Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine) 4th Ed.



Heat and Cold Illness

Sean M. Fox


• While there are physiologic differences that exist between children and adults, the primary risk factor for heat illness in children is inadequate or inappropriate supervision.

• Heat-related illnesses comprise a continuum of conditions ranging from minor entities such as heat cramps to more serious conditions including heat exhaustion and heatstroke.

• Heatstroke is the most severe form of heat illness, with reported mortality between 17% and 80%.

• Heat exhaustion is a syndrome of dizziness, postural hypotension, nausea, vomiting, headache, weakness, and, occasionally, syncope.

• Special glass or electronic thermometers are required for accurate measurement of temperatures in hypothermic patients.

• Extracorporeal rewarming is the most rapid method of rewarming and is indicated in hypothermic cardiac arrest and with patients who present with completely frozen extremities.


Heat-related illness garners much publicity and may lead to significant morbidity and mortality. The spectrum of heat illness ranges from mild, self-limited problems to major, life-threatening conditions. The majority of patients who are evaluated in the emergency department for heat illness can be appropriately treated and discharged, with only approximately 7% requiring transfer or hospitalization.1Unfortunately, there has been a 133.5% increase in exertion-related heat illness between 1997 and 2006.2 The average annual number of deaths attributed to heat illness in the United States over the past decade was 618 per year.3 While there are multiple factors that influence these numbers, it is currently believed that the majority of the morbidity and mortality associated with heat illness is preventable.

Traditionally, pediatric patients are included in the group who is considered to be at greater risk for developing heat-related illness. Commonly cited reasons for the pediatric patient’s increased risk include a greater body surface to mass ratio adversely affecting heat absorption, higher metabolic rate leading to greater heat production, lower perspiration rate leading to decreased heat dissipation, and reduced acclimatization.47 Recent research investigating the validity of these potential causes challenges the notion that children are at physiologic disadvantage compared to adults.8,9 While there are obvious physiologic and metabolic differences between children and adults, it is difficult to determine whether these variances lead to increased risk. The different thermoregulatory strategies in pediatric patients do not, necessarily, constitute an inferior response to heat stress.9,10

What is known is that children interact with the environment differently than adults and this often places them at greater risk for injury. Infants, especially those under one year of age, who are dependent upon adult supervision to ensure their safety, are at greatest risk for heat-related mortality.11 Excessive bundling alone can lead to heat illness in the very young. The development of heat illness in small children left in closed cars on hot days is a tragic situation that is entirely preventable through parental education.12 While the dependent infant is at high risk of heat injury because of inadequate guardian protection, adult supervision also influences older children’s and adolescent’s risk for heat injury. Older children are susceptible to heat illness when they exercise vigorously under hot, humid conditions.4 Patients less than 19 years of age accounted for the largest proportion of exertion-related heat illness.2Several factors influence this association of the young athlete and heat illness. Some athletes are actually dehydrated before participating in their sport.13 The specific activity also plays a role: Those who participate in football have been shown to have a 10-fold higher rate of heat illness compared to other sports.14 Naturally, the older children’s zeal for competitive athletics, coupled with a sense of invulnerability, can lead to serious heat illness; however, guidelines and prevention strategies exist to assist supervising coaches to manage the young athletes in a safe manner.1517 Appropriate education for both adults and children is an important strategy to help prevent heat illness from occurring.

In addition to poor supervision and exertion with poor acclimatization, there are other factors that influence development of heat illness in pediatric patients. Drug-related heat illness is seen with increasing incidence in the adolescent population. Obesity has also been found to increase risk for heat-related illness.18 Infections and chronic medical problems also influence a child’s risk by affecting their thermoregulatory systems. Children with cystic fibrosis (see Chapter 45) are prone to develop a form of heat illness characterized by excessive electrolyte loss with sweating. In addition, any patient who has had a previous episode of heatstroke is markedly predisposed to recurrence.19


The body’s metabolic processes constantly generate heat. At rest, the body generates enough heat to raise the body temperature by approximately 1°C/h. Heavy exertion can increase heat production to 12 times this level. The environment also influences the body’s temperature. When the ambient temperature exceeds the body temperature, there is a net heat gain from the environment. The body can dissipate heat by radiation, conduction, convection, and evaporation20 (Table 139-1). Heat injury occurs when the body’s internal temperature rises faster than it can dissipate the heat.

Table 139-1

Primary Mechanisms of Heat Dissipation Related to Heat Illness



The spectrum of heat-related illnesses comprises conditions ranging from minor entities such as heat cramps to more serious conditions including heat exhaustion and heatstroke. Depending upon the condition, the management priorities are varied (Table 139-2).

Table 139-2

Spectrum of Heat-Related Illness


Heat Cramps

Heat cramps are extremely painful muscle spasms that occur with heavy exertion. The body temperature remains normal, and there is associated sweating. There are no central nervous system signs. Heat cramps can occur regardless of whether exercise is performed in hot or cold weather. The underlying cause has long been described as dilutional hyponatremia, which usually occurs in conditioned athletes who replace fluid losses with water; however, there is no clear evidence to support this as a cause.5 Another theory suggests that the underlying mechanism is due to alterations in the spinal neural reflex activity stimulated by fatigue in susceptible individuals.20 Clinically, fluid rehydration is paramount as the pain associated with the muscle spasms can be resistant to narcotics in the absence of adequate fluid rehydration.21

Heat Exhaustion

Unlike heat cramps, heat exhaustion manifests with systemic symptoms. Heat exhaustion is a syndrome of dizziness, postural hypotension, nausea, vomiting, headache, weakness, and, occasionally, syncope. It may be associated with normal body temperature or moderate temperature elevation (39–41.1°C).22 The skin is usually wet from profuse sweating. Generally, it occurs in unacclimated individuals but has a low associated morbidity.22

The cause of heat exhaustion may be either salt or water depletion. Salt depletion occurs when fluid losses are replaced by water or other hypotonic solutions and hyponatremia results. Although severe hyponatremia can result in significant mental status changes and/or seizures, the mental status in heat exhaustion patients tends to be normal. Water depletion occurs when victims are unable to replace fluid losses, resulting in hypernatremic dehydration. This can occur in infants or mentally retarded children, who cannot communicate their thirst.5,19,23


Heatstroke is the most severe form of heat illness and represents a state of complete thermoregulatory failure. The reported mortality for heatstroke ranges from 17% to 80%.1922 Patients with heatstroke can present with disorientation, seizures, or coma. Classic heatstroke is typically seen at the extremes of age (infants and elderly) and develops over a period of days.24 The skin is usually hot and dry. With exertional heatstroke, which is much more likely in the pediatric population, the skin may be dry or sweating may continue. The temperature ranges from 41.1 to 42.2°C. There is no clear scientific evidence to indicate that heatstroke results from fluid and electrolyte abnormalities. The risk of developing exertional heatstroke appears greater in individuals performing high-intensity exercise for a relatively short time span.20

Predisposing conditions for classic heatstroke include dehydration, obesity, neurologic disorders, hyperthyroidism, extremes of age, alcohol consumption, sickle cell trait, and medications that interfere with heat dissipation (e.g., phenothiazines, anticholinergics, and diuretics).19,21

The high mortality rate is due to systemic complications that commonly develop. All organ systems are potentially affected and patients may present with neurologic dysfunction, renal insufficiency secondary to acute tubular necrosis, hepatic damage, disseminated intravascular coagulation, and respiratory distress syndrome. Multiorgan system dysfunction may also develop.20,22,25 These include encephalopathy, hemorrhagic complications, intestinal ischemia or infarction, rhabdomyolysis, and sepsis.20,21 In-hospital mortality is reported at 21% while residual moderate-to-severe functional impairment is seen in 33% of those patients who can be discharged from the hospital. In follow-up, the functional impairment was found to persist at 1 year.20,22 While the outcome may be somewhat better for the young, otherwise healthy individual, mortality and morbidity remain unquestionably significant.


With each heat-related illness, prompt recognition and initiation of therapy is imperative. In addition to rapid assessment and management of airway, breathing, and circulation, expedient reversal of hyperthermia, if present, is the key component of therapy. Management is directed by proper identification of the suspected condition (Fig. 139-1Table 139-2).


FIGURE 139-1. Approach to the patient with heat exposure.

Heat cramps are treated by having the patient rest and placing the patient in a cool environment. Providing rest and oral electrolyte solutions is often all that is needed. Salt tablets are not recommended as they may cause gastrointestinal cramping. If commercially prepared electrolyte replacement fluids are not available, a solution of 1-tsp table salt in 500-mL water can be used to initiate therapy. Avoid use of replacement fluids that contain caffeine or alcohol because of their diuretic effects.20,21

Heat exhaustion is also treated by removal to a cool environment and providing rest, but generally intravenous rehydration is recommended as the patient’s clinical symptoms often prevent adequate oral rehydration. Initial intravenous rehydration can start with 20 mL/kg of normal saline over 30 minutes and rehydration continued as outlined in Chapter 10. If hypernatremic dehydration is suspected on clinical or laboratory grounds, slower replacement is indicated.19,23 Victims of heat exhaustion may require observation in the hospital; however, if all symptoms have resolved during emergency department treatment and observation, the patient may be released to continue rest and rehydration in a cool environment.

Heatstroke, on the other hand, is an immediately life-threatening entity and must be treated vigorously. After assessment and stabilization of the airway, breathing, and circulation, cooling should be instituted immediately.26 An effective and practical method to begin cooling is by spraying the skin with room-temperature water and directing an electric fan onto the patient’s skin. This method will usually result in rapid reduction of the core temperature. Ice packs may be used in the groin and axilla, but ice water should not be applied widely to the skin as this may cause vasoconstriction and impair the dissipation of heat. Submersion in cold water is very effective in lowering the temperature but makes other resuscitative efforts practically impossible. Invasive lavage to lower the body temperature has not been adequately studied and is not currently recommended. During resuscitation, intravenous fluids are required and should initially be given as isotonic crystalloid at a rate of 20 mL/kg over the first hour. Antipyretics are generally ineffective.4,21 The core temperature should be monitored continuously during treatment and active cooling should continue until the core temperature falls to 39°C.20 Due to the potential multisystem involvement and injury, continuous venous–venous hemofiltration can also be a useful tool to lower the body’s temperature while supporting the multiorgan functions.27

Since the effects of heatstroke are widespread and the potential clinical scenarios vast, a broad differential diagnosis should be considered during the evaluation and management. (Fig. 139-1Table 139-3). Individual strategies should be adjusted to specifically address the patient’s suspected complications. Patients with heatstroke may have significant derangement in oxygenation, ventilation, and acid–base status. Changes in body temperature alter blood gas values, but whether corrections in the values are helpful before treatment decisions are made is controversial.19,21 Heatstroke is also associated with other basic laboratory value alterations. Electrolyte studies may reveal abnormal sodium levels. Hemoglobin and hematocrit values are usually elevated due to dehydration. A low hemoglobin level should prompt consideration for potential trauma. It is also important to keep rhabdomyolysis on the differential and look for abnormal renal function, hyperkalemia, and evidence of muscle breakdown. Urinalysis will often show a high specific gravity as a reflection of the hydration status. A urinalysis that is positive for hemoglobin in the absence of red blood cells on the microscopic evaluation, is concerning for rhabdomyolysis. In addition, the liver is very susceptible to injury due to hyperthermia, and liver enzymes may be elevated. Transaminase levels correlate well with the severity of injury and peak in 24 to 48 hours. Very high levels (aspartate transaminase >1000 IU) are predictive of severe illness and complications. Serum glucose levels are variable but should be monitored to assess the need for replacement or control. Coagulation studies are needed to detect the development of disseminated intravascular coagulation.

Table 139-3

Differential Diagnosis of Heatstroke: Symptom Complex—Altered Mental Status, Hyperthermia


Considering potential concurrent infectious etiologies is also important. The complete blood count will usually show an elevated white blood cell count in patients with heatstroke. Counts >20,000/mm3 and elevated band counts are more consistent with an underlying infection, though, and should prompt a complete septic workup. Often, because the clinical picture is poorly defined initially in the patient with possible heatstroke, it is most practical to act conservatively and obtain cultures and consider initiating empiric antibiotics.

As part of the further evaluation of the poorly differentiated patient presenting with altered mental status, possibly due to heatstroke, a number of other studies are potentially useful to obtain. A chest radiograph looking for potential traumatic explanations of infectious etiologies can be beneficial. Computed tomographic scanning of the brain may also be indicated to rule out intracranial pathology, especially if the mental status does not promptly improve with lowering of the temperature. An electrocardiogram is also helpful to evaluate for myocardial ischemia, electrolyte abnormalities, and possible toxic ingestions.

After initial stabilization, patients with heatstroke require admission to an intensive care setting for continued monitoring and aggressive treatment.


Similar to heat illness, cold illness represents a significant public health issue that is often preventable. In the United States, cold exposure leads to a total of 16,911 deaths from 1999 to 2011, which is an average of 1301 per year. 2010 saw the highest yearly total of hypothermia-related deaths with 1536 deaths.28 Hypothermia is defined as an unintentional drop in core body temperature of <35°C. Hypothermia can be classified into three categories: mild (core body temperature 35–32°C), moderate (core body temperature 32–30°C), and severe (core body temperature <30°C).29 A low body temperature may develop as a result of exposure to low ambient temperature or may be secondary to a disease process (Table 139-4).

Table 139-4

Causes of Hypothermia in Infants and Children


Once again, similar to heat-related illness, pediatric patients are included in the group that is at greater risk for having cold illness. Age is an important factor in determining the susceptibility to hypothermia and the morbidity and mortality associated with it. Neonates are particularly at high risk for developing hypothermia due to their large surface area compared with body mass and the relative paucity of subcutaneous tissue.30 Neonates have also been postulated to have poorly developed thermoregulatory systems. The newly born is particularly susceptible to hypothermia due to the evaporation of amniotic fluid from the skin. Throughout infancy and young childhood, children remain susceptible to hypothermia with exposure to cold, although less so with advancing age. Most cases of accidental hypothermia in older children and adolescents are associated with submersion events in cold water.31 Recently, there has been an increase in exposure-related hypothermia in older children and adolescents, which is believed to be associated with the increased popularity of winter sports.31 The greater the environmental stress, the higher the potential for development of hypothermia.29 Inexperience and lack of caution, which are common among adolescents, increase the likelihood of their becoming victims of hypothermia. Appropriate supervision, education, and adequate preparation have the potential to positively affect the number of hypothermia cases.

Thermoregulatory measures control the normal body’s temperature over a narrow range usually. The primary mechanisms of heat loss related to cold illness are outlined in Table 139-5.

Table 139-5

Primary Mechanisms of Heat Dissipation Related to Cold Illness


Exposure to cold stimulates skin receptors, resulting in peripheral vasoconstriction and conservation of heat. As the temperature of the blood declines, the preoptic anterior hypothalamus is stimulated to initiate mechanisms to generate more heat. Shivering is one of the initial mechanisms appreciated, but metabolic and endocrine means of thermogenesis, primarily mediated by thyroid hormones and adrenal axis, also play a role (Fig. 139-2).32


FIGURE 139-2. Physiologic responses in hypothermia. (Adapted with permission from Cooper MA, Danzl DF. Hypothermia. In: Hamilton GC, Sanders GR, Trott AT, eds. Emergency Medicine: An Approach to Clinical Problem-Solving. Philadelphia, PA: W. B. Saunders; 1991.)

Cold stress potentially affects all organ systems (Fig. 139-3). The most prominent effects are seen in the cardiovascular, central nervous, respiratory, renal, and gastrointestinal systems.29,33 The effects of hypothermia on the cardiovascular system are often the most noticeable. After an initial tachycardia, the heart rate falls as temperature falls. Mean arterial pressure also falls progressively, along with cardiac output.29,34,35 Atrial dysrhythmias commonly appear at temperatures below 32°C but are usually considered innocent because the ventricular response is slow. Ventricular ectopy is seen with temperatures <30°C and the risk of ventricular fibrillation is greatly increased. Electrocardiogram may demonstrate J waves (Osborn waves) at the junction of the QRS complex and ST segment (Fig. 139-4).29,34 Although considered pathognomonic for hypothermia, the Osborn or J wave has no prognostic or predictive value in cases of hypothermia.29 As hypothermia worsens, the cardiovascular system continues to be adversely affected and at 19°C asystole can occur.


FIGURE 139-3. A schematic showing the multisystem effects of hypothermia on the cardiovascular, central nervous, respiratory, renal, and gastrointestinal systems.


FIGURE 139-4. In severe hypothermia, the electrocardiogram (ECG) demonstrates the prominent elevation of the J deflection, so-called Osborn waves. The height of the J wave is proportionate to the degree of hypothermia, and this finding is usually most marked in the midprecordial leads. As the rewarming continues, the Osborn waves lessen in amplitude, and it disappears after 24 hours (Reproduced with permission from Alhaddad IA1, Khalil M, Brown EJ Jr. Osborn waves of hypothermia. Circulation. 2000;101(25):E233–244.)

Central nervous system is also greatly affected by cold stress. As the core body temperature drops below 33°C, the patient becomes confused and ataxic. Brain enzymes are less functional with declining temperature, resulting in a linear decrease in cerebral metabolism. Cerebral perfusion is maintained until autoregulation fails at approximately 25°C. At 20°C, the electroencephalogram shows a flat line.

While hypothermia may affect the respiratory system through influencing the central nervous system, it can also directly impact the pulmonary system. Cold initially stimulates the respiratory drive, but as temperature falls, a progressive decline in minute ventilation supervenes. Bronchorrhea, because of the local effect of cold air, can be severe, simulating pulmonary edema29,35

In addition to cardiac, central nervous system, and pulmonary injury, cold illness also affects other organ systems. Vasoconstriction in the extremities results in an initial central hypervolemia. The kidney responds rapidly, producing a large “cold diuresis” of dilute glomerular filtrate. Ethanol and immersion in cold water increase this early diuresis. Gastrointestinal motility is decreased and gastric dilatation, ileus, constipation, and poor rectal tone commonly result. Inflammatory changes in the pancreas are also often found. When managing a patient with hypothermia, all organ systems need to be considered and evaluated.


The diagnosis of hypothermia may be obvious when a history of exposure is known; however, hypothermia may develop insidiously because of causes other than environmental exposure or to exposure in relatively warm environments. Unfortunately, the hypothermic patient is often not able to give an adequate history, so other sources of information should be sought. Attempts should be made to obtain a thorough history of the exposure, including the circumstances, location, ambient temperature, the length of exposure, and presence or absence of submersion or wet skin. If significant exposure is unlikely, an extensive history is required to search for clues for other causes of hypothermia (Table 139-4).

The core temperature defines the presence and severity of hypothermia. Most thermometers for routine clinical use will record a temperature down to only 34.4°C.35 Special glass or electronic thermometers are required for accurate measurement of temperatures in hypothermic patients. Continuous monitoring of rectal, esophageal, or tympanic temperature is very useful during treatment.29,34

The physical examination will help reveal the severity of the hypothermia. The key physical findings in patients with hypothermia, and the temperature level at which they occur, are depicted in Table 139-6. The skin is typically cold, firm, pale, or mottled. Localized damage due to frostbite may be present.36 Shivering will often be present in the older child or adolescent but ceases by the time the temperature reaches 31°C. Shivering can increase heat production by four to five times. Shivering is absent in neonates, making them entirely dependent on care from others, vasoconstriction, and heat generated by lipolysis.32 Behavioral responses, such as seeking a warm environment or putting on protective clothing, are major preventive mechanisms that are entirely absent in the infant.

In older children and adolescents, the affects on the central nervous system become a prominent clinical feature. Early neurologic signs of hypothermia include confusion, apathy, poor judgment, slurred speech, and ataxia. Focal neurologic defects may also be present. Coma usually supervenes by the time the temperature reaches 27°C. Due to the significant central nervous system effects, other pathology can be masked. It is imperative to actively search for signs of trauma, toxic ingestion, and endocrine disturbance. Serial physical examinations repeated at intervals during treatment can aid in the discovery of clues to problems that were initially masked by the hypothermia.

Table 139-6

Pathophysiologic Changes During Hypothermia



Since hypothermia impacts all organ systems, a high suspicion should be maintained for end-organ injury. Often extensive diagnostic testing may be indicated (Table 139-7).30 In hypothermia, there is decreased tissue perfusion and the oxyhemoglobin dissociation curve is shifted to the left. Arterial blood gases are useful for the evaluation of oxygenation, ventilation, and acid–base status. Although some authorities have recommended correcting blood gas results for body temperature, correction can lead to false elevation of Po2. Metabolic acidosis is usually present and the buffering capacity of the blood is markedly reduced.

Table 139-7

Key Diagnostic and Laboratory Testing in the Evaluation of Hypothermia


Typically, the hematocrit increases 2% for each 1°C drop in temperature. A baseline complete blood count is useful to help assess trends. In addition, the hemoglobin level may be decreased due to blood loss or chronic illness. Occult trauma should always be considered as a cause of low hemoglobin levels. Hypothermia can also lead to alterations in the white blood count. It may be reduced by sequestration and bone marrow depression. Even in the presence of severe infection, leukocytosis may not be seen.

Basic chemistry panels can also be useful in the evaluation of the patient with cold-related injury. Renal function tests are useful for establishing baseline renal function but are poor indicators of fluid status in hypothermia. During continued care, acute tubular necrosis may develop after rewarming. Serum glucose values may be elevated due to catecholamine effect and insulin inactivity below 30°C. Persistently elevated levels suggest pancreatitis or diabetic ketoacidosis. Hypoglycemia may develop due to inadequate glycogen stores in neonates and malnourished children.

Considering that hypothermia can also lead to clotting dysfunction, platelet count, coagulation studies, and fibrinogen level can be helpful in moderate-to-severe hypothermia. Cold injury induces thrombocytopenia and prolongs clotting times. Persistent changes after rewarming suggest the development of disseminated intravascular coagulation.

In addition, numerous other studies may prove to be beneficial. Amylase and lipase may be elevated and, because of the unreliability of the abdominal examination, may be the only indicators of the development of pancreatitis, which is associated with poor outcomes in the setting of hypothermia. Urinalysis will demonstrate a low specific gravity due to cold diuresis. Toxicologic studies are frequently indicated to detect causative or predisposing agents. Cultures of body fluids are indicated in all cases of moderate-to-severe hypothermia. Sepsis is a common cause of hypothermia in infants and may also develop as a complication of hypothermia due to other causes.

Radiologic imaging should include a chest radiograph in all cases of significant hypothermia. Pulmonary edema may develop during rewarming and aspiration is relatively common. Cervical spine films may be indicated if there is suspicion of trauma. Cranial computed tomographic scanning may be indicated in the setting of trauma or to search for other etiologic factors, especially when mental status does not clear with rewarming. An electrocardiogram is indicated for all patients with a core temperature <32°C to detect dysrhythmias or evidence of myocardial ischemia. The J wave (Osborn wave) (Fig. 139-4) is usually seen when the temperature falls below 32°C.


While the diagnosis of cold injury can be difficult to make in the emergency department, it requires a high index of suspicion to diagnose hypothermia in the field. Prehospital providers should presume hypothermia in situations where exposure, even at moderate temperatures, has occurred.37

One particular instance that requires consideration is the transport of the newly born or the neonate. Great caution is needed to prevent hypothermia and to initiate its early treatment in neonates. The neonate should immediately be dried and wrapped in warm blankets. Alternatively, after drying, the neonate can be placed against the body of the mother and then covered.

For other potentially hypothermic patients, simple strategies can be very helpful. All wet clothing should be removed, and dry blankets applied. Resuscitation fluids should be warmed whenever possible. While supporting ventilation, heated, humidified oxygen, if available, may minimize further core temperature loss and significantly add to other rewarming techniques. Cardiac monitoring is indicated to detect dysrhythmias. Because pulse and respiratory rates may be very slow in severe hypothermia, assessment for breathing and pulselessness is carried out over a 30- to 45-second period. If there is no pulse, chest compressions are started immediately. Basic life support measures should not be withheld while the patient is being rewarmed.


The management of previously healthy patients who is only mildly hypothermic (35–33°C) is generally straightforward. Passive external rewarming with placing the patient in a dry, warm environment and providing dry insulating coverings is usually sufficient to safely reheat the patient. For these patients, if there is no obvious environmental exposure, it is important to consider other causes of hypothermia, particularly infectious etiologies in the very young or immunocompromised.

For the patient with moderate or severe hypothermia, the initial approach to the patient is the same as that for any seriously ill patient, with evaluation and stabilization of the airway, breathing, and circulation before moving to other aspects of treatment.34 The path of further management of hypothermia is directed by the results of the assessment of the patient’s airway, breathing, and circulation (Fig. 139-5). Since the spectrum of illness ranges from mild symptoms to profound illness, the approach will need to be tailored for the individual. Patients without protective airway reflexes require endotracheal intubation, which should not be withheld for fear of precipitating ventricular fibrillation. As those patients with hypothermia are prone to arrhythmia, cardiac monitoring should be initiated and vascular access obtained. In addition, continuous monitoring of temperature is very helpful during treatment. A urinary catheter is also necessary to adequately monitor output.


FIGURE 139-5. Approach to the patient with cold exposure. IV, intravenous; CPR, cardiopulmonary resuscitation. (Reproduced with permission from McCullough L, Arora S. Diagnosis and treatment of hypothermia. Am Fam Physician. 2004;70(12):2325–2332.)

In the unfortunate circumstance of a patient arriving without pulses, cardiopulmonary resuscitation should be started. Focus should be on ensuring appropriate and adequate chest compressions. The cold myocardium may be resistant to defibrillation and to pharmacologic agents. During hypothermia, protein binding of drugs is increased, and most drugs will be ineffective in normal doses. Pharmacologic attempts to alter the pulse or blood pressure are to be avoided because drugs can accumulate in the peripheral circulation and subsequently lead to toxicity as rewarming occurs. If the initial, three defibrillation attempts fail to establish a rhythm, CPR should be resumed with minimal interruptions. Additional defibrillation attempts are unlikely to be successful until the patient is rewarmed to 30°C. Many patients spontaneously convert to an organized rhythm once achieving a core temperature of 32 to 35°C. It is important to remember that infants and children who have sustained prolonged hypothermic cardiac arrest have recovered with little or no neurologic impairment. In general, resuscitative efforts should continue until the hypothermic child is warmed to at least 30°C.29,30,35 Unfortunately there are no consistently reliable prognostic laboratory values that can help guide the reasonable duration of resuscitative measures.

While prompt basic life-supporting techniques are paramount, moderate-to-severe cases of hypothermia require active rewarming to be initiated as soon as possible. Heated, humidified oxygen and intravenous fluids warmed to 40°C have been shown to be safe and efficacious and are used from the onset of therapy. For neonates and infants, using radiant warmers prevents further heat loss. The older child and adolescent should be covered with dry, warm blankets. Attention should be paid to trying to limit heat loss from the head and often a warm blanket covering the scalp will help the rewarming process while not hindering resuscitation. Forced air rewarming systems are also very useful and have been described as effective, noninvasive, and not associated with an after-drop phenomenon. Another noninvasive means of rewarming involves applying subatmospheric pressure to the hand and forearm, along with heat. This technique is described as immediately resulting in subcutaneous vasodilatation and rapid heat acquisition, rapidly eliminating shivering, and subjective improvement. Further studies of these techniques are needed.29,38 Hot packs and electric blankets can be dangerous, because cold, vasoconstricted skin is very susceptible to thermal injury.

Simple rewarming measures like warm intravenous fluids, blankets, and warm, humidified oxygen are all effective strategies, but active core rewarming is used in most cases of moderate-to-severe hypothermia.24,29,30 Active core rewarming can be accomplished by irrigation of the stomach, bladder, and colon. Heat transfer by these techniques is somewhat limited. Rapid rewarming by irrigation of the mediastinum or pleural cavity via a thoracostomy tube is effective but very invasive. Peritoneal lavage with heated fluid (40–45°C) is probably a more effective method of active core rewarming. Another viable option for rewarming in severe conditions is extracorporeal rewarming, which is the most rapid method. Extracorporeal rewarming is indicated in patients with hypothermic cardiac arrest and with patients who present with completely frozen extremities. Using this technique, young, otherwise healthy people have survived deep hypothermia with no or minimal cerebral impairment.29,30,34


A special consideration in pediatric hypothermia is submersion events in cold water. (See Chapter 136.)


Another special consideration for cold-related injury is frostbite, which may occur in conjunction with hypothermia or as an isolated localized injury. Once primarily a military problem, frostbite is now more prevalent in the civilian population as a result of occupational and recreational exposures. In frostbite, the body parts most susceptible are those areas farthest from the body’s core; the earlobes, nose, hands, and feet. Predisposing factors to the development of frostbite include environmental, individual, behavioral, and occasion-linked factors (Fig. 139-6).36,39


FIGURE 139-6. Predisposing factors for development of frostbite. (The environmental, individual, behavioral, and occasion-linked factors that may predispose individuals for the development of frostbite.)

The pathophysiology of frostbite includes three distinct pathways of tissue freezing:1 extracellular formation of ice crystals,2 hypoxia secondary to cold-induced local vasoconstriction, and3 release of inflammatory mediators such as prostaglandins PGF2 and thromboxane A2. All pathways can occur simultaneously thereby intensifying tissue damage. Cold exposure also increases blood viscosity, promotes vasospasm, and precipitates microthrombus formation. The release of inflammatory mediators has been shown to peak during the rewarming process and cycles of recurrent freezing and rewarming further increase the tissue levels.29,40

Classification of Frostbite Injuries The clinical signs and symptoms of frostbite differ according to the depth of injury. Traditionally, frostbite has been classified by degree. First-degree frostbite is limited to the superficial epidermis. Erythema and edema occur and resolve without sequelae. Second-degree frostbite results in deeper epidermal involvement. Third-degree injury consists of full thickness skin injury. Recent studies have suggested that frostbite may be more usefully classified as superficial or deep (Table 139-8).29,30,36,39 With superficial frostbite, the rewarmed skin develops clear blisters in contrast to the hemorrhagic blisters seen upon rewarming with deep frostbite (Figs. 139-7 and 139-8).

Table 139-8

Classification of Frostbite Injuries



FIGURE 139-7. Clear blisters as commonly seen with superficial frostbite injuries.


FIGURE 139-8. Hemorrhagic blister as commonly seen with deep frostbite injuries.


The treatment of frostbite is rapid rewarming. The preferred initial technique is immersion of the affected part in circulating warm water (40–42°C). Narcotic analgesics are often required to control pain during rewarming. A number of adjunctive therapies, such as vasodilators, hyperbaric oxygen, and sympathectomy, have been recommended, but definitive evidence for their effectiveness is still lacking. Recently, the utility of thrombolytic therapy has been reported.41,42 While this is as of yet a novel approach, advances in imaging and interventional radiology have led to this technique being potentially viable on a larger scale.41

It is very difficult to determine tissue viability after significant hypothermic injury. Debridement of nonviable tissue is traditionally delayed for several days to weeks to preserve as much tissue as possible; however, recent improvements in radiologic assessment of tissue viability have led to the possibility of earlier surgery and more rapid rehabilitation times.29,36 Topical aloe vera cream and ibuprofen may be used for outpatient treatment after rewarming. More extensively injured patients will require continued inpatient treatment and pain control.

Rewarmed body parts are highly susceptible to refreezing, leading to even greater tissue loss. If exposure is anticipated, it is better not to rewarm the tissue.

Patients with mild accidental hypothermia (35–32°C) may be rewarmed and discharged to a safe environment if there is no evidence of underlying disease.

Most patients with hypothermia will require hospitalization for further treatment and evaluation. Those patients with a core temperature of <32°C will require cardiac monitoring. Profoundly, hypothermic patients with cardiac arrest and those with completely frozen extremities are candidates for extracorporeal rewarming and may require transfer to a tertiary care facility with this capability.


Proper preparation and planning in conjunction with adequate supervision can prevent most injuries. The first step is to be aware of cold risks. While little true acclimatization to the cold probably occurs, there is some value to practicing tasks that are to be performed in the cold and building up endurance before beginning a major cold activity. Good nutrition and hydration are helpful in resisting the stresses of cold weather activity. Sufficient clothing, either in layers or made of good insulating materials, is essential. Spare clothing is also essential since it may be necessary to change into dry clothing if clothing becomes wet. Going slowly and avoiding exhaustion or excessive sweating is also helpful. Alcohol and tobacco should be strictly avoided, as should contact with metallic objects. Appropriate education about the potential hazards of cold exposure is vital to the effort to reduce the incidence of cold-related injuries.


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