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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

Chapter 208: Cold Injuries T. Paddock Michael

INTRODUCTION

The occurrence of cold-related injuries depends on the degree of cold exposure, as well as environmentaland individual factors. Frostbite is the prototypical freezing injury and is seen when ambient temperaturesare well below freezing. Nonfreezing cold injuries occur as a result of exposure to wet conditions whentemperatures are above freezing. The most common nonfreezing cold injuries are trench foot and chilblains.Although frostbite may result in permanent tissue damage, nonfreezing cold injuries are characterized byusually mild but uncomfortable inflammatory lesions of the skin. This chapter describes the occurrence, riskfactors, treatment, and prevention of the nonfreezing cold injuries—trench foot and immersion foot,chilblains or pernio, panniculitis, and cold urticaria—and the freezing injury—frostbite.

NONFREEZING COLD INJURIES

TRENCH FOOT

Trench foot and its more severe variant, immersion foot, are rare conditions in civilians but can be asignificant problem in military operations. The pathophysiology of trench foot is multifactorial but involvesdirect injury to so� tissue sustained from prolonged cooling, accelerated by wet conditions. The peripheralnerves seem to be the most sensitive to this form of injury.

Early symptoms progress from tingling to numbness of the a�ected tissues. On initial examination, the foot ispale, mottled, anesthetic, pulseless, and immobile, with no immediate change a�er rewarming. A hyperemicphase begins within hours a�er rewarming and is associated with severe burning pain and reappearance ofproximal sensation. As perfusion returns to the foot over 2 to 3 days, edema and possibly bullae form, andhyperemia may worsen. Anesthesia frequently persists for weeks and may be permanent. In more severecases, tissue sloughing and gangrene may develop. Hyperhidrosis and cold sensitivity are common latefeatures and may persist for months to years. Severe cases may be associated with prolonged convalescence

and permanent disability.1

Treatment is supportive, but vasodilator drugs may be tried. Oral prostaglandins can increase skin

temperatures, which suggests improved circulation.2 Feet should be kept clean, warm, dryly bandaged,elevated, and closely monitored for early signs of infection. Prophylaxis for trench foot includes keepingLoading [Contrib]/a11y/accessibility-menu.js

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warm, ensuring good boot fit, changing out of wet socks several times a day, never sleeping in wet socks andboots, and, once early symptoms are identified, maximizing e�orts to warm, dry, and elevate the feet.

CHILBLAINS OR PERNIO

Chilblains, or pernio, are characterized by mild but uncomfortable inflammatory lesions of the skin causedby long-term intermittent exposure to damp, nonfreezing ambient temperatures. Symptoms are precipitated

by acute exposure to cold.3 The most common areas a�ected are the feet (toes), hands, ears, and lower legs.Chilblains are primarily a disease of women and children, and although rare in the United States, the disease

is common in the United Kingdom and other countries with a cold or temperate, damp climate.3 In addition,young females with Raynaud's phenomenon and other immunologic abnormalities such as lupuserythematosus, as well as those in households with inadequate heating and lack of warm clothing, are at

greatest risk. Some studies suggest that a low body mass index may be associated with increased risk.3,4

Early symptoms progress from tingling to numbness of the a�ected tissues. The cutaneous manifestations,which appear up to 12 to 24 hours a�er acute exposure, include localized edema, erythema, cyanosis,plaques, nodules, and, in rare cases, ulcerations, vesicles, and bullae. Patients may complain of pruritus andburning paresthesias. Rewarming may result in the formation of tender blue nodules, which may persist forseveral days.

Management is supportive. The a�ected skin should be rewarmed, gently bandaged, and elevated. SomeEuropean studies support the use of nifedipine, 20 milligrams PO three times daily; pentoxifylline, 400milligrams PO three times daily; or an analog of prostaglandin E1, limaprost, 20 micrograms PO three times

daily, as both prophylactic and therapeutic treatment for local cold injury.2,5 Topical corticosteroids (0.1%

triamcinolone cream) are also e�ective.6

PANNICULITIS

Panniculitis is characterized by mild degrees of necrosis of the subcutaneous fat tissue that develops duringprolonged exposure to temperatures just above freezing. It is observed in children (e.g., "popsiclepanniculitis" of the cheeks) and on the thighs and buttocks of young women involved in equestrian

activities.7 During resolution of the mild inflammation, adipose fibrosis may result in cosmetic defects, suchas unevenness of the skin. There is no e�ective treatment for the injury.

COLD URTICARIA

Cold urticaria is a distinctive example of hypersensitivity to cold air or water, which in rare cases may lead to

fatal anaphylaxis.8 Most cases are idiopathic,9 but they can also be associated with increased a�inity of

immunoglobulin E to mast cells and viral infections.9 The diagnosis can be confirmed with the cold water testduring follow-up. Young adults and children and those with atopy or other forms of inducible urticaria are

most commonly a�ected.8,10Loading [Contrib]/a11y/accessibility-menu.js

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Cold urticaria is treated similarly to urticarial lesions from other causes. Antihistamines (H1) are

recommended for acute cases, although higher than usual dosing may be required.11 Other potential

therapies include leukotriene receptor antagonists (zafirlukast, montelukast)12,13 and topical capsaicin. Forpersistent cold urticaria, ketotifen or doxantrazole may be tried, but oral preparations of these mast cellstabilizers are not available in the United States. Prescribe epinephrine autoinjectors for patients with ahistory of cold-induced anaphylaxis.

FREEZING INJURIES

EPIDEMIOLOGY

Groups at high risk for frostbite include military personnel, winter sports enthusiasts, outdoor workers, theelderly, the homeless, people who abuse drugs or alcohol, and those with psychiatric disorders. Individualattributes, such as anthropometry, physiology, behavior, and general health, a�ect an individual's likelihood

of developing cold-related injuries14,15 (Table 208-1).

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TABLE 208-1

Factors Influencing the Likelihood of Frostbite

Environmental

Temperature

Wind

Wetness

Contact with cold objects or liquids (e.g., metals, petroleum, oil, lubricants)

Duration of cold exposure

Geographical area

Hypoxia

Altitude

Physical/Anthropometric Characteristics

Age

Gender

Race

Behavioral

Cold acclimatization

Alcohol use

Fatigue

Dehydration

Smoking

Use of protective ointments

Inappropriate or wet clothing

Constrictive clothing (e.g., tight boots)

Prolonged stationary posture

Health-Related/Physiologic

Raynaud's phenomenon

Vibration-induced white finger

Cold-induced vasodilation reactivity

Other peripheral vascular diseases

Diabetes

Peripheral neuropathies

Certain medications (e.g., vasoconstrictive drugs)

Previous cold injury

Psychiatric disorders or altered mental status

The areas most commonly a�ected by frostbite are the head (31% to 39.1% of cases), hands (20% to 27.9%),

and feet (15% to 24.9%).16-18 Studies vary regarding which of these sites is most commonly a�ected, withLoading [Contrib]/a11y/accessibility-menu.js

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Notes: Study population = 5839. Some persons had multiple locations and degrees of frostbite.

military personnel reporting higher incidences of foot and hand involvement than civilians.18 Although mostcases of frostbite are mild (frostnip), 12% of cases are more severe (Table 208-2).

TABLE 208-2

Body Parts A�ected by Frostbite (Lifetime Cumulative Incidence)

Degree of FrostbiteNumber of Frostbite Episodes

All Head Hands Feet

All frostbite cases 2555 (44%) 1668 (31%) 1154 (20%) 810 (15%)

First degree 2333 (41%) 1462 (28%) 1064 (19%) 738 (14%)

Higher than first degree, deep 671 (12%) 459 (9%) 213 (4%) 174 (3%)

RISK FACTORS FOR FROSTBITE

Age and Gender

Both age and gender influence the incidence of frostbite. Among Finnish teens, twice as many teenage boysas girls report having had frostbite of at least blister grade during the previous year (4.1% of boys and 2.4% of

girls).19 Young men entering the military service report a cumulative lifetime incidence of 44%.16 Although

frostbite injuries occur more frequently in men as they age, the same is not true of women.19 In general, the

occurrence of frostbite is higher in men than in women,19,20 which is possibly related to di�erentoccupational and leisure time activity patterns. The smaller size of women and their larger surface area–to–

mass ratio increase the cooling rate, which makes women more susceptible to cooling and cold injuries.15,21

Temperature and Windchill

The incidence of frostbite among civilians is governed by latitude of residence, the annual number of days on

which the ambient temperature is below –15°C (5°F), and the length of daily cold exposure.19 In the UnitedStates, the majority of occupational outdoor cold injuries occur during the few coldest days of winter. Windstrongly increases the injury rate. Rates of injury begin to increase when temperatures fall below –12°C

(10.4°F) and wind speeds exceed 4.5 m/s (10 mph).22 Wind markedly increases the cooling rate by increasingconvective heat loss and reducing the insulation value of clothing, thus increasing the risk of frostbite. In

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addition, the colder temperatures at high altitudes, combined with high wind speeds, increase the risk of

frostbite. Frostbite risk is clearly increased above 5182 m (17,000 �).23,24

The National Weather Service windchill temperature index provides the relative risk for frostbite andpredicted time for freezing risk at given air temperatures and wind speeds. The risk of frostbite is <5% whenthe ambient temperature is above –15°C (5°F), but increased surveillance is warranted when the windchill

temperature falls below –27°C (–16.6°F).15

Frostbite most o�en occurs at environmental temperatures below –20°C (–4°F). Exposure times for injuryvary from hours to several days depending on magnitude of exposure, degree of protective clothing, andphysical activity level.

Skin temperature is <0°C (<32°F) when frostbite occurs. Of note, the risk of finger frostbite increases linearly

from 5% to 95% when temperature at the skin surface decreases from –4.8°C to –7.8°C (23.4°F to 18.0°F).25 Inaddition to ambient temperature and wind, merely touching cold materials (e.g., metal) is a risk factor forfrostbite. Contact cooling is dependent on the surface temperature, type of material, duration of contact, andseveral individual factors. Frostbite can develop within 2 to 3 seconds when metal surfaces that are at or

below –15°C (5°F) are touched.26 Touching surfaces at ambient temperatures of <0°C (<32°F) with bare handsis not recommended. Other factors that increase heat loss and cooling rate and raise the risk of frostbite arewetting of the skin and contact with supercooled liquids (petroleum, oil).

Behavioral and Physiologic Risk Factors for Cold Injuries

Multiple behavioral factors influence the risk of cold-related injuries. Alcohol consumption and smoking

increase the occurrence of frostbite.19,23 Inappropriate clothing (e.g., lack of gloves, headgear, or scarf, orwet clothes), constrictive clothing, and prolonged stationary posture increase the incidence of both freezingand nonfreezing injuries. Interestingly, the use of protective ointments is associated with an increased risk of

frostbite on the head and face.17

Among military personnel, lower level of education or training and lower military rank, as well as situationalmisjudgments, accidental situations, fatigue, and insu�icient nutrition, are all associated with a higher

incidence of frostbite.17 U.S. military studies suggest that black soldiers and those from warmer climatic

regions are more susceptible to frostbite.18

Certain disease states, such as peripheral vascular disease, atherosclerosis, arteritis, Raynaud's disease,vibration-induced white finger, hypovolemia, diabetes, vascular injury secondary to trauma or infection, and

previous cold-related injuries, may predispose to cold-related injury.16,17,23 In addition, medications that

a�ect the circulation, such as vasoconstrictors, may increase the risk of frostbite14,19 (Table 208-1).

PATHOPHYSIOLOGYLoading [Contrib]/a11y/accessibility-menu.js

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It is generally agreed that freezing alone is usually not su�icient to cause tissue death, and o�en theconsequences of thawing contribute markedly to the degree of injury. The depth of tissue freezing dependson the temperature, the duration of exposure, and the velocity of freezing.

Endothelial damage, beginning at the point of thaw, is the likely critical event in frostbite. Immediately a�erfreezing and thawing, an arachidonic acid cascade forms and promotes vasoconstriction, plateletaggregation, leukocyte sludging, and erythrostasis, which results in venule and arterial thrombosis and

subsequent ischemia, necrosis, and dry gangrene.27 The necrosis of tissue following frostbite either is due to

cellular injury or is secondary to a vascular lesion.28

Frostbite injury can be divided into three zones. The zone of coagulation is the most severe and is usuallydistal, and the damage is irreversible. The zone of hyperemia is the most superficial, is typically proximal, hasthe least cellular damage, and generally recovers without treatment in <10 days. The zone of stasis is themiddle ground and is characterized by severe, but possibly reversible, cell damage. It is this middle zone forwhich treatment may have benefit if the circulation in the frozen area can be restored.

Tissue susceptibility to frostbite varies. The least to most sensitive tissues are, in order, cartilage, ligament,blood vessel, cutis, epidermis, bone, muscle, nerve, and bone marrow.

CLINICAL FEATURES AND DIAGNOSIS

Frostbite injuries are frequently classified by the depth of injury and amount of tissue damage based onappearance a�er rewarming (Table 208-3). Visual determination of tissue viability is di�icult during the firstfew weeks a�er the injury, and viable tissue can o�en be identified only a�er gangrenous tissue hasdemarcated and sloughed.

TABLE 208-3

Classification of Frostbite Injuries

First degree Numbness, central pallor with surrounding erythema and edema, desquamation, dysesthesia

Second

degree

Blisters of the skin with surrounding edema and erythema

Third

degree

Tissue loss involving the entire thickness of the skin; hemorrhagic blisters

Fourth

degree

Tissue loss involving the entire thickness of the part, including deep structures, resulting in

the loss of the part

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First-degree injury (frostnip) is characterized by partial skin freezing, erythema, mild edema, lack of blisters,and occasional skin desquamation several days later. The patient may complain of stinging and burning,followed by throbbing. Prognosis is excellent. Second-degree injury is characterized by full-thickness skinfreezing, formation of substantial edema over 3 to 4 hours, erythema, and formation of clear blisters filledwith fluid rich in thromboxane and prostaglandins (Figure 208-1). The blisters form within 6 to 24 hours,extend to the end of the digit, and usually desquamate and form hard black eschars over several days. Thepatient complains of numbness, followed later by aching and throbbing. Prognosis is good. Third-degreeinjury is characterized by damage that extends into the subdermal plexus. Hemorrhagic blisters form and areassociated with skin necrosis and a blue-gray discoloration of the skin (Figure 208-2). The patient maycomplain that the involved extremity feels like a "block of wood," which is followed later by burning,throbbing, and shooting pains. Prognosis is o�en poor. Fourth-degree injury is characterized by extensioninto subcutaneous tissues, muscle, bone, and tendon. There is little edema. The skin is mottled, withnonblanching cyanosis, and eventually forms a deep, dry, black, mummified eschar. Vesicles o�en presentlate, if at all, and may be small, bloody blebs that do not extend to the digit tips. The patient may complain ofa deep, aching joint pain. Prognosis is extremely poor (Figures 208-3 and 208-4).

FIGURE 208-1.

Second-degree frostbite in the hand with blisters. [Photo contributed by Scott Sherman, MD.]

FIGURE 208-2.

Second- and third-degree frostbite in the hand with blisters. [Photo contributed by Edward Lew, MD.]

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FIGURE 208-3.

Third- and fourth-degree frostbite of bilateral feet. [Photo contributed by Edward Lew, MD.]

FIGURE 208-4.

A. Fourth-degree frostbite 1 month a�er injury. Note the clear demarcation line in the fingers. B. The samehands 2 months later a�er surgical treatment.

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DIAGNOSIS

Frostbite may occur anywhere on the skin but is generally limited to the distal part of the extremities, face,nose, and ears. The injured area looks pale and waxy and feels hard and cold. Patients frequently complain ofstinging and numbness.

Because it is initially di�icult to estimate the depth of the cold injury, early injuries are best classified simplyas either superficial or deep. Prognostic considerations of ultimate tissue loss should take into accountduration of exposure, environmental conditions (temperature, wind, and precipitation), type of clothingworn, level of physical activity, possible contact with metal or moisture, and associated use of recreationaldrugs, alcohol, or tobacco in addition to physical findings. Patients with frostbite may have concomitant

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cold-related problems such as hypothermia and dehydration, and patients with hypothermia may also havefrostbite.

Although some chemical liquids and burn injuries may cause blister formation, a history of cold exposuredi�erentiates chemically induced blisters from cold-induced injuries.

The diagnosis of frostbite is clinical. No specific laboratory tests are indicated when treating patients withfrostbite, and specific laboratory evaluation should be guided by the clinical situation including associatedtrauma or medical illness. Early imaging is rarely helpful, either for diagnostic or prognostic purposes,

although the use of technetium-99 scintigraphy may have prognostic value outside of the ED setting.29

TREATMENT

Prehospital Care

Initial field management of frostbite includes prevention of further cold injury, hypothermia, anddehydration. Remove wet and constrictive clothing, cover with dry clothing, and protect against wind. In mildcases, and if the patient is conscious, warm drinks can be administered. Do not heat the frozen area, because

dry heat may cause further injury. Do not attempt rewarming until the risk of refreezing is eliminated.30,31

Refreezing will cause even more severe damage and is an important concern. Provide analgesia, because therewarming process is very painful. Immobilize and elevate frozen extremities, and handle gently. Do notambulate on edematous and blistered feet. Home remedies such as rubbing the a�ected area or rubbing

snow on frostbitten tissue increase tissue damage.30,31 Locally applied creams should not be used in thefield.

ED Management

Rapid rewarming is the first definitive step of frostbite therapy and should be initiated as soon as

possible.30,31 Place the injured extremity in gently circulating water heated to a temperature of 37°C to 39°C(98.6°F to 102.2°F), for approximately 20 to 30 minutes, until the distal extremity is pliable and

erythematous.30,31 Frostbitten faces can be thawed using moistened compresses soaked in warm water.Some patients may tolerate immersion of the ears in a bowl or pool of warmed water. Anticipate severe painduring rewarming and treat with parenteral opiates.

Local care is directed toward tissue preservation and infection prevention. Management of clear blisters andthe use of prophylactic antibiotics are somewhat controversial. The blister fluid is rich in destructivethromboxane and prostaglandins. Although removal theoretically limits damage from these chemicals andenables access to the underlying tissue for topical therapy, not all experts agree that removal is indicated.Hemorrhagic blisters should not be debrided, because this o�en results in tissue desiccation and worseoutcome. However, there is some controversy as to whether aspiration is helpful. Both blister types shouldbe treated with topical aloe vera cream every 6 hours, which helps to combat the arachidonic acidLoading [Contrib]/a11y/accessibility-menu.js

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cascade.30,31 A�ected digits should be separated with cotton and wrapped with sterile, dry gauze. Othera�ected areas should be dressed in bulky, loose-fitting dry gauze dressings to allow room for the expectedsubsequent edema. Elevation of the involved extremities helps decrease edema and pain.

Tetanus immunization status should be assessed and appropriate vaccination administered if needed,because frostbite is a tetanus-prone wound (see chapter 156, "Tetanus").

Because microvascular thrombosis plays a role in tissue injury, thrombolysis has been advocated by some

for use in cases at risk for proximal or multiple digit amputations32,33 and, when given a�er rapid rewarming,

appears to reduce digit amputations.30,34-36 The evidence in support of IV or intra-arterial tissueplasminogen activator is limited to retrospective studies, and bleeding risks must be weighed againstpotential benefit.

The role of prophylactic antibiotics is unclear. The edema that is present on the first several days a�er injurydoes appear to predispose to infection. Staphylococcus aureus, Staphylococcus epidermidis, and β-hemolytic streptococci account for nearly half of infections, but anaerobes, Pseudomonas, and Enterococcusare important pathogens as well. Therapy with penicillin G, 500,000 units IV every 6 hours for 48 to 72 hours,is recommended in several successful protocols and seems to be beneficial. However, infection prophylaxisusing topical bacitracin may be as good as or better than IV penicillin. The use of silver sulfadiazine creamalso has been advocated by some, but it has not been shown to be consistently beneficial. One disadvantageof using topical antibiotics is that they complicate the concurrent use of aloe vera cream.

Several agents besides aloe vera cream have been recommended to battle the arachidonic acid cascade andthereby limit tissue damage. The most commonly advocated oral medication is ibuprofen, 12milligrams/kg/d PO in divided doses. Animal studies suggest possible future roles for oral methimazole (athromboxane synthetase inhibitor) and topical 1% methylprednisolone acetate (a phospholipase A2inhibitor) in preventing the formation of arachidonic acid.

Another controversial area is the use of sympathetic blockade with either intra-arterial reserpine or surgicalsympathectomy to relieve vasospasm and edema. There is no role for early sympathectomy. Prolongedsympathetic blockade using a long-acting anesthetic drug (bupivacaine) may improve blood flow to thehand, relieve pain, and speed recovery. Continuous epidural anesthesia may relieve peripheral vasospasmand perhaps prevent retrograde arterial and venous thrombosis.

Heparin and hyperbaric oxygen therapy appear to be of little value, although case reports of improvement in

isolated cases have been published.37,38 IV low-molecular-weight dextran has theoretical benefits, but dose

and e�ectiveness have not been validated.39

Early surgical intervention is not indicated in the management of frostbite. Premature surgery has been animportant contributor to unnecessary tissue loss and poor results in the past. This is due primarily to theinability to assess the depth of frostbite at early stages and the fact that the blackened, mummified carapace

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protects the underlying regenerating tissue. Limited early escharotomy may be indicated if the eschar ispreventing adequate range of motion or circulation. Fasciotomy is rarely, if ever, indicated.

Table 208-4 presents the core treatment of frostbite.

TABLE 208-4

Treatment of Frostbite

Core Treatment

1. Immersion in or application of water at 37°C to 39°C (98.6°F to 102.2°F) until a�ected area is pliable and

erythematous; do not begin rewarming until risk of refreezing is eliminated

2. Parenteral narcotics for pain management

3. Topical aloe vera cream every 6 h

4. No blister or so� tissue debridement acutely

5. Meticulous local care

6. Tetanus immunization

7. Ibuprofen, 12 milligrams/kg/d PO, in divided doses

Optional Treatment

1. Topical bacitracin ointment for infection prophylaxis

2. Penicillin G, 500,000 units IV every 6 h, for prophylaxis for susceptible organisms

3. Topical silver sulfadiazine cream for prophylaxis (do not use on face)

SEQUELAE

Up to 65% of persons with frostbite injuries experience sequelae from their injuries.1 Sequelae may be seenin patients with mild injuries but are generally more intense with more severe frostbite. The most typicalsequelae are hypersensitivity to cold, pain, and ongoing numbness. Neuropathies have also been described.The clinical and functional limitations associated with late sequelae are dependent on the type and severityof the frostbite injury and the related anatomic deformities and amputations.

DISPOSITION AND FOLLOW-UP

Because it is di�icult to determine the extent of frostbite on initial examination, it is best to be conservativewhen contemplating admission. Consider social and medical issues. The homeless or elderly, especiallywhen unable to care for themselves adequately, should never be discharged into subfreezing temperatures.If the frostbite is extensive and the hospital and sta� are not equipped to treat injury of that degree ofseverity, consider transfer to a tertiary hospital a�er initial rewarming and treatment.

Patients with only superficial local frostbite may be discharged home if social circumstances allow. Patientswith deeper frostbite injuries should be hospitalized. At discharge from the ED, patients must be provided

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1. 

2. 

3. 

with su�icient guidelines for self-care and clear instructions for close short-term and long-term follow-up,preferably with local burn center or plastic surgery providers. They must also be instructed to contact theirdoctor at an early stage if problems or concerns arise. Patients who are discharged from the ED should betreated with topical aloe vera cream and oral ibuprofen and encouraged not to smoke or drink alcohol. Table208-5 lists prevention strategies.

TABLE 208-5

Cold Injury Prevention Strategy

Risk Assessment

Assessment of environmental conditions

Assessment of expected duration of exposure and physical activity level

Risk Management

Raising of awareness

Identification of susceptible population groups, education to recognize personal warning signals of adverse

cooling, provision of training and information, distribution of learning and guidance materials

Organizational Preventive Measures

Advance planning; appropriate scheduling of activities; assessment of physical activity level; provision of

facilities for warming; establishment of mandatory clothing changes, breaks, etc.

Technical Preventive Measures

Attention to shelters, tools, external heating, work areas, slippery surfaces, lighting, etc.

Protective Clothing

Whole-body protection, hand and footwear, head protection, face and respiratory protection, use of personal

protective equipment together with cold protective clothing

Health Care

Individual recommendations based on special needs

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