Physiology

The only way humans can avoid functional impairment in cold environments is by maintaining their core temperature within a 4°C range. This core temperature can be maintained by two mechanisms: increasing heat production and decreasing heat loss.

Pathophysiology

Clinical Manifestations

With mild hypothermia, vasoconstriction is maximal, causing the extremities to be cool and pale. Performing fine movements of the hands is difficult. Increased urinary frequency and volume, called cold diuresis , occurs at this stage. The patient is at maximal levels of involuntary thermogenesis and has uncontrollable shivering. The mental status is altered and manifested by listlessness, confusion, and disorientation. Speech may be dysarthric. Victims are often ambulatory but ataxic. Mild degrees of tachycardia, tachypnea, and hypertension may be present, but vital signs are stable.

The condition of a person with moderate hypothermia is more serious. He or she exhibits a markedly altered mental status with slurred speech, apathy, and amnesia. The mental status may deteriorate into stupor and coma. The phenomenon of paradoxical undressing may occur at this stage, with the person inexplicably disrobing despite the conditions and worsening physiologic state. Deep tendon reflexes diminish and become absent. Vital signs become unstable; hypotension follows with worsening dehydration, and bradycardia emerges. Atrial dysrhythmias, namely atrial fibrillation, begin to occur. Shivering slows and ceases. Without the ability to generate heat, the body will quickly begin to cool to the ambient temperature. Death is inevitable without treatment.

A person with severe hypothermia is often comatose and may appear dead. His or her pupils may be fixed and dilated. Hypotension and bradycardia are severe. In fact, blood pressure and pulse readings may be difficult to obtain. Arrhythmias such as ventricular fibrillation and asystole are common. The respiratory rate decreases to the point of apnea. Muscles become rigid. Urine output falls precipitously, and oliguria occurs. Persons with severe hypothermia have the highest mortality rate.

Diagnosis

The diagnosis of hypothermia requires accurate and reliable measurement of the core temperature. Rectal or esophageal probes that can read temperatures below 34°C are required to make the diagnosis. Oral or axillary probes do not reflect core temperature and often can be much lower. The amount of decrease in core temperature determines the severity of the patient’s condition, and mortality is directly related to severity. ECG monitoring is also helpful in diagnosing cardiac manifestations of hypothermia. Laboratory evaluation should include blood glucose and arterial blood gas levels, a complete blood cell count, levels of electrolytes, blood urea nitrogen, creatinine, serum calcium, serum magnesium, serum amylase, and lipase, prothrombin time/international normalized ratio, partial thromboplastin time, and fibrinogen level. Intensive care monitoring is essential in cases of moderate to severe hypothermia because of the multiple organ systems that may be involved.

Treatment

In general, treatment depends on the severity of the hypothermia and the treatment setting. Rewarming is the primary treatment for hypothermia. Methods of rewarming may be categorized as passive rewarming, active external rewarming, active internal rewarming, and extracorporeal rewarming. Passive rewarming consists of insulating the patient and allowing thermogenesis, specifically shivering, to increase the core temperature. Examples of methods for active external rewarming include chemical heat packs, heat lamps, warming blankets, and hot baths. Active internal rewarming has been attempted using warmed air for inhalation, warmed intravenous fluids, and warmed fluids instilled into the gastrointestinal tract. Extracorporeal rewarming refers specifically to shunting blood from the body, usually by cardiopulmonary bypass or venoarterial or venovenous shunt, to a machine that rewarms the blood and returns it to the body.

After hypothermia is confirmed with an accurate temperature, reduction of further heat loss becomes a priority. All wet clothes should be immediately replaced with dry garments. However, the clothing of persons with a markedly altered mental status should not be removed; rather, warm blankets should be placed over them. Care should be observed when moving moderately to severely hypothermic patients to prevent the precipitation of ventricular fibrillation that can result from myocardial instability. All persons with hypothermia can be assumed to have some degree of volume depletion, and thus fluid resuscitation with intravenous fluids is recommended. Passive rewarming is usually adequate for persons with mild hypothermia. Passive rewarming has been successfully accomplished in persons with core temperatures as low as 32°C.

Persons with moderate hypothermia require active external rewarming. When instituting active rewarming, care must be taken to avoid thermal burns to the skin. Another hazard of active external rewarming is the phenomenon known as afterdrop , in which core temperature drops precipitously after rewarming is started because of shunting of cold blood away from the periphery to the core. Rewarming the trunk before rewarming the limbs is recommended to avoid afterdrop.

Severe hypothermia requires active rewarming. Methods of active internal rewarming are invasive to varying degrees, from instillation of warm water into the gut to peritoneal or thoracic lavage. Extracorporeal rewarming is highly invasive and should be carried out only in centers with experience in these techniques. Cardiac arrest can occur either as a direct result of the hypothermia or during the rewarming process. Defibrillation is recommended in these circumstances to convert to a pulse-generating rhythm. Moderate and severe forms of hypothermia may induce several metabolic changes that can affect cardiac and other organ function, including acidosis, hyperkalemia, and intravascular coagulation. Patients must be monitored carefully for these changes.

Prevention

For athletes exercising in cold conditions, hypothermia is a preventable condition. Competitions in cold weather should be very organized, with numerous marshals using well-developed communication networks to attend quickly to victims. Athletes should know the weather conditions and dress appropriately. Wearing too many layers may cause excessive sweating and increase heat loss through evaporation. Athletes undertaking long training routes in remote areas should train with a partner and carry a cell phone, which cannot substitute for a partner because of the potential for the cell phone to fail. Athletes participating in winter sports must pay close attention to energy stores; even so, thermogenesis causes muscle glycogen to be used at a faster rate. Increased intake of carbohydrate is recommended. Adequate hydration is important because of the possibility of hypovolemia from cold diuresis. Athletes participating in winter sports should be aware of the warning signs of hypothermia, and if they find themselves lost in the cold, they should remember that their chances for survival are better if they take temporary shelter and conserve heat than if they continue to trek in the cold.

Epidemiology

With increasing numbers of persons participating in outdoor activities and sports in cold weather, one would expect an increasing incidence of frostbite. However, large-scale incidence studies have not been performed. The military has traditionally been a group with higher risk of frostbite, particularly in wartime. Mountaineering also is a particularly high-risk activity for frostbite. Harirchi described an incidence of 366/1000 population per year in a survey study of mountaineers. In urban environments, homelessness is a significant risk factor for frostbite. In a Canadian study it was found that alcohol consumption and psychiatric illness were the most common predisposing factors for urban cases of frostbite.

Pathophysiology

Frostbite injury occurs through four pathologic phases—prefreeze, freeze-thaw, vascular stasis, and late ischemic—with overlap occurring between them. In the prefreeze phase, vasoconstriction occurs as heat is lost in an effort to shunt blood to the core. Vasodilation will intermittently relieve this vasoconstriction approximately every 5 to 7 minutes in a phenomenon known as cold-induced vasodilation. At the freeze-thaw phase, ice crystals form at the cellular level. Ice crystal formation alters protein structure and causes cell dehydration, shrinkage, and death. As thawing then occurs, inflammatory mediators are released and accumulate—namely, arachidonic acid metabolites. Vascular endothelial damage occurs, causing blood leakage and thrombus formation. These changes mark the vascular stasis phase. Affected tissues undergo progressive ischemia, and further inflammatory mediators accumulate. The local microvasculature is then destroyed and further cell death occurs. With continued exposure to the cold environment, the pathophysiologic phases progress and frostbite progresses from distal to proximal and from superficial to deep.

Clinical Manifestations

During the early stage of frostbite, most patients notice that the involved extremity becomes cold and numb. Patients present with a somewhat mottled or yellowish injured area, and early symptoms are similar in all persons with frostbite. Numbness gives way to significant pain with rewarming. Rewarming also leads to marked edema and hyperemia. In persons with moderate frostbite, blisters develop in the involved area and can be clear or hemorrhagic, with hemorrhagic blisters indicating a deeper injury. After a few weeks, dark eschars and mummification will develop in persons with severe frostbite. Injured tissues are clearly demarcated from healthy tissues. Pain, burning, and electric shock–like sensations can persist for weeks to months after the initial injury. These symptoms are typically the result of an ischemic neuritis. Long-term sensory deficits occur in virtually all persons with frostbite.

Diagnosis

Diagnosing frostbite is not difficult because, as previously mentioned, patients present with a cold and sometimes frozen extremity. Determining the severity and prognosis of frostbite can be a difficult task, however. Most persons with frostbite present similarly early in the course of the injury. Numerous tests have been described to predict severity, with duplex ultrasonography, magnetic resonance angiography, and technetium-99m scanning among the most promising modalities. Cauchy et al. described a classification system using technetium bone scanning and clinical appearance after rewarming that could reliably predict which persons with frostbite would eventually require amputation and the extent of that amputation. The Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Frostbite recommend using imaging to assess tissue viability and to guide the timing and extent of amputation.

Treatment

The mainstay of treatment is rewarming of the extremity. Initial treatment in the field, however, should consist of removing the patient from the hazardous environment. Rewarming should not be initiated in the field if refreezing is a possibility, because refreezing can cause more extensive tissue injury. Treatment of hypothermia should take precedence in any initial treatment. If conditions in the field and during transport to a medical facility allow for slow thawing of the extremity, then the thawing process should be undertaken. Once the patient is in an environment where refreezing is not a risk, rapid rewarming should commence. Rapid rewarming is performed in warm (not hot) water with a temperature in the range of 37°C to 42°C (98.6°F to 107.6°F). Care must be taken to ensure that the water temperature remains constant, which can be facilitated by keeping the water continually circulating. The extremity must not be allowed to touch the sides of the vessel that contains the water to prevent damage to fragile, injured tissue. Rewarming should proceed until the extremity becomes red-purple and the skin is pliable, which typically occurs in 30 to 45 minutes. The rewarming process is extremely painful, and opioid analgesics are required for pain control.

In addition to undergoing rapid rewarming, the patient should take nonsteroidal antiinflammatory medication. The Wilderness Medical Society recommends ibuprofen in a dose of 12 mg/kg/day in two divided doses, because this medication helps block formation of inflammatory mediators. Tetanus prophylaxis should be administered. Common practice is to perform needle aspiration of any clear blisters but to leave hemorrhagic blisters alone. The injured extremity should be gently cleaned and allowed to air dry. Dry bulky dressings should be applied, which help to minimize any further tissue trauma, and the extremity should be elevated. Aloe vera is a thromboxane inhibitor and can be used topically in cream or gel form as an adjunctive treatment for persons with frostbite. Prophylactic antibiotic treatment for sepsis is not recommended. Antibiotics should only be given if signs or symptoms of infection/sepsis develop.

Because part of the pathophysiology of frostbite involves microthrombi formation, thrombolytic therapy can be instituted in severe cases of frostbite. Use of tissue intravenous or intraarterial tissue plasminogen activator within 24 hours of thawing has been shown to be of potential benefit in salvaging tissue at risk for necrosis. Treatment with tissue plasminogen activator has significant potential risks, however, and should only be undertaken at a medical facility with intensive-care monitoring and experience in using it in cases of frostbite.

Early surgical intervention with amputation should not be undertaken too early in the course of frostbite. Necrotic tissue demarcation can take up to 3 months. Most experts recommend early amputation only in cases of sepsis due to frostbitten tissue.

Prevention

The best ultimate treatment of frostbite is to prevent its occurrence. The following general points can help prevent a potentially devastating injury :

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  Maintain adequate hydration

  
  
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  Keep skin protected from wind and moisture

  
  
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  Wear appropriate layers and wear mittens instead of gloves

  
  
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  Do not wear tight footwear

  
  
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  Use chemical or electrical warmers for hands and feet

  
  
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  Avoid exposure to cold temperatures when under the influence of alcohol or drugs

  
  
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  Minimize duration of exposure to cold conditions

  
  
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  Know signs and symptoms of frostbite and check for them frequently

  
  
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  Move to a sheltered environment at the earliest signs of frostbite

Definition

Heat exhaustion is primarily due to dehydration. Athletes with heat exhaustion typically lose 10% or more of their body weight through sweating, resulting in a diminished ability to exercise. The athlete’s thermoregulatory mechanisms are seldom able to maintain the core temperature within normal limits.

Pathophysiology

Heat exhaustion is likely due to a combination of dehydration, central nervous system fatigue, depletion of muscle energy stores, and in some cases, electrolyte imbalance. Heat exhaustion typically occurs in high-temperature environments but may also occur in moderate- to low-temperature environments with high humidity. The relative contributions of temperature and humidity to an athlete’s heat stress are quantified by the heat index (see http://www.nws.noaa.gov/om/heat/index.shtml ). Dehydration may be normonatremic, hypernatremic, or hyponatremic. In a prospective study of 133 collapsed ultramarathon runners, 53% were isonatremic, 45% were hypernatremic, and 2% were hyponatremic.

Diagnosis

The diagnosis of heat exhaustion is made clinically. Symptoms include fatigue, weakness, dizziness, muscle cramps, abdominal pain, headache, and nausea. Mild mental status changes may be observed, including mild confusion, irritability, and emotional lability. Common physical signs include pallor, listlessness, and weakness.

Treatment

The athlete should rest in a cool place. Oral rehydration is the initial treatment of choice, with the goal of replacing 1.5 L of fluid for every kg of decreased body weight. If body weight was not previously recorded, adequate rehydration is evidenced by an overall sense of well-being. Cooled fluids and fluids containing less than 8% carbohydrate are absorbed more rapidly than plain water. Rehydration fluids that contain sodium appear to restore total body water levels more completely than water alone. Intravenous (IV) hydration may be required in persons who are vomiting or have orthostatic symptoms. The recommended IV hydration solution is 5% dextrose in normal saline solution. Physiologic markers of dehydration in athletes do not normalize more quickly with IV hydration. Furthermore, the World Anti-Doping Agency has recently banned the use of IV fluids to accelerate rehydration in otherwise healthy athletes.

Return to Play

No evidence-based guidelines have been developed for return to play after heat exhaustion. Our recommendations for return to play are listed in Box 25-1 . Preparation for return to play should address risk factors including deconditioning, chronic hypohydration, habitual fatigue, and excess body weight.

Prevention

Definition

Hyponatremic dehydration is defined as dehydration that results in a low serum sodium level (<135 mEq/L). It may lead to collapse, coma, seizures, and death.

Pathophysiology

Athletes who experience hyponatremia typically have a high loss of sodium through sweat. Overhydration with plain water before and during exercise can also result in hyponatremia. Other risk factors include a history of endurance exercise, inexperience with racing, female gender, low sodium intake before exercise, and use of nonsteroidal antiinflammatory drugs.

Diagnosis

The diagnosis of hyponatremic dehydration is usually made clinically in the athlete with apparent heat exhaustion whose symptoms fail to improve with water rehydration.

Treatment

Suspected hyponatremic dehydration should be considered a medical emergency, and emergency medical services (EMS) should be activated. An athlete with mild symptoms should be given an oral rehydration solution that contains sodium. Oral fluid should be withheld from an athlete who appears to be worsening to avoid further diluting the serum. An athlete who is obtunded or encephalopathic or who experiences seizures must be treated immediately with IV hypertonic saline solution (3%).

Return to Play

Athletes who have hyponatremia without encephalopathy or seizures may return to activity according to the previously described guidelines for athletes with heat exhaustion. An athlete with encephalopathy will require a more gradual return to activity after recovery, and it is recommended that each case be evaluated on an individual basis to prevent complications.

Prevention

Athletes should be educated about the need to avoid overhydration with plain water before exercise and to avoid continued ingestion of plain water during prolonged exercise (>1 hour).

Definition

Exertional heat stroke (EHS) has been defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction, with a preponderance of encephalopathy.” EHS usually occurs in otherwise healthy, fit persons participating in high-intensity exercise in the heat, although it has also been reported with an ambient temperature of 14°C (57°F) in a heavily clad soldier.

Pathophysiology

The initial responses to increasing core temperature include sweating, rising cardiac output, vasodilation, and redistribution of blood away from the splanchnic organs to the muscles and skin. Continued heat stress with increased shunting of blood flow from the core to the periphery may lead to organ hypoxia and acidosis. Organ damage allows endotoxins to enter the circulation, resulting in hypotension. Further cell injury causes the release of inflammatory cytokines, which results in increased intracranial pressure, decreased cerebral blood flow, and neuronal injury, which lead to lethargy and seizure activity. Muscle injury results in hyperkalemia and hypercalcemia, whereas hypoperfusion forces anaerobic metabolism and depletion of carbohydrate stores, all of which compound organ damage. Death usually occurs as a result of shock.

Diagnosis

EHS occurs in otherwise healthy, often fit persons participating in high-intensity exercise, usually in the heat, who present with mental status changes, tachycardia, and hyperthermia. The person with EHS may be lethargic or obtunded, and early neurologic signs may include throbbing headache, dizziness, nausea, and confusion. Physical examination typically reveals hot skin and a rapid pulse. Failure to recognize these symptoms may delay cooling treatment, dramatically increasing the likelihood of encephalopathy and death. Body temperature is typically above 40°C (104°F). Rectal temperature measurement is the most reliable method of monitoring core body temperature in persons experiencing heat stroke.

Treatment

The keys to a favorable outcome for a person with EHS are (1) early recognition and (2) a minimal delay in initiating cooling. Cooling should never be delayed while awaiting the measurement of rectal temperature in an athlete suspected of having EHS. The first responder should initiate basic cardiopulmonary resuscitation and activate EMS. Clothing and equipment should be removed immediately. Immersion of the entire body in cold water is the treatment of choice. Adequate cooling can also be achieved by pouring cold water continuously over the entire body, placing ice bags on the scalp, neck, axillae, groin, and popliteal fossae, and performing ice massage of large muscles. More invasive methods of cooling, such as peritoneal lavage and intravenous cooling catheters, have not been shown to cool more effectively than cold water immersion. Cooling should continue until the rectal temperature reaches 38.6°C (101.4°F) to prevent overcooling.

Return to Play

Recommendations for return-to-play criteria are summarized in Box 25-2 . All athletes should be evaluated with a follow-up examination 7 days after discharge from the hospital. Athletes may return to play when they are clinically normal after 2 to 4 weeks of monitored, progressive training. Before making return-to-play decisions, it is imperative for clinicians to consider that athletes may have neurologic damage as the result of varying degrees of heart, liver, and kidney failure. Furthermore, no validated tests are available to measure responses to graded exercise in the heat to assist in making return-to-play decisions.

Box 25-2

Return-to-Play Criteria After Heat Stroke

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  Demonstration of normal mental status

  
  
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  Return to normal dietary and elimination habits

  
  
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  Normal variation in daily body temperature

  
  
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  Normal complete blood cell count, blood urea nitrogen/creatinine, anion gap, liver enzymes, creatine phosphokinase, and urinalysis, including specific gravity

  
  
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  Normal echocardiogram

  
  
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  Persons with complicated heat stroke (i.e., significant organ failure and extensive rhabdomyolysis) should refrain from exercise for 1 month

  
  
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  Persons with uncomplicated heat stroke (i.e., a brief emergency department or hospital stay) should refrain from exercise for 1 week

  
  
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  Begin exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure

  
  
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  Athletes who demonstrate heat tolerance after 2 to 4 weeks of training may return to competition

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