CHAPTER KEY WORDS

• Altitude
  
• Cold
  
• Environmental
  
• Heat
  
• Lightning

CHAPTER SCENARIO

A 17-year-old male high school football player becomes dizzy and lightheaded, and starts vomiting during practice. On initial evaluation, he appears to be confused and cannot stand up without leaning on a teammate.

SCENARIO RESOLUTION

Possible heat illness is immediately recognized. The athlete is moved to a shaded area, and his equipment is removed. Vital signs show a slight tachycardia of 110 beats/minute, blood pressure of 118/68, and a rectal temperature of 105°F. Ice bath immersion is completed, and his core temperature drops to 102°F within 9 minutes. After cooling, he is transported to the nearest local hospital via ambulance for further monitoring.

INTRODUCTION

Medical professionals share a unique objective when caring for the athlete. Although the competitor’s focus is sharply aimed at winning, the medical professional is concentrating on success and safety. Many factors can alter the athlete’s success, health, and safety while competing. Outcomes on the field of play are directly related to factors that include conditioning, strength, ability, and preparation. Much less considered is the effect the environment has on health, safety, and performance.

Environmental conditions not only affect how an athlete performs, but may also put an athlete at significant risk for a catastrophic medical complication. Heat illness, hypothermia, altitude sickness, and lightning are some of the more common conditions experienced, and many other environmental risk factors affect the athlete population. In this chapter, we will discuss temperature extremes, high altitude, and lightning, with goal of providing a basic understanding and systematic approach to their management.

Exertional Heat Illness

Exertional heat illness (EHI) is a common environmental-related condition with which all medical providers need to be familiar. Although debated and not universally agreed upon, EHI is often thought of as a continuum. Regardless, degrees of severity vary from mild to moderate to severe.^1,2

Heat cramps and heat rash are forms of mild EHI. Heat cramps are common, but do not predispose the athlete to more severe forms of EHI. These painful, involuntary skeletal muscle contractions are typically brought on by prolonged exertion and more commonly occur at higher temperatures. Heat cramps are treated with rest, rehydration, stretching, and massage. The athlete may return to play when properly rehydrated and the cramping has subsided.3

Heat rash is simply a pruritic, maculopapular, erythematous rash that develops in areas of maximal warmth and tight-fitting clothing. The sweat glands become clogged, swell, and rupture. This self-limiting rash is best treated with loose fitting clothing and antihistamines.^2,4

The clinical signs and symptoms of moderate and severe EHI (heat exhaustion and heat stroke) often overlap. Athletes commonly present with some combination of profuse sweating, lethargy, headache, dizziness, cool and clammy skin, nausea, tachycardia, hypotension, hyperventilation, and an elevated core body temperature (CBT). These are the signs of the vascular strain the body is experiencing in an attempt to thermoregulate.

Ominous signs of potential progression toward heat stroke include cessation of profuse sweating and the lack of spontaneous cooling when exertion has been stopped.^1,2,4 The American College of Sports Medicine (ACSM) defines heat stroke as an elevated core body temperature greater than 40°C, or 104°F, plus central nervous system alterations such as seizure or disordered thought. Early recognition of EHI is crucial in successful treatment and prevention of long-term effects or death. The suspicion of EHI for any collapsed athlete should be high, and early CBT measurement is needed. Rectal temperatures are considered the gold standard measurement of CBT, and treatment must be provided rapidly when the suspicion or diagnosis is made.

Thermoregulation occurs through radiation, conduction, convection, and evaporation, with the latter 3 employed in the medical professional’s cooling efforts. In evaporation, the most commonly understood form, heat is lost as liquid changes phase to vapor, such as during sweating. Conduction is the transfer of heat between unmoving objects. This can be achieved by cold-water immersion, ice vests, or simply ice packs within the groin and axilla. Convection is the transfer of heat from an object to moving air or water. This is classically accomplished with the use of a cooling fan, mist, or even immersion within a cold river or creek.

Early treatment, ideally within less than 30 minutes, has profound effects on return to normal thermoregulation and prevention of progression to heat stroke. The gold standard of treatment is cooling performed by full-body ice water immersion. The athlete should be removed from activity and taken to a shaded area if possible. If ice-water immersion is not available, other forms of cooling, such as misting, fanning, and ice packs, should be undertaken. Attempts to cool continue until the CBT reaches 39°C, or 102.2°F, and then the athlete may be transferred. It is important to avoid antipyretics, as this condition is a result of the overproduction of heat, and the body’s hypothalamic set point is unaffected, rendering medications such as acetaminophen more detrimental than beneficial.

Rehydration is another important step in treatment of exertional heat illness. A rehydration goal of 1 to 2 L/hour is recommended. This fluid should contain 20 to 30 mEq/L of sodium, 2 to 5 mEq/L of potassium, and 5% to 10% carbohydrate. Most commercially sold sports drink fit these criteria.³

Athletes who are diagnosed and respond to treatment of exertional heat illness should avoid further exertion for the next 24 to 48 hours to avoid the increased, albeit transient, risk of recurrent EHI.¹

Activity planning and reduction should be guided by the wet-bulb globe temperature (WBGT). The frequency of EHI increases proportionately with the increase in WBGT, which is calculated with the following formula⁵:

WBGT = (wet bulb temp × 0.7) + (dry bulb × 0.1) + (black bulb × 0.2)

The WBGT represents humidity, dry bulb is air temperature, and black bulb is radiant heat. High-risk individuals include obese athletes, those with poor physical fitness or a recent episode of heat illness, athletes with a concomitant febrile illness, and those taking medications or supplements that alter thermoregulation, such as antihistamines, caffeine, and diuretics. It is generally considered low risk for heat illness when the WBGT is less than 65°F, but the ACSM offers the following recommendations for temperatures above this threshold (Table 7-1).¹

Activity in cold temperatures places athletes at risk of hypothermia or other peripheral cold injuries. Unfortunately, our physiologic response to low temperature is less effective when compared to our warm-weather adaptive changes. Luckily, the incidence of cold injury is low in athletics, with hypothermia and frostbite accounting for only 20% of cross-country skiing injuries and fewer than 5% of injuries in mountaineers.6 Other at-risk events include ultramarathons and triathlons, particularly due to the duration of competition and swimming. With the increasing popularity of these activities, there should continue to be heightened awareness of the physiologic changes our bodies go through in cold temperatures, as well as the classic injuries.

Our bodies transfer heat in 4 primary ways. In the setting of cold injury, we primarily focus on convective heat loss. Tolerance to cold varies by the individual and hinges on duration of exposure, environmental factors, and preexisting risk factors unique to the athlete. The amount of heat exchanged from our skin to the environment is directly affected by the ambient temperature, humidity, wind speed, precipitation, and the insulating properties of our clothing.^6,7 The human body works to maintain a CBT near 37°C, or 98.6°F. To combat a dropping core temperature, our bodies must create more heat and decrease lost heat. To increase heat production, the body involuntarily begins to shiver. We can additionally increase heat production by exertion. To minimize heat loss, peripheral vessel vasoconstriction occurs when the skin temperatures reach 35°C or below to shunt blood away from the skin and subcutaneous tissue. The most challenging environment combines cold, wind, and wet. Temperature alone cannot be the only factor considered, and a perfect example is wind chill, the actual temperature when wind is factored. It is calculated by the following formula:

WC (°F) = 35.74 + 0.6215T – 35.75(V^0.16) + 0.4275T(V^0.16)

where T is air temperature and V is the wind speed (mph).

Other risk factors for cold injury include inactivity, inappropriate attire, impaired thermoregulation, previous cold injury, age, and preexisting medical conditions. Athletes with prior frostbite have a 2- to 4-fold increased risk of repeat injury. Young children and adults older than 60 years have a greater risk. Our shiver response can be blunted by hypoglycemia, poor caloric intake, and endocrine abnormalities, leading to poor heat production. Disorders such as hyperhidrosis, chronic dermatologic conditions, and low-percent body fat may lead to increased heat loss. Athletes with known reactive airway disease have an increased risk of cold-induced bronchospasm. Finally, there is an increased rate of cardiovascular events secondary to cold-induced increases in mean arterial pressure, total peripheral resistance, and increased cardiac output and oxygen demand.⁸

Hypothermia is defined as a drop in CBT below 35°C. In the early stages, shivering, lethargy, apathy, and cold extremities can occur.⁹ However, as this progresses, the athlete experiences confusion, impaired gross motor control, and slurred speech. Core temperatures below 35°C lead to bradycardia, hypotension, and decreased cardiac output, which strain the myocardium and predispose the patient to spontaneous dysrhythmias. In the severe stages, hypothermia causes pulmonary edema, muscle rigidity, and loss of consciousness. General considerations in immediate management include ABCs (Airway, Breathing, Circulation), gentle handling of affected extremities, and removal of any wet clothing.^6,9

Rewarming is either passive or active, depending on the degree of hypothermia. Passive external rewarming is for athletes with a CBT of greater than 32°C, and consists of removing wet clothing and covering the victim with warm blankets. The goal rewarming rate is 0.5°C to 2.0°C/hour. Active external rewarming consists of fires, hot water bottles, and heating pads. Active core rewarming is accomplished in a controlled setting with intravenous 5% dextrose in normal saline warmed to 40°C to 42°C, inhalation of warmed oxygen, or, more intensively, a warmed peritoneal lavage. These active forms of rewarming are reserved for CBTs below 32°C.

Care must be taken to avoid afterdrop, a phenomenon that occurs with active external rewarming. In chronic hypothermia, dehydration leads to general hypotension and hypovolemia. The cold extremity vessels are vasoconstricted, and the blood returning is cold and acidic. By rewarming the extremity, there is peripheral vasodilation and a resultant drop in CBT, pH, and blood pressure, which decrease coronary perfusion and increase risk of arrhythmia. For this reason, it is imperative to rewarm the core first before addressing the extremities.⁹

Peripheral cold injuries can be further broken down into freezing and nonfreezing injuries. Some nonfreezing injuries (often termed cold–wet injuries) such as trench foot are not high yield in athletics, as these tend to occur after more than 12 hours of exposure. Other nonfreezing injuries include chilblains and cold urticaria.^6,10 Chilblains are superficial, cold-induced erythrocyanotic skin lesions that develop within 24 hours of cold exposure. Athletes experience tender, pruritic erythematous papules in sites of cold exposure. There is concern that blistering and ulceration may develop secondary infection; however, the condition is otherwise self-limiting. Athletes should avoid further cold exposure, and lesions resolve within 2 to 3 weeks. Cold urticaria, much like chilblains, develops on exposed skin and presents as erythematous, pruritic hives. However, these typically develop within minutes of exposure. These are also self-limiting, and treatment consists of removing from cold, limiting reexposure, and giving antihistamines for pruritus.10

Frostbite, generally considered the most common cold injury, falls into the freezing category of peripheral cold injuries. Frostbite develops when the skin and deeper tissue reach temperatures at or below 0°C, or 31°F.⁶ The most commonly affected areas include ears, nose, cheeks, chin, fingers, and toes. Athletes will initially complain of numbness, cold, insensate skin with difficulty moving digits, and white or gray discoloration of surrounding skin. It is further classified into the following 4 stages:

• First-degree injuries are limited to the epidermis.
  
• Second-degree injury is characterized by full-thickness involvement of the dermis, leading to edema and the formation of clear blisters. Over a 2- to 3-week period, these blisters contract and form dark eschars. Sequelae include persistent cold sensitivity, paresthesia, and hyperhidrosis.
  
• Third-degree frostbite is distinguished from second degree by formation of hemorrhagic blisters, deep burning pain on rewarming, and thick gangrenous eschar formation.
  
• Fourth-degree frostbite involves deeper muscle, bone, and tendons.

Prehospital management consists of removing the athlete from cold environment and removing any wet clothing. Handle the affected area with care, as vigorous manipulation of involved tissue will lead to further damage. Do not begin rewarming until there is no further risk of cold exposure, and be careful with active rewarming, as the skin is insensate and will burn without the athlete knowing. When in a controlled setting, the affected skin may be actively rewarmed with warm water immersion at a temperature around 98°F. Too-high temperatures may risk burning, lead to increased pain, and will not hasten the process. Tetanus prophylaxis is recommended, but antibiotics remain controversial. Further wound management should be handled by an expert.^7,10

High-Altitude Illness

Competitive and recreational athletes exerting at elevation face certain risks to health and performance. Health care personnel should be familiar with common altitude-related illnesses such as acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema, as well as the physiologic effects of elevation, risk factors, and preventative measures of such conditions.

At high altitudes, our bodies are exposed to lower levels of ambient oxygen and increased thermal radiation. The primary driving force behind high-altitude illness (HAI) is believed to be hypoxemia, secondary to low partial pressure of inspired oxygen, which acts as the driving force behind oxygen diffusion as we inhale. As elevation increases, the barometric pressure and available oxygen fall.¹¹ During activity, tissue oxygen demands are high. At high altitude, the marked reduction in pressure and oxygen availability results in tissue hypoxia. An individual’s response to high altitude is highly variable and depends on individual fitness levels, exertion on arrival at altitude, prior residence at low altitude, sensitivity to hypoxia, the blood’s oxygen-carrying capacity, nutritional status, obesity, and prior episodes of HAI.^11–13

The most important preventative measure is slow ascent, especially at altitudes greater than 2000 to 3000 m. Consensus guidelines recommend an ascent of 300 to 600 m/day when above 3000 m. In addition, for every 1000 m gained, there should be a planned 24 hours of rest. Maintaining appropriate hydration is imperative at high elevation, as there is an increase of insensible losses and thus an increased risk of dehydration. Appropriate clothing and application of sunscreen reduce the risk of sun-related injuries, which have high incidence due to increased ultraviolet radiation at high elevation. Finally, and typically reserved for those with prior cases of HAI or a need to ascend rapidly, medications (eg, acetazolamide, dexamethasone, and nifedipine) have been used to decrease the incidence of HAI. Special consideration must be taken with use of acetazolamide and dexamethasone, as these substances are banned by the World Anti-Doping Agency.¹³

Acute mountain sickness (AMS) is the most common form of HAI and is considered the early, more benign side of a spectrum containing high-altitude cerebral edema (HACE). AMS is characterized by a high-altitude headache plus one of the following: nausea or vomiting, fatigue, dizziness, or insomnia. Generally, this is a delayed reaction occurring 6 to 12 hours after arrival; however, it may present as quickly as 1 to 2 hours or as late as 24 hours. AMS is self-limiting, and, if no further ascent is obtained, the symptoms will gradually resolve within 48 hours.^11,13 This is not considered life-threatening, but it may significantly impact performance. Aside from resting, symptomatic treatment is provided for issues such as headaches and nausea. Concern for HACE arises if the athlete develops ataxia, altered level of consciousness, or other signs of neurologic impact. These symptoms develop as a result of brain edema secondary to increased permeability of the blood–brain barrier. The mechanism of the increased permeability is not completely understood.¹³ This is considered a medical emergency, and early recognition is critical. The definitive treatment of HACE is descent; however, this is not always possible, given level of consciousness and weather. If not possible, supplemental oxygen or hyperbaric therapy may be applied. In addition, dexamethasone may be initiated until descent is completed.^11,13

High-altitude pulmonary edema is the abnormal accumulation of fluid in the lungs secondary to a breakdown in the pulmonary blood–gas barrier.11 This is separate from the AMS-HACE continuum and is believed to be secondary to maladaptive responses to hypobaric hypoxia experienced in high altitude. High-altitude pulmonary edema generally develops 2 to 5 days after arrival and is characterized by shortness of breath, cough, and poor exercise tolerance.¹⁴ Like HACE, high-altitude pulmonary edema is a medical emergency and can rapidly progress to severe shortness of breath at rest. Additional signs are tachycardia, tachypnea, and a low-grade fever. First-line treatment is rest and oxygen. Again, definitive treatment is descent, but hyperbaric therapy is an option if oxygen is not available and descent is delayed. Finally, nifedipine may be used; however, the clinical evidence is modest, and, in most cases, does not offer benefit compared with oxygen and descent.^13,14

Lightning

Mother Nature can be most unpredictable regarding severe-weather storms. Lightning strikes can lead to both injuries and death. Approximately 15% of all lightning deaths occur during sporting events. This is concerning, as many of these fatalities could be avoided if proper precautions were taken. In 2013, the National Athletic Trainers’ Association released a position statement outlining lightning safety recommendations. They included the following guidelines:

1. Establish a lightning-specific emergency action plan for each venue.
   
2. Ensure lightning and general weather awareness.
   
3. Prepare large-venue planning protocol.
   
4. Provide first aid.

Currently, we have access to weather forecast resources at our fingertips. However, a team or individual may be traveling to a remote location, and proper steps need to be taken to ensure safety. During a lightning storm, take shelter indoors, such as in an enclosed building, vehicle, or even a basement. If those are not readily available, alternatives may include picnic shelters or even covered bus stops.

If a lightning strike is visualized or thunder is heard, activity should be halted for a minimum of 30 minutes. The clock starts after the most recent event. An individual should be put in charge of coordinating the evacuation of a venue. These protocols should be made, reviewed, and practiced prior to holding an event.

Should lightning strike an individual, a first responder needs to make sure his or her safety is not compromised before attending to a victim. When it is determined as safe, the victim should be moved to a safe location. An automated external defibrillator should be available, and basic life support should be initiated if indicated.

CHAPTER SUMMARY

Environmental conditions play a large role in the management of the athlete. A medical professional must be aware of the clear and present dangers to which an athlete may be exposed and how to appropriately manage these individuals. Be aware of local and forecasted weather conditions, and, if traveling to an unfamiliar environment, research and gain a better understanding of the conditions with which you and the athlete may be confronted.

CHAPTER REVIEW QUESTIONS

1. What is the gold standard for taking an individual’s body temperature if heat illness is suspected?
   
2. The American College of Sports Medicine defines heat stroke as a temperature greater than 40°C (104°F) plus what?
   
3. True or False: In hypothermia, it is imperative to warm the core first before addressing the extremities.
   
4. What is the definitive treatment for high-altitude cerebral edema?
   
5. An athletic event should be suspended for how many minutes from the last witnessed lightning strike or sound of thunder?

ANSWERS

1. Rectal temperature
   
2. Central nervous system alteration
   
3. True
   
4. Descent
   
5. 30 minutes

REFERENCES

1.     Armstrong L, Casa DJ, Milliard-Stafford M, Moran D, Pyne S, Roberts W. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sport Exerc. 2007;39(3):556-572.

2.     Asplund CA, O’Connor FG, Noakes TD. Exercise-associated collapse: an evidence-based review and primer for clinicians. Br J Sports Med. 2011;45(14):1157-1162.

3.     Schwellnus MP, Drew N, Collins M. Muscle cramping in athletes—risk factors, clinical assessment, and management. Clin Sports Med. 2008:27(1):183-194.

4.     Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainers’ Association position statement: exertional heat illnesses. J Athl Train. 2015;50(9):986-1000.

5.     Racinais S, Alonso JM, Coutts AJ, et al. Consensus recommendations on training and competing in the heat. Br J Sports Med. 2015;49(18):1164-1173.

6.     Fudge MD, Bennett BL, Simanis JP, Roberts WO. Medical evaluation for exposure extremes:cold. Clin J Sport Med. 2015;25:432-436.

7.     Castellani JW, Young AJ, Ducharme MB, et al. Position stand: prevention of cold injuries during exercise. Med Sci Sports Exerc. 2006;37:2012-2029.

8.     Castellani JW, Young AJ. Health and performance challenges during sports training and competition in cold weather. Br J Sports Med. 2012;46:788-791.

9.     Brown DJ, Brugger H, Boyd J, Paal P. Accidental hypothermia. N Engl J Med. 2012;367(20):1930-8.

10.   Harirchi I, Arvin A, Vash JH, Zafarmand V. Frostbite: incidence and predisposing factors in mountaineers. Br J Sports Med. 2005;39:898-901.

11.   Bartsch P, Swenson ER. Clinical practice: acute high-altitude illnesses. N Engl J Med. 2013;368:2294-2302.

12.   West JB, American College of Physicians, American Physiological Society. The physiologic basis of high-altitude diseases. Ann Intern Med. 2004;141(10):789-800.

13.   Koehle MS, Cheng I, Sporer B. Canadian academy of sport and exercise medicine position statement: athletes at high altitude. Clin J Sport Med. 2014;24(2):120-127.

14.   Stream JO, Grissom CK. Update on high-altitude pulmonary edema: pathogenesis, prevention, and treatment. Wilderness Environ Med. 2008;19(4):293-303.

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