Management of heat stroke is directed at reducing core temperature as rapidly as possible and treating subsequent complications. Heat stroke is often fatal despite rapid treatment. Maintenance of airway, breathing, and circulation (ABCs) is crucial for patient recovery. Establish an airway, and administer supplemental oxygen by the method most appropriate for the patient’s level of consciousness. Fluid volume is not depleted in most victims of hyperthermia; therefore 1 to 2 L of 0.9% saline solution during the first 4 hours is usually adequate. Lactated Ringer’s solution is not recommended because the liver may not be able to metabolize lactate. Hemodynamic monitoring is indicated until normal vital signs are restored. After the ABCs are secured, rapid, aggressive cooling becomes the next intervention.

Prehospital treatment starts with removing the patient from the external source of heat and removing all clothing. Aggressive ice- or cold-water cooling should be avoided in the field to prevent shivering and seizure activity, which will only increase the core body temperature. Spray the patient with tepid water while fanning the entire body to promote cooling by evaporation. Well-padded ice packs in vascular areas such as the groin, axilla, and neck are also useful. Ice water or cold water immersion is an effective method of rapidly lowering core body temperature; however, its use is one the of the more hotly debated topics in the heatstroke literature. In addition to being unpleasant for the patient and caregiver, access to the patient is limited. Ice water immersion can also cause shivering, which dramatically increases oxygen consumption and can increase body temperature. Intravenous chlorpromazine (Thorazine), 10 to 25 mg, may be used to prevent shivering during the cooling process. Massive peripheral vasoconstriction from ice water immersion can act as an insulator and prevent adequate cooling. After the patient is in the emergency department (ED), aggressive cooling measures such as ice water gastric and peritoneal lavage can also be used. Cooling blankets may be used; however, cooling from wet skin is 25 times more effective than cooling from dry skin

Cooling should be continued until the rectal temperature is 102° F (38.8° C) or less. Core temperature should be monitored frequently during the cooling phase to prevent inadvertent hypothermia. Aspirin and acetaminophen have not proved effective in reducing hyperthermia secondary to heat stroke. Corticosteroid therapy, usually with methylprednisolone, may be used to treat cerebral edema. Intracranial pressure monitoring may be helpful for some patients. To increase renal blood flow, intravenous mannitol, 0.2 g/kg over 3 to 5 minutes, is recommended in patients over 12 years of age whose urinary output is less than 50 mL/hr.

High-output cardiac failure may develop with heat stroke; therefore patients should be placed on a cardiac monitor. Central venous pressure and pulmonary capillary wedge pressure monitoring may be considered in the critical phase to evaluate fluid status. Protecting the kidneys and liver from thermal and low-flow damage is critical. Myoglobinuria and poor renal perfusion put the kidneys at risk for renal failure; therefore urine should be carefully monitored for color, amount, pH, and myoglobin. ^{1.12. and 23.}

Chilblains are localized areas of itching and redness accompanied by recurrent edema to exposed or poorly insulated body parts such as the ears, fingers, and toes. Chilblains are usually seen in cool, damp climates with temperatures above freezing. Chilblains are probably a mild form of frostbite with gradual onset of symptoms. There is generally no pain; however, the patient may experience transient numbness and tingling. Initial pallor or redness of the nose, digits, or ears may evolve into plaques and small, superficial ulcerations over chronically exposed areas.

Prehospital treatment begins with removal to a warm area in conjunction with covering the affected area with a warm hand or placing fingers under the axilla. ¹⁹ Elevation of the affected area decreases edema, which increases circulation and allows gradual warming at room temperature. Never rub or massage injured tissue. Avoid direct heat application. Tissue damage is rarely seen with chilblains; however, the patient should be instructed to protect the area from injury and further environmental exposure and to watch for signs of secondary infection. ^{11. and 18.}

Nonfreezing cold injury, a syndrome also known as immersion foot or trench foot, results from damage to peripheral tissues from prolonged (hours to days) contact between a wet foot and cold temperature. This usually occurs when the patient is wearing a watertight boot that does not allow normal evaporative “breathing.” This condition is commonly seen in hunters and soldiers on outdoor maneuvers. Feet initially are cold, damp, numb, and edematous but within 24 to 48 hours will appear warm. Vasodilation and hyperemia, which result from warming, cause intense burning and tingling. Prolonged and repeated exposure can lead to lymphangitis, cellulitis, thrombophlebitis, and liquefaction gangrene.

Therapeutic interventions include drying the feet and changing frequently into dry socks. After the patient is in a controlled environment, rewarm injured areas gradually by exposing them to air or soaking them in warm water (100° F to 105° F [37.7° C to 40.5° C]) before drying. Some clinicians recommend daily air-drying of the feet for 8 hours. ³ Immersion foot is reversible with timely treatment. Patients are usually hospitalized for observation and prevention of complications.

Frostbite, the most prevalent injury caused by extreme cold, occurs when ice crystals form in intracellular spaces as tissue freezes. These crystals enlarge and compress cells, causing membrane rupture, interruption of enzymatic activity, and altered metabolic processes. Histamine release increases capillary permeability, red cell aggregation, and microvascular occlusion. ¹ Once frostbite occurs, damage is irreversible. Further exposure to extreme cold or trauma increases tissue damage and worsens the injury. The patient with frostbite may also have hypothermia. Treatment of hypothermia takes priority over management of frostbite. Frostbite can be superficial or deep, depending on the degree of the cold and the length of exposure. Estimation of the extent of injury may not be possible until several days after exposure. ^{6. and 12.}

Hypothermia can occur in many different situations, including cold ambient air, cold water immersion, or cold water submersion. Hypothermia can also occur as the result of a disease process (e.g., hypoglycemia), infusion of room temperature fluids, alcohol consumption, and ingestion of some medications. Hypothermia is defined as a core temperature below 95° F (35° C). Severe hypothermia is a core temperature less than 90° F (32.2° C). The American Heart Association has established 86° F (30° C) as the temperature for initiation of aggressive internal rewarming procedures. ¹⁷ The body’s metabolic responses depend on a normal core temperature. As the core temperature drops, there is a progressive decrease in cellular activity and organ function. When the temperature drops by 18° F (10° C), the basal metabolic rate drops by two to three times the normal rate. The most obvious response is seen in the central nervous system (CNS). The patient becomes apathetic, weak, and easily fatigued, with impaired reasoning, coordination, and gait. The patient’s speech is slow or slurred. Renal blood flow decreases, causing a decline in the glomerular filtration rate. Impaired water reabsorption leads to dehydration. Decreased respiratory rate and effort lead to carbon dioxide retention, hypoxia, and acidosis. Shivering consumes glucose stores, so the patient becomes hypoglycemic. Insulin levels fall, so available glucose decreases, forcing the body to metabolize fat for energy. Drug metabolism in the liver is sluggish, so medication effects may last longer. ^{8. and 17.}

The cardiovascular system is also dramatically affected. Cold heart muscle is irritable and prone to dysrhythmias. The Osborne or J wave is a striking feature seen on electrocardiogram in approximately one third of hypothermic patients³² (Figure 40-3). The J wave is described as a “humplike” deflection between the QRS complex and the early part of the ST segment. The most common dysrhythmias are atrial and ventricular fibrillation. The cold patient is in great danger of ventricular fibrillation when core temperature falls below 82° F (27.8° C). Ventricular fibrillation at these extremely cold temperatures does not respond to conventional treatment without prior rewarming. Defibrillation is limited to three shocks until core temperature is greater than 86° F (30° C). ¹⁰ Intravenous medications are also limited until the core temperature is greater than 86° F (30° C). Careful handling of hypothermic patients, especially when their temperatures reach the vulnerable mid-80s range, is imperative because even turning may cause ventricular fibrillation. Rewarming procedures are active or passive, based on external warming or internal warming. ¹⁷Table 40-1 lists various procedures by category.

The goal in mild hypothermia (93.2° F to 96.8° F [34° C to 36° C]), in which the patient is still shivering, alert, and oriented, is to prevent further heat loss and rewarm the patient as rapidly as possible. ^{8.16. and 17.} Passive external rewarming techniques such as moving the patient to a warm environment, replacing wet clothing with dry material, and wrapping with warm blankets may be effective. However, many patients require internal rewarming using warmed humidified oxygen. Giving the patient warmed, oral fluids that contain glucose or other sugars provides more heat through calories. Passive rewarming raises the temperature 1° F to 4° F (0.5° C to 2.0° C) per hour. Gradual rewarming minimizes the risk for active rewarming shock.

In moderate hypothermia (86° F to 93.2° F [30° C to 34° C]), rewarm truncal areas at 1° F (0.5° C) per hour using heating blankets such as Bair Hugger Therapy, radiant heating lamps, and hot water bottles. Monitor closely for marked vasodilatation and subsequent hypotension. American Heart Association guidelines recommend active internal rewarming when core temperature is less than 86° F (30° C) (see Table 40-1). Warmed humidified oxygen via endotracheal tube (108° F to 111° F [42.2° C to 43.8° C]), mechanically warmed intravenous fluid, peritoneal lavage, esophageal rewarming tubes, gastrointestinal irrigation, bladder irrigation, extracorporeal rewarming cardiopulmonary bypass, and hemodialysis may all be used.

In severe hypothermia (lower than 78.8° F [26° C]), active internal (core) rewarming in conjunction with active external rewarming procedures is essential to prevent rewarming shock. Rewarming shock can occur after rewarming is initiated. Cold peripheral blood returns to the central circulation, causing a continual drop in core temperature. Circulation of cold blood through the heart also increases ventricular irritability and leads to fibrillation. Rewarming may also cause peripheral vasodilatation, which can precipitate hypotension and cardiovascular collapse.

The continuous arteriovenous rewarming (CAVR) method, developed at the University of Washington, employs a modified bypass technique for rapid blood rewarming using a Level One fluid warmer normally used for trauma resuscitation. The treatment is preferred for patients with profound hypothermia. A spontaneous pulse is necessary because the patient’s intrinsic blood pressure drives flow through the countercurrent module. (In true cardiothoracic bypass, an external pump is built into the machine.) The catheters are placed into a femoral artery and venous cordis, the blood is warmed as it flows through the countercurrent module. The CAVR method has rewarmed profoundly hypothermic patients five times more rapidly (39 minus versus 199 minutes) than standard methods and was demonstrated to decrease mortality rate. ¹³

Successful rewarming depends on the patient’s age, general condition before the hypothermic event, length of the patient’s exposure, and careful handling by the ED team. To prevent hyperthermia secondary to aggressive rewarming, discontinue active rewarming when core temperature reaches 89.6° F to 93.2° F (32° C to 34° C).