Emergency Medicine

THE EMERGENT PATIENT: Cold-Related Injuries

The authors discuss the clinical characteristics of nonfreezing injuries such as chilblain and the management of frostbite, including the risk of "core temperature after-drop."

By Thomas M. Cruz, MD, and Barry Knapp, MD

Like burns, cold-related injuries exist on a spectrum of severity ranging from minor tissue injury to devastating injuries causing permanent damage to deep structures. Minor injury is often sustained as a result of prolonged exposure to cold conditions at nonfreezing temperatures; it includes frostnip, chilblain (or pernio), and trench foot (or immersion foot). True frostbite is caused by exposure to freezing conditions and implies damage to involved tissue. All frostbite victims experience some sensory loss that can last up to four years or may even be permanent.

Although temperature plays a key role in the severity of cold-related injuries, it is the duration of exposure to cold conditions that determines the extent of injury. In addition to temperature, other environmental factors contributing to cold-related injury include contact time, humidity, wind-chill factor, wind velocity, and wet skin. Host factors, such as lack of proper clothing, alcohol or drug intoxication, and malnutrition, also play a major role. Some of the earliest and most dramatic reports of cold-related injuries come from military accounts during times of war. Probably the most famous of these is the cold weather that claimed the lives of 2500 of George WashingtonÕs soldiers at Valley Forge, Pennsylvania, during the winter of 1777-78.

Epidemiologic data reveal that most patients who sustain cold-related injuries are men who are improperly clothed during the winter months. As many as 80% have abnormal mental status with psychiatric illness or alcohol intoxication, or both, as a major predisposing factor leading to prolonged exposure. Alcohol contributes to cold-related injury by altering physiologic protective mechanisms. Specifically, it causes vasodilation of pores, which promotes heat loss and ultimately hypothermia. Once hypothermia develops, compensatory vasoconstriction compounds injury by limiting blood flow to peripheral tissue, which increases the risk of frostbite.

Other medical comorbidities for cold-related injury include atherosclerosis, hypovolemia, hypothyroidism, diabetes, trauma, and infection. Another high-risk group is sports enthusiasts, especially those who engage in mountain climbing, hiking, skiing, snowmobiling, and water-related recreation.

NONFREEZING INJURY

Chilblain results from chronic exposure to dry, cold conditions. Recurrent vasospastic episodes may ultimately lead to the development of inflammatory lesions and nodules on the hands, feet, and pretibial areas (see photo). In addition to these superficial skin ulcers, cyanotic-appearing tissue and bullae may be seen. The physiologic mechanism of injury puts individuals with a history of RaynaudÕs phenomenon at increased risk for chilblain. Some sources recommend the use of nifedipine 20 to 60 mg daily in the management of persistent vasospasm.

Trench foot, usually a more severe injury than chilblain, results from prolonged exposure to wet, cold conditions and develops over several days. Although originally designed to preserve body heat, some new synthetic materials, such as neoprene, actually retain moisture and may increase the risk of trench foot. Patients may report numbness and tingling in their extremities, which may appear cyanotic, edematous, or even black from subsequent development of superficial gangrene.

Unlike patients with chilblain, patients with trench foot are more likely to experience prolonged effects following rewarming. Erythema, cold sensitivity, pain with ambulation, vasomotor paralysis, and vesicular ulcerations have been reported.

Frostnip is a superficial cold injury that presents with temporary numbness and tingling. No tissue destruction occurs and symptoms resolve with rewarming.

FREEZING INJURY

Compromised circulation plays a central role in the pathophysiology of cold-related injury. Damage to the vascular endothelium is the first step in the progressive pathway of frostbite. Following endothelial destruction of arterioles, capillaries, and venules, fibrin deposition and extravasations of fluid into interstitial spaces occur. Between the temperatures of 37.4¼ and 51.8¼F, approximately 40% of blood flow from the arterioles to venules ceases, which promotes sludging and thrombosis. This progressive ischemia incites further injury by inducing responses mediated by inflammation.

The symptoms and effects of frostbite injury vary greatly, depending on whether or not tissue loss has been sustained. Common symptoms of frostbite include diminished light touch and temperature sensation, with numbness being the most common reported symptom (about 75% of patients). Intermittent pain is a sign of incomplete tissue destruction, while complete anesthesia of an involved extremity suggests severe injury. It has also been reported that a sensation of an electric current shock may be an indicator of tissue loss. In contrast, a burning sensation experienced early in the presentation is an indicator of tissue preservation.

Patients who sustain tissue loss often report symptoms that last up to six months or longer. In contrast, symptoms may resolve within one month when tissue is preserved. Regardless of the extent of the injury, almost all patients will experience an exacerbation of pain or discomfort on rewarming of the affected areas. As with nonfreezing injuries, areas of the body most commonly affected include the extremities, ears, nose, and penis.

The diagnosis of frostbite is sometimes difficult to make on initial presentation. Affected tissue may appear pale or waxy and often reveals hyperemia on rewarming. Following the initial thaw stage, patients typically report a partial return of sensation. Over the next 6 to 24 hours, the formation of vesicles and large blebs is expected with true frostbite injury.

To determine the extent of freezing injuries, attempts have been made to classify frostbite based on degree. However, such classifications have limited utility with regard to treatment and prognosis. Instead, there is a trend toward classifying these injuries as either superficial or deep. Superficial frostbite is limited to involvement of the subcutaneous tissue and skin. Affected areas appear pale or white, with a firm surface that can be depressed with gentle pressure. Rewarmed areas may develop a swollen appearance with occasional blister formation over the next 24 hours. These blisters will contain either clear or milk-colored fluid. Ultimately, there is no permanent tissue damage and the involved area recovers fully, although sometimes not for years.

Deep frostbite extends beyond subcutaneous layers to include muscle, tendon, nerve, and sometimes even bone. Initially, patients may report a pins-and-needles sensation or numbness. However, on rewarming, patients experience severe pain with a throbbing sensation. Affected areas become indurated and cyanotic, sometimes taking on what is often described as a ÒstonyÓ or ÒwoodyÓ appearance. Skin tissue loses pliability and will not roll over bony prominences.

In contrast to the clear blisters seen with superficial injury, hemorrhagic bullae develop and the skin takes on a violaceous hue. Presentation of a black, necrotic eschar with clear demarcation indicates severe frostbite injury and increases the risk of gangrene. Long-term effects from freezing injuries may include the development of neuropathic pain, sensory deficits, hyperhydrosis of involved areas, RaynaudÕs disease, and arthritis.

In addition to tissue injury of the extremities, other injuries associated with prolonged exposure to cold conditions need to be considered. Ophthalmologic injury such as corneal freezing and abrasions may occur in conditions of high wind chill and wind velocity. These injuries are more likely to occur in recreational sports such as snowmobiling and skiing. Diagnosis requires adequate ophthalmologic evaluation with a slit lamp and fluorescein examination.

WORKUP AND INITIAL TREATMENT

Laboratory evaluation of patients sustaining cold-related injuries must be tailored to each individual case and should take into account pre-existing comorbidities. For instance, a complete blood count, metabolic panel, and blood cultures should be obtained for a diabetic patient in whom infection or dehydration is suspected. Imaging studies such as x-rays and computed tomography (CT) scans may assist in ruling in or ruling out other sources of infection or altered mental status that may compound the patientÕs presentation. Magnetic resonance angiography or magnetic resonance imaging may become the modality of choice in assessing tissue viability and the extent of damage. In the emergency care setting, however, these studies are of little utility and are better used by surgeons weeks later to determine the need for amputation or debridement.

Initial management of cold-related injuries is dictated by the setting. If there is any risk of refreezing, which may occur during transport to a primary care facility, thawing should be avoided; refreezing will only exacerbate the damage already done. If refreezing is a risk, the affected areas should be wrapped in protective padding, followed by application of clean dry gauze and a splint, if possible.

Before definitive treatment of frostbite is initiated, any existing hypothermia should be corrected. Once the patientÕs core temperature is at least 93¼F, treatment should begin with immersion of the affected areas in warm water (100.4¼ to 104¼F) for 15 to 30 minutes. Use of a thermometer is recommended; temperatures exceeding 107.6¼F have been shown to cause thermal injury to transition zones of tissue. This active form of rewarming should continue until tissues develop some erythema and pliability returns. Dry heat and the rubbing of tissue to promote warming will only cause more damage and should never be attempted. However, some active movement of the extremity should be encouraged during thawing.

PREVENTING PROGRESSIVE EFFECTS

While rapid rewarming effectively halts immediate injury produced by initial ice crystal formation, it does not prevent the progressive effects of cold injury that ensue. A treatment protocol designed by McCauley focuses on limiting these effects. This protocol has resulted in better patient outcomes, as indicated by shorter hospital stays, less tissue loss, and lower amputation rates compared with other treatment modalities. In addition to the immediate active rewarming techniques discussed above, the protocol recommends debridement of only white or clear blisters, which contain the proinflammatory components prostaglandin F2 alpha and thromboxane A2.

In contrast to white or clear blisters, which represent superficial injury, hemorrhagic blisters indicate damage to the subdermal vascular beds. Debridement of these blisters may result in dessication of the dermis, with progression of a partial-thickness injury to a full-thickness injury.

It should be noted that many sources suggest leaving all blisters intact.

Nonsteroidal anti-inflammatories (400 mg every 8 hours) may also be administered to diminish the inflammatory effects of arachidonic acid and promote fibrinolysis. Affected extremities should be elevated to decrease edema formation. The McCauley protocol recommends the use of parenteral antibiotics (particularly penicillin) during the edematous phase, since edema has been reported to inhibit the protective barriers of the skin. However, the use of prophylactic antibiotics remains controversial. The patientÕs tetanus status should be updated and all vasoconstrictors, such as nicotine, should be avoided.

CORE TEMPERATURE AFTER-DROP

As previously mentioned, tissue reperfusion during thawing commonly causes intense pain. As a result, use of a parenteral analgesic is recommended. Fluid resuscitation and electrolyte abnormalities are rarely a concern unless patients have sustained prolonged exposure to harsh conditions with complete freezing of an extremity. In these cases, rewarming of extensively injured areas puts patients at risk for what has been referred to as Òcore temperature after-drop.Ó As areas are rewarmed, the ensuing vasodilation of large muscular areas returns significant amounts of cold blood to the central circulation. This resulting drop in core temperature is also exacerbated by the acidotic, hyperkalemic nature of the previously frozen tissue. In such severe cases, administration of warm crystalloid fluids is warranted and extracorporeal rewarming should be considered.

Following the thaw period, involved extremities should be wrapped in sterile dressings and elevated to minimize edema. Tissue pressures should be closely monitored in extremities that remain cyanotic after thawing; this may be an indication of impending compartment syndrome. Decisions regarding surgical intervention are often delayed until the full extent of injury has manifested itself, a process that may take weeks to months.

In an attempt to limit the physiologic inflammatory effects and thrombosis caused by cold-related injury, many other treatment options have been explored. Both urokinase and low-molecular-weight dextran have shown some benefit by improving blood flow in severely frostbitten limbs. However, such treatment modalities have been studied mostly in animals and will require more extensive evaluation before they become accepted practice. Also, despite numerous references to the use of topical aloe vera as a thromboxane inhibitor, it has not been demonstrated to improve tissue outcome.

DISPOSITION OF PATIENTS

Due to the progressive nature of cold-related injuries, admission is recommended for all frostbite patients. Victims of nonfreezing injuries such as chilblain or trench foot obviously should not be discharged in subfreezing conditions with inadequate clothing. When patients are discharged, they should be instructed to avoid reinjury by wearing woolen socks, hats, and mittens (which are preferable to gloves). They should also be told that they are susceptible to refreezing due to the initial injury.

All cold-related injuries should be re-evaluated in follow-up visits until wounds are stable. In addition to keeping the involved extremities elevated, patients with open lesions should continue to take ibuprofen 400 mg two to three times daily.