heat and Cold 551

tablets by themselves because these can cause gastrointestinal
(GI) distress.

Heat Syncope

Heat syncope is seen with prolonged standing in warm envi-
ronments and is caused by low blood pressure that results in
fainting or feeling faint or light-headed. Heat exposure causes
vasodilation and venous blood pooling in the legs, causing low
blood pressure. The effects are commonly experienced on tran-
sition from sitting to standing.

Management

After removal to a cool environment, patients rest in a recum-
bent position and are provided oral or IV rehydration. If a fall
occurred, patients should be thoroughly evaluated for any iitjury.
Patients with a signtlicant history of cardiac or neurologic disor-
ders need further evaluation for the cause of their syncopal epi-
sode. Monitoring of vital signs and the electrocardiogram (ECG)
during transport is essential.

Major Heat-Related Disorders

The major heat-related disorders include exertion-associated
collapse, heat exhaustion, and heatstroke (classic and exertional
forms) and may pose a life threat if allowed to progress.

Figure 21-6 Heat rash. Exertion-Associated Collapse
Source:© Wellcome Images Library I Custom Medical Stock Photo
This disorder occurs when an individual collapses after strenu-
diaphragm, and bulbar muscles (muscles involved with speech, ous exercise.34-39 During exercise, contraction of the muscles of
chewing, and swallowing) are not involved. Muscle cramps can the lower extremities assists in augmenting venous blood return
occur alone or in association with heat exhaustion. to the heart. When exercise stops, such as at the end of a jog,
the muscle contraction that assisted blood return to the heart
The cause of muscle cramping is unknown, but it is believed slows significantly. This in turn causes venous blood return to
to be related to muscle fatigue commonly from exercise, body the heart to decrease, resulting in a decreased cardiac output
water loss, and large sodium and other electrolyte losses. It is to the brain.
more commonly seen when individuals exercise in hot and
humid environments. Salt supplementation in the diet has been Assessment
shown to reduce the incidence of muscle cramps.
Signs and symptoms include nausea, light-headedness, collapse,
Management orsyncope. Patientsmay feel better when lying down but become
light-headed when they attempt to stand or sit (orthostati c hypo-
Treatment consists of rest in a cool environment, prolonged tension). Profuse sweating is not unusual. Ventilations and pulse
stretching ofthe affected muscle, and consuming oral fluids and rates may be rapid. The patient's core body temperature may be
food containing sodium chloride (i.e., l;8 to 114 teaspoon of table normal or slightly elevated. It is difficult to rule out dehydration,
salt added to 10 to 16 ounces [300 to 500 ml] of fluids or sport but this type of postexercise collapse is not from hypovolemia.
drinks, 1 to 2 salt tablets with 10 to 16 ounces of fluid, bullion In contrast, collapse that occurs during exercise requires imme-
broth, or salty snacks). Intravenous (IV) fluids are rarely needed, diate evaluation for other causes (e.g., cardiovascular).
but prolonged and severe diffuse muscle cramps can be resolved
more rapidly with IV normal saline (NS). Avoid the use of salt Management

The patient is removed to a cool environment and rests in a
recumbent position. IV rehydration is provided if truly needed
for moderate to severe dehydration; otherwise provide cool

5 5 2 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

fluids by mouth. Since many of these patients experienced It is important to obtain a good history of prior heat illness
collapse because of the decreased venous return at the end of and the current heat exposure incident because these patients
exercise and not from dehydration, it is highly recommended to may display signs and symptoms of other conditions of fluid
withhold IV therapy until further assessment is completed fol- and sodium loss (e.g., hyponatremia; see later discussion).
lowing recumbent rest (Trendelenburg position) and passive Reassessment is critical since heat exhaustion may progress to
"cool down." As with any form of collapse, further evaluation is heatstroke. Continuously look for any changes in mentation and
necessary to rule out other disorders (e.g., exercise-associated personality (i.e., confusion, disorientation, irrational or unusual
hyponatremia, cardiac or neurologic causes). Monitoring ofvital behavior). Any such change should be taken as a progressive
signs and ECG during transport is essential to detect cardiac sign of hyperthermia indicating heatstroke---a life-threatening
dysrhythmias. condition!

Heat Exhaustion Management

Heat exhaustion is the most common heat-related disorder seen Immediately remove the patient from the hot environment (e.g.,
by prehospital care providers. This condition can develop over sun, hot pavement, hot vehicle) to a cooler location either in
days ofexposure, as in elderly persons living in poorly ventilated the shade or air-conditioned space (i.e., ambulance). Place the
spaces, or acutely, as in athletes. Heat exhaustion results from patientina supine resting position. Remove clothing andanything
cardiac output that is insufficient to support the increased cir- restricting heat dissipation, such as a hat or any excess cloth-
culatory load caused by competing demands of thermoregula- ing. Assess the patient's heart rate, blood pressure, ventilatory
tory heat dissipation, increased skin blood flow, reduced plasma rate, and rectal temperature (if a thermometer is available and
volume, reduced venous return to the heart from vasodilation, conditions permit), and be alert particularly for central nervous
and sweat-induced depletion of salt and water.25 Patients with system status changes as an early indicator of life-threatening
heat exhaustion normally present with a rectal temperature less heatstroke.
than 104°F (40°C), but this is a guide and not always a reliable
finding.38 Oral rehydration should be considered for any patient who
can take fluids by mouth and who is not at risk of aspirating,
Another form of heat exhaustion is known as exertional using sport electrolyte fluids diluted to half-strength. Large
heat exhaustion. This occurs with physical exercise or heavy amounts of oral fluids may increase bloating, nausea, and vomit-
exertion in all temperatures. It is defined as the inability to con- ing. Normally IV fluids are not needed as long as blood pressure,
tinue the exercise or exertion and may or may not be associ- pulse, and rectal temperature are normal. However, in patients
ated with physical collapse.23 The key predisposing factors are who are not able to consume fluids by mouth, IV fluids provide
dehydration and high body mass index that place an individual rapid recovery from heat exhaustion.23 If IV fluids are needed,
at greater risk for exertional heat exhaustion. lactated Ringer's (LR) solution or NS should be used. IV solu-
tions produce more rapid fluid recovery than fluids by mouth due
Distinguishing severe heat exhaustion from heatstroke to delays in gastric emptying and absorption in the small intes-
often may be difficult, but a quick mental status assessment tine caused by dehydration.
will determine the level of neurologic involvement. If heat
exhaustion is not effectively treated, it may lead to heatstroke, a In exertional heat exhaustion, most exercising patients
life-threatening form of heatillness. Heat exhaustion is a diagrw- recover with recumbent rest and oral fluids. Before any deci-
sis of exclusion when there is no evidence of heatstroke. These sion is made for IV therapy in these patients, there needs to
patients will need further physical and laboratory evaluation in be a thorough assessment for signs and symptoms of dehy-
the ED. dration, orthostatic (postural) pulse, blood pressure changes,
and the ability to ingest oral fluids. Ongoing mental status
Assessment changes should prompt further evaluation for hyponatremia,
hypoglycemia, and other medical problems. In the exertional
Signs and symptoms of heat exhaustion are neither specific heat exhaustion patient, the recommended IV fluids are NS or
nor sensitive. They include low fluid intake, decreased urine 5% dextrose in NS for patients who are mildly hypoglycemic.
output, frontal headache, drowsiness, euphoria, nausea, vom- However, caution should be used to ensure that large amounts
iting, light-headedness, anxiety, fatigue, irritability, decreased of IV fluids are not administered t o a patient who has been
coordination, heat sensation on head and neck, chills, and apa- participating in prolonged exercise (greater than 4 hours),
thy. Patients may feel better when lying down but may become especially individuals who do not have obvious clinical signs
light-headed when they attempt to stand or sit (orthostatic hypo- of dehydration, or in a collapsed athlete with suspected heat
tension). During the acute stage of heat exhaustion, the blood exhaustion who has been drinking a large amount of water.
pressure is low, and the pulse and ventilatory rates are rapid. This type of patient may have exercise-associated hyponatre-
The radial pulse may feel thready. The patient generally appears mia (low serum sodium level), and providing oral and/or IV
sweaty, pale, and ashen. The patient's core body temperature fluids will cause further dilutional hyponatremia, potentially
may be either normal or slightly elevated, but generally below causing a life-threatening condition.40•41 See the discussion on
104°F (40°C). exercise-associated hyponatremia for information on how

CHAPTER 21 Environmental Trauma I: Heat and Cold 5 5 3

best to correctly assess the patient for heat-related illness or which may be compounded by the risk factors listed in Figure 21-4
exercise-associated hyponatremia.
(e.g., medications). A classic presentation is a patient who is
Because heat exhaustion may be difficult to distinguish exposed to elevated humidity and high room temperatures over
from heatstroke and because patients with heatstroke should be several days without air conditioning, leading to dehydration and
cooled rapidly to reduce core temperature, the best course of high core temperature. Often this patient's sweating mechanism
actionis to provide some active coolingprocedures to all patients has stopped, known as anhidrosis. This is especially common
with heat exhaustion. Active cooling can be done simply and in large cities during summer heat waves, when effective home
quickly by wetting the head and upper torso with water or a wet ventilation is either not possible or not used.15 Scene assessment
cloth and then fanning or positioning the patient into the wind will provide information helpful in the identification of classic
to increase convective body heat dissipation. Body-cooling pro- heatstroke.
cedures will also improve mental status. Transport all patients
who are unconscious, who do not recover rapidly, or who have Exertional heatstroke (EHS) is a preventable disorder
a significant medical history. Proper environmental temperature often seen in those individuals with poor physical fitness or lack
control and monitoring ofvital signs and mental status are essen- of heat acclimatization who are involved in short-term, strenu-
tial during transport. ous physical activity (e.g., industrial workers, athletes, military
recruits, fire fighters, and other public safety personnel) in a hot,
Heatstroke humid environment. These conditions can rapidly elevate inter-
nal heat production and limit the body's ability to dissipate heat.
Heatstroke is considered the most emergent and life-threatening Almost all EHS patients exhibit sweat-soaked and pale skin at
form ofheat illness. Heatstroke is a form of hyperthermia result-
ing in failure of the thermoregulatory system-a failure of the Figure 21-7
body's physiologic systems to dissipate heat and cool down.
Heatstroke is characterized by an elevated core temperature of Classic ExertionaI
104°F (40°C) or greater and central nervous system dysfunction,
resulting in delirium, convulsions, or coma.31·36•42 Patient Elderly Men (15 to
45 years)
The most significant difference in heatstroke compared characteristics
with heat exhaustion is neurologic disability, which presents
to the prehospital care provider as mental status changes. Health status Chronically ill Healthy
Pathophysiologic changes often result in multiple organ fail-
ure.33·43 These pathophysiologic changes occur when organ tis- Concurrent Sedent ary Strenuous
sue temperatures rise above a critical level. Cell membranes activity exercise
are damaged, leading to disruption in cell volume, metabolism,
acid-base balance, and membrane permeability that causes cel- Drug use Diuretics, Usually none
lular and a whole organ dysfunction with ultimate cell death antidepressants,
and organ failure.23 The degree of complications in patients with anti hypertensives,
heatstroke is not entirely related to the magnitude of core tem- anticholinergics,
perature elevation. anti psychotics

This whole-body pathophysiologic dysfunction is the under- Sweating May be absent Usually present
lying reason for the need for early heatstroke recognition by pre-
hospital care providers. With early recognition, prehospital care Lactic acidosis Usually absent; Common
providers can quickly provide aggressive whole-body cooling in poor prognosis if
an effort to rapidly reduce core temperature and decrease the present
associated heatstroke morbidity and mortality too frequently
seen in the emergency department (ED). Hyperkalemia Usually absent Often present

Morbidity and mortality are directly associated with the Hypocalcemia Uncommon Frequent
duration of elevated core temperature, and a positive patient
outcome is directly related to how fast the core temperature can Hypoglycemia Uncommon Common
be decreased below 102°F (38.9°C). Even with aggressive pre-
hospital intervention and in-hospital management, heatstroke Creatine Mildly elevated Greatly elevated
can be fatal, and many patients who survive have permanent
neurologic disability. Rhabdomyolysis Mild Frequent ly
severe
Heatstroke has two different clinical presentations: classic
heatstroke and exertional heatstroke (Figure 21-7). Source: Modified from Knochel JP, Reed G. Disorders of heat regulation.
In: Kleeman CR, Maxwell MH, Narin RG, eds. Clinical Disorders of Fluid and
Classic heatstroke is a disorder of infants, febrile children, Electrolyte Metabolism. New York, NY: McGraw -Hill; 1987.
poor people, the elderly, alcoholic persons, and sick patients,

554 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

time of collapse as compared to dry, hot, and flushed skin in the provider assesses and stabilizes the patient's ABCs. Cooling of
classic heatstroke patient.23 Even though drinking fluids can slow the patient begins immediately with whatever means are avail-
the rate of dehydration during strenuous activity and reduce the able (e.g., garden hose, fire hose, bottled water, IV saline liter
rate at which core temperature rises, hyperthermia and EHS may bags), even before removing clothing. Application of ice or
still occur in the absence of significant dehydration. cold-water immersion are the fastest two methods of cooling,
but these approaches are generally limited in the prehospital
With aggressive treatment, no one should die from EHS if setting.35,4547
prompt care begins within 10 minutes of collapse. Some of the
common reasons that death from EHS may occur are listed Since the late 1950s, it has been thought that cold- or
in Figure 21-8.= The motto to "cool first, transport second" ice-water immersion will cause vasoconstriction sufficient to
is meant to avoid any delays in initiating the lowering of core decrease heat loss from the body and cause the onset of shiver-
temperature. ing so that internal heat is produced, thus limiting the exchange
of heat. Empirical evidence now refutes this concern that cool-
Assessment ing rates in these patients are blunted. Therefore, this form of
cooling, if available, should not be withheld from a patient with
The appearance of signs and symptoms depends on the degree heatstroke.39
and duration of hyperthermia.28 Patients with heatstroke typ-
ically present with hot, flushed skin. They may or may not be If cold water and ice are not immediately available, remove
sweating, depending on where they are found and whether they the patient's excess clothing, wet down the patient head to toe,
have classic or exertional heatstroke. Blood pressure may be ele- and provide continuous fanning of the skin. It is essential that
vated or diminished, and the radial pulse is usually tachycardic this procedure begin immediately and not be delayed before pre-
and thready; 25% of these patients are hypotensive. The patient's paring to transport the patient from the scene to the ambulance.
level of consciousness can range from confused to unconscious, Patient wetting and fanning is the next most effective cooling
and seizure activity may also be present, particularly during cool- technique, causing evaporation and convective heat loss.45
ing.44 As confirmed in hospitals, rectal temperature may range Individuals who rapidly become lucid during whole-body cool-
from 104° to 116°F (40°C to 46.7°C).33•44 ing usually have the best prognosis. The most important inter-
vention prehospital care providers can deliver to a patient
The keys to distinguishing heatstrokefrom one ofthe other with heatstroke (along with ABCs) is immediate and rapid
heat-related conditions are the elevation in body temperature whole-body cooling to reduce core temperature.
and altered mental status. Any patient who is warm to the
touch with an altered mental status (confused, disoriented, During transport, the patient should be placed in a prepared,
combative, orunconscious) should be suspected ofhaving heat- air-conditioned ambulance. It is an error to place a patient with
stroke and managed immediately and aggressively to reduce heatstroke in a hot internal cabin of the ambulance even if it is a
core temperature. short transfer time to the hospital. Remove any additional cloth-
ing, cover the patient with a sheet, and wet down the sheet with
Management irrigation fluids along with providing continuous fanning, ideally
by powered fans from the cabin overhead. Ice packs, if avail-
Heatstroke is a true emergency. Immediately remove the patient able and time allows, can be placed in the groin area, in the axil-
from the source of heat. Cooling the patient should begin imme- lae, and around the anterior-lateral neck because blood vessels
diately in the field by one prehospital care provider as another are closest to the skin surface in these areas. The widespread

Figure 21-8

1. Inaccurate temperature assessment or misdiagnosis. 3. Inefficient whole-body cooling techniques. The goal to
This is often due to the inability to rule out other reduce core temperature rapidly below 104°F (40°C)
similar medical conditions. Oral, axillary, and tympanic within 30 minutes is critical. Th is is recognized as the
temperature measurements may underestimate "golden half-hour" of heatstroke management and is
the degree of temperature elevation; therefore, the standard to meet with rapid whole-body cooling.
prehospital care providers should rely only on the
rectal temperature to determine the degree of 4. Immediate transport. With EHS it is critical to begin
hyperthermia. whole-body cooling to reduce the core temperature
at the scene and not to transport until this treatment
2. No care or a treatment delay. Failing to recognize the gets started. Cooling should continue during transport
potential for EHS and delaying the response to provide with rectal temperature assessment to ensure core
effective care can have disastrous results. temperature drops below 104°F (40°C).

CHAPTER 21 Environmental Trauma I: Heat and Cold 5 5 5

recommendation ofusing ice packs alone is a much inferior core malaise, confusion, and seizures to coma, permanent brain
cooling technique. They are completely insufficient to rapidly damage, brain stem herniation, and death.40•41•51 These indi-
lower core body temperature and should be considered only as viduals are said to have exercise-associated hyponatremic
an extra cooling method and not a priority in patient care.4,44,45 encephalopathy (EAHE).40•41•51

If possible, the patient's rectal temperature should be Symptomatic EAHE patients generally have a serum sodium
measured every 5 to 10 minutes during transport to ensure concentration below 126 milliequivalents (mEq)/liter (normal
effective cooling. Other means to assess the patient's tempera- range, 135 to 145 mEq/liter) with rapidly developing (less than 48
ture (e.g., oral, skin, axillary) should not be used for treatment hours) hyponatremia, as seen frequently in prolonged endurance
decisions since they do not adequately reflect the patient's core activities.40•41•48•52 Alternatively, the milder form of EAH generally
temperature.23 presents with isolated serum sodium levels of 135 to 128 mEq(
liter, without easily discemable symptoms (i.e., weakness, nau-
Active cooling should stop when the patient's rectal tem- sea/vomiting, headache, or no symptoms), and is self-limiting
perature reaches 101.5°F to 102°F (38.6°C to 38.9°C) since the with rest, food, and electrolyte fluids. Even with the initial pre-
core temperature will continue to drop even after cooling pro- senting mild signs and symptoms of EAH, a patient can progress
cedures stop and could end up below 98°F (36.7°C).as,47 Provide into EAHE. It has been suggested that there is an acute drop in
high-flow oxygen, support ventilations with a bag-mask device as serum sodium concentration at the end of an endurance event
needed, and monitor the patient's cardiac rhythm. caused by the absorption of water retained in the GI tract.40•41
This may account for a transient lucid period after finishing an
Patients with heatstroke generally do not require exten- endurance activity followed by the acute development of clinic
sive fluid resuscitation and typically are initially given IV fluids signs of EAHE within about 30 minutes following the cessation
consisting of 1.0 to 1.5 liter of NS. Provide a 500-milliliter (ml) of the activity.
fluid challenge and assess vital signs. Fluid volume should not
exceed 1 to 2 liters in the first hour, or follow local medical Studies have reported that 18%to 23%of ultra-marathoners
protocol. Monitor blood glucose because these patients are fre- and 29% of the Hawaiian Ironman Triathlete finishers had
quently hypoglycemic and may require a bolus of 50% dextrose EAH.38·43-56 In 2003, 32 cases of EAH were reported in hikers in the
IV. Seizures can be managed with 5 to 10 milligrams (mg) of diaz- Grand Canyon National Park, requiring extensive rescue efforts
epam or other benzodiazepines as per local protocol. Transport by park rangers and paramedics in many cases.57
the patient in a right or left lateral recumbent position to main-
tain an open airway and to avoid aspiration. EAH can occur in the following situations:

Exercise-Associated Hyponatremia 1. Excessive sodium and water loss in sweat through-
out an endurance event, resulting in dehydration and
Exercise-associated hyponatremia (EAH), also known as exer- sodium depletion
tional hyponatremia or water intoxication, is a life-threatening
condition that has been increasingly described after pro- 2. Overhydration solely with water while maintain-
longed physical exertion in recreational hikers, marathoners, ing plasma sodium, creating a dilution of sodium
ultra-marathoners, triathletes, adventure racers, and military concentration
infantry personnel.48-52 With the increasing popularity of these
outdoor activities, the incidence of mild to severe EAH has 3. Combination of excessive sodium and fluid loss in
steadily increased since it was first reported in the mid-1980s.51 sweat and an excessive overhydration with water only
It is now known to be one of the most severe medical compli-
cations of endurance activities and is an important cause of The evidence indicates that EAH is a result offluid retention
event-related fatalities.40•41 in the extracellular space (dilutiona[) rather than fluid remain-
ing unabsorbed in the intestine.48 Typically, these patients have
EAH is commonly associated with excessive consumption not consumed sport electrolyte drinks, have consumed energy
of water (1.5 quarts (1.4 liters] or greater per hour) during pro- food supplements containing no salt, or have consumed salt in
longed activities.52 Two major pathogenic mechanisms largely insufficient quantity to balance the loss ofsodium in sweat or the
account for the development of EAH: (1) excessive fluid intake dilution from excessive water intake.
and (2) impaired urinary water excretion due largely to per-
sistent secretion of arginine vasopressin (AVP), also referred The following are a few key risk factors that have been
to as antidiuretic hormone (ADH).40•41 EAH can take two forms, linked to the development of EAH34•35•58:
mild or severe, depending on presenting symptoms.
1. Activity or exercise duration (greater than 4 hours) or
In the severe form, low plasma sodium concentration dis- slow running/exercise pace
turbs the osmotic balance across the blood- brain barrier, result-
ing in the rapid influx of water into the brain, which causes 2. Female gender (may be explained by lower body
cerebral edema.40•4 1•51•52 In similar fashion to the signs and symp- weight)
toms of increased intracranial pressure in head trauma (see the
Head Trauma chapter), a progression of neurologic symptoms 3. Low or high body mass index
from hyponatremia will occur, including headache, vomiting, 4. Excessive drinking (greater than 1.5 liters/hour) during

an event or activity
5. Use ofnonsteroidal anti-inflammatory drugs (NSAIDs),

which decrease renal filtration

5 5 6 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

EAH has been described as the "other heat-related illness" headache, and nausea. Other forms of neurologic changes
because the symptoms are nonspecific and are similar to those include slowed speech, ataxia, and cognitive changes, including
exhibited in minor and major heat-related disorders.57 Many irrational behavior, combativeness, and fear. These patients also
endurance events and multiday adventure activities are con- often report that they have a sense of "impending doom."
ducted in warm to hot environments; therefore, it is assumed
that the signs and symptoms of EAH are some form of heat Management
illness, and patients are managed with standard protocols that
address the presumed hypovolemia and excessive body heat. The first step in treatment is recognizing the disorder and deter-
Standard protocols that provide body cooling and IV fluid chal- mining the severity. Management is based on the severity of EAH
lenge to correct hyperthermia, sweat-induced dehydration, and and what portable diagnostic tools are available to measure
mental status changes can complicate the dilutional hyponatre- serum sodium.59 Figure 21-10 provides an algorithm for assess-
mia and place the patient at further risk for seizure and coma ing patients to determine whether EAH or a heat-related illness
Treating a patient with EAH with fluids and rest will worsen the is present. Mild symptoms should be managed conservatively by
patient's condition, unlike the heat exhaustion patient. observing the patient to ensure no further progression to EAHE
and waiting for normal diuresis of excessive fluid.
This "other heat-related disorder" is becoming more widely
recognized and correctly treated today by EMS and ED person- Symptomatic patients should be placed in an upright posi-
nel, largely because of an increased effort to educate medical tion to maintain their airway and to minimize any positional
personnel and the public in its prevention, early recognition, and effect on intracranial pressure. These patients are known to
management (Figure 21-9). Prehospital care providers directly have projectile vomiting when transported. Place unconscious
supporting or responding to calls at physical endurance events patients in the left lateral recumbent position, anticipate vomit-
in the cities or in the wilderness settings need to be aware that ing, and consider active airway management. Provide high-flow
EAH is more frequently reported today. It is important to remem- oxygen, establish IV access at the keep vein open (KVO) rate,
ber that, in general, dehydration is more common in prolonged and monitor for seizures.
exertional activities and that it can lead to impaired perfor-
mance during exercise or work-related tasks and to serious heat As needed, administer anticonvulsant therapy (e.g., titrate
illness; however, symptomatic hyponatremia brought on by over- benzodiazepine IV, per medical protocol). Check with medical
drinking is more dangerous and potentially a life-threatening control for volume ofNS fluid, ifany, to be administered, depend-
illness.58 ing on patient severity and transport time to hospital. Because
these patients are already fluid-overloaded, infusion of IV hypo-
Assessment tonic fluids is contraindicated, as this can worsen the degree of
hyponatremia and fluid overload.60•61
A wide range of signs and symptoms may be found in
the endurance-athlete population with hyponatremia (see Patients with extensive signs and symptoms of EAHE
Figure 21-5). Core temperature is usually normal but can be (i.e., cerebral edema and pulmonary edema) need to have their
low or slightly elevated, depending on the ambient tempera- plasma sodium concentration increased. The current consen-
ture, body heat dissipation, and recent exercise intensity at sus for management in the prehospital setting is to provide a
assessment. Heart rate and blood pressure can be low, normal, 100-ml bolus infusion of 3% hypertonic saline over 10 minutes
or elevated, depending on core temperature, exercise intensity, to acutely reduce brain edema. Each dose will raise sodium
hypovolemia, or shock. Ventilatory rate ranges from within nor- by 2 to 3 mEq/L, if this solution is available.60•61 If no clinical
mal limits to slightly elevated. Hyperventilation observed with improvement is noted, up to two additional 100-ml, 3% bolus
EAH can account for vision disturbances, dizziness, tingling in infusions can be given per medical protocol.59•60 These severe
hands, and paresthesias in the extremities. The hallmark assess- cases of EAHE have a poor outcome if they do not receive
ment and findings are mental status changes, fatigue, malaise, hypertonic saline.62 Keep the patient calm while en route to
the ED, and continue to monitor for mental status changes or
seizures.

Figure 21-9 Prevention of
Heat-Related Illness
Recently, the Wilderness Medical Society published
practice guidelines for managing EAH and EAHE, Because heat stress is a significant public health factor in the
with an emphasis on how patients competing in United States, methods for preventing heat illness are vital to
endurance events should be managed in the prehospital any community, particularly for those individuals who must
environment by a medical director and staff or by work in high-heat occupational settings. For example, from 2002
responding EMS personnel.59 to 2011, fire fighter (volunteer, career, wildland) deaths in the
United States from all causes totaled 1,054,61 for a yearly average
of 105 fire fighter deaths. The lowest fire fighter all-cause mor-
tality total was recorded in 2011, at 83 deaths (downward trend
2009 to 2011). Of these total deaths, 50 fire fighter deaths (60%)

CHAPTER 21 Environmental Trauma I: Heat and Cold 5 5 7

- Unconscious or Irrational Patient
Rectal temperature Last urine within one hour?
or
1os· F or higher
Fluid intake > 1 liter/hr

Hyponatremia Findings: 'Heat Exhaustion Findings:
Heat Stroke Findings:

Tachycardia or bradycardia Water intake> 1 liter/hour Water intake < 1 liter/hour

Hypotensive Resting pulse< 110 Resting pulse > 11 O

Rapid and shallow breathing Normal or low rectal temp Temperature low, normal, high

Mental status changes Normal vital signs BP normal or low

Seizure Negative orthostatic vital signs Positive orthostatic signs

Coma Bloated stomach Syncope

Severe fatigue Dry mucus membrane

Initiate aggressive body cooling Chills Diarrhea

Provide high-flow oxygen Loss of coordination Oliguria

Maintain airway Headache Nausea/vomiting

Initiate 1-2 IVs with fluid challenge Dizziness Chills

Prepare for seizures Seizure Dizziness

Use diazepam per protocol Provide oral fluids if ALERT or
Transport via air or ground initiate IV with fluid challenge

CNS changes? Transport

• -~--11
Withhold oral fluids Withhold oral fluids
Establish IV w/saline TKO Establish IV w/ saline TKO
Seek Medical Control for additional direction Transport

of IV saline flow rate, possible use of 3%
hypertonic saline, and use of a diuretic
if delayed evac
Transport air or ground
Monitor patient
Reassessment
Transport

Figure 21-10 Treatment algorithm for heat exhaustion, heatstroke, and hyponatremia.

occurred at the scene due to stress/overexertion, which includes strategies, which include administrative policies, procedures,
heat illness as a cause of death in this category.61 engineering controls, use of equipment, and medical surveil-
lance programs, are designed to help minimize the overall
Prehospital care providers and their EMS agencies are a impact from acute or chronic heat exposure. The implemen-
good resource as partners for community education on heat tation of simple preventive procedures can have a dramatic
stress prevention strategies in many different formats, including impact on lowering the incidence of heat illness, but individ-
workshops, educational handouts, agency website or newsletter, uals in an organization often do not consider these strategies.
community presentations, and local newspaper. Figure 21-11 provides an overview of heat stress prevention
strategies for prehospital care providers, fire fighters, and other
As with the general public, it may not be possible to public safety personnel.63
prevent all forms of heat-related illness in prehospital care pro-
viders; therefore, EMS and other public safety personnel need A complex interaction offactors that combine to exceed the
to use prevention strategies and prepare for exposure to high tolerance limits for individual heat exposure can eventually lead
ambient temperature and high occupational exposures. These

5 5 8 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Figure 21-11

You can prevent the serious consequences of heat disorders illness, you must hydrate before, during, and after exercise
by improving your level of fitness and becoming acclimated or physical work. Individual characteristics (e.g., body
to the heat. weight, genetic predisposition, heat acclimatization state,
and metabolic state) will influence sweat rate for a given
Maintaining a high level of aerobic fitness is one of the activity. These factors will result in large individual sweat
best ways to protect yourself against heat stress. The fit rates and total sweat loss. For example, long-distance
prehospital care provider has a well-developed circulatory running is known to cause an average sweat rate of 1.5
system and increased blood volume. Both are important to to 2 quarts (1 .4 to 1.9 liters) per hour in summer months,
regulate body temperature. Fit prehospital care providers whereas football players (large body mass and wearing
start to sweat sooner, so they work with a lower heart protective gear) are known to sweat on average over
rate and body temperature. They adjust to the heat twice 2 quarts (1.9 liters) per hour and up to 9 quarts (8.5 liters)
as fast as the unfit prehospital care provider. They lose per day.48 There needs to be a commitment to frequent
acclimatization more slowly and regain it quickly. hydration breaks to ensure dehydration does not exceed
greater than 2% of body weight (based on preactivity nude
Heat acclimatization occurs in 5 to 1O days of heat body weight) throughout the duration of physical activity.
exposure as the body:
Before work, you should take extra fluids to prepare for the
• Increases sweat production heat. Drink 8 to 16 ounces (0.2 to 0.5 liters) of water, juice,
• Improves blood distribution or a sport drink before work. Avoid excess caffeine; it hastens
• Decreases the heart rate fluid loss in the urine. There is no physiologic advantage
• Lowers the skin and body temperatures to excessively consuming large amounts of fluid prior to
As a prehospital care provider, you can acclimatize by physical activity. The American College of Sports Medicine
gradually increasing work time in the heat, taking care now recommends prehydrating slowly for several hours
to replace fluids, and resting as needed. Acclimatization before a physical activity and consuming 0.16 to 0.24 ounces
is maintained with periodic work or exercise in a hot (approximately 5 to 7 ml) per kg of body weight. The goal is to
environment. produce urine output that is clear to straw color in appearance
and prevent starting an activity in a dehydrated state.
On the Job
The heat stress index (Figure 21-12) illustrates how While working, take several fluid breaks every hour, drinking
temperature and humidity combine to create moderate-heat approximately 1 quart (0.9 liter) of fluid per hour. Individual
or high-heat stress conditions. Be alert for heat stress when sweat rates will vary, as will the amount of water needed
radiant heat from the sun or nearby flames is high, when the to consume per hour. Caution should be used to prevent
air is still, or when working hard, creating large amounts of consumption of excessive fluids greater than 1.5 quarts/
metabolic heat. Heat stress indexes do not take into account hour (1 .4 liters/hour) for prolonged periods unless you have
the effects of long hours of hard work, dehydration, or the determined your individualized sweat loss rate per hour. The
impact of personal protective clothing and equipment. American College of Sports Medicine now recommends a
starting point of 14 to 28 ounces (0.4 to 0.8 liters) on average
When heat stress conditions exist, you must modify per hour for exercise activities (e.g., marathon running) and
the way you work or exercise. Pace yourself. There are adjusting the amount consumed based on individual lower or
individual differences in fitness, acclimatization, and heat higher sweat rates for activities in cool or warm temperature
tolerance. Push too hard and you will become a candidate conditions, and for lighter or heavier individuals.48
for a heat disorder.
Water is the body's greatest need during work in the
When possible, you should: heat. Studies show that workers drink more when lightly
• Avoid working close to heat sources flavored beverages are available. Providing a portion of
• Do harder work during cooler morning and evening hours fluid replacement with a carbohydrate/electrolyte sport
• Change tools or tasks to minimize fatigue beverage will help to retain fluids and maintain energy and
• Take frequent rest breaks electrolyte levels. Unfortunately, many sport drinks contain
Most important, maintain hydration by replacing lost fluids. large amounts of sugar, which can actually slow absorption
of ingested fluid.
Hydration
Maintaining body fluids is essential for sweating and After work, you need to continue drinking to replace
the removal of internal heat generated during physical fluid losses. To achieve rapid and complete recovery for
activities. To minimize dehydration and the risk of heat

(Continues on next page)

CHAPTER 21 Environmental Trauma I: Heat and Cold 5 5 9

Figure 21 -11

activities resulting is large sweat loss (i.e., firefighting), Individual Differences
drink approximately 24 ounces for each pound of body Individuals differ in their response to heat. Some emergency
weight loss (1. 5 liters for each kilogram of body weight responders, such as fire fighters, are at greater risk for heat
loss).48 Thirst always underestimates fluid needs, so you disorders. The reasons include inherited differences in heat
should drink more than you think you need. Rehydration tolerance and sweat rate; excess body weight, which raises
is enhanced when fluids contain sodium and potassium or metabolic heat production; and illness, illicit drugs, and
when foods with these electrolytes are consumed along medications, which can also influence the body's response
with the fluid. to work in a hot environment. Check with your physician or
pharmacist if you are using prescription or over-the-counter
Sodium lost in sweat is easily replaced at meals with medications, or if you have a medical condition.
liberal use of the salt shaker. Unacclimatized prehospital
care providers lose more salt in the heat, so they need to You should always train and work with a partner w ho
pay particular attention to salt replacement. Do not overdo can help in the event of a problem. Remind each other to
salt intake; too much salt impairs temperature regulation . drink lots of fluids, and watch each other. If your partner
Excessive salt can cause stomach distress, fatigue, and other develops a heat disorder, start treatment immediately.
problems.
Summary
Make potassium-rich foods such as bananas and Prevention
citrus fruits a regular part of your diet, and drink lots of
lemonade, orange juice, or tomato juice. Limit the amount • Improve or maintain aerobic fitness.
of caffeine drinks such as coffee and colas because • Acclimate to the heat.
caffeine increases fluid loss in the urine. Avoid alcoholic
drinks because they also cause dehydration. To avoid On the Job
common viruses, avoid sharing water bottles except in • Be aware of conditions (temperature, humidity, air
emergencies. movement).
• Take frequent rest breaks.
Hydration can be reassessed by observing your urine's • Avoid extra layers of clothing.
volume, color, and concentration. Low volumes of dark, • Maintain a steady pace.
concentrated urine and painful urination indicate a serious
need for rehydration. Other signs of dehydration include Hydrate
a rapid heart rate, weakness, excessive fatigue, and • The hydration goal is to prevent dehydration (sweat
dizziness. Rapid loss of several pounds of body weight is loss) of greater than 2% of nude body weight.
a certain sign of dehydration. Rehydrate before returning • Before work, drink several cups of water, juice, or a
to work. Continuing to work in a dehydrated state can sport drink.
lead to serious consequences, including heatstroke, muscle • During work, take frequent flu id breaks.
breakdown, and kidney failure. • After work, keep drinking to ensure rehydration.
• Remember, "Only you can prevent dehydration. "
Clothing
Personal protective clothing strikes a balance between Partners
protection and comfort. Australian researchers have • Always work or train with a partner.
concluded that the task for personnel wearing personal
protective equipment is not to keep heat out, but to let it Drinks
out. About 70% of the heat load comes from within, from • Sport drinkswith carbohydrates (no more than 6% to
metabolic heat generated during hard work. Only 30% 8%; -30 to 60 grams/hour) and electrolytes (e.g., sodium
comes from the environment. Wear loose-fitting garments 460 to 1150 mg/liter or 20 to 50 mEq/liter) encourage
to enhance air movement. Wear cotton T-shirts and fluid intake, provide energy, and diminish urinary water
underwear to help sweat evaporate. Avoid extra layers of loss. The carbohydrates also help maintain immune
clothing that insulate, restrict air movement, and contribute function and mental performance duri ng prolonged,
to heat stress. arduous work. Drinks with caffeine and alcohol interfere
with rehydration by increasing urine production.

Source: Modified from U.S. Department of Agriculture, U.S. Forest Service. Heat stress brochure, http://www.fs.fed.us/fire/safety/fitness/heat_stress/hs_pgl .html.
Accessed January 11, 20 14. See also: American College of Sports Medicine, Sawka MN, Burke LM, et al. American College of Sports Medicine position stand: exercise
and fluid replacement. Med Sci Sports Exerc. 2007;39(2):377.

5 6 0 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

to the onset of signs and symptoms of heat-related illness. The large amounts of heat, or in heavy protective clothing, 10°F
capacity of humans to work in moderate to hot environments (-5.5°C) should be added to the value in the table.
can be maximized through advanced preparation of physical fit-
ness, heat acclimatization, living and working conditions, per- A more widely used method for measurement of environ-
sonal hygiene, and use of food and beverages to maintain and mental heat strain used in many industrial and military settings is
replace electrolytes and water in the body. Environment, fluid the wet-bulb globe temperature (WBGT) index 21•60 (Figure 21-13).
hydration, physical fitness, and heat acclimatization are essential This index uses the combination of a dry bulb for ambient tem-
factors to understand. perature, wet bulb for humidity measurement, black globe for radi-
ant heat, and air movement to provide a more accurate impact of
Environment the environmental conditions. Integrated in the five-level WBGT
index range of temperatures are hourly work/rest (minutes) and
Prehospital care providers and other public safety personnel are hydration (quarts) guidelines. A color flag (no flag, green, yellow,
subjected to high heat environments as part oftheir occupational red, or black) represent each of the five WBGT ranges of tempera-
requirements. During training or an emergency response, many tures. The WBGT can be monitored hourly and the corresponding
personnel will encounter high levels of heat stress while working color flag placed on a flagpole outdoors for all personnel to see
in personal protective equipment (PPE) (impermeable clothing), throughout the day. When applicable, the appropriate adjustments
such as turnout gear, hazardous material suit, or chemical/bio- of clothing, physical activity, work/rest cycles, and fluid intake can
logic protective garment. This heat stress is further compounded then be made based on these WBGT conditions. This integrated
by the need to enter poorly ventilated or confined spaces or to WBGT system and related policies can easily be developed at var-
work on a multivehicle crash in the sun on a hot, humid day. ious public safety locations and training sites to ensure that effec-
tive heat illness prevention programs are in use to reduce fatigue,
PPE compromises the body's ability to dissipate body heat injuries, and heat illness.
and prevents the evaporation of sweat during a heavy workload.
With high sweat rates from internal h eat production during phys- Hydration
ically demanding tasks and the external heat exposure, person-
nel are at a high risk of dehydration and heat illness. Thus, the Ifthe WBGTflagsystemisnotusedto provideguidelinesforhydra-
use of PPE diminishes the phys iologic advantage gained through tion, another excellent resource is published by the American
heat acclimatization and physical fitness. College of Sports Medicine, based on years of research.58 These
guidelines are easily applied to any individual engaged in phys-
These risks can be minimized by measuring the environmen- ical activity. Hydration guidelines should be established within
tal heat conditions and, when applicable, following the recom- an agency in an effort to prevent excessive dehydration (greater
mended work/rest and hydration guidelines for work in highly than 2% body weight loss) by creating easy access to water and
thermal environments.21•64 sport electrolyte drinks, particularly during activity in warm envi-
ronments (Figure 21-14). Studies show that the average individ-
One traditional method for measuring the thermal load is by ual does not drink sufficient quantities of fluids before, during,
use of the heat stress index (see Figure 21-12). This index uses and after work or exercise to recover body fluids lost from
the combination of ambient temperature (read on a thermom- sweating, even though these individuals believe they are con-
eter) and relative humidity. This is a better method of predict- suming enough fluids.58 Although overconsumption of fluids can
ing potential systemic heat injury than the ambient temperature
alone. If working in direct sunlight, near surfaces that radiate

Temperature (°F) versus Relative Humidity(%)
90% 80% 70% 60% 50% 40%

80 85 84 82 81 80 79 High Possible Heat Disorder

85 101 96 92 90 86 84 9o·F - 9o· F Fatigue possible with prolonged exposure and physical activity.

90 121 113 105 99 94 90 9o· F- 105·F Sunstroke, heat cramps, and heat exhaustion possible.
OF
105·F - 13o· F Sunstroke, heat cramps, and heat exhaustion likely, and
95 133 122 113 105 98 heat stroke possible.

100 142 129 11 8 109 130•F or greater Heat stroke highly likely with continued exposure.

105 148 133 121

110 135

Due to the nature of the heat index calculation, the values in the tables have an error +/- 1.3° F.

Figure 21-12 Heat stress index.

Source: Courtesy of the National Weather Service, Pueblo, Colorado (http://www.crh.noaa.gov/pub/heat.htm).

CHAPTER 21 Environmental Trauma I: Heat and Cold 561

Figure 21-13

Easy Work Moderate Work Hard Work

78 to 81.9 NL 1/2 NL 314 40/20 314

2 82 to 84.9 NL 1/2 50/10 314 30130

3 85 to 87.9 NL 314 40/20 3/4 30130

4 88 to 89.9 NL 314 30130 3/4 20/40

5 > 90 50/10 20/40 10/50

Easy Work Moderate Work Hard Work

Walking on hard surface at Walking on hard surface at Walking on hard surface at
2.5 mph, less than 31-lb 3.5 mph, less than 41-lb 3.5 mph, greater than
load. load. 40-lb load.

Walking in loose sand at 2.5 Walking in loose sand at
mph, no load. Calisthenics. 2.5 mph w ith load.

lb, pound; mph, miles per hour; NL, no limit to work time; WBGT, wet-bulb g lobe temperature.
The work/rest times and fluid replacement volumes w ill sustain performance and hydration for at least 4 hours of work in the specified heat category. Individual w at er
needs will vary. Rest means minimal physical adivity (sitting or standing), accomplished in shade if possible.
Caution: Hourly fluid intake should not exceed 1.5 quarts. Daily fluid intake should not exceed 12 quarts. W hen wearing body armor: Add 5°F (-2.75°( ) to WBGT index
in humid climates. When wearing PPE over garment: Add 10° F (-5.5°C) to WBGT index for easy work and 20°F (-11 °C) for moderate and hard work.
Source: Current version of WBGT, hydration, and work/rest g uidelines as updated by U.S. Army Research Institute for Environmental Medicine (USARIEM) and published
by Montain SJ, Latzka WA, Sawka MN. Mi/ Med. 1999;164:502.

lead to hyponatremia (see the preceding Exercise-Associated Heat Acclimatization
Hyponatremia section), it is more common for individuals to
become dehydrated (greater than 2% of body weight) during A policy and protocol for heat acclimatization should be pro-
a given physical activity. Ideally, fluid-replacement programs vided within a public safety organization.68 Heat acclimatization
should be customized based on individualized sweat rate loss, can be achieved with 60 to 90 minutes of exercise a day in hot
body mass, and exercise intensity as determined from a pre- or conditions for approximately 7 to 14 days.69 The benefits of heat
post-physical activity nude body weight loss measurement. acclimatization are increased work performance, heat toler-
ance, and reduced physiologic strain. These adjustments include
Fitness increased blood volume, increased stroke volume, decreased
heart rate at a given activity level, reduced sodium concentra-
To increase heat tolerance effectively in high-heat conditions, tion in sweat, sodium conserved in the body, earlier onset of
prehospital care providers should increase their aerobic fitness sweating, and increased sweat volume rate (Figure 21-15). These
through individualized programs (e.g., walking, jogging, biking, changes improve the transfer of body heat from the core to the
swimming, stair stepping, using elliptical exercise machines).65 skin in an effort to increase the heat transfer from the skin to
These programs will provide the cardiac reserve to sustain the the environment. Although heat tolerance is improved in these
cardiac output required to meet the competing demands of phys- individuals (e.g., endurance athletes, military infantry personnel)
ical (muscular) work and heat dissipation mechanisms (thermo- and is considered desirable, the greater sweat-volume produc-
regulation) in a high-temperature environment.66•67 The American tion (1 to 2 liters/hour) results in large fluid losses, leading to
College of Sports Medicine, American Heart Association, and dehydration. Consequently, the greater volume of sweat loss in
Department of Health and Human Services have collaborated heat-acclimatized individuals increases the hydration require-
recently to establish updated nationwide physical activity rec- ments during heat exposure, particularly when the person does
ommendations to maintain health and well-being.67 not adhere to a rigorous oral hydration schedule. Figure 21-16
provides an overview of heat acclimatization guidelines.

5 6 2 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

Figure 21-14

General Principles When you do not drink enough during exertion, be sure
It is important to maintain hydration, especially when to replenish fl uids afterwards. Also remember: do not use
exercising or performing activities that involve heavy dehydration as a weight loss technique.
physical exertion. A person's hydration needs will differ
depending on how heavily the person sweats. General Type of Drink
principles to remember include: In addition to remembering to drink sufficient amounts, it
is important to know what type of fluid to drink. Drinking
1. Drink before and during exertion. only water during heavy exertion can lead to electrolyte
2. Use water and electrolyte drinks to replace lost imbalance. Sport electrolyte drinks are designed to replace
electrolytes lost t hrough sw eat. During exercise, stay alert
fluids. for swelling of the hands and feet, headache, and bloating,
3. Note your weight before and after exertion to w hich could indicate hyponatremia.

help track whether your fluid intake is sufficient, In addition, if you are an athlete or work in a profession
deficient, or excessive. that requires heavy exertion, include a moderate amount of
Make sure you drink sufficiently even when not salt in your diet to help fu lfi ll your body's increased need for
exercising. If you postpone drinking during your regular sodium chloride.
day, your body may dehydrate more quickly once you exert
yourself.

Weight Fluid Intake Recommendations
Weight is a factor used to determine hydration (or Recommendations for replacing fluid (wit h water and
dehydration). It is important to replace fluid lost during sports electrolyte drinks) are as follows:
physical exertion. If a person does not replace this fluid,
he or she will weigh less after exertion. Conversely, if a Time frame Quantity
person drinks excessive amounts during physical exertion,
he or she may gain weight due to the fluid intake. Ideally, 2-3 hours before exertion 2-3 cups
a person will weigh approximately the same before and
after exercise; this indicates that the person maintained t he 30 minutes before exertion 5-1 O oz.
appropriate fluid level.
During exertion 5-10 oz. every 10-20 min.

Source: Data fro m: M urray B, Eichner ER, Stofan J. Hyponatremia in athletes.
Sports Sci Exchange. 2003;16(1):88.

Figure 21-15 6. Exercise performance: improved
7. Sweating: earlier and greater
1. Thermal comfort: improved 8. Body heat production: lower
2. Core temperature: reduced 9. Thirst improved
3. Skin blood flow: earlier 10. Organ protection: improved
4. Heart rate: lowered
5. Salt losses (sweat and urine): reduced

Emergency Incident Rehabilitation impact upon the safety and health ofthe individual emergency
responder. Members who are not provided adequate rest and
In 1992, the U.S. Fire Administration (USFA) stated the rehydration during emergency operations and training exer-
following: cises are at increased risk for illness, and may jeopardize
the safety of others on the incident scene. When emergency
The physical and mental demands of EMS, firefighting and responders become fatigued, their ability to operate safely is
emergency operations that are associated with extreme heat impaired. As a result, their reaction time is reduced, and their
and hwnidity create conditions that can have an adverse ability to make critical decisions diminishes. Rehabilitation is

CHAPTER 21 Environmental Trauma I: Heat and Cold 5 6 3

Figure 21-16

The following is a modified version of the heat The benefits of heat acclimatization will be retained
acclimatization guidelines designed for healthy and for about 1 week and then decay, with about 75% lost
physically fit infantry personnel in preparation for physical by about 3 weeks, once heat exposure ends. One or 2
activity in hot environments. days of intervening cool weather will not interfere with
acclimatization to hot weather.
Should You Be Concerned About Hot Weather?
If you are used to working in cool or temperate climates, How Quickly Can You Become Heat Acclimatized?
exposure to hot weather will make it much more difficult to For the average individual, heat acclimatization requires
complete your advanced training course. Hot weather will about 2 weeks of heat exposure and progressive increases
make you feel fatigued, make it more difficult to recover, in physical work. By the second day of acclimatization,
and increase your risk of becoming a casualty to heat. significant reductions in physiologic strain are observed. By
Individuals with the same abilities but who are used to the end of the first week and second week, greater than
training in hot weather will have a greater heat tolerance 60% and greater than 80% of the physiologic adaptations
and physical ability during heat exposure. are complete, respectively. Less fit individuals or those
unusually susceptible to heat exposure may require several
What Is Heat Acclimatization? days or weeks more to fully acclimatize.
Heat acclimatization refers to biologic adaptations
that reduce physiologic strain (e.g., heart rate, body Physically fit individuals should be able to achieve heat
temperature), improve physical work capabilities, improve acclimatization in about 1 week. However, several weeks of
comfort, and protect vital organs (brain, liver, kidneys, living and working in the heat (seasoning) may be required
muscles) from heat injury. The most important biologic to maximize tolerance to high body temperatures.
adaptation from heat acclimatization is an earlier and
greater sweating response, and for this response to What Are the Best Heat Acclimatization Strategies?
improve, it needs to be invoked. 1. Maximize physical fitness and heat acclimatization

Heat acclimatization is specific to the climate (desert) before hot weather exposure. Maintain physical
and physical activity level. However, acclimatization to fitness w ith maintenance programs tailored to the
desert climates greatly improves the ability to work in environment, such as physical training in the cooler
other climates. Individuals who perform only light or brief morning or evening hours.
physical work will achieve the level of heat acclimatization 2. Integrate training and heat acclimatization. Train in the
needed to perform that task. If they attempt a more coolest part of the day and acclimatize in the heat of
strenuous or prolonged task, additional acclimatization and the day. Start slowly by reducing your usual training
improved physical fitness will be needed to perform that intensity and duration (compared to what you could
task successf ully in the heat. achieve in temperate climates). Increase training and
heat exposure volume as your heat tolerance permits.
How Do You Become Heat Acclimatized? Use interval training to modify your activity level.
Heat acclimatization occurs when repeated heat exposures 3. If the new climate is much hotter than what you
are sufficiently stressful to elevate body temperature are accustomed to, recreational activities may be
and provoke profuse sweating. Resting in the heat, with appropriate for the first 2 days with periods of run/
physical activity limited to that required for existence, walk. By the third day, you should be able to integrate
results in only partial acclimatization. Physical exercise in the training runs (20 to 40 minutes) at a reduced pace.
heat is required to achieve optimal heat acclimatization for 4. Consume sufficient water to replace sweat losses.
that exercise intensity in a given hot environment. Sweat rates of more than 1 quart (0.9 liter) per hour are
common. Heat acclimatization increases the sweating
Generally, about 2 weeks of daily heat exposure is rate and, therefore, increases water requirements. As
needed to induce heat acclimatization. Heat acclimatization a result, heat-acclimatized individuals will dehydrate
requires a minimum daily heat exposure of about 2 hours faster if they do not consume fl uids. Dehydration
(can be broken into two 1-hour exposures) combined with negates many of the thermoregulatory advantages
physical exercise that requires cardiovascular endurance conferred by heat acclimatization and high physical
(e.g., jogging) rather than strength training. Gradually fitness.
increase the exercise intensity or duration each day. Work For the complete report, visit http://www.usariem.army.
up to an appropriate physical training schedule adapted to mil/assets/docs/partnering/HeatAcclimatizationGuide.pdf .
the required physical activity.

5 6 4 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

an essential element on the incident scene to prevent more a. Presence of chest pain, dizziness, shortness of
serious conditions such as heat exhaustion or heatstroke from breath, wealmess, nausea, or headache.
occurring.
b. General complaints such as cramps or aches and
Due to the importance of rehabilitation for emergency pains.

responders, the USFA created a standardized approach for eval- c. Symptoms of heat- or cold-related stress.
d. Changes in gait, speech, or behavior.
uating and rehabilitating fire fighters and emergency person- e. Alertness and orientationto person, place, and time.
f. Any vital signs considered abnormal in local pro-
nel during environmental extremes (Figure 21-17). NFPA 1584,
tocol. The specific vital signs and the definitions of
Standard on the Rehabilitation Process for Members During "normal" are entirely up to local medical control
and department medical authorities. Vital signs
Emergency Operations and Training Exercises, complements listed in the NFPA 1584 annex include temperature,
pulse, respirations, blood pressure, pulse oximetry,
the USFA standard and the standards set by other agencies (e.g., and carbon monoxide assessment, using either an
exhaled breath carbon monoxide monitor ora pulse
the Occupational Safety and Health Administration). The 2008 carbon monoxide-oximeter (i.e., a pulse oximeter
designed to measure carboxyhemoglobin).
edition of NFPA 1584 reflects current science and lmowledge on 7. EMS treatment in accordance with local protocol.
Services must be available on scene for emergency
rehabilitation and upgrades the previous document from a rec- responders who require treatment or transport. Note
that medical monitoring is documented in the fire
ommended practice to a s ta n da rd .71 2 The introduction of NFPA department data collection system. When EMS treat-
}.7 ment or transport is provided, a medical report must be
generated and included in the emergency responder's
1584 as a standard means that every fire department and EMS employee medical record.
8. Accountability. A personnel accountability system
agency must have standardized procedures outlining how they must track emergency responders assigned to rehabil-
itation by incident command as they enter and leave.
provide rehabilitation at incidents and training exercises. 9. Release. Prior to leaving rehabilitation, EMS must con-
firm that emergency responders are able to safely per-
The nine key components of rehabilitation required by form full duty.61

NFPA 1584 are: EMS Drug Storage in
Thermal Extremes
1. Relief from climactic conditions. An area free of
smoke, away from vehicle exhaust fumes, and shel- Prehospital care providers work in regions within the United
tered from extreme heat or cold is provided. This might States and elsewhere where annual weather extremes range
be a nonfire floor in a high-rise building, a shaded area from below freezing to high heat and humidity. Their vehicles,
upwind from a brush fire, or the heated fire apparatus including mobile intensive care units, paramedic units, and
cab during cold winter months. The theme is provid- medical helicopters, and the medications stored in those vehi-
ing shelter from environmental extremes and on-scene cles, are also subjected to the environmental extremes unless a
hazards. temperature-controlled storage device is on board. Medications
used by prehospital care providers are intended for storage at
2. Rest and recovery. Emergency responders are afforded controlled room temperature according to recommendations of
the ability to rest for at least 10 minutes or as long as the drug manufacturers. The U.S. Pharmacopeia (USP) has over-
needed to recover work capacity. sight responsibilities in the United States for establishing drug
standards intended to ensure the quality of medications, and the
3. Cooling or rewarming. Emergency responders who USP defines controlled room temperature as follows:
feel hot should be able to remove their PPE and
drink water and should have the means to cool off. A temperature maintained thermostatically that encompasses
Emergency responders who are cold should be able to the usual and customary working environment of 68°F to 77°F
add clothing and wrap in blankets and should have the (20°C to 25°C); that results in a mean kinetic temperature
means to warm themselves. calculated to be not more than 77°F (25°C); and allows for
excursions between 59°F to 86°F (15°C to 30°C) that are expe-
4. Rehydration (fluid replacement). Fluid volume rienced in pharmacies, hospitals and warehouses. Provided
requirements were eliminated from the standard
with the exception of prehydration with 16 ounces
(500 ml) offluids consumed 2 hours prior to scheduled
events. On-scene, potable fluids must be provided so
members can satisfy their thirst. Fluids should also be
provided to encourage continued hydration after the
incide n t.

5. Calorie and electrolyte replacement. This component is
intended for longer duration events, such as incidents
exceeding 3 hours or situations in which emergency
responders are likely to work for more than 1 hour. Of
note, whenever food is available, means for emergency
responders to wash their hands and faces must also be
provided.

6. Medical monitoring. This component specifies a min-
imum of six conditions that EMS must assess in each
emergency responder during rehabilitation:

CHAPTER 21 Environmental Trauma I: Heat and Cold 5 6 5

Figure 21-17

Purpose Nourishment
To ensure that the physical and mental conditions of The department will provide food at the scene of an
members operating at the scene of an emergency or a extended incident when units are engaged for 3 or
training exercise do not deteriorate to a point that affects more hours. A cup of soup, broth, or stew is highly
the safety of each member or that jeopardizes the safety recommended because it is digested much faster than
and integrity of the operation. sandwiches and fast-food products.

Scope Rest
This procedure will apply to all emergency operations and The "two-bottle rule," or 45 minutes of work time, is
training exercises in which strenuous physical activity or recommended as an acceptable level before mandatory
exposure to heat or cold exists. rehabilitation. Members will rehydrate (at least 8 ounces
(250 ml]) while self-contained breathing apparatus (SCBA)
Responsibilities cylinders are charged. Fire fighters having worked for
The incident commander will consider the circumstances two full 30-minute-rated bottles, or 45 minutes, will be
of each incident and make adequate provisions early in immediately placed in the rehabilitation area for rest and
the incident for the rest and rehabilitation for all members evaluation. Rest will not be less than 10 minutes and may
operating at the scene. These provisions will include medical exceed an hour, as determined by the rehabilitation officer.
evaluation, treatment, and monitoring; food and fluid
replenishment; mental rest; and relief from extreme climatic Recovery
conditions and the other environmental parameters of the Members in the rehabilitation area should maintain a
incident. The rehabilitation will include the provision of EMS high level of hydration. Certain drugs impair the body's
at the basic life support (BLS) level or higher. The incident ability to sweat, and extreme caution must be exercised if
commander will establish a rehabilitation sector or group the member has taken antihistamines, such as Actifed or
when conditions indicate rest and rehabilitation is needed for Benadryl, or has taken diuretics or stimulants.
persons operating at the incident scene or training evaluation.
Medical Evaluation
Gu id e lin es EMS should be staffed and provided by the most highly
Climatic or environmental conditions of the emergency trained and qualified prehospital care providers on the
scene should not be the sole justification for establishing scene (at a minimum of BLS level). They will evaluate vital
a rehabilitation area. Any activity or incident that is large signs, examine members, and make proper disposition
in size, long in duration, or labor intensive will rapidly (return to duty, continued rehabilitation, or treatment and
deplete the energy and strength of personnel and, transport to medical facility). Continued rehabilitation
therefore, merits consideration for rehabilitation. Climatic should consist of additional monitoring of vital signs,
or environmental conditions that indicate the need to providing rest, and providing fluids for rehydration.
establish a rehabilitation area are a heat stress index above Prehospital care providers will be assertive in an effort
90°F (32.2°C) (see Figure 21 -12) or windchill index below to find potential medical problems early; considerations
10°F (-12 .2°C) (see Figure 21 -30). include the following:
• If a member's heart rate exceeds 110 beats/minute, an
Hydration
During heat stress, the member should consume at least oral temperature should be taken.
1 quart (0.9 liter) per hour and should not exceed • If the member's temperature exceeds 100.6°F (38.1°C),
1.5 quarts (1.4 liters) per hour. The rehydration should be
a 50/50 mixture of water and a commercially prepared he or she should not be permitted to wear protective
activity beverage (sport electrolyte beverage) and should be equipment.
administered at about 40°F (4.4°C). Alcohol and caffeine • If it is below 100.6°Fand heart rate remains above
beverages should be avoided before and during heat stress 11Obeats/minute, rehabilitation time should be
because both interfere with the body's water conservation increased .
mechanisms. Carbonated beverages should also be avoided. • If the heart rate is less than 11O beats/minute, the chance
of heat stress is negligible.
• EMS should document all medical evaluations.

5 6 6 PREHOSPITAL TRAUMA LIFE SUPPORT, EIGHTH EDITION

the mean kinetic temperature remains in the allowed range, Cold-induced diuresis is a normal physiologic response
transient spikes up to 104°F (40°C) may be permitted if the resulting from skin vasoconstriction from prolonged cold expo-
manufacturer so instructs.73 sure. This is the body's response to reduce body heat loss by
shunting blood away from the colder periphery to deeper veins
Manufacturers will guarantee a medication's stability, qual- of the body. This response causes a central blood volume expan-
ity, and potency only when the drugs are stored within the rec- sion, which results in a rise in the mean arterial pressure, stroke
ommendedtemperature range. In many cases across the country, volume, and cardiac output.71 The expanded blood volume can
EMS vehicles have been shown periodicallyto have stored medi- produce a diuresis, manifested by frequent urination. Cold-
cations attemperatures outside the USP-recommended range.74-77 induced diuresis can reduce plasma volume by 7%to 15%, result-
These studies have examined thermal exposure of drugs in both ing in hemoconcentration and acute dehydration from almost a
field and laboratory settings for short (1to4 weeks) and long (12 twofold :fluid loss over normal.
to 26 weeks) durations.74 What remains unclear is the effect of
these thermal fluctuations on the bioavailability of many com- As with exposure to heat, adherence to fluid hydration
mon prehospital drugs. Laboratory assessment shows that the guidelines while working in cold environments is necessary to
majority of these drugs remain stable, except for epinephrine, minimize dehydration along with the associated fatigue, and
which significantly degrades in extreme cold and heat.74•78•79 physical and cognitive changes. Because thirst is suppressed in
cold environments, dehydration is a significant risk.
To improve compliance with the USP standards and man-
ufacturers' recommendations, some states have implemented Minor Cold-Related Disorders
specific rules regarding storage of medication. For example, the
New Jersey Office of Emergency Medical Services (Department Contact Freeze Injury
of Health and Senior Services) passed regulations requiring the
following: When cold material comes into contact with unprotected skin, it
can produce local frostbite immediately. Do not touch any metal
Each vehicle and cabinet orotherstorage place for medications surface, alcohol, gasoline, antifreeze, ice, or snow with the hands.
shall be sufficiently climate controlled so that the medications (See the Frostbite section for assessment and management.)
and solutions are kept within temperature range recommended
by the manufacturer. Each vehicle shall have a temperature Frostnip
recording device which shall, at least, record the highest and
lowest temperature during a specified time period.'° Frostnip is a precursor to frostbite and produces reversible signs
ofskin blanching and numbness in localized tissue. It is typically
EMS agencies need to consider how they will deal with this seen on the face, nose, and ears. Frostnip is a self-limited tissue
concern for the efficacy of the medications used in their vehi- injury as long as cold exposure does not continue; it does not
cles to assure that these drugs always work as intended when require prehospital care provider intervention and transport.
used by the EMS personnel. The cost for implementing environ-
mentally controlled storage for all advanced life support (ALS) Cold Urticaria
units, as recommended by each drug manufacturer and the USP,
is certainly not insignificant, but to take no action based on these Cold urticaria ("hives") is a disorder characterized by the rapid
studies is unacceptable as well. It is suggested that each EMS onset (within minutes) of itchiness, redness, and swelling of the
agency develop a policy to investigate the thermal conditions skin after exposure to cold. The sensation of burning may be a
in the vehicle medication storage area and consider a medica- prominent feature. This condition, caused by a local release of
tion rotation system during periods of extreme cold and heat, or histamine, is sometimes observed when ice is applied directly to
some other system to minimize the exposure of medications to the skin during cold therapy for sprains and strains. Individuals
thermal extremes in their region.74 with a history of cold urticaria are advised to avoid cold-water
immersion, which could potentially cause death from systemic
Injuries Produced anaphylaxis. Treatment includes avoiding the cold and possibly
taking antihistamines.
by Cold

Dehydration Chilblains (Pernio)

Dehydration occurs very easily in the cold, particularly with Chilblains are small skin lesions that are itchy and tender,
increased physical activity. This occurs for three primary reasons: appearing as red or purple bumps that occur on the extensor
skin surface of the finger or any skin surface (e.g., ears, face)
• Evaporation ofsweat from chronic cold exposure. Chilblains occur several hours
• Increased respiratory heat and fluid losses caused by after exposure to the cold in temperate humid climates. They are
sometimes aggravated by sun exposure. Cold causes constric-
the dryness of cold air tion of the small arteries and veins in the skin, and rewarming
• Cold-induced diuresis

CHAPTER 21 Environmental Trauma I: Heat and Cold 5 6 7

results in leakage of blood into the tissues and swelling of frostbite. With an increase in adventure sports and other recre-
the skin. ational activities conducted in the winter season, localized cold
injuries are now seen more often.
Chilblains are more likely to develop in those with poor
peripheral circulation. Some contributing factors are a familial Prehospital care providers need to prevent body heat loss
tendency, peripheral vascular disease caused by diabetes, smok- and protect exposed skin from frostbite in patients during pro-
ing, hyperlipidemia (increased serum lipid levels), poor nutrition longed exposure to cold conditions. For example, in patients
(e.g., anorexia nervosa), connective tissue disease, and bone needing vehicular extrication, in scenarios resulting in the inabil-
marrow disorders. Each chilblain comes up over a few hours as ity to move the patient, and in patients in cold environments with
an itchy, red swelling and subsides over the next 7 to 14 days. soft-tissue swelling, impaired circulation can lead to an increased
In severe cases, blistering, pustules, scabs, and ulceration can incidence oflocalized cold injury.
occur. Occasionally the lesions may be ring shaped. They may
become thickened and persistfor months. Nonfreezing Cold Injury

Symptoms will subside with removal of the individual from Nonfreezing cold injury (NFCI), a syndrome also called immer-
the cold. Management involves protection from cold with appro- sion foot and trench foot, results from damage to peripheral tis-
priate gloves and clothing. sues caused by prolonged (hours to days) wet/cold exposure.SWl6
NFCI does not involve freezing of tissue but may coexist with
Solar Keratitis (Snow Blindness) freezing injury such as frostbite. This syndrome involves pri-
marily the feet and is reflected in two types of NFCI. Trench
Without protection from dry air and from exposure to bright foot occurs primarily in military personnel during infantry
reflections on snow, the risk ofultraviolet burns to skin and eyes operations and is related to the combined effects of prolonged
increases. This risk is greatly enhanced at higher altitudes. Solar cold exposure and restricted circulation in the feet; it does not
keratitis is insidious during the exposure phase, with corneal involve immersion in water.84 Immersion foot is caused by pro-
burns occurring within 1 hour, but not becoming apparent until 6 longed immersion of extremities in moisture that is cool to cold.
to 12 hours after exposure. Prehospital care providers may see immersion foot in persons
who are homeless, persons with alcoholism, or elderly persons;
Management of snow blindness is based on symptoms, in hikers and hunters; in multiday adventure sport athletes; and
which include excessive tearing, pain, redness, swollen eye- in ocean survivors.84•87•88 Frequently, this syndrome goes unrecog-
lids, pain when looking at light, headache, a gritty sensation in nized during assessment of individuals who have been exposed
the eyes, and decreased (hazy) vision. Prehospital care provid- to cold or wet conditions because of the lack of formal medical
ers need to consider patching affected eyes if there is no other training in NFCI.84
method to prevent further ultraviolet exposure (e.g., sunglasses),
then transport the patient. Topical ophthalmic anesthetic drops, This syndrome occurs as a result ofmany hours ofcooling of
if available, may be used to provide symptomatic relief. Medical the lower extremities in temperatures ranging from 32°F to 65°F
attention is required to determine the level of severity and the (0°C to 18.3°C). Soft-tissue injury occurs to the skin of the feet,
need for antibiotics and analgesics. known as maceration. The breakdown of the skin will predis-
pose individuals to infection as well. The greatest injury is seen
Major Cold-Related Disorders to the peripheral nerves and blood vessels, caused by secondary
ischemic injury. Mild NFCI is self-limited initially, but with con-
Localized Cutaneous Cold Injury tinued prolonged cold exposure, it becomes irreversible. When
the feet are wet and cold, they are at increased risk and the inju-
Cold injuries occur at peripheral sites on the body and are classi- ry's course is accelerated because wet socks insulate poorly, and
fied as eitherfreezing (e.g., frostbite) or nonfreezing (e.g., immer- water cools more effectively than air at the same temperature.
sion foot) injuries. Localized cold injuries are preventable with Any factors that reduce circulation to the extremities also con-
proper preparation for cold exposure, early recognition of cold tribute to the injury, such as constrictive clothing, boots, pro-
injury, and effective medical care. However, frostbite, potentially longed immobility, hypothermia, and crouched posture.
the most serious form of freezing injury because of the risk of
limb loss, is the primary injury of concern in this section. NFCI is classified in four degrees of severity, as follows:

It is imperative to recognize, manage, and prevent fur- • Minimal. Hyperemia or engorgement caused by an
ther tissue freezing in mild to severe forms of freezing injury. increase in blood flow to the feet and slight sensory
Nicotine, alcohol intoxication, homelessness, and major psychi- change will remain 2 to 3 days after injury. Condition is
atric disorders remain important predisposing factors.81 When self-limited, and no signs of injury remain after 7 days.
comparing cold weather injuries by ethnicity, African Americans Occasionally, cold sensitivity will remain.
are reported to be at greater risk for cold weather injuries,
including frostbite. This relationship is related to the greater sus- • Mild. Edema, hyperemia, and slight sensory change
ceptibility of pigmented cells to freeze compared with nonpig- remain 2 to 3 days after injury. Seven days after injury,
mented cells.82•83 Tight or constricting clothes, too many socks, anesthesia is found on the plantar surface of the foot
and tight-fitting footwear are predicable factors in the onset of and tips of the toes and lasts 4 to 9 weeks. Blisters


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