Heat illnesses exist on a spectrum of seriousness. An athlete need not experience symptoms of mild then moderate then severe heat illness to have heat stroke. The exact epidemiology is poorly defined and varies widely dependent on the study population and environmental conditions.
Definitions, pathogenesis, clinical presentations, and key principles of treatment of heat-related illnesses are summarized in Table 38-1.1–8
Illness | Definition | Pathophysiology | Clinical Presentation | Treatment |
|---|---|---|---|---|
Heat edema | Swelling of the distal extremities when exposed to exercise in a warm environment. Usually transient and subsides within the first few days of the acclimatization period. | Neuroendocrine system response to real or relative decreased plasma volume early in the period of exposure to exercise in a warm environment. It is believed that this decrease causes increased secretion of aldosterone and therefore leads to sodium retention. | Swelling and puffiness, more notable in the ankles, and less commonly the hands. Typically in the first few days in heat exposure. Heat edema is uncommon in the face and therefore any facial edema should be evaluated accordingly. | Elevation of the swollen extremities. Self limiting and resolves within the few first days of heat exposure. |
Heat syncope | Transient hypovolemia, orthostatic hypotension that usually affects an unacclimatized athlete. Likely related to dehydration and venous pooling secondary to vasodilatation in the body’s attempt to regulate core body temperature. | Explained by the vasodilation. As the athlete decreases activity the resulting decreased cardiac output along with possible dehydration, results in hypotension. This, in turn, leads to vasovagal insufficiency and cerebral hypoperfusion. | Manifests in the early acclimatizing period as a sudden fainting that resolves shortly after the young athlete comes to rest on the ground. Occurs after completion of a sustained activity, and typically in the first few days of exposure to the warm environment. | Evaluate for injuries secondary to the syncopal episode, including head and neck injuries. The athlete should be moved to a cool environment and re-hydrated. Evaluate need for cardiac workup prior to the return to activity. |
Exercise-associated cramps | Involuntary spasms of the muscles, commonly affecting the lower extremity but may occur in the arms or abdomen; occurring during or after the physical activity. | Multiple theories including alterations in spinal neural reflex activity, local electrolyte abnormalities, and exertional muscle damage. | Can occur at any ambient temperature; more common in warmer environments. Present as uncontrolled and involuntary contractions of the muscles, most commonly the lower extremity. Abdominal, back and upper extremity may be involved. Common with longer duration sports as the muscle approaches fatigue. | Cessation of the activity, gentle stretching, massage, and oral hydration. With severe cramping, intravenous hydration with normal saline may be required. When the cramping resolves, and provided the athlete re-hydrates, he/she can generally return to activity. |
Exertional heat exhaustion | Inability to sustain exercise that has occurred during heavy exertion that may or may not be associated with collapse. | Represent the body’s attempt to prevent further perturbations of thermal regulation where central fatigue causes peripheral vasodilatation and ultimately collapse. Core temperature need not be elevated. The primary differentiation between exertional heat exhaustion and exertional heat stroke is the presence of central nervous dysfunction and multisystem dysfunction that are present with exertional heat stroke. | Initially dizziness or faintness and fatigue. The athlete usually is typically sweating which may be on the spectrum from mild to perfuse. Chills, nausea, thirst, anxiety, weakness, and poor coordination, among other nonspecific symptoms. The major distinction between heat exhaustion and heat stroke is mental confusion, and at times the fatigue and faintness can be difficult to differentiate from altered mental status. | Prompt cooling and re-hydration to maintain intravascular volume. Active cooling may include water spray; fanning, and ice bag or ice towel application to the neck, groin, and axilla. Oral hydration with a dilute electrolyte drink should commence immediately. Any athlete who shows deterioration to exertional heat stroke requires emergent care. Return to participation can be considered 24 to 48 hours after the athlete is asymptomatic and re-hydrated. |
Heat stroke | Body core temperature above 40oC, associated with altered mental status and multisystem dysfunction that occurs during or following heavy physical exertion. | Damage at the cell and organ level secondary to elevated core temperature. As tissue temperatures reach a critical level, cell membranes are damaged, energy systems are disrupted, and electrolyte and acid–base disturbances are induced. The degree of damage to organ systems is dependent on the duration of thermal stress. | Most commonly presents as collapse during a sustained activity in the warm environment. More common in the early period of acclimatization. The skin is usually warm and dry, but minimal perspiration may still be present. The athlete will have tachycardia, tachypnea, and an altered mental status. | Active cooling should be implemented at the site, cooling with ice water emersion with continuous rectal temperature monitoring. Other measures for aggressive cooling including cold water spray, ice bag or ice towel, and fanning should be implemented emergently. Aggressive cooling should continue until core temperature reaches 38.3°C (101°F). Intravenous fluid resuscitation should be initiated as soon as possible to prevent a decrease in perfusion that is expected in exertional heat stroke. Emergent transport via EMS to a medical facility. |
Pathogenesis is summarized in Table 38-1.1–8 Risk factors are summarized in Table 38-2. Core body temperature is determined by the balance of heat generation and dissipation. A major contribution to the total thermal load is the generation of heat from exercising muscle. At maximal effort, skeletal muscle generates as much as 20 times the energy at rest. However, muscle energy generation is inefficient and as much as 75% is converted to heat, providing a major thermal load to the body systems. Additional thermal load is provided by the environment itself through radiant heat and convection in the environment. Dissipation of heat from the body to the environment is a combination of convection, radiation, and evaporative loss. But as the ambient temperature and humidity increase, the body becomes dependent on evaporative loss. At 23°C (74°F), 71% of heat dissipation is dependent on evaporative loss versus 100% dependence on evaporative loss at 35°C (95°F).9 Logic dictates that ambient temperatures approaching 35°C, and high relative humidity, will decrease the efficacy of evaporative heat loss. It is noted that although core temperature above 40°C (104°F) is the definition for exertional heat stroke, higher core temperatures have been recorded in asymptomatic elite athletes. Therefore, the elevation of core temperature alone does not indicate heat illness.
Intensity and duration of activity |
Extremes of age |
Acclimatization to exercise |
Heat stress |
Individual work capacity |
Individual sweat loss |
Physical conditioning |
Hydration status |
Medications, supplements |
Sleep deprivation |
Recent illness |
Increased ambient temperature |
Increased relative humidity |
Wind |
Increased radiant heat |
Multiple consecutive days of elevated temperatures |
Specifics factors in children
|
The body’s response to increasing core temperature is vasodilatation of the skin capillaries to dissipate heat. At the same time, there is vasodilatation of the skeletal muscle to provide oxygen and nutrients to the working muscle. As the skin temperature increases, neural regulation increases sweat loss. This sweat loss is hypotonic or isotonic. Thus, initially there may be no significant electrolyte loss. However, as exercise and sweating continues over longer endurance activities, continued loss of sweat can influence the loss of electrolytes.
Clinical presentation, diagnosis, and treatment are summarized in Table 38-1.
Prevention of heat-related illnesses includes providing for a period of acclimatization, modification of activities based on the heat index, and access to electrolyte sports beverages. The process of acclimatization includes physiological adaptations that allow for increased peripheral blood flow, earlier onset of sweating, and greater volume of sweat. Acclimatization occurs over a period of 7 to 14 days where the athlete is gradually introduced to increasing levels and duration of physical activity.
Although weather forecasts may provide some information regarding the ambient temperature, relative humidity, and heat index, it is advisable to perform measurements at the site on a regular basis. Instruments for measurement of environmental conditions vary from the sling psychrometer to more expensive heat stress monitors. Figure 38-1 provides a table for determination of the heat index using temperature and relative humidity. Physical activities for children in hot climate should be modified based on the wet bulb globe temperatures (Table 38-3).3 Similar guidelines for adults can be accessed from American College of Sports Medicine at www.acsm.org.
Wet Bulb Globe Temperature | Restraints on Activities | |
|---|---|---|
(°C) | (°F) | |
<24 | <75 | All activities allowed, but be alert for prodromes of heat-related illness in prolonged events |
24.0–25.9 | 75.0–78.6 | Longer rest periods in the shade; enforce drinking every 15 min |
26–29 | 79–84 | Stop activity of unacclimatized persons and other persons with high risk; limit activities of all others (disallow long-distance races, cut down further duration of other activities) |
>29 | >85 | Cancel all athletic activities |
Maintenance of proper hydration before, during, and after physical activities is paramount to preventing dehydration and associated exertional heat illnesses. Loss of 2% of the total body weight to fluid losses increases physiologic strain and has a negative effect on physical and cognitive performance. Detailed information regarding fluid replacement is available through the position statements of American College of Sports Medicine (ACSM) and the National Athletic Trainers’ Association (NATA).4,5
Athletes should be euhydrated prior to beginning practice or competition. First morning urine osmolarity or specific gravity and morning body weight monitoring can be used to evaluate individual hydration status. This information can be used by the athlete during training along with the fluids consumed to develop an individual hydration plan. Urine should not be dark and generally should have a specific gravity lower than 1.020. Four hours prior to competition, the athlete should slowly consume fluids to ensure urine production. The use of hyperhydration has not been shown to prevent dehydration and may increase the need to void during competition.
The quantity of fluid needed during exercise is highly variable between athletes as sweating rates have been reported between 400 mL/h and 1800 mL/h. General starting quantities recommended are 400 to 800 mL per hour, or 200 to 300 mL every 20 minutes, with regular monitoring of body weight and urine color or specific gravity so that the athletes may customize their fluid intake to individual needs.4–8 Larger volumes may be required depending on sport-specific demands. For example, American football players in full gear have been shown to have losses of 8 L per day.
The major loss to sweat is water; however, there are losses of sodium, potassium, and chloride. Carbohydrate intake of 30 to 60 g during longer competition, more than 90 minutes may be beneficial to maintain blood glucose levels as well as promoting absorption and retention of fluids. Beverages should be chilled and flavored to encourage consumption. Commercial sports drinks generally provide approximately 20–30 meq/L of sodium chloride, 2–5 meq/L of potassium chloride, and 60–80 g/L of carbohydrate. It would be appropriate for these nutrients to be supplied in other sources besides a sport drink as well.
Rehydration following exercise is best accomplished with normal meals and beverages. The general guideline is that 1.5 L of fluid are consumed for every 1 kg of body weight loss. If it is impractical to consume a full meal, sodium containing snacks and carbohydrates are beneficial in promoting fluid absorption and retention.
Lightening causes a vast array of injuries and is one of the top causes of weather-related fatalities. In the US, over 100 fatalities and many more injuries are related to lightening strikes annually.9 Athletes are at risk of lightening injuries because of the fact that many athletic events take place in the afternoons during thunderstorm seasons. Additionally, the flat cleared fields used for practice and competition afford no protection.
The electrical current from lightening preferentially travels through the human body because of the high electrolyte-rich medium (i.e., serum, extracellular fluid) that composes the human body. There are five major mechanisms of lightening injury as listed in Table 38-4. Because lightening strike victims do not remain in contact with the electrical source, the body does not remain energized, and therefore can be approached and touched.9
Direct strike |
Contact with object that is struck |
Side strike from an object that is struck |
Step-voltage or ground current (preferential pathway through the feet apart in contact with the ground near a strike) |
Blunt injury |
After a lightening strike, victims may present with a wide range of injuries dependent on the mechanism of the contact with lightening. Victims in cardiopulmonary arrest may be found unresponsive, apneic, pulseless, and with dilated and fixed pupils. Many of these findings are secondary to the charge of energy in the body, and despite these findings, victims can still be revived. Other injuries include burns, fractures, blast injuries, and tympanic membrane perforations.
The diagnosis is based on the history.
Initial on-field treatment begins with ensuring a safe environment for the rescuer. In many circumstances the victim may need to be emergently moved from the site of injury to a safe area for the rescuer, followed by management based on the standard principles of basic and advanced life support by appropriately trained personnel. Data shows that recovery from cardiopulmonary arrest secondary to lightening strikes is favorable, therefore the general triage principles are modified, and the pulseless, apneic patient should be treated first. Table 38-5 lists the steps for prehospital treatment of lightening injuries.
Perform steps in the following order:
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