29.1

Environmental Injuries

Chapter 29

Environmental Injuries

Introduction

The successful prevention and control of cold, heat, and altitude

injuries depend on vigorous command interest, the provision

of adequate clothing, and a number of individual and group

measures. The medical officer must ensure that he or she

understands how military duties impact the occurrence and

severity of environmental conditions and advise the commander

on preventive measures.

Cold Injuries

Trench foot and frostbite together have accounted for over 1 million

US casualties in WW I, WW II, and the Korean War. Influencing

factors include previous cold injury; fatigue; concomitant injury

resulting in significant blood loss or shock; geographic origin;

nutrition; tobacco use; activity; drugs and medication; alcohol;

duration and exposure; dehydration; environment (temperature,

humidity, precipitation, and wind); and clothing.

Non–Freezing Cold Injury

 Chilblain.

ο Results from intermittent exposure to temperatures above

freezing, usually accompanied by high humidity and

moisture; 1 to 6 hours of exposure.

ο Swelling, tingling pain, and numbness with pink-to-red

flushing of skin (especially the fingers).

ο Extremities will be pruritic as they warm up.

ο Symptoms usually subside overnight; some superficial

scaling may occur.

ο Mild joint stiffness may occur acutely but subsides in a

few hours.

ο No permanent damage occurs.
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Emergency War Surgery

 Pernio.

ο Continuum of events from chilblain.

ο Exposure for > 12 hours to cold and/or wet conditions.

ο Tight-fitting footwear can shorten exposure time and

increase severity of injury.

ο Swelling is more severe; pain is more persistent than with

chilblain.

ο Thin, partial-skin thickness, and necrotic patches (from

dorsum of the hands or feet).

ο Plaques may slough without scarring but may be

particularly painful for months or years.

 Trench foot.

ο Epidemiology/clinical appearance.

♦ Occurs from prolonged exposure to cold, wet conditions

or prolonged immersion of feet at temperatures as high

as 17°C for > 12 hours. Shorter duration at or near 0°C

results in the same injury.

♦ Occurs in nonfreezing temperatures 0°C–12°C.

♦ Can occur at higher temperatures from prolonged water

immersion.

♦ Blunt trauma of marching can produce more serious injury.

♦ First symptom often is the feet becoming cold, mildly

painful, and numb.

♦ Tight footwear increases risk of trench foot.

♦ Common symptoms are “cold and numb” or “walking

on wood.”

♦ Foot may appear swollen, with the skin mildly blue,

red, or black.

♦ Limb is hot and often hyperhidrotic.

♦ On rewarming, pain is excruciating and does not

respond to pain medication, including morphine.

♦ As time progresses, liquefaction necrosis occurs distally,

but more proximal tissue may also be compromised.

♦ No sharp line of demarcation of dead from viable tissue.

♦ Nerve, muscle, and endothelial cells are most susceptible to this long-term cooling.

♦ Microvascular vasospasm with tissue ischemia is the

apparent etiology of trench foot.
29.3

Environmental Injuries

♦ Postinjury sequelae include pain, numbness, loss of

proprioception, and cold feet. Hyperhidrosis with

subsequent paronychial fungal infections are common.

♦ Life-long, life-changing injury.

ο Treatment.

♦ Prevent further cold exposure.

♦ Do not massage.

♦ Dry extremity, warm torso, and allow slow passive

rewarming of feet. Never immerse feet in warm or hot

water.

♦ Elevate feet.

♦ Rehydrate.

♦ If vesicles develop do not debride.

♦ Pain medication. The only effective approach is

amitriptyline 50–150 mg at bedtime. Other analgesics

are either completely ineffective, or (as with narcotics)

do not actually relieve pain.

♦ Blisters should be left intact; ruptured blisters require

meticulous antisepsis after unroofing.

♦ Systemic antibiotics and tetanus prophylaxis are

indicated when there are nonviable tissues, as with any

other contaminated wound, or when there is evidence

of infection.

♦ Debridement of necrotic tissue may be required in

trench foot.

♦ Macerated or damaged skin requires topical antibacterial precautions.

♦ Avoid trauma.

♦ Early mobilization is vital to prevent long-term

immobility.

♦ Recovery is protracted and may require evacuation

because trench foot may lead to weeks-to-months of

pain and disability.

♦ Long-term sequelae are very common and include

sensitivity to the cold (secondary Raynaud’s phenomenon), chronic pain, neurological impairment, and

hyperhidrosis.
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Emergency War Surgery

 Frostnip.

ο Exposed skin appears red or minimally swollen.

ο Tissue is not actually damaged.

ο Not true frostbite; freezing is limited to skin surface only.

ο Signals imminent likelihood of frostbite developing.

ο Resolves quickly with warming.

 Frostbite.

ο Results from crystallization of water in the skin and

adjacent tissues exposed to temperatures below freezing.

ο Depth and severity of injury is a function of temperature

and duration—the lower the temperature, the shorter the

time required to produce injury.

ο At low temperatures in the presence of wind, exposed skin

can freeze within a few seconds—starts distally and

progresses up the finger or toe.

ο Freeze-front (line where the ice is formed in the tissues) is

where liquefaction and necrosis occur. Tissues immediately

proximal to this line may also die, but therapeutic

modalities are directed at improving their survival.

ο Clinical appearance.

♦ Skin initially becomes numb and feels stiff or woody.

♦ Mottled, bluish, yellowish, “waxy,” or “frozen.”

♦ Depth of involvement may be difficult to determine

until demarcation occurs, which may take an extended

period.

ο Frostbite grading.

♦ Classification into degrees is primarily a retrospective

evaluation and has little treatment value.

♦ A more clinically useful grading typically divides

injuries into superficial or deep.

♦ Superficial frostbite.

◊ Involves only the skin with swelling, mild pain, and

minor joint stiffness.

◊ No blisters form.

◊ Nonmedical personnel can manage simply by

rewarming.

♦ Deep frostbite.

◊ Involves deeper tissues to include bone.

◊ White-hard, anesthetic, blanched, and inflexible.
29.5

Environmental Injuries

◊ Skin will not move over joints.

◊ On rewarming, there is great pain and a blue-grayto-burgundy color change.

◊ Blisters form and are clear, fluid-filled, or hemorrhagic (the latter indicates a more severe, deeper

injury). They should be left in place; will slough in

7–10 days without consequence.

◊ Failure to form vesicles in an obviously deep-frozen

extremity is a grave sign.

◊ Postinjury sequelae include Raynaud’s phenomenon;

pain; paraesthesias; hyperhidrosis; loss of proprioception; cold, discolored feet; and gait modification.

 Field treatment (first aid).

ο Superficial (blanched cheeks, nose, ears, fingertips).

♦ Warm with palm of hand or warm, wet cloth; warm

fingers in armpits.

♦ Emollients may help prevent skin from drying or

cracking.

♦ Do not massage, rub with snow, or warm part by an

open fire or high-heat source.

♦ Meticulous skin care is required.

ο Deep frostbite.

♦ Prevent further cooling of body part as well as the

patient as a whole.

♦ Apply dry, sterile bandage and elevate involved

extremity.

♦ Protect from refreezing during evacuation.

♦ Evacuate promptly to definitive medical care.

Avoid thawing and refreezing; this leads to the greatest

damage to tissue and the poorest outcome.

 MTF treatment.

ο The outcome of a frozen extremity is not directly related

to length of time frozen, but more importantly to the

method of rewarming and any subsequent refreezing.

♦ If the soldier will again be at risk for refreezing, no

attempt at rewarming should be initiated; the soldier
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Emergency War Surgery

should ambulate on the frozen extremities until he

reaches definitive care.

♦ For transport, the patient’s extremity should be splinted,

and padded with dry dressings and protected from heat

sources that would slowly rewarm the extremity.

ο Rapid rewarming (without the possibility of refreezing)

is the treatment of choice.

♦ Immerse in gently circulating water (whirlpool bath) at

40°C (104°F) for at least 30 minutes longer than could

be needed to defrost all affected tissues. If deep freezing

of the leg or arm has taken place, thorough surgical

fasciotomy is mandatory prior to rewarming, to prevent

lethal increase in deep tissue pressures as ice melts.

Extremities are rewarmed until pliable and erythematous

at the most distal areas.

♦ Twice daily whirlpool baths at 40°C with topical

antibacterial added to the water, together with oral

ethanol. The alcohol reduces the need for analgesia and

may improve outcome. Other drug regimens remain

unproven.

♦ After rewarming, edema will appear within a few hours

and vesicles form within the next 6–24 hours.

♦ Intensive mobilization is essential to avoid long-term

immobility.

ο Vesicles.

♦ Frostbite vesicles are typically left intact.

♦ Debridement is not recommended. Early surgery is only

indicated in severely infected cases. Normally surgery

should be delayed for at least 6 months.

ο General considerations.

♦ Ibuprofen or ketorolac should be given as systemic

thromboxane/prostaglandin inhibitors.

♦ Systemic antibiotics and tetanus prophylaxis are

indicated when there are dead tissues, as with any other

contaminated wound, or when there is evidence of

infection.

♦ Dry, loose dressings may be applied.

♦ Cigarette smoking and/or nicotine use is contraindicated

during treatment due to its effect on the microvasculature.
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Environmental Injuries

♦ Daily hydrotherapy is recommended. Pain control with

NSAIDs and narcotics will be needed.

♦ Sequelae include contractures, cold sensitivity, chronic

ulceration, arthritis, and hyperhidrosis.

♦ Frostbite cases will require prolonged hospital care (9 d

on average); therefore, all but those with the most trivial

injuries should be evacuated to more definitive care as

soon as possible.

♦ Early surgery is indicated only in the most severe freezethaw-refreeze cases, where massive tissue destruction

has taken place, and in some more severely infected

cases. Normally, surgery should be delayed for at least

6 months (“Freeze in January, operate in July”).

Due to the inability to reliably predict the outcome in

the postthaw period, there is no role for debridement/

amputation of necrotic or potentially necrotic tissue in

the initial treatment of frostbite.

Hypothermia

Hypothermia is classically defined as whole-body cooling below

35°C. Degree of hypothermia is further defined according to

the body’s core temperature and the clinical effects seen in a

given temperature range.

 Causative factors and prevention.

ο Water immersion.

ο Rain and wind.

ο Prolonged exposure to severe weather without adequate

clothing. The insulation effect of clothing is markedly

decreased with wetness, which increases the conductive

heat loss.

ο Stay dry and avoid windy exposure.

ο Shivering can provide five times the normal metabolic heat

production. Exhaustion and glycogen depletion decrease

the time of shivering. Compromise of shivering due to

inadequate food intake (skipping meals), exhaustion,

heavy exercise, alcohol, and drugs increases threat of

hypothermia.
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Emergency War Surgery

 Mild hypothermia > 33°C (> 91°F).

ο Shivering, hyperreflexia.

ο Amnesia, dysarthria, poor judgment, ataxia, apathy.

ο Cold diuresis.

 Moderate hypothermia 28°C–33°C (82°F–91°F).

ο Standard hospital thermometers, mercury as well as

digital, cannot measure temperatures below 34°C (93°F).

ο Stupor, loss of shivering.

ο Onset of atrial fibrillation and other arrhythmias.

ο Progressive decrease in level of consciousness, respiration,

and pupillary reaction, eventual pupil dilation.

 Severe hypothermia < 28°C (< 82°F).

ο Increased incidence of ventricular fibrillation, which often

occurs spontaneously.

ο Loss of motion and reflexes, areflexic at approximately

23°C (72°F).

ο Marked hypotension/bradycardia.

 Profound hypothermia < 20oC (< 68°F).

ο Asystole.

ο Lowest known adult survival from accidental hypothermia

is 13.7oC (56°F).

Treatment

 Prehospital (field) treatment.

ο Awake patients.

♦ Remove wet clothing; dry and insulate the patient.

♦ Give oral sugar solutions to hydrate.

♦ Walk out or transport to MTF. (This should be attempted

if it is the only alternative because it is likely to worsen

the condition.)

♦ Although walking may deepen hypothermia due to the

return of peripheral colder blood to the core, adequate

prehydration decreases the postexposure cooling.

ο Comatose patients.

♦ Patient should remain horizontal and be handled gently

to avoid inducing arrhythmias; do not massage.

♦ IV fluids, warmed to 40°C–42°C, if possible.

♦ Do not use lactated Ringer’s solution because the cold

liver cannot metabolize lactate; warm (40°C–42°C
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Environmental Injuries

[104°F–107.5°F]), D5NS is the fluid of choice.

♦ Remove wet clothes, dry, insulate, and add an outer

vapor barrier. Wrap patient in multiple layers of

insulation.

♦ Limit active rewarming principally to the body’s center/

core only.

◊ Heated (40°C–45°C), humidified air/O2 is the method

of choice.

◊ Norwegian personal heater pack (charcoal heater),

with warming tube placed into insulation wrap.

◊ Forced air (Bair Hugger) with rigid chest frame.

◊ Hot water bottles in groin/axilla.

♦ Intubation and heated ventilation may be performed.

♦ If apneic and asystolic, consider CPR, because the brain

may survive longer.

Remember: The patient is not dead until he is warm and

dead. Continue resuscitation, if possible, until patient

has been rewarmed.

 Medical treatment.

ο Ventilate; apply CPR if asystolic or in ventricular

fibrillation.

ο As the body cools, the peripheral vasculature constricts,

causing pooling of cold acidotic blood.

ο Rewarming the periphery of the body rather than the core

causes an inrush of this cold acidotic blood into the core,

further dropping the core temperature (afterdrop), and

worsening cardiac instability.

ο Core rewarming—peritoneal dialysis, thoracic lavage,

heated and humidified oxygen, external warm blankets,

and warm-water torso immersion.

ο For ventricular fibrillation.

♦ Bretylium tosylate, 10 mg/kg. Bretylium is the only known

effective antidefibrillation drug for hypothermia. It

remains functional in a cold heart. Other medications

have not proven effective.

♦ Warmed IV (lactate and potassium-free).
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Emergency War Surgery

♦ Monitor core temperature via esophageal (preferred) or

rectal probes.

♦ Careful correction of acid/base balance.

♦ Rewarm core to 32°C (90°F) and attempt cardioversion

(360 J). Continue rewarming and repeat. Defibrillate

after every 1°C rise in temperature.

♦ Monitor potassium, glucose, temperature, and pH.

♦ Major causes of failure to resuscitate include elevating

central venous pressure too fast or too early; attempting

defibrillation when core temperature is below 32°C, or

continuing to rewarm past 33°C when potassium levels

are high and pH is low. If serum potassium levels are

high, consider the use of intravenous glucose and

insulin.

♦ Avoid other antiarrhythmics and other medications.

♦ Patients with core temperature (rectal) above 30°C can

generally be rewarmed externally in a variety of

methods including warm blankets, warm-water torso

immersion. Patients below 30°C rectal should be

considered more fragile and will often require internal

methods of rewarming (ie, warm gastric, colonic, and/

or bladder lavage; warm peritoneal lavage dialysis;

warm thoracic lavage; and arteriovenous (blood

rewarming). Lavage fluids should be warmed to 40°C–

42°C (104°F–107.5°F).

♦ Core temperature will continue to drop after the patient

is removed from the cold exposure. Continued

temperature drop can have grave prognostic implication

and increases the likelihood of fibrillation. Postrewarming collapse of an apparently functional heart

often leads to a nonresuscitable heart and death.

 Cardiopulmonary resuscitation.

ο If cardiac monitor shows any electrical complexes, check

carefully for apical and carotid pulses before initiating

CPR. If any pulse—however thready—is present, do NOT

initiate CPR.
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Environmental Injuries

Trauma patients should be considered to have hypothermia more profound than the core temperature indicates

and be warmed more aggressively.

 Treatment of mild stable hypothermia.

ο Insulation.

ο Heat lamps.

ο Warmed IV fluids.

ο Warmed forced air (Bair Hugger). Hair dryers have been

jury-rigged for this purpose.

ο Consider arteriovenous anastomoses (AVA) warming.

♦ Immerse hand, forearms, feet, calves in water heated to

44°C–45°C (111°F–113°F).

♦ Opens AVAs in the digits causing increased flow of

warmed venous blood to the heart and decreases

afterdrop.

 Treatment of severe hypothermia with hemodynamic

instability.

ο Cardiopulmonary bypass with rewarming, when available,

is the ideal technique in this circumstance because it

provides core rewarming while ensuring circulatory stability.

Heat Injury

In the military setting, heat illness occurs in otherwise healthy

individuals, and ranges from mild (heat cramps) to life

threatening (heatstroke). Individuals typically present with

exertional heat illness and are hot and sweaty, not hot and dry

as seen in classic heatstroke.

Lack of sweating is not a criterion for heatstroke. Some

military casualties of heatstroke have profuse sweating;

especially with rapid onset of heatstroke.

Minor heat illnesses include heat cramps and heat exhaustion.

Major heat injuries include exertional heat injury (EHI),

exertional rhabdomyolysis, and heat stroke. The diagnostic

categories of heat exhaustion, EHI, and heat stroke have

overlapping features and should be thought of as different
29.12

Emergency War Surgery

regions on the continuum rather than discrete disorders, each

with its own distinct pathogenesis.

 Heat injury prevention.

ο Easier to prevent than treat.

ο Occurs most commonly in unacclimatized individuals.

♦ Acclimatization to heat requires 7–10 days.

♦ Predeployment training in artificially warm environments does aid heat acclimatization.

♦ One hour of progressively more difficult exercise sufficient

to induce moderate sweating each day will maximize

acclimatization. (Regular strenuous exercise sufficient to

stimulate sweating and increase body temperature will

result in a significant degree of heat acclimation.) Aerobic

fitness provides cardiovascular reserve to maintain the

extra cardiac output required to sustain thermoregulation,

muscular work, and vital organs in the face of heat stress.

ο Utilize published work–rest cycle guides (eg, FM 21-10/

MCRP 4-11.1D) or work–rest cycles tailored to the

individual’s physical capacity by direct medical oversight.

ο Water restriction/discipline leads to increased heat injury

and is contraindicated.

♦ Acclimatization does not reduce, and may actually

increase, water requirements.

♦ Service members will on average not feel thirsty until

1.5 L (1%–2%) dehydrated.

♦ Fluid intake should be monitored to ensure urine

appears dilute. Additionally, soldiers should be

monitored for body weight changes and orthostatic

blood pressure changes due to hydration.

♦ The GI tract can absorb only 1–1.5 L/h.

♦ Daily rehydration should not exceed 12 L/d orally. Too

much hydration can also be dangerous and lead to

water intoxication!

♦ Leaders must reinforce hydration by planning for all

aspects of adequate hydration—elimination as well as

consumption. (Soldiers may not drink at night to avoid

awakening and having to dress to urinate, or soldiers

may not drink prior to a convoy because no rest stops

are planned.)
29.13

Environmental Injuries

ο MOPP gear will increase fluid losses and the incidence of

heat injuries.

ο In the first few days of acclimatization, sweat–salt

conservation will not be fully developed. Salt depletion is

a risk if soldiers are exposed during this time to sufficient

heat or work stress to induce high sweating rates (> several

liters per day), particularly if ration consumption is

reduced. Salt depletion can be avoided by providing a salt

supplement in the form of salted water (0.05%–0.1%).

Acclimation should eventually eliminate the need for salt

supplementation

ο Salt supplements are not routinely required and are only

recommended in rare instances where adequate rations

are not consumed.

ο Coincidental illnesses increase heat casualty risk through

fever and dehydration. Fever reduces thermoregulatory

capacity leading to increased risk, even after clinical

evidence of illness has disappeared. Requires increased

command supervision and moderate work schedule.

ο Sunburn and other skin diseases of hot environments reduce

the ability of the skin to thermoregulate. Sunburn must be

prevented by adequate clothing, shade, and sunscreen. Skin

diseases are best prevented by adequate hygiene.

ο Medications that effect thermoregulatory adaptations and

increase risk of heat injury include anticholinergics,

antihistamines, diuretics, tricyclic antidepressants, major

tranquilizers, stimulants, and beta blockers.

Despite preventive measures, service members may suffer from

heat illness. One case of heat illness is a warning sign that many

others are imminent. The most life-threatening condition is

heatstroke. Severity of heat illness depends on the maximum

core temperature and duration.

 Heatstroke.

Heat stroke is distinguished from heat exhaustion by the

presence of clinically significant tissue injury and/or altered

mental status. Degree of injury appears to relate to both the

degree of temperature elevation and duration of exposure.
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Emergency War Surgery

ο Clinical presentation.

♦ Heat stroke is a true emergency. Involves five organ

systems: brain, hemostatic, liver, kidneys, and muscles.

♦ Encephalopathy ranges from syncope and confusion to

seizures or coma with decerebrate rigidity. Profound

neuropsychiatric impairments present early and universally in casualties of advanced exertional heat stroke.

♦ Coagulopathy: thermal damage to endothelium,

rhabdomyolysis, and direct thermal platelet activation

causes intravascular microthrombi. Fibrinolysis is

secondarily activated. Hepatic dysfunction and thermal

injury to megakaryocytes slow the repletion of clotting

factors. Hepatic injury is common. Transaminase

enzyme elevation (values 100 or more times the upper

normal limit), clotting factor deficiencies, and jaundice

(within 24–36 h of onset). Transaminase levels may be

transient and reversible, but if they persist 48 hours, it

is indicative of more severe injury. Hypoglycemia is a

frequent complication of exertional heat stroke.

♦ Renal failure: myoglobinuria from rhabdomyolysis in

exertional heat stroke, acute tubular necrosis due to

hypoperfusion, glomerulopathy due to disseminated

intravascular coagulation (DIC), direct thermal injury,

and hyperuricemia.

♦ Muscles are often rigid and contracted: Rhabdomyolysis

is a frequent acute complication of exertional heat stroke.

Acute muscular necrosis releases large quantities of

potassium, myoglobin, phosphate, uric acid, and creatine,

and sequesters calcium in exposed contractile proteins.

If heat stroke is suspected and temperature is elevated,

cooling should not be delayed to accomplish a diagnostic

evaluation. Cooling and evaluation should proceed

simultaneously.

The patient with heat stroke requires immediate

evacuation to medical facilities with intensive care

capabilities. Active cooling should be started immediately

and continued during evacuation.
29.15

Environmental Injuries

♦ Prodromal symptoms include headache, dizziness

(lightheadedness), restlessness, weakness, ataxia,

confusion, disorientation, drowsiness, irrational or

aggressive behavior, syncope, seizures, or coma.

♦ Collapse is a universal feature of heat stroke.

♦ An individual with a core temperature of ≥ 40oC (104°F)

and CNS dysfunction that results in delirium, convulsions, or coma has heat stroke.

ο Casualties who are unconscious and have a core

temperature of ≥ 39°C (102.2°F) have heatstroke.

♦ Core temperature is often lower on arrival at a treatment

area.

♦ Seizures.

◊ Occur frequently (> 50% of cases) with heatstroke.

◊ Hinder cooling efforts.

◊ Treat with diazepam 5–10 mg.

ο Treatment.

♦ Rapid cooling can reduce heat stroke mortality

anywhere from 50% down to 5%. Cooling by spraying

cool water over the body and vigorous fanning can be

effective though not as effective as ice water immersion.

Any effective means of cooling is acceptable.

♦ A variety of techniques have been used, and, while

evaporative cooling is less effective, the ice immersion

method may prevent safe cardiac monitoring or rapid

resuscitation.

♦ Cool water immersion (20°C) with skin massage is the

classic technique. It provides rapid cooling. Closely

monitor patient for, and prevent, shivering.

♦ Cooling with cool-water–soaked sheets or ice chips and

vigorous fanning is highly effective.

♦ Do not use alcohol in the cooling solution because

freezing of the skin can occur.

The goal of treatment is to effect a rapid lowering of the

core temperature to 38°C (101°F), without inducing

shivering.
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Emergency War Surgery

♦ Rectal temperature should be closely monitored during

cooling. Discontinue cooling efforts when core temperature reaches 38.3°C (101°F) to avoid hypothermia.

♦ Aspirin and acetaminophen should NOT be given to

casualties of heatstroke.

♦ Aggressive fluid resuscitation is not required. Fluid

requirements of 1 L in the first 30 minutes, with an

additional 2 L or more in the next 2 hours may be

sufficient. Because heat stroke patients are frequently

hypoglycemic, the initial fluid should include dextrose

(chilled IV fluid is of limited benefit).

◊ Base further hydration on fluid status/urinary

output (Foley required).

◊ Overhydration can lead to congestive heart failure,

cerebral edema, and pulmonary edema in the heatstressed lung.

♦ If shivering develops, treat with diazepam (5–10 mg IV)

or chlorpromazine (50 mg IV).

♦ Patients are frequently agitated, combative, or seizing.

Diazepam is effective for control and can be administered IV, endotracheally, or rectally, but should be used

with caution.

♦ Airway control is essential. Vomiting is common and

endotracheal intubation should be used in any patient

with a reduced level of consciousness, or otherwise

unable to protect the airway. Supplemental oxygen

should be provided when available.

♦ Hypotensive patients who do not respond to saline

should receive inotropic support. Careful titrated use of

dopamine or dobutamine is reasonable and has the

potential added advantage of improving renal perfusion.

♦ Pulmonary artery wedge pressure monitoring should

be used in patients with persistent hemodynamic

instability.

♦ Management of encephalopathy is supportive in nature

and is directed at minimizing cerebral edema by

avoiding fluid overreplacement and by assuring

hemodynamic, thermal, and metabolic stability. IV

mannitol has been used to treat life-threatening cerebral
29.17

Environmental Injuries

edema, but is questionable unless renal function is

adequate and the patient is fully hydrated. The efficacy

of dexamethasone for treating heat-stroke–induced

cerebral edema is not known.

ο Complications.

♦ Rhabdomyolysis and secondary renal failure due to

myoglobinuria and hyperuricemia; hyperkalemia;

hypocalcemia; and compartment syndromes due to

muscle swelling.

◊ Elevated creatine phosphokinase (CPK) (in the

thousands).

◊ Administer IV fluid and possibly furosemide to

maintain urinary output > 50 cc/h. (Assurance of

adequate renal perfusion and urine flow will

moderate the nephrotoxic effects of myoglobin and

uric acid.)

◊ Hyperkalemia can be managed by K/Na ion

exchange resin (Kayexalate) given orally or rectally

as an enema. If available, dialysis may occasionally

be indicated.

◊ Hypocalcemia does not usually require treatment.

◊ Increasing tenderness or tension in a muscle

compartment may represent increasing intracompartmental pressures. Direct measurement of

intramuscular pressure or fasciotomy should be

considered. Pain and paresthesia from a compartment syndrome may not be present until after

permanent damage has occurred.

♦ Alkalinize urine with sodium bicarbonate IV (2 amps

NaHCO3/L D5W). Management of acute renal failure

requires exquisite attention to fluid and electrolyte

balance. Uremic metabolic acidosis and hyperkalemia

require dialysis for control.

♦ Coagulopathy due to hepatic injury.

◊ Hepatic injury is common, resulting in transaminase

enzyme elevation, clotting factor deficiencies, and

jaundice. Transaminase levels may be transient and

reversible, but if they persist 48 hours, then it is

indicative of more severe injury.
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Emergency War Surgery

◊ Worst prothrombin time occurs at 48–72 hours

postinjury.

◊ Thrombocytopenia and disseminated intravascular

coagulation (DIC) peak at 18–36 hours postinjury.

◊ Beware of the coagulopathy timeframe when

planning evacuation.

◊ Subclinical coagulopathy does not require active

management. Clinically significant bleeding is an

ominous sign. Treatment is directed at reducing the

rate of coagulation and replacement of depleted

clotting factors. Intravascular coagulation can be

slowed by cautious heparin infusion (5–7 U/kg/h),

followed in 2–3 hours by FFP and platelets. Successful

management leads to a decline in indices of

fibrinolysis (eg, fibrin split products). Heparin is

tapered gradually over 2–3 days as directed by

laboratory evidence of control.

◊ Monitor for hypo- or hyperglycemia.

♦ Prognosis is worse in patients with more severe degrees

of encephalopathy. Permanent neurologic sequelae can

develop after heat stroke, including cerebellar ataxia,

paresis, seizure disorder, and cognitive dysfunction.

♦ Neurologic deterioration after initial recovery may

represent intracranial hemorrhage related to diffuse

intravascular coagulation or hematoma related to

trauma unrecognized at the time of initial presentation.

♦ Other complications include gastrointestinal bleeding,

jaundice, aspiration pneumonia, noncardiogenic

pulmonary edema, and myocardial infarction. Immune

incompetence and infection are late complications,

particularly in patients with severe renal failure.

♦ Hyperkalemia is the most life-threatening early clinical

problem. Measurement of serum potassium is an early

priority.

 Heat cramps.

ο Clinical presentation.

♦ Brief, intermittent, recurring, and often excruciating

tonic muscle contractions that last 2–3 minutes.

Preceded by palpable or visible fasciculations.
29.19

Environmental Injuries

♦ Typically involve muscles of the abdomen, legs, and

arms (voluntary muscles of the trunk and extremities).

Smooth muscle, cardiac muscle, the diaphragm, and

bulbar muscles are not involved.

♦ Occur often with heat exhaustion. (Despite the salt

depletion associated with heat cramps, frank signs and

symptoms of heat exhaustion are unusual.)

♦ There are no systemic manifestations except those

attributable to pain.

♦ Occur in healthy individuals who exercise for prolonged

periods in warm environments.

♦ Occur in salt-depleted patients, generally during a

period of recovery after a period of work in the heat.

♦ Differential diagnosis: tetany due to alkalosis (hyperventilation, severe gastroenteritis, cholera), hypocalcemia,

strychnine poisoning, black widow spider envenomation,

and abdominal colic.

ο Treatment.

♦ Mild cases can be treated with oral 0.1%–0.2% salt

solutions. Salt tablets should not used as an oral salt

source.

♦ Most “sports drinks” (diluted 1:1 with water) effective

for mild cases.

♦ IV NS provides rapid relief in more severe cases

♦ Patients with heat cramps usually have substantial salt

deficits (15–30 g over 2–3 days, usual dietary intake).

These individuals should be allowed 2–3 days to

replenish salt and water deficits before returning to

work in the heat.

 Heat exhaustion.

ο Clinical presentation.

♦ Thirst, headache, dyspnea, lightheadedness (orthostatic

dizziness), profound physical fatigue, anorexia,

confusion, anxiety, agitation, mood change, chills,

piloerection, nausea, and vomiting. There is no

combination of presenting symptoms and signs that is

pathognomonic.

♦ Often accompanied by heat cramps.

♦ Oliguria, clinical dehydration, ataxia, tachycardia, and
29.20

Emergency War Surgery

tachypnea resulting in symptomatic hyperventilation

with acroparesthesia and carpopedal spasm.

♦ Syncope may occur.

♦ Core temperature is < 39°C (102.2°F), even at time of

collapse.

ο Treatment.

♦ Oral rehydration (if patient is not vomiting).

♦ Parenteral fluids produce more rapid recovery: no more

than 250 mL NS bolus without laboratory surveillance;

after 2.5 L of plain saline, add dextrose as a source of

energy (D2.51

/2NaCl); subsequent fluid replacement

should be D51/2NS or D51/4NS. Individuals with

significant salt depletion have coincident potassium

depletion, often amounting to 300–400 mEq of KCl. To

begin restoration of potassium deficit, inclusion of

potassium in parenteral fluids after volume resuscitation is appropriate if there is no evidence of renal

insufficiency or rhabdomyolysis.

♦ Does not require active cooling; however, because

symptoms are difficult to distinguish from heat stroke,

the safest course is to provide active cooling for all

casualties who are at risk for heat stroke.

♦ Removal from hot environment.

♦ Stop exercising, move out of the sun.

 Minor heat illnesses.

ο Miliaria rubra, miliaria profunda, and anhidrotic heat

exhaustion.

♦ Subacute (miliaria rubra) pruritic inflamed papulovesicular skin eruption that appears in actively sweating

skin exposed to high humidity. Becomes generalized

and prolonged (miliaria profunda); lesions are truncal,

noninflamed papular, with less evidence of vesiculation

than the lesions of miliaria rubra.

♦ Each miliarial papulovesicle represents an eccrine sweat

gland whose duct is occluded at the level of the

epidermal stratum granulosum by inspissated organic

debris.

♦ Eccrine secretions accumulate in the glandular portion

of the gland and infiltrate into the surrounding dermis.
29.21

Environmental Injuries

♦ Pruritus is increased with increased sweating.

♦ Miliarial skin cannot fully participate in thermoregulatory

sweating, therefore the risk of heat illness increases in

proportion to the amount of skin surface involved.

Sweat does not appear on the surface of affected skin.

♦ Sleeplessness due to pruritus and secondary infection

of occluded glands has systemic effects that further

degrade optimal thermoregulation.

♦ Miliaria is treated by cooling and drying affected skin,

avoiding conditions that induce sweating, controlling

infection, and relieving pruritus. Eccrine gland function

recovers with desquamation of the affected epidermis,

which takes 7–10 days.

♦ Miliaria profunda causes an uncommon but disabling

disorder: anhidrotic heat exhaustion (or tropical

anhidrotic asthenia). Miliaria profunda causes a marked

inhibition of thermoregulatory sweating and heat

intolerance similar to that of ectodermal dysplasia. That

individual is more at risk for heat exhaustion and at

high risk of heat stroke in conditions tolerated by others.

♦ Evacuation to a cooler environment until restoration of

normal eccrine gland function.

ο Heat-induced syncope.

♦ Due to a reduced effective blood volume. (Thermal

stress increases risk of classic neurally mediated

[vasovagal] syncope by aggravating peripheral pooling

of blood in dilated cutaneous vessels.)

♦ Symptoms range from light-headedness to loss of

consciousness.

♦ Typically someone standing in a hot environment.

♦ Greatest risk on first day of heat exposure, subsequent

risk decreases daily.

♦ Risk almost zero after 1 week of heat exposure; however,

syncope occurring during or after work in the heat, or

after more than 5 days of heat exposure, should be

considered evidence of heat exhaustion.

♦ Core temperature is not elevated or only very minimally so.

♦ Patient regains consciousness immediately after syncope.
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Emergency War Surgery

♦ Clinical evaluation and management should be

directed toward the syncopal episode, not potential heat

illness. Treatment is oral hydration and continued

acclimatization.

ο Heat edema.

♦ Seen early in heat exposure.

♦ Plasma volume expanding to compensate for the

increased need for thermoregulatory blood flow.

♦ In absence of other disease, condition is of no clinical

significance.

♦ Will resolve spontaneously.

♦ Diuretic therapy is not appropriate and may increase

risk of heat illness.

ο Sunburn.

♦ Reduces thermoregulatory capacity of skin.

♦ Systemic effect: hyperthermia.

♦ Preventable.

♦ Affected soldiers should be kept from significant heat

strain until the burn has healed.

ο Heat tetany.

♦ Rare; occurs in individuals acutely exposed to

overwhelming heat stress.

♦ Extremely severe heat stress induces hyperventilation.

♦ Manifestations include respiratory alkalosis, carpopedal

spasm, and syncope.

♦ Treatment: removal from heat source and control of

hyperventilation (rebreathing into paper bag to reverse

respiratory alkalosis).

♦ Dehydration and salt depletion are not prominent

features.

Altitude Illness

Exposure of troops to the hypobaric hypoxia of altitude results

in a decrement of performance, as well as the possible

development of altitude illness. Altitude illness spans a

spectrum from high-altitude bronchitis, to acute mountain

sickness (AMS), to death from high-altitude pulmonary edema

(HAPE) and high-altitude cerebral edema (HACE).
29.23

Environmental Injuries

 Altitude basics.

The occurrence of altitude illness is based on altitude and

rapidity of ascent. Contributory factors include level of exertion,

physiologic susceptibility, age, and coexisting medical

conditions.

ο Physiologic changes due to altitude begin to occur at just

over 1,500 m (4,900 ft).

ο These changes are the body’s attempt to acclimatize to

altitude.

ο Symptoms occurring below 2,250 m (7,400 ft) are rarely

due to altitude illness.

♦ Rapid ascent to high altitudes results in a high incidence

of altitude illness.

♦ Climbing Mt. Rainier brings one from sea level to 14,500

ft (4,400 m) in 36 hours and results in a 70% incidence

of altitude illness. An ascent to a similar height over

the course of 5 days would only result in a 5% incidence

of altitude illness.

♦ 10%–20% of soldiers who ascend rapidly (< 24 h) to

altitudes between 1,800 to 2,500 m (6,000–8,000 ft)

experience some mild symptoms

♦ Rapid ascent to elevations of 3,600 to 4,300 m (12,000–

14,000 ft) results in moderate symptoms in over 50% of

the soldiers, and 12%–18% may have severe symptoms.

♦ Rapid ascent to 5,300 m (17,500 ft) causes severe,

incapacitating symptoms in almost all individuals.

 Descent basics.

ο Almost everything improves with prompt descent.

ο For illness requiring descent, one should try to descend at

least 1,000 m (3,300 ft) if not more.

ο A Gamow bag (USA) (portable fabric hyperbaric chamber)

or Certec SA (Europe) can temporize a patient if evacuation

/descent is not possible.

ο Symptoms typically resolve quickly with descent, but may

linger for several days.

ο Victims of HACE and HAPE should not reascend until 72

hours after symptoms abate, and then must ascend much

slower than previously.
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Emergency War Surgery

ο Victims of HACE or HAPE should descend at the earliest

sign, before they become moribund and incapable of aiding

in their own descent.

ο There are no reliable predictors of susceptibility to AMS

except prior experience at altitude.

Incidence and severity of symptoms vary with initial

altitude, rate of ascent, level of exertion, and individual

susceptibility.

ο Vigorous physical activity during ascent or within 24 hours

after ascent will increase both the incidence and severity

of symptoms.

♦ If a soldier became ill previously at a given altitude he

or she will likely become ill at the same altitude unless

the ascent is slower to allow for better acclimatization.

♦ Physical fitness level has no effect on susceptibility to

altitude illness.

♦ Oral sildenafil (Viagra) 50 mg qd increases exercise

tolerance in healthy volunteers at altitude (5,200 m

[17,000 ft]), although it has not been approved for this

purpose. The role of this drug in the treatment and/or

prophylaxis of AMS and HAPE has not been established.

♦ If a rapid ascent to altitude must be made, use

prophylaxis against AMS.

 Acute mountain sickness.

ο AMS is the most common form of altitude illness.

ο Onset is shortly after arrival at high altitude. Onset occurs

3–24 hours after ascent. Symptoms reach peak severity in

24–72 hours and usually subside over the course of 3–7

days.

ο Further ascent without an acclimation period usually

exacerbates symptoms and can result in increased

incidence of HAPE and HACE. The majority of AMS cases

do not progress to more serious altitude illness without

continued ascent.

ο Symptoms.

♦ Headache: Symmetric, global in location, and throbbing

in character. Most intense during night and shortly after
29.25

Environmental Injuries

arising in the morning, attributed to increased

hypoxemia caused by altitude-induced sleep apnea.

♦ Anorexia.

♦ Nausea.

♦ Fatigue (weakness).

♦ General malaise.

♦ Decreased coordination.

♦ Dizziness or light-headedness.

♦ Oliguria.

♦ Emesis (vomiting).

♦ Lassitude.

♦ Insomnia: Sleep disturbances with periodic breathing

with recurrent apneic periods during sleep are usually

present, but are not necessarily a component of AMS.

ο Diagnosis.

♦ Occurrence of a headache and at least one other sign/

symptom in an individual who ascended from low

(1,524 m or < 5,000 ft) to high altitude, or high altitude

to higher altitude in the previous 24–48 hours.

♦ Differential diagnosis includes viral gastroenteritis,

hangover, exhaustion, dehydration, carbon monoxide

poisoning, and HACE.

♦ Presence of neurologic symptoms such as incoordination, ataxia, and excessive lethargy or cognitive

dysfunction is indicative of progression to HACE, which

requires immediate therapeutic intervention.

ο Prophylaxis for AMS.

♦ Gradual acclimation.

◊ Staged ascent: Soldiers ascend to intermediate

altitudes and remain there for 3 or more days before

ascending further.

◊ Graded ascent: Limits daily altitude gain to allow

partial acclimation. Sleep altitude is most important.

Have soldiers spend 2 nights at 2,743 m (9,000 ft) and

limit the sleeping altitude to no more than 305 m

(1,000 ft) per day above previous night’s sleep

altitude.

◊ Combination of both staged and graded ascent is the

safest and most effective prevention method.
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Emergency War Surgery

♦ Diet: High carbohydrate diet (< 70% of total energy

intake as carbohydrates) (stimulation of ventilation

through increased carbon dioxide produced from

metabolism of carbohydrates).

♦ Acetazolamide, 250 mg qid or 500 mg bid po, starting

48 hours before ascent, continuing for 48 hours after

ascent. Side effects include peripheral paresthesias,

fatigue, increased urination (polyuria), and altered taste

imparted to carbonated beverages. It prevents AMS in

50%–75% of soldiers and reduces symptoms in most

others. Short-term use when changing altitude

significantly (400 m). Contraindicated in sulfa allergy.

♦ Dexamethasone, 4 mg qid po is the prophylaxis of choice

in sulfa-allergic individuals. Dexamethasone does not

aid acclimatization and effects are gone when it is

stopped. Dexamethasone +/– acetazolamide is also

prophylaxis of choice for missions of a rapid, high (over

4,000 m [13,000 ft]), short-duration profile (raids,

rescues).

♦ Cyanosis: Oxygen 2–6 L/min. Do not delay descent.

ο Treatment.

♦ AMS alone does NOT mandate descent.

♦ Remain at the same elevation; do not ascend until

symptoms abate.

♦ Acetazolamide, 125 mg qid to 500 mg, tid, po—do not

use in patients with sulfa allergies. (If already receiving

a preventive dose of acetazolamide (1,000 mg/d) and

still symptomatic, 500 mg can be added with caution.

♦ Dexamethasone in doses of 2–4 mg q6h (has the same

potentially serious side effects as when used as a

prophylaxis). Symptoms may recur when medication

stopped.

♦ Oxygen by nasal cannula 2–6 L/min (severe headache).

♦ Do NOT advance sleeping altitude.

♦ Symptomatic treatment with ASA, acetaminophen,

prochlorperazine for nausea and vomiting 5–10 mg tid–

qid, po or IM, or 25 mg bid prn also stimulates

respiration; ibuprofen for headache.

♦ Minimize utilization of sleeping agents at altitude; they
29.27

Environmental Injuries

can worsen illness. Acetazolamide for sleep disorders,

250 mg qid or tid po. Temazepam for insomnia 30 mg

qhs po; triazolam for insomnia 0.125–0.25 mg qhs po.

Short-term use only. Possible short-term memory loss.

 High-altitude pharyngitis and bronchitis.

ο Common condition occurring after 2–3 weeks at altitude.

ο Common at altitudes over 5,486 m (18,000 ft).

ο Sore throat, chronic cough, and severe cough spasms

(severe enough to cause rib fractures).

ο Environmental, from breathing cold dry air.

ο Altitude-induced tachypnea aggravates the problem.

ο Cold-induced vasomotor rhinitis, especially at night,

stimulates mouth breathing and also aggravates problem.

ο Usually not caused by infection, although infection can

occur.

ο Patient will not have dyspnea at rest.

ο Symptomatic treatment with lozenges, mild cough

suppressant, and decongestant nasal sprays. Personnel can

use a mask or a porous, breathable silk balaclava as a

mouth covering to reduce respiratory heat and moisture

loss.

ο Maintain hydration.

 High-altitude peripheral edema.

ο Altitude-related edema of hands and face.

ο Hypoxia-induced retention of sodium and water.

ο Not considered related to AMS/HACE edema-spectrum

or HAPE.

ο Decreased urine output and weight gain of 2.7–5.4 kg

(6–12 lb) over several days; most evident upon awakening.

ο Diagnosis based on association of characteristic peripheral

edema with ascent to high altitude; recurs consistently with

repeat ascents; more common in females.

ο Differential diagnosis includes cardiogenic edema, allergic

reactions, and edema of the upper extremities caused by

pack straps or binding by tight clothes.

ο Prophylaxis includes salt restriction. The acetazolamide

regimen used to prevent AMS is often successful in

preventing peripheral edema.
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Emergency War Surgery

ο Treatment with diuretics (one 20–40 mg dose of furosemide,

or 250 mg of acetazolamide every 8 h for 3 doses) and salt

restriction.

 High-altitude retinal hemorrhage (HARH).

ο Bleeding from retinal vessels during altitude exposure.

One of the manifestations of hypoxia-induced retinopathy.

ο Caused by BP “surges” within the distended vessels.

ο Usually asymptomatic; normally does not adversely affect

military operations; however, can affect an individual

soldier’s vision.

ο Hemorrhages are self-limiting and resolve in 1–2 weeks

after descent.

 Thromboembolic events.

ο Increased possibility of thromboembolic event with ascent

to high altitude: thrombophlebitis, deep venous thrombosis,

pulmonary embolus, transient ischemic attacks (TIAs), and

stroke.

ο Probably result from hypoxia-induced polycythemia and

clotting abnormalities but also may result from environmental and mission factors such as dehydration, cold, and

venous stasis caused by prolonged periods of inactivity

during inclement weather or by constriction of tight-fitting

clothing and equipment.

ο Unusual below 4,267 m (14,000 ft). At very high and

extreme altitudes (> 4,200 m [13,700 ft]) these events are

not uncommon, and thrombophlebitis appears to be

relatively common.

ο Clinical manifestations are similar to manifestations of

thromboembolic events at low altitude, except for their

occurrence in young and otherwise healthy personnel.

ο Prevention relies on reducing the risk factors by maintaining adequate hydration and warmth and by avoiding

conditions that might cause venous stasis.

ο Evacuation to lower altitude is required. Treatment follows

standard treatment guidelines, including appropriate anticoagulation. In the field setting, fractionated heparin (one dose

of 250 IU/d) can be used prior to and during evacuation.

 Subacute mountain sickness.
29.29

Environmental Injuries

ο Prolonged deployment (weeks to months) to elevations

above 3,658 m (12,000 ft).

ο Common manifestations include sleep disturbances,

anorexia, weight loss, fatigue, daytime somnolence, and

subnormal mentation.

ο Caused by failure to acclimatize adequately.

ο Some relief of symptoms obtained from low-flow oxygen

and from acetazolamide.

ο Evacuate to lower altitude as soon as practical.

ο Some degree of immune suppression and poor wound

healing occurs in personnel at very high and extreme

altitudes. Injuries resulting from burns, ballistics, and

physical trauma should be considered more clinically

significant at high altitude.

 High-altitude pulmonary edema.

ο Potentially fatal, noncardiogenic pulmonary edema.

ο Occurs in < 10% of personnel ascending above 3,700 m

(12,000 ft).

ο Onset 2–4 days after rapid ascent to altitudes greater than

2,438 m (8,000 ft).

ο Repeated ascents and descents above 3,700 m (12,000 ft)

increase susceptibility.

ο Risk factors.

♦ Moderate to severe exertion.

♦ Cold exposure.

♦ Anxiety.

♦ Young age.

♦ Male sex.

♦ Obesity (possibly).

ο Early symptoms (pulmonary edema).

♦ Nonproductive cough.

♦ Rales (few).

♦ Dyspnea on exertion.

♦ Fatigue.

♦ Weakness with decreased tolerance for physical activity

and increased time for recovery after physical exertion.

♦ Resting tachycardia and tachypnea greater than induced

by altitude alone.
29.30

Emergency War Surgery

♦ Once symptoms appear, HAPE can progress very

rapidly (< 12 hours) to coma and death.

♦ Nail beds and lips may be more cyanotic than other unit

members.

ο Progressing pulmonary edema.

♦ Productive cough of frothy and sometimes pink or

bloodstained sputum.

♦ Rales more numerous and widespread.

♦ Wheezing may develop.

♦ Lung sounds become audible even without stethoscope,

especially when individual is supine.

♦ Orthopnea may occur (< 20%).

♦ Progressive hypoxemia causes dyspnea and cyanosis.

♦ Arterial blood gas (if available) documents hypoxemia,

hypocapnia, and slight increase in pH.

♦ Mental status deteriorates with progressive confusion

and sometimes vivid hallucinations.

♦ Obtundation, coma, and death occur without treatment.

♦ Subfebrile temperature < 38°C (100.5°F) and a mild

increase in white blood cell count may be present.

♦ Dyspnea at rest.

♦ Marked hypoxia by oximetry.

♦ Dyspnea at rest and cough should be considered to

be the onset of HAPE.

DELAY IN TREATMENT OF PROGRESSIVE PULMONARY EDEMA AT

ALTITUDE USUALLY RESULTS IN DEATH.

ο Treatment.

♦ Depends on severity.

♦ Immediate descent is mandatory! Descent of even a few

hundred meters (300–1,000 m) can be helpful or even

lifesaving in severe cases.

♦ Mortality can approach 50% if descent cannot be

accomplished rapidly.

♦ Oxygen by cannula 2–6 L/min (mild), or by mask 4–6

L/min (moderate and severe). DO NOT DELAY

DESCENT!
29.31

Environmental Injuries

♦ Portable fabric hyperbaric chamber may be lifesaving—

Gamow bag/Certec SA.

♦ Nifedipine, 10 mg tid sublingually, or 20 mg po. A

second 10-mg, sublingual dose can be administered in

15–20 minutes if no improvement in symptoms is

apparent, followed by 30 mg qid.

Nifedipine should not be used in lieu of descent,

supplemental oxygen, or treatment in a hyperbaric bag.

It may be used in conjunction with other therapies.

♦ Immediate descent to lower elevation; if symptoms

resolve, wait at least 72 hours before attempted return

to previous elevation.

Neither furosemide nor morphine sulfate should be used

in the treatment of HAPE unless other more effective

treatment options are not available.

♦ Treatment after descent, at an MTF, is directed toward

ensuring adequate oxygenation and reducing pulmonary

artery pressure; includes bed rest, supplemental oxygen,

and nifedipine.

♦ Invasive diagnostic procedures such as bronchoscopy

or pulmonary artery catheterization are NOT indicated

unless clinical course deteriorates and the diagnosis is

in doubt. Endotracheal intubation is seldom necessary.

ο HAPE Prophylaxis.

♦ Nifedipine, 20 mg tid, po, 24 hours before ascent,

continuing 72 hours after ascent.

 High-altitude cerebral edema.

ο Onset following ascent is highly variable and occurs later

than either AMS or HAPE. Mean duration of onset 5 days

with a range of 1–13 days.

ο Incidence lower than AMS or HAPE (< 1% of individuals

making rapid ascent).

ο Potentially fatal, uncommon (< 2% above 3,700 m). Can

occur as low as 2,430 m (8,000 ft) but vast majority of cases
29.32

Emergency War Surgery

above 3,600 m (12,000 ft). Untreated HACE can progress

to death over 1–3 days or become more fulminant with

death occurring in < 12 hours.

ο Exacerbation of unresolved, severe AMS.

ο Most often occurs in people who have AMS symptoms

and continue to ascend.

ο Signs and symptoms.

♦ Most signs and symptoms are a manifestation of

progressive cerebral edema.

♦ Early signs resemble AMS (these symptoms are not

invariably present).

♦ Severe headache

♦ Nausea

♦ Vomiting.

♦ Extreme lassitude.

ο Progressing signs.

♦ Mental status changes: Confusion, disorientation,

drowsiness, and impaired mentation.

♦ Truncal ataxia (swaying of upper body, especially when

walking). As the edema progresses, soldier may also

exhibit an ataxic gait in addition to the truncal ataxia.

♦ Soldier appears withdrawn, and behavior is mistakenly

attributed to fatigue or anxiety.

♦ Cyanosis and general pallor are common.

♦ Symptoms of HAPE.

ο Untreated HACE.

♦ Variety of focal and generalized neurologic abnormalities

may develop: visual changes, anesthesias, paresthesias,

clonus, pathological reflexes, hyperreflexia, bladder and

bowel dysfunction, hallucinations, and seizures.

♦ Papilledema may be present in up to 50% of the soldiers,

but is NOT universal.

ο Coma.

Ataxia at altitude is HACE.

ο Prophylaxis.
29.33

Environmental Injuries

No definitive evidence; however, due to similarity with

AMS, prophylactic measures for HACE include use of

staged or graded ascent, high carbohydrate diet, and use

of acetazolamide.

ο Treatment.

♦ Immediate descent is mandatory. Definitive treatment

of HACE is immediate descent. In general, the greater

the descent the better the outcome. Descent of more than

300 m (1,000 ft) may be required for clinical improvement,

and descents to altitudes of less than 2,500 m (8,000 ft)

is optimal.

♦ If descent is delayed, treatment with a portable cloth

hyperbaric chamber may be lifesaving. May require at

least 6 hours of pressurization in chamber.

♦ Oxygen by mask or cannula 2–6 L/m; should not be

used as a substitute for descent.

♦ Dexamethasone, 4–8 mg initially and then 4 mg qid,

po, IV, or IM. DO NOT DELAY DESCENT! Few side

effects if used only 3–4 days.

♦ Loop diuretics and osmotic diuretic agents, such as

mannitol, urea, and glycerol, have been suggested, but

there is little experience with them in this role. Careful

attention is required before diuretics are used.

Individual may have altitude-induced decrease in

intravascular volume concomitant with cerebral edema.

♦ Hospital management consists of supplemental oxygen

(if needed to maintain arterial oxygen levels), supportive

care, and possibly diuretics. Comatose patients may

require intubation and bladder catheterization.

HACE and HAPE often coexist. Individuals with HACE

will often have HAPE; however, most individuals with

HAPE do not have concomitant HACE.
29.34

Emergency War Surgery