Environmental Illness

Pathophysiology

Exertional heat exhaustion (EHE) 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.

Diagnosis

The diagnosis of EHE is made clinically. Symptoms include fatigue, dizziness, muscle cramps, headache, and nausea. Mild mental status changes may be observed (mild confusion, irritability, and emotional lability). Common physical signs include pallor and weakness. Vital signs will show elevated heart rate and body temperature (<39.5°C) with normal to low blood pressure.

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 kilogram of body weight lost. If body weight is unknown, adequate rehydration is evidenced by improved vital signs, ability to urinate, less orthostasis, and generally “feeling better.” Cooled fluids containing less than 8% carbohydrate are absorbed more rapidly than plain water. Rehydration fluids containing sodium appear to restore total body water levels more completely than water alone. Intravenous (IV) hydration may be required for vomiting or significant orthostatic issues. Recommended IV solutions are normal saline (NS) and 5% dextrose in NS (D5NS). The authors prefer D5NS to help limit the depletion of glycogen stores in the post-exercise hypermetabolic state. The infusion of IV fluids in heat exhaustion patients does not improve dehydration quicker than oral fluid, and IV infusions are prohibited by the World Anti-Doping Agency for athletes who are able to drink.

Return to Play

No evidence-based guidelines have been developed for return to play (RTP) after heat exhaustion. Our recommendations are listed in Box 21.1 . RTP should address risk factors including deconditioning, chronic dehydration, habitual fatigue, and excess body weight.

Prevention

Several sports organizations recommend modifying outdoor physical activity when heat index values are in the “extreme caution” or “danger” zones. Modifications include reducing the number of practices, scheduling practices during cooler times of the day, shedding equipment, and increasing access to water. These recommendations pertain especially to North American football, which is responsible for more cases of heat-related illness and deaths than any other sport. In addition, athletes should be educated about gauging hydration status based on urine color; urine the color of apple juice reflects dehydration, whereas lemonade-colored urine reflects adequate hydration.

Acclimatization to hot environments occurs by a number of physiologic adaptations, including initiation of sweating at a lower core temperature and thirst at a lower serum osmolality, increased sweat rate, increased sodium absorption from sweat and urine, and expanded plasma volume. The time required for acclimatization depends on age, baseline level of conditioning, practice and equipment requirements, and environmental factors. College athletes have been shown to acclimatize in as few as 12 days of practice. Younger athletes typically require a longer period of acclimatization.

Diagnosis

The person with EHS may start out as dizzy, nauseated, and confused, but lethargy, obtundation, or unresponsiveness indicate more advanced, critical EHS. Physical examination typically reveals hot, sweaty skin, rapid pulse, and low blood pressure. Body temperature is above 40°C (104°F). Rectal temperature measurement is the most reliable method of monitoring core body temperature in the exercising athlete.

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 wait for rectal temperature measurement in an athlete suspected of having EHS. The first responder should initiate basic cardiopulmonary resuscitation if necessary and activate EMS. Clothing and equipment should be removed immediately. Immersion should occur first if removing cumbersome equipment would delay treatment. Immersion of the entire body in cold water is the treatment of choice. Alternatives include pouring cold ice 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. Cooling continues until the rectal temperature reaches 38.6°C (101.4°F) to prevent overcooling.

Return to Play

Recommendations for RTP criteria are summarized in Box 21.2 . No validated tests are available to measure responses to graded exercise in the heat to assist in making return-to-play decisions.

Pathophysiology

Exercise-associated muscle cramps (EAMC), commonly known as heat cramps , are involuntary, painful muscular contractions during exercise. Several hypotheses have been proposed to explain EAMC, including excessive sodium losses, muscle fatigue, and central nervous system fatigue. Prospective studies have failed to correlate sodium losses with the onset of EAMC. Fatigue causes an increased firing rate of type Ia and II (excitatory) muscle spindle afferents and a decrease in afferent activity from the Golgi tendon organ (inhibitory) that results in sustained alpha motor neuron firing. Poor conditioning may be result in premature fatigue.

Diagnosis

EAMC are usually self-evident. The athlete who has been exercising vigorously experiences painful cramping and is unable to function normally.

Treatment

The most effective treatment for EAMC appears to be passive stretching, which presumably increases the inhibitory activity of the Golgi tendon organ. Cooling the muscles with ice massage may provide additional relief. Little evidence indicates that ingestion of an electrolyte solution or pickle juice consistently resolves EAMC.

Prevention

Athletes who are prone to cramping should be encouraged to consume more than normal amounts of salt in their diet and to use oral hydration fluids that contain sodium during and after practice. Adequate conditioning and improved rest may also help prevent EAMC.

Return to Play

Athletes may return to the field of play after the resolution of muscle cramps if they are able to perform sports-specific drills without recurrence of EAMC.

Pathophysiology

Heat syncope (HS) and exercise-associated collapse (EAC) occur immediately following the stress of heat exposure and/or exercise. Upon cessation of exercise (i.e., the finish line of a marathon), the absence of rhythmic muscular contraction combined with dehydration limits, venous return, and thus cerebral perfusion pressure, results in syncope in susceptible individuals. Syncope may occur similarly after prolonged standing in the heat or sudden rising from a sitting or lying position after exercise.

Diagnosis

Syncope that occurs upon stopping prolonged exercise in the absence of any other cause of syncope is EAC. Likewise, syncope in the heat after prolonged standing or sudden postural changes is likely HS. Orthostatic blood pressure changes may be present.

Treatment

Supportive care to restore normal perfusion of the brain is essential. Placing patients in the Trendelenburg position for 15 to 30 minutes will help to restore cerebral blood flow. Squeezing crossed legs together and making a strong fist have been useful in increasing venous return and reestablishing adequate perfusion.

Prevention

Adequate hydration with sufficient salt intake is important to maintaining normal fluid volume. Continuing to walk after completing a running race can minimize the risk for EAC. Moving or contracting the muscles of the legs during prolonged standing in the heat can help to maintain adequate perfusion.

Return to Play

Athletes may RTP after resolution of symptoms as long as they have reestablished normal blood pressure without orthostasis and have no signs of dehydration.

Pathophysiology

Exertional rhabdomyolysis (ER) is characterized by the breakdown of skeletal muscle during and after exercise that exceeds the working ability of the muscles.

Excessive exercise will result in elevated intracellular free ionized calcium (Ca) especially in the mitochondria, compounded by depletion of ATP causing dysfunction in the Ca-ATPase pump. This elevated calcium results in the activation of proteases and oxygen free radicals that cause myocyte death. Muscle injury causes intense muscular pain, weakness, swelling and elevated levels of serum CPK at least five times the upper limit of normal. Risk factors for ER include dehydration, acidosis, excess ambient temperature, and hypoxia. In persons with ER, large amounts of myoglobin, proteases, and inflammatory mediators enter the circulation. Filtration of myoglobin results in glomerular injury, and proteases damage the respiratory epithelium, which may lead to respiratory distress. Rarely, inborn errors of metabolism may present with ER in apparently healthy persons.

Diagnosis

Affected persons typically present with severe muscle pain especially those muscles involved in the extreme exercise. The muscles are tender to palpation and may be swollen. Severely affected patients may present with tachypnea and edema. Severe consequences include renal failure, disseminated intravascular coagulopathy, and acidosis.

Treatment

Treatment usually requires hospitalization for the correction of acidosis, careful hydration to aid in the clearance of myoglobin without inducing fluid overload, monitoring renal function, and supporting cardiac and pulmonary function. If CPK does not improve after 72 hours, renal consultation should be considered. Persons who meet the following criteria may be treated as outpatients with close follow-up: (1) CPK less than 15,000 IU/L; (2) normal renal function and mild dehydration; and (3) the absence of sickle cell trait, infectious disease, or an underlying metabolic syndrome. These persons should be encouraged to recover in a cool environment, refrain from exercise, and drink plenty of fluids.

Return to Play

Our RTP criteria are listed in Box 21.3 .

Prevention

ER can be prevented by gradually increasing training intensity and volume, and by ensuring adequate hydration and recovery between exercise bouts. ER has occurred in persons involved in activities, such as physical education, band, cheerleading, drill team, and Reserve Officers’ Training Corps, especially when excessive exercise is used as a reprimand. Persons involved in these activities should be provided free access to water and sufficient rest during exercise, and they should be educated about symptoms and signs of heat illness and muscle injury.