Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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CARE OF PATIENTS WITH ENVIRONMENTAL INJURIES

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cerebral edema can occur in severe cases. Although many

patients recover without neurologic sequelae, residual cere-

bellar symptoms, quadriparesis, hemiparesis, and memory

loss may be present.

Hypovolemia results from dehydration, intracellular vol-

ume shifts, decreased peripheral vascular resistance, or poor

myocardial function. Myocardial depression follows heat-

induced myocardial necrosis.

Disseminated intravascular coagulation can result from

heat stroke. Denaturation of the proteins involved in the

coagulation cascade may produce prolongation of the pro-

thrombin time and partial thromboplastin time. Direct ther-

mal injury may result in platelet dysfunction. Megakaryocytes

in the bone marrow also may show thermal damage.

Coagulation abnormalities cause hemorrhage within the CNS

resulting in secondary neurologic deterioration.

Thermal injury results in direct muscle damage and

necrosis. It may occur in nonexertional heat stroke as well as

in heat stroke associated with exertion. Rhabdomyolysis

results in the release of large amounts of myoglobin and

muscle enzymes.

Renal failure may result from direct thermal damage to

the tubules. Hypoperfusion of the kidneys results in acute

tubular necrosis. Myoglobinuria may exacerbate renal failure

owing to direct toxic effects.

Death in heat stroke can occur from direct heat injury to

the brain. Other causes of death and morbidity include cere-

bral hemorrhage, aspiration pneumonia, cardiac failure,

renal failure, and hepatic failure.

Clinical Features of Heat Stroke

A. Symptoms and Signs—Heat stroke can develop sud-

denly, with loss of consciousness, and need not be preceded

by prodromal symptoms such as headache, dizziness, muscle

cramps, nausea, and fainting. Although hot, flushed skin is

associated with heat stroke, about half of patients exhibit

sweating. Depression of neurologic status is present in nearly

all cases, and most patients are unconscious at presentation.

Signs of cerebellar dysfunction and seizures also may occur.

Sinus tachycardia and hypotension are common in patients

with heat stroke. Hypovolemia with dehydration causes these

changes in most cases, but cardiac dysfunction also may

occur as a result of direct injury or acidosis. In the later stages

of heat stroke, acute respiratory failure, renal failure, and

severe coagulation disorders may develop.

B. Laboratory Findings—Serum concentrations of sodium,

potassium, phosphate, calcium, and magnesium are usually

low during the early stages of heat stroke. Hematocrit is usu-

ally elevated as a result of hemoconcentration. In the later

stages of heat stroke, hyperkalemia may develop as a result of

rhabdomyolysis. This also results in serum enzyme eleva-

tions of creatine kinase (CK), lactate dehydrogenase (LDH),

and aspartate aminotransferase (AST). Coagulation studies

may be abnormal in the later stages of the syndrome.

Elevation of fibrin split products suggests disseminated

intravascular coagulation and is associated with a poor prog-

nosis. Arterial blood gases usually reveal a mixed disorder,

with respiratory alkalosis owing to hyperventilation and a

profound metabolic acidosis. Arterial blood gases should

be interpreted without temperature correction to avoid

misinterpretation.

Differential Diagnosis

The diagnosis of exertional heat stroke is usually straightfor-

ward and based on a history of strenuous physical activity in

a hot environment. In the elderly patient presenting with

fever, hypotension, tachycardia, and mental status changes,

sepsis must be considered. A thorough physical examination

should be performed and appropriate cultures obtained to

exclude this possibility. Heat stroke also must be differenti-

ated from neuroleptic malignant syndrome. In this syndrome,

hyperthermia is triggered by major antipsychotic medications

such as phenothiazines, thioxanthenes, and the butyrophe-

nones. Neuroleptic malignant syndrome occurs in as many as

1% of patients receiving these medications, and its recogni-

tion is important because effective treatment is available with

the nondepolarizing muscle relaxants and dantrolene.

It is important to differentiate between fever and the

hyperthermia of heat stroke. In the febrile patient, the regu-

latory set point is increased owing to endogenous or exoge-

nous pyrogens, and body temperature is balanced at a new

set point. Heat stroke represents a failure of thermoregula-

tory mechanisms. Therefore, antipyretics are ineffective in

patients with heat stroke, and the peripheral cooling used to

lower body temperature in these patients generally is not

effective in treating patients with fever.

Treatment of Heat Stroke

A. Prompt Lowering of Body Temperature—The patient

should be placed in a cool environment. If the patient is

unconscious, endotracheal intubation should be performed

and mechanical ventilation with supplemental oxygen insti-

tuted to maintain adequate gas exchange. Fluid resuscitation

is required to reverse hypovolemia. In almost all cases, cen-

tral venous pressure monitoring will be necessary to evaluate

fluid status. In the elderly patient with evidence of cardiac

dysfunction, pulmonary artery catheterization may be

required. After rapid resuscitation, the rapid reduction of

body temperature is the major priority. The optimal method

for cooling the patient remains controversial. Immediate

treatment usually consists of surface cooling with immersion

in ice water or cold water or the use of cooling blankets. Cold

water immersion has been shown to be as effective as ice

water immersion and may be less uncomfortable for the

patient. The disadvantages of ice water immersion include

peripheral vasoconstriction and shivering. Shivering is unde-

sirable because of increased heat production and metabolic

demand. In this setting, shivering can be abolished by the

administration of nondepolarizing muscle relaxants. The use

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of phenothiazines should be avoided because of the risk of

toxicity and the possibility of a decrease in the seizure

threshold. Other techniques for cooling include cold intra-

venous fluids, cold water gastric or rectal lavage, peritoneal

dialysis with cold fluids, and the use of external cooling with

circulatory bypass. Once the temperature has been reduced

to 39°C, cooling efforts should be discontinued to prevent

the development of hypothermia. The use of antipyretics

such as aspirin or acetaminophen is ineffective for the rea-

sons previously stated, and their use is contraindicated

because they may worsen an existing coagulopathy or exac-

erbate hepatic injury. The use of alcohol sponge baths is also

contraindicated because of the risk of systemic absorption

and resulting toxicity.

B. Physiologic Monitoring—Continued monitoring in the

ICU is essential because many of the complications of hyper-

thermia, such as pulmonary failure, renal failure, and coagu-

lopathy, may take 24–48 hours to develop. Electrolytes

should be monitored frequently to detect life-threatening

electrolyte disorders. If rhabdomyolysis develops, osmotic

diuresis and alkalinization of the urine may help to prevent

renal damage from myoglobinuria. Organ system dysfunc-

tion may necessitate continued mechanical ventilation or

hemodialysis.

Current Controversies and Unresolved Issues

Investigations continue to focus on the relationship between

heat stroke and malignant hyperthermia and the role of

inflammatory mediators in the pathogenesis of heat stroke.

Clinical heat stroke may be associated with an underlying

inherited abnormality of skeletal muscle similar to that of

malignant hyperthermia. Skeletal muscle biopsies performed

in patients who developed heat stroke have shown abnormal

responses similar to those seen in malignant hyperthermia.

Such an association might suggest that certain patients are

more susceptible to heat stroke than others. Several authors

have suggested that dantrolene may be effective in the treat-

ment of heat stroke patients. However, the scant data avail-

able are still inconclusive.

There is evidence that inflammatory mediators may have

a role in the pathogenesis of heat stroke and subsequent

organ-system dysfunction. Patients with heat stroke have

been found to have elevated levels of tumor necrosis factor

and interleukin-1α. These elevated levels persisted even after

cooling was completed. Heat stroke also has been associated

with excessive nitric oxide (NO) production, the magnitude

of which is proportional to the severity of illness. It has been

suggested that NO may be an important mediator and inte-

gral part of the pathophysiologic processes resulting in heat

stroke and may be a central factor linking the observed neu-

rologic and cardiovascular abnormalities. If a role is estab-

lished for these mediators, new management strategies may

be possible by modulation of the inflammatory response or

specific blocking agents.

Lugo-Amador NM et al: Heat-related illness. Emerg Med Clin

North Am 2004;22:315–27. [PMID: 15163570]

Rav-Acha M et al: Fatal exertional heat stroke: A case series. Am J

Med Sci 2004;328:84–7. [PMID: 15311166]



Hypothermia

ESSENTIALS OF DIAGNOSIS



History of events.



Early hypothermia (35–37°C): shivering, cool cyanotic

extremities, tachycardia.



Mild hypothermia (32.2–35°C): confusion, disorienta-

tion, hyperventilation.



Moderate hypothermia (28–32.2°C): amnesia, lethargy,

J-wave on ECG, atrial fibrillation.



Severe hypothermia (<28°C): coma, dilated pupils and

absent tendon reflexes, absence of shivering, ventricu-

lar fibrillation, asystole, apnea.

General Considerations

Hypothermia is defined as an unintentional decline in the

core body temperature. Below 35°C, the systems responsible

for thermoregulation begin to fail because the compensatory

physiologic responses to minimize heat loss are ineffective.

Hypothermia may occur as a result of environmental expo-

sure or during prolonged surgical procedures. Prompt diag-

nosis and treatment are necessary in severe cases to reverse

organ dysfunction and to prevent death. Frostbite results

from local cold injury and threatens mainly function. Cold

injuries are being encountered with increasing frequency in

the elderly, in the homeless, and in individuals participating

in winter sports without proper protective clothing.

Hypothermia develops because of an imbalance between

body heat generation and environmental losses. Body heat is

generated as a by-product of metabolic processes and as a

result of muscular contraction. Heat is lost from the body by

radiation, convection, conduction, and evaporation.

Immersion injuries result in rapid conductive heat loss to the

cold water. Radiation and evaporation are the mechanisms by

which heat is lost during prolonged open-cavity surgical pro-

cedures. Hypothermia may occur in individuals with normal

thermoregulation following prolonged exposure to extreme

cold. Neurologic disorders, drug intoxication, myxedema, and

malnutrition may cause thermoregulatory malfunction, and

hypothermia may occur after only mild to moderate cold

exposure in individuals with these conditions. Hypothermia

may be classified as acute if the patient has been hypothermic

for less than 6 hours and chronic if for more than 6 hours.

Dehydration and electrolyte imbalance are more likely to

occur in patients with chronic hypothermia.

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When the core body temperature falls below 36°C,

increased sympathetic activity, shivering, and peripheral

vasoconstriction develop. These mechanisms have the effect

of increasing heat production and preventing further heat

loss. Shivering may result in a profound increase in meta-

bolic rate with a sixfold increase in oxygen consumption.

The principal defense against cold is peripheral vasocon-

striction. Cold-induced vasoconstriction may lead to an initial

rise in central venous pressure from redistribution of blood to

the central circulation. Patients with severely compromised

cardiac function may develop pulmonary edema as a result of

this central circulatory overload. Limb ischemia may develop,

and the resulting anaerobic metabolism may contribute to

metabolic acidosis. As the core body temperature falls below

35°C, many patients no longer complain of being cold. When

the core body temperature falls below 32°C, shivering ceases.

The metabolic rate falls rapidly, and the muscles become rigid.

With profound hypothermia, the metabolic rate is reduced to

less than 50% of the basal level. Amnesia and lethargy develop,

progressing to coma. Bradycardia is prominent, and cardiac

output falls. The respiratory rate decreases, but a relative alka-

losis is maintained. This alkalosis may be protective of protein

and enzyme function, myocardial function, and cerebral

autoregulation. The cerebral ischemic tolerance during

hypothermia is considerably increased compared with the

normothermic state. This may, in some cases, contribute to

full neurologic recovery. For this reason, most patients with

hypothermia should be rewarmed and reevaluated before a

diagnosis of brain death is made. An additional consequence

of the altered level of consciousness is that normal protective

airway reflexes are abolished. This probably accounts for the

high incidence of aspiration pneumonia in hypothermic

patients. Atrial fibrillation, heart block, ventricular fibrillation,

or asystole may develop when the core body temperature falls

below 28°C. Ventricular fibrillation may occur spontaneously

or may be induced by line placement or other therapeutic

maneuvers. When ventricular fibrillation develops in this set-

ting, it is difficult to convert by countershock or pharmaco-

logic agents without further rewarming.

As the core body temperature falls below 26°C, hypoten-

sion and decreased systemic vascular resistance develop. An

additional factor contributing to hypotension may be the

hypovolemia that is commonly observed in accidental

hypothermia victims. The hypovolemia is frequently related

to a preexisting medical condition and may be exacerbated

by hypothermia-induced diuresis. Although renal blood flow

and the glomerular filtration rate decrease with hypother-

mia, cold diuresis usually results from the redistribution of

blood to the central circulation and from a decreased

response of the renal tubule to antidiuretic hormone. With

profound hypothermia, severe oliguria develops as a result of

generalized hypoperfusion and also may be related to acute

tubular necrosis secondary to rhabdomyolysis.

Hypothermia has profound effects on the hematologic

and coagulation systems. The hematocrit and the viscosity of

the blood increase owing to hemoconcentration, and viscosity

is further increased by the fall in temperature. Coagulation is

impaired as a result of platelet dysfunction and decreased

enzymatic protein activity. These coagulation disorders are

usually reversed on rewarming.

Hypothermia may result in severe GI complications,

including ileus, pancreatitis, and gastric stress ulcers. Depressed

hepatic function may result in alterations in the pharmacoki-

netics of many drugs and reduced clearance of toxins.

As core body temperature falls below 26°C, spontaneous

respirations cease, asystole develops, and electrocerebral

silence occurs.

Clinical Features

A. Symptoms and Signs—The history of the events prior to

presentation is essential for the diagnosis of hypothermia. In

cases such as cold water immersion or prolonged exposure to

winter temperatures, the diagnosis will be obvious. The diag-

nosis may be less obvious in a patient with associated injuries

or in the elderly patient with multiple medical problems.

Suspicion of hypothermia is particularly relevant when the

history suggests that an injury or disease has resulted in a

prolonged period of immobility with or without the associa-

tion of a cold environment.

Patients experiencing early hypothermia (35–37°C) usu-

ally present with shivering. The extremities are cool and

cyanotic as a result of reflex vasoconstriction. Tachycardia

results from increased sympathetic activity. In patients with

mild hypothermia (33–35°C), confusion and disorientation

are common. Hyperventilation may develop in response to

increased metabolic activity. Patients with moderate

hypothermia (30–33°C) are amnesic, obtunded, and often

progress to coma. When the core temperature falls below

32°C, shivering ceases and bradycardia develops. Terminal

additions to the QRS complex known as Osborne waves or

J waves develop in the ECG, and the PR and QT intervals may

be prolonged. Atrioventricular block or atrial fibrillation can

develop. Patients with severe hypothermia (<30°C) present

with coma, dilated pupils, and absent tendon reflexes. Life-

threatening cardiac arrhythmias or asystole may be present.

B. Temperature Monitoring—Body temperatures should

be accurately measured in all patients suspected of being

hypothermic. Standard clinical thermometers have a low

temperature limit of 32–33°C and should not be used.

Electronic temperature-sensing systems accurate down to

25°C are desirable, and many of these systems provide for

continuous temperature monitoring. If electronic equip-

ment is not available, standard glass laboratory thermome-

ters can be used to monitor temperature. In addition to

sublingual, axillary, and rectal sites, specialized electronic

systems allow for temperature monitoring in the esophagus,

pulmonary artery, bladder, and tympanic membrane.

Monitoring temperature at the tympanic membrane may

offer some advantage because this area is warmed by cerebral

blood flow, but temperature always should be recorded at

several sites to ensure accuracy.

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790

C. Laboratory Findings—A complete blood count, arterial

blood gas measurements, and blood cultures should be

obtained in all patients with hypothermia. The arterial blood

gas should be interpreted with and without temperature cor-

rection to avoid misinterpretation. Coagulation studies are

not usually of benefit because the blood sample is heated to

physiologic temperature prior to testing, and the results thus

do not correlate with the clinical situation.

D. Electrocardiography—Continuous electrocardiographic

monitoring should be established immediately. In cases of

moderate hypothermia, a complete ECG should be obtained

to determine intervals and to check for the presence of J waves.

Differential Diagnosis

The signs and symptoms of early hypothermia are nonspe-

cific. Accurate temperature determination is essential to

establish or exclude the diagnosis. Hypothermia may compli-

cate other disorders, including drug or alcohol intoxication

and endocrinopathies—that is, hypoglycemia, hyperosmolar

coma, diabetic ketoacidosis, and myxedema. Hypothermia

also may occur as a complication of sepsis. Patients with

severe trauma or burns are particularly at risk for the devel-

opment of hypothermia.

Treatment

A. Airway—Orotracheal intubation is indicated for all

hypothermic patients with altered mental status.

Nasotracheal intubation should be avoided because nasal

bleeding can be a significant problem in the patient with a

coagulation disorder. Cricothyroid pressure should be main-

tained during intubation attempts to prevent aspiration. It

should be recognized that even a cuffed endotracheal tube

will not offer complete protection against aspiration, and an

orogastric tube should be passed and placed on continuous

suction to evacuate the stomach contents. During the

rewarming process, endotracheal tube cuff pressures must be

monitored frequently to avoid tracheal injury because the

volume and pressure in the cuff will increase.

B. Breathing—Patients with moderate to severe hypothermia

require mechanical ventilation. Warm humidified gases should

be used to prevent further heat loss, but they will not play a

major role in rewarming owing to the small amount of heat

they convey. Adjustment of mechanical ventilation should be

guided by non-temperature-corrected blood gas values for pH

and Pa

.However,temperature correction is required for

accurate determination of Pa

and hemoglobin saturation.

C. Circulation—Most patients with moderate to severe

hypothermia also will be hypovolemic. These patients may

require as many as 10 L of crystalloid during rewarming.

Ideally, all intravenous fluids should be warmed to 39°C. This

can be accomplished in a number of ways, including use of

microwave ovens, but care must be taken to avoid overheat-

ing, which can lead to hemolysis. Heating units allow for

rapid fluid administration with precise temperature control

and should be used if available. Central venous pressure or

pulmonary artery pressure monitoring may be necessary in

patients who do not respond to aggressive volume adminis-

tration. Inotropic and vasoconstrictive agents such as

dopamine should be avoided because they are usually inef-

fective and may result in cardiac arrhythmias.

D. Rewarming—The faster the patient is warmed, the better

is the prognosis. Once the diagnosis of hypothermia is sus-

pected, all efforts should be directed toward reducing further

heat loss and rewarming the patient. In addition to the use of

warm intravenous fluids and heated respiratory gases, warm

blankets should be applied to prevent radiant heat loss during

resuscitation and evaluation. There are three options for

rewarming: (1) passive rewarming, (2) active external rewarm-

ing, and (3) active internal rewarming. The overall condition

of the patient will determine the most appropriate method.

Most patients with mild to moderate hypothermia will be

able to rewarm themselves, and passive external measures to

prevent further heat loss will be all that are necessary. Active

external rewarming, achieved by conductive surface warming

with methods such as warm water immersion or heating blan-

kets, is often ineffective in adults because of the low body-

surface-to-body-volume ratio. The vasodilation resulting from

these methods also may worsen hypotension. In addition, the

reestablishment of flow in peripheral circulatory beds may

lead to increased transport of colder peripheral blood to the

central core, resulting in a paradoxical decrease in core tem-

perature. To effect external rewarming, air circulating systems

may prove to be more effective because they provide for addi-

tional heat exchange by convection. These devices are usually

readily available in the operating room or recovery area. To

minimize adverse circulatory effects, these systems can be

applied initially only to the trunk. In most cases of moderate

to severe hypothermia, active external rewarming will need to

be combined with active internal rewarming.

Active internal rewarming is achieved by gastric, colonic, or

bladder lavage with heated saline, pleural lavage, peritoneal

lavage, and cardiopulmonary bypass. Gastric, colonic, and

bladder lavage can be performed easily without specialized

equipment or facilities. Although rewarming is relatively slow

by these methods because of limited surface area, it may be

enough to make the difference in cases of moderate hypother-

mia. Lavage fluid temperatures should not exceed 40.5°C to

avoid mucosal injury. With gastric lavage, care should be taken

to minimize the risk of aspiration. Gastric lavage should not be

performed on a patient receiving chest compressions for car-

diopulmonary resuscitation. Although more invasive, peri-

toneal lavage will result in more rapid warming. Lavage fluid up

to 43°C can be used, and the placement of two catheters will

provide for a continuous flow rate of up to 6 L/h. An intact car-

diovascular status is necessary to provide adequate perfusion so

that heat exchange can take place. If the patient has severe

hypothermia and cardiac arrest, open cardiac massage and

mediastinal and pleural lavage with warm saline is indicated.

The methods available for extracorporeal blood rewarm-

ing include hemodialysis, arteriovenous rewarming, venovenous

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CARE OF PATIENTS WITH ENVIRONMENTAL INJURIES

791

rewarming, and cardiopulmonary bypass. Hemodialysis

offers the advantage of requiring only a single venous cannu-

lation with a two-way flow catheter. The femoral approach is

preferred to avoid cardiac irritation. Hemodialysis may offer

additional advantages in patients with renal failure and drug

or other toxicity.

In addition to providing circulatory support for the patient

with cardiac arrest or arrhythmia, cardiopulmonary bypass

will allow for rapid rewarming. A major drawback of car-

diopulmonary bypass is that systemic heparinization is

required. Therefore, the technique may be contraindicated in

patients who have sustained severe trauma. The use of systems

with heparin-bonded tubing may overcome some of these

problems. Standard cannulation techniques may be used in

the patient with a thoracotomy for open cardiac massage.

Alternatively, femoral venoarterial bypass can be instituted by

cutdown or by percutaneously placed catheters in the patient

with intact cardiovascular function. Portable systems using

percutaneous access may allow the institution of bypass

warming in the ICU. The long-term outcome of patients with

severe hypothermia treated with cardiopulmonary bypass has

been favorable.

Prognosis

The outcome depends on a number of factors, including the

severity and duration of hypothermia and the presence of

coexisting medical conditions. Aggressive treatment is indi-

cated because any hypothermic patient has the potential for

full recovery despite severely depressed cardiac or respiratory

function. Successful resuscitation with full recovery has been

reported after documented ice water submersion for as long

as 66 minutes in a small child. Success such as this probably

depends on rapid symmetric cooling of the entire body,

including the brain.

Current Controversies and Unresolved Issues

Techniques such as the use of very high temperature intra-

venous fluids are being explored for the treatment of moder-

ate to severe hypothermia. Intravenous fluids heated to 65°C

have been used in animal studies and have resulted in rewarm-

ing rates of 2.9–3.7°C per hour with minimal intimal injuries.

Diathermy involves the conversion of energy waves into

heat. Ultrasound or low-frequency microwave radiation

can deliver large amounts of heat to deep tissues. Although

animal studies have yielded some promising results, further

investigation is needed to determine the optimal clinical

use of diathermy. There is controversy about when and

when not to resuscitate the victim of hypothermia. The

techniques necessary to reverse severe hypothermia require

a major allocation of personnel and resources. Although it

has been stated that no person is dead until “warm and

dead,” in many cases additional information will establish a

definitive diagnosis. Severe hyperkalemia (>10 meq/L) sug-

gests that the patient died prior to the development of

hypothermia because the potassium level is usually normal

or low in patients with hypothermia. Of course, other

causes of hyperkalemia such as renal failure or crush injury

must be ruled out.

Once instituted, resuscitation should proceed until a core

temperature of 30°C is achieved. At this temperature, some

signs of life should be evident, and successful cardioversion is

usually possible.

Eddy VA et al: Hypothermia, coagulopathy, and acidosis. Surg Clin

North Am 2000;80:845–54. [PMID: 10897264]

Giesbrecht GG et al: Cold stress, near-drowning and accidental

hypothermia: A review. Aviat Space Environ Med 2000;71:

733–52. [PMID: 10902937]

Kempainen RR et al: The evaluation and management of acciden-

tal hypothermia. Respir Care 2004;49:192–205. [PMID:

14744270]

Mallet ML: Pathophysiology of accidental hypothermia. QJM

2002;95:775–85. [PMID: 12454320]

Megarbane B et al: Hypothermia with indoor occurrence is associ-

ated with a worse outcome. Intensive Care Med 2000;26:

1843–9.

Mizushima Y et al: Should normothermia be restored and main-

tained during resuscitation after trauma and hemorrhage?

J Trauma 2000;48:58–65. [PMID: 10647566]

Owda A, Osama S: Hemodialysis in management of hypothermia.

Am J Kidney Dis 2001;38:E8. [PMID: 11479182]

Silvas T et al: Outcome from severe accidental hypothermia in

southern Finland: A 10-year review. Resuscitation 2003;59:

285–90. [PMID: 14659598]

Ujhelyi MR et al: Defibrillation energy requirements and electrical

heterogeneity during total body hypothermia. Crit Care Med

2001;29:1006–11. [PMID: 11378613]

Vassal T et al: Severe accidental hypothermia treated in an ICU:

Prognosis and outcome. Chest 2001;120:1998–2003.

Voelckel WG et al: Intraosseous blood gases during hypothermia:

Correlation with arterial, mixed venous, and sagittal sinus

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9366581]



Frostbite

ESSENTIALS OF DIAGNOSIS



First degree: hyperemia and edema after rewarming;

no blister formation.



Second degree: hyperemia, edema, and serous blister

formation; severe pain during rewarming.



Third degree: full-thickness skin injury resulting in skin

necrosis, black eschars, and hemorrhagic blister formation.



Fourth degree: complete necrosis of soft tissue, muscle,

and bone; after rewarming, the tissue is cyanotic and

ischemic; mummification with minimal edema.

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792

General Considerations

Local injuries owing to cold include chilblains, immersion

foot, and frostbite. Chilblains and immersion foot result

from prolonged exposure of the extremities in wet condi-

tions to temperatures above freezing. Severe neurovascular

damage may result, and ulcerations with chronic infections

may be incapacitating.

Frostbite occurs when the tissues are actually frozen.

Edema and blister formation develop after thawing or partial

thawing. These areas may progress to gangrene.

There are two phases of injury that occur with frostbite:

Phase 1: direct cellular cryotoxicity—As ice crystals

form within the affected area, cell death occurs as a result of

both dehydration and mechanical disruption owing to

expanding ice crystals. The most severe injuries occur after

partial thawing and refreezing of tissues.

Phase 2: progressive vascular thrombosis—Cold

exposure results in reflex arterial vasoconstriction and freez-

ing of the tissues that result in capillary injuries. In addition,

cold increases blood viscosity. When thawing occurs, the cir-

culatory stasis and tissue swelling result in intravascular

thrombosis. Tissue necrosis will occur when reperfusion can-

not be sustained following rewarming.

Clinical Features

Freezing begins distally and progresses centrally. Therefore,

the fingers and toes are most susceptible to severe injury.

There is usually a line of demarcation between the frozen and

unfrozen areas. However, the severity of injury and the extent

of nonviable tissue will not become apparent until several

days after thawing. In classifying frostbite, it is most impor-

tant to differentiate between superficial frostbite with skin

injury only and deep frostbite with injury to deeper struc-

tures of the extremities. Frostbite traditionally has been clas-

sified in somewhat the same way as burns.

Frostbitten extremities are painless, numb, and have a

blanched, waxy appearance. Superficial frostbite involves

only the skin and subcutaneous tissues. Deep frostbite

extends deeper and produces a woody consistency. However,

a wide range of frostbite injuries may appear similar at the

time of the initial evaluation. Therefore, classification of

frostbite should be applied after rewarming.

Treatment

The injury associated with freezing is progressive, and expo-

sure should be limited as soon as possible. However, thawing

should be avoided if refreezing is likely because this will

increase the severity of injury.

A. Rapid Rewarming—Extremities can be rewarmed most

effectively by immersion in a warm water bath with a mild

antibacterial agent such as povidone-iodine at a temperature

between 40 and 42°C. Lower temperatures may compromise

tissue survival. Higher temperatures should be avoided

because of the risk of thermal injury. Thawing should con-

tinue until all the blanched tissues of the injured extremity are

perfused with blood. A red to purple color and pliability of the

tissues will indicate that warming is complete. Active motion

during thawing may be beneficial, but it is important to avoid

rubbing the affected area because this may worsen the injury.

Severe pain is likely to develop during the warming process,

and opioid analgesics are usually required. Unfortunately, the

high opioid doses often required lead to side effects such as

heavy sedation, respiratory depression, and nausea that may

become a serious problem. In cases of frostbite injury of the

lower extremities, epidural blockade has been demonstrated to

provide good pain relief with fewer of these complications.

B. Postthaw Care—The affected area must be carefully pro-

tected after rewarming. White blisters should be debrided

and hemorrhagic ones left intact. Aloe vera (available in

generic preparations), a topical inhibitor of thromboxane,

should be applied to the injured tissue every 6 hours. The

extremity can be splinted in a position of function with ele-

vation, for both protection and comfort. Tetanus prophylaxis

should be administered if required. The use of ibuprofen as

a systemic antithromboxane agent is preferable to aspirin

because aspirin has been shown to inhibit prostaglandins

beneficial to wound healing. Ibuprofen 400 mg should be

given orally every 6 hours. Penicillin, with excellent coverage

of Streptococcus, is the antibiotic of choice for prophylaxis

and is usually continued for 48–72 hours. Daily hydrother-

apy at 40°C for 30–45 minutes aids debridement of devital-

ized tissue. Range-of-motion exercises are essential for

preservation of function. Adequate analgesia is necessary to

permit effective physical therapy.

C. Avoid Early or Inappropriately High Amputation—

Amputation should not be performed until the degree of tis-

sue loss is clearly determined. This may not be possible until

weeks or months after injury. In most cases, skin necrosis will

not be associated with deep tissue loss. Occasionally, digital

escharotomy or fasciotomy is necessary because a compart-

ment syndrome develops or because the range of motion

becomes severely limited. Imaging studies such as tech-

netium scanning and MRI may allow for precise determina-

tion of viable tissue and earlier debridement and

reconstruction with no loss in stump length. In some cases,

the survival of deeper structures may be improved by cover-

age with vascularized tissue.

Prognosis

Patients who sustain superficial frostbite usually achieve

complete recovery with minimal loss of tissue and no loss of

function. Complete recovery is unlikely for patients with

more severe degrees of frostbite injury. Amputation may

result in loss of function and severe cosmetic defects. Patients

may be incapacitated by the development of reflex sympathetic

dystrophy. Numbness, hypertrophic skin changes, chronic



CARE OF PATIENTS WITH ENVIRONMENTAL INJURIES

793

pain, hyperhidrosis, stiffness, and cold intolerance are all

potential sequelae of frostbite. Regional sympathectomy may

improve some of the symptoms of vasospasticity related to

sympathetic hyperactivity.

Children exposed to extreme cold may develop early epi-

physial closure as a result of injury to the growth plate. This

injury results in shortened phalanges. Hand function usually

remains excellent, and reconstructive surgery is rarely required.

Current Controversies and Unresolved Issues

Current interest in frostbite management centers around

heparin anticoagulation, low-molecular-weight dextran

administration, and the role of early sympathectomy.

Frostbite necrosis develops when reperfusion cannot be sus-

tained following rewarming. This has led to the development

of experimental treatments designed to maintain blood flow

in the microcirculation during the period of reperfusion.

However, none of these treatments has been proved to be

effective in controlled trials. Low-molecular-weight dextran

may improve circulation by decreasing blood viscosity and

red blood cell clumping. Animal experiments have demon-

strated a decrease in tissue loss, but this has yet to be estab-

lished in a clinical trial. Clinical studies on the use of heparin

anticoagulation have been inconclusive. Thrombolytic

agents have resulted in significant improvement in tissue sur-

vival in animal models of frostbite. These studies have yet to

be validated in human trials.

Murphy JV et al: Frostbite: pathogenesis and treatment. J Trauma

2000;48:171–8. [PMID: 10647591]

Petron P et al. Surgical management and strategies in the treat-

ment of hypothermia and cold injury. Emerg Med Clin North

Am 2003;21:1165–78. [PMID: 14708823]

Wittmers LE Jr: Pathophysiology of cold exposure. Minn Med

2001;84:31–6. [PMID: 11816961]



Near-Drowning

ESSENTIALS OF DIAGNOSIS



History.



Hypoxemia.



Metabolic or mixed acidosis.



Hypovolemia.



Profound electrolyte abnormalities.



Hypothermia.



Associated injuries.

General Considerations

Drowning is death from asphyxia while submerged. The

near-drowning victim, having survived the acute episode, is

at major risk of developing severe organ dysfunction and of

subsequent mortality.

Pathogenic mechanisms of near-drowning are related to

hypoxemia and aspiration. The physiologic effects of aspira-

tion differ depending on whether the drowning medium is

fresh or salt water. Compared with plasma, these fluids are

hypo- and hypertonic, respectively. Although it is possible for

a drowning victim to die of hypoxemia without aspiration,

this rarely occurs. When fresh water is aspirated, the fluid is

rapidly absorbed from the alveoli, producing intravascular

hypervolemia, hypotonicity, dilution of serum electrolytes,

and intravascular hemolysis. Saltwater aspiration produces

the opposite effects as water is drawn into the alveoli from the

vascular space, producing hypovolemia, hemoconcentration,

and hypertonicity. Hemolysis is not a major problem after

saltwater drowning.

The initial contact of water with the upper respiratory

tract usually stimulates severe laryngospasm. This occasion-

ally results in hypoxia without significant aspiration of water.

Aspiration of water into the trachea and bronchi can result in

airway obstruction. Additional effects of water aspiration

include bronchoconstriction, loss of surfactant, damage to

alveolar and capillary endothelium, and direct alveolar

flooding. Aspiration of gastric contents is common in near-

drowning victims and dramatically increases the severity of

the direct injury.

Hypoxemia occurs most often as a result of intrapul-

monary shunting. Approximately 50% of near-drowning

victims develop acute respiratory distress syndrome (ARDS),

in most cases reversible.

The pathophysiology of brain injury is directly related

to hypoxia and diffuse neuronal damage. The resulting

brain edema may increase intracranial pressure, which may

further compromise cerebral perfusion. In children, the

diving reflex may play a protective role in cases of cold

water submersion. Owing to a high surface-to-volume

ratio, prompt hypothermia results in decreased cerebral

metabolism, with shunting of the circulation to the cerebral

and coronary systems.

Atrial and ventricular arrhythmias occur in the near-

drowning victim owing to hypoxia, metabolic and respira-

tory acidosis, and catecholamine excess. Vagally mediated

cardiac arrhythmias can develop as well. Electrolyte distur-

bances contribute to the generation of cardiac arrhythmias.

Acute tubular necrosis in the drowning victim develops as

a result of hypotension and hypoxemia. Renal failure is exac-

erbated by rhabdomyolysis and hemolysis associated with

disseminated intravascular coagulation.

Clinical Features

The diagnosis of near-drowning is necessarily based on the

history. In the surviving victim, the severity of injury is

determined by evaluation of the level of pulmonary and neu-

rologic function, metabolic and respiratory acidosis, elec-

trolyte abnormalities, and hypovolemia. Victims should be



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794

examined carefully to exclude associated injuries that may

require additional management decisions.

Differential Diagnosis

When a history of diving with compressed gas is obtained,

several additional diagnoses must be considered. Pulmonary

barotrauma occurs when expanding gases are unable to

escape from the alveoli during ascent from a dive.

Pneumothorax with arterial gas embolization then may

occur. Arterial gas embolization may result in neurologic

dysfunction and cardiovascular collapse. These diagnoses

should be suspected in any case of near-drowning associated

with compressed air diving.

The use of compressed air while diving may cause other

problems owing to the release of excess gas from tissues on

ascent. Severe pain is the usual clinical manifestation of

decompression sickness and is due to the presence of gas

bubbles in body tissues. Gas bubble formation also may

result in spinal cord injury or CNS dysfunction. In some

cases, this may have precipitated the drowning episode.

A blood alcohol level and a drug screen should be

obtained in all adolescent and adult victims of near-

drowning because intoxication is a factor in more than half

the cases.

Treatment

A. Airway—Since a successful outcome in the near-

drowning victim depends on early correction of hypoxia,

endotracheal intubation should be performed early if there is

any evidence of pulmonary dysfunction. Prior to intubation,

it is important to clear the airway of vomitus or debris.

Cervical spine precautions should be maintained in any vic-

tim who suffers a near-drowning episode after diving.

B. Breathing—The arterial oxygen saturation should be

maintained at a level greater than 90%. If this level cannot be

maintained with high concentrations of inspired oxygen or

with continuous positive airway pressure, mechanical ventila-

tion with positive end-expiratory pressure should be insti-

tuted. Alveolar flooding, with loss of surfactant and direct

capillary injury, results in atelectasis and pulmonary edema.

Aspiration injury may result from vomiting and aspiration of

gastric contents. Aspiration of polluted water and foreign

materials can result in additional lung injury. Early chest radi-

ographs may be normal, with pulmonary infiltrates becoming

evident 48–72 hours after injury. Delayed pulmonary compli-

cations include ARDS and aspiration pneumonia.

C. Circulation—The hypotensive near-drowning victim

requires vigorous fluid resuscitation. Central venous pressure

monitoring is instituted in patients who do not respond to

volume resuscitation and in those with hypoperfusion

despite fluid challenges.

D. Acid-Base Status—Metabolic acidosis is best managed

by optimization of fluid status. In most cases, bicarbonate

should not be administered. Mechanical hyperventilation

may be used to establish a compensatory respiratory alkalo-

sis in victims with severe metabolic acidosis.

E. Correction of Electrolyte Abnormalities—Electrolyte

abnormalities are usually not significant in victims of fresh-

water near-drowning. In the case of saltwater victims, critical

elevations of sodium and chloride may occur. Treatment

requires aggressive diuresis, adjustment of intravenous flu-

ids, and in some cases hemodialysis. Hypermagnesemia and

hypercalcemia also may develop in victims of saltwater

drowning and require hemodialysis.

The kidney may be adversely affected if significant

intravascular hemolysis has occurred. Hemoglobinuria is

treated initially by establishing an osmotic diuresis and by

alkalinization of the urine. Despite these measures, acute

tubular necrosis can develop and require dialysis.

Prognosis

The outcome depends on a number of factors, including the

length of submersion, water temperature, time to first

breath, initial pH, and the initial neurologic evaluation. A

recent review reported 58% survival, with no neurologic

deficit, in a group of pediatric victims of near-drowning. The

major factors that improved outcome were the presence of a

detectable heartbeat and hypothermia on admission to the

hospital. Neurologic outcome in adults is also improved in

cases of cold water near-drowning.

Current Controversies and Unresolved Issues

Emergency cardiopulmonary bypass may have a role in the

resuscitation of the profoundly hypothermic near-drowning

victim. Survival with subsequent normal neurologic func-

tion has been reported in victims with severe hypothermia

and no vital signs on admission. An obvious limitation of

this technique is the necessity for immediate availability of

equipment and personnel to institute bypass and the need

for systemic anticoagulation. However, it is unlikely that any

other method of resuscitation would prove successful in this

select group of patients.

Concern regarding the sequelae of cerebral edema in the

near-drowning victim has prompted the consideration of

various therapeutic interventions to prevent cerebral injury.

Unfortunately, the use of steroids, intracerebral monitoring,

hypothermia, and controlled hyperventilation have not

resulted in improved outcomes in controlled clinical trials.

The potential benefits of calcium channel blockers,

prostaglandin inhibitors, free-radical inhibition, and hemod-

ilution to decrease tissue injury remain unproved.

Gheen KM: Near-drowning and cold water submersion. Semin

Pediatr Surg 2001;10:26–7. [PMID: 11172569]

Giesbrecht GG: Cold stress, near drowning and accidental

hypothermia: A review. Aviat Space Environ Med 2000;71:

733–52. [PMID: 10902937]



CARE OF PATIENTS WITH ENVIRONMENTAL INJURIES

795

Harries M. Near-drowning. Br Med J 2003;327:336–8. [PMID:

14656846]

Thalmann M et al. Resuscitation in near drowning with extracor-

poreal membrane oxygenation. Ann Thorac Surg 2001;72:

607–8. [PMID: 11515909]



Envenomation

1. Snakebite

ESSENTIALS OF DIAGNOSIS

Crotalidae:



Swelling, erythema, ecchymosis.



Coagulopathy.



Metallic taste, perioral paresthesias.



Hypotension.



Tachypnea.



Respiratory compromise.

Elapidae:



Respiratory compromise, generalized paralysis.

General Considerations

It is estimated that 1500 snakebites are inflicted annually in

the United States by 19 species of venomous snakes.

Depending on the degree of envenomation, significant mor-

bidity and potential mortality can result. Ninety-five percent

of poisonous snakebites in the United States are caused by pit

vipers (Crotalidae), which include rattlesnakes, cotton-

mouths and copperheads; only 4–5% of bites are inflicted by

coral snakes (Elapidae).

The main functions of crotalid venom are immobiliza-

tion, death, and digestion of prey. These venoms are complex

mixtures of enzymes and toxic proteins. Other components

include metalloproteins, glycoproteins, lipids, and biogenic

amines. Crotalid venom causes local tissue injury, coagulopa-

thy, and systemic manifestations. The local injury is due to a

combination of direct toxic damage to tissue as well as to

ischemic damage owing to elevated compartment pressure

resulting from local tissue edema. The coagulopathy is

caused by procoagulant esterases that act on fibrinogen and

split off fibrinopeptides. This results in depletion of fibrino-

gen and elevation of the prothrombin and partial thrombo-

plastin times. The platelet count usually remains normal.

Bradykinin is released by the action of arginine ester hydrox-

ylase on plasma kininogen and may cause vasodilation and

pooling of blood in the pulmonary and splanchnic beds,

resulting in decreased venous return, hypotension, and

shock. Interstitial loss of intravascular fluid further worsens

the hypotension. Myocardial ischemia and depression of

contractility also have been associated with pit viper venom.

Renal failure probably results from hypotension, from the

direct effects of the venom, and from myoglobinuria.

Disseminated intravascular coagulation further contributes

to the development of renal failure.

The Mojave rattlesnake has a different type of venom

containing a toxin that immobilizes prey by neuromuscular

blockade. This toxin is present to some extent in other cro-

talid species, but in Mojave rattlesnake venom the higher

concentration significantly increases the risk of airway and

breathing complications. For these reasons, Mojave rat-

tlesnake venom has the lowest median lethal dose level of any

North American crotalid venom.

Venom from the Elapidae causes symptoms that are pri-

marily neurologic in nature, with little or no local tissue tox-

icity. The neurotoxic elements are polypeptides that bind

postsynaptically and effect nondepolarizing blockade of the

acetylcholine receptors. Generalized paralysis, bulbar paraly-

sis, and respiratory arrest may occur. The neurotoxic effects

of these venoms are severe and in some cases irreversible.

The signs and symptoms of envenomation can be delayed for

more than 12 hours and often occur precipitously.

Clinical Features

A. Signs and Symptoms—The symptoms in each individ-

ual case of snakebite vary depending on the degree of enven-

omation. It is estimated that approximately 3% of

snakebites are “dry,” with no evidence of venom injection.

In the case of crotalid bites, the degree of envenomation can

be estimated by the presence and progression of signs and

symptoms. The bites of elapid snakes usually cause minimal

early symptoms—it is only after 1–12 hours that severe

systemic symptoms suddenly appear.

Minimal envenomation is characterized by the presence

of local findings with slow progression and the absence of

systemic signs and symptoms. In the case of severe enveno-

mation, local findings will progress rapidly, and systemic

complications appear early and are particularly severe.

B. Laboratory Findings—Determination of coagulation

parameters helps to evaluate the degree of envenomation in cro-

talid bites. Prothrombin time, partial thromboplastin time,

platelet count, fibrinogen levels, and fibrin degradation prod-

ucts should be determined initially and repeated at regular

intervals to estimate the severity and monitor the progression of

coagulopathy. Serial red blood cell counts should be obtained to

evaluate for the development of hemoconcentration caused by

third spacing of fluid or to detect anemia owing to bleeding or

hemolysis. Urinary myoglobin indicates myonecrosis.

Laboratory data should be obtained on admission, again after

the administration of antivenin, and then every 4 hours until

the data have returned to near-normal levels.

Differential Diagnosis

Identification of the type of snake is necessary to secure the

appropriate antivenin. In cases where the snake has not been

identified, the diagnosis of venomous snakebite often can be



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796

made by examination of the fang marks. Crotalid bites are char-

acterized by two such marks. Remember that elapid bites may

not result in local signs or symptoms despite envenomation.

Treatment

A. Resuscitation—The adequacy of the airway and ventila-

tion should be verified. The primary survey and resuscitation

should follow standard protocols available from the

American College of Surgeons Advanced Trauma Life

Support Course. The airway should be secured promptly in

patients with envenomation to the head or neck. Subsequent

swelling could make endotracheal intubation difficult or

impossible. Hypotension is best treated with rapid crystal-

loid infusion. Fluid resuscitation should be aggressive to pre-

serve organ function. Prophylactic antibiotics are not

recommended.

B. Antivenin—In the patient with major systemic signs and

symptoms owing to severe envenomation, antivenin should

be administered as quickly as possible. Antivenin is recom-

mended for moderate to severe envenomation and for any

envenomation with symptoms of progression—particularly

worsening local injury, progressive coagulopathy, and hemol-

ysis. A skin test is performed with the antivenin prior to

administration in an attempt to predict the likelihood of an

allergic reaction. The test is performed by intradermal injec-

tion of 0.2 mL of antivenin diluted 1:10 with normal saline.

Erythema and a wheal reaction within 30 minutes is a posi-

tive reaction indicating the need for treatment. Antivenin

should be given only by slow intravenous infusion. The use

of antivenin should be considered early because it may have

to be obtained from a distance. The time required to prepare

the antivenin will result in an additional delay. Patients may

require additional doses of antivenin if their symptoms

progress after the initial administration.

Moderate to severe antivenin reactions occur in 15–20%

of patients who receive antivenin. Mild reactions can be

treated with intravenous diphenhydramine and epinephrine;

severe reactions require increased doses.

In cases of severe envenomation, further antivenin ther-

apy should be strongly considered after treatment of a reac-

tion. In less severe cases, antivenin should be withheld if

possible after a reaction because there have been cases of

death owing to anaphylaxis. Antivenin information can be

obtained from local poison control centers or from a

national service by calling 1-800-222-1222.

Exotic envenomations may occur occasionally in the United

States from foreign snakes or lizards kept in zoos or private col-

lections. The principles of management are the same: support-

ive care and administration of appropriate antivenin. Most

exotic antivenins are available at the institutions that maintain

the snakes. The availability of these antivenins also can be

determined through the Antivenin Index.

C. Local Treatment—Local therapy consists of elevation and

immobilization of the affected area until swelling recedes.

Extremities should be observed for the development of

compartment syndrome. If muscle compartments become

firm, or if pain increases, the compartment pressure should

be measured. In some cases, fasciotomy may be required to

prevent ischemic necrosis. Cruciate incisions should not be

performed in an attempt to extract venom.

D. Tetanus Prophylaxis—Tetanus prophylaxis should be

administered if the patient’s immunization status is not cur-

rent or is unknown.

Current Controversies and Unresolved Issues

Immediate excision of the bite down to fascia and including

damaged fascia and muscle has been advocated to reduce the

incidence of local necrosis and to reduce systemic symptoms.

This therapy can be effective only in cases of recent enveno-

mation and in the absence of local diffusion of venom or sys-

temic symptoms. Surgical excision of the envenomation site

cannot be recommended for a number of reasons: Most vic-

tims of snakebite do not reach medical care for several hours

and are therefore beyond the point where local excision

would be expected to have any benefit. In addition, wide

local excision can increase morbidity in cases of minimal

envenomation without offering any benefit.

A polyvalent antivenin, CroTAb, has been approved for

clinical use. This antivenin is produced by immunizing sheep

with venom from the eastern and western diamondback rat-

tlesnakes, the Mojave rattlesnake, and the eastern cottonmouth.

In a randomized trial in the United States, CroTAb was demon-

strated to effectively terminate venom effects. In another study,

CroTAb was successful in immediately and completely revers-

ing neurotoxicity resulting from Mojave rattlesnake envenoma-

tion. Conventional polyvalent antivenin is often ineffective in

the treatment of venom-induced neurotoxicity.

2. Spider & Scorpion Bites

ESSENTIALS OF DIAGNOSIS

Black widow spider:



Numbing pain at the site of the bite.



Muscle cramps and low back pain.



Severe abdominal pain.



Respiratory insufficiency.



Cardiac conduction abnormalities.

Brown recluse spider:



Pain beginning 1–4 hours after bite.



Erythema, central pustule, bull’s-eye lesion.



Fever, malaise, arthralgias, rash, hemolysis.

Scorpions:



Pain with little erythema or swelling.



Generalized reactions within 1 hour.