Perspective

Accidental hypothermia is responsible for approximately 700 deaths per year in the United States.¹ It primarily affects those least able to ward off the effects of cold weather: the very young, the very old, and the poor, disabled, pharmacologically inquisitive, environmentally adventurous, and mentally ill. Urban people are common victims. Hypothermia can occur in many latitudes, with episodes reported even in Florida.² It occurs when a person’s ability to generate heat and remain warm is outstripped by the ambient temperature.

In the United States, frostbite is often a disease of the indigent, the intoxicated, the mentally ill, and winter outdoor recreation enthusiasts. For both frostbite and hypothermia the literature consists of primarily case reports, case series, and reviews.

Epidemiology

Accidental hypothermia is generally manifested as progression from an initial state of catecholamine release and stimulation (mild hypothermia) to one marked by a predictable slowing of metabolism and all critical body functions to the extent that patients may appear dead. The profound physiologic changes and metabolic slowing all reverse with rapid rewarming, and reports of remarkable neurologically intact survival despite hours of pulselessness and resuscitation are not infrequent. This has given rise to the adage “No one is dead until they are warm and dead.” Not surprisingly, there is little strong scientific evidence for treatment recommendations because trials cannot be conducted. The medical literature is composed mostly of animal experiments, case reports and series, and retrospective reviews. Still, rational approaches can be inferred from the extant literature for this uncommon but serious problem (Table 131.1).

Table 131.1 Definitions of Hypothermia

Frostbite is a freezing injury to soft tissues secondary to cold exposure and results in loss of circulation to and therefore viability of the affected area. The extremities, nose, ears, and male genitalia are the most commonly affected areas.

Pathophysiology

Mechanisms of Heat Loss

The mechanisms of heat loss are as follows:

• Radiation of heat occurs when the ambient temperature is less than body temperature and heat is lost directly to the environment via electromagnetic radiation.

• Conduction is heat transfer from one (warmer) solid to another (cooler) when they are in contact.

• Convection is loss of heat from a surface to a (usually moving) gas or fluid, typically air or water. It can be considered an adjunct to conduction.

• Evaporation causes heat loss through the energy required to vaporize water (i.e., sweat).

As a person cools, a fairly predictable procession of pathophysiologic changes occurs, as seen in Table 131.2 and Figure 131 .1.

Table 131.2 Pathologic Changes Seen with Hypothermia

Fig. 131.1 Osborn wave seen on the electrocardiogram of a patient with hypothermia.

The wave is usually seen at body temperatures lower than 30° C; however, it is neither diagnostic nor prognostic of hypothermia and is thus of academic interest only.

Presenting Signs and Symptoms

Patients with mild hypothermia are awake, occasionally drowsy, uncomfortable, and shivering. They simply need insulation (blanket), dry clothes, and food. They will recover completely and can be discharged when normothermic and feeling better.

Patients with moderate hypothermia are generally confused and lethargic, often have slurred speech, and are typically not shivering. They require more energetic rewarming measures, including heated blankets, resistive and hot air blankets (Bair Hugger), and close monitoring, including core temperature. Though strictly considered active internal rewarming, the use of heated, humidified oxygen and warmed intravenous (IV) fluids is reasonable in this situation. Patients whose hypothermia responds to these measures may be discharged when normothermic, awake, alert, and ambulatory. Patients with severe hypothermia require prompt intervention, close monitoring, and potentially aggressive, invasive rewarming therapies.

It is of the utmost importance to learn the circumstances that led to the patient becoming hypothermic. The possibility of a verify drug overdose, trauma, infection, drowning, or decompensated comorbid conditions—to name but a few examples—must be considered, sought, and treated along with the hypothermia.

The critical element of the diagnosis of hypothermia is accurate measurement of core temperature. Several methods exist, all of which have potential drawbacks (Table 131.3). Laboratory and physiologic changes are correlated with the temperature. For example, a normal hematocrit value in a severely hypothermic patient should prompt concern for hemorrhage because the hematocrit should rise in a predictable fashion with ever-lowering temperature. Alternatively, arterial blood gas values should be interpreted as though the patient is normothermic (the alpha-stat method) and not corrected for the actual core temperature (the pH-stat method). Evaluation for infection, metabolic derangement, and cardiac, neurologic, renal, and other organ system abnormalities is important because comorbid conditions are common as a cause, a consequence, or coincidence of hypothermia.

Table 131.3 Methods of Measuring Core Temperature

Treatment

Next Steps in Care

Patients with mild hypothermia and (most) patients with moderate hypothermia can be treated in the emergency department and released when normothermic. This statement relies on the assumption that no other complicating social or medical problems are present that must be addressed. All patients with severe hypothermia should be admitted to the hospital, usually to an intensive care unit. Successful revival of these patients will require considerable time and resources.

Clear, universally accepted criteria on declaration of death in hypothermic patients are lacking, beyond the obvious recommendations regarding terminal injuries, rigidity that precludes chest compressions, and physical blockage of the mouth or nose by ice.

Numerous case reports have described neurologically intact survival after prolonged, severe hypothermia with cardiac arrest.^7,12 A serum potassium level higher than 10 mmol/L has been postulated to be a marker of irreversible cell and therefore patient death¹³; however, another case report has called this approach into question.¹⁴ Pronouncement of death in a severely hypothermic patient should be made with reluctance until the patient’s core temperature has been warmed to higher than 30° C to 32° C and signs of life remain absent.

A reasonable approach to the hypothermic patient is presented in Figure 131.2.

Fig. 131.2 Algorithmic approach to patients with hypothermia.

ACLS, Advanced cardiac life support; CPR, cardiopulmonary resuscitation; PEA, pulseless electrical activity; VFib, ventricular fibrillation.

(From EB Medicine, publisher of EM Critical Care and Emergency Medicine Practice: Mulcahy AR, Watts MR. Accidental hypothermia: an evidence-based approach. Emerg Med Prac 2009;11:1–24. Available at www.ebmedicine.net.)

see Figure 131.2, Algorithmic Approach to Patiens with Hypothermia, online at www.expertconsult.com

Pathophysiology

Frostbite is a freezing injury to tissues. During this process it is believed that deposits of ice crystals causing interstitial, cellular, and vascular endothelial cell damage are one part of the pathophysiologic process.¹⁵ The vascular endothelial damage results in activation of the clotting cascade with resulting thrombosis, which leads to hypoperfusion, ischemia, and eventually tissue necrosis. The prominence of the clotting that can cause vascular occlusion can be seen on angiography and is the basis for the concept of treating selected patients with thrombolysis.

Presenting Signs and Symptoms

The classic victim of frostbite has either a dusky or a white affected area that is brawny to solid in texture, insensate, and without capillary refill. Variations are time dependent, and patients seen in delayed fashion may have blisters that are either hemorrhagic or clear and even some tissue loss or frank necrosis already evident. Classification systems exist for frostbite, but they are controversial and are also problematic for the emergency physician because the initial clinical appearance can be misleading and it takes time for the full extent of the damage to become clear. It is simpler and more realistic to start to treat the affected part and consult surgeons for ongoing wound care and treatment (Fig. 131.3).

Fig. 131.3 Frostbitten feet of a young man who had been running barefoot all night in winter secondary to drug-induced paranoia.

Treatment

Frostbite is a clinical diagnosis. Other cold-related tissue injuries to be considered are frostnip, pernio (chilblains), and trench foot. These injuries, however, are nonfreezing ones, in contrast to frostbite.

For a concise summation of nonfreezing injuries, see www.expertconsult.com

Prehospital Management

Treatment of frostbite in the field consists of the application of dry sterile dressings to separate the involved digits and elevation of the affected extremity. Avoid rewarming with dry heat, such as with fires or heaters, and also assiduously prevent further cold injury. Rubbing the affected part with snow is soundly condemned. It is paramount to avoid a freeze-thaw-freeze cycle, which worsens the tissue damage.

Hospital Management

Once the patient is in the hospital, the mainstay of treatment is rapid rewarming with a circulating bath of water heated to 40° C to 42° C for 10 to 30 minutes until the involved area is erythematous and pliable. Because rewarming is extraordinarily painful, liberal use of parenteral analgesics is usually necessary. Clear, large blisters should generally be débrided, but hemorrhagic ones should be left intact (their presence implies much deeper damage, and desiccation of the area is a concern). Débridement removes fluid that is rich in thromboxanes and prostaglandins, which are thought to be destructive to tissue. Aloe vera may be applied topically every 6 hours and the wounds bandaged.

Prophylactic antibiotics are controversial. Penicillin G has been advocated. Additionally, ibuprofen, 400 mg by mouth twice daily, is recommended in an attempt to interrupt the arachidonic acid cascade.^15,16 Both catheter-directed intraarterial and systemic thrombolytic therapies have been used with impressive success in preventing amputations (Figs. 131.4 and 131.5). This novel therapy holds considerable promise but does have several limitations, including restriction to patients initially seen within 24 hours of the injury and risk for bleeding.^17,18

Fig. 131.4 Angiogram of the left foot of a young female with frostbite after she wandered in the desert all night under the influence of illicit drugs.

Fig. 131.5 Angiogram of the foot shown in Figure. 131.3 after approximately 30 hours of tissue plasminogen activator infusion showing restoration of perfusion.

An amputation was averted with this therapy.

Most recently, a small, randomized trial of frostbite therapies showed remarkable success with intravenous iloprost, a prostacyclin (no digit amputations), over an IV nonsteroidal antiinflammatory drug (≈40% digit amputation rate) or recombinant tissue plasminogen activator plus iloprost (≈3% digit amputation rate).¹⁹ Whether this promising success can be repeated and confirmed elsewhere remains to be seen.

Early surgical management is not indicated for frostbite because of the difficulty of ascertaining the full extent of the tissue damage initially. Typically, the affected area is left to mummify and essentially autoamputate before the formal procedure is carried out. Some newer imaging modalities, such as nuclear scanning and magnetic resonance angiography, may be able to shorten the time to definitive surgery by delineating viable tissue earlier than possible with simple observation.