FROSTBITE INJURY
CLINICAL PEARLS AND PITFALLS
Care should be taken not to rub or apply pressure to the affected areas.
Rewarming is painful and analgesics should be provided.

Clinical Recognition
Frostbite is injury or destruction of the skin and its underlying tissue that can
occur in temperatures below the freezing point of water. Damage is caused by
tissue freezing, hypoxia, and inflammatory response with microvascular thrombus
formation mediated by the release of bradykinin, prostaglandin F2α, thromboxane
β2, and histamine. Children are at greater risk for frostbite injuries due to their
high body surface area-to-mass ratios and less subcutaneous fat. The most typical
body parts affected include the fingers, toes, ears, and nose. Emergency
physicians should be suspicious when adolescents present with geometrical burn
injuries and unexplained circumstances and be aware of the “salt and ice
challenge,” which involves putting salt on the skin and then applying ice cubes on
top of the salt with the goal to resist the pain from the resultant frostbite for as
long as possible.
The clinical presentation of frostbite can range from superficial areas of pallor
and edema to more severe hemorrhagic blisters and necrosis. Severe injury can
lead to amputations, chronic pain, and premature fusion of the epiphyseal
cartilage that can affect growth.
The treatment goals are to minimize dermal ischemia and promote timely
healing. Treatment can be described in three phases. The initial prethaw period,
usually performed by prehospital personnel, involves getting the patient out of the
cold environment and then removing wet clothing. Soft padding should be
applied to protect the affected area; care must be taken not to rub any of these
tissues as this may cause further damage. The second phase, the actual rewarming
process, will take place over the next 15 to 30 minutes with the affected area
being immersed in water that is preheated to 40° to 42°C. Because rewarming is
quite painful, IV analgesics will likely be required. The third phase, the postthaw

period, involves careful wound management and application of loose, sterile
dressings. Digits are typically separated with cotton, and extremities are splinted.
A follow-up with a wound care specialist is highly recommended.
Tetanus prophylaxis is warranted. Prophylactic antibiotic use is controversial;
however, coverage for staphylococci, streptococci, and pseudomonas should be


considered if there is any indication of infection.

HIGH-ALTITUDE ILLNESS
Goals of Treatment
Early recognition and treatment can lead to complete recovery. Severe illness
needs to be treated with cardiopulmonary resuscitation and descent to prevent
pulmonary edema and cerebral edema.
CLINICAL PEARLS AND PITFALLS
The four major illnesses seen with altitude include high-altitude
headache (HAH), acute mountain sickness (AMS), high-altitude
cerebral edema (HACE), and high-altitude pulmonary edema (HAPE).
Treatment for HAH or mild AMS includes acetazolamide, analgesics,
hydration, and antiemetics.
For more severe AMS or HACE, oxygen, hyperbaric therapy, and
dexamethasone are indicated, along with immediate descent if feasible.

Current Evidence
Physiologic changes accompanying altitude may be attributed to hypobaric
hypoxia. As altitude increases, barometric pressure decreases, resulting in a
reduction in the partial pressure of oxygen. Temperature also decreases with
altitude, so hypothermia can compound these hypoxic effects. The individual’s
response to hypoxia is to increase ventilation, which raises alveolar oxygen while
reducing alveolar carbon dioxide simultaneously. Hypocapnia produces an

alkalosis that, in turn, will serve as a “check and balance” for the body by limiting
further increases in the respiratory rate. With time the pH returns to neutral as the
kidneys excrete bicarbonate in response to this alkalosis. Acetazolamide
(Diamox) is used to inhibit carbonic anhydrase-dependent bicarbonate resorption
in the tubules to facilitate bicarbonate excretion, inducing a metabolic acidosis
that allows the ventilatory rate to remain high and to maintain better oxygenation.

Clinical Recognition
The four major illnesses seen with altitude include high-altitude headache (HAH),
acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and highaltitude pulmonary edema (HAPE). Headache is typically the initial symptom
upon climbing to higher altitudes; it may occur alone as in HAH or progress to


AMS. AMS is defined as having a headache in the setting of at least one of four
other symptoms: nausea/vomiting, fatigue, difficulty sleeping, and dizziness.
Vasogenic edema is believed to explain the pathophysiology underlying AMS,
with clinical progression to encephalopathy occurring as cerebral edema, or
HACE, worsens. HAPE is the most common cause of death when exposed to
high altitudes; younger individuals may be more susceptible to HAPE because of
immature control of breathing and frequent respiratory illnesses. Pulmonary
vascular leak leads to elevated pulmonary artery pressures. Pediatric patients with
HAPE should undergo evaluation for cardiopulmonary abnormalities such as
structural heart disease and pulmonary hypertension.

Triage and Initial Assessment
The recognition of altitude illness depends mainly on a compatible history of
exposure to high altitude. Children may be at risk for high-altitude illness when
traveling from low altitude to high altitude (sporting events, family vacations,
school activities), returning to high altitude after traveling to low altitude, or
when having a respiratory illness at high altitude without changes in elevation.

Intermediate altitude is defined as 1,520 to 2,440 m (5,000 to 8,000 ft), high
altitude as 2,440 to 4,270 m (8,000 to 14,000 ft), very high altitude as 4,270 to
5,490 m (14,000 to 18,000 ft) and extreme altitude as greater than 5,490 m
(18,000 ft).
Initial Assessment
The diagnosis of altitude illness in children can be challenging, especially in the
preverbal age group. Factors that affect whether an individual gets sick include
the altitude itself, rate of ascent, the altitude where sleeping occurs routinely, and
the individual’s physiology. Information regarding any potential genetic basis of
high-altitude illness is limited. However, from an anatomical perspective, those
who are able to tolerate brain swelling (i.e., the elderly whose brain size
diminishes with age, or infants with their immature sutures and open fontanelles)
are less susceptible to altitude illnesses.

Management and Diagnostic Studies
Treatment for HAH and mild AMS includes stopping the ascent and
acclimatizing at the current altitude; acetazolamide given early will hasten this
process and remains the best choice for prevention of AMS. Analgesics,
hydration, and antiemetics are also given for supportive care. Phosphodiesterase
inhibitors such as sildenafil have shown promise in prevention of HAPE in
patients with AMS.


Once AMS worsens, low-flow oxygen should be given in conjunction with
acetazolamide and/or dexamethasone, and either HBO therapy with a portable
compartment or immediate descent should occur. Therapy should be more
aggressive if HACE ensues, with dexamethasone administered in addition to
oxygen, HBO, head elevation to 30 degrees in the supine position, and immediate
descent or evacuation. The addition of the calcium-channel blocker nifedipine
will reduce pulmonary vascular pressures in patients with HAPE. Exertion should

be limited, oxygen provided, and either HBO or immediate descent arranged.
Recently, portable hyperbaric chambers that weigh less than 4 kg have been
developed and can be lifesaving if descent is not possible. Descent is the
definitive treatment for all forms of altitude illness but may not always be feasible
due to weather or other barriers.

Prevention
Prevention efforts may minimize an individual’s chance of developing altitude
illness. For example, different formulas exist regarding ideal ascent rates (i.e.,
above 3,000 m [9,842 ft], sleeping elevations should not exceed the previous day
by more than 300 to 500 m and rest should occur every 3 days), following the
mantra of “climb high, sleep low.” If physically fit individuals follow such
climbing guidelines, prophylaxis with acetazolamide is not typically required.
However, because of the ease of getting to high elevations via car or airplane,
individuals who ascend quickly, and/or have significant underlying diseases
(hepatic, renal, or cardiopulmonary dysfunction in particular) may warrant
acetazolamide prophylaxis. Most sources recommend using 250 mg
acetazolamide twice daily, with pediatric dosing extrapolated from acetazolamide
dosing for edema at 5 to 10 mg/kg/dose every 6 hours, not to exceed 1 g/day.
Care should be taken in the individual with a sulfa allergy because acetazolamide
contains a sulfa moiety. While the incidence of cross-reactivity is low at 7% to
10% in patients with a self-reported sulfa allergy, anaphylaxis has been reported,
and thus use of dexamethasone may be more prudent in these cases.

ELECTRICAL INJURIES
Goals of Treatment
The goals of emergency therapy are stabilization of cardiopulmonary status,
treatment of external injuries, and assessment for potential internal injuries.
CLINICAL PEARLS AND PITFALLS