1. Rovell D. NFL most popular for 30th year in row. ESPN. Accessed August 28, 2015.
  2. DeMaria C. What are the most popular youth sports? May 27, 2015. Accessed August 28, 2015.
  3. Wallerson R. Youth participation weakens in basketball, football, baseball, soccer. Wall Street Journal. January 31, 2014. Accessed August 28, 2015.
  4. Pietrosimone B, Golightly YM, Mihalik JP, Guskiewicz KM. Concussion frequency associates with musculoskeletal injury in retired NFL players. Med Sci Sports Exerc. 2015 Apr 11. [Epub ahead of print]
  5. Lykissas MG, Eismann EA, Parikh SN. Trends in pediatric sports-related and recreation-related Injuries in the United States in the last decade. J Pediatr Orthop. 2013;33:803-810.
  6. Kucera KL, Klossner D, Colgate B, Cantu RC. Annual survey of football injury research: 1931-2014. March 2015. Accessed September 1, 2015.
  7. Olson D, Sikka RS, Labounty A, Christensen T. Injuries in professional football: current concepts. Curr Sports Med Rep. 2013;12:381-390.
  8. George T. Heat kills a pro football player; NFL orders a training review. New York Times. August 2, 2001. Accessed August 29, 2015.
  9. Kerr ZY, Casa DJ, Marshall SW, Comstock RD. Epidemiology of exertional heat illness among U.S. high school athletes. Am J Prev Med. 2013;44:8-14.
  10. Casa DJ, DeMartini JK, Bergeron MF, et al. National Athletic Trainers' Association position statement: exertional heat illnesses. J Athl Train. 2015 Aug 18. [Epub ahead of print]
  11. Centers for Disease Control and Prevention (CDC). Heat illness among high school athletes—United States, 2005-2009. MMWR Morb Mortal Wkly Rep. 2010;59:1009-1013.
  12. Allen SB, Cross KP. Out of the frying pan, into the fire: a case of heat shock and its fatal complications. Pediatr Emerg Care. 2014;30:904-910.
  13. Associated Press. Coroner: 49ers' Herrion died of heart disease. ESPN. September 6, 2005. Accessed September 15, 2015.
  14. Pugh A, Bourke JP, Kunadian V. Sudden cardiac death among competitive adult athletes: a review. Postgrad Med J. 2012;88:382-390.
  15. Alattar A, Maffulli N. The validity of adding ECG to the preparticipation screening of athletes: an evidence-based literature review. Transl Med UniSa. 2015;11:2-13.
  16. Harmon KG, Drezner JA, Maleszewski JJ, et al. Pathogenesis of sudden cardiac death in national collegiate athletic association athletes. Circ Arrhythm Electrophysiol. 2014;7:198-204.
  17. Maron BJ. Hypertrophic cardiomyopathy and other causes of sudden cardiac death in young competitive athletes, with considerations for preparticipation screening and criteria for disqualification. Cardiol Clin. 2007;25:399-414.
  18. Maron BJ. Sudden death in young athletes. N Engl J Med. 2003;349:1064-1075.
  19. Semsarian C, Ingles J, Maron MS, Maron BJ. New perspectives on the prevalence of hypertrophic cardiomyopathy. J Am Coll Cardiol. 2015;65:1249-1254.
  20. Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE. Triggering of sudden death from cardiac causes by vigorous exertion. N Engl J Med. 2000;343:1355-1361.
  21. Halabchi F, Seif-Barghi T, Mazaheri R. Sudden cardiac death in young athletes; a literature review and special considerations in Asia. Asian J Sports Med. 2011;2:1-15.
  22. Harmon KG, Zigman M, Drezner JA. The effectiveness of screening history, physical exam, and ECG to detect potentially lethal cardiac disorders in athletes: a systematic review/meta-analysis. J Electrocardiol. 2015;48:329-338.
  23. Maron BJ, Friedman RA, Kligfield P, et al; American Heart Association Council on Clinical Cardiology; Advocacy Coordinating Committee; Council on Cardiovascular Disease in the Young; Council on Cardiovascular Surgery and Anesthesia; Council on Epidemiology and Prevention; Council on Functional Genomics and Translational Biology; Council on Quality of Care and Outcomes Research, and American College of Cardiology. Assessment of the 12-lead electrocardiogram as a screening test for detection of cardiovascular disease in healthy general populations of young people (12-25 years of age): a scientific statement from the American Heart Association and the American College of Cardiology. J Am Coll Cardiol. 2014;64:1479-1514.
  24. Aziz PF, Sweeten T, Vogel RL, Froelicher V. Update: causes and symptoms of sudden cardiac death in young athletes. Phys Sportsmed. 2015;43:44-53.
  25. Johnson JN, Ackerman MJ. Return to play? Athletes with congenital long QT syndrome. Br J Sports Med. 2013;47:28-33.
  26. Rossenbacker T, Priori S. [New insights into the long QT syndrome]. Rev Esp Cardiol. 2007;60:675-682.
  27. Boggs W. Sports possible for children with genotype-positive long QT syndrome. Consultant 360 for Pediatricians. April 21, 2015. Accessed August 31, 2015.
  28. Aziz PF, Sweeten T, Vogel RL, et al. Sports participation in genotype positive children with long QT syndrome. JACC Clin Electrophysiol. 2015;1:62-70.
  29. Baltsezak S. Bowing, kneeling and 'prostration': athlete's collapse patterns during sudden cardiac arrhythmia/arrest on the field of play. Emerg Med J. 2014;31:939-941.
  30. Bhalla MC, Dick-Perez R. Exercise induced rhabdomyolysis with compartment syndrome and renal failure. Case Rep Emerg Med. 2014;2014:735820.
  31. Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: rhabdomyolysis—an overview for clinicians. Crit Care. 2005;9:158-169.
  32. La Canfora J. No headache: Haynesworth likely suffers from rhabdomyolysis. NFL Network Insider. August 22, 2010. Accessed August 30, 2015.
  33. Niesen J. There are some things Rahim Moore doesn't want to remember. MMQB. May 28, 2014. Accessed August 30, 2015.
  34. Krogstad JM. Report: Iowa football team should drop squat workout. Hawk Central. March 22, 2011. Accessed September 1, 2015.
  35. USA Today. Bills quarterback Trent Edwards suffers concussion. October 5, 2008. Accessed September 2, 2015.
  36. Pellman EJ, Viano DC; National Football League's Committee on Mild Traumatic Brain Injury. Concussion in professional football: summary of the research conducted by the National Football League's Committee on Mild Traumatic Brain Injury. Neurosurg Focus. 2006;21:E12. Accessed August 27, 2015.
  37. Dompier TP, Kerr ZY, Marshall SW, et al. Incidence of concussion during practice and games in youth, high school, and collegiate American football players. JAMA Pediatr. 2015;169:659-665.
  38. ESPN. NFL: concussions down 25 percent. January 29, 2015. Accessed August 27, 2015.
  39. Bey T, Ostick B. Second impact syndrome. West J Emerg Med. 2009;10:6-10. Accessed August 27, 2015.
  40. Boden BP, Tacchetti RL, Cantu RC, Knowles SB, Mueller FO. Catastrophic head injuries in high school and college football players. Am J Sports Med. 2007;35:1075-1081.
  41. Omalu BI, DeKosky ST, Minster RL, Kamboh MI, Hamilton RL, Wecht CH. Chronic traumatic encephalopathy in a National Football League player. Neurosurgery. 2005;57:128-134.
  42. Chappell B. Study of Junior Seau's brain finds signs of neurodegenerative disease. NPR. January 10, 2013. Accessed August 27, 2015.
  43. Boren C. Jovan Belcher likely had CTE, a study of his brain shows. Washington Post. September 29, 2014. Accessed August 27, 2015.
  44. Meehan W 3rd, Mannix R, Zafonte R, Pascual-Leone A. Chronic traumatic encephalopathy and athletes. Neurology. 2015 Aug 7. [Epub ahead of print]
  45. Stamm JM, Bourlas AP, Baugh CM, et al. Age of first exposure to football and later-life cognitive impairment in former NFL players. Neurology. 2015;84:1114-1120.
  46. Stamm JM, Koerte IK, Muehlmann M, et al. Age at first exposure to football is associated with altered corpus callosum white matter microstructure in former professional football players. J Neurotrauma. 2015 Jul 22. [Epub ahead of print]
  47. Rihn JA, Anderson DT, Lamb K, et al. Cervical spine injuries in American football. Sports Med. 2009;39:697-708.
  48. Breslow MJ, Rosen JE. Cervical spine injuries in football. Bull Hosp Jt Dis. 2000;59:201-210.
  49. Litsky F. Darryl Stingley, 55, paralyzed player, dies. New York Times. April 6, 2007. Accessed August 27, 2015.
  50. Altman LK. Jackson's case is dividing the doctors. New York Times. March 20, 1991. Accessed August 27, 2015.
  51. Moorman CT 3rd, Warren RF, Hershman EB, et al. Traumatic posterior hip subluxation in American football. J Bone Joint Surg Am. 2003;85:1190-1196.
  52. Rotter J. NFL legend and Super Bowl winner Joe Theismann chats about his life-changing leg injury, his recovery process, and even Tim Tebow, and Joe Paterno. Healthline. January 12, 2012. Accessed August 27, 2015.
  53. Waldén M, Krosshaug T, Bjørneboe J, Andersen TE, Faul O, Hägglund M. Three distinct mechanisms predominate in non-contact anterior cruciate ligament injuries in male professional football players: a systematic video analysis of 39 cases. Br J Sports Med. 2015 Apr 23. [Epub ahead of print]
  54. Dragoo JL, Braun HJ, Harris AH. The effect of playing surface on the incidence of ACL injuries in National Collegiate Athletic Association American Football. Knee. 2013;20:191-195.
  55. McCall A, Carling C, Nedelec M, et al. Risk factors, testing and preventative strategies for non-contact injuries in professional football: current perceptions and practices of 44 teams from various premier leagues. Br J Sports Med. 2014;48:1352-1357.
  56. Schub D, Brophy RH, Wuerz TH, et al. Video analysis of the mechanism of anterior cruciate ligament injuries in the National Football League. Program and abstracts of the American Academy of Orthopaedic Surgeons 2015 Annual Meeting; March 24-28, 2015; Las Vegas, Nevada. Poster P474. Accessed August 30, 2015.
  57. McCormick JJ, Anderson RB. Turf toe. Anatomy, diagnosis, and treatment. Sports Health. 2010;2:487-494. Accessed August 28, 2015.
  58. Mann JB, Bryant K, Johnstone B, Ivey P, Sayers SP. The effect of physical and academic stress on illness and injury in division 1 college football players. J Strength Cond Res. 2015 May 30. [Epub ahead of print]
  59. Turbeville SD, Cowan LD, Owen WL, Asal NR, Anderson MA. Risk factors for injury in high school football players. Am J Sports Med. 2003;31:974-980.
  60. Stuart MJ. Gridiron football injuries. Med Sport Sci. 2005;49:62-85.
  61. Lions player is paralyzed after his neck surgery. New York Times. November 19, 1991. Accessed August 30, 2015.
  62. Bissinger B. NFL playoffs: why football needs violence. Daily Beast. January 17, 2011. Accessed August 30, 2015.
  63. Brinson W. Aaron Rodgers pokes fun at Stephen Tulloch's season-ending celebration. CBS News. December 10, 2014. Accessed August 31, 2015.
  64. Shapiro L, Barr J. Head-butt turns into real pain in the neck. Washington Post. November 24, 1997. Accessed August 31, 2015.
  65. Feldman B. Ginn starts on right foot, ends with bad left foot. ESPN. January 9, 2007. Accessed September 1, 2015.
  66. Associated Press. Ravens cheerleader injured, team says she's OK. USA Today. November 9, 2014. Accessed August 31, 2015.
  67. Welch TR. Dangers of cheerleading. J Pediatr. 2013;163:929-931.
  68. Shields BJ, Smith GA. Cheerleading-related injuries in the United States: a prospective surveillance study. J Athl Train. 2009;44:567-577.
  69. Shields BJ, Smith GA. Cheerleading-related injuries to children 5 to 18 years of age: United States, 1990-2002. Pediatrics. 2006;117:122-129.
  70. LaBella CR, Mjaanes J; Council on Sports Medicine and Fitness. Cheerleading injuries: epidemiology and recommendations for prevention. Pediatrics. 2012;130:966-971.

Contributor Information

Laurie Scudder, DNP, NP
Executive Editor

Laura Stokowski, RN, MS
Senior Editor


Close<< Medscape

Are You Ready to Tackle Some Football Maladies?

Laurie Scudder DNP, NP; Laura Stokowski, RN, MS  |  September 11, 2015

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Slide 1

Football and Its Injuries and Maladies

Updated January 30, 2017. Football is said to be the most popular sport in America. Polls show that professional football has held the top spot in the hearts of US sport fans for the past 30 years.[1] In terms of youth sport participation, football comes in third place behind basketball and baseball.[2] Participation in high school football declined by 2.3% in 2012-2013 compared with 2008-2009.[3] With participation in all organized youth sports (age 6-17 years) on the decline, this might reflect a general trend toward inactivity, but football faces the extra hurdle of concern about concussions and other injuries that can cause permanent harm.[3]

These concerns are well-founded. Recent data show that 61% of retired players in the National Football League (NFL) report having had a concussion.[4] Among 5- to 24-year-olds, football is a leading cause of visits to emergency departments for nonfatal injuries, easily outnumbering motor vehicle-related injuries among teenage boys.[5]

Watching from the safety of a sofa or stadium seat is one thing, where the greatest dangers to one's health are posed by alcohol, high-calorie snack foods, and prolonged sitting. But playing the game brings risk of another order of magnitude. The constellation of football-associated injuries is wide, ranging from the well-known contact head injuries to heat stroke, stress injuries, catastrophic joint injuries, rhabdomyolysis, and even sudden death.[6] In 2014, six fatalities were directly related to football played at any level.[7] In time for Super Bowl LI, Medscape brings you this review of common and not-so-common injuries and events associated with this sometimes dangerous sport.

Image courtesy of AP Photo/David J. Phillip

Slide 2

Exertional Heat Stroke

In 2001, a preventable tragedy took place at the Minnesota Vikings' training camp. During early morning drills, 335-lb offensive tackle Korey Stringer (pictured above), dressed in full pads and helmet, vomited several times and collapsed. Despite medical intervention, he developed organ failure and died 15 hours later. The ambient temperature was 91°F, and Stringer's body temperature had reached 108°F.[8]

Exertional heat illness (EHI) can occur in any sport and in any geographic area.[9] In football, the risk is particularly high during the preseason months of July and August. Football players begin training during the hottest and most humid days of summer, often wearing up to 50 lb of gear. Being overweight or obese, a condition common in this era of super-sized linemen, increases risk for EHI.[10] Without precautions, EHI can lead to exertional heat stroke (EHS), a potentially fatal emergency.

More than 9000 high school football athletes are treated annually for EHI,[9] and EHS is now the third leading cause of death in this population.[10] From 2005 to 2009, more EHS-related deaths (a mean of 3.6 per year) occurred in organized sports than during any other 5-year period in the past 35 years.[6,11] From 2010 to 2014, EHS-related deaths declined slightly, to 2.6 deaths per year.[6] Of note, this year, two additional deaths resulted from athletes overhydrating to prevent heat-related issues. Prevention messages must go beyond simply hydrating, to emphasize how to properly hydrate.[12]

Although prompt treatment of EHI/EHS can be lifesaving, primary prevention is far more critical and is mandated in many states. The National Athletic Trainers' Association offers a position statement[6] outlining the prevention, recognition, treatment, and return-to-play considerations for EHI, and a printable infographic. To honor his legacy, the Korey Stringer Institute at the University of Connecticut provides information, resources, assistance, and advocacy for the prevention of sudden death in sports.

Image courtesy of AP Photo/File, Tom Olmscheid

Slide 3

Sudden Cardiac Death

In football, a first down is a good thing. A player down is not. It is difficult to comprehend a healthy athlete dropping dead on the field or the basketball court—yet it happens. San Francisco 49ers offensive lineman Thomas Herrion (#72, pictured above) collapsed and died after a preseason game in 2005. On autopsy, he had evidence of ischemic heart disease.[13]

Sudden cardiac death (SCD) is defined as "an event that is non-traumatic, non-violent, unexpected, and resulting from sudden cardiac arrest within 6 hours of previously witnessed normal health."[14] SCD is not common, but it is the leading cause of death among young athletes, with an incidence of 1-2 per 100,000 athletes annually.[15] In the United States, two thirds of SCDs occur in basketball and football players,[16] and SCD is more frequent among black athletes[17]; however, precise incidence figures are elusive, owing to a lack of mandatory reporting.

For many years, the evidence has pointed to structural cardiovascular abnormalities as the most common cause of SCD in young athletes in the United States.[18] Hypertrophic cardiomyopathy (HCM), a condition that might be more common in the general population than previously believed[19], tops the list, followed by commotio cordis (a nonstructural problem), coronary artery anomalies, left ventricular hypertrophy of indeterminate origin, myocarditis, and ruptured aortic aneurysm in players with Marfan syndrome. SCD is triggered by exertion,[20] and in patients with HCM, this leads to primary ventricular tachycardia or fibrillation.[21]

Despite being a relatively low-event phenomenon, when SCD occurs in a presumably healthy athlete, the public reacts with shock and dismay, and questions arise as to how such a death could have been prevented. Preparticipation athletic screening to detect potentially lethal cardiovascular disease is typically part of this conversation. The value of the most sensitive screening test[22]—the 12-lead ECG—is controversial, and universal screening is not currently recommended.[23] One limitation is the fact that the 12-lead ECG will detect only 60% of patients with HCM.[17]

Image courtesy of Michael Zagaris/Getty Images

Slide 4

Long QT Syndrome

Some athletes who died suddenly were found to have normal cardiac structures on autopsy. These deaths might be caused by hereditary ion channelopathies, long QT syndrome (LQTS), catecholaminergic polymorphic ventricular tachycardia, or Brugada syndrome.[24] Patients with LQTS exhibit QT interval prolongation on ECG, and this delayed cardiac repolarization predisposes to syncope, seizures, and death due to polymorphic ventricular tachycardia, a potentially lethal arrhythmia known as torsades de pointes.[25]

The first arrhythmic manifestations of LQTS occur during adolescence and largely are triggered by increased sympathetic activity.[26] Identification of a prolonged corrected QT interval (QTc) in athletes is usually a cause for disqualification from competitive sports, according to prevailing guidelines.[26]

But are the "goal posts moving on long QT syndrome"?[27] Recent evidence suggests that complete avoidance of physical activity and sports in children with genetically diagnosed LQTS might be unnecessary. Several recent studies have demonstrated good outcomes when children with LQTS continued participation in sports while adhering to treatment and monitoring.[25,28]

As with all sudden cardiac events in athletes, prompt intervention on the field can be lifesaving. In the absence of head injury, any athlete who is observed to be bowing and/or kneeling, followed by collapse, should be assumed to have a life-threatening cardiac event, and an automatic external defibrillator should be obtained immediately.[29]

Image from iStock

Slide 5

Compartment Syndrome/Exertional Rhabdomyolysis

A 22-year-old black college football player presented to the emergency department 2 days after an off-season workout with his team.[30] He had severe bilateral thigh pain, back pain, and dark urine. Lab studies showed hyperkalemia, an elevated creatine kinase (CK) level, and marked renal impairment requiring dialysis. Measurement of compartment pressures indicated bilateral anterolateral compartment syndrome due to rhabdomyolysis, requiring emergency fasciotomies.

Rhabdomyolysis is caused by muscle injury through trauma or exertion.[30] Muscle breakdown and necrosis cause leakage of cellular enzymes and myoglobinemia, and eventually myoglobinuria. Rhabdomyolysis can range from asymptomatic to life-threatening, with extreme elevation of CK, electrolyte imbalances, acute renal failure, and disseminated intravascular coagulation.[31] Weakness, myalgia, and tea-colored urine are the main clinical manifestations, and the most sensitive laboratory finding is an elevated plasma CK level. Vigorous hydration is the primary mode of initial management of suspected rhabdomyolysis,[31] an intervention that requires prompt recognition of the condition. In this case, the football player had initially presented to urgent care but was sent home with pain medication, so he received no specific treatment for rhabdomyolysis for another 24 hours.

Although anyone can develop rhabdomyolysis, the risk is higher in poorly conditioned individuals who suddenly begin vigorous exercise, such as military recruits or players returning to practice after the off-season, especially in the presence of dehydration. An overly aggressive workout can also lead to exertional rhabdomyolysis. Pro football players who have been reported to have rhabdomyolysis include Washington Redskins defensive lineman Albert Haynesworth [32] and Denver Broncos safety Rahim Moore (pictured above), who developed acute compartment syndrome and nearly lost his leg.[33] In 2011, intense squat workouts were blamed for the hospitalization of 13 University of Iowa football players.[34] Three members of the University of Oregon football team were hospitalized in January 2017 after a series of grueling workouts, and at least one was diagnosed with rhabdomyolysis. The university's strength coach was subsequently fired and the school issued an apology.

Image courtesy of John Leyba/The Denver Post/Getty Images

Slide 6


Trent Edwards (pictured above), quarterback for the Buffalo Bills, sustained a concussion in a 2008 game against the Arizona Cardinals after being slammed to the ground.[35] A large body of evidence underpins the growing concern about both the short- and long-term effects of concussion, particularly repeated concussions and those occurring in younger players. Although the long-term effects can be severe and unpredictable in an individual athlete, most concussions are classified as mild. Even in the NFL, with crushing tackles and high-impact injuries, only a minority (9.3%; 95% confidence interval, 7%-11.6%) of these events are accompanied by loss of consciousness.[36] However, the sheer volume of athletes who sustain concussion is daunting. A recent study[37] exploring the incidence of concussion in youth, high school, and college football players found that concussions comprise 4% to almost 10% of all injuries, depending on player age, with a higher concussion rate occurring during practice rather than games. With over 4 million individuals between the ages of 5 and 23 years playing competitive football, that rate translates to a huge number of events. The tide may be starting to turn as a result of greater awareness; the NFL reports that concussions sustained during practices, regular games, and preseason games decreased 12% in the 2014-2015 season compared with the previous year.[38]

Image courtesy of Donald Miralle/Getty Images

Slide 7

Second Impact Syndrome

For many years, the most feared consequence of a concussion was not long-term neurologic deficits, but rather another concussion. Second impact syndrome (SIS) can occur when an athlete with postconcussive symptoms returns to play and sustains a second head injury, which can cause diffuse cerebral swelling, brain herniation, and potentially death.[39] There is controversy as to whether SIS exists, and its incidence is unknown. One study[40] of high school and college athletes found 94 possible events over a 13-year period, only two of which occurred at the collegiate level. These findings may underscore concerns about comparatively less rigorous monitoring of younger players. In the NFL study of traumatic brain injury, no cases of SIS, death, prolonged coma, or diffuse cerebral edema were detected during the 6-year study period.[36] Furthermore, there have been no case reports of SIS in the history of the NFL.

Images from iStock

Slide 8

Chronic Traumatic Encephalopathy

Chronic traumatic encephalopathy (CTE) was first reported in the NFL in 2005.[41] Since then, its devastating effects have been dramatized by the suicides of such well-known players as Junior Seau (pictured top right above) and Jovan Belcher (pictured bottom right above). Autopsies of both men's brains confirmed changes consistent with CTE.[42,43] Although news reports indicate that both Seau and Belcher attributed their symptoms to repeated head injuries sustained during their years as players, the evidence supporting a link between head injury and CTE in athletes is case-based.[44] Some data suggest that subconcussive blows—that is, those that do not result in signs and symptoms needed to diagnose concussion—may cause both the clinical and pathologic findings seen in CTE. Evidence suggesting a link between CTE and other neurodegenerative disorders, including Alzheimer disease and Parkinson disease, is less clear-cut. Former New York Jets player Mark Gastineau announced in January 2017 that he has both disorders, and suggested that they were indeed the result of his years in the NFL and numerous head blows. In addition, the age at which an athlete first participates in tackle football may be a factor; one study[45] of former NFL players found an association between participation beginning before the age of 12 years and greater cognitive impairment later in life. Another study,[46] also conducted in former NFL players, found changes in the corpus callosum microstructure in players who began participation at a young age. Together, the two studies suggest that head injuries sustained at a younger age may disrupt neurodevelopmental processes.

Images courtesy of (clockwise left to right) Wikipedia; AP Foto/Denis Poroy; AP Photo/Seth Perlman

Slide 9

Spinal Cord Injury

Spinal cord injuries, less common than head injuries, are potentially catastrophic. The risk for serious neurologic sequelae has decreased over the past 30 years, probably owing to rule changes that prohibit head-first blocking and tackling as well as improved sideline care.[47] Fortunately, the majority of cervical spine injuries in football are relatively minor, with most players experiencing a full recovery.[48] Incidence is approximately 0.2 per 100,000 participants at the high school level and 2 per 100,000 participants at the collegiate level.[47] Despite the relatively lower incidence, cervical spine injuries account for a significant proportion of the permanent injuries sustained in football. Darryl Stingley (pictured above), an acclaimed wide receiver selected by the New England Patriots in the first round of the NFL draft in 1973, sustained a cervical vertebral fracture with resultant quadriplegia after a head-first tackle (pictured above left) in a preseason game—the kind of hit that is now outlawed by the league.[49]

Images courtesy of (left) Ron Riesterer/Sporting News via Getty Images and (right) John F. Jaqua /Sports Illustrated/Getty Images

Slide 10

Catastrophic Contact Injury

In addition to head and neck injuries, football players are at risk for any number of other potentially career-ending injuries. An important, albeit relatively rare, example is hip subluxation or dislocation, the injury that ended the career of acclaimed Oakland Raiders running back and Heisman Trophy winner Bo Jackson (#34, pictured above).[50] Hip dislocation is the event, but the subsequent avascular necrosis is the real problem. Jackson sustained a fracture and posterior hip subluxation during a playoff game in January 1991, and the severity of the resultant damage was not apparent until 1 month later. A recent review article concluded that prompt diagnosis and proper treatment of hip subluxation—which in many cases is dismissed simply as a hip "sprain" or "strain"—is important, because 25% of these injuries may disrupt blood supply, leading to necrosis of the femoral head.[51] Fortunately, the widespread use of MRI to evaluate players who sustain hip injuries that result in limited range of motion makes recognition and treatment more likely. Players with osteonecrosis visible on MRI at 6 weeks postevent are at significant risk for joint degeneration and should be advised to not return to play.

Although the severity of Jackson's injury was not initially recognized, most football fans are familiar with numerous other examples of cringe-worthy, catastrophic, contact injuries that no one would miss. Washington Redskins quarterback Joe Theismann's comminuted compound leg fracture sustained during a Monday Night Football game in 1985 was voted "The Hit That No One Who Saw It Can Ever Forget" and ended his career.[52]

Image courtesy of Focus on Sport/Getty Images

Slide 11

Noncontact Injuries

More common than the events that make football fans gasp are injuries that result from the wear-and-tear that football's repetitive stresses and strains place on the body. In fact, fully 85% of anterior cruciate ligament (ACL) injuries result from noncontact or indirect contact mechanisms.[53] These injuries are 1.39 times higher in athletes playing on artificial surfaces compared with natural grass surfaces.[54] Increasing emphasis is now placed on both recognizing player risk for this type of injury and appropriate preventive strategies. A survey[55] of professional sports teams identified the top 5 risk factors for noncontact injury, four of which are modifiable: fatigue, muscle imbalance, fitness, and movement efficiency. The final risk factor, previous injury, is not. Studies have also identified specific actions, notably planting or cutting to change direction, that increase risk for ACL injury.[56] Whereas other sports leagues, most notably the Fédération Internationale de Football Association (FIFA), have instituted structured injury-prevention programs, the NFL has not.[55]

Image from iStock

Slide 12

Recognizing and Addressing Injury Risk

Risk factors specific for many injuries have been identified and, in many cases, mitigated by new rules or better equipment. Rules against head-to-head tackles, stricter return-to-play guidelines, and better helmet technology have reduced incidence of concussion. Turf toe, a hyperdorsiflexion injury of the first metatarsophalangeal joint that is more common in athletes playing on artificial turf, is better identified through newer imaging techniques and treated with conservative measures, including turf-toe plates and orthotics.[57] But what about general injury risk? Are there player factors that increase the likelihood of risk, regardless of injury type? A recent study[58] of Division I college football players found that injury was more likely during periods of higher academic stress. Other global risk factors are now also recognized, including player age and experience, inadequate conditioning, poor technique, and ill-fitting equipment.[59,60]

Image from iStock

Slide 13

Will There Ever Be Risk-Free Football?

Pundits would argue that playing football is inherently risky. Player speed and size have combined with a collision sport to create high-impact injuries. All the risk recognition and mitigation in the world may not compensate for sheer bad luck. Mike Utley (pictured above as he was transported off the field in 1991, and in the inset photo in 2014), a Detroit Lions offensive lineman, sustained a severe cervical spine injury when an opposing player leaped into the air to deflect a pass and came down on him. The Lions coach said at the time, "It was an accident. It wasn't an illegal play or an illegal block. It was just one of those freak things that happens on the football field."[61] Utley later established the Mike Utley Foundation, whose mission is to support research into function-restoring treatments for spinal cord injuries. Of note, the foundation does not call for an end to football. As Buzz Bissinger, a Pulitzer prize-winning sports journalist, argues, violence is an intrinsic part of football and players accept it as part of the game[62]—which will forever leave healthcare professionals with the need to put players back together again.

Image courtesy of Sporting News/Getty Images; inset: Wikipedia

Slide 14

And Sometimes It's Not About Luck

A discussion of injury in football would not be complete without at least a brief mention of completely preventable injuries—that is, those caused by operator (ie, player) error. Over-the-top celebrations after a play have become routine, and most are harmless. Not so for Detroit Lions linebacker Stephen Tulloch, who saw his season end after tearing his ACL while celebrating a sack.[63] Washington Redskins quarterback Gus Ferrotte got so carried away after running 1 yard for a touchdown that he ran through the end zone all the way to the concrete back wall and head-butted it, injuring his neck and having to leave the game.[64] And sometimes the injury is the result of teammates celebrating. After Ohio State's Ted Ginn, Jr, returned the opening kickoff in the 2007 Bowl Championship Series title game against University of Florida for a touchdown, he injured his ankle in the post-touchdown end-zone celebration, presumably the result of a tackle by a teammate.[65] He was forced to leave the game, and without him, Ohio State sputtered and eventually lost.

Image from iStock

Slide 15

Cheerleading: The Height of Danger

Last November, during a football game, a Baltimore Ravens cheerleader was tossed high into the air as part of a stunt, but instead of being caught by her team, she landed on her head and neck, and was carried off the field on a stretcher.[66] She was lucky. She suffered no catastrophic injury, but the risk for harm was high.

In terms of the injury rate, cheerleading is one of the most dangerous sports for females.[67] Cheerleading is no longer about hand-clapping and doing splits. Cheerleading routines now incorporate tumbling runs and partner stunts, human pyramids, lifts, catches, and tosses—acrobatics and gymnastics that are much more likely to result in injury.[68] Competition and more difficult routines resulted in a doubling of cheerleader injury rates between 1990 and 2002.[69]

Among college-aged and younger cheerleaders, most injuries occur during practice, and often while the cheerleader was basing or spotting another cheerleader. The top 5 types of injury are strain or sprain (53%); abrasion, contusion, or hematoma (13%); fracture (10%); laceration or puncture (4%); and concussion or closed head injury (4%). Performing stunts causes the most injuries, and nearly all concussions. Collegiate cheerleaders have the highest overall injury rates and are more likely than their younger counterparts to sustain concussions.[68]

In recognition of the popularity of cheerleading, and the potential for catastrophic injury, in 2012 the American Academy of Pediatrics released a policy statement describing the epidemiology of cheerleading injuries and provides recommendations for injury prevention.[70]

Image from iStock

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