Cold Injuries

Updated: Apr 15, 2021
  • Author: Blair Peters, MD; Chief Editor: Deepak Narayan, MD, FRCS  more...
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Practice Essentials

There are several key take-home points from this article with regard to cold injuries:

  • Patient education is critical and prevention is best if at all possible
  • The most imminent threat to life in cold injuries is systemic hypothermia; this must not be missed
  • When hypothermia is identified, treatment should be instituted immediately with both passive and active rewarming measures, as indicated [1]
  • Peripheral cold injury occurs on a spectrum from frost nip to varying depths of frostbite [2, 3]
  • Once cold injury is identified and the affected parts rewarmed, it is vital to avoid refreezing; if refreezing occurs, the subsequent tissue damage will be catastrophic
  • Simple management measures include rewarming, analgesia, blister débridement, the use of nonsteroidal anti-inflammatory drugs (NSAIDs), and aloe vera application
  • It is difficult to predict the depth and severity of frostbite injury in the acute setting; it is best to allow the tissue to slowly demarcate over time (often 60-90 days) prior to the patient undergoing any form of surgical débridement
  • Newer techniques for the attempted avoidance of amputation (such as the use of tissue plasminogen activator [tPA]) are being investigated and may have a role in the future routine care of these injuries


Exposure to cold can produce a spectrum of injuries resulting from the human body's inability to adapt to low temperatures. [4] These injuries can be divided into localized injury to a body part or parts (peripheral cold injuries), systemic injury due to generalized cooling of the entire body (systemic hypothermia), or a combination of both. The frequency of cold injuries varies according to geographic region, with more cases typically occurring in areas with cooler climates. Within the general population, specific subgroups at higher risk of cold injury, either because they are at risk of prolonged cold exposure or because they have an inability to compensate for decreased environmental temperature. Examples would include the homeless, military personnel, patients with psychiatric illness, or the young or old (who may not be able to remove themselves from a cold environment). Patients with peripheral vascular disease or diabetic neuropathy who are unable to either feel or tolerate decreased temperatures are also at higher risk.


Systemic Hypothermia

If a patient presents with severe frostbite, the obvious damage to the involved areas, especially the extremities, can be quite distracting. Although it is important for these injuries to be addressed in a timely manner, the physician must never forget that the most imminent threat to life and limb is systemic hypothermia. This must be treated and corrected prior to focusing on peripheral cold injury.

Body temperature may fall as a result of heat loss by radiation, evaporation, conduction, and/or convection. [5] Radiation causes 55-65% of the body's heat loss. Evaporation occurs via the skin and airway and accounts for 30% of the heat loss (this is often referred to as "insensible loss"). Normally, in a dry environment, only 15% of the body's heat loss results from conduction. However, the thermal conductivity of water is approximately 30 times that of air, so the body loses heat rapidly when immersed in water or covered in wet clothing, leading to a rapid decline in body temperature. Convection accounts for a minor amount of heat loss, but it becomes more significant in a windy environment. The amount of heat dissipated by any of these mechanisms is proportional to the temperature difference between the body and environment. In simpler terms, the body will lose a greater amount of heat, and at a more rapid pace, if exposed to an environment that is not just cold, but wet and/or windy as well.

Opposing the loss of body heat are the mechanisms of heat conservation and gain. In general, a thermostat in the preoptic region of the hypothalamus controls these mechanisms. This human thermostat is set to a precise reference temperature, usually very close to 37°C (98.6°F). It responds to thermoregulatory mechanisms, the temperature of blood, and temperature receptors deep within the body and in the skin.

When the preoptic area of the hypothalamus is stimulated by the above mechanisms, various heat conservation and production mechanisms become activated. When the sympathetic nerves are excited, they cause the blood vessels in the skin to markedly constrict. The flow of warm blood from the core to the skin surface is depressed, thereby decreasing the transfer of heat to the body surface and reducing heat loss. This reduction of blood flow in the skin is the prime physiologic regulator of heat loss from the body. The temperature of the skin decreases to approach the temperature of surrounding air, which lowers the temperature gradient and further decreases heat loss. Although this mechanism is protective in terms of safeguarding the more vital organs of the body from hypothermia, it places the extremities at particular risk for peripheral cold injury.

Stimulation of the sympathetic nerves also causes secretion of epinephrine and norepinephrine by the adrenal medullae. These hormones increase the metabolic rate of all cells, thereby enhancing heat production. In addition, impulses from the preoptic hypothalamus activate the primary motor center for shivering, which, in turn, increases the tone of skeletal muscles. The resulting enhancement of muscle metabolism can increase heat production by as much as 500%. Although these mechanisms greatly enhance the human ability to adjust to extreme temperatures, if they are overwhelmed, systemic hypothermia results.


Hypothermia, or systemic cold injury, is a clinical condition in which the core body temperature has decreased to 35°C (95°F) or less. The causes of hypothermia are either primary or secondary. Primary, or accidental, hypothermia occurs in healthy individuals inadequately clothed and exposed to severe cooling. [6] Accidental hypothermia can be divided into immersion and nonimmersion cold exposure. The high thermal conductivity of water leads to the rapid development of immersion hypothermia. Although the rate of heat loss is determined by water temperature, immersion in any water less than 16°C (60.8°F) may lead to hypothermia within minutes. It cannot be stressed enough how much higher a person's risk for hypothermia is when he or she is in a wet environment. Indeed, if a patient is in a wet environment or is damp, the practitioner's index of suspicion for systemic hypothermia must be heightened and proper treatment instituted immediately.

The added danger from moisture is why individuals buried in snow by an avalanche must be extricated from the scene as soon as possible. [7] In fact, rapid extrication is the most important determinant of positive outcome in snow avalanche victims.

In secondary hypothermia, another illness predisposes the individual to accidental hypothermia. The mechanism of secondary hypothermia appears to be an acute failure of thermoregulation; shivering often does not occur in these patients. In many reports, alcohol seems to be a predominant cause of cutaneous vasodilation, loss of shivering, hypothalamic dysfunction, and lack of concern regarding the environment. [8] Other factors that predispose an individual to acute hypothermia include the following:

Clinical presentation

Hypothermia affects multiple organs. [12] Initially, the metabolic rate increases, with tachycardia, tachypnea, increased muscle tone, and peripheral vascular resistance to generate maximal shivering. Once hypothermia sets in, the body loses the ability to cope; with continued hypothermia, the metabolism progressively declines, with bradycardia and hypoventilation and subsequent carbon dioxide retention. The heart rate drops to half its normal rate at 28°C (82.4°F), and ventricular contractility decreases. The risk of ventricular fibrillation increases at temperatures below 28°C (82.4°F). Cerebral metabolism is decreased 6-7% per every 1°C drop in temperature, which results in the declining level of consciousness that is often seen in these patients. Autoregulation of cerebral blood flow is impaired at temperatures below 25°C (77°F). The shivering mechanism of thermoregulation stops at 31°C (87.8°F).

The symptoms of hypothermia vary depending on the severity of the cold injury. In mild hypothermia, clinical symptoms are often vague and include dizziness, fatigue, joint stiffness, nausea, and pruritus. The skin is pale and cool as a result of peripheral vasoconstriction. The patient may exhibit lethargy, flat affect, impaired judgment, and mild confusion progressing to motor incoordination, ataxia, and slurred speech. This should not be mistaken for intoxication, although these two states can coexist.

In severe hypothermia, mental status is further impaired, leading to hallucinations, stupor, and even coma. Atrial and ventricular arrhythmias are common with moderate hypothermia. The Osborn (J) point, an upward deflection at the junction of the QRS complex and the ST segment, can usually be seen on the ECG. The patient may appear clinically dead, with nonpalpable peripheral pulses, fixed and dilated pupils, loss of ocular reflexes, and stiff extensor posturing. Cardiac standstill usually occurs at 20°C (68°F), but one report described a survivor whose temperature was 15°C (60.8°F).


The diagnosis of hypothermia is easy if the history is straightforward (eg, a patient who is a mountaineer who was stranded in cold weather). [13, 14] However, diagnosis may be more difficult in an elderly patient who has been exposed to a cold external environment, an intoxicated patient with an unknown history, or other similar situations. In either case, the rectal temperature should be checked with a low-reading thermometer. The diagnosis of accidental hypothermia has proved elusive, largely because clinical thermometers do not record temperatures below 35°C (95°F). The only inexpensive low-reading thermometer is the Zeal (Zeal Group Ltd; London). Electronic thermometers with digital readouts and remote electric probes are made by several companies. Rectal temperature measurements are influenced by lower body temperature and probe placement. An inaccurate reading may result if the rectal probe was inserted in cold feces or to a depth of less than 15 cm.

Other methods of determining core body temperature include infrared tympanic thermometers, esophageal probes in intubated patients, and bladder thermistors embedded in a urinary catheter. The tympanic probe accurately measures hypothalamic temperature and most rapidly changes to reflect variations in core body temperature. On the basis of temperature measurements, the arbitrary classification of the level of hypothermia is mild (< 34°C [93.2°F]), moderate (28-34°C [82.4-93.2°F]), and severe, with a boundary core temperature of less than 28°C (82.4°F).


Treatment & Management


Prevention of cold injuries is always preferable, and education of persons working or living in cold environments (or those with risk factors for secondary hypothermia) should focus on the modification of risk factors, as well as on the selection and application of appropriate clothing.

Field First Aid and Prehospital Management

The general principles of prehospital management are to (1) prevent further heat loss, (2) rewarm the body core temperature in advance of the shell, and (3) avoid precipitating ventricular fibrillation. The application of these principles depends on the patient's core temperature, the equipment available, and the presence of complicating illnesses or injuries.

In general, the patient should be moved out of the cold environment and out of the wind, provided with warm shelter, and given warmed fluids. Any wet clothing should be removed and replaced with warm, dry articles. It should be noted that rubbing affected parts of the body is not recommended because this potentially can worsen tissue injury.

Mild hypothermia

For a person with mild hypothermia (≥33°C [91°F]) found in a cold environment, the first priority is to search for other injuries in that person and/or other affected individuals, since often these patients have been involved in some form of accident (eg, a motor vehicle accident from which they cannot extricate themselves) that has placed them at risk for hypothermia. Therefore, these cases should be approached with an advanced trauma life support (ATLS) algorithm. While performing an ATLS protocol, duration of patient exposure should be limited in order to avoid further heat loss. The second priority is to increase the patient's core temperature to normal before and during transport to the hospital. The patient should be moved into a tent or other dry shelter for protection from the wind. Wet clothing should be removed by cutting along the seams. Insulation, such as a sleeping bag, should be placed under and over the patient, who should not be allowed to stand or sit and whose head should be covered. A fire should be built or a stove lit. No fluids should be given by mouth. The patient should be transported to the hospital in an ambulance heated to 30°C (86°F). It is important for the transport vehicle to be heated, even if the transport staff is uncomfortably warm.

Severe hypothermia

Severe hypothermia (< 28°C [82.4°F]) should be treated as a life-threatening emergency. Attention should be directed first to the cardiopulmonary system. If the patient is breathing, humidified and warmed vented oxygen (10 L/min) should be administered using a nonrebreathing reservoir mask. If the patient is not breathing, ventilation should be initiated with a bag-valve-mask ventilator or a pocket mask connected to a humidified, heated oxygen delivery system.

The patient should not be hyperventilated because this may induce ventricular fibrillation. If bradycardia and hypotension are evident, do not perform cardiac compressions because this, too, may precipitate ventricular fibrillation. To avoid inappropriate chest compressions, prehospital personnel must examine the patient for a full minute before diagnosing pulselessness. If the patient is pulseless, external cardiac compressions with ventilations should be initiated unless the exterior wall is frozen and not compressible. Cardiopulmonary resuscitation should continue until the patient is evaluated and treated in the hospital.

Always follow the dictum that patients with severe hypothermia are never dead until they are warm and dead. Even with prolonged cardiac arrest, resuscitation is possible and has been reported. Many physicians who are specialists in hypothermia believe that patients with severe hypothermia should not be rewarmed in the field, but, rather, kept in a "metabolic icebox" until in a hospital setting in which physiologic monitoring and advanced life-support equipment are available.

Hospital Treatment

Upon the patient's arrival in the emergency department, the physician must focus on cardiopulmonary function. If the patient is still not breathing, endotracheal intubation should be undertaken immediately to maintain the airway. Frozen skin may require cricothyroidotomy. External cardiac compressions must be continued in pulseless patients with compressible chest walls. A central venous access line should be established to obtain blood for laboratory studies and to administer warmed fluids for volume expansion. A venous cutdown may be necessary because vasoconstriction and hypovolemia may make percutaneous catheterization impossible. Central venous pressure monitoring is useful to determine the results of volume expansion in patients with severe hypothermia and hypovolemic shock.

Baseline laboratory determinations should include a complete blood cell count; levels of blood glucose, electrolyte, phosphorus, creatinine, amylase, lactic dehydrogenase isoenzyme, and creatine kinase isoenzyme; prothrombin time; activated partial thromboplastin time (aPTT); and arterial blood gas values. These laboratory studies should be repeated as indicated. A toxicologic evaluation is recommended for any patient whose history is unknown or who may have ingested a drug or poison. An initial 12-lead ECG should be obtained, after which the patient should have continuous cardiac monitoring. Intensely cold skin may preclude adequate transmission of electrical impulses to the electrocardiographic electrodes. A Foley catheter is introduced into the bladder to monitor urine output and to provide specimens for urinalysis and toxicology screening, including urine myoglobin levels. The Foley catheter can also be used for warm fluid irrigation, to assist in active rewarming.

Treatment of hypothermic patients should include volume expansion, cardiopulmonary support, and rewarming. Blood volume should be expanded using heated crystalloid solutions to maintain blood pressure and coronary perfusion. It cannot be overemphasized how crucial it is that intravenous (IV) fluids be run through a warmer. In adults, 300-500 mL should be administered rapidly, with the subsequent rate of infusion adjusted according to blood pressure. The solution should be warmed to 45°C (111°F) by heat exchangers or blood warmers. Fluid replacement may lead to increased ventricular filling pressures, increased cardiac work, and pulmonary edema. Although fluid resuscitation is important, avoid overresuscitation.

Supplemental oxygen is necessary to prevent hypoxia, reduce the risk of ventricular fibrillation, and treat pulmonary edema. Oxygen delivery to hypothermic patients should be maximized by the use of 100% oxygen during rewarming. Hyperventilation should be avoided because it may trigger ventricular fibrillation. If possible, any oxygen administered should be in the form of warmed, humidified air.

Although severe cardiac arrhythmias in hypothermic patients may represent an immediate threat to life, most rhythm disturbances (eg, sinus bradycardia, atrial fibrillation or flutter) require no therapy and revert spontaneously with rewarming. Indeed, the most important step in treating cardiac arrhythmias in these cases is rewarming the patient. Ventricular fibrillation may be refractory to therapy until the patient is rewarmed to at least 34°C (93.2°F). At core body temperatures below 30°C (86°F), the heart is usually unresponsive to defibrillation, pacemaker stimulation, and cardioactive drugs.

Patients with ventricular fibrillation should receive 1-2 attempts at electrical defibrillation once the temperature is above 28°C (82.4°F). One dose of 10 mg/kg of bretylium (Bretylol) may be given; it is the only antiarrhythmic drug effective at low temperatures. If this is unsuccessful, cardiopulmonary resuscitation should be started or continued with active rewarming until the patient's core body temperature is above 32°C (89.6°F). As the myocardium warms, the rhythm may revert spontaneously or in response to electrical defibrillation.

The hypothermic heart is poorly responsive to the pharmacologic effects of medications (with the exception of bretylium). Excessive medication levels can accumulate as a result of decreased hepatic metabolism and increased protein binding, resulting in toxicity when rewarming occurs. Therefore, nonessential medications should not be given until after rewarming, and rewarming should not be delayed for medication administration. For information on various medication toxicities, see the Medscape Drugs & Diseases Emergency Medicine Toxicology section.

Coagulopathy is an underappreciated cause of morbidity in patients with moderate and profound hypothermia. Hypothermia itself will increase bleeding risk and precipitate coagulopathy. Platelets are sequestered in frostbitten areas and in the lungs, causing thrombocytopenia and failure of platelets to clot. The aPTT becomes prolonged as core temperatures decrease. The combination of a prolonged aPTT and thrombocytopenia produces clinical disseminated intravascular coagulation. The passage of a nasogastric tube through friable nasal passages may produce torrential bleeding; this must be kept in mind when any interventions are performed in a patient who is suffering from systemic hypothermia.

Because a large proportion of hypothermic patients are thiamine-depleted and alcoholic, they should be given thiamine at 100 mg intramuscularly, followed by 50-100 mL of 50% dextrose. Administration of antibiotics, steroids, and thyroid hormones must be considered if secondary hypothermia is thought to play a role. Very cold patients are immunosuppressed, and antibiotics are usually withheld until a definite infection is evident. Hydrocortisone should be administered to patients with a history of adrenal suppression or insufficiency and to hypothermic patients with cachexia and/or generalized weight loss. Levothyroxine (Synthroid) is necessary for patients in a myxedema coma and may be helpful in elderly persons.

A multicenter study of regional care of hypothermia, by Rasmussen et al, reported that greater hypothermic severity positively correlated with worsening dysrhythmia, acute kidney injury, and frostbite risk. The highest mortality was found in patients with mixed primary/secondary hypothermia (39%) and in patients over age 65 years (33%). However, individuals with severe, moderate, and mild hypothermia had similar 30-day mortality rates. [15]


Rewarming Techniques

The two general techniques of rewarming are passive rewarming and active rewarming. [16] The capacity of humans with mild to moderate hypothermia to rewarm spontaneously after removal from the hypothermic condition accounts for the beneficial effects of passive rewarming. Because patients often become hypothermic over a period of days or hours, passive rewarming is physiologically sound. Rapid changes in temperature can affect the cardiovascular status, and these rapid changes are often the cause of complications associated with active rewarming methods. Passive rewarming is a safe and simple method of treating mild hypothermia, and it is frequently the only method available for field management. Passive rewarming and noninvasive methods can also be used for patients with severe hypothermia (< 28°C [91.4°F]) with a stable cardiac rhythm (including sinus bradycardia and atrial fibrillation) and stable vital signs. However, it is not recommended for patients with cardiovascular compromise.

Passive rewarming involves effective insulation of the patient, allowing the patient's spontaneous metabolic heat to rewarm the body. With this technique, the patient is covered with 1-2 blankets and rewarmed at a room temperature of 25-33°C (77-91.4°F). The increase in core temperature varies from 0.5-2°C/h; 24 hours may be required to achieve a normal temperature. If the increase in temperature is less than 0.5°C/h, the presence of a complicating disease, such as hypothyroidism, should be considered. In other words, consideration of secondary hypothermia should be triggered.

Active rewarming involves the internal or external addition of heat to the body. Active is an appropriate term, as active intervention is being made to increase body temperature at a rate that is much faster than could be achieved with passive rewarming alone. Active external rewarming works best for patients with mild or moderate hypothermia because it applies exogenous heat to the surface of the body in the form of warm packs, heating blankets, radiant heat, and warm water immersion. Concern has been raised about the efficacy of actively rewarming from the surface because of inherent physiologic changes that may aggravate the effects of hypothermia on dermal tissues that are poorly perfused because of vasoconstriction.

Active external rewarming may precipitate hypovolemic rewarming shock by decreasing the circulating blood volume secondary to peripheral vasodilation in an already hypovolemic patient. This peripheral vasodilation paradoxically causes central cooling by shunting stagnant, cold blood to the core, thus further chilling the myocardium, depressing contractility, and increasing its vulnerability to ventricular fibrillation. Active external rewarming should therefore be used with caution, and the physician must remember that it places the patient at risk of cardiac compromise.

The safest method of active rewarming of patients with severe hypothermia is internal rewarming that increases the core temperature. Active core rewarming should be used in patients with core temperatures lower than 32°C (90°F), who are hemodynamically unstable, or in whom more conservative rewarming methods have failed. Internal or core rewarming has the advantage of minimizing rewarming shock by warming the central core circulation first, as opposed to the peripheral circulation, which can take place with active external rewarming measures. Heat may be added internally by heated, humidified inhalation; peritoneal dialysis with warmed fluids; mediastinal irrigation (ie, through chest tubes); gastrointestinal tract irrigation; arterial venous shunting including hemodialysis; extracorporeal bypass; or warm irrigation through a Foley catheter inserted into the bladder.

Airway rewarming at 40-45°C (104-113°F) prevents respiratory heat loss and raises body temperature 1-2°C/h. It also provides warm blood to the coronary arteries, with the blood warming through the pulmonary circulation before returning to the left side of the heart and perfusing the coronary arteries. In patients with severe hypothermia, air rewarming should be used as an adjunct to more rapid rewarming methods. This is a simple and reliable way of active rewarming.

Peritoneal lavage with warmed potassium-free dialysate 40-45°C (104-113°F) is more effective, raising the body temperature 2-4°C/h. Irrigation of the stomach or colon with warm fluids produces minimal rewarming because the surface area available for heat exchange is small; also, this may cause mucosal sloughing in the very cold tissues, which can precipitate bleeding, as it must be remembered that hypothermia itself will cause coagulopathy. Arterial venous shunts and hemodialysis warm the blood directly but require cannulas to be inserted into arteriotomies.

Extracorporeal rewarming is the most rapid and efficient method of rewarming and is indicated in patients with cardiac arrest or impending cardiac arrest. Cutdowns may be necessary to place cannulas in the heart, aorta, or femoral vessels. A cardiopulmonary bypass circuit can achieve rewarming of 1-2°C every 3-5 minutes, but it mandates anticoagulation. Cardiopulmonary bypass resuscitation has been successful even after prolonged cardiac arrest unresponsive to other resuscitative and rewarming methods. Contraindications to the use of cardiopulmonary bypass for rewarming are severe brain injury, hyperkalemia (potassium level >7 mEq/L), and clotted or gelled blood in the arteries. This intervention also requires the availability of a perfusionist on call. Not all centers have the capability of performing cardiopulmonary bypass resuscitation, but if available, it can be extremely effective.

Gilbert et al reported the results of resuscitation of a 29-year-old skier who sustained accidental hypothermia after skiing down a waterfall gully. She responded to treatment using an extracorporeal membrane oxygenation (ECMO) machine for 5 days. During that time, several organ dysfunctions developed that required hemodiafiltration and respiratory support, in addition to ECMO. Hemodiafiltration is an extracorporeal renal-replacement technique using a highly permeable membrane in which diffusion and convection are conveniently combined to enhance solute removal in a wide spectrum of molecular weights. Transitory hemorrhagic diathesis, atrophic gastritis, ischemic colitis, and polyneuropathy also occurred. At follow-up, 5 months after the accident, the patient had residual but improving partial pareses of the upper and lower extremities. Her mental function was excellent, and she was gradually returning to work. She also resumed hiking and skiing. This case provides an example of the profound effect that ECMO can have in very severe cases of hypothermia. However, patient selection is critical, and this treatment should not be offered if the case is deemed futile. [17]

ECMO has even been reported to be successful in near drowning associated with deep hypothermia. Thalmann et al described a case of near drowning of a 3-year-old girl who was admitted to the emergency department with a core temperature of 18.4° C. [18] After rewarming on cardiopulmonary bypass and restitution of her circulation, respiratory failure resistant to conventional respiratory therapy prohibited weaning from cardiopulmonary bypass. Consequently, the medical team instituted ECMO. Fifteen hours later, the patient could be weaned from ECMO but required assisted ventilation for 12 days. Twenty months later, no neurologic deficits were in evidence. [18]

A study by Ohbe et al indicated that in patients with accidental hypothermia and no vital signs, the survival rate and neurologic outcomes are better in association with venoarterial ECMO than with conventional cardiopulmonary resuscitation (CPR) alone. Using propensity score-matching analysis, the investigators found that the risk difference in inhospital mortality between patients receiving venoarterial ECMO and those who underwent only conventional CPR was -13%, while the risk difference with regard to “alert consciousness” at discharge was 8.3%. [19]

Cardiopulmonary bypass and ECMO are not available in hospitals without cardiopulmonary bypass capabilities. Therefore, other methods of active rewarming should be instituted at these sites. Winegard reported an instance in which closed thoracic cavity lavage was used successfully in the treatment of severe hypothermia. [20] In Winegard’s patient, closed thoracic cavity lavage was initiated through a 28-mL straight chest tube inserted into the left pleural cavity. Closed thoracic cavity lavage was performed with a saline solution at a temperature of 40°C. This lavage was continued after the patient began to make spontaneous respirations and was successfully defibrillated. The patient was discharged 10 days after admission. Follow-up neurological examination revealed relatively minor neurological sequelae. Two months after the accident, the victim had minor numbness, mostly in his feet. This was considered a cold neuropathy rather than a pressure palsy neuropathy. [20]


Peripheral Cold Injuries

The mechanisms of peripheral cold injuries can be divided into phenomena that affect cells and extracellular fluids (direct effects) and those that disrupt the function of the organized tissue and the integrity of the circulation (indirect effects). [21] Generally, no serious damage is seen until tissue freezing occurs. During frostbite, ice crystals many times the size of individual cells form from the available extracellular compartment, producing intracellular dehydration. The cell content becomes hyperosmolar, and toxic concentrations of electrolytes may cause cell death. [22] Usually, no gross rupture of the cell membrane is evident. A reversal of this process probably occurs during thawing of frozen tissues. After tissue thawing, vasodilation and leakage from capillaries occur, causing tissue edema. This edema can often be quite marked and alarming to practitioners who do not expect this normal response. Alternating freeze-thaw cycles potentiate the vascular injury and lead to ischemic infarction. It is critical that once rewarmed, the affected parts not be reexposed to the cold environment. A second cycle of freezing will lead to catastrophic tissue damage.

The indirect effects of frostbite, a fulminating vascular reaction and stasis, are associated with the release of prostaglandins that have been implicated in progressive dermal ischemia. Both prostaglandin F2 and thromboxane A2 cause platelet aggregation and vasoconstriction. These substances have been found in high quantities in the blisters that form as part of the tissue response to cold injury. Therapy with antiprostaglandin agents and thromboxane inhibitors has been shown in experimental and clinical studies to increase tissue survival. If the patient has no contraindications to the use of NSAIDs, it is recommended that he or she be started on a course of high-dose NSAID therapy when initially seen.

A study by Carlsson et al indicated that the effects of local freezing cold injuries can persist for years. The study involved 15 patients who had sustained such injuries to one or both hands and/or feet during military training. Four months after the injury, it was determined that abnormalities in one or both cold-injured hands with regard to vibrotactile, warmth, and cold perception thresholds were exhibited in 6, 4, and 1 patient, respectively. The same was true for one or both feet in 8, 6, and 4 patients, respectively. In addition, after 4 months, out of 13 patient responses, 10 patients reported feeling pain when their affected hands or feet were exposed to cold; after 4 years, out of 12 responses, 7 patients reported that the problem persisted. Other neurovascular symptoms, including whiteness and cold sensation in the affected digits, also persisted in patients after 4 years. Any practitioner who sees a reasonable amount of frostbite is familiar with this phenomenon; despite healing of the involved areas, there is long-term sequelae including chronic pain and often extreme cold sensitivity. [23]


Peripheral cold injuries occur on a spectrum of severity. The mildest form of peripheral cold injury is frostnip, which tends to occur in apical structures (nose, ears, hands, feet), where blood flow is most variable because of the richly innervated arteriovenous anastomoses. Frostnip most often occurs in skiers exposed to fast-moving, very cold air. Simple warming either by pressure of a warm hand or by placing the hand in the axilla is sufficient treatment. More consequential local cold injuries may be divided into freezing (frostbite) and nonfreezing (chilblains and immersion [trench] foot) injuries. The diagnosis of freezing and nonfreezing injuries can generally be made on the basis of history and clinical manifestations.

Chilblain (perniones)

Chilblain represents a more severe form of cold injury than frostnip and occurs after exposure to nonfreezing temperatures and damp conditions. This condition is characterized by a chronic, recurrent vasculitis manifested by red-to-violaceous, raised lesions in unprotected extremities, such as the hands, feet, and face. Blisters, erosions, or ulcers are sometimes seen. Chilblain commonly affects young and middle-aged women and is associated with a variety of chronic disorders, especially Raynaud phenomenon.

The lesions usually resolve spontaneously in 1-3 weeks, but they may recur in some individuals when exposed to cold triggers. Management involves local heat, gentle massage, and lubricants to keep the skin supple. Nifedipine (Procardia) at 20-60 mg/d may be used to reduce the pain and speed the resolution of the lesions. Once the diagnosis of chilblain has been made, it is important to educate patients to avoid triggers.

Immersion (trench) foot

Immersion foot, or trench foot, a disease of the sympathetic nerves and blood vessels in the feet, is observed in shipwreck survivors or in soldiers whose feet have been wet, but not freezing, for prolonged periods of time. [24] It may occur at ambient temperatures near or slightly above freezing and is usually associated with dependency and immobilization of the lower extremities with constriction of the limb by shoes and clothing. This clinical entity can also be seen in the homeless population during periods of wet, cool weather. Immediate symptoms include numbness and tingling pain with itching, progressing to leg cramps and complete numbness. Initially, the skin is red; later, it becomes progressively pale and mottled and then gray and blue. The soles of the feet are wrinkled and very tender to palpation.

The progression of this cold injury has three stages. The first is a prehyperemic phase, lasting for a few hours to a few days, in which the limb is cold, slightly swollen, discolored, and possibly numb. Major pulses are barely palpable. The second, or hyperemic phase, lasts 2-6 weeks. It is characterized by bounding, pulsatile circulation in a red, swollen foot. The third, or posthyperemic, phase lasts for weeks or months. The limb may be warm, with increased sensitivity to cold. The injury often produces a superficial, moist, liquefaction gangrene quite dissimilar to the dry, mummification gangrene that occurs with severe frostbite.

Management of this injury entails careful washing and air-drying of the feet, gentle rewarming, bed rest, and slight elevation of the extremity. Improvement occurs within 24-48 hours, while the injury completely resolves in 1-2 weeks. Early physical therapy is essential. The patient should be warned that subsequent chilling will preferentially affect the previously injured area. This again cannot be overemphasized. Once injured, the involved area will always be more prone to cold injury than will unaffected areas of the body. Key to prevention of immersion foot injury is keeping the feet dry for at least 8 h/d.


Patients with frostbite frequently present with multisystem injuries (eg, systemic hypothermia, blunt trauma, substance abuse). The health professional must detect these injuries and appropriately triage care according to those that are most life threatening. Often, the occurrence of frostbite is a reflection of a patient's inability to remove himself or herself from a cold environment, frequently because of trauma, associated injury, or intoxication. [25]

Several days after the injury, frostbite can be classified into four degrees of severity. In first-degree frostbite, hyperemia and edema are evident. Second-degree frostbite is characterized by hyperemia and edema, with large, clear blisters that may extend the entire length of the involved limb, digit, or facial feature. The blisters can be quite large and interfere with function, especially if they involve the digits of the hand or the soles of the feet. Third-degree frostbite is characterized by hyperemia, edema, and vesicles filled with hemorrhagic fluid that are usually smaller than those of second-degree frostbite and do not extend to the tip of the involved digit. The hemorrhagic component of the blisters is a sign of underlying deeper tissue injury. Fourth-degree frostbite, the most severe type, involves complete necrosis, with gangrene and loss of the affected part.

The classification of frostbite into four degrees of severity is not favored by clinicians, who find assessing the full extent of tissue injury difficult in the acute setting. A simpler classification divides frostbite injury into two types: superficial and deep. Superficial frostbite (first- and second-degree frostbite) involves the skin and subcutaneous tissues. The skin is cold, waxy white, and nonblanching. The frozen part is anesthetic but becomes painful and flushed with thawing. Edema develops, and clear bullae filled with serous fluid appear within the first 24 hours.

Deep frostbite (third- and fourth-degree frostbite) involves the muscle, tendons, neurovascular structures, and bone, in addition to the skin and subcutaneous tissues. The frozen part is hard, woodlike, and anesthetic. It appears ashen-gray, cyanotic, or mottled and may remain unchanged even after rewarming. Edema develops, but bullae may be absent or delayed. Bullae, if present, are filled with hemorrhagic fluid. Despite these "classic" findings, in reality it can be quite difficult to predict the depth of tissue injury in deep frostbite, especially in the acute setting. Conservative management is key, with the tissues allowed to demarcate over time. It is unwise to débride early and sacrifice tissue that is potentially viable. Allowing time for the tissue to declare also gives the patient time to adjust psychologically to the impending loss of digits. This is a helpful approach in clinical practice and can mitigate some of the psychological stress that amputation imposes.

Initially, as the tissue is freezing, the patient experiences discomfort or pain. This progresses to numbness and loss of sensation. Upon examination, the frozen tissue is white and anesthetic, owing to intense vasoconstriction. Tissues that remain frozen can appear mottled, violaceous, pale yellow, or waxy. Favorable signs include warmth, normal color, and some sensation. Several factors predispose to this cold injury. Clinical experience suggests that frostbite occurs at higher temperatures in patients with preexisting arterial disease. [26] In addition, a physiologic basis seems to exist for the reported susceptibility of black persons to frostbite. Finally, it has been demonstrated repeatedly that a person who previously suffered frostbite is more prone to develop this cold injury in the same body part than an individual with no history of such a cold injury.

Several principles of frostbite treatment are universally accepted. The patient must be removed from the cold environment. Treatment should not be attempted in the field if a hospital is available within a short distance or if a risk exists that the extremity will be refrozen. Once the rewarming process has begun, weight-bearing on the affected part is almost certain to result in additional injury. Rubbing the frostbitten part with snow or exercising it in an attempt to hasten rewarming is absolutely contraindicated. Contrary to popular belief, walking some distance on frostbitten feet can result in tissue fracture. Consequently, this ambulation should be avoided.

Upon arrival at the emergency department, normal body temperature should be restored before treating the local injury. Always assume that the patient has systemic hypothermia until proven otherwise. The preferred initial treatment for frostbite is rapid rewarming in a water bath at a temperature of 39-42°C (102.2-107.6°F). Strict aseptic technique (eg, mask, powder-free gloves) should be used by all personnel during the warming procedure and during subsequent wound treatments. The rewarming bath should be large enough so that the frostbitten part does not rapidly reduce the temperature of the water. The temperature of the bath is monitored carefully as the bath cools. Additional hot water is added to the bath only after the extremity is removed from it. After hot water is added, the bath is stirred and the temperature retested before the extremity is reintroduced.

Rewarming is continued until the frostbitten tissue has a flushed appearance, demonstrating that circulation has been reestablished. This rewarming procedure usually lasts 30-45 minutes. Because rewarming is painful, narcotics are often required. After rewarming, the skin is washed gently to remove any residual dirt. The skin is then carefully dried. Tetanus prophylaxis is indicated with a tetanus vaccine (Td) without thimerosal because frostbite injuries are considered tetanus-prone wounds. [27] A vaccine information statement, which outlines the adverse effects of the vaccine, should be given to the patient or a family member, along with the National Vaccine Information Compensation Program. [28]

Prophylactic antibiotics should not be administered. Antibiotics should only be prescribed in the event of signs and symptoms of infection. It is important to closely follow patients with frostbite and to educate them on the signs of infection to look for.

Heggers et al recommended a therapeutic approach devised to prevent the progressive dermal ischemia of frostbite. [29] The combination of the systemic prostaglandin inhibitor ibuprofen (Motrin) and the topical antithromboxane agent aloe vera was used to inhibit localized thromboxane production, which had been implicated as the cause of dermal ischemia. [29] The prescription of a course of ibuprofen and the application of aloe vera are simple interventions that can easily be applied to cases with no contraindications to their use.

The clear blisters of frostbite are immediately débrided, especially if they are deemed to interfere with function such as hand range of motion, and the aloe vera (Dermaide Aloe) is applied directly to the débrided wound. In contrast, hemorrhagic blisters are left intact and treated with aloe vera. The aloe vera is reapplied to the frostbitten wounds every 6 hours. When the hemorrhagic blisters rupture, the blisters are débrided, facilitating application of the aloe vera to the wound. Unless contraindicated by medical history (eg, aspirin allergy, peptic ulcer disease), ibuprofen (12 mg/kg/d for 1 wk) is administered orally to counteract the deleterious effects of increased thromboxane production. These treatments should reduce the length of hospital stay and the morbidity of patients with frostbite.

The affected part should be protected from trauma and infection, and it should be elevated above the patient's heart to minimize edema. A protective cradle should cover frostbitten lower extremities to prevent trauma. An environmental temperature of 21-26°C (69.8-78.8°F) in the hospital room is usually comfortable for the patient. Tobacco should be avoided because of its vasoconstrictive effect.

In cases of first- or second-degree frostbite of the feet, it usually takes two weeks of rest before the edema has receded and the vesicles and bullae have dried. It is important to keep the involved areas elevated to aid in resolution of tissue edema. Early consultation with occupational and physical therapy practitioners is also important, since these patients are at high risk of developing stiff contractures of involved joints and early range of motion therapy is critical to obtaining good outcomes. Additionally, depending on the areas involved, occupational therapy can be very helpful in terms of instituting the use of splints and walking aids in order to preserve functional independence during the healing and demarcation process. Avoidance of joint stiffness and wound contraction is an essential goal of the rehabilitation program. The intrinsic muscles of the hands are particularly sensitive to frostbite injury; night splinting of the hand in the intrinsic-plus position is recommended.

Severe frostbite can have devastating consequences, including the loss of limbs and digits. One of the mechanisms of cold injury to human tissue is vascular thrombosis. The effect of tissue plasminogen activator and heparin in limb and digit preservation was demonstrated by Twomey et al. [30] Patients with severe frostbite were divided into two groups. A group of six patients was treated with intra-arterial tissue plasminogen activator (tPA) and intravenous heparin. A group of 13 patients was treated with intravenous tPA and intravenous heparin.

Patients eligible for this study included all patients with severe frostbite between January 1, 1989 and February 1, 2003 whose symptoms were not improved by rapid rewarming, who had absent Doppler pulses in distal limb or digits, who did not have perfusion by technetium-99m (99mTc) three-phase bone scan, and who had no contraindications to tPA use. [30] Efficacy was assessed on the basis of predicted digit amputation before therapy, given the clinical and 99mTc scan results versus partial or complete digits removed. Fortunately, no serious complications with intravenous tPA occurred. Two patients with intra-arterial tissue plasminogen activator experienced bleeding complications. On the basis of historical 99mTc scan data, the investigators predicted which digits were at risk for amputation. In their study, 174 digits were at risk in 18 patients, and only 33 were amputated.

In 2007, Bruen et al further confirmed the reduction of the incidence of amputation in frostbite injury with thrombolytic therapy. [31] From 2001-2006, their patients with severe frostbite within 24 hours of injury underwent digital angiography and treatment with intra-arterial tPA if abnormal perfusion was documented. These patients were compared with those treated from 1995-2006 who did not receive tPA. In their study, 32 patients with digital involvement were identified. Seven patients received tPA (6 within 24 h of injury). The incidence of digital amputation in patients who did not receive tPA was 41%. In those patients who received tPA within 24 hours of injury, the incidence of amputation was decreased to 10%. The authors concluded that the use of tPA represented the first clinically significant advancement in the treatment of frostbite in more than 25 years.

It is important to note, however, that in cold injury, digit amputation, in terms of number of digits and level of amputation, is very unpredictable. Therefore, it is possible that the number of at-risk digits in these studies was overpredicted. If a practitioner is at a center where intensive care unit (ICU) monitoring and tPA treatment are available, the patient should be thoroughly apprised of the risks and benefits of tPA therapy. Although tPA use can potentially lead to the amputation of fewer digits, there is a well-documented bleeding risk, which can have catastrophic or even fatal consequences. Therefore, tPA should be reserved for very severe cases in which multiple digits are at risk.

A study by Gonzaga et al indicated that late amputations related to frostbite can be decreased through the use of angiography to detect impaired arterial blood flow and aid in catheter-directed thrombolytic drug therapy. The study included 62 patients (472 digits) revealed by angiography to have frostbite injury and impaired arterial perfusion. The complete digit salvage rate was 68.6% following intraarterial thrombolytic treatment. [32]

The difficulty in determining the depth of tissue destruction has led to a conservative approach to the care of local cold injuries. As a general rule, amputation and surgical débridement should be delayed for 60-90 days unless severe infection with sepsis develops. The natural history of most injuries is one of gradual demarcation of the injured area, followed by dry gangrene or mummification of the area, with later sloughing of necrotic tissue, resulting in a viable, but shortened, extremity beneath the eschar.

Emergency surgery is occasionally required for patients with a frostbitten extremity. Open amputations are indicated in patients with persistent infection with sepsis that is refractory to débridement and antibiotics. Compartment syndrome may be encountered in a frostbitten extremity, which mandates fasciotomy.

The intense vasoconstrictive effects of increased sympathetic tone in cold injuries have attracted attention for many years. The theoretical benefit from sympathetic blockade is the release of vasospasm that may precipitate thrombosis in injured vessels. The vasospastic effects may, therefore, be counteracted by intra-arterial drugs, such as tolazoline, or by surgical sympathectomy. However, a controlled clinical study by Bouwman et al demonstrated no subsequent differences in the natural history of acute frostbite injury between patients who underwent early operative sympathectomy within 20 hours of hospitalization and those who underwent intra-arterial drug infusion within the first hour of hospitalization followed by operative sympathectomy. [33]  Neither operative sympathectomy nor intra-arterial drugs are currently recommended.


Predicting Tissue Loss

As mentioned previously, predicting tissue loss is one of the greatest challenges in the management of peripheral cold injuries. The classic strategy is to allow the damaged tissue to demarcate, a process that typically takes 60-90 days to complete. This can be helpful in terms of giving patients time to come to terms with the impending digit loss; it also allows them to see the very clear definition between the viable part of the digit and the distal, nonviable, dry gangrenous part. Despite the perceived benefits of this approach, however, there are drawbacks. Typically, patients are off work during this phase and require prolonged dressing changes and support. Various imaging modalities have been studied to assess their value in terms of predicting tissue loss, the idea being that an imaging modality that can accurately predict the final level of amputation will permit surgical intervention to take place earlier. This will allow the patient to return to a more normal life more quickly than will the typical conservative watch-and-wait approach.

Many imaging modalities have been used for such predictions, but angiography and 99mTc triple-phase bone scanning give the best prognostic information for directing therapy. A retrospective review by Cauchy et al of 92 patients with severe frostbite of the extremities showed that 99mTc scans obtained a few days after the injury can accurately predict the level of amputation in over 84% of cases. [34] Case reports suggest that magnetic resonance imaging (MRI)/magnetic resonance angiography (MRA) [35] may be superior to 99mTc bone scanning, as they permit direct visualization of occluded vessels, allow surrounding tissues to be imaged, and may show a clearer level of demarcation with regard to ischemic tissue. However, this has yet to be confirmed by larger studies. Of note, MRA may be easier to access than 99mTc bone scanning in many hospital units.


Adjunctive Treatment

Multiple experimental therapies have been proposed for the treatment of frostbite. Calcium channel blockers, steroids, and hyperbaric oxygen have not been shown to enhance tissue salvage. Pentoxifylline (Trental), 400 mg every 8 hours, may aid small vessel perfusion. Phenoxybenzamine (Dibenzyline), 10-60 mg/d, may reduce refractory vasospasm in some patients.

Despite the lack of effectiveness in the acute phase, sympathectomy does appear to provide prophylaxis against the deleterious effects of subsequent cold exposure. This observation may have clinical implications in patients who need such prophylaxis for occupational reasons, such as professional skiers with cold sensitivity. In addition, the results of digital sympathectomy in the management of chronic vasospastic frostbite sequelae, such as vasospastic pain, are encouraging.

A body part that suffers frostbite seldom recovers completely. Some degree of cold sensitivity and hyperhidrosis are common. Neuropathies, decreased nail and hair growth, lymphedema, ulcerations, and persistent Raynaud phenomenon in the affected part are other residua of the injury. Permanent tissue damage, such as subcutaneous tissue atrophy, bony defects on radiographic examination, and abnormal epiphyseal growth, may occur. In children, the healed frostbitten hand frequently develops shortening of the digits, skin redundancy, joint laxity, and distal interphalangeal joint radial deviation. Surgical management options for the sequelae of frostbite of the juvenile hand include epiphyseal arrest, arthrodesis, and angular osteotomy. Specific treatment must be tailored to the patient, as cases can evolve in a variety of ways over time. The important take-home point is that most patients, especially those with severe initial injury, will have long-term sequelae that may require ongoing care.


Ophthalmic Injuries

Freezing of the corneas, though rare, has been reported to occur in individuals who have kept their eyes open in high-windchill situations without protective goggles (eg, snowmobilers, cross-country skiers). Initial corneal flare and pain during rewarming are signs of this injury. Keratitis and corneal opacification may require corneal transplantation. If this injury is suspected, an ophthalmologist should be consulted early in the course of the patient's care.

Snow blindness is produced by ultraviolet (UV) solar radiation reflected from snow, ice, or water. It tends to be more common at high altitudes, where the air filtration of UV radiation is diminished. Excess radiation produces corneal pitting and disruption of the epithelium. Retinal damage may also occur. Symptoms develop 4-12 hours after exposure and include a painful eye and excessive tearing. The lids and corneas of the eyes may be swollen and red. Treatment includes induced cycloplegia, mydriasis, and eyelid closure with a dressing. Artificial tears and antibiotics are indicated early in the treatment. Again, if this injury is suspected, an ophthalmologist should be consulted early.