Environmental Injuries and

Altitude Injuries

Yuddy Imowanto
Departement of Emergency Medicine
Faculty of Medicine – University of Brawijaya
Malang 2020
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References…
• ROSEN’S EMERGENCY MEDICINE: CONCEPTS AND CLINICAL
PRACTICE 8th edition. Copyright © 2014 by Saunders, an imprint
of Elsevier Inc.
• TINTINALLI’S EMERGENCY MEDICINE: A COMPREHENSIVE
STUDI GUIDE 8th edition, American College of Emergency
Physicians. Copyright © 2016 by McGraw-Hill Education.

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Epidemiology…
• High-altitude illness represents a spectrum of clinical entities
that have hampered the activities of mountaineers, merchants,
military forces, aviators, and explorers throughout time.
• This illness is seen clinically in one of several forms that overlap
and share a common pathophysiologic mechanism.
• Acute mountain sickness (AMS) is the relatively benign and self-
limited presentation, whereas highaltitude pulmonary edema
(HAPE) and high-altitude cerebral edema (HACE) represent the
potentially life-threatening manifestations of high-altitude
illness.

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Epidemiology…
• The incidence of high-altitude illness depends on many variables,
including the rate of ascent, previous altitude exposure, and
individual genetic susceptibility.
• Sleeping altitude, final altitude reached, and duration of stay at
altitude are also risk factors for AMS development. AMS is
common (67% incidence) among mountain climbers on Mt. Rainier
who ascend quickly (1 or 2 days) to 14,410 feet.
• Trekkers who fly into the Khumbu region to explore the Mt.
Everest (29,029 feet), area have a higher incidence of AMS
(47%) compared with those who walk (23%).
• Among this population, AMS occurs in approximately 25%
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Mount Bromo, is an active volcano & part of the Tengger massif, in East
Java, Indonesia. At 2,329 metres (7,641 ft) it is not the highest peak of
the massif, but is the most well known. The massif area is one of the most
visited tourist attractions in East Java, Indonesia.

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Epidemiology…
• Age may be a relative risk factor. Most studies of children
suggest that they have the same incidence of AMS as adults do.
• One small study of tourists in Chile evaluated children 4 to 48
months old and found higher AMS scores and lower oxygen
saturations compared with those of their parents.
• Younger individuals (< 20 yo) are more likely to have HAPE,
although HAPE is extremely rare in children younger than 2
years.
• Gender does not affect the incidence of AMS; however, women
may have less risk for development of HAPE. No relationship
appears to exist between AMS development and the menstrual
cycle.
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Epidemiology…
• The number of older travelers visiting mountain resorts is increasing.
Many of these individuals have underlying health problems, including
lung disease (10%), heart disease (25%), and hypertension (30%).
• Despite these conditions, the risk for AMS development in adults
older than 50 years may be less than in younger age groups.
• One study found no difference in the incidence or severity of AMS in
climbers older than 50 years compared with a matched cohort of
younger climbers. There are indications that elders may not react well
to acute highaltitude exposure.
• Pulmonary vital capacity decreases almost one third in elders
ascending from sea level to 14,000 feet for 1 week, producing a large
decrease in both oxygen saturation & maximal oxygen uptake during
exercise. 8
 Definitions …
• Moderate altitude is between 8000 and 10,000 feet of elevation.
• Although most people do not experience signifcant arterial
oxygen desaturation until they reach higher altitudes, high-
altitude illness is common with rapid ascent above 8000 feet, and
individuals with underlying medical problems may be predisposed
to development of altitude illness at lower levels.

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 Definitions…
• High altitude is between 10,000 and 18,000 feet. Most serious
altitude illness occurs at these levels. The pathophysiologic effects of
high altitude begin when the oxygen saturation of the arterial blood
begins to fall below the 90% level.
• The sigmoidal shape of the oxyhemoglobin dissociation curve prevents
a signifcant fall of arterial oxygen saturation in most individuals until
an altitude of approximately 12,000 feet.
• At this altitude, the steep portion of the curve is encountered, and
marked oxygen desaturation may occur with relatively small increases
in altitude. Some predisposed individuals may desaturate < 90% at
altitudes as low as 8000 feet.
• Extreme altitude is above 18,000 feet.
• At this height, complete acclimatization generally is not possible, and
long visits above this level result in progressive deterioration.
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 Oxygen-hemoglobin dissociation curve

Approximate oxygen saturations are marked for several altitudes. PO2, partial pressure of
oxygen. (Data for 15,000-29,029 feet from Sutton JR, et al: Operation Everest II: Oxygen
transport during exercise at extreme simulated altitude. J Appl Physiol 64:1309, 1988.) 11
 ACCLIMATIZATION …
• Refers to the series of integrated adaptations that take place at high
altitude, which tend to restore the oxygen pressures within the
tissues toward normal sea-level values despite the lowered PO2 of the
atmosphere.
• These processes occur gradually and involve multiple systems from
protein synthesis to respiratory, cardiovascular, and hematologic
adjustments.
• Gradual ascents made by mountaineers during several weeks have
allowed the successful summiting of many of the world’s highest peaks,
including Mt. Everest (29,029 feet), without supplemental oxygen.
• Without this gradual approach to allow acclimatization, however, rapid
exposure to extreme altitude results in loss of consciousness, and
death may occur in a matter of minutes.
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ACCLIMATIZATION …
• One of the most important physiologic changes is an increase in minute
ventilation, causing a decrease in the partial pressure of carbon dioxide.
• The alveolar gas equation states that as the PaCO2 decreases, a
corresponding increase in PaO2 occurs, thereby increasing arterial
oxygenation. Thus the level of ventilation determines alveolar oxygen for a
given inspired oxygen tension.
• When a person arrives at high altitude, the peripheral chemoreceptors in
the carotid bodies respond to a decrease in PaO2 and signal the
respiratory control center in the medulla to increase ventilation.
• This increase in ventilation is known as the hypoxic ventilatory response
(HVR), which may be inhibited or stimulated by numerous factors, including
ethanol, sleep medications, caffeine, cocoa, prochlorperazine, and
progesterone. The magnitude of the HVR varies among individuals and may
be genetically predetermined.
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ACCLIMATIZATION
• As ventilation increases, a respiratory alkalosis occurs that acts as a
negative feedback system on the central respiratory center, limiting
any further increase in ventilation.
• Within 24 to 48 hours of ascent, the kidneys excrete bicarbonate in
an effort to compensate for the alkalosis. As the pH normalizes,
ventilation rises slowly, reaching a maximum after 6 to 8 days.
• This process is enhanced by acetazolamide. The ability to achieve an
adequate HVR varies and is related to the ability to acclimatize. A low
HVR and relative hypoventilation are implicated in the pathogenesis of
both AMS and HAPE.
• For the majority of people with intermediate HVRs, however,
ventilatory drive probably has no predictive value for AMS
development.
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ACCLIMATIZATION…
• The release of catecholamines on ascent stimulates the
circulatory system to increase cardiac output.
• This is manifested by an elevation in heart rate, blood pressure,
cardiac output, and venous tone.
• Except at extreme altitudes, acclimatization results in the
gradual return of the resting heart rate to near sea-level
values.
• Resting relative tachycardia is evidence of poor acclimatization.
• As the altitude increases, a decrease in maximal heart rate
capacity occurs, and at the limits of acclimatization, maximal
and resting heart rates converge.
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ACCLIMATIZATION…
• The hematopoietic response to high-altitude acclimatization consists
of an increase in both hemoglobin and the number of red blood cells.
An early increase of up to 15% occurs in mean corpuscular
hemoglobin concentration after rapid ascent to high altitude.
• This is primarily a result of a fluid shift into the extravascular space.
Long-term acclimatization leads to an increase in plasma volume and
total blood volume.
• Erythropoietin is secreted in response to hypoxemia within hours of
ascent, which in turn stimulates the production of red blood cells,
leading to new circulatory red blood cells in 4 or 5 days.
• During the next 2 months, red blood cell mass increases in proportion
to the degree of hypoxemia.
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ACCLIMATIZATION…
• Hypoxemia also results in an increase in 2,3-diphosphoglycerate,
causing a rightward shift of the oxyhemoglobin dissociation curve,
which favors a release of oxygen from the blood to the tissues.
• This is counteracted by the leftward shift of the oxyhemoglobin
dissociation curve caused by the respiratory alkalosis from
hyperventilation.
• The result is a net null change in the oxyhemoglobin curve and an
increase in oxygen-hemoglobin binding in the lung, which raises Sao2.
• Some individuals with mutant hemoglobin and high oxygen-hemoglobin
affnity are found to acclimatize more effciently than their normal
counterparts at moderate altitudes.

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PATHOPHYSIOLOGY…
• The clinical syndromes of high-altitude illness are not discrete
entities but represent a spectrum of intertwined pathophysiologic
mechanisms.
• AMS and HACE appear to represent differing manifestations of
altitude illness on the same continuum, whereas HAPE appears to have
a somewhat independent pathophysiologic mechanism.
• The symptoms of AMS develop several hours after arrival at high
altitude, whereas the development of HAPE and HACE generally
requires several days of altitude exposure. Because hypobaric
hypoxemia occurs within minutes of arrival, it cannot be the direct
cause of high-altitude illness.
• It appears to be the initiating factor for a complex pathologic
process that leads to the development of the various clinical
syndromes.

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Mechanisms for the development of
acute mountain sickness (AMS), high-
altitude pulmonary edema (HAPE), and
high-altitude cerebral edema (HACE).
CNS, central nervous system; ICP,
intracranial pressure.

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ACUTE MOUNTAIN SICKNESS…
• For the diagnosis of AMS, a patient must be in the setting of a
recent gain in altitude, be at the new altitude for at least several
hours, and report a headache plus at least one of the following
symptoms: gastrointestinal upset (anorexia, nausea, or vomiting),
general weakness or fatigue, dizziness or lightheadedness, or
diffculty in sleeping.
• The headache may vary from mild to severe, is generally bitemporal
and throbbing in nature, and is worse during the night and on
awakening or on suddenly becoming upright.
• Anorexia and nausea, with or without vomiting, are common, and the
other symptoms described can range in severity from mild to
incapacitating.

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ACUTE MOUNTAIN SICKNESS…
• Ultrasonography is emerging as an early, noninvasive diagnostic
tool to assess intracranial pressure.
• Studies have demonstrated that elevated intracranial pressure
is associated with AMS and HACE. Increasing intracranial
pressure correlates directly with optic nerve sheath diameter.
• It is possible to demonstrate that subjects with symptoms and
signs of AMS or HACE have enlarged optic nerve sheath
diameters, which may be a useful adjunct in the diagnosis of
AMS and HACE.

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ACUTE MOUNTAIN SICKNESS…
• Most mild AMS is treated by stopping of further ascent and
waiting for acclimatization.
• This may take 1 to 4 days. AMS that becomes worse or does not
respond to maintenance of altitude, rest, and pharmacologic
intervention necessitates descent.
• A descent of 1500 to 3000 feet effectively reverses high-
altitude illness in most cases. Descent should be continued until
improvement is seen, and efforts to minimize exertion should be
instituted during the descent.

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ACUTE MOUNTAIN SICKNESS…
• Acetazolamide accelerates acclimatization and, if it is given early in the
development of AMS, rapidly resolves symptoms. A dose of 250 mg of
acetazolamide at the onset of symptoms and repeated twice daily is effective
therapy for AMS.
• The dose for children is 2.5 mg/kg/dose given twice daily to a max of 250 mg.
Acetazolamide is a carbonic anhydrase inhibitor that induces a renal bicarbonate
diuresis, causing a metabolic acidosis that increases ventilation and arterial
oxygenation. This respiratory stimulation improves sleep when the hypoxemia
caused by periodic breathing is eradicated by acetazolamide.
• The diuretic effects attenuate fluid retention common in patients with AMS. This
agent also lowers CSF volume and pressure, which may play an additional role in
its therapeutic and prophylactic use.
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ACUTE MOUNTAIN SICKNESS…
• Dexamethasone is an effective alternative treatment of AMS. An initial dose of 8
mg is followed by 4 mg every 6 hours. No signifcant adverse reactions are
reported; however, symptoms can recur when the treatment is withdrawn.
• Although dexamethasone can resolve the symptoms of AMS, it does not play a role
in acclimatization. Concurrent use with acetazolamide is advocated by some to
promote acclimatization.
• It is known to have and this weight-based approach may reduce side effects in
smaller adults. Ibuprofen compared with acetazolamide is equally effcacious in
preventing headache. Dexamethasone also prevents AMS.
• The lowest effective dosage is 2 mg every 6 hours or 4 mg every 12 hours. Some
patients experience the rapid onset of AMS after dexamethasone is discontinued.
Dexamethasone does not facilitate acclimatization but rather reduces nausea and
enhances mood. In most cases, dexamethasone use should be reserved for
treatment of AMS rather than for prophylaxis.
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High Altitude Pulmonary Edema
• Marked dyspnea on exertion, fatigue with minimal-to-moderate effort,
prolonged recovery time, and dry cough are early manifestations of the
disease. The symptoms of AMS usually occur concurrently with the
development of HAPE.
• As the HAPE patient deteriorates, usually through the night, the dyspnea
intensifes with effort and is unrelieved by rest. Dyspnea at rest should be
recognized as a red flag that warns of the development of a serious
pulmonary problem. The cough becomes productive of copious amounts of
clear, watery sputum, and hemoptysis may be seen in severe cases.
• As the condition intensifes, cerebral edema or simply severe hypoxemia
causes
central nervous system dysfunction, such as ataxia and altered mentation.
• Coma may follow and precede death in a few hours if oxygen therapy or
descent is not instituted.
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Chest radiograph of a patient with high-altitude pulmonary edema. A, Before treatment. B, After treatment. (Courtesy Richard Nicholas, MD.)

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High Altitude Pulmonary Edema
• Hyperbaric therapy simulates descent without the
administration of supplemental oxygen.
• Several portable, lightweight (approximately 15 pounds), fabric
hyperbaric chambers are available and pressurized manually.
These chambers generate 103 mm Hg (2 psi) above the ambient
pressure. This simulates a descent of 4000 to 5000 feet at
moderate altitudes, and at the summit of Mt. Everest it would
simulate a descent of approximately 9000 feet.
• These devices can be lifesaving in patients with HAPE and
HACE. Some nonambulatory patients are able to descend under
their own power after a few hours in hyperbaric chambers.
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High Altitude
Pulmonary
Edema

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HIGH-ALTITUDE CEREBRAL EDEMA
• HACE is the least common but most severe form of high-
altitude illness.
• Death from HACE at as low as 8200 feet is reported, although
most cases occur above 12,000 feet.
• Mild AMS can progress to severe HACE with coma in as few as
12 hours. Although the usual time course is 1 to 3 days for the
development of severe symptoms, it may occur in 5 to 9 days.

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HIGH-ALTITUDE CEREBRAL EDEMA
• HACE-specifc signs include ataxia, generalized seizures, slurred
speech, rarely focal neurologic defcits, and altered mentation, which
can range from mild emotional lability or confusion to hallucinations
and decreased levels of consciousness that may proceed to coma and
death. MRI of patients with HACE reveals white matter changes
consistent with vasogenic edema
• Altered consciousness and cerebellar ataxia are the most sensitive
signs for early recognition of HACE. The early appearance of ataxia
reflects the particular sensitivity of the cerebellum to hypoxia.
Ataxia alone is an indication for immediate descent.
• Retinal hemorrhages are common but often occur as an isolated
finding. Papilledema and occasionally cranial nerve palsy also occur in
the setting of increased intracranial pressure.
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HIGH-ALTITUDE CEREBRAL EDEMA

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HIGH-ALTITUDE CEREBRAL EDEMA
• Early recognition and initiation of descent are the keys to successful
therapy for HACE. High-flow oxygen should be administered if it is
available because oxygen alone reduces intracranial blood flow at high
altitude.
• Steroid therapy is recommended and may result in recovery from HACE
without neurologic defcits. The initial dose of dexamethasone is 8 mg
parenterally or orally in mild cases, followed by 4 mg every 6 hours.
Patients with severely altered levels of consciousness require tracheal
intubation.
• Hyperventilation, diuretics (e.g., furosemide), and hypertonic solutions (e.g.,
mannitol) may be used to manage severely elevated intracranial pressure.
Caution is warranted because many patients with HACE are already volume
depleted from poor fluid intake; diuretic use could compromise adequate iv
volume and reduce cerebral perfusion pressure.
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HIGH-ALTITUDE CEREBRAL EDEMA…
• Hyperbaric treatment of HACE is also effective and may result in
temporary improvement and allow self-rescue. Conversely, coma may
persist for several days after descent to lower altitudes, so placement of
HACE patients in a hyperbaric device may only delay the more
comprehensive care available in the hospital setting.
• Long-term neurologic defcits, such as ataxia and cognitive impairment, are
reported after recovery from acute episodes of HACE.
• Both transient and long-lasting neurobehavioral impairments can occur in
mountaineers after climbing to extreme altitude without experiencing
clinical HACE.
• Some of these sequelae can persist for 1 year. Early treatment of HACE
generally results in good outcomes, but after coma is present, the
mortality rate exceeds 60%.
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HIGH-ALTITUDE RETINAL HEMORRHAGE
• Is the most common type of retinopathy in visitors to high altitude.
• These hemorrhages are common at altitudes above 17,500 feet, although
they can occur at lower levels.
• The exact incidence of HARH is unknown because most patients are
asymptomatic, with HARH noted only on retinoscopy. HARH is not generally
related to the presence of mild AMS but does seem to be related to
strenuous exercise at high altitude. At any altitude, in the setting of
severe HAPE or HACE, retinal hemorrhages are commonly noted, but the
mechanism remains unclear.
• Hemorrhages usually spare the macula. Retinal hemorrhages usually resolve
without treatment in 2 or 3 weeks. With macular involvement, central
scotomas may be noticed for several years, gradually resolving. In some
cases, however, these visual defects are permanent.
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CARBON MONOXIDE TOXICITY
• can occur at altitude from the use of fres and combustion stoves to
keep warm and to prepare food in the high-altitude environment.
• If CO poisoning occurs at altitude, it can be more devastating
because of the lower oxygen pressures and the body’s baseline
hypoxic state. CO binds to hemoglobin and prevents oxygen release
to the body’s tissues that are already, relative to sea level, hypoxic.
• It is easy to confuse the symptoms and signs of CO poisoning and
AMS as both include headache, nausea, dizziness, dyspnea, and
lassitude (kelesuan).
• If there is doubt, a person should leave the enclosed space and
descend or use supplemental oxygen if it is available.

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Heat Injuries
Yuddy Imowanto
Departemen Ilmu Kedokteran Emergensi
Fakultas Kedokteran Universitas Brawijaya

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Heat Cramps - Physiology
Heat cramps are brief, intermittent, and often severe muscle
cramps occurring typically in muscles that are fatigued by heavy
work.
Heat cramps appear to be related to a salt deficiency.
Heat cramps occur most commonly during the first days of work
in a hot environment and develop in persons who produce large
amounts of thermal sweat and subsequently drink copious
amounts of hypotonic fluid.

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Heat Cramps - Clinical Factors
Heat cramps are occasionally confused with hyperventilation
tetany, which can occur during heat exhaustion.
Hyperventilation tetany can be distinguished by the presence of
carpopedal spasm and paresthesias in the distal extremities and
perioral area.
Heat cramps accompanied by systemic symptoms may be part of
salt depletion heat exhaustion.
Heat cramp victims exhibit hyponatremia, hypochloremia, and low
serum sodium and chloride levels.
Rhabdomyolysis or resultant renal damage is not present with
isolated heat cramps

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Heat Cramps - Management
Heat cramps are usually rapidly relieved by salt solutions.
Commercially available flavored electrolyte solutions are
commonly ingested.
Mild cases without concurrent dehydration are treated orally
with 0.1 or 0.2% salt solution (two to four 10-grain salt tablets
[56-112 mEq] or ¼ to ½ teaspoon of table salt dissolved in a quart
of water), which is the general limit of palatability.
Severe cases respond rapidly to intravenous isotonic solution
(0.9% NaCl). Salt tablets are gastric irritants, delay gastric
emptying, and are not recommended.

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Heat Cramps - Diagnostis

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Heat Edema
Physiology and Clinical Features
Swollen feet and ankles are often reported by nonacclimatized
individuals, especially the elderly, who encounter climatic
stresses of tropical and semitropical areas.
Such individuals often have no underlying cardiac, hepatic,
venous, or lymphatic disease.
They commonly have assumed rigorous schedules with long
periods of sitting or standing. The edema is usually minimal, is not
accompanied by any significant impairment in function, and often
resolves after several days of acclimatization.
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Heat Edema
Physiology and Clinical Features
It is presumed that hydrostatic pressure and vasodilation of
cutaneous vessels, combined with some degree of orthostatic
pooling, lead to vascular leak and accumulation of interstitial fluid
in the lower extremities. Simultaneously, aldosterone increases in
response to the heat stress and perceived central volume deficit.
Brief diagnostic evaluation to rule out thrombophlebitis,
lymphedema, or congestive heart failure is appropriate, but
invasive diagnostic techniques or vigorous pharmacologic therapy
is not indicated.

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Heat Edema
Management
Diuretic therapy is not effective. Rather, simple leg
elevation or thigh-high support hose should be used.
In most individuals, the problem resolves either through
adequate acclimatization or with the individual’s return
to a temperate climate.

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Heat Syncope
Physiology and Clinical Features
The elderly have a special predilection for this disorder. Individuals
adapt to a hot, humid environment by dilation of cutaneous vessels to
deliver heat to the body surface.
Thus an increased portion of the iv pool is located in the periphery at
any given time.
Increasing blood flow to compliant cutaneous veins raises skin vascular
volume at the expense of thoracic blood volume. Individuals who stand
for protracted periods tend to pool blood in the lower extremities.
Combined with volume loss and peripheral vasodilation, this pooling can
result in inadequate central venous return, a concomitant drop in CO &
cerebral perfusion inadequate to maintain consciousness.
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Heat Syncope
Management
The disorder is self-limited because assumption of a horizontal
position is curative.
Individuals at risk for heat syncope should be warned to move
often, to flex leg muscles repeatedly when standing stationary,
to avoid protracted standing in hot environments, and to assume
a sitting or horizontal position when prodromal warning symptoms
or signs occur.
These include scintillating scotomas, tunnel vision, vertigo,
nausea, diaphoresis, and weakness.

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Prickly Heat
Physiology and Clinical Features
Prickly heat, also known as miliaria rubra, lichen tropicus, & heat rash,
is an acute inflammatory disorder of the skin that occurs in tropical
climates. It is the result of blockage of sweat gland pores by
macerated stratum corneum and secondary staphylococcal infection.
The acute phase is characterized by vesicles in the malpighian layer of
the skin caused by dilation and rupture of the obstructed sweat gland
ducts. The rash is confined to clothed areas, and the affected area is
often completely anhidrotic.
During approximately the next week, a keratin plug arises and fills
these vesicles, causing a deeper obstruction of the sweat gland duct.

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Prickly Heat
Physiology and Clinical Features
The obstructed duct then ruptures a second time, producing a
deeper vesicle within the dermis
This is known as the profunda stage, and it can persist for weeks.
Profunda vesicles are not pruritic and closely resemble the white
papules of piloerection; chronic dermatitis is a common
complication.

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Prickly Heat

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Prickly Heat
Management
Chlorhexidine in a light cream or lotion is the antibacterial
treatment of choice during the acute phase. Salicylic acid, 1%,
can be applied three times daily to localized, affected areas to
assist in desquamation, but it should not be used in children or
over large areas because of possible salicylate intoxication.
For diffuse or pustular rashes, erythromycin can be helpful.
Prickly heat can be prevented by wearing of light, loose-fitting,
clean clothing and the avoidance of situations that produce
continuous sweating.
Routine use of talcum or baby powder should be avoided.
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HEAT EXHAUSTION - Physiology
a clinical syndrome characterized by volume depletion that occurs
under conditions of heat stress. Two types of heat exhaustion
are classically described: water depletion and salt depletion.
Water depletion heat exhaustion results from inadequate fluid
replacement by individuals working in a hot environment, usually
laborers, athletes, military personnel, and incapacitated
individuals without free access to water.
Those working in the heat seldom drink as much as they lose &
replace only approximately two thirds of net water loss.
This voluntary dehydration results in progressive hypovolemia.
Left untreated, water depletion heat exhaustion will progress to
heatstroke.

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HEAT EXHAUSTION - Physiology
It differs from heat cramps in that systemic symptoms occur.
This syndrome is characterized by hyponatremia, hypochloremia,
and low urinary sodium and chloride concentrations.
Symptoms are similar to those seen in water depletion heat
exhaustion; body temperature usually remains nearly normal.

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HEAT EXHAUSTION - Clinical Features
The symptoms and signs associated with both types of heat
exhaustion are variable and nonspecific and include weakness,
fatigue, frontal headache, impaired judgment, vertigo, nausea and
vomiting, and occasionally muscle cramps.
Orthostatic dizziness and syncope can occur. Sweating persists
and may be profuse.
The core temperature is only moderately elevated, usually below
40° C, and signs of severe CNS dysfunction are not present.

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HEAT EXHAUSTION - Clinical Features
Clinical Features
Mild heat exhaustion and full-blown heatstroke represent extremes of
the spectrum of heat illness, and intermediate cases may prove
difficult to differentiate.
Nevertheless, heat exhaustion should not be diagnosed in the
presence of major CNS dysfunction (seizures & coma) or severe
hyperthermia (40.5° C).
Measurement of hepatic transaminases may prove helpful. Elevations
to several thousand units can be seen in patients with heat exhaustion
or in healthy runners after a marathon, whereas in patients with
heatstroke, such levels are usually in the tens of thousands after 24
hour.

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HEAT EXHAUSTION - Management
Pure forms of either type of heat exhaustion are rare, and most
cases of heat exhaustion involve mixed salt and water depletion.
Heat exhaustion is primarily a volume depletion problem, and
rapid recovery generally follows fluid administration.
Decisions regarding the type of fluid & electrolyte replacements
should be based on serum electrolyte measurements and the
estimation of hydration status by clinical and laboratory
parameters.

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HEAT EXHAUSTION - Management
Patients with significant volume depletion or electrolyte
abnormalities require intravenous fluids.
If the patient is orthostatic, normal saline should be
administered until the patient is hemodynamically stable.
Free water deficits should be replaced slowly during 48 hours to
avoid a decrease of serum osmolality more than 2 mOsm/hr.
Overly rapid correction of hypernatremia is associated with
seizures caused by cerebral edema → CPM (Central Pontine
Myelinolysis)

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 HEAT STROKE - Physiology
Energy will be insufficient to sustain thermoregulatory
mechanisms, resulting in dramatic increases in core temperature
and the clinical manifestations of heatstroke.
An exact temperature at which cellular damage begins to occur in
an individual patient varies. Credible reports exist of full recovery
despite rectal temperatures of 44.4 to 46.5° C.
Damage is a function not only of temperature but also of the
exposure time.The resultant damage to tissues is a function of a
complex interaction of body temperature, exposure time, workload,
tissue perfusion, and individual factors, which vary markedly.

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HEAT STROKE - Physiology
Neurologic dysfunction is a hallmark of heatstroke, and cerebral
edema is common. Other pathologic changes include petechiae in
the walls of the third and fourth ventricles and marked
cerebellar Purkinje cell damage.
Interestingly, the hypothalamus, the predominant site of central
thermoregulatory control, is usually not damaged.
Heat stress creates tremendous demands on the cardiovascular
system, and patients who succumb to heatstroke show signs of
circulatory failure. Although such pathologic changes are common,
cardiac damage alone is not lethal.

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HEAT STROKE - Physiology
If severe heat stress continues, compensatory splanchnic
vasoconstriction will eventually fail.
Failure to perfuse the skin with heated blood from the core
results in a dramatically increased rate of heat storage.
This produces elevated ICP, which in combination with a reduction
in mean arterial pressure caused by failure of compensatory
splanchnic vasoconstriction, conspires to produce a decrease in
cerebral blood flow.
This results in the major CNS dysfunction characteristic of
heatstroke.

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HEAT STROKE - Diagnosis

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HEAT STROKE - Physiology
Malignant hyperthermia and neuroleptic malignant syndrome are
characterized by lead-pipe rigidity.The serotonin syndrome can also
mimic heatstroke because of the elevated body temperature tremors
and CNS alterations that occur.
Serotonin syndrome is classically a triad of mental status changes,
autonomic hyperactivity, and neuromuscular abnormalities secondary
to increased CNS serotonergic activity.
A history of recent exposure to illicit or therapeutic medication is an
important clue.
Hepatic transaminase elevations may be diagnostically helpful.
In most febrile states that include altered mental status or coma,
these enzymes will be normal or minimally elevated, although they are
usually dramatically elevated early in the course of heatstroke.
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Management - Cooling
Immediate cooling is the cornerstone of treatment. Mortality
correlates with the temperature and the number of dysfunctional
organ systems, with an increased risk of death if patients present with
anuria, coma, or cardiovascular failure.
Patients who present to the hospital with heat stroke have high
mortality rates ranging from 21 to 63%, and mortality increases
significantly when cooling is delayed.
Cooling efforts take precedence over any time-consuming search for
the cause. In the out-of-hospital setting, cooling should be initiated
after removal of the patient from the hot environment.
When the patient arrives at the hospital, clothes should be removed, a
thermistor probe should be inserted & the temperature should be
continuously monitored. 72
Management – Cooling
The ideal method of evaporative cooling uses a body cooling unit on
which the patient lies suspended on a net surface while being sprayed
with atomized 15° C water from above and below.
Air warmed to 45 to 48° C is blown over the skin surface at 3 m/min.
The unit, not widely available, maximizes evaporative cooling by
maintaining cutaneous vasodilation and avoiding heat generation caused
by shivering.
Less complex equipment can also be used to maximize evaporative
cooling, which is the most widely used cooling method.
The combination of atomized tepid water at 40° C from a spray bottle
and standing fans cools at rates comparable to both body cooling unit
and immersion.
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75
COLD INJURIES

76
INTRODUCTION
Frostbite is the prototypical freezing injury and is seen when ambient
temperatures are well below freezing. Nonfreezing cold injuries occur
as a result of exposure to wet conditions when temperatures are above
freezing. The most common nonfreezing cold injuries are trench foot
and chilblains.
Although frostbite may result in permanent tissue damage, nonfreezing
cold injuries are characterized by usually mild but uncomfortable
inflammatory lesions of the skin.
This chapter describes the occurrence, risk factors, treatment, and
prevention of the nonfreezing cold injuries—trench foot and immersion
foot, chilblains or pernio, panniculitis, and cold urticaria—and the
freezing injury—frostbite.

77
TRENCH FOOT
Early symptoms progress from tingling to numbness of the affected tissues.
On initial examination, the foot is pale, mottled, anesthetic, pulseless, and
immobile, with no immediate change after rewarming.
A hyperemic phase begins within hours after rewarming and is associated
with severe burning pain and reappearance of proximal sensation.
As perfusion returns to the foot over 2 to 3 days, edema and possibly bullae
form, and hyperemia may worsen.
Anesthesia frequently persists for weeks and may be permanent. In more
severe cases, tissue sloughing and gangrene may develop.
Hyperhidrosis and cold sensitivity are common late features and may persist
for months to years. Severe cases may be associated with prolonged
convalescence and permanent disability.
78
MANAGEMENT - TRENCH FOOT
Treatment is supportive, but vasodilator drugs may be tried.
Oral prostaglandins can increase skin temperatures, which
suggests improved circulation.
Feet should be kept clean, warm, dryly bandaged, elevated, and
closely monitored for early signs of infection.
Prophylaxis for trench foot includes keeping warm, ensuring good
boot fit, changing out of wet socks several times a day, never
sleeping in wet socks and boots, and, once early symptoms are
identified, maximizing efforts to warm, dry & elevate the feet.

79
CHILBLAINS OR PERNIO
• are characterized by mild but uncomfortable inflammatory lesions of
the skin caused by long-term intermittent exposure to damp,
nonfreezing ambient temperatures. Symptoms are precipitated by
acute exposure to cold.The most common areas affected are the
feet (toes), hands, ears, and lower legs.
• Chilblains are primarily a disease of women and children, and although
rare in the US, the disease is common in the United Kingdom and
other countries with a cold or temperate, damp climate.
• Young females with Raynaud’s phenomenon and other immunologic
abnormalities such as lupus erythematosus, as well as those in
households with inadequate heating and lack of warm clothing, are at
greatest risk. Some studies suggest that a low BMI may be
associated with increased risk.
80
MANAGEMENT CHILBLAINS OR PERNIO
Management is supportive.
The affected skin should be rewarmed, gently bandaged, and
elevated. Some European studies support the use of nifedipine,
20 milligrams PO three times daily; pentoxifylline, 400 milligrams
PO three times daily; or an analog of prostaglandin E1, limaprost,
20 micrograms PO three times daily, as both prophylactic and
therapeutic treatment for local cold injury.2
Topical corticosteroids (0.1% triamcinolone cream) are also
effective.

81
PANNICULITIS
is characterized by mild degrees of necrosis of the subcutaneous
fat tissue that develops during prolonged exposure to
temperatures just above freezing.
It is observed in children (e.g., “popsicle panniculitis” of the
cheeks) and on the thighs and buttocks of young women involved
in equestrian activities.
During resolution of the mild inflammation, adipose fibrosis may
result in cosmetic defects, such as unevenness of the skin. There
is no effective treatment for the injury.

82
COLD URTICARIA
is a distinctive example of hypersensitivity to cold air or water,
which in rare cases may lead to fatal anaphylaxis.
Most cases are idiopathic, but they can also be associated with
increased affinity of immunoglobulin E to mast cells and viral
infections.
The diagnosis can be confirmed with the cold water test during
follow-up. Young adults and children and those with atopy or
other forms of inducible urticaria are most commonly affected.
Cold urticaria is treated similarly to urticarial lesions from other
causes.

83
Management cold urticaria
• Antihistamines (H1) are recommended for acute cases, although
higher than usual dosing may be required.
• Other potential therapies include leukotriene receptor
antagonists (zafirlukast, montelukast) and topical capsaicin.
• For persistent cold urticaria, ketotifen or doxantrazole may be
tried, but oral preparations of these mast cell stabilizers are
not available in the United States.
• Prescribe epinephrine autoinjectors for patients with a history
of cold-induced anaphylaxis.

84
FREEZING INJURIES – FROSTBITE
• Groups at high risk for frostbite include military personnel,
winter sports enthusiasts, outdoor workers, the elderly, the
homeless, people who abuse drugs or alcohol, and those with
psychiatric disorders.
• Endothelial damage, beginning at the point of thaw, is the likely
critical event in frostbite. Immediately after freezing and
thawing, an arachidonic acid cascade forms and promotes
vasoconstriction, platelet aggregation, leukocyte sludging, and
erythrostasis, which results in venule and arterial thrombosis
and subsequent ischemia, necrosis, and dry gangrene.
• The necrosis of tissue following frostbite either is due
tocellular injury or is secondary to a vascular lesion.
85
86
FROSTBITE DEGREE

87
FROSTBITE INJURY
• Can be divided into three zones.
• The zone of coagulation is the most severe and is usually distal, and
the damage is irreversible.
• The zone of hyperemia is the most superficial, is typically proximal,
has the least cellular damage, and generally recovers without
treatment in < 10 days.
• The zone of stasis is the middle ground and is characterized by
severe, but possibly reversible, cell damage.
• It is this middle zone for which treatment may have benefit if the
circulation in the frozen area can be restored. Tissue susceptibility
to frostbite varies. The least to most sensitive tissues are, in order,
cartilage, ligament, blood vessel, cutis, epidermis, bone, muscle,
nerve, and bone marrow

88
89
FROSTBITE DEGREE
• First-degree injury (frostnip) is characterized by partial skin
freezing, erythema, mild edema, lack of blisters, and occasional skin
desquamation several days later. The patient may complain of stinging
and burning, followed by throbbing. Prognosis is excellent.
• Second-degree injury is characterized by full-thickness skin
freezing, formation of substantial edema over 3 to 4 hours,
erythema, and formation of clear blisters filled with fluid rich in
thromboxane and prostaglandins. The blisters form within 6 to 24
hours, extend to the end of the digit, and usually desquamate and
form hard black eschars over several days.
• The patient complains of numbness, followed later by aching and
throbbing. Prognosis is good.

90
FROSTBITE DEGREE
• Third-degree injury is characterized by damage that extends into
the subdermal plexus. Hemorrhagic blisters form and are associated
with skin necrosis & a blue-gray discoloration of the skin. The patient
may complain that the involved extremity feels like a “block of wood,”
which is followed later by burning, throbbing, and shooting pains.
Prognosis is often poor.
• Fourth-degree injury is characterized by extension into
subcutaneous tissues, muscle, bone, and tendon. There is little edema.
The skin is mottled, with nonblanching cyanosis, and eventually forms
a deep, dry, black, mummified eschar. Vesicles often present late, if
at all, and may be small, bloody blebs that do not extend to the digit
tips. The patient may complain of a deep, aching joint pain. Prognosis
is extremely poor.

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92
DIAGNOSIS FROSTBITE
• Frostbite may occur anywhere on the skin but is generally limited to
the distal part of the extremities, face, nose, and ears. The injured
area looks pale and waxy and feels hard and cold. Patients frequently
complain of stinging and numbness.
• It is initially difficult to estimate the depth of the cold injury, early
injuries are best classified simply as either superficial or deep.
Prognostic considerations of ultimate tissue loss should take into
account duration of exposure, environmental conditions (temperature,
wind, and precipitation), type of clothing worn, level of physical
activity, possible contact with metal or moisture & associated use of
recreational drugs, alcohol, or tobacco in addition to physical findings.
• Patients with frostbite may have concomitant cold-related problems
such as hypothermia and dehydration, and patients with hypothermia
may also have frostbite. 93
DIAGNOSIS FROSTBITE
• Although some chemical liquids and burn injuries may cause
blister formation, a history of cold exposure differentiates
chemically induced blisters from cold-induced injuries.
• The diagnosis of frostbite is clinical. No specific laboratory
tests are indicated when treating patients with frostbite, and
specific laboratory evaluation should be guided by the clinical
situation including associated trauma or medical illness.
• Early imaging is rarely helpful, either for diagnostic or
prognostic purposes, although the use of technetium-99
scintigraphy may have prognostic value outside of the ED
setting.

94
TREATMENT - PREHOSPITAL
• Initial field management of frostbite includes prevention of further
cold injury, hypothermia & dehydration. Remove wet and constrictive
clothing, cover with dry clothing, and protect against wind. In mild
cases & if the patient is conscious, warm drinks can be administered.
Do not heat the frozen area, because dry heat may cause further
injury. Do not attempt rewarming until the risk of refreezing is
eliminated.
• Refreezing will cause even more severe damage and is an important
concern. Provide analgesia, because the rewarming process is very
painful. Immobilize and elevate frozen extremities, and handle gently.
Do not ambulate on edematous and blistered feet. Home remedies
such as rubbing the affected area or rubbing snow on frostbitten
tissue increase tissue damage.
• Locally applied creams should not be used in the field. 95
TREATMENT – ED MANAGEMENT
• Rapid rewarming is the first definitive step of frostbite
therapy and should be initiated as soon as possible.
• Place the injured extremity in gently circulating water heated
to a temperature of 37°C to 39°C (98.6°F to 102.2°F), for
approximately 20 to 30 minutes, until the distal extremity is
pliable and erythematous. Frostbitten faces can be thawed
using moistened compresses soaked in warm water.
• Some patients may tolerate immersion of the ears in a bowl or
pool of warmed water. Anticipate severe pain during rewarming
and treat with parenteral opiates.

96
TREATMENT – ED MANAGEMENT
• Local care is directed toward tissue preservation and infection prevention.
Management of clear blisters and the use of prophylactic antibiotics are
somewhat controversial. The blister fluid is rich in destructive
thromboxane and prostaglandins. Although removal theoretically limits
damage from these chemicals and enables access to the underlying tissue
for topical therapy, not all experts agree that removal is indicated.
• Hemorrhagic blisters should not be debrided, because this often results in
tissue desiccation and worse outcome.
There is some controversy as to whether aspiration is helpful. Both blister
types should be treated with topical aloe vera cream every 6 hours, which
helps to combat the arachidonic acid cascade.
• Affected digits should be separated with cotton and wrapped with sterile,
dry gauze. Other affected areas should be dressed in bulky, loose-fitting
dry gauze dressings to allow room for the expected subsequent edema.
Elevation of the involved extremities helps decrease edema and pain.
97
TREATMENT – ED MANAGEMENT
• Tetanus immunization status should be assessed and appropriate
vaccination administered if needed, because frostbite is a
tetanusprone wound.
• Because microvascular thrombosis plays a role in tissue injury,
thrombolysis has been advocated by some for use in cases at risk for
proximal or multiple digit amputations and, when given after rapid
rewarming, appears to reduce digit amputations.
• The evidence in support of IV or intra-arterial tissue plasminogen
activator is limited to retrospective studies, and bleeding risks must
be weighed against potential benefit.

98
TREATMENT – ED MANAGEMENT
• The role of prophylactic antibiotics is unclear. The edema that is
present on the first several days after injury does appear to
predispose to infection. Staphylococcus aureus, Staphylococcus
epidermidis, and β-hemolytic streptococci account for nearly half of
infections, but anaerobes, Pseudomonas, and Enterococcus are
important pathogens as well.
• Therapy with penicillin G, 500,000 units IV every 6 hours for 48 to
72 hours, is recommended in several successful protocols and seems
to be beneficial. However, infection prophylaxis using topical
bacitracin may be as good as or better than IV penicillin.
• The use of silver sulfadiazine cream also has been advocated by some,
but it has not been shown to be consistently beneficial. One
disadvantage of using topical antibiotics is that they complicate the
concurrent use of aloe vera cream.
99
TREATMENT – ED MANAGEMENT
• Several agents besides aloe vera cream have been recommended to
battle the arachidonic acid cascade and thereby limit tissue damage.
• The most commonly advocated oral medication is ibuprofen, 12 mg/
kg/d PO in divided doses. Animal studies suggest possible future roles
for oral methimazole (a thromboxane synthetase inhibitor) and
topical 1% methylprednisolone acetate (a phospholipase A2 inhibitor)
in preventing the formation of arachidonic acid.
• Another controversial area is the use of sympathetic blockade with
either intra-arterial reserpine or surgical sympathectomy to relieve
vasospasm and edema.There is no role for early sympathectomy.
• Prolonged sympathetic blockade using a long-acting anesthetic drug
(bupivacaine) may improve blood flow to the hand, relieve pain, and
speed recovery.
100
TREATMENT – ED MANAGEMENT
• Continuous epidural anesthesia may relieve peripheral vasospasm and
perhaps prevent retrograde arterial and venous thrombosis. Heparin
& hyperbaric oxygen therapy appear to be of little value, although
case reports of improvement in isolated cases have been published.
• IV low-molecular-weight dextran has theoretical benefits, but dose
and effectiveness have not been validated.
• Early surgical intervention is not indicated in the management of
frostbite. Premature surgery has been an important contributor to
unnecessary tissue loss and poor results in the past. This is due
primarily to the inability to assess the depth of frostbite at early
stages & the fact that the blackened, mummified carapace protects
the underlying regenerating tissue. Limited early escharotomy may be
indicated if the eschar is preventing adequate range of motion or
circulation. Fasciotomy is rarely if ever, indicated. 101
SEQUELAE - FROSTBITE
• Up to 65% of persons with frostbite injuries experience
sequelae from their injuries. Sequelae may be seen in patients
with mild injuries but are generally more intense with more
severe frostbite.
• The most typical sequelae are hypersensitivity to cold, pain, and
ongoing numbness. Neuropathies have also been described.
• The clinical & functional limitations associated with late sequelae
are dependent on the type and severity of the frostbite injury
and the related anatomic deformities and amputations.

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103
FROSTBITE - DISPOSITION AND
FOLLOW-UP
• Because it is difficult to determine the extent of frostbite on
initial examination, it is best to be conservative when
contemplating admission. Consider social and medical issues.
• The homeless or elderly, especially when unable to care for
themselves adequately, should never be discharged into
subfreezing temperatures.
• If the frostbite is extensive and the hospital and staff are not
equipped to treat injury of that degree of severity, consider
transfer to a tertiary hospital after initial rewarming and
treatment.
104
FROSTBITE - DISPOSITION AND
FOLLOW-UP
• Patients with only superficial local frostbite may be discharged home
if social circumstances allow. Patients with deeper frostbite injuries
should be hospitalized.
• At discharge from the ED, patients must be provided with sufficient
guidelines for self-care and clear instructions for close short-term
and long-term follow-up, preferably with local burn center or plastic
surgery providers. They must also be instructed to contact their
doctor at an early stage if problems or concerns arise.
• Patients who are discharged from the ED should be treated with
topical aloe vera cream and oral ibuprofen and encouraged not to
smoke or drink alcohol.
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THANK YOU

107