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The Three H’s: Head, Heart, and Heat Considerations in Soccer
ABSTRACT
Soccer requires significant physical conditioning and endurance, as well as the physicality required for contact play. In order to keep athletes safe, it is important that coaches, medical staff, and the players themselves are educated on the most common dangers to their health that they may encounter on a soccer pitch. This article aims to review the current literature and recommendations on concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer, with a goal of educating all those who help to keep athletes healthy and competing to their full potential.
Continue to: Soccer is one of the most popular sports...
Soccer is one of the most popular sports in the modern world and requires significant physical conditioning and endurance, as well as the physicality required for contact play. This article covers the topics of concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer players. We provide a review of the prevention, recognition, and management required to keep athletes safe on the soccer pitch, both in practice and in competitive play.
HEAD
With an estimated 1.6 to 3.8 million sports-related mild traumatic brain injuries (ie, concussions) occurring annually in the United States,1 there has been an appropriate increase in the focus on prevention and treatment of these injuries. For more than a decade the spotlight has been on concussions that occur in American football, but other sports have also had to examine the prevalence of concussions in their sport. This is certainly true for soccer.
There has been a steady increase in soccer participation in the United States. From 1973 to 2014 there was a 4-fold increase in high school boys and a 35-fold increase in high school girls playing soccer.2 Currently, there are more than 3.7 million youth who play on teams under the supervision of the US Soccer Federation, the sport’s national governing body.3 With the growth of the sport, there has also been an intensified focus on injury prevention in soccer players, including concussive brain injuries.
A recent study examined injury rates in high school soccer players and noted that concussion is the second most common injury (17.9%), after ligament sprains (29.7%).4 The overall injury rate was 2.06 per 1000 athletic exposures (AEs [defined as participation in practice or game play]), but higher in games (4.42 per 1000 AEs) than during practices (1.05 per 1000 AEs). The overall concussion rate was 0.36 per 1000 AEs.4
Most concussions (54.8%) resulted in missing play between 1 to 3 weeks, but a sizeable portion of the athletes (14.9%) were out of play for more than 3 weeks. Additionally, 10.7% of all medical disqualifications were due to concussive injuries. Khodaee and colleagues4 found no statistically significant difference in concussion rates between male and female soccer players over the 9-year period of time that they examined, however previous studies have found higher rates in female athletes.5
In soccer, as in other sports, there is a concern about both the adequate recognition of concussions during practice and play and the underreporting of concussions by athletes. The US Soccer Federation has taken a proactive stance on addressing concussion in youth soccer by developing the “Recognize to Recover” program.6 Recognize to Recover is the US Soccer Federation’s “comprehensive player health and safety program aimed at promoting safe play and reducing injuries in soccer players of all ages.” The website provides an educational video geared toward players, along with links to concussion assessment tools, the US Soccer Federation Concussion Protocol, and US Soccer Federation-Centers for Disease Control fact sheets for athletes, parents, and coaches.6
Continue to: A challenge for all sports...
A challenge for all sports is allowing adequate evaluation of a suspected concussion by properly trained healthcare professionals. The 2017 Berlin Concussion in Sport Group position paper stated, “when a concussion is suspected, the athlete should be removed from the sporting environment and a multimodal assessment should be conducted in standardized fashion (eg, Sport Concussion Assessment Tool- 5th edition). Sporting bodies should allow adequate time to conduct this evaluation.”7 However, the International Federation of Football Association (FIFA) rules limit substitutions to 3 over the course of the game, which can make a thorough evaluation of players difficult as trainers and coaches are under increased pressure to quickly determine whether to use one of their valuable substitutions. Fortunately, the National Collegiate Athletic Association (NCAA) soccer has mitigated this issue by allowing unlimited substitutions during matches, and high school teams generally follow similar rules.
One of the goals of any safety education program is not only to raise the awareness of the signs and symptoms of concussion by all those involved in the sport, but also to increase the number of athletes who self-report their symptoms and decrease those who hide any possible concussions. A study found that a majority (58.6%) of middle school soccer players continued to play while experiencing concussion symptoms.5 However, in a very recent (not yet published) study, 92% of US Soccer Federation players reported that they did seek out a medical evaluation for their concussion.8 This is certainly a positive sign and further research needs to clarify what methods of education or training will maintain this level of self-reporting in soccer players.
There has also been an increased focus on understanding the mechanism of injury of concussions. In soccer, concussions can occur from player-to-player contact, contact with the player surface, contact with playing apparatus (eg, goal posts) and non-contact mechanisms. While there has been a focus on concussions from heading the ball, player-to-player contact is the most common cause of concussions. A 2017 study of 7- to 12-year-old soccer players in 4 European countries found that about 1 out of 10 concussions were caused by heading the ball.9 Comstock and colleageues10 found slightly higher numbers, roughly 25% to 30% (depending on gender), but 70% to 78% (again depending on gender) of those were caused by player-to-player contact rather than contact with the ball.
To date there has not been any meta-analytic review evaluating the cognitive and physical symptoms associated with heading in soccer. A recent review paper stated that the “current evidence seems insufficient to support a ban of heading in children’s football (soccer).”10 However, in December 2015 the US Soccer Federation included age-specific heading limitations. Players ages 10 years and under “shall not engage in heading, either in practices or in games” and players age 11 years and 12 years should have “limited heading in practice; maximum of 30 minutes of heading training per week, with no more than 15-20 headers per player, per week.”11 US Soccer Federation officials acknowledged the limitations in the current science regarding heading in young soccer players but chose to err on the side of caution until further empirical evidence regarding the risks associated with repetitive heading is available.
The US Soccer Federation is also exploring other ways to reduce the incidence rate of concussions, including ensuring that the age-appropriate sized ball is used in practice and play, possible rule changes, evaluation of different playing surfaces, and equipment usage. To date, there is no strong evidence to support the use of mouth guards or helmets to reduce concussions in soccer. Additionally, the current data about the value of head impact sensors in soccer has not supported its widespread use.
Continue to: Finally, the issue of the prevalence...
Finally, the issue of the prevalence of chronic traumatic encephalopathy (CTE) in soccer players is beyond the scope of this article. The expert opinion from the 2017 US Soccer Federation, Major League Soccer (MLS), and National Women’s Soccer League (NWSL) conference concluded, “At present, no data exist that support that soccer participation is a risk factor for the development of neurodegenerative disease. Similarly, at this time, consistent with evidence discussed in the Berlin Concussion in Sport Group (CISG) Consensus Conference, our review suggests no causal relationship has been demonstrated between soccer and CTE pathology.”12
The more we know about concussions, both in general and those sustained during soccer play, the better we are able to diagnose and manage these injuries in our athletes. An important step is creating evidence-based protocols that evolve as our knowledge of concussions does as well. In April 2017, the US Soccer Federation, MLS, and the NWSL held a joint summit entitled, “Head Injury in Soccer: From Science to the Field” to address the current evidence-based science of concussions in soccer.8 An article discussing the findings of this meeting is forthcoming and will undoubtedly guide further development of concussion protocols for soccer players of all ages.
HEART
The physiologic demands of soccer place considerable stress on the cardiovascular system. Participation in training and competition is characterized by a combination of aerobic and anaerobic physiology with the typical athlete covering approximately 10 km over the course of the 90-minute match. The primary role of the heart and blood vessels is to supply the exercising skeletal muscle with oxygen and energy substrate and to clear the byproducts of metabolism. Among healthy athletes without cardiovascular disease, these processes are typically well tolerated and may be associated with beneficial cardiovascular adaptations over time. However, competitive soccer players are not completely immune to cardiovascular disease. Athletes across the age and competition spectrum may develop symptoms suggestive of underlying cardiovascular disease during play including exertional chest pain, inappropriate shortness of breath, palpitations, and syncope. These athletes require timely clinical evaluation. In extremely rare but high visibility cases, competitive soccer players may succumb to cardiac arrest on the pitch, underscoring the need for comprehensive emergency action plans (EAPs). We provide the practicing clinician with an overview of cardiovascular issues relevant to the competitive soccer athlete.
CARDIOVASCULAR ADAPTATIONS TO SPORT
The pressure (ie, repetitive surges in systemic blood pressure) and volume (ie, sustained increases in high cardiac output) challenges inherent in soccer participation place stress on the cardiovascular system. Healthy athletes across the age spectrum typically tolerate the hemodynamic stressors of participation without issues. Athletes that engage in training and competition over months to years often develop beneficial adaptations of the cardiovascular system that enhance on-field performance and contribute to optimal long-term health. Detailed discussion of how the heart and blood vessels respond to exercise training is beyond the scope of this article, but the interested reader is referred to several prior publications.13,14 In brief, the heart of the healthy soccer athlete demonstrates the balanced mild chamber dilation and wall thickening characteristic of left ventricular eccentric remodeling. This form of exercise-induced cardiac remodeling facilitates maintenance of high stroke volume during exercise with minimal increases in cardiac work. In parallel, routine aerobic exercise training confers favorable changes in the systemic arterial system, which leads to reductions in age-associated ventricular stiffening and maintenance of healthy low blood pressure. It must be emphasized that the healthy heart muscle dilation and thickening that develop in response to sports participation, regardless of age, ethnicity, or gender, are relatively mild and should not be confused with common forms of heart muscle disease that may be seen in athletes at risk for adverse outcomes. In some situations, consultation with an extreme sports cardiologist may be required to differentiate exercise-induced remodeling from over heart muscle pathology.15
Continue to: THE SYMPTOMATIC ATHLETE...
THE SYMPTOMATIC ATHLETE
Any athlete presenting with symptoms suggestive of underlying cardiovascular disease should be withheld from training and competition until a comprehensive clinical evaluation has been completed. Common manifestations of underlying heart disease that occur in soccer players include exertional chest pain/pressure/tightness, shortness of breath that is out of proportion to workload, palpitations or the perception of irregular cardiac activity, and syncope. Chest discomfort, inappropriate shortness of breath, and palpitations that occur during training or competition should be managed with immediate removal from the playing field and prompt medical assessment. In many cases, thorough evaluation will involve collaboration between sports medicine and sports cardiology providers. Evaluations must be individualized on a case-by-case basis as tailored to the athlete’s presenting chief complaint and prior medical history. Most of these assessments will include a detailed medical history and physical examination, a 12-lead electrocardiogram (ECG), provocative exercise testing in a controlled environment, noninvasive cardiac imaging, and in some cases ambulatory rhythm monitoring. Uniformly, the athlete should be withheld from further training and competition until high-risk cardiovascular disease has been excluded. We refer the interested reader to a comprehensive discussion of symptom-based assessment of the athlete with suspected cardiovascular disease.16
Syncope (sudden and abrupt loss of consciousness with spontaneous neurologic recovery) is common among trained athletes. The vast majority of syncope is caused by “neurocardiogenic” mechanisms and carries a benign prognosis. Benign neurally-mediated syncope most often occurs outside of training and competition among athletes with heightened vagal tone and a predisposed susceptibility to triggers including pain, anxiety, emotional stimulation, and sudden postural change. Athletes who experience neurally-mediated syncope outside of training and competition routinely report a pre-event prodrome or aura that permits them to lower themselves to the ground, thereby avoiding injury. A distinct, but similarly benign and common, form of neurally-mediated fainting is post-exertional syncope. Here, fainting occurs within seconds of abrupt termination of exercise due to a rapid reduction cardiac preload and corollary cerebral blood supply. When either form of neurally-mediated syncope is suggested by a comprehensive medical history, normal physical examination, and a normal 12- lead ECG, further evaluation is unnecessary. However, the athlete and their coaching staff should be educated about avoidance tactics including hydration, dietary sodium supplementation, and avoidance of abrupt exercise termination as neutrally-mediated syncope tends to be recurrent without such measures. Fainting episodes that occur during training or competition that are not clearly post-exertional should be considered a medical emergency and should prompt comprehensive evaluation by a qualified cardiovascular specialist. Working closely with team physicians and athletic training staff, it is the responsibility of sports cardiologists to exclude potentially life-threatening forms of electrical, muscular, coronary, and valvular heart disease. Ideally, this evaluation should be conducted rapidly to avoid unnecessary delays in return to play.
CARDIAC ARREST AND SUDDEN DEATH
Numerous high-visibility cases of cardiac arrest on the soccer pitch have alerted the sporting community to the potential for these rare and potentially tragic events. Definitive incidence statistics defining the risk of cardiac arrest among soccer players are lacking. Data from the NCAA database suggest a sudden death incidence rate among collegiate male soccer athletes of approximately 1:24,000 athlete years.8 Similar data documenting incidence among female athletes and among those at lower (ie, youth level and high school) and higher (ie, professional) levels of play are unavailable. Underlying cardiovascular disease in the forms of heart muscle abnormalities (ie, genetic and acquired cardiomyopathy), coronary artery abnormalities (ie, genetic coronary anomalies and atherosclerotic coronary disease), valvular heart problems (ie, congenitally malformed aortic valves), and primary disturbances of the cardiac electrical system (ie, Wolf-Parkinson-White syndrome, long QT syndrome, etc.) explain a substantial percentage of on-pitch cardiac arrest. However, it is increasingly recognized that a significant minority of sudden cardiac deaths among athletes occur in the absence of attributable cardiovascular abnormality.17 Such cases, often referred to as “sudden unexplained death,” present unique challenges in the context of pre-participation screening, as they are undetectable and thus unpredictable.
Reduction of cardiac arrest and sudden death may best be accomplished through a combination of focused pre-participation screening and the development and implementation of a comprehensive EAP. Pre-participation involves the performance of a battery of tests prior to training and competition that are geared toward the detection of occult high-risk cardiovascular disease. Recommendations regarding pre-participation screening vary both across and within countries. Current US recommendations call for a focused medical history and physical examination prior to training and competition with consideration of the addition of a 12-lead ECG on a local level based on expertise and available resources.18 Conversely, current European guidelines including those endorsed by FIFA, suggest routine inclusion of a 12-lead ECG and in some cases, a transthoracic ECG.19 It must be emphasized that no screening approach has been confirmed to reduce the incidence of sudden death, and the decision to extend screening beyond the medical history and physical examination to include a 12-lead ECG or echocardiogram may come at the cost of increased false positive testing. In practice, decisions about how and when to screen are ideally made at a local level after consideration of medical and financial resources.20
Continue to: Even the most comprehensive approach...
Even the most comprehensive approach to screening and evaluation of symptomatic athletes will not completely eliminate on-pitch cardiac arrest. Thus, all stakeholders that engage in the oversight of organized soccer must be committed to the development and implementation of an EAP.21 Key components of an effective EAP include the training of coaching staff, athletic trainers, and players in basic cardiopulmonary resuscitation, access to and training in the use of automated external defibrillators, and a triage/transport protocol that ensures timely access to advanced cardiac life support. Much like screening, emergency action planning involving these key core components must be developed and tailored locally. In the era of contemporary organized athletics, the absence of an EAP at any level of competition, from youth to professional leagues, is unacceptable. Effective EAPs must be developed, documented, and rehearsed at regular intervals. For the health and safety of competitive soccer players, as well as coaching staff and spectators, these steps are of critical importance.
HEAT
Heat-related illnesses can be serious and, at times, even life threatening. It is important for athletic staff and athletes to be well versed in the prevention, signs and symptoms, and treatment of heat-related illnesses in order to prevent serious and lasting injury. We aim to educate physicians about the prevention, recognition, and management of heat-related injury, and stress the importance of similarly educating athletes and coaching staff.
Exertional heat illnesses most often occur at temperatures >86°F, however they can occur at any temperature with heavy exertion.22 Signs and symptoms can be nonspecific early on, including weakness, fatigue, headache, nausea, and dizziness. Later signs can include imbalance, altered mentation, confusion, and behavior that is out of character such as irritability or aggression.23 It is easy to see how the later signs can be confused for concussion in the right context. We cover the recognition and treatment of two common and serious heat-related illnesses: heat exhaustion and exertional heat stroke (EHS).
HEAT EXHAUSTION
Heat exhaustion occurs when an athlete cannot continue to exercise due to weakness and fatigue. While the exact mechanism is not well understood, it has been established that the combined effect of heat and dehydration have been proven to decrease exercise capacity and performance to a greater degree than either alone. The heat created by the body during exercise is 15 to 20 times greater than when at rest, and can increase core body temperature by 1°C every 5 minutes if no heat is lost, such as through sweating.24 Additionally, when fluid deficits reach >3% to 5% of total body water, sweat production and skin blood flow decline, blunting the ability for the body to cool itself and causing progressive elevation of core body temperature if the athlete continues exerting him or herself. When fluid deficits reach 6% to 10%, cardiac output, sweat, and muscle blood flow decrease, likely leading to the symptoms seen with heat exhaustion: weakness, profound fatigue, and occasionally confusion and disorientation. Athletes with suspected heat exhaustion should be moved to a cooler area, laid down with legs elevated, and orally rehydrated. If they do not improve with oral rehydration, they may require intravenous fluids. The diagnosis of heat exhaustion hinges on a rectal temperature of <104°F; if >104°F the athlete should be presumed to have heat stroke, which will be addressed in the following paragraphs. Players can be cleared to return to play in mild cases within 24 to 48 hours with gradual increases in exercise intensity.24
EXERTIONAL HEAT STROKE
EHS occurs when the body can no longer regulate the core body temperature and it rises to upwards of 104°F. In EHS, elevated core body temperature is associated with evidence of end organ dysfunction. The most easily identified on the playing field is likely central nervous system dysfunction, including irritability, confusion, irrational behavior, lethargy, dizziness, confusion, and even loss of consciousness. Temperature should be measured with rectal temperature only, as other methods of measurement have been shown to be consistently inaccurate.22 Heat stroke can be confused with exertional hyponatremia, heat exhaustion, or concussion, especially when core body temperature cannot be determined. However, EHS should always be the presumed cause of altered mentation when no rectal temperature is available because rapid cooling is critical to minimizing lasting effects. Morbidity and mortality are directly related to the length of time required to cool the athlete under 40°C (104°F).24 Cooling should be completed on site prior to transport to a medical facility and is best achieved with submersion in an ice bath (ie, a kiddie pool or soaking tub full of ice and water).22,25 If an ice bath is not available, ice bags should be applied to the neck axilla and groin and exchanged for fresh bags every 2 to 3 minutes.22 Ice bags have been shown to be inferior to whole body cooling, only cooling the athlete .04°C to .08°C/min compared to .15°C to .24°C/min with the ice bath.24 All other tests should be delayed until cooling is achieved, unless they can be completed while cooling the athlete. The athlete can be removed from the ice bath once rectal temperatures reach <101°F to 102°F.23 If the athlete returns to baseline after cooling, transportation to a medical facility may not be necessary. However, they should refrain from physical activity and heat exposure for at least 7 days and should be evaluated by a physician at that time. If all labs are normal and the athlete is asymptomatic, they can start progressive return to play under the direction of an athletic trainer or a sports medicine physician.23
Continue to: HEAT-RELATED ILLNESS...
HEAT-RELATED ILLNESS
It is impossible to predict exactly which athletes will be most at risk for heat-related illness, so it is important to have a high degree of suspicion when environmental conditions are right. Athletes with recent illness, fever, or lack of sleep are at higher risk. Additional intrinsic risk factors include low fitness level, obesity, and inadequate hydration. Athletes who are highly competitive or motivated can be more likely to push through the early signs of illness or be reluctant to report symptoms.23 Those with a history of exertional heat illness are more at risk for developing it again in the future.23
The extrinsic risk factors for the development of heat-related illness are much easier to identify and modify in order to keep athletes safe. High temperature and high humidity conditions, heavy sun exposure, and exposure to similar conditions the preceding day put athletes at risk for exertional heat illness. Risks are even greater when the exercise is prolonged or intense with few breaks and access to hydration is limited.23 Therefore, prevention of exertional heat illness is centered on these external risk factors.
Each team should have a heat policy as part of their EAP aimed at prevention and early recognition of heat-related illness. This policy should be shared with all athletes and coaches. The plan should be centered on acclimatization, activity modification, and early recognition and management as previously discussed. The US Soccer Federation “Recognize to Recover” Heat Guidelines suggest a 3-step process for appropriate activity modification:22
1. Find the wet bulb globe temperature, either using a wet bulb globe thermometer or the temperature and humidity (Figure 1).
2. Find your regional weather category on the map (Figure 2).
3. Find your alert level and work to rest ratio recommendations (Figure 3).
Scheduled hydration breaks should be given as listed in Figure 3. Breaks of 4 minutes should be given for each 30 minutes of continuous practice or play. In a regulation 90-minute match, a hydration break should be given at 30 and 75 minutes (with half time at 45 minutes) at minimum. Athletes should be educated about where hydration can be accessed, and given unlimited access to hydration even outside of planned breaks.22
Acclimatization to conditions is another integral part of preventing heat-related illness. It allows the body time to adapt to exercising in heat gradually, with a measured progression of exertion over the course of 10 to 14 days. The “Recognize to Recover” Heat Guidelines also provide guidance on acclimatization, and specifics can be found on the website.1 Generally speaking, the warmest part of the day, usually between 11 AM and 4 PM, should be avoided for all training sessions, and length of practice and exertion should be gradually increased over 2 weeks.22
In summary, appropriate acclimatization, hydration, activity modification, and education of athletes and staff are essential for the prevention of heat-related illness. Athletes and staff should understand the signs and symptoms of heat-related illness so that it can be recognized early and treated appropriately. If an athlete is altered in the heat and rectal temperature is >104°F or rectal temperature cannot be obtained, rapid cooling using an ice bath or ice bags is essential to prevent the morbidity and mortality associated with EHS. Above all, teams should have an explicit plan that includes protocols for acclimatization, activity modification, and all necessary equipment to prevent and treat heat-related illnesses should they occur, and ultimately keep athletes safe and healthy.
1. Langlois JA, Rutland-Brown W, Wald MM. The epidemiology and impact of traumatic brain Injury: a brief overview. J Head Trauma Rehabil. 2006;21(5):375-378.
2. The National Federation of State High School Associations. 2013-14 high school athletics participation survey. http://www.nfhs.org/ParticipationStatics/PDF/2013-14_Participation_Survey_PDF.pdf. Accessed August 6, 2018.
3. Youth Council. US Soccer Federation Web site. https://www.ussoccer.com/about/affiliates/youth-council. Accessed July 31, 2018.
4. Khodaee M, Currie DW, Asif IM, Comstock RD. Nine-year study of US high school soccer injuries: data from a national sports injury surveillance programme. Br J Sports Med. 2017;51(3):185-193. doi:10.1136/bjsports-2015-095946.
5. Schallmo MS, Weiner JA, Hsu WK. Sport and sex-specific trends in the epidemiology of concussions sustained by high school athletes. J Bone Joint Surg Am. 2017;99(15):1314-1320. doi:10.2106/JBJS.16.01573.
6. US Soccer Federation. U.S. Soccer’s comprehensive player health and safety program. Recognize to Recover Web site. http://www.recognizetorecover.org/#us-soccers-comprehensive-player-health-and-safety-program. Accessed July 31, 2018.
7. McCrory P, Meeuwisse W, Dvořák J, et al. Consensus statement on concussion in sport-the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;51(11):838-847. doi:10.1136/bjsports-2017-097699.
8. Harmon KG, Asif IM, Klossner D, Drezner JA. Incidence of sudden cardiac death in National Collegiate Athletic Association athletes. Circulation. 2011;123(15):1594-1600. doi:10.1161/CIRCULATIONAHA.110.004622.
9. Faude O, Rössler R, Junge A, et al. Head injuries in children’s football-results from two prospective cohort studies in four European countries. Scand J Med Sci Sports. 2017;27(12):1986-1992. doi:10.1111/sms.12839.
10. Comstock RD, Currie DW, Pierpoint LA, Grubenhoff JA, Fields SK. An evidence-based discussion of heading the ball and concussions in high school soccer. JAMA Pediatr. 2015;169(9):830-837. doi:10.1001/jamapediatrics.2015.1062.
11. Tarnutzer AA. Should heading be forbidden in children’s football? Sci Med Football. 2018;2(1):75-79.
12. US Soccer Federation. US Soccer, NWSL and MLS to host “head injury in soccer; science to field”. https://www.ussoccer.com/stories/2017/04/18/17/35/20170418-news-us-soccer-nwsl-mls-host-head-injury-in-soccer-science-to-field. Published April 18, 2017. Accessed August 6, 2018.
13. Weiner RB, Baggish AL. Exercise-induced cardiac remodeling. Prog Cardiovasc Dis. 2012;54(5):380-386. doi:10.1016/j.pcad.2012.01.006.
14. Baggish AL, Wood MJ. Athlete's heart and cardiovascular care of the athlete: scientific and clinical update. Circulation. 2011;123(23):2723-2735. doi:10.1161/CIRCULATIONAHA.110.981571.
15. Kim JH, Baggish AL. Differentiating exercise-induced cardiac adaptations from cardiac pathology: the "Grey Zone" of clinical uncertainty. Can J Cardiol. 2016;32(4):429-437. doi:10.1016/j.cjca.2015.11.025.
16. Baggish AL, Battle RW, Beckerman JG, et al; ACC’s Sports and Exercise Council Leadership Group. Sports cardiology: core curriculum for providing cardiovascular care to competitive athletes and highly active people. J Am Coll Cardiol. 2017;70(15):1902-1918. doi:10.1016/j.jacc.2017.08.055.
17. Harmon KG, Asif IM, Maleszewski JJ, et al. Incidence, cause, and comparative frequency of sudden cardiac death in National Collegiate Athletic Association athletes: a decade in review. Circulation. 2015;132(1):10-19. doi:10.1161/CIRCULATIONAHA.115.015431.
18. Maron BJ, Levine BD, Washington RL, Baggish AL, Kovacs RJ, Maron MS. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: task force 2: preparticipation screening for cardiovascular disease in competitive athletes: a scientific statement from the American Heart Association and American College of Cardiology. J Am Coll Cardiol. 2015;66(21):2356-2361. doi:10.1016/j.jacc.2015.09.034.
19. Corrado D, Pelliccia A, Bjørnstad HH, et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus Statement of the Study Group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J. 2005;26(5):516-524.
20. Baggish AL, Kovacs RJ. Preparticipation cardiovascular screening: clinical partnership is the only certainty. Br J Sports Med. 2017;51(3):150-151. doi:10.1136/bjsports-2016-096954.
21. Hainline B, Drezner J, Baggish A, et al. Interassociation consensus statement on cardiovascular care of college student-athletes. J Athl Train. 2016;51(4):344-357. doi:10.4085/j.jacc.2016.03.527.
22. US Soccer Federation. Environmental conditions. Recognize to Recover Web site. http://www.recognizetorecover.org/environmental/#environmental-conditions. Accessed April 15, 2018.
23. Korey Stringer Institute. Emergency conditions: heat illnesses. University of Connecticut Web site. https://ksi.uconn.edu/. Accessed April 15, 2018.
24. American College of Sports Medicine, Armstrong LE, Casa DJ, et al. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556-572.
25. Belval LN, Casa DJ, Adams WM, et al. Consensus statement- prehospital care of exertional heat stroke. Prehosp Emerg Care. 2018;22(3):392-397. doi:10.1080/10903127.2017.1392666.
ABSTRACT
Soccer requires significant physical conditioning and endurance, as well as the physicality required for contact play. In order to keep athletes safe, it is important that coaches, medical staff, and the players themselves are educated on the most common dangers to their health that they may encounter on a soccer pitch. This article aims to review the current literature and recommendations on concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer, with a goal of educating all those who help to keep athletes healthy and competing to their full potential.
Continue to: Soccer is one of the most popular sports...
Soccer is one of the most popular sports in the modern world and requires significant physical conditioning and endurance, as well as the physicality required for contact play. This article covers the topics of concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer players. We provide a review of the prevention, recognition, and management required to keep athletes safe on the soccer pitch, both in practice and in competitive play.
HEAD
With an estimated 1.6 to 3.8 million sports-related mild traumatic brain injuries (ie, concussions) occurring annually in the United States,1 there has been an appropriate increase in the focus on prevention and treatment of these injuries. For more than a decade the spotlight has been on concussions that occur in American football, but other sports have also had to examine the prevalence of concussions in their sport. This is certainly true for soccer.
There has been a steady increase in soccer participation in the United States. From 1973 to 2014 there was a 4-fold increase in high school boys and a 35-fold increase in high school girls playing soccer.2 Currently, there are more than 3.7 million youth who play on teams under the supervision of the US Soccer Federation, the sport’s national governing body.3 With the growth of the sport, there has also been an intensified focus on injury prevention in soccer players, including concussive brain injuries.
A recent study examined injury rates in high school soccer players and noted that concussion is the second most common injury (17.9%), after ligament sprains (29.7%).4 The overall injury rate was 2.06 per 1000 athletic exposures (AEs [defined as participation in practice or game play]), but higher in games (4.42 per 1000 AEs) than during practices (1.05 per 1000 AEs). The overall concussion rate was 0.36 per 1000 AEs.4
Most concussions (54.8%) resulted in missing play between 1 to 3 weeks, but a sizeable portion of the athletes (14.9%) were out of play for more than 3 weeks. Additionally, 10.7% of all medical disqualifications were due to concussive injuries. Khodaee and colleagues4 found no statistically significant difference in concussion rates between male and female soccer players over the 9-year period of time that they examined, however previous studies have found higher rates in female athletes.5
In soccer, as in other sports, there is a concern about both the adequate recognition of concussions during practice and play and the underreporting of concussions by athletes. The US Soccer Federation has taken a proactive stance on addressing concussion in youth soccer by developing the “Recognize to Recover” program.6 Recognize to Recover is the US Soccer Federation’s “comprehensive player health and safety program aimed at promoting safe play and reducing injuries in soccer players of all ages.” The website provides an educational video geared toward players, along with links to concussion assessment tools, the US Soccer Federation Concussion Protocol, and US Soccer Federation-Centers for Disease Control fact sheets for athletes, parents, and coaches.6
Continue to: A challenge for all sports...
A challenge for all sports is allowing adequate evaluation of a suspected concussion by properly trained healthcare professionals. The 2017 Berlin Concussion in Sport Group position paper stated, “when a concussion is suspected, the athlete should be removed from the sporting environment and a multimodal assessment should be conducted in standardized fashion (eg, Sport Concussion Assessment Tool- 5th edition). Sporting bodies should allow adequate time to conduct this evaluation.”7 However, the International Federation of Football Association (FIFA) rules limit substitutions to 3 over the course of the game, which can make a thorough evaluation of players difficult as trainers and coaches are under increased pressure to quickly determine whether to use one of their valuable substitutions. Fortunately, the National Collegiate Athletic Association (NCAA) soccer has mitigated this issue by allowing unlimited substitutions during matches, and high school teams generally follow similar rules.
One of the goals of any safety education program is not only to raise the awareness of the signs and symptoms of concussion by all those involved in the sport, but also to increase the number of athletes who self-report their symptoms and decrease those who hide any possible concussions. A study found that a majority (58.6%) of middle school soccer players continued to play while experiencing concussion symptoms.5 However, in a very recent (not yet published) study, 92% of US Soccer Federation players reported that they did seek out a medical evaluation for their concussion.8 This is certainly a positive sign and further research needs to clarify what methods of education or training will maintain this level of self-reporting in soccer players.
There has also been an increased focus on understanding the mechanism of injury of concussions. In soccer, concussions can occur from player-to-player contact, contact with the player surface, contact with playing apparatus (eg, goal posts) and non-contact mechanisms. While there has been a focus on concussions from heading the ball, player-to-player contact is the most common cause of concussions. A 2017 study of 7- to 12-year-old soccer players in 4 European countries found that about 1 out of 10 concussions were caused by heading the ball.9 Comstock and colleageues10 found slightly higher numbers, roughly 25% to 30% (depending on gender), but 70% to 78% (again depending on gender) of those were caused by player-to-player contact rather than contact with the ball.
To date there has not been any meta-analytic review evaluating the cognitive and physical symptoms associated with heading in soccer. A recent review paper stated that the “current evidence seems insufficient to support a ban of heading in children’s football (soccer).”10 However, in December 2015 the US Soccer Federation included age-specific heading limitations. Players ages 10 years and under “shall not engage in heading, either in practices or in games” and players age 11 years and 12 years should have “limited heading in practice; maximum of 30 minutes of heading training per week, with no more than 15-20 headers per player, per week.”11 US Soccer Federation officials acknowledged the limitations in the current science regarding heading in young soccer players but chose to err on the side of caution until further empirical evidence regarding the risks associated with repetitive heading is available.
The US Soccer Federation is also exploring other ways to reduce the incidence rate of concussions, including ensuring that the age-appropriate sized ball is used in practice and play, possible rule changes, evaluation of different playing surfaces, and equipment usage. To date, there is no strong evidence to support the use of mouth guards or helmets to reduce concussions in soccer. Additionally, the current data about the value of head impact sensors in soccer has not supported its widespread use.
Continue to: Finally, the issue of the prevalence...
Finally, the issue of the prevalence of chronic traumatic encephalopathy (CTE) in soccer players is beyond the scope of this article. The expert opinion from the 2017 US Soccer Federation, Major League Soccer (MLS), and National Women’s Soccer League (NWSL) conference concluded, “At present, no data exist that support that soccer participation is a risk factor for the development of neurodegenerative disease. Similarly, at this time, consistent with evidence discussed in the Berlin Concussion in Sport Group (CISG) Consensus Conference, our review suggests no causal relationship has been demonstrated between soccer and CTE pathology.”12
The more we know about concussions, both in general and those sustained during soccer play, the better we are able to diagnose and manage these injuries in our athletes. An important step is creating evidence-based protocols that evolve as our knowledge of concussions does as well. In April 2017, the US Soccer Federation, MLS, and the NWSL held a joint summit entitled, “Head Injury in Soccer: From Science to the Field” to address the current evidence-based science of concussions in soccer.8 An article discussing the findings of this meeting is forthcoming and will undoubtedly guide further development of concussion protocols for soccer players of all ages.
HEART
The physiologic demands of soccer place considerable stress on the cardiovascular system. Participation in training and competition is characterized by a combination of aerobic and anaerobic physiology with the typical athlete covering approximately 10 km over the course of the 90-minute match. The primary role of the heart and blood vessels is to supply the exercising skeletal muscle with oxygen and energy substrate and to clear the byproducts of metabolism. Among healthy athletes without cardiovascular disease, these processes are typically well tolerated and may be associated with beneficial cardiovascular adaptations over time. However, competitive soccer players are not completely immune to cardiovascular disease. Athletes across the age and competition spectrum may develop symptoms suggestive of underlying cardiovascular disease during play including exertional chest pain, inappropriate shortness of breath, palpitations, and syncope. These athletes require timely clinical evaluation. In extremely rare but high visibility cases, competitive soccer players may succumb to cardiac arrest on the pitch, underscoring the need for comprehensive emergency action plans (EAPs). We provide the practicing clinician with an overview of cardiovascular issues relevant to the competitive soccer athlete.
CARDIOVASCULAR ADAPTATIONS TO SPORT
The pressure (ie, repetitive surges in systemic blood pressure) and volume (ie, sustained increases in high cardiac output) challenges inherent in soccer participation place stress on the cardiovascular system. Healthy athletes across the age spectrum typically tolerate the hemodynamic stressors of participation without issues. Athletes that engage in training and competition over months to years often develop beneficial adaptations of the cardiovascular system that enhance on-field performance and contribute to optimal long-term health. Detailed discussion of how the heart and blood vessels respond to exercise training is beyond the scope of this article, but the interested reader is referred to several prior publications.13,14 In brief, the heart of the healthy soccer athlete demonstrates the balanced mild chamber dilation and wall thickening characteristic of left ventricular eccentric remodeling. This form of exercise-induced cardiac remodeling facilitates maintenance of high stroke volume during exercise with minimal increases in cardiac work. In parallel, routine aerobic exercise training confers favorable changes in the systemic arterial system, which leads to reductions in age-associated ventricular stiffening and maintenance of healthy low blood pressure. It must be emphasized that the healthy heart muscle dilation and thickening that develop in response to sports participation, regardless of age, ethnicity, or gender, are relatively mild and should not be confused with common forms of heart muscle disease that may be seen in athletes at risk for adverse outcomes. In some situations, consultation with an extreme sports cardiologist may be required to differentiate exercise-induced remodeling from over heart muscle pathology.15
Continue to: THE SYMPTOMATIC ATHLETE...
THE SYMPTOMATIC ATHLETE
Any athlete presenting with symptoms suggestive of underlying cardiovascular disease should be withheld from training and competition until a comprehensive clinical evaluation has been completed. Common manifestations of underlying heart disease that occur in soccer players include exertional chest pain/pressure/tightness, shortness of breath that is out of proportion to workload, palpitations or the perception of irregular cardiac activity, and syncope. Chest discomfort, inappropriate shortness of breath, and palpitations that occur during training or competition should be managed with immediate removal from the playing field and prompt medical assessment. In many cases, thorough evaluation will involve collaboration between sports medicine and sports cardiology providers. Evaluations must be individualized on a case-by-case basis as tailored to the athlete’s presenting chief complaint and prior medical history. Most of these assessments will include a detailed medical history and physical examination, a 12-lead electrocardiogram (ECG), provocative exercise testing in a controlled environment, noninvasive cardiac imaging, and in some cases ambulatory rhythm monitoring. Uniformly, the athlete should be withheld from further training and competition until high-risk cardiovascular disease has been excluded. We refer the interested reader to a comprehensive discussion of symptom-based assessment of the athlete with suspected cardiovascular disease.16
Syncope (sudden and abrupt loss of consciousness with spontaneous neurologic recovery) is common among trained athletes. The vast majority of syncope is caused by “neurocardiogenic” mechanisms and carries a benign prognosis. Benign neurally-mediated syncope most often occurs outside of training and competition among athletes with heightened vagal tone and a predisposed susceptibility to triggers including pain, anxiety, emotional stimulation, and sudden postural change. Athletes who experience neurally-mediated syncope outside of training and competition routinely report a pre-event prodrome or aura that permits them to lower themselves to the ground, thereby avoiding injury. A distinct, but similarly benign and common, form of neurally-mediated fainting is post-exertional syncope. Here, fainting occurs within seconds of abrupt termination of exercise due to a rapid reduction cardiac preload and corollary cerebral blood supply. When either form of neurally-mediated syncope is suggested by a comprehensive medical history, normal physical examination, and a normal 12- lead ECG, further evaluation is unnecessary. However, the athlete and their coaching staff should be educated about avoidance tactics including hydration, dietary sodium supplementation, and avoidance of abrupt exercise termination as neutrally-mediated syncope tends to be recurrent without such measures. Fainting episodes that occur during training or competition that are not clearly post-exertional should be considered a medical emergency and should prompt comprehensive evaluation by a qualified cardiovascular specialist. Working closely with team physicians and athletic training staff, it is the responsibility of sports cardiologists to exclude potentially life-threatening forms of electrical, muscular, coronary, and valvular heart disease. Ideally, this evaluation should be conducted rapidly to avoid unnecessary delays in return to play.
CARDIAC ARREST AND SUDDEN DEATH
Numerous high-visibility cases of cardiac arrest on the soccer pitch have alerted the sporting community to the potential for these rare and potentially tragic events. Definitive incidence statistics defining the risk of cardiac arrest among soccer players are lacking. Data from the NCAA database suggest a sudden death incidence rate among collegiate male soccer athletes of approximately 1:24,000 athlete years.8 Similar data documenting incidence among female athletes and among those at lower (ie, youth level and high school) and higher (ie, professional) levels of play are unavailable. Underlying cardiovascular disease in the forms of heart muscle abnormalities (ie, genetic and acquired cardiomyopathy), coronary artery abnormalities (ie, genetic coronary anomalies and atherosclerotic coronary disease), valvular heart problems (ie, congenitally malformed aortic valves), and primary disturbances of the cardiac electrical system (ie, Wolf-Parkinson-White syndrome, long QT syndrome, etc.) explain a substantial percentage of on-pitch cardiac arrest. However, it is increasingly recognized that a significant minority of sudden cardiac deaths among athletes occur in the absence of attributable cardiovascular abnormality.17 Such cases, often referred to as “sudden unexplained death,” present unique challenges in the context of pre-participation screening, as they are undetectable and thus unpredictable.
Reduction of cardiac arrest and sudden death may best be accomplished through a combination of focused pre-participation screening and the development and implementation of a comprehensive EAP. Pre-participation involves the performance of a battery of tests prior to training and competition that are geared toward the detection of occult high-risk cardiovascular disease. Recommendations regarding pre-participation screening vary both across and within countries. Current US recommendations call for a focused medical history and physical examination prior to training and competition with consideration of the addition of a 12-lead ECG on a local level based on expertise and available resources.18 Conversely, current European guidelines including those endorsed by FIFA, suggest routine inclusion of a 12-lead ECG and in some cases, a transthoracic ECG.19 It must be emphasized that no screening approach has been confirmed to reduce the incidence of sudden death, and the decision to extend screening beyond the medical history and physical examination to include a 12-lead ECG or echocardiogram may come at the cost of increased false positive testing. In practice, decisions about how and when to screen are ideally made at a local level after consideration of medical and financial resources.20
Continue to: Even the most comprehensive approach...
Even the most comprehensive approach to screening and evaluation of symptomatic athletes will not completely eliminate on-pitch cardiac arrest. Thus, all stakeholders that engage in the oversight of organized soccer must be committed to the development and implementation of an EAP.21 Key components of an effective EAP include the training of coaching staff, athletic trainers, and players in basic cardiopulmonary resuscitation, access to and training in the use of automated external defibrillators, and a triage/transport protocol that ensures timely access to advanced cardiac life support. Much like screening, emergency action planning involving these key core components must be developed and tailored locally. In the era of contemporary organized athletics, the absence of an EAP at any level of competition, from youth to professional leagues, is unacceptable. Effective EAPs must be developed, documented, and rehearsed at regular intervals. For the health and safety of competitive soccer players, as well as coaching staff and spectators, these steps are of critical importance.
HEAT
Heat-related illnesses can be serious and, at times, even life threatening. It is important for athletic staff and athletes to be well versed in the prevention, signs and symptoms, and treatment of heat-related illnesses in order to prevent serious and lasting injury. We aim to educate physicians about the prevention, recognition, and management of heat-related injury, and stress the importance of similarly educating athletes and coaching staff.
Exertional heat illnesses most often occur at temperatures >86°F, however they can occur at any temperature with heavy exertion.22 Signs and symptoms can be nonspecific early on, including weakness, fatigue, headache, nausea, and dizziness. Later signs can include imbalance, altered mentation, confusion, and behavior that is out of character such as irritability or aggression.23 It is easy to see how the later signs can be confused for concussion in the right context. We cover the recognition and treatment of two common and serious heat-related illnesses: heat exhaustion and exertional heat stroke (EHS).
HEAT EXHAUSTION
Heat exhaustion occurs when an athlete cannot continue to exercise due to weakness and fatigue. While the exact mechanism is not well understood, it has been established that the combined effect of heat and dehydration have been proven to decrease exercise capacity and performance to a greater degree than either alone. The heat created by the body during exercise is 15 to 20 times greater than when at rest, and can increase core body temperature by 1°C every 5 minutes if no heat is lost, such as through sweating.24 Additionally, when fluid deficits reach >3% to 5% of total body water, sweat production and skin blood flow decline, blunting the ability for the body to cool itself and causing progressive elevation of core body temperature if the athlete continues exerting him or herself. When fluid deficits reach 6% to 10%, cardiac output, sweat, and muscle blood flow decrease, likely leading to the symptoms seen with heat exhaustion: weakness, profound fatigue, and occasionally confusion and disorientation. Athletes with suspected heat exhaustion should be moved to a cooler area, laid down with legs elevated, and orally rehydrated. If they do not improve with oral rehydration, they may require intravenous fluids. The diagnosis of heat exhaustion hinges on a rectal temperature of <104°F; if >104°F the athlete should be presumed to have heat stroke, which will be addressed in the following paragraphs. Players can be cleared to return to play in mild cases within 24 to 48 hours with gradual increases in exercise intensity.24
EXERTIONAL HEAT STROKE
EHS occurs when the body can no longer regulate the core body temperature and it rises to upwards of 104°F. In EHS, elevated core body temperature is associated with evidence of end organ dysfunction. The most easily identified on the playing field is likely central nervous system dysfunction, including irritability, confusion, irrational behavior, lethargy, dizziness, confusion, and even loss of consciousness. Temperature should be measured with rectal temperature only, as other methods of measurement have been shown to be consistently inaccurate.22 Heat stroke can be confused with exertional hyponatremia, heat exhaustion, or concussion, especially when core body temperature cannot be determined. However, EHS should always be the presumed cause of altered mentation when no rectal temperature is available because rapid cooling is critical to minimizing lasting effects. Morbidity and mortality are directly related to the length of time required to cool the athlete under 40°C (104°F).24 Cooling should be completed on site prior to transport to a medical facility and is best achieved with submersion in an ice bath (ie, a kiddie pool or soaking tub full of ice and water).22,25 If an ice bath is not available, ice bags should be applied to the neck axilla and groin and exchanged for fresh bags every 2 to 3 minutes.22 Ice bags have been shown to be inferior to whole body cooling, only cooling the athlete .04°C to .08°C/min compared to .15°C to .24°C/min with the ice bath.24 All other tests should be delayed until cooling is achieved, unless they can be completed while cooling the athlete. The athlete can be removed from the ice bath once rectal temperatures reach <101°F to 102°F.23 If the athlete returns to baseline after cooling, transportation to a medical facility may not be necessary. However, they should refrain from physical activity and heat exposure for at least 7 days and should be evaluated by a physician at that time. If all labs are normal and the athlete is asymptomatic, they can start progressive return to play under the direction of an athletic trainer or a sports medicine physician.23
Continue to: HEAT-RELATED ILLNESS...
HEAT-RELATED ILLNESS
It is impossible to predict exactly which athletes will be most at risk for heat-related illness, so it is important to have a high degree of suspicion when environmental conditions are right. Athletes with recent illness, fever, or lack of sleep are at higher risk. Additional intrinsic risk factors include low fitness level, obesity, and inadequate hydration. Athletes who are highly competitive or motivated can be more likely to push through the early signs of illness or be reluctant to report symptoms.23 Those with a history of exertional heat illness are more at risk for developing it again in the future.23
The extrinsic risk factors for the development of heat-related illness are much easier to identify and modify in order to keep athletes safe. High temperature and high humidity conditions, heavy sun exposure, and exposure to similar conditions the preceding day put athletes at risk for exertional heat illness. Risks are even greater when the exercise is prolonged or intense with few breaks and access to hydration is limited.23 Therefore, prevention of exertional heat illness is centered on these external risk factors.
Each team should have a heat policy as part of their EAP aimed at prevention and early recognition of heat-related illness. This policy should be shared with all athletes and coaches. The plan should be centered on acclimatization, activity modification, and early recognition and management as previously discussed. The US Soccer Federation “Recognize to Recover” Heat Guidelines suggest a 3-step process for appropriate activity modification:22
1. Find the wet bulb globe temperature, either using a wet bulb globe thermometer or the temperature and humidity (Figure 1).
2. Find your regional weather category on the map (Figure 2).
3. Find your alert level and work to rest ratio recommendations (Figure 3).
Scheduled hydration breaks should be given as listed in Figure 3. Breaks of 4 minutes should be given for each 30 minutes of continuous practice or play. In a regulation 90-minute match, a hydration break should be given at 30 and 75 minutes (with half time at 45 minutes) at minimum. Athletes should be educated about where hydration can be accessed, and given unlimited access to hydration even outside of planned breaks.22
Acclimatization to conditions is another integral part of preventing heat-related illness. It allows the body time to adapt to exercising in heat gradually, with a measured progression of exertion over the course of 10 to 14 days. The “Recognize to Recover” Heat Guidelines also provide guidance on acclimatization, and specifics can be found on the website.1 Generally speaking, the warmest part of the day, usually between 11 AM and 4 PM, should be avoided for all training sessions, and length of practice and exertion should be gradually increased over 2 weeks.22
In summary, appropriate acclimatization, hydration, activity modification, and education of athletes and staff are essential for the prevention of heat-related illness. Athletes and staff should understand the signs and symptoms of heat-related illness so that it can be recognized early and treated appropriately. If an athlete is altered in the heat and rectal temperature is >104°F or rectal temperature cannot be obtained, rapid cooling using an ice bath or ice bags is essential to prevent the morbidity and mortality associated with EHS. Above all, teams should have an explicit plan that includes protocols for acclimatization, activity modification, and all necessary equipment to prevent and treat heat-related illnesses should they occur, and ultimately keep athletes safe and healthy.
ABSTRACT
Soccer requires significant physical conditioning and endurance, as well as the physicality required for contact play. In order to keep athletes safe, it is important that coaches, medical staff, and the players themselves are educated on the most common dangers to their health that they may encounter on a soccer pitch. This article aims to review the current literature and recommendations on concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer, with a goal of educating all those who help to keep athletes healthy and competing to their full potential.
Continue to: Soccer is one of the most popular sports...
Soccer is one of the most popular sports in the modern world and requires significant physical conditioning and endurance, as well as the physicality required for contact play. This article covers the topics of concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer players. We provide a review of the prevention, recognition, and management required to keep athletes safe on the soccer pitch, both in practice and in competitive play.
HEAD
With an estimated 1.6 to 3.8 million sports-related mild traumatic brain injuries (ie, concussions) occurring annually in the United States,1 there has been an appropriate increase in the focus on prevention and treatment of these injuries. For more than a decade the spotlight has been on concussions that occur in American football, but other sports have also had to examine the prevalence of concussions in their sport. This is certainly true for soccer.
There has been a steady increase in soccer participation in the United States. From 1973 to 2014 there was a 4-fold increase in high school boys and a 35-fold increase in high school girls playing soccer.2 Currently, there are more than 3.7 million youth who play on teams under the supervision of the US Soccer Federation, the sport’s national governing body.3 With the growth of the sport, there has also been an intensified focus on injury prevention in soccer players, including concussive brain injuries.
A recent study examined injury rates in high school soccer players and noted that concussion is the second most common injury (17.9%), after ligament sprains (29.7%).4 The overall injury rate was 2.06 per 1000 athletic exposures (AEs [defined as participation in practice or game play]), but higher in games (4.42 per 1000 AEs) than during practices (1.05 per 1000 AEs). The overall concussion rate was 0.36 per 1000 AEs.4
Most concussions (54.8%) resulted in missing play between 1 to 3 weeks, but a sizeable portion of the athletes (14.9%) were out of play for more than 3 weeks. Additionally, 10.7% of all medical disqualifications were due to concussive injuries. Khodaee and colleagues4 found no statistically significant difference in concussion rates between male and female soccer players over the 9-year period of time that they examined, however previous studies have found higher rates in female athletes.5
In soccer, as in other sports, there is a concern about both the adequate recognition of concussions during practice and play and the underreporting of concussions by athletes. The US Soccer Federation has taken a proactive stance on addressing concussion in youth soccer by developing the “Recognize to Recover” program.6 Recognize to Recover is the US Soccer Federation’s “comprehensive player health and safety program aimed at promoting safe play and reducing injuries in soccer players of all ages.” The website provides an educational video geared toward players, along with links to concussion assessment tools, the US Soccer Federation Concussion Protocol, and US Soccer Federation-Centers for Disease Control fact sheets for athletes, parents, and coaches.6
Continue to: A challenge for all sports...
A challenge for all sports is allowing adequate evaluation of a suspected concussion by properly trained healthcare professionals. The 2017 Berlin Concussion in Sport Group position paper stated, “when a concussion is suspected, the athlete should be removed from the sporting environment and a multimodal assessment should be conducted in standardized fashion (eg, Sport Concussion Assessment Tool- 5th edition). Sporting bodies should allow adequate time to conduct this evaluation.”7 However, the International Federation of Football Association (FIFA) rules limit substitutions to 3 over the course of the game, which can make a thorough evaluation of players difficult as trainers and coaches are under increased pressure to quickly determine whether to use one of their valuable substitutions. Fortunately, the National Collegiate Athletic Association (NCAA) soccer has mitigated this issue by allowing unlimited substitutions during matches, and high school teams generally follow similar rules.
One of the goals of any safety education program is not only to raise the awareness of the signs and symptoms of concussion by all those involved in the sport, but also to increase the number of athletes who self-report their symptoms and decrease those who hide any possible concussions. A study found that a majority (58.6%) of middle school soccer players continued to play while experiencing concussion symptoms.5 However, in a very recent (not yet published) study, 92% of US Soccer Federation players reported that they did seek out a medical evaluation for their concussion.8 This is certainly a positive sign and further research needs to clarify what methods of education or training will maintain this level of self-reporting in soccer players.
There has also been an increased focus on understanding the mechanism of injury of concussions. In soccer, concussions can occur from player-to-player contact, contact with the player surface, contact with playing apparatus (eg, goal posts) and non-contact mechanisms. While there has been a focus on concussions from heading the ball, player-to-player contact is the most common cause of concussions. A 2017 study of 7- to 12-year-old soccer players in 4 European countries found that about 1 out of 10 concussions were caused by heading the ball.9 Comstock and colleageues10 found slightly higher numbers, roughly 25% to 30% (depending on gender), but 70% to 78% (again depending on gender) of those were caused by player-to-player contact rather than contact with the ball.
To date there has not been any meta-analytic review evaluating the cognitive and physical symptoms associated with heading in soccer. A recent review paper stated that the “current evidence seems insufficient to support a ban of heading in children’s football (soccer).”10 However, in December 2015 the US Soccer Federation included age-specific heading limitations. Players ages 10 years and under “shall not engage in heading, either in practices or in games” and players age 11 years and 12 years should have “limited heading in practice; maximum of 30 minutes of heading training per week, with no more than 15-20 headers per player, per week.”11 US Soccer Federation officials acknowledged the limitations in the current science regarding heading in young soccer players but chose to err on the side of caution until further empirical evidence regarding the risks associated with repetitive heading is available.
The US Soccer Federation is also exploring other ways to reduce the incidence rate of concussions, including ensuring that the age-appropriate sized ball is used in practice and play, possible rule changes, evaluation of different playing surfaces, and equipment usage. To date, there is no strong evidence to support the use of mouth guards or helmets to reduce concussions in soccer. Additionally, the current data about the value of head impact sensors in soccer has not supported its widespread use.
Continue to: Finally, the issue of the prevalence...
Finally, the issue of the prevalence of chronic traumatic encephalopathy (CTE) in soccer players is beyond the scope of this article. The expert opinion from the 2017 US Soccer Federation, Major League Soccer (MLS), and National Women’s Soccer League (NWSL) conference concluded, “At present, no data exist that support that soccer participation is a risk factor for the development of neurodegenerative disease. Similarly, at this time, consistent with evidence discussed in the Berlin Concussion in Sport Group (CISG) Consensus Conference, our review suggests no causal relationship has been demonstrated between soccer and CTE pathology.”12
The more we know about concussions, both in general and those sustained during soccer play, the better we are able to diagnose and manage these injuries in our athletes. An important step is creating evidence-based protocols that evolve as our knowledge of concussions does as well. In April 2017, the US Soccer Federation, MLS, and the NWSL held a joint summit entitled, “Head Injury in Soccer: From Science to the Field” to address the current evidence-based science of concussions in soccer.8 An article discussing the findings of this meeting is forthcoming and will undoubtedly guide further development of concussion protocols for soccer players of all ages.
HEART
The physiologic demands of soccer place considerable stress on the cardiovascular system. Participation in training and competition is characterized by a combination of aerobic and anaerobic physiology with the typical athlete covering approximately 10 km over the course of the 90-minute match. The primary role of the heart and blood vessels is to supply the exercising skeletal muscle with oxygen and energy substrate and to clear the byproducts of metabolism. Among healthy athletes without cardiovascular disease, these processes are typically well tolerated and may be associated with beneficial cardiovascular adaptations over time. However, competitive soccer players are not completely immune to cardiovascular disease. Athletes across the age and competition spectrum may develop symptoms suggestive of underlying cardiovascular disease during play including exertional chest pain, inappropriate shortness of breath, palpitations, and syncope. These athletes require timely clinical evaluation. In extremely rare but high visibility cases, competitive soccer players may succumb to cardiac arrest on the pitch, underscoring the need for comprehensive emergency action plans (EAPs). We provide the practicing clinician with an overview of cardiovascular issues relevant to the competitive soccer athlete.
CARDIOVASCULAR ADAPTATIONS TO SPORT
The pressure (ie, repetitive surges in systemic blood pressure) and volume (ie, sustained increases in high cardiac output) challenges inherent in soccer participation place stress on the cardiovascular system. Healthy athletes across the age spectrum typically tolerate the hemodynamic stressors of participation without issues. Athletes that engage in training and competition over months to years often develop beneficial adaptations of the cardiovascular system that enhance on-field performance and contribute to optimal long-term health. Detailed discussion of how the heart and blood vessels respond to exercise training is beyond the scope of this article, but the interested reader is referred to several prior publications.13,14 In brief, the heart of the healthy soccer athlete demonstrates the balanced mild chamber dilation and wall thickening characteristic of left ventricular eccentric remodeling. This form of exercise-induced cardiac remodeling facilitates maintenance of high stroke volume during exercise with minimal increases in cardiac work. In parallel, routine aerobic exercise training confers favorable changes in the systemic arterial system, which leads to reductions in age-associated ventricular stiffening and maintenance of healthy low blood pressure. It must be emphasized that the healthy heart muscle dilation and thickening that develop in response to sports participation, regardless of age, ethnicity, or gender, are relatively mild and should not be confused with common forms of heart muscle disease that may be seen in athletes at risk for adverse outcomes. In some situations, consultation with an extreme sports cardiologist may be required to differentiate exercise-induced remodeling from over heart muscle pathology.15
Continue to: THE SYMPTOMATIC ATHLETE...
THE SYMPTOMATIC ATHLETE
Any athlete presenting with symptoms suggestive of underlying cardiovascular disease should be withheld from training and competition until a comprehensive clinical evaluation has been completed. Common manifestations of underlying heart disease that occur in soccer players include exertional chest pain/pressure/tightness, shortness of breath that is out of proportion to workload, palpitations or the perception of irregular cardiac activity, and syncope. Chest discomfort, inappropriate shortness of breath, and palpitations that occur during training or competition should be managed with immediate removal from the playing field and prompt medical assessment. In many cases, thorough evaluation will involve collaboration between sports medicine and sports cardiology providers. Evaluations must be individualized on a case-by-case basis as tailored to the athlete’s presenting chief complaint and prior medical history. Most of these assessments will include a detailed medical history and physical examination, a 12-lead electrocardiogram (ECG), provocative exercise testing in a controlled environment, noninvasive cardiac imaging, and in some cases ambulatory rhythm monitoring. Uniformly, the athlete should be withheld from further training and competition until high-risk cardiovascular disease has been excluded. We refer the interested reader to a comprehensive discussion of symptom-based assessment of the athlete with suspected cardiovascular disease.16
Syncope (sudden and abrupt loss of consciousness with spontaneous neurologic recovery) is common among trained athletes. The vast majority of syncope is caused by “neurocardiogenic” mechanisms and carries a benign prognosis. Benign neurally-mediated syncope most often occurs outside of training and competition among athletes with heightened vagal tone and a predisposed susceptibility to triggers including pain, anxiety, emotional stimulation, and sudden postural change. Athletes who experience neurally-mediated syncope outside of training and competition routinely report a pre-event prodrome or aura that permits them to lower themselves to the ground, thereby avoiding injury. A distinct, but similarly benign and common, form of neurally-mediated fainting is post-exertional syncope. Here, fainting occurs within seconds of abrupt termination of exercise due to a rapid reduction cardiac preload and corollary cerebral blood supply. When either form of neurally-mediated syncope is suggested by a comprehensive medical history, normal physical examination, and a normal 12- lead ECG, further evaluation is unnecessary. However, the athlete and their coaching staff should be educated about avoidance tactics including hydration, dietary sodium supplementation, and avoidance of abrupt exercise termination as neutrally-mediated syncope tends to be recurrent without such measures. Fainting episodes that occur during training or competition that are not clearly post-exertional should be considered a medical emergency and should prompt comprehensive evaluation by a qualified cardiovascular specialist. Working closely with team physicians and athletic training staff, it is the responsibility of sports cardiologists to exclude potentially life-threatening forms of electrical, muscular, coronary, and valvular heart disease. Ideally, this evaluation should be conducted rapidly to avoid unnecessary delays in return to play.
CARDIAC ARREST AND SUDDEN DEATH
Numerous high-visibility cases of cardiac arrest on the soccer pitch have alerted the sporting community to the potential for these rare and potentially tragic events. Definitive incidence statistics defining the risk of cardiac arrest among soccer players are lacking. Data from the NCAA database suggest a sudden death incidence rate among collegiate male soccer athletes of approximately 1:24,000 athlete years.8 Similar data documenting incidence among female athletes and among those at lower (ie, youth level and high school) and higher (ie, professional) levels of play are unavailable. Underlying cardiovascular disease in the forms of heart muscle abnormalities (ie, genetic and acquired cardiomyopathy), coronary artery abnormalities (ie, genetic coronary anomalies and atherosclerotic coronary disease), valvular heart problems (ie, congenitally malformed aortic valves), and primary disturbances of the cardiac electrical system (ie, Wolf-Parkinson-White syndrome, long QT syndrome, etc.) explain a substantial percentage of on-pitch cardiac arrest. However, it is increasingly recognized that a significant minority of sudden cardiac deaths among athletes occur in the absence of attributable cardiovascular abnormality.17 Such cases, often referred to as “sudden unexplained death,” present unique challenges in the context of pre-participation screening, as they are undetectable and thus unpredictable.
Reduction of cardiac arrest and sudden death may best be accomplished through a combination of focused pre-participation screening and the development and implementation of a comprehensive EAP. Pre-participation involves the performance of a battery of tests prior to training and competition that are geared toward the detection of occult high-risk cardiovascular disease. Recommendations regarding pre-participation screening vary both across and within countries. Current US recommendations call for a focused medical history and physical examination prior to training and competition with consideration of the addition of a 12-lead ECG on a local level based on expertise and available resources.18 Conversely, current European guidelines including those endorsed by FIFA, suggest routine inclusion of a 12-lead ECG and in some cases, a transthoracic ECG.19 It must be emphasized that no screening approach has been confirmed to reduce the incidence of sudden death, and the decision to extend screening beyond the medical history and physical examination to include a 12-lead ECG or echocardiogram may come at the cost of increased false positive testing. In practice, decisions about how and when to screen are ideally made at a local level after consideration of medical and financial resources.20
Continue to: Even the most comprehensive approach...
Even the most comprehensive approach to screening and evaluation of symptomatic athletes will not completely eliminate on-pitch cardiac arrest. Thus, all stakeholders that engage in the oversight of organized soccer must be committed to the development and implementation of an EAP.21 Key components of an effective EAP include the training of coaching staff, athletic trainers, and players in basic cardiopulmonary resuscitation, access to and training in the use of automated external defibrillators, and a triage/transport protocol that ensures timely access to advanced cardiac life support. Much like screening, emergency action planning involving these key core components must be developed and tailored locally. In the era of contemporary organized athletics, the absence of an EAP at any level of competition, from youth to professional leagues, is unacceptable. Effective EAPs must be developed, documented, and rehearsed at regular intervals. For the health and safety of competitive soccer players, as well as coaching staff and spectators, these steps are of critical importance.
HEAT
Heat-related illnesses can be serious and, at times, even life threatening. It is important for athletic staff and athletes to be well versed in the prevention, signs and symptoms, and treatment of heat-related illnesses in order to prevent serious and lasting injury. We aim to educate physicians about the prevention, recognition, and management of heat-related injury, and stress the importance of similarly educating athletes and coaching staff.
Exertional heat illnesses most often occur at temperatures >86°F, however they can occur at any temperature with heavy exertion.22 Signs and symptoms can be nonspecific early on, including weakness, fatigue, headache, nausea, and dizziness. Later signs can include imbalance, altered mentation, confusion, and behavior that is out of character such as irritability or aggression.23 It is easy to see how the later signs can be confused for concussion in the right context. We cover the recognition and treatment of two common and serious heat-related illnesses: heat exhaustion and exertional heat stroke (EHS).
HEAT EXHAUSTION
Heat exhaustion occurs when an athlete cannot continue to exercise due to weakness and fatigue. While the exact mechanism is not well understood, it has been established that the combined effect of heat and dehydration have been proven to decrease exercise capacity and performance to a greater degree than either alone. The heat created by the body during exercise is 15 to 20 times greater than when at rest, and can increase core body temperature by 1°C every 5 minutes if no heat is lost, such as through sweating.24 Additionally, when fluid deficits reach >3% to 5% of total body water, sweat production and skin blood flow decline, blunting the ability for the body to cool itself and causing progressive elevation of core body temperature if the athlete continues exerting him or herself. When fluid deficits reach 6% to 10%, cardiac output, sweat, and muscle blood flow decrease, likely leading to the symptoms seen with heat exhaustion: weakness, profound fatigue, and occasionally confusion and disorientation. Athletes with suspected heat exhaustion should be moved to a cooler area, laid down with legs elevated, and orally rehydrated. If they do not improve with oral rehydration, they may require intravenous fluids. The diagnosis of heat exhaustion hinges on a rectal temperature of <104°F; if >104°F the athlete should be presumed to have heat stroke, which will be addressed in the following paragraphs. Players can be cleared to return to play in mild cases within 24 to 48 hours with gradual increases in exercise intensity.24
EXERTIONAL HEAT STROKE
EHS occurs when the body can no longer regulate the core body temperature and it rises to upwards of 104°F. In EHS, elevated core body temperature is associated with evidence of end organ dysfunction. The most easily identified on the playing field is likely central nervous system dysfunction, including irritability, confusion, irrational behavior, lethargy, dizziness, confusion, and even loss of consciousness. Temperature should be measured with rectal temperature only, as other methods of measurement have been shown to be consistently inaccurate.22 Heat stroke can be confused with exertional hyponatremia, heat exhaustion, or concussion, especially when core body temperature cannot be determined. However, EHS should always be the presumed cause of altered mentation when no rectal temperature is available because rapid cooling is critical to minimizing lasting effects. Morbidity and mortality are directly related to the length of time required to cool the athlete under 40°C (104°F).24 Cooling should be completed on site prior to transport to a medical facility and is best achieved with submersion in an ice bath (ie, a kiddie pool or soaking tub full of ice and water).22,25 If an ice bath is not available, ice bags should be applied to the neck axilla and groin and exchanged for fresh bags every 2 to 3 minutes.22 Ice bags have been shown to be inferior to whole body cooling, only cooling the athlete .04°C to .08°C/min compared to .15°C to .24°C/min with the ice bath.24 All other tests should be delayed until cooling is achieved, unless they can be completed while cooling the athlete. The athlete can be removed from the ice bath once rectal temperatures reach <101°F to 102°F.23 If the athlete returns to baseline after cooling, transportation to a medical facility may not be necessary. However, they should refrain from physical activity and heat exposure for at least 7 days and should be evaluated by a physician at that time. If all labs are normal and the athlete is asymptomatic, they can start progressive return to play under the direction of an athletic trainer or a sports medicine physician.23
Continue to: HEAT-RELATED ILLNESS...
HEAT-RELATED ILLNESS
It is impossible to predict exactly which athletes will be most at risk for heat-related illness, so it is important to have a high degree of suspicion when environmental conditions are right. Athletes with recent illness, fever, or lack of sleep are at higher risk. Additional intrinsic risk factors include low fitness level, obesity, and inadequate hydration. Athletes who are highly competitive or motivated can be more likely to push through the early signs of illness or be reluctant to report symptoms.23 Those with a history of exertional heat illness are more at risk for developing it again in the future.23
The extrinsic risk factors for the development of heat-related illness are much easier to identify and modify in order to keep athletes safe. High temperature and high humidity conditions, heavy sun exposure, and exposure to similar conditions the preceding day put athletes at risk for exertional heat illness. Risks are even greater when the exercise is prolonged or intense with few breaks and access to hydration is limited.23 Therefore, prevention of exertional heat illness is centered on these external risk factors.
Each team should have a heat policy as part of their EAP aimed at prevention and early recognition of heat-related illness. This policy should be shared with all athletes and coaches. The plan should be centered on acclimatization, activity modification, and early recognition and management as previously discussed. The US Soccer Federation “Recognize to Recover” Heat Guidelines suggest a 3-step process for appropriate activity modification:22
1. Find the wet bulb globe temperature, either using a wet bulb globe thermometer or the temperature and humidity (Figure 1).
2. Find your regional weather category on the map (Figure 2).
3. Find your alert level and work to rest ratio recommendations (Figure 3).
Scheduled hydration breaks should be given as listed in Figure 3. Breaks of 4 minutes should be given for each 30 minutes of continuous practice or play. In a regulation 90-minute match, a hydration break should be given at 30 and 75 minutes (with half time at 45 minutes) at minimum. Athletes should be educated about where hydration can be accessed, and given unlimited access to hydration even outside of planned breaks.22
Acclimatization to conditions is another integral part of preventing heat-related illness. It allows the body time to adapt to exercising in heat gradually, with a measured progression of exertion over the course of 10 to 14 days. The “Recognize to Recover” Heat Guidelines also provide guidance on acclimatization, and specifics can be found on the website.1 Generally speaking, the warmest part of the day, usually between 11 AM and 4 PM, should be avoided for all training sessions, and length of practice and exertion should be gradually increased over 2 weeks.22
In summary, appropriate acclimatization, hydration, activity modification, and education of athletes and staff are essential for the prevention of heat-related illness. Athletes and staff should understand the signs and symptoms of heat-related illness so that it can be recognized early and treated appropriately. If an athlete is altered in the heat and rectal temperature is >104°F or rectal temperature cannot be obtained, rapid cooling using an ice bath or ice bags is essential to prevent the morbidity and mortality associated with EHS. Above all, teams should have an explicit plan that includes protocols for acclimatization, activity modification, and all necessary equipment to prevent and treat heat-related illnesses should they occur, and ultimately keep athletes safe and healthy.
1. Langlois JA, Rutland-Brown W, Wald MM. The epidemiology and impact of traumatic brain Injury: a brief overview. J Head Trauma Rehabil. 2006;21(5):375-378.
2. The National Federation of State High School Associations. 2013-14 high school athletics participation survey. http://www.nfhs.org/ParticipationStatics/PDF/2013-14_Participation_Survey_PDF.pdf. Accessed August 6, 2018.
3. Youth Council. US Soccer Federation Web site. https://www.ussoccer.com/about/affiliates/youth-council. Accessed July 31, 2018.
4. Khodaee M, Currie DW, Asif IM, Comstock RD. Nine-year study of US high school soccer injuries: data from a national sports injury surveillance programme. Br J Sports Med. 2017;51(3):185-193. doi:10.1136/bjsports-2015-095946.
5. Schallmo MS, Weiner JA, Hsu WK. Sport and sex-specific trends in the epidemiology of concussions sustained by high school athletes. J Bone Joint Surg Am. 2017;99(15):1314-1320. doi:10.2106/JBJS.16.01573.
6. US Soccer Federation. U.S. Soccer’s comprehensive player health and safety program. Recognize to Recover Web site. http://www.recognizetorecover.org/#us-soccers-comprehensive-player-health-and-safety-program. Accessed July 31, 2018.
7. McCrory P, Meeuwisse W, Dvořák J, et al. Consensus statement on concussion in sport-the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;51(11):838-847. doi:10.1136/bjsports-2017-097699.
8. Harmon KG, Asif IM, Klossner D, Drezner JA. Incidence of sudden cardiac death in National Collegiate Athletic Association athletes. Circulation. 2011;123(15):1594-1600. doi:10.1161/CIRCULATIONAHA.110.004622.
9. Faude O, Rössler R, Junge A, et al. Head injuries in children’s football-results from two prospective cohort studies in four European countries. Scand J Med Sci Sports. 2017;27(12):1986-1992. doi:10.1111/sms.12839.
10. Comstock RD, Currie DW, Pierpoint LA, Grubenhoff JA, Fields SK. An evidence-based discussion of heading the ball and concussions in high school soccer. JAMA Pediatr. 2015;169(9):830-837. doi:10.1001/jamapediatrics.2015.1062.
11. Tarnutzer AA. Should heading be forbidden in children’s football? Sci Med Football. 2018;2(1):75-79.
12. US Soccer Federation. US Soccer, NWSL and MLS to host “head injury in soccer; science to field”. https://www.ussoccer.com/stories/2017/04/18/17/35/20170418-news-us-soccer-nwsl-mls-host-head-injury-in-soccer-science-to-field. Published April 18, 2017. Accessed August 6, 2018.
13. Weiner RB, Baggish AL. Exercise-induced cardiac remodeling. Prog Cardiovasc Dis. 2012;54(5):380-386. doi:10.1016/j.pcad.2012.01.006.
14. Baggish AL, Wood MJ. Athlete's heart and cardiovascular care of the athlete: scientific and clinical update. Circulation. 2011;123(23):2723-2735. doi:10.1161/CIRCULATIONAHA.110.981571.
15. Kim JH, Baggish AL. Differentiating exercise-induced cardiac adaptations from cardiac pathology: the "Grey Zone" of clinical uncertainty. Can J Cardiol. 2016;32(4):429-437. doi:10.1016/j.cjca.2015.11.025.
16. Baggish AL, Battle RW, Beckerman JG, et al; ACC’s Sports and Exercise Council Leadership Group. Sports cardiology: core curriculum for providing cardiovascular care to competitive athletes and highly active people. J Am Coll Cardiol. 2017;70(15):1902-1918. doi:10.1016/j.jacc.2017.08.055.
17. Harmon KG, Asif IM, Maleszewski JJ, et al. Incidence, cause, and comparative frequency of sudden cardiac death in National Collegiate Athletic Association athletes: a decade in review. Circulation. 2015;132(1):10-19. doi:10.1161/CIRCULATIONAHA.115.015431.
18. Maron BJ, Levine BD, Washington RL, Baggish AL, Kovacs RJ, Maron MS. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: task force 2: preparticipation screening for cardiovascular disease in competitive athletes: a scientific statement from the American Heart Association and American College of Cardiology. J Am Coll Cardiol. 2015;66(21):2356-2361. doi:10.1016/j.jacc.2015.09.034.
19. Corrado D, Pelliccia A, Bjørnstad HH, et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus Statement of the Study Group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J. 2005;26(5):516-524.
20. Baggish AL, Kovacs RJ. Preparticipation cardiovascular screening: clinical partnership is the only certainty. Br J Sports Med. 2017;51(3):150-151. doi:10.1136/bjsports-2016-096954.
21. Hainline B, Drezner J, Baggish A, et al. Interassociation consensus statement on cardiovascular care of college student-athletes. J Athl Train. 2016;51(4):344-357. doi:10.4085/j.jacc.2016.03.527.
22. US Soccer Federation. Environmental conditions. Recognize to Recover Web site. http://www.recognizetorecover.org/environmental/#environmental-conditions. Accessed April 15, 2018.
23. Korey Stringer Institute. Emergency conditions: heat illnesses. University of Connecticut Web site. https://ksi.uconn.edu/. Accessed April 15, 2018.
24. American College of Sports Medicine, Armstrong LE, Casa DJ, et al. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556-572.
25. Belval LN, Casa DJ, Adams WM, et al. Consensus statement- prehospital care of exertional heat stroke. Prehosp Emerg Care. 2018;22(3):392-397. doi:10.1080/10903127.2017.1392666.
1. Langlois JA, Rutland-Brown W, Wald MM. The epidemiology and impact of traumatic brain Injury: a brief overview. J Head Trauma Rehabil. 2006;21(5):375-378.
2. The National Federation of State High School Associations. 2013-14 high school athletics participation survey. http://www.nfhs.org/ParticipationStatics/PDF/2013-14_Participation_Survey_PDF.pdf. Accessed August 6, 2018.
3. Youth Council. US Soccer Federation Web site. https://www.ussoccer.com/about/affiliates/youth-council. Accessed July 31, 2018.
4. Khodaee M, Currie DW, Asif IM, Comstock RD. Nine-year study of US high school soccer injuries: data from a national sports injury surveillance programme. Br J Sports Med. 2017;51(3):185-193. doi:10.1136/bjsports-2015-095946.
5. Schallmo MS, Weiner JA, Hsu WK. Sport and sex-specific trends in the epidemiology of concussions sustained by high school athletes. J Bone Joint Surg Am. 2017;99(15):1314-1320. doi:10.2106/JBJS.16.01573.
6. US Soccer Federation. U.S. Soccer’s comprehensive player health and safety program. Recognize to Recover Web site. http://www.recognizetorecover.org/#us-soccers-comprehensive-player-health-and-safety-program. Accessed July 31, 2018.
7. McCrory P, Meeuwisse W, Dvořák J, et al. Consensus statement on concussion in sport-the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;51(11):838-847. doi:10.1136/bjsports-2017-097699.
8. Harmon KG, Asif IM, Klossner D, Drezner JA. Incidence of sudden cardiac death in National Collegiate Athletic Association athletes. Circulation. 2011;123(15):1594-1600. doi:10.1161/CIRCULATIONAHA.110.004622.
9. Faude O, Rössler R, Junge A, et al. Head injuries in children’s football-results from two prospective cohort studies in four European countries. Scand J Med Sci Sports. 2017;27(12):1986-1992. doi:10.1111/sms.12839.
10. Comstock RD, Currie DW, Pierpoint LA, Grubenhoff JA, Fields SK. An evidence-based discussion of heading the ball and concussions in high school soccer. JAMA Pediatr. 2015;169(9):830-837. doi:10.1001/jamapediatrics.2015.1062.
11. Tarnutzer AA. Should heading be forbidden in children’s football? Sci Med Football. 2018;2(1):75-79.
12. US Soccer Federation. US Soccer, NWSL and MLS to host “head injury in soccer; science to field”. https://www.ussoccer.com/stories/2017/04/18/17/35/20170418-news-us-soccer-nwsl-mls-host-head-injury-in-soccer-science-to-field. Published April 18, 2017. Accessed August 6, 2018.
13. Weiner RB, Baggish AL. Exercise-induced cardiac remodeling. Prog Cardiovasc Dis. 2012;54(5):380-386. doi:10.1016/j.pcad.2012.01.006.
14. Baggish AL, Wood MJ. Athlete's heart and cardiovascular care of the athlete: scientific and clinical update. Circulation. 2011;123(23):2723-2735. doi:10.1161/CIRCULATIONAHA.110.981571.
15. Kim JH, Baggish AL. Differentiating exercise-induced cardiac adaptations from cardiac pathology: the "Grey Zone" of clinical uncertainty. Can J Cardiol. 2016;32(4):429-437. doi:10.1016/j.cjca.2015.11.025.
16. Baggish AL, Battle RW, Beckerman JG, et al; ACC’s Sports and Exercise Council Leadership Group. Sports cardiology: core curriculum for providing cardiovascular care to competitive athletes and highly active people. J Am Coll Cardiol. 2017;70(15):1902-1918. doi:10.1016/j.jacc.2017.08.055.
17. Harmon KG, Asif IM, Maleszewski JJ, et al. Incidence, cause, and comparative frequency of sudden cardiac death in National Collegiate Athletic Association athletes: a decade in review. Circulation. 2015;132(1):10-19. doi:10.1161/CIRCULATIONAHA.115.015431.
18. Maron BJ, Levine BD, Washington RL, Baggish AL, Kovacs RJ, Maron MS. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: task force 2: preparticipation screening for cardiovascular disease in competitive athletes: a scientific statement from the American Heart Association and American College of Cardiology. J Am Coll Cardiol. 2015;66(21):2356-2361. doi:10.1016/j.jacc.2015.09.034.
19. Corrado D, Pelliccia A, Bjørnstad HH, et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus Statement of the Study Group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J. 2005;26(5):516-524.
20. Baggish AL, Kovacs RJ. Preparticipation cardiovascular screening: clinical partnership is the only certainty. Br J Sports Med. 2017;51(3):150-151. doi:10.1136/bjsports-2016-096954.
21. Hainline B, Drezner J, Baggish A, et al. Interassociation consensus statement on cardiovascular care of college student-athletes. J Athl Train. 2016;51(4):344-357. doi:10.4085/j.jacc.2016.03.527.
22. US Soccer Federation. Environmental conditions. Recognize to Recover Web site. http://www.recognizetorecover.org/environmental/#environmental-conditions. Accessed April 15, 2018.
23. Korey Stringer Institute. Emergency conditions: heat illnesses. University of Connecticut Web site. https://ksi.uconn.edu/. Accessed April 15, 2018.
24. American College of Sports Medicine, Armstrong LE, Casa DJ, et al. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556-572.
25. Belval LN, Casa DJ, Adams WM, et al. Consensus statement- prehospital care of exertional heat stroke. Prehosp Emerg Care. 2018;22(3):392-397. doi:10.1080/10903127.2017.1392666.
TAKE-HOME POINTS
- Current concussion education programs such as “Recognize to Recover” aim to increase self-reporting of concussion symptoms by players, and recognition and appropriate evaluation by medical and coaching staff.
- Athletes who develop symptoms suggestive of underlying cardiovascular disease during play, including exertional chest pain, inappropriate shortness of breath, palpitations, and syncope should be withheld from play until they can be evaluated by a qualified medical professional.
- Key components of an effective EAP include the training of coaching staff, athletic trainers, and players in basic cardiopulmonary resuscitation, access to and training in the use of automated external defibrillators, and a triage/transport protocol that ensures timely access to advanced cardiac life support.
- Exertional heat stroke should always be the presumed cause of altered mentation when no rectal temperature is available because rapid cooling is critical to minimizing lasting effects.
- Prevention of exertional heat illness should center around appropriate acclimatization, access to adequate hydration and scheduled hydration breaks, and avoiding exertion all together when conditions are too dangerous.