Sarah Manspeaker, PhD, LAT, ATC and Kelley Henderson, EdD, LAT, ATC
CHAPTER KEY WORDS
- Creatine kinase
- Exercise-associated hyponatremia
- Exertional rhabdomyolysis
- Sickle cell trait
Martin, a Division I football player, traveled from his home university in Tampa, FL, (elevation: 48 feet) to Boulder, CO, (elevation: 5,328 feet) to play in a conference game. In the first half of the game, Martin reported to the athletic trainer with cramping in his left leg. He was treated with stretching exercises, given oral hydration products, and returned to the game. During the second quarter, Martin began to experience significant pain, rated 10/10, in his low back, as well as in his left side beneath his ribs, and shortness of breath. He was immediately removed from the game and transported to a local hospital for further evaluation. Throughout the evening at the hospital, Martin began to develop a fever, which topped out at 1020F. A complete blood count revealed elevated white blood cell count.
Following an abdominal computed tomography scan, Martin was diagnosed with a splenic infarct as a result of the decreased oxygen to the spleen at the high altitude. Martin was hospitalized for 5 days, and he was then released to fly back to Florida, with instructions for conservative treatment and rest until the spleen had healed. He did not participate in any activity for 3 weeks and began an acclimation protocol to return to full participation that took 3 weeks.
The incidence of medical emergencies directly related to participation in conditioning and exercise is rare. When such emergencies occur, the associated conditions are characterized by the development of signs and symptoms often related to the timing, location, and intensity of the physical activity. Even though these conditions could be fatal, proper recognition and treatment can prevent sudden death in athletes.
Health care providers should be familiar with the signs and symptoms associated with conditions such as exercise-associated hyponatremia, exertional collapse associated with sickle cell trait, and exertional rhabdomyolysis. In addition, they should understand the contributing environmental and exercise intensity factors that may increase risk for development of such conditions. Being able to quickly recognize signs and symptoms of these conditions should lead to decreased time to diagnosis, with subsequent increase in effective treatment methods, prevention of catastrophic outcomes, and ultimate return to activity. This chapter will present an overview of each of the mentioned conditions, the predisposing factors or causes of the conditions, the related signs and symptoms, and treatment and return to activity guidelines.
The body requires a delicate balance between fluid and electrolytes, particularly among individuals involved in physical activity.1 Fluid intake before, during, and after exercise is important, given the concern about hypohydration2; however, it is possible to drink excessive amounts of fluid to become overhydrated. This overhydration results in more water than nutrients in the cells,3,4 thus resulting in hyponatremia. During exercise, the fluid balance and subsequent increase in water rather than nutrients can be termed exercise-associated hyponatremia (EAH).
EAH is closely related to the amount of water present in the body. The terms hypohydration, or loss of body water, and dehydration, or deficit of body water caused by hypohydration, are important to understand in relation to the differences from EAH.2 The condition of EAH refers not to body water content, but rather to the amounts of electrolytes, specifically sodium, present within the body. Hyponatremia is simply the decrease in blood sodium concentrate.3 From a clinical standpoint, EAH occurs during or within 24 hours after physical activity and is marked by a serum, plasma, or blood sodium concentration less than 135 mmol/L (normal values range from 135 to 145 mmol/L).3 It can be considered a potential medical emergency.2
Causes and Predisposing Factors
Several contributing factors may lead to the development of EAH. During exercise, these factors may include excessive fluid consumption, failure to excrete excess volume, and excessive sodium loss.2,3 Furthermore, prolonged exercise may particularly influence the development of EAH. Each of these topics will be discussed further in this chapter.
Excessive fluid consumption, or overdrinking, is often accomplished when a person consumes more fluid than he or she can expel.3,5 In simpler terms, a person drinks more fluid or water than is released through sweat and urine.3 Timing of this ingestion typically matches periods of hydration and rehydration (eg, before or after physical activity). Sometimes, patients may show signs and symptoms of EAH (Table 13-1) but be diagnosed with hypohydration and given more water, thus increasing the likelihood for EAH. It is possible for someone to be both hypohydrated and hyponatremic.
In contrast to excessive fluid consumption, the lack of ability to excrete excess volume may also lead to EAH. For example, sweating is the primary mechanism for the body to dissipate heat.5 The contents of sweat include water and electrolytes such as sodium, chloride, and potassium.5 If a person does not sweat as much as he or she drinks water or other hypotonic fluids, the balance of nutrients in the body will decrease. This imbalance becomes even more pronounced during long periods of exercise as well as heat.5 Specifically, these environmental factors have been linked to decreased blood flow and urine output, thus contributing to the development of EAH.5
Excessive sodium loss, which often occurs through sweating, may also lead to EAH.3 Serum sodium levels are determined through the total content of exchangeable sodium and potassium in relation to body water.3 When loss of these electrolytes occurs or when the amount of body water increases, hyponatremia results. For example, if a person sweats excessively, the nutrient balance may decrease significantly.1,5 In athletics, this imbalance is often due to prolonged exercise, lack of acclimation to the environment, or inexperience in the activity being performed.3,5 Additionally, general sodium content in the body may be decreased in those who have a low-sodium diet or those who do not consume drinks containing sodium.5
Prolonged exercise may be a direct contributor to the development of EAH. Physical activity lasting longer than 4 to 5 hours typically falls into this category.3 During an event such as an ultramarathon or marathon, it is important to prevent both hypohydration and hyperhydration. Other participants who may be at risk for EAH are those who did not adequately train or who are inexperienced in the event, those with a slower running or performance pace, and individuals with a high or low body mass index.1,3
Signs and Symptoms
The signs and symptoms of EAH may vary, but they should always be considered by the athletic trainer. Some patients may be asymptomatic and not present with any significant signs or symptoms. As the sodium imbalance increases, symptoms may develop and can be categorized as either mild or severe. Mild EAH is often characterized by signs and symptoms of dizziness, lightheadedness, nausea, and/or weight gain.3,5 More severe forms of EAH may present with the signs and symptoms of headache, nausea or vomiting, confusion or other change in mental status, dyspnea, or frothy sputum.3,5 If left unrecognized or untreated, EAH may develop into a sequelae of seizure or coma, thus elevating the emergent nature of the patient’s condition.3 Table 13-1 provides an overview of the differential signs and symptoms between EAH and hypohydration.
Diagnosis of EAH is best achieved through analysis of blood sodium concentrate. In the athletic training clinical setting, a finger stick and an express blood analyzer may be used.6 In the hospital setting, a physician may order an electrolyte panel or base metabolic panel to determine the levels of sodium present in the blood. From a combined diagnostic and clinical symptom standpoint, a blood sodium value of less than 135 mmol/L would elicit symptoms. Values below 125 mmol/L would warrant immediate administration of treatment to increase sodium levels; whereas patients with values less than 120 mmol/L of sodium would likely present in a comatose state and require advanced emergency medical attention.3
Adapted from National Athletic Trainers’ Association. Consensus statement: Sickle cell trait and the athlete. 2007. www.nata.org/sites/default/files/sicklecelltraitandtheathlete.pdf. Accessed September 28, 2018.
Asymptomatic patients can transition to symptomatic if hypotonic fluids are ingested; therefore, it is of utmost importance to recognize and treat EAH early.3 When identified, EAH should be treated on an individual basis to address the specific severity of presenting signs and symptoms.7 While onsite at an event, a patient displaying mild EAH should be under observation for progression into a symptomatic stage. Hypotonic and isotonic fluids should be restricted until the patient is urinating freely. Treatment may consist of administration of either oral hypertonic saline (HTS) such as concentrated bouillon or 3% to 5% sodium chloride (NaCl) with added flavoring, or intravenous HTS.3 Those individuals presenting with severe EAH should receive immediate administration of intravenous (IV) HTS and be prepared for transport to the emergency department.3 Clinical practice guidelines for treatment of EAH in the hospital setting have been established and should be based on severity of symptoms and the serum sodium values. Treatment guidelines include 3% NaCl administered intravenously over a 20-minute period, followed by a blood sodium retest. This treatment should be continued until there is a 5-mmol/L increase in serum sodium.7
Return to Activity
Currently, no consistent body of literature supports return-to-activity guidelines following treatment for EAH. When symptoms, including a normal serum sodium level, have resolved and the athlete has been cleared by a physician, he or she may begin to transition back to activity. There should be an individualized hydration plan developed as well as further education on excessive fluid intake.
Prevention of EAH begins with education regarding drinking behaviors and monitoring hydration through body weight. Athletes, parents, coaches, and event support crews need to understand the dangers of overdrinking. The thirst sensation can prevent excess dehydration while also preventing the excessive fluid intake contributing to the development of EAH. Individuals should be educated on the importance of not drinking in excess of sweat rate. If an athlete secretes salty sweat and will be involved in events lasting longer than 4 to 6 hours, he or she may consider consuming food or drinks containing sodium.5 Although sodium supplementation equal to fluid loss may be beneficial, it will not prevent EAH if there is excessive fluid intake.3,8 Due to the wide variety of sweat rates and renal excretion capacity, specific guidelines for fluid consumption should be individualized.3,5 For event management and support teams, it may be beneficial to decrease the number of fluid stations as well as provide appropriate drinking advice to event participants.3 Educational programs for athletes, parents, coaches, and onsite medical staff should also include recognition of signs and symptoms of EAH, management of EAH, and the immediate need for medical attention if EAH is suspected.3
Sickle Cell Trait
Sickle cell trait (SCT) is a hereditary condition in which the red blood cells of the body are not uniform. Specifically, one hemoglobin gene (A) is shaped normally, and the other hemoglobin gene (S) is abnormally shaped.9 An estimated more than 4-million people in the United States have SCT. In general, most people identified as carrying the SCT have no adverse health effects due to the trait.10,13 For people with SCT, the abnormal shape of the red blood cells decreases the ability to carry oxygen through the blood to the rest of the body.9,11 If this oxygen delivery is impaired for a period of time, life-threatening impacts on the body may occur.
Sickle cell abnormalities are identified most often in people who have connections to locations where malaria is prevalent. The ethnicities associated with SCT may be traced to ancestry in areas such as Africa, South/Central America, Mediterranean countries, Hispanic countries, south Asian countries, Middle Eastern areas, and the Caribbean.12 People who carry the SCT do not necessarily have sickle cell anemia, and the SCT cannot turn into sickle cell disease. To have sickle cell disease, a person must have 2 abnormal hemoglobin genes.13
Of primary concern to the athletic trainer is exercise collapse associated with SCT (ECAST).14,15 During exercise or exertion, the abnormal hemoglobin may change from a round shape to more of a quarter-moon shape, known as sickling. This is a medical emergency called exertional sickling, and it poses a significant risk to athletes, as it may result in sudden death.14,15 SCT has also been identified as a potential contributor to the development of exertional rhabdomyolysis, which will be presented later in the chapter.
Another potential complication associated with SCT and activity is impact on the spleen. The spleen is one of the most-often affected organs in SCT carriers, and complications may result in splenomegaly.16 Clinicians should be aware of the potential for splenomegaly and potential complications, such as rupture, during activity. Complications due to splenic enlargement have direct associations with increased morbidity of SCT and may, in some cases, lead to mortality.16
Causes and Predisposing Factors
During exercise or exertion, the oxygen carrying abilities of the blood may be decreased due to the resultant S-shape of the abnormal hemoglobin.9 Specifically, these sickled red blood cells may build up and block normal blood flow to muscle and other tissue.15 It has been theorized that there may be a quick increase in epinephrine during exercise that could contribute to the sickled red blood cells becoming sticky, thus further cutting off blood flow to muscles.15
Athletes who carry the SCT may be at increased risk of developing ECAST based on their environment, hydration level, and presence of asthma.9,13,17 Environmental factors include high heat, high humidity, and high altitude. High heat and humidity influence the body’s ability to maintain hydration levels. Hydration is an important consideration for proper athletic performance. Altitude is of significant note, as the higher the elevation, the less oxygen is available. Due to the decreased ability of red blood cells to carry oxygen when sickled, the already-decreased oxygen levels at high altitude can further decrease the body’s ability to circulate the much-needed oxygen. Sickling events may often be seen in athletes who have participated in maximal exertion exercise over a short time frame, such as a few minutes.9,13,17
Signs and Symptoms of Exercise Collapse Associated With Sickle Cell Trait
For athletes experiencing a sickling event, several signs and symptoms may occur. Initially, the patient will present with muscle pain, cramping, and weakness, particularly in the lower extremity and back.13,17,18 Further evaluation will likely reveal that the muscle weakness is greater than pain, and the muscles feel normal upon palpation. Many athletes have been noted to slump to the ground during a sickling event or report that they cannot go any further, and just stop activity.13,18 Additional signs may include shortness of breath during or immediately following exercise, as well as fatigue and difficulty recovering after exertion.17,19 In many cases, this clinical presentation may warrant a differential diagnosis with heat illness and/or cardiac conditions.13 In comparison to these conditions, the patient will often be able to communicate clearly, at least at first, and will have a rectal temperature below 103oF.18 Not all patients will present the same. Some will have leg and low back symptoms, whereas others will have chest tightness. It is all individualized18 (Table 13-2).
Reprinted with permission from Eichner, ER. Sickle Cell Trait in Sport. Curr Sports Med Rep. 2010; 9(6): 347-351. © 2010 Wolters Kluwer