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Up in Arms: Bilateral Luxatio Erecta Fracture-Dislocations
Unilateral inferior shoulder dislocation (luxatio erecta) is uncommon, accounting for only 0.5% of all shoulder dislocations.1 Bilateral luxatio erecta is extremely rare, having been described fewer than 20 times in the literature. The most common etiology is hyperabduction causing the humerus to lever on the acromion; less common is axial loading onto a fully abducted arm and an extended elbow.2 Hyperabduction can occur when a person grabs an object in an attempt to stop a fall, as occurred in the present case. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 58-year-old man with a trauma injury presented to our emergency department. For his open right elbow fracture, emergency medical services had given him fentanyl en route, and when he arrived he was less responsive. As the patient reported, he had been on a scaffold 16 feet high when it began to give way. He jumped for another scaffold, 3 to 4 feet away, but came up short and, in an attempt to stop himself from falling, grabbed onto it with arms extended and above his head. His hands and arms were immediately pulled up in full extension. When both shoulders became dislocated, he could not hold on and fell to the ground, landing on a buttock. He did not lose consciousness.
Physical examination revealed both arms abducted at the shoulder, and elbows extended (Figure 1). 
Radiographs confirmed the diagnosis and showed bilateral nondisplaced proximal humeral fractures of the greater tuberosity (Figure 2). 
For the shoulder reductions, we administered propofol for conscious sedation and fentanyl for analgesia. Then, a sheet was wrapped supraclavicular and pulled across the torso inferiorly to allow countertraction when pulling the arm superiorly on the axial line. Another countertraction sheet was placed on the opposite side. For each arm, the countertraction was pulled inferiorly when the arm was pulled superiorly, both on the longitudinal plane. The arm was then gently rotated in adduction until reduction was achieved.
The right shoulder reduced relatively easily. The left shoulder reduced into an anterior dislocation—a relatively uncommon outcome in in-line traction attempts.3 (Reduction into anterior dislocation can also be a desired result in a specific technique of 2-step reduction, as described by Nho and colleagues.4) The patient’s anterior dislocation was then easily reduced into anatomical position with use of the Kocher technique of arm adduction with elbow flexion, followed by external rotation, and then finally into anatomical position with internal rotation.5 Both arms were then immobilized in full adduction with bilateral slings. The patient was admitted for further treatment of multiple fractures of the arms and vertebrae.
He was discharged in bilateral shoulder slings to an extended-care facility for physical therapy. One month after discharge, he could not elevate his arms and had minimal use of them. Two weeks later, magnetic resonance imaging showed a “comminuted greater tuberosity fracture with new displacement of fragments involving the attachment of the supraspinatus and infraspinatus; posterior subluxation of the glenohumeral joint with evidence of posterior and anterior labral tears; and large glenohumeral joint effusion.” The patient opted for surgical repair and underwent left shoulder arthroscopy with extensive débridement, open rotator cuff repair, open greater tuberosity reduction and internal fixation, and open biceps tenodesis. He was then discharged back to an extended-care facility to continue rehabilitation. One and a half months after surgery, he started the physical therapy phase of the massive rotator cuff repair protocol. He declined reverse total shoulder arthroplasty (RTSA).
Four and a half months after injury (3 months after surgery), the left shoulder demonstrated 20° of flexion and 70° to 110° of abduction (external rotation not tested), and the right shoulder demonstrated 30° of flexion and 70° to 110° of abduction (external rotation not tested). He had no instability and no lag with good external rotation.
Six months after injury, the patient still could not lift his arms above his head. He likely would not be able to do so without RTSA, which he again declined. He continued physical therapy and clinical follow-ups.
Discussion
Although inferior shoulder dislocations are rare, they carry a higher rate of complications, most of which our patient experienced. Our patient had bilateral humeral head fractures, which occur in 80% of cases.6 Postreduction CT showed the degree of his fractures (Figure 3).
Our patient also had reduced sensation in the axillary nerve distribution, which occurs in 60% of inferior dislocations.6 Axillary nerve injuries produce numbness in the lateral arm or posterior shoulder and weakness with shoulder flexion, abduction, and external rotation.7 In our patient’s case, sensation returned after reduction, which is typical (most patients have a positive prognosis).8 As the shoulder dislocates inferiorly, the humeral head tears the glenohumeral capsule inferiorly, which can damage the axillary artery. This artery becomes the brachial and eventually the radial and ulnar arteries, which can have decreased or absent pulses with injury.
Inferior dislocations are also associated with abundant soft-tissue injuries, including torn rotator cuff, shoulder capsule avulsion, and disruption of adjacent muscles (supraspinatus, infraspinatus, teres minor, subscapularis, pectoralis major).9Luxatio erecta is relatively easy to diagnose given the unmistakable arm positioning. The key for the physician is first to assess for the many possible complications, then to administer the proper sedation and analgesia for reduction, and finally to reassess for complications.
Am J Orthop. 2016;45(6):E328-E330. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Camarda L, Martorana U, D’Arienzo M. A case of bilateral luxatio erecta. J Orthop Traumatol. 2009;10(2):97-99.
2. Musmeci E, Gaspari D, Sandri A, Regis D, Bartolozzi P. Bilateral luxatio erecta humeri associated with a unilateral brachial plexus and bilateral rotator cuff injuries: a case report. J Orthop Trauma. 2008;22(7):498-500.
3. Lam AC, Shih RD. Luxatio erecta complicated by anterior shoulder dislocation during reduction. West J Emerg Med. 2010;11(1):28-30.
4. Nho SJ, Dodson CC, Bardzik KF, Brophy RH, Domb BG, MacGillivray JD. The two-step maneuver for closed reduction of inferior glenohumeral dislocation (luxatio erecta to anterior dislocation to reduction). J Orthop Trauma. 2006;20(5):354-357.
5. Beattie TF, Steedman DJ, McGowan A, Robertson CE. A comparison of the Milch and Kocher techniques for acute anterior dislocation of the shoulder. Injury. 1986;17(5):349-352.
6. Mallon WJ, Bassett FH 3rd, Goldner RD. Luxatio erecta: the inferior glenohumeral dislocation. J Orthop Trauma. 1990;4(1):19-24.
7. Miller T. Peripheral nerve injuries at the shoulder. J Manipulative Physiol Ther. 1998;6(4):170-183.
8. Groh GI, Wirth MA, Rockwood CA Jr. Results of treatment of luxatio erecta (inferior shoulder dislocation). J Shoulder Elbow Surg. 2010;19(3):423-426.
9. Garcia R, Ponsky T, Brody F, Long J. Bilateral luxatio erecta complicated by venous thrombosis. J Trauma. 2006;60(5):1132-1134.
Unilateral inferior shoulder dislocation (luxatio erecta) is uncommon, accounting for only 0.5% of all shoulder dislocations.1 Bilateral luxatio erecta is extremely rare, having been described fewer than 20 times in the literature. The most common etiology is hyperabduction causing the humerus to lever on the acromion; less common is axial loading onto a fully abducted arm and an extended elbow.2 Hyperabduction can occur when a person grabs an object in an attempt to stop a fall, as occurred in the present case. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 58-year-old man with a trauma injury presented to our emergency department. For his open right elbow fracture, emergency medical services had given him fentanyl en route, and when he arrived he was less responsive. As the patient reported, he had been on a scaffold 16 feet high when it began to give way. He jumped for another scaffold, 3 to 4 feet away, but came up short and, in an attempt to stop himself from falling, grabbed onto it with arms extended and above his head. His hands and arms were immediately pulled up in full extension. When both shoulders became dislocated, he could not hold on and fell to the ground, landing on a buttock. He did not lose consciousness.
Physical examination revealed both arms abducted at the shoulder, and elbows extended (Figure 1).
Radiographs confirmed the diagnosis and showed bilateral nondisplaced proximal humeral fractures of the greater tuberosity (Figure 2).
For the shoulder reductions, we administered propofol for conscious sedation and fentanyl for analgesia. Then, a sheet was wrapped supraclavicular and pulled across the torso inferiorly to allow countertraction when pulling the arm superiorly on the axial line. Another countertraction sheet was placed on the opposite side. For each arm, the countertraction was pulled inferiorly when the arm was pulled superiorly, both on the longitudinal plane. The arm was then gently rotated in adduction until reduction was achieved.
The right shoulder reduced relatively easily. The left shoulder reduced into an anterior dislocation—a relatively uncommon outcome in in-line traction attempts.3 (Reduction into anterior dislocation can also be a desired result in a specific technique of 2-step reduction, as described by Nho and colleagues.4) The patient’s anterior dislocation was then easily reduced into anatomical position with use of the Kocher technique of arm adduction with elbow flexion, followed by external rotation, and then finally into anatomical position with internal rotation.5 Both arms were then immobilized in full adduction with bilateral slings. The patient was admitted for further treatment of multiple fractures of the arms and vertebrae.
He was discharged in bilateral shoulder slings to an extended-care facility for physical therapy. One month after discharge, he could not elevate his arms and had minimal use of them. Two weeks later, magnetic resonance imaging showed a “comminuted greater tuberosity fracture with new displacement of fragments involving the attachment of the supraspinatus and infraspinatus; posterior subluxation of the glenohumeral joint with evidence of posterior and anterior labral tears; and large glenohumeral joint effusion.” The patient opted for surgical repair and underwent left shoulder arthroscopy with extensive débridement, open rotator cuff repair, open greater tuberosity reduction and internal fixation, and open biceps tenodesis. He was then discharged back to an extended-care facility to continue rehabilitation. One and a half months after surgery, he started the physical therapy phase of the massive rotator cuff repair protocol. He declined reverse total shoulder arthroplasty (RTSA).
Four and a half months after injury (3 months after surgery), the left shoulder demonstrated 20° of flexion and 70° to 110° of abduction (external rotation not tested), and the right shoulder demonstrated 30° of flexion and 70° to 110° of abduction (external rotation not tested). He had no instability and no lag with good external rotation.
Six months after injury, the patient still could not lift his arms above his head. He likely would not be able to do so without RTSA, which he again declined. He continued physical therapy and clinical follow-ups.
Discussion
Although inferior shoulder dislocations are rare, they carry a higher rate of complications, most of which our patient experienced. Our patient had bilateral humeral head fractures, which occur in 80% of cases.6 Postreduction CT showed the degree of his fractures (Figure 3).
Our patient also had reduced sensation in the axillary nerve distribution, which occurs in 60% of inferior dislocations.6 Axillary nerve injuries produce numbness in the lateral arm or posterior shoulder and weakness with shoulder flexion, abduction, and external rotation.7 In our patient’s case, sensation returned after reduction, which is typical (most patients have a positive prognosis).8 As the shoulder dislocates inferiorly, the humeral head tears the glenohumeral capsule inferiorly, which can damage the axillary artery. This artery becomes the brachial and eventually the radial and ulnar arteries, which can have decreased or absent pulses with injury.
Inferior dislocations are also associated with abundant soft-tissue injuries, including torn rotator cuff, shoulder capsule avulsion, and disruption of adjacent muscles (supraspinatus, infraspinatus, teres minor, subscapularis, pectoralis major).9Luxatio erecta is relatively easy to diagnose given the unmistakable arm positioning. The key for the physician is first to assess for the many possible complications, then to administer the proper sedation and analgesia for reduction, and finally to reassess for complications.
Am J Orthop. 2016;45(6):E328-E330. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Unilateral inferior shoulder dislocation (luxatio erecta) is uncommon, accounting for only 0.5% of all shoulder dislocations.1 Bilateral luxatio erecta is extremely rare, having been described fewer than 20 times in the literature. The most common etiology is hyperabduction causing the humerus to lever on the acromion; less common is axial loading onto a fully abducted arm and an extended elbow.2 Hyperabduction can occur when a person grabs an object in an attempt to stop a fall, as occurred in the present case. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 58-year-old man with a trauma injury presented to our emergency department. For his open right elbow fracture, emergency medical services had given him fentanyl en route, and when he arrived he was less responsive. As the patient reported, he had been on a scaffold 16 feet high when it began to give way. He jumped for another scaffold, 3 to 4 feet away, but came up short and, in an attempt to stop himself from falling, grabbed onto it with arms extended and above his head. His hands and arms were immediately pulled up in full extension. When both shoulders became dislocated, he could not hold on and fell to the ground, landing on a buttock. He did not lose consciousness.
Physical examination revealed both arms abducted at the shoulder, and elbows extended (Figure 1).
Radiographs confirmed the diagnosis and showed bilateral nondisplaced proximal humeral fractures of the greater tuberosity (Figure 2).
For the shoulder reductions, we administered propofol for conscious sedation and fentanyl for analgesia. Then, a sheet was wrapped supraclavicular and pulled across the torso inferiorly to allow countertraction when pulling the arm superiorly on the axial line. Another countertraction sheet was placed on the opposite side. For each arm, the countertraction was pulled inferiorly when the arm was pulled superiorly, both on the longitudinal plane. The arm was then gently rotated in adduction until reduction was achieved.
The right shoulder reduced relatively easily. The left shoulder reduced into an anterior dislocation—a relatively uncommon outcome in in-line traction attempts.3 (Reduction into anterior dislocation can also be a desired result in a specific technique of 2-step reduction, as described by Nho and colleagues.4) The patient’s anterior dislocation was then easily reduced into anatomical position with use of the Kocher technique of arm adduction with elbow flexion, followed by external rotation, and then finally into anatomical position with internal rotation.5 Both arms were then immobilized in full adduction with bilateral slings. The patient was admitted for further treatment of multiple fractures of the arms and vertebrae.
He was discharged in bilateral shoulder slings to an extended-care facility for physical therapy. One month after discharge, he could not elevate his arms and had minimal use of them. Two weeks later, magnetic resonance imaging showed a “comminuted greater tuberosity fracture with new displacement of fragments involving the attachment of the supraspinatus and infraspinatus; posterior subluxation of the glenohumeral joint with evidence of posterior and anterior labral tears; and large glenohumeral joint effusion.” The patient opted for surgical repair and underwent left shoulder arthroscopy with extensive débridement, open rotator cuff repair, open greater tuberosity reduction and internal fixation, and open biceps tenodesis. He was then discharged back to an extended-care facility to continue rehabilitation. One and a half months after surgery, he started the physical therapy phase of the massive rotator cuff repair protocol. He declined reverse total shoulder arthroplasty (RTSA).
Four and a half months after injury (3 months after surgery), the left shoulder demonstrated 20° of flexion and 70° to 110° of abduction (external rotation not tested), and the right shoulder demonstrated 30° of flexion and 70° to 110° of abduction (external rotation not tested). He had no instability and no lag with good external rotation.
Six months after injury, the patient still could not lift his arms above his head. He likely would not be able to do so without RTSA, which he again declined. He continued physical therapy and clinical follow-ups.
Discussion
Although inferior shoulder dislocations are rare, they carry a higher rate of complications, most of which our patient experienced. Our patient had bilateral humeral head fractures, which occur in 80% of cases.6 Postreduction CT showed the degree of his fractures (Figure 3).
Our patient also had reduced sensation in the axillary nerve distribution, which occurs in 60% of inferior dislocations.6 Axillary nerve injuries produce numbness in the lateral arm or posterior shoulder and weakness with shoulder flexion, abduction, and external rotation.7 In our patient’s case, sensation returned after reduction, which is typical (most patients have a positive prognosis).8 As the shoulder dislocates inferiorly, the humeral head tears the glenohumeral capsule inferiorly, which can damage the axillary artery. This artery becomes the brachial and eventually the radial and ulnar arteries, which can have decreased or absent pulses with injury.
Inferior dislocations are also associated with abundant soft-tissue injuries, including torn rotator cuff, shoulder capsule avulsion, and disruption of adjacent muscles (supraspinatus, infraspinatus, teres minor, subscapularis, pectoralis major).9Luxatio erecta is relatively easy to diagnose given the unmistakable arm positioning. The key for the physician is first to assess for the many possible complications, then to administer the proper sedation and analgesia for reduction, and finally to reassess for complications.
Am J Orthop. 2016;45(6):E328-E330. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Camarda L, Martorana U, D’Arienzo M. A case of bilateral luxatio erecta. J Orthop Traumatol. 2009;10(2):97-99.
2. Musmeci E, Gaspari D, Sandri A, Regis D, Bartolozzi P. Bilateral luxatio erecta humeri associated with a unilateral brachial plexus and bilateral rotator cuff injuries: a case report. J Orthop Trauma. 2008;22(7):498-500.
3. Lam AC, Shih RD. Luxatio erecta complicated by anterior shoulder dislocation during reduction. West J Emerg Med. 2010;11(1):28-30.
4. Nho SJ, Dodson CC, Bardzik KF, Brophy RH, Domb BG, MacGillivray JD. The two-step maneuver for closed reduction of inferior glenohumeral dislocation (luxatio erecta to anterior dislocation to reduction). J Orthop Trauma. 2006;20(5):354-357.
5. Beattie TF, Steedman DJ, McGowan A, Robertson CE. A comparison of the Milch and Kocher techniques for acute anterior dislocation of the shoulder. Injury. 1986;17(5):349-352.
6. Mallon WJ, Bassett FH 3rd, Goldner RD. Luxatio erecta: the inferior glenohumeral dislocation. J Orthop Trauma. 1990;4(1):19-24.
7. Miller T. Peripheral nerve injuries at the shoulder. J Manipulative Physiol Ther. 1998;6(4):170-183.
8. Groh GI, Wirth MA, Rockwood CA Jr. Results of treatment of luxatio erecta (inferior shoulder dislocation). J Shoulder Elbow Surg. 2010;19(3):423-426.
9. Garcia R, Ponsky T, Brody F, Long J. Bilateral luxatio erecta complicated by venous thrombosis. J Trauma. 2006;60(5):1132-1134.
1. Camarda L, Martorana U, D’Arienzo M. A case of bilateral luxatio erecta. J Orthop Traumatol. 2009;10(2):97-99.
2. Musmeci E, Gaspari D, Sandri A, Regis D, Bartolozzi P. Bilateral luxatio erecta humeri associated with a unilateral brachial plexus and bilateral rotator cuff injuries: a case report. J Orthop Trauma. 2008;22(7):498-500.
3. Lam AC, Shih RD. Luxatio erecta complicated by anterior shoulder dislocation during reduction. West J Emerg Med. 2010;11(1):28-30.
4. Nho SJ, Dodson CC, Bardzik KF, Brophy RH, Domb BG, MacGillivray JD. The two-step maneuver for closed reduction of inferior glenohumeral dislocation (luxatio erecta to anterior dislocation to reduction). J Orthop Trauma. 2006;20(5):354-357.
5. Beattie TF, Steedman DJ, McGowan A, Robertson CE. A comparison of the Milch and Kocher techniques for acute anterior dislocation of the shoulder. Injury. 1986;17(5):349-352.
6. Mallon WJ, Bassett FH 3rd, Goldner RD. Luxatio erecta: the inferior glenohumeral dislocation. J Orthop Trauma. 1990;4(1):19-24.
7. Miller T. Peripheral nerve injuries at the shoulder. J Manipulative Physiol Ther. 1998;6(4):170-183.
8. Groh GI, Wirth MA, Rockwood CA Jr. Results of treatment of luxatio erecta (inferior shoulder dislocation). J Shoulder Elbow Surg. 2010;19(3):423-426.
9. Garcia R, Ponsky T, Brody F, Long J. Bilateral luxatio erecta complicated by venous thrombosis. J Trauma. 2006;60(5):1132-1134.
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), 
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). 
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). 
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%).
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). 
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. 
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). 
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.
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.
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),
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).
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).
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%).
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).
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.
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).
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),
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).
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).
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%).
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).
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.
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).
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.
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.
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.
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). 
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 
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 
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). 
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 
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. 
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). 
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. 
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
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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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).
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
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
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).
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
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.
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).
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.
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
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).
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
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
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).
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
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.
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).
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.
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
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.
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.
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.
Back to Basics: The Role of the Team Physician
Editor’s Note: AJO Deputy Editor-in-Chief Robin West, MD, is the Head Team Physician for the Washington Redskins and the Washington Nationals. She has previously served as a team physician for 2 Super Bowl-winning Pittsburgh Steelers teams. I am pleased to “hand off” this issue to her.
—Bryan T. Hanypsiak, MD
The summer is over, football season has begun, and team physicians are busy trying to manage and treat the plethora of injuries that come with the game. Football is one of the most popular sports played by young athletes. Youth participation (ages 6-14 years) in tackle football was 2.169 million in 2015, according to a study conducted by the Physical Activity Council and presented by USA Football. There were 1.084 million boys (and 1500 girls) playing high school football in the 2014-2015 season, nearly twice the number of the next most popular sport, track and field, according to the National Federation of State High School Associations.Due to the sheer volume of athletes and high-impact nature of the game, football leads all other sports in the number of sustained injuries.
Team physicians have the leadership role in the organization, management, and provision of care of the athletes on the team. The roles and responsibilities of the team physician are ever-evolving. The team physician has to meet certain medical qualifications and education requirements, and understand the ethical and medicolegal issues.
The American Academy of Orthopaedic Surgeons and several other medical associations have put together a Team Physician Consensus Statement (available at http://bit.ly/2b8rOzS). All team physicians, coaches, and athletic trainers should read and understand this statement, as it delineates the qualifications, duties, and responsibilities of the team physician.
Our Football Issue focuses on the most common injuries that the team physician will encounter during the season. Our goal is to create a comprehensive guide for the team physician on the acute management of these injuries. As team physicians, we have to make quick return-to-play decisions that are often difficult, as we are dealing with extremely competitive athletes and coaches in the heat of the moment. Since we can’t control the high levels of adrenalin, loud stadium, or rapid speed of the game, we need to be prepared to perform a comprehensive evaluation and diagnosis under these circumstances. This return-to-play decision should be based solely on the severity of the injury and safety of the player. As a team physician, you are responsible for making the “final call” on when the player is safe to return to the game.
This issue includes a section on the most common medical issues (ophthalmology, dental, and dermatology), concussion, exertional heat stroke, knee injuries, and foot and ankle injuries. We also have a special list of the most common items to include in the athletic trainer’s medical bag when covering a high school or collegiate football game (see page 376). Our prominent contributing authors all have extensive experience covering high school, collegiate, and professional teams.
I hope that our Football Issue helps you to keep your athletes safe and injury-free, which is necessary to have a successful season. Remember, as the team physician, your primary focus is the well being of the players. The success of the team only comes when the players are healthy. A cohesive, well-organized medical team, led by the head athletic trainer and team physician, is a key component to the care of the athletes. It truly takes a village to provide top-notch medical care to a football team.
Am J Orthop. 2016;45(6):338. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Editor’s Note: AJO Deputy Editor-in-Chief Robin West, MD, is the Head Team Physician for the Washington Redskins and the Washington Nationals. She has previously served as a team physician for 2 Super Bowl-winning Pittsburgh Steelers teams. I am pleased to “hand off” this issue to her.
—Bryan T. Hanypsiak, MD
The summer is over, football season has begun, and team physicians are busy trying to manage and treat the plethora of injuries that come with the game. Football is one of the most popular sports played by young athletes. Youth participation (ages 6-14 years) in tackle football was 2.169 million in 2015, according to a study conducted by the Physical Activity Council and presented by USA Football. There were 1.084 million boys (and 1500 girls) playing high school football in the 2014-2015 season, nearly twice the number of the next most popular sport, track and field, according to the National Federation of State High School Associations.Due to the sheer volume of athletes and high-impact nature of the game, football leads all other sports in the number of sustained injuries.
Team physicians have the leadership role in the organization, management, and provision of care of the athletes on the team. The roles and responsibilities of the team physician are ever-evolving. The team physician has to meet certain medical qualifications and education requirements, and understand the ethical and medicolegal issues.
The American Academy of Orthopaedic Surgeons and several other medical associations have put together a Team Physician Consensus Statement (available at http://bit.ly/2b8rOzS). All team physicians, coaches, and athletic trainers should read and understand this statement, as it delineates the qualifications, duties, and responsibilities of the team physician.
Our Football Issue focuses on the most common injuries that the team physician will encounter during the season. Our goal is to create a comprehensive guide for the team physician on the acute management of these injuries. As team physicians, we have to make quick return-to-play decisions that are often difficult, as we are dealing with extremely competitive athletes and coaches in the heat of the moment. Since we can’t control the high levels of adrenalin, loud stadium, or rapid speed of the game, we need to be prepared to perform a comprehensive evaluation and diagnosis under these circumstances. This return-to-play decision should be based solely on the severity of the injury and safety of the player. As a team physician, you are responsible for making the “final call” on when the player is safe to return to the game.
This issue includes a section on the most common medical issues (ophthalmology, dental, and dermatology), concussion, exertional heat stroke, knee injuries, and foot and ankle injuries. We also have a special list of the most common items to include in the athletic trainer’s medical bag when covering a high school or collegiate football game (see page 376). Our prominent contributing authors all have extensive experience covering high school, collegiate, and professional teams.
I hope that our Football Issue helps you to keep your athletes safe and injury-free, which is necessary to have a successful season. Remember, as the team physician, your primary focus is the well being of the players. The success of the team only comes when the players are healthy. A cohesive, well-organized medical team, led by the head athletic trainer and team physician, is a key component to the care of the athletes. It truly takes a village to provide top-notch medical care to a football team.
Am J Orthop. 2016;45(6):338. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Editor’s Note: AJO Deputy Editor-in-Chief Robin West, MD, is the Head Team Physician for the Washington Redskins and the Washington Nationals. She has previously served as a team physician for 2 Super Bowl-winning Pittsburgh Steelers teams. I am pleased to “hand off” this issue to her.
—Bryan T. Hanypsiak, MD
The summer is over, football season has begun, and team physicians are busy trying to manage and treat the plethora of injuries that come with the game. Football is one of the most popular sports played by young athletes. Youth participation (ages 6-14 years) in tackle football was 2.169 million in 2015, according to a study conducted by the Physical Activity Council and presented by USA Football. There were 1.084 million boys (and 1500 girls) playing high school football in the 2014-2015 season, nearly twice the number of the next most popular sport, track and field, according to the National Federation of State High School Associations.Due to the sheer volume of athletes and high-impact nature of the game, football leads all other sports in the number of sustained injuries.
Team physicians have the leadership role in the organization, management, and provision of care of the athletes on the team. The roles and responsibilities of the team physician are ever-evolving. The team physician has to meet certain medical qualifications and education requirements, and understand the ethical and medicolegal issues.
The American Academy of Orthopaedic Surgeons and several other medical associations have put together a Team Physician Consensus Statement (available at http://bit.ly/2b8rOzS). All team physicians, coaches, and athletic trainers should read and understand this statement, as it delineates the qualifications, duties, and responsibilities of the team physician.
Our Football Issue focuses on the most common injuries that the team physician will encounter during the season. Our goal is to create a comprehensive guide for the team physician on the acute management of these injuries. As team physicians, we have to make quick return-to-play decisions that are often difficult, as we are dealing with extremely competitive athletes and coaches in the heat of the moment. Since we can’t control the high levels of adrenalin, loud stadium, or rapid speed of the game, we need to be prepared to perform a comprehensive evaluation and diagnosis under these circumstances. This return-to-play decision should be based solely on the severity of the injury and safety of the player. As a team physician, you are responsible for making the “final call” on when the player is safe to return to the game.
This issue includes a section on the most common medical issues (ophthalmology, dental, and dermatology), concussion, exertional heat stroke, knee injuries, and foot and ankle injuries. We also have a special list of the most common items to include in the athletic trainer’s medical bag when covering a high school or collegiate football game (see page 376). Our prominent contributing authors all have extensive experience covering high school, collegiate, and professional teams.
I hope that our Football Issue helps you to keep your athletes safe and injury-free, which is necessary to have a successful season. Remember, as the team physician, your primary focus is the well being of the players. The success of the team only comes when the players are healthy. A cohesive, well-organized medical team, led by the head athletic trainer and team physician, is a key component to the care of the athletes. It truly takes a village to provide top-notch medical care to a football team.
Am J Orthop. 2016;45(6):338. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
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).
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.
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.
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).
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).
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.
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.
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.
Setting Up Your New Physician for Success
Practices and hospitals invest significant time and money in recruiting a new physician. From phone interviews to site visits to contract negotiations, it’s a long and involved process.
Beyond setting up a new physician’s office and appointment schedule, completing human resources paperwork, and ordering business cards, what does your practice do to support new physicians to ensure they are successful? Although a new colleague may arrive with excellent clinical skills, even the most promising surgeon can fall short if not provided with the right expectations, training, and collegial support. Here’s how to fast track your new physician to professional heights.
Credentialing Is Key
At the crux of a new physician’s success is credentialing him or her with hospitals and insurance plans before the official start date to see patients.
“A state medical license is the first domino,” says orthopedic surgeon Michael R. Marks, MD, MBA, consultant and coding educator with KarenZupko & Associates, Inc. Marks has led or participated in physician recruitment in orthopedic and multispecialty groups. The firm has developed a comprehensive New Physician Onboarding Checklist, available at https://www.karenzupko.com/new-physician-onboarding-checklist/.
“Without a medical license,” Marks continues, “you can’t get the new physician hospital privileges and you can’t get him or her credentialed with plans. Without being credentialed, the physician can’t bill for patients treated.” Because commercial carriers won’t allow retrospective billing for services already rendered, “even a 3-month delay in credentialing could cost an orthopedic practice $60,000 to $180,000 in lost revenue.”
And if you think you can bill the new physician’s services under another partner’s name, you are incorrect. “The billing physician will have signed the note, but not have treated the patient,” warns Marks. “This is improper billing. Don’t do it.”
The remedy for ensuring that the new physician is credentialed is simple: get organized and plan ahead.
“When I first started participating in recruitment, I remember telling physicians, ‘I need you tomorrow!’” admits Amon T. Ferry, MD, a practicing orthopedist who leads recruitment efforts at IMS Orthopedics, a division of Integrated Medical Specialists in Phoenix, Arizona. “So they’d get hired before the practice was prepared and before credentialing was completed. Now, I set more realistic expectations,” he says, noting that in Arizona it takes 3 months to get a medical license, 6 months to contract with the hospital, and 9 months to get on insurance plans. And even after a plan has credentialed a new physician, “sometimes it still takes 4 to 6 weeks before the physician’s data is loaded into the plan’s computer systems.”
“The way to do credentialing right is to get all departments communicating,” Marks says. “If you keep everyone siloed, staff don’t understand that a lack of timeliness on their part impacts other areas of the practice.”
Ferry agrees, and says his group learned to organize its multiple departments after making mistakes and missing deadlines. “We now have an 8-page pre-employment application for new physicians,” he explains. “In addition to asking for contact information and everything we need to know in order to get the physician credentialed, we ask questions about malpractice suit history and whether there are issues with the medical board. We also ask about gaps in employment and details about where the physician has practiced in the past.” All of this is done to identify early whether credentialing will require more time and effort. Ferry says that the application has solved a number of processing problems the practice had in the past.
And whether credentialing is done within the practice or outsourced, Ferry says that it pays to be persistent. “Don’t sit back and assume it will get done. Even if you have outsourced credentialing to a company, someone must check with payers and hospitals weekly and provide the practice a status update.”
In one case, when getting a new physician contracted at a hospital was taking forever, Ferry directed the staff to call. “Turns out, they had been trying to reach us and had the wrong phone number,” he says. “When people are processing thousands of physician renewals, things get lost. You have to be proactive and be your own advocate. Don’t be afraid to be the squeaky wheel.”
Staff Relationships and Operational Wisdom
Marks points out that in many practices, the new physician is shown the examination rooms and his or her office, gets electronic health record (EHR) training, and that’s it. To be successful, Marks insists that the new physician must build relationships with personnel and understand operational basics. “In other business industries, successful leaders understand at least the basics of what everyone does. Part of how they do this is by getting to know the employees.”
Ideally, Marks advises that new physicians spend time with each staff member. “The best time to do this is in the first few weeks of employment,” he suggests. “Odds are, the new orthopedist doesn’t have 40 patients a day on the schedule. So schedule conversations within the first few weeks or month, and schedule observation time as well. When a patient complains about check-in, the physician will have an understanding of how things work up there if he or she knows the basic processes.” The new doctor should also spend time in the billing office getting to know the challenges faced by staff, and sit with the surgery coordinator to understand the process of getting cases booked and scheduled.
Plan for an initial and then periodic meetings with the practice administrator and other supervisors. Transparency about business operations, data, and strategy will help the new physician get up to speed faster.
“The executive director of our group was an absolutely invaluable information resource,” says Kathryn J. McCarthy, MD, an orthopedic spine surgeon with Arkansas Specialty Orthopaedics in Little Rock, Arkansas. McCarthy has been with the group for 3 years.
The practice’s executive director developed and presented a PowerPoint (Microsoft) explaining general business procedures, expectations for the coding and billing process, and pertinent compliance and risk issues. She had also developed an interactive model of the compensation formula and buy-in program, using Excel (Microsoft). McCarthy met with the executive director at 3 months, 6 months, and 9 months to review her patient and case volumes and how they were trending against the estimates made about her income, bonus, and buy-in status.
From the new physician’s perspective, McCarthy says having the new physician understand the complexities of certain business systems helps them understand things better. “If you sit in the business meetings long enough, you figure it out,” she says, “but it would have made some of the growing pains less painful if I understood what my overhead charge was going to, or more about the workflow of the clinic.” She adds that an overview of hospital relationships and any overlapping ownership interests will benefit new physicians as well.
“I think it’s useful to provide new physicians with a history of the practice and the vision of where things are going,” McCarthy says. “It’s important to outline the business vision, especially for subspecialties. If you explain to the new physician where you want to grow and when the practice plans on bringing on the next physician, it could really drive someone to grow their practice.”
Don’t Underestimate the Need for Coding Training
“When fellows come out of training, they are comfortable with clinical activity but uncomfortable with business administration,” Marks says. “And we know they don’t get training on coding and billing.”
Marks cites a recent conversation at an American Academy of Orthopaedic Surgeons (AAOS) coding workshop. “A surgeon new in practice told me, ‘I’ve been in practice for 4 months. I understand the clinical side but nobody educated me about coding and billing before this course.’” Practices must provide new physicians with coding and documentation training, and coach them to make sure they feel up to speed and comfortable. “The practice’s future revenue depends on it,” Marks says.
McCarthy agrees. “Having an administrative mentorship for coding is incredibly valuable. They don’t teach it in school.”
So from a practical standpoint, purchase AAOS’ Orthopaedic Code-X, a software tool that will help the new physician navigate and integrate Current Procedural Terminology (CPT), ICD-10 (International Classification of Diseases, Tenth Revision), and other coding data easily and accurately. Send him or her to one of the Academy’s regional coding and reimbursement workshops as well. “It will behoove the practice to send them even before they start seeing patients,” Marks says.
And don’t just stop there. High-performing groups conduct peer reviews of evaluation and management (E/M) and operative notes, blinding the codes billed and discussing which CPT and ICD-10 codes are appropriate for the visit or case. “It will take time for the new physician to completely integrate coding with their clinical care,” says Marks. “Peer review sessions, as well as having a partner review codes before they go to the billing office, can help speed learning.”
Collegial Coaching Counts
The week before her official start day, Mc-Carthy scrubbed in as a first assist with each of her new partners. “It was a great way to start ramping up,” she says. “I could see what kind of equipment was present in the hospitals, and got a touch point for hospital logistics. Plus, as a young surgeon it’s great to see how your skill sets match up with your new partners, and which best practices are being deployed by the group.”
This kind of “collegial coaching” is a vital part of the clinical and cultural integration to the practice. Beyond providing clinical support, it builds relationships and trust among the group, and fosters collaboration.
Arkansas Specialty Orthopaedics organized McCarthy’s clinic and operating room (OR) schedules so that a partner was always present. “There was also someone I could bounce ideas off of,” McCarthy explains. “Every day in the OR, there was a partner there at the same time. If I got into a sticky situation, one of my colleagues was willing to come in and scrub in the OR.”
McCarthy says that patients responded favorably when she told them her plan was developed in conjunction with her partners. “Patients find comfort in knowing that several people’s opinions were considered,” she says. “And as a young surgeon, knowing that you have backup, even if you don’t use it, when caring for high-risk and complex cases really means a lot,” she says.
And although her group didn’t offer a formal mentoring program, McCarthy found that an informal mentorship grew organically when a friendship developed with one of her new partners. “In the first 6 months, every single weekend we sat by the pool and rolled through a ton of cases,” she says. “That was fabulous and it alleviated so much stress for me.” And when it was time for McCarthy to move into board case selection, this colleague and another were instrumental in her board preparation because, “they knew my style and where I would need to focus.”
IMS Orthopedics’ approach is to provide the staff and systems that allow new physicians to step up and take responsibility. “If they want to scrub in with me, that’s great. If they’d like to visit additional facilities and get the lay of the land, we encourage it. But we don’t do a lot of handholding. We set them up for success and make sure people are in place to help them,” says Ferry.
A Marketing Plan Is a Must
“The vast majority of practices do very little when it comes to thinking about how to market and build the practice of their new physician,” Marks says. “Practice-building is more of a challenge for surgical specialists today than it was in the old days when new surgeons could easily meet internists as they were rounding at the hospital. Now, a new physician and the practice must come up with a game plan.”
That game plan starts with the easy things: order business cards, schedule a photo shoot, and update the practice’s Web site pages with the physician’s biography and an introductory video. But with social media, online reviews, and subspecialty competition, Marks says practices must think beyond the basics. Think through each element of marketing, from online to outreach to developing referral relationships.
“I tell practices to draft a written marketing plan,” he says. “Not only does it provide a roadmap for the new physician, but also indicates that the practice has put some thought into how he or she can build a practice. It can make the new physician feel less overwhelmed knowing that he or she doesn’t have to do the marketing alone.” Once you’ve developed a list of actions, Marks suggests creating a spreadsheet with deadlines, and ensuring each action is completed.
McCarthy was scheduled to visit family practice clinics, and joined by the administrator who “handed out cookies and cards while I talked,” she says. Arkansas Specialty Orthopaedics also hired an external marketing firm to develop promotional opportunities for her. For example, “I was scheduled to appear on news channels, where I discussed new and interesting procedures,” she says. “It got my name out into the community.”
If your practice is too small to hire an outside firm, Marks suggests reaching out to agencies such as nursing homes, fitness centers, or the YMCA, which frequently offers educational programs for members. “Contact the administrators or medical directors in these organizations. A few minutes on the phone or a short visit can go a long way to building these relationships and getting your new physician on the map.”
As the old saying goes, an ounce of prevention is worth a pound of cure. Scheduling time for orientation, training, staff integration, and collegial coaching will speed up a new physician’s integration into the practice, and increase his or her opportunity for success.
Practices and hospitals invest significant time and money in recruiting a new physician. From phone interviews to site visits to contract negotiations, it’s a long and involved process.
Beyond setting up a new physician’s office and appointment schedule, completing human resources paperwork, and ordering business cards, what does your practice do to support new physicians to ensure they are successful? Although a new colleague may arrive with excellent clinical skills, even the most promising surgeon can fall short if not provided with the right expectations, training, and collegial support. Here’s how to fast track your new physician to professional heights.
Credentialing Is Key
At the crux of a new physician’s success is credentialing him or her with hospitals and insurance plans before the official start date to see patients.
“A state medical license is the first domino,” says orthopedic surgeon Michael R. Marks, MD, MBA, consultant and coding educator with KarenZupko & Associates, Inc. Marks has led or participated in physician recruitment in orthopedic and multispecialty groups. The firm has developed a comprehensive New Physician Onboarding Checklist, available at https://www.karenzupko.com/new-physician-onboarding-checklist/.
“Without a medical license,” Marks continues, “you can’t get the new physician hospital privileges and you can’t get him or her credentialed with plans. Without being credentialed, the physician can’t bill for patients treated.” Because commercial carriers won’t allow retrospective billing for services already rendered, “even a 3-month delay in credentialing could cost an orthopedic practice $60,000 to $180,000 in lost revenue.”
And if you think you can bill the new physician’s services under another partner’s name, you are incorrect. “The billing physician will have signed the note, but not have treated the patient,” warns Marks. “This is improper billing. Don’t do it.”
The remedy for ensuring that the new physician is credentialed is simple: get organized and plan ahead.
“When I first started participating in recruitment, I remember telling physicians, ‘I need you tomorrow!’” admits Amon T. Ferry, MD, a practicing orthopedist who leads recruitment efforts at IMS Orthopedics, a division of Integrated Medical Specialists in Phoenix, Arizona. “So they’d get hired before the practice was prepared and before credentialing was completed. Now, I set more realistic expectations,” he says, noting that in Arizona it takes 3 months to get a medical license, 6 months to contract with the hospital, and 9 months to get on insurance plans. And even after a plan has credentialed a new physician, “sometimes it still takes 4 to 6 weeks before the physician’s data is loaded into the plan’s computer systems.”
“The way to do credentialing right is to get all departments communicating,” Marks says. “If you keep everyone siloed, staff don’t understand that a lack of timeliness on their part impacts other areas of the practice.”
Ferry agrees, and says his group learned to organize its multiple departments after making mistakes and missing deadlines. “We now have an 8-page pre-employment application for new physicians,” he explains. “In addition to asking for contact information and everything we need to know in order to get the physician credentialed, we ask questions about malpractice suit history and whether there are issues with the medical board. We also ask about gaps in employment and details about where the physician has practiced in the past.” All of this is done to identify early whether credentialing will require more time and effort. Ferry says that the application has solved a number of processing problems the practice had in the past.
And whether credentialing is done within the practice or outsourced, Ferry says that it pays to be persistent. “Don’t sit back and assume it will get done. Even if you have outsourced credentialing to a company, someone must check with payers and hospitals weekly and provide the practice a status update.”
In one case, when getting a new physician contracted at a hospital was taking forever, Ferry directed the staff to call. “Turns out, they had been trying to reach us and had the wrong phone number,” he says. “When people are processing thousands of physician renewals, things get lost. You have to be proactive and be your own advocate. Don’t be afraid to be the squeaky wheel.”
Staff Relationships and Operational Wisdom
Marks points out that in many practices, the new physician is shown the examination rooms and his or her office, gets electronic health record (EHR) training, and that’s it. To be successful, Marks insists that the new physician must build relationships with personnel and understand operational basics. “In other business industries, successful leaders understand at least the basics of what everyone does. Part of how they do this is by getting to know the employees.”
Ideally, Marks advises that new physicians spend time with each staff member. “The best time to do this is in the first few weeks of employment,” he suggests. “Odds are, the new orthopedist doesn’t have 40 patients a day on the schedule. So schedule conversations within the first few weeks or month, and schedule observation time as well. When a patient complains about check-in, the physician will have an understanding of how things work up there if he or she knows the basic processes.” The new doctor should also spend time in the billing office getting to know the challenges faced by staff, and sit with the surgery coordinator to understand the process of getting cases booked and scheduled.
Plan for an initial and then periodic meetings with the practice administrator and other supervisors. Transparency about business operations, data, and strategy will help the new physician get up to speed faster.
“The executive director of our group was an absolutely invaluable information resource,” says Kathryn J. McCarthy, MD, an orthopedic spine surgeon with Arkansas Specialty Orthopaedics in Little Rock, Arkansas. McCarthy has been with the group for 3 years.
The practice’s executive director developed and presented a PowerPoint (Microsoft) explaining general business procedures, expectations for the coding and billing process, and pertinent compliance and risk issues. She had also developed an interactive model of the compensation formula and buy-in program, using Excel (Microsoft). McCarthy met with the executive director at 3 months, 6 months, and 9 months to review her patient and case volumes and how they were trending against the estimates made about her income, bonus, and buy-in status.
From the new physician’s perspective, McCarthy says having the new physician understand the complexities of certain business systems helps them understand things better. “If you sit in the business meetings long enough, you figure it out,” she says, “but it would have made some of the growing pains less painful if I understood what my overhead charge was going to, or more about the workflow of the clinic.” She adds that an overview of hospital relationships and any overlapping ownership interests will benefit new physicians as well.
“I think it’s useful to provide new physicians with a history of the practice and the vision of where things are going,” McCarthy says. “It’s important to outline the business vision, especially for subspecialties. If you explain to the new physician where you want to grow and when the practice plans on bringing on the next physician, it could really drive someone to grow their practice.”
Don’t Underestimate the Need for Coding Training
“When fellows come out of training, they are comfortable with clinical activity but uncomfortable with business administration,” Marks says. “And we know they don’t get training on coding and billing.”
Marks cites a recent conversation at an American Academy of Orthopaedic Surgeons (AAOS) coding workshop. “A surgeon new in practice told me, ‘I’ve been in practice for 4 months. I understand the clinical side but nobody educated me about coding and billing before this course.’” Practices must provide new physicians with coding and documentation training, and coach them to make sure they feel up to speed and comfortable. “The practice’s future revenue depends on it,” Marks says.
McCarthy agrees. “Having an administrative mentorship for coding is incredibly valuable. They don’t teach it in school.”
So from a practical standpoint, purchase AAOS’ Orthopaedic Code-X, a software tool that will help the new physician navigate and integrate Current Procedural Terminology (CPT), ICD-10 (International Classification of Diseases, Tenth Revision), and other coding data easily and accurately. Send him or her to one of the Academy’s regional coding and reimbursement workshops as well. “It will behoove the practice to send them even before they start seeing patients,” Marks says.
And don’t just stop there. High-performing groups conduct peer reviews of evaluation and management (E/M) and operative notes, blinding the codes billed and discussing which CPT and ICD-10 codes are appropriate for the visit or case. “It will take time for the new physician to completely integrate coding with their clinical care,” says Marks. “Peer review sessions, as well as having a partner review codes before they go to the billing office, can help speed learning.”
Collegial Coaching Counts
The week before her official start day, Mc-Carthy scrubbed in as a first assist with each of her new partners. “It was a great way to start ramping up,” she says. “I could see what kind of equipment was present in the hospitals, and got a touch point for hospital logistics. Plus, as a young surgeon it’s great to see how your skill sets match up with your new partners, and which best practices are being deployed by the group.”
This kind of “collegial coaching” is a vital part of the clinical and cultural integration to the practice. Beyond providing clinical support, it builds relationships and trust among the group, and fosters collaboration.
Arkansas Specialty Orthopaedics organized McCarthy’s clinic and operating room (OR) schedules so that a partner was always present. “There was also someone I could bounce ideas off of,” McCarthy explains. “Every day in the OR, there was a partner there at the same time. If I got into a sticky situation, one of my colleagues was willing to come in and scrub in the OR.”
McCarthy says that patients responded favorably when she told them her plan was developed in conjunction with her partners. “Patients find comfort in knowing that several people’s opinions were considered,” she says. “And as a young surgeon, knowing that you have backup, even if you don’t use it, when caring for high-risk and complex cases really means a lot,” she says.
And although her group didn’t offer a formal mentoring program, McCarthy found that an informal mentorship grew organically when a friendship developed with one of her new partners. “In the first 6 months, every single weekend we sat by the pool and rolled through a ton of cases,” she says. “That was fabulous and it alleviated so much stress for me.” And when it was time for McCarthy to move into board case selection, this colleague and another were instrumental in her board preparation because, “they knew my style and where I would need to focus.”
IMS Orthopedics’ approach is to provide the staff and systems that allow new physicians to step up and take responsibility. “If they want to scrub in with me, that’s great. If they’d like to visit additional facilities and get the lay of the land, we encourage it. But we don’t do a lot of handholding. We set them up for success and make sure people are in place to help them,” says Ferry.
A Marketing Plan Is a Must
“The vast majority of practices do very little when it comes to thinking about how to market and build the practice of their new physician,” Marks says. “Practice-building is more of a challenge for surgical specialists today than it was in the old days when new surgeons could easily meet internists as they were rounding at the hospital. Now, a new physician and the practice must come up with a game plan.”
That game plan starts with the easy things: order business cards, schedule a photo shoot, and update the practice’s Web site pages with the physician’s biography and an introductory video. But with social media, online reviews, and subspecialty competition, Marks says practices must think beyond the basics. Think through each element of marketing, from online to outreach to developing referral relationships.
“I tell practices to draft a written marketing plan,” he says. “Not only does it provide a roadmap for the new physician, but also indicates that the practice has put some thought into how he or she can build a practice. It can make the new physician feel less overwhelmed knowing that he or she doesn’t have to do the marketing alone.” Once you’ve developed a list of actions, Marks suggests creating a spreadsheet with deadlines, and ensuring each action is completed.
McCarthy was scheduled to visit family practice clinics, and joined by the administrator who “handed out cookies and cards while I talked,” she says. Arkansas Specialty Orthopaedics also hired an external marketing firm to develop promotional opportunities for her. For example, “I was scheduled to appear on news channels, where I discussed new and interesting procedures,” she says. “It got my name out into the community.”
If your practice is too small to hire an outside firm, Marks suggests reaching out to agencies such as nursing homes, fitness centers, or the YMCA, which frequently offers educational programs for members. “Contact the administrators or medical directors in these organizations. A few minutes on the phone or a short visit can go a long way to building these relationships and getting your new physician on the map.”
As the old saying goes, an ounce of prevention is worth a pound of cure. Scheduling time for orientation, training, staff integration, and collegial coaching will speed up a new physician’s integration into the practice, and increase his or her opportunity for success.
Practices and hospitals invest significant time and money in recruiting a new physician. From phone interviews to site visits to contract negotiations, it’s a long and involved process.
Beyond setting up a new physician’s office and appointment schedule, completing human resources paperwork, and ordering business cards, what does your practice do to support new physicians to ensure they are successful? Although a new colleague may arrive with excellent clinical skills, even the most promising surgeon can fall short if not provided with the right expectations, training, and collegial support. Here’s how to fast track your new physician to professional heights.
Credentialing Is Key
At the crux of a new physician’s success is credentialing him or her with hospitals and insurance plans before the official start date to see patients.
“A state medical license is the first domino,” says orthopedic surgeon Michael R. Marks, MD, MBA, consultant and coding educator with KarenZupko & Associates, Inc. Marks has led or participated in physician recruitment in orthopedic and multispecialty groups. The firm has developed a comprehensive New Physician Onboarding Checklist, available at https://www.karenzupko.com/new-physician-onboarding-checklist/.
“Without a medical license,” Marks continues, “you can’t get the new physician hospital privileges and you can’t get him or her credentialed with plans. Without being credentialed, the physician can’t bill for patients treated.” Because commercial carriers won’t allow retrospective billing for services already rendered, “even a 3-month delay in credentialing could cost an orthopedic practice $60,000 to $180,000 in lost revenue.”
And if you think you can bill the new physician’s services under another partner’s name, you are incorrect. “The billing physician will have signed the note, but not have treated the patient,” warns Marks. “This is improper billing. Don’t do it.”
The remedy for ensuring that the new physician is credentialed is simple: get organized and plan ahead.
“When I first started participating in recruitment, I remember telling physicians, ‘I need you tomorrow!’” admits Amon T. Ferry, MD, a practicing orthopedist who leads recruitment efforts at IMS Orthopedics, a division of Integrated Medical Specialists in Phoenix, Arizona. “So they’d get hired before the practice was prepared and before credentialing was completed. Now, I set more realistic expectations,” he says, noting that in Arizona it takes 3 months to get a medical license, 6 months to contract with the hospital, and 9 months to get on insurance plans. And even after a plan has credentialed a new physician, “sometimes it still takes 4 to 6 weeks before the physician’s data is loaded into the plan’s computer systems.”
“The way to do credentialing right is to get all departments communicating,” Marks says. “If you keep everyone siloed, staff don’t understand that a lack of timeliness on their part impacts other areas of the practice.”
Ferry agrees, and says his group learned to organize its multiple departments after making mistakes and missing deadlines. “We now have an 8-page pre-employment application for new physicians,” he explains. “In addition to asking for contact information and everything we need to know in order to get the physician credentialed, we ask questions about malpractice suit history and whether there are issues with the medical board. We also ask about gaps in employment and details about where the physician has practiced in the past.” All of this is done to identify early whether credentialing will require more time and effort. Ferry says that the application has solved a number of processing problems the practice had in the past.
And whether credentialing is done within the practice or outsourced, Ferry says that it pays to be persistent. “Don’t sit back and assume it will get done. Even if you have outsourced credentialing to a company, someone must check with payers and hospitals weekly and provide the practice a status update.”
In one case, when getting a new physician contracted at a hospital was taking forever, Ferry directed the staff to call. “Turns out, they had been trying to reach us and had the wrong phone number,” he says. “When people are processing thousands of physician renewals, things get lost. You have to be proactive and be your own advocate. Don’t be afraid to be the squeaky wheel.”
Staff Relationships and Operational Wisdom
Marks points out that in many practices, the new physician is shown the examination rooms and his or her office, gets electronic health record (EHR) training, and that’s it. To be successful, Marks insists that the new physician must build relationships with personnel and understand operational basics. “In other business industries, successful leaders understand at least the basics of what everyone does. Part of how they do this is by getting to know the employees.”
Ideally, Marks advises that new physicians spend time with each staff member. “The best time to do this is in the first few weeks of employment,” he suggests. “Odds are, the new orthopedist doesn’t have 40 patients a day on the schedule. So schedule conversations within the first few weeks or month, and schedule observation time as well. When a patient complains about check-in, the physician will have an understanding of how things work up there if he or she knows the basic processes.” The new doctor should also spend time in the billing office getting to know the challenges faced by staff, and sit with the surgery coordinator to understand the process of getting cases booked and scheduled.
Plan for an initial and then periodic meetings with the practice administrator and other supervisors. Transparency about business operations, data, and strategy will help the new physician get up to speed faster.
“The executive director of our group was an absolutely invaluable information resource,” says Kathryn J. McCarthy, MD, an orthopedic spine surgeon with Arkansas Specialty Orthopaedics in Little Rock, Arkansas. McCarthy has been with the group for 3 years.
The practice’s executive director developed and presented a PowerPoint (Microsoft) explaining general business procedures, expectations for the coding and billing process, and pertinent compliance and risk issues. She had also developed an interactive model of the compensation formula and buy-in program, using Excel (Microsoft). McCarthy met with the executive director at 3 months, 6 months, and 9 months to review her patient and case volumes and how they were trending against the estimates made about her income, bonus, and buy-in status.
From the new physician’s perspective, McCarthy says having the new physician understand the complexities of certain business systems helps them understand things better. “If you sit in the business meetings long enough, you figure it out,” she says, “but it would have made some of the growing pains less painful if I understood what my overhead charge was going to, or more about the workflow of the clinic.” She adds that an overview of hospital relationships and any overlapping ownership interests will benefit new physicians as well.
“I think it’s useful to provide new physicians with a history of the practice and the vision of where things are going,” McCarthy says. “It’s important to outline the business vision, especially for subspecialties. If you explain to the new physician where you want to grow and when the practice plans on bringing on the next physician, it could really drive someone to grow their practice.”
Don’t Underestimate the Need for Coding Training
“When fellows come out of training, they are comfortable with clinical activity but uncomfortable with business administration,” Marks says. “And we know they don’t get training on coding and billing.”
Marks cites a recent conversation at an American Academy of Orthopaedic Surgeons (AAOS) coding workshop. “A surgeon new in practice told me, ‘I’ve been in practice for 4 months. I understand the clinical side but nobody educated me about coding and billing before this course.’” Practices must provide new physicians with coding and documentation training, and coach them to make sure they feel up to speed and comfortable. “The practice’s future revenue depends on it,” Marks says.
McCarthy agrees. “Having an administrative mentorship for coding is incredibly valuable. They don’t teach it in school.”
So from a practical standpoint, purchase AAOS’ Orthopaedic Code-X, a software tool that will help the new physician navigate and integrate Current Procedural Terminology (CPT), ICD-10 (International Classification of Diseases, Tenth Revision), and other coding data easily and accurately. Send him or her to one of the Academy’s regional coding and reimbursement workshops as well. “It will behoove the practice to send them even before they start seeing patients,” Marks says.
And don’t just stop there. High-performing groups conduct peer reviews of evaluation and management (E/M) and operative notes, blinding the codes billed and discussing which CPT and ICD-10 codes are appropriate for the visit or case. “It will take time for the new physician to completely integrate coding with their clinical care,” says Marks. “Peer review sessions, as well as having a partner review codes before they go to the billing office, can help speed learning.”
Collegial Coaching Counts
The week before her official start day, Mc-Carthy scrubbed in as a first assist with each of her new partners. “It was a great way to start ramping up,” she says. “I could see what kind of equipment was present in the hospitals, and got a touch point for hospital logistics. Plus, as a young surgeon it’s great to see how your skill sets match up with your new partners, and which best practices are being deployed by the group.”
This kind of “collegial coaching” is a vital part of the clinical and cultural integration to the practice. Beyond providing clinical support, it builds relationships and trust among the group, and fosters collaboration.
Arkansas Specialty Orthopaedics organized McCarthy’s clinic and operating room (OR) schedules so that a partner was always present. “There was also someone I could bounce ideas off of,” McCarthy explains. “Every day in the OR, there was a partner there at the same time. If I got into a sticky situation, one of my colleagues was willing to come in and scrub in the OR.”
McCarthy says that patients responded favorably when she told them her plan was developed in conjunction with her partners. “Patients find comfort in knowing that several people’s opinions were considered,” she says. “And as a young surgeon, knowing that you have backup, even if you don’t use it, when caring for high-risk and complex cases really means a lot,” she says.
And although her group didn’t offer a formal mentoring program, McCarthy found that an informal mentorship grew organically when a friendship developed with one of her new partners. “In the first 6 months, every single weekend we sat by the pool and rolled through a ton of cases,” she says. “That was fabulous and it alleviated so much stress for me.” And when it was time for McCarthy to move into board case selection, this colleague and another were instrumental in her board preparation because, “they knew my style and where I would need to focus.”
IMS Orthopedics’ approach is to provide the staff and systems that allow new physicians to step up and take responsibility. “If they want to scrub in with me, that’s great. If they’d like to visit additional facilities and get the lay of the land, we encourage it. But we don’t do a lot of handholding. We set them up for success and make sure people are in place to help them,” says Ferry.
A Marketing Plan Is a Must
“The vast majority of practices do very little when it comes to thinking about how to market and build the practice of their new physician,” Marks says. “Practice-building is more of a challenge for surgical specialists today than it was in the old days when new surgeons could easily meet internists as they were rounding at the hospital. Now, a new physician and the practice must come up with a game plan.”
That game plan starts with the easy things: order business cards, schedule a photo shoot, and update the practice’s Web site pages with the physician’s biography and an introductory video. But with social media, online reviews, and subspecialty competition, Marks says practices must think beyond the basics. Think through each element of marketing, from online to outreach to developing referral relationships.
“I tell practices to draft a written marketing plan,” he says. “Not only does it provide a roadmap for the new physician, but also indicates that the practice has put some thought into how he or she can build a practice. It can make the new physician feel less overwhelmed knowing that he or she doesn’t have to do the marketing alone.” Once you’ve developed a list of actions, Marks suggests creating a spreadsheet with deadlines, and ensuring each action is completed.
McCarthy was scheduled to visit family practice clinics, and joined by the administrator who “handed out cookies and cards while I talked,” she says. Arkansas Specialty Orthopaedics also hired an external marketing firm to develop promotional opportunities for her. For example, “I was scheduled to appear on news channels, where I discussed new and interesting procedures,” she says. “It got my name out into the community.”
If your practice is too small to hire an outside firm, Marks suggests reaching out to agencies such as nursing homes, fitness centers, or the YMCA, which frequently offers educational programs for members. “Contact the administrators or medical directors in these organizations. A few minutes on the phone or a short visit can go a long way to building these relationships and getting your new physician on the map.”
As the old saying goes, an ounce of prevention is worth a pound of cure. Scheduling time for orientation, training, staff integration, and collegial coaching will speed up a new physician’s integration into the practice, and increase his or her opportunity for success.
Surgical Pearls in Total Knee Arthroplasty: A Lifetime of Lessons Learned
After over 4 decades of experience with total knee arthroplasty (TKA), I have learned many lessons regarding surgical technique. These include exposure issues, alignment methods, bone preparation, correction of deformity, and implantation techniques. Most of these lessons have been self-taught, but some have been suggested by or modified from colleague and student interaction. Attribution is given when possible.
The Incision
The skin incision should be marked in flexion rather than extension because the skin moves approximately 1 cm laterally from extension to flexion.1 This occurs because the tibia internally rotates beneath the skin as the knee is flexed and externally rotates as full extension is achieved. This lateral movement of the skin could bring an incision marked in extension on top of the tibial tubercle when the knee is flexed and may result in pain and dysfunction when the patient attempts to kneel. A review of kneeling ability after TKA showed that most patients are hesitant to kneel initially after their arthroplasty, but gain confidence and improved comfort and ability as their scar matures.2
Exposure
Patellar eversion can be difficult in a markedly obese or ankylosed knee, especially when the patella is difficult to grasp. This is facilitated by the use of a standard patellar clamp that is normally used to compress the patella during component cementation (Figure 1).3
Exposing the Ankylosed Knee and Protecting the Patellar Tendon From Avulsion
A tibial tubercle osteotomy is often recommended in the ankylosed knee but can be avoided by making a short inverted “V” incision in the proximal quadriceps tendon (Figure 2).4
Protecting the Soft Tissues During Surgery
Moist wound towels sewn into the joint capsule protect the underlying soft tissues from debris and desiccation during the procedure and will intuitively lower the chance of wound infection from contamination and tissue injury (Figures 4A, 4B).
Locating and Coagulating the Lateral Inferior Genicular Vessels
The lateral inferior genicular artery and vein can be easily located and coagulated just outside the posterior rim of the lateral meniscus near the popliteus hiatus. This will minimize both intraoperative and postoperative blood loss.
Determining the Entry Point in the Distal Femur for Intramedullary Alignment Devices
Templating the femoral entry point for insertion of an intramedullary alignment device on a preoperative radiograph will help avoid inadvertent excessive distal femoral valgus resection. This is especially important in valgus knees that have a valgus metaphyseal bow (Figure 5).
Avoiding Notching of the Anterior Femoral Cortex
Notching the anterior femoral cortex when in-between femoral sizes or when there is a preexisting dysplastic or shallow trochlea (Figure 6)
Obtaining a Medial Release by Removing Peripheral Medial Tibial Bone
Varus deformities can be corrected without performing a formal medial collateral ligament (MCL) release by a so-called reduction tibial osteotomy.5,6 In mild varus deformity, sufficient medial release can be achieved by removing medial femoral and tibial peripheral osteophytes that tent up the MCL and medial capsule. When this is insufficient, removal of additional peripheral tibial bone further shortens the distance between the origin and insertion of the MCL, effectively lengthening the ligament (Figure 7).
An Inverted Cruciform Lateral Retinacular Release to Correct Severe Valgus Deformity
An inverted cruciform lateral retinacular release effectively corrects a severe valgus deformity and avoids the need for a lateral collateral ligament (LCL) release.7
Relieving Posterior Femoral Impingement
Uncapped posterior condylar bone or retained posterior osteophytes can limit both flexion and extension and cause impingement. Trimming the posterior femoral condyles and removing posterior osteophytes is best accomplished using a trial femoral component as a template.4 A curved osteotome is passed tangential to the metallic condyles to define the bone requiring resection. After removal of the trial, the outlined bone can be easily and accurately resected.
Minimizing Postoperative Posterior Condylar Bone-Cement Radiolucencies
Zone 4 femoral bone-cement radiolucencies8 can be minimized using the “smear” technique.4 These radiolucencies are common because most prosthetic femoral components have posterior condyles that are parallel to the femoral fixation lugs and do not allow for compression of this interface during implantation. Most surgeons put no cement on the posterior condylar bone but place it on the inside of the prosthetic condyle instead. The lack of compression upon insertion leads to a poor interface and the resultant lucencies. In the long term, these lucencies could allow access of wear debris to the posterior condylar bone, with the potential for osteolysis and loosening. To improve this interface, cement can be smeared or packed into the posterior condyles and also placed on the posterior condyles of the prosthesis. This could lead to posterior extrusion of some cement during polymerization, so a removable trial insert should be utilized to allow access posteriorly after polymerization is complete.
Predicting Potential Postoperative Flexion
The best indicator of potential postoperative flexion for any individual patient is not preoperative flexion but is intraoperative flexion against gravity measured after capsular closure.9 Surgeons should measure and record this value for reference if a patient has difficulty regaining flexion during their recovery (Figure 9).
Summary
The short- and long-term success of TKA is highly dependent on surgical technique that allows proper and safe exposure under all circumstances, correction of deformity, and accurate component implantation while minimizing intraoperative and postoperative complications. The surgical pearls shared above will hopefully aid in achieving these goals.
Am J Orthop. 2016;45(6):384-388. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Yacoubian SV, Scott RD. Skin incision translation in total knee arthroplasty: the difference between flexion and extension. J Arthroplasty. 2007;22(3):353-355.
2. Schai PA, Gibbon AJ, Scott RD. Kneeling ability after total knee arthroplasty. Perception and reality. Clin Orthop Relat Res. 1999;367:195-200.
3. Springorum HP, Scott RD. A technique to facilitate everting the patella in stiff or obese knees in total knee arthroplasty. Am J Orthop. 2009;38(10):507-508.
4. Scott RD. Total Knee Arthroplasty. 2nd ed. Philadelphia, PA: Elsevier; 2014.
5. Dixon MC, Parsch D, Brown RR, Scott RD. The correction of severe varus deformity in total knee arthroplasty by tibial component downsizing and resection of uncapped proximal medial bone. J Arthroplasty. 2004;19(1):19-22.
6. Mullaji AB, Padmanabhan V, Jindal G. Total knee arthroplasty for profound varus deformity: technique and radiological results in 173 knees with varus of more than 20 degrees. J Arthroplasty. 2005;20(5):550-561.
7. Politi J, Scott RD. Balancing severe valgus deformity in total knee arthroplasty using a lateral cruciform retinacular release. J Arthroplasty. 2004;19(5):553-557.
8. Huddleston JI, Wiley JW, Scott RD. Zone 4 femoral radiolucent lines in hybrid versus cemented total knee arthroplasties: are they clinically significant? Clin Orthop Relat Res. 2005;441:334-339.
9. Lee DC, Kim DH, Scott RD, Suthers K. Intraoperative flexion against gravity as an indication of ultimate range of motion in individual cases after total knee arthroplasty. J Arthroplasty. 1998;13(5):500-503.
After over 4 decades of experience with total knee arthroplasty (TKA), I have learned many lessons regarding surgical technique. These include exposure issues, alignment methods, bone preparation, correction of deformity, and implantation techniques. Most of these lessons have been self-taught, but some have been suggested by or modified from colleague and student interaction. Attribution is given when possible.
The Incision
The skin incision should be marked in flexion rather than extension because the skin moves approximately 1 cm laterally from extension to flexion.1 This occurs because the tibia internally rotates beneath the skin as the knee is flexed and externally rotates as full extension is achieved. This lateral movement of the skin could bring an incision marked in extension on top of the tibial tubercle when the knee is flexed and may result in pain and dysfunction when the patient attempts to kneel. A review of kneeling ability after TKA showed that most patients are hesitant to kneel initially after their arthroplasty, but gain confidence and improved comfort and ability as their scar matures.2
Exposure
Patellar eversion can be difficult in a markedly obese or ankylosed knee, especially when the patella is difficult to grasp. This is facilitated by the use of a standard patellar clamp that is normally used to compress the patella during component cementation (Figure 1).3
Exposing the Ankylosed Knee and Protecting the Patellar Tendon From Avulsion
A tibial tubercle osteotomy is often recommended in the ankylosed knee but can be avoided by making a short inverted “V” incision in the proximal quadriceps tendon (Figure 2).4
Protecting the Soft Tissues During Surgery
Moist wound towels sewn into the joint capsule protect the underlying soft tissues from debris and desiccation during the procedure and will intuitively lower the chance of wound infection from contamination and tissue injury (Figures 4A, 4B).
Locating and Coagulating the Lateral Inferior Genicular Vessels
The lateral inferior genicular artery and vein can be easily located and coagulated just outside the posterior rim of the lateral meniscus near the popliteus hiatus. This will minimize both intraoperative and postoperative blood loss.
Determining the Entry Point in the Distal Femur for Intramedullary Alignment Devices
Templating the femoral entry point for insertion of an intramedullary alignment device on a preoperative radiograph will help avoid inadvertent excessive distal femoral valgus resection. This is especially important in valgus knees that have a valgus metaphyseal bow (Figure 5).
Avoiding Notching of the Anterior Femoral Cortex
Notching the anterior femoral cortex when in-between femoral sizes or when there is a preexisting dysplastic or shallow trochlea (Figure 6)
Obtaining a Medial Release by Removing Peripheral Medial Tibial Bone
Varus deformities can be corrected without performing a formal medial collateral ligament (MCL) release by a so-called reduction tibial osteotomy.5,6 In mild varus deformity, sufficient medial release can be achieved by removing medial femoral and tibial peripheral osteophytes that tent up the MCL and medial capsule. When this is insufficient, removal of additional peripheral tibial bone further shortens the distance between the origin and insertion of the MCL, effectively lengthening the ligament (Figure 7).
An Inverted Cruciform Lateral Retinacular Release to Correct Severe Valgus Deformity
An inverted cruciform lateral retinacular release effectively corrects a severe valgus deformity and avoids the need for a lateral collateral ligament (LCL) release.7
Relieving Posterior Femoral Impingement
Uncapped posterior condylar bone or retained posterior osteophytes can limit both flexion and extension and cause impingement. Trimming the posterior femoral condyles and removing posterior osteophytes is best accomplished using a trial femoral component as a template.4 A curved osteotome is passed tangential to the metallic condyles to define the bone requiring resection. After removal of the trial, the outlined bone can be easily and accurately resected.
Minimizing Postoperative Posterior Condylar Bone-Cement Radiolucencies
Zone 4 femoral bone-cement radiolucencies8 can be minimized using the “smear” technique.4 These radiolucencies are common because most prosthetic femoral components have posterior condyles that are parallel to the femoral fixation lugs and do not allow for compression of this interface during implantation. Most surgeons put no cement on the posterior condylar bone but place it on the inside of the prosthetic condyle instead. The lack of compression upon insertion leads to a poor interface and the resultant lucencies. In the long term, these lucencies could allow access of wear debris to the posterior condylar bone, with the potential for osteolysis and loosening. To improve this interface, cement can be smeared or packed into the posterior condyles and also placed on the posterior condyles of the prosthesis. This could lead to posterior extrusion of some cement during polymerization, so a removable trial insert should be utilized to allow access posteriorly after polymerization is complete.
Predicting Potential Postoperative Flexion
The best indicator of potential postoperative flexion for any individual patient is not preoperative flexion but is intraoperative flexion against gravity measured after capsular closure.9 Surgeons should measure and record this value for reference if a patient has difficulty regaining flexion during their recovery (Figure 9).
Summary
The short- and long-term success of TKA is highly dependent on surgical technique that allows proper and safe exposure under all circumstances, correction of deformity, and accurate component implantation while minimizing intraoperative and postoperative complications. The surgical pearls shared above will hopefully aid in achieving these goals.
Am J Orthop. 2016;45(6):384-388. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
After over 4 decades of experience with total knee arthroplasty (TKA), I have learned many lessons regarding surgical technique. These include exposure issues, alignment methods, bone preparation, correction of deformity, and implantation techniques. Most of these lessons have been self-taught, but some have been suggested by or modified from colleague and student interaction. Attribution is given when possible.
The Incision
The skin incision should be marked in flexion rather than extension because the skin moves approximately 1 cm laterally from extension to flexion.1 This occurs because the tibia internally rotates beneath the skin as the knee is flexed and externally rotates as full extension is achieved. This lateral movement of the skin could bring an incision marked in extension on top of the tibial tubercle when the knee is flexed and may result in pain and dysfunction when the patient attempts to kneel. A review of kneeling ability after TKA showed that most patients are hesitant to kneel initially after their arthroplasty, but gain confidence and improved comfort and ability as their scar matures.2
Exposure
Patellar eversion can be difficult in a markedly obese or ankylosed knee, especially when the patella is difficult to grasp. This is facilitated by the use of a standard patellar clamp that is normally used to compress the patella during component cementation (Figure 1).3
Exposing the Ankylosed Knee and Protecting the Patellar Tendon From Avulsion
A tibial tubercle osteotomy is often recommended in the ankylosed knee but can be avoided by making a short inverted “V” incision in the proximal quadriceps tendon (Figure 2).4
Protecting the Soft Tissues During Surgery
Moist wound towels sewn into the joint capsule protect the underlying soft tissues from debris and desiccation during the procedure and will intuitively lower the chance of wound infection from contamination and tissue injury (Figures 4A, 4B).
Locating and Coagulating the Lateral Inferior Genicular Vessels
The lateral inferior genicular artery and vein can be easily located and coagulated just outside the posterior rim of the lateral meniscus near the popliteus hiatus. This will minimize both intraoperative and postoperative blood loss.
Determining the Entry Point in the Distal Femur for Intramedullary Alignment Devices
Templating the femoral entry point for insertion of an intramedullary alignment device on a preoperative radiograph will help avoid inadvertent excessive distal femoral valgus resection. This is especially important in valgus knees that have a valgus metaphyseal bow (Figure 5).
Avoiding Notching of the Anterior Femoral Cortex
Notching the anterior femoral cortex when in-between femoral sizes or when there is a preexisting dysplastic or shallow trochlea (Figure 6)
Obtaining a Medial Release by Removing Peripheral Medial Tibial Bone
Varus deformities can be corrected without performing a formal medial collateral ligament (MCL) release by a so-called reduction tibial osteotomy.5,6 In mild varus deformity, sufficient medial release can be achieved by removing medial femoral and tibial peripheral osteophytes that tent up the MCL and medial capsule. When this is insufficient, removal of additional peripheral tibial bone further shortens the distance between the origin and insertion of the MCL, effectively lengthening the ligament (Figure 7).
An Inverted Cruciform Lateral Retinacular Release to Correct Severe Valgus Deformity
An inverted cruciform lateral retinacular release effectively corrects a severe valgus deformity and avoids the need for a lateral collateral ligament (LCL) release.7
Relieving Posterior Femoral Impingement
Uncapped posterior condylar bone or retained posterior osteophytes can limit both flexion and extension and cause impingement. Trimming the posterior femoral condyles and removing posterior osteophytes is best accomplished using a trial femoral component as a template.4 A curved osteotome is passed tangential to the metallic condyles to define the bone requiring resection. After removal of the trial, the outlined bone can be easily and accurately resected.
Minimizing Postoperative Posterior Condylar Bone-Cement Radiolucencies
Zone 4 femoral bone-cement radiolucencies8 can be minimized using the “smear” technique.4 These radiolucencies are common because most prosthetic femoral components have posterior condyles that are parallel to the femoral fixation lugs and do not allow for compression of this interface during implantation. Most surgeons put no cement on the posterior condylar bone but place it on the inside of the prosthetic condyle instead. The lack of compression upon insertion leads to a poor interface and the resultant lucencies. In the long term, these lucencies could allow access of wear debris to the posterior condylar bone, with the potential for osteolysis and loosening. To improve this interface, cement can be smeared or packed into the posterior condyles and also placed on the posterior condyles of the prosthesis. This could lead to posterior extrusion of some cement during polymerization, so a removable trial insert should be utilized to allow access posteriorly after polymerization is complete.
Predicting Potential Postoperative Flexion
The best indicator of potential postoperative flexion for any individual patient is not preoperative flexion but is intraoperative flexion against gravity measured after capsular closure.9 Surgeons should measure and record this value for reference if a patient has difficulty regaining flexion during their recovery (Figure 9).
Summary
The short- and long-term success of TKA is highly dependent on surgical technique that allows proper and safe exposure under all circumstances, correction of deformity, and accurate component implantation while minimizing intraoperative and postoperative complications. The surgical pearls shared above will hopefully aid in achieving these goals.
Am J Orthop. 2016;45(6):384-388. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Yacoubian SV, Scott RD. Skin incision translation in total knee arthroplasty: the difference between flexion and extension. J Arthroplasty. 2007;22(3):353-355.
2. Schai PA, Gibbon AJ, Scott RD. Kneeling ability after total knee arthroplasty. Perception and reality. Clin Orthop Relat Res. 1999;367:195-200.
3. Springorum HP, Scott RD. A technique to facilitate everting the patella in stiff or obese knees in total knee arthroplasty. Am J Orthop. 2009;38(10):507-508.
4. Scott RD. Total Knee Arthroplasty. 2nd ed. Philadelphia, PA: Elsevier; 2014.
5. Dixon MC, Parsch D, Brown RR, Scott RD. The correction of severe varus deformity in total knee arthroplasty by tibial component downsizing and resection of uncapped proximal medial bone. J Arthroplasty. 2004;19(1):19-22.
6. Mullaji AB, Padmanabhan V, Jindal G. Total knee arthroplasty for profound varus deformity: technique and radiological results in 173 knees with varus of more than 20 degrees. J Arthroplasty. 2005;20(5):550-561.
7. Politi J, Scott RD. Balancing severe valgus deformity in total knee arthroplasty using a lateral cruciform retinacular release. J Arthroplasty. 2004;19(5):553-557.
8. Huddleston JI, Wiley JW, Scott RD. Zone 4 femoral radiolucent lines in hybrid versus cemented total knee arthroplasties: are they clinically significant? Clin Orthop Relat Res. 2005;441:334-339.
9. Lee DC, Kim DH, Scott RD, Suthers K. Intraoperative flexion against gravity as an indication of ultimate range of motion in individual cases after total knee arthroplasty. J Arthroplasty. 1998;13(5):500-503.
1. Yacoubian SV, Scott RD. Skin incision translation in total knee arthroplasty: the difference between flexion and extension. J Arthroplasty. 2007;22(3):353-355.
2. Schai PA, Gibbon AJ, Scott RD. Kneeling ability after total knee arthroplasty. Perception and reality. Clin Orthop Relat Res. 1999;367:195-200.
3. Springorum HP, Scott RD. A technique to facilitate everting the patella in stiff or obese knees in total knee arthroplasty. Am J Orthop. 2009;38(10):507-508.
4. Scott RD. Total Knee Arthroplasty. 2nd ed. Philadelphia, PA: Elsevier; 2014.
5. Dixon MC, Parsch D, Brown RR, Scott RD. The correction of severe varus deformity in total knee arthroplasty by tibial component downsizing and resection of uncapped proximal medial bone. J Arthroplasty. 2004;19(1):19-22.
6. Mullaji AB, Padmanabhan V, Jindal G. Total knee arthroplasty for profound varus deformity: technique and radiological results in 173 knees with varus of more than 20 degrees. J Arthroplasty. 2005;20(5):550-561.
7. Politi J, Scott RD. Balancing severe valgus deformity in total knee arthroplasty using a lateral cruciform retinacular release. J Arthroplasty. 2004;19(5):553-557.
8. Huddleston JI, Wiley JW, Scott RD. Zone 4 femoral radiolucent lines in hybrid versus cemented total knee arthroplasties: are they clinically significant? Clin Orthop Relat Res. 2005;441:334-339.
9. Lee DC, Kim DH, Scott RD, Suthers K. Intraoperative flexion against gravity as an indication of ultimate range of motion in individual cases after total knee arthroplasty. J Arthroplasty. 1998;13(5):500-503.
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
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).
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).
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).
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).
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 (
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.
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.
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
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).
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).
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).
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).
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 (
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
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).
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).
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).
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).
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 (
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.
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.
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.
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
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
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
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
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.
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.
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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.
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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.
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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.
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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
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
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.
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.
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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.
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