LayerRx Mapping ID
677
Slot System
Featured Buckets
Featured Buckets Admin
Reverse Chronological Sort
Medscape Lead Concept
3003382

Historical Patterns and Variation in Treatment of Injuries in NFL (National Football League) Players and NCAA (National Collegiate Athletic Association) Division I Football Players

Article Type
Changed
Thu, 09/19/2019 - 13:24
Display Headline
Historical Patterns and Variation in Treatment of Injuries in NFL (National Football League) Players and NCAA (National Collegiate Athletic Association) Division I Football Players

Among National Football League (NFL) and National Collegiate Athletic Association (NCAA) team physicians, there is no consensus on the management of various injuries. At national and regional meetings, the management of football injuries often is debated.

Given the high level of interest in the treatment of elite football players, we wanted to determine treatment patterns by surveying orthopedic team physicians. We conducted a study to determine the demographics of NFL and NCAA team physicians and to identify patterns and variations in the management of common injuries in these groups of elite football players.

Materials and Methods

The study was reviewed by an Institutional Review Board before data collection and was classified as exempt. The study population consisted of head orthopedic team physicians for NFL teams and NCAA Division I universities. The survey (Appendix),

which included questions about team physician experience, team medical coverage, reimbursement issues, and management of common football injuries, was emailed to the head orthopedic team physicians (a paper version of the survey was mailed to those who had no known email address or who preferred a hard copy). Data were collected from May 1, 2007 through July 15, 2008.

Chi-square tests were used to determine significant differences between groups. P < .05 was considered statistically significant.

Results

Responses were received from 31 (97%) of the 32 NFL and 111 (93%) of the 119 NCAA team physicians. The 2 groups’ surveys were identical with the exception of question 3, regarding NFL division or NCAA conference.

Team Physician Demographics

All survey respondents were the head orthopedic physicians for their teams. Seventy-one percent were the head team physicians as well; another 25% named a primary care physician as the head team physician. Thirty-nine percent of the NFL team physicians had been a team physician at the NFL level for more than 15 years, and 58% of the NCAA team physicians had been a team physician at the Division I level for more than 15 years. Eighty-one percent of NFL and 66% of NCAA team physicians had fellowship training in sports medicine. For away games, 10% of NFL vs 65% of NCAA teams traveled with 2 physicians; 90% of NFL and 28% of NCAA teams traveled with 3 or more physicians.

Only a small percentage of respondents (NFL, 10%; NCAA, 14%) indicated they had received advertising in exchange for services. Most respondents (NFL, 93%; NCAA, 89%) did not pay to provide team coverage. In contrast, 97% of NFL vs only 31% of NCAA physicians indicated they received a monetary stipend for providing orthopedic coverage.

Anterior Cruciate Ligament Reconstructions

Eighty-seven percent of NFL and 67% of NCAA respondents indicated that patellar tendon autograft was their preferred graft choice (Table 1).

The percentage of NCAA physicians who allowed return to football 6 months or less after anterior cruciate ligament (ACL) reconstruction was significantly (P = .03) higher than that of NFL physicians
(Figure 1).

Anterior Shoulder Dislocations (Without Bony Bankart)

Sling use after reduction of anterior shoulder dislocation was varied, with most physicians using a sling 2 weeks or less (Table 2).

Ninety-three percent of the team physicians in each group had athletes play with a harness when they returned from an in-season injury. For anterior stabilization, most team physicians (NFL, 79%; NCAA, 69%) performed arthroscopic repair. A minority indicated that, after anterior stabilization, they always required use of a harness; a higher proportion based their decision on the player’s position (Table 3).
Return to contact was similarly allowed by both groups, and 90% allowed return to contact within 4 to 6 months (Figure 2).

Acromioclavicular Joint Injuries

Roughly two-thirds of respondents (NFL, 60%; NCAA, 69%) indicated that, during a game, they managed acute acromioclavicular (AC) joint injuries (type I/II) with injection of a local anesthetic that allowed return to play. In addition, a majority (NFL, 90%; NCAA, 87%) indicated they gave such athletes pregame injections that allowed them to play. About half the physicians (NFL, 57%; NCAA, 52%) injected the AC joint with cortisone during the acute/subacute period (<1 month) to decrease inflammation.

No significant difference was found between the 2 groups in terms of proportion of surgeons electing to treat type III AC joint injuries operatively versus nonoperatively (Table 4).

Medial Collateral Ligament Injuries

There was a significant (P < .0001) difference in use of prophylactic bracing for medial collateral ligament (MCL) injuries (NFL, 28%; NCAA, 89%).

Bracing was most commonly used in offensive linemen (Figure 3).

 

 

Posterior Cruciate Ligament Injuries

The percentage of physicians who allowed athletes to return to play after a grade I/II posterior cruciate ligament (PCL) injury was significantly (P = .01) higher in NFL physicians (22%) than in NCAA physicians (7%). The amount of time varied up to more than 4 weeks (Figure 4).

When athletes returned to play after a grade I/II PCL injury, significantly (P < .01) more NCAA physicians (64%) than NFL physicians (37%) required bracing.

Physicians varied in their responses about how often grade III PCL injuries would be managed (Table 5). Both groups’ preferred method of operative repair was the arthroscopic single-bundle technique (Figure 5).

Elbow Ulnar Collateral Ligament Tears

A majority of respondents indicated they would treat a complete elbow ulnar collateral ligament (UCL) tear in a quarterback; a much smaller percentage preferred operative repair in athletes playing other positions (Table 6).

Thumb Ulnar Collateral Ligament Tears

For athletes with in-season thumb UCL tears, 63% of NFL and 54% of NCAA physicians indicated they cast the thumb and allowed return to play. Others recommended operative repair and either cast the thumb and allowed return to play (NFL, 30%; NCAA, 41%) or let the thumb heal before allowing return to play (NFL, 7%; NCAA, 5%).

Fifth Metatarsal Fractures

For a large majority of physicians (NFL, 100%; NCAA, 94%), the preferred treatment for fifth metatarsal fractures was screw fixation.

The percentage of physicians who allowed return to play by 6 weeks was significantly (P < .01) higher in NCAA (55%) than NFL (24%) physicians (Figure 6).

Tibia Fractures

In the 5-year period before the survey, 43% of NFL and 75% of NCAA physicians managed at least one tibia fracture (P < .001) (Figure 7).

The treatment preferred by all NFL physicians and 96% of NCAA physicians was intramedullary nailing. Only 2 respondents, both in the NCAA, removed the nail before allowing return to play. Five physicians, all in the NCAA, reported nonunions occurring after tibia fractures. Reported complications (NFL, 8%; NCAA, 13%) included 4 cases of fatty embolism, 1 death, infection, compartment syndrome, muscular contracture, and persistent pain.

Ketorolac Injections

Intramuscular ketorolac injections were frequently given to elite football players, significantly (P < .01) more so in the NFL (93%) than in the NCAA (62%). The average number of injections varied among physicians, though a significantly (P < .0001) higher percentage of NFL (79%) than NCAA (13%) physicians gave 5 or more injections per game.

Discussion

This survey on managing common injuries in elite football players had an overall response rate of 94%. All NFL divisions and NCAA conferences were represented in physicians’ responses. Ninety percent of NFL and 65% of NCAA head team physicians were orthopedists. These findings differ from those of Stockard1 (1997), who surveyed athletic directors at Division I schools and reported 45% of head team physicians were family medicine-trained and 41% were orthopedists.

Given the high visibility of team coverage and the economics of college football’s highest division, one might expect team physicians to receive financial remuneration. This was not the case, according to our survey: Only 30% of physicians received a monetary stipend for team coverage, and only 14% received advertising in exchange for their services. Twelve NCAA team physicians indicated they pay to be allowed to provide team coverage.

Injury Management

Anterior Cruciate Ligament Injuries. For NFL and NCAA team physicians, the preferred graft choice for ACL reconstruction was patellar tendon autograft. This finding is similar to what Erickson and colleagues2 reported from a survey of NFL and NCAA team physicians: 86% of surgeons preferred bone–patellar tendon–bone (BPTB) autograft. However, only 1 surgeon (0.7%) in that study, vs 16% in ours, preferred allograft. Allograft use may be somewhat controversial, as relevant data on competitive athletes are lacking, and it has been shown that the graft rupture rate3 is higher for BPTB allograft than for BPTB autograft in young patients. However, much of the data on higher failure rates with use of allograft in young patients4,5 has appeared since our data were collected.

Our return-to-play data are similar to data from other studies.2,6 According to our survey, the most common length of time from ACL reconstruction to return to football was 6 months, and 94% of team physicians allowed return to football by 9 months. In the survey by Erickson and colleagues,2 55% of surgeons waited a minimum of 6 months before returning athletes to play, and only 12% waited at least 9 months. In the study by Bradley and colleagues6 (2002), 84% of surgeons waited at least 6 months before returning athletes to play. Of note, we found a significantly higher percentage of NCAA football players than NFL players returning within 6 months after surgery. The difference may be attributable to a more cautious approach being taken with NFL players, whereas most NCAA players are limited in the time remaining in their football careers and want to return to the playing field as soon as possible.

Shoulder Dislocations. Responses to the 5 survey questions on anterior shoulder dislocation showed little consensus with respect to management. The exception pertained to use of a harness for in-season return to play with a dislocation—92% of physicians preferred management with a harness. Of note, 7 of 10 team surgeons performed anterior stabilization through an arthroscopic approach. Despite historical recommendations to perform open anterior stabilization in collision athletes, NFL and NCAA physicians’ practice patterns have evolved.7 Although return to contact activity was varied among responses, 94% of physicians allowed return to contact within 6 months.

Acromioclavicular Joint Injuries. For college football players, AC joint injuries are the most common shoulder injuries.8 In the NFL Combine, the incidence of AC joint injuries was 15.7 per 100 players.8 Several studies have cited favorable results with nonoperative management of type III AC joint injuries.9-12 Nonoperative management was the preferred treatment in our study as well, yet 26% of surgeons still preferred operative treatment in quarterbacks. Opinions about operative repair of type III injuries in overhead athletes vary,13 but nonoperative management clearly is the preferred method for elite football players. A 2013 study by Lynch and colleagues14 found that only 2 of 40 NFL players with type III AC joint injuries underwent surgery.

For type I and II AC joint injuries that occur during a game, more than two-thirds of the NCAA team physicians in our study favored injecting a local anesthetic to reduce pain and allow return to play in the same game. An even larger majority indicated they gave a pregame injection of an anesthetic to allow play. Similar use of injections for AC joint injuries has been reported in Australian-rules football and rugby.15Medial Collateral Ligament Injuries. Whether bracing is prophylactic against MCL injuries is controversial.16 Some studies have found it effective.17,18 According to our survey, 89% of Division I football teams used prophylactic knee bracing, mainly in offensive linemen but frequently in defensive linemen, too. No schools used bracing in athletes who played skill positions, except quarterbacks. Six schools used bracing on a quarterback’s front leg.

The percentage of teams that used prophylactic MCL bracing was significantly higher in the NCAA than in the NFL. NCAA team physicians generally have more control over players and therefore can implement widespread use of this bracing.

Posterior Cruciate Ligament Injuries. These injuries are infrequent. According to Parolie and Bergfeld,19 only 2% of college football players at the NFL Combine had a PCL injury. Treatment in athletes remains controversial. Our survey showed physicians’ willingness to return players to competition within 4 weeks after grade I/II PCL injuries. There is no consensus on management or on postinjury bracing. In operative cases, however, the preferred graft is allograft, and the preferred repair method is the arthroscopic single-bundle technique. These findings mirror those of a 2004 survey of the Herodicus Society by Dennis and colleagues.20 Elbow Ulnar Collateral Ligament Tears. In throwing athletes with UCL tears, operative treatment has been recommended.21,22 A majority of our survey respondents preferred operative treatment for quarterbacks. However, operative treatment is still controversial, and quarterbacks differ from baseball players in their throwing motions and in the stresses acting on the UCLs during throwing. Two systematic reviews of UCL reconstruction have affirmed the positive outcomes of operative treatment in throwing athletes.21,22 However, most of the studies covered by these reviews focused on baseball players. In athletes playing positions other than quarterback, these injuries were typically treated nonoperatively.

Thumb Ulnar Collateral Ligament Tears. Our survey respondents differed in their opinions on treating thumb UCL tears. About half recommended cast treatment, and the other half recommended operative treatment. Previous data suggest that delaying surgical treatment may be deleterious to the eventual outcome.23,24Fifth Metatarsal Fractures. For fifth metatarsal fractures, screw fixation was preferred by 90% of our survey respondents—vs 73% of NFL team physicians in a 2004 study by Low and colleagues.25 What remains controversial is the length of time before return to play. Our most frequent response was 4 to 6 weeks, and 46% of our respondents indicated they would wait 7 weeks or longer. These times differ significantly from what Low and colleagues25 reported: 86% of their physicians allowed return to competition after 6 to 12 weeks.

Tibia Fractures. Management of tibia fractures in US football players has not been reported. Chang and colleagues26 described 24 tibial shaft fractures in UK soccer players. Eleven fractures (~50%) were treated with intramedullary nails, 2 with plating, and 11 with conservative management. All players returned to activity, the operative group at 23.3 weeks and the nonoperative group at 27.6 weeks. Our respondents reported treating at least 150 tibial shaft fractures in the 5-year period before our survey, demonstrating the incidence and importance of this type of injury. A vast majority of team surgeons (96%) opted for treatment with intramedullary nailing. This choice may reflect an ability to return to play earlier—the ability to move the knee and maintain strength in the legs. Some have suggested it is important to remove the nail before the player returns to the football field, but this was not common practice among our groups of team surgeons. Other studies have not found any advantage to tibial nail removal.27Ketorolac Injections. Authors have described using ketorolac for the treatment of acute or pregame pain in professional football players.28-30 According to a 2000 survey, 93% of NFL teams used intramuscular ketorolac, and on average 15 players per team were treated, primarily on game day. Our survey found frequent use of ketorolac, with almost two-thirds of team orthopedists indicating pregame use. Ketorolac use was popular, particularly because of its effect in reducing postoperative pain and its potent effect in reducing pain on game day. However, injections by football team physicians have declined significantly in recent years, ever since an NFL Physician Society task force published recommendations on ketorolac use.31

 

 

Conclusion

There is a wide variety of patterns in treating athletes who play football at the highest levels of competition. Our findings can initiate further discussion on these topics and assist orthopedists providing game coverage at all levels of play in their decision-making process by helping to define the standard of care for their injured players.

Am J Orthop. 2016;45(6):E319-E327. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Stockard AR. Team physician preferences at National Collegiate Athletic Association Division I universities. J Am Osteopath Assoc. 1997;97(2):89-95.

2. Erickson BJ, Harris JD, Fillingham YA, et al. Anterior cruciate ligament reconstruction practice patterns by NFL and NCAA football team physicians. Arthroscopy. 2014;30(6):731-738.

3. Kraeutler MJ, Bravman JT, McCarty EC. Bone-patellar tendon-bone autograft versus allograft in outcomes of anterior cruciate ligament reconstruction: a meta-analysis of 5182 patients. Am J Sports Med. 2013;41(10):2439-2448.

4. Bottoni CR, Smith EL, Shaha J, et al. Autograft versus allograft anterior cruciate ligament reconstruction: a prospective, randomized clinical study with a minimum 10-year follow-up. Am J Sports Med. 2015;43(10):2501-2509.

5. Sun K, Tian S, Zhang J, Xia C, Zhang C, Yu T. Anterior cruciate ligament reconstruction with BPTB autograft, irradiated versus non-irradiated allograft: a prospective randomized clinical study. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):464-474.

6. Bradley JP, Klimkiewicz JJ, Rytel MJ, Powell JW. Anterior cruciate ligament injuries in the National Football League: epidemiology and current treatment trends among team physicians. Arthroscopy. 2002;18(5):502-509.

7. Rhee YG, Ha JH, Cho NS. Anterior shoulder stabilization in collision athletes: arthroscopic versus open Bankart repair. Am J Sports Med. 2006;34(6):979-985.

8. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine—trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.

9. Bishop JY, Kaeding C. Treatment of the acute traumatic acromioclavicular separation. Sports Med Arthrosc. 2006;14(4):237-245.

10. Mazzocca AD, Arciero RA, Bicos J. Evaluation and treatment of acromioclavicular joint injuries. Am J Sports Med. 2007;35(2):316-329.

11. Schlegel TF, Burks RT, Marcus RL, Dunn HK. A prospective evaluation of untreated acute grade III acromioclavicular separations. Am J Sports Med. 2001;29(6):699-703.

12. Spencer EE Jr. Treatment of grade III acromioclavicular joint injuries: a systematic review. Clin Orthop Relat Res. 2007;(455):38-44.

13. Kraeutler MJ, Williams GR Jr, Cohen SB, et al. Inter- and intraobserver reliability of the radiographic diagnosis and treatment of acromioclavicular joint separations. Orthopedics. 2012;35(10):e1483-e1487.

14. Lynch TS, Saltzman MD, Ghodasra JH, Bilimoria KY, Bowen MK, Nuber GW. Acromioclavicular joint injuries in the National Football League: epidemiology and management. Am J Sports Med. 2013;41(12):2904-2908.

15. Orchard JW. Benefits and risks of using local anaesthetic for pain relief to allow early return to play in professional football. Br J Sports Med. 2002;36(3):209-213.

16. Salata MJ, Gibbs AE, Sekiya JK. The effectiveness of prophylactic knee bracing in American football: a systematic review. Sports Health. 2010;2(5):375-379.

17. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee sprains in college football. Effectiveness of preventive braces. Am J Sports Med. 1994;22(1):12-18.

18. Sitler M, Ryan J, Hopkinson W, et al. The efficacy of a prophylactic knee brace to reduce knee injuries in football. A prospective, randomized study at West Point. Am J Sports Med. 1990;18(3):310-315.

19. Parolie JM, Bergfeld JA. Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med. 1986;14(1):35-38.

20. Dennis MG, Fox JA, Alford JW, Hayden JK, Bach BR Jr. Posterior cruciate ligament reconstruction: current trends. J Knee Surg. 2004;17(3):133-139.

21. Purcell DB, Matava MJ, Wright RW. Ulnar collateral ligament reconstruction: a systematic review. Clin Orthop Relat Res. 2007;(455):72-77.

22. Vitale MA, Ahmad CS. The outcome of elbow ulnar collateral ligament reconstruction in overhead athletes: a systematic review. Am J Sports Med. 2008;36(6):1193-1205.

23. Fricker R, Hintermann B. Skier’s thumb. Treatment, prevention and recommendations. Sports Med. 1995;19(1):73-79.

24. Smith RJ. Post-traumatic instability of the metacarpophalangeal joint of the thumb. J Bone Joint Surg Am. 1977;59(1):14-21.

25. Low K, Noblin JD, Browne JE, Barnthouse CD, Scott AR. Jones fractures in the elite football player. J Surg Orthop Adv. 2004;13(3):156-160.

26. Chang WR, Kapasi Z, Daisley S, Leach WJ. Tibial shaft fractures in football players. J Orthop Surg Res. 2007;2:11.

27. Karladani AH, Ericsson PA, Granhed H, Karlsson L, Nyberg P. Tibial intramedullary nails—should they be removed? A retrospective study of 71 patients. Acta Orthop. 2007;78(5):668-671.

28. Eichner ER. Intramuscular ketorolac injections: the pregame Toradol parade. Curr Sports Med Rep. 2012;11(4):169-170.

29. Nepple JJ, Matava MJ. Soft tissue injections in the athlete. Sports Health. 2009;1(5):396-404.

30. Powell ET, Tokish JM, Hawkins RJ. Toradol use in the athletic population. Curr Sports Med Rep. 2002;1(4):191.

31. Matava M, Brater DC, Gritter N, et al. Recommendations of the National Football League physician society task force on the use of toradol® ketorolac in the National Football League. Sports Health. 2012;4(5):377-383.

Article PDF
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Issue
The American Journal of Orthopedics - 45(6)
Publications
Topics
Page Number
E319-E327
Sections
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Article PDF
Article PDF

Among National Football League (NFL) and National Collegiate Athletic Association (NCAA) team physicians, there is no consensus on the management of various injuries. At national and regional meetings, the management of football injuries often is debated.

Given the high level of interest in the treatment of elite football players, we wanted to determine treatment patterns by surveying orthopedic team physicians. We conducted a study to determine the demographics of NFL and NCAA team physicians and to identify patterns and variations in the management of common injuries in these groups of elite football players.

Materials and Methods

The study was reviewed by an Institutional Review Board before data collection and was classified as exempt. The study population consisted of head orthopedic team physicians for NFL teams and NCAA Division I universities. The survey (Appendix),

which included questions about team physician experience, team medical coverage, reimbursement issues, and management of common football injuries, was emailed to the head orthopedic team physicians (a paper version of the survey was mailed to those who had no known email address or who preferred a hard copy). Data were collected from May 1, 2007 through July 15, 2008.

Chi-square tests were used to determine significant differences between groups. P < .05 was considered statistically significant.

Results

Responses were received from 31 (97%) of the 32 NFL and 111 (93%) of the 119 NCAA team physicians. The 2 groups’ surveys were identical with the exception of question 3, regarding NFL division or NCAA conference.

Team Physician Demographics

All survey respondents were the head orthopedic physicians for their teams. Seventy-one percent were the head team physicians as well; another 25% named a primary care physician as the head team physician. Thirty-nine percent of the NFL team physicians had been a team physician at the NFL level for more than 15 years, and 58% of the NCAA team physicians had been a team physician at the Division I level for more than 15 years. Eighty-one percent of NFL and 66% of NCAA team physicians had fellowship training in sports medicine. For away games, 10% of NFL vs 65% of NCAA teams traveled with 2 physicians; 90% of NFL and 28% of NCAA teams traveled with 3 or more physicians.

Only a small percentage of respondents (NFL, 10%; NCAA, 14%) indicated they had received advertising in exchange for services. Most respondents (NFL, 93%; NCAA, 89%) did not pay to provide team coverage. In contrast, 97% of NFL vs only 31% of NCAA physicians indicated they received a monetary stipend for providing orthopedic coverage.

Anterior Cruciate Ligament Reconstructions

Eighty-seven percent of NFL and 67% of NCAA respondents indicated that patellar tendon autograft was their preferred graft choice (Table 1).

The percentage of NCAA physicians who allowed return to football 6 months or less after anterior cruciate ligament (ACL) reconstruction was significantly (P = .03) higher than that of NFL physicians
(Figure 1).

Anterior Shoulder Dislocations (Without Bony Bankart)

Sling use after reduction of anterior shoulder dislocation was varied, with most physicians using a sling 2 weeks or less (Table 2).

Ninety-three percent of the team physicians in each group had athletes play with a harness when they returned from an in-season injury. For anterior stabilization, most team physicians (NFL, 79%; NCAA, 69%) performed arthroscopic repair. A minority indicated that, after anterior stabilization, they always required use of a harness; a higher proportion based their decision on the player’s position (Table 3).
Return to contact was similarly allowed by both groups, and 90% allowed return to contact within 4 to 6 months (Figure 2).

Acromioclavicular Joint Injuries

Roughly two-thirds of respondents (NFL, 60%; NCAA, 69%) indicated that, during a game, they managed acute acromioclavicular (AC) joint injuries (type I/II) with injection of a local anesthetic that allowed return to play. In addition, a majority (NFL, 90%; NCAA, 87%) indicated they gave such athletes pregame injections that allowed them to play. About half the physicians (NFL, 57%; NCAA, 52%) injected the AC joint with cortisone during the acute/subacute period (<1 month) to decrease inflammation.

No significant difference was found between the 2 groups in terms of proportion of surgeons electing to treat type III AC joint injuries operatively versus nonoperatively (Table 4).

Medial Collateral Ligament Injuries

There was a significant (P < .0001) difference in use of prophylactic bracing for medial collateral ligament (MCL) injuries (NFL, 28%; NCAA, 89%).

Bracing was most commonly used in offensive linemen (Figure 3).

 

 

Posterior Cruciate Ligament Injuries

The percentage of physicians who allowed athletes to return to play after a grade I/II posterior cruciate ligament (PCL) injury was significantly (P = .01) higher in NFL physicians (22%) than in NCAA physicians (7%). The amount of time varied up to more than 4 weeks (Figure 4).

When athletes returned to play after a grade I/II PCL injury, significantly (P < .01) more NCAA physicians (64%) than NFL physicians (37%) required bracing.

Physicians varied in their responses about how often grade III PCL injuries would be managed (Table 5). Both groups’ preferred method of operative repair was the arthroscopic single-bundle technique (Figure 5).

Elbow Ulnar Collateral Ligament Tears

A majority of respondents indicated they would treat a complete elbow ulnar collateral ligament (UCL) tear in a quarterback; a much smaller percentage preferred operative repair in athletes playing other positions (Table 6).

Thumb Ulnar Collateral Ligament Tears

For athletes with in-season thumb UCL tears, 63% of NFL and 54% of NCAA physicians indicated they cast the thumb and allowed return to play. Others recommended operative repair and either cast the thumb and allowed return to play (NFL, 30%; NCAA, 41%) or let the thumb heal before allowing return to play (NFL, 7%; NCAA, 5%).

Fifth Metatarsal Fractures

For a large majority of physicians (NFL, 100%; NCAA, 94%), the preferred treatment for fifth metatarsal fractures was screw fixation.

The percentage of physicians who allowed return to play by 6 weeks was significantly (P < .01) higher in NCAA (55%) than NFL (24%) physicians (Figure 6).

Tibia Fractures

In the 5-year period before the survey, 43% of NFL and 75% of NCAA physicians managed at least one tibia fracture (P < .001) (Figure 7).

The treatment preferred by all NFL physicians and 96% of NCAA physicians was intramedullary nailing. Only 2 respondents, both in the NCAA, removed the nail before allowing return to play. Five physicians, all in the NCAA, reported nonunions occurring after tibia fractures. Reported complications (NFL, 8%; NCAA, 13%) included 4 cases of fatty embolism, 1 death, infection, compartment syndrome, muscular contracture, and persistent pain.

Ketorolac Injections

Intramuscular ketorolac injections were frequently given to elite football players, significantly (P < .01) more so in the NFL (93%) than in the NCAA (62%). The average number of injections varied among physicians, though a significantly (P < .0001) higher percentage of NFL (79%) than NCAA (13%) physicians gave 5 or more injections per game.

Discussion

This survey on managing common injuries in elite football players had an overall response rate of 94%. All NFL divisions and NCAA conferences were represented in physicians’ responses. Ninety percent of NFL and 65% of NCAA head team physicians were orthopedists. These findings differ from those of Stockard1 (1997), who surveyed athletic directors at Division I schools and reported 45% of head team physicians were family medicine-trained and 41% were orthopedists.

Given the high visibility of team coverage and the economics of college football’s highest division, one might expect team physicians to receive financial remuneration. This was not the case, according to our survey: Only 30% of physicians received a monetary stipend for team coverage, and only 14% received advertising in exchange for their services. Twelve NCAA team physicians indicated they pay to be allowed to provide team coverage.

Injury Management

Anterior Cruciate Ligament Injuries. For NFL and NCAA team physicians, the preferred graft choice for ACL reconstruction was patellar tendon autograft. This finding is similar to what Erickson and colleagues2 reported from a survey of NFL and NCAA team physicians: 86% of surgeons preferred bone–patellar tendon–bone (BPTB) autograft. However, only 1 surgeon (0.7%) in that study, vs 16% in ours, preferred allograft. Allograft use may be somewhat controversial, as relevant data on competitive athletes are lacking, and it has been shown that the graft rupture rate3 is higher for BPTB allograft than for BPTB autograft in young patients. However, much of the data on higher failure rates with use of allograft in young patients4,5 has appeared since our data were collected.

Our return-to-play data are similar to data from other studies.2,6 According to our survey, the most common length of time from ACL reconstruction to return to football was 6 months, and 94% of team physicians allowed return to football by 9 months. In the survey by Erickson and colleagues,2 55% of surgeons waited a minimum of 6 months before returning athletes to play, and only 12% waited at least 9 months. In the study by Bradley and colleagues6 (2002), 84% of surgeons waited at least 6 months before returning athletes to play. Of note, we found a significantly higher percentage of NCAA football players than NFL players returning within 6 months after surgery. The difference may be attributable to a more cautious approach being taken with NFL players, whereas most NCAA players are limited in the time remaining in their football careers and want to return to the playing field as soon as possible.

Shoulder Dislocations. Responses to the 5 survey questions on anterior shoulder dislocation showed little consensus with respect to management. The exception pertained to use of a harness for in-season return to play with a dislocation—92% of physicians preferred management with a harness. Of note, 7 of 10 team surgeons performed anterior stabilization through an arthroscopic approach. Despite historical recommendations to perform open anterior stabilization in collision athletes, NFL and NCAA physicians’ practice patterns have evolved.7 Although return to contact activity was varied among responses, 94% of physicians allowed return to contact within 6 months.

Acromioclavicular Joint Injuries. For college football players, AC joint injuries are the most common shoulder injuries.8 In the NFL Combine, the incidence of AC joint injuries was 15.7 per 100 players.8 Several studies have cited favorable results with nonoperative management of type III AC joint injuries.9-12 Nonoperative management was the preferred treatment in our study as well, yet 26% of surgeons still preferred operative treatment in quarterbacks. Opinions about operative repair of type III injuries in overhead athletes vary,13 but nonoperative management clearly is the preferred method for elite football players. A 2013 study by Lynch and colleagues14 found that only 2 of 40 NFL players with type III AC joint injuries underwent surgery.

For type I and II AC joint injuries that occur during a game, more than two-thirds of the NCAA team physicians in our study favored injecting a local anesthetic to reduce pain and allow return to play in the same game. An even larger majority indicated they gave a pregame injection of an anesthetic to allow play. Similar use of injections for AC joint injuries has been reported in Australian-rules football and rugby.15Medial Collateral Ligament Injuries. Whether bracing is prophylactic against MCL injuries is controversial.16 Some studies have found it effective.17,18 According to our survey, 89% of Division I football teams used prophylactic knee bracing, mainly in offensive linemen but frequently in defensive linemen, too. No schools used bracing in athletes who played skill positions, except quarterbacks. Six schools used bracing on a quarterback’s front leg.

The percentage of teams that used prophylactic MCL bracing was significantly higher in the NCAA than in the NFL. NCAA team physicians generally have more control over players and therefore can implement widespread use of this bracing.

Posterior Cruciate Ligament Injuries. These injuries are infrequent. According to Parolie and Bergfeld,19 only 2% of college football players at the NFL Combine had a PCL injury. Treatment in athletes remains controversial. Our survey showed physicians’ willingness to return players to competition within 4 weeks after grade I/II PCL injuries. There is no consensus on management or on postinjury bracing. In operative cases, however, the preferred graft is allograft, and the preferred repair method is the arthroscopic single-bundle technique. These findings mirror those of a 2004 survey of the Herodicus Society by Dennis and colleagues.20 Elbow Ulnar Collateral Ligament Tears. In throwing athletes with UCL tears, operative treatment has been recommended.21,22 A majority of our survey respondents preferred operative treatment for quarterbacks. However, operative treatment is still controversial, and quarterbacks differ from baseball players in their throwing motions and in the stresses acting on the UCLs during throwing. Two systematic reviews of UCL reconstruction have affirmed the positive outcomes of operative treatment in throwing athletes.21,22 However, most of the studies covered by these reviews focused on baseball players. In athletes playing positions other than quarterback, these injuries were typically treated nonoperatively.

Thumb Ulnar Collateral Ligament Tears. Our survey respondents differed in their opinions on treating thumb UCL tears. About half recommended cast treatment, and the other half recommended operative treatment. Previous data suggest that delaying surgical treatment may be deleterious to the eventual outcome.23,24Fifth Metatarsal Fractures. For fifth metatarsal fractures, screw fixation was preferred by 90% of our survey respondents—vs 73% of NFL team physicians in a 2004 study by Low and colleagues.25 What remains controversial is the length of time before return to play. Our most frequent response was 4 to 6 weeks, and 46% of our respondents indicated they would wait 7 weeks or longer. These times differ significantly from what Low and colleagues25 reported: 86% of their physicians allowed return to competition after 6 to 12 weeks.

Tibia Fractures. Management of tibia fractures in US football players has not been reported. Chang and colleagues26 described 24 tibial shaft fractures in UK soccer players. Eleven fractures (~50%) were treated with intramedullary nails, 2 with plating, and 11 with conservative management. All players returned to activity, the operative group at 23.3 weeks and the nonoperative group at 27.6 weeks. Our respondents reported treating at least 150 tibial shaft fractures in the 5-year period before our survey, demonstrating the incidence and importance of this type of injury. A vast majority of team surgeons (96%) opted for treatment with intramedullary nailing. This choice may reflect an ability to return to play earlier—the ability to move the knee and maintain strength in the legs. Some have suggested it is important to remove the nail before the player returns to the football field, but this was not common practice among our groups of team surgeons. Other studies have not found any advantage to tibial nail removal.27Ketorolac Injections. Authors have described using ketorolac for the treatment of acute or pregame pain in professional football players.28-30 According to a 2000 survey, 93% of NFL teams used intramuscular ketorolac, and on average 15 players per team were treated, primarily on game day. Our survey found frequent use of ketorolac, with almost two-thirds of team orthopedists indicating pregame use. Ketorolac use was popular, particularly because of its effect in reducing postoperative pain and its potent effect in reducing pain on game day. However, injections by football team physicians have declined significantly in recent years, ever since an NFL Physician Society task force published recommendations on ketorolac use.31

 

 

Conclusion

There is a wide variety of patterns in treating athletes who play football at the highest levels of competition. Our findings can initiate further discussion on these topics and assist orthopedists providing game coverage at all levels of play in their decision-making process by helping to define the standard of care for their injured players.

Am J Orthop. 2016;45(6):E319-E327. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Among National Football League (NFL) and National Collegiate Athletic Association (NCAA) team physicians, there is no consensus on the management of various injuries. At national and regional meetings, the management of football injuries often is debated.

Given the high level of interest in the treatment of elite football players, we wanted to determine treatment patterns by surveying orthopedic team physicians. We conducted a study to determine the demographics of NFL and NCAA team physicians and to identify patterns and variations in the management of common injuries in these groups of elite football players.

Materials and Methods

The study was reviewed by an Institutional Review Board before data collection and was classified as exempt. The study population consisted of head orthopedic team physicians for NFL teams and NCAA Division I universities. The survey (Appendix),

which included questions about team physician experience, team medical coverage, reimbursement issues, and management of common football injuries, was emailed to the head orthopedic team physicians (a paper version of the survey was mailed to those who had no known email address or who preferred a hard copy). Data were collected from May 1, 2007 through July 15, 2008.

Chi-square tests were used to determine significant differences between groups. P < .05 was considered statistically significant.

Results

Responses were received from 31 (97%) of the 32 NFL and 111 (93%) of the 119 NCAA team physicians. The 2 groups’ surveys were identical with the exception of question 3, regarding NFL division or NCAA conference.

Team Physician Demographics

All survey respondents were the head orthopedic physicians for their teams. Seventy-one percent were the head team physicians as well; another 25% named a primary care physician as the head team physician. Thirty-nine percent of the NFL team physicians had been a team physician at the NFL level for more than 15 years, and 58% of the NCAA team physicians had been a team physician at the Division I level for more than 15 years. Eighty-one percent of NFL and 66% of NCAA team physicians had fellowship training in sports medicine. For away games, 10% of NFL vs 65% of NCAA teams traveled with 2 physicians; 90% of NFL and 28% of NCAA teams traveled with 3 or more physicians.

Only a small percentage of respondents (NFL, 10%; NCAA, 14%) indicated they had received advertising in exchange for services. Most respondents (NFL, 93%; NCAA, 89%) did not pay to provide team coverage. In contrast, 97% of NFL vs only 31% of NCAA physicians indicated they received a monetary stipend for providing orthopedic coverage.

Anterior Cruciate Ligament Reconstructions

Eighty-seven percent of NFL and 67% of NCAA respondents indicated that patellar tendon autograft was their preferred graft choice (Table 1).

The percentage of NCAA physicians who allowed return to football 6 months or less after anterior cruciate ligament (ACL) reconstruction was significantly (P = .03) higher than that of NFL physicians
(Figure 1).

Anterior Shoulder Dislocations (Without Bony Bankart)

Sling use after reduction of anterior shoulder dislocation was varied, with most physicians using a sling 2 weeks or less (Table 2).

Ninety-three percent of the team physicians in each group had athletes play with a harness when they returned from an in-season injury. For anterior stabilization, most team physicians (NFL, 79%; NCAA, 69%) performed arthroscopic repair. A minority indicated that, after anterior stabilization, they always required use of a harness; a higher proportion based their decision on the player’s position (Table 3).
Return to contact was similarly allowed by both groups, and 90% allowed return to contact within 4 to 6 months (Figure 2).

Acromioclavicular Joint Injuries

Roughly two-thirds of respondents (NFL, 60%; NCAA, 69%) indicated that, during a game, they managed acute acromioclavicular (AC) joint injuries (type I/II) with injection of a local anesthetic that allowed return to play. In addition, a majority (NFL, 90%; NCAA, 87%) indicated they gave such athletes pregame injections that allowed them to play. About half the physicians (NFL, 57%; NCAA, 52%) injected the AC joint with cortisone during the acute/subacute period (<1 month) to decrease inflammation.

No significant difference was found between the 2 groups in terms of proportion of surgeons electing to treat type III AC joint injuries operatively versus nonoperatively (Table 4).

Medial Collateral Ligament Injuries

There was a significant (P < .0001) difference in use of prophylactic bracing for medial collateral ligament (MCL) injuries (NFL, 28%; NCAA, 89%).

Bracing was most commonly used in offensive linemen (Figure 3).

 

 

Posterior Cruciate Ligament Injuries

The percentage of physicians who allowed athletes to return to play after a grade I/II posterior cruciate ligament (PCL) injury was significantly (P = .01) higher in NFL physicians (22%) than in NCAA physicians (7%). The amount of time varied up to more than 4 weeks (Figure 4).

When athletes returned to play after a grade I/II PCL injury, significantly (P < .01) more NCAA physicians (64%) than NFL physicians (37%) required bracing.

Physicians varied in their responses about how often grade III PCL injuries would be managed (Table 5). Both groups’ preferred method of operative repair was the arthroscopic single-bundle technique (Figure 5).

Elbow Ulnar Collateral Ligament Tears

A majority of respondents indicated they would treat a complete elbow ulnar collateral ligament (UCL) tear in a quarterback; a much smaller percentage preferred operative repair in athletes playing other positions (Table 6).

Thumb Ulnar Collateral Ligament Tears

For athletes with in-season thumb UCL tears, 63% of NFL and 54% of NCAA physicians indicated they cast the thumb and allowed return to play. Others recommended operative repair and either cast the thumb and allowed return to play (NFL, 30%; NCAA, 41%) or let the thumb heal before allowing return to play (NFL, 7%; NCAA, 5%).

Fifth Metatarsal Fractures

For a large majority of physicians (NFL, 100%; NCAA, 94%), the preferred treatment for fifth metatarsal fractures was screw fixation.

The percentage of physicians who allowed return to play by 6 weeks was significantly (P < .01) higher in NCAA (55%) than NFL (24%) physicians (Figure 6).

Tibia Fractures

In the 5-year period before the survey, 43% of NFL and 75% of NCAA physicians managed at least one tibia fracture (P < .001) (Figure 7).

The treatment preferred by all NFL physicians and 96% of NCAA physicians was intramedullary nailing. Only 2 respondents, both in the NCAA, removed the nail before allowing return to play. Five physicians, all in the NCAA, reported nonunions occurring after tibia fractures. Reported complications (NFL, 8%; NCAA, 13%) included 4 cases of fatty embolism, 1 death, infection, compartment syndrome, muscular contracture, and persistent pain.

Ketorolac Injections

Intramuscular ketorolac injections were frequently given to elite football players, significantly (P < .01) more so in the NFL (93%) than in the NCAA (62%). The average number of injections varied among physicians, though a significantly (P < .0001) higher percentage of NFL (79%) than NCAA (13%) physicians gave 5 or more injections per game.

Discussion

This survey on managing common injuries in elite football players had an overall response rate of 94%. All NFL divisions and NCAA conferences were represented in physicians’ responses. Ninety percent of NFL and 65% of NCAA head team physicians were orthopedists. These findings differ from those of Stockard1 (1997), who surveyed athletic directors at Division I schools and reported 45% of head team physicians were family medicine-trained and 41% were orthopedists.

Given the high visibility of team coverage and the economics of college football’s highest division, one might expect team physicians to receive financial remuneration. This was not the case, according to our survey: Only 30% of physicians received a monetary stipend for team coverage, and only 14% received advertising in exchange for their services. Twelve NCAA team physicians indicated they pay to be allowed to provide team coverage.

Injury Management

Anterior Cruciate Ligament Injuries. For NFL and NCAA team physicians, the preferred graft choice for ACL reconstruction was patellar tendon autograft. This finding is similar to what Erickson and colleagues2 reported from a survey of NFL and NCAA team physicians: 86% of surgeons preferred bone–patellar tendon–bone (BPTB) autograft. However, only 1 surgeon (0.7%) in that study, vs 16% in ours, preferred allograft. Allograft use may be somewhat controversial, as relevant data on competitive athletes are lacking, and it has been shown that the graft rupture rate3 is higher for BPTB allograft than for BPTB autograft in young patients. However, much of the data on higher failure rates with use of allograft in young patients4,5 has appeared since our data were collected.

Our return-to-play data are similar to data from other studies.2,6 According to our survey, the most common length of time from ACL reconstruction to return to football was 6 months, and 94% of team physicians allowed return to football by 9 months. In the survey by Erickson and colleagues,2 55% of surgeons waited a minimum of 6 months before returning athletes to play, and only 12% waited at least 9 months. In the study by Bradley and colleagues6 (2002), 84% of surgeons waited at least 6 months before returning athletes to play. Of note, we found a significantly higher percentage of NCAA football players than NFL players returning within 6 months after surgery. The difference may be attributable to a more cautious approach being taken with NFL players, whereas most NCAA players are limited in the time remaining in their football careers and want to return to the playing field as soon as possible.

Shoulder Dislocations. Responses to the 5 survey questions on anterior shoulder dislocation showed little consensus with respect to management. The exception pertained to use of a harness for in-season return to play with a dislocation—92% of physicians preferred management with a harness. Of note, 7 of 10 team surgeons performed anterior stabilization through an arthroscopic approach. Despite historical recommendations to perform open anterior stabilization in collision athletes, NFL and NCAA physicians’ practice patterns have evolved.7 Although return to contact activity was varied among responses, 94% of physicians allowed return to contact within 6 months.

Acromioclavicular Joint Injuries. For college football players, AC joint injuries are the most common shoulder injuries.8 In the NFL Combine, the incidence of AC joint injuries was 15.7 per 100 players.8 Several studies have cited favorable results with nonoperative management of type III AC joint injuries.9-12 Nonoperative management was the preferred treatment in our study as well, yet 26% of surgeons still preferred operative treatment in quarterbacks. Opinions about operative repair of type III injuries in overhead athletes vary,13 but nonoperative management clearly is the preferred method for elite football players. A 2013 study by Lynch and colleagues14 found that only 2 of 40 NFL players with type III AC joint injuries underwent surgery.

For type I and II AC joint injuries that occur during a game, more than two-thirds of the NCAA team physicians in our study favored injecting a local anesthetic to reduce pain and allow return to play in the same game. An even larger majority indicated they gave a pregame injection of an anesthetic to allow play. Similar use of injections for AC joint injuries has been reported in Australian-rules football and rugby.15Medial Collateral Ligament Injuries. Whether bracing is prophylactic against MCL injuries is controversial.16 Some studies have found it effective.17,18 According to our survey, 89% of Division I football teams used prophylactic knee bracing, mainly in offensive linemen but frequently in defensive linemen, too. No schools used bracing in athletes who played skill positions, except quarterbacks. Six schools used bracing on a quarterback’s front leg.

The percentage of teams that used prophylactic MCL bracing was significantly higher in the NCAA than in the NFL. NCAA team physicians generally have more control over players and therefore can implement widespread use of this bracing.

Posterior Cruciate Ligament Injuries. These injuries are infrequent. According to Parolie and Bergfeld,19 only 2% of college football players at the NFL Combine had a PCL injury. Treatment in athletes remains controversial. Our survey showed physicians’ willingness to return players to competition within 4 weeks after grade I/II PCL injuries. There is no consensus on management or on postinjury bracing. In operative cases, however, the preferred graft is allograft, and the preferred repair method is the arthroscopic single-bundle technique. These findings mirror those of a 2004 survey of the Herodicus Society by Dennis and colleagues.20 Elbow Ulnar Collateral Ligament Tears. In throwing athletes with UCL tears, operative treatment has been recommended.21,22 A majority of our survey respondents preferred operative treatment for quarterbacks. However, operative treatment is still controversial, and quarterbacks differ from baseball players in their throwing motions and in the stresses acting on the UCLs during throwing. Two systematic reviews of UCL reconstruction have affirmed the positive outcomes of operative treatment in throwing athletes.21,22 However, most of the studies covered by these reviews focused on baseball players. In athletes playing positions other than quarterback, these injuries were typically treated nonoperatively.

Thumb Ulnar Collateral Ligament Tears. Our survey respondents differed in their opinions on treating thumb UCL tears. About half recommended cast treatment, and the other half recommended operative treatment. Previous data suggest that delaying surgical treatment may be deleterious to the eventual outcome.23,24Fifth Metatarsal Fractures. For fifth metatarsal fractures, screw fixation was preferred by 90% of our survey respondents—vs 73% of NFL team physicians in a 2004 study by Low and colleagues.25 What remains controversial is the length of time before return to play. Our most frequent response was 4 to 6 weeks, and 46% of our respondents indicated they would wait 7 weeks or longer. These times differ significantly from what Low and colleagues25 reported: 86% of their physicians allowed return to competition after 6 to 12 weeks.

Tibia Fractures. Management of tibia fractures in US football players has not been reported. Chang and colleagues26 described 24 tibial shaft fractures in UK soccer players. Eleven fractures (~50%) were treated with intramedullary nails, 2 with plating, and 11 with conservative management. All players returned to activity, the operative group at 23.3 weeks and the nonoperative group at 27.6 weeks. Our respondents reported treating at least 150 tibial shaft fractures in the 5-year period before our survey, demonstrating the incidence and importance of this type of injury. A vast majority of team surgeons (96%) opted for treatment with intramedullary nailing. This choice may reflect an ability to return to play earlier—the ability to move the knee and maintain strength in the legs. Some have suggested it is important to remove the nail before the player returns to the football field, but this was not common practice among our groups of team surgeons. Other studies have not found any advantage to tibial nail removal.27Ketorolac Injections. Authors have described using ketorolac for the treatment of acute or pregame pain in professional football players.28-30 According to a 2000 survey, 93% of NFL teams used intramuscular ketorolac, and on average 15 players per team were treated, primarily on game day. Our survey found frequent use of ketorolac, with almost two-thirds of team orthopedists indicating pregame use. Ketorolac use was popular, particularly because of its effect in reducing postoperative pain and its potent effect in reducing pain on game day. However, injections by football team physicians have declined significantly in recent years, ever since an NFL Physician Society task force published recommendations on ketorolac use.31

 

 

Conclusion

There is a wide variety of patterns in treating athletes who play football at the highest levels of competition. Our findings can initiate further discussion on these topics and assist orthopedists providing game coverage at all levels of play in their decision-making process by helping to define the standard of care for their injured players.

Am J Orthop. 2016;45(6):E319-E327. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Stockard AR. Team physician preferences at National Collegiate Athletic Association Division I universities. J Am Osteopath Assoc. 1997;97(2):89-95.

2. Erickson BJ, Harris JD, Fillingham YA, et al. Anterior cruciate ligament reconstruction practice patterns by NFL and NCAA football team physicians. Arthroscopy. 2014;30(6):731-738.

3. Kraeutler MJ, Bravman JT, McCarty EC. Bone-patellar tendon-bone autograft versus allograft in outcomes of anterior cruciate ligament reconstruction: a meta-analysis of 5182 patients. Am J Sports Med. 2013;41(10):2439-2448.

4. Bottoni CR, Smith EL, Shaha J, et al. Autograft versus allograft anterior cruciate ligament reconstruction: a prospective, randomized clinical study with a minimum 10-year follow-up. Am J Sports Med. 2015;43(10):2501-2509.

5. Sun K, Tian S, Zhang J, Xia C, Zhang C, Yu T. Anterior cruciate ligament reconstruction with BPTB autograft, irradiated versus non-irradiated allograft: a prospective randomized clinical study. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):464-474.

6. Bradley JP, Klimkiewicz JJ, Rytel MJ, Powell JW. Anterior cruciate ligament injuries in the National Football League: epidemiology and current treatment trends among team physicians. Arthroscopy. 2002;18(5):502-509.

7. Rhee YG, Ha JH, Cho NS. Anterior shoulder stabilization in collision athletes: arthroscopic versus open Bankart repair. Am J Sports Med. 2006;34(6):979-985.

8. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine—trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.

9. Bishop JY, Kaeding C. Treatment of the acute traumatic acromioclavicular separation. Sports Med Arthrosc. 2006;14(4):237-245.

10. Mazzocca AD, Arciero RA, Bicos J. Evaluation and treatment of acromioclavicular joint injuries. Am J Sports Med. 2007;35(2):316-329.

11. Schlegel TF, Burks RT, Marcus RL, Dunn HK. A prospective evaluation of untreated acute grade III acromioclavicular separations. Am J Sports Med. 2001;29(6):699-703.

12. Spencer EE Jr. Treatment of grade III acromioclavicular joint injuries: a systematic review. Clin Orthop Relat Res. 2007;(455):38-44.

13. Kraeutler MJ, Williams GR Jr, Cohen SB, et al. Inter- and intraobserver reliability of the radiographic diagnosis and treatment of acromioclavicular joint separations. Orthopedics. 2012;35(10):e1483-e1487.

14. Lynch TS, Saltzman MD, Ghodasra JH, Bilimoria KY, Bowen MK, Nuber GW. Acromioclavicular joint injuries in the National Football League: epidemiology and management. Am J Sports Med. 2013;41(12):2904-2908.

15. Orchard JW. Benefits and risks of using local anaesthetic for pain relief to allow early return to play in professional football. Br J Sports Med. 2002;36(3):209-213.

16. Salata MJ, Gibbs AE, Sekiya JK. The effectiveness of prophylactic knee bracing in American football: a systematic review. Sports Health. 2010;2(5):375-379.

17. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee sprains in college football. Effectiveness of preventive braces. Am J Sports Med. 1994;22(1):12-18.

18. Sitler M, Ryan J, Hopkinson W, et al. The efficacy of a prophylactic knee brace to reduce knee injuries in football. A prospective, randomized study at West Point. Am J Sports Med. 1990;18(3):310-315.

19. Parolie JM, Bergfeld JA. Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med. 1986;14(1):35-38.

20. Dennis MG, Fox JA, Alford JW, Hayden JK, Bach BR Jr. Posterior cruciate ligament reconstruction: current trends. J Knee Surg. 2004;17(3):133-139.

21. Purcell DB, Matava MJ, Wright RW. Ulnar collateral ligament reconstruction: a systematic review. Clin Orthop Relat Res. 2007;(455):72-77.

22. Vitale MA, Ahmad CS. The outcome of elbow ulnar collateral ligament reconstruction in overhead athletes: a systematic review. Am J Sports Med. 2008;36(6):1193-1205.

23. Fricker R, Hintermann B. Skier’s thumb. Treatment, prevention and recommendations. Sports Med. 1995;19(1):73-79.

24. Smith RJ. Post-traumatic instability of the metacarpophalangeal joint of the thumb. J Bone Joint Surg Am. 1977;59(1):14-21.

25. Low K, Noblin JD, Browne JE, Barnthouse CD, Scott AR. Jones fractures in the elite football player. J Surg Orthop Adv. 2004;13(3):156-160.

26. Chang WR, Kapasi Z, Daisley S, Leach WJ. Tibial shaft fractures in football players. J Orthop Surg Res. 2007;2:11.

27. Karladani AH, Ericsson PA, Granhed H, Karlsson L, Nyberg P. Tibial intramedullary nails—should they be removed? A retrospective study of 71 patients. Acta Orthop. 2007;78(5):668-671.

28. Eichner ER. Intramuscular ketorolac injections: the pregame Toradol parade. Curr Sports Med Rep. 2012;11(4):169-170.

29. Nepple JJ, Matava MJ. Soft tissue injections in the athlete. Sports Health. 2009;1(5):396-404.

30. Powell ET, Tokish JM, Hawkins RJ. Toradol use in the athletic population. Curr Sports Med Rep. 2002;1(4):191.

31. Matava M, Brater DC, Gritter N, et al. Recommendations of the National Football League physician society task force on the use of toradol® ketorolac in the National Football League. Sports Health. 2012;4(5):377-383.

References

1. Stockard AR. Team physician preferences at National Collegiate Athletic Association Division I universities. J Am Osteopath Assoc. 1997;97(2):89-95.

2. Erickson BJ, Harris JD, Fillingham YA, et al. Anterior cruciate ligament reconstruction practice patterns by NFL and NCAA football team physicians. Arthroscopy. 2014;30(6):731-738.

3. Kraeutler MJ, Bravman JT, McCarty EC. Bone-patellar tendon-bone autograft versus allograft in outcomes of anterior cruciate ligament reconstruction: a meta-analysis of 5182 patients. Am J Sports Med. 2013;41(10):2439-2448.

4. Bottoni CR, Smith EL, Shaha J, et al. Autograft versus allograft anterior cruciate ligament reconstruction: a prospective, randomized clinical study with a minimum 10-year follow-up. Am J Sports Med. 2015;43(10):2501-2509.

5. Sun K, Tian S, Zhang J, Xia C, Zhang C, Yu T. Anterior cruciate ligament reconstruction with BPTB autograft, irradiated versus non-irradiated allograft: a prospective randomized clinical study. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):464-474.

6. Bradley JP, Klimkiewicz JJ, Rytel MJ, Powell JW. Anterior cruciate ligament injuries in the National Football League: epidemiology and current treatment trends among team physicians. Arthroscopy. 2002;18(5):502-509.

7. Rhee YG, Ha JH, Cho NS. Anterior shoulder stabilization in collision athletes: arthroscopic versus open Bankart repair. Am J Sports Med. 2006;34(6):979-985.

8. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine—trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.

9. Bishop JY, Kaeding C. Treatment of the acute traumatic acromioclavicular separation. Sports Med Arthrosc. 2006;14(4):237-245.

10. Mazzocca AD, Arciero RA, Bicos J. Evaluation and treatment of acromioclavicular joint injuries. Am J Sports Med. 2007;35(2):316-329.

11. Schlegel TF, Burks RT, Marcus RL, Dunn HK. A prospective evaluation of untreated acute grade III acromioclavicular separations. Am J Sports Med. 2001;29(6):699-703.

12. Spencer EE Jr. Treatment of grade III acromioclavicular joint injuries: a systematic review. Clin Orthop Relat Res. 2007;(455):38-44.

13. Kraeutler MJ, Williams GR Jr, Cohen SB, et al. Inter- and intraobserver reliability of the radiographic diagnosis and treatment of acromioclavicular joint separations. Orthopedics. 2012;35(10):e1483-e1487.

14. Lynch TS, Saltzman MD, Ghodasra JH, Bilimoria KY, Bowen MK, Nuber GW. Acromioclavicular joint injuries in the National Football League: epidemiology and management. Am J Sports Med. 2013;41(12):2904-2908.

15. Orchard JW. Benefits and risks of using local anaesthetic for pain relief to allow early return to play in professional football. Br J Sports Med. 2002;36(3):209-213.

16. Salata MJ, Gibbs AE, Sekiya JK. The effectiveness of prophylactic knee bracing in American football: a systematic review. Sports Health. 2010;2(5):375-379.

17. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee sprains in college football. Effectiveness of preventive braces. Am J Sports Med. 1994;22(1):12-18.

18. Sitler M, Ryan J, Hopkinson W, et al. The efficacy of a prophylactic knee brace to reduce knee injuries in football. A prospective, randomized study at West Point. Am J Sports Med. 1990;18(3):310-315.

19. Parolie JM, Bergfeld JA. Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med. 1986;14(1):35-38.

20. Dennis MG, Fox JA, Alford JW, Hayden JK, Bach BR Jr. Posterior cruciate ligament reconstruction: current trends. J Knee Surg. 2004;17(3):133-139.

21. Purcell DB, Matava MJ, Wright RW. Ulnar collateral ligament reconstruction: a systematic review. Clin Orthop Relat Res. 2007;(455):72-77.

22. Vitale MA, Ahmad CS. The outcome of elbow ulnar collateral ligament reconstruction in overhead athletes: a systematic review. Am J Sports Med. 2008;36(6):1193-1205.

23. Fricker R, Hintermann B. Skier’s thumb. Treatment, prevention and recommendations. Sports Med. 1995;19(1):73-79.

24. Smith RJ. Post-traumatic instability of the metacarpophalangeal joint of the thumb. J Bone Joint Surg Am. 1977;59(1):14-21.

25. Low K, Noblin JD, Browne JE, Barnthouse CD, Scott AR. Jones fractures in the elite football player. J Surg Orthop Adv. 2004;13(3):156-160.

26. Chang WR, Kapasi Z, Daisley S, Leach WJ. Tibial shaft fractures in football players. J Orthop Surg Res. 2007;2:11.

27. Karladani AH, Ericsson PA, Granhed H, Karlsson L, Nyberg P. Tibial intramedullary nails—should they be removed? A retrospective study of 71 patients. Acta Orthop. 2007;78(5):668-671.

28. Eichner ER. Intramuscular ketorolac injections: the pregame Toradol parade. Curr Sports Med Rep. 2012;11(4):169-170.

29. Nepple JJ, Matava MJ. Soft tissue injections in the athlete. Sports Health. 2009;1(5):396-404.

30. Powell ET, Tokish JM, Hawkins RJ. Toradol use in the athletic population. Curr Sports Med Rep. 2002;1(4):191.

31. Matava M, Brater DC, Gritter N, et al. Recommendations of the National Football League physician society task force on the use of toradol® ketorolac in the National Football League. Sports Health. 2012;4(5):377-383.

Issue
The American Journal of Orthopedics - 45(6)
Issue
The American Journal of Orthopedics - 45(6)
Page Number
E319-E327
Page Number
E319-E327
Publications
Publications
Topics
Article Type
Display Headline
Historical Patterns and Variation in Treatment of Injuries in NFL (National Football League) Players and NCAA (National Collegiate Athletic Association) Division I Football Players
Display Headline
Historical Patterns and Variation in Treatment of Injuries in NFL (National Football League) Players and NCAA (National Collegiate Athletic Association) Division I Football Players
Sections
Disallow All Ads
Article PDF Media

Thigh Injuries in American Football

Article Type
Changed
Thu, 09/19/2019 - 13:24
Display Headline
Thigh Injuries in American Football

American football has the highest injury rate of any team sport in the United States at the high school, collegiate, and professional levels.1-3 Muscle strains and contusions constitute a large proportion of football injuries. For example, at the high school level, muscle strains comprise 12% to 24% of all injuries;2 at the collegiate level, they account for approximately 20% of all practice injuries, with nearly half of all strains occurring within the thigh.1,4 Among a single National Football League (NFL) team, Feeley and colleagues5 reported that muscle strains accounted for 46% of practice and 22% of preseason game injuries. The hamstrings, followed by the quadriceps, are the most commonly strained muscle groups among both professional and amateur athletes,5,6 with hamstring and quadriceps injuries making up approximately 13% of all injuries among NFL players.7 Given the relatively large surface area and muscle volume of the anterior and posterior thigh, as well as the activities and maneuvers necessitated by the various football positions, it is not surprising that the thigh is frequently involved in football-related injuries.

The purpose of this review is to describe the clinical manifestations of thigh-related soft-tissue injuries seen in football players. Two of these conditions—muscle strains and contusions—are relatively common, while a third condition—the Morel-Lavallée lesion—is a rare, yet relevant injury that warrants discussion.

Quadriceps Contusion

Pathophysiology

Contusion to the quadriceps muscle is a common injury in contact sports generally resulting from a direct blow from a helmet, knee, or shoulder.8 Bleeding within the musculature causes swelling, pain, stiffness, and limitation of quadriceps excursion, ultimately resulting in loss of knee flexion and an inability to run or squat. The injury is typically confined to a single quadriceps muscle.8 The use of thigh padding, though helpful, does not completely eliminate the risk of this injury.

History and Physical Examination

Immediately after injury, the athlete may complain only of thigh pain. However, swelling, pain, and diminished range of knee motion may develop within the first 24 hours depending on the severity of injury and how quickly treatment is instituted.8 Jackson and Feagin9 developed an injury grading system for quadriceps contusions based on the limitation of knee flexion observed (Table 1).

Fortunately, the majority of contusions in these athletes are of a mild to moderate severity.9,10

Imaging

A quadriceps contusion is a clinical diagnosis based on a typical history and physical examination; therefore, advanced imaging usually does not need to be obtained except to gauge the severity of injury, to rule out concurrent injuries (ie, tendon rupture), and to identify the presence of a hematoma that may necessitate aspiration. Plain radiographs are typically unremarkable in the acute setting. Appearance on magnetic resonance imaging (MRI) varies by injury severity, with increased signal throughout the affected muscle belly and a diffuse, feathery appearance centered at the point of impact on short TI inversion recovery (STIR) and T2-weighted images reflecting edema and possibly hematoma (Figures 1A-1C).8,11

Resolution of these MRI findings may lag behind functional recovery.8 Therefore, the athlete is often able to return to competition once he has recovered full lower extremity motion and function despite the persistence of abnormal findings on MRI.

Treatment

Treatment of a quadriceps contusion is nonoperative and consists of a 3-phase recovery.10 The first phase lasts approximately 2 days and consists of rest, ice, compression, and elevation (RICE) to limit hemorrhage. The knee should be rested in a flexed position to maintain quadriceps muscle fiber length in order to promote muscle compression and limit knee stiffness. For severe contusions in which there is a question of an acute thigh compartment syndrome, compression should be avoided with appropriate treatment based on typical symptoms and intra-compartmental pressure measurement.12 Nonsteroidal anti-inflammatory drugs (NSAIDs) may be administered to diminish pain as well as the risk of myositis ossificans. While there is no data on the efficacy of NSAIDs in preventing myositis ossificans following quadriceps contusions, both COX-2 selective (ie, celecoxib) and nonselective (ie, naproxen, indomethacin) COX inhibitors have been demonstrated to significantly reduce the incidence of heterotopic ossification following hip surgery—a condition occurring from a similar pathophysiologic process as myositis ossificans.13-17 However, this class of drugs should not be given any sooner than 48 to 72 hours after injury to decrease further bleeding risk, given its inhibitory effect on platelet function.18 Narcotic pain medications are rarely required.

The second phase focuses on restoring active and passive knee and hip flexion and begins when permitted by pain.8 Icing, pain control, and physical therapy modalities are also continued in order to reduce pain and swelling as knee motion is progressed. The third phase begins once full range of knee and hip motion is restored and consists of quadriceps strengthening and functional rehabilitation of the lower extremity.8,19 Return to athletic activities and eventually competition should take place when a full, painless range of motion is restored and strength returns to baseline. Isokinetic strength testing may be utilized to more accurately assess strength and endurance. Noncontact, position-specific drills are incorporated as clinical improvement allows. A full recovery should be expected within 4 weeks of injury, with faster resolution and return to play seen in less severe contusions depending on the athlete’s position.8 Continued quadriceps stretching is recommended to prevent recurrence once the athlete returns to play. A protective hard shell may also be utilized both during rehabilitation as well as once the athlete returns to play in order to protect the thigh from reinjury, which may increase the risk of myositis ossificans.8

 

 

Complications

A prolonged recovery or persistent symptoms should alert the treating physician to the possibility of complications, including myositis ossificans.8,20 Myositis ossificans typically results from moderate to severe contusions, which may present initially as a painful, indurated mass that later becomes quite firm. This mass may be seen on plain radiographs as early as 2 to 4 weeks following injury if the athlete complains of persistent pain or a palpable thigh mass (Figure 2).9

The risk of myositis ossificans increases in proportion to the severity of injury.18 Among US military academy members, the incidence of myositis ossificans following quadriceps contusions ranges from 9% to 20%.9,10 These masses often masquerade as a neoplasm that results in an unnecessary biopsy which reveals an “aggressive” lesion leading to an incorrect diagnosis of a soft-tissue sarcoma. MRI and/or computed tomography scanning may confirm the diagnosis of a benign process in these questionable cases as the lesion matures, with ossification demonstrated on both T1- and T2-weight imaging.21 Even in the presence of myositis ossificans, most patients regain full knee and hip motion and return to sports without residual weakness or pain.20 Very rarely, persistent symptoms and limitation of motion may warrant consideration for surgical excision of the symptomatic mass once it is considered mature, which generally occurs within 6 months to 1 year, in order to avoid the risk of recurrence resulting from the surgical trauma.9, 22

Mani-Babu and colleagues23 reported a case of a 14-year-old male football player who sustained a quadriceps contusion after a direct blow from an opponent’s helmet to the lateral thigh. Persistent pain and limitation of motion at 2 months follow-up prompted imaging studies that demonstrated myositis ossificans. The patient was treated with intravenous pamidronate (a bisphosphonate) twice over a 3-month period and demonstrated a full recovery within 5 months.

Acute compartment syndrome of the thigh has also been reported following severe quadriceps contusions, with the majority occurring in the anterior compartment.12,24-28 When injury from blunt trauma extends into and disrupts the muscular layer adjacent to the femur, vascular disruption can cause hematoma formation, muscle edema, and significant swelling, thereby increasing intracompartmental pressure. The relatively large volume of the anterior thigh compartment and lack of a rigid deep fascial envelope may be protective from the development of compartment syndrome compared to other sites.28 It can be difficult to distinguish a severe contusion from a compartment syndrome, as both can occur from the same mechanism and have similar presenting signs and symptoms. Signs of a compartment syndrome include pain out of proportion to the injury that is aggravated by passive stretch of the quadriceps muscles, an increasingly firm muscle compartment to palpation, and neurovascular deficits.29 Both acute compartment syndrome and a severe contusion may present with significant pain, inability to bear weight, tense swelling, tenderness to palpation, and pain with passive knee flexion.24 While the successful conservative treatment of athletes with acute compartment syndrome of the thigh has been reported, it is important to closely monitor the patient’s condition and consider intracompartmental pressure monitoring if the patient’s clinical condition deteriorates.12 An acute fasciotomy should be strongly considered when intracompartmental pressures are within 30 mm Hg of diastolic pressure.24-27 Fortunately, it is highly uncommon for thigh compartment pressure to rise to this level. Percutaneous compartment decompression using liposuction equipment or a large cannula has been described to decrease intracompartmental pressure, potentially expediting recovery and minimizing morbidity.18 Interestingly, reports of fasciotomies for acute thigh compartment syndrome following closed athletic injuries have not described necrotic or non-contractile muscle typical of an acute compartment syndrome, calling into question the need for fasciotomy following closed blunt athletic trauma to the thigh.18

Quadriceps Strain

Pathophysiology

Acute quadriceps strains occur during sudden forceful eccentric contraction of the extensor mechanism. Occasionally, in the absence of a clear mechanism, these injuries mistakenly appear as a contusion resulting from a direct blow to the thigh.30,31 The rectus femoris is the most frequently strained quadriceps muscle due, in part, to its superficial location and predominance of type II muscle fibers, which are more likely to be strained.11,32 Although classically described as occurring along the distal portion of the rectus femoris at the musculotendinous junction, quadriceps strains most commonly occur at the mid to proximal aspect of the rectus femoris.30,33 The quadriceps muscle complex crosses 2 joints and, as a result, is more predisposed to eccentric injury than mono-articular muscles.34 We have had a subset of complete myotendinous tears of the rectus femoris that occur in the plant leg of placekickers that result in significant disability.

 

 

Risk Factors

Quadriceps and thigh injuries comprise approximately 4.5% of injuries among NFL players.7 Several risk factors for quadriceps strains have been described. In a study of Australian Rules football players, Orchard35 demonstrated that for all muscle strains, the strongest risk factor was a recent history of the same injury, with the next strongest risk factor being a past history of the same injury. Increasing age was found to be a risk factor for hamstring strains but not quadriceps strains. Muscle fatigue may also contribute to injury susceptibility.36

History and Physical Examination

Injuries typically occur during kicking, jumping, or a sudden change in direction while running.30 Athletes may localize pain anywhere along the quadriceps muscle, although strains most commonly occur at the proximal to mid portion of the rectus femoris.30,33 The grading system for quadriceps strains described by Kary30 is based on level of pain, quadriceps strength, and the presence or absence of a palpable defect (Table 2).

In high-grade strains, a sharp pain occurs immediately following the injury and often causes variable degrees of functional loss to the quadriceps.30

The athlete typically walks with an antalgic gait. Visible swelling and/or ecchymosis may be present depending on when the athlete is seen, as ecchymosis may develop within the first 24 hours of injury. The examiner should palpate along the entire length of the injured muscle. High-grade strains or complete tears may present with a bulge or defect in the muscle belly, but in most cases no defect will be palpable. There may be loss of knee flexion similar to a quadriceps contusion. Strength testing should be performed in both the sitting and prone position with the hip both flexed and extended to assess resisted knee extension strength.30 Loss of strength is proportional to the degree of injury.

Imaging

While most quadriceps strains are adequately diagnosed clinically without the need for imaging studies, ultrasound or MRI can be used to evaluate for partial or complete rupture.30,33 In milder cases, MRI usually demonstrates interstitial edema and hemorrhage with a feathery appearance on STIR and T2-weighted imaging (Figures 3A-3C).11

Myotendinous strains can be classified based on the extent of fiber disruption.11,32 Cross and colleagues33 demonstrated that strains of the central tendon of the rectus femoris seen on MRI correlated with a significantly longer rehabilitation period than those occurring at the periphery of the rectus or within other quadriceps muscles.
Ultrasound is a more economical imaging modality that can dynamically assess the quadriceps musculature for fiber disruption and hematoma formation but is user-dependent, requiring a skilled technician (Figures 4A, 4B).30

Treatment

Acute treatment of quadriceps strains focuses on minimizing bleeding using the principles of RICE treatment.37 NSAIDs may be used immediately to assist with pain control.30 COX-2-specific NSAIDs are preferred due to their lack of any inhibitory effect on platelet function in order to reduce the risk of further bleeding within the muscle compartment. For the first 24 to 72 hours following injury, the quadriceps should be maintained relatively immobilized to prevent further injury.38 High-grade injuries might necessitate crutches for ambulatory assistance.

Depending on injury severity, the active phase of treatment usually begins within 5 days of injury and consists of stretching and knee/hip range of motion. An active warm-up should precede rehabilitation exercises to activate neural pathways within the muscle and improve muscle elasticity.38 Ballistic stretching should be avoided to prevent additional injury to the muscle fibers. Strengthening should proceed when the athlete recovers a pain-free range of motion. When isometric exercises can be completed at increasing degrees of knee flexion, isotonic exercises may be implemented into the rehabilitation program.30 Return to football can be considered when the athlete has recovered knee and hip range of motion, is pain-free, and has near-normal strength compared to the contralateral side. The athlete should also perform satisfactorily in simulated position-specific activities in a noncontact fashion prior to return to full competition.30

Hamstring Strain

Pathophysiology

Hamstring strains are the most common noncontact injuries in football resulting from excessive muscle stretching during eccentric contraction generally occurring at the musculotendinous junction.5,39 Because the hamstrings cross both the hip and knee, simultaneous hip flexion and knee extension results in maximal lengthening, making them most vulnerable to injury at the terminal swing phase of gait just prior to heel strike.39-42 The long head of the biceps femoris undergoes the greatest stretch, reaching 110% of resting length during terminal swing phase and is the most commonly injured hamstring muscle.43,44 Injury occurs when the force of eccentric contraction, and resulting muscle strain, exceeds the mechanical limits of the tissue.42,45 It remains to be shown whether hamstring strains occur as a result of accumulated microscopic muscle damage or secondary to a single event that exceeds the mechanical limits of the muscle.42

 

 

Epidemiology and Risk Factors

The majority of hamstring strains are sustained during noncontact activities, with most athletes citing sprinting as the activity at the time of injury.3 Approximately 93% of injuries occur during noncontact activities among defensive backs and wide receivers.3 Hamstring strains are the second-most common injury among NFL players, comprising approximately 9% of all injuries,5,7 with 16% to 31% of these injuries associated with recurrence.3,5,35,46 Using the NFL’s Injury Surveillance System, Elliott and colleagues3 reported 1716 hamstring strains over a 10-year period (1989-1998). Fifty-one percent of hamstring strains occurred during the 7-week preseason, with a greater than 4-fold increased injury rate noted during the preseason compared to the 16-week regular season. An increased incidence in the preseason is partially attributable to relative deconditioning over the offseason. Defensive backs, wide receivers, and special teams players accounted for the majority of injured players, suggesting that speed position players and those who must “backpedal” (run backwards) are at an increased risk for injury.

Several risk factors for hamstring strain have been described, including prior injury, older age, quadriceps-hamstring strength imbalances, limited hip and knee flexibility, and fatigue.39,42,47 Inadequate rehabilitation and premature return to competition are also likely important factors predisposing to recurrent injury.39,48

History and Physical Examination

The majority of hamstring strains occur in the acute setting when the player experiences the sudden onset of pain in the posterior thigh during strenuous exercise, most commonly while sprinting.39 The injury typically occurs in the early or late stage of practice or competition due, in part, to inadequate warm-up or fatigue. The athlete may describe an audible pop and an inability to continue play, depending on injury severity.

Physical examination may demonstrate palpable induration and tenderness immediately or shortly after injury. In the setting of severe strains, there can be significant thigh swelling and ecchymosis, and in complete ruptures, a palpable defect.39 The affected muscle should be palpated along its entire length, and is best performed prone with the knee flexed to 90° as well as with the knee partially extended to place it under mild tension. Injury severity can be assessed by determining the restriction of passive knee extension while the athlete is lying supine with the hip flexed to 90°. The severity of hamstring strains varies from minor damage of a few myofibers without loss of structural integrity to complete muscle rupture.

Hamstring strains are classified into 3 groups based on the amount of myotendinous disruption (Table 3).49

Imaging

Similar to other muscle strains, hamstring strains are a clinical diagnosis and generally do not necessitate advanced imaging studies except to assess the degree of damage (ie, partial vs complete rupture) and to rule out other injuries, especially if the athlete fails to respond to treatment. Plain radiographs in acute cases are usually unremarkable. However, more severe injuries may go on to develop myositis ossificans similar to quadriceps soft tissue injuries (Figure 5).

The MRI appearance of hamstring strains shows increased signal within and surrounding the affected muscle belly on T2-weighted imaging as well as the degree of muscle fiber disruption (Figures 6A, 6B).
MRI can also be beneficial to confirm the diagnosis of myositis ossificans in chronic cases with a palpable mass.

Treatment

Most hamstring strains respond to conservative treatment, with operative intervention rarely indicated except for proximal or distal tendon avulsions.39 Like other muscle strains, initial management consists of RICE. COX-2-selective NSAIDs are preferred initially following injury. During a brief period of immobilization, the leg should be extended as much as tolerated to maximize muscle length, limit hematoma formation, and reduce the risk of contracture.39 Controlled mobilization should begin as soon as tolerated by the athlete.39 Isometric exercises and a stretching program should be started early in the rehabilitation period, with isotonic exercises added as motion and pain improve. Active stretching should be initiated and progressed to passive, static stretching as guided by pain.

The late phase of rehabilitation and long-term conditioning protocols should incorporate eccentric training once the athlete is pain-free, performing isotonic and isokinetic exercises. Eccentric exercises best strengthen the hamstrings at their most susceptible point, prepares the athlete for functional activities, and minimizes the risk of reinjury,3,50,51 Elliot and colleagues3 reported an order of magnitude decrease in hamstring injuries in high-risk athletes with identifiable hamstring muscle weakness after implementing an eccentric strengthening program and progressive sprint training. Similarly, in a large cohort of elite soccer players, correction of strength deficits in players with prior hamstring injuries led to similar rates of injury compared to athletes without strength deficits or prior injury.52 Those athletes with persistent weakness who did not undergo rehabilitation had significantly higher rates of reinjury.

Various injections containing local anesthetics, corticosteroids, platelet-rich plasma (PRP), and other substances have been administered to football players following acute muscle strains in an effort to alleviate pain and safely return the athlete to competition. Some practitioners have been reluctant to administer injections (especially those containing corticosteroids) due to a potentially increased risk of tendinopathy or rupture.31 Drakos and colleagues53 reported their outcomes following muscle and ligament strains treated with combined corticosteroid and local anesthetic injections on one NFL team. While quadriceps and hamstring strains were associated with the most missed games among all muscle strains, these injections resulted in no adverse events or progression of injury severity. Similarly, Levine and colleagues 51 administered intramuscular corticosteroid injections to 58 NFL players with high-grade hamstring injuries that had a palpable defect within the muscle belly. They reported no complications or strength deficits at final examination. In a case-control study, Rettig and colleagues46 administered PRP injections under ultrasound guidance in 5 NFL players with hamstring injuries. Compared to players treated with a focused rehabilitation program only, there were no significant differences in recovery or return to play.

The decision to return to play should be based on a clinical assessment considering pain, strength, motion, and flexibility. Player position should also be considered. Return-to-play guidelines describing the appropriate progression through rehabilitation and return to sport have been described and can be used as a template for the rehabilitation of football players.54 It should be noted that primary hamstring strains are associated with decreased athletic performance and an increased risk of more severe reinjury after return to sport.55,56

 

 

Morel-Lavallée Lesion

Pathophysiology

Morel-Lavallée lesions (MLLs) are uncommon football injuries, but often occur in the thigh.57,58 An MLL is a posttraumatic soft tissue injury in which deforming forces of pressure and shear cause a closed, soft tissue degloving injury; in this injury, the skin and subcutaneous tissues are separated from the underlying fascia, disrupting perforating blood vessels. The resulting space between the fascia and subcutaneous tissue fills with blood, lymphatics, and necrotic fat, resulting in a hematoma/seroma that can be a nidus for bacterial infection.58 The most common anatomic regions are the anterior distal thigh and lateral hip. Both of these areas are commonly involved in both direct contact and shear forces following a fall to the ground.

History and Physical Examination

Athletes with MLLs typically present with the insidious onset of a fluid collection within the thigh following a fall to the ground, usually while sliding or diving on the playing surface.57,58 The fluid collection can be associated with thigh tightness and may extend distally into the suprapatellar region or proximally over the greater trochanter. Thigh swelling, ecchymosis, and palpable fluctuance are seen in most cases. Progressive increases in pain and thigh swelling may be seen in severe injuries, but thigh compartments generally remain soft and nontender. Signs and symptoms of an MLL do not typically manifest immediately following the athletic event. Tejwani and colleagues58 reported a case series of MLLs of the knee in 27 NFL players from a single team over a 14-year period, with an average of 3 days between injury and evaluation by the medical staff. The mechanism of injury was a shearing blow from the knee striking the playing surface in 81% of cases and direct contact to the knee from another player in 19% of cases; all cases occurred in game situations. No affected players were wearing kneepads at the time of injury.

Imaging

Plain radiography may reveal a noncalcified soft tissue mass over the involved area and is not usually helpful except to rule out an underlying fracture. The appearance of an MLL on ultrasound is nonspecific and variable, often described as anechoic, hypoechoic, or hyperechoic depending on the presence of hemolymphatic fluid sedimentation and varying amounts of internal fat debris. MRI is the imaging modality of choice and typically shows a well-defined oval or fusiform, fluid-filled mass with tapering margins blending with adjacent fascial planes.

These lesions may show fluid-fluid levels, septations, and variable internal signal intensity depending on the acuity of the lesion (Figures 7A-7C).59

Treatment

Similar to quadriceps contusions, treatment goals for MLLs are evacuation of the fluid collection, prevention of fluid recurrence, a full range of active knee flexion, and prompt return to play.57,58 Initial treatment for smaller lesions consists of cryotherapy, compression wrapping of the involved area, and immediate active and passive range of motion of the hip and knee. While MLLs were traditionally treated with serial open debridements, less invasive approaches—including elastic compression, aspiration, percutaneous irrigation with debridement and suction drainage, or liposuction and drainage followed by suction therapy—have been recently described.57,58,60,61 Less invasive approaches aim to minimize soft tissue dissection and disruption of the vascular supply while accelerating rehabilitation. The presence of a surrounding capsule on MRI makes conservative or minimally invasive approaches less likely to be successful and may necessitate an open procedure.62 Antibiotics should be used preoperatively due to the presence of a dead space containing necrotic debris that makes infection a potential complication. While elite contact athletes can expect to return to competition long before complete resolution of an MLL, there is a risk of further delamination and lesion expansion due to re-injury prior to compete healing.

Tejwani and colleagues58 performed aspiration at the area of palpable fluctuance in the thigh or suprapatellar region using a 14-gauge needle in those athletes who failed to improve with conservative treatments alone. Mean time to resolution of the fluid collection was 16 days following aspiration. Fifty-two percent of the athletes were successfully treated with cryotherapy, compression, and motion exercises alone; 48% were treated with at least one aspiration, with a mean of 2.7 aspirations per knee. In 11% of cases that failed to resolve after multiple aspirations, doxycycline sclerodesis was performed immediately following an aspiration. Patients treated with sclerodesis had no return of the fluid collection and returned to play the following day.

Matava and colleagues57 described the case of an NFL player who sustained a closed MLL of the lateral hip while diving onto an artificial turf surface attempting to catch a pass. Despite immediate thigh pain and swelling, he was able to continue play. Immediately following the game, the player was examined and had a tense thigh with ecchymosis extending into the trochanteric region. Aspiration of the fluctuant area was unsuccessful. Progressive increases in pain and thigh swelling prompted hospital admission. Percutaneous irrigation and debridement was performed as described by Tseng and Tornetta.61 A suction drain was placed within the residual dead space, and constant wall suction was applied in addition to hip compression using a spica wrap. The player returned to practice 22 days after the injury and missed a total of 3 games without any residual deficit.

 

 

Conclusion

Quadriceps and hamstring injuries occur frequently in football and are generally treated conservatively. While return to competition following hamstring strains is relatively quick, a high rate of injury recurrence highlights the importance of targeted rehabilitation and conditioning. Rarely, complications from quadriceps contusions, including acute compartment syndrome and myositis ossificans, may require operative intervention if unresponsive to conservative treatment. MLLs are rare in sports, but usually involve the thigh when they occur in football players. Team physicians must maintain a heightened degree of awareness of this injury as it may require operative intervention.

 

Acknowledgements: The authors would like to thank Jonathon Baker, MD and David Rubin, MD for their assistance in providing radiographic images for this paper.


Am J Orthop. 2016;45(6):E308-E318. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train. 2007;42(2):311-319.

2. Rechel JA, Yard EE, Comstock RD. An epidemiologic comparison of high school sports injuries sustained in practice and competition. J Athl Train. 2008;43(2):197-204.

3. Elliott MC, Zarins B, Powell JW, Kenyon CD. Hamstring muscle strains in professional football players: a 10-year review. Am J Sports Med. 2011;39(4):843-850.

4. Dick R, Ferrara MS, Agel J, et al. Descriptive epidemiology of collegiate men’s football injuries: National Collegiate Athletic Association Injury Surveillance System, 1988-1989 through 2003-2004. J Athl Train. 2007;42(2):221-233.

5. Feeley BT, Kennelly S, Barnes RP, et al. Epidemiology of National Football League training camp injuries from 1998 to 2007. Am J Sports Med. 2008;36(8):1597-1603.

6. Garrett WE Jr. Muscle strain injuries. Am J Sports Med. 1996;24(6 Suppl):S2-S8.

7. Lawrence DW, Hutchison MG, Comper P. Descriptive epidemiology of musculoskeletal injuries and concussions in the National Football League, 2012-2014. Orthop J Sports Med. 2015;3(5):2325967115583653.

8. Diaz JA, Fischer DA, Rettig AC, Davis TJ, Shelbourne KD. Severe quadriceps muscle contusions in athletes. A report of three cases. Am J Sports Med. 2003;31(2):289-293.

9. Jackson DW, Feagin JA. Quadriceps contusions in young athletes. Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am. 1973;55(1):95-105.

10. Ryan JB, Wheeler JH, Hopkinson WJ, Arciero RA, Kolakowski KR. Quadriceps contusions. West Point update. Am J Sports Med. 1991;19(3):299-304.

11. Bencardino JT, Rosenberg ZS, Brown RR, Hassankhani A, Lustrin ES, Beltran J. Traumatic musculotendinous injuries of the knee: diagnosis with MR imaging. Radiographics. 2000;20 Spec No:S103-S120.

12. Robinson D, On E, Halperin N. Anterior compartment syndrome of the thigh in athletes--indications for conservative treatment. J Trauma. 1992;32(2):183-186.

13. Beckmann JT, Wylie JD, Kapron AL, Hanson JA, Maak TG, Aoki SK. The effect of NSAID prophylaxis and operative variables on heterotopic ossification after hip arthroscopy. Am J Sports Med. 2014;42(6):1359-1364.

14. Shehab D, Elgazzar AH, Collier BD. Heterotopic ossification. J Nucl Med. 2002;43(3):346-353.

15. Beckmann JT, Wylie JD, Potter MQ, Maak TG, Greene TH, Aoki SK. Effect of naproxen prophylaxis on heterotopic ossification following hip arthroscopy: a double-blind randomized placebo-controlled trial. J Bone Joint Surg Am. 2015;97(24):2032-2037.

16. Yeung M, Jamshidi S, Horner N, Simunovic N, Karlsson J, Ayeni OR. Efficacy of nonsteroidal anti-inflammatory drug prophylaxis for heterotrophic ossification in hip arthroscopy: a systematic review. Arthroscopy. 2016;32(3):519-525.

17. Goyal K, Pettis CR, Bancroft AE, Wasyliw CW, Scherer KF. Myositis ossificans in the thigh of a lacrosse player. Orthopedics. 2015;38(8):468,515-518.

18. Cooper DE. Severe quadriceps muscle contusions in athletes. Am J Sports Med. 2004;32(3):820.

19. Bonsell S, Freudigman PT, Moore HA. Quadriceps muscle contusion resulting in osteomyelitis of the femur in a high school football player. A case report. Am J Sports Med. 2001;29(6):818-820.

20. Rothwell AG. Quadriceps hematoma. A prospective clinical study. Clin Orthop Relat Res. 1982;(171):97-103.

21. Armfield DR, Kim DH, Towers JD, Bradley JP, Robertson DD. Sports-related muscle injury in the lower extremity. Clin Sports Med. 2006;25(4):803-842.

22. Lipscomb AB, Thomas ED, Johnston RK. Treatment of myositis ossificans traumatica in athletes. Am J Sports Med. 1976;4(3):111-120.

23. Mani-Babu S, Wolman R, Keen R. Quadriceps traumatic myositis ossificans in a football player: management with intravenous pamidronate. Clin J Sport Med. 2014;24(5):e56-e58.

24. McCaffrey DD, Clarke J, Bunn J, McCormack MJ. Acute compartment syndrome of the anterior thigh in the absence of fracture secondary to sporting trauma. J Trauma. 2009;66(4):1238-1242.

25. Klasson SC, Vander Schilden JL. Acute anterior thigh compartment syndrome complicating quadriceps hematoma. Two case reports and review of the literature. Orthop Rev. 1990;19(5):421-427.

26. Rooser B. Quadriceps contusion with compartment syndrome. Evacuation of hematoma in 2 cases. Acta Orthop Scand. 1987;58(2):170-172.

27. Rooser B, Bengtson S, Hagglund G. Acute compartment syndrome from anterior thigh muscle contusion: a report of eight cases. J Orthop Trauma. 1991;5(1):57-59.

28. Schwartz JT Jr, Brumback RJ, Lakatos R, Poka A, Bathon GH, Burgess AR. Acute compartment syndrome of the thigh. A spectrum of injury. J Bone Joint Surg Am. 1989;71(3):392-400.

29. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg Br. 2003;85(5):625-632.

30. Kary JM. Diagnosis and management of quadriceps strains and contusions. Curr Rev Musculoskelet Med. 2010;3(1-4):26-31.

31. Boublik M, Schlegel TF, Koonce RC, Genuario JW, Kinkartz JD. Quadriceps tendon injuries in national football league players. Am J Sports Med. 2013;41(8):1841-1846.

32. Palmer WE, Kuong SJ, Elmadbouh HM. MR imaging of myotendinous strain. AJR Am J Roentgenol. 1999;173(3):703-709.

33. Cross TM, Gibbs N, Houang MT, Cameron M. Acute quadriceps muscle strains: magnetic resonance imaging features and prognosis. Am J Sports Med. 2004;32(3):710-719.

34. Hughes C 4th, Hasselman CT, Best TM, Martinez S, Garrett WE Jr. Incomplete, intrasubstance strain injuries of the rectus femoris muscle. Am J Sports Med. 1995;23(4):500-506.

35. Orchard JW. Intrinsic and extrinsic risk factors for muscle strains in Australian football. Am J Sports Med. 2001;29(3):300-303.36. Mair SD, Seaber AV, Glisson RR, Garrett WE, Jr. The role of fatigue in susceptibility to acute muscle strain injury. Am J Sports Med. 1996;24(2):137-143.

37. Bleakley C, McDonough S, MacAuley D. The use of ice in the treatment of acute soft-tissue injury: a systematic review of randomized controlled trials. Am J Sports Med. 2004;32(1):251-261.

38. Jarvinen TA, Jarvinen TL, Kaariainen M, Kalimo H, Jarvinen M. Muscle injuries: biology and treatment. Am J Sports Med. 2005;33(5):745-764.

39. Clanton TO, Coupe KJ. Hamstring strains in athletes: diagnosis and treatment. J Am Acad Orthop Surg. 1998;6(4):237-248.

40. Novacheck TF. The biomechanics of running. Gait Posture. 1998;7(1):77-95.

41. Yu B, Queen RM, Abbey AN, Liu Y, Moorman CT, Garrett WE. Hamstring muscle kinematics and activation during overground sprinting. J Biomech. 2008;41(15):3121-3126.

42. Opar DA, Williams MD, Shield AJ. Hamstring strain injuries: factors that lead to injury and re-injury. Sports Med. 2012;42(3):209-226.

43. Askling CM, Tengvar M, Saartok T, Thorstensson A. Acute first-time hamstring strains during high-speed running: a longitudinal study including clinical and magnetic resonance imaging findings. Am J Sports Med. 2007;35(2):197-206.

44. Thelen DG, Chumanov ES, Hoerth DM, et al. Hamstring muscle kinematics during treadmill sprinting. Med Sci Sports Exerc. 2005;37(1):108-114.

45. Chumanov ES, Heiderscheit BC, Thelen DG. The effect of speed and influence of individual muscles on hamstring mechanics during the swing phase of sprinting. J Biomech. 2007;40(16):3555-3562.

46. Rettig AC, Meyer S, Bhadra AK. Platelet-rich plasma in addition to rehabilitation for acute hamstring injuries in NFL players: clinical effects and time to return to play. Orthop J Sports Med. 2013;1(1):2325967113494354.

47. Zvijac JE, Toriscelli TA, Merrick S, Kiebzak GM. Isokinetic concentric quadriceps and hamstring strength variables from the NFL Scouting Combine are not predictive of hamstring injury in first-year professional football players. Am J Sports Med. 2013;41(7):1511-1518.

48. Arnason A, Sigurdsson SB, Gudmundsson A, Holme I, Engebretsen L, Bahr R. Risk factors for injuries in football. Am J Sports Med. 2004;32(1 Suppl):5S-16S.

49. Zarins B, Ciullo JV. Acute muscle and tendon injuries in athletes. Clin Sports Med. 1983;2(1):167-182.

50. Arnason A, Andersen TE, Holme I, Engebretsen L, Bahr R. Prevention of hamstring strains in elite soccer: an intervention study. Scand J Med Sci Sports. 2008;18(1):40-48.

51. Levine WN, Bergfeld JA, Tessendorf W, Moorman CT 3rd. Intramuscular corticosteroid injection for hamstring injuries. A 13-year experience in the National Football League. Am J Sports Med. 2000;28(3):297-300.

52. Croisier JL, Ganteaume S, Binet J, Genty M, Ferret JM. Strength imbalances and prevention of hamstring injury in professional soccer players: a prospective study. Am J Sports Med. 2008;36(8):1469-1475.

53. Drakos M, Birmingham P, Delos D, et al. Corticosteroid and anesthetic injections for muscle strains and ligament sprains in the NFL. HSS J. 2014;10(2):136-142.

54. Worrell TW. Factors associated with hamstring injuries. An approach to treatment and preventative measures. Sports Med. 1994;17(5):338-345.

55. Brooks JH, Fuller CW, Kemp SP, Reddin DB. Incidence, risk, and prevention of hamstring muscle injuries in professional rugby union. Am J Sports Med. 2006;34(8):1297-1306.

56. Verrall GM, Kalairajah Y, Slavotinek JP, Spriggins AJ. Assessment of player performance following return to sport after hamstring muscle strain injury. J Sci Med Sport. 2006;9(1-2):87-90.

57. Matava MJ, Ellis E, Shah NR, Pogue D, Williams T. Morel-lavallee lesion in a professional american football player. Am J Orthop. 2010;39(3):144-147.

58. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the national football league. Am J Sports Med. 2007;35(7):1162-1167.

59. Mellado JM, Bencardino JT. Morel-Lavallee lesion: review with emphasis on MR imaging. Magn Reson Imaging Clin N Am. 2005;13(4):775-782.

60. Harma A, Inan M, Ertem K. [The Morel-Lavallee lesion: a conservative approach to closed degloving injuries]. Acta Orthop Traumatol Turc. 2004;38(4):270-273.

61. Tseng S, Tornetta P 3rd. Percutaneous management of Morel-Lavallee lesions. J Bone Joint Surg Am. 2006;88(1):92-96.

62. Gilbert BC, Bui-Mansfield LT, Dejong S. MRI of a Morel-Lavellee lesion. AJR Am J Roentgenol. 2004;182(5):1347-1348.

Article PDF
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Issue
The American Journal of Orthopedics - 45(6)
Publications
Topics
Page Number
E308-E318
Sections
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Article PDF
Article PDF

American football has the highest injury rate of any team sport in the United States at the high school, collegiate, and professional levels.1-3 Muscle strains and contusions constitute a large proportion of football injuries. For example, at the high school level, muscle strains comprise 12% to 24% of all injuries;2 at the collegiate level, they account for approximately 20% of all practice injuries, with nearly half of all strains occurring within the thigh.1,4 Among a single National Football League (NFL) team, Feeley and colleagues5 reported that muscle strains accounted for 46% of practice and 22% of preseason game injuries. The hamstrings, followed by the quadriceps, are the most commonly strained muscle groups among both professional and amateur athletes,5,6 with hamstring and quadriceps injuries making up approximately 13% of all injuries among NFL players.7 Given the relatively large surface area and muscle volume of the anterior and posterior thigh, as well as the activities and maneuvers necessitated by the various football positions, it is not surprising that the thigh is frequently involved in football-related injuries.

The purpose of this review is to describe the clinical manifestations of thigh-related soft-tissue injuries seen in football players. Two of these conditions—muscle strains and contusions—are relatively common, while a third condition—the Morel-Lavallée lesion—is a rare, yet relevant injury that warrants discussion.

Quadriceps Contusion

Pathophysiology

Contusion to the quadriceps muscle is a common injury in contact sports generally resulting from a direct blow from a helmet, knee, or shoulder.8 Bleeding within the musculature causes swelling, pain, stiffness, and limitation of quadriceps excursion, ultimately resulting in loss of knee flexion and an inability to run or squat. The injury is typically confined to a single quadriceps muscle.8 The use of thigh padding, though helpful, does not completely eliminate the risk of this injury.

History and Physical Examination

Immediately after injury, the athlete may complain only of thigh pain. However, swelling, pain, and diminished range of knee motion may develop within the first 24 hours depending on the severity of injury and how quickly treatment is instituted.8 Jackson and Feagin9 developed an injury grading system for quadriceps contusions based on the limitation of knee flexion observed (Table 1).

Fortunately, the majority of contusions in these athletes are of a mild to moderate severity.9,10

Imaging

A quadriceps contusion is a clinical diagnosis based on a typical history and physical examination; therefore, advanced imaging usually does not need to be obtained except to gauge the severity of injury, to rule out concurrent injuries (ie, tendon rupture), and to identify the presence of a hematoma that may necessitate aspiration. Plain radiographs are typically unremarkable in the acute setting. Appearance on magnetic resonance imaging (MRI) varies by injury severity, with increased signal throughout the affected muscle belly and a diffuse, feathery appearance centered at the point of impact on short TI inversion recovery (STIR) and T2-weighted images reflecting edema and possibly hematoma (Figures 1A-1C).8,11

Resolution of these MRI findings may lag behind functional recovery.8 Therefore, the athlete is often able to return to competition once he has recovered full lower extremity motion and function despite the persistence of abnormal findings on MRI.

Treatment

Treatment of a quadriceps contusion is nonoperative and consists of a 3-phase recovery.10 The first phase lasts approximately 2 days and consists of rest, ice, compression, and elevation (RICE) to limit hemorrhage. The knee should be rested in a flexed position to maintain quadriceps muscle fiber length in order to promote muscle compression and limit knee stiffness. For severe contusions in which there is a question of an acute thigh compartment syndrome, compression should be avoided with appropriate treatment based on typical symptoms and intra-compartmental pressure measurement.12 Nonsteroidal anti-inflammatory drugs (NSAIDs) may be administered to diminish pain as well as the risk of myositis ossificans. While there is no data on the efficacy of NSAIDs in preventing myositis ossificans following quadriceps contusions, both COX-2 selective (ie, celecoxib) and nonselective (ie, naproxen, indomethacin) COX inhibitors have been demonstrated to significantly reduce the incidence of heterotopic ossification following hip surgery—a condition occurring from a similar pathophysiologic process as myositis ossificans.13-17 However, this class of drugs should not be given any sooner than 48 to 72 hours after injury to decrease further bleeding risk, given its inhibitory effect on platelet function.18 Narcotic pain medications are rarely required.

The second phase focuses on restoring active and passive knee and hip flexion and begins when permitted by pain.8 Icing, pain control, and physical therapy modalities are also continued in order to reduce pain and swelling as knee motion is progressed. The third phase begins once full range of knee and hip motion is restored and consists of quadriceps strengthening and functional rehabilitation of the lower extremity.8,19 Return to athletic activities and eventually competition should take place when a full, painless range of motion is restored and strength returns to baseline. Isokinetic strength testing may be utilized to more accurately assess strength and endurance. Noncontact, position-specific drills are incorporated as clinical improvement allows. A full recovery should be expected within 4 weeks of injury, with faster resolution and return to play seen in less severe contusions depending on the athlete’s position.8 Continued quadriceps stretching is recommended to prevent recurrence once the athlete returns to play. A protective hard shell may also be utilized both during rehabilitation as well as once the athlete returns to play in order to protect the thigh from reinjury, which may increase the risk of myositis ossificans.8

 

 

Complications

A prolonged recovery or persistent symptoms should alert the treating physician to the possibility of complications, including myositis ossificans.8,20 Myositis ossificans typically results from moderate to severe contusions, which may present initially as a painful, indurated mass that later becomes quite firm. This mass may be seen on plain radiographs as early as 2 to 4 weeks following injury if the athlete complains of persistent pain or a palpable thigh mass (Figure 2).9

The risk of myositis ossificans increases in proportion to the severity of injury.18 Among US military academy members, the incidence of myositis ossificans following quadriceps contusions ranges from 9% to 20%.9,10 These masses often masquerade as a neoplasm that results in an unnecessary biopsy which reveals an “aggressive” lesion leading to an incorrect diagnosis of a soft-tissue sarcoma. MRI and/or computed tomography scanning may confirm the diagnosis of a benign process in these questionable cases as the lesion matures, with ossification demonstrated on both T1- and T2-weight imaging.21 Even in the presence of myositis ossificans, most patients regain full knee and hip motion and return to sports without residual weakness or pain.20 Very rarely, persistent symptoms and limitation of motion may warrant consideration for surgical excision of the symptomatic mass once it is considered mature, which generally occurs within 6 months to 1 year, in order to avoid the risk of recurrence resulting from the surgical trauma.9, 22

Mani-Babu and colleagues23 reported a case of a 14-year-old male football player who sustained a quadriceps contusion after a direct blow from an opponent’s helmet to the lateral thigh. Persistent pain and limitation of motion at 2 months follow-up prompted imaging studies that demonstrated myositis ossificans. The patient was treated with intravenous pamidronate (a bisphosphonate) twice over a 3-month period and demonstrated a full recovery within 5 months.

Acute compartment syndrome of the thigh has also been reported following severe quadriceps contusions, with the majority occurring in the anterior compartment.12,24-28 When injury from blunt trauma extends into and disrupts the muscular layer adjacent to the femur, vascular disruption can cause hematoma formation, muscle edema, and significant swelling, thereby increasing intracompartmental pressure. The relatively large volume of the anterior thigh compartment and lack of a rigid deep fascial envelope may be protective from the development of compartment syndrome compared to other sites.28 It can be difficult to distinguish a severe contusion from a compartment syndrome, as both can occur from the same mechanism and have similar presenting signs and symptoms. Signs of a compartment syndrome include pain out of proportion to the injury that is aggravated by passive stretch of the quadriceps muscles, an increasingly firm muscle compartment to palpation, and neurovascular deficits.29 Both acute compartment syndrome and a severe contusion may present with significant pain, inability to bear weight, tense swelling, tenderness to palpation, and pain with passive knee flexion.24 While the successful conservative treatment of athletes with acute compartment syndrome of the thigh has been reported, it is important to closely monitor the patient’s condition and consider intracompartmental pressure monitoring if the patient’s clinical condition deteriorates.12 An acute fasciotomy should be strongly considered when intracompartmental pressures are within 30 mm Hg of diastolic pressure.24-27 Fortunately, it is highly uncommon for thigh compartment pressure to rise to this level. Percutaneous compartment decompression using liposuction equipment or a large cannula has been described to decrease intracompartmental pressure, potentially expediting recovery and minimizing morbidity.18 Interestingly, reports of fasciotomies for acute thigh compartment syndrome following closed athletic injuries have not described necrotic or non-contractile muscle typical of an acute compartment syndrome, calling into question the need for fasciotomy following closed blunt athletic trauma to the thigh.18

Quadriceps Strain

Pathophysiology

Acute quadriceps strains occur during sudden forceful eccentric contraction of the extensor mechanism. Occasionally, in the absence of a clear mechanism, these injuries mistakenly appear as a contusion resulting from a direct blow to the thigh.30,31 The rectus femoris is the most frequently strained quadriceps muscle due, in part, to its superficial location and predominance of type II muscle fibers, which are more likely to be strained.11,32 Although classically described as occurring along the distal portion of the rectus femoris at the musculotendinous junction, quadriceps strains most commonly occur at the mid to proximal aspect of the rectus femoris.30,33 The quadriceps muscle complex crosses 2 joints and, as a result, is more predisposed to eccentric injury than mono-articular muscles.34 We have had a subset of complete myotendinous tears of the rectus femoris that occur in the plant leg of placekickers that result in significant disability.

 

 

Risk Factors

Quadriceps and thigh injuries comprise approximately 4.5% of injuries among NFL players.7 Several risk factors for quadriceps strains have been described. In a study of Australian Rules football players, Orchard35 demonstrated that for all muscle strains, the strongest risk factor was a recent history of the same injury, with the next strongest risk factor being a past history of the same injury. Increasing age was found to be a risk factor for hamstring strains but not quadriceps strains. Muscle fatigue may also contribute to injury susceptibility.36

History and Physical Examination

Injuries typically occur during kicking, jumping, or a sudden change in direction while running.30 Athletes may localize pain anywhere along the quadriceps muscle, although strains most commonly occur at the proximal to mid portion of the rectus femoris.30,33 The grading system for quadriceps strains described by Kary30 is based on level of pain, quadriceps strength, and the presence or absence of a palpable defect (Table 2).

In high-grade strains, a sharp pain occurs immediately following the injury and often causes variable degrees of functional loss to the quadriceps.30

The athlete typically walks with an antalgic gait. Visible swelling and/or ecchymosis may be present depending on when the athlete is seen, as ecchymosis may develop within the first 24 hours of injury. The examiner should palpate along the entire length of the injured muscle. High-grade strains or complete tears may present with a bulge or defect in the muscle belly, but in most cases no defect will be palpable. There may be loss of knee flexion similar to a quadriceps contusion. Strength testing should be performed in both the sitting and prone position with the hip both flexed and extended to assess resisted knee extension strength.30 Loss of strength is proportional to the degree of injury.

Imaging

While most quadriceps strains are adequately diagnosed clinically without the need for imaging studies, ultrasound or MRI can be used to evaluate for partial or complete rupture.30,33 In milder cases, MRI usually demonstrates interstitial edema and hemorrhage with a feathery appearance on STIR and T2-weighted imaging (Figures 3A-3C).11

Myotendinous strains can be classified based on the extent of fiber disruption.11,32 Cross and colleagues33 demonstrated that strains of the central tendon of the rectus femoris seen on MRI correlated with a significantly longer rehabilitation period than those occurring at the periphery of the rectus or within other quadriceps muscles.
Ultrasound is a more economical imaging modality that can dynamically assess the quadriceps musculature for fiber disruption and hematoma formation but is user-dependent, requiring a skilled technician (Figures 4A, 4B).30

Treatment

Acute treatment of quadriceps strains focuses on minimizing bleeding using the principles of RICE treatment.37 NSAIDs may be used immediately to assist with pain control.30 COX-2-specific NSAIDs are preferred due to their lack of any inhibitory effect on platelet function in order to reduce the risk of further bleeding within the muscle compartment. For the first 24 to 72 hours following injury, the quadriceps should be maintained relatively immobilized to prevent further injury.38 High-grade injuries might necessitate crutches for ambulatory assistance.

Depending on injury severity, the active phase of treatment usually begins within 5 days of injury and consists of stretching and knee/hip range of motion. An active warm-up should precede rehabilitation exercises to activate neural pathways within the muscle and improve muscle elasticity.38 Ballistic stretching should be avoided to prevent additional injury to the muscle fibers. Strengthening should proceed when the athlete recovers a pain-free range of motion. When isometric exercises can be completed at increasing degrees of knee flexion, isotonic exercises may be implemented into the rehabilitation program.30 Return to football can be considered when the athlete has recovered knee and hip range of motion, is pain-free, and has near-normal strength compared to the contralateral side. The athlete should also perform satisfactorily in simulated position-specific activities in a noncontact fashion prior to return to full competition.30

Hamstring Strain

Pathophysiology

Hamstring strains are the most common noncontact injuries in football resulting from excessive muscle stretching during eccentric contraction generally occurring at the musculotendinous junction.5,39 Because the hamstrings cross both the hip and knee, simultaneous hip flexion and knee extension results in maximal lengthening, making them most vulnerable to injury at the terminal swing phase of gait just prior to heel strike.39-42 The long head of the biceps femoris undergoes the greatest stretch, reaching 110% of resting length during terminal swing phase and is the most commonly injured hamstring muscle.43,44 Injury occurs when the force of eccentric contraction, and resulting muscle strain, exceeds the mechanical limits of the tissue.42,45 It remains to be shown whether hamstring strains occur as a result of accumulated microscopic muscle damage or secondary to a single event that exceeds the mechanical limits of the muscle.42

 

 

Epidemiology and Risk Factors

The majority of hamstring strains are sustained during noncontact activities, with most athletes citing sprinting as the activity at the time of injury.3 Approximately 93% of injuries occur during noncontact activities among defensive backs and wide receivers.3 Hamstring strains are the second-most common injury among NFL players, comprising approximately 9% of all injuries,5,7 with 16% to 31% of these injuries associated with recurrence.3,5,35,46 Using the NFL’s Injury Surveillance System, Elliott and colleagues3 reported 1716 hamstring strains over a 10-year period (1989-1998). Fifty-one percent of hamstring strains occurred during the 7-week preseason, with a greater than 4-fold increased injury rate noted during the preseason compared to the 16-week regular season. An increased incidence in the preseason is partially attributable to relative deconditioning over the offseason. Defensive backs, wide receivers, and special teams players accounted for the majority of injured players, suggesting that speed position players and those who must “backpedal” (run backwards) are at an increased risk for injury.

Several risk factors for hamstring strain have been described, including prior injury, older age, quadriceps-hamstring strength imbalances, limited hip and knee flexibility, and fatigue.39,42,47 Inadequate rehabilitation and premature return to competition are also likely important factors predisposing to recurrent injury.39,48

History and Physical Examination

The majority of hamstring strains occur in the acute setting when the player experiences the sudden onset of pain in the posterior thigh during strenuous exercise, most commonly while sprinting.39 The injury typically occurs in the early or late stage of practice or competition due, in part, to inadequate warm-up or fatigue. The athlete may describe an audible pop and an inability to continue play, depending on injury severity.

Physical examination may demonstrate palpable induration and tenderness immediately or shortly after injury. In the setting of severe strains, there can be significant thigh swelling and ecchymosis, and in complete ruptures, a palpable defect.39 The affected muscle should be palpated along its entire length, and is best performed prone with the knee flexed to 90° as well as with the knee partially extended to place it under mild tension. Injury severity can be assessed by determining the restriction of passive knee extension while the athlete is lying supine with the hip flexed to 90°. The severity of hamstring strains varies from minor damage of a few myofibers without loss of structural integrity to complete muscle rupture.

Hamstring strains are classified into 3 groups based on the amount of myotendinous disruption (Table 3).49

Imaging

Similar to other muscle strains, hamstring strains are a clinical diagnosis and generally do not necessitate advanced imaging studies except to assess the degree of damage (ie, partial vs complete rupture) and to rule out other injuries, especially if the athlete fails to respond to treatment. Plain radiographs in acute cases are usually unremarkable. However, more severe injuries may go on to develop myositis ossificans similar to quadriceps soft tissue injuries (Figure 5).

The MRI appearance of hamstring strains shows increased signal within and surrounding the affected muscle belly on T2-weighted imaging as well as the degree of muscle fiber disruption (Figures 6A, 6B).
MRI can also be beneficial to confirm the diagnosis of myositis ossificans in chronic cases with a palpable mass.

Treatment

Most hamstring strains respond to conservative treatment, with operative intervention rarely indicated except for proximal or distal tendon avulsions.39 Like other muscle strains, initial management consists of RICE. COX-2-selective NSAIDs are preferred initially following injury. During a brief period of immobilization, the leg should be extended as much as tolerated to maximize muscle length, limit hematoma formation, and reduce the risk of contracture.39 Controlled mobilization should begin as soon as tolerated by the athlete.39 Isometric exercises and a stretching program should be started early in the rehabilitation period, with isotonic exercises added as motion and pain improve. Active stretching should be initiated and progressed to passive, static stretching as guided by pain.

The late phase of rehabilitation and long-term conditioning protocols should incorporate eccentric training once the athlete is pain-free, performing isotonic and isokinetic exercises. Eccentric exercises best strengthen the hamstrings at their most susceptible point, prepares the athlete for functional activities, and minimizes the risk of reinjury,3,50,51 Elliot and colleagues3 reported an order of magnitude decrease in hamstring injuries in high-risk athletes with identifiable hamstring muscle weakness after implementing an eccentric strengthening program and progressive sprint training. Similarly, in a large cohort of elite soccer players, correction of strength deficits in players with prior hamstring injuries led to similar rates of injury compared to athletes without strength deficits or prior injury.52 Those athletes with persistent weakness who did not undergo rehabilitation had significantly higher rates of reinjury.

Various injections containing local anesthetics, corticosteroids, platelet-rich plasma (PRP), and other substances have been administered to football players following acute muscle strains in an effort to alleviate pain and safely return the athlete to competition. Some practitioners have been reluctant to administer injections (especially those containing corticosteroids) due to a potentially increased risk of tendinopathy or rupture.31 Drakos and colleagues53 reported their outcomes following muscle and ligament strains treated with combined corticosteroid and local anesthetic injections on one NFL team. While quadriceps and hamstring strains were associated with the most missed games among all muscle strains, these injections resulted in no adverse events or progression of injury severity. Similarly, Levine and colleagues 51 administered intramuscular corticosteroid injections to 58 NFL players with high-grade hamstring injuries that had a palpable defect within the muscle belly. They reported no complications or strength deficits at final examination. In a case-control study, Rettig and colleagues46 administered PRP injections under ultrasound guidance in 5 NFL players with hamstring injuries. Compared to players treated with a focused rehabilitation program only, there were no significant differences in recovery or return to play.

The decision to return to play should be based on a clinical assessment considering pain, strength, motion, and flexibility. Player position should also be considered. Return-to-play guidelines describing the appropriate progression through rehabilitation and return to sport have been described and can be used as a template for the rehabilitation of football players.54 It should be noted that primary hamstring strains are associated with decreased athletic performance and an increased risk of more severe reinjury after return to sport.55,56

 

 

Morel-Lavallée Lesion

Pathophysiology

Morel-Lavallée lesions (MLLs) are uncommon football injuries, but often occur in the thigh.57,58 An MLL is a posttraumatic soft tissue injury in which deforming forces of pressure and shear cause a closed, soft tissue degloving injury; in this injury, the skin and subcutaneous tissues are separated from the underlying fascia, disrupting perforating blood vessels. The resulting space between the fascia and subcutaneous tissue fills with blood, lymphatics, and necrotic fat, resulting in a hematoma/seroma that can be a nidus for bacterial infection.58 The most common anatomic regions are the anterior distal thigh and lateral hip. Both of these areas are commonly involved in both direct contact and shear forces following a fall to the ground.

History and Physical Examination

Athletes with MLLs typically present with the insidious onset of a fluid collection within the thigh following a fall to the ground, usually while sliding or diving on the playing surface.57,58 The fluid collection can be associated with thigh tightness and may extend distally into the suprapatellar region or proximally over the greater trochanter. Thigh swelling, ecchymosis, and palpable fluctuance are seen in most cases. Progressive increases in pain and thigh swelling may be seen in severe injuries, but thigh compartments generally remain soft and nontender. Signs and symptoms of an MLL do not typically manifest immediately following the athletic event. Tejwani and colleagues58 reported a case series of MLLs of the knee in 27 NFL players from a single team over a 14-year period, with an average of 3 days between injury and evaluation by the medical staff. The mechanism of injury was a shearing blow from the knee striking the playing surface in 81% of cases and direct contact to the knee from another player in 19% of cases; all cases occurred in game situations. No affected players were wearing kneepads at the time of injury.

Imaging

Plain radiography may reveal a noncalcified soft tissue mass over the involved area and is not usually helpful except to rule out an underlying fracture. The appearance of an MLL on ultrasound is nonspecific and variable, often described as anechoic, hypoechoic, or hyperechoic depending on the presence of hemolymphatic fluid sedimentation and varying amounts of internal fat debris. MRI is the imaging modality of choice and typically shows a well-defined oval or fusiform, fluid-filled mass with tapering margins blending with adjacent fascial planes.

These lesions may show fluid-fluid levels, septations, and variable internal signal intensity depending on the acuity of the lesion (Figures 7A-7C).59

Treatment

Similar to quadriceps contusions, treatment goals for MLLs are evacuation of the fluid collection, prevention of fluid recurrence, a full range of active knee flexion, and prompt return to play.57,58 Initial treatment for smaller lesions consists of cryotherapy, compression wrapping of the involved area, and immediate active and passive range of motion of the hip and knee. While MLLs were traditionally treated with serial open debridements, less invasive approaches—including elastic compression, aspiration, percutaneous irrigation with debridement and suction drainage, or liposuction and drainage followed by suction therapy—have been recently described.57,58,60,61 Less invasive approaches aim to minimize soft tissue dissection and disruption of the vascular supply while accelerating rehabilitation. The presence of a surrounding capsule on MRI makes conservative or minimally invasive approaches less likely to be successful and may necessitate an open procedure.62 Antibiotics should be used preoperatively due to the presence of a dead space containing necrotic debris that makes infection a potential complication. While elite contact athletes can expect to return to competition long before complete resolution of an MLL, there is a risk of further delamination and lesion expansion due to re-injury prior to compete healing.

Tejwani and colleagues58 performed aspiration at the area of palpable fluctuance in the thigh or suprapatellar region using a 14-gauge needle in those athletes who failed to improve with conservative treatments alone. Mean time to resolution of the fluid collection was 16 days following aspiration. Fifty-two percent of the athletes were successfully treated with cryotherapy, compression, and motion exercises alone; 48% were treated with at least one aspiration, with a mean of 2.7 aspirations per knee. In 11% of cases that failed to resolve after multiple aspirations, doxycycline sclerodesis was performed immediately following an aspiration. Patients treated with sclerodesis had no return of the fluid collection and returned to play the following day.

Matava and colleagues57 described the case of an NFL player who sustained a closed MLL of the lateral hip while diving onto an artificial turf surface attempting to catch a pass. Despite immediate thigh pain and swelling, he was able to continue play. Immediately following the game, the player was examined and had a tense thigh with ecchymosis extending into the trochanteric region. Aspiration of the fluctuant area was unsuccessful. Progressive increases in pain and thigh swelling prompted hospital admission. Percutaneous irrigation and debridement was performed as described by Tseng and Tornetta.61 A suction drain was placed within the residual dead space, and constant wall suction was applied in addition to hip compression using a spica wrap. The player returned to practice 22 days after the injury and missed a total of 3 games without any residual deficit.

 

 

Conclusion

Quadriceps and hamstring injuries occur frequently in football and are generally treated conservatively. While return to competition following hamstring strains is relatively quick, a high rate of injury recurrence highlights the importance of targeted rehabilitation and conditioning. Rarely, complications from quadriceps contusions, including acute compartment syndrome and myositis ossificans, may require operative intervention if unresponsive to conservative treatment. MLLs are rare in sports, but usually involve the thigh when they occur in football players. Team physicians must maintain a heightened degree of awareness of this injury as it may require operative intervention.

 

Acknowledgements: The authors would like to thank Jonathon Baker, MD and David Rubin, MD for their assistance in providing radiographic images for this paper.


Am J Orthop. 2016;45(6):E308-E318. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

American football has the highest injury rate of any team sport in the United States at the high school, collegiate, and professional levels.1-3 Muscle strains and contusions constitute a large proportion of football injuries. For example, at the high school level, muscle strains comprise 12% to 24% of all injuries;2 at the collegiate level, they account for approximately 20% of all practice injuries, with nearly half of all strains occurring within the thigh.1,4 Among a single National Football League (NFL) team, Feeley and colleagues5 reported that muscle strains accounted for 46% of practice and 22% of preseason game injuries. The hamstrings, followed by the quadriceps, are the most commonly strained muscle groups among both professional and amateur athletes,5,6 with hamstring and quadriceps injuries making up approximately 13% of all injuries among NFL players.7 Given the relatively large surface area and muscle volume of the anterior and posterior thigh, as well as the activities and maneuvers necessitated by the various football positions, it is not surprising that the thigh is frequently involved in football-related injuries.

The purpose of this review is to describe the clinical manifestations of thigh-related soft-tissue injuries seen in football players. Two of these conditions—muscle strains and contusions—are relatively common, while a third condition—the Morel-Lavallée lesion—is a rare, yet relevant injury that warrants discussion.

Quadriceps Contusion

Pathophysiology

Contusion to the quadriceps muscle is a common injury in contact sports generally resulting from a direct blow from a helmet, knee, or shoulder.8 Bleeding within the musculature causes swelling, pain, stiffness, and limitation of quadriceps excursion, ultimately resulting in loss of knee flexion and an inability to run or squat. The injury is typically confined to a single quadriceps muscle.8 The use of thigh padding, though helpful, does not completely eliminate the risk of this injury.

History and Physical Examination

Immediately after injury, the athlete may complain only of thigh pain. However, swelling, pain, and diminished range of knee motion may develop within the first 24 hours depending on the severity of injury and how quickly treatment is instituted.8 Jackson and Feagin9 developed an injury grading system for quadriceps contusions based on the limitation of knee flexion observed (Table 1).

Fortunately, the majority of contusions in these athletes are of a mild to moderate severity.9,10

Imaging

A quadriceps contusion is a clinical diagnosis based on a typical history and physical examination; therefore, advanced imaging usually does not need to be obtained except to gauge the severity of injury, to rule out concurrent injuries (ie, tendon rupture), and to identify the presence of a hematoma that may necessitate aspiration. Plain radiographs are typically unremarkable in the acute setting. Appearance on magnetic resonance imaging (MRI) varies by injury severity, with increased signal throughout the affected muscle belly and a diffuse, feathery appearance centered at the point of impact on short TI inversion recovery (STIR) and T2-weighted images reflecting edema and possibly hematoma (Figures 1A-1C).8,11

Resolution of these MRI findings may lag behind functional recovery.8 Therefore, the athlete is often able to return to competition once he has recovered full lower extremity motion and function despite the persistence of abnormal findings on MRI.

Treatment

Treatment of a quadriceps contusion is nonoperative and consists of a 3-phase recovery.10 The first phase lasts approximately 2 days and consists of rest, ice, compression, and elevation (RICE) to limit hemorrhage. The knee should be rested in a flexed position to maintain quadriceps muscle fiber length in order to promote muscle compression and limit knee stiffness. For severe contusions in which there is a question of an acute thigh compartment syndrome, compression should be avoided with appropriate treatment based on typical symptoms and intra-compartmental pressure measurement.12 Nonsteroidal anti-inflammatory drugs (NSAIDs) may be administered to diminish pain as well as the risk of myositis ossificans. While there is no data on the efficacy of NSAIDs in preventing myositis ossificans following quadriceps contusions, both COX-2 selective (ie, celecoxib) and nonselective (ie, naproxen, indomethacin) COX inhibitors have been demonstrated to significantly reduce the incidence of heterotopic ossification following hip surgery—a condition occurring from a similar pathophysiologic process as myositis ossificans.13-17 However, this class of drugs should not be given any sooner than 48 to 72 hours after injury to decrease further bleeding risk, given its inhibitory effect on platelet function.18 Narcotic pain medications are rarely required.

The second phase focuses on restoring active and passive knee and hip flexion and begins when permitted by pain.8 Icing, pain control, and physical therapy modalities are also continued in order to reduce pain and swelling as knee motion is progressed. The third phase begins once full range of knee and hip motion is restored and consists of quadriceps strengthening and functional rehabilitation of the lower extremity.8,19 Return to athletic activities and eventually competition should take place when a full, painless range of motion is restored and strength returns to baseline. Isokinetic strength testing may be utilized to more accurately assess strength and endurance. Noncontact, position-specific drills are incorporated as clinical improvement allows. A full recovery should be expected within 4 weeks of injury, with faster resolution and return to play seen in less severe contusions depending on the athlete’s position.8 Continued quadriceps stretching is recommended to prevent recurrence once the athlete returns to play. A protective hard shell may also be utilized both during rehabilitation as well as once the athlete returns to play in order to protect the thigh from reinjury, which may increase the risk of myositis ossificans.8

 

 

Complications

A prolonged recovery or persistent symptoms should alert the treating physician to the possibility of complications, including myositis ossificans.8,20 Myositis ossificans typically results from moderate to severe contusions, which may present initially as a painful, indurated mass that later becomes quite firm. This mass may be seen on plain radiographs as early as 2 to 4 weeks following injury if the athlete complains of persistent pain or a palpable thigh mass (Figure 2).9

The risk of myositis ossificans increases in proportion to the severity of injury.18 Among US military academy members, the incidence of myositis ossificans following quadriceps contusions ranges from 9% to 20%.9,10 These masses often masquerade as a neoplasm that results in an unnecessary biopsy which reveals an “aggressive” lesion leading to an incorrect diagnosis of a soft-tissue sarcoma. MRI and/or computed tomography scanning may confirm the diagnosis of a benign process in these questionable cases as the lesion matures, with ossification demonstrated on both T1- and T2-weight imaging.21 Even in the presence of myositis ossificans, most patients regain full knee and hip motion and return to sports without residual weakness or pain.20 Very rarely, persistent symptoms and limitation of motion may warrant consideration for surgical excision of the symptomatic mass once it is considered mature, which generally occurs within 6 months to 1 year, in order to avoid the risk of recurrence resulting from the surgical trauma.9, 22

Mani-Babu and colleagues23 reported a case of a 14-year-old male football player who sustained a quadriceps contusion after a direct blow from an opponent’s helmet to the lateral thigh. Persistent pain and limitation of motion at 2 months follow-up prompted imaging studies that demonstrated myositis ossificans. The patient was treated with intravenous pamidronate (a bisphosphonate) twice over a 3-month period and demonstrated a full recovery within 5 months.

Acute compartment syndrome of the thigh has also been reported following severe quadriceps contusions, with the majority occurring in the anterior compartment.12,24-28 When injury from blunt trauma extends into and disrupts the muscular layer adjacent to the femur, vascular disruption can cause hematoma formation, muscle edema, and significant swelling, thereby increasing intracompartmental pressure. The relatively large volume of the anterior thigh compartment and lack of a rigid deep fascial envelope may be protective from the development of compartment syndrome compared to other sites.28 It can be difficult to distinguish a severe contusion from a compartment syndrome, as both can occur from the same mechanism and have similar presenting signs and symptoms. Signs of a compartment syndrome include pain out of proportion to the injury that is aggravated by passive stretch of the quadriceps muscles, an increasingly firm muscle compartment to palpation, and neurovascular deficits.29 Both acute compartment syndrome and a severe contusion may present with significant pain, inability to bear weight, tense swelling, tenderness to palpation, and pain with passive knee flexion.24 While the successful conservative treatment of athletes with acute compartment syndrome of the thigh has been reported, it is important to closely monitor the patient’s condition and consider intracompartmental pressure monitoring if the patient’s clinical condition deteriorates.12 An acute fasciotomy should be strongly considered when intracompartmental pressures are within 30 mm Hg of diastolic pressure.24-27 Fortunately, it is highly uncommon for thigh compartment pressure to rise to this level. Percutaneous compartment decompression using liposuction equipment or a large cannula has been described to decrease intracompartmental pressure, potentially expediting recovery and minimizing morbidity.18 Interestingly, reports of fasciotomies for acute thigh compartment syndrome following closed athletic injuries have not described necrotic or non-contractile muscle typical of an acute compartment syndrome, calling into question the need for fasciotomy following closed blunt athletic trauma to the thigh.18

Quadriceps Strain

Pathophysiology

Acute quadriceps strains occur during sudden forceful eccentric contraction of the extensor mechanism. Occasionally, in the absence of a clear mechanism, these injuries mistakenly appear as a contusion resulting from a direct blow to the thigh.30,31 The rectus femoris is the most frequently strained quadriceps muscle due, in part, to its superficial location and predominance of type II muscle fibers, which are more likely to be strained.11,32 Although classically described as occurring along the distal portion of the rectus femoris at the musculotendinous junction, quadriceps strains most commonly occur at the mid to proximal aspect of the rectus femoris.30,33 The quadriceps muscle complex crosses 2 joints and, as a result, is more predisposed to eccentric injury than mono-articular muscles.34 We have had a subset of complete myotendinous tears of the rectus femoris that occur in the plant leg of placekickers that result in significant disability.

 

 

Risk Factors

Quadriceps and thigh injuries comprise approximately 4.5% of injuries among NFL players.7 Several risk factors for quadriceps strains have been described. In a study of Australian Rules football players, Orchard35 demonstrated that for all muscle strains, the strongest risk factor was a recent history of the same injury, with the next strongest risk factor being a past history of the same injury. Increasing age was found to be a risk factor for hamstring strains but not quadriceps strains. Muscle fatigue may also contribute to injury susceptibility.36

History and Physical Examination

Injuries typically occur during kicking, jumping, or a sudden change in direction while running.30 Athletes may localize pain anywhere along the quadriceps muscle, although strains most commonly occur at the proximal to mid portion of the rectus femoris.30,33 The grading system for quadriceps strains described by Kary30 is based on level of pain, quadriceps strength, and the presence or absence of a palpable defect (Table 2).

In high-grade strains, a sharp pain occurs immediately following the injury and often causes variable degrees of functional loss to the quadriceps.30

The athlete typically walks with an antalgic gait. Visible swelling and/or ecchymosis may be present depending on when the athlete is seen, as ecchymosis may develop within the first 24 hours of injury. The examiner should palpate along the entire length of the injured muscle. High-grade strains or complete tears may present with a bulge or defect in the muscle belly, but in most cases no defect will be palpable. There may be loss of knee flexion similar to a quadriceps contusion. Strength testing should be performed in both the sitting and prone position with the hip both flexed and extended to assess resisted knee extension strength.30 Loss of strength is proportional to the degree of injury.

Imaging

While most quadriceps strains are adequately diagnosed clinically without the need for imaging studies, ultrasound or MRI can be used to evaluate for partial or complete rupture.30,33 In milder cases, MRI usually demonstrates interstitial edema and hemorrhage with a feathery appearance on STIR and T2-weighted imaging (Figures 3A-3C).11

Myotendinous strains can be classified based on the extent of fiber disruption.11,32 Cross and colleagues33 demonstrated that strains of the central tendon of the rectus femoris seen on MRI correlated with a significantly longer rehabilitation period than those occurring at the periphery of the rectus or within other quadriceps muscles.
Ultrasound is a more economical imaging modality that can dynamically assess the quadriceps musculature for fiber disruption and hematoma formation but is user-dependent, requiring a skilled technician (Figures 4A, 4B).30

Treatment

Acute treatment of quadriceps strains focuses on minimizing bleeding using the principles of RICE treatment.37 NSAIDs may be used immediately to assist with pain control.30 COX-2-specific NSAIDs are preferred due to their lack of any inhibitory effect on platelet function in order to reduce the risk of further bleeding within the muscle compartment. For the first 24 to 72 hours following injury, the quadriceps should be maintained relatively immobilized to prevent further injury.38 High-grade injuries might necessitate crutches for ambulatory assistance.

Depending on injury severity, the active phase of treatment usually begins within 5 days of injury and consists of stretching and knee/hip range of motion. An active warm-up should precede rehabilitation exercises to activate neural pathways within the muscle and improve muscle elasticity.38 Ballistic stretching should be avoided to prevent additional injury to the muscle fibers. Strengthening should proceed when the athlete recovers a pain-free range of motion. When isometric exercises can be completed at increasing degrees of knee flexion, isotonic exercises may be implemented into the rehabilitation program.30 Return to football can be considered when the athlete has recovered knee and hip range of motion, is pain-free, and has near-normal strength compared to the contralateral side. The athlete should also perform satisfactorily in simulated position-specific activities in a noncontact fashion prior to return to full competition.30

Hamstring Strain

Pathophysiology

Hamstring strains are the most common noncontact injuries in football resulting from excessive muscle stretching during eccentric contraction generally occurring at the musculotendinous junction.5,39 Because the hamstrings cross both the hip and knee, simultaneous hip flexion and knee extension results in maximal lengthening, making them most vulnerable to injury at the terminal swing phase of gait just prior to heel strike.39-42 The long head of the biceps femoris undergoes the greatest stretch, reaching 110% of resting length during terminal swing phase and is the most commonly injured hamstring muscle.43,44 Injury occurs when the force of eccentric contraction, and resulting muscle strain, exceeds the mechanical limits of the tissue.42,45 It remains to be shown whether hamstring strains occur as a result of accumulated microscopic muscle damage or secondary to a single event that exceeds the mechanical limits of the muscle.42

 

 

Epidemiology and Risk Factors

The majority of hamstring strains are sustained during noncontact activities, with most athletes citing sprinting as the activity at the time of injury.3 Approximately 93% of injuries occur during noncontact activities among defensive backs and wide receivers.3 Hamstring strains are the second-most common injury among NFL players, comprising approximately 9% of all injuries,5,7 with 16% to 31% of these injuries associated with recurrence.3,5,35,46 Using the NFL’s Injury Surveillance System, Elliott and colleagues3 reported 1716 hamstring strains over a 10-year period (1989-1998). Fifty-one percent of hamstring strains occurred during the 7-week preseason, with a greater than 4-fold increased injury rate noted during the preseason compared to the 16-week regular season. An increased incidence in the preseason is partially attributable to relative deconditioning over the offseason. Defensive backs, wide receivers, and special teams players accounted for the majority of injured players, suggesting that speed position players and those who must “backpedal” (run backwards) are at an increased risk for injury.

Several risk factors for hamstring strain have been described, including prior injury, older age, quadriceps-hamstring strength imbalances, limited hip and knee flexibility, and fatigue.39,42,47 Inadequate rehabilitation and premature return to competition are also likely important factors predisposing to recurrent injury.39,48

History and Physical Examination

The majority of hamstring strains occur in the acute setting when the player experiences the sudden onset of pain in the posterior thigh during strenuous exercise, most commonly while sprinting.39 The injury typically occurs in the early or late stage of practice or competition due, in part, to inadequate warm-up or fatigue. The athlete may describe an audible pop and an inability to continue play, depending on injury severity.

Physical examination may demonstrate palpable induration and tenderness immediately or shortly after injury. In the setting of severe strains, there can be significant thigh swelling and ecchymosis, and in complete ruptures, a palpable defect.39 The affected muscle should be palpated along its entire length, and is best performed prone with the knee flexed to 90° as well as with the knee partially extended to place it under mild tension. Injury severity can be assessed by determining the restriction of passive knee extension while the athlete is lying supine with the hip flexed to 90°. The severity of hamstring strains varies from minor damage of a few myofibers without loss of structural integrity to complete muscle rupture.

Hamstring strains are classified into 3 groups based on the amount of myotendinous disruption (Table 3).49

Imaging

Similar to other muscle strains, hamstring strains are a clinical diagnosis and generally do not necessitate advanced imaging studies except to assess the degree of damage (ie, partial vs complete rupture) and to rule out other injuries, especially if the athlete fails to respond to treatment. Plain radiographs in acute cases are usually unremarkable. However, more severe injuries may go on to develop myositis ossificans similar to quadriceps soft tissue injuries (Figure 5).

The MRI appearance of hamstring strains shows increased signal within and surrounding the affected muscle belly on T2-weighted imaging as well as the degree of muscle fiber disruption (Figures 6A, 6B).
MRI can also be beneficial to confirm the diagnosis of myositis ossificans in chronic cases with a palpable mass.

Treatment

Most hamstring strains respond to conservative treatment, with operative intervention rarely indicated except for proximal or distal tendon avulsions.39 Like other muscle strains, initial management consists of RICE. COX-2-selective NSAIDs are preferred initially following injury. During a brief period of immobilization, the leg should be extended as much as tolerated to maximize muscle length, limit hematoma formation, and reduce the risk of contracture.39 Controlled mobilization should begin as soon as tolerated by the athlete.39 Isometric exercises and a stretching program should be started early in the rehabilitation period, with isotonic exercises added as motion and pain improve. Active stretching should be initiated and progressed to passive, static stretching as guided by pain.

The late phase of rehabilitation and long-term conditioning protocols should incorporate eccentric training once the athlete is pain-free, performing isotonic and isokinetic exercises. Eccentric exercises best strengthen the hamstrings at their most susceptible point, prepares the athlete for functional activities, and minimizes the risk of reinjury,3,50,51 Elliot and colleagues3 reported an order of magnitude decrease in hamstring injuries in high-risk athletes with identifiable hamstring muscle weakness after implementing an eccentric strengthening program and progressive sprint training. Similarly, in a large cohort of elite soccer players, correction of strength deficits in players with prior hamstring injuries led to similar rates of injury compared to athletes without strength deficits or prior injury.52 Those athletes with persistent weakness who did not undergo rehabilitation had significantly higher rates of reinjury.

Various injections containing local anesthetics, corticosteroids, platelet-rich plasma (PRP), and other substances have been administered to football players following acute muscle strains in an effort to alleviate pain and safely return the athlete to competition. Some practitioners have been reluctant to administer injections (especially those containing corticosteroids) due to a potentially increased risk of tendinopathy or rupture.31 Drakos and colleagues53 reported their outcomes following muscle and ligament strains treated with combined corticosteroid and local anesthetic injections on one NFL team. While quadriceps and hamstring strains were associated with the most missed games among all muscle strains, these injections resulted in no adverse events or progression of injury severity. Similarly, Levine and colleagues 51 administered intramuscular corticosteroid injections to 58 NFL players with high-grade hamstring injuries that had a palpable defect within the muscle belly. They reported no complications or strength deficits at final examination. In a case-control study, Rettig and colleagues46 administered PRP injections under ultrasound guidance in 5 NFL players with hamstring injuries. Compared to players treated with a focused rehabilitation program only, there were no significant differences in recovery or return to play.

The decision to return to play should be based on a clinical assessment considering pain, strength, motion, and flexibility. Player position should also be considered. Return-to-play guidelines describing the appropriate progression through rehabilitation and return to sport have been described and can be used as a template for the rehabilitation of football players.54 It should be noted that primary hamstring strains are associated with decreased athletic performance and an increased risk of more severe reinjury after return to sport.55,56

 

 

Morel-Lavallée Lesion

Pathophysiology

Morel-Lavallée lesions (MLLs) are uncommon football injuries, but often occur in the thigh.57,58 An MLL is a posttraumatic soft tissue injury in which deforming forces of pressure and shear cause a closed, soft tissue degloving injury; in this injury, the skin and subcutaneous tissues are separated from the underlying fascia, disrupting perforating blood vessels. The resulting space between the fascia and subcutaneous tissue fills with blood, lymphatics, and necrotic fat, resulting in a hematoma/seroma that can be a nidus for bacterial infection.58 The most common anatomic regions are the anterior distal thigh and lateral hip. Both of these areas are commonly involved in both direct contact and shear forces following a fall to the ground.

History and Physical Examination

Athletes with MLLs typically present with the insidious onset of a fluid collection within the thigh following a fall to the ground, usually while sliding or diving on the playing surface.57,58 The fluid collection can be associated with thigh tightness and may extend distally into the suprapatellar region or proximally over the greater trochanter. Thigh swelling, ecchymosis, and palpable fluctuance are seen in most cases. Progressive increases in pain and thigh swelling may be seen in severe injuries, but thigh compartments generally remain soft and nontender. Signs and symptoms of an MLL do not typically manifest immediately following the athletic event. Tejwani and colleagues58 reported a case series of MLLs of the knee in 27 NFL players from a single team over a 14-year period, with an average of 3 days between injury and evaluation by the medical staff. The mechanism of injury was a shearing blow from the knee striking the playing surface in 81% of cases and direct contact to the knee from another player in 19% of cases; all cases occurred in game situations. No affected players were wearing kneepads at the time of injury.

Imaging

Plain radiography may reveal a noncalcified soft tissue mass over the involved area and is not usually helpful except to rule out an underlying fracture. The appearance of an MLL on ultrasound is nonspecific and variable, often described as anechoic, hypoechoic, or hyperechoic depending on the presence of hemolymphatic fluid sedimentation and varying amounts of internal fat debris. MRI is the imaging modality of choice and typically shows a well-defined oval or fusiform, fluid-filled mass with tapering margins blending with adjacent fascial planes.

These lesions may show fluid-fluid levels, septations, and variable internal signal intensity depending on the acuity of the lesion (Figures 7A-7C).59

Treatment

Similar to quadriceps contusions, treatment goals for MLLs are evacuation of the fluid collection, prevention of fluid recurrence, a full range of active knee flexion, and prompt return to play.57,58 Initial treatment for smaller lesions consists of cryotherapy, compression wrapping of the involved area, and immediate active and passive range of motion of the hip and knee. While MLLs were traditionally treated with serial open debridements, less invasive approaches—including elastic compression, aspiration, percutaneous irrigation with debridement and suction drainage, or liposuction and drainage followed by suction therapy—have been recently described.57,58,60,61 Less invasive approaches aim to minimize soft tissue dissection and disruption of the vascular supply while accelerating rehabilitation. The presence of a surrounding capsule on MRI makes conservative or minimally invasive approaches less likely to be successful and may necessitate an open procedure.62 Antibiotics should be used preoperatively due to the presence of a dead space containing necrotic debris that makes infection a potential complication. While elite contact athletes can expect to return to competition long before complete resolution of an MLL, there is a risk of further delamination and lesion expansion due to re-injury prior to compete healing.

Tejwani and colleagues58 performed aspiration at the area of palpable fluctuance in the thigh or suprapatellar region using a 14-gauge needle in those athletes who failed to improve with conservative treatments alone. Mean time to resolution of the fluid collection was 16 days following aspiration. Fifty-two percent of the athletes were successfully treated with cryotherapy, compression, and motion exercises alone; 48% were treated with at least one aspiration, with a mean of 2.7 aspirations per knee. In 11% of cases that failed to resolve after multiple aspirations, doxycycline sclerodesis was performed immediately following an aspiration. Patients treated with sclerodesis had no return of the fluid collection and returned to play the following day.

Matava and colleagues57 described the case of an NFL player who sustained a closed MLL of the lateral hip while diving onto an artificial turf surface attempting to catch a pass. Despite immediate thigh pain and swelling, he was able to continue play. Immediately following the game, the player was examined and had a tense thigh with ecchymosis extending into the trochanteric region. Aspiration of the fluctuant area was unsuccessful. Progressive increases in pain and thigh swelling prompted hospital admission. Percutaneous irrigation and debridement was performed as described by Tseng and Tornetta.61 A suction drain was placed within the residual dead space, and constant wall suction was applied in addition to hip compression using a spica wrap. The player returned to practice 22 days after the injury and missed a total of 3 games without any residual deficit.

 

 

Conclusion

Quadriceps and hamstring injuries occur frequently in football and are generally treated conservatively. While return to competition following hamstring strains is relatively quick, a high rate of injury recurrence highlights the importance of targeted rehabilitation and conditioning. Rarely, complications from quadriceps contusions, including acute compartment syndrome and myositis ossificans, may require operative intervention if unresponsive to conservative treatment. MLLs are rare in sports, but usually involve the thigh when they occur in football players. Team physicians must maintain a heightened degree of awareness of this injury as it may require operative intervention.

 

Acknowledgements: The authors would like to thank Jonathon Baker, MD and David Rubin, MD for their assistance in providing radiographic images for this paper.


Am J Orthop. 2016;45(6):E308-E318. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train. 2007;42(2):311-319.

2. Rechel JA, Yard EE, Comstock RD. An epidemiologic comparison of high school sports injuries sustained in practice and competition. J Athl Train. 2008;43(2):197-204.

3. Elliott MC, Zarins B, Powell JW, Kenyon CD. Hamstring muscle strains in professional football players: a 10-year review. Am J Sports Med. 2011;39(4):843-850.

4. Dick R, Ferrara MS, Agel J, et al. Descriptive epidemiology of collegiate men’s football injuries: National Collegiate Athletic Association Injury Surveillance System, 1988-1989 through 2003-2004. J Athl Train. 2007;42(2):221-233.

5. Feeley BT, Kennelly S, Barnes RP, et al. Epidemiology of National Football League training camp injuries from 1998 to 2007. Am J Sports Med. 2008;36(8):1597-1603.

6. Garrett WE Jr. Muscle strain injuries. Am J Sports Med. 1996;24(6 Suppl):S2-S8.

7. Lawrence DW, Hutchison MG, Comper P. Descriptive epidemiology of musculoskeletal injuries and concussions in the National Football League, 2012-2014. Orthop J Sports Med. 2015;3(5):2325967115583653.

8. Diaz JA, Fischer DA, Rettig AC, Davis TJ, Shelbourne KD. Severe quadriceps muscle contusions in athletes. A report of three cases. Am J Sports Med. 2003;31(2):289-293.

9. Jackson DW, Feagin JA. Quadriceps contusions in young athletes. Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am. 1973;55(1):95-105.

10. Ryan JB, Wheeler JH, Hopkinson WJ, Arciero RA, Kolakowski KR. Quadriceps contusions. West Point update. Am J Sports Med. 1991;19(3):299-304.

11. Bencardino JT, Rosenberg ZS, Brown RR, Hassankhani A, Lustrin ES, Beltran J. Traumatic musculotendinous injuries of the knee: diagnosis with MR imaging. Radiographics. 2000;20 Spec No:S103-S120.

12. Robinson D, On E, Halperin N. Anterior compartment syndrome of the thigh in athletes--indications for conservative treatment. J Trauma. 1992;32(2):183-186.

13. Beckmann JT, Wylie JD, Kapron AL, Hanson JA, Maak TG, Aoki SK. The effect of NSAID prophylaxis and operative variables on heterotopic ossification after hip arthroscopy. Am J Sports Med. 2014;42(6):1359-1364.

14. Shehab D, Elgazzar AH, Collier BD. Heterotopic ossification. J Nucl Med. 2002;43(3):346-353.

15. Beckmann JT, Wylie JD, Potter MQ, Maak TG, Greene TH, Aoki SK. Effect of naproxen prophylaxis on heterotopic ossification following hip arthroscopy: a double-blind randomized placebo-controlled trial. J Bone Joint Surg Am. 2015;97(24):2032-2037.

16. Yeung M, Jamshidi S, Horner N, Simunovic N, Karlsson J, Ayeni OR. Efficacy of nonsteroidal anti-inflammatory drug prophylaxis for heterotrophic ossification in hip arthroscopy: a systematic review. Arthroscopy. 2016;32(3):519-525.

17. Goyal K, Pettis CR, Bancroft AE, Wasyliw CW, Scherer KF. Myositis ossificans in the thigh of a lacrosse player. Orthopedics. 2015;38(8):468,515-518.

18. Cooper DE. Severe quadriceps muscle contusions in athletes. Am J Sports Med. 2004;32(3):820.

19. Bonsell S, Freudigman PT, Moore HA. Quadriceps muscle contusion resulting in osteomyelitis of the femur in a high school football player. A case report. Am J Sports Med. 2001;29(6):818-820.

20. Rothwell AG. Quadriceps hematoma. A prospective clinical study. Clin Orthop Relat Res. 1982;(171):97-103.

21. Armfield DR, Kim DH, Towers JD, Bradley JP, Robertson DD. Sports-related muscle injury in the lower extremity. Clin Sports Med. 2006;25(4):803-842.

22. Lipscomb AB, Thomas ED, Johnston RK. Treatment of myositis ossificans traumatica in athletes. Am J Sports Med. 1976;4(3):111-120.

23. Mani-Babu S, Wolman R, Keen R. Quadriceps traumatic myositis ossificans in a football player: management with intravenous pamidronate. Clin J Sport Med. 2014;24(5):e56-e58.

24. McCaffrey DD, Clarke J, Bunn J, McCormack MJ. Acute compartment syndrome of the anterior thigh in the absence of fracture secondary to sporting trauma. J Trauma. 2009;66(4):1238-1242.

25. Klasson SC, Vander Schilden JL. Acute anterior thigh compartment syndrome complicating quadriceps hematoma. Two case reports and review of the literature. Orthop Rev. 1990;19(5):421-427.

26. Rooser B. Quadriceps contusion with compartment syndrome. Evacuation of hematoma in 2 cases. Acta Orthop Scand. 1987;58(2):170-172.

27. Rooser B, Bengtson S, Hagglund G. Acute compartment syndrome from anterior thigh muscle contusion: a report of eight cases. J Orthop Trauma. 1991;5(1):57-59.

28. Schwartz JT Jr, Brumback RJ, Lakatos R, Poka A, Bathon GH, Burgess AR. Acute compartment syndrome of the thigh. A spectrum of injury. J Bone Joint Surg Am. 1989;71(3):392-400.

29. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg Br. 2003;85(5):625-632.

30. Kary JM. Diagnosis and management of quadriceps strains and contusions. Curr Rev Musculoskelet Med. 2010;3(1-4):26-31.

31. Boublik M, Schlegel TF, Koonce RC, Genuario JW, Kinkartz JD. Quadriceps tendon injuries in national football league players. Am J Sports Med. 2013;41(8):1841-1846.

32. Palmer WE, Kuong SJ, Elmadbouh HM. MR imaging of myotendinous strain. AJR Am J Roentgenol. 1999;173(3):703-709.

33. Cross TM, Gibbs N, Houang MT, Cameron M. Acute quadriceps muscle strains: magnetic resonance imaging features and prognosis. Am J Sports Med. 2004;32(3):710-719.

34. Hughes C 4th, Hasselman CT, Best TM, Martinez S, Garrett WE Jr. Incomplete, intrasubstance strain injuries of the rectus femoris muscle. Am J Sports Med. 1995;23(4):500-506.

35. Orchard JW. Intrinsic and extrinsic risk factors for muscle strains in Australian football. Am J Sports Med. 2001;29(3):300-303.36. Mair SD, Seaber AV, Glisson RR, Garrett WE, Jr. The role of fatigue in susceptibility to acute muscle strain injury. Am J Sports Med. 1996;24(2):137-143.

37. Bleakley C, McDonough S, MacAuley D. The use of ice in the treatment of acute soft-tissue injury: a systematic review of randomized controlled trials. Am J Sports Med. 2004;32(1):251-261.

38. Jarvinen TA, Jarvinen TL, Kaariainen M, Kalimo H, Jarvinen M. Muscle injuries: biology and treatment. Am J Sports Med. 2005;33(5):745-764.

39. Clanton TO, Coupe KJ. Hamstring strains in athletes: diagnosis and treatment. J Am Acad Orthop Surg. 1998;6(4):237-248.

40. Novacheck TF. The biomechanics of running. Gait Posture. 1998;7(1):77-95.

41. Yu B, Queen RM, Abbey AN, Liu Y, Moorman CT, Garrett WE. Hamstring muscle kinematics and activation during overground sprinting. J Biomech. 2008;41(15):3121-3126.

42. Opar DA, Williams MD, Shield AJ. Hamstring strain injuries: factors that lead to injury and re-injury. Sports Med. 2012;42(3):209-226.

43. Askling CM, Tengvar M, Saartok T, Thorstensson A. Acute first-time hamstring strains during high-speed running: a longitudinal study including clinical and magnetic resonance imaging findings. Am J Sports Med. 2007;35(2):197-206.

44. Thelen DG, Chumanov ES, Hoerth DM, et al. Hamstring muscle kinematics during treadmill sprinting. Med Sci Sports Exerc. 2005;37(1):108-114.

45. Chumanov ES, Heiderscheit BC, Thelen DG. The effect of speed and influence of individual muscles on hamstring mechanics during the swing phase of sprinting. J Biomech. 2007;40(16):3555-3562.

46. Rettig AC, Meyer S, Bhadra AK. Platelet-rich plasma in addition to rehabilitation for acute hamstring injuries in NFL players: clinical effects and time to return to play. Orthop J Sports Med. 2013;1(1):2325967113494354.

47. Zvijac JE, Toriscelli TA, Merrick S, Kiebzak GM. Isokinetic concentric quadriceps and hamstring strength variables from the NFL Scouting Combine are not predictive of hamstring injury in first-year professional football players. Am J Sports Med. 2013;41(7):1511-1518.

48. Arnason A, Sigurdsson SB, Gudmundsson A, Holme I, Engebretsen L, Bahr R. Risk factors for injuries in football. Am J Sports Med. 2004;32(1 Suppl):5S-16S.

49. Zarins B, Ciullo JV. Acute muscle and tendon injuries in athletes. Clin Sports Med. 1983;2(1):167-182.

50. Arnason A, Andersen TE, Holme I, Engebretsen L, Bahr R. Prevention of hamstring strains in elite soccer: an intervention study. Scand J Med Sci Sports. 2008;18(1):40-48.

51. Levine WN, Bergfeld JA, Tessendorf W, Moorman CT 3rd. Intramuscular corticosteroid injection for hamstring injuries. A 13-year experience in the National Football League. Am J Sports Med. 2000;28(3):297-300.

52. Croisier JL, Ganteaume S, Binet J, Genty M, Ferret JM. Strength imbalances and prevention of hamstring injury in professional soccer players: a prospective study. Am J Sports Med. 2008;36(8):1469-1475.

53. Drakos M, Birmingham P, Delos D, et al. Corticosteroid and anesthetic injections for muscle strains and ligament sprains in the NFL. HSS J. 2014;10(2):136-142.

54. Worrell TW. Factors associated with hamstring injuries. An approach to treatment and preventative measures. Sports Med. 1994;17(5):338-345.

55. Brooks JH, Fuller CW, Kemp SP, Reddin DB. Incidence, risk, and prevention of hamstring muscle injuries in professional rugby union. Am J Sports Med. 2006;34(8):1297-1306.

56. Verrall GM, Kalairajah Y, Slavotinek JP, Spriggins AJ. Assessment of player performance following return to sport after hamstring muscle strain injury. J Sci Med Sport. 2006;9(1-2):87-90.

57. Matava MJ, Ellis E, Shah NR, Pogue D, Williams T. Morel-lavallee lesion in a professional american football player. Am J Orthop. 2010;39(3):144-147.

58. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the national football league. Am J Sports Med. 2007;35(7):1162-1167.

59. Mellado JM, Bencardino JT. Morel-Lavallee lesion: review with emphasis on MR imaging. Magn Reson Imaging Clin N Am. 2005;13(4):775-782.

60. Harma A, Inan M, Ertem K. [The Morel-Lavallee lesion: a conservative approach to closed degloving injuries]. Acta Orthop Traumatol Turc. 2004;38(4):270-273.

61. Tseng S, Tornetta P 3rd. Percutaneous management of Morel-Lavallee lesions. J Bone Joint Surg Am. 2006;88(1):92-96.

62. Gilbert BC, Bui-Mansfield LT, Dejong S. MRI of a Morel-Lavellee lesion. AJR Am J Roentgenol. 2004;182(5):1347-1348.

References

1. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train. 2007;42(2):311-319.

2. Rechel JA, Yard EE, Comstock RD. An epidemiologic comparison of high school sports injuries sustained in practice and competition. J Athl Train. 2008;43(2):197-204.

3. Elliott MC, Zarins B, Powell JW, Kenyon CD. Hamstring muscle strains in professional football players: a 10-year review. Am J Sports Med. 2011;39(4):843-850.

4. Dick R, Ferrara MS, Agel J, et al. Descriptive epidemiology of collegiate men’s football injuries: National Collegiate Athletic Association Injury Surveillance System, 1988-1989 through 2003-2004. J Athl Train. 2007;42(2):221-233.

5. Feeley BT, Kennelly S, Barnes RP, et al. Epidemiology of National Football League training camp injuries from 1998 to 2007. Am J Sports Med. 2008;36(8):1597-1603.

6. Garrett WE Jr. Muscle strain injuries. Am J Sports Med. 1996;24(6 Suppl):S2-S8.

7. Lawrence DW, Hutchison MG, Comper P. Descriptive epidemiology of musculoskeletal injuries and concussions in the National Football League, 2012-2014. Orthop J Sports Med. 2015;3(5):2325967115583653.

8. Diaz JA, Fischer DA, Rettig AC, Davis TJ, Shelbourne KD. Severe quadriceps muscle contusions in athletes. A report of three cases. Am J Sports Med. 2003;31(2):289-293.

9. Jackson DW, Feagin JA. Quadriceps contusions in young athletes. Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am. 1973;55(1):95-105.

10. Ryan JB, Wheeler JH, Hopkinson WJ, Arciero RA, Kolakowski KR. Quadriceps contusions. West Point update. Am J Sports Med. 1991;19(3):299-304.

11. Bencardino JT, Rosenberg ZS, Brown RR, Hassankhani A, Lustrin ES, Beltran J. Traumatic musculotendinous injuries of the knee: diagnosis with MR imaging. Radiographics. 2000;20 Spec No:S103-S120.

12. Robinson D, On E, Halperin N. Anterior compartment syndrome of the thigh in athletes--indications for conservative treatment. J Trauma. 1992;32(2):183-186.

13. Beckmann JT, Wylie JD, Kapron AL, Hanson JA, Maak TG, Aoki SK. The effect of NSAID prophylaxis and operative variables on heterotopic ossification after hip arthroscopy. Am J Sports Med. 2014;42(6):1359-1364.

14. Shehab D, Elgazzar AH, Collier BD. Heterotopic ossification. J Nucl Med. 2002;43(3):346-353.

15. Beckmann JT, Wylie JD, Potter MQ, Maak TG, Greene TH, Aoki SK. Effect of naproxen prophylaxis on heterotopic ossification following hip arthroscopy: a double-blind randomized placebo-controlled trial. J Bone Joint Surg Am. 2015;97(24):2032-2037.

16. Yeung M, Jamshidi S, Horner N, Simunovic N, Karlsson J, Ayeni OR. Efficacy of nonsteroidal anti-inflammatory drug prophylaxis for heterotrophic ossification in hip arthroscopy: a systematic review. Arthroscopy. 2016;32(3):519-525.

17. Goyal K, Pettis CR, Bancroft AE, Wasyliw CW, Scherer KF. Myositis ossificans in the thigh of a lacrosse player. Orthopedics. 2015;38(8):468,515-518.

18. Cooper DE. Severe quadriceps muscle contusions in athletes. Am J Sports Med. 2004;32(3):820.

19. Bonsell S, Freudigman PT, Moore HA. Quadriceps muscle contusion resulting in osteomyelitis of the femur in a high school football player. A case report. Am J Sports Med. 2001;29(6):818-820.

20. Rothwell AG. Quadriceps hematoma. A prospective clinical study. Clin Orthop Relat Res. 1982;(171):97-103.

21. Armfield DR, Kim DH, Towers JD, Bradley JP, Robertson DD. Sports-related muscle injury in the lower extremity. Clin Sports Med. 2006;25(4):803-842.

22. Lipscomb AB, Thomas ED, Johnston RK. Treatment of myositis ossificans traumatica in athletes. Am J Sports Med. 1976;4(3):111-120.

23. Mani-Babu S, Wolman R, Keen R. Quadriceps traumatic myositis ossificans in a football player: management with intravenous pamidronate. Clin J Sport Med. 2014;24(5):e56-e58.

24. McCaffrey DD, Clarke J, Bunn J, McCormack MJ. Acute compartment syndrome of the anterior thigh in the absence of fracture secondary to sporting trauma. J Trauma. 2009;66(4):1238-1242.

25. Klasson SC, Vander Schilden JL. Acute anterior thigh compartment syndrome complicating quadriceps hematoma. Two case reports and review of the literature. Orthop Rev. 1990;19(5):421-427.

26. Rooser B. Quadriceps contusion with compartment syndrome. Evacuation of hematoma in 2 cases. Acta Orthop Scand. 1987;58(2):170-172.

27. Rooser B, Bengtson S, Hagglund G. Acute compartment syndrome from anterior thigh muscle contusion: a report of eight cases. J Orthop Trauma. 1991;5(1):57-59.

28. Schwartz JT Jr, Brumback RJ, Lakatos R, Poka A, Bathon GH, Burgess AR. Acute compartment syndrome of the thigh. A spectrum of injury. J Bone Joint Surg Am. 1989;71(3):392-400.

29. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg Br. 2003;85(5):625-632.

30. Kary JM. Diagnosis and management of quadriceps strains and contusions. Curr Rev Musculoskelet Med. 2010;3(1-4):26-31.

31. Boublik M, Schlegel TF, Koonce RC, Genuario JW, Kinkartz JD. Quadriceps tendon injuries in national football league players. Am J Sports Med. 2013;41(8):1841-1846.

32. Palmer WE, Kuong SJ, Elmadbouh HM. MR imaging of myotendinous strain. AJR Am J Roentgenol. 1999;173(3):703-709.

33. Cross TM, Gibbs N, Houang MT, Cameron M. Acute quadriceps muscle strains: magnetic resonance imaging features and prognosis. Am J Sports Med. 2004;32(3):710-719.

34. Hughes C 4th, Hasselman CT, Best TM, Martinez S, Garrett WE Jr. Incomplete, intrasubstance strain injuries of the rectus femoris muscle. Am J Sports Med. 1995;23(4):500-506.

35. Orchard JW. Intrinsic and extrinsic risk factors for muscle strains in Australian football. Am J Sports Med. 2001;29(3):300-303.36. Mair SD, Seaber AV, Glisson RR, Garrett WE, Jr. The role of fatigue in susceptibility to acute muscle strain injury. Am J Sports Med. 1996;24(2):137-143.

37. Bleakley C, McDonough S, MacAuley D. The use of ice in the treatment of acute soft-tissue injury: a systematic review of randomized controlled trials. Am J Sports Med. 2004;32(1):251-261.

38. Jarvinen TA, Jarvinen TL, Kaariainen M, Kalimo H, Jarvinen M. Muscle injuries: biology and treatment. Am J Sports Med. 2005;33(5):745-764.

39. Clanton TO, Coupe KJ. Hamstring strains in athletes: diagnosis and treatment. J Am Acad Orthop Surg. 1998;6(4):237-248.

40. Novacheck TF. The biomechanics of running. Gait Posture. 1998;7(1):77-95.

41. Yu B, Queen RM, Abbey AN, Liu Y, Moorman CT, Garrett WE. Hamstring muscle kinematics and activation during overground sprinting. J Biomech. 2008;41(15):3121-3126.

42. Opar DA, Williams MD, Shield AJ. Hamstring strain injuries: factors that lead to injury and re-injury. Sports Med. 2012;42(3):209-226.

43. Askling CM, Tengvar M, Saartok T, Thorstensson A. Acute first-time hamstring strains during high-speed running: a longitudinal study including clinical and magnetic resonance imaging findings. Am J Sports Med. 2007;35(2):197-206.

44. Thelen DG, Chumanov ES, Hoerth DM, et al. Hamstring muscle kinematics during treadmill sprinting. Med Sci Sports Exerc. 2005;37(1):108-114.

45. Chumanov ES, Heiderscheit BC, Thelen DG. The effect of speed and influence of individual muscles on hamstring mechanics during the swing phase of sprinting. J Biomech. 2007;40(16):3555-3562.

46. Rettig AC, Meyer S, Bhadra AK. Platelet-rich plasma in addition to rehabilitation for acute hamstring injuries in NFL players: clinical effects and time to return to play. Orthop J Sports Med. 2013;1(1):2325967113494354.

47. Zvijac JE, Toriscelli TA, Merrick S, Kiebzak GM. Isokinetic concentric quadriceps and hamstring strength variables from the NFL Scouting Combine are not predictive of hamstring injury in first-year professional football players. Am J Sports Med. 2013;41(7):1511-1518.

48. Arnason A, Sigurdsson SB, Gudmundsson A, Holme I, Engebretsen L, Bahr R. Risk factors for injuries in football. Am J Sports Med. 2004;32(1 Suppl):5S-16S.

49. Zarins B, Ciullo JV. Acute muscle and tendon injuries in athletes. Clin Sports Med. 1983;2(1):167-182.

50. Arnason A, Andersen TE, Holme I, Engebretsen L, Bahr R. Prevention of hamstring strains in elite soccer: an intervention study. Scand J Med Sci Sports. 2008;18(1):40-48.

51. Levine WN, Bergfeld JA, Tessendorf W, Moorman CT 3rd. Intramuscular corticosteroid injection for hamstring injuries. A 13-year experience in the National Football League. Am J Sports Med. 2000;28(3):297-300.

52. Croisier JL, Ganteaume S, Binet J, Genty M, Ferret JM. Strength imbalances and prevention of hamstring injury in professional soccer players: a prospective study. Am J Sports Med. 2008;36(8):1469-1475.

53. Drakos M, Birmingham P, Delos D, et al. Corticosteroid and anesthetic injections for muscle strains and ligament sprains in the NFL. HSS J. 2014;10(2):136-142.

54. Worrell TW. Factors associated with hamstring injuries. An approach to treatment and preventative measures. Sports Med. 1994;17(5):338-345.

55. Brooks JH, Fuller CW, Kemp SP, Reddin DB. Incidence, risk, and prevention of hamstring muscle injuries in professional rugby union. Am J Sports Med. 2006;34(8):1297-1306.

56. Verrall GM, Kalairajah Y, Slavotinek JP, Spriggins AJ. Assessment of player performance following return to sport after hamstring muscle strain injury. J Sci Med Sport. 2006;9(1-2):87-90.

57. Matava MJ, Ellis E, Shah NR, Pogue D, Williams T. Morel-lavallee lesion in a professional american football player. Am J Orthop. 2010;39(3):144-147.

58. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the national football league. Am J Sports Med. 2007;35(7):1162-1167.

59. Mellado JM, Bencardino JT. Morel-Lavallee lesion: review with emphasis on MR imaging. Magn Reson Imaging Clin N Am. 2005;13(4):775-782.

60. Harma A, Inan M, Ertem K. [The Morel-Lavallee lesion: a conservative approach to closed degloving injuries]. Acta Orthop Traumatol Turc. 2004;38(4):270-273.

61. Tseng S, Tornetta P 3rd. Percutaneous management of Morel-Lavallee lesions. J Bone Joint Surg Am. 2006;88(1):92-96.

62. Gilbert BC, Bui-Mansfield LT, Dejong S. MRI of a Morel-Lavellee lesion. AJR Am J Roentgenol. 2004;182(5):1347-1348.

Issue
The American Journal of Orthopedics - 45(6)
Issue
The American Journal of Orthopedics - 45(6)
Page Number
E308-E318
Page Number
E308-E318
Publications
Publications
Topics
Article Type
Display Headline
Thigh Injuries in American Football
Display Headline
Thigh Injuries in American Football
Sections
Disallow All Ads
Article PDF Media

Collagen Meniscus Implant

Article Type
Changed
Thu, 09/19/2019 - 13:25
Display Headline
Collagen Meniscus Implant

Ivy Sports Medicine (http://www.ivysportsmed.com/en)

Collagen Meniscus Implant

The number of patients undergoing arthroscopic partial meniscectomy has continued to increase. However, this is potentially not a benign procedure, as there are increased contact pressures on the articular cartilage even with the removal of only a segment of the meniscus.

The Collagen Meniscus Implant (CMI, Ivy Sports Medicine) is a resorbable and biocompatible Type I collagen matrix that was developed to restore the segmental loss of meniscal tissue in the knee. It consists of a porous cross-linked matrix scaffold that allows for the ingrowth of the body’s own cells. The CMI is the only meniscal implant composed of purely biological materials and is available in an off-the-shelf supply.

The CMI is available in the United States for use in the restoration of segmental loss of the medial meniscus. The CMI can be utilized in either an acute or chronic situation. In the acute case, it would be indicated when the medial meniscus is irreparable, and that segment must be removed. In the chronic case, the patient would have had a previous partial meniscectomy and/or failed meniscus repair and had developed either pain or signs of early articular cartilage wear in the compartment. The procedure can be done arthroscopically and as an outpatient. The CMI can be kept on the shelf to be available as needed; it has a 2-year shelf life. There are specialized instruments for measuring the length of implant needed and for delivery of the implant.

The CMI has been utilized clinically for 18 years with excellent clinical results. Patients treated with CMI have benefited in over 80% of cases. Studies have demonstrated improved knee function, activity levels, and pain values from the pre- to postoperative periods.1,2 In addition, functional improvements have been maintained for over 10 years. The reoperation rate has been demonstrated to be 10% to 20%, which is comparable to the reoperation rate after meniscal repair.

Surgical pearl: The surgical technique for insertion of the CMI is relatively uncomplicated (Figures A, B).

Figure.
The first step is the resection of all dysfunctional meniscus and then creating 90° walls to attach to posteriorly and anteriorly, and a firm peripheral rim to attach the CMI into.

The second step is to measure the length of your meniscus defect with the measuring rod.

Once measured, you want to oversize the implant 10% to 15% (ie, if you measure 30 mm, you will cut at least 34 mm). Use the measuring rod to measure the length of the CMI and mark your length. Use a new scalpel blade to cut the CMI.

 

 

Place the measured CMI into the delivery clamp and insert through a mini-arthrotomy into the meniscal defect. The fixation technique of the CMI is entirely up to the implanting surgeon. Most surgeons have used a combination of all-inside and inside-out meniscus repair techniques. It is recommended to start fixing the CMI first posteriorly. The posterior stitch is usually an all-inside horizontal mattress stitch. Coming 1 cm anteriorly, place a vertical mattress stitch. Continue this method sequentially while moving anteriorly. The anterior suture is the surgeon’s choice for device, but it should be a horizontal mattress like the most posterior stitch. It is important while tightening your suture tension to apply the concept of “approximated and not strangulated.” Once completed, close wounds in typical fashion.
References

1. Zaffagnini S, Marcheggiani Muccioli GM, Lopomo N, et al. Prospective long-term outcomes of the medial collagen meniscus implant versus partial medial meniscectomy: a minimum 10-year follow-up study. Am J Sports Med. 2011;39(5):977-985

2. Bulgheroni P, Murena L, Ratti C, Bulgheroni E, Ronga M, Cherubino P. Follow-up of collagen meniscus implant patients: clinical, radiological, and magnetic resonance imaging results at 5 years. Knee. 2010;17(3):224-229.

Article PDF
Author and Disclosure Information

Author’s Disclosure Statement: Dr. Gersoff reports that he is a consultant for Ivy Sports Medicine and Vericell.

Issue
The American Journal of Orthopedics - 45(6)
Publications
Topics
Page Number
394
Sections
Author and Disclosure Information

Author’s Disclosure Statement: Dr. Gersoff reports that he is a consultant for Ivy Sports Medicine and Vericell.

Author and Disclosure Information

Author’s Disclosure Statement: Dr. Gersoff reports that he is a consultant for Ivy Sports Medicine and Vericell.

Article PDF
Article PDF

Ivy Sports Medicine (http://www.ivysportsmed.com/en)

Collagen Meniscus Implant

The number of patients undergoing arthroscopic partial meniscectomy has continued to increase. However, this is potentially not a benign procedure, as there are increased contact pressures on the articular cartilage even with the removal of only a segment of the meniscus.

The Collagen Meniscus Implant (CMI, Ivy Sports Medicine) is a resorbable and biocompatible Type I collagen matrix that was developed to restore the segmental loss of meniscal tissue in the knee. It consists of a porous cross-linked matrix scaffold that allows for the ingrowth of the body’s own cells. The CMI is the only meniscal implant composed of purely biological materials and is available in an off-the-shelf supply.

The CMI is available in the United States for use in the restoration of segmental loss of the medial meniscus. The CMI can be utilized in either an acute or chronic situation. In the acute case, it would be indicated when the medial meniscus is irreparable, and that segment must be removed. In the chronic case, the patient would have had a previous partial meniscectomy and/or failed meniscus repair and had developed either pain or signs of early articular cartilage wear in the compartment. The procedure can be done arthroscopically and as an outpatient. The CMI can be kept on the shelf to be available as needed; it has a 2-year shelf life. There are specialized instruments for measuring the length of implant needed and for delivery of the implant.

The CMI has been utilized clinically for 18 years with excellent clinical results. Patients treated with CMI have benefited in over 80% of cases. Studies have demonstrated improved knee function, activity levels, and pain values from the pre- to postoperative periods.1,2 In addition, functional improvements have been maintained for over 10 years. The reoperation rate has been demonstrated to be 10% to 20%, which is comparable to the reoperation rate after meniscal repair.

Surgical pearl: The surgical technique for insertion of the CMI is relatively uncomplicated (Figures A, B).

Figure.
The first step is the resection of all dysfunctional meniscus and then creating 90° walls to attach to posteriorly and anteriorly, and a firm peripheral rim to attach the CMI into.

The second step is to measure the length of your meniscus defect with the measuring rod.

Once measured, you want to oversize the implant 10% to 15% (ie, if you measure 30 mm, you will cut at least 34 mm). Use the measuring rod to measure the length of the CMI and mark your length. Use a new scalpel blade to cut the CMI.

 

 

Place the measured CMI into the delivery clamp and insert through a mini-arthrotomy into the meniscal defect. The fixation technique of the CMI is entirely up to the implanting surgeon. Most surgeons have used a combination of all-inside and inside-out meniscus repair techniques. It is recommended to start fixing the CMI first posteriorly. The posterior stitch is usually an all-inside horizontal mattress stitch. Coming 1 cm anteriorly, place a vertical mattress stitch. Continue this method sequentially while moving anteriorly. The anterior suture is the surgeon’s choice for device, but it should be a horizontal mattress like the most posterior stitch. It is important while tightening your suture tension to apply the concept of “approximated and not strangulated.” Once completed, close wounds in typical fashion.

Ivy Sports Medicine (http://www.ivysportsmed.com/en)

Collagen Meniscus Implant

The number of patients undergoing arthroscopic partial meniscectomy has continued to increase. However, this is potentially not a benign procedure, as there are increased contact pressures on the articular cartilage even with the removal of only a segment of the meniscus.

The Collagen Meniscus Implant (CMI, Ivy Sports Medicine) is a resorbable and biocompatible Type I collagen matrix that was developed to restore the segmental loss of meniscal tissue in the knee. It consists of a porous cross-linked matrix scaffold that allows for the ingrowth of the body’s own cells. The CMI is the only meniscal implant composed of purely biological materials and is available in an off-the-shelf supply.

The CMI is available in the United States for use in the restoration of segmental loss of the medial meniscus. The CMI can be utilized in either an acute or chronic situation. In the acute case, it would be indicated when the medial meniscus is irreparable, and that segment must be removed. In the chronic case, the patient would have had a previous partial meniscectomy and/or failed meniscus repair and had developed either pain or signs of early articular cartilage wear in the compartment. The procedure can be done arthroscopically and as an outpatient. The CMI can be kept on the shelf to be available as needed; it has a 2-year shelf life. There are specialized instruments for measuring the length of implant needed and for delivery of the implant.

The CMI has been utilized clinically for 18 years with excellent clinical results. Patients treated with CMI have benefited in over 80% of cases. Studies have demonstrated improved knee function, activity levels, and pain values from the pre- to postoperative periods.1,2 In addition, functional improvements have been maintained for over 10 years. The reoperation rate has been demonstrated to be 10% to 20%, which is comparable to the reoperation rate after meniscal repair.

Surgical pearl: The surgical technique for insertion of the CMI is relatively uncomplicated (Figures A, B).

Figure.
The first step is the resection of all dysfunctional meniscus and then creating 90° walls to attach to posteriorly and anteriorly, and a firm peripheral rim to attach the CMI into.

The second step is to measure the length of your meniscus defect with the measuring rod.

Once measured, you want to oversize the implant 10% to 15% (ie, if you measure 30 mm, you will cut at least 34 mm). Use the measuring rod to measure the length of the CMI and mark your length. Use a new scalpel blade to cut the CMI.

 

 

Place the measured CMI into the delivery clamp and insert through a mini-arthrotomy into the meniscal defect. The fixation technique of the CMI is entirely up to the implanting surgeon. Most surgeons have used a combination of all-inside and inside-out meniscus repair techniques. It is recommended to start fixing the CMI first posteriorly. The posterior stitch is usually an all-inside horizontal mattress stitch. Coming 1 cm anteriorly, place a vertical mattress stitch. Continue this method sequentially while moving anteriorly. The anterior suture is the surgeon’s choice for device, but it should be a horizontal mattress like the most posterior stitch. It is important while tightening your suture tension to apply the concept of “approximated and not strangulated.” Once completed, close wounds in typical fashion.
References

1. Zaffagnini S, Marcheggiani Muccioli GM, Lopomo N, et al. Prospective long-term outcomes of the medial collagen meniscus implant versus partial medial meniscectomy: a minimum 10-year follow-up study. Am J Sports Med. 2011;39(5):977-985

2. Bulgheroni P, Murena L, Ratti C, Bulgheroni E, Ronga M, Cherubino P. Follow-up of collagen meniscus implant patients: clinical, radiological, and magnetic resonance imaging results at 5 years. Knee. 2010;17(3):224-229.

References

1. Zaffagnini S, Marcheggiani Muccioli GM, Lopomo N, et al. Prospective long-term outcomes of the medial collagen meniscus implant versus partial medial meniscectomy: a minimum 10-year follow-up study. Am J Sports Med. 2011;39(5):977-985

2. Bulgheroni P, Murena L, Ratti C, Bulgheroni E, Ronga M, Cherubino P. Follow-up of collagen meniscus implant patients: clinical, radiological, and magnetic resonance imaging results at 5 years. Knee. 2010;17(3):224-229.

Issue
The American Journal of Orthopedics - 45(6)
Issue
The American Journal of Orthopedics - 45(6)
Page Number
394
Page Number
394
Publications
Publications
Topics
Article Type
Display Headline
Collagen Meniscus Implant
Display Headline
Collagen Meniscus Implant
Sections
Disallow All Ads
Article PDF Media

Medical Issues in American Football: Eyes, Teeth, and Skin

Article Type
Changed
Thu, 09/19/2019 - 13:25
Display Headline
Medical Issues in American Football: Eyes, Teeth, and Skin

Orthopedic conditions are only one of the many medical issues football team physicians may face. In this review, we cover the management of a few of the most common nonorthopedic medical issues football team physicians are likely to encounter, including eye injuries, dental concerns, and skin conditions.

Eye Injuries

More than 2.5 million eye injuries occur each year, with 50,000 people permanently losing part or all of their vision.1 Eye injuries account for over 600,000 yearly emergency department visits; over 30% of these eye injuries were attributed to a sports injury.1 Football is classified as high risk for eye injury, along with baseball, hockey, basketball, and lacrosse.2 Common eye injury mechanisms are categorized as blunt, penetrating, and radiating. Blunt injuries are most common.2 When evaluating an athlete on the sideline, relevant history would include the size of the object, the level of force, and the direction from which the impact occurred. An examination should include best-corrected visual acuity using an eye chart, confrontational visual fields, assessment of extraocular movements, assessment of red reflex, and pupil evaluation with a light source.2

Cornea Injuries

The outermost layer of the eye, the cornea, can be subject to blunt and penetrating injuries. Corneal abrasions often occur from mechanical trauma, such as one from the fingernail of an opposing player, that disrupts the integrity of the corneal epithelium. A corneal abrasion can be identified by applying fluorescein strips after application of a topical anesthetic. Abrasions appear fluorescent green when viewed with a cobalt blue light. If an abrasion is identified, management includes preventing infection and treating pain. Prophylactic topical antibiotics can be applied, particularly for contact lens wearers. Patching has not shown benefit in treatment of pain.3 The physician can consider using topical nonsteroidal anti-inflammatory drugs, such as diclofenac or ketorolac, with a soft contact lens to treat the pain.4 The patient should follow up frequently for monitoring for infection and healing.

Orbital Fractures

Orbital fractures should be considered when an object larger than the orbital opening, such as an elbow or knee, causes blunt trauma to the surrounding bony structures, or a digital poke occurs to the globe.5 The floor of the orbit and medial wall are thin bones that often break sacrificially to protect the globe from rupture. Examination findings may include diplopia, sunken globe, numbness in the distribution of infraorbital nerve, or periorbital emphysema.6 Urgent evaluation should be considered to rule out associated intraocular damage. Imaging and a physical examination can help guide surgical management, if indicated. The most common outcome after this injury is diplopia with upper field gaze.5

Retina Issues

Trauma to the face or head may result in a separation of the retina from the underlying retinal pigment epithelium and allow vitreous fluid to seep in and further separate the layers, causing a retinal detachment. Symptoms may include flashes of light (photopsia), floaters, and visual field defects. Emergent referral is indicated, as the outcomes from this condition are time-sensitive. Consider placing an eye shield to prevent any further pressure on the globe.

Globe Injuries and Rupture

Another emergent ophthalmologic condition that can occur in football is globe rupture. Clinical findings usually prompt the clinician to consider this diagnosis. Hyphema (the collection of blood in the anterior chamber) may be seen in globe injuries. The most common clinical finding of athletes requiring hospitalization after an ocular injury is macroscopic hyphema (Figure 1).7-9

Figure 1.
Hyphema should be monitored with serial intraocular pressure evaluations, as increased pressure may lead to secondary complications. Another clinical finding that should cause the physician to consider possible globe rupture is the presence of severe subconjunctival hemorrhage encompassing 360° of the cornea.8 Pain and decreased vision occur with globe rupture. Placement of an eye shield to protect the globe from further pressure and immediate referral should be arranged. Prevention of endophthalmitis is key and prophylactic antibiotics are utilized.

Prompt referral is warranted when there is a sudden decrease or change in vision, pain during movements, photophobia, and floaters and/or flashes.2 Consideration of return to play should take into account the patient’s vision and comfort level, which should not be masked by topical analgesics. Protective eyewear has been mandated in several sports, and has decreased the rate of eye injuries.10 Polycarbonate lenses of 3-mm thickness are recommended due to the significant comparable strength and impact-resistance.2 During the preparticipation physical for high-risk sports, the utilization of protective eyewear should be discussed.

 

 

Dental Concerns

Dental injuries may present a challenge for the sports medicine clinician. Contact injuries from elbows, fists, and other nonprojectile objects typically result in low-speed, lower-energy injuries, such as soft tissue lacerations and contusions. On the other hand, high-speed injuries occurring from balls, pucks, and sticks may result in more significant trauma. Baseball accounts for the highest percentage of sports-related dental injuries (40.2%), while basketball was second (20.2%) and football third (12.5%). Over 75% of these injuries occurred in males.11

On-field management of dental injuries should always start with the primary trauma survey, including assessment of the athlete’s airway, breathing, and circulatory function, as well as a targeted cervical spine evaluation. When obtaining a history, one should recognize the mechanism of injury and assess for signs of concomitant injuries, ie, respiratory compromise, concussion, leakage of cerebrospinal fluid, and teeth alignment. Findings from this initial evaluation may reveal critical conditions that will require management in addition to the dental injury.

Of central concern in managing dental trauma is preserving the viability of the injured structures. Therefore, much attention is paid to the pulpal and root vitality of injured teeth. The International Association of Dental Traumology Dental Trauma Guidelines recommend a biological approach to the urgent care of dental injuries:12

1. Stabilize the injury by carefully repositioning displaced entities and suturing soft tissue lacerations.

2. Eliminate or reduce the complications from bacterial contamination by rinsing and flushing with available liquids and use of chlorhexidine when possible.

3. Promote the opportunity for healing by replanting avulsed teeth and repositioning displaced teeth.

4. Make every effort to allow continued development of alveolar ridges in children.

Mouth guards are the single most effective prevention strategy for most contact sport dental injuries. One meta-analysis demonstrated a pooled 86% increased risk of orofacial injuries in nonusers.13

To review the anatomy (and injuries) of the tooth, one must consider the Ellis classification of enamel, dentin, and pulp injuries (Figure 2).

Figure 2.
Class I involves only the enamel, class II involves the dentin and enamel, and class III involves the pulp, dentin, and enamel.

Tooth Subluxation

Tooth subluxations usually occur secondary to trauma and cause loosening of the tooth in its alveolar socket. A root fracture should be suspected in the setting of a subluxation. On exam, the tooth may be excessively mobile with gentle pressure. If unstable, immobilization with gauze packing or aluminum foil with dental follow-up is recommended.

Fractures

Ellis class I fractures are small chips in the enamel. There should be uniform color at the fracture site. A dental referral may be warranted to smooth rough enamel edges, but if no other injuries are present, these athletes may continue playing with some protection of the fractured surface. A mouth guard may be helpful to avoid mucosal lacerations.

Ellis class II fractures often present with sensitivity to inhaled air and to hot and cold temperatures. Yellow dentin is visible at the fracture site (Figure 3).

Figure 3.
The athletes should be restricted from contact activities, a calcium hydroxide dressing should be placed, and the fracture site should be covered with gauze or aluminum for protection. The athlete should be evaluated by a dentist within 24 hours.

Ellis class III fractures may also present with air and temperature sensitivity. Finger pressure may expose a large fracture. Pink or red pulp is visible at the fracture site. Wiping the fracture site with sterile gauze may reveal bleeding from the pulp. This is considered a dental emergency. Immediate restriction from contact sports participation and urgent dental evaluation is indicated for root canal and capping and to prevent abscess formation.

Tooth Avulsion

Tooth avulsions occur when a tooth is completely displaced from the socket (Figure 4).

Figure 4.
Primary teeth should not be re-implanted, but every attempt should be made to preserve the viability of adult teeth. When adult teeth are re-implanted within 20 minutes, there is an up to 90% rate of preserving the tooth’s viability. Ideally, this should be done in 5 to 10 minutes. If the tooth is out more than 6 hours, then there is a <5% chance of preserving tooth viability. Before attempting re-implantation immediately after the injury, gently trickle or rinse any debris from the tooth with sterile saline. Do not rub or scrub the root, as this will efface and damage the delicate periodontal ligaments crucial for the health of the root. Close attention should be paid to ensure the tooth is re-implanted in the correct orientation. Prophylactic antibiotics (such as amoxicillin-clavulanate) are indicated and a tetanus booster if the athlete’s immunization status is unknown or not up-to-date. If unable to re-implant, transport in sterile saline, Hank’s Balanced Salt Solution, milk, or in the athlete’s cheek. If any teeth are aspirated, they should be removed by bronchoscopy. Dental referral is warranted for repositioning, splinting, possible root canal therapy, and long-term follow-up. After consultation with a dentist, a number of athletes may return to play in 2 to 4 weeks with a splint, mouth guard, or mask.

 

 

Skin Issues

Dermatological issues are some of the most common medical conditions faced by a football team physician. Skin infections in particular can pose a significant challenge both diagnostically as well as from a clearance-to-play perspective, given the potential for infections to affect other participants, such as other members of the team. Skin infection rates vary by sport and age group, with one study reporting 28.56 infections per 100,000 athletic exposures in high school wrestlers, which was more than 10 times that of football.14 Still, football players are at a higher risk of skin infections given the contact nature of the sport and close person-to-person proximity. A precise diagnosis may be difficult early in the course of a skin eruption, and with differing guidelines from various professional societies, it may be best suited for medical personnel familiar with these conditions, such as a sports medicine physician or dermatologist, to manage these athletes. A thorough and systematic evaluation is recommended, as athletes are often treated with unnecessary antibiotics, which contributes to antibiotic resistance. Previous antibiotic use may also be a risk factor for developing community-­acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).15

Two terms sports medicine clinicians must be familiar with are “adequately protected” and “properly covered.” The National Collegiate Athletic Association (NCAA) defines a wound or skin condition as adequately protected when the condition is considered noninfectious, adequately treated by a healthcare provider, and is able to be properly covered. A skin infection is considered properly covered when the lesion is covered by a securely attached bandage or dressing that will contain all drainage and remain intact throughout the sport activity.16

Impetigo

Impetigo is often caused by Staphylococcus and Streptococcus subspecies. The classic presentation is a dry, honey-crusted lesion with an erythematous base. Culture or gram stain may be helpful, but treatment may be initiated on a clinical basis without these studies. Topical antibiotics may be used, but in the setting of multiple lesions or an outbreak, systemic (eg, oral) antibiotics are preferred. Oral antibiotics may also shorten the time to return to play. If not responsive to the initial treatment, MRSA should be considered. No new lesions for 48 hours and a minimum of 72 hours of therapy with no moist, exudative, or draining lesions are required prior to return to play. These lesions cannot be covered as the sole means of return to play.

Methicillin-Resistant Staphylococcus aureus

MRSA is one of the most challenging skin infections for the sports medicine clinician to manage. Several outbreaks have been reported in the high school, college, and professional settings.17-20 Standardized precautions and a proactive approach are key in preventing MRSA outbreaks. It appears that different activities within a given sport may contribute to MRSA risk. One study reported football linemen had the highest attack rate, while another study reported cornerbacks and wide receivers to have the highest rate of MRSA infections.17,20 The elbow area was the most common site infected in both studies.

Abscesses are best initially managed by incision and drainage as well as obtaining wound cultures (Figure 5).

Figure 5.
In the absence of systemic symptoms or cellulitis, oral antibiotics may not be necessary. However, should antibiotics be considered, depending on local resistance patterns, antibiotic choices include sulfamethoxazole-trimethoprim, doxycycline, or clindamycin.

Preventative measures are thought to be useful, especially in the management of teams. The Centers for Disease Control and Prevention has published guidelines for both clinicians and patients. Precautions including hand washing; encouraging good overall hygiene; avoiding whirlpools; discouraging the sharing of towels, razors, and athletic gear; maintaining clean equipment/facilities; and encouraging early reporting of skin lesions.14,17,21,22 Isolated cases of MRSA do not need to be reported, but if more than one athlete is infected, one should notify the athletic training and team coaching staff. In the setting of an outbreak, the physician may need to notify local or state health agencies. No new lesions for 48 hours and a minimum of 72 hours of therapy with no moist, exudative, or draining lesions are required prior to returning to play. These lesions cannot be covered as the sole means of return to play.

Tinea Pedis

Tinea pedis is a common dermatophyte infection involving the feet and is most commonly caused by Trichophyton rubrum. Its distribution is usually interdigital or along the plantar surface of the foot. Topical antifungals with either allylamines or azoles are usually sufficient. Terbinafine has been shown to have a shorter duration of treatment. Athletes with tinea pedis are not restricted from sports participation during treatment, as long as the lesions are properly covered.

 

 

Tinea Corporis

Tinea corporis is a common superficial fungal infection of the body. It classically presents as pruritic, annular lesions, with well-demarcated borders and central clearing (Figure 6).

Figure 6.
The periphery is often scaly. Evaluating a skin scrapping via culture or with potassium hydroxide (KOH) preparation may be helpful when a diagnosis is uncertain. Allylamines may be more efficacious than azoles. For small areas, topical agents should be sufficient, whereas larger areas may better respond to oral agents. This infection requires 72 hours of treatment, absence of new active lesions, and covering with a bio-occlusive dressing before return to play. Athletes with extensive lesions may need to be disqualified from contact sports activities.

Tinea Cruris

Commonly known as “jock-itch,” this fungal infection is often very pruritic and involves the groin or genital region. The area is also inflamed and scaly. Treatment usually consists of topical allylamines or azoles. Allylamines amines are often preferred, as they require a shorter duration of treatment. There are no specific guidelines on the return to play with these athletes. Clearance is at the team physician’s discretion, but usually there are no restrictions. Athletes with extensive lesions may need to be disqualified from contact sports activities.


Am J Orthop. 2016;45(6):377-382. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Owens PL, Mutter R. Emergency Department Visits Related to Eye Injuries, 2008. Agency for Healthcare Research and Quality Web site. http://www.hcup-us.ahrq.gov/reports/statbriefs/sb112.pdf. Published May 2011. Accessed August 18, 2016.

2. Rodriguez JO, Lavina AM, Agarwai A. Prevention and treatment of common eye injuries in sports. Am Fam Physician. 2003;67(7):1481-1496.

3. Lim CH, Turner A, Lim BX. Patching for corneal abrasion. Cochrane Database Syst Rev. 2016;7:CD004764.

4. Weaver CS, Terrell KM. Evidence-based emergency medicine. Update: do ophthalmic nonsteroidal anti-inflammatory drugs reduce the pain associated with simple corneal abrasion without delaying healing? Ann Emerg Med. 2003;41(1):134-140.

5. Williams RJ 3rd, Marx RG, Barnes R, O’Brien SJ, Warren RF. Fractures about the orbit in professional American football players. Am J Sports Med. 2001;29(1):55-57.

6. Forrest LA, Schuller DE, Strauss RH. Management of orbital blow-out fractures. Case reports and discussion. Am J Sports Med. 1989;17(2):217-220.

7. Barr A, Baines PS, Desai P, MacEwen CJ. Ocular sports injuries: the current picture. Br J Sports Med. 2000;34(6):456-458.

8. Pokhrel PK, Loftus SA. Ocular emergencies. Am Fam Physician. 2007;76(6):829-836.

9. Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. Eye Trauma—Hyphema. The Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013.

10. Lincoln AE, Caswell SV, Almquist JL, et al. Effectiveness of the women’s lacrosse protective eyewear mandate in the reduction of eye injuries. Am J Sports Med. 2012;40(3):611-614.

11. Stewart GB, Shields BJ, Fields S, Comstock RD, Smith GA. Consumer products and activities associated with dental injuries to children treated in United States emergency departments, 1990-2003. Dental Traumatol. 2009;25(4):399-405.

12. Bakland LK. Dental trauma guidelines. Pediatric Dent. 2013;35(2):106-108.

13. Knapik J, Marshall SW, Lee RB, et al. Mouthguards in sport activities: history, physical properties and Injury prevention effectiveness. Sports Med. 2007;37(2):117-144.

14. Ashack KA, Burton KA, Johnson TR, Currie DW, Comstock RD, Dellavalle RP. Skin infections among US high school athletes: a national survey. J Am Acad Dermatol. 2016;74(4):679-684.e1.

15. Ellis MW, Hospenthal DR, Dooley DP, Gray PJ, Murray CK. Natural history of community-acquired methicillin-resistant Staphylococcus aureus colonization and infection in soldiers. Clin Infect Dis. 2004;39(7):971-979.

16. The National Collegiate Athletic Association. 2014-15 NCAA Sports Medicine Handbook. http://www.ncaapublications.com/productdownloads/MD15.pdf. Revised June 2008. Accessed August 18, 2016.

17. Anderson BJ. The effectiveness of valacyclovir in preventing reactivation of herpes gladiatorum in wrestlers. Clin J Sport Med. 1999;9(2):86-90.

18. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis. 2011;52(3):e18-e55.

19. Jeffords MD, Batts K. Dermatology. In: O’Connor FG, Casa DJ, Davis BA, Pierre PS, Sallis RE, Wilder RP, eds. ACSM’s Sports Medicine: A Comprehensive Review. Riverwoods, IL: Wolters Kluwer; 2016:181-188.

20. Kazakova SV, Hageman JC, Matava M, et al. A clone of methicillin-resistant Staphylococcus aureus among professional football players. N Engl J Med. 2005;352(5):468-475.

21. Begier EM, Frenette K, Barrett NL, et al. A high-morbidity outbreak of methicillin-resistant Staphylococcus aureus among players on a college football team, facilitated by cosmetic body shaving and turf burns. Clin Infect Dis. 2004;39(10):1446-1453.

22. Geissler KE, Borchers JR. More than meets the eye: a rapidly progressive skin infection in a football player. Clin J Sport Med. 2015;25(3):e54-e56.

Article PDF
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Issue
The American Journal of Orthopedics - 45(6)
Publications
Topics
Page Number
377-382
Sections
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Article PDF
Article PDF

Orthopedic conditions are only one of the many medical issues football team physicians may face. In this review, we cover the management of a few of the most common nonorthopedic medical issues football team physicians are likely to encounter, including eye injuries, dental concerns, and skin conditions.

Eye Injuries

More than 2.5 million eye injuries occur each year, with 50,000 people permanently losing part or all of their vision.1 Eye injuries account for over 600,000 yearly emergency department visits; over 30% of these eye injuries were attributed to a sports injury.1 Football is classified as high risk for eye injury, along with baseball, hockey, basketball, and lacrosse.2 Common eye injury mechanisms are categorized as blunt, penetrating, and radiating. Blunt injuries are most common.2 When evaluating an athlete on the sideline, relevant history would include the size of the object, the level of force, and the direction from which the impact occurred. An examination should include best-corrected visual acuity using an eye chart, confrontational visual fields, assessment of extraocular movements, assessment of red reflex, and pupil evaluation with a light source.2

Cornea Injuries

The outermost layer of the eye, the cornea, can be subject to blunt and penetrating injuries. Corneal abrasions often occur from mechanical trauma, such as one from the fingernail of an opposing player, that disrupts the integrity of the corneal epithelium. A corneal abrasion can be identified by applying fluorescein strips after application of a topical anesthetic. Abrasions appear fluorescent green when viewed with a cobalt blue light. If an abrasion is identified, management includes preventing infection and treating pain. Prophylactic topical antibiotics can be applied, particularly for contact lens wearers. Patching has not shown benefit in treatment of pain.3 The physician can consider using topical nonsteroidal anti-inflammatory drugs, such as diclofenac or ketorolac, with a soft contact lens to treat the pain.4 The patient should follow up frequently for monitoring for infection and healing.

Orbital Fractures

Orbital fractures should be considered when an object larger than the orbital opening, such as an elbow or knee, causes blunt trauma to the surrounding bony structures, or a digital poke occurs to the globe.5 The floor of the orbit and medial wall are thin bones that often break sacrificially to protect the globe from rupture. Examination findings may include diplopia, sunken globe, numbness in the distribution of infraorbital nerve, or periorbital emphysema.6 Urgent evaluation should be considered to rule out associated intraocular damage. Imaging and a physical examination can help guide surgical management, if indicated. The most common outcome after this injury is diplopia with upper field gaze.5

Retina Issues

Trauma to the face or head may result in a separation of the retina from the underlying retinal pigment epithelium and allow vitreous fluid to seep in and further separate the layers, causing a retinal detachment. Symptoms may include flashes of light (photopsia), floaters, and visual field defects. Emergent referral is indicated, as the outcomes from this condition are time-sensitive. Consider placing an eye shield to prevent any further pressure on the globe.

Globe Injuries and Rupture

Another emergent ophthalmologic condition that can occur in football is globe rupture. Clinical findings usually prompt the clinician to consider this diagnosis. Hyphema (the collection of blood in the anterior chamber) may be seen in globe injuries. The most common clinical finding of athletes requiring hospitalization after an ocular injury is macroscopic hyphema (Figure 1).7-9

Figure 1.
Hyphema should be monitored with serial intraocular pressure evaluations, as increased pressure may lead to secondary complications. Another clinical finding that should cause the physician to consider possible globe rupture is the presence of severe subconjunctival hemorrhage encompassing 360° of the cornea.8 Pain and decreased vision occur with globe rupture. Placement of an eye shield to protect the globe from further pressure and immediate referral should be arranged. Prevention of endophthalmitis is key and prophylactic antibiotics are utilized.

Prompt referral is warranted when there is a sudden decrease or change in vision, pain during movements, photophobia, and floaters and/or flashes.2 Consideration of return to play should take into account the patient’s vision and comfort level, which should not be masked by topical analgesics. Protective eyewear has been mandated in several sports, and has decreased the rate of eye injuries.10 Polycarbonate lenses of 3-mm thickness are recommended due to the significant comparable strength and impact-resistance.2 During the preparticipation physical for high-risk sports, the utilization of protective eyewear should be discussed.

 

 

Dental Concerns

Dental injuries may present a challenge for the sports medicine clinician. Contact injuries from elbows, fists, and other nonprojectile objects typically result in low-speed, lower-energy injuries, such as soft tissue lacerations and contusions. On the other hand, high-speed injuries occurring from balls, pucks, and sticks may result in more significant trauma. Baseball accounts for the highest percentage of sports-related dental injuries (40.2%), while basketball was second (20.2%) and football third (12.5%). Over 75% of these injuries occurred in males.11

On-field management of dental injuries should always start with the primary trauma survey, including assessment of the athlete’s airway, breathing, and circulatory function, as well as a targeted cervical spine evaluation. When obtaining a history, one should recognize the mechanism of injury and assess for signs of concomitant injuries, ie, respiratory compromise, concussion, leakage of cerebrospinal fluid, and teeth alignment. Findings from this initial evaluation may reveal critical conditions that will require management in addition to the dental injury.

Of central concern in managing dental trauma is preserving the viability of the injured structures. Therefore, much attention is paid to the pulpal and root vitality of injured teeth. The International Association of Dental Traumology Dental Trauma Guidelines recommend a biological approach to the urgent care of dental injuries:12

1. Stabilize the injury by carefully repositioning displaced entities and suturing soft tissue lacerations.

2. Eliminate or reduce the complications from bacterial contamination by rinsing and flushing with available liquids and use of chlorhexidine when possible.

3. Promote the opportunity for healing by replanting avulsed teeth and repositioning displaced teeth.

4. Make every effort to allow continued development of alveolar ridges in children.

Mouth guards are the single most effective prevention strategy for most contact sport dental injuries. One meta-analysis demonstrated a pooled 86% increased risk of orofacial injuries in nonusers.13

To review the anatomy (and injuries) of the tooth, one must consider the Ellis classification of enamel, dentin, and pulp injuries (Figure 2).

Figure 2.
Class I involves only the enamel, class II involves the dentin and enamel, and class III involves the pulp, dentin, and enamel.

Tooth Subluxation

Tooth subluxations usually occur secondary to trauma and cause loosening of the tooth in its alveolar socket. A root fracture should be suspected in the setting of a subluxation. On exam, the tooth may be excessively mobile with gentle pressure. If unstable, immobilization with gauze packing or aluminum foil with dental follow-up is recommended.

Fractures

Ellis class I fractures are small chips in the enamel. There should be uniform color at the fracture site. A dental referral may be warranted to smooth rough enamel edges, but if no other injuries are present, these athletes may continue playing with some protection of the fractured surface. A mouth guard may be helpful to avoid mucosal lacerations.

Ellis class II fractures often present with sensitivity to inhaled air and to hot and cold temperatures. Yellow dentin is visible at the fracture site (Figure 3).

Figure 3.
The athletes should be restricted from contact activities, a calcium hydroxide dressing should be placed, and the fracture site should be covered with gauze or aluminum for protection. The athlete should be evaluated by a dentist within 24 hours.

Ellis class III fractures may also present with air and temperature sensitivity. Finger pressure may expose a large fracture. Pink or red pulp is visible at the fracture site. Wiping the fracture site with sterile gauze may reveal bleeding from the pulp. This is considered a dental emergency. Immediate restriction from contact sports participation and urgent dental evaluation is indicated for root canal and capping and to prevent abscess formation.

Tooth Avulsion

Tooth avulsions occur when a tooth is completely displaced from the socket (Figure 4).

Figure 4.
Primary teeth should not be re-implanted, but every attempt should be made to preserve the viability of adult teeth. When adult teeth are re-implanted within 20 minutes, there is an up to 90% rate of preserving the tooth’s viability. Ideally, this should be done in 5 to 10 minutes. If the tooth is out more than 6 hours, then there is a <5% chance of preserving tooth viability. Before attempting re-implantation immediately after the injury, gently trickle or rinse any debris from the tooth with sterile saline. Do not rub or scrub the root, as this will efface and damage the delicate periodontal ligaments crucial for the health of the root. Close attention should be paid to ensure the tooth is re-implanted in the correct orientation. Prophylactic antibiotics (such as amoxicillin-clavulanate) are indicated and a tetanus booster if the athlete’s immunization status is unknown or not up-to-date. If unable to re-implant, transport in sterile saline, Hank’s Balanced Salt Solution, milk, or in the athlete’s cheek. If any teeth are aspirated, they should be removed by bronchoscopy. Dental referral is warranted for repositioning, splinting, possible root canal therapy, and long-term follow-up. After consultation with a dentist, a number of athletes may return to play in 2 to 4 weeks with a splint, mouth guard, or mask.

 

 

Skin Issues

Dermatological issues are some of the most common medical conditions faced by a football team physician. Skin infections in particular can pose a significant challenge both diagnostically as well as from a clearance-to-play perspective, given the potential for infections to affect other participants, such as other members of the team. Skin infection rates vary by sport and age group, with one study reporting 28.56 infections per 100,000 athletic exposures in high school wrestlers, which was more than 10 times that of football.14 Still, football players are at a higher risk of skin infections given the contact nature of the sport and close person-to-person proximity. A precise diagnosis may be difficult early in the course of a skin eruption, and with differing guidelines from various professional societies, it may be best suited for medical personnel familiar with these conditions, such as a sports medicine physician or dermatologist, to manage these athletes. A thorough and systematic evaluation is recommended, as athletes are often treated with unnecessary antibiotics, which contributes to antibiotic resistance. Previous antibiotic use may also be a risk factor for developing community-­acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).15

Two terms sports medicine clinicians must be familiar with are “adequately protected” and “properly covered.” The National Collegiate Athletic Association (NCAA) defines a wound or skin condition as adequately protected when the condition is considered noninfectious, adequately treated by a healthcare provider, and is able to be properly covered. A skin infection is considered properly covered when the lesion is covered by a securely attached bandage or dressing that will contain all drainage and remain intact throughout the sport activity.16

Impetigo

Impetigo is often caused by Staphylococcus and Streptococcus subspecies. The classic presentation is a dry, honey-crusted lesion with an erythematous base. Culture or gram stain may be helpful, but treatment may be initiated on a clinical basis without these studies. Topical antibiotics may be used, but in the setting of multiple lesions or an outbreak, systemic (eg, oral) antibiotics are preferred. Oral antibiotics may also shorten the time to return to play. If not responsive to the initial treatment, MRSA should be considered. No new lesions for 48 hours and a minimum of 72 hours of therapy with no moist, exudative, or draining lesions are required prior to return to play. These lesions cannot be covered as the sole means of return to play.

Methicillin-Resistant Staphylococcus aureus

MRSA is one of the most challenging skin infections for the sports medicine clinician to manage. Several outbreaks have been reported in the high school, college, and professional settings.17-20 Standardized precautions and a proactive approach are key in preventing MRSA outbreaks. It appears that different activities within a given sport may contribute to MRSA risk. One study reported football linemen had the highest attack rate, while another study reported cornerbacks and wide receivers to have the highest rate of MRSA infections.17,20 The elbow area was the most common site infected in both studies.

Abscesses are best initially managed by incision and drainage as well as obtaining wound cultures (Figure 5).

Figure 5.
In the absence of systemic symptoms or cellulitis, oral antibiotics may not be necessary. However, should antibiotics be considered, depending on local resistance patterns, antibiotic choices include sulfamethoxazole-trimethoprim, doxycycline, or clindamycin.

Preventative measures are thought to be useful, especially in the management of teams. The Centers for Disease Control and Prevention has published guidelines for both clinicians and patients. Precautions including hand washing; encouraging good overall hygiene; avoiding whirlpools; discouraging the sharing of towels, razors, and athletic gear; maintaining clean equipment/facilities; and encouraging early reporting of skin lesions.14,17,21,22 Isolated cases of MRSA do not need to be reported, but if more than one athlete is infected, one should notify the athletic training and team coaching staff. In the setting of an outbreak, the physician may need to notify local or state health agencies. No new lesions for 48 hours and a minimum of 72 hours of therapy with no moist, exudative, or draining lesions are required prior to returning to play. These lesions cannot be covered as the sole means of return to play.

Tinea Pedis

Tinea pedis is a common dermatophyte infection involving the feet and is most commonly caused by Trichophyton rubrum. Its distribution is usually interdigital or along the plantar surface of the foot. Topical antifungals with either allylamines or azoles are usually sufficient. Terbinafine has been shown to have a shorter duration of treatment. Athletes with tinea pedis are not restricted from sports participation during treatment, as long as the lesions are properly covered.

 

 

Tinea Corporis

Tinea corporis is a common superficial fungal infection of the body. It classically presents as pruritic, annular lesions, with well-demarcated borders and central clearing (Figure 6).

Figure 6.
The periphery is often scaly. Evaluating a skin scrapping via culture or with potassium hydroxide (KOH) preparation may be helpful when a diagnosis is uncertain. Allylamines may be more efficacious than azoles. For small areas, topical agents should be sufficient, whereas larger areas may better respond to oral agents. This infection requires 72 hours of treatment, absence of new active lesions, and covering with a bio-occlusive dressing before return to play. Athletes with extensive lesions may need to be disqualified from contact sports activities.

Tinea Cruris

Commonly known as “jock-itch,” this fungal infection is often very pruritic and involves the groin or genital region. The area is also inflamed and scaly. Treatment usually consists of topical allylamines or azoles. Allylamines amines are often preferred, as they require a shorter duration of treatment. There are no specific guidelines on the return to play with these athletes. Clearance is at the team physician’s discretion, but usually there are no restrictions. Athletes with extensive lesions may need to be disqualified from contact sports activities.


Am J Orthop. 2016;45(6):377-382. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Orthopedic conditions are only one of the many medical issues football team physicians may face. In this review, we cover the management of a few of the most common nonorthopedic medical issues football team physicians are likely to encounter, including eye injuries, dental concerns, and skin conditions.

Eye Injuries

More than 2.5 million eye injuries occur each year, with 50,000 people permanently losing part or all of their vision.1 Eye injuries account for over 600,000 yearly emergency department visits; over 30% of these eye injuries were attributed to a sports injury.1 Football is classified as high risk for eye injury, along with baseball, hockey, basketball, and lacrosse.2 Common eye injury mechanisms are categorized as blunt, penetrating, and radiating. Blunt injuries are most common.2 When evaluating an athlete on the sideline, relevant history would include the size of the object, the level of force, and the direction from which the impact occurred. An examination should include best-corrected visual acuity using an eye chart, confrontational visual fields, assessment of extraocular movements, assessment of red reflex, and pupil evaluation with a light source.2

Cornea Injuries

The outermost layer of the eye, the cornea, can be subject to blunt and penetrating injuries. Corneal abrasions often occur from mechanical trauma, such as one from the fingernail of an opposing player, that disrupts the integrity of the corneal epithelium. A corneal abrasion can be identified by applying fluorescein strips after application of a topical anesthetic. Abrasions appear fluorescent green when viewed with a cobalt blue light. If an abrasion is identified, management includes preventing infection and treating pain. Prophylactic topical antibiotics can be applied, particularly for contact lens wearers. Patching has not shown benefit in treatment of pain.3 The physician can consider using topical nonsteroidal anti-inflammatory drugs, such as diclofenac or ketorolac, with a soft contact lens to treat the pain.4 The patient should follow up frequently for monitoring for infection and healing.

Orbital Fractures

Orbital fractures should be considered when an object larger than the orbital opening, such as an elbow or knee, causes blunt trauma to the surrounding bony structures, or a digital poke occurs to the globe.5 The floor of the orbit and medial wall are thin bones that often break sacrificially to protect the globe from rupture. Examination findings may include diplopia, sunken globe, numbness in the distribution of infraorbital nerve, or periorbital emphysema.6 Urgent evaluation should be considered to rule out associated intraocular damage. Imaging and a physical examination can help guide surgical management, if indicated. The most common outcome after this injury is diplopia with upper field gaze.5

Retina Issues

Trauma to the face or head may result in a separation of the retina from the underlying retinal pigment epithelium and allow vitreous fluid to seep in and further separate the layers, causing a retinal detachment. Symptoms may include flashes of light (photopsia), floaters, and visual field defects. Emergent referral is indicated, as the outcomes from this condition are time-sensitive. Consider placing an eye shield to prevent any further pressure on the globe.

Globe Injuries and Rupture

Another emergent ophthalmologic condition that can occur in football is globe rupture. Clinical findings usually prompt the clinician to consider this diagnosis. Hyphema (the collection of blood in the anterior chamber) may be seen in globe injuries. The most common clinical finding of athletes requiring hospitalization after an ocular injury is macroscopic hyphema (Figure 1).7-9

Figure 1.
Hyphema should be monitored with serial intraocular pressure evaluations, as increased pressure may lead to secondary complications. Another clinical finding that should cause the physician to consider possible globe rupture is the presence of severe subconjunctival hemorrhage encompassing 360° of the cornea.8 Pain and decreased vision occur with globe rupture. Placement of an eye shield to protect the globe from further pressure and immediate referral should be arranged. Prevention of endophthalmitis is key and prophylactic antibiotics are utilized.

Prompt referral is warranted when there is a sudden decrease or change in vision, pain during movements, photophobia, and floaters and/or flashes.2 Consideration of return to play should take into account the patient’s vision and comfort level, which should not be masked by topical analgesics. Protective eyewear has been mandated in several sports, and has decreased the rate of eye injuries.10 Polycarbonate lenses of 3-mm thickness are recommended due to the significant comparable strength and impact-resistance.2 During the preparticipation physical for high-risk sports, the utilization of protective eyewear should be discussed.

 

 

Dental Concerns

Dental injuries may present a challenge for the sports medicine clinician. Contact injuries from elbows, fists, and other nonprojectile objects typically result in low-speed, lower-energy injuries, such as soft tissue lacerations and contusions. On the other hand, high-speed injuries occurring from balls, pucks, and sticks may result in more significant trauma. Baseball accounts for the highest percentage of sports-related dental injuries (40.2%), while basketball was second (20.2%) and football third (12.5%). Over 75% of these injuries occurred in males.11

On-field management of dental injuries should always start with the primary trauma survey, including assessment of the athlete’s airway, breathing, and circulatory function, as well as a targeted cervical spine evaluation. When obtaining a history, one should recognize the mechanism of injury and assess for signs of concomitant injuries, ie, respiratory compromise, concussion, leakage of cerebrospinal fluid, and teeth alignment. Findings from this initial evaluation may reveal critical conditions that will require management in addition to the dental injury.

Of central concern in managing dental trauma is preserving the viability of the injured structures. Therefore, much attention is paid to the pulpal and root vitality of injured teeth. The International Association of Dental Traumology Dental Trauma Guidelines recommend a biological approach to the urgent care of dental injuries:12

1. Stabilize the injury by carefully repositioning displaced entities and suturing soft tissue lacerations.

2. Eliminate or reduce the complications from bacterial contamination by rinsing and flushing with available liquids and use of chlorhexidine when possible.

3. Promote the opportunity for healing by replanting avulsed teeth and repositioning displaced teeth.

4. Make every effort to allow continued development of alveolar ridges in children.

Mouth guards are the single most effective prevention strategy for most contact sport dental injuries. One meta-analysis demonstrated a pooled 86% increased risk of orofacial injuries in nonusers.13

To review the anatomy (and injuries) of the tooth, one must consider the Ellis classification of enamel, dentin, and pulp injuries (Figure 2).

Figure 2.
Class I involves only the enamel, class II involves the dentin and enamel, and class III involves the pulp, dentin, and enamel.

Tooth Subluxation

Tooth subluxations usually occur secondary to trauma and cause loosening of the tooth in its alveolar socket. A root fracture should be suspected in the setting of a subluxation. On exam, the tooth may be excessively mobile with gentle pressure. If unstable, immobilization with gauze packing or aluminum foil with dental follow-up is recommended.

Fractures

Ellis class I fractures are small chips in the enamel. There should be uniform color at the fracture site. A dental referral may be warranted to smooth rough enamel edges, but if no other injuries are present, these athletes may continue playing with some protection of the fractured surface. A mouth guard may be helpful to avoid mucosal lacerations.

Ellis class II fractures often present with sensitivity to inhaled air and to hot and cold temperatures. Yellow dentin is visible at the fracture site (Figure 3).

Figure 3.
The athletes should be restricted from contact activities, a calcium hydroxide dressing should be placed, and the fracture site should be covered with gauze or aluminum for protection. The athlete should be evaluated by a dentist within 24 hours.

Ellis class III fractures may also present with air and temperature sensitivity. Finger pressure may expose a large fracture. Pink or red pulp is visible at the fracture site. Wiping the fracture site with sterile gauze may reveal bleeding from the pulp. This is considered a dental emergency. Immediate restriction from contact sports participation and urgent dental evaluation is indicated for root canal and capping and to prevent abscess formation.

Tooth Avulsion

Tooth avulsions occur when a tooth is completely displaced from the socket (Figure 4).

Figure 4.
Primary teeth should not be re-implanted, but every attempt should be made to preserve the viability of adult teeth. When adult teeth are re-implanted within 20 minutes, there is an up to 90% rate of preserving the tooth’s viability. Ideally, this should be done in 5 to 10 minutes. If the tooth is out more than 6 hours, then there is a <5% chance of preserving tooth viability. Before attempting re-implantation immediately after the injury, gently trickle or rinse any debris from the tooth with sterile saline. Do not rub or scrub the root, as this will efface and damage the delicate periodontal ligaments crucial for the health of the root. Close attention should be paid to ensure the tooth is re-implanted in the correct orientation. Prophylactic antibiotics (such as amoxicillin-clavulanate) are indicated and a tetanus booster if the athlete’s immunization status is unknown or not up-to-date. If unable to re-implant, transport in sterile saline, Hank’s Balanced Salt Solution, milk, or in the athlete’s cheek. If any teeth are aspirated, they should be removed by bronchoscopy. Dental referral is warranted for repositioning, splinting, possible root canal therapy, and long-term follow-up. After consultation with a dentist, a number of athletes may return to play in 2 to 4 weeks with a splint, mouth guard, or mask.

 

 

Skin Issues

Dermatological issues are some of the most common medical conditions faced by a football team physician. Skin infections in particular can pose a significant challenge both diagnostically as well as from a clearance-to-play perspective, given the potential for infections to affect other participants, such as other members of the team. Skin infection rates vary by sport and age group, with one study reporting 28.56 infections per 100,000 athletic exposures in high school wrestlers, which was more than 10 times that of football.14 Still, football players are at a higher risk of skin infections given the contact nature of the sport and close person-to-person proximity. A precise diagnosis may be difficult early in the course of a skin eruption, and with differing guidelines from various professional societies, it may be best suited for medical personnel familiar with these conditions, such as a sports medicine physician or dermatologist, to manage these athletes. A thorough and systematic evaluation is recommended, as athletes are often treated with unnecessary antibiotics, which contributes to antibiotic resistance. Previous antibiotic use may also be a risk factor for developing community-­acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).15

Two terms sports medicine clinicians must be familiar with are “adequately protected” and “properly covered.” The National Collegiate Athletic Association (NCAA) defines a wound or skin condition as adequately protected when the condition is considered noninfectious, adequately treated by a healthcare provider, and is able to be properly covered. A skin infection is considered properly covered when the lesion is covered by a securely attached bandage or dressing that will contain all drainage and remain intact throughout the sport activity.16

Impetigo

Impetigo is often caused by Staphylococcus and Streptococcus subspecies. The classic presentation is a dry, honey-crusted lesion with an erythematous base. Culture or gram stain may be helpful, but treatment may be initiated on a clinical basis without these studies. Topical antibiotics may be used, but in the setting of multiple lesions or an outbreak, systemic (eg, oral) antibiotics are preferred. Oral antibiotics may also shorten the time to return to play. If not responsive to the initial treatment, MRSA should be considered. No new lesions for 48 hours and a minimum of 72 hours of therapy with no moist, exudative, or draining lesions are required prior to return to play. These lesions cannot be covered as the sole means of return to play.

Methicillin-Resistant Staphylococcus aureus

MRSA is one of the most challenging skin infections for the sports medicine clinician to manage. Several outbreaks have been reported in the high school, college, and professional settings.17-20 Standardized precautions and a proactive approach are key in preventing MRSA outbreaks. It appears that different activities within a given sport may contribute to MRSA risk. One study reported football linemen had the highest attack rate, while another study reported cornerbacks and wide receivers to have the highest rate of MRSA infections.17,20 The elbow area was the most common site infected in both studies.

Abscesses are best initially managed by incision and drainage as well as obtaining wound cultures (Figure 5).

Figure 5.
In the absence of systemic symptoms or cellulitis, oral antibiotics may not be necessary. However, should antibiotics be considered, depending on local resistance patterns, antibiotic choices include sulfamethoxazole-trimethoprim, doxycycline, or clindamycin.

Preventative measures are thought to be useful, especially in the management of teams. The Centers for Disease Control and Prevention has published guidelines for both clinicians and patients. Precautions including hand washing; encouraging good overall hygiene; avoiding whirlpools; discouraging the sharing of towels, razors, and athletic gear; maintaining clean equipment/facilities; and encouraging early reporting of skin lesions.14,17,21,22 Isolated cases of MRSA do not need to be reported, but if more than one athlete is infected, one should notify the athletic training and team coaching staff. In the setting of an outbreak, the physician may need to notify local or state health agencies. No new lesions for 48 hours and a minimum of 72 hours of therapy with no moist, exudative, or draining lesions are required prior to returning to play. These lesions cannot be covered as the sole means of return to play.

Tinea Pedis

Tinea pedis is a common dermatophyte infection involving the feet and is most commonly caused by Trichophyton rubrum. Its distribution is usually interdigital or along the plantar surface of the foot. Topical antifungals with either allylamines or azoles are usually sufficient. Terbinafine has been shown to have a shorter duration of treatment. Athletes with tinea pedis are not restricted from sports participation during treatment, as long as the lesions are properly covered.

 

 

Tinea Corporis

Tinea corporis is a common superficial fungal infection of the body. It classically presents as pruritic, annular lesions, with well-demarcated borders and central clearing (Figure 6).

Figure 6.
The periphery is often scaly. Evaluating a skin scrapping via culture or with potassium hydroxide (KOH) preparation may be helpful when a diagnosis is uncertain. Allylamines may be more efficacious than azoles. For small areas, topical agents should be sufficient, whereas larger areas may better respond to oral agents. This infection requires 72 hours of treatment, absence of new active lesions, and covering with a bio-occlusive dressing before return to play. Athletes with extensive lesions may need to be disqualified from contact sports activities.

Tinea Cruris

Commonly known as “jock-itch,” this fungal infection is often very pruritic and involves the groin or genital region. The area is also inflamed and scaly. Treatment usually consists of topical allylamines or azoles. Allylamines amines are often preferred, as they require a shorter duration of treatment. There are no specific guidelines on the return to play with these athletes. Clearance is at the team physician’s discretion, but usually there are no restrictions. Athletes with extensive lesions may need to be disqualified from contact sports activities.


Am J Orthop. 2016;45(6):377-382. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Owens PL, Mutter R. Emergency Department Visits Related to Eye Injuries, 2008. Agency for Healthcare Research and Quality Web site. http://www.hcup-us.ahrq.gov/reports/statbriefs/sb112.pdf. Published May 2011. Accessed August 18, 2016.

2. Rodriguez JO, Lavina AM, Agarwai A. Prevention and treatment of common eye injuries in sports. Am Fam Physician. 2003;67(7):1481-1496.

3. Lim CH, Turner A, Lim BX. Patching for corneal abrasion. Cochrane Database Syst Rev. 2016;7:CD004764.

4. Weaver CS, Terrell KM. Evidence-based emergency medicine. Update: do ophthalmic nonsteroidal anti-inflammatory drugs reduce the pain associated with simple corneal abrasion without delaying healing? Ann Emerg Med. 2003;41(1):134-140.

5. Williams RJ 3rd, Marx RG, Barnes R, O’Brien SJ, Warren RF. Fractures about the orbit in professional American football players. Am J Sports Med. 2001;29(1):55-57.

6. Forrest LA, Schuller DE, Strauss RH. Management of orbital blow-out fractures. Case reports and discussion. Am J Sports Med. 1989;17(2):217-220.

7. Barr A, Baines PS, Desai P, MacEwen CJ. Ocular sports injuries: the current picture. Br J Sports Med. 2000;34(6):456-458.

8. Pokhrel PK, Loftus SA. Ocular emergencies. Am Fam Physician. 2007;76(6):829-836.

9. Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. Eye Trauma—Hyphema. The Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013.

10. Lincoln AE, Caswell SV, Almquist JL, et al. Effectiveness of the women’s lacrosse protective eyewear mandate in the reduction of eye injuries. Am J Sports Med. 2012;40(3):611-614.

11. Stewart GB, Shields BJ, Fields S, Comstock RD, Smith GA. Consumer products and activities associated with dental injuries to children treated in United States emergency departments, 1990-2003. Dental Traumatol. 2009;25(4):399-405.

12. Bakland LK. Dental trauma guidelines. Pediatric Dent. 2013;35(2):106-108.

13. Knapik J, Marshall SW, Lee RB, et al. Mouthguards in sport activities: history, physical properties and Injury prevention effectiveness. Sports Med. 2007;37(2):117-144.

14. Ashack KA, Burton KA, Johnson TR, Currie DW, Comstock RD, Dellavalle RP. Skin infections among US high school athletes: a national survey. J Am Acad Dermatol. 2016;74(4):679-684.e1.

15. Ellis MW, Hospenthal DR, Dooley DP, Gray PJ, Murray CK. Natural history of community-acquired methicillin-resistant Staphylococcus aureus colonization and infection in soldiers. Clin Infect Dis. 2004;39(7):971-979.

16. The National Collegiate Athletic Association. 2014-15 NCAA Sports Medicine Handbook. http://www.ncaapublications.com/productdownloads/MD15.pdf. Revised June 2008. Accessed August 18, 2016.

17. Anderson BJ. The effectiveness of valacyclovir in preventing reactivation of herpes gladiatorum in wrestlers. Clin J Sport Med. 1999;9(2):86-90.

18. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis. 2011;52(3):e18-e55.

19. Jeffords MD, Batts K. Dermatology. In: O’Connor FG, Casa DJ, Davis BA, Pierre PS, Sallis RE, Wilder RP, eds. ACSM’s Sports Medicine: A Comprehensive Review. Riverwoods, IL: Wolters Kluwer; 2016:181-188.

20. Kazakova SV, Hageman JC, Matava M, et al. A clone of methicillin-resistant Staphylococcus aureus among professional football players. N Engl J Med. 2005;352(5):468-475.

21. Begier EM, Frenette K, Barrett NL, et al. A high-morbidity outbreak of methicillin-resistant Staphylococcus aureus among players on a college football team, facilitated by cosmetic body shaving and turf burns. Clin Infect Dis. 2004;39(10):1446-1453.

22. Geissler KE, Borchers JR. More than meets the eye: a rapidly progressive skin infection in a football player. Clin J Sport Med. 2015;25(3):e54-e56.

References

1. Owens PL, Mutter R. Emergency Department Visits Related to Eye Injuries, 2008. Agency for Healthcare Research and Quality Web site. http://www.hcup-us.ahrq.gov/reports/statbriefs/sb112.pdf. Published May 2011. Accessed August 18, 2016.

2. Rodriguez JO, Lavina AM, Agarwai A. Prevention and treatment of common eye injuries in sports. Am Fam Physician. 2003;67(7):1481-1496.

3. Lim CH, Turner A, Lim BX. Patching for corneal abrasion. Cochrane Database Syst Rev. 2016;7:CD004764.

4. Weaver CS, Terrell KM. Evidence-based emergency medicine. Update: do ophthalmic nonsteroidal anti-inflammatory drugs reduce the pain associated with simple corneal abrasion without delaying healing? Ann Emerg Med. 2003;41(1):134-140.

5. Williams RJ 3rd, Marx RG, Barnes R, O’Brien SJ, Warren RF. Fractures about the orbit in professional American football players. Am J Sports Med. 2001;29(1):55-57.

6. Forrest LA, Schuller DE, Strauss RH. Management of orbital blow-out fractures. Case reports and discussion. Am J Sports Med. 1989;17(2):217-220.

7. Barr A, Baines PS, Desai P, MacEwen CJ. Ocular sports injuries: the current picture. Br J Sports Med. 2000;34(6):456-458.

8. Pokhrel PK, Loftus SA. Ocular emergencies. Am Fam Physician. 2007;76(6):829-836.

9. Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. Eye Trauma—Hyphema. The Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013.

10. Lincoln AE, Caswell SV, Almquist JL, et al. Effectiveness of the women’s lacrosse protective eyewear mandate in the reduction of eye injuries. Am J Sports Med. 2012;40(3):611-614.

11. Stewart GB, Shields BJ, Fields S, Comstock RD, Smith GA. Consumer products and activities associated with dental injuries to children treated in United States emergency departments, 1990-2003. Dental Traumatol. 2009;25(4):399-405.

12. Bakland LK. Dental trauma guidelines. Pediatric Dent. 2013;35(2):106-108.

13. Knapik J, Marshall SW, Lee RB, et al. Mouthguards in sport activities: history, physical properties and Injury prevention effectiveness. Sports Med. 2007;37(2):117-144.

14. Ashack KA, Burton KA, Johnson TR, Currie DW, Comstock RD, Dellavalle RP. Skin infections among US high school athletes: a national survey. J Am Acad Dermatol. 2016;74(4):679-684.e1.

15. Ellis MW, Hospenthal DR, Dooley DP, Gray PJ, Murray CK. Natural history of community-acquired methicillin-resistant Staphylococcus aureus colonization and infection in soldiers. Clin Infect Dis. 2004;39(7):971-979.

16. The National Collegiate Athletic Association. 2014-15 NCAA Sports Medicine Handbook. http://www.ncaapublications.com/productdownloads/MD15.pdf. Revised June 2008. Accessed August 18, 2016.

17. Anderson BJ. The effectiveness of valacyclovir in preventing reactivation of herpes gladiatorum in wrestlers. Clin J Sport Med. 1999;9(2):86-90.

18. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis. 2011;52(3):e18-e55.

19. Jeffords MD, Batts K. Dermatology. In: O’Connor FG, Casa DJ, Davis BA, Pierre PS, Sallis RE, Wilder RP, eds. ACSM’s Sports Medicine: A Comprehensive Review. Riverwoods, IL: Wolters Kluwer; 2016:181-188.

20. Kazakova SV, Hageman JC, Matava M, et al. A clone of methicillin-resistant Staphylococcus aureus among professional football players. N Engl J Med. 2005;352(5):468-475.

21. Begier EM, Frenette K, Barrett NL, et al. A high-morbidity outbreak of methicillin-resistant Staphylococcus aureus among players on a college football team, facilitated by cosmetic body shaving and turf burns. Clin Infect Dis. 2004;39(10):1446-1453.

22. Geissler KE, Borchers JR. More than meets the eye: a rapidly progressive skin infection in a football player. Clin J Sport Med. 2015;25(3):e54-e56.

Issue
The American Journal of Orthopedics - 45(6)
Issue
The American Journal of Orthopedics - 45(6)
Page Number
377-382
Page Number
377-382
Publications
Publications
Topics
Article Type
Display Headline
Medical Issues in American Football: Eyes, Teeth, and Skin
Display Headline
Medical Issues in American Football: Eyes, Teeth, and Skin
Sections
Disallow All Ads
Article PDF Media

In My Athletic Trainer’s Bag

Article Type
Changed
Thu, 09/19/2019 - 13:25
Display Headline
In My Athletic Trainer’s Bag

Editor’s Note: Doug Quon, MAT, ATC, PES, is the Assistant Athletic Trainer for the Washington Redskins. Click the PDF button below to view and download his list of the essential components of an athletic trainer’s bag for high school football and Division II and III collegiate football.

 

Article PDF
Author and Disclosure Information

Author’s Disclosure Statement: Mr. Quon reports no actual or potential conflict of interest in relation to this article.

Issue
The American Journal of Orthopedics - 45(6)
Publications
Topics
Page Number
376
Sections
Author and Disclosure Information

Author’s Disclosure Statement: Mr. Quon reports no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Author’s Disclosure Statement: Mr. Quon reports no actual or potential conflict of interest in relation to this article.

Article PDF
Article PDF

Editor’s Note: Doug Quon, MAT, ATC, PES, is the Assistant Athletic Trainer for the Washington Redskins. Click the PDF button below to view and download his list of the essential components of an athletic trainer’s bag for high school football and Division II and III collegiate football.

 

Editor’s Note: Doug Quon, MAT, ATC, PES, is the Assistant Athletic Trainer for the Washington Redskins. Click the PDF button below to view and download his list of the essential components of an athletic trainer’s bag for high school football and Division II and III collegiate football.

 

Issue
The American Journal of Orthopedics - 45(6)
Issue
The American Journal of Orthopedics - 45(6)
Page Number
376
Page Number
376
Publications
Publications
Topics
Article Type
Display Headline
In My Athletic Trainer’s Bag
Display Headline
In My Athletic Trainer’s Bag
Sections
Disallow All Ads
Article PDF Media

Knee Injuries in American Football: An Epidemiological Review

Article Type
Changed
Thu, 09/19/2019 - 13:25
Display Headline
Knee Injuries in American Football: An Epidemiological Review

Football is one of the most popular sports in the United States. Every year more than 1 million high school males and over 60,000 collegiate males participate in organized football. The number of males who play football is greater than the combined number of males and females who participate in track and field or basketball.1 Football has the highest injury rate amongst popular American sports.2 From 2001 to 2005, there was an estimated 1.1 million emergency room visits as a direct result of football.3 Injuries are more likely to occur during games,1,2,4,5 more likely to require surgery,4 and more likely to end the player’s season or career when compared to other sports.6 Of those injuries that end seasons or careers, the knee is the most common culprit.6 This is of particular concern because knee injuries are most common in football.1,2,5,7 This article reviews the epidemiology of 4 of the most common knee injuries in American football: tears of the anterior cruciate ligament (ACL), medial collateral ligament (MCL), medial patellofemoral ligament (MPFL), and posterior cruciate ligament (PCL).

Anterior Cruciate Ligament

The ACL is the primary structure preventing anterior tibial translation. It is composed of 2 anatomic bundles: the anteromedial and posterolateral bundles. The ACL originates from the posteromedial portion of the lateral femoral condyle and inserts between and slightly anterior to the tibial intercondylar eminence. The bundles are named for their relative insertions onto the tibia.

Injury to the ACL occurs both through noncontact and contact mechanisms. Typical noncontact mechanism is a forceful valgus collapse with the knee close to full extension with combined external or internal rotation of the tibia.8 This is often the result of a sudden deceleration prior to a change in direction.9 Contact injuries to the ACL are the result of a direct blow to the knee causing valgus collapse.9 The majority of ACL injuries amongst all sports are a result of a noncontact mechanism. However, Dragoo and colleagues10 found the majority of football ACL injuries (55%-60%) were from contact. As a result, football players are 4 times more likely to sustain ACL injuries than in other sports.11

ACL injuries are associated with significant time loss from sport. At the high school level, they are the most likely injury to end a season or career.6 Because these are higher-energy injuries, they are frequently associated with damage to additional structures. ACL injuries that occur in football are associated with increased rates of meniscus, chondral, and multi-ligamentous injuries.12,13

The incidence of ACL injuries increases with level of competition. In high school athletes it is 11.1 per 100,000 athlete exposures (AE).1,11 In collegiate football, the rate increases to 14.2 to 18 per 100,000 AE.2,14 Though no incidence data per AE was found in our review of the literature, there were 219 ACL injuries in the National Football League (NFL) from 2010 to 2013.15 In addition, 14.2% of retired NFL athletes in one survey reported a history of ACL injury.16

The most common high-risk positions are running backs and linebackers. Brophy and colleagues17 found that 9.7% of running backs and 8.9% of linebackers participating in the NFL Combine had a history of ACL injury. This may be because both the running back and linebacker are involved in frequent high-energy collisions and often quickly change direction. Other studies have also identified running backs and linebackers as high risk, in addition to tight ends, wide receivers, and interior linemen.13,15,18

Treatment of choice for elite level athletes with ACL injury is reconstruction.19 Of those who undergo ACL reconstruction, the rate of return to play ranges from 63% to 80%.20-22 The average time to return to play is 9 to 13 months. The odds of making a successful return hinges on how successful the athlete was prior to injury. Factors such as prior game experience, position on depth chart, being on scholarship, and draft position for NFL athletes have all been shown to have a positive predictive value on a patient’s chance of returning from ACL reconstruction.20,21

Players who return have variable levels of success afterwards. In a study of NFL quarterbacks who sustained ACL injuries, 12 out of 13 were able to return to game action with no appreciable dropoff in performance based on in-game production.23 Carey and colleagues24 looked specifically at NFL wide receivers and running backs and found an 80% return to play rate but with an approximate decrease in production of one-third upon return. Furthermore, in the Multicenter Orthopaedic Outcomes Network (MOON) cohort study, only 43% of participants felt they returned to their preoperative level.22

 

 

Medial Collateral Ligament

The MCL consists of superficial and deep components. The superficial MCL is the primary restraint to valgus laxity at the knee. The superficial MCL has 1 femoral and 2 tibial attachments. The deep MCL is a thickening of the medial joint capsule and runs deep and parallel to the superficial MCL. The amount of medial joint gapping with a valgus force on examination is used to grade severity of MCL injuries. Grade I is a <5-mm opening; Grade II, 5- to 10-mm opening; and grade III, >10-mm opening.

The MCL is the most common knee injury in high school, collegiate, and professional football.1,18,25-28 Injuries are typically due to contact when a valgus force is applied to the knee.29 The annual incidence of MCL injuries amongst high school football players is 24.2 per 100,000 AE.1 The positions that appear to be at greatest risk for MCL injuries are offensive and defensive linemen.18,30-32 In a review of 5047 collegiate athletes participating in the NFL Combine from 1987 to 2000, 23% of offensive linemen had a history of MCL injury, compared to the overall rate of 16%.33 In a similar study, Bradley and colleagues18 performed medical histories on athletes invited to the 2005 NFL Combine and also found offensive linemen had the highest rate of MCL injury at 33%, compared to the overall rate of 22%. They reasonably hypothesized that “chop blocks” and other players “rolling up” on the outside of linemen’s knees were responsible for these injuries. Albright and colleagues32 found that prophylactic knee braces decreased the incidence of MCL injuries in collegiate offensive lineman. However, additional studies have not been able to reproduce these results and the use of prophylactic knee braces remains controversial.26

Treatment of MCL injuries depends upon the grade of injury, associated injuries, and anatomical location of injury. Management of MCL injuries is for the most part nonsurgical. In 1974, Ellsasser and colleagues34 were the first to publish data on nonoperative management of Grade I and Grade II injuries with immediate motion and rehabilitation instead of cast immobilization. They found 93% of patients returned to football in 3 to 8 weeks.34 Derscheid and Garrick27 observed nonoperative treatment of Grade I and II sprains in collegiate football players, with a time loss of 10.6 days and 19.5 days for Grade I and II injuries, respectively. Holden and colleagues35 evaluated nonoperative management of Grade I and II MCL injuries in collegiate football players and found an average return to play of 21 days.

Grade III injury treatment is more controversial. Indelicato and colleagues36 demonstrated successful nonoperative management of Grade III MCL injuries in collegiate football players, with an average return to play of 64.4 days. Jones and colleagues37 had similar success with high school football players, with an average return to play of 34 days. However, isolated Grade III injuries are rare and therefore treatment is likely to be dictated by concomitant injuries. Fetto and Marshall38 found that 78% of Grade III injuries were associated with an additional ligamentous injury. Of those additional injuries, 95% were ACL tears.

Finally, one must consider the location of the MCL injury. Injuries of the distal MCL at its tibial insertion may result in poor healing, as the ligament is displaced away from its insertion. Therefore, some authors recommend surgical management for these injuries.39,40

Medial Patellofemoral Ligament

The patellofemoral joint is a complex structure in which the patella is stabilized within the trochlear groove of the femur by both bony and soft tissue structures. The MPFL is one of the most important soft tissue stabilizers. The MPFL is the primary restraint to lateral patellar translation within the first 20° of knee flexion, contributing to 60% of the total restraining force.41 The MPFL originates on the medial femoral condyle and inserts on the superomedial aspect of the patella.

Patellar instability is the subluxation or dislocation of the patella out of the trochlear groove. Patellar subluxation and dislocation account for approximately 3% of all knee injuries.42 Patella dislocations are more common in younger populations43-45 with the majority (52%-63%) occurring during sports.43,44,46 Mitchell and colleagues47 reported an incidence of 4.1 patellar subluxations/dislocations per 100,000 AE in high school football players.

Dislocation is most commonly the result of knee flexion with the tibia in a valgus position.44,48 The majority of patellar dislocations occur via a noncontact mechanism.44,48 However, the majority of these injuries in football are from contact (63%).47

Acute patellar dislocations are associated with more soft tissue damage than those with recurrent dislocations.46 In acute patella dislocations, the MPFL is almost always ruptured.44 In contrast, Fithian and colleagues46 found only 38% of recurrent dislocators had MPFL injury. As a result, it is thought that those with recurrent instability dislocate without trauma and do not have the same characteristics as those who dislocate from high-energy trauma in sport. Risk factors for atraumatic dislocation are numerous and have been well described in the literature.49 However, traumatic dislocators usually do not have risk factors.50

Traumatic patella dislocations are higher energy and are associated with chondral injury in up to 95%of cases 51 and osteochondral injury 58% to 76% of the time.52,53 In contrast, people with “articular hypermobility” are less likely to sustain articular damage.54 This concept is important when considering risk for recurrent patella dislocation. The literature reports a 17% to 50% rate of recurrent instability after acute patella dislocation.46,55,56 However, most studies do not distinguish between traumatic and atraumatic injuries. Because the majority of patellar dislocations in football occur through contact mechanisms, the rate of recurrent instability in these athletes may in fact be less than what is reported in the literature.

First-time patella dislocations are generally treated nonoperatively. Mitchell and colleagues47 reported that 72.6% of high school athletes with patella subluxation treated conservatively were able to return to sports within 3 weeks, compared to only 34.1% of those with patellar dislocations. In the same study, patellar dislocations were season-ending 37% of the time.47 Atkin and colleagues50 followed 74 patients treated conservatively for first-time patellar dislocation and noted 58% at 6 months still had difficulty in squatting, jumping, or cutting.

Those who have failed conservative management and have an additional dislocation are 7 times more likely to redislocate.46 Therefore, they are usually treated operatively with MPFL reconstruction. Return to sport ranges from 3 to 6 months,57 with 53% to 77.3% reporting return to their previous functionality.57-59 Overall, 84.1% of patients are able to return to sport with 1.2% risk of recurrent dislocation.60

 

 

Posterior Cruciate Ligament

The PCL is the primary posterior stabilizer of the knee.61,62 It consists of the anterolateral and posteromedial bundles, named by their insertion on the posterior tibial plateau. The larger, stronger anterolateral bundle is the primary restraint to posterior tibial translation.63

Due to the relative infrequency of PCL injuries, there is a paucity of epidemiological data on sports-related PCL injuries. These injuries in the literature are commonly found due to traffic accidents (45%-57%) or from sports (33%-40%).64,65 According to Swensen and colleagues,1 PCL injuries account for 2.4% of all high school sport knee injuries. In a cohort of 62 knees with PCL injuries, Patel and colleagues66 found football was the most common cause of injury (19.3%).

The most common mechanism of injury in athletes is knee hyperflexion or a direct blow to the tibia in a flexed knee.67 In football, contact mechanisms are the most common. In a 16-year review of the National Collegiate Athletic Association (NCAA) injury surveillance system, the incidence of contact PCL injuries during games were 7.3 times higher than noncontact.68 The most common activity was being tackled, which accounted for 22.9% of all PCL injuries.68

Due to the high energy of these injuries, isolated PCL injuries are rare. In one trauma center’s experience, 96.5% of PCL injuries had an additional ligament injury.64 In that study, injuries to the PCL were associated with posterolateral corner, ACL, and MCL injuries 62%, 46%, and 31% of the time, respectively.64,69

Because isolated PCL injuries are rare, clinicians must rely on a thorough history and physical examination when evaluating athletes with knee injuries. Classification of PCL injuries is based on the amount of posterior tibial translation in relation to the femur with the knee bent to 90°. Grade I is 1 to 5 mm; Grade II, 6 to 10 mm; and Grade III, >10 mm. If there is suspicion of a PCL injury, there should be a very low threshold for magnetic resonance imaging, given the high association with additional injuries.

Natural history of Grade I and II isolated PCL injuries is generally favorable compared to Grade III and multi-ligamentous injuries.70 As a result, isolated Grade I and II PCL injuries are generally treated nonoperatively. Treatment consists of physical therapy with emphasis on quadriceps strengthening. Return to play can be considered as early as 2 to 4 weeks from injury.71 Recent long-term data have shown successful conservative management of Grade I and II injuries with quadriceps strength to 97% of contralateral leg and full range of motion.72 However, there was 11% moderate to severe osteoarthritis in these patients at a mean follow-up of 14.3 years.72 Fowler and Messieh67 managed athletes with 7 isolated complete PCL tears and 5 partial tears nonoperatively, all of whom were able to return to sport without limitation. Parolie and Bergfeld73 managed 25 athletes with isolated PCL tears conservatively. In this study, 80% of athletes reported satisfaction and 68% returned to previous level of play.73 Neither of the aforementioned studies specify the grades of the injuries. Finally, Patel and colleagues66 managed 6 NFL athletes with Grade I and II injuries nonoperatively, and all were able to return to sport.

Treatment of isolated Grade III PCL injuries is more controversial, and no consensus exists in the literature. In an epidemiological study, Dick and colleagues68 found that only 39% of NCAA football athletes underwent surgery for their torn PCLs, compared to 79% of ACL injuries. However, their study makes no mention to the severity of these injuries. Numerous options exist for PCL reconstruction, with no consensus on the preferred method.

Conclusion

Knee injuries are the most common injury in football. Knowledge of the natural history of these injuries, as well as treatment options and expected outcomes, will help treating physicians educate their patients on the optimal treatment and manage return to play expectations.

Am J Orthop. 2016;45(6):368-373. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Swenson DM, Collins CL, Best TM, Flanigan DC, Fields SK, Comstock RD. Epidemiology of knee injuries among U.S. high school athletes, 2005/2006-2010/2011. Med Sci Sports Exerc. 2013;45(3):462-469.

2. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train. 2007;42(2):311-319.

3. Mello MJ, Myers R, Christian JB, Palmisciano L, Linakis JG. Injuries in youth football: national emergency department visits during 2001-2005 for young and adolescent players. Acad Emerg Med. 2009;16(3):243-248.

4. Rechel JA, Collins CL, Comstock RD. Epidemiology of injuries requiring surgery among high school athletes in the United States, 2005 to 2010. J Trauma. 2011;71(4):982-989.

5. Ingram JG, Fields SK, Yard EE, Comstock RD. Epidemiology of knee injuries among boys and girls in US high school athletics. Am J Sports Med. 2008;36(6):1116-1122.

6. Tirabassi J, Brou L, Khodaee M, Lefort R, Fields SK, Comstock RD. Epidemiology of high school sports-related injuries resulting in medical disqualification: 2005-2006 through 2013-2014 academic years. Am J Sports Med. 2016 May 10. [Epub ahead of print]

7. Fernandez WG, Yard EE, Comstock RD. Epidemiology of lower extremity injuries among U.S. high school athletes. Acad Emerg Med. 2007;14(7):641-645.

8. Olsen OE, Myklebust G, Engebretsen L, Bahr R. Injury mechanisms for anterior cruciate ligament injuries in team handball: a systematic video analysis. Am J Sports Med. 2004;32(4):1002-1012.

9. Boden BP, Dean GS, Feagin JA Jr, Garrett WE Jr. Mechanisms of anterior cruciate ligament injury. Orthopedics. 2000;23(6):573-578.

10. 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(3):191-195.

11. Joseph AM, Collins CL, Henke NM, Yard EE, Fields SK, Comstock RD. A multisport epidemiologic comparison of anterior cruciate ligament injuries in high school athletics. J Athl Train. 2013;48(6):810-817.

12. Granan LP, Inacio MC, Maletis GB, Funahashi TT, Engebretsen L. Sport-specific injury pattern recorded during anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(12):2814-2818.

13. Bradley JP, Klimkiewicz JJ, Rytel MJ, Powell JW. Anterior cruciate ligament injuries in the National Football League: epidemiology and current treatment trends among team physicians. Arthroscopy. 2002;18(5):502-509.

14. Dragoo JL, Braun HJ, Durham JL, Chen MR, Harris AH. Incidence and risk factors for injuries to the anterior cruciate ligament in National Collegiate Athletic Association football: data from the 2004-2005 through 2008-2009 National Collegiate Athletic Association Injury Surveillance System. Am J Sports Med. 2012;40(5):990-995.

15. Dodson CC, Secrist ES, Bhat SB, Woods DP, Deluca PF. Anterior cruciate ligamenti in National Football League athletes from 2010 to 2013: a descriptive epidemiology study. Orthop J Sports Med. 2016;4(3):2325967116631949.

16. Golightly YM, Marshall SW, Callahan LF, Guskiewicz K. Early-onset arthritis in retired National Football League players. J Phys Act Health. 2009;6(5):638-643.

17. Brophy RH, Lyman S, Chehab EL, Barnes RP, Rodeo SA, Warren RF. Predictive value of prior injury on career in professional American football is affected by player position. Am J Sports Med. 2009;37(4):768-775.

18. Bradley J, Honkamp NJ, Jost P, West R, Norwig J, Kaplan LD. Incidence and variance of knee injuries in elite college football players. Am J Orthop. 2008;37(6):310-314.

19. Erickson BJ, Harris JD, Fillingham YA, et al. Anterior cruciate ligament reconstruction practice patterns by NFL and NCAA football team physicians. Arthroscopy. 2014;30(6):731-738.

20. Daruawalla JH, Greis PE, Hancock R; ASP Collaborative Group, Xerogeanes JW. Rates and determinants of return to play after anterior cruciate ligament reconstruction in NCAA Division 1 college football athletes: a study of the ACC, SEC, and PAC-12 conferences. Orthop J Sports Med. 2014;2(8):2325967114543901.

21. Shah VM, Andrews JR, Fleisig GS, McMichael CS, Lemak LJ. Return to play after anterior cruciate ligament reconstruction in National Football League athletes. Am J Sports Med. 2010;38(11):2233-2239.

22. McCullough KA, Phelps KD, Spindler KP, et al. Return to high school- and college-level football after anterior cruciate ligament reconstruction: a Multicenter Orthopaedic Outcomes Network (MOON) cohort study. Am J Sports Med. 2012;40(11):2523-2529.

23. Erickson BJ, Harris JD, Heninger JR, et al. Performance and return-to-sport after ACL reconstruction in NFL quarterbacks. Orthopedics. 2014;37(8):e728-e734.

24. Carey JL, Huffman GR, Parekh SG, Sennett BJ. Outcomes of anterior cruciate ligament injuries to running backs and wide receivers in the National Football League. Am J Sports Med. 2006;34(12):1911-1917.

25. Hershman EB, Anderson R, Bergfeld JA, et al. An analysis of specific lower extremity injury rates on grass and FieldTurf playing surfaces in National Football League Games: 2000-2009 seasons. Am J Sports Med. 2012;40(10):2200-2205.

26. Salata MJ, Gibbs AE, Sekiya JK. The effectiveness of prophylactic knee bracing in American football: a systematic review. Sports Health. 2010;2(5):375-379.

27. Derscheid GL, Garrick JG. Medial collateral ligament injuries in football. Nonoperative management of grade I and grade II sprains. Am J Sports Med. 1981;9(6):365-368.

28. Meyers MC, Barnhill BS. Incidence, causes, and severity of high school football injuries on FieldTurf versus natural grass: a 5-year prospective study. Am J Sports Med. 2004;32(7):1626-1638.

29. Lundblad M, Waldén M, Magnusson H, Karlsson J, Ekstrand J. The UEFA injury study: 11-year data concerning 346 MCL injuries and time to return to play. Br J Sports Med. 2013;47(12):759-762.

30. Hewson GF Jr, Mendini RA, Wang JB. Prophylactic knee bracing in college football. Am J Sports Med. 1986;14(4):262-266.

31. Rovere GD, Haupt HA, Yates CS. Prophylactic knee bracing in college football. Am J Sports Med. 1987;15(2):111-116.

32. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee sprains in college football. Brace wear preferences and injury risk. Am J Sports Med. 1994;22(1):2-11.

33. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine--trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.

34. Ellsasser JC, Reynolds FC, Omohundro JR. The non-operative treatment of collateral ligament injuries of the knee in professional football players. An analysis of seventy-four injuries treated non-operatively and twenty-four injuries treated surgically. J Bone Joint Surg Am. 1974;56(6):1185-1190.

35. Holden DL, Eggert AW, Butler JE. The nonoperative treatment of grade I and II medial collateral ligament injuries to the knee. Am J Sports Med. 1983;11(5):340-344.

36. Indelicato PA, Hermansdorfer J, Huegel M. Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate football players. Clin Orthop Relat Res. 1990;(256):174-177.

37. Jones RE, Henley MB, Francis P. Nonoperative management of isolated grade III collateral ligament injury in high school football players. Clin Orthop Relat Res. 1986;(213):137-140.

38. Fetto JF, Marshall JL. Medial collateral ligament injuries of the knee: a rationale for treatment. Clin Orthop Relat Res. 1978;(132):206-218.

39. Corten K, Hoser C, Fink C, Bellemans J. Case reports: a Stener-like lesion of the medial collateral ligament of the knee. Clin Orthop Relat Res. 2010;468(1):289-293.

40. Marchant MH Jr, Tibor LM, Sekiya JK, Hardaker WT Jr, Garrett WE Jr, Taylor DC. Management of medial-sided knee injuries, part 1: medial collateral ligament. Am J Sports Med. 2011;39(5):1102-1113.

41. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 1998;26(1):59-65.

42. Casteleyn PP, Handelberg F. Arthroscopy in the diagnosis of occult dislocation of the patella. Acta Orthop Belg. 1989;55(3):381-383.

43. Waterman BR, Belmont PJ Jr, Owens BD. Patellar dislocation in the United States: role of sex, age, race, and athletic participation. J Knee Surg. 2012;25(1):51-57.

44. Sillanpää P, Mattila VM, Iivonen T, Visuri T, Pihlajamäki H. Incidence and risk factors of acute traumatic primary patellar dislocation. Med Sci Sports Exerc. 2008;40(4):606-611.

45. Hsiao M, Owens BD, Burks R, Sturdivant RX, Cameron KL. Incidence of acute traumatic patellar dislocation among active-duty United States military service members. Am J Sports Med. 2010;38(10):1997-2004.

46. Fithian DC, Paxton EW, Stone ML, et al. Epidemiology and natural history of acute patellar dislocation. Am J Sports Med. 2004;32(5):1114-1121.

47. Mitchell J, Magnussen RA, Collins CL, et al. Epidemiology of patellofemoral instability injuries among high school athletes in the United States. Am J Sports Med. 2015;43(7):1676-1682.

48. Nikku R, Nietosvaara Y, Aalto K, Kallio PE. The mechanism of primary patellar dislocation: trauma history of 126 patients. Acta Orthop. 2009;80(4):432-434.

49. Tsai CH, Hsu CJ, Hung CH, Hsu HC. Primary traumatic patellar dislocation. J Orthop Surg Res. 2012;7:21.

50. Atkin DM, Fithian DC, Marangi KS, Stone ML, Dobson BE, Mendelsohn C. Characteristics of patients with primary acute lateral patellar dislocation and their recovery within the first 6 months of injury. Am J Sports Med. 2000;28(4):472-479.

51. Nomura E, Inoue M, Kurimura M. Chondral and osteochondral injuries associated with acute patellar dislocation. Arthroscopy. 2003;19(7):717-721.

52. Kirsch MD, Fitzgerald SW, Friedman H, Rogers LF. Transient lateral patellar dislocation: diagnosis with MR imaging. AJR Am J Roentgenol. 1993;161(1):109-113.

53. Virolainen H, Visuri T, Kuusela T. Acute dislocation of the patella: MR findings. Radiology. 1993;189(1):243-246.

54. Stanitski CL. Articular hypermobility and chondral injury in patients with acute patellar dislocation. Am J Sports Med. 1995;23(2):146-150.

55. Mäenpää H, Huhtala H, Lehto MU. Recurrence after patellar dislocation. Redislocation in 37/75 patients followed for 6-24 years. Acta Orthop Scand. 1997;68(5):424-426.

56. Buchner M, Baudendistel B, Sabo D, Schmitt H. Acute traumatic primary patellar dislocation: long-term results comparing conservative and surgical treatment. Clin J Sport Med. 2005;15(2):62-66.

57. Fisher B, Nyland J, Brand E, Curtin B. Medial patellofemoral ligament reconstruction for recurrent patellar dislocation: a systematic review including rehabilitation and return-to-sports efficacy. Arthroscopy. 2010;26(10):1384-1394.

58. Lippacher S, Dreyhaupt J, Williams SR, Reichel H, Nelitz M. Reconstruction of the medial patellofemoral ligament: clinical outcomes and return to sports. Am J Sports Med. 2014;42(7):1661-1668.

59. Panni AS, Alam M, Cerciello S, Vasso M, Maffulli N. Medial patellofemoral ligament reconstruction with a divergent patellar transverse 2-tunnel technique. Am J Sports Med. 2011;39(12):2647-1655.

60. Schneider DK, Grawe B, Magnussen RA, et al. Outcomes after isolated medial patellofemoral ligament reconstruction for the treatment of recurrent lateral patellar dislocations: a systematic review and meta-analysis. Am J Sports Med. 2016 Feb 12. [Epub ahead of print]

61. Amis AA, Bull AM, Gupte CM, Hijazi I, Race A, Robinson JR. Biomechanics of the PCL and related structures: posterolateral, posteromedial and meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc. 2003;11(5):271-281.

62. Fu FH, Harner CD, Johnson DL, Miller MD, Woo SL. Biomechanics of knee ligaments: basic concepts and clinical application. Instr Course Lect. 1994;43:137-148.

63. Markolf KL, Feeley BT, Tejwani SG, Martin DE, McAllister DR. Changes in knee laxity and ligament force after sectioning the posteromedial bundle of the posterior cruciate ligament. Arthroscopy. 2006; 22(10):1100-1106.

64. Ganelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: Part II. Arthroscopy. 1995;11(5):526-529.

65. Schulz MS, Russe K, Weiler A, Eichhorn HJ, Strobel MJ. Epidemiology of posterior cruciate ligament injuries. Arch Orthop Trauma Surg. 2003;123(4):186-191.

66. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The nonoperative treatment of acute, isolated (partial or complete) posterior cruciate ligament-deficient knees: an intermediate-term follow-up study. HSS J. 2007;3(2):137-146.

67. Fowler PJ, Messieh SS. Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med. 1987;15(6):553-557.

68. Dick R, Ferrara MS, Agel J, et al. Descriptive epidemiology of collegiate men’s football injuries: National Collegiate Athletic Association Injury Surveillance System, 1988-1989 through 2003-2004. J Athl Train. 2007;42(2):221-233.

69. LaPrade CM, Civitarese DM, Rasmussen MT, LaPrade RF. Emerging updates on the posterior cruciate ligament: a review of the current literature. Am J Sports Med. 2015;43(12):3077-3092.

70. Torg JS, Barton TM, Pavlov H, Stine R. Natural history of the posterior cruciate ligament-deficient knee. Clin Orthop Relat Res. 1989(246):208-216.

71. Miller MD. Orthopaedic Knowledge Update: Sports Medicine 5. Rosemont, IL; American Academy of Orthopaedic Surgeons; 2016.

72. Shelbourne KD, Clark M, Gray T. Minimum 10-year follow-up of patients after an acute, isolated posterior cruciate ligament injury treated nonoperatively. Am J Sports Med. 2013;41(7):1526-1533.

73. Parolie JM, Bergfeld JA. Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med. 1986;14(1):35-38.

Article PDF
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Issue
The American Journal of Orthopedics - 45(6)
Publications
Topics
Page Number
368-373
Sections
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Article PDF
Article PDF

Football is one of the most popular sports in the United States. Every year more than 1 million high school males and over 60,000 collegiate males participate in organized football. The number of males who play football is greater than the combined number of males and females who participate in track and field or basketball.1 Football has the highest injury rate amongst popular American sports.2 From 2001 to 2005, there was an estimated 1.1 million emergency room visits as a direct result of football.3 Injuries are more likely to occur during games,1,2,4,5 more likely to require surgery,4 and more likely to end the player’s season or career when compared to other sports.6 Of those injuries that end seasons or careers, the knee is the most common culprit.6 This is of particular concern because knee injuries are most common in football.1,2,5,7 This article reviews the epidemiology of 4 of the most common knee injuries in American football: tears of the anterior cruciate ligament (ACL), medial collateral ligament (MCL), medial patellofemoral ligament (MPFL), and posterior cruciate ligament (PCL).

Anterior Cruciate Ligament

The ACL is the primary structure preventing anterior tibial translation. It is composed of 2 anatomic bundles: the anteromedial and posterolateral bundles. The ACL originates from the posteromedial portion of the lateral femoral condyle and inserts between and slightly anterior to the tibial intercondylar eminence. The bundles are named for their relative insertions onto the tibia.

Injury to the ACL occurs both through noncontact and contact mechanisms. Typical noncontact mechanism is a forceful valgus collapse with the knee close to full extension with combined external or internal rotation of the tibia.8 This is often the result of a sudden deceleration prior to a change in direction.9 Contact injuries to the ACL are the result of a direct blow to the knee causing valgus collapse.9 The majority of ACL injuries amongst all sports are a result of a noncontact mechanism. However, Dragoo and colleagues10 found the majority of football ACL injuries (55%-60%) were from contact. As a result, football players are 4 times more likely to sustain ACL injuries than in other sports.11

ACL injuries are associated with significant time loss from sport. At the high school level, they are the most likely injury to end a season or career.6 Because these are higher-energy injuries, they are frequently associated with damage to additional structures. ACL injuries that occur in football are associated with increased rates of meniscus, chondral, and multi-ligamentous injuries.12,13

The incidence of ACL injuries increases with level of competition. In high school athletes it is 11.1 per 100,000 athlete exposures (AE).1,11 In collegiate football, the rate increases to 14.2 to 18 per 100,000 AE.2,14 Though no incidence data per AE was found in our review of the literature, there were 219 ACL injuries in the National Football League (NFL) from 2010 to 2013.15 In addition, 14.2% of retired NFL athletes in one survey reported a history of ACL injury.16

The most common high-risk positions are running backs and linebackers. Brophy and colleagues17 found that 9.7% of running backs and 8.9% of linebackers participating in the NFL Combine had a history of ACL injury. This may be because both the running back and linebacker are involved in frequent high-energy collisions and often quickly change direction. Other studies have also identified running backs and linebackers as high risk, in addition to tight ends, wide receivers, and interior linemen.13,15,18

Treatment of choice for elite level athletes with ACL injury is reconstruction.19 Of those who undergo ACL reconstruction, the rate of return to play ranges from 63% to 80%.20-22 The average time to return to play is 9 to 13 months. The odds of making a successful return hinges on how successful the athlete was prior to injury. Factors such as prior game experience, position on depth chart, being on scholarship, and draft position for NFL athletes have all been shown to have a positive predictive value on a patient’s chance of returning from ACL reconstruction.20,21

Players who return have variable levels of success afterwards. In a study of NFL quarterbacks who sustained ACL injuries, 12 out of 13 were able to return to game action with no appreciable dropoff in performance based on in-game production.23 Carey and colleagues24 looked specifically at NFL wide receivers and running backs and found an 80% return to play rate but with an approximate decrease in production of one-third upon return. Furthermore, in the Multicenter Orthopaedic Outcomes Network (MOON) cohort study, only 43% of participants felt they returned to their preoperative level.22

 

 

Medial Collateral Ligament

The MCL consists of superficial and deep components. The superficial MCL is the primary restraint to valgus laxity at the knee. The superficial MCL has 1 femoral and 2 tibial attachments. The deep MCL is a thickening of the medial joint capsule and runs deep and parallel to the superficial MCL. The amount of medial joint gapping with a valgus force on examination is used to grade severity of MCL injuries. Grade I is a <5-mm opening; Grade II, 5- to 10-mm opening; and grade III, >10-mm opening.

The MCL is the most common knee injury in high school, collegiate, and professional football.1,18,25-28 Injuries are typically due to contact when a valgus force is applied to the knee.29 The annual incidence of MCL injuries amongst high school football players is 24.2 per 100,000 AE.1 The positions that appear to be at greatest risk for MCL injuries are offensive and defensive linemen.18,30-32 In a review of 5047 collegiate athletes participating in the NFL Combine from 1987 to 2000, 23% of offensive linemen had a history of MCL injury, compared to the overall rate of 16%.33 In a similar study, Bradley and colleagues18 performed medical histories on athletes invited to the 2005 NFL Combine and also found offensive linemen had the highest rate of MCL injury at 33%, compared to the overall rate of 22%. They reasonably hypothesized that “chop blocks” and other players “rolling up” on the outside of linemen’s knees were responsible for these injuries. Albright and colleagues32 found that prophylactic knee braces decreased the incidence of MCL injuries in collegiate offensive lineman. However, additional studies have not been able to reproduce these results and the use of prophylactic knee braces remains controversial.26

Treatment of MCL injuries depends upon the grade of injury, associated injuries, and anatomical location of injury. Management of MCL injuries is for the most part nonsurgical. In 1974, Ellsasser and colleagues34 were the first to publish data on nonoperative management of Grade I and Grade II injuries with immediate motion and rehabilitation instead of cast immobilization. They found 93% of patients returned to football in 3 to 8 weeks.34 Derscheid and Garrick27 observed nonoperative treatment of Grade I and II sprains in collegiate football players, with a time loss of 10.6 days and 19.5 days for Grade I and II injuries, respectively. Holden and colleagues35 evaluated nonoperative management of Grade I and II MCL injuries in collegiate football players and found an average return to play of 21 days.

Grade III injury treatment is more controversial. Indelicato and colleagues36 demonstrated successful nonoperative management of Grade III MCL injuries in collegiate football players, with an average return to play of 64.4 days. Jones and colleagues37 had similar success with high school football players, with an average return to play of 34 days. However, isolated Grade III injuries are rare and therefore treatment is likely to be dictated by concomitant injuries. Fetto and Marshall38 found that 78% of Grade III injuries were associated with an additional ligamentous injury. Of those additional injuries, 95% were ACL tears.

Finally, one must consider the location of the MCL injury. Injuries of the distal MCL at its tibial insertion may result in poor healing, as the ligament is displaced away from its insertion. Therefore, some authors recommend surgical management for these injuries.39,40

Medial Patellofemoral Ligament

The patellofemoral joint is a complex structure in which the patella is stabilized within the trochlear groove of the femur by both bony and soft tissue structures. The MPFL is one of the most important soft tissue stabilizers. The MPFL is the primary restraint to lateral patellar translation within the first 20° of knee flexion, contributing to 60% of the total restraining force.41 The MPFL originates on the medial femoral condyle and inserts on the superomedial aspect of the patella.

Patellar instability is the subluxation or dislocation of the patella out of the trochlear groove. Patellar subluxation and dislocation account for approximately 3% of all knee injuries.42 Patella dislocations are more common in younger populations43-45 with the majority (52%-63%) occurring during sports.43,44,46 Mitchell and colleagues47 reported an incidence of 4.1 patellar subluxations/dislocations per 100,000 AE in high school football players.

Dislocation is most commonly the result of knee flexion with the tibia in a valgus position.44,48 The majority of patellar dislocations occur via a noncontact mechanism.44,48 However, the majority of these injuries in football are from contact (63%).47

Acute patellar dislocations are associated with more soft tissue damage than those with recurrent dislocations.46 In acute patella dislocations, the MPFL is almost always ruptured.44 In contrast, Fithian and colleagues46 found only 38% of recurrent dislocators had MPFL injury. As a result, it is thought that those with recurrent instability dislocate without trauma and do not have the same characteristics as those who dislocate from high-energy trauma in sport. Risk factors for atraumatic dislocation are numerous and have been well described in the literature.49 However, traumatic dislocators usually do not have risk factors.50

Traumatic patella dislocations are higher energy and are associated with chondral injury in up to 95%of cases 51 and osteochondral injury 58% to 76% of the time.52,53 In contrast, people with “articular hypermobility” are less likely to sustain articular damage.54 This concept is important when considering risk for recurrent patella dislocation. The literature reports a 17% to 50% rate of recurrent instability after acute patella dislocation.46,55,56 However, most studies do not distinguish between traumatic and atraumatic injuries. Because the majority of patellar dislocations in football occur through contact mechanisms, the rate of recurrent instability in these athletes may in fact be less than what is reported in the literature.

First-time patella dislocations are generally treated nonoperatively. Mitchell and colleagues47 reported that 72.6% of high school athletes with patella subluxation treated conservatively were able to return to sports within 3 weeks, compared to only 34.1% of those with patellar dislocations. In the same study, patellar dislocations were season-ending 37% of the time.47 Atkin and colleagues50 followed 74 patients treated conservatively for first-time patellar dislocation and noted 58% at 6 months still had difficulty in squatting, jumping, or cutting.

Those who have failed conservative management and have an additional dislocation are 7 times more likely to redislocate.46 Therefore, they are usually treated operatively with MPFL reconstruction. Return to sport ranges from 3 to 6 months,57 with 53% to 77.3% reporting return to their previous functionality.57-59 Overall, 84.1% of patients are able to return to sport with 1.2% risk of recurrent dislocation.60

 

 

Posterior Cruciate Ligament

The PCL is the primary posterior stabilizer of the knee.61,62 It consists of the anterolateral and posteromedial bundles, named by their insertion on the posterior tibial plateau. The larger, stronger anterolateral bundle is the primary restraint to posterior tibial translation.63

Due to the relative infrequency of PCL injuries, there is a paucity of epidemiological data on sports-related PCL injuries. These injuries in the literature are commonly found due to traffic accidents (45%-57%) or from sports (33%-40%).64,65 According to Swensen and colleagues,1 PCL injuries account for 2.4% of all high school sport knee injuries. In a cohort of 62 knees with PCL injuries, Patel and colleagues66 found football was the most common cause of injury (19.3%).

The most common mechanism of injury in athletes is knee hyperflexion or a direct blow to the tibia in a flexed knee.67 In football, contact mechanisms are the most common. In a 16-year review of the National Collegiate Athletic Association (NCAA) injury surveillance system, the incidence of contact PCL injuries during games were 7.3 times higher than noncontact.68 The most common activity was being tackled, which accounted for 22.9% of all PCL injuries.68

Due to the high energy of these injuries, isolated PCL injuries are rare. In one trauma center’s experience, 96.5% of PCL injuries had an additional ligament injury.64 In that study, injuries to the PCL were associated with posterolateral corner, ACL, and MCL injuries 62%, 46%, and 31% of the time, respectively.64,69

Because isolated PCL injuries are rare, clinicians must rely on a thorough history and physical examination when evaluating athletes with knee injuries. Classification of PCL injuries is based on the amount of posterior tibial translation in relation to the femur with the knee bent to 90°. Grade I is 1 to 5 mm; Grade II, 6 to 10 mm; and Grade III, >10 mm. If there is suspicion of a PCL injury, there should be a very low threshold for magnetic resonance imaging, given the high association with additional injuries.

Natural history of Grade I and II isolated PCL injuries is generally favorable compared to Grade III and multi-ligamentous injuries.70 As a result, isolated Grade I and II PCL injuries are generally treated nonoperatively. Treatment consists of physical therapy with emphasis on quadriceps strengthening. Return to play can be considered as early as 2 to 4 weeks from injury.71 Recent long-term data have shown successful conservative management of Grade I and II injuries with quadriceps strength to 97% of contralateral leg and full range of motion.72 However, there was 11% moderate to severe osteoarthritis in these patients at a mean follow-up of 14.3 years.72 Fowler and Messieh67 managed athletes with 7 isolated complete PCL tears and 5 partial tears nonoperatively, all of whom were able to return to sport without limitation. Parolie and Bergfeld73 managed 25 athletes with isolated PCL tears conservatively. In this study, 80% of athletes reported satisfaction and 68% returned to previous level of play.73 Neither of the aforementioned studies specify the grades of the injuries. Finally, Patel and colleagues66 managed 6 NFL athletes with Grade I and II injuries nonoperatively, and all were able to return to sport.

Treatment of isolated Grade III PCL injuries is more controversial, and no consensus exists in the literature. In an epidemiological study, Dick and colleagues68 found that only 39% of NCAA football athletes underwent surgery for their torn PCLs, compared to 79% of ACL injuries. However, their study makes no mention to the severity of these injuries. Numerous options exist for PCL reconstruction, with no consensus on the preferred method.

Conclusion

Knee injuries are the most common injury in football. Knowledge of the natural history of these injuries, as well as treatment options and expected outcomes, will help treating physicians educate their patients on the optimal treatment and manage return to play expectations.

Am J Orthop. 2016;45(6):368-373. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football is one of the most popular sports in the United States. Every year more than 1 million high school males and over 60,000 collegiate males participate in organized football. The number of males who play football is greater than the combined number of males and females who participate in track and field or basketball.1 Football has the highest injury rate amongst popular American sports.2 From 2001 to 2005, there was an estimated 1.1 million emergency room visits as a direct result of football.3 Injuries are more likely to occur during games,1,2,4,5 more likely to require surgery,4 and more likely to end the player’s season or career when compared to other sports.6 Of those injuries that end seasons or careers, the knee is the most common culprit.6 This is of particular concern because knee injuries are most common in football.1,2,5,7 This article reviews the epidemiology of 4 of the most common knee injuries in American football: tears of the anterior cruciate ligament (ACL), medial collateral ligament (MCL), medial patellofemoral ligament (MPFL), and posterior cruciate ligament (PCL).

Anterior Cruciate Ligament

The ACL is the primary structure preventing anterior tibial translation. It is composed of 2 anatomic bundles: the anteromedial and posterolateral bundles. The ACL originates from the posteromedial portion of the lateral femoral condyle and inserts between and slightly anterior to the tibial intercondylar eminence. The bundles are named for their relative insertions onto the tibia.

Injury to the ACL occurs both through noncontact and contact mechanisms. Typical noncontact mechanism is a forceful valgus collapse with the knee close to full extension with combined external or internal rotation of the tibia.8 This is often the result of a sudden deceleration prior to a change in direction.9 Contact injuries to the ACL are the result of a direct blow to the knee causing valgus collapse.9 The majority of ACL injuries amongst all sports are a result of a noncontact mechanism. However, Dragoo and colleagues10 found the majority of football ACL injuries (55%-60%) were from contact. As a result, football players are 4 times more likely to sustain ACL injuries than in other sports.11

ACL injuries are associated with significant time loss from sport. At the high school level, they are the most likely injury to end a season or career.6 Because these are higher-energy injuries, they are frequently associated with damage to additional structures. ACL injuries that occur in football are associated with increased rates of meniscus, chondral, and multi-ligamentous injuries.12,13

The incidence of ACL injuries increases with level of competition. In high school athletes it is 11.1 per 100,000 athlete exposures (AE).1,11 In collegiate football, the rate increases to 14.2 to 18 per 100,000 AE.2,14 Though no incidence data per AE was found in our review of the literature, there were 219 ACL injuries in the National Football League (NFL) from 2010 to 2013.15 In addition, 14.2% of retired NFL athletes in one survey reported a history of ACL injury.16

The most common high-risk positions are running backs and linebackers. Brophy and colleagues17 found that 9.7% of running backs and 8.9% of linebackers participating in the NFL Combine had a history of ACL injury. This may be because both the running back and linebacker are involved in frequent high-energy collisions and often quickly change direction. Other studies have also identified running backs and linebackers as high risk, in addition to tight ends, wide receivers, and interior linemen.13,15,18

Treatment of choice for elite level athletes with ACL injury is reconstruction.19 Of those who undergo ACL reconstruction, the rate of return to play ranges from 63% to 80%.20-22 The average time to return to play is 9 to 13 months. The odds of making a successful return hinges on how successful the athlete was prior to injury. Factors such as prior game experience, position on depth chart, being on scholarship, and draft position for NFL athletes have all been shown to have a positive predictive value on a patient’s chance of returning from ACL reconstruction.20,21

Players who return have variable levels of success afterwards. In a study of NFL quarterbacks who sustained ACL injuries, 12 out of 13 were able to return to game action with no appreciable dropoff in performance based on in-game production.23 Carey and colleagues24 looked specifically at NFL wide receivers and running backs and found an 80% return to play rate but with an approximate decrease in production of one-third upon return. Furthermore, in the Multicenter Orthopaedic Outcomes Network (MOON) cohort study, only 43% of participants felt they returned to their preoperative level.22

 

 

Medial Collateral Ligament

The MCL consists of superficial and deep components. The superficial MCL is the primary restraint to valgus laxity at the knee. The superficial MCL has 1 femoral and 2 tibial attachments. The deep MCL is a thickening of the medial joint capsule and runs deep and parallel to the superficial MCL. The amount of medial joint gapping with a valgus force on examination is used to grade severity of MCL injuries. Grade I is a <5-mm opening; Grade II, 5- to 10-mm opening; and grade III, >10-mm opening.

The MCL is the most common knee injury in high school, collegiate, and professional football.1,18,25-28 Injuries are typically due to contact when a valgus force is applied to the knee.29 The annual incidence of MCL injuries amongst high school football players is 24.2 per 100,000 AE.1 The positions that appear to be at greatest risk for MCL injuries are offensive and defensive linemen.18,30-32 In a review of 5047 collegiate athletes participating in the NFL Combine from 1987 to 2000, 23% of offensive linemen had a history of MCL injury, compared to the overall rate of 16%.33 In a similar study, Bradley and colleagues18 performed medical histories on athletes invited to the 2005 NFL Combine and also found offensive linemen had the highest rate of MCL injury at 33%, compared to the overall rate of 22%. They reasonably hypothesized that “chop blocks” and other players “rolling up” on the outside of linemen’s knees were responsible for these injuries. Albright and colleagues32 found that prophylactic knee braces decreased the incidence of MCL injuries in collegiate offensive lineman. However, additional studies have not been able to reproduce these results and the use of prophylactic knee braces remains controversial.26

Treatment of MCL injuries depends upon the grade of injury, associated injuries, and anatomical location of injury. Management of MCL injuries is for the most part nonsurgical. In 1974, Ellsasser and colleagues34 were the first to publish data on nonoperative management of Grade I and Grade II injuries with immediate motion and rehabilitation instead of cast immobilization. They found 93% of patients returned to football in 3 to 8 weeks.34 Derscheid and Garrick27 observed nonoperative treatment of Grade I and II sprains in collegiate football players, with a time loss of 10.6 days and 19.5 days for Grade I and II injuries, respectively. Holden and colleagues35 evaluated nonoperative management of Grade I and II MCL injuries in collegiate football players and found an average return to play of 21 days.

Grade III injury treatment is more controversial. Indelicato and colleagues36 demonstrated successful nonoperative management of Grade III MCL injuries in collegiate football players, with an average return to play of 64.4 days. Jones and colleagues37 had similar success with high school football players, with an average return to play of 34 days. However, isolated Grade III injuries are rare and therefore treatment is likely to be dictated by concomitant injuries. Fetto and Marshall38 found that 78% of Grade III injuries were associated with an additional ligamentous injury. Of those additional injuries, 95% were ACL tears.

Finally, one must consider the location of the MCL injury. Injuries of the distal MCL at its tibial insertion may result in poor healing, as the ligament is displaced away from its insertion. Therefore, some authors recommend surgical management for these injuries.39,40

Medial Patellofemoral Ligament

The patellofemoral joint is a complex structure in which the patella is stabilized within the trochlear groove of the femur by both bony and soft tissue structures. The MPFL is one of the most important soft tissue stabilizers. The MPFL is the primary restraint to lateral patellar translation within the first 20° of knee flexion, contributing to 60% of the total restraining force.41 The MPFL originates on the medial femoral condyle and inserts on the superomedial aspect of the patella.

Patellar instability is the subluxation or dislocation of the patella out of the trochlear groove. Patellar subluxation and dislocation account for approximately 3% of all knee injuries.42 Patella dislocations are more common in younger populations43-45 with the majority (52%-63%) occurring during sports.43,44,46 Mitchell and colleagues47 reported an incidence of 4.1 patellar subluxations/dislocations per 100,000 AE in high school football players.

Dislocation is most commonly the result of knee flexion with the tibia in a valgus position.44,48 The majority of patellar dislocations occur via a noncontact mechanism.44,48 However, the majority of these injuries in football are from contact (63%).47

Acute patellar dislocations are associated with more soft tissue damage than those with recurrent dislocations.46 In acute patella dislocations, the MPFL is almost always ruptured.44 In contrast, Fithian and colleagues46 found only 38% of recurrent dislocators had MPFL injury. As a result, it is thought that those with recurrent instability dislocate without trauma and do not have the same characteristics as those who dislocate from high-energy trauma in sport. Risk factors for atraumatic dislocation are numerous and have been well described in the literature.49 However, traumatic dislocators usually do not have risk factors.50

Traumatic patella dislocations are higher energy and are associated with chondral injury in up to 95%of cases 51 and osteochondral injury 58% to 76% of the time.52,53 In contrast, people with “articular hypermobility” are less likely to sustain articular damage.54 This concept is important when considering risk for recurrent patella dislocation. The literature reports a 17% to 50% rate of recurrent instability after acute patella dislocation.46,55,56 However, most studies do not distinguish between traumatic and atraumatic injuries. Because the majority of patellar dislocations in football occur through contact mechanisms, the rate of recurrent instability in these athletes may in fact be less than what is reported in the literature.

First-time patella dislocations are generally treated nonoperatively. Mitchell and colleagues47 reported that 72.6% of high school athletes with patella subluxation treated conservatively were able to return to sports within 3 weeks, compared to only 34.1% of those with patellar dislocations. In the same study, patellar dislocations were season-ending 37% of the time.47 Atkin and colleagues50 followed 74 patients treated conservatively for first-time patellar dislocation and noted 58% at 6 months still had difficulty in squatting, jumping, or cutting.

Those who have failed conservative management and have an additional dislocation are 7 times more likely to redislocate.46 Therefore, they are usually treated operatively with MPFL reconstruction. Return to sport ranges from 3 to 6 months,57 with 53% to 77.3% reporting return to their previous functionality.57-59 Overall, 84.1% of patients are able to return to sport with 1.2% risk of recurrent dislocation.60

 

 

Posterior Cruciate Ligament

The PCL is the primary posterior stabilizer of the knee.61,62 It consists of the anterolateral and posteromedial bundles, named by their insertion on the posterior tibial plateau. The larger, stronger anterolateral bundle is the primary restraint to posterior tibial translation.63

Due to the relative infrequency of PCL injuries, there is a paucity of epidemiological data on sports-related PCL injuries. These injuries in the literature are commonly found due to traffic accidents (45%-57%) or from sports (33%-40%).64,65 According to Swensen and colleagues,1 PCL injuries account for 2.4% of all high school sport knee injuries. In a cohort of 62 knees with PCL injuries, Patel and colleagues66 found football was the most common cause of injury (19.3%).

The most common mechanism of injury in athletes is knee hyperflexion or a direct blow to the tibia in a flexed knee.67 In football, contact mechanisms are the most common. In a 16-year review of the National Collegiate Athletic Association (NCAA) injury surveillance system, the incidence of contact PCL injuries during games were 7.3 times higher than noncontact.68 The most common activity was being tackled, which accounted for 22.9% of all PCL injuries.68

Due to the high energy of these injuries, isolated PCL injuries are rare. In one trauma center’s experience, 96.5% of PCL injuries had an additional ligament injury.64 In that study, injuries to the PCL were associated with posterolateral corner, ACL, and MCL injuries 62%, 46%, and 31% of the time, respectively.64,69

Because isolated PCL injuries are rare, clinicians must rely on a thorough history and physical examination when evaluating athletes with knee injuries. Classification of PCL injuries is based on the amount of posterior tibial translation in relation to the femur with the knee bent to 90°. Grade I is 1 to 5 mm; Grade II, 6 to 10 mm; and Grade III, >10 mm. If there is suspicion of a PCL injury, there should be a very low threshold for magnetic resonance imaging, given the high association with additional injuries.

Natural history of Grade I and II isolated PCL injuries is generally favorable compared to Grade III and multi-ligamentous injuries.70 As a result, isolated Grade I and II PCL injuries are generally treated nonoperatively. Treatment consists of physical therapy with emphasis on quadriceps strengthening. Return to play can be considered as early as 2 to 4 weeks from injury.71 Recent long-term data have shown successful conservative management of Grade I and II injuries with quadriceps strength to 97% of contralateral leg and full range of motion.72 However, there was 11% moderate to severe osteoarthritis in these patients at a mean follow-up of 14.3 years.72 Fowler and Messieh67 managed athletes with 7 isolated complete PCL tears and 5 partial tears nonoperatively, all of whom were able to return to sport without limitation. Parolie and Bergfeld73 managed 25 athletes with isolated PCL tears conservatively. In this study, 80% of athletes reported satisfaction and 68% returned to previous level of play.73 Neither of the aforementioned studies specify the grades of the injuries. Finally, Patel and colleagues66 managed 6 NFL athletes with Grade I and II injuries nonoperatively, and all were able to return to sport.

Treatment of isolated Grade III PCL injuries is more controversial, and no consensus exists in the literature. In an epidemiological study, Dick and colleagues68 found that only 39% of NCAA football athletes underwent surgery for their torn PCLs, compared to 79% of ACL injuries. However, their study makes no mention to the severity of these injuries. Numerous options exist for PCL reconstruction, with no consensus on the preferred method.

Conclusion

Knee injuries are the most common injury in football. Knowledge of the natural history of these injuries, as well as treatment options and expected outcomes, will help treating physicians educate their patients on the optimal treatment and manage return to play expectations.

Am J Orthop. 2016;45(6):368-373. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Swenson DM, Collins CL, Best TM, Flanigan DC, Fields SK, Comstock RD. Epidemiology of knee injuries among U.S. high school athletes, 2005/2006-2010/2011. Med Sci Sports Exerc. 2013;45(3):462-469.

2. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train. 2007;42(2):311-319.

3. Mello MJ, Myers R, Christian JB, Palmisciano L, Linakis JG. Injuries in youth football: national emergency department visits during 2001-2005 for young and adolescent players. Acad Emerg Med. 2009;16(3):243-248.

4. Rechel JA, Collins CL, Comstock RD. Epidemiology of injuries requiring surgery among high school athletes in the United States, 2005 to 2010. J Trauma. 2011;71(4):982-989.

5. Ingram JG, Fields SK, Yard EE, Comstock RD. Epidemiology of knee injuries among boys and girls in US high school athletics. Am J Sports Med. 2008;36(6):1116-1122.

6. Tirabassi J, Brou L, Khodaee M, Lefort R, Fields SK, Comstock RD. Epidemiology of high school sports-related injuries resulting in medical disqualification: 2005-2006 through 2013-2014 academic years. Am J Sports Med. 2016 May 10. [Epub ahead of print]

7. Fernandez WG, Yard EE, Comstock RD. Epidemiology of lower extremity injuries among U.S. high school athletes. Acad Emerg Med. 2007;14(7):641-645.

8. Olsen OE, Myklebust G, Engebretsen L, Bahr R. Injury mechanisms for anterior cruciate ligament injuries in team handball: a systematic video analysis. Am J Sports Med. 2004;32(4):1002-1012.

9. Boden BP, Dean GS, Feagin JA Jr, Garrett WE Jr. Mechanisms of anterior cruciate ligament injury. Orthopedics. 2000;23(6):573-578.

10. 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(3):191-195.

11. Joseph AM, Collins CL, Henke NM, Yard EE, Fields SK, Comstock RD. A multisport epidemiologic comparison of anterior cruciate ligament injuries in high school athletics. J Athl Train. 2013;48(6):810-817.

12. Granan LP, Inacio MC, Maletis GB, Funahashi TT, Engebretsen L. Sport-specific injury pattern recorded during anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(12):2814-2818.

13. Bradley JP, Klimkiewicz JJ, Rytel MJ, Powell JW. Anterior cruciate ligament injuries in the National Football League: epidemiology and current treatment trends among team physicians. Arthroscopy. 2002;18(5):502-509.

14. Dragoo JL, Braun HJ, Durham JL, Chen MR, Harris AH. Incidence and risk factors for injuries to the anterior cruciate ligament in National Collegiate Athletic Association football: data from the 2004-2005 through 2008-2009 National Collegiate Athletic Association Injury Surveillance System. Am J Sports Med. 2012;40(5):990-995.

15. Dodson CC, Secrist ES, Bhat SB, Woods DP, Deluca PF. Anterior cruciate ligamenti in National Football League athletes from 2010 to 2013: a descriptive epidemiology study. Orthop J Sports Med. 2016;4(3):2325967116631949.

16. Golightly YM, Marshall SW, Callahan LF, Guskiewicz K. Early-onset arthritis in retired National Football League players. J Phys Act Health. 2009;6(5):638-643.

17. Brophy RH, Lyman S, Chehab EL, Barnes RP, Rodeo SA, Warren RF. Predictive value of prior injury on career in professional American football is affected by player position. Am J Sports Med. 2009;37(4):768-775.

18. Bradley J, Honkamp NJ, Jost P, West R, Norwig J, Kaplan LD. Incidence and variance of knee injuries in elite college football players. Am J Orthop. 2008;37(6):310-314.

19. Erickson BJ, Harris JD, Fillingham YA, et al. Anterior cruciate ligament reconstruction practice patterns by NFL and NCAA football team physicians. Arthroscopy. 2014;30(6):731-738.

20. Daruawalla JH, Greis PE, Hancock R; ASP Collaborative Group, Xerogeanes JW. Rates and determinants of return to play after anterior cruciate ligament reconstruction in NCAA Division 1 college football athletes: a study of the ACC, SEC, and PAC-12 conferences. Orthop J Sports Med. 2014;2(8):2325967114543901.

21. Shah VM, Andrews JR, Fleisig GS, McMichael CS, Lemak LJ. Return to play after anterior cruciate ligament reconstruction in National Football League athletes. Am J Sports Med. 2010;38(11):2233-2239.

22. McCullough KA, Phelps KD, Spindler KP, et al. Return to high school- and college-level football after anterior cruciate ligament reconstruction: a Multicenter Orthopaedic Outcomes Network (MOON) cohort study. Am J Sports Med. 2012;40(11):2523-2529.

23. Erickson BJ, Harris JD, Heninger JR, et al. Performance and return-to-sport after ACL reconstruction in NFL quarterbacks. Orthopedics. 2014;37(8):e728-e734.

24. Carey JL, Huffman GR, Parekh SG, Sennett BJ. Outcomes of anterior cruciate ligament injuries to running backs and wide receivers in the National Football League. Am J Sports Med. 2006;34(12):1911-1917.

25. Hershman EB, Anderson R, Bergfeld JA, et al. An analysis of specific lower extremity injury rates on grass and FieldTurf playing surfaces in National Football League Games: 2000-2009 seasons. Am J Sports Med. 2012;40(10):2200-2205.

26. Salata MJ, Gibbs AE, Sekiya JK. The effectiveness of prophylactic knee bracing in American football: a systematic review. Sports Health. 2010;2(5):375-379.

27. Derscheid GL, Garrick JG. Medial collateral ligament injuries in football. Nonoperative management of grade I and grade II sprains. Am J Sports Med. 1981;9(6):365-368.

28. Meyers MC, Barnhill BS. Incidence, causes, and severity of high school football injuries on FieldTurf versus natural grass: a 5-year prospective study. Am J Sports Med. 2004;32(7):1626-1638.

29. Lundblad M, Waldén M, Magnusson H, Karlsson J, Ekstrand J. The UEFA injury study: 11-year data concerning 346 MCL injuries and time to return to play. Br J Sports Med. 2013;47(12):759-762.

30. Hewson GF Jr, Mendini RA, Wang JB. Prophylactic knee bracing in college football. Am J Sports Med. 1986;14(4):262-266.

31. Rovere GD, Haupt HA, Yates CS. Prophylactic knee bracing in college football. Am J Sports Med. 1987;15(2):111-116.

32. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee sprains in college football. Brace wear preferences and injury risk. Am J Sports Med. 1994;22(1):2-11.

33. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine--trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.

34. Ellsasser JC, Reynolds FC, Omohundro JR. The non-operative treatment of collateral ligament injuries of the knee in professional football players. An analysis of seventy-four injuries treated non-operatively and twenty-four injuries treated surgically. J Bone Joint Surg Am. 1974;56(6):1185-1190.

35. Holden DL, Eggert AW, Butler JE. The nonoperative treatment of grade I and II medial collateral ligament injuries to the knee. Am J Sports Med. 1983;11(5):340-344.

36. Indelicato PA, Hermansdorfer J, Huegel M. Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate football players. Clin Orthop Relat Res. 1990;(256):174-177.

37. Jones RE, Henley MB, Francis P. Nonoperative management of isolated grade III collateral ligament injury in high school football players. Clin Orthop Relat Res. 1986;(213):137-140.

38. Fetto JF, Marshall JL. Medial collateral ligament injuries of the knee: a rationale for treatment. Clin Orthop Relat Res. 1978;(132):206-218.

39. Corten K, Hoser C, Fink C, Bellemans J. Case reports: a Stener-like lesion of the medial collateral ligament of the knee. Clin Orthop Relat Res. 2010;468(1):289-293.

40. Marchant MH Jr, Tibor LM, Sekiya JK, Hardaker WT Jr, Garrett WE Jr, Taylor DC. Management of medial-sided knee injuries, part 1: medial collateral ligament. Am J Sports Med. 2011;39(5):1102-1113.

41. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 1998;26(1):59-65.

42. Casteleyn PP, Handelberg F. Arthroscopy in the diagnosis of occult dislocation of the patella. Acta Orthop Belg. 1989;55(3):381-383.

43. Waterman BR, Belmont PJ Jr, Owens BD. Patellar dislocation in the United States: role of sex, age, race, and athletic participation. J Knee Surg. 2012;25(1):51-57.

44. Sillanpää P, Mattila VM, Iivonen T, Visuri T, Pihlajamäki H. Incidence and risk factors of acute traumatic primary patellar dislocation. Med Sci Sports Exerc. 2008;40(4):606-611.

45. Hsiao M, Owens BD, Burks R, Sturdivant RX, Cameron KL. Incidence of acute traumatic patellar dislocation among active-duty United States military service members. Am J Sports Med. 2010;38(10):1997-2004.

46. Fithian DC, Paxton EW, Stone ML, et al. Epidemiology and natural history of acute patellar dislocation. Am J Sports Med. 2004;32(5):1114-1121.

47. Mitchell J, Magnussen RA, Collins CL, et al. Epidemiology of patellofemoral instability injuries among high school athletes in the United States. Am J Sports Med. 2015;43(7):1676-1682.

48. Nikku R, Nietosvaara Y, Aalto K, Kallio PE. The mechanism of primary patellar dislocation: trauma history of 126 patients. Acta Orthop. 2009;80(4):432-434.

49. Tsai CH, Hsu CJ, Hung CH, Hsu HC. Primary traumatic patellar dislocation. J Orthop Surg Res. 2012;7:21.

50. Atkin DM, Fithian DC, Marangi KS, Stone ML, Dobson BE, Mendelsohn C. Characteristics of patients with primary acute lateral patellar dislocation and their recovery within the first 6 months of injury. Am J Sports Med. 2000;28(4):472-479.

51. Nomura E, Inoue M, Kurimura M. Chondral and osteochondral injuries associated with acute patellar dislocation. Arthroscopy. 2003;19(7):717-721.

52. Kirsch MD, Fitzgerald SW, Friedman H, Rogers LF. Transient lateral patellar dislocation: diagnosis with MR imaging. AJR Am J Roentgenol. 1993;161(1):109-113.

53. Virolainen H, Visuri T, Kuusela T. Acute dislocation of the patella: MR findings. Radiology. 1993;189(1):243-246.

54. Stanitski CL. Articular hypermobility and chondral injury in patients with acute patellar dislocation. Am J Sports Med. 1995;23(2):146-150.

55. Mäenpää H, Huhtala H, Lehto MU. Recurrence after patellar dislocation. Redislocation in 37/75 patients followed for 6-24 years. Acta Orthop Scand. 1997;68(5):424-426.

56. Buchner M, Baudendistel B, Sabo D, Schmitt H. Acute traumatic primary patellar dislocation: long-term results comparing conservative and surgical treatment. Clin J Sport Med. 2005;15(2):62-66.

57. Fisher B, Nyland J, Brand E, Curtin B. Medial patellofemoral ligament reconstruction for recurrent patellar dislocation: a systematic review including rehabilitation and return-to-sports efficacy. Arthroscopy. 2010;26(10):1384-1394.

58. Lippacher S, Dreyhaupt J, Williams SR, Reichel H, Nelitz M. Reconstruction of the medial patellofemoral ligament: clinical outcomes and return to sports. Am J Sports Med. 2014;42(7):1661-1668.

59. Panni AS, Alam M, Cerciello S, Vasso M, Maffulli N. Medial patellofemoral ligament reconstruction with a divergent patellar transverse 2-tunnel technique. Am J Sports Med. 2011;39(12):2647-1655.

60. Schneider DK, Grawe B, Magnussen RA, et al. Outcomes after isolated medial patellofemoral ligament reconstruction for the treatment of recurrent lateral patellar dislocations: a systematic review and meta-analysis. Am J Sports Med. 2016 Feb 12. [Epub ahead of print]

61. Amis AA, Bull AM, Gupte CM, Hijazi I, Race A, Robinson JR. Biomechanics of the PCL and related structures: posterolateral, posteromedial and meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc. 2003;11(5):271-281.

62. Fu FH, Harner CD, Johnson DL, Miller MD, Woo SL. Biomechanics of knee ligaments: basic concepts and clinical application. Instr Course Lect. 1994;43:137-148.

63. Markolf KL, Feeley BT, Tejwani SG, Martin DE, McAllister DR. Changes in knee laxity and ligament force after sectioning the posteromedial bundle of the posterior cruciate ligament. Arthroscopy. 2006; 22(10):1100-1106.

64. Ganelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: Part II. Arthroscopy. 1995;11(5):526-529.

65. Schulz MS, Russe K, Weiler A, Eichhorn HJ, Strobel MJ. Epidemiology of posterior cruciate ligament injuries. Arch Orthop Trauma Surg. 2003;123(4):186-191.

66. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The nonoperative treatment of acute, isolated (partial or complete) posterior cruciate ligament-deficient knees: an intermediate-term follow-up study. HSS J. 2007;3(2):137-146.

67. Fowler PJ, Messieh SS. Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med. 1987;15(6):553-557.

68. Dick R, Ferrara MS, Agel J, et al. Descriptive epidemiology of collegiate men’s football injuries: National Collegiate Athletic Association Injury Surveillance System, 1988-1989 through 2003-2004. J Athl Train. 2007;42(2):221-233.

69. LaPrade CM, Civitarese DM, Rasmussen MT, LaPrade RF. Emerging updates on the posterior cruciate ligament: a review of the current literature. Am J Sports Med. 2015;43(12):3077-3092.

70. Torg JS, Barton TM, Pavlov H, Stine R. Natural history of the posterior cruciate ligament-deficient knee. Clin Orthop Relat Res. 1989(246):208-216.

71. Miller MD. Orthopaedic Knowledge Update: Sports Medicine 5. Rosemont, IL; American Academy of Orthopaedic Surgeons; 2016.

72. Shelbourne KD, Clark M, Gray T. Minimum 10-year follow-up of patients after an acute, isolated posterior cruciate ligament injury treated nonoperatively. Am J Sports Med. 2013;41(7):1526-1533.

73. Parolie JM, Bergfeld JA. Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med. 1986;14(1):35-38.

References

1. Swenson DM, Collins CL, Best TM, Flanigan DC, Fields SK, Comstock RD. Epidemiology of knee injuries among U.S. high school athletes, 2005/2006-2010/2011. Med Sci Sports Exerc. 2013;45(3):462-469.

2. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train. 2007;42(2):311-319.

3. Mello MJ, Myers R, Christian JB, Palmisciano L, Linakis JG. Injuries in youth football: national emergency department visits during 2001-2005 for young and adolescent players. Acad Emerg Med. 2009;16(3):243-248.

4. Rechel JA, Collins CL, Comstock RD. Epidemiology of injuries requiring surgery among high school athletes in the United States, 2005 to 2010. J Trauma. 2011;71(4):982-989.

5. Ingram JG, Fields SK, Yard EE, Comstock RD. Epidemiology of knee injuries among boys and girls in US high school athletics. Am J Sports Med. 2008;36(6):1116-1122.

6. Tirabassi J, Brou L, Khodaee M, Lefort R, Fields SK, Comstock RD. Epidemiology of high school sports-related injuries resulting in medical disqualification: 2005-2006 through 2013-2014 academic years. Am J Sports Med. 2016 May 10. [Epub ahead of print]

7. Fernandez WG, Yard EE, Comstock RD. Epidemiology of lower extremity injuries among U.S. high school athletes. Acad Emerg Med. 2007;14(7):641-645.

8. Olsen OE, Myklebust G, Engebretsen L, Bahr R. Injury mechanisms for anterior cruciate ligament injuries in team handball: a systematic video analysis. Am J Sports Med. 2004;32(4):1002-1012.

9. Boden BP, Dean GS, Feagin JA Jr, Garrett WE Jr. Mechanisms of anterior cruciate ligament injury. Orthopedics. 2000;23(6):573-578.

10. 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(3):191-195.

11. Joseph AM, Collins CL, Henke NM, Yard EE, Fields SK, Comstock RD. A multisport epidemiologic comparison of anterior cruciate ligament injuries in high school athletics. J Athl Train. 2013;48(6):810-817.

12. Granan LP, Inacio MC, Maletis GB, Funahashi TT, Engebretsen L. Sport-specific injury pattern recorded during anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(12):2814-2818.

13. Bradley JP, Klimkiewicz JJ, Rytel MJ, Powell JW. Anterior cruciate ligament injuries in the National Football League: epidemiology and current treatment trends among team physicians. Arthroscopy. 2002;18(5):502-509.

14. Dragoo JL, Braun HJ, Durham JL, Chen MR, Harris AH. Incidence and risk factors for injuries to the anterior cruciate ligament in National Collegiate Athletic Association football: data from the 2004-2005 through 2008-2009 National Collegiate Athletic Association Injury Surveillance System. Am J Sports Med. 2012;40(5):990-995.

15. Dodson CC, Secrist ES, Bhat SB, Woods DP, Deluca PF. Anterior cruciate ligamenti in National Football League athletes from 2010 to 2013: a descriptive epidemiology study. Orthop J Sports Med. 2016;4(3):2325967116631949.

16. Golightly YM, Marshall SW, Callahan LF, Guskiewicz K. Early-onset arthritis in retired National Football League players. J Phys Act Health. 2009;6(5):638-643.

17. Brophy RH, Lyman S, Chehab EL, Barnes RP, Rodeo SA, Warren RF. Predictive value of prior injury on career in professional American football is affected by player position. Am J Sports Med. 2009;37(4):768-775.

18. Bradley J, Honkamp NJ, Jost P, West R, Norwig J, Kaplan LD. Incidence and variance of knee injuries in elite college football players. Am J Orthop. 2008;37(6):310-314.

19. Erickson BJ, Harris JD, Fillingham YA, et al. Anterior cruciate ligament reconstruction practice patterns by NFL and NCAA football team physicians. Arthroscopy. 2014;30(6):731-738.

20. Daruawalla JH, Greis PE, Hancock R; ASP Collaborative Group, Xerogeanes JW. Rates and determinants of return to play after anterior cruciate ligament reconstruction in NCAA Division 1 college football athletes: a study of the ACC, SEC, and PAC-12 conferences. Orthop J Sports Med. 2014;2(8):2325967114543901.

21. Shah VM, Andrews JR, Fleisig GS, McMichael CS, Lemak LJ. Return to play after anterior cruciate ligament reconstruction in National Football League athletes. Am J Sports Med. 2010;38(11):2233-2239.

22. McCullough KA, Phelps KD, Spindler KP, et al. Return to high school- and college-level football after anterior cruciate ligament reconstruction: a Multicenter Orthopaedic Outcomes Network (MOON) cohort study. Am J Sports Med. 2012;40(11):2523-2529.

23. Erickson BJ, Harris JD, Heninger JR, et al. Performance and return-to-sport after ACL reconstruction in NFL quarterbacks. Orthopedics. 2014;37(8):e728-e734.

24. Carey JL, Huffman GR, Parekh SG, Sennett BJ. Outcomes of anterior cruciate ligament injuries to running backs and wide receivers in the National Football League. Am J Sports Med. 2006;34(12):1911-1917.

25. Hershman EB, Anderson R, Bergfeld JA, et al. An analysis of specific lower extremity injury rates on grass and FieldTurf playing surfaces in National Football League Games: 2000-2009 seasons. Am J Sports Med. 2012;40(10):2200-2205.

26. Salata MJ, Gibbs AE, Sekiya JK. The effectiveness of prophylactic knee bracing in American football: a systematic review. Sports Health. 2010;2(5):375-379.

27. Derscheid GL, Garrick JG. Medial collateral ligament injuries in football. Nonoperative management of grade I and grade II sprains. Am J Sports Med. 1981;9(6):365-368.

28. Meyers MC, Barnhill BS. Incidence, causes, and severity of high school football injuries on FieldTurf versus natural grass: a 5-year prospective study. Am J Sports Med. 2004;32(7):1626-1638.

29. Lundblad M, Waldén M, Magnusson H, Karlsson J, Ekstrand J. The UEFA injury study: 11-year data concerning 346 MCL injuries and time to return to play. Br J Sports Med. 2013;47(12):759-762.

30. Hewson GF Jr, Mendini RA, Wang JB. Prophylactic knee bracing in college football. Am J Sports Med. 1986;14(4):262-266.

31. Rovere GD, Haupt HA, Yates CS. Prophylactic knee bracing in college football. Am J Sports Med. 1987;15(2):111-116.

32. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee sprains in college football. Brace wear preferences and injury risk. Am J Sports Med. 1994;22(1):2-11.

33. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine--trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.

34. Ellsasser JC, Reynolds FC, Omohundro JR. The non-operative treatment of collateral ligament injuries of the knee in professional football players. An analysis of seventy-four injuries treated non-operatively and twenty-four injuries treated surgically. J Bone Joint Surg Am. 1974;56(6):1185-1190.

35. Holden DL, Eggert AW, Butler JE. The nonoperative treatment of grade I and II medial collateral ligament injuries to the knee. Am J Sports Med. 1983;11(5):340-344.

36. Indelicato PA, Hermansdorfer J, Huegel M. Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate football players. Clin Orthop Relat Res. 1990;(256):174-177.

37. Jones RE, Henley MB, Francis P. Nonoperative management of isolated grade III collateral ligament injury in high school football players. Clin Orthop Relat Res. 1986;(213):137-140.

38. Fetto JF, Marshall JL. Medial collateral ligament injuries of the knee: a rationale for treatment. Clin Orthop Relat Res. 1978;(132):206-218.

39. Corten K, Hoser C, Fink C, Bellemans J. Case reports: a Stener-like lesion of the medial collateral ligament of the knee. Clin Orthop Relat Res. 2010;468(1):289-293.

40. Marchant MH Jr, Tibor LM, Sekiya JK, Hardaker WT Jr, Garrett WE Jr, Taylor DC. Management of medial-sided knee injuries, part 1: medial collateral ligament. Am J Sports Med. 2011;39(5):1102-1113.

41. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 1998;26(1):59-65.

42. Casteleyn PP, Handelberg F. Arthroscopy in the diagnosis of occult dislocation of the patella. Acta Orthop Belg. 1989;55(3):381-383.

43. Waterman BR, Belmont PJ Jr, Owens BD. Patellar dislocation in the United States: role of sex, age, race, and athletic participation. J Knee Surg. 2012;25(1):51-57.

44. Sillanpää P, Mattila VM, Iivonen T, Visuri T, Pihlajamäki H. Incidence and risk factors of acute traumatic primary patellar dislocation. Med Sci Sports Exerc. 2008;40(4):606-611.

45. Hsiao M, Owens BD, Burks R, Sturdivant RX, Cameron KL. Incidence of acute traumatic patellar dislocation among active-duty United States military service members. Am J Sports Med. 2010;38(10):1997-2004.

46. Fithian DC, Paxton EW, Stone ML, et al. Epidemiology and natural history of acute patellar dislocation. Am J Sports Med. 2004;32(5):1114-1121.

47. Mitchell J, Magnussen RA, Collins CL, et al. Epidemiology of patellofemoral instability injuries among high school athletes in the United States. Am J Sports Med. 2015;43(7):1676-1682.

48. Nikku R, Nietosvaara Y, Aalto K, Kallio PE. The mechanism of primary patellar dislocation: trauma history of 126 patients. Acta Orthop. 2009;80(4):432-434.

49. Tsai CH, Hsu CJ, Hung CH, Hsu HC. Primary traumatic patellar dislocation. J Orthop Surg Res. 2012;7:21.

50. Atkin DM, Fithian DC, Marangi KS, Stone ML, Dobson BE, Mendelsohn C. Characteristics of patients with primary acute lateral patellar dislocation and their recovery within the first 6 months of injury. Am J Sports Med. 2000;28(4):472-479.

51. Nomura E, Inoue M, Kurimura M. Chondral and osteochondral injuries associated with acute patellar dislocation. Arthroscopy. 2003;19(7):717-721.

52. Kirsch MD, Fitzgerald SW, Friedman H, Rogers LF. Transient lateral patellar dislocation: diagnosis with MR imaging. AJR Am J Roentgenol. 1993;161(1):109-113.

53. Virolainen H, Visuri T, Kuusela T. Acute dislocation of the patella: MR findings. Radiology. 1993;189(1):243-246.

54. Stanitski CL. Articular hypermobility and chondral injury in patients with acute patellar dislocation. Am J Sports Med. 1995;23(2):146-150.

55. Mäenpää H, Huhtala H, Lehto MU. Recurrence after patellar dislocation. Redislocation in 37/75 patients followed for 6-24 years. Acta Orthop Scand. 1997;68(5):424-426.

56. Buchner M, Baudendistel B, Sabo D, Schmitt H. Acute traumatic primary patellar dislocation: long-term results comparing conservative and surgical treatment. Clin J Sport Med. 2005;15(2):62-66.

57. Fisher B, Nyland J, Brand E, Curtin B. Medial patellofemoral ligament reconstruction for recurrent patellar dislocation: a systematic review including rehabilitation and return-to-sports efficacy. Arthroscopy. 2010;26(10):1384-1394.

58. Lippacher S, Dreyhaupt J, Williams SR, Reichel H, Nelitz M. Reconstruction of the medial patellofemoral ligament: clinical outcomes and return to sports. Am J Sports Med. 2014;42(7):1661-1668.

59. Panni AS, Alam M, Cerciello S, Vasso M, Maffulli N. Medial patellofemoral ligament reconstruction with a divergent patellar transverse 2-tunnel technique. Am J Sports Med. 2011;39(12):2647-1655.

60. Schneider DK, Grawe B, Magnussen RA, et al. Outcomes after isolated medial patellofemoral ligament reconstruction for the treatment of recurrent lateral patellar dislocations: a systematic review and meta-analysis. Am J Sports Med. 2016 Feb 12. [Epub ahead of print]

61. Amis AA, Bull AM, Gupte CM, Hijazi I, Race A, Robinson JR. Biomechanics of the PCL and related structures: posterolateral, posteromedial and meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc. 2003;11(5):271-281.

62. Fu FH, Harner CD, Johnson DL, Miller MD, Woo SL. Biomechanics of knee ligaments: basic concepts and clinical application. Instr Course Lect. 1994;43:137-148.

63. Markolf KL, Feeley BT, Tejwani SG, Martin DE, McAllister DR. Changes in knee laxity and ligament force after sectioning the posteromedial bundle of the posterior cruciate ligament. Arthroscopy. 2006; 22(10):1100-1106.

64. Ganelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: Part II. Arthroscopy. 1995;11(5):526-529.

65. Schulz MS, Russe K, Weiler A, Eichhorn HJ, Strobel MJ. Epidemiology of posterior cruciate ligament injuries. Arch Orthop Trauma Surg. 2003;123(4):186-191.

66. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The nonoperative treatment of acute, isolated (partial or complete) posterior cruciate ligament-deficient knees: an intermediate-term follow-up study. HSS J. 2007;3(2):137-146.

67. Fowler PJ, Messieh SS. Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med. 1987;15(6):553-557.

68. Dick R, Ferrara MS, Agel J, et al. Descriptive epidemiology of collegiate men’s football injuries: National Collegiate Athletic Association Injury Surveillance System, 1988-1989 through 2003-2004. J Athl Train. 2007;42(2):221-233.

69. LaPrade CM, Civitarese DM, Rasmussen MT, LaPrade RF. Emerging updates on the posterior cruciate ligament: a review of the current literature. Am J Sports Med. 2015;43(12):3077-3092.

70. Torg JS, Barton TM, Pavlov H, Stine R. Natural history of the posterior cruciate ligament-deficient knee. Clin Orthop Relat Res. 1989(246):208-216.

71. Miller MD. Orthopaedic Knowledge Update: Sports Medicine 5. Rosemont, IL; American Academy of Orthopaedic Surgeons; 2016.

72. Shelbourne KD, Clark M, Gray T. Minimum 10-year follow-up of patients after an acute, isolated posterior cruciate ligament injury treated nonoperatively. Am J Sports Med. 2013;41(7):1526-1533.

73. Parolie JM, Bergfeld JA. Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med. 1986;14(1):35-38.

Issue
The American Journal of Orthopedics - 45(6)
Issue
The American Journal of Orthopedics - 45(6)
Page Number
368-373
Page Number
368-373
Publications
Publications
Topics
Article Type
Display Headline
Knee Injuries in American Football: An Epidemiological Review
Display Headline
Knee Injuries in American Football: An Epidemiological Review
Sections
Disallow All Ads
Article PDF Media

Foot and Ankle Injuries in American Football

Article Type
Changed
Thu, 09/19/2019 - 13:25
Display Headline
Foot and Ankle Injuries in American Football

Foot and ankle injuries are common in American football, with injury rates significantly increasing over the past decade.1-5 Epidemiologic studies of collegiate football players have shown an annual incidence of foot and ankle injuries ranging from 9% to 39%,3,6 with as many as 72% of all collegiate players presenting to the National Football League (NFL) Combine with a history of a foot or ankle injury and 13% undergoing surgical treatment.5 Player position influences the rate and type of foot and ankle injury. Offensive and “skill position” players, including linemen, running backs, and wide receivers, are particularly susceptible to foot and ankle injuries due to high levels of force and torque placed on the distal extremity during running, cutting, and tackling. Shoe wear changes, playing field conditions, increasing player size and speed, and improved reporting of injuries are also contributing to increasing injury rates.

The interaction between player cleats and the playing surface is a central issue of foot and ankle injuries in football. Improved traction relates to performance, but increased subsequent torque on the lower extremity is associated with injury. While lateral ankle sprains are the most common foot and ankle injury experienced by football players,7 numerous other injuries can occur, including turf toe, Jones fractures, Lisfranc injuries, syndesmotic disruption, deltoid complex avulsion, and Achilles ruptures. It is important for physicians to be able to recognize, diagnose, and appropriately treat these injuries in players in order to expedite recovery, restore function, and help prevent future injury and long-term sequelae. This review focuses on updated treatment principles, surgical advances, and rehabilitation protocols for common football foot and ankle injuries.

Turf Toe

The term “turf toe” was first used in 1976 to refer to hyperextension injuries and plantar capsule-ligament sprains of the hallux metatarsophalangeal (MTP) joint that can lead to progressive cock-up deformity.8 While these injuries can occur on any surface and disrupt soft tissue balance with functional implications, predisposing factors include increasing playing surface hardness and decreasing shoe stiffness. In a classic scenario, the foot is fixed in equinus as an axial load is placed on the back of the heel, resulting in forced dorsiflexion of the hallux MTP joint.9 As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the metatarsal head articular surface bears the majority of the load, causing partial or complete tearing of the plantar plate with or without hallux MTP dislocation. Osteochondral lesions of the MTP joint and subchondral edema of the metatarsal head can occur concurrently as the proximal phalanx impacts or shears across the metatarsal head articular surface.

Clinical examination should focus on hallux swelling, alignment, and flexor hallucis longus (FHL) function along with vertical instability of the hallux MTP joint using a Lachman test. Radiographs should be evaluated for proximal migration of the sesamoids or diastasis (Figures W1A-W1C).

Figures W1A-W1C
Forced hallux MTP dorsiflexion lateral view can help assess the distance from the distal sesamoid to the base of the phalanx. A small fleck of bone pulled off of the proximal phalanx or distal sesamoid may indicate a capsular avulsion or disruption. Live fluoroscopy can be very helpful in diagnosing turf toe, as the physician can assess the trailing motion of the sesamoids with increasing dorsiflexion and evaluate instability in all planes. Magnetic resonance imaging (MRI) is useful for subtle capsular injuries and can also identify osseous and articular damage that may occur and FHL disruption (Figures W2A, W2B).
Figures W2A, W2B
Nonoperative intervention focuses on rest, ice, compression, and elevation (RICE) and nonsteroidal anti-inflammatory drugs (NSAIDs). The hallux is temporarily immobilized in a plantarflexed position using a short leg cast or walking boot with toe spica or turf toe plate with tape for 2 to 3 weeks.

Indications for surgical intervention include loss of push-off strength, gross MTP instability, proximal migration of the sesamoids, and progressive hallux malalignment or clawing after immobilization. Cases can involve one or a combination of the following: (1) large capsular avulsion with unstable MTP joint; (2) diastasis of bipartite sesamoid; (3) diastasis of sesamoid fracture; (4) retraction of sesamoid; (5) traumatic hallux valgus deformity; (6) vertical instability (positive Lachman test); (7) loose body in MTP joint; or (8) chondral injury in MTP joint. The goal of surgery is the restoration of anatomy in order to restore normal function of the hallux MTP joint.

We have found that using dual medial and plantar incisions places less traction on the plantar medial cutaneous nerve, improves lateral exposure, and provides better wound healing. The medial capsulotomy extends from the metatarsal neck to the mid-phalanx to provide complete visualization of the sesamoid complex (Figures 1A-1F).
Figures 1A-1F
The collateral ligaments are often torn away from the metatarsal head during the initial dissection and the plantar plate tear is distal to the sesamoid complex. The soft tissue defect in the plantar complex must be closed distal to the sesamoids followed by advancement of the plantar plate to the proximal phalanx in a distal to proximal fashion and advancement of the medial capsule. The plantar incision is made along the lateral border of hallux MTP-sesamoid complex just lateral to the weight-bearing surface of the hallux and the plantar lateral cutaneous nerve is carefully dissected and retracted out of the way. Sutures are placed in a figure-of-eight fashion through the plantar capsule and plantar plate starting lateral to medial to reduce injury to the nerve. If the tear cannot be primarily repaired due to inadequate healthy tissue, a plantar plate advancement can be performed directly onto the base of the proximal phalanx using drill holes or suture anchors. Proper alignment and motion of the sesamoids should be verified with fluoroscopy and compared to the contralateral hallux (Figures W3A, W3B).
Figures W3A, W3B


It is important to recognize that not all turf toe injuries involve pure hyperextension on artificial playing surfaces. In recent years, we have found an increasing rate of medial variant turf toe injuries in which a forceful valgus stress on the hallux leads to rupture of the medial collateral ligament, medial or plantar-medial capsule, and/or abductor halluces. Medial variant turf toe can lead to progressive hallux valgus and a traumatic bunion with a significant loss of push-off strength and difficulty with cutting maneuvers. Surgical treatment requires a modified McBride bunionectomy with adductor tenotomy and direct repair of the medial soft tissue defect.

Postoperative management is just as important as proper surgical technique for these injuries and involves a delicate balance between protecting the repair and starting early range of motion (ROM). Patients are immobilized non-weight-bearing (NWB) for 5 to 7 days maximum followed immediately with the initiation of passive hallux plantarflexion to keep the sesamoids moving. Active hallux plantarflexion is started at 4 weeks after surgery with active dorsiflexion from 6 to 8 weeks. Patients are transitioned to an accommodative shoe with stiff hallux insert 8 weeks postoperative with continued therapy focusing on hallux ROM. Running is initiated at 12 weeks and return to play (RTP) is typically allowed 4 months after surgery.

 

 

Jones Fractures

Jones fractures are fractures of the 5th metatarsal at the metaphyseal-diaphyseal junction, where there is a watershed area of decreased vascularity between the intramedullary nutrient and metaphyseal arteries. Current thought is that the rising rate of Jones fractures among football players is partially caused by the use of flexible, narrow cleats that do not provide enough stiffness and lateral support for the 5th metatarsal during running and cutting. Additionally, lateral overload from a baseline cavovarus foot posture with or without metatarsus adductus and/or skewfoot is thought to contribute to Jones fractures.10 Preoperative radiographs should be evaluated for fracture location, orientation, amount of cortical thickening, and overall geometry of the foot and 5th metatarsal. In elite athletes, the threshold for surgical intervention is decreasing in order to expedite healing and recovery and decrease re-fracture risk. This rationale is based on delayed union rates of 25% to 66%, nonunion rates of 7% to 28%,11 and re-fracture rates of up to 33% associated with nonoperative treatment.12 Nonoperative management is usually not feasible in the competitive athlete, as it typically involves a period of protected weight-bearing in a tall controlled ankle motion (CAM) boot for 6 to 8 weeks with serial radiographs to evaluate healing.

Our preference for surgical intervention involves percutaneous screw fixation with a “high and inside” starting point on fluoroscopy (Figures 2A-2D).

Figures 2A-2D
The guidewire is inserted percutaneously through the skin 2 cm proximal to the base of the 5th metatarsal. Incorrect starting point can lead to a prominent screw head laterally or perforation of the medial cortex. A 1-cm incision is made around the guidewire entry point and intramedullary cannulated drilling enters the proximal third of the metatarsal, removing any thickened lateral cortex. Due to the natural curve of the 5th metatarsal, cannulated drilling is not continued distally but can be safely completed with a 3.2-mm solid drill bit. Proper tap sizing should generate enough torque to begin to rotate the entire foot as the tap is advanced (Figures W4A-W4F).
Figures W4A-W4F
The largest solid screw with a low-profile head that “comfortably” fits the intramedullary canal of the 5th metatarsal should be inserted (Carolina Jones Fracture System, Wright Medical Technology).13 In elite athletes, we will typically use a 5.5-mm or 6.5-mm screw that is 45 to 55 mm in length. Screw threads should pass just across the fracture site, avoiding “straightening” of the curved 5th metatarsal that will create a lateral gap and increase the rate of nonunion. We do not recommend headless tapered screws due to inconsistent compression and difficulty with later removal if re-fracture or nonunion occurs.

In career athletes, we augment the fracture site using a mixture of bone marrow aspirate concentrate (BMA) (Magellan, Arteriocyte Medical Systems) and demineralized bone matrix (DBM) (Mini Ignite, Wright Medical Technology) injected percutaneously in and around the fracture site under fluoroscopic guidance. Using this technique in a cohort of 25 NFL players treated operatively for Jones fractures, we found that 100% of athletes were able to RTP in the NFL in an average of 9.5 weeks.14 Two patients (7.5%) suffered re-fractures requiring revision surgery with iliac crest bone graft and repeat screw placement with a RTP after 15 weeks. We did not find an association between RTP and re-fracture rate.

The appropriate rehabilitation protocol for Jones fractures after surgery remains controversial and dependent on individual needs and abilities.15,16 For athletes in-season, we recommend a brief period of NWB for 1 to 2 weeks followed by toe-touch weight-bearing in a tall CAM boot for 2 to 4 weeks. After 4 weeks, patients begin gentle exercises on a stationary bike and pool therapy to reduce impact on the fracture site. Low-intensity pulsed ultrasound bone stimulators (Exogen, Bioventus) are frequently used directly over fracture site throughout the postoperative protocol as an adjuvant therapy. If clinically nontender over the fracture site, patients are allowed to begin running in modified protective shoe wear 4 weeks after surgery with an average RTP of 6 to 8 weeks. RTP is determined clinically, as radiographic union may not be evident for 12 to 16 weeks. Useful custom orthoses include turf toe plates with a cushioned lateral column and lateral heel wedge if hindfoot varus is present preoperatively.10 The solid intramedullary screw is left in place permanently.

In our experience, we have found the average re-fracture and nonunion rate to be approximately 8% across all athletes. Our observation that union rates do not appear to be related to RTP times suggests that underlying biology such as Vitamin D deficiency may play a larger role in union rates than previously thought. We have found that most Jones re-fractures occur in the first year after the initial injury, but can occur up to 2.5 years afterwards as well.14 For the management of symptomatic re-fractures and nonunions, the previous screw must be first removed. This can be difficult if the screw is bent or broken, and may require a lateral corticotomy of the metatarsal.

After hardware removal, we advocate open bone grafting of the fracture site using bone from the iliac crest retrieved with a small, percutaneous trephine. Re-fixation should be achieved using a larger, solid screw and postoperative adjuvants may include bone stimulators, Vitamin D and calcium supplemention, and possible teriparatide use (Forteo, Eli Lilly), depending on individual patient profile. In a cohort of 21 elite athletes treated for Jones fracture revision surgery with screw exchange and bone grafting, we found that 100% of patients had computed tomography (CT) evidence of union, with an average RTP of 12.3 weeks.17

 

 

Lisfranc Injuries

Lisfranc injuries include any bony or ligamentous damage that involves the tarsometatarsal (TMT) joints. While axial loading of a fixed, plantarflexed foot has traditionally been thought of as the most common mechanism of Lisfranc injury, we have found that noncontact twisting injuries leading to Lisfranc disruption are actually more common among NFL players. This mechanism is similar to noncontact turf toe and results in a purely ligamentous injury. We have found this to be particularly true in the case of defensive ends engaged with offensive linemen in which no axial loading or contact of the foot occurs. Clinically, patients often have painful weight-bearing, inability to perform a single limb heel rise, plantar ecchymosis, and swelling and point tenderness across the bases of the 1st and 2nd metatarsals.

It is critical to obtain comparison weight-bearing radiographs of both feet during initial work-up to look for evidence of instability. Subtle radiographic findings of Lisfranc injury include a bony “fleck” sign, compression fracture of the cuboid, and diastasis between the base of the 1st and 2nd metatarsals and/or medial and middle cuneiforms (Figures 3A, 3B).

Figures 3A, 3B
Stress testing involves pronation and adduction of the foot under live fluoroscopy to evaluate for diastasis. MRI can be helpful in cases of vague pain with negative radiographs and subtle displacement. Nonoperative treatment for cases of no instability or displacement involved protected weight-bearing for 4 weeks followed by progressive increase in activities, with RTP 6 to 8 weeks after injury.

The goal of surgical intervention is to obtain and maintain anatomic reduction of all unstable joints in order to restore a normal foot posture. One of the difficulties with Lisfranc injuries is that there are no exact diastasis parameters and individuals should be treated based on symptoms, functional needs, and degree of instability. It has been shown that 5 mm of displacement can have good long-term clinical results in select cases without surgery.18 For surgery, we recommend open reduction to remove interposed soft tissue debris and directly assess the articular surfaces (Figures 4A-4D).
Figures 4A-4D
A freer can be placed in the individual joints to assess for areas of instability. We prefer solid screw fixation (Charlotte Lisfranc Reconstruction System, Wright Medical Technology) to decrease the risk of later screw breakage. A homerun screw from the proximal aspect of the medial cuneiform to the distal-lateral aspect of the 2nd metatarsal base should be placed first. Bridge plates can be used over the 1st and 2nd TMT joints to avoid articular cartilage damage without a loss of rigidity.19

Proximal-medial column Lisfranc injury variants are increasingly common among football players.20 In these injuries, the force of injury extends through the intercuneiform joint and exits out the naviculocuneiform joint, thus causing instability at multiple joints and an unstable 1st ray. Patients often have minimal clinical findings and normal radiographs and stress radiographs. MRI of the foot often reveals edema at the naviculocuneiform joint. Often patients fail to improve with nonoperative immobilization with continued inability to push off from the hallux. Unrecognized or untreated instability will lead to rapid deterioration of the naviculocuneiform joint. Surgical intervention requires a homerun screw and intercuneiform screw. We do not recommend primary arthrodesis in athletes due to significant risk of malunion and nonunion unless severe articular damage is present.

Patients are typically kept NWB in a splint for 2 weeks after surgery followed by NWB in a tall CAM from 3 to 4 weeks postoperative. Progressive weight-bearing and ROM exercises are initiated from 4 to 8 weeks, followed by return to accommodative shoe wear from 10 to 12 weeks. Hardware removal is performed 4 to 6 months after surgery, typically in the off-season to allow for 6 to 8 weeks or protected recovery afterwards. Premature hardware removal can lead to loss of reduction, particularly at the intercuneiform joints. All hardware crossing the TMT joints should be removed, while the homerun screw can be left in place in addition to the intercuneiform screw. RTP in football typically occurs 6 to 7 months after surgery. Final functional outcome is related to the adequacy of initial reduction and severity of the initial injury.21

Syndesmotic Disruption

Syndesmotic injuries comprise 1% to 18% of ankle sprains in the general population, but occur at much higher rates in football due to the increased rotation forces placed on the ankle during cutting and tackling. RTP after syndesmotic injury often takes twice as long when compared to isolated lateral ankle ligamentous injury.22 Missed injuries are common and if not treated properly can lead to chronic ankle instability and posttraumatic ankle arthritis.23 Syndesmotic injury can occur in isolation or with concomitant adjacent bony, cartilaginous, or ligamentous injuries. Therefore, clinical examination and imaging work-up are critical to successful management.

 

 

Syndesmotic injuries often result from an external rotation force applied to a hyperdorsiflexed ankle while the foot is planted. This mechanism causes the fibula to externally rotate while translating posteriorly and laterally, resulting in rupture of the anterior inferior tibiofibular ligament (AITFL) first, followed by the deep deltoid ligament, interosseous ligament (IOL), and lastly posterior talofibular ligament.24 Most syndesmotic injuries involve rupture of only the AITFL and IOL.25 Multiple clinical stress tests have been designed to assess syndesmotic stability, including the squeeze test, external rotation stress test, crossed-leg test, and fibula-translation test.26-29 However, no physical examination maneuver has been shown to reliably predict the presence or degree of syndesmotic injury and therefore imaging studies are necessary.30

Initial imaging should include standing radiographs of the affected ankle. An increase in the medial clear space between the medial malleolus and talus can occur with a combined syndesmotic and deltoid disruption. In the case of subtle syndesmotic injuries, contralateral comparison weight-bearing radiographs are recommended. CT and MRI can provide additional information, but these static imaging tests cannot identify instability. Fluoroscopic stress evaluation is beneficial but has a high false-negative rate in low-grade injuries and may not detect partial rupture of the AITFL and IOL.31 It has been shown that malrotation of as much as 30° of external rotation can occur if relying on intraoperative fluoroscopy alone.32 It has been our practice to recommend surgical reduction and stabilization for any syndesmotic injury with documented diastasis or instability seen on imaging and/or arthroscopy.

Nonoperative treatment is indicated for truly stable grade I syndesmotic injuries. This involves rest and immobilization followed by a progressive rehabilitation program consisting of stretching, strengthening, and proprioceptive exercises.33 After 1 week of protected weight-bearing in a cast or tall CAM boot, progression to full weight-bearing should occur over the following week. Active-assisted ankle ROM exercises and light proprioceptive training should then be initiated followed by sport-specific exercises 2 to 3 weeks after injury.

Arthroscopy can be a valuable diagnostic tool in the setting of subtle syndesmotic injury with negative radiographs, positive MRI for edema, and a protracted recovery course with vague pain (Figures W5A-W5E).

Figures W5A-W5E
In these situations, an examination under anesthesia is performed, the syndesmosis is probed under direct arthroscopic visualization, and distal tibiofibular instability is evaluated while performing an external rotation stress test. For surgical intervention of these subtle varieties or any athlete with documented instability, we prefer the use of dynamic stabilization with a knotless suture-button construct (TightRope, Arthrex) or hybrid fixation with screws (3.5/4.5 mm) and suture-buttons. Advantages of a knotless suture-button construct include more physiologic motion at the syndesmosis and decreased hardware irritation and implant removal.

Implants are placed above the true syndesmotic joint (at least 15 mm above the tibial plafond) angled 30° posterior to anterior to follow the normal relationship of the fibula to the distal tibia in the incisura. Typically 2 suture-buttons are used, with the devices placed in a divergent fashion. We highly recommend the use of a fibular buttress plate with button placement in individuals returning to contact activity. This construct increases surface area distribution while preventing stress risers and the risk of fibula fractures. In a cadaver model with deliberate syndesmotic malreduction, suture-button stabilization resulted in decreased postoperative displacement as opposed to conventional screw fixation.34 Therefore, dynamic syndesmotic fixation may help to decrease the negative sequelae of iatrogenic clamp malreduction. 
Postoperative rehabilitation involves NWB in a cast or tall CAM boot for 4 weeks followed by ankle ROM exercises and progressive weight-bearing and physical therapy. Patients are transitioned to a lace-up ankle brace and athletic shoe from 6 to 12 weeks postoperative with increasing activity. Running and jumping is permitted 4 months after surgery with RTP typically at 6 to 7 months. Athletes who have had surgical stabilization for documented instability without any diastasis may engage in a more rapid recovery and RTP as symptoms and function allow.

Deltoid Complex Avulsion

Missed or neglected deltoid ligament injuries can lead to progressive chondral injury and joint degeneration. These injuries are often subtle and difficult to diagnose. An inability to perform a single limb heel rise, persistent pain with activity, and lack of normal functional improvement despite appropriate care are indicators of subtle ligament instability. These injuries often require an examination under anesthesia with combined ankle arthroscopy. Valgus stress testing of the ankle while directly visualizing the deltoid ligament from the anterolateral portal can reveal medial laxity in addition to potential osteochondral lesions along the anterolateral talar dome.

In American football players, we have observed that infolding and retraction of an avulsed superficial deltoid ligament complex after an ankle fracture, Maisonneuve injury, or severe high ankle sprain can be a source of persistent increased medial clear space, malreduction, and postoperative pain and medial instability. We have found that there is often complete avulsion of the superficial deltoid complex off the proximal aspect of the medial malleolus during high-energy ankle fractures in football players that is amenable to direct repair to bone (Figures W6A-W6E).

Figures W6A-W6E
In a cohort of 14 NFL players who underwent ankle fracture fixation with ankle arthroscopy and debridement, fibula fixation with plate and screws, syndesmotic fixation with suture-button devices, and open deltoid complex repair with suture anchors, all athletes were able to return to running and cutting maneuvers by 6 months after surgery.35 There were no intraoperative or postoperative complications noted, and no players had clinical evidence of medial pain or instability at final follow-up with radiographic maintenance of anatomic mortise alignment.

During surgical repair, an incision is made along the anterior aspect of the medial malleolus and the superficial deltoid ligament complex can often be found flipped and interposed in the medial gutter. A rongeur is used to create a bleeding cancellous bone surface for soft-tissue healing and 1 to 2 suture anchors are used to repair and imbricate the deltoid ligament complex back to the medial malleolus. The goal of these sutures is to repair the tibionavicular and tibial spring ligaments back to the medial malleolus. We believe that superficial deltoid complex avulsion during high-energy ankle fractures is a distinct injury pattern that should be recognized and may benefit from primary open repair.

We currently open explore every deltoid ligament complex in athletes with unstable syndesmotic injuries, as we believe that deltoid avulsion injuries are underrecognized and do not heal in an anatomic fashion if left alone. Postoperative recovery follows the same immobilization, progressive weight-bearing, and physical therapy protocol as that for syndesmotic disruption.

 

 

Achilles Ruptures

Acute midsubstance Achilles tendon ruptures are an increasingly common injury in patients 30 to 50 years of age, with more than 50% of all injuries occurring during basketball.36,37 Among NFL players, we have found that Achilles ruptures tend to occur at a higher rate during training camp, when athletes are deconditioned and quickly returning to explosive push-off activities. Physical examination should include a Thompson test, palpation of a gap within the tendon, and evaluation of resting ankle dorsiflexion in the affected extremity in the prone position with the knees bent. Lateral radiographs should be analyzed for the presence of a bony avulsion fragment indicative of an insertional avulsion injury or midsubstance calcium deposition reflecting chronic Achilles tendinosis, as both of these conditions will change surgical management. MRI is not recommended with acute midsubstance ruptures but may be helpful in the case of chronic ruptures or more proximal tears of the musculotendinous junction.

The management of acute midsubstance Achilles tendon ruptures is controversial, with no general consensus in the literature regarding nonoperative treatment, surgical repair, and ideal repair technique.36,38-42 American Academy of Orthopaedic Surgeons clinical practice guidelines report moderate evidence that nonoperative treatment of Achilles tendon ruptures has lower wound healing complications but higher rates of re-rupture.38,39 Additionally, limited incision approaches have been found to have fewer overall complications compared with traditional open repair. In an effort to reduce the incidence of postoperative wound complications while improving functional recovery, modern repair techniques focus on a limited incision repair using percutaneous suture insertion and management (PARS Achilles Jig System, Arthrex).36 The limited incision technique utilizes a 2-cm transverse incision and non-disposable jig with divergent needle passes and locking suture fixation options to secure and fixate both tendon ends with minimal dissection of skin, subcutaneous tissue, and paratenon. Limited incision repair is ideally performed within 2 weeks of the injury to ensure that both tendon ends are easy to identify, mobilize, and repair. An open repair is generally recommended for midsubstance ruptures more than 4 weeks old and cases of insertional rupture and Achilles tendinopathy.

In a cohort of 9 NFL players treated for midsubstance Achilles ruptures using the PARS technique, we found no re-ruptures, no wound complications, and no sural nerve issues after surgery.43 A comparative review of 270 cases of operatively treated Achilles tendon ruptures (101 PARS, 169 traditional open repair) showed that the PARS group had significantly shorter operative times and a higher number of patients able to return to baseline physical activities by 5 months compared to open repair.36 Although not statistically significant, the overall PARS complication rate was 5% while the open complication rate was 11%. The PARS group had no cases of sural neuritis or deep infection requiring reoperation. We currently use a limited incision technique for all acute midsubstance Achilles ruptures in athletes regardless of sport, patient size, or position played.

During surgery, a 2-cm transverse incision is made over the gap in the Achilles tendon and dissection is carried down to the rupture site with minimal manipulation of the skin (Figures 5A-5F).

Figures 5A-5F
A transverse incision is made through the paratenon and typically a hematoma is expressed. An Allis clamp is inserted and the proximal tendon stump is grabbed securely and pulled through the wound approximately 1 to 2 cm. The PARS jig is inserted around the proximal tendon and centered so that the needle and sutures will pass through tendon. Needles and sutures are passed in a stepwise fashion and then the entire jig is removed from the wound. Sutures are passed to create 2 non-locking and 1 locking suture. The jig and suture passing process is repeated for the distal tendon stump. Then, each pair of sutures is tied together with the ankle in maximum plantarflexion to obtain a secure end-to-end repair. The knots are cut short and tucked into tendon so that they do not protrude and cause subcutaneous tissue irritation. Absorbable sutures are used to close the paratenon, followed by closure of subcutaneous tissues and skin followed by placement of a short leg posterior mold NWB splint with the ankle in resting plantar flexion.

A key aspect of postoperative recovery is avoiding excessive ankle dorsiflexion while the tendon is healing during the first 4 weeks after surgery, as this can lead to an elongated tendon with loss of push-off strength. Patients are kept in a plantarflexion splint NWB for 2 weeks after surgery. If the incision is healed at 2 weeks, sutures are removed and patients are transitioned into a NWB tall CAM boot for 2 weeks with gentle ankle ROM exercises. If there is any concern regarding wound healing status, sutures are maintained for an additional 1 to 2 weeks.

From 4 to 8 weeks after surgery, progressive weight-bearing with continued ankle ROM exercises is initiated with peel-away heel lifts (~2 cm thick total, 3 layers). Each layer of the heel lift is gradually removed as pain allows every 2 to 3 days with the goal of being full weight-bearing with the foot flat at 6 weeks postoperative. Physical therapy focusing on ankle ROM and gentle Achilles stretching and strengthening is also started 6 weeks after surgery. From 8 to 12 weeks postoperative, patients are transitioned out of the tall CAM boot into normal, accommodative shoe wear with full weight-bearing. We avoid ankle dorsiflexion past neutral until 12 weeks after surgery, as overlengthening of the Achilles complex and the subsequent loss of push-off power can be devastating to running athletes. Activity levels are increased as tolerated, with no running or jumping from 12 to 16 weeks with full release to all activities after 16 weeks. RTP often takes 5 to 6 months after surgery, depending on the position played.

Am J Orthop. 2016;45(6):358-367. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Canale ST, Cantler ED Jr, Sisk TD, Freeman BL 3rd. A chronicle of injuries of an American intercollegiate football team. Am J Sports Med. 1981;9(6):384-389.2. Robey JM, Blyth CS, Mueller FO. Athletic injuries. Application of epidemiologic methods. JAMA. 1971;217(2):184-189.

3. Saal JA. Common American football injuries. Sports Med. 1991;12(2):132-147.

4. Thompson N, Halpern B, Curl WW, et al. High school football injuries: evaluation. Am J Sports Med. 1987;15(2):117-124.

5. Kaplan LD, Jost PW, Honkamp N, Norwig J, West R, Bradley JP. Incidence and variance of foot and ankle injuries in elite college football players. Am J Orthop. 2011;40(1):40-44.

6. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.

7. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine--trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.

8. Bowers KD Jr, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8(2):81-83.

9. McCormick JJ, Anderson RB. Turf toe: anatomy, diagnosis, and treatment. Sports Health. 2010;2(6):487-494.

10. Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367-1372.

11. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete. Orthop Clin North Am. 2002;33(3):587-598.

12. Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am. 1995;26(2):353-361.

13. Nunley JA, Glisson RR. A new option for intramedullary fixation of Jones fractures: the Charlotte Carolina Jones Fracture System. Foot Ankle Int. 2008;29(12):1216-1221.

14. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8-16.

15. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones fractures. Analysis of failure. Am J Sports Med. 2002;30(1):55-60.

16. Portland G, Kelikian A, Kodros S. Acute surgical management of Jones’ fractures. Foot Ankle Int. 2003;24(11):829-833.

17. Hunt KJ, Anderson RB. Treatment of Jones fracture nonunions and refractures in the elite athlete: outcomes of intramedullary screw fixation with bone grafting. Am J Sports Med. 2011;39(9):1948-1954.

18. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871-878.

19. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw fixation. Foot Ankle Int. 2005;26(6):462-473.

20. Ardoin GT, Anderson RB. Subtle Lisfranc injury. Tech Foot Ankle Surg. 2010;9(3):100-106.

21. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A(11):1609-1618.

22. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.

23. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35(7):1197-1207.

24. Beumer A, Valstar ER, Garling EH, et al. Effects of ligament sectioning on the kinematics of the distal tibiofibular syndesmosis: a radiostereometric study of 10 cadaveric specimens based on presumed trauma mechanisms with suggestions for treatment. Acta Orthop. 2006;77(3):531-540.

25. McCollum GA, van den Bekerom MP, Kerkhoffs GM, Calder JD, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1328-1337.

26. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.

27. Nussbaum ED, Hosea TM, Sieler SD, Incremona BR, Kessler DE. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med. 2001;29(1):31-35.

28. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle syndesmosis injuries. Foot Ankle Int. 2005;26(2):187-188.

29. Beumer A, van Hemert WL, Swierstra BA, Jasper LE, Belkoff SM. A biomechanical evaluation of clinical stress tests for syndesmotic ankle instability. Foot Ankle Int. 2003;24(4):358-363.

30. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14(4):232-236.

31. Beumer A, Valstar ER, Garling EH, et al. External rotation stress imaging in syndesmotic injuries of the ankle: comparison of lateral radiography and radiostereometry in a cadaveric model. Acta Orthop Scand. 2003;74(2):201-205.

32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.

33. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2(6):460-470.

34. Westermann RW, Rungprai C, Goetz JE, Femino J, Amendola A, Phisitkul P. The effect of suture-button fixation on simulated syndesmotic malreduction: a cadaveric study. J Bone Joint Surg Am. 2014;96(20):1732-1738.

35. Hsu AR, Lareau CR, Anderson RB. Repair of acute superficial deltoid complex avulsion during ankle fracture fixation in National Football League players. Foot Ankle Int. 2015;36(11):1272-1278.

36. Hsu AR, Jones CP, Cohen BE, Davis WH, Ellington JK, Anderson RB. Clinical outcomes and complications of percutaneous Achilles repair system versus open technique for acute achilles tendon ruptures. Foot Ankle Int. 2015;36(11):1279-1286.

37. Raikin SM, Garras DN, Krapchev PV. Achilles tendon injuries in a United States population. Foot Ankle Int. 2013;34(4):475-480.

38. Chiodo CP, Glazebrook M, Bluman EM, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on treatment of achilles tendon rupture. J Bone Joint Surg Am. 2010;92(14):2466-2468.

39. Chiodo CP, Glazebrook M, Bluman EM, et al. Diagnosis and treatment of acute achilles tendon rupture. J Am Acad Orthop Surg. 2010;18(8):503-510.

40. Khan RJ, Fick D, Keogh A, Crawford J, Brammar T, Parker M. Treatment of acute achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2005;87(10):2202-2210.

41. Renninger CH, Kuhn K, Fellars T, Youngblood S, Bellamy J. Operative and nonoperative management of achilles tendon ruptures in active duty military population. Foot Ankle Int. 2016;37(3):269-273.

42. Khan RJ, Carey Smith RL. Surgical interventions for treating acute achilles tendon ruptures. Cochrane Database Syst Rev. 2010;(9):CD003674.

43. McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv. 2014;23(4):179-183.

Article PDF
Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Hsu reports that he is a paid speaker/presenter for Arthrex. Dr. Anderson reports that he receives royalties from Arthrex, DJ Orthopaedics, and Wright Medical Technology; is a paid consultant for Amniox, Wright Medical Technology, and Arthrex; and receives research support from Wright Medical Technology.

Issue
The American Journal of Orthopedics - 45(6)
Publications
Topics
Page Number
358-367
Sections
Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Hsu reports that he is a paid speaker/presenter for Arthrex. Dr. Anderson reports that he receives royalties from Arthrex, DJ Orthopaedics, and Wright Medical Technology; is a paid consultant for Amniox, Wright Medical Technology, and Arthrex; and receives research support from Wright Medical Technology.

Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Hsu reports that he is a paid speaker/presenter for Arthrex. Dr. Anderson reports that he receives royalties from Arthrex, DJ Orthopaedics, and Wright Medical Technology; is a paid consultant for Amniox, Wright Medical Technology, and Arthrex; and receives research support from Wright Medical Technology.

Article PDF
Article PDF

Foot and ankle injuries are common in American football, with injury rates significantly increasing over the past decade.1-5 Epidemiologic studies of collegiate football players have shown an annual incidence of foot and ankle injuries ranging from 9% to 39%,3,6 with as many as 72% of all collegiate players presenting to the National Football League (NFL) Combine with a history of a foot or ankle injury and 13% undergoing surgical treatment.5 Player position influences the rate and type of foot and ankle injury. Offensive and “skill position” players, including linemen, running backs, and wide receivers, are particularly susceptible to foot and ankle injuries due to high levels of force and torque placed on the distal extremity during running, cutting, and tackling. Shoe wear changes, playing field conditions, increasing player size and speed, and improved reporting of injuries are also contributing to increasing injury rates.

The interaction between player cleats and the playing surface is a central issue of foot and ankle injuries in football. Improved traction relates to performance, but increased subsequent torque on the lower extremity is associated with injury. While lateral ankle sprains are the most common foot and ankle injury experienced by football players,7 numerous other injuries can occur, including turf toe, Jones fractures, Lisfranc injuries, syndesmotic disruption, deltoid complex avulsion, and Achilles ruptures. It is important for physicians to be able to recognize, diagnose, and appropriately treat these injuries in players in order to expedite recovery, restore function, and help prevent future injury and long-term sequelae. This review focuses on updated treatment principles, surgical advances, and rehabilitation protocols for common football foot and ankle injuries.

Turf Toe

The term “turf toe” was first used in 1976 to refer to hyperextension injuries and plantar capsule-ligament sprains of the hallux metatarsophalangeal (MTP) joint that can lead to progressive cock-up deformity.8 While these injuries can occur on any surface and disrupt soft tissue balance with functional implications, predisposing factors include increasing playing surface hardness and decreasing shoe stiffness. In a classic scenario, the foot is fixed in equinus as an axial load is placed on the back of the heel, resulting in forced dorsiflexion of the hallux MTP joint.9 As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the metatarsal head articular surface bears the majority of the load, causing partial or complete tearing of the plantar plate with or without hallux MTP dislocation. Osteochondral lesions of the MTP joint and subchondral edema of the metatarsal head can occur concurrently as the proximal phalanx impacts or shears across the metatarsal head articular surface.

Clinical examination should focus on hallux swelling, alignment, and flexor hallucis longus (FHL) function along with vertical instability of the hallux MTP joint using a Lachman test. Radiographs should be evaluated for proximal migration of the sesamoids or diastasis (Figures W1A-W1C).

Figures W1A-W1C
Forced hallux MTP dorsiflexion lateral view can help assess the distance from the distal sesamoid to the base of the phalanx. A small fleck of bone pulled off of the proximal phalanx or distal sesamoid may indicate a capsular avulsion or disruption. Live fluoroscopy can be very helpful in diagnosing turf toe, as the physician can assess the trailing motion of the sesamoids with increasing dorsiflexion and evaluate instability in all planes. Magnetic resonance imaging (MRI) is useful for subtle capsular injuries and can also identify osseous and articular damage that may occur and FHL disruption (Figures W2A, W2B).
Figures W2A, W2B
Nonoperative intervention focuses on rest, ice, compression, and elevation (RICE) and nonsteroidal anti-inflammatory drugs (NSAIDs). The hallux is temporarily immobilized in a plantarflexed position using a short leg cast or walking boot with toe spica or turf toe plate with tape for 2 to 3 weeks.

Indications for surgical intervention include loss of push-off strength, gross MTP instability, proximal migration of the sesamoids, and progressive hallux malalignment or clawing after immobilization. Cases can involve one or a combination of the following: (1) large capsular avulsion with unstable MTP joint; (2) diastasis of bipartite sesamoid; (3) diastasis of sesamoid fracture; (4) retraction of sesamoid; (5) traumatic hallux valgus deformity; (6) vertical instability (positive Lachman test); (7) loose body in MTP joint; or (8) chondral injury in MTP joint. The goal of surgery is the restoration of anatomy in order to restore normal function of the hallux MTP joint.

We have found that using dual medial and plantar incisions places less traction on the plantar medial cutaneous nerve, improves lateral exposure, and provides better wound healing. The medial capsulotomy extends from the metatarsal neck to the mid-phalanx to provide complete visualization of the sesamoid complex (Figures 1A-1F).
Figures 1A-1F
The collateral ligaments are often torn away from the metatarsal head during the initial dissection and the plantar plate tear is distal to the sesamoid complex. The soft tissue defect in the plantar complex must be closed distal to the sesamoids followed by advancement of the plantar plate to the proximal phalanx in a distal to proximal fashion and advancement of the medial capsule. The plantar incision is made along the lateral border of hallux MTP-sesamoid complex just lateral to the weight-bearing surface of the hallux and the plantar lateral cutaneous nerve is carefully dissected and retracted out of the way. Sutures are placed in a figure-of-eight fashion through the plantar capsule and plantar plate starting lateral to medial to reduce injury to the nerve. If the tear cannot be primarily repaired due to inadequate healthy tissue, a plantar plate advancement can be performed directly onto the base of the proximal phalanx using drill holes or suture anchors. Proper alignment and motion of the sesamoids should be verified with fluoroscopy and compared to the contralateral hallux (Figures W3A, W3B).
Figures W3A, W3B


It is important to recognize that not all turf toe injuries involve pure hyperextension on artificial playing surfaces. In recent years, we have found an increasing rate of medial variant turf toe injuries in which a forceful valgus stress on the hallux leads to rupture of the medial collateral ligament, medial or plantar-medial capsule, and/or abductor halluces. Medial variant turf toe can lead to progressive hallux valgus and a traumatic bunion with a significant loss of push-off strength and difficulty with cutting maneuvers. Surgical treatment requires a modified McBride bunionectomy with adductor tenotomy and direct repair of the medial soft tissue defect.

Postoperative management is just as important as proper surgical technique for these injuries and involves a delicate balance between protecting the repair and starting early range of motion (ROM). Patients are immobilized non-weight-bearing (NWB) for 5 to 7 days maximum followed immediately with the initiation of passive hallux plantarflexion to keep the sesamoids moving. Active hallux plantarflexion is started at 4 weeks after surgery with active dorsiflexion from 6 to 8 weeks. Patients are transitioned to an accommodative shoe with stiff hallux insert 8 weeks postoperative with continued therapy focusing on hallux ROM. Running is initiated at 12 weeks and return to play (RTP) is typically allowed 4 months after surgery.

 

 

Jones Fractures

Jones fractures are fractures of the 5th metatarsal at the metaphyseal-diaphyseal junction, where there is a watershed area of decreased vascularity between the intramedullary nutrient and metaphyseal arteries. Current thought is that the rising rate of Jones fractures among football players is partially caused by the use of flexible, narrow cleats that do not provide enough stiffness and lateral support for the 5th metatarsal during running and cutting. Additionally, lateral overload from a baseline cavovarus foot posture with or without metatarsus adductus and/or skewfoot is thought to contribute to Jones fractures.10 Preoperative radiographs should be evaluated for fracture location, orientation, amount of cortical thickening, and overall geometry of the foot and 5th metatarsal. In elite athletes, the threshold for surgical intervention is decreasing in order to expedite healing and recovery and decrease re-fracture risk. This rationale is based on delayed union rates of 25% to 66%, nonunion rates of 7% to 28%,11 and re-fracture rates of up to 33% associated with nonoperative treatment.12 Nonoperative management is usually not feasible in the competitive athlete, as it typically involves a period of protected weight-bearing in a tall controlled ankle motion (CAM) boot for 6 to 8 weeks with serial radiographs to evaluate healing.

Our preference for surgical intervention involves percutaneous screw fixation with a “high and inside” starting point on fluoroscopy (Figures 2A-2D).

Figures 2A-2D
The guidewire is inserted percutaneously through the skin 2 cm proximal to the base of the 5th metatarsal. Incorrect starting point can lead to a prominent screw head laterally or perforation of the medial cortex. A 1-cm incision is made around the guidewire entry point and intramedullary cannulated drilling enters the proximal third of the metatarsal, removing any thickened lateral cortex. Due to the natural curve of the 5th metatarsal, cannulated drilling is not continued distally but can be safely completed with a 3.2-mm solid drill bit. Proper tap sizing should generate enough torque to begin to rotate the entire foot as the tap is advanced (Figures W4A-W4F).
Figures W4A-W4F
The largest solid screw with a low-profile head that “comfortably” fits the intramedullary canal of the 5th metatarsal should be inserted (Carolina Jones Fracture System, Wright Medical Technology).13 In elite athletes, we will typically use a 5.5-mm or 6.5-mm screw that is 45 to 55 mm in length. Screw threads should pass just across the fracture site, avoiding “straightening” of the curved 5th metatarsal that will create a lateral gap and increase the rate of nonunion. We do not recommend headless tapered screws due to inconsistent compression and difficulty with later removal if re-fracture or nonunion occurs.

In career athletes, we augment the fracture site using a mixture of bone marrow aspirate concentrate (BMA) (Magellan, Arteriocyte Medical Systems) and demineralized bone matrix (DBM) (Mini Ignite, Wright Medical Technology) injected percutaneously in and around the fracture site under fluoroscopic guidance. Using this technique in a cohort of 25 NFL players treated operatively for Jones fractures, we found that 100% of athletes were able to RTP in the NFL in an average of 9.5 weeks.14 Two patients (7.5%) suffered re-fractures requiring revision surgery with iliac crest bone graft and repeat screw placement with a RTP after 15 weeks. We did not find an association between RTP and re-fracture rate.

The appropriate rehabilitation protocol for Jones fractures after surgery remains controversial and dependent on individual needs and abilities.15,16 For athletes in-season, we recommend a brief period of NWB for 1 to 2 weeks followed by toe-touch weight-bearing in a tall CAM boot for 2 to 4 weeks. After 4 weeks, patients begin gentle exercises on a stationary bike and pool therapy to reduce impact on the fracture site. Low-intensity pulsed ultrasound bone stimulators (Exogen, Bioventus) are frequently used directly over fracture site throughout the postoperative protocol as an adjuvant therapy. If clinically nontender over the fracture site, patients are allowed to begin running in modified protective shoe wear 4 weeks after surgery with an average RTP of 6 to 8 weeks. RTP is determined clinically, as radiographic union may not be evident for 12 to 16 weeks. Useful custom orthoses include turf toe plates with a cushioned lateral column and lateral heel wedge if hindfoot varus is present preoperatively.10 The solid intramedullary screw is left in place permanently.

In our experience, we have found the average re-fracture and nonunion rate to be approximately 8% across all athletes. Our observation that union rates do not appear to be related to RTP times suggests that underlying biology such as Vitamin D deficiency may play a larger role in union rates than previously thought. We have found that most Jones re-fractures occur in the first year after the initial injury, but can occur up to 2.5 years afterwards as well.14 For the management of symptomatic re-fractures and nonunions, the previous screw must be first removed. This can be difficult if the screw is bent or broken, and may require a lateral corticotomy of the metatarsal.

After hardware removal, we advocate open bone grafting of the fracture site using bone from the iliac crest retrieved with a small, percutaneous trephine. Re-fixation should be achieved using a larger, solid screw and postoperative adjuvants may include bone stimulators, Vitamin D and calcium supplemention, and possible teriparatide use (Forteo, Eli Lilly), depending on individual patient profile. In a cohort of 21 elite athletes treated for Jones fracture revision surgery with screw exchange and bone grafting, we found that 100% of patients had computed tomography (CT) evidence of union, with an average RTP of 12.3 weeks.17

 

 

Lisfranc Injuries

Lisfranc injuries include any bony or ligamentous damage that involves the tarsometatarsal (TMT) joints. While axial loading of a fixed, plantarflexed foot has traditionally been thought of as the most common mechanism of Lisfranc injury, we have found that noncontact twisting injuries leading to Lisfranc disruption are actually more common among NFL players. This mechanism is similar to noncontact turf toe and results in a purely ligamentous injury. We have found this to be particularly true in the case of defensive ends engaged with offensive linemen in which no axial loading or contact of the foot occurs. Clinically, patients often have painful weight-bearing, inability to perform a single limb heel rise, plantar ecchymosis, and swelling and point tenderness across the bases of the 1st and 2nd metatarsals.

It is critical to obtain comparison weight-bearing radiographs of both feet during initial work-up to look for evidence of instability. Subtle radiographic findings of Lisfranc injury include a bony “fleck” sign, compression fracture of the cuboid, and diastasis between the base of the 1st and 2nd metatarsals and/or medial and middle cuneiforms (Figures 3A, 3B).

Figures 3A, 3B
Stress testing involves pronation and adduction of the foot under live fluoroscopy to evaluate for diastasis. MRI can be helpful in cases of vague pain with negative radiographs and subtle displacement. Nonoperative treatment for cases of no instability or displacement involved protected weight-bearing for 4 weeks followed by progressive increase in activities, with RTP 6 to 8 weeks after injury.

The goal of surgical intervention is to obtain and maintain anatomic reduction of all unstable joints in order to restore a normal foot posture. One of the difficulties with Lisfranc injuries is that there are no exact diastasis parameters and individuals should be treated based on symptoms, functional needs, and degree of instability. It has been shown that 5 mm of displacement can have good long-term clinical results in select cases without surgery.18 For surgery, we recommend open reduction to remove interposed soft tissue debris and directly assess the articular surfaces (Figures 4A-4D).
Figures 4A-4D
A freer can be placed in the individual joints to assess for areas of instability. We prefer solid screw fixation (Charlotte Lisfranc Reconstruction System, Wright Medical Technology) to decrease the risk of later screw breakage. A homerun screw from the proximal aspect of the medial cuneiform to the distal-lateral aspect of the 2nd metatarsal base should be placed first. Bridge plates can be used over the 1st and 2nd TMT joints to avoid articular cartilage damage without a loss of rigidity.19

Proximal-medial column Lisfranc injury variants are increasingly common among football players.20 In these injuries, the force of injury extends through the intercuneiform joint and exits out the naviculocuneiform joint, thus causing instability at multiple joints and an unstable 1st ray. Patients often have minimal clinical findings and normal radiographs and stress radiographs. MRI of the foot often reveals edema at the naviculocuneiform joint. Often patients fail to improve with nonoperative immobilization with continued inability to push off from the hallux. Unrecognized or untreated instability will lead to rapid deterioration of the naviculocuneiform joint. Surgical intervention requires a homerun screw and intercuneiform screw. We do not recommend primary arthrodesis in athletes due to significant risk of malunion and nonunion unless severe articular damage is present.

Patients are typically kept NWB in a splint for 2 weeks after surgery followed by NWB in a tall CAM from 3 to 4 weeks postoperative. Progressive weight-bearing and ROM exercises are initiated from 4 to 8 weeks, followed by return to accommodative shoe wear from 10 to 12 weeks. Hardware removal is performed 4 to 6 months after surgery, typically in the off-season to allow for 6 to 8 weeks or protected recovery afterwards. Premature hardware removal can lead to loss of reduction, particularly at the intercuneiform joints. All hardware crossing the TMT joints should be removed, while the homerun screw can be left in place in addition to the intercuneiform screw. RTP in football typically occurs 6 to 7 months after surgery. Final functional outcome is related to the adequacy of initial reduction and severity of the initial injury.21

Syndesmotic Disruption

Syndesmotic injuries comprise 1% to 18% of ankle sprains in the general population, but occur at much higher rates in football due to the increased rotation forces placed on the ankle during cutting and tackling. RTP after syndesmotic injury often takes twice as long when compared to isolated lateral ankle ligamentous injury.22 Missed injuries are common and if not treated properly can lead to chronic ankle instability and posttraumatic ankle arthritis.23 Syndesmotic injury can occur in isolation or with concomitant adjacent bony, cartilaginous, or ligamentous injuries. Therefore, clinical examination and imaging work-up are critical to successful management.

 

 

Syndesmotic injuries often result from an external rotation force applied to a hyperdorsiflexed ankle while the foot is planted. This mechanism causes the fibula to externally rotate while translating posteriorly and laterally, resulting in rupture of the anterior inferior tibiofibular ligament (AITFL) first, followed by the deep deltoid ligament, interosseous ligament (IOL), and lastly posterior talofibular ligament.24 Most syndesmotic injuries involve rupture of only the AITFL and IOL.25 Multiple clinical stress tests have been designed to assess syndesmotic stability, including the squeeze test, external rotation stress test, crossed-leg test, and fibula-translation test.26-29 However, no physical examination maneuver has been shown to reliably predict the presence or degree of syndesmotic injury and therefore imaging studies are necessary.30

Initial imaging should include standing radiographs of the affected ankle. An increase in the medial clear space between the medial malleolus and talus can occur with a combined syndesmotic and deltoid disruption. In the case of subtle syndesmotic injuries, contralateral comparison weight-bearing radiographs are recommended. CT and MRI can provide additional information, but these static imaging tests cannot identify instability. Fluoroscopic stress evaluation is beneficial but has a high false-negative rate in low-grade injuries and may not detect partial rupture of the AITFL and IOL.31 It has been shown that malrotation of as much as 30° of external rotation can occur if relying on intraoperative fluoroscopy alone.32 It has been our practice to recommend surgical reduction and stabilization for any syndesmotic injury with documented diastasis or instability seen on imaging and/or arthroscopy.

Nonoperative treatment is indicated for truly stable grade I syndesmotic injuries. This involves rest and immobilization followed by a progressive rehabilitation program consisting of stretching, strengthening, and proprioceptive exercises.33 After 1 week of protected weight-bearing in a cast or tall CAM boot, progression to full weight-bearing should occur over the following week. Active-assisted ankle ROM exercises and light proprioceptive training should then be initiated followed by sport-specific exercises 2 to 3 weeks after injury.

Arthroscopy can be a valuable diagnostic tool in the setting of subtle syndesmotic injury with negative radiographs, positive MRI for edema, and a protracted recovery course with vague pain (Figures W5A-W5E).

Figures W5A-W5E
In these situations, an examination under anesthesia is performed, the syndesmosis is probed under direct arthroscopic visualization, and distal tibiofibular instability is evaluated while performing an external rotation stress test. For surgical intervention of these subtle varieties or any athlete with documented instability, we prefer the use of dynamic stabilization with a knotless suture-button construct (TightRope, Arthrex) or hybrid fixation with screws (3.5/4.5 mm) and suture-buttons. Advantages of a knotless suture-button construct include more physiologic motion at the syndesmosis and decreased hardware irritation and implant removal.

Implants are placed above the true syndesmotic joint (at least 15 mm above the tibial plafond) angled 30° posterior to anterior to follow the normal relationship of the fibula to the distal tibia in the incisura. Typically 2 suture-buttons are used, with the devices placed in a divergent fashion. We highly recommend the use of a fibular buttress plate with button placement in individuals returning to contact activity. This construct increases surface area distribution while preventing stress risers and the risk of fibula fractures. In a cadaver model with deliberate syndesmotic malreduction, suture-button stabilization resulted in decreased postoperative displacement as opposed to conventional screw fixation.34 Therefore, dynamic syndesmotic fixation may help to decrease the negative sequelae of iatrogenic clamp malreduction. 
Postoperative rehabilitation involves NWB in a cast or tall CAM boot for 4 weeks followed by ankle ROM exercises and progressive weight-bearing and physical therapy. Patients are transitioned to a lace-up ankle brace and athletic shoe from 6 to 12 weeks postoperative with increasing activity. Running and jumping is permitted 4 months after surgery with RTP typically at 6 to 7 months. Athletes who have had surgical stabilization for documented instability without any diastasis may engage in a more rapid recovery and RTP as symptoms and function allow.

Deltoid Complex Avulsion

Missed or neglected deltoid ligament injuries can lead to progressive chondral injury and joint degeneration. These injuries are often subtle and difficult to diagnose. An inability to perform a single limb heel rise, persistent pain with activity, and lack of normal functional improvement despite appropriate care are indicators of subtle ligament instability. These injuries often require an examination under anesthesia with combined ankle arthroscopy. Valgus stress testing of the ankle while directly visualizing the deltoid ligament from the anterolateral portal can reveal medial laxity in addition to potential osteochondral lesions along the anterolateral talar dome.

In American football players, we have observed that infolding and retraction of an avulsed superficial deltoid ligament complex after an ankle fracture, Maisonneuve injury, or severe high ankle sprain can be a source of persistent increased medial clear space, malreduction, and postoperative pain and medial instability. We have found that there is often complete avulsion of the superficial deltoid complex off the proximal aspect of the medial malleolus during high-energy ankle fractures in football players that is amenable to direct repair to bone (Figures W6A-W6E).

Figures W6A-W6E
In a cohort of 14 NFL players who underwent ankle fracture fixation with ankle arthroscopy and debridement, fibula fixation with plate and screws, syndesmotic fixation with suture-button devices, and open deltoid complex repair with suture anchors, all athletes were able to return to running and cutting maneuvers by 6 months after surgery.35 There were no intraoperative or postoperative complications noted, and no players had clinical evidence of medial pain or instability at final follow-up with radiographic maintenance of anatomic mortise alignment.

During surgical repair, an incision is made along the anterior aspect of the medial malleolus and the superficial deltoid ligament complex can often be found flipped and interposed in the medial gutter. A rongeur is used to create a bleeding cancellous bone surface for soft-tissue healing and 1 to 2 suture anchors are used to repair and imbricate the deltoid ligament complex back to the medial malleolus. The goal of these sutures is to repair the tibionavicular and tibial spring ligaments back to the medial malleolus. We believe that superficial deltoid complex avulsion during high-energy ankle fractures is a distinct injury pattern that should be recognized and may benefit from primary open repair.

We currently open explore every deltoid ligament complex in athletes with unstable syndesmotic injuries, as we believe that deltoid avulsion injuries are underrecognized and do not heal in an anatomic fashion if left alone. Postoperative recovery follows the same immobilization, progressive weight-bearing, and physical therapy protocol as that for syndesmotic disruption.

 

 

Achilles Ruptures

Acute midsubstance Achilles tendon ruptures are an increasingly common injury in patients 30 to 50 years of age, with more than 50% of all injuries occurring during basketball.36,37 Among NFL players, we have found that Achilles ruptures tend to occur at a higher rate during training camp, when athletes are deconditioned and quickly returning to explosive push-off activities. Physical examination should include a Thompson test, palpation of a gap within the tendon, and evaluation of resting ankle dorsiflexion in the affected extremity in the prone position with the knees bent. Lateral radiographs should be analyzed for the presence of a bony avulsion fragment indicative of an insertional avulsion injury or midsubstance calcium deposition reflecting chronic Achilles tendinosis, as both of these conditions will change surgical management. MRI is not recommended with acute midsubstance ruptures but may be helpful in the case of chronic ruptures or more proximal tears of the musculotendinous junction.

The management of acute midsubstance Achilles tendon ruptures is controversial, with no general consensus in the literature regarding nonoperative treatment, surgical repair, and ideal repair technique.36,38-42 American Academy of Orthopaedic Surgeons clinical practice guidelines report moderate evidence that nonoperative treatment of Achilles tendon ruptures has lower wound healing complications but higher rates of re-rupture.38,39 Additionally, limited incision approaches have been found to have fewer overall complications compared with traditional open repair. In an effort to reduce the incidence of postoperative wound complications while improving functional recovery, modern repair techniques focus on a limited incision repair using percutaneous suture insertion and management (PARS Achilles Jig System, Arthrex).36 The limited incision technique utilizes a 2-cm transverse incision and non-disposable jig with divergent needle passes and locking suture fixation options to secure and fixate both tendon ends with minimal dissection of skin, subcutaneous tissue, and paratenon. Limited incision repair is ideally performed within 2 weeks of the injury to ensure that both tendon ends are easy to identify, mobilize, and repair. An open repair is generally recommended for midsubstance ruptures more than 4 weeks old and cases of insertional rupture and Achilles tendinopathy.

In a cohort of 9 NFL players treated for midsubstance Achilles ruptures using the PARS technique, we found no re-ruptures, no wound complications, and no sural nerve issues after surgery.43 A comparative review of 270 cases of operatively treated Achilles tendon ruptures (101 PARS, 169 traditional open repair) showed that the PARS group had significantly shorter operative times and a higher number of patients able to return to baseline physical activities by 5 months compared to open repair.36 Although not statistically significant, the overall PARS complication rate was 5% while the open complication rate was 11%. The PARS group had no cases of sural neuritis or deep infection requiring reoperation. We currently use a limited incision technique for all acute midsubstance Achilles ruptures in athletes regardless of sport, patient size, or position played.

During surgery, a 2-cm transverse incision is made over the gap in the Achilles tendon and dissection is carried down to the rupture site with minimal manipulation of the skin (Figures 5A-5F).

Figures 5A-5F
A transverse incision is made through the paratenon and typically a hematoma is expressed. An Allis clamp is inserted and the proximal tendon stump is grabbed securely and pulled through the wound approximately 1 to 2 cm. The PARS jig is inserted around the proximal tendon and centered so that the needle and sutures will pass through tendon. Needles and sutures are passed in a stepwise fashion and then the entire jig is removed from the wound. Sutures are passed to create 2 non-locking and 1 locking suture. The jig and suture passing process is repeated for the distal tendon stump. Then, each pair of sutures is tied together with the ankle in maximum plantarflexion to obtain a secure end-to-end repair. The knots are cut short and tucked into tendon so that they do not protrude and cause subcutaneous tissue irritation. Absorbable sutures are used to close the paratenon, followed by closure of subcutaneous tissues and skin followed by placement of a short leg posterior mold NWB splint with the ankle in resting plantar flexion.

A key aspect of postoperative recovery is avoiding excessive ankle dorsiflexion while the tendon is healing during the first 4 weeks after surgery, as this can lead to an elongated tendon with loss of push-off strength. Patients are kept in a plantarflexion splint NWB for 2 weeks after surgery. If the incision is healed at 2 weeks, sutures are removed and patients are transitioned into a NWB tall CAM boot for 2 weeks with gentle ankle ROM exercises. If there is any concern regarding wound healing status, sutures are maintained for an additional 1 to 2 weeks.

From 4 to 8 weeks after surgery, progressive weight-bearing with continued ankle ROM exercises is initiated with peel-away heel lifts (~2 cm thick total, 3 layers). Each layer of the heel lift is gradually removed as pain allows every 2 to 3 days with the goal of being full weight-bearing with the foot flat at 6 weeks postoperative. Physical therapy focusing on ankle ROM and gentle Achilles stretching and strengthening is also started 6 weeks after surgery. From 8 to 12 weeks postoperative, patients are transitioned out of the tall CAM boot into normal, accommodative shoe wear with full weight-bearing. We avoid ankle dorsiflexion past neutral until 12 weeks after surgery, as overlengthening of the Achilles complex and the subsequent loss of push-off power can be devastating to running athletes. Activity levels are increased as tolerated, with no running or jumping from 12 to 16 weeks with full release to all activities after 16 weeks. RTP often takes 5 to 6 months after surgery, depending on the position played.

Am J Orthop. 2016;45(6):358-367. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Foot and ankle injuries are common in American football, with injury rates significantly increasing over the past decade.1-5 Epidemiologic studies of collegiate football players have shown an annual incidence of foot and ankle injuries ranging from 9% to 39%,3,6 with as many as 72% of all collegiate players presenting to the National Football League (NFL) Combine with a history of a foot or ankle injury and 13% undergoing surgical treatment.5 Player position influences the rate and type of foot and ankle injury. Offensive and “skill position” players, including linemen, running backs, and wide receivers, are particularly susceptible to foot and ankle injuries due to high levels of force and torque placed on the distal extremity during running, cutting, and tackling. Shoe wear changes, playing field conditions, increasing player size and speed, and improved reporting of injuries are also contributing to increasing injury rates.

The interaction between player cleats and the playing surface is a central issue of foot and ankle injuries in football. Improved traction relates to performance, but increased subsequent torque on the lower extremity is associated with injury. While lateral ankle sprains are the most common foot and ankle injury experienced by football players,7 numerous other injuries can occur, including turf toe, Jones fractures, Lisfranc injuries, syndesmotic disruption, deltoid complex avulsion, and Achilles ruptures. It is important for physicians to be able to recognize, diagnose, and appropriately treat these injuries in players in order to expedite recovery, restore function, and help prevent future injury and long-term sequelae. This review focuses on updated treatment principles, surgical advances, and rehabilitation protocols for common football foot and ankle injuries.

Turf Toe

The term “turf toe” was first used in 1976 to refer to hyperextension injuries and plantar capsule-ligament sprains of the hallux metatarsophalangeal (MTP) joint that can lead to progressive cock-up deformity.8 While these injuries can occur on any surface and disrupt soft tissue balance with functional implications, predisposing factors include increasing playing surface hardness and decreasing shoe stiffness. In a classic scenario, the foot is fixed in equinus as an axial load is placed on the back of the heel, resulting in forced dorsiflexion of the hallux MTP joint.9 As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the metatarsal head articular surface bears the majority of the load, causing partial or complete tearing of the plantar plate with or without hallux MTP dislocation. Osteochondral lesions of the MTP joint and subchondral edema of the metatarsal head can occur concurrently as the proximal phalanx impacts or shears across the metatarsal head articular surface.

Clinical examination should focus on hallux swelling, alignment, and flexor hallucis longus (FHL) function along with vertical instability of the hallux MTP joint using a Lachman test. Radiographs should be evaluated for proximal migration of the sesamoids or diastasis (Figures W1A-W1C).

Figures W1A-W1C
Forced hallux MTP dorsiflexion lateral view can help assess the distance from the distal sesamoid to the base of the phalanx. A small fleck of bone pulled off of the proximal phalanx or distal sesamoid may indicate a capsular avulsion or disruption. Live fluoroscopy can be very helpful in diagnosing turf toe, as the physician can assess the trailing motion of the sesamoids with increasing dorsiflexion and evaluate instability in all planes. Magnetic resonance imaging (MRI) is useful for subtle capsular injuries and can also identify osseous and articular damage that may occur and FHL disruption (Figures W2A, W2B).
Figures W2A, W2B
Nonoperative intervention focuses on rest, ice, compression, and elevation (RICE) and nonsteroidal anti-inflammatory drugs (NSAIDs). The hallux is temporarily immobilized in a plantarflexed position using a short leg cast or walking boot with toe spica or turf toe plate with tape for 2 to 3 weeks.

Indications for surgical intervention include loss of push-off strength, gross MTP instability, proximal migration of the sesamoids, and progressive hallux malalignment or clawing after immobilization. Cases can involve one or a combination of the following: (1) large capsular avulsion with unstable MTP joint; (2) diastasis of bipartite sesamoid; (3) diastasis of sesamoid fracture; (4) retraction of sesamoid; (5) traumatic hallux valgus deformity; (6) vertical instability (positive Lachman test); (7) loose body in MTP joint; or (8) chondral injury in MTP joint. The goal of surgery is the restoration of anatomy in order to restore normal function of the hallux MTP joint.

We have found that using dual medial and plantar incisions places less traction on the plantar medial cutaneous nerve, improves lateral exposure, and provides better wound healing. The medial capsulotomy extends from the metatarsal neck to the mid-phalanx to provide complete visualization of the sesamoid complex (Figures 1A-1F).
Figures 1A-1F
The collateral ligaments are often torn away from the metatarsal head during the initial dissection and the plantar plate tear is distal to the sesamoid complex. The soft tissue defect in the plantar complex must be closed distal to the sesamoids followed by advancement of the plantar plate to the proximal phalanx in a distal to proximal fashion and advancement of the medial capsule. The plantar incision is made along the lateral border of hallux MTP-sesamoid complex just lateral to the weight-bearing surface of the hallux and the plantar lateral cutaneous nerve is carefully dissected and retracted out of the way. Sutures are placed in a figure-of-eight fashion through the plantar capsule and plantar plate starting lateral to medial to reduce injury to the nerve. If the tear cannot be primarily repaired due to inadequate healthy tissue, a plantar plate advancement can be performed directly onto the base of the proximal phalanx using drill holes or suture anchors. Proper alignment and motion of the sesamoids should be verified with fluoroscopy and compared to the contralateral hallux (Figures W3A, W3B).
Figures W3A, W3B


It is important to recognize that not all turf toe injuries involve pure hyperextension on artificial playing surfaces. In recent years, we have found an increasing rate of medial variant turf toe injuries in which a forceful valgus stress on the hallux leads to rupture of the medial collateral ligament, medial or plantar-medial capsule, and/or abductor halluces. Medial variant turf toe can lead to progressive hallux valgus and a traumatic bunion with a significant loss of push-off strength and difficulty with cutting maneuvers. Surgical treatment requires a modified McBride bunionectomy with adductor tenotomy and direct repair of the medial soft tissue defect.

Postoperative management is just as important as proper surgical technique for these injuries and involves a delicate balance between protecting the repair and starting early range of motion (ROM). Patients are immobilized non-weight-bearing (NWB) for 5 to 7 days maximum followed immediately with the initiation of passive hallux plantarflexion to keep the sesamoids moving. Active hallux plantarflexion is started at 4 weeks after surgery with active dorsiflexion from 6 to 8 weeks. Patients are transitioned to an accommodative shoe with stiff hallux insert 8 weeks postoperative with continued therapy focusing on hallux ROM. Running is initiated at 12 weeks and return to play (RTP) is typically allowed 4 months after surgery.

 

 

Jones Fractures

Jones fractures are fractures of the 5th metatarsal at the metaphyseal-diaphyseal junction, where there is a watershed area of decreased vascularity between the intramedullary nutrient and metaphyseal arteries. Current thought is that the rising rate of Jones fractures among football players is partially caused by the use of flexible, narrow cleats that do not provide enough stiffness and lateral support for the 5th metatarsal during running and cutting. Additionally, lateral overload from a baseline cavovarus foot posture with or without metatarsus adductus and/or skewfoot is thought to contribute to Jones fractures.10 Preoperative radiographs should be evaluated for fracture location, orientation, amount of cortical thickening, and overall geometry of the foot and 5th metatarsal. In elite athletes, the threshold for surgical intervention is decreasing in order to expedite healing and recovery and decrease re-fracture risk. This rationale is based on delayed union rates of 25% to 66%, nonunion rates of 7% to 28%,11 and re-fracture rates of up to 33% associated with nonoperative treatment.12 Nonoperative management is usually not feasible in the competitive athlete, as it typically involves a period of protected weight-bearing in a tall controlled ankle motion (CAM) boot for 6 to 8 weeks with serial radiographs to evaluate healing.

Our preference for surgical intervention involves percutaneous screw fixation with a “high and inside” starting point on fluoroscopy (Figures 2A-2D).

Figures 2A-2D
The guidewire is inserted percutaneously through the skin 2 cm proximal to the base of the 5th metatarsal. Incorrect starting point can lead to a prominent screw head laterally or perforation of the medial cortex. A 1-cm incision is made around the guidewire entry point and intramedullary cannulated drilling enters the proximal third of the metatarsal, removing any thickened lateral cortex. Due to the natural curve of the 5th metatarsal, cannulated drilling is not continued distally but can be safely completed with a 3.2-mm solid drill bit. Proper tap sizing should generate enough torque to begin to rotate the entire foot as the tap is advanced (Figures W4A-W4F).
Figures W4A-W4F
The largest solid screw with a low-profile head that “comfortably” fits the intramedullary canal of the 5th metatarsal should be inserted (Carolina Jones Fracture System, Wright Medical Technology).13 In elite athletes, we will typically use a 5.5-mm or 6.5-mm screw that is 45 to 55 mm in length. Screw threads should pass just across the fracture site, avoiding “straightening” of the curved 5th metatarsal that will create a lateral gap and increase the rate of nonunion. We do not recommend headless tapered screws due to inconsistent compression and difficulty with later removal if re-fracture or nonunion occurs.

In career athletes, we augment the fracture site using a mixture of bone marrow aspirate concentrate (BMA) (Magellan, Arteriocyte Medical Systems) and demineralized bone matrix (DBM) (Mini Ignite, Wright Medical Technology) injected percutaneously in and around the fracture site under fluoroscopic guidance. Using this technique in a cohort of 25 NFL players treated operatively for Jones fractures, we found that 100% of athletes were able to RTP in the NFL in an average of 9.5 weeks.14 Two patients (7.5%) suffered re-fractures requiring revision surgery with iliac crest bone graft and repeat screw placement with a RTP after 15 weeks. We did not find an association between RTP and re-fracture rate.

The appropriate rehabilitation protocol for Jones fractures after surgery remains controversial and dependent on individual needs and abilities.15,16 For athletes in-season, we recommend a brief period of NWB for 1 to 2 weeks followed by toe-touch weight-bearing in a tall CAM boot for 2 to 4 weeks. After 4 weeks, patients begin gentle exercises on a stationary bike and pool therapy to reduce impact on the fracture site. Low-intensity pulsed ultrasound bone stimulators (Exogen, Bioventus) are frequently used directly over fracture site throughout the postoperative protocol as an adjuvant therapy. If clinically nontender over the fracture site, patients are allowed to begin running in modified protective shoe wear 4 weeks after surgery with an average RTP of 6 to 8 weeks. RTP is determined clinically, as radiographic union may not be evident for 12 to 16 weeks. Useful custom orthoses include turf toe plates with a cushioned lateral column and lateral heel wedge if hindfoot varus is present preoperatively.10 The solid intramedullary screw is left in place permanently.

In our experience, we have found the average re-fracture and nonunion rate to be approximately 8% across all athletes. Our observation that union rates do not appear to be related to RTP times suggests that underlying biology such as Vitamin D deficiency may play a larger role in union rates than previously thought. We have found that most Jones re-fractures occur in the first year after the initial injury, but can occur up to 2.5 years afterwards as well.14 For the management of symptomatic re-fractures and nonunions, the previous screw must be first removed. This can be difficult if the screw is bent or broken, and may require a lateral corticotomy of the metatarsal.

After hardware removal, we advocate open bone grafting of the fracture site using bone from the iliac crest retrieved with a small, percutaneous trephine. Re-fixation should be achieved using a larger, solid screw and postoperative adjuvants may include bone stimulators, Vitamin D and calcium supplemention, and possible teriparatide use (Forteo, Eli Lilly), depending on individual patient profile. In a cohort of 21 elite athletes treated for Jones fracture revision surgery with screw exchange and bone grafting, we found that 100% of patients had computed tomography (CT) evidence of union, with an average RTP of 12.3 weeks.17

 

 

Lisfranc Injuries

Lisfranc injuries include any bony or ligamentous damage that involves the tarsometatarsal (TMT) joints. While axial loading of a fixed, plantarflexed foot has traditionally been thought of as the most common mechanism of Lisfranc injury, we have found that noncontact twisting injuries leading to Lisfranc disruption are actually more common among NFL players. This mechanism is similar to noncontact turf toe and results in a purely ligamentous injury. We have found this to be particularly true in the case of defensive ends engaged with offensive linemen in which no axial loading or contact of the foot occurs. Clinically, patients often have painful weight-bearing, inability to perform a single limb heel rise, plantar ecchymosis, and swelling and point tenderness across the bases of the 1st and 2nd metatarsals.

It is critical to obtain comparison weight-bearing radiographs of both feet during initial work-up to look for evidence of instability. Subtle radiographic findings of Lisfranc injury include a bony “fleck” sign, compression fracture of the cuboid, and diastasis between the base of the 1st and 2nd metatarsals and/or medial and middle cuneiforms (Figures 3A, 3B).

Figures 3A, 3B
Stress testing involves pronation and adduction of the foot under live fluoroscopy to evaluate for diastasis. MRI can be helpful in cases of vague pain with negative radiographs and subtle displacement. Nonoperative treatment for cases of no instability or displacement involved protected weight-bearing for 4 weeks followed by progressive increase in activities, with RTP 6 to 8 weeks after injury.

The goal of surgical intervention is to obtain and maintain anatomic reduction of all unstable joints in order to restore a normal foot posture. One of the difficulties with Lisfranc injuries is that there are no exact diastasis parameters and individuals should be treated based on symptoms, functional needs, and degree of instability. It has been shown that 5 mm of displacement can have good long-term clinical results in select cases without surgery.18 For surgery, we recommend open reduction to remove interposed soft tissue debris and directly assess the articular surfaces (Figures 4A-4D).
Figures 4A-4D
A freer can be placed in the individual joints to assess for areas of instability. We prefer solid screw fixation (Charlotte Lisfranc Reconstruction System, Wright Medical Technology) to decrease the risk of later screw breakage. A homerun screw from the proximal aspect of the medial cuneiform to the distal-lateral aspect of the 2nd metatarsal base should be placed first. Bridge plates can be used over the 1st and 2nd TMT joints to avoid articular cartilage damage without a loss of rigidity.19

Proximal-medial column Lisfranc injury variants are increasingly common among football players.20 In these injuries, the force of injury extends through the intercuneiform joint and exits out the naviculocuneiform joint, thus causing instability at multiple joints and an unstable 1st ray. Patients often have minimal clinical findings and normal radiographs and stress radiographs. MRI of the foot often reveals edema at the naviculocuneiform joint. Often patients fail to improve with nonoperative immobilization with continued inability to push off from the hallux. Unrecognized or untreated instability will lead to rapid deterioration of the naviculocuneiform joint. Surgical intervention requires a homerun screw and intercuneiform screw. We do not recommend primary arthrodesis in athletes due to significant risk of malunion and nonunion unless severe articular damage is present.

Patients are typically kept NWB in a splint for 2 weeks after surgery followed by NWB in a tall CAM from 3 to 4 weeks postoperative. Progressive weight-bearing and ROM exercises are initiated from 4 to 8 weeks, followed by return to accommodative shoe wear from 10 to 12 weeks. Hardware removal is performed 4 to 6 months after surgery, typically in the off-season to allow for 6 to 8 weeks or protected recovery afterwards. Premature hardware removal can lead to loss of reduction, particularly at the intercuneiform joints. All hardware crossing the TMT joints should be removed, while the homerun screw can be left in place in addition to the intercuneiform screw. RTP in football typically occurs 6 to 7 months after surgery. Final functional outcome is related to the adequacy of initial reduction and severity of the initial injury.21

Syndesmotic Disruption

Syndesmotic injuries comprise 1% to 18% of ankle sprains in the general population, but occur at much higher rates in football due to the increased rotation forces placed on the ankle during cutting and tackling. RTP after syndesmotic injury often takes twice as long when compared to isolated lateral ankle ligamentous injury.22 Missed injuries are common and if not treated properly can lead to chronic ankle instability and posttraumatic ankle arthritis.23 Syndesmotic injury can occur in isolation or with concomitant adjacent bony, cartilaginous, or ligamentous injuries. Therefore, clinical examination and imaging work-up are critical to successful management.

 

 

Syndesmotic injuries often result from an external rotation force applied to a hyperdorsiflexed ankle while the foot is planted. This mechanism causes the fibula to externally rotate while translating posteriorly and laterally, resulting in rupture of the anterior inferior tibiofibular ligament (AITFL) first, followed by the deep deltoid ligament, interosseous ligament (IOL), and lastly posterior talofibular ligament.24 Most syndesmotic injuries involve rupture of only the AITFL and IOL.25 Multiple clinical stress tests have been designed to assess syndesmotic stability, including the squeeze test, external rotation stress test, crossed-leg test, and fibula-translation test.26-29 However, no physical examination maneuver has been shown to reliably predict the presence or degree of syndesmotic injury and therefore imaging studies are necessary.30

Initial imaging should include standing radiographs of the affected ankle. An increase in the medial clear space between the medial malleolus and talus can occur with a combined syndesmotic and deltoid disruption. In the case of subtle syndesmotic injuries, contralateral comparison weight-bearing radiographs are recommended. CT and MRI can provide additional information, but these static imaging tests cannot identify instability. Fluoroscopic stress evaluation is beneficial but has a high false-negative rate in low-grade injuries and may not detect partial rupture of the AITFL and IOL.31 It has been shown that malrotation of as much as 30° of external rotation can occur if relying on intraoperative fluoroscopy alone.32 It has been our practice to recommend surgical reduction and stabilization for any syndesmotic injury with documented diastasis or instability seen on imaging and/or arthroscopy.

Nonoperative treatment is indicated for truly stable grade I syndesmotic injuries. This involves rest and immobilization followed by a progressive rehabilitation program consisting of stretching, strengthening, and proprioceptive exercises.33 After 1 week of protected weight-bearing in a cast or tall CAM boot, progression to full weight-bearing should occur over the following week. Active-assisted ankle ROM exercises and light proprioceptive training should then be initiated followed by sport-specific exercises 2 to 3 weeks after injury.

Arthroscopy can be a valuable diagnostic tool in the setting of subtle syndesmotic injury with negative radiographs, positive MRI for edema, and a protracted recovery course with vague pain (Figures W5A-W5E).

Figures W5A-W5E
In these situations, an examination under anesthesia is performed, the syndesmosis is probed under direct arthroscopic visualization, and distal tibiofibular instability is evaluated while performing an external rotation stress test. For surgical intervention of these subtle varieties or any athlete with documented instability, we prefer the use of dynamic stabilization with a knotless suture-button construct (TightRope, Arthrex) or hybrid fixation with screws (3.5/4.5 mm) and suture-buttons. Advantages of a knotless suture-button construct include more physiologic motion at the syndesmosis and decreased hardware irritation and implant removal.

Implants are placed above the true syndesmotic joint (at least 15 mm above the tibial plafond) angled 30° posterior to anterior to follow the normal relationship of the fibula to the distal tibia in the incisura. Typically 2 suture-buttons are used, with the devices placed in a divergent fashion. We highly recommend the use of a fibular buttress plate with button placement in individuals returning to contact activity. This construct increases surface area distribution while preventing stress risers and the risk of fibula fractures. In a cadaver model with deliberate syndesmotic malreduction, suture-button stabilization resulted in decreased postoperative displacement as opposed to conventional screw fixation.34 Therefore, dynamic syndesmotic fixation may help to decrease the negative sequelae of iatrogenic clamp malreduction. 
Postoperative rehabilitation involves NWB in a cast or tall CAM boot for 4 weeks followed by ankle ROM exercises and progressive weight-bearing and physical therapy. Patients are transitioned to a lace-up ankle brace and athletic shoe from 6 to 12 weeks postoperative with increasing activity. Running and jumping is permitted 4 months after surgery with RTP typically at 6 to 7 months. Athletes who have had surgical stabilization for documented instability without any diastasis may engage in a more rapid recovery and RTP as symptoms and function allow.

Deltoid Complex Avulsion

Missed or neglected deltoid ligament injuries can lead to progressive chondral injury and joint degeneration. These injuries are often subtle and difficult to diagnose. An inability to perform a single limb heel rise, persistent pain with activity, and lack of normal functional improvement despite appropriate care are indicators of subtle ligament instability. These injuries often require an examination under anesthesia with combined ankle arthroscopy. Valgus stress testing of the ankle while directly visualizing the deltoid ligament from the anterolateral portal can reveal medial laxity in addition to potential osteochondral lesions along the anterolateral talar dome.

In American football players, we have observed that infolding and retraction of an avulsed superficial deltoid ligament complex after an ankle fracture, Maisonneuve injury, or severe high ankle sprain can be a source of persistent increased medial clear space, malreduction, and postoperative pain and medial instability. We have found that there is often complete avulsion of the superficial deltoid complex off the proximal aspect of the medial malleolus during high-energy ankle fractures in football players that is amenable to direct repair to bone (Figures W6A-W6E).

Figures W6A-W6E
In a cohort of 14 NFL players who underwent ankle fracture fixation with ankle arthroscopy and debridement, fibula fixation with plate and screws, syndesmotic fixation with suture-button devices, and open deltoid complex repair with suture anchors, all athletes were able to return to running and cutting maneuvers by 6 months after surgery.35 There were no intraoperative or postoperative complications noted, and no players had clinical evidence of medial pain or instability at final follow-up with radiographic maintenance of anatomic mortise alignment.

During surgical repair, an incision is made along the anterior aspect of the medial malleolus and the superficial deltoid ligament complex can often be found flipped and interposed in the medial gutter. A rongeur is used to create a bleeding cancellous bone surface for soft-tissue healing and 1 to 2 suture anchors are used to repair and imbricate the deltoid ligament complex back to the medial malleolus. The goal of these sutures is to repair the tibionavicular and tibial spring ligaments back to the medial malleolus. We believe that superficial deltoid complex avulsion during high-energy ankle fractures is a distinct injury pattern that should be recognized and may benefit from primary open repair.

We currently open explore every deltoid ligament complex in athletes with unstable syndesmotic injuries, as we believe that deltoid avulsion injuries are underrecognized and do not heal in an anatomic fashion if left alone. Postoperative recovery follows the same immobilization, progressive weight-bearing, and physical therapy protocol as that for syndesmotic disruption.

 

 

Achilles Ruptures

Acute midsubstance Achilles tendon ruptures are an increasingly common injury in patients 30 to 50 years of age, with more than 50% of all injuries occurring during basketball.36,37 Among NFL players, we have found that Achilles ruptures tend to occur at a higher rate during training camp, when athletes are deconditioned and quickly returning to explosive push-off activities. Physical examination should include a Thompson test, palpation of a gap within the tendon, and evaluation of resting ankle dorsiflexion in the affected extremity in the prone position with the knees bent. Lateral radiographs should be analyzed for the presence of a bony avulsion fragment indicative of an insertional avulsion injury or midsubstance calcium deposition reflecting chronic Achilles tendinosis, as both of these conditions will change surgical management. MRI is not recommended with acute midsubstance ruptures but may be helpful in the case of chronic ruptures or more proximal tears of the musculotendinous junction.

The management of acute midsubstance Achilles tendon ruptures is controversial, with no general consensus in the literature regarding nonoperative treatment, surgical repair, and ideal repair technique.36,38-42 American Academy of Orthopaedic Surgeons clinical practice guidelines report moderate evidence that nonoperative treatment of Achilles tendon ruptures has lower wound healing complications but higher rates of re-rupture.38,39 Additionally, limited incision approaches have been found to have fewer overall complications compared with traditional open repair. In an effort to reduce the incidence of postoperative wound complications while improving functional recovery, modern repair techniques focus on a limited incision repair using percutaneous suture insertion and management (PARS Achilles Jig System, Arthrex).36 The limited incision technique utilizes a 2-cm transverse incision and non-disposable jig with divergent needle passes and locking suture fixation options to secure and fixate both tendon ends with minimal dissection of skin, subcutaneous tissue, and paratenon. Limited incision repair is ideally performed within 2 weeks of the injury to ensure that both tendon ends are easy to identify, mobilize, and repair. An open repair is generally recommended for midsubstance ruptures more than 4 weeks old and cases of insertional rupture and Achilles tendinopathy.

In a cohort of 9 NFL players treated for midsubstance Achilles ruptures using the PARS technique, we found no re-ruptures, no wound complications, and no sural nerve issues after surgery.43 A comparative review of 270 cases of operatively treated Achilles tendon ruptures (101 PARS, 169 traditional open repair) showed that the PARS group had significantly shorter operative times and a higher number of patients able to return to baseline physical activities by 5 months compared to open repair.36 Although not statistically significant, the overall PARS complication rate was 5% while the open complication rate was 11%. The PARS group had no cases of sural neuritis or deep infection requiring reoperation. We currently use a limited incision technique for all acute midsubstance Achilles ruptures in athletes regardless of sport, patient size, or position played.

During surgery, a 2-cm transverse incision is made over the gap in the Achilles tendon and dissection is carried down to the rupture site with minimal manipulation of the skin (Figures 5A-5F).

Figures 5A-5F
A transverse incision is made through the paratenon and typically a hematoma is expressed. An Allis clamp is inserted and the proximal tendon stump is grabbed securely and pulled through the wound approximately 1 to 2 cm. The PARS jig is inserted around the proximal tendon and centered so that the needle and sutures will pass through tendon. Needles and sutures are passed in a stepwise fashion and then the entire jig is removed from the wound. Sutures are passed to create 2 non-locking and 1 locking suture. The jig and suture passing process is repeated for the distal tendon stump. Then, each pair of sutures is tied together with the ankle in maximum plantarflexion to obtain a secure end-to-end repair. The knots are cut short and tucked into tendon so that they do not protrude and cause subcutaneous tissue irritation. Absorbable sutures are used to close the paratenon, followed by closure of subcutaneous tissues and skin followed by placement of a short leg posterior mold NWB splint with the ankle in resting plantar flexion.

A key aspect of postoperative recovery is avoiding excessive ankle dorsiflexion while the tendon is healing during the first 4 weeks after surgery, as this can lead to an elongated tendon with loss of push-off strength. Patients are kept in a plantarflexion splint NWB for 2 weeks after surgery. If the incision is healed at 2 weeks, sutures are removed and patients are transitioned into a NWB tall CAM boot for 2 weeks with gentle ankle ROM exercises. If there is any concern regarding wound healing status, sutures are maintained for an additional 1 to 2 weeks.

From 4 to 8 weeks after surgery, progressive weight-bearing with continued ankle ROM exercises is initiated with peel-away heel lifts (~2 cm thick total, 3 layers). Each layer of the heel lift is gradually removed as pain allows every 2 to 3 days with the goal of being full weight-bearing with the foot flat at 6 weeks postoperative. Physical therapy focusing on ankle ROM and gentle Achilles stretching and strengthening is also started 6 weeks after surgery. From 8 to 12 weeks postoperative, patients are transitioned out of the tall CAM boot into normal, accommodative shoe wear with full weight-bearing. We avoid ankle dorsiflexion past neutral until 12 weeks after surgery, as overlengthening of the Achilles complex and the subsequent loss of push-off power can be devastating to running athletes. Activity levels are increased as tolerated, with no running or jumping from 12 to 16 weeks with full release to all activities after 16 weeks. RTP often takes 5 to 6 months after surgery, depending on the position played.

Am J Orthop. 2016;45(6):358-367. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Canale ST, Cantler ED Jr, Sisk TD, Freeman BL 3rd. A chronicle of injuries of an American intercollegiate football team. Am J Sports Med. 1981;9(6):384-389.2. Robey JM, Blyth CS, Mueller FO. Athletic injuries. Application of epidemiologic methods. JAMA. 1971;217(2):184-189.

3. Saal JA. Common American football injuries. Sports Med. 1991;12(2):132-147.

4. Thompson N, Halpern B, Curl WW, et al. High school football injuries: evaluation. Am J Sports Med. 1987;15(2):117-124.

5. Kaplan LD, Jost PW, Honkamp N, Norwig J, West R, Bradley JP. Incidence and variance of foot and ankle injuries in elite college football players. Am J Orthop. 2011;40(1):40-44.

6. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.

7. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine--trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.

8. Bowers KD Jr, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8(2):81-83.

9. McCormick JJ, Anderson RB. Turf toe: anatomy, diagnosis, and treatment. Sports Health. 2010;2(6):487-494.

10. Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367-1372.

11. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete. Orthop Clin North Am. 2002;33(3):587-598.

12. Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am. 1995;26(2):353-361.

13. Nunley JA, Glisson RR. A new option for intramedullary fixation of Jones fractures: the Charlotte Carolina Jones Fracture System. Foot Ankle Int. 2008;29(12):1216-1221.

14. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8-16.

15. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones fractures. Analysis of failure. Am J Sports Med. 2002;30(1):55-60.

16. Portland G, Kelikian A, Kodros S. Acute surgical management of Jones’ fractures. Foot Ankle Int. 2003;24(11):829-833.

17. Hunt KJ, Anderson RB. Treatment of Jones fracture nonunions and refractures in the elite athlete: outcomes of intramedullary screw fixation with bone grafting. Am J Sports Med. 2011;39(9):1948-1954.

18. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871-878.

19. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw fixation. Foot Ankle Int. 2005;26(6):462-473.

20. Ardoin GT, Anderson RB. Subtle Lisfranc injury. Tech Foot Ankle Surg. 2010;9(3):100-106.

21. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A(11):1609-1618.

22. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.

23. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35(7):1197-1207.

24. Beumer A, Valstar ER, Garling EH, et al. Effects of ligament sectioning on the kinematics of the distal tibiofibular syndesmosis: a radiostereometric study of 10 cadaveric specimens based on presumed trauma mechanisms with suggestions for treatment. Acta Orthop. 2006;77(3):531-540.

25. McCollum GA, van den Bekerom MP, Kerkhoffs GM, Calder JD, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1328-1337.

26. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.

27. Nussbaum ED, Hosea TM, Sieler SD, Incremona BR, Kessler DE. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med. 2001;29(1):31-35.

28. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle syndesmosis injuries. Foot Ankle Int. 2005;26(2):187-188.

29. Beumer A, van Hemert WL, Swierstra BA, Jasper LE, Belkoff SM. A biomechanical evaluation of clinical stress tests for syndesmotic ankle instability. Foot Ankle Int. 2003;24(4):358-363.

30. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14(4):232-236.

31. Beumer A, Valstar ER, Garling EH, et al. External rotation stress imaging in syndesmotic injuries of the ankle: comparison of lateral radiography and radiostereometry in a cadaveric model. Acta Orthop Scand. 2003;74(2):201-205.

32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.

33. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2(6):460-470.

34. Westermann RW, Rungprai C, Goetz JE, Femino J, Amendola A, Phisitkul P. The effect of suture-button fixation on simulated syndesmotic malreduction: a cadaveric study. J Bone Joint Surg Am. 2014;96(20):1732-1738.

35. Hsu AR, Lareau CR, Anderson RB. Repair of acute superficial deltoid complex avulsion during ankle fracture fixation in National Football League players. Foot Ankle Int. 2015;36(11):1272-1278.

36. Hsu AR, Jones CP, Cohen BE, Davis WH, Ellington JK, Anderson RB. Clinical outcomes and complications of percutaneous Achilles repair system versus open technique for acute achilles tendon ruptures. Foot Ankle Int. 2015;36(11):1279-1286.

37. Raikin SM, Garras DN, Krapchev PV. Achilles tendon injuries in a United States population. Foot Ankle Int. 2013;34(4):475-480.

38. Chiodo CP, Glazebrook M, Bluman EM, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on treatment of achilles tendon rupture. J Bone Joint Surg Am. 2010;92(14):2466-2468.

39. Chiodo CP, Glazebrook M, Bluman EM, et al. Diagnosis and treatment of acute achilles tendon rupture. J Am Acad Orthop Surg. 2010;18(8):503-510.

40. Khan RJ, Fick D, Keogh A, Crawford J, Brammar T, Parker M. Treatment of acute achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2005;87(10):2202-2210.

41. Renninger CH, Kuhn K, Fellars T, Youngblood S, Bellamy J. Operative and nonoperative management of achilles tendon ruptures in active duty military population. Foot Ankle Int. 2016;37(3):269-273.

42. Khan RJ, Carey Smith RL. Surgical interventions for treating acute achilles tendon ruptures. Cochrane Database Syst Rev. 2010;(9):CD003674.

43. McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv. 2014;23(4):179-183.

References

1. Canale ST, Cantler ED Jr, Sisk TD, Freeman BL 3rd. A chronicle of injuries of an American intercollegiate football team. Am J Sports Med. 1981;9(6):384-389.2. Robey JM, Blyth CS, Mueller FO. Athletic injuries. Application of epidemiologic methods. JAMA. 1971;217(2):184-189.

3. Saal JA. Common American football injuries. Sports Med. 1991;12(2):132-147.

4. Thompson N, Halpern B, Curl WW, et al. High school football injuries: evaluation. Am J Sports Med. 1987;15(2):117-124.

5. Kaplan LD, Jost PW, Honkamp N, Norwig J, West R, Bradley JP. Incidence and variance of foot and ankle injuries in elite college football players. Am J Orthop. 2011;40(1):40-44.

6. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.

7. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine--trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27.

8. Bowers KD Jr, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8(2):81-83.

9. McCormick JJ, Anderson RB. Turf toe: anatomy, diagnosis, and treatment. Sports Health. 2010;2(6):487-494.

10. Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367-1372.

11. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete. Orthop Clin North Am. 2002;33(3):587-598.

12. Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am. 1995;26(2):353-361.

13. Nunley JA, Glisson RR. A new option for intramedullary fixation of Jones fractures: the Charlotte Carolina Jones Fracture System. Foot Ankle Int. 2008;29(12):1216-1221.

14. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8-16.

15. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones fractures. Analysis of failure. Am J Sports Med. 2002;30(1):55-60.

16. Portland G, Kelikian A, Kodros S. Acute surgical management of Jones’ fractures. Foot Ankle Int. 2003;24(11):829-833.

17. Hunt KJ, Anderson RB. Treatment of Jones fracture nonunions and refractures in the elite athlete: outcomes of intramedullary screw fixation with bone grafting. Am J Sports Med. 2011;39(9):1948-1954.

18. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871-878.

19. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw fixation. Foot Ankle Int. 2005;26(6):462-473.

20. Ardoin GT, Anderson RB. Subtle Lisfranc injury. Tech Foot Ankle Surg. 2010;9(3):100-106.

21. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A(11):1609-1618.

22. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.

23. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35(7):1197-1207.

24. Beumer A, Valstar ER, Garling EH, et al. Effects of ligament sectioning on the kinematics of the distal tibiofibular syndesmosis: a radiostereometric study of 10 cadaveric specimens based on presumed trauma mechanisms with suggestions for treatment. Acta Orthop. 2006;77(3):531-540.

25. McCollum GA, van den Bekerom MP, Kerkhoffs GM, Calder JD, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1328-1337.

26. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.

27. Nussbaum ED, Hosea TM, Sieler SD, Incremona BR, Kessler DE. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med. 2001;29(1):31-35.

28. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle syndesmosis injuries. Foot Ankle Int. 2005;26(2):187-188.

29. Beumer A, van Hemert WL, Swierstra BA, Jasper LE, Belkoff SM. A biomechanical evaluation of clinical stress tests for syndesmotic ankle instability. Foot Ankle Int. 2003;24(4):358-363.

30. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14(4):232-236.

31. Beumer A, Valstar ER, Garling EH, et al. External rotation stress imaging in syndesmotic injuries of the ankle: comparison of lateral radiography and radiostereometry in a cadaveric model. Acta Orthop Scand. 2003;74(2):201-205.

32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.

33. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2(6):460-470.

34. Westermann RW, Rungprai C, Goetz JE, Femino J, Amendola A, Phisitkul P. The effect of suture-button fixation on simulated syndesmotic malreduction: a cadaveric study. J Bone Joint Surg Am. 2014;96(20):1732-1738.

35. Hsu AR, Lareau CR, Anderson RB. Repair of acute superficial deltoid complex avulsion during ankle fracture fixation in National Football League players. Foot Ankle Int. 2015;36(11):1272-1278.

36. Hsu AR, Jones CP, Cohen BE, Davis WH, Ellington JK, Anderson RB. Clinical outcomes and complications of percutaneous Achilles repair system versus open technique for acute achilles tendon ruptures. Foot Ankle Int. 2015;36(11):1279-1286.

37. Raikin SM, Garras DN, Krapchev PV. Achilles tendon injuries in a United States population. Foot Ankle Int. 2013;34(4):475-480.

38. Chiodo CP, Glazebrook M, Bluman EM, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on treatment of achilles tendon rupture. J Bone Joint Surg Am. 2010;92(14):2466-2468.

39. Chiodo CP, Glazebrook M, Bluman EM, et al. Diagnosis and treatment of acute achilles tendon rupture. J Am Acad Orthop Surg. 2010;18(8):503-510.

40. Khan RJ, Fick D, Keogh A, Crawford J, Brammar T, Parker M. Treatment of acute achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2005;87(10):2202-2210.

41. Renninger CH, Kuhn K, Fellars T, Youngblood S, Bellamy J. Operative and nonoperative management of achilles tendon ruptures in active duty military population. Foot Ankle Int. 2016;37(3):269-273.

42. Khan RJ, Carey Smith RL. Surgical interventions for treating acute achilles tendon ruptures. Cochrane Database Syst Rev. 2010;(9):CD003674.

43. McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv. 2014;23(4):179-183.

Issue
The American Journal of Orthopedics - 45(6)
Issue
The American Journal of Orthopedics - 45(6)
Page Number
358-367
Page Number
358-367
Publications
Publications
Topics
Article Type
Display Headline
Foot and Ankle Injuries in American Football
Display Headline
Foot and Ankle Injuries in American Football
Sections
Disallow All Ads
Article PDF Media

Concussions in American Football

Article Type
Changed
Thu, 09/19/2019 - 13:25
Display Headline
Concussions in American Football

Football is an important component of American culture, with approximately 3 million youth athletes, 1.1 million high school athletes, and 100,000 college athletes participating each year.1 Participation in football provides athletes with physical, social, psychological, and academic benefits. Despite these benefits, widespread focus has been placed on the safety of football due to the risk for sport-related concussion (SRC) and potentially long-term effects; however, little recognition has been given to the advancements in concussion management across time and occurrence of concussions during most life activities. Although it is reasonable for concerns to be presented, it is important to better understand SRC and the current factors leading to prolonged recoveries, increased risk for injury, and potentially long-term effects.

What Is a Concussion?

Concussions occur after sustaining direct or indirect injury to the head or other parts of the body, as long as the injury force is transmitted to the head. Athletes often experience physical, cognitive, emotional, and sleep-related symptoms post-concussion secondary to an “energy crisis” within the brain.2 The energy crisis occurs as the result of transient neurological dysfunction triggered by changes in the brain (eg, release of neurotransmitters, impaired axonal function).2,3 Concussion is undetectable with traditional imaging; however, advanced imaging techniques (eg, diffuse tensor imaging) have shown progress in assessing axonal injury.3 Symptom duration post-concussion is highly variable due to individual differences; a recent study showed recovery took 3 to 4 weeks for memory and symptoms.4,5

Previous Concussion Management

Identification techniques and return-to-play guidelines for concussion have significantly changed across time. In the past, concussion grading scales were utilized for diagnosis and return to play was possible within the same contest.6,7 It has since been recognized that initial concussion severity makes it difficult to predict recovery.3 For example, research revealed memory decline and increased symptoms 36 hours post-injury for athletes with a grade 1 concussion (ie, transient confusion, no loss of consciousness, concussion symptoms or mental status changes that resolve within 15 minutes of injury) compared to baseline.7 Another study found duration of mental status changes to be related to slower symptom resolution and memory impairment 36 hours to 7 days post-injury.6 Consequently, return to play within the same contest was likely too liberal. Guidelines today recommend immediate removal from play with suspected SRC. Nevertheless, the “play through pain” culture has led athletes to continue playing after SRC, contributing to prolonged recoveries and potentially long-term effects.

Current Concussion Management: Continued Concerns and Areas of Improvement

Despite increased awareness of concussions, recent estimates revealed high rates (ie, 27:1 ratio for general players) of underreporting in college football, particularly amongst offensive linemen.8 Researchers have studied recovery implications for remaining in play, with one study revealing a 2.2 times greater risk for prolonged recovery in college athletes with delayed vs immediate removal.9 Another similar study discovered an 8.8 times greater risk for prolonged recovery in adolescent and young adult athletes not removed vs removed from play.10 Further analysis found remaining in play to be the greatest risk factor for prolonged recovery compared to other previously studied risk factors (eg, age, sex, posttraumatic migraine).10 Additionally, significant differences in neurocognitive data were seen between the “removed” and “not removed” groups for verbal memory, visual memory, processing speed, and reaction time at 1 to 7 days and 8 to 30 days.10 The recovery implications of remaining in play and the additional risk for second impact syndrome (SIS), or repeat concussion when recovering from another injury, emphasizes the need for further education efforts amongst athletes to encourage immediate reporting of injury.11

Sideline Assessment

Sideline assessment has become a vital component of concussion management to rule out concussion and/or significant injury other than concussion. Assessment should include observation, cognitive/balance testing, neurologic examination, and possible exertion testing to ensure a comprehensive evaluation of all areas of potential dysfunction.12 Indications for emergency department evaluation include suspicion for cervical spine injury, intracranial hemorrhage, or skull fracture as well as prolonged loss of consciousness, high-risk mechanisms, posttraumatic seizure(s), and/or significant worsening of symptoms.12

Observation

On the sideline, it is important to identify any immediate signs of injury (ie, loss of consciousness, anterograde/retrograde amnesia, and disorientation/confusion). Since immediate signs are not always present, it is important to be aware of the most commonly reported symptoms, including headache, difficulty concentrating, fatigue, drowsiness, and dizziness.13 If symptoms are not reported by the athlete, balance problems, lack of coordination, increased emotionality, and difficulty following instructions may be observed during play.12

On-Field Assessment

Cognitive and balance testing are essential in determining if an athlete has sustained a concussion. Immediate declines in memory, concentration abilities, and balance abilities are common. Given limitations in administering long testing batteries on the sideline, brief standardized tests such as the Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and Sport Concussion Assessment Tool (SCAT) are commonly utilized. Identification of cognitive and/or balance abnormalities can help the athlete recognize deficits following injury.12 Balance problems are experienced due to abnormalities in sensory organization and generally resolve during the acute recovery period.14,15 Cognitive difficulties typically persist longer than balance problems, though duration varies widely.

 

 

Neurologic Evaluation

A neurologic evaluation including cranial nerve testing and evaluation of motor-sensory function (ie, assessment for the strength and sensation of upper and lower extremities) is important to identify focal deficits (ie, sensation changes, loss of fine motor control) indicative of serious intracranial pathology.12 Additionally, clinicians have suggested inclusion of vestibular and oculomotor assessments due to frequent dysfunction post-concussion.12,15,16 Examination of the vestibular/oculomotor systems through tools such as the Vestibular/Ocular Motor Screening (VOMS) assessment (assesses both the vestibular and oculomotor systems) and King-Devick Test (primarily assesses saccadic eye movements) can elicit symptoms that may not present immediately. If assessment appears normal, exertion testing can be utilized to determine if symptoms are provoked through physical exercise that should include cardio, dynamic, and sport-specific activities to stress the vestibular system.12

Risk Factors for Injury and Prolonged Recovery

Medical professionals must consider the presence of risk factors when managing concussion in order to make appropriate treatment recommendations and return-to-play decisions. Research has demonstrated the role of female gender, learning disability, attention-deficit/hyperactivity disorder, psychiatric history, young age, motion sickness, sleep problems, somatization, concussion history, on-field dizziness, posttraumatic migraine, and fogginess in increased risk for injury and/or prolonged recovery.17-25 Additionally, athletes with ongoing symptoms from a previous injury are at risk for sustaining another injury.

Acute Home Concussion Management

Although strict rest has been recommended post-concussion, recent research evaluating strict rest vs usual care for adolescents revealed greater symptom reports and longer recovery periods for the strict rest group.26 Based on these findings and emphasis for regulation within the migraine literature (due to the common pathophysiology between migraine and concussion27), we recommend that athletes follow a regulated daily schedule post-concussion including: 1) regular sleep-wake schedule with avoidance of naps, 2) regular meals, 3) adequate fluid hydration, 4) light noncontact physical activity (ie, walking, with progressions recommended by a physician), and 5) stress management techniques. Use of these strategies immediately can help in preventing against increased symptoms and stress, and decreases the need for medication in select cases. Additionally, over-the-counter medications should be limited to 2 to 3 doses per week to avoid rebound headaches.28

In-Office Concussion Management

Athletes diagnosed with SRC will experience different symptoms based on the injury mechanism, risk factors, and management approach. Comprehensive evaluation should include assessment of risk factors, injury details, symptoms, neurocognitive functioning, vestibular/oculomotor dysfunction, tolerance of physical exertion, balance functioning, and cervical spine integrity (if necessary).29,30 Due to individual differences and the heterogeneous symptom profiles, concussion management must move beyond a “one size fits all” approach to avoid nonspecific treatment strategies and consequently prolonged recoveries.29 Clinicians and researchers at University of Pittsburgh Medical Center have identified 6 concussion clinical profiles (ie, vestibular, ocular, posttraumatic migraine, cervical, anxiety/mood, and cognitive/fatigue) that are generally identifiable 48 hours after injury.29,30 Identification of the clinical profile(s) through a comprehensive evaluation guides the development of individualized treatment plans and targeted rehabilitation strategies.29,30

Vestibular. The vestibular system is responsible for stabilizing vision while the head moves and balance control.15 Athletes can experience central and/or peripheral vestibular dysfunction to include benign paroxysmal positional vertigo (BPPV), visual motion sensitivity, vestibular ocular reflex impairment, and balance impairment.30,31 Symptoms typically include dizziness, impaired balance, blurry vision, difficulty focusing, and environmental sensitivity.15,29,30 Potential treatment options include vestibular rehabilitation, exertion therapy, and school/work accommodations.

Ocular. The oculomotor system is responsible for control of eye movements. Athletes can experience many different posttraumatic vision changes, including convergence problems, eye-tracking difficulties, refractive error, difficulty with pursuits/saccades, and accommodation insufficiency. Symptoms typically include light sensitivity, blurred vision, double vision, headaches, fatigue, and memory difficulties.15,29,30 Potential treatment options include vision therapy, vestibular rehabilitation, and school/work accommodations.32

Posttraumatic Migraine. Headache, the most common post-concussion symptom, can persist and meet criteria for posttraumatic migraine (ie, unilateral headache with accompanying nausea and/or photophobia and phonophobia).29,30,33 Implementation of a routine schedule, daily physical activity, exertion therapy, pharmacologic intervention, and school/work accommodations are potential treatment options.

Cervical. The cervical spine can be injured during whiplash-type injuries. Therefore, determining the location, onset, and typical exacerbations of pain can be helpful in identifying cervical involvement.29,30 Symptoms typically include headaches, neck pain, numbness, and tingling. Evaluation and therapy by a certified physical therapist and pharmacologic intervention (eg, muscle relaxants) are potential treatment options. 29,30

Anxiety/Mood. Anxiety, or worry and fear about everyday situations, is common post-concussion and can sometimes be related to ongoing vestibular impairment. Symptoms typically include ruminative thoughts, avoidance of specific situations, hypervigilance, feelings of being overwhelmed, and difficulty falling asleep.29,30 Potential treatment options include implementation of a routine schedule, exposure to provocative situations, psychotherapy, pharmacologic intervention, and school/work accommodations.34

 

 


Cognitive/Fatigue. A global concussion factor (including cognitive, fatigue, and migraine symptoms) has been identified within 1 to 7 days of injury. Although this factor of symptoms generally resolves during the acute recovery period, it persists in select cases.13 Symptoms typically include fatigue, decreased energy levels, nonspecific headaches, potential sleep disruption, increased symptoms towards the end of the day, difficulty concentrating, and increased headache with cognitive activities.29,30,35 Routine schedule, daily physical activity, exertion therapy, pharmacologic intervention (eg, amantadine), and school/work accommodations are potential treatment options.30

Conclusion

Advancements in SRC management warrant change in the conversations regarding concussion in football. Specifically, conversations should address the current understanding of concussion and improvements in the safety of football through stricter concussion guidelines, detailed sideline evaluations, recognition of risk factors, improved acute management, and identification of concussion profiles that help to direct individualized treatment plans and targeted rehabilitation strategies. The biggest concerns related to concussions in football include underreporting of injury, premature return to play, and receiving routine rather than individualized treatment. Therefore, to further improve the safety of football and management of concussion it is essential that future efforts focus on the following 6 areas:

Education: Improved understanding of concussion is imperative to reducing poor outcomes and widespread concerns.

Immediate reporting: Reporting of concussion must be expected and encouraged through consistent responses by coaches to reduce underreporting and fear of reporting in athletes.

Prevention techniques: Athletes must be taught proper form and playing techniques to reduce the risk for concussion. Proper form and technique should be incentivized.

Targeted treatment: Individualized treatment plans and targeted rehabilitation strategies must be developed based on the identified clinical profile(s) to avoid nonspecific treatment recommendations.

Multidisciplinary treatment teams: Given the heterogeneous symptoms profiles and need for care provided by different medical specialties, multidisciplinary teams are essential.

Remain current: With the progress in understanding concussion, providers must remain vigilant of future advances in concussion management to further improve the safety of football.


Am J Orthop. 2016;45(6):352-356. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. 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 Pediatrics. 2015;169(7):659-665.

2. Giza C, Hovda D. The new neurometabolic cascade of concussion. Neurosurgery. 2014;75 Suppl 4:S24-S33.

3. Barkhoudarian G, Hovda DA, Giza CC. The molecular pathophysiology of concussive brain injury - an update. Phys Med Rehabil Clin N Am. 2016;27:373-393.

4. Henry L, Elbin R, Collins M, Marchetti G, Kontos A. Examining recovery trajectories after sport-related concussion with a multimodal clinical assessment approach. Neurosurgery. 2016;78(2):232-241.

5. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Brit J Sports Med. 2013;47(5):250-258.

6. Lovell MR, Collins MW, Iverson GL, et al. Recovery from mild concussion in high school athletes. J Neurosurg. 2003;98(2):296-301.

7. Lovell MR, Collins MW, Iverson GL, Johnston KM, Bradley JP. Grade 1 or “ding” concussions in high school athletes. Am J Sports Med. 2004;32(1):47-54.

8. Baugh CM, Kroshus E, Daneshvar DH, Filali NA, Hiscox MJ, Glantz LH. Concussion management in United States college sports: compliance with National Collegiate Athletic Association concussion policy and areas for improvement. Am J Sports Med. 2015;43(1):47-56.

9. Asken BM, McCrea MA, Clugston JR, Snyder AR, Houck ZM, Bauer RM. “Playing through it”: Delayed reporting and removal from athletic activity after concussion predicts prolonged recovery. J Athl Train. 2016;51(4):329-335.

10. Elbin RJ, Sufrinko A, Schatz P, et al. Athletes that continue to play with concussion demonstrate worse recovery outcomes than athletes immediately removed from play. J Pediatr. In press.

11. Signoretti S, Lazzarino G, Tavazzi B, Vagnozzi R. The pathophysiology of concussion. PM R. 2011;3(10 Suppl 2):S359-S368.

12. Bloom J, Blount JG. Sideline evaluation of concussion. UpToDate. 2016. http://www.uptodate.com/contents/sideline-evaluation-of-concussion. Accessed July 13, 2016.

13. Kontos AP, Elbin RJ, Schatz P, et al. A revised factor structure for the post-concussion symptom scale: baseline and postconcussion factors. Am J Sports Med. 2012;40(10):2375-2384.

14. Guskiewicz KM, Ross SE, Marshall SW. Postural stability and neuropsychological deficits after concussion in collegiate athletes. J Athl Train. 2001;36(3):263.

15. Mucha A, Collins MW, Elbin R, et al. A brief Vestibular/Ocular Motor Screening (VOMS) assessment to evaluate concussions preliminary findings. Am J Sports Med. 2014;42(10):2479-2486.

16. Bloom J. Vestibular and ocular motor assessments: Important pieces to the concussion puzzle. Athletic Training and Sports Health Care. 2013;5(6):246-248.

17. Covassin T, Elbin R, Harris W, Parker T, Kontos A. The role of age and sex in symptoms, neurocognitive performance, and postural stability in athletes after concussion. Am J Sports Med. 2012;40(6):1303-1312.

18. Kontos A, Sufrinko A, Elbin R, Puskar A, Collins M. Reliability and associated risk factors for performance on the Vestibular/Ocular Motor Screening (VOMS) tool in healthy collegiate athletes. Am J Sports Med. 2016;44(6):1400-1406.

19. Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA. 2003;290(19):2549-2555.

20. Lau B, Lovell MR, Collins MW, Pardini J. Neurocognitive and symptom predictors of recovery in high school athletes. Clin J Sport Med. 2009;19(3):216-221.

21. Lau BC, Kontos AP, Collins MW, Mucha A, Lovell MR. Which on-field signs/symptoms predict protracted recovery from sport-related concussion among high school football players? Am J Sports Med. 2011;39(11):2311-2318.

22. Mihalik JP, Register-Mihalik J, Kerr ZY, Marshall SW, McCrea MC, Guskiewicz KM. Recovery of posttraumatic migraine characteristics in patients after mild traumatic brain injury. Am J Sports Med. 2013;41(7):1490-1496.

23. Covassin T, Moran R, Elbin RJ. Sex differences in reported concussion injury rates and time loss from participation: An update of the National Collegiate Athletic Association injury surveillance program from 2004-2005 through 2008-2009. J Athl Train. 2016;51(3):189-194.

24. Root JM, Zuckerbraun NS, Wang L, et al. History of somatization is associated with prolonged recovery from concussion. J Pediatr. 2016;174:39-44.

25. Sufrinko A, Pearce K, Elbin RJ, et al. The effect of preinjury sleep difficulties on neurocognitive impairment and symptoms after sport-related concussion. Am J Sports Med. 2015;43(4):830-838.

26. Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135(2):213-223.

27. Choe M, Blume H. Pediatric posttraumatic Headache: a review. J Child Neurol. 2016;31(1):76-85.

28. Tepper SJ, Tepper DE. Breaking the cycle of medication overuse. Cleve Clin J Med. 2010;77(4):236-242.

29. Collins M, Kontos A, Reynolds E, Murawski C, Fu F. A comprehensive, targeted approach to the clinical care of athletes following sport-related concussion. Knee Surg Sports Traumatol Arthrosc. 2014;22(2):235-246.

30. Reynolds E, Collins MW, Mucha A, Troutman-Ensecki C. Establishing a clinical service for the management of sports-related concussions. Neurosurgery. 2014;75 Suppl 4:S71-S81.

31. Broglio SP, Collins MW, Williams RM, Mucha A, Kontos AP. Current and emerging rehabilitation for concussion: a review of the evidence. Clin Sports Med. 2015;34(2):213-231.

32. Master C, Scheiman M, Gallaway M, et al. Vision diagnoses are common after concussion in adolescents. Clin Pediatr (Phila). 2016;55(3):260-267.

33. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33(9):629-808.

34. Kontos A, Deitrick JM, Reynolds E. Mental health implication and consequences following sport-related concussion. Brit J Sports Med. 2016;50(3):139-140.

35. Kontos AP, Covassin T, Elbin R, Parker T. Depression and neurocognitive performance after concussion among male and female high school and collegiate athletes. Arch Phys Med Rehabil. 2012;93(10):1751-1756.

Article PDF
Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Collins is a cofounder of ImPACT Applications, Inc. However, the ImPACT test is not the focus of this article. The authors report no actual or potential conflict of interest in relation to this article.

Issue
The American Journal of Orthopedics - 45(6)
Publications
Topics
Page Number
352-356
Sections
Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Collins is a cofounder of ImPACT Applications, Inc. However, the ImPACT test is not the focus of this article. The authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Collins is a cofounder of ImPACT Applications, Inc. However, the ImPACT test is not the focus of this article. The authors report no actual or potential conflict of interest in relation to this article.

Article PDF
Article PDF

Football is an important component of American culture, with approximately 3 million youth athletes, 1.1 million high school athletes, and 100,000 college athletes participating each year.1 Participation in football provides athletes with physical, social, psychological, and academic benefits. Despite these benefits, widespread focus has been placed on the safety of football due to the risk for sport-related concussion (SRC) and potentially long-term effects; however, little recognition has been given to the advancements in concussion management across time and occurrence of concussions during most life activities. Although it is reasonable for concerns to be presented, it is important to better understand SRC and the current factors leading to prolonged recoveries, increased risk for injury, and potentially long-term effects.

What Is a Concussion?

Concussions occur after sustaining direct or indirect injury to the head or other parts of the body, as long as the injury force is transmitted to the head. Athletes often experience physical, cognitive, emotional, and sleep-related symptoms post-concussion secondary to an “energy crisis” within the brain.2 The energy crisis occurs as the result of transient neurological dysfunction triggered by changes in the brain (eg, release of neurotransmitters, impaired axonal function).2,3 Concussion is undetectable with traditional imaging; however, advanced imaging techniques (eg, diffuse tensor imaging) have shown progress in assessing axonal injury.3 Symptom duration post-concussion is highly variable due to individual differences; a recent study showed recovery took 3 to 4 weeks for memory and symptoms.4,5

Previous Concussion Management

Identification techniques and return-to-play guidelines for concussion have significantly changed across time. In the past, concussion grading scales were utilized for diagnosis and return to play was possible within the same contest.6,7 It has since been recognized that initial concussion severity makes it difficult to predict recovery.3 For example, research revealed memory decline and increased symptoms 36 hours post-injury for athletes with a grade 1 concussion (ie, transient confusion, no loss of consciousness, concussion symptoms or mental status changes that resolve within 15 minutes of injury) compared to baseline.7 Another study found duration of mental status changes to be related to slower symptom resolution and memory impairment 36 hours to 7 days post-injury.6 Consequently, return to play within the same contest was likely too liberal. Guidelines today recommend immediate removal from play with suspected SRC. Nevertheless, the “play through pain” culture has led athletes to continue playing after SRC, contributing to prolonged recoveries and potentially long-term effects.

Current Concussion Management: Continued Concerns and Areas of Improvement

Despite increased awareness of concussions, recent estimates revealed high rates (ie, 27:1 ratio for general players) of underreporting in college football, particularly amongst offensive linemen.8 Researchers have studied recovery implications for remaining in play, with one study revealing a 2.2 times greater risk for prolonged recovery in college athletes with delayed vs immediate removal.9 Another similar study discovered an 8.8 times greater risk for prolonged recovery in adolescent and young adult athletes not removed vs removed from play.10 Further analysis found remaining in play to be the greatest risk factor for prolonged recovery compared to other previously studied risk factors (eg, age, sex, posttraumatic migraine).10 Additionally, significant differences in neurocognitive data were seen between the “removed” and “not removed” groups for verbal memory, visual memory, processing speed, and reaction time at 1 to 7 days and 8 to 30 days.10 The recovery implications of remaining in play and the additional risk for second impact syndrome (SIS), or repeat concussion when recovering from another injury, emphasizes the need for further education efforts amongst athletes to encourage immediate reporting of injury.11

Sideline Assessment

Sideline assessment has become a vital component of concussion management to rule out concussion and/or significant injury other than concussion. Assessment should include observation, cognitive/balance testing, neurologic examination, and possible exertion testing to ensure a comprehensive evaluation of all areas of potential dysfunction.12 Indications for emergency department evaluation include suspicion for cervical spine injury, intracranial hemorrhage, or skull fracture as well as prolonged loss of consciousness, high-risk mechanisms, posttraumatic seizure(s), and/or significant worsening of symptoms.12

Observation

On the sideline, it is important to identify any immediate signs of injury (ie, loss of consciousness, anterograde/retrograde amnesia, and disorientation/confusion). Since immediate signs are not always present, it is important to be aware of the most commonly reported symptoms, including headache, difficulty concentrating, fatigue, drowsiness, and dizziness.13 If symptoms are not reported by the athlete, balance problems, lack of coordination, increased emotionality, and difficulty following instructions may be observed during play.12

On-Field Assessment

Cognitive and balance testing are essential in determining if an athlete has sustained a concussion. Immediate declines in memory, concentration abilities, and balance abilities are common. Given limitations in administering long testing batteries on the sideline, brief standardized tests such as the Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and Sport Concussion Assessment Tool (SCAT) are commonly utilized. Identification of cognitive and/or balance abnormalities can help the athlete recognize deficits following injury.12 Balance problems are experienced due to abnormalities in sensory organization and generally resolve during the acute recovery period.14,15 Cognitive difficulties typically persist longer than balance problems, though duration varies widely.

 

 

Neurologic Evaluation

A neurologic evaluation including cranial nerve testing and evaluation of motor-sensory function (ie, assessment for the strength and sensation of upper and lower extremities) is important to identify focal deficits (ie, sensation changes, loss of fine motor control) indicative of serious intracranial pathology.12 Additionally, clinicians have suggested inclusion of vestibular and oculomotor assessments due to frequent dysfunction post-concussion.12,15,16 Examination of the vestibular/oculomotor systems through tools such as the Vestibular/Ocular Motor Screening (VOMS) assessment (assesses both the vestibular and oculomotor systems) and King-Devick Test (primarily assesses saccadic eye movements) can elicit symptoms that may not present immediately. If assessment appears normal, exertion testing can be utilized to determine if symptoms are provoked through physical exercise that should include cardio, dynamic, and sport-specific activities to stress the vestibular system.12

Risk Factors for Injury and Prolonged Recovery

Medical professionals must consider the presence of risk factors when managing concussion in order to make appropriate treatment recommendations and return-to-play decisions. Research has demonstrated the role of female gender, learning disability, attention-deficit/hyperactivity disorder, psychiatric history, young age, motion sickness, sleep problems, somatization, concussion history, on-field dizziness, posttraumatic migraine, and fogginess in increased risk for injury and/or prolonged recovery.17-25 Additionally, athletes with ongoing symptoms from a previous injury are at risk for sustaining another injury.

Acute Home Concussion Management

Although strict rest has been recommended post-concussion, recent research evaluating strict rest vs usual care for adolescents revealed greater symptom reports and longer recovery periods for the strict rest group.26 Based on these findings and emphasis for regulation within the migraine literature (due to the common pathophysiology between migraine and concussion27), we recommend that athletes follow a regulated daily schedule post-concussion including: 1) regular sleep-wake schedule with avoidance of naps, 2) regular meals, 3) adequate fluid hydration, 4) light noncontact physical activity (ie, walking, with progressions recommended by a physician), and 5) stress management techniques. Use of these strategies immediately can help in preventing against increased symptoms and stress, and decreases the need for medication in select cases. Additionally, over-the-counter medications should be limited to 2 to 3 doses per week to avoid rebound headaches.28

In-Office Concussion Management

Athletes diagnosed with SRC will experience different symptoms based on the injury mechanism, risk factors, and management approach. Comprehensive evaluation should include assessment of risk factors, injury details, symptoms, neurocognitive functioning, vestibular/oculomotor dysfunction, tolerance of physical exertion, balance functioning, and cervical spine integrity (if necessary).29,30 Due to individual differences and the heterogeneous symptom profiles, concussion management must move beyond a “one size fits all” approach to avoid nonspecific treatment strategies and consequently prolonged recoveries.29 Clinicians and researchers at University of Pittsburgh Medical Center have identified 6 concussion clinical profiles (ie, vestibular, ocular, posttraumatic migraine, cervical, anxiety/mood, and cognitive/fatigue) that are generally identifiable 48 hours after injury.29,30 Identification of the clinical profile(s) through a comprehensive evaluation guides the development of individualized treatment plans and targeted rehabilitation strategies.29,30

Vestibular. The vestibular system is responsible for stabilizing vision while the head moves and balance control.15 Athletes can experience central and/or peripheral vestibular dysfunction to include benign paroxysmal positional vertigo (BPPV), visual motion sensitivity, vestibular ocular reflex impairment, and balance impairment.30,31 Symptoms typically include dizziness, impaired balance, blurry vision, difficulty focusing, and environmental sensitivity.15,29,30 Potential treatment options include vestibular rehabilitation, exertion therapy, and school/work accommodations.

Ocular. The oculomotor system is responsible for control of eye movements. Athletes can experience many different posttraumatic vision changes, including convergence problems, eye-tracking difficulties, refractive error, difficulty with pursuits/saccades, and accommodation insufficiency. Symptoms typically include light sensitivity, blurred vision, double vision, headaches, fatigue, and memory difficulties.15,29,30 Potential treatment options include vision therapy, vestibular rehabilitation, and school/work accommodations.32

Posttraumatic Migraine. Headache, the most common post-concussion symptom, can persist and meet criteria for posttraumatic migraine (ie, unilateral headache with accompanying nausea and/or photophobia and phonophobia).29,30,33 Implementation of a routine schedule, daily physical activity, exertion therapy, pharmacologic intervention, and school/work accommodations are potential treatment options.

Cervical. The cervical spine can be injured during whiplash-type injuries. Therefore, determining the location, onset, and typical exacerbations of pain can be helpful in identifying cervical involvement.29,30 Symptoms typically include headaches, neck pain, numbness, and tingling. Evaluation and therapy by a certified physical therapist and pharmacologic intervention (eg, muscle relaxants) are potential treatment options. 29,30

Anxiety/Mood. Anxiety, or worry and fear about everyday situations, is common post-concussion and can sometimes be related to ongoing vestibular impairment. Symptoms typically include ruminative thoughts, avoidance of specific situations, hypervigilance, feelings of being overwhelmed, and difficulty falling asleep.29,30 Potential treatment options include implementation of a routine schedule, exposure to provocative situations, psychotherapy, pharmacologic intervention, and school/work accommodations.34

 

 


Cognitive/Fatigue. A global concussion factor (including cognitive, fatigue, and migraine symptoms) has been identified within 1 to 7 days of injury. Although this factor of symptoms generally resolves during the acute recovery period, it persists in select cases.13 Symptoms typically include fatigue, decreased energy levels, nonspecific headaches, potential sleep disruption, increased symptoms towards the end of the day, difficulty concentrating, and increased headache with cognitive activities.29,30,35 Routine schedule, daily physical activity, exertion therapy, pharmacologic intervention (eg, amantadine), and school/work accommodations are potential treatment options.30

Conclusion

Advancements in SRC management warrant change in the conversations regarding concussion in football. Specifically, conversations should address the current understanding of concussion and improvements in the safety of football through stricter concussion guidelines, detailed sideline evaluations, recognition of risk factors, improved acute management, and identification of concussion profiles that help to direct individualized treatment plans and targeted rehabilitation strategies. The biggest concerns related to concussions in football include underreporting of injury, premature return to play, and receiving routine rather than individualized treatment. Therefore, to further improve the safety of football and management of concussion it is essential that future efforts focus on the following 6 areas:

Education: Improved understanding of concussion is imperative to reducing poor outcomes and widespread concerns.

Immediate reporting: Reporting of concussion must be expected and encouraged through consistent responses by coaches to reduce underreporting and fear of reporting in athletes.

Prevention techniques: Athletes must be taught proper form and playing techniques to reduce the risk for concussion. Proper form and technique should be incentivized.

Targeted treatment: Individualized treatment plans and targeted rehabilitation strategies must be developed based on the identified clinical profile(s) to avoid nonspecific treatment recommendations.

Multidisciplinary treatment teams: Given the heterogeneous symptoms profiles and need for care provided by different medical specialties, multidisciplinary teams are essential.

Remain current: With the progress in understanding concussion, providers must remain vigilant of future advances in concussion management to further improve the safety of football.


Am J Orthop. 2016;45(6):352-356. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football is an important component of American culture, with approximately 3 million youth athletes, 1.1 million high school athletes, and 100,000 college athletes participating each year.1 Participation in football provides athletes with physical, social, psychological, and academic benefits. Despite these benefits, widespread focus has been placed on the safety of football due to the risk for sport-related concussion (SRC) and potentially long-term effects; however, little recognition has been given to the advancements in concussion management across time and occurrence of concussions during most life activities. Although it is reasonable for concerns to be presented, it is important to better understand SRC and the current factors leading to prolonged recoveries, increased risk for injury, and potentially long-term effects.

What Is a Concussion?

Concussions occur after sustaining direct or indirect injury to the head or other parts of the body, as long as the injury force is transmitted to the head. Athletes often experience physical, cognitive, emotional, and sleep-related symptoms post-concussion secondary to an “energy crisis” within the brain.2 The energy crisis occurs as the result of transient neurological dysfunction triggered by changes in the brain (eg, release of neurotransmitters, impaired axonal function).2,3 Concussion is undetectable with traditional imaging; however, advanced imaging techniques (eg, diffuse tensor imaging) have shown progress in assessing axonal injury.3 Symptom duration post-concussion is highly variable due to individual differences; a recent study showed recovery took 3 to 4 weeks for memory and symptoms.4,5

Previous Concussion Management

Identification techniques and return-to-play guidelines for concussion have significantly changed across time. In the past, concussion grading scales were utilized for diagnosis and return to play was possible within the same contest.6,7 It has since been recognized that initial concussion severity makes it difficult to predict recovery.3 For example, research revealed memory decline and increased symptoms 36 hours post-injury for athletes with a grade 1 concussion (ie, transient confusion, no loss of consciousness, concussion symptoms or mental status changes that resolve within 15 minutes of injury) compared to baseline.7 Another study found duration of mental status changes to be related to slower symptom resolution and memory impairment 36 hours to 7 days post-injury.6 Consequently, return to play within the same contest was likely too liberal. Guidelines today recommend immediate removal from play with suspected SRC. Nevertheless, the “play through pain” culture has led athletes to continue playing after SRC, contributing to prolonged recoveries and potentially long-term effects.

Current Concussion Management: Continued Concerns and Areas of Improvement

Despite increased awareness of concussions, recent estimates revealed high rates (ie, 27:1 ratio for general players) of underreporting in college football, particularly amongst offensive linemen.8 Researchers have studied recovery implications for remaining in play, with one study revealing a 2.2 times greater risk for prolonged recovery in college athletes with delayed vs immediate removal.9 Another similar study discovered an 8.8 times greater risk for prolonged recovery in adolescent and young adult athletes not removed vs removed from play.10 Further analysis found remaining in play to be the greatest risk factor for prolonged recovery compared to other previously studied risk factors (eg, age, sex, posttraumatic migraine).10 Additionally, significant differences in neurocognitive data were seen between the “removed” and “not removed” groups for verbal memory, visual memory, processing speed, and reaction time at 1 to 7 days and 8 to 30 days.10 The recovery implications of remaining in play and the additional risk for second impact syndrome (SIS), or repeat concussion when recovering from another injury, emphasizes the need for further education efforts amongst athletes to encourage immediate reporting of injury.11

Sideline Assessment

Sideline assessment has become a vital component of concussion management to rule out concussion and/or significant injury other than concussion. Assessment should include observation, cognitive/balance testing, neurologic examination, and possible exertion testing to ensure a comprehensive evaluation of all areas of potential dysfunction.12 Indications for emergency department evaluation include suspicion for cervical spine injury, intracranial hemorrhage, or skull fracture as well as prolonged loss of consciousness, high-risk mechanisms, posttraumatic seizure(s), and/or significant worsening of symptoms.12

Observation

On the sideline, it is important to identify any immediate signs of injury (ie, loss of consciousness, anterograde/retrograde amnesia, and disorientation/confusion). Since immediate signs are not always present, it is important to be aware of the most commonly reported symptoms, including headache, difficulty concentrating, fatigue, drowsiness, and dizziness.13 If symptoms are not reported by the athlete, balance problems, lack of coordination, increased emotionality, and difficulty following instructions may be observed during play.12

On-Field Assessment

Cognitive and balance testing are essential in determining if an athlete has sustained a concussion. Immediate declines in memory, concentration abilities, and balance abilities are common. Given limitations in administering long testing batteries on the sideline, brief standardized tests such as the Standardized Assessment of Concussion (SAC), Balance Error Scoring System (BESS), and Sport Concussion Assessment Tool (SCAT) are commonly utilized. Identification of cognitive and/or balance abnormalities can help the athlete recognize deficits following injury.12 Balance problems are experienced due to abnormalities in sensory organization and generally resolve during the acute recovery period.14,15 Cognitive difficulties typically persist longer than balance problems, though duration varies widely.

 

 

Neurologic Evaluation

A neurologic evaluation including cranial nerve testing and evaluation of motor-sensory function (ie, assessment for the strength and sensation of upper and lower extremities) is important to identify focal deficits (ie, sensation changes, loss of fine motor control) indicative of serious intracranial pathology.12 Additionally, clinicians have suggested inclusion of vestibular and oculomotor assessments due to frequent dysfunction post-concussion.12,15,16 Examination of the vestibular/oculomotor systems through tools such as the Vestibular/Ocular Motor Screening (VOMS) assessment (assesses both the vestibular and oculomotor systems) and King-Devick Test (primarily assesses saccadic eye movements) can elicit symptoms that may not present immediately. If assessment appears normal, exertion testing can be utilized to determine if symptoms are provoked through physical exercise that should include cardio, dynamic, and sport-specific activities to stress the vestibular system.12

Risk Factors for Injury and Prolonged Recovery

Medical professionals must consider the presence of risk factors when managing concussion in order to make appropriate treatment recommendations and return-to-play decisions. Research has demonstrated the role of female gender, learning disability, attention-deficit/hyperactivity disorder, psychiatric history, young age, motion sickness, sleep problems, somatization, concussion history, on-field dizziness, posttraumatic migraine, and fogginess in increased risk for injury and/or prolonged recovery.17-25 Additionally, athletes with ongoing symptoms from a previous injury are at risk for sustaining another injury.

Acute Home Concussion Management

Although strict rest has been recommended post-concussion, recent research evaluating strict rest vs usual care for adolescents revealed greater symptom reports and longer recovery periods for the strict rest group.26 Based on these findings and emphasis for regulation within the migraine literature (due to the common pathophysiology between migraine and concussion27), we recommend that athletes follow a regulated daily schedule post-concussion including: 1) regular sleep-wake schedule with avoidance of naps, 2) regular meals, 3) adequate fluid hydration, 4) light noncontact physical activity (ie, walking, with progressions recommended by a physician), and 5) stress management techniques. Use of these strategies immediately can help in preventing against increased symptoms and stress, and decreases the need for medication in select cases. Additionally, over-the-counter medications should be limited to 2 to 3 doses per week to avoid rebound headaches.28

In-Office Concussion Management

Athletes diagnosed with SRC will experience different symptoms based on the injury mechanism, risk factors, and management approach. Comprehensive evaluation should include assessment of risk factors, injury details, symptoms, neurocognitive functioning, vestibular/oculomotor dysfunction, tolerance of physical exertion, balance functioning, and cervical spine integrity (if necessary).29,30 Due to individual differences and the heterogeneous symptom profiles, concussion management must move beyond a “one size fits all” approach to avoid nonspecific treatment strategies and consequently prolonged recoveries.29 Clinicians and researchers at University of Pittsburgh Medical Center have identified 6 concussion clinical profiles (ie, vestibular, ocular, posttraumatic migraine, cervical, anxiety/mood, and cognitive/fatigue) that are generally identifiable 48 hours after injury.29,30 Identification of the clinical profile(s) through a comprehensive evaluation guides the development of individualized treatment plans and targeted rehabilitation strategies.29,30

Vestibular. The vestibular system is responsible for stabilizing vision while the head moves and balance control.15 Athletes can experience central and/or peripheral vestibular dysfunction to include benign paroxysmal positional vertigo (BPPV), visual motion sensitivity, vestibular ocular reflex impairment, and balance impairment.30,31 Symptoms typically include dizziness, impaired balance, blurry vision, difficulty focusing, and environmental sensitivity.15,29,30 Potential treatment options include vestibular rehabilitation, exertion therapy, and school/work accommodations.

Ocular. The oculomotor system is responsible for control of eye movements. Athletes can experience many different posttraumatic vision changes, including convergence problems, eye-tracking difficulties, refractive error, difficulty with pursuits/saccades, and accommodation insufficiency. Symptoms typically include light sensitivity, blurred vision, double vision, headaches, fatigue, and memory difficulties.15,29,30 Potential treatment options include vision therapy, vestibular rehabilitation, and school/work accommodations.32

Posttraumatic Migraine. Headache, the most common post-concussion symptom, can persist and meet criteria for posttraumatic migraine (ie, unilateral headache with accompanying nausea and/or photophobia and phonophobia).29,30,33 Implementation of a routine schedule, daily physical activity, exertion therapy, pharmacologic intervention, and school/work accommodations are potential treatment options.

Cervical. The cervical spine can be injured during whiplash-type injuries. Therefore, determining the location, onset, and typical exacerbations of pain can be helpful in identifying cervical involvement.29,30 Symptoms typically include headaches, neck pain, numbness, and tingling. Evaluation and therapy by a certified physical therapist and pharmacologic intervention (eg, muscle relaxants) are potential treatment options. 29,30

Anxiety/Mood. Anxiety, or worry and fear about everyday situations, is common post-concussion and can sometimes be related to ongoing vestibular impairment. Symptoms typically include ruminative thoughts, avoidance of specific situations, hypervigilance, feelings of being overwhelmed, and difficulty falling asleep.29,30 Potential treatment options include implementation of a routine schedule, exposure to provocative situations, psychotherapy, pharmacologic intervention, and school/work accommodations.34

 

 


Cognitive/Fatigue. A global concussion factor (including cognitive, fatigue, and migraine symptoms) has been identified within 1 to 7 days of injury. Although this factor of symptoms generally resolves during the acute recovery period, it persists in select cases.13 Symptoms typically include fatigue, decreased energy levels, nonspecific headaches, potential sleep disruption, increased symptoms towards the end of the day, difficulty concentrating, and increased headache with cognitive activities.29,30,35 Routine schedule, daily physical activity, exertion therapy, pharmacologic intervention (eg, amantadine), and school/work accommodations are potential treatment options.30

Conclusion

Advancements in SRC management warrant change in the conversations regarding concussion in football. Specifically, conversations should address the current understanding of concussion and improvements in the safety of football through stricter concussion guidelines, detailed sideline evaluations, recognition of risk factors, improved acute management, and identification of concussion profiles that help to direct individualized treatment plans and targeted rehabilitation strategies. The biggest concerns related to concussions in football include underreporting of injury, premature return to play, and receiving routine rather than individualized treatment. Therefore, to further improve the safety of football and management of concussion it is essential that future efforts focus on the following 6 areas:

Education: Improved understanding of concussion is imperative to reducing poor outcomes and widespread concerns.

Immediate reporting: Reporting of concussion must be expected and encouraged through consistent responses by coaches to reduce underreporting and fear of reporting in athletes.

Prevention techniques: Athletes must be taught proper form and playing techniques to reduce the risk for concussion. Proper form and technique should be incentivized.

Targeted treatment: Individualized treatment plans and targeted rehabilitation strategies must be developed based on the identified clinical profile(s) to avoid nonspecific treatment recommendations.

Multidisciplinary treatment teams: Given the heterogeneous symptoms profiles and need for care provided by different medical specialties, multidisciplinary teams are essential.

Remain current: With the progress in understanding concussion, providers must remain vigilant of future advances in concussion management to further improve the safety of football.


Am J Orthop. 2016;45(6):352-356. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. 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 Pediatrics. 2015;169(7):659-665.

2. Giza C, Hovda D. The new neurometabolic cascade of concussion. Neurosurgery. 2014;75 Suppl 4:S24-S33.

3. Barkhoudarian G, Hovda DA, Giza CC. The molecular pathophysiology of concussive brain injury - an update. Phys Med Rehabil Clin N Am. 2016;27:373-393.

4. Henry L, Elbin R, Collins M, Marchetti G, Kontos A. Examining recovery trajectories after sport-related concussion with a multimodal clinical assessment approach. Neurosurgery. 2016;78(2):232-241.

5. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Brit J Sports Med. 2013;47(5):250-258.

6. Lovell MR, Collins MW, Iverson GL, et al. Recovery from mild concussion in high school athletes. J Neurosurg. 2003;98(2):296-301.

7. Lovell MR, Collins MW, Iverson GL, Johnston KM, Bradley JP. Grade 1 or “ding” concussions in high school athletes. Am J Sports Med. 2004;32(1):47-54.

8. Baugh CM, Kroshus E, Daneshvar DH, Filali NA, Hiscox MJ, Glantz LH. Concussion management in United States college sports: compliance with National Collegiate Athletic Association concussion policy and areas for improvement. Am J Sports Med. 2015;43(1):47-56.

9. Asken BM, McCrea MA, Clugston JR, Snyder AR, Houck ZM, Bauer RM. “Playing through it”: Delayed reporting and removal from athletic activity after concussion predicts prolonged recovery. J Athl Train. 2016;51(4):329-335.

10. Elbin RJ, Sufrinko A, Schatz P, et al. Athletes that continue to play with concussion demonstrate worse recovery outcomes than athletes immediately removed from play. J Pediatr. In press.

11. Signoretti S, Lazzarino G, Tavazzi B, Vagnozzi R. The pathophysiology of concussion. PM R. 2011;3(10 Suppl 2):S359-S368.

12. Bloom J, Blount JG. Sideline evaluation of concussion. UpToDate. 2016. http://www.uptodate.com/contents/sideline-evaluation-of-concussion. Accessed July 13, 2016.

13. Kontos AP, Elbin RJ, Schatz P, et al. A revised factor structure for the post-concussion symptom scale: baseline and postconcussion factors. Am J Sports Med. 2012;40(10):2375-2384.

14. Guskiewicz KM, Ross SE, Marshall SW. Postural stability and neuropsychological deficits after concussion in collegiate athletes. J Athl Train. 2001;36(3):263.

15. Mucha A, Collins MW, Elbin R, et al. A brief Vestibular/Ocular Motor Screening (VOMS) assessment to evaluate concussions preliminary findings. Am J Sports Med. 2014;42(10):2479-2486.

16. Bloom J. Vestibular and ocular motor assessments: Important pieces to the concussion puzzle. Athletic Training and Sports Health Care. 2013;5(6):246-248.

17. Covassin T, Elbin R, Harris W, Parker T, Kontos A. The role of age and sex in symptoms, neurocognitive performance, and postural stability in athletes after concussion. Am J Sports Med. 2012;40(6):1303-1312.

18. Kontos A, Sufrinko A, Elbin R, Puskar A, Collins M. Reliability and associated risk factors for performance on the Vestibular/Ocular Motor Screening (VOMS) tool in healthy collegiate athletes. Am J Sports Med. 2016;44(6):1400-1406.

19. Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA. 2003;290(19):2549-2555.

20. Lau B, Lovell MR, Collins MW, Pardini J. Neurocognitive and symptom predictors of recovery in high school athletes. Clin J Sport Med. 2009;19(3):216-221.

21. Lau BC, Kontos AP, Collins MW, Mucha A, Lovell MR. Which on-field signs/symptoms predict protracted recovery from sport-related concussion among high school football players? Am J Sports Med. 2011;39(11):2311-2318.

22. Mihalik JP, Register-Mihalik J, Kerr ZY, Marshall SW, McCrea MC, Guskiewicz KM. Recovery of posttraumatic migraine characteristics in patients after mild traumatic brain injury. Am J Sports Med. 2013;41(7):1490-1496.

23. Covassin T, Moran R, Elbin RJ. Sex differences in reported concussion injury rates and time loss from participation: An update of the National Collegiate Athletic Association injury surveillance program from 2004-2005 through 2008-2009. J Athl Train. 2016;51(3):189-194.

24. Root JM, Zuckerbraun NS, Wang L, et al. History of somatization is associated with prolonged recovery from concussion. J Pediatr. 2016;174:39-44.

25. Sufrinko A, Pearce K, Elbin RJ, et al. The effect of preinjury sleep difficulties on neurocognitive impairment and symptoms after sport-related concussion. Am J Sports Med. 2015;43(4):830-838.

26. Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135(2):213-223.

27. Choe M, Blume H. Pediatric posttraumatic Headache: a review. J Child Neurol. 2016;31(1):76-85.

28. Tepper SJ, Tepper DE. Breaking the cycle of medication overuse. Cleve Clin J Med. 2010;77(4):236-242.

29. Collins M, Kontos A, Reynolds E, Murawski C, Fu F. A comprehensive, targeted approach to the clinical care of athletes following sport-related concussion. Knee Surg Sports Traumatol Arthrosc. 2014;22(2):235-246.

30. Reynolds E, Collins MW, Mucha A, Troutman-Ensecki C. Establishing a clinical service for the management of sports-related concussions. Neurosurgery. 2014;75 Suppl 4:S71-S81.

31. Broglio SP, Collins MW, Williams RM, Mucha A, Kontos AP. Current and emerging rehabilitation for concussion: a review of the evidence. Clin Sports Med. 2015;34(2):213-231.

32. Master C, Scheiman M, Gallaway M, et al. Vision diagnoses are common after concussion in adolescents. Clin Pediatr (Phila). 2016;55(3):260-267.

33. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33(9):629-808.

34. Kontos A, Deitrick JM, Reynolds E. Mental health implication and consequences following sport-related concussion. Brit J Sports Med. 2016;50(3):139-140.

35. Kontos AP, Covassin T, Elbin R, Parker T. Depression and neurocognitive performance after concussion among male and female high school and collegiate athletes. Arch Phys Med Rehabil. 2012;93(10):1751-1756.

References

1. 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 Pediatrics. 2015;169(7):659-665.

2. Giza C, Hovda D. The new neurometabolic cascade of concussion. Neurosurgery. 2014;75 Suppl 4:S24-S33.

3. Barkhoudarian G, Hovda DA, Giza CC. The molecular pathophysiology of concussive brain injury - an update. Phys Med Rehabil Clin N Am. 2016;27:373-393.

4. Henry L, Elbin R, Collins M, Marchetti G, Kontos A. Examining recovery trajectories after sport-related concussion with a multimodal clinical assessment approach. Neurosurgery. 2016;78(2):232-241.

5. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Brit J Sports Med. 2013;47(5):250-258.

6. Lovell MR, Collins MW, Iverson GL, et al. Recovery from mild concussion in high school athletes. J Neurosurg. 2003;98(2):296-301.

7. Lovell MR, Collins MW, Iverson GL, Johnston KM, Bradley JP. Grade 1 or “ding” concussions in high school athletes. Am J Sports Med. 2004;32(1):47-54.

8. Baugh CM, Kroshus E, Daneshvar DH, Filali NA, Hiscox MJ, Glantz LH. Concussion management in United States college sports: compliance with National Collegiate Athletic Association concussion policy and areas for improvement. Am J Sports Med. 2015;43(1):47-56.

9. Asken BM, McCrea MA, Clugston JR, Snyder AR, Houck ZM, Bauer RM. “Playing through it”: Delayed reporting and removal from athletic activity after concussion predicts prolonged recovery. J Athl Train. 2016;51(4):329-335.

10. Elbin RJ, Sufrinko A, Schatz P, et al. Athletes that continue to play with concussion demonstrate worse recovery outcomes than athletes immediately removed from play. J Pediatr. In press.

11. Signoretti S, Lazzarino G, Tavazzi B, Vagnozzi R. The pathophysiology of concussion. PM R. 2011;3(10 Suppl 2):S359-S368.

12. Bloom J, Blount JG. Sideline evaluation of concussion. UpToDate. 2016. http://www.uptodate.com/contents/sideline-evaluation-of-concussion. Accessed July 13, 2016.

13. Kontos AP, Elbin RJ, Schatz P, et al. A revised factor structure for the post-concussion symptom scale: baseline and postconcussion factors. Am J Sports Med. 2012;40(10):2375-2384.

14. Guskiewicz KM, Ross SE, Marshall SW. Postural stability and neuropsychological deficits after concussion in collegiate athletes. J Athl Train. 2001;36(3):263.

15. Mucha A, Collins MW, Elbin R, et al. A brief Vestibular/Ocular Motor Screening (VOMS) assessment to evaluate concussions preliminary findings. Am J Sports Med. 2014;42(10):2479-2486.

16. Bloom J. Vestibular and ocular motor assessments: Important pieces to the concussion puzzle. Athletic Training and Sports Health Care. 2013;5(6):246-248.

17. Covassin T, Elbin R, Harris W, Parker T, Kontos A. The role of age and sex in symptoms, neurocognitive performance, and postural stability in athletes after concussion. Am J Sports Med. 2012;40(6):1303-1312.

18. Kontos A, Sufrinko A, Elbin R, Puskar A, Collins M. Reliability and associated risk factors for performance on the Vestibular/Ocular Motor Screening (VOMS) tool in healthy collegiate athletes. Am J Sports Med. 2016;44(6):1400-1406.

19. Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA. 2003;290(19):2549-2555.

20. Lau B, Lovell MR, Collins MW, Pardini J. Neurocognitive and symptom predictors of recovery in high school athletes. Clin J Sport Med. 2009;19(3):216-221.

21. Lau BC, Kontos AP, Collins MW, Mucha A, Lovell MR. Which on-field signs/symptoms predict protracted recovery from sport-related concussion among high school football players? Am J Sports Med. 2011;39(11):2311-2318.

22. Mihalik JP, Register-Mihalik J, Kerr ZY, Marshall SW, McCrea MC, Guskiewicz KM. Recovery of posttraumatic migraine characteristics in patients after mild traumatic brain injury. Am J Sports Med. 2013;41(7):1490-1496.

23. Covassin T, Moran R, Elbin RJ. Sex differences in reported concussion injury rates and time loss from participation: An update of the National Collegiate Athletic Association injury surveillance program from 2004-2005 through 2008-2009. J Athl Train. 2016;51(3):189-194.

24. Root JM, Zuckerbraun NS, Wang L, et al. History of somatization is associated with prolonged recovery from concussion. J Pediatr. 2016;174:39-44.

25. Sufrinko A, Pearce K, Elbin RJ, et al. The effect of preinjury sleep difficulties on neurocognitive impairment and symptoms after sport-related concussion. Am J Sports Med. 2015;43(4):830-838.

26. Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135(2):213-223.

27. Choe M, Blume H. Pediatric posttraumatic Headache: a review. J Child Neurol. 2016;31(1):76-85.

28. Tepper SJ, Tepper DE. Breaking the cycle of medication overuse. Cleve Clin J Med. 2010;77(4):236-242.

29. Collins M, Kontos A, Reynolds E, Murawski C, Fu F. A comprehensive, targeted approach to the clinical care of athletes following sport-related concussion. Knee Surg Sports Traumatol Arthrosc. 2014;22(2):235-246.

30. Reynolds E, Collins MW, Mucha A, Troutman-Ensecki C. Establishing a clinical service for the management of sports-related concussions. Neurosurgery. 2014;75 Suppl 4:S71-S81.

31. Broglio SP, Collins MW, Williams RM, Mucha A, Kontos AP. Current and emerging rehabilitation for concussion: a review of the evidence. Clin Sports Med. 2015;34(2):213-231.

32. Master C, Scheiman M, Gallaway M, et al. Vision diagnoses are common after concussion in adolescents. Clin Pediatr (Phila). 2016;55(3):260-267.

33. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33(9):629-808.

34. Kontos A, Deitrick JM, Reynolds E. Mental health implication and consequences following sport-related concussion. Brit J Sports Med. 2016;50(3):139-140.

35. Kontos AP, Covassin T, Elbin R, Parker T. Depression and neurocognitive performance after concussion among male and female high school and collegiate athletes. Arch Phys Med Rehabil. 2012;93(10):1751-1756.

Issue
The American Journal of Orthopedics - 45(6)
Issue
The American Journal of Orthopedics - 45(6)
Page Number
352-356
Page Number
352-356
Publications
Publications
Topics
Article Type
Display Headline
Concussions in American Football
Display Headline
Concussions in American Football
Sections
Disallow All Ads
Article PDF Media

Exertional Heat Stroke and American Football: What the Team Physician Needs to Know

Article Type
Changed
Thu, 09/19/2019 - 13:25
Display Headline
Exertional Heat Stroke and American Football: What the Team Physician Needs to Know

Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.1 USA Football estimates that an additional 3 million youth participate in community football leagues.1 The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.1 While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues2 reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.2The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).

The Challenge

EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”3 EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.

During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,5 which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.6 Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.7

An estimated 9000 cases of EHI occur annually across all high school sports,8 with an incidence of 1.6:100,000 athlete-exposures.8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.10 The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.8,9 Between 2000 and 2014, 41 football players died from EHS.1 In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.8

Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.

Prevention

EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.

Primary Prevention

Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).

 

 

Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.

Table 1
While identifying at-risk athletes is important in mitigating the risk of developing EHI, it will not identify all possible cases: a study of military recruits found that up to 50% of Marines who developed EHI lacked an identifiable risk factor.13Wet Bulb Globe Temperature. Humidity can heighten a player’s risk of developing thermogenic dysregulation during hot temperatures. As ambient temperature nears internal body temperature, heat may actually be absorbed by the skin rather than dissipated into the air. As a result, the body must increasingly rely on sweat evaporation to encourage heat loss; this process is hindered in very humid climates. Wet bulb globe temperature (WBGT) is a measure of heat stress that accounts for temperature, humidity, wind speed, and cloud cover. WBGT should be utilized to determine the relative risk of EHI based on local environmental conditions, as there is a direct correlation between elevated WBGT and risk of EHI.11,14 The greatest risk for EHS is performing high-intensity exercise (>75% VO2max) when WBGT >28°C (82°F).7 A study of hyperthermia-related deaths in football found that a majority of fatalities occurred on days classified as high risk (23°C-28°C) or extreme risk (>28°C) by WBGT.14 Consensus guidelines recommend that activities be modified based on WBGT (Table 2).7,12
Table 2.
The impact of WBGT does not end solely on the day of practice. Athletes who exercise in elevated WBGT environments on 2 consecutive days are at increased risk of EHI due to cumulative effects of exercise in heat.11Clothing. In football, required protective equipment may cover up to 60% of body surfaces. Studies have shown that wearing full uniform with pads increases internal body temperature and decreases time to exhaustion when compared to light clothing.5,15 In addition, athletic equipment traps heat close to the body and inhibits evaporation of sweat into the environment, thereby inhibiting radiant and evaporative heat dissipation.5,11 Likewise, wearing dark clothing encourages radiant absorption of heat, further contributing to potential thermal dysregulation.5 Use of a helmet is a specific risk factor for EHI, as significant heat dissipation occurs through the head.11 To mitigate these risk factors, the introduction of padded equipment should occur incrementally over the heat acclimatization period (see below). In addition, athletes should be encouraged to remove their helmets during rest periods to promote added heat dissipation and recovery.

Heat Acclimatization. The risk of EHI escalates significantly when athletes are subjected to multiple stressors during periods of heat exposure, such as sudden increases in intensity or duration of exercise; prolonged new exposures to heat; dehydration; and sleep loss.5 When football season begins in late summer, athletes are least conditioned as temperatures reach their seasonal peak, causing increased risk of EHI.15 Planning for heat acclimatization is vital for all athletes who exercise in hot environments. Acclimatization procedures place progressively mounting physiologic strains on the body to improve athletes’ ability to dissipate heat, diminishing thermoregulatory and cardiovascular exertion.4,5 Acclimatization begins with expansion of plasma volume on days 3 to 6, causing improvements in cardiac efficiency and resulting in an overall decrease in basal internal body temperature.4,5,15 This process results in improvements in heat tolerance and exercise performance, evolving over 10 to 14 days of gradual escalation of exercise intensity and duration.5,10,11,16 However, poor fitness levels and extreme temperatures can prolong this period, requiring up to 2 to 3 months to fully take effect.5,7

The National Athletic Trainers Association (NATA) and National Collegiate Athletic Association (NCAA) have released consensus guidelines regarding heat acclimatization protocols for football athletes at the high school and college levels (Tables 3 and 4). Each of these guidelines involves an initial period without use of protective equipment, followed by a gradual addition of further equipment.11,16
Table 3.

Secondary Prevention

Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.

Table 4.

 

 

Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.6 Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.7 After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.7 If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.

Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,6 a deficit that is most marked during the first week of practices.17 This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.6 Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.

The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;6 it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.6 Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.

Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),6 a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.6Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.19

Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;4 a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.19 Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.19 Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.4

Tertiary Prevention

The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.

Diagnosis and Management

Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.7 Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.20

 

 

EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.21 EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.7,12,15

Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.11 On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.11 In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.15

Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.15 Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;12 however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.20,21,22

If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.20 None of these methods have been shown to be as effective as CWI.23

Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.

Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation20 and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).

Figure.


Rapid cooling is more crucial than transport; transport poses a risk of delayed cooling, which can dramatically increase an individual’s risk of morbidity and mortality.20,23 In situations where a patient can be cooled on-site, physicians should pursue cooling before transporting the patient to a medical treatment facility.

Emergency Action Plan

Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.12 All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.12,15,20 This tub should be set up and functional for all high-risk activities, including practices.12

Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.15 A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.

Table 5.


EHS is a unique life-threatening situation where it is best to treat the patient on the sideline before transport.15 Those athletes transported before cooling risk spending an increased amount of time above critical temperatures for cell damage, which has been associated with increased morbidity and mortality. This mantra of “cool first, transport second” cannot be overemphasized, as those individuals with EHS who present to the ED with a persisting rectal temperature >41°F may risk up to an 80% mortality rate.24 Conversely, a recent large, retrospective study of 274 EHS events sustained during the Falmouth Road Race found a 100% survival rate when athletes were rapidly identified via rectal thermometry and treated with aggressive, rapid cooling through CWI.21

 

 

Return to Play

Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.7 The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.11 Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.11 The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:7

  • No exercise for at least 7 days following release from medical care.
  • Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
  • Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
  • Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
  • The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.

Heat tolerance testing (HTT) in these athletes remains controversial.5 26 The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.27 The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.

Conclusion

While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement28 further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.

 

Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Kucera KL, Klossner D, Colgate B, Cantu RC. Annual Survey of Football Injury Research: 1931-2014. National Center for Catastrophic Sport Injury Research Web site. https://nccsir.unc.edu/files/2013/10/Annual-Football-2014-Fatalities-Final.pdf. Accessed May 31, 2016.

2. Boden BP, Breit I, Beachler JA, Williams A, Mueller FO. Fatalities in high school and college football players. Am J Sports Med. 2013;41(5):1108-1116.

3. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346(25):1978-1988.

4. Racinais S, Alonso JM, Coutts AJ, et al. Consensus recommendations on training and competing in the heat. Scand J Med Sci Sports. 2015;25 Suppl 1:6-19.

5. Pryor RR, Casa DJ, Adams WM, et al. Maximizing athletic performance in the heat. Strength Cond J. 2013;35(6):24-33.

6. Adams WM, Casa DJ. Hydration for football athletes. Sports Sci Exchange. 2015;28(141):1-5.

7. 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.

8. Yard EE, Gilchrist J, Haileyesus T, et al. Heat illness among high school athletes--United States, 2005-2009. J Safety Res. 2010;41(6):471-474.

9. Huffman EA, Yard EE, Fields SK, Collins CL, Comstock RD. Epidemiology of rare injuries and conditions among United States high school athletes during the 2005-2006 and 2006-2007 school years. J Athl Train. 2008;43(6):624-630.

10. 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(1):8-14.

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

12. Casa DJ, Almquist J, Anderson SA. The inter-association task force for preventing sudden death in secondary school athletics programs: best-practices recommendations. J Athl Train. 2013;48(4):546-553.

13. Gardner JW, Kark JA, Karnei K, et al. Risk factors predicting exertional heat illness in male Marine Corps recruits. Med Sci Sports Exerc. 1996;28(8):939-944.

14. Gundstein AJ, Ramseyer C, Zhao F, et al. A retrospective analysis of American football hyperthermia deaths in the United States. Int J Biometerol. 2012;56(1):11-20.

15. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform: uncompensable heat stress and hyperthermic exhaustion. J Athl Train. 2010;45(2):117-127.

16. Casa DJ, Csillan D; Inter-Association Task Force for Preseason Secondary School Athletics Participants, et al. Preseason heat-acclimatization guidelines for secondary school athletics. J Athl Train. 2009;44(3):332-333.

17. Godek SF, Godek JJ, Bartolozzi AR. Hydration status in college football players during consecutive days of twice-a-day preseason practices. Am J Sports Med. 2005;33(6):843-851.

18. Stover EA, Zachwieja J, Stofan J, Murray R, Horswill CA. Consistently high urine specific gravity in adolescent American football players and the impact of an acute drinking strategy. Int J Sports Med. 2006;27(4):330-335.

19. Bongers CC, Thijssen DH, Veltmeijer MTW, Hopman MT, Eijsvogels TM. Precooling and percooling (cooling during exercise) both improve performance in the heat: a meta-analytical review. Br J Sports Med. 2015;49(6):377-384.

20. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev. 2007;35(3):141-149.

21. DeMartini JK, Casa DJ, Stearns R, et al. Effectiveness of cold water immersion in the treatment of exertional heat stroke at the Falmouth Road Race. Med Sci Sports Exerc. 2015;47(2):240-245.

22. Casa DJ, Kenny GP, Taylor NA. Immersion treatment for exertional hyperthermia: cold or temperate water? Med Sci Sports Exerc. 2010;42(7):1246-1252.

23. Casa DJ, Armstrong LE, Kenny GP, O’Connor FG, Huggins RA. Exertional heat stroke: new concepts regarding cause and care. Curr Sports Med Rep. 2012;11(3):115-122.

24. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heat stroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183.

25. O’Connor FG, Casa DJ, Bergeron MF, et al. American College of Sports Medicine Roundtable on exertional heat stroke--return to duty/return to play: conference proceedings. Curr Sports Med Rep. 2010;9(5):314-321.

26. Kazman JB, Heled Y, Lisman PJ, Druyan A, Deuster PA, O’Connor FG. Exertional heat illness: the role of heat tolerance testing. Curr Sports Med Rep. 2013;12(2):101-105.

27. Moran DS, Heled Y, Still L, Laor A, Shapiro Y. Assessment of heat tolerance for post exertional heat stroke individuals. Med Sci Monit. 2004;10(6):CR252-CR257.

28. Herring SA, Kibler WB, Putukian M. Team Physician Consensus Statement: 2013 update. Med Sci Sports Exerc. 2013;45(8):1618-1622.

29. Heat stroke treatment. Korey Stringer Institute University of Connecticut Web site. http://ksi.uconn.edu/emergency-conditions/heat-illnesses/exertional-heat-stroke/heat-stroke-treatment/. Accessed June 14, 2016.

30. Headquarters, Department of the Army and the Air Force. Heat Stress Control and Heat Casualty Management. Technical Bulletin Medical 507. http://www.dir.ca.gov/oshsb/documents/Heat_illness_prevention_tbmed507.pdf. Published March 7, 2003. Accessed June 14, 2016.

Article PDF
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article. The opinions and assertions contained herein are private views and are not to be construed as official or as reflecting the views of the US Army Medical Department, US Air Force Medical Corps, Uniformed Services University, or the Department of Defense at large.

Issue
The American Journal of Orthopedics - 45(6)
Publications
Topics
Page Number
340-348
Sections
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article. The opinions and assertions contained herein are private views and are not to be construed as official or as reflecting the views of the US Army Medical Department, US Air Force Medical Corps, Uniformed Services University, or the Department of Defense at large.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article. The opinions and assertions contained herein are private views and are not to be construed as official or as reflecting the views of the US Army Medical Department, US Air Force Medical Corps, Uniformed Services University, or the Department of Defense at large.

Article PDF
Article PDF

Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.1 USA Football estimates that an additional 3 million youth participate in community football leagues.1 The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.1 While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues2 reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.2The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).

The Challenge

EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”3 EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.

During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,5 which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.6 Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.7

An estimated 9000 cases of EHI occur annually across all high school sports,8 with an incidence of 1.6:100,000 athlete-exposures.8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.10 The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.8,9 Between 2000 and 2014, 41 football players died from EHS.1 In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.8

Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.

Prevention

EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.

Primary Prevention

Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).

 

 

Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.

Table 1
While identifying at-risk athletes is important in mitigating the risk of developing EHI, it will not identify all possible cases: a study of military recruits found that up to 50% of Marines who developed EHI lacked an identifiable risk factor.13Wet Bulb Globe Temperature. Humidity can heighten a player’s risk of developing thermogenic dysregulation during hot temperatures. As ambient temperature nears internal body temperature, heat may actually be absorbed by the skin rather than dissipated into the air. As a result, the body must increasingly rely on sweat evaporation to encourage heat loss; this process is hindered in very humid climates. Wet bulb globe temperature (WBGT) is a measure of heat stress that accounts for temperature, humidity, wind speed, and cloud cover. WBGT should be utilized to determine the relative risk of EHI based on local environmental conditions, as there is a direct correlation between elevated WBGT and risk of EHI.11,14 The greatest risk for EHS is performing high-intensity exercise (>75% VO2max) when WBGT >28°C (82°F).7 A study of hyperthermia-related deaths in football found that a majority of fatalities occurred on days classified as high risk (23°C-28°C) or extreme risk (>28°C) by WBGT.14 Consensus guidelines recommend that activities be modified based on WBGT (Table 2).7,12
Table 2.
The impact of WBGT does not end solely on the day of practice. Athletes who exercise in elevated WBGT environments on 2 consecutive days are at increased risk of EHI due to cumulative effects of exercise in heat.11Clothing. In football, required protective equipment may cover up to 60% of body surfaces. Studies have shown that wearing full uniform with pads increases internal body temperature and decreases time to exhaustion when compared to light clothing.5,15 In addition, athletic equipment traps heat close to the body and inhibits evaporation of sweat into the environment, thereby inhibiting radiant and evaporative heat dissipation.5,11 Likewise, wearing dark clothing encourages radiant absorption of heat, further contributing to potential thermal dysregulation.5 Use of a helmet is a specific risk factor for EHI, as significant heat dissipation occurs through the head.11 To mitigate these risk factors, the introduction of padded equipment should occur incrementally over the heat acclimatization period (see below). In addition, athletes should be encouraged to remove their helmets during rest periods to promote added heat dissipation and recovery.

Heat Acclimatization. The risk of EHI escalates significantly when athletes are subjected to multiple stressors during periods of heat exposure, such as sudden increases in intensity or duration of exercise; prolonged new exposures to heat; dehydration; and sleep loss.5 When football season begins in late summer, athletes are least conditioned as temperatures reach their seasonal peak, causing increased risk of EHI.15 Planning for heat acclimatization is vital for all athletes who exercise in hot environments. Acclimatization procedures place progressively mounting physiologic strains on the body to improve athletes’ ability to dissipate heat, diminishing thermoregulatory and cardiovascular exertion.4,5 Acclimatization begins with expansion of plasma volume on days 3 to 6, causing improvements in cardiac efficiency and resulting in an overall decrease in basal internal body temperature.4,5,15 This process results in improvements in heat tolerance and exercise performance, evolving over 10 to 14 days of gradual escalation of exercise intensity and duration.5,10,11,16 However, poor fitness levels and extreme temperatures can prolong this period, requiring up to 2 to 3 months to fully take effect.5,7

The National Athletic Trainers Association (NATA) and National Collegiate Athletic Association (NCAA) have released consensus guidelines regarding heat acclimatization protocols for football athletes at the high school and college levels (Tables 3 and 4). Each of these guidelines involves an initial period without use of protective equipment, followed by a gradual addition of further equipment.11,16
Table 3.

Secondary Prevention

Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.

Table 4.

 

 

Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.6 Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.7 After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.7 If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.

Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,6 a deficit that is most marked during the first week of practices.17 This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.6 Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.

The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;6 it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.6 Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.

Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),6 a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.6Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.19

Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;4 a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.19 Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.19 Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.4

Tertiary Prevention

The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.

Diagnosis and Management

Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.7 Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.20

 

 

EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.21 EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.7,12,15

Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.11 On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.11 In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.15

Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.15 Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;12 however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.20,21,22

If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.20 None of these methods have been shown to be as effective as CWI.23

Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.

Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation20 and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).

Figure.


Rapid cooling is more crucial than transport; transport poses a risk of delayed cooling, which can dramatically increase an individual’s risk of morbidity and mortality.20,23 In situations where a patient can be cooled on-site, physicians should pursue cooling before transporting the patient to a medical treatment facility.

Emergency Action Plan

Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.12 All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.12,15,20 This tub should be set up and functional for all high-risk activities, including practices.12

Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.15 A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.

Table 5.


EHS is a unique life-threatening situation where it is best to treat the patient on the sideline before transport.15 Those athletes transported before cooling risk spending an increased amount of time above critical temperatures for cell damage, which has been associated with increased morbidity and mortality. This mantra of “cool first, transport second” cannot be overemphasized, as those individuals with EHS who present to the ED with a persisting rectal temperature >41°F may risk up to an 80% mortality rate.24 Conversely, a recent large, retrospective study of 274 EHS events sustained during the Falmouth Road Race found a 100% survival rate when athletes were rapidly identified via rectal thermometry and treated with aggressive, rapid cooling through CWI.21

 

 

Return to Play

Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.7 The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.11 Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.11 The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:7

  • No exercise for at least 7 days following release from medical care.
  • Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
  • Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
  • Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
  • The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.

Heat tolerance testing (HTT) in these athletes remains controversial.5 26 The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.27 The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.

Conclusion

While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement28 further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.

 

Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Football, one of the most popular sports in the United States, is additionally recognized as a leading contributor to sports injury secondary to the contact collision nature of the endeavor. There are an estimated 1.1 million high school football players with another 100,000 participants combined in the National Football League (NFL), college, junior college, Arena Football League, and semipro levels of play.1 USA Football estimates that an additional 3 million youth participate in community football leagues.1 The National Center for Catastrophic Sports Injury Research recently calculated a fatality rate of 0.14 per 100,000 participants in 2014 for the 4.2 million who play football at all levels—and 0.45 per 100,000 in high school.1 While direct deaths from head and spine injury remain a significant contributor to the number of catastrophic injuries, indirect deaths (systemic failure) predominate. Exertional heat stroke (EHS) has emerged as one of the leading indirect causes of death in high school and collegiate football. Boden and colleagues2 reported that high school and college football players sustain approximately 12 fatalities annually, with indirect systemic causes being twice as common as direct blunt trauma.2The most common indirect causes identified included cardiac failure, heat illness, and complications of sickle cell trait (SCT). It was also noted that the risk of SCT, heat-related, and cardiac deaths increased during the second decade of the study, indicating these conditions may require a greater emphasis on diagnosis, treatment, and prevention. This review details for the team physician the unique challenge of exercising in the heat to the football player, and the prevention, diagnosis, management and return-to-play issues pertinent to exertional heat illness (EHI).

The Challenge

EHS represents the most severe manifestation of EHI—a gamut of diseases commonly encountered during the hot summer months when American football season begins. The breadth of EHI includes several important clinical diagnoses: exercise-associated muscle cramps (heat cramps); heat exhaustion with and without syncope; heat injury with evidence of end organ injury (eg, rhabdomyolysis); and EHS. EHS is defined as “a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates.”3 EHS, if left untreated, or even if clinical treatment is delayed, may result in significant end organ morbidity and/or mortality.

During exercise, the human thermoregulatory system mitigates heat gain by increasing skin blood flow and sweating, causing an increased dissipation of heat to the surrounding environment by leveraging conduction, convection, and evaporation.4,5 Elevated environmental temperatures, increased humidity, and dehydration can impede the body’s ability to dissipate heat at a rate needed to maintain thermoregulation. This imbalance can result in hyperthermia secondary to uncompensated heat stress,5 which in turn can lead to EHI. Football players have unique challenges that make them particularly vulnerable to EHI. The summer heat during early-season participation and the requirement for equipment that covers nearly 60% of body surfaces pose increased risk of volume losses and hyperthermia that trigger the onset of EHI.6 Football athletes’ body compositions and physical size are additional contributing risk factors; the relatively high muscle and fat content increase thermogenicity, which require their bodies to dissipate more heat.7

An estimated 9000 cases of EHI occur annually across all high school sports,8 with an incidence of 1.6:100,000 athlete-exposures.8,9 Studies have demonstrated, however, that EHI occurs in football 11.4 times more often than in all other high school sports combined.10 The incidence of nonfatal EHI in all levels of football is 4.42-5:100,000.8,9 Between 2000 and 2014, 41 football players died from EHS.1 In football, approximately 75% of all EHI events occurred during practices, while only 25% of incidents occurred during games.8

Given these potentially deadly consequences, it is important that football team physicians are not only alert to the early symptoms of heat illness and prepared to intervene to prevent the progression to EHS, but are critical leaders in educating coaches and players in evidence-based EHI prevention practices and policies.

Prevention

EHS is a preventable condition, arguably the most common cause of preventable nontraumatic exertional death in young athletes in the United States. Close attention to mitigating risk factors should begin prior to the onset of preseason practice and continue through the early season, where athletes are at the highest risk of developing heat illness.

Primary Prevention

Primary prevention is fundamental to minimizing the occurrences of EHI. It focuses on the following methods: recognition of inherent risk factors, acclimatization, hydration, and avoidance of inciting substances (including supplements).

 

 

Pre-Participation Examination. The purpose of the pre-participation examination (PPE) is to maximize an athlete’s safety by identifying medical conditions that place the athlete at risk.11,12 The Preparticipation Physical Evaluation, 4th edition, the most widely used consensus publication, specifically queries if an athlete has a previous history of heat injury. However, it only indirectly addresses intrinsic risk factors that may predispose an athlete to EHI who has never had an EHI before. Therefore, providers should take the opportunity of the PPE to inquire about additional risk factors that may make an athlete high risk for sustaining a heat injury. Common risk factors for EHI are listed in Table 1.

Table 1
While identifying at-risk athletes is important in mitigating the risk of developing EHI, it will not identify all possible cases: a study of military recruits found that up to 50% of Marines who developed EHI lacked an identifiable risk factor.13Wet Bulb Globe Temperature. Humidity can heighten a player’s risk of developing thermogenic dysregulation during hot temperatures. As ambient temperature nears internal body temperature, heat may actually be absorbed by the skin rather than dissipated into the air. As a result, the body must increasingly rely on sweat evaporation to encourage heat loss; this process is hindered in very humid climates. Wet bulb globe temperature (WBGT) is a measure of heat stress that accounts for temperature, humidity, wind speed, and cloud cover. WBGT should be utilized to determine the relative risk of EHI based on local environmental conditions, as there is a direct correlation between elevated WBGT and risk of EHI.11,14 The greatest risk for EHS is performing high-intensity exercise (>75% VO2max) when WBGT >28°C (82°F).7 A study of hyperthermia-related deaths in football found that a majority of fatalities occurred on days classified as high risk (23°C-28°C) or extreme risk (>28°C) by WBGT.14 Consensus guidelines recommend that activities be modified based on WBGT (Table 2).7,12
Table 2.
The impact of WBGT does not end solely on the day of practice. Athletes who exercise in elevated WBGT environments on 2 consecutive days are at increased risk of EHI due to cumulative effects of exercise in heat.11Clothing. In football, required protective equipment may cover up to 60% of body surfaces. Studies have shown that wearing full uniform with pads increases internal body temperature and decreases time to exhaustion when compared to light clothing.5,15 In addition, athletic equipment traps heat close to the body and inhibits evaporation of sweat into the environment, thereby inhibiting radiant and evaporative heat dissipation.5,11 Likewise, wearing dark clothing encourages radiant absorption of heat, further contributing to potential thermal dysregulation.5 Use of a helmet is a specific risk factor for EHI, as significant heat dissipation occurs through the head.11 To mitigate these risk factors, the introduction of padded equipment should occur incrementally over the heat acclimatization period (see below). In addition, athletes should be encouraged to remove their helmets during rest periods to promote added heat dissipation and recovery.

Heat Acclimatization. The risk of EHI escalates significantly when athletes are subjected to multiple stressors during periods of heat exposure, such as sudden increases in intensity or duration of exercise; prolonged new exposures to heat; dehydration; and sleep loss.5 When football season begins in late summer, athletes are least conditioned as temperatures reach their seasonal peak, causing increased risk of EHI.15 Planning for heat acclimatization is vital for all athletes who exercise in hot environments. Acclimatization procedures place progressively mounting physiologic strains on the body to improve athletes’ ability to dissipate heat, diminishing thermoregulatory and cardiovascular exertion.4,5 Acclimatization begins with expansion of plasma volume on days 3 to 6, causing improvements in cardiac efficiency and resulting in an overall decrease in basal internal body temperature.4,5,15 This process results in improvements in heat tolerance and exercise performance, evolving over 10 to 14 days of gradual escalation of exercise intensity and duration.5,10,11,16 However, poor fitness levels and extreme temperatures can prolong this period, requiring up to 2 to 3 months to fully take effect.5,7

The National Athletic Trainers Association (NATA) and National Collegiate Athletic Association (NCAA) have released consensus guidelines regarding heat acclimatization protocols for football athletes at the high school and college levels (Tables 3 and 4). Each of these guidelines involves an initial period without use of protective equipment, followed by a gradual addition of further equipment.11,16
Table 3.

Secondary Prevention

Despite physicians’ best efforts to prevent all cases of EHI, athletes will still experience the effects of exercise-induced hyperthermia. The goal of secondary prevention is to slow the progression of this hyperthermia so that it does not progress to more dangerous EHI.

Table 4.

 

 

Hydration. Dehydration is an important risk factor for EHI. Sweat maintains thermoregulation by dissipating heat generated during exercise; however, it also contributes to body water losses. Furthermore, intravascular depletion decreases stroke volume, thereby increasing cardiovascular strain. It is estimated that for every 1% loss in body mass from dehydration, body temperature rises 0.22°C in comparison to a euhydrated state.6 Dehydration occurs more rapidly in hot environments, as fluid is lost through increased sweat production.7 After approximately 6% to 10% body weight volume loss, cardiac output cannot be maintained, diminishing sweat production and blood flow to both skin and muscle and causing diminished performance and a significant risk of heat exhaustion.7 If left unchecked, these physiologic changes result in further elevations in body temperature and increased cardiovascular strain, ultimately placing the athlete at significant risk for development of EHS.

Adequate hydration to maintain euvolemia is an important step in avoiding possible EHI. Multiple studies have shown that football players experience a baseline hypovolemia during their competition season,6 a deficit that is most marked during the first week of practices.17 This deficit is multifactorial, as football players expend a significant amount of fluid through sweat, are not able to adequately replace these losses during practice, and do not appropriately hydrate off the field.6,18 Some players, especially linemen, sweat at a higher rate than their teammates, posing a possible risk of significant dehydration.6 Coaches and players alike should be educated on the importance of adequate hydration to meet their fluid needs.

The goal of hydration during exercise is to prevent large fluid losses that can adversely affect performance and increase risk of EHI;6 it may be unrealistic to replace all fluid losses during the practice period. Instead, athletes should target complete volume replacement over the post-exercise period.6 Some recommend hydrating based upon thirst drive; however, thirst is activated following a volume loss of approximately 2% body mass, the same degree of losses that place athletes at an increased risk for performance impairment and EHI.4,6,11,12 Individuals should have access to fluids throughout practice and competition and be encouraged to hydrate as needed.6,12,15 Furthermore, staff should modify their practices based upon WBGT and acclimatization status to provide more frequent hydration breaks.

Hyperhydration and Salt Intake. Of note, there are inherent risks to hyperhydration. Athletes with low sweat rates have an increased risk of overhydration and the development of exercise-associated hyponatremia (EAH),6 a condition whose presentation is very similar to EHS. In addition, inadequate sodium intake and excessive sweating can also contribute to the development of EAH. EAH has been implicated in the deaths of 2 football players in 2014.1,6 Establishing team hydration guidelines and educating players and staff on appropriate hydration and dietary salt intake is essential to reduce the risk of both dehydration and hyperhydration and their complications.6Intra-Event Cooling. During exercise, team physicians can employ strategies for cooling athletes during exertion to mitigate their risk of EHI by decreasing thermal and cardiovascular strain.4,19 Cooling during exercise is hypothesized to allow for accelerated heat dissipation, where heat is lost from the body more effectively. This accelerated loss enables athletes to maintain a higher heat storage capacity over the duration of exercise, avoiding uncompensated heat stresses that ultimately cause EHI.19

Some intra-event cooling strategies include the use of cooling garments, cooling packs, and cold water/slurry ingestion. Cooling garments lower skin temperature, which in turn can decrease thermoregulatory strains;4 a recent meta-analysis of intra-event cooling modalities revealed that wearing an ice vest during exercise resulted in the greatest decrease in thermal heat strain.19 Internal cooling strategies—namely ingestion of cold fluids/ice slurry—have shown some mild benefit in decreasing internal temperatures; however, some studies have demonstrated some decrease in sweat production associated with cold oral intake used in isolation.19 Overall, studies have shown that combining external (cooling clothing, ice packs, fanning) and internal (cold water, ice slurry) cooling methods result in a greater cooling effect than a use of a single method.4

Tertiary Prevention

The goal of tertiary prevention is to mitigate the risk of long-term adverse outcomes following an EHS event. The most effective means of reducing risk for morbidity and mortality is rapid identification and treatment of EHS as well as close evaluation of an athlete’s return to activity in heat. This process is spearheaded by an effective and well-rehearsed emergency action plan.

Diagnosis and Management

Rapid identification and treatment of EHS is crucial to minimizing the risk of poor outcomes.7 Any delay in the treatment of EHS can dramatically increase the likelihood of associated morbidity and mortality.20

 

 

EHS is diagnosed by an elevated rectal temperature ≥40°C (104°F) and associated central nervous system (CNS) dysfunction.21 EHS should be strongly suspected in any athlete exercising in heat who exhibits signs of CNS dysfunction, including disorientation, confusion, dizziness, erratic behavior, irritability, headache, loss of coordination, delirium, collapse, or seizures.7,12,15 EHS may also present with symptoms of heat exhaustion, including fatigue, hyperventilation, tachycardia, vomiting, diarrhea, and hypotension.7,12,15

Rectal temperature should be taken for any athlete with suspected EHS, as other modalities—oral, skin, axillary, and aural—can be inaccurate and easily modified by ambient confounders such as ambient and skin temperature, athlete hyperventilation, and consumption of liquids.7,11,12 Athletes exhibiting CNS symptoms with moderately elevated rectal temperatures that do not exceed 40°C should also be assumed to be suffering from EHS and treated with rapid cooling.11 On the other hand, athletes with CNS symptoms who are normothermic should be assumed to have EAH until ruled out by electrolyte assessment; IV fluids should be at no more than keep vein open (KVO) pending this determination.11 In some cases, an athlete may initially present with altered mental status but return to “normal.” However, this improvement may represent a “lucid period”; evaluation should continue with rectal temperature and treatment, as EHS in these cases may progress quickly.15

Treatment is centered on rapid, whole body cooling initiated at the first sign of heat illness.7,22 The goal of treatment is to achieve a rectal temperature <38.9°C within 30 minutes of the onset of EHS.15 Upon diagnosis, the athlete should be quickly placed in a tub of ice water to facilitate cold water immersion (CWI) therapy. Some guidelines suggest the athlete’s clothing be removed to potentiate evaporative cooling during CWI;12 however, cooling should not be delayed due to difficulties in removing equipment. CWI, where a heat stroke victim is submerged in ice water up to their neck while water is continuously circulated, is generally considered to be the gold standard treatment as it is the modality with the highest recorded cooling rates and the lowest rate of morbidity and mortality.7,20,21 Multiple studies of CWI have shown that survival nears 100% when aggressive cooling starts within 5 minutes of collapse or identification of EHS.20,21,22

If whole body CWI is unavailable, alternative methods of rapid cooling should be employed. Partial CWI, with torso immersion being preferable to the extremities, has been shown to achieve an acceptable rate of cooling to achieve sufficient drops in internal body temperature.20,23 However, one popular treatment—applying ice packs to the whole body, in particular to the groin and axillae—has not been shown to be sufficient to achieve standard cooling goals.20 None of these methods have been shown to be as effective as CWI.23

Intravenous access should be initiated with fluid resuscitation dictated by the provider’s assessment. Normal saline is recommended as the resuscitative fluid of choice, with the rate dictated by clinical judgment and adjusted as guided by electrolyte determination and clinical response. It cannot be overstated that in normothermic patients with confusion, EAH is the diagnosis of exclusion and aggressive fluid resuscitation should be withheld until electrolyte determination.

Once rectal temperature descends appropriately (~38.9°C), the cooling process should stop and the individual should be transported to a hospital for further observation20 and evaluation of possible sequelae, including rhabdomyolysis and renal injury, cardiac dysfunction and arrhythmia, severe electrolyte abnormalities, acute respiratory distress syndrome, lactic acidosis, and other forms of end-organ failure (Figure).

Figure.


Rapid cooling is more crucial than transport; transport poses a risk of delayed cooling, which can dramatically increase an individual’s risk of morbidity and mortality.20,23 In situations where a patient can be cooled on-site, physicians should pursue cooling before transporting the patient to a medical treatment facility.

Emergency Action Plan

Team physicians should be proactive in developing an emergency action plan to address possible EHS events. These plans should be site-specific, addressing procedures for all practice and home competition locations.12 All competition venues should have a CWI tub on-site in events where there is an increased risk of EHS.12,15,20 This tub should be set up and functional for all high-risk activities, including practices.12

Following recognition of a potential case of EHS, treatment teams should have procedures in place to transport athletes to the treatment area, obtain rectal temperature, initiate rapid cooling, and stabilize the athlete for transport to an emergency department (ED) for further evaluation.12,15 A written record of treatments and medications provided during athlete stabilization should be maintained and transported with the athlete to the ED.15 A list of helpful equipment and supplies for treatment of EHS can be found in Table 5.

Table 5.


EHS is a unique life-threatening situation where it is best to treat the patient on the sideline before transport.15 Those athletes transported before cooling risk spending an increased amount of time above critical temperatures for cell damage, which has been associated with increased morbidity and mortality. This mantra of “cool first, transport second” cannot be overemphasized, as those individuals with EHS who present to the ED with a persisting rectal temperature >41°F may risk up to an 80% mortality rate.24 Conversely, a recent large, retrospective study of 274 EHS events sustained during the Falmouth Road Race found a 100% survival rate when athletes were rapidly identified via rectal thermometry and treated with aggressive, rapid cooling through CWI.21

 

 

Return to Play

Perhaps the most challenging and important role the team physician has is determining an athlete’s return to play following EHI, as there currently are no evidence-based guidelines for return to activity for these athletes.7 The decisions surrounding return to play are highly individualized, as recovery from EHS and heat injury is associated with the duration of internal body temperature elevation above the critical level (40°C).7,20 Guidelines for return to activity following recovery from EHI differ among experts and institutions.7,25 The general consensus from these guidelines is that, at minimum, athletes should not participate in any physical activity until they are asymptomatic and all blood tests have normalized.11 Following this asymptomatic period, most guidelines advocate for a slow, deliberate return to activity.11 The American College of Sports Medicine (ACSM) offers one reasonable approach to the returning athlete following EHS:7

  • No exercise for at least 7 days following release from medical care.
  • Follow-up with a physician 1 week after release from medical care for physical examination and any warranted lab or radiologic studies (based upon organ systems affected during EHS).
  • Once cleared to return to activity, the athlete begins exercise in a cool environment, gradually increasing the duration, intensity, and heat exposure over 2 weeks to demonstrate heat tolerance and acclimatization.
  • Athletes who cannot resume vigorous activity due to recurrent symptoms (eg, excessive fatigue) should be reevaluated after 4 weeks. Laboratory exercise-heat tolerance testing may be useful in this setting.
  • The athlete may resume full competition once they are able to participate in full training in the heat for 2 to 4 weeks without adverse effects.

Heat tolerance testing (HTT) in these athletes remains controversial.5 26 The ACSM recommends that HTT be considered only for those unable to return to vigorous activity after a suitable period (approximately 4 weeks). In contrast, the Israeli Defense Force (IDF) uses HTT to evaluate soldiers following EHS to guide decision-making about return to duty.27 The IDF HTT assumes that individuals will respond differently to heat stresses. They identify individuals who are “heat intolerant” as being unable to tolerate specific heat challenges, indicated by increases in body temperature occurring more rapidly than normal responders under identical environmental and exercise conditions. However, despite being used for more than 30 years, there is no clear evidence that HTT adequately predicts who will experience subsequent episodes of EHS.

Conclusion

While the recognized cornerstone of being a team physician is the provision of medical care, the ACSM Team Physician Consensus Statement28 further delineates the medical and administrative responsibilities as both (1) understanding medical management and prevention of injury and illness in athletes; and (2) awareness of or involvement in the development and rehearsal of an emergency action plan. These tenets are critical for the team physician who accepts the responsibility to cover sports at the high school level or higher. Football team physicians play an essential role in mitigating risk of EHI in their athletes. Through development and execution of both comprehensive prevention strategies and emergency action plans, physicians can work to minimize athletes’ risk of both developing and experiencing significant adverse outcomes from an EHI.

 

Am J Orthop. 2016;45(6):340-348. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Kucera KL, Klossner D, Colgate B, Cantu RC. Annual Survey of Football Injury Research: 1931-2014. National Center for Catastrophic Sport Injury Research Web site. https://nccsir.unc.edu/files/2013/10/Annual-Football-2014-Fatalities-Final.pdf. Accessed May 31, 2016.

2. Boden BP, Breit I, Beachler JA, Williams A, Mueller FO. Fatalities in high school and college football players. Am J Sports Med. 2013;41(5):1108-1116.

3. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346(25):1978-1988.

4. Racinais S, Alonso JM, Coutts AJ, et al. Consensus recommendations on training and competing in the heat. Scand J Med Sci Sports. 2015;25 Suppl 1:6-19.

5. Pryor RR, Casa DJ, Adams WM, et al. Maximizing athletic performance in the heat. Strength Cond J. 2013;35(6):24-33.

6. Adams WM, Casa DJ. Hydration for football athletes. Sports Sci Exchange. 2015;28(141):1-5.

7. 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.

8. Yard EE, Gilchrist J, Haileyesus T, et al. Heat illness among high school athletes--United States, 2005-2009. J Safety Res. 2010;41(6):471-474.

9. Huffman EA, Yard EE, Fields SK, Collins CL, Comstock RD. Epidemiology of rare injuries and conditions among United States high school athletes during the 2005-2006 and 2006-2007 school years. J Athl Train. 2008;43(6):624-630.

10. 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(1):8-14.

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

12. Casa DJ, Almquist J, Anderson SA. The inter-association task force for preventing sudden death in secondary school athletics programs: best-practices recommendations. J Athl Train. 2013;48(4):546-553.

13. Gardner JW, Kark JA, Karnei K, et al. Risk factors predicting exertional heat illness in male Marine Corps recruits. Med Sci Sports Exerc. 1996;28(8):939-944.

14. Gundstein AJ, Ramseyer C, Zhao F, et al. A retrospective analysis of American football hyperthermia deaths in the United States. Int J Biometerol. 2012;56(1):11-20.

15. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform: uncompensable heat stress and hyperthermic exhaustion. J Athl Train. 2010;45(2):117-127.

16. Casa DJ, Csillan D; Inter-Association Task Force for Preseason Secondary School Athletics Participants, et al. Preseason heat-acclimatization guidelines for secondary school athletics. J Athl Train. 2009;44(3):332-333.

17. Godek SF, Godek JJ, Bartolozzi AR. Hydration status in college football players during consecutive days of twice-a-day preseason practices. Am J Sports Med. 2005;33(6):843-851.

18. Stover EA, Zachwieja J, Stofan J, Murray R, Horswill CA. Consistently high urine specific gravity in adolescent American football players and the impact of an acute drinking strategy. Int J Sports Med. 2006;27(4):330-335.

19. Bongers CC, Thijssen DH, Veltmeijer MTW, Hopman MT, Eijsvogels TM. Precooling and percooling (cooling during exercise) both improve performance in the heat: a meta-analytical review. Br J Sports Med. 2015;49(6):377-384.

20. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev. 2007;35(3):141-149.

21. DeMartini JK, Casa DJ, Stearns R, et al. Effectiveness of cold water immersion in the treatment of exertional heat stroke at the Falmouth Road Race. Med Sci Sports Exerc. 2015;47(2):240-245.

22. Casa DJ, Kenny GP, Taylor NA. Immersion treatment for exertional hyperthermia: cold or temperate water? Med Sci Sports Exerc. 2010;42(7):1246-1252.

23. Casa DJ, Armstrong LE, Kenny GP, O’Connor FG, Huggins RA. Exertional heat stroke: new concepts regarding cause and care. Curr Sports Med Rep. 2012;11(3):115-122.

24. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heat stroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183.

25. O’Connor FG, Casa DJ, Bergeron MF, et al. American College of Sports Medicine Roundtable on exertional heat stroke--return to duty/return to play: conference proceedings. Curr Sports Med Rep. 2010;9(5):314-321.

26. Kazman JB, Heled Y, Lisman PJ, Druyan A, Deuster PA, O’Connor FG. Exertional heat illness: the role of heat tolerance testing. Curr Sports Med Rep. 2013;12(2):101-105.

27. Moran DS, Heled Y, Still L, Laor A, Shapiro Y. Assessment of heat tolerance for post exertional heat stroke individuals. Med Sci Monit. 2004;10(6):CR252-CR257.

28. Herring SA, Kibler WB, Putukian M. Team Physician Consensus Statement: 2013 update. Med Sci Sports Exerc. 2013;45(8):1618-1622.

29. Heat stroke treatment. Korey Stringer Institute University of Connecticut Web site. http://ksi.uconn.edu/emergency-conditions/heat-illnesses/exertional-heat-stroke/heat-stroke-treatment/. Accessed June 14, 2016.

30. Headquarters, Department of the Army and the Air Force. Heat Stress Control and Heat Casualty Management. Technical Bulletin Medical 507. http://www.dir.ca.gov/oshsb/documents/Heat_illness_prevention_tbmed507.pdf. Published March 7, 2003. Accessed June 14, 2016.

References

1. Kucera KL, Klossner D, Colgate B, Cantu RC. Annual Survey of Football Injury Research: 1931-2014. National Center for Catastrophic Sport Injury Research Web site. https://nccsir.unc.edu/files/2013/10/Annual-Football-2014-Fatalities-Final.pdf. Accessed May 31, 2016.

2. Boden BP, Breit I, Beachler JA, Williams A, Mueller FO. Fatalities in high school and college football players. Am J Sports Med. 2013;41(5):1108-1116.

3. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346(25):1978-1988.

4. Racinais S, Alonso JM, Coutts AJ, et al. Consensus recommendations on training and competing in the heat. Scand J Med Sci Sports. 2015;25 Suppl 1:6-19.

5. Pryor RR, Casa DJ, Adams WM, et al. Maximizing athletic performance in the heat. Strength Cond J. 2013;35(6):24-33.

6. Adams WM, Casa DJ. Hydration for football athletes. Sports Sci Exchange. 2015;28(141):1-5.

7. 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.

8. Yard EE, Gilchrist J, Haileyesus T, et al. Heat illness among high school athletes--United States, 2005-2009. J Safety Res. 2010;41(6):471-474.

9. Huffman EA, Yard EE, Fields SK, Collins CL, Comstock RD. Epidemiology of rare injuries and conditions among United States high school athletes during the 2005-2006 and 2006-2007 school years. J Athl Train. 2008;43(6):624-630.

10. 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(1):8-14.

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

12. Casa DJ, Almquist J, Anderson SA. The inter-association task force for preventing sudden death in secondary school athletics programs: best-practices recommendations. J Athl Train. 2013;48(4):546-553.

13. Gardner JW, Kark JA, Karnei K, et al. Risk factors predicting exertional heat illness in male Marine Corps recruits. Med Sci Sports Exerc. 1996;28(8):939-944.

14. Gundstein AJ, Ramseyer C, Zhao F, et al. A retrospective analysis of American football hyperthermia deaths in the United States. Int J Biometerol. 2012;56(1):11-20.

15. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform: uncompensable heat stress and hyperthermic exhaustion. J Athl Train. 2010;45(2):117-127.

16. Casa DJ, Csillan D; Inter-Association Task Force for Preseason Secondary School Athletics Participants, et al. Preseason heat-acclimatization guidelines for secondary school athletics. J Athl Train. 2009;44(3):332-333.

17. Godek SF, Godek JJ, Bartolozzi AR. Hydration status in college football players during consecutive days of twice-a-day preseason practices. Am J Sports Med. 2005;33(6):843-851.

18. Stover EA, Zachwieja J, Stofan J, Murray R, Horswill CA. Consistently high urine specific gravity in adolescent American football players and the impact of an acute drinking strategy. Int J Sports Med. 2006;27(4):330-335.

19. Bongers CC, Thijssen DH, Veltmeijer MTW, Hopman MT, Eijsvogels TM. Precooling and percooling (cooling during exercise) both improve performance in the heat: a meta-analytical review. Br J Sports Med. 2015;49(6):377-384.

20. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev. 2007;35(3):141-149.

21. DeMartini JK, Casa DJ, Stearns R, et al. Effectiveness of cold water immersion in the treatment of exertional heat stroke at the Falmouth Road Race. Med Sci Sports Exerc. 2015;47(2):240-245.

22. Casa DJ, Kenny GP, Taylor NA. Immersion treatment for exertional hyperthermia: cold or temperate water? Med Sci Sports Exerc. 2010;42(7):1246-1252.

23. Casa DJ, Armstrong LE, Kenny GP, O’Connor FG, Huggins RA. Exertional heat stroke: new concepts regarding cause and care. Curr Sports Med Rep. 2012;11(3):115-122.

24. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heat stroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183.

25. O’Connor FG, Casa DJ, Bergeron MF, et al. American College of Sports Medicine Roundtable on exertional heat stroke--return to duty/return to play: conference proceedings. Curr Sports Med Rep. 2010;9(5):314-321.

26. Kazman JB, Heled Y, Lisman PJ, Druyan A, Deuster PA, O’Connor FG. Exertional heat illness: the role of heat tolerance testing. Curr Sports Med Rep. 2013;12(2):101-105.

27. Moran DS, Heled Y, Still L, Laor A, Shapiro Y. Assessment of heat tolerance for post exertional heat stroke individuals. Med Sci Monit. 2004;10(6):CR252-CR257.

28. Herring SA, Kibler WB, Putukian M. Team Physician Consensus Statement: 2013 update. Med Sci Sports Exerc. 2013;45(8):1618-1622.

29. Heat stroke treatment. Korey Stringer Institute University of Connecticut Web site. http://ksi.uconn.edu/emergency-conditions/heat-illnesses/exertional-heat-stroke/heat-stroke-treatment/. Accessed June 14, 2016.

30. Headquarters, Department of the Army and the Air Force. Heat Stress Control and Heat Casualty Management. Technical Bulletin Medical 507. http://www.dir.ca.gov/oshsb/documents/Heat_illness_prevention_tbmed507.pdf. Published March 7, 2003. Accessed June 14, 2016.

Issue
The American Journal of Orthopedics - 45(6)
Issue
The American Journal of Orthopedics - 45(6)
Page Number
340-348
Page Number
340-348
Publications
Publications
Topics
Article Type
Display Headline
Exertional Heat Stroke and American Football: What the Team Physician Needs to Know
Display Headline
Exertional Heat Stroke and American Football: What the Team Physician Needs to Know
Sections
Disallow All Ads
Article PDF Media

FDA: New labeling warns against combining opioids, benzodiazepines

Article Type
Changed
Fri, 01/18/2019 - 16:10
Display Headline
FDA: New labeling warns against combining opioids, benzodiazepines

Labeling for prescription opioid pain or cough medicines and benzodiazepines will now carry the strongest available warning regarding serious side effects and death associated with their combined use, according to the Food and Drug Administration.

The new boxed warnings urge health care professionals to limit prescribing opioid pain medicines with benzodiazepines or other central nervous system depressants only to patients for whom alternative treatment options are inadequate, and to limit dosages and treatment duration to the minimum possible while achieving the desired clinical effect.

 

“First, the FDA is requiring companies to update their product labeling for ... benzodiazepines and opioids to include possible harms when they are used together. Second, we are requiring new or updated medication guides for these drugs reflecting those same warnings,” said Doug Throckmorton, MD, deputy director of the FDA’s Center for Drug Evaluation and Research, during a telebriefing.

Opioids will include a warning regarding prescribing with benzodiazepines and other central nervous system depressants, including alcohol. Benzodiazepines will include a warning regarding prescribing with opioids.

In addition, the FDA has issued a safety communication to “warn the public about the serious risk of taking these products together to help make doctors more cautious and patients better informed,” Dr. Throckmorton said.

The action comes amid ongoing efforts to address an epidemic of opioid addiction across the United States, and in response to a first-of-its-kind “citizen petition” calling for the boxed warnings.

A coalition of health officials from multiple cities, states, and U.S. territories initiated that petition in February, and thousands of concerned community members started an additional online petition. Those petitions were in response to both the increasing combined use of opioids and benzodiazepines and a concomitant increase in the risk of serious side effects and deaths associated with their combined use, according to Baltimore City Health Commissioner Leana Wen, MD.

As an emergency physician, Dr. Wen said that she has seen firsthand the alarming trends; one in three unintentional overdose deaths from prescribed opioids also involve benzodiazepines, she noted.

“In my state of Maryland in 2014, benzodiazepines were associated with 19% of prescription opioid deaths, and 59% of benzodiazepine-associated deaths involved prescription opioids. We also noted the growing biological evidence that combining these medications caused sleepiness and slowed breathing, increasing the likelihood of a fatal overdose,” she said.

Dr. Throckmorton further noted that emergency department visits and deaths involving patients prescribed both opioids and benzodiazepines have increased significantly over time. From 2004 to 2011, the rate of nonmedical use–related emergency department visits increased significantly each year, and overdose deaths involving both drug classes during that period nearly tripled on an annual basis.

 

Dr. Robert Califf

“Communities have been seeing this trend for some time, but ultimately we needed data in order to act today,” FDA Commissioner Robert Califf, MD, said during the telebriefing.

The current action is just “one part of a larger effort to address this epidemic.

“We remain focused and deeply committed to contributing to the comprehensive effort to address the opioid epidemic,” Dr. Califf said. The FDA “will continue to monitor these products carefully and take additional actions as needed, and will share updates with the public as necessary as we work to address this public health crisis.”

Dr. Califf noted that the current action is part of the FDA’s Opioids Action Plan, which is “importantly not meant just to cover illicit or abusive use of opioids.”

“So, you’ll be hearing a lot more from us, because this is a national crisis that is not going away. We’re making progress on the prescribing, and we’re seeing a reduction in the use of opioids now,” he noted. “But we’re still seeing many overdoses.

“This is a continuum, and we’ll continue to try to do everything we can to address the epidemic,” Dr. Califf concluded.

[email protected]

Publications
Topics
Legacy Keywords
opioids, benzodiazepines, FDA, abuse, overdose
Sections

Labeling for prescription opioid pain or cough medicines and benzodiazepines will now carry the strongest available warning regarding serious side effects and death associated with their combined use, according to the Food and Drug Administration.

The new boxed warnings urge health care professionals to limit prescribing opioid pain medicines with benzodiazepines or other central nervous system depressants only to patients for whom alternative treatment options are inadequate, and to limit dosages and treatment duration to the minimum possible while achieving the desired clinical effect.

 

“First, the FDA is requiring companies to update their product labeling for ... benzodiazepines and opioids to include possible harms when they are used together. Second, we are requiring new or updated medication guides for these drugs reflecting those same warnings,” said Doug Throckmorton, MD, deputy director of the FDA’s Center for Drug Evaluation and Research, during a telebriefing.

Opioids will include a warning regarding prescribing with benzodiazepines and other central nervous system depressants, including alcohol. Benzodiazepines will include a warning regarding prescribing with opioids.

In addition, the FDA has issued a safety communication to “warn the public about the serious risk of taking these products together to help make doctors more cautious and patients better informed,” Dr. Throckmorton said.

The action comes amid ongoing efforts to address an epidemic of opioid addiction across the United States, and in response to a first-of-its-kind “citizen petition” calling for the boxed warnings.

A coalition of health officials from multiple cities, states, and U.S. territories initiated that petition in February, and thousands of concerned community members started an additional online petition. Those petitions were in response to both the increasing combined use of opioids and benzodiazepines and a concomitant increase in the risk of serious side effects and deaths associated with their combined use, according to Baltimore City Health Commissioner Leana Wen, MD.

As an emergency physician, Dr. Wen said that she has seen firsthand the alarming trends; one in three unintentional overdose deaths from prescribed opioids also involve benzodiazepines, she noted.

“In my state of Maryland in 2014, benzodiazepines were associated with 19% of prescription opioid deaths, and 59% of benzodiazepine-associated deaths involved prescription opioids. We also noted the growing biological evidence that combining these medications caused sleepiness and slowed breathing, increasing the likelihood of a fatal overdose,” she said.

Dr. Throckmorton further noted that emergency department visits and deaths involving patients prescribed both opioids and benzodiazepines have increased significantly over time. From 2004 to 2011, the rate of nonmedical use–related emergency department visits increased significantly each year, and overdose deaths involving both drug classes during that period nearly tripled on an annual basis.

 

Dr. Robert Califf

“Communities have been seeing this trend for some time, but ultimately we needed data in order to act today,” FDA Commissioner Robert Califf, MD, said during the telebriefing.

The current action is just “one part of a larger effort to address this epidemic.

“We remain focused and deeply committed to contributing to the comprehensive effort to address the opioid epidemic,” Dr. Califf said. The FDA “will continue to monitor these products carefully and take additional actions as needed, and will share updates with the public as necessary as we work to address this public health crisis.”

Dr. Califf noted that the current action is part of the FDA’s Opioids Action Plan, which is “importantly not meant just to cover illicit or abusive use of opioids.”

“So, you’ll be hearing a lot more from us, because this is a national crisis that is not going away. We’re making progress on the prescribing, and we’re seeing a reduction in the use of opioids now,” he noted. “But we’re still seeing many overdoses.

“This is a continuum, and we’ll continue to try to do everything we can to address the epidemic,” Dr. Califf concluded.

[email protected]

Labeling for prescription opioid pain or cough medicines and benzodiazepines will now carry the strongest available warning regarding serious side effects and death associated with their combined use, according to the Food and Drug Administration.

The new boxed warnings urge health care professionals to limit prescribing opioid pain medicines with benzodiazepines or other central nervous system depressants only to patients for whom alternative treatment options are inadequate, and to limit dosages and treatment duration to the minimum possible while achieving the desired clinical effect.

 

“First, the FDA is requiring companies to update their product labeling for ... benzodiazepines and opioids to include possible harms when they are used together. Second, we are requiring new or updated medication guides for these drugs reflecting those same warnings,” said Doug Throckmorton, MD, deputy director of the FDA’s Center for Drug Evaluation and Research, during a telebriefing.

Opioids will include a warning regarding prescribing with benzodiazepines and other central nervous system depressants, including alcohol. Benzodiazepines will include a warning regarding prescribing with opioids.

In addition, the FDA has issued a safety communication to “warn the public about the serious risk of taking these products together to help make doctors more cautious and patients better informed,” Dr. Throckmorton said.

The action comes amid ongoing efforts to address an epidemic of opioid addiction across the United States, and in response to a first-of-its-kind “citizen petition” calling for the boxed warnings.

A coalition of health officials from multiple cities, states, and U.S. territories initiated that petition in February, and thousands of concerned community members started an additional online petition. Those petitions were in response to both the increasing combined use of opioids and benzodiazepines and a concomitant increase in the risk of serious side effects and deaths associated with their combined use, according to Baltimore City Health Commissioner Leana Wen, MD.

As an emergency physician, Dr. Wen said that she has seen firsthand the alarming trends; one in three unintentional overdose deaths from prescribed opioids also involve benzodiazepines, she noted.

“In my state of Maryland in 2014, benzodiazepines were associated with 19% of prescription opioid deaths, and 59% of benzodiazepine-associated deaths involved prescription opioids. We also noted the growing biological evidence that combining these medications caused sleepiness and slowed breathing, increasing the likelihood of a fatal overdose,” she said.

Dr. Throckmorton further noted that emergency department visits and deaths involving patients prescribed both opioids and benzodiazepines have increased significantly over time. From 2004 to 2011, the rate of nonmedical use–related emergency department visits increased significantly each year, and overdose deaths involving both drug classes during that period nearly tripled on an annual basis.

 

Dr. Robert Califf

“Communities have been seeing this trend for some time, but ultimately we needed data in order to act today,” FDA Commissioner Robert Califf, MD, said during the telebriefing.

The current action is just “one part of a larger effort to address this epidemic.

“We remain focused and deeply committed to contributing to the comprehensive effort to address the opioid epidemic,” Dr. Califf said. The FDA “will continue to monitor these products carefully and take additional actions as needed, and will share updates with the public as necessary as we work to address this public health crisis.”

Dr. Califf noted that the current action is part of the FDA’s Opioids Action Plan, which is “importantly not meant just to cover illicit or abusive use of opioids.”

“So, you’ll be hearing a lot more from us, because this is a national crisis that is not going away. We’re making progress on the prescribing, and we’re seeing a reduction in the use of opioids now,” he noted. “But we’re still seeing many overdoses.

“This is a continuum, and we’ll continue to try to do everything we can to address the epidemic,” Dr. Califf concluded.

[email protected]

Publications
Publications
Topics
Article Type
Display Headline
FDA: New labeling warns against combining opioids, benzodiazepines
Display Headline
FDA: New labeling warns against combining opioids, benzodiazepines
Legacy Keywords
opioids, benzodiazepines, FDA, abuse, overdose
Legacy Keywords
opioids, benzodiazepines, FDA, abuse, overdose
Sections
Disallow All Ads