Running for Rare Team Raises Funds for NORD Program for Undiagnosed Patients

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Collagen Meniscus Implant

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

Collagen Meniscus Implant

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

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

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

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

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

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

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

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

 

 

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

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

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

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

Collagen Meniscus Implant

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

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

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

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

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

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

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

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

 

 

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

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

Collagen Meniscus Implant

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

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

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

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

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

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

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

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

 

 

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

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

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

References

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

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

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Setting Up Your New Physician for Success

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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.”(These figures are based on typical revenue generated by several specialties, as well as professional experience with multiple practices.)

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.

10 Tips for New Physician Success


“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.

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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.”(These figures are based on typical revenue generated by several specialties, as well as professional experience with multiple practices.)

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.

10 Tips for New Physician Success


“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.”(These figures are based on typical revenue generated by several specialties, as well as professional experience with multiple practices.)

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.

10 Tips for New Physician Success


“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.

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Surgical Pearls in Total Knee Arthroplasty: A Lifetime of Lessons Learned

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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

Figure 1.
When using this technique, remember to protect the patellar tendon from avulsion by using the techniques described below.

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

Figure 2.
This maneuver, along with a smooth 1/8-inchpin in the tibial tubercle, also protects the patellar tendon from avulsing (Figure 3).
Figure 3.
The patella can be easily everted and access to the lateral parapatellar scar tissue allows a lateral release to be performed from inside out to further mobilize the knee and enhance exposure. The inverted “V” incision can be closed anatomically, and no modifications of the postoperative physical therapy program are necessary.

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).

Figure 4.
Since I have done this routinely in both hip and knee arthroplasty over the last 7000 consecutive primary arthroplasties, I have had no operative deep infections. This experience is without the use of antibiotics in the bone cement.

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).

Figure 5.
In these cases, the entry point must be moved medially and/or the valgus angle chosen must be diminished.

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)

Figure 6.
can be avoided by making the distal femoral resection in an extra 3° of flexion. In most TKA systems, the prosthetic trochlear flange diverges 3° or 4° away from the posterior femoral condyles. If the distal femoral resection is made in an extra 3° of flexion, the femoral component utilized can be anatomically sized off the patient’s posterior femoral condyles and the diverging trochlear flange will avoid notching the anterior femoral cortex while providing increased surface contact with the trochlear bone, enhancing prosthetic fixation. The only potential adverse effects of increased femoral component flexion would occur in a system that does not allow hyperextension of the femoral/tibial articulation without loss of articular contact or in a posterior-stabilized articulation where there could be post impingement in hyperextension. Total knee systems vary in the amount of hyperextension that can be tolerated.

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

Figure 7.
The release is best done after bone resection but without trial components in place, because this facilitates exposure to the lateral retinaculum (Figure 8).
Figure 8.
The lateral superior genicular vessels should be identified and preserved. The vertical part of the release begins distal to the vessels and ends at the tibial resection. The horizontal limbs extend posteriorly short of the LCL and anteriorly short of the patellar tendon. If the extent of this release does not sufficiently balance the knee, it can be propagated by placing trial components with an insert thickness that stabilizes the medial side. Under this circumstance, the tight lateral side will now prohibit full passive extension. With gentle manipulation of the knee into extension, the lateral release will be propagated to its appropriate length. Postoperative perineal nerve palsies are rare with this technique. Immediate postoperative assessment, however, should always be done and the patient’s dressing loosened and their knee placed in flexion if there is any concern. Almost all of these rare palsies make a complete recovery.

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).

Figure 9.
If a patient had 120° of flexion against gravity after capsular closure but achieves only 80° at 2 months, a knee manipulation is probably indicated. If their flexion after closure was only 80°, a manipulation is unlikely to lead to any improvement.

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.

References

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.

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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

Figure 1.
When using this technique, remember to protect the patellar tendon from avulsion by using the techniques described below.

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

Figure 2.
This maneuver, along with a smooth 1/8-inchpin in the tibial tubercle, also protects the patellar tendon from avulsing (Figure 3).
Figure 3.
The patella can be easily everted and access to the lateral parapatellar scar tissue allows a lateral release to be performed from inside out to further mobilize the knee and enhance exposure. The inverted “V” incision can be closed anatomically, and no modifications of the postoperative physical therapy program are necessary.

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).

Figure 4.
Since I have done this routinely in both hip and knee arthroplasty over the last 7000 consecutive primary arthroplasties, I have had no operative deep infections. This experience is without the use of antibiotics in the bone cement.

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).

Figure 5.
In these cases, the entry point must be moved medially and/or the valgus angle chosen must be diminished.

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)

Figure 6.
can be avoided by making the distal femoral resection in an extra 3° of flexion. In most TKA systems, the prosthetic trochlear flange diverges 3° or 4° away from the posterior femoral condyles. If the distal femoral resection is made in an extra 3° of flexion, the femoral component utilized can be anatomically sized off the patient’s posterior femoral condyles and the diverging trochlear flange will avoid notching the anterior femoral cortex while providing increased surface contact with the trochlear bone, enhancing prosthetic fixation. The only potential adverse effects of increased femoral component flexion would occur in a system that does not allow hyperextension of the femoral/tibial articulation without loss of articular contact or in a posterior-stabilized articulation where there could be post impingement in hyperextension. Total knee systems vary in the amount of hyperextension that can be tolerated.

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

Figure 7.
The release is best done after bone resection but without trial components in place, because this facilitates exposure to the lateral retinaculum (Figure 8).
Figure 8.
The lateral superior genicular vessels should be identified and preserved. The vertical part of the release begins distal to the vessels and ends at the tibial resection. The horizontal limbs extend posteriorly short of the LCL and anteriorly short of the patellar tendon. If the extent of this release does not sufficiently balance the knee, it can be propagated by placing trial components with an insert thickness that stabilizes the medial side. Under this circumstance, the tight lateral side will now prohibit full passive extension. With gentle manipulation of the knee into extension, the lateral release will be propagated to its appropriate length. Postoperative perineal nerve palsies are rare with this technique. Immediate postoperative assessment, however, should always be done and the patient’s dressing loosened and their knee placed in flexion if there is any concern. Almost all of these rare palsies make a complete recovery.

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).

Figure 9.
If a patient had 120° of flexion against gravity after capsular closure but achieves only 80° at 2 months, a knee manipulation is probably indicated. If their flexion after closure was only 80°, a manipulation is unlikely to lead to any improvement.

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

Figure 1.
When using this technique, remember to protect the patellar tendon from avulsion by using the techniques described below.

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

Figure 2.
This maneuver, along with a smooth 1/8-inchpin in the tibial tubercle, also protects the patellar tendon from avulsing (Figure 3).
Figure 3.
The patella can be easily everted and access to the lateral parapatellar scar tissue allows a lateral release to be performed from inside out to further mobilize the knee and enhance exposure. The inverted “V” incision can be closed anatomically, and no modifications of the postoperative physical therapy program are necessary.

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).

Figure 4.
Since I have done this routinely in both hip and knee arthroplasty over the last 7000 consecutive primary arthroplasties, I have had no operative deep infections. This experience is without the use of antibiotics in the bone cement.

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).

Figure 5.
In these cases, the entry point must be moved medially and/or the valgus angle chosen must be diminished.

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)

Figure 6.
can be avoided by making the distal femoral resection in an extra 3° of flexion. In most TKA systems, the prosthetic trochlear flange diverges 3° or 4° away from the posterior femoral condyles. If the distal femoral resection is made in an extra 3° of flexion, the femoral component utilized can be anatomically sized off the patient’s posterior femoral condyles and the diverging trochlear flange will avoid notching the anterior femoral cortex while providing increased surface contact with the trochlear bone, enhancing prosthetic fixation. The only potential adverse effects of increased femoral component flexion would occur in a system that does not allow hyperextension of the femoral/tibial articulation without loss of articular contact or in a posterior-stabilized articulation where there could be post impingement in hyperextension. Total knee systems vary in the amount of hyperextension that can be tolerated.

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

Figure 7.
The release is best done after bone resection but without trial components in place, because this facilitates exposure to the lateral retinaculum (Figure 8).
Figure 8.
The lateral superior genicular vessels should be identified and preserved. The vertical part of the release begins distal to the vessels and ends at the tibial resection. The horizontal limbs extend posteriorly short of the LCL and anteriorly short of the patellar tendon. If the extent of this release does not sufficiently balance the knee, it can be propagated by placing trial components with an insert thickness that stabilizes the medial side. Under this circumstance, the tight lateral side will now prohibit full passive extension. With gentle manipulation of the knee into extension, the lateral release will be propagated to its appropriate length. Postoperative perineal nerve palsies are rare with this technique. Immediate postoperative assessment, however, should always be done and the patient’s dressing loosened and their knee placed in flexion if there is any concern. Almost all of these rare palsies make a complete recovery.

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).

Figure 9.
If a patient had 120° of flexion against gravity after capsular closure but achieves only 80° at 2 months, a knee manipulation is probably indicated. If their flexion after closure was only 80°, a manipulation is unlikely to lead to any improvement.

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.

References

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.

References

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.

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

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

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

Eye Injuries

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

Cornea Injuries

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

Orbital Fractures

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

Retina Issues

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

Globe Injuries and Rupture

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

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

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

 

 

Dental Concerns

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

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

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

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

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

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

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

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

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

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

Tooth Subluxation

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

Fractures

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

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

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

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

Tooth Avulsion

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

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

 

 

Skin Issues

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

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

Impetigo

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

Methicillin-Resistant Staphylococcus aureus

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

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

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

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

Tinea Pedis

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

 

 

Tinea Corporis

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

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

Tinea Cruris

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


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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Eye Injuries

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

Cornea Injuries

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

Orbital Fractures

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

Retina Issues

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

Globe Injuries and Rupture

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

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

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

 

 

Dental Concerns

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

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

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

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

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

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

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

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

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

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

Tooth Subluxation

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

Fractures

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

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

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

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

Tooth Avulsion

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

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

 

 

Skin Issues

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

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

Impetigo

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

Methicillin-Resistant Staphylococcus aureus

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

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

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

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

Tinea Pedis

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

 

 

Tinea Corporis

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

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

Tinea Cruris

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


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

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

Eye Injuries

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

Cornea Injuries

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

Orbital Fractures

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

Retina Issues

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

Globe Injuries and Rupture

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

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

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

 

 

Dental Concerns

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

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

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

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

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

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

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

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

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

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

Tooth Subluxation

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

Fractures

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

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

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

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

Tooth Avulsion

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

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

 

 

Skin Issues

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

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

Impetigo

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

Methicillin-Resistant Staphylococcus aureus

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

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

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

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

Tinea Pedis

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

 

 

Tinea Corporis

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

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

Tinea Cruris

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


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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

 

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Knee Injuries in American Football: An Epidemiological Review

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Knee Injuries in American Football: An Epidemiological Review

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

Anterior Cruciate Ligament

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

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

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

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

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

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

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

 

 

Medial Collateral Ligament

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

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

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

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

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

Medial Patellofemoral Ligament

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

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

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

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

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

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

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

 

 

Posterior Cruciate Ligament

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

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

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

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

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

Natural history of Grade I and II isolated PCL injuries is generally favorable compared to Grade III and multi-ligamentous injuries.70 As a result, isolated Grade I and II PCL injuries are generally treated nonoperatively. Treatment consists of physical therapy with emphasis on quadriceps strengthening. Return to play can be considered as early as 2 to 4 weeks from injury.71 Recent long-term data have shown successful conservative management of Grade I and II injuries with quadriceps strength to 97% of contralateral leg and full range of motion.72 However, there was 11% moderate to severe osteoarthritis in these patients at a mean follow-up of 14.3 years.72 Fowler and Messieh67 managed athletes with 7 isolated complete PCL tears and 5 partial tears nonoperatively, all of whom were able to return to sport without limitation. Parolie and Bergfeld73 managed 25 athletes with isolated PCL tears conservatively. In this study, 80% of athletes reported satisfaction and 68% returned to previous level of play.73 Neither of the aforementioned studies specify the grades of the injuries. Finally, Patel and colleagues66 managed 6 NFL athletes with Grade I and II injuries nonoperatively, and all were able to return to sport.

Treatment of isolated Grade III PCL injuries is more controversial, and no consensus exists in the literature. In an epidemiological study, Dick and colleagues68 found that only 39% of NCAA football athletes underwent surgery for their torn PCLs, compared to 79% of ACL injuries. However, their study makes no mention to the severity of these injuries. Numerous options exist for PCL reconstruction, with no consensus on the preferred method.

Conclusion

Knee injuries are the most common injury in football. Knowledge of the natural history of these injuries, as well as treatment options and expected outcomes, will help treating physicians educate their patients on the optimal treatment and manage return to play expectations.

Am J Orthop. 2016;45(6):368-373. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Swenson DM, Collins CL, Best TM, Flanigan DC, Fields SK, Comstock RD. Epidemiology of knee injuries among U.S. high school athletes, 2005/2006-2010/2011. Med Sci Sports Exerc. 2013;45(3):462-469.

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

3. Mello MJ, Myers R, Christian JB, Palmisciano L, Linakis JG. Injuries in youth football: national emergency department visits during 2001-2005 for young and adolescent players. Acad Emerg Med. 2009;16(3):243-248.

4. Rechel JA, Collins CL, Comstock RD. Epidemiology of injuries requiring surgery among high school athletes in the United States, 2005 to 2010. J Trauma. 2011;71(4):982-989.

5. Ingram JG, Fields SK, Yard EE, Comstock RD. Epidemiology of knee injuries among boys and girls in US high school athletics. Am J Sports Med. 2008;36(6):1116-1122.

6. Tirabassi J, Brou L, Khodaee M, Lefort R, Fields SK, Comstock RD. Epidemiology of high school sports-related injuries resulting in medical disqualification: 2005-2006 through 2013-2014 academic years. Am J Sports Med. 2016 May 10. [Epub ahead of print]

7. Fernandez WG, Yard EE, Comstock RD. Epidemiology of lower extremity injuries among U.S. high school athletes. Acad Emerg Med. 2007;14(7):641-645.

8. Olsen OE, Myklebust G, Engebretsen L, Bahr R. Injury mechanisms for anterior cruciate ligament injuries in team handball: a systematic video analysis. Am J Sports Med. 2004;32(4):1002-1012.

9. Boden BP, Dean GS, Feagin JA Jr, Garrett WE Jr. Mechanisms of anterior cruciate ligament injury. Orthopedics. 2000;23(6):573-578.

10. Dragoo JL, Braun HJ, Harris AH. The effect of playing surface on the incidence of ACL injuries in National Collegiate Athletic Association American Football. Knee. 2013;20(3):191-195.

11. Joseph AM, Collins CL, Henke NM, Yard EE, Fields SK, Comstock RD. A multisport epidemiologic comparison of anterior cruciate ligament injuries in high school athletics. J Athl Train. 2013;48(6):810-817.

12. Granan LP, Inacio MC, Maletis GB, Funahashi TT, Engebretsen L. Sport-specific injury pattern recorded during anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(12):2814-2818.

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

14. Dragoo JL, Braun HJ, Durham JL, Chen MR, Harris AH. Incidence and risk factors for injuries to the anterior cruciate ligament in National Collegiate Athletic Association football: data from the 2004-2005 through 2008-2009 National Collegiate Athletic Association Injury Surveillance System. Am J Sports Med. 2012;40(5):990-995.

15. Dodson CC, Secrist ES, Bhat SB, Woods DP, Deluca PF. Anterior cruciate ligamenti in National Football League athletes from 2010 to 2013: a descriptive epidemiology study. Orthop J Sports Med. 2016;4(3):2325967116631949.

16. Golightly YM, Marshall SW, Callahan LF, Guskiewicz K. Early-onset arthritis in retired National Football League players. J Phys Act Health. 2009;6(5):638-643.

17. Brophy RH, Lyman S, Chehab EL, Barnes RP, Rodeo SA, Warren RF. Predictive value of prior injury on career in professional American football is affected by player position. Am J Sports Med. 2009;37(4):768-775.

18. Bradley J, Honkamp NJ, Jost P, West R, Norwig J, Kaplan LD. Incidence and variance of knee injuries in elite college football players. Am J Orthop. 2008;37(6):310-314.

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

20. Daruawalla JH, Greis PE, Hancock R; ASP Collaborative Group, Xerogeanes JW. Rates and determinants of return to play after anterior cruciate ligament reconstruction in NCAA Division 1 college football athletes: a study of the ACC, SEC, and PAC-12 conferences. Orthop J Sports Med. 2014;2(8):2325967114543901.

21. Shah VM, Andrews JR, Fleisig GS, McMichael CS, Lemak LJ. Return to play after anterior cruciate ligament reconstruction in National Football League athletes. Am J Sports Med. 2010;38(11):2233-2239.

22. McCullough KA, Phelps KD, Spindler KP, et al. Return to high school- and college-level football after anterior cruciate ligament reconstruction: a Multicenter Orthopaedic Outcomes Network (MOON) cohort study. Am J Sports Med. 2012;40(11):2523-2529.

23. Erickson BJ, Harris JD, Heninger JR, et al. Performance and return-to-sport after ACL reconstruction in NFL quarterbacks. Orthopedics. 2014;37(8):e728-e734.

24. Carey JL, Huffman GR, Parekh SG, Sennett BJ. Outcomes of anterior cruciate ligament injuries to running backs and wide receivers in the National Football League. Am J Sports Med. 2006;34(12):1911-1917.

25. Hershman EB, Anderson R, Bergfeld JA, et al. An analysis of specific lower extremity injury rates on grass and FieldTurf playing surfaces in National Football League Games: 2000-2009 seasons. Am J Sports Med. 2012;40(10):2200-2205.

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

27. Derscheid GL, Garrick JG. Medial collateral ligament injuries in football. Nonoperative management of grade I and grade II sprains. Am J Sports Med. 1981;9(6):365-368.

28. Meyers MC, Barnhill BS. Incidence, causes, and severity of high school football injuries on FieldTurf versus natural grass: a 5-year prospective study. Am J Sports Med. 2004;32(7):1626-1638.

29. Lundblad M, Waldén M, Magnusson H, Karlsson J, Ekstrand J. The UEFA injury study: 11-year data concerning 346 MCL injuries and time to return to play. Br J Sports Med. 2013;47(12):759-762.

30. Hewson GF Jr, Mendini RA, Wang JB. Prophylactic knee bracing in college football. Am J Sports Med. 1986;14(4):262-266.

31. Rovere GD, Haupt HA, Yates CS. Prophylactic knee bracing in college football. Am J Sports Med. 1987;15(2):111-116.

32. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee sprains in college football. Brace wear preferences and injury risk. Am J Sports Med. 1994;22(1):2-11.

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

34. Ellsasser JC, Reynolds FC, Omohundro JR. The non-operative treatment of collateral ligament injuries of the knee in professional football players. An analysis of seventy-four injuries treated non-operatively and twenty-four injuries treated surgically. J Bone Joint Surg Am. 1974;56(6):1185-1190.

35. Holden DL, Eggert AW, Butler JE. The nonoperative treatment of grade I and II medial collateral ligament injuries to the knee. Am J Sports Med. 1983;11(5):340-344.

36. Indelicato PA, Hermansdorfer J, Huegel M. Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate football players. Clin Orthop Relat Res. 1990;(256):174-177.

37. Jones RE, Henley MB, Francis P. Nonoperative management of isolated grade III collateral ligament injury in high school football players. Clin Orthop Relat Res. 1986;(213):137-140.

38. Fetto JF, Marshall JL. Medial collateral ligament injuries of the knee: a rationale for treatment. Clin Orthop Relat Res. 1978;(132):206-218.

39. Corten K, Hoser C, Fink C, Bellemans J. Case reports: a Stener-like lesion of the medial collateral ligament of the knee. Clin Orthop Relat Res. 2010;468(1):289-293.

40. Marchant MH Jr, Tibor LM, Sekiya JK, Hardaker WT Jr, Garrett WE Jr, Taylor DC. Management of medial-sided knee injuries, part 1: medial collateral ligament. Am J Sports Med. 2011;39(5):1102-1113.

41. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 1998;26(1):59-65.

42. Casteleyn PP, Handelberg F. Arthroscopy in the diagnosis of occult dislocation of the patella. Acta Orthop Belg. 1989;55(3):381-383.

43. Waterman BR, Belmont PJ Jr, Owens BD. Patellar dislocation in the United States: role of sex, age, race, and athletic participation. J Knee Surg. 2012;25(1):51-57.

44. Sillanpää P, Mattila VM, Iivonen T, Visuri T, Pihlajamäki H. Incidence and risk factors of acute traumatic primary patellar dislocation. Med Sci Sports Exerc. 2008;40(4):606-611.

45. Hsiao M, Owens BD, Burks R, Sturdivant RX, Cameron KL. Incidence of acute traumatic patellar dislocation among active-duty United States military service members. Am J Sports Med. 2010;38(10):1997-2004.

46. Fithian DC, Paxton EW, Stone ML, et al. Epidemiology and natural history of acute patellar dislocation. Am J Sports Med. 2004;32(5):1114-1121.

47. Mitchell J, Magnussen RA, Collins CL, et al. Epidemiology of patellofemoral instability injuries among high school athletes in the United States. Am J Sports Med. 2015;43(7):1676-1682.

48. Nikku R, Nietosvaara Y, Aalto K, Kallio PE. The mechanism of primary patellar dislocation: trauma history of 126 patients. Acta Orthop. 2009;80(4):432-434.

49. Tsai CH, Hsu CJ, Hung CH, Hsu HC. Primary traumatic patellar dislocation. J Orthop Surg Res. 2012;7:21.

50. Atkin DM, Fithian DC, Marangi KS, Stone ML, Dobson BE, Mendelsohn C. Characteristics of patients with primary acute lateral patellar dislocation and their recovery within the first 6 months of injury. Am J Sports Med. 2000;28(4):472-479.

51. Nomura E, Inoue M, Kurimura M. Chondral and osteochondral injuries associated with acute patellar dislocation. Arthroscopy. 2003;19(7):717-721.

52. Kirsch MD, Fitzgerald SW, Friedman H, Rogers LF. Transient lateral patellar dislocation: diagnosis with MR imaging. AJR Am J Roentgenol. 1993;161(1):109-113.

53. Virolainen H, Visuri T, Kuusela T. Acute dislocation of the patella: MR findings. Radiology. 1993;189(1):243-246.

54. Stanitski CL. Articular hypermobility and chondral injury in patients with acute patellar dislocation. Am J Sports Med. 1995;23(2):146-150.

55. Mäenpää H, Huhtala H, Lehto MU. Recurrence after patellar dislocation. Redislocation in 37/75 patients followed for 6-24 years. Acta Orthop Scand. 1997;68(5):424-426.

56. Buchner M, Baudendistel B, Sabo D, Schmitt H. Acute traumatic primary patellar dislocation: long-term results comparing conservative and surgical treatment. Clin J Sport Med. 2005;15(2):62-66.

57. Fisher B, Nyland J, Brand E, Curtin B. Medial patellofemoral ligament reconstruction for recurrent patellar dislocation: a systematic review including rehabilitation and return-to-sports efficacy. Arthroscopy. 2010;26(10):1384-1394.

58. Lippacher S, Dreyhaupt J, Williams SR, Reichel H, Nelitz M. Reconstruction of the medial patellofemoral ligament: clinical outcomes and return to sports. Am J Sports Med. 2014;42(7):1661-1668.

59. Panni AS, Alam M, Cerciello S, Vasso M, Maffulli N. Medial patellofemoral ligament reconstruction with a divergent patellar transverse 2-tunnel technique. Am J Sports Med. 2011;39(12):2647-1655.

60. Schneider DK, Grawe B, Magnussen RA, et al. Outcomes after isolated medial patellofemoral ligament reconstruction for the treatment of recurrent lateral patellar dislocations: a systematic review and meta-analysis. Am J Sports Med. 2016 Feb 12. [Epub ahead of print]

61. Amis AA, Bull AM, Gupte CM, Hijazi I, Race A, Robinson JR. Biomechanics of the PCL and related structures: posterolateral, posteromedial and meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc. 2003;11(5):271-281.

62. Fu FH, Harner CD, Johnson DL, Miller MD, Woo SL. Biomechanics of knee ligaments: basic concepts and clinical application. Instr Course Lect. 1994;43:137-148.

63. Markolf KL, Feeley BT, Tejwani SG, Martin DE, McAllister DR. Changes in knee laxity and ligament force after sectioning the posteromedial bundle of the posterior cruciate ligament. Arthroscopy. 2006; 22(10):1100-1106.

64. Ganelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: Part II. Arthroscopy. 1995;11(5):526-529.

65. Schulz MS, Russe K, Weiler A, Eichhorn HJ, Strobel MJ. Epidemiology of posterior cruciate ligament injuries. Arch Orthop Trauma Surg. 2003;123(4):186-191.

66. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The nonoperative treatment of acute, isolated (partial or complete) posterior cruciate ligament-deficient knees: an intermediate-term follow-up study. HSS J. 2007;3(2):137-146.

67. Fowler PJ, Messieh SS. Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med. 1987;15(6):553-557.

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

69. LaPrade CM, Civitarese DM, Rasmussen MT, LaPrade RF. Emerging updates on the posterior cruciate ligament: a review of the current literature. Am J Sports Med. 2015;43(12):3077-3092.

70. Torg JS, Barton TM, Pavlov H, Stine R. Natural history of the posterior cruciate ligament-deficient knee. Clin Orthop Relat Res. 1989(246):208-216.

71. Miller MD. Orthopaedic Knowledge Update: Sports Medicine 5. Rosemont, IL; American Academy of Orthopaedic Surgeons; 2016.

72. Shelbourne KD, Clark M, Gray T. Minimum 10-year follow-up of patients after an acute, isolated posterior cruciate ligament injury treated nonoperatively. Am J Sports Med. 2013;41(7):1526-1533.

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

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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

Medial Patellofemoral Ligament

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

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

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

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

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

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

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

 

 

Posterior Cruciate Ligament

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

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

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

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

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

Natural history of Grade I and II isolated PCL injuries is generally favorable compared to Grade III and multi-ligamentous injuries.70 As a result, isolated Grade I and II PCL injuries are generally treated nonoperatively. Treatment consists of physical therapy with emphasis on quadriceps strengthening. Return to play can be considered as early as 2 to 4 weeks from injury.71 Recent long-term data have shown successful conservative management of Grade I and II injuries with quadriceps strength to 97% of contralateral leg and full range of motion.72 However, there was 11% moderate to severe osteoarthritis in these patients at a mean follow-up of 14.3 years.72 Fowler and Messieh67 managed athletes with 7 isolated complete PCL tears and 5 partial tears nonoperatively, all of whom were able to return to sport without limitation. Parolie and Bergfeld73 managed 25 athletes with isolated PCL tears conservatively. In this study, 80% of athletes reported satisfaction and 68% returned to previous level of play.73 Neither of the aforementioned studies specify the grades of the injuries. Finally, Patel and colleagues66 managed 6 NFL athletes with Grade I and II injuries nonoperatively, and all were able to return to sport.

Treatment of isolated Grade III PCL injuries is more controversial, and no consensus exists in the literature. In an epidemiological study, Dick and colleagues68 found that only 39% of NCAA football athletes underwent surgery for their torn PCLs, compared to 79% of ACL injuries. However, their study makes no mention to the severity of these injuries. Numerous options exist for PCL reconstruction, with no consensus on the preferred method.

Conclusion

Knee injuries are the most common injury in football. Knowledge of the natural history of these injuries, as well as treatment options and expected outcomes, will help treating physicians educate their patients on the optimal treatment and manage return to play expectations.

Am J Orthop. 2016;45(6):368-373. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

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

Anterior Cruciate Ligament

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

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

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

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

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

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

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

 

 

Medial Collateral Ligament

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

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

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

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

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

Medial Patellofemoral Ligament

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

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

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

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

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

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

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

 

 

Posterior Cruciate Ligament

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

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

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

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

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

Natural history of Grade I and II isolated PCL injuries is generally favorable compared to Grade III and multi-ligamentous injuries.70 As a result, isolated Grade I and II PCL injuries are generally treated nonoperatively. Treatment consists of physical therapy with emphasis on quadriceps strengthening. Return to play can be considered as early as 2 to 4 weeks from injury.71 Recent long-term data have shown successful conservative management of Grade I and II injuries with quadriceps strength to 97% of contralateral leg and full range of motion.72 However, there was 11% moderate to severe osteoarthritis in these patients at a mean follow-up of 14.3 years.72 Fowler and Messieh67 managed athletes with 7 isolated complete PCL tears and 5 partial tears nonoperatively, all of whom were able to return to sport without limitation. Parolie and Bergfeld73 managed 25 athletes with isolated PCL tears conservatively. In this study, 80% of athletes reported satisfaction and 68% returned to previous level of play.73 Neither of the aforementioned studies specify the grades of the injuries. Finally, Patel and colleagues66 managed 6 NFL athletes with Grade I and II injuries nonoperatively, and all were able to return to sport.

Treatment of isolated Grade III PCL injuries is more controversial, and no consensus exists in the literature. In an epidemiological study, Dick and colleagues68 found that only 39% of NCAA football athletes underwent surgery for their torn PCLs, compared to 79% of ACL injuries. However, their study makes no mention to the severity of these injuries. Numerous options exist for PCL reconstruction, with no consensus on the preferred method.

Conclusion

Knee injuries are the most common injury in football. Knowledge of the natural history of these injuries, as well as treatment options and expected outcomes, will help treating physicians educate their patients on the optimal treatment and manage return to play expectations.

Am J Orthop. 2016;45(6):368-373. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Swenson DM, Collins CL, Best TM, Flanigan DC, Fields SK, Comstock RD. Epidemiology of knee injuries among U.S. high school athletes, 2005/2006-2010/2011. Med Sci Sports Exerc. 2013;45(3):462-469.

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

3. Mello MJ, Myers R, Christian JB, Palmisciano L, Linakis JG. Injuries in youth football: national emergency department visits during 2001-2005 for young and adolescent players. Acad Emerg Med. 2009;16(3):243-248.

4. Rechel JA, Collins CL, Comstock RD. Epidemiology of injuries requiring surgery among high school athletes in the United States, 2005 to 2010. J Trauma. 2011;71(4):982-989.

5. Ingram JG, Fields SK, Yard EE, Comstock RD. Epidemiology of knee injuries among boys and girls in US high school athletics. Am J Sports Med. 2008;36(6):1116-1122.

6. Tirabassi J, Brou L, Khodaee M, Lefort R, Fields SK, Comstock RD. Epidemiology of high school sports-related injuries resulting in medical disqualification: 2005-2006 through 2013-2014 academic years. Am J Sports Med. 2016 May 10. [Epub ahead of print]

7. Fernandez WG, Yard EE, Comstock RD. Epidemiology of lower extremity injuries among U.S. high school athletes. Acad Emerg Med. 2007;14(7):641-645.

8. Olsen OE, Myklebust G, Engebretsen L, Bahr R. Injury mechanisms for anterior cruciate ligament injuries in team handball: a systematic video analysis. Am J Sports Med. 2004;32(4):1002-1012.

9. Boden BP, Dean GS, Feagin JA Jr, Garrett WE Jr. Mechanisms of anterior cruciate ligament injury. Orthopedics. 2000;23(6):573-578.

10. Dragoo JL, Braun HJ, Harris AH. The effect of playing surface on the incidence of ACL injuries in National Collegiate Athletic Association American Football. Knee. 2013;20(3):191-195.

11. Joseph AM, Collins CL, Henke NM, Yard EE, Fields SK, Comstock RD. A multisport epidemiologic comparison of anterior cruciate ligament injuries in high school athletics. J Athl Train. 2013;48(6):810-817.

12. Granan LP, Inacio MC, Maletis GB, Funahashi TT, Engebretsen L. Sport-specific injury pattern recorded during anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(12):2814-2818.

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

14. Dragoo JL, Braun HJ, Durham JL, Chen MR, Harris AH. Incidence and risk factors for injuries to the anterior cruciate ligament in National Collegiate Athletic Association football: data from the 2004-2005 through 2008-2009 National Collegiate Athletic Association Injury Surveillance System. Am J Sports Med. 2012;40(5):990-995.

15. Dodson CC, Secrist ES, Bhat SB, Woods DP, Deluca PF. Anterior cruciate ligamenti in National Football League athletes from 2010 to 2013: a descriptive epidemiology study. Orthop J Sports Med. 2016;4(3):2325967116631949.

16. Golightly YM, Marshall SW, Callahan LF, Guskiewicz K. Early-onset arthritis in retired National Football League players. J Phys Act Health. 2009;6(5):638-643.

17. Brophy RH, Lyman S, Chehab EL, Barnes RP, Rodeo SA, Warren RF. Predictive value of prior injury on career in professional American football is affected by player position. Am J Sports Med. 2009;37(4):768-775.

18. Bradley J, Honkamp NJ, Jost P, West R, Norwig J, Kaplan LD. Incidence and variance of knee injuries in elite college football players. Am J Orthop. 2008;37(6):310-314.

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

20. Daruawalla JH, Greis PE, Hancock R; ASP Collaborative Group, Xerogeanes JW. Rates and determinants of return to play after anterior cruciate ligament reconstruction in NCAA Division 1 college football athletes: a study of the ACC, SEC, and PAC-12 conferences. Orthop J Sports Med. 2014;2(8):2325967114543901.

21. Shah VM, Andrews JR, Fleisig GS, McMichael CS, Lemak LJ. Return to play after anterior cruciate ligament reconstruction in National Football League athletes. Am J Sports Med. 2010;38(11):2233-2239.

22. McCullough KA, Phelps KD, Spindler KP, et al. Return to high school- and college-level football after anterior cruciate ligament reconstruction: a Multicenter Orthopaedic Outcomes Network (MOON) cohort study. Am J Sports Med. 2012;40(11):2523-2529.

23. Erickson BJ, Harris JD, Heninger JR, et al. Performance and return-to-sport after ACL reconstruction in NFL quarterbacks. Orthopedics. 2014;37(8):e728-e734.

24. Carey JL, Huffman GR, Parekh SG, Sennett BJ. Outcomes of anterior cruciate ligament injuries to running backs and wide receivers in the National Football League. Am J Sports Med. 2006;34(12):1911-1917.

25. Hershman EB, Anderson R, Bergfeld JA, et al. An analysis of specific lower extremity injury rates on grass and FieldTurf playing surfaces in National Football League Games: 2000-2009 seasons. Am J Sports Med. 2012;40(10):2200-2205.

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

27. Derscheid GL, Garrick JG. Medial collateral ligament injuries in football. Nonoperative management of grade I and grade II sprains. Am J Sports Med. 1981;9(6):365-368.

28. Meyers MC, Barnhill BS. Incidence, causes, and severity of high school football injuries on FieldTurf versus natural grass: a 5-year prospective study. Am J Sports Med. 2004;32(7):1626-1638.

29. Lundblad M, Waldén M, Magnusson H, Karlsson J, Ekstrand J. The UEFA injury study: 11-year data concerning 346 MCL injuries and time to return to play. Br J Sports Med. 2013;47(12):759-762.

30. Hewson GF Jr, Mendini RA, Wang JB. Prophylactic knee bracing in college football. Am J Sports Med. 1986;14(4):262-266.

31. Rovere GD, Haupt HA, Yates CS. Prophylactic knee bracing in college football. Am J Sports Med. 1987;15(2):111-116.

32. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee sprains in college football. Brace wear preferences and injury risk. Am J Sports Med. 1994;22(1):2-11.

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

34. Ellsasser JC, Reynolds FC, Omohundro JR. The non-operative treatment of collateral ligament injuries of the knee in professional football players. An analysis of seventy-four injuries treated non-operatively and twenty-four injuries treated surgically. J Bone Joint Surg Am. 1974;56(6):1185-1190.

35. Holden DL, Eggert AW, Butler JE. The nonoperative treatment of grade I and II medial collateral ligament injuries to the knee. Am J Sports Med. 1983;11(5):340-344.

36. Indelicato PA, Hermansdorfer J, Huegel M. Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate football players. Clin Orthop Relat Res. 1990;(256):174-177.

37. Jones RE, Henley MB, Francis P. Nonoperative management of isolated grade III collateral ligament injury in high school football players. Clin Orthop Relat Res. 1986;(213):137-140.

38. Fetto JF, Marshall JL. Medial collateral ligament injuries of the knee: a rationale for treatment. Clin Orthop Relat Res. 1978;(132):206-218.

39. Corten K, Hoser C, Fink C, Bellemans J. Case reports: a Stener-like lesion of the medial collateral ligament of the knee. Clin Orthop Relat Res. 2010;468(1):289-293.

40. Marchant MH Jr, Tibor LM, Sekiya JK, Hardaker WT Jr, Garrett WE Jr, Taylor DC. Management of medial-sided knee injuries, part 1: medial collateral ligament. Am J Sports Med. 2011;39(5):1102-1113.

41. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 1998;26(1):59-65.

42. Casteleyn PP, Handelberg F. Arthroscopy in the diagnosis of occult dislocation of the patella. Acta Orthop Belg. 1989;55(3):381-383.

43. Waterman BR, Belmont PJ Jr, Owens BD. Patellar dislocation in the United States: role of sex, age, race, and athletic participation. J Knee Surg. 2012;25(1):51-57.

44. Sillanpää P, Mattila VM, Iivonen T, Visuri T, Pihlajamäki H. Incidence and risk factors of acute traumatic primary patellar dislocation. Med Sci Sports Exerc. 2008;40(4):606-611.

45. Hsiao M, Owens BD, Burks R, Sturdivant RX, Cameron KL. Incidence of acute traumatic patellar dislocation among active-duty United States military service members. Am J Sports Med. 2010;38(10):1997-2004.

46. Fithian DC, Paxton EW, Stone ML, et al. Epidemiology and natural history of acute patellar dislocation. Am J Sports Med. 2004;32(5):1114-1121.

47. Mitchell J, Magnussen RA, Collins CL, et al. Epidemiology of patellofemoral instability injuries among high school athletes in the United States. Am J Sports Med. 2015;43(7):1676-1682.

48. Nikku R, Nietosvaara Y, Aalto K, Kallio PE. The mechanism of primary patellar dislocation: trauma history of 126 patients. Acta Orthop. 2009;80(4):432-434.

49. Tsai CH, Hsu CJ, Hung CH, Hsu HC. Primary traumatic patellar dislocation. J Orthop Surg Res. 2012;7:21.

50. Atkin DM, Fithian DC, Marangi KS, Stone ML, Dobson BE, Mendelsohn C. Characteristics of patients with primary acute lateral patellar dislocation and their recovery within the first 6 months of injury. Am J Sports Med. 2000;28(4):472-479.

51. Nomura E, Inoue M, Kurimura M. Chondral and osteochondral injuries associated with acute patellar dislocation. Arthroscopy. 2003;19(7):717-721.

52. Kirsch MD, Fitzgerald SW, Friedman H, Rogers LF. Transient lateral patellar dislocation: diagnosis with MR imaging. AJR Am J Roentgenol. 1993;161(1):109-113.

53. Virolainen H, Visuri T, Kuusela T. Acute dislocation of the patella: MR findings. Radiology. 1993;189(1):243-246.

54. Stanitski CL. Articular hypermobility and chondral injury in patients with acute patellar dislocation. Am J Sports Med. 1995;23(2):146-150.

55. Mäenpää H, Huhtala H, Lehto MU. Recurrence after patellar dislocation. Redislocation in 37/75 patients followed for 6-24 years. Acta Orthop Scand. 1997;68(5):424-426.

56. Buchner M, Baudendistel B, Sabo D, Schmitt H. Acute traumatic primary patellar dislocation: long-term results comparing conservative and surgical treatment. Clin J Sport Med. 2005;15(2):62-66.

57. Fisher B, Nyland J, Brand E, Curtin B. Medial patellofemoral ligament reconstruction for recurrent patellar dislocation: a systematic review including rehabilitation and return-to-sports efficacy. Arthroscopy. 2010;26(10):1384-1394.

58. Lippacher S, Dreyhaupt J, Williams SR, Reichel H, Nelitz M. Reconstruction of the medial patellofemoral ligament: clinical outcomes and return to sports. Am J Sports Med. 2014;42(7):1661-1668.

59. Panni AS, Alam M, Cerciello S, Vasso M, Maffulli N. Medial patellofemoral ligament reconstruction with a divergent patellar transverse 2-tunnel technique. Am J Sports Med. 2011;39(12):2647-1655.

60. Schneider DK, Grawe B, Magnussen RA, et al. Outcomes after isolated medial patellofemoral ligament reconstruction for the treatment of recurrent lateral patellar dislocations: a systematic review and meta-analysis. Am J Sports Med. 2016 Feb 12. [Epub ahead of print]

61. Amis AA, Bull AM, Gupte CM, Hijazi I, Race A, Robinson JR. Biomechanics of the PCL and related structures: posterolateral, posteromedial and meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc. 2003;11(5):271-281.

62. Fu FH, Harner CD, Johnson DL, Miller MD, Woo SL. Biomechanics of knee ligaments: basic concepts and clinical application. Instr Course Lect. 1994;43:137-148.

63. Markolf KL, Feeley BT, Tejwani SG, Martin DE, McAllister DR. Changes in knee laxity and ligament force after sectioning the posteromedial bundle of the posterior cruciate ligament. Arthroscopy. 2006; 22(10):1100-1106.

64. Ganelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: Part II. Arthroscopy. 1995;11(5):526-529.

65. Schulz MS, Russe K, Weiler A, Eichhorn HJ, Strobel MJ. Epidemiology of posterior cruciate ligament injuries. Arch Orthop Trauma Surg. 2003;123(4):186-191.

66. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The nonoperative treatment of acute, isolated (partial or complete) posterior cruciate ligament-deficient knees: an intermediate-term follow-up study. HSS J. 2007;3(2):137-146.

67. Fowler PJ, Messieh SS. Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med. 1987;15(6):553-557.

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

69. LaPrade CM, Civitarese DM, Rasmussen MT, LaPrade RF. Emerging updates on the posterior cruciate ligament: a review of the current literature. Am J Sports Med. 2015;43(12):3077-3092.

70. Torg JS, Barton TM, Pavlov H, Stine R. Natural history of the posterior cruciate ligament-deficient knee. Clin Orthop Relat Res. 1989(246):208-216.

71. Miller MD. Orthopaedic Knowledge Update: Sports Medicine 5. Rosemont, IL; American Academy of Orthopaedic Surgeons; 2016.

72. Shelbourne KD, Clark M, Gray T. Minimum 10-year follow-up of patients after an acute, isolated posterior cruciate ligament injury treated nonoperatively. Am J Sports Med. 2013;41(7):1526-1533.

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

References

1. Swenson DM, Collins CL, Best TM, Flanigan DC, Fields SK, Comstock RD. Epidemiology of knee injuries among U.S. high school athletes, 2005/2006-2010/2011. Med Sci Sports Exerc. 2013;45(3):462-469.

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

3. Mello MJ, Myers R, Christian JB, Palmisciano L, Linakis JG. Injuries in youth football: national emergency department visits during 2001-2005 for young and adolescent players. Acad Emerg Med. 2009;16(3):243-248.

4. Rechel JA, Collins CL, Comstock RD. Epidemiology of injuries requiring surgery among high school athletes in the United States, 2005 to 2010. J Trauma. 2011;71(4):982-989.

5. Ingram JG, Fields SK, Yard EE, Comstock RD. Epidemiology of knee injuries among boys and girls in US high school athletics. Am J Sports Med. 2008;36(6):1116-1122.

6. Tirabassi J, Brou L, Khodaee M, Lefort R, Fields SK, Comstock RD. Epidemiology of high school sports-related injuries resulting in medical disqualification: 2005-2006 through 2013-2014 academic years. Am J Sports Med. 2016 May 10. [Epub ahead of print]

7. Fernandez WG, Yard EE, Comstock RD. Epidemiology of lower extremity injuries among U.S. high school athletes. Acad Emerg Med. 2007;14(7):641-645.

8. Olsen OE, Myklebust G, Engebretsen L, Bahr R. Injury mechanisms for anterior cruciate ligament injuries in team handball: a systematic video analysis. Am J Sports Med. 2004;32(4):1002-1012.

9. Boden BP, Dean GS, Feagin JA Jr, Garrett WE Jr. Mechanisms of anterior cruciate ligament injury. Orthopedics. 2000;23(6):573-578.

10. Dragoo JL, Braun HJ, Harris AH. The effect of playing surface on the incidence of ACL injuries in National Collegiate Athletic Association American Football. Knee. 2013;20(3):191-195.

11. Joseph AM, Collins CL, Henke NM, Yard EE, Fields SK, Comstock RD. A multisport epidemiologic comparison of anterior cruciate ligament injuries in high school athletics. J Athl Train. 2013;48(6):810-817.

12. Granan LP, Inacio MC, Maletis GB, Funahashi TT, Engebretsen L. Sport-specific injury pattern recorded during anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(12):2814-2818.

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

14. Dragoo JL, Braun HJ, Durham JL, Chen MR, Harris AH. Incidence and risk factors for injuries to the anterior cruciate ligament in National Collegiate Athletic Association football: data from the 2004-2005 through 2008-2009 National Collegiate Athletic Association Injury Surveillance System. Am J Sports Med. 2012;40(5):990-995.

15. Dodson CC, Secrist ES, Bhat SB, Woods DP, Deluca PF. Anterior cruciate ligamenti in National Football League athletes from 2010 to 2013: a descriptive epidemiology study. Orthop J Sports Med. 2016;4(3):2325967116631949.

16. Golightly YM, Marshall SW, Callahan LF, Guskiewicz K. Early-onset arthritis in retired National Football League players. J Phys Act Health. 2009;6(5):638-643.

17. Brophy RH, Lyman S, Chehab EL, Barnes RP, Rodeo SA, Warren RF. Predictive value of prior injury on career in professional American football is affected by player position. Am J Sports Med. 2009;37(4):768-775.

18. Bradley J, Honkamp NJ, Jost P, West R, Norwig J, Kaplan LD. Incidence and variance of knee injuries in elite college football players. Am J Orthop. 2008;37(6):310-314.

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

20. Daruawalla JH, Greis PE, Hancock R; ASP Collaborative Group, Xerogeanes JW. Rates and determinants of return to play after anterior cruciate ligament reconstruction in NCAA Division 1 college football athletes: a study of the ACC, SEC, and PAC-12 conferences. Orthop J Sports Med. 2014;2(8):2325967114543901.

21. Shah VM, Andrews JR, Fleisig GS, McMichael CS, Lemak LJ. Return to play after anterior cruciate ligament reconstruction in National Football League athletes. Am J Sports Med. 2010;38(11):2233-2239.

22. McCullough KA, Phelps KD, Spindler KP, et al. Return to high school- and college-level football after anterior cruciate ligament reconstruction: a Multicenter Orthopaedic Outcomes Network (MOON) cohort study. Am J Sports Med. 2012;40(11):2523-2529.

23. Erickson BJ, Harris JD, Heninger JR, et al. Performance and return-to-sport after ACL reconstruction in NFL quarterbacks. Orthopedics. 2014;37(8):e728-e734.

24. Carey JL, Huffman GR, Parekh SG, Sennett BJ. Outcomes of anterior cruciate ligament injuries to running backs and wide receivers in the National Football League. Am J Sports Med. 2006;34(12):1911-1917.

25. Hershman EB, Anderson R, Bergfeld JA, et al. An analysis of specific lower extremity injury rates on grass and FieldTurf playing surfaces in National Football League Games: 2000-2009 seasons. Am J Sports Med. 2012;40(10):2200-2205.

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

27. Derscheid GL, Garrick JG. Medial collateral ligament injuries in football. Nonoperative management of grade I and grade II sprains. Am J Sports Med. 1981;9(6):365-368.

28. Meyers MC, Barnhill BS. Incidence, causes, and severity of high school football injuries on FieldTurf versus natural grass: a 5-year prospective study. Am J Sports Med. 2004;32(7):1626-1638.

29. Lundblad M, Waldén M, Magnusson H, Karlsson J, Ekstrand J. The UEFA injury study: 11-year data concerning 346 MCL injuries and time to return to play. Br J Sports Med. 2013;47(12):759-762.

30. Hewson GF Jr, Mendini RA, Wang JB. Prophylactic knee bracing in college football. Am J Sports Med. 1986;14(4):262-266.

31. Rovere GD, Haupt HA, Yates CS. Prophylactic knee bracing in college football. Am J Sports Med. 1987;15(2):111-116.

32. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee sprains in college football. Brace wear preferences and injury risk. Am J Sports Med. 1994;22(1):2-11.

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

34. Ellsasser JC, Reynolds FC, Omohundro JR. The non-operative treatment of collateral ligament injuries of the knee in professional football players. An analysis of seventy-four injuries treated non-operatively and twenty-four injuries treated surgically. J Bone Joint Surg Am. 1974;56(6):1185-1190.

35. Holden DL, Eggert AW, Butler JE. The nonoperative treatment of grade I and II medial collateral ligament injuries to the knee. Am J Sports Med. 1983;11(5):340-344.

36. Indelicato PA, Hermansdorfer J, Huegel M. Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate football players. Clin Orthop Relat Res. 1990;(256):174-177.

37. Jones RE, Henley MB, Francis P. Nonoperative management of isolated grade III collateral ligament injury in high school football players. Clin Orthop Relat Res. 1986;(213):137-140.

38. Fetto JF, Marshall JL. Medial collateral ligament injuries of the knee: a rationale for treatment. Clin Orthop Relat Res. 1978;(132):206-218.

39. Corten K, Hoser C, Fink C, Bellemans J. Case reports: a Stener-like lesion of the medial collateral ligament of the knee. Clin Orthop Relat Res. 2010;468(1):289-293.

40. Marchant MH Jr, Tibor LM, Sekiya JK, Hardaker WT Jr, Garrett WE Jr, Taylor DC. Management of medial-sided knee injuries, part 1: medial collateral ligament. Am J Sports Med. 2011;39(5):1102-1113.

41. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 1998;26(1):59-65.

42. Casteleyn PP, Handelberg F. Arthroscopy in the diagnosis of occult dislocation of the patella. Acta Orthop Belg. 1989;55(3):381-383.

43. Waterman BR, Belmont PJ Jr, Owens BD. Patellar dislocation in the United States: role of sex, age, race, and athletic participation. J Knee Surg. 2012;25(1):51-57.

44. Sillanpää P, Mattila VM, Iivonen T, Visuri T, Pihlajamäki H. Incidence and risk factors of acute traumatic primary patellar dislocation. Med Sci Sports Exerc. 2008;40(4):606-611.

45. Hsiao M, Owens BD, Burks R, Sturdivant RX, Cameron KL. Incidence of acute traumatic patellar dislocation among active-duty United States military service members. Am J Sports Med. 2010;38(10):1997-2004.

46. Fithian DC, Paxton EW, Stone ML, et al. Epidemiology and natural history of acute patellar dislocation. Am J Sports Med. 2004;32(5):1114-1121.

47. Mitchell J, Magnussen RA, Collins CL, et al. Epidemiology of patellofemoral instability injuries among high school athletes in the United States. Am J Sports Med. 2015;43(7):1676-1682.

48. Nikku R, Nietosvaara Y, Aalto K, Kallio PE. The mechanism of primary patellar dislocation: trauma history of 126 patients. Acta Orthop. 2009;80(4):432-434.

49. Tsai CH, Hsu CJ, Hung CH, Hsu HC. Primary traumatic patellar dislocation. J Orthop Surg Res. 2012;7:21.

50. Atkin DM, Fithian DC, Marangi KS, Stone ML, Dobson BE, Mendelsohn C. Characteristics of patients with primary acute lateral patellar dislocation and their recovery within the first 6 months of injury. Am J Sports Med. 2000;28(4):472-479.

51. Nomura E, Inoue M, Kurimura M. Chondral and osteochondral injuries associated with acute patellar dislocation. Arthroscopy. 2003;19(7):717-721.

52. Kirsch MD, Fitzgerald SW, Friedman H, Rogers LF. Transient lateral patellar dislocation: diagnosis with MR imaging. AJR Am J Roentgenol. 1993;161(1):109-113.

53. Virolainen H, Visuri T, Kuusela T. Acute dislocation of the patella: MR findings. Radiology. 1993;189(1):243-246.

54. Stanitski CL. Articular hypermobility and chondral injury in patients with acute patellar dislocation. Am J Sports Med. 1995;23(2):146-150.

55. Mäenpää H, Huhtala H, Lehto MU. Recurrence after patellar dislocation. Redislocation in 37/75 patients followed for 6-24 years. Acta Orthop Scand. 1997;68(5):424-426.

56. Buchner M, Baudendistel B, Sabo D, Schmitt H. Acute traumatic primary patellar dislocation: long-term results comparing conservative and surgical treatment. Clin J Sport Med. 2005;15(2):62-66.

57. Fisher B, Nyland J, Brand E, Curtin B. Medial patellofemoral ligament reconstruction for recurrent patellar dislocation: a systematic review including rehabilitation and return-to-sports efficacy. Arthroscopy. 2010;26(10):1384-1394.

58. Lippacher S, Dreyhaupt J, Williams SR, Reichel H, Nelitz M. Reconstruction of the medial patellofemoral ligament: clinical outcomes and return to sports. Am J Sports Med. 2014;42(7):1661-1668.

59. Panni AS, Alam M, Cerciello S, Vasso M, Maffulli N. Medial patellofemoral ligament reconstruction with a divergent patellar transverse 2-tunnel technique. Am J Sports Med. 2011;39(12):2647-1655.

60. Schneider DK, Grawe B, Magnussen RA, et al. Outcomes after isolated medial patellofemoral ligament reconstruction for the treatment of recurrent lateral patellar dislocations: a systematic review and meta-analysis. Am J Sports Med. 2016 Feb 12. [Epub ahead of print]

61. Amis AA, Bull AM, Gupte CM, Hijazi I, Race A, Robinson JR. Biomechanics of the PCL and related structures: posterolateral, posteromedial and meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc. 2003;11(5):271-281.

62. Fu FH, Harner CD, Johnson DL, Miller MD, Woo SL. Biomechanics of knee ligaments: basic concepts and clinical application. Instr Course Lect. 1994;43:137-148.

63. Markolf KL, Feeley BT, Tejwani SG, Martin DE, McAllister DR. Changes in knee laxity and ligament force after sectioning the posteromedial bundle of the posterior cruciate ligament. Arthroscopy. 2006; 22(10):1100-1106.

64. Ganelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: Part II. Arthroscopy. 1995;11(5):526-529.

65. Schulz MS, Russe K, Weiler A, Eichhorn HJ, Strobel MJ. Epidemiology of posterior cruciate ligament injuries. Arch Orthop Trauma Surg. 2003;123(4):186-191.

66. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The nonoperative treatment of acute, isolated (partial or complete) posterior cruciate ligament-deficient knees: an intermediate-term follow-up study. HSS J. 2007;3(2):137-146.

67. Fowler PJ, Messieh SS. Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med. 1987;15(6):553-557.

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

69. LaPrade CM, Civitarese DM, Rasmussen MT, LaPrade RF. Emerging updates on the posterior cruciate ligament: a review of the current literature. Am J Sports Med. 2015;43(12):3077-3092.

70. Torg JS, Barton TM, Pavlov H, Stine R. Natural history of the posterior cruciate ligament-deficient knee. Clin Orthop Relat Res. 1989(246):208-216.

71. Miller MD. Orthopaedic Knowledge Update: Sports Medicine 5. Rosemont, IL; American Academy of Orthopaedic Surgeons; 2016.

72. Shelbourne KD, Clark M, Gray T. Minimum 10-year follow-up of patients after an acute, isolated posterior cruciate ligament injury treated nonoperatively. Am J Sports Med. 2013;41(7):1526-1533.

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

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Knee Injuries in American Football: An Epidemiological Review
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Foot and Ankle Injuries in American Football

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Foot and Ankle Injuries in American Football

Foot and ankle injuries are common in American football, with injury rates significantly increasing over the past decade.1-5 Epidemiologic studies of collegiate football players have shown an annual incidence of foot and ankle injuries ranging from 9% to 39%,3,6 with as many as 72% of all collegiate players presenting to the National Football League (NFL) Combine with a history of a foot or ankle injury and 13% undergoing surgical treatment.5 Player position influences the rate and type of foot and ankle injury. Offensive and “skill position” players, including linemen, running backs, and wide receivers, are particularly susceptible to foot and ankle injuries due to high levels of force and torque placed on the distal extremity during running, cutting, and tackling. Shoe wear changes, playing field conditions, increasing player size and speed, and improved reporting of injuries are also contributing to increasing injury rates.

The interaction between player cleats and the playing surface is a central issue of foot and ankle injuries in football. Improved traction relates to performance, but increased subsequent torque on the lower extremity is associated with injury. While lateral ankle sprains are the most common foot and ankle injury experienced by football players,7 numerous other injuries can occur, including turf toe, Jones fractures, Lisfranc injuries, syndesmotic disruption, deltoid complex avulsion, and Achilles ruptures. It is important for physicians to be able to recognize, diagnose, and appropriately treat these injuries in players in order to expedite recovery, restore function, and help prevent future injury and long-term sequelae. This review focuses on updated treatment principles, surgical advances, and rehabilitation protocols for common football foot and ankle injuries.

Turf Toe

The term “turf toe” was first used in 1976 to refer to hyperextension injuries and plantar capsule-ligament sprains of the hallux metatarsophalangeal (MTP) joint that can lead to progressive cock-up deformity.8 While these injuries can occur on any surface and disrupt soft tissue balance with functional implications, predisposing factors include increasing playing surface hardness and decreasing shoe stiffness. In a classic scenario, the foot is fixed in equinus as an axial load is placed on the back of the heel, resulting in forced dorsiflexion of the hallux MTP joint.9 As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the metatarsal head articular surface bears the majority of the load, causing partial or complete tearing of the plantar plate with or without hallux MTP dislocation. Osteochondral lesions of the MTP joint and subchondral edema of the metatarsal head can occur concurrently as the proximal phalanx impacts or shears across the metatarsal head articular surface.

Clinical examination should focus on hallux swelling, alignment, and flexor hallucis longus (FHL) function along with vertical instability of the hallux MTP joint using a Lachman test. Radiographs should be evaluated for proximal migration of the sesamoids or diastasis (Figures W1A-W1C).

Figures W1A-W1C
Forced hallux MTP dorsiflexion lateral view can help assess the distance from the distal sesamoid to the base of the phalanx. A small fleck of bone pulled off of the proximal phalanx or distal sesamoid may indicate a capsular avulsion or disruption. Live fluoroscopy can be very helpful in diagnosing turf toe, as the physician can assess the trailing motion of the sesamoids with increasing dorsiflexion and evaluate instability in all planes. Magnetic resonance imaging (MRI) is useful for subtle capsular injuries and can also identify osseous and articular damage that may occur and FHL disruption (Figures W2A, W2B).
Figures W2A, W2B
Nonoperative intervention focuses on rest, ice, compression, and elevation (RICE) and nonsteroidal anti-inflammatory drugs (NSAIDs). The hallux is temporarily immobilized in a plantarflexed position using a short leg cast or walking boot with toe spica or turf toe plate with tape for 2 to 3 weeks.

Indications for surgical intervention include loss of push-off strength, gross MTP instability, proximal migration of the sesamoids, and progressive hallux malalignment or clawing after immobilization. Cases can involve one or a combination of the following: (1) large capsular avulsion with unstable MTP joint; (2) diastasis of bipartite sesamoid; (3) diastasis of sesamoid fracture; (4) retraction of sesamoid; (5) traumatic hallux valgus deformity; (6) vertical instability (positive Lachman test); (7) loose body in MTP joint; or (8) chondral injury in MTP joint. The goal of surgery is the restoration of anatomy in order to restore normal function of the hallux MTP joint.

We have found that using dual medial and plantar incisions places less traction on the plantar medial cutaneous nerve, improves lateral exposure, and provides better wound healing. The medial capsulotomy extends from the metatarsal neck to the mid-phalanx to provide complete visualization of the sesamoid complex (Figures 1A-1F).
Figures 1A-1F
The collateral ligaments are often torn away from the metatarsal head during the initial dissection and the plantar plate tear is distal to the sesamoid complex. The soft tissue defect in the plantar complex must be closed distal to the sesamoids followed by advancement of the plantar plate to the proximal phalanx in a distal to proximal fashion and advancement of the medial capsule. The plantar incision is made along the lateral border of hallux MTP-sesamoid complex just lateral to the weight-bearing surface of the hallux and the plantar lateral cutaneous nerve is carefully dissected and retracted out of the way. Sutures are placed in a figure-of-eight fashion through the plantar capsule and plantar plate starting lateral to medial to reduce injury to the nerve. If the tear cannot be primarily repaired due to inadequate healthy tissue, a plantar plate advancement can be performed directly onto the base of the proximal phalanx using drill holes or suture anchors. Proper alignment and motion of the sesamoids should be verified with fluoroscopy and compared to the contralateral hallux (Figures W3A, W3B).
Figures W3A, W3B


It is important to recognize that not all turf toe injuries involve pure hyperextension on artificial playing surfaces. In recent years, we have found an increasing rate of medial variant turf toe injuries in which a forceful valgus stress on the hallux leads to rupture of the medial collateral ligament, medial or plantar-medial capsule, and/or abductor halluces. Medial variant turf toe can lead to progressive hallux valgus and a traumatic bunion with a significant loss of push-off strength and difficulty with cutting maneuvers. Surgical treatment requires a modified McBride bunionectomy with adductor tenotomy and direct repair of the medial soft tissue defect.

Postoperative management is just as important as proper surgical technique for these injuries and involves a delicate balance between protecting the repair and starting early range of motion (ROM). Patients are immobilized non-weight-bearing (NWB) for 5 to 7 days maximum followed immediately with the initiation of passive hallux plantarflexion to keep the sesamoids moving. Active hallux plantarflexion is started at 4 weeks after surgery with active dorsiflexion from 6 to 8 weeks. Patients are transitioned to an accommodative shoe with stiff hallux insert 8 weeks postoperative with continued therapy focusing on hallux ROM. Running is initiated at 12 weeks and return to play (RTP) is typically allowed 4 months after surgery.

 

 

Jones Fractures

Jones fractures are fractures of the 5th metatarsal at the metaphyseal-diaphyseal junction, where there is a watershed area of decreased vascularity between the intramedullary nutrient and metaphyseal arteries. Current thought is that the rising rate of Jones fractures among football players is partially caused by the use of flexible, narrow cleats that do not provide enough stiffness and lateral support for the 5th metatarsal during running and cutting. Additionally, lateral overload from a baseline cavovarus foot posture with or without metatarsus adductus and/or skewfoot is thought to contribute to Jones fractures.10 Preoperative radiographs should be evaluated for fracture location, orientation, amount of cortical thickening, and overall geometry of the foot and 5th metatarsal. In elite athletes, the threshold for surgical intervention is decreasing in order to expedite healing and recovery and decrease re-fracture risk. This rationale is based on delayed union rates of 25% to 66%, nonunion rates of 7% to 28%,11 and re-fracture rates of up to 33% associated with nonoperative treatment.12 Nonoperative management is usually not feasible in the competitive athlete, as it typically involves a period of protected weight-bearing in a tall controlled ankle motion (CAM) boot for 6 to 8 weeks with serial radiographs to evaluate healing.

Our preference for surgical intervention involves percutaneous screw fixation with a “high and inside” starting point on fluoroscopy (Figures 2A-2D).

Figures 2A-2D
The guidewire is inserted percutaneously through the skin 2 cm proximal to the base of the 5th metatarsal. Incorrect starting point can lead to a prominent screw head laterally or perforation of the medial cortex. A 1-cm incision is made around the guidewire entry point and intramedullary cannulated drilling enters the proximal third of the metatarsal, removing any thickened lateral cortex. Due to the natural curve of the 5th metatarsal, cannulated drilling is not continued distally but can be safely completed with a 3.2-mm solid drill bit. Proper tap sizing should generate enough torque to begin to rotate the entire foot as the tap is advanced (Figures W4A-W4F).
Figures W4A-W4F
The largest solid screw with a low-profile head that “comfortably” fits the intramedullary canal of the 5th metatarsal should be inserted (Carolina Jones Fracture System, Wright Medical Technology).13 In elite athletes, we will typically use a 5.5-mm or 6.5-mm screw that is 45 to 55 mm in length. Screw threads should pass just across the fracture site, avoiding “straightening” of the curved 5th metatarsal that will create a lateral gap and increase the rate of nonunion. We do not recommend headless tapered screws due to inconsistent compression and difficulty with later removal if re-fracture or nonunion occurs.

In career athletes, we augment the fracture site using a mixture of bone marrow aspirate concentrate (BMA) (Magellan, Arteriocyte Medical Systems) and demineralized bone matrix (DBM) (Mini Ignite, Wright Medical Technology) injected percutaneously in and around the fracture site under fluoroscopic guidance. Using this technique in a cohort of 25 NFL players treated operatively for Jones fractures, we found that 100% of athletes were able to RTP in the NFL in an average of 9.5 weeks.14 Two patients (7.5%) suffered re-fractures requiring revision surgery with iliac crest bone graft and repeat screw placement with a RTP after 15 weeks. We did not find an association between RTP and re-fracture rate.

The appropriate rehabilitation protocol for Jones fractures after surgery remains controversial and dependent on individual needs and abilities.15,16 For athletes in-season, we recommend a brief period of NWB for 1 to 2 weeks followed by toe-touch weight-bearing in a tall CAM boot for 2 to 4 weeks. After 4 weeks, patients begin gentle exercises on a stationary bike and pool therapy to reduce impact on the fracture site. Low-intensity pulsed ultrasound bone stimulators (Exogen, Bioventus) are frequently used directly over fracture site throughout the postoperative protocol as an adjuvant therapy. If clinically nontender over the fracture site, patients are allowed to begin running in modified protective shoe wear 4 weeks after surgery with an average RTP of 6 to 8 weeks. RTP is determined clinically, as radiographic union may not be evident for 12 to 16 weeks. Useful custom orthoses include turf toe plates with a cushioned lateral column and lateral heel wedge if hindfoot varus is present preoperatively.10 The solid intramedullary screw is left in place permanently.

In our experience, we have found the average re-fracture and nonunion rate to be approximately 8% across all athletes. Our observation that union rates do not appear to be related to RTP times suggests that underlying biology such as Vitamin D deficiency may play a larger role in union rates than previously thought. We have found that most Jones re-fractures occur in the first year after the initial injury, but can occur up to 2.5 years afterwards as well.14 For the management of symptomatic re-fractures and nonunions, the previous screw must be first removed. This can be difficult if the screw is bent or broken, and may require a lateral corticotomy of the metatarsal.

After hardware removal, we advocate open bone grafting of the fracture site using bone from the iliac crest retrieved with a small, percutaneous trephine. Re-fixation should be achieved using a larger, solid screw and postoperative adjuvants may include bone stimulators, Vitamin D and calcium supplemention, and possible teriparatide use (Forteo, Eli Lilly), depending on individual patient profile. In a cohort of 21 elite athletes treated for Jones fracture revision surgery with screw exchange and bone grafting, we found that 100% of patients had computed tomography (CT) evidence of union, with an average RTP of 12.3 weeks.17

 

 

Lisfranc Injuries

Lisfranc injuries include any bony or ligamentous damage that involves the tarsometatarsal (TMT) joints. While axial loading of a fixed, plantarflexed foot has traditionally been thought of as the most common mechanism of Lisfranc injury, we have found that noncontact twisting injuries leading to Lisfranc disruption are actually more common among NFL players. This mechanism is similar to noncontact turf toe and results in a purely ligamentous injury. We have found this to be particularly true in the case of defensive ends engaged with offensive linemen in which no axial loading or contact of the foot occurs. Clinically, patients often have painful weight-bearing, inability to perform a single limb heel rise, plantar ecchymosis, and swelling and point tenderness across the bases of the 1st and 2nd metatarsals.

It is critical to obtain comparison weight-bearing radiographs of both feet during initial work-up to look for evidence of instability. Subtle radiographic findings of Lisfranc injury include a bony “fleck” sign, compression fracture of the cuboid, and diastasis between the base of the 1st and 2nd metatarsals and/or medial and middle cuneiforms (Figures 3A, 3B).

Figures 3A, 3B
Stress testing involves pronation and adduction of the foot under live fluoroscopy to evaluate for diastasis. MRI can be helpful in cases of vague pain with negative radiographs and subtle displacement. Nonoperative treatment for cases of no instability or displacement involved protected weight-bearing for 4 weeks followed by progressive increase in activities, with RTP 6 to 8 weeks after injury.

The goal of surgical intervention is to obtain and maintain anatomic reduction of all unstable joints in order to restore a normal foot posture. One of the difficulties with Lisfranc injuries is that there are no exact diastasis parameters and individuals should be treated based on symptoms, functional needs, and degree of instability. It has been shown that 5 mm of displacement can have good long-term clinical results in select cases without surgery.18 For surgery, we recommend open reduction to remove interposed soft tissue debris and directly assess the articular surfaces (Figures 4A-4D).
Figures 4A-4D
A freer can be placed in the individual joints to assess for areas of instability. We prefer solid screw fixation (Charlotte Lisfranc Reconstruction System, Wright Medical Technology) to decrease the risk of later screw breakage. A homerun screw from the proximal aspect of the medial cuneiform to the distal-lateral aspect of the 2nd metatarsal base should be placed first. Bridge plates can be used over the 1st and 2nd TMT joints to avoid articular cartilage damage without a loss of rigidity.19

Proximal-medial column Lisfranc injury variants are increasingly common among football players.20 In these injuries, the force of injury extends through the intercuneiform joint and exits out the naviculocuneiform joint, thus causing instability at multiple joints and an unstable 1st ray. Patients often have minimal clinical findings and normal radiographs and stress radiographs. MRI of the foot often reveals edema at the naviculocuneiform joint. Often patients fail to improve with nonoperative immobilization with continued inability to push off from the hallux. Unrecognized or untreated instability will lead to rapid deterioration of the naviculocuneiform joint. Surgical intervention requires a homerun screw and intercuneiform screw. We do not recommend primary arthrodesis in athletes due to significant risk of malunion and nonunion unless severe articular damage is present.

Patients are typically kept NWB in a splint for 2 weeks after surgery followed by NWB in a tall CAM from 3 to 4 weeks postoperative. Progressive weight-bearing and ROM exercises are initiated from 4 to 8 weeks, followed by return to accommodative shoe wear from 10 to 12 weeks. Hardware removal is performed 4 to 6 months after surgery, typically in the off-season to allow for 6 to 8 weeks or protected recovery afterwards. Premature hardware removal can lead to loss of reduction, particularly at the intercuneiform joints. All hardware crossing the TMT joints should be removed, while the homerun screw can be left in place in addition to the intercuneiform screw. RTP in football typically occurs 6 to 7 months after surgery. Final functional outcome is related to the adequacy of initial reduction and severity of the initial injury.21

Syndesmotic Disruption

Syndesmotic injuries comprise 1% to 18% of ankle sprains in the general population, but occur at much higher rates in football due to the increased rotation forces placed on the ankle during cutting and tackling. RTP after syndesmotic injury often takes twice as long when compared to isolated lateral ankle ligamentous injury.22 Missed injuries are common and if not treated properly can lead to chronic ankle instability and posttraumatic ankle arthritis.23 Syndesmotic injury can occur in isolation or with concomitant adjacent bony, cartilaginous, or ligamentous injuries. Therefore, clinical examination and imaging work-up are critical to successful management.

 

 

Syndesmotic injuries often result from an external rotation force applied to a hyperdorsiflexed ankle while the foot is planted. This mechanism causes the fibula to externally rotate while translating posteriorly and laterally, resulting in rupture of the anterior inferior tibiofibular ligament (AITFL) first, followed by the deep deltoid ligament, interosseous ligament (IOL), and lastly posterior talofibular ligament.24 Most syndesmotic injuries involve rupture of only the AITFL and IOL.25 Multiple clinical stress tests have been designed to assess syndesmotic stability, including the squeeze test, external rotation stress test, crossed-leg test, and fibula-translation test.26-29 However, no physical examination maneuver has been shown to reliably predict the presence or degree of syndesmotic injury and therefore imaging studies are necessary.30

Initial imaging should include standing radiographs of the affected ankle. An increase in the medial clear space between the medial malleolus and talus can occur with a combined syndesmotic and deltoid disruption. In the case of subtle syndesmotic injuries, contralateral comparison weight-bearing radiographs are recommended. CT and MRI can provide additional information, but these static imaging tests cannot identify instability. Fluoroscopic stress evaluation is beneficial but has a high false-negative rate in low-grade injuries and may not detect partial rupture of the AITFL and IOL.31 It has been shown that malrotation of as much as 30° of external rotation can occur if relying on intraoperative fluoroscopy alone.32 It has been our practice to recommend surgical reduction and stabilization for any syndesmotic injury with documented diastasis or instability seen on imaging and/or arthroscopy.

Nonoperative treatment is indicated for truly stable grade I syndesmotic injuries. This involves rest and immobilization followed by a progressive rehabilitation program consisting of stretching, strengthening, and proprioceptive exercises.33 After 1 week of protected weight-bearing in a cast or tall CAM boot, progression to full weight-bearing should occur over the following week. Active-assisted ankle ROM exercises and light proprioceptive training should then be initiated followed by sport-specific exercises 2 to 3 weeks after injury.

Arthroscopy can be a valuable diagnostic tool in the setting of subtle syndesmotic injury with negative radiographs, positive MRI for edema, and a protracted recovery course with vague pain (Figures W5A-W5E).

Figures W5A-W5E
In these situations, an examination under anesthesia is performed, the syndesmosis is probed under direct arthroscopic visualization, and distal tibiofibular instability is evaluated while performing an external rotation stress test. For surgical intervention of these subtle varieties or any athlete with documented instability, we prefer the use of dynamic stabilization with a knotless suture-button construct (TightRope, Arthrex) or hybrid fixation with screws (3.5/4.5 mm) and suture-buttons. Advantages of a knotless suture-button construct include more physiologic motion at the syndesmosis and decreased hardware irritation and implant removal.

Implants are placed above the true syndesmotic joint (at least 15 mm above the tibial plafond) angled 30° posterior to anterior to follow the normal relationship of the fibula to the distal tibia in the incisura. Typically 2 suture-buttons are used, with the devices placed in a divergent fashion. We highly recommend the use of a fibular buttress plate with button placement in individuals returning to contact activity. This construct increases surface area distribution while preventing stress risers and the risk of fibula fractures. In a cadaver model with deliberate syndesmotic malreduction, suture-button stabilization resulted in decreased postoperative displacement as opposed to conventional screw fixation.34 Therefore, dynamic syndesmotic fixation may help to decrease the negative sequelae of iatrogenic clamp malreduction. 
Postoperative rehabilitation involves NWB in a cast or tall CAM boot for 4 weeks followed by ankle ROM exercises and progressive weight-bearing and physical therapy. Patients are transitioned to a lace-up ankle brace and athletic shoe from 6 to 12 weeks postoperative with increasing activity. Running and jumping is permitted 4 months after surgery with RTP typically at 6 to 7 months. Athletes who have had surgical stabilization for documented instability without any diastasis may engage in a more rapid recovery and RTP as symptoms and function allow.

Deltoid Complex Avulsion

Missed or neglected deltoid ligament injuries can lead to progressive chondral injury and joint degeneration. These injuries are often subtle and difficult to diagnose. An inability to perform a single limb heel rise, persistent pain with activity, and lack of normal functional improvement despite appropriate care are indicators of subtle ligament instability. These injuries often require an examination under anesthesia with combined ankle arthroscopy. Valgus stress testing of the ankle while directly visualizing the deltoid ligament from the anterolateral portal can reveal medial laxity in addition to potential osteochondral lesions along the anterolateral talar dome.

In American football players, we have observed that infolding and retraction of an avulsed superficial deltoid ligament complex after an ankle fracture, Maisonneuve injury, or severe high ankle sprain can be a source of persistent increased medial clear space, malreduction, and postoperative pain and medial instability. We have found that there is often complete avulsion of the superficial deltoid complex off the proximal aspect of the medial malleolus during high-energy ankle fractures in football players that is amenable to direct repair to bone (Figures W6A-W6E).

Figures W6A-W6E
In a cohort of 14 NFL players who underwent ankle fracture fixation with ankle arthroscopy and debridement, fibula fixation with plate and screws, syndesmotic fixation with suture-button devices, and open deltoid complex repair with suture anchors, all athletes were able to return to running and cutting maneuvers by 6 months after surgery.35 There were no intraoperative or postoperative complications noted, and no players had clinical evidence of medial pain or instability at final follow-up with radiographic maintenance of anatomic mortise alignment.

During surgical repair, an incision is made along the anterior aspect of the medial malleolus and the superficial deltoid ligament complex can often be found flipped and interposed in the medial gutter. A rongeur is used to create a bleeding cancellous bone surface for soft-tissue healing and 1 to 2 suture anchors are used to repair and imbricate the deltoid ligament complex back to the medial malleolus. The goal of these sutures is to repair the tibionavicular and tibial spring ligaments back to the medial malleolus. We believe that superficial deltoid complex avulsion during high-energy ankle fractures is a distinct injury pattern that should be recognized and may benefit from primary open repair.

We currently open explore every deltoid ligament complex in athletes with unstable syndesmotic injuries, as we believe that deltoid avulsion injuries are underrecognized and do not heal in an anatomic fashion if left alone. Postoperative recovery follows the same immobilization, progressive weight-bearing, and physical therapy protocol as that for syndesmotic disruption.

 

 

Achilles Ruptures

Acute midsubstance Achilles tendon ruptures are an increasingly common injury in patients 30 to 50 years of age, with more than 50% of all injuries occurring during basketball.36,37 Among NFL players, we have found that Achilles ruptures tend to occur at a higher rate during training camp, when athletes are deconditioned and quickly returning to explosive push-off activities. Physical examination should include a Thompson test, palpation of a gap within the tendon, and evaluation of resting ankle dorsiflexion in the affected extremity in the prone position with the knees bent. Lateral radiographs should be analyzed for the presence of a bony avulsion fragment indicative of an insertional avulsion injury or midsubstance calcium deposition reflecting chronic Achilles tendinosis, as both of these conditions will change surgical management. MRI is not recommended with acute midsubstance ruptures but may be helpful in the case of chronic ruptures or more proximal tears of the musculotendinous junction.

The management of acute midsubstance Achilles tendon ruptures is controversial, with no general consensus in the literature regarding nonoperative treatment, surgical repair, and ideal repair technique.36,38-42 American Academy of Orthopaedic Surgeons clinical practice guidelines report moderate evidence that nonoperative treatment of Achilles tendon ruptures has lower wound healing complications but higher rates of re-rupture.38,39 Additionally, limited incision approaches have been found to have fewer overall complications compared with traditional open repair. In an effort to reduce the incidence of postoperative wound complications while improving functional recovery, modern repair techniques focus on a limited incision repair using percutaneous suture insertion and management (PARS Achilles Jig System, Arthrex).36 The limited incision technique utilizes a 2-cm transverse incision and non-disposable jig with divergent needle passes and locking suture fixation options to secure and fixate both tendon ends with minimal dissection of skin, subcutaneous tissue, and paratenon. Limited incision repair is ideally performed within 2 weeks of the injury to ensure that both tendon ends are easy to identify, mobilize, and repair. An open repair is generally recommended for midsubstance ruptures more than 4 weeks old and cases of insertional rupture and Achilles tendinopathy.

In a cohort of 9 NFL players treated for midsubstance Achilles ruptures using the PARS technique, we found no re-ruptures, no wound complications, and no sural nerve issues after surgery.43 A comparative review of 270 cases of operatively treated Achilles tendon ruptures (101 PARS, 169 traditional open repair) showed that the PARS group had significantly shorter operative times and a higher number of patients able to return to baseline physical activities by 5 months compared to open repair.36 Although not statistically significant, the overall PARS complication rate was 5% while the open complication rate was 11%. The PARS group had no cases of sural neuritis or deep infection requiring reoperation. We currently use a limited incision technique for all acute midsubstance Achilles ruptures in athletes regardless of sport, patient size, or position played.

During surgery, a 2-cm transverse incision is made over the gap in the Achilles tendon and dissection is carried down to the rupture site with minimal manipulation of the skin (Figures 5A-5F).

Figures 5A-5F
A transverse incision is made through the paratenon and typically a hematoma is expressed. An Allis clamp is inserted and the proximal tendon stump is grabbed securely and pulled through the wound approximately 1 to 2 cm. The PARS jig is inserted around the proximal tendon and centered so that the needle and sutures will pass through tendon. Needles and sutures are passed in a stepwise fashion and then the entire jig is removed from the wound. Sutures are passed to create 2 non-locking and 1 locking suture. The jig and suture passing process is repeated for the distal tendon stump. Then, each pair of sutures is tied together with the ankle in maximum plantarflexion to obtain a secure end-to-end repair. The knots are cut short and tucked into tendon so that they do not protrude and cause subcutaneous tissue irritation. Absorbable sutures are used to close the paratenon, followed by closure of subcutaneous tissues and skin followed by placement of a short leg posterior mold NWB splint with the ankle in resting plantar flexion.

A key aspect of postoperative recovery is avoiding excessive ankle dorsiflexion while the tendon is healing during the first 4 weeks after surgery, as this can lead to an elongated tendon with loss of push-off strength. Patients are kept in a plantarflexion splint NWB for 2 weeks after surgery. If the incision is healed at 2 weeks, sutures are removed and patients are transitioned into a NWB tall CAM boot for 2 weeks with gentle ankle ROM exercises. If there is any concern regarding wound healing status, sutures are maintained for an additional 1 to 2 weeks.

From 4 to 8 weeks after surgery, progressive weight-bearing with continued ankle ROM exercises is initiated with peel-away heel lifts (~2 cm thick total, 3 layers). Each layer of the heel lift is gradually removed as pain allows every 2 to 3 days with the goal of being full weight-bearing with the foot flat at 6 weeks postoperative. Physical therapy focusing on ankle ROM and gentle Achilles stretching and strengthening is also started 6 weeks after surgery. From 8 to 12 weeks postoperative, patients are transitioned out of the tall CAM boot into normal, accommodative shoe wear with full weight-bearing. We avoid ankle dorsiflexion past neutral until 12 weeks after surgery, as overlengthening of the Achilles complex and the subsequent loss of push-off power can be devastating to running athletes. Activity levels are increased as tolerated, with no running or jumping from 12 to 16 weeks with full release to all activities after 16 weeks. RTP often takes 5 to 6 months after surgery, depending on the position played.

Am J Orthop. 2016;45(6):358-367. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Canale ST, Cantler ED Jr, Sisk TD, Freeman BL 3rd. A chronicle of injuries of an American intercollegiate football team. Am J Sports Med. 1981;9(6):384-389.2. Robey JM, Blyth CS, Mueller FO. Athletic injuries. Application of epidemiologic methods. JAMA. 1971;217(2):184-189.

3. Saal JA. Common American football injuries. Sports Med. 1991;12(2):132-147.

4. Thompson N, Halpern B, Curl WW, et al. High school football injuries: evaluation. Am J Sports Med. 1987;15(2):117-124.

5. Kaplan LD, Jost PW, Honkamp N, Norwig J, West R, Bradley JP. Incidence and variance of foot and ankle injuries in elite college football players. Am J Orthop. 2011;40(1):40-44.

6. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.

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

8. Bowers KD Jr, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8(2):81-83.

9. McCormick JJ, Anderson RB. Turf toe: anatomy, diagnosis, and treatment. Sports Health. 2010;2(6):487-494.

10. Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367-1372.

11. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete. Orthop Clin North Am. 2002;33(3):587-598.

12. Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am. 1995;26(2):353-361.

13. Nunley JA, Glisson RR. A new option for intramedullary fixation of Jones fractures: the Charlotte Carolina Jones Fracture System. Foot Ankle Int. 2008;29(12):1216-1221.

14. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8-16.

15. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones fractures. Analysis of failure. Am J Sports Med. 2002;30(1):55-60.

16. Portland G, Kelikian A, Kodros S. Acute surgical management of Jones’ fractures. Foot Ankle Int. 2003;24(11):829-833.

17. Hunt KJ, Anderson RB. Treatment of Jones fracture nonunions and refractures in the elite athlete: outcomes of intramedullary screw fixation with bone grafting. Am J Sports Med. 2011;39(9):1948-1954.

18. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871-878.

19. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw fixation. Foot Ankle Int. 2005;26(6):462-473.

20. Ardoin GT, Anderson RB. Subtle Lisfranc injury. Tech Foot Ankle Surg. 2010;9(3):100-106.

21. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A(11):1609-1618.

22. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.

23. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35(7):1197-1207.

24. Beumer A, Valstar ER, Garling EH, et al. Effects of ligament sectioning on the kinematics of the distal tibiofibular syndesmosis: a radiostereometric study of 10 cadaveric specimens based on presumed trauma mechanisms with suggestions for treatment. Acta Orthop. 2006;77(3):531-540.

25. McCollum GA, van den Bekerom MP, Kerkhoffs GM, Calder JD, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1328-1337.

26. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.

27. Nussbaum ED, Hosea TM, Sieler SD, Incremona BR, Kessler DE. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med. 2001;29(1):31-35.

28. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle syndesmosis injuries. Foot Ankle Int. 2005;26(2):187-188.

29. Beumer A, van Hemert WL, Swierstra BA, Jasper LE, Belkoff SM. A biomechanical evaluation of clinical stress tests for syndesmotic ankle instability. Foot Ankle Int. 2003;24(4):358-363.

30. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14(4):232-236.

31. Beumer A, Valstar ER, Garling EH, et al. External rotation stress imaging in syndesmotic injuries of the ankle: comparison of lateral radiography and radiostereometry in a cadaveric model. Acta Orthop Scand. 2003;74(2):201-205.

32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.

33. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2(6):460-470.

34. Westermann RW, Rungprai C, Goetz JE, Femino J, Amendola A, Phisitkul P. The effect of suture-button fixation on simulated syndesmotic malreduction: a cadaveric study. J Bone Joint Surg Am. 2014;96(20):1732-1738.

35. Hsu AR, Lareau CR, Anderson RB. Repair of acute superficial deltoid complex avulsion during ankle fracture fixation in National Football League players. Foot Ankle Int. 2015;36(11):1272-1278.

36. Hsu AR, Jones CP, Cohen BE, Davis WH, Ellington JK, Anderson RB. Clinical outcomes and complications of percutaneous Achilles repair system versus open technique for acute achilles tendon ruptures. Foot Ankle Int. 2015;36(11):1279-1286.

37. Raikin SM, Garras DN, Krapchev PV. Achilles tendon injuries in a United States population. Foot Ankle Int. 2013;34(4):475-480.

38. Chiodo CP, Glazebrook M, Bluman EM, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on treatment of achilles tendon rupture. J Bone Joint Surg Am. 2010;92(14):2466-2468.

39. Chiodo CP, Glazebrook M, Bluman EM, et al. Diagnosis and treatment of acute achilles tendon rupture. J Am Acad Orthop Surg. 2010;18(8):503-510.

40. Khan RJ, Fick D, Keogh A, Crawford J, Brammar T, Parker M. Treatment of acute achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2005;87(10):2202-2210.

41. Renninger CH, Kuhn K, Fellars T, Youngblood S, Bellamy J. Operative and nonoperative management of achilles tendon ruptures in active duty military population. Foot Ankle Int. 2016;37(3):269-273.

42. Khan RJ, Carey Smith RL. Surgical interventions for treating acute achilles tendon ruptures. Cochrane Database Syst Rev. 2010;(9):CD003674.

43. McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv. 2014;23(4):179-183.

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Foot and ankle injuries are common in American football, with injury rates significantly increasing over the past decade.1-5 Epidemiologic studies of collegiate football players have shown an annual incidence of foot and ankle injuries ranging from 9% to 39%,3,6 with as many as 72% of all collegiate players presenting to the National Football League (NFL) Combine with a history of a foot or ankle injury and 13% undergoing surgical treatment.5 Player position influences the rate and type of foot and ankle injury. Offensive and “skill position” players, including linemen, running backs, and wide receivers, are particularly susceptible to foot and ankle injuries due to high levels of force and torque placed on the distal extremity during running, cutting, and tackling. Shoe wear changes, playing field conditions, increasing player size and speed, and improved reporting of injuries are also contributing to increasing injury rates.

The interaction between player cleats and the playing surface is a central issue of foot and ankle injuries in football. Improved traction relates to performance, but increased subsequent torque on the lower extremity is associated with injury. While lateral ankle sprains are the most common foot and ankle injury experienced by football players,7 numerous other injuries can occur, including turf toe, Jones fractures, Lisfranc injuries, syndesmotic disruption, deltoid complex avulsion, and Achilles ruptures. It is important for physicians to be able to recognize, diagnose, and appropriately treat these injuries in players in order to expedite recovery, restore function, and help prevent future injury and long-term sequelae. This review focuses on updated treatment principles, surgical advances, and rehabilitation protocols for common football foot and ankle injuries.

Turf Toe

The term “turf toe” was first used in 1976 to refer to hyperextension injuries and plantar capsule-ligament sprains of the hallux metatarsophalangeal (MTP) joint that can lead to progressive cock-up deformity.8 While these injuries can occur on any surface and disrupt soft tissue balance with functional implications, predisposing factors include increasing playing surface hardness and decreasing shoe stiffness. In a classic scenario, the foot is fixed in equinus as an axial load is placed on the back of the heel, resulting in forced dorsiflexion of the hallux MTP joint.9 As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the metatarsal head articular surface bears the majority of the load, causing partial or complete tearing of the plantar plate with or without hallux MTP dislocation. Osteochondral lesions of the MTP joint and subchondral edema of the metatarsal head can occur concurrently as the proximal phalanx impacts or shears across the metatarsal head articular surface.

Clinical examination should focus on hallux swelling, alignment, and flexor hallucis longus (FHL) function along with vertical instability of the hallux MTP joint using a Lachman test. Radiographs should be evaluated for proximal migration of the sesamoids or diastasis (Figures W1A-W1C).

Figures W1A-W1C
Forced hallux MTP dorsiflexion lateral view can help assess the distance from the distal sesamoid to the base of the phalanx. A small fleck of bone pulled off of the proximal phalanx or distal sesamoid may indicate a capsular avulsion or disruption. Live fluoroscopy can be very helpful in diagnosing turf toe, as the physician can assess the trailing motion of the sesamoids with increasing dorsiflexion and evaluate instability in all planes. Magnetic resonance imaging (MRI) is useful for subtle capsular injuries and can also identify osseous and articular damage that may occur and FHL disruption (Figures W2A, W2B).
Figures W2A, W2B
Nonoperative intervention focuses on rest, ice, compression, and elevation (RICE) and nonsteroidal anti-inflammatory drugs (NSAIDs). The hallux is temporarily immobilized in a plantarflexed position using a short leg cast or walking boot with toe spica or turf toe plate with tape for 2 to 3 weeks.

Indications for surgical intervention include loss of push-off strength, gross MTP instability, proximal migration of the sesamoids, and progressive hallux malalignment or clawing after immobilization. Cases can involve one or a combination of the following: (1) large capsular avulsion with unstable MTP joint; (2) diastasis of bipartite sesamoid; (3) diastasis of sesamoid fracture; (4) retraction of sesamoid; (5) traumatic hallux valgus deformity; (6) vertical instability (positive Lachman test); (7) loose body in MTP joint; or (8) chondral injury in MTP joint. The goal of surgery is the restoration of anatomy in order to restore normal function of the hallux MTP joint.

We have found that using dual medial and plantar incisions places less traction on the plantar medial cutaneous nerve, improves lateral exposure, and provides better wound healing. The medial capsulotomy extends from the metatarsal neck to the mid-phalanx to provide complete visualization of the sesamoid complex (Figures 1A-1F).
Figures 1A-1F
The collateral ligaments are often torn away from the metatarsal head during the initial dissection and the plantar plate tear is distal to the sesamoid complex. The soft tissue defect in the plantar complex must be closed distal to the sesamoids followed by advancement of the plantar plate to the proximal phalanx in a distal to proximal fashion and advancement of the medial capsule. The plantar incision is made along the lateral border of hallux MTP-sesamoid complex just lateral to the weight-bearing surface of the hallux and the plantar lateral cutaneous nerve is carefully dissected and retracted out of the way. Sutures are placed in a figure-of-eight fashion through the plantar capsule and plantar plate starting lateral to medial to reduce injury to the nerve. If the tear cannot be primarily repaired due to inadequate healthy tissue, a plantar plate advancement can be performed directly onto the base of the proximal phalanx using drill holes or suture anchors. Proper alignment and motion of the sesamoids should be verified with fluoroscopy and compared to the contralateral hallux (Figures W3A, W3B).
Figures W3A, W3B


It is important to recognize that not all turf toe injuries involve pure hyperextension on artificial playing surfaces. In recent years, we have found an increasing rate of medial variant turf toe injuries in which a forceful valgus stress on the hallux leads to rupture of the medial collateral ligament, medial or plantar-medial capsule, and/or abductor halluces. Medial variant turf toe can lead to progressive hallux valgus and a traumatic bunion with a significant loss of push-off strength and difficulty with cutting maneuvers. Surgical treatment requires a modified McBride bunionectomy with adductor tenotomy and direct repair of the medial soft tissue defect.

Postoperative management is just as important as proper surgical technique for these injuries and involves a delicate balance between protecting the repair and starting early range of motion (ROM). Patients are immobilized non-weight-bearing (NWB) for 5 to 7 days maximum followed immediately with the initiation of passive hallux plantarflexion to keep the sesamoids moving. Active hallux plantarflexion is started at 4 weeks after surgery with active dorsiflexion from 6 to 8 weeks. Patients are transitioned to an accommodative shoe with stiff hallux insert 8 weeks postoperative with continued therapy focusing on hallux ROM. Running is initiated at 12 weeks and return to play (RTP) is typically allowed 4 months after surgery.

 

 

Jones Fractures

Jones fractures are fractures of the 5th metatarsal at the metaphyseal-diaphyseal junction, where there is a watershed area of decreased vascularity between the intramedullary nutrient and metaphyseal arteries. Current thought is that the rising rate of Jones fractures among football players is partially caused by the use of flexible, narrow cleats that do not provide enough stiffness and lateral support for the 5th metatarsal during running and cutting. Additionally, lateral overload from a baseline cavovarus foot posture with or without metatarsus adductus and/or skewfoot is thought to contribute to Jones fractures.10 Preoperative radiographs should be evaluated for fracture location, orientation, amount of cortical thickening, and overall geometry of the foot and 5th metatarsal. In elite athletes, the threshold for surgical intervention is decreasing in order to expedite healing and recovery and decrease re-fracture risk. This rationale is based on delayed union rates of 25% to 66%, nonunion rates of 7% to 28%,11 and re-fracture rates of up to 33% associated with nonoperative treatment.12 Nonoperative management is usually not feasible in the competitive athlete, as it typically involves a period of protected weight-bearing in a tall controlled ankle motion (CAM) boot for 6 to 8 weeks with serial radiographs to evaluate healing.

Our preference for surgical intervention involves percutaneous screw fixation with a “high and inside” starting point on fluoroscopy (Figures 2A-2D).

Figures 2A-2D
The guidewire is inserted percutaneously through the skin 2 cm proximal to the base of the 5th metatarsal. Incorrect starting point can lead to a prominent screw head laterally or perforation of the medial cortex. A 1-cm incision is made around the guidewire entry point and intramedullary cannulated drilling enters the proximal third of the metatarsal, removing any thickened lateral cortex. Due to the natural curve of the 5th metatarsal, cannulated drilling is not continued distally but can be safely completed with a 3.2-mm solid drill bit. Proper tap sizing should generate enough torque to begin to rotate the entire foot as the tap is advanced (Figures W4A-W4F).
Figures W4A-W4F
The largest solid screw with a low-profile head that “comfortably” fits the intramedullary canal of the 5th metatarsal should be inserted (Carolina Jones Fracture System, Wright Medical Technology).13 In elite athletes, we will typically use a 5.5-mm or 6.5-mm screw that is 45 to 55 mm in length. Screw threads should pass just across the fracture site, avoiding “straightening” of the curved 5th metatarsal that will create a lateral gap and increase the rate of nonunion. We do not recommend headless tapered screws due to inconsistent compression and difficulty with later removal if re-fracture or nonunion occurs.

In career athletes, we augment the fracture site using a mixture of bone marrow aspirate concentrate (BMA) (Magellan, Arteriocyte Medical Systems) and demineralized bone matrix (DBM) (Mini Ignite, Wright Medical Technology) injected percutaneously in and around the fracture site under fluoroscopic guidance. Using this technique in a cohort of 25 NFL players treated operatively for Jones fractures, we found that 100% of athletes were able to RTP in the NFL in an average of 9.5 weeks.14 Two patients (7.5%) suffered re-fractures requiring revision surgery with iliac crest bone graft and repeat screw placement with a RTP after 15 weeks. We did not find an association between RTP and re-fracture rate.

The appropriate rehabilitation protocol for Jones fractures after surgery remains controversial and dependent on individual needs and abilities.15,16 For athletes in-season, we recommend a brief period of NWB for 1 to 2 weeks followed by toe-touch weight-bearing in a tall CAM boot for 2 to 4 weeks. After 4 weeks, patients begin gentle exercises on a stationary bike and pool therapy to reduce impact on the fracture site. Low-intensity pulsed ultrasound bone stimulators (Exogen, Bioventus) are frequently used directly over fracture site throughout the postoperative protocol as an adjuvant therapy. If clinically nontender over the fracture site, patients are allowed to begin running in modified protective shoe wear 4 weeks after surgery with an average RTP of 6 to 8 weeks. RTP is determined clinically, as radiographic union may not be evident for 12 to 16 weeks. Useful custom orthoses include turf toe plates with a cushioned lateral column and lateral heel wedge if hindfoot varus is present preoperatively.10 The solid intramedullary screw is left in place permanently.

In our experience, we have found the average re-fracture and nonunion rate to be approximately 8% across all athletes. Our observation that union rates do not appear to be related to RTP times suggests that underlying biology such as Vitamin D deficiency may play a larger role in union rates than previously thought. We have found that most Jones re-fractures occur in the first year after the initial injury, but can occur up to 2.5 years afterwards as well.14 For the management of symptomatic re-fractures and nonunions, the previous screw must be first removed. This can be difficult if the screw is bent or broken, and may require a lateral corticotomy of the metatarsal.

After hardware removal, we advocate open bone grafting of the fracture site using bone from the iliac crest retrieved with a small, percutaneous trephine. Re-fixation should be achieved using a larger, solid screw and postoperative adjuvants may include bone stimulators, Vitamin D and calcium supplemention, and possible teriparatide use (Forteo, Eli Lilly), depending on individual patient profile. In a cohort of 21 elite athletes treated for Jones fracture revision surgery with screw exchange and bone grafting, we found that 100% of patients had computed tomography (CT) evidence of union, with an average RTP of 12.3 weeks.17

 

 

Lisfranc Injuries

Lisfranc injuries include any bony or ligamentous damage that involves the tarsometatarsal (TMT) joints. While axial loading of a fixed, plantarflexed foot has traditionally been thought of as the most common mechanism of Lisfranc injury, we have found that noncontact twisting injuries leading to Lisfranc disruption are actually more common among NFL players. This mechanism is similar to noncontact turf toe and results in a purely ligamentous injury. We have found this to be particularly true in the case of defensive ends engaged with offensive linemen in which no axial loading or contact of the foot occurs. Clinically, patients often have painful weight-bearing, inability to perform a single limb heel rise, plantar ecchymosis, and swelling and point tenderness across the bases of the 1st and 2nd metatarsals.

It is critical to obtain comparison weight-bearing radiographs of both feet during initial work-up to look for evidence of instability. Subtle radiographic findings of Lisfranc injury include a bony “fleck” sign, compression fracture of the cuboid, and diastasis between the base of the 1st and 2nd metatarsals and/or medial and middle cuneiforms (Figures 3A, 3B).

Figures 3A, 3B
Stress testing involves pronation and adduction of the foot under live fluoroscopy to evaluate for diastasis. MRI can be helpful in cases of vague pain with negative radiographs and subtle displacement. Nonoperative treatment for cases of no instability or displacement involved protected weight-bearing for 4 weeks followed by progressive increase in activities, with RTP 6 to 8 weeks after injury.

The goal of surgical intervention is to obtain and maintain anatomic reduction of all unstable joints in order to restore a normal foot posture. One of the difficulties with Lisfranc injuries is that there are no exact diastasis parameters and individuals should be treated based on symptoms, functional needs, and degree of instability. It has been shown that 5 mm of displacement can have good long-term clinical results in select cases without surgery.18 For surgery, we recommend open reduction to remove interposed soft tissue debris and directly assess the articular surfaces (Figures 4A-4D).
Figures 4A-4D
A freer can be placed in the individual joints to assess for areas of instability. We prefer solid screw fixation (Charlotte Lisfranc Reconstruction System, Wright Medical Technology) to decrease the risk of later screw breakage. A homerun screw from the proximal aspect of the medial cuneiform to the distal-lateral aspect of the 2nd metatarsal base should be placed first. Bridge plates can be used over the 1st and 2nd TMT joints to avoid articular cartilage damage without a loss of rigidity.19

Proximal-medial column Lisfranc injury variants are increasingly common among football players.20 In these injuries, the force of injury extends through the intercuneiform joint and exits out the naviculocuneiform joint, thus causing instability at multiple joints and an unstable 1st ray. Patients often have minimal clinical findings and normal radiographs and stress radiographs. MRI of the foot often reveals edema at the naviculocuneiform joint. Often patients fail to improve with nonoperative immobilization with continued inability to push off from the hallux. Unrecognized or untreated instability will lead to rapid deterioration of the naviculocuneiform joint. Surgical intervention requires a homerun screw and intercuneiform screw. We do not recommend primary arthrodesis in athletes due to significant risk of malunion and nonunion unless severe articular damage is present.

Patients are typically kept NWB in a splint for 2 weeks after surgery followed by NWB in a tall CAM from 3 to 4 weeks postoperative. Progressive weight-bearing and ROM exercises are initiated from 4 to 8 weeks, followed by return to accommodative shoe wear from 10 to 12 weeks. Hardware removal is performed 4 to 6 months after surgery, typically in the off-season to allow for 6 to 8 weeks or protected recovery afterwards. Premature hardware removal can lead to loss of reduction, particularly at the intercuneiform joints. All hardware crossing the TMT joints should be removed, while the homerun screw can be left in place in addition to the intercuneiform screw. RTP in football typically occurs 6 to 7 months after surgery. Final functional outcome is related to the adequacy of initial reduction and severity of the initial injury.21

Syndesmotic Disruption

Syndesmotic injuries comprise 1% to 18% of ankle sprains in the general population, but occur at much higher rates in football due to the increased rotation forces placed on the ankle during cutting and tackling. RTP after syndesmotic injury often takes twice as long when compared to isolated lateral ankle ligamentous injury.22 Missed injuries are common and if not treated properly can lead to chronic ankle instability and posttraumatic ankle arthritis.23 Syndesmotic injury can occur in isolation or with concomitant adjacent bony, cartilaginous, or ligamentous injuries. Therefore, clinical examination and imaging work-up are critical to successful management.

 

 

Syndesmotic injuries often result from an external rotation force applied to a hyperdorsiflexed ankle while the foot is planted. This mechanism causes the fibula to externally rotate while translating posteriorly and laterally, resulting in rupture of the anterior inferior tibiofibular ligament (AITFL) first, followed by the deep deltoid ligament, interosseous ligament (IOL), and lastly posterior talofibular ligament.24 Most syndesmotic injuries involve rupture of only the AITFL and IOL.25 Multiple clinical stress tests have been designed to assess syndesmotic stability, including the squeeze test, external rotation stress test, crossed-leg test, and fibula-translation test.26-29 However, no physical examination maneuver has been shown to reliably predict the presence or degree of syndesmotic injury and therefore imaging studies are necessary.30

Initial imaging should include standing radiographs of the affected ankle. An increase in the medial clear space between the medial malleolus and talus can occur with a combined syndesmotic and deltoid disruption. In the case of subtle syndesmotic injuries, contralateral comparison weight-bearing radiographs are recommended. CT and MRI can provide additional information, but these static imaging tests cannot identify instability. Fluoroscopic stress evaluation is beneficial but has a high false-negative rate in low-grade injuries and may not detect partial rupture of the AITFL and IOL.31 It has been shown that malrotation of as much as 30° of external rotation can occur if relying on intraoperative fluoroscopy alone.32 It has been our practice to recommend surgical reduction and stabilization for any syndesmotic injury with documented diastasis or instability seen on imaging and/or arthroscopy.

Nonoperative treatment is indicated for truly stable grade I syndesmotic injuries. This involves rest and immobilization followed by a progressive rehabilitation program consisting of stretching, strengthening, and proprioceptive exercises.33 After 1 week of protected weight-bearing in a cast or tall CAM boot, progression to full weight-bearing should occur over the following week. Active-assisted ankle ROM exercises and light proprioceptive training should then be initiated followed by sport-specific exercises 2 to 3 weeks after injury.

Arthroscopy can be a valuable diagnostic tool in the setting of subtle syndesmotic injury with negative radiographs, positive MRI for edema, and a protracted recovery course with vague pain (Figures W5A-W5E).

Figures W5A-W5E
In these situations, an examination under anesthesia is performed, the syndesmosis is probed under direct arthroscopic visualization, and distal tibiofibular instability is evaluated while performing an external rotation stress test. For surgical intervention of these subtle varieties or any athlete with documented instability, we prefer the use of dynamic stabilization with a knotless suture-button construct (TightRope, Arthrex) or hybrid fixation with screws (3.5/4.5 mm) and suture-buttons. Advantages of a knotless suture-button construct include more physiologic motion at the syndesmosis and decreased hardware irritation and implant removal.

Implants are placed above the true syndesmotic joint (at least 15 mm above the tibial plafond) angled 30° posterior to anterior to follow the normal relationship of the fibula to the distal tibia in the incisura. Typically 2 suture-buttons are used, with the devices placed in a divergent fashion. We highly recommend the use of a fibular buttress plate with button placement in individuals returning to contact activity. This construct increases surface area distribution while preventing stress risers and the risk of fibula fractures. In a cadaver model with deliberate syndesmotic malreduction, suture-button stabilization resulted in decreased postoperative displacement as opposed to conventional screw fixation.34 Therefore, dynamic syndesmotic fixation may help to decrease the negative sequelae of iatrogenic clamp malreduction. 
Postoperative rehabilitation involves NWB in a cast or tall CAM boot for 4 weeks followed by ankle ROM exercises and progressive weight-bearing and physical therapy. Patients are transitioned to a lace-up ankle brace and athletic shoe from 6 to 12 weeks postoperative with increasing activity. Running and jumping is permitted 4 months after surgery with RTP typically at 6 to 7 months. Athletes who have had surgical stabilization for documented instability without any diastasis may engage in a more rapid recovery and RTP as symptoms and function allow.

Deltoid Complex Avulsion

Missed or neglected deltoid ligament injuries can lead to progressive chondral injury and joint degeneration. These injuries are often subtle and difficult to diagnose. An inability to perform a single limb heel rise, persistent pain with activity, and lack of normal functional improvement despite appropriate care are indicators of subtle ligament instability. These injuries often require an examination under anesthesia with combined ankle arthroscopy. Valgus stress testing of the ankle while directly visualizing the deltoid ligament from the anterolateral portal can reveal medial laxity in addition to potential osteochondral lesions along the anterolateral talar dome.

In American football players, we have observed that infolding and retraction of an avulsed superficial deltoid ligament complex after an ankle fracture, Maisonneuve injury, or severe high ankle sprain can be a source of persistent increased medial clear space, malreduction, and postoperative pain and medial instability. We have found that there is often complete avulsion of the superficial deltoid complex off the proximal aspect of the medial malleolus during high-energy ankle fractures in football players that is amenable to direct repair to bone (Figures W6A-W6E).

Figures W6A-W6E
In a cohort of 14 NFL players who underwent ankle fracture fixation with ankle arthroscopy and debridement, fibula fixation with plate and screws, syndesmotic fixation with suture-button devices, and open deltoid complex repair with suture anchors, all athletes were able to return to running and cutting maneuvers by 6 months after surgery.35 There were no intraoperative or postoperative complications noted, and no players had clinical evidence of medial pain or instability at final follow-up with radiographic maintenance of anatomic mortise alignment.

During surgical repair, an incision is made along the anterior aspect of the medial malleolus and the superficial deltoid ligament complex can often be found flipped and interposed in the medial gutter. A rongeur is used to create a bleeding cancellous bone surface for soft-tissue healing and 1 to 2 suture anchors are used to repair and imbricate the deltoid ligament complex back to the medial malleolus. The goal of these sutures is to repair the tibionavicular and tibial spring ligaments back to the medial malleolus. We believe that superficial deltoid complex avulsion during high-energy ankle fractures is a distinct injury pattern that should be recognized and may benefit from primary open repair.

We currently open explore every deltoid ligament complex in athletes with unstable syndesmotic injuries, as we believe that deltoid avulsion injuries are underrecognized and do not heal in an anatomic fashion if left alone. Postoperative recovery follows the same immobilization, progressive weight-bearing, and physical therapy protocol as that for syndesmotic disruption.

 

 

Achilles Ruptures

Acute midsubstance Achilles tendon ruptures are an increasingly common injury in patients 30 to 50 years of age, with more than 50% of all injuries occurring during basketball.36,37 Among NFL players, we have found that Achilles ruptures tend to occur at a higher rate during training camp, when athletes are deconditioned and quickly returning to explosive push-off activities. Physical examination should include a Thompson test, palpation of a gap within the tendon, and evaluation of resting ankle dorsiflexion in the affected extremity in the prone position with the knees bent. Lateral radiographs should be analyzed for the presence of a bony avulsion fragment indicative of an insertional avulsion injury or midsubstance calcium deposition reflecting chronic Achilles tendinosis, as both of these conditions will change surgical management. MRI is not recommended with acute midsubstance ruptures but may be helpful in the case of chronic ruptures or more proximal tears of the musculotendinous junction.

The management of acute midsubstance Achilles tendon ruptures is controversial, with no general consensus in the literature regarding nonoperative treatment, surgical repair, and ideal repair technique.36,38-42 American Academy of Orthopaedic Surgeons clinical practice guidelines report moderate evidence that nonoperative treatment of Achilles tendon ruptures has lower wound healing complications but higher rates of re-rupture.38,39 Additionally, limited incision approaches have been found to have fewer overall complications compared with traditional open repair. In an effort to reduce the incidence of postoperative wound complications while improving functional recovery, modern repair techniques focus on a limited incision repair using percutaneous suture insertion and management (PARS Achilles Jig System, Arthrex).36 The limited incision technique utilizes a 2-cm transverse incision and non-disposable jig with divergent needle passes and locking suture fixation options to secure and fixate both tendon ends with minimal dissection of skin, subcutaneous tissue, and paratenon. Limited incision repair is ideally performed within 2 weeks of the injury to ensure that both tendon ends are easy to identify, mobilize, and repair. An open repair is generally recommended for midsubstance ruptures more than 4 weeks old and cases of insertional rupture and Achilles tendinopathy.

In a cohort of 9 NFL players treated for midsubstance Achilles ruptures using the PARS technique, we found no re-ruptures, no wound complications, and no sural nerve issues after surgery.43 A comparative review of 270 cases of operatively treated Achilles tendon ruptures (101 PARS, 169 traditional open repair) showed that the PARS group had significantly shorter operative times and a higher number of patients able to return to baseline physical activities by 5 months compared to open repair.36 Although not statistically significant, the overall PARS complication rate was 5% while the open complication rate was 11%. The PARS group had no cases of sural neuritis or deep infection requiring reoperation. We currently use a limited incision technique for all acute midsubstance Achilles ruptures in athletes regardless of sport, patient size, or position played.

During surgery, a 2-cm transverse incision is made over the gap in the Achilles tendon and dissection is carried down to the rupture site with minimal manipulation of the skin (Figures 5A-5F).

Figures 5A-5F
A transverse incision is made through the paratenon and typically a hematoma is expressed. An Allis clamp is inserted and the proximal tendon stump is grabbed securely and pulled through the wound approximately 1 to 2 cm. The PARS jig is inserted around the proximal tendon and centered so that the needle and sutures will pass through tendon. Needles and sutures are passed in a stepwise fashion and then the entire jig is removed from the wound. Sutures are passed to create 2 non-locking and 1 locking suture. The jig and suture passing process is repeated for the distal tendon stump. Then, each pair of sutures is tied together with the ankle in maximum plantarflexion to obtain a secure end-to-end repair. The knots are cut short and tucked into tendon so that they do not protrude and cause subcutaneous tissue irritation. Absorbable sutures are used to close the paratenon, followed by closure of subcutaneous tissues and skin followed by placement of a short leg posterior mold NWB splint with the ankle in resting plantar flexion.

A key aspect of postoperative recovery is avoiding excessive ankle dorsiflexion while the tendon is healing during the first 4 weeks after surgery, as this can lead to an elongated tendon with loss of push-off strength. Patients are kept in a plantarflexion splint NWB for 2 weeks after surgery. If the incision is healed at 2 weeks, sutures are removed and patients are transitioned into a NWB tall CAM boot for 2 weeks with gentle ankle ROM exercises. If there is any concern regarding wound healing status, sutures are maintained for an additional 1 to 2 weeks.

From 4 to 8 weeks after surgery, progressive weight-bearing with continued ankle ROM exercises is initiated with peel-away heel lifts (~2 cm thick total, 3 layers). Each layer of the heel lift is gradually removed as pain allows every 2 to 3 days with the goal of being full weight-bearing with the foot flat at 6 weeks postoperative. Physical therapy focusing on ankle ROM and gentle Achilles stretching and strengthening is also started 6 weeks after surgery. From 8 to 12 weeks postoperative, patients are transitioned out of the tall CAM boot into normal, accommodative shoe wear with full weight-bearing. We avoid ankle dorsiflexion past neutral until 12 weeks after surgery, as overlengthening of the Achilles complex and the subsequent loss of push-off power can be devastating to running athletes. Activity levels are increased as tolerated, with no running or jumping from 12 to 16 weeks with full release to all activities after 16 weeks. RTP often takes 5 to 6 months after surgery, depending on the position played.

Am J Orthop. 2016;45(6):358-367. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Foot and ankle injuries are common in American football, with injury rates significantly increasing over the past decade.1-5 Epidemiologic studies of collegiate football players have shown an annual incidence of foot and ankle injuries ranging from 9% to 39%,3,6 with as many as 72% of all collegiate players presenting to the National Football League (NFL) Combine with a history of a foot or ankle injury and 13% undergoing surgical treatment.5 Player position influences the rate and type of foot and ankle injury. Offensive and “skill position” players, including linemen, running backs, and wide receivers, are particularly susceptible to foot and ankle injuries due to high levels of force and torque placed on the distal extremity during running, cutting, and tackling. Shoe wear changes, playing field conditions, increasing player size and speed, and improved reporting of injuries are also contributing to increasing injury rates.

The interaction between player cleats and the playing surface is a central issue of foot and ankle injuries in football. Improved traction relates to performance, but increased subsequent torque on the lower extremity is associated with injury. While lateral ankle sprains are the most common foot and ankle injury experienced by football players,7 numerous other injuries can occur, including turf toe, Jones fractures, Lisfranc injuries, syndesmotic disruption, deltoid complex avulsion, and Achilles ruptures. It is important for physicians to be able to recognize, diagnose, and appropriately treat these injuries in players in order to expedite recovery, restore function, and help prevent future injury and long-term sequelae. This review focuses on updated treatment principles, surgical advances, and rehabilitation protocols for common football foot and ankle injuries.

Turf Toe

The term “turf toe” was first used in 1976 to refer to hyperextension injuries and plantar capsule-ligament sprains of the hallux metatarsophalangeal (MTP) joint that can lead to progressive cock-up deformity.8 While these injuries can occur on any surface and disrupt soft tissue balance with functional implications, predisposing factors include increasing playing surface hardness and decreasing shoe stiffness. In a classic scenario, the foot is fixed in equinus as an axial load is placed on the back of the heel, resulting in forced dorsiflexion of the hallux MTP joint.9 As the proximal phalanx extends, the sesamoids are drawn distally and the more dorsal portion of the metatarsal head articular surface bears the majority of the load, causing partial or complete tearing of the plantar plate with or without hallux MTP dislocation. Osteochondral lesions of the MTP joint and subchondral edema of the metatarsal head can occur concurrently as the proximal phalanx impacts or shears across the metatarsal head articular surface.

Clinical examination should focus on hallux swelling, alignment, and flexor hallucis longus (FHL) function along with vertical instability of the hallux MTP joint using a Lachman test. Radiographs should be evaluated for proximal migration of the sesamoids or diastasis (Figures W1A-W1C).

Figures W1A-W1C
Forced hallux MTP dorsiflexion lateral view can help assess the distance from the distal sesamoid to the base of the phalanx. A small fleck of bone pulled off of the proximal phalanx or distal sesamoid may indicate a capsular avulsion or disruption. Live fluoroscopy can be very helpful in diagnosing turf toe, as the physician can assess the trailing motion of the sesamoids with increasing dorsiflexion and evaluate instability in all planes. Magnetic resonance imaging (MRI) is useful for subtle capsular injuries and can also identify osseous and articular damage that may occur and FHL disruption (Figures W2A, W2B).
Figures W2A, W2B
Nonoperative intervention focuses on rest, ice, compression, and elevation (RICE) and nonsteroidal anti-inflammatory drugs (NSAIDs). The hallux is temporarily immobilized in a plantarflexed position using a short leg cast or walking boot with toe spica or turf toe plate with tape for 2 to 3 weeks.

Indications for surgical intervention include loss of push-off strength, gross MTP instability, proximal migration of the sesamoids, and progressive hallux malalignment or clawing after immobilization. Cases can involve one or a combination of the following: (1) large capsular avulsion with unstable MTP joint; (2) diastasis of bipartite sesamoid; (3) diastasis of sesamoid fracture; (4) retraction of sesamoid; (5) traumatic hallux valgus deformity; (6) vertical instability (positive Lachman test); (7) loose body in MTP joint; or (8) chondral injury in MTP joint. The goal of surgery is the restoration of anatomy in order to restore normal function of the hallux MTP joint.

We have found that using dual medial and plantar incisions places less traction on the plantar medial cutaneous nerve, improves lateral exposure, and provides better wound healing. The medial capsulotomy extends from the metatarsal neck to the mid-phalanx to provide complete visualization of the sesamoid complex (Figures 1A-1F).
Figures 1A-1F
The collateral ligaments are often torn away from the metatarsal head during the initial dissection and the plantar plate tear is distal to the sesamoid complex. The soft tissue defect in the plantar complex must be closed distal to the sesamoids followed by advancement of the plantar plate to the proximal phalanx in a distal to proximal fashion and advancement of the medial capsule. The plantar incision is made along the lateral border of hallux MTP-sesamoid complex just lateral to the weight-bearing surface of the hallux and the plantar lateral cutaneous nerve is carefully dissected and retracted out of the way. Sutures are placed in a figure-of-eight fashion through the plantar capsule and plantar plate starting lateral to medial to reduce injury to the nerve. If the tear cannot be primarily repaired due to inadequate healthy tissue, a plantar plate advancement can be performed directly onto the base of the proximal phalanx using drill holes or suture anchors. Proper alignment and motion of the sesamoids should be verified with fluoroscopy and compared to the contralateral hallux (Figures W3A, W3B).
Figures W3A, W3B


It is important to recognize that not all turf toe injuries involve pure hyperextension on artificial playing surfaces. In recent years, we have found an increasing rate of medial variant turf toe injuries in which a forceful valgus stress on the hallux leads to rupture of the medial collateral ligament, medial or plantar-medial capsule, and/or abductor halluces. Medial variant turf toe can lead to progressive hallux valgus and a traumatic bunion with a significant loss of push-off strength and difficulty with cutting maneuvers. Surgical treatment requires a modified McBride bunionectomy with adductor tenotomy and direct repair of the medial soft tissue defect.

Postoperative management is just as important as proper surgical technique for these injuries and involves a delicate balance between protecting the repair and starting early range of motion (ROM). Patients are immobilized non-weight-bearing (NWB) for 5 to 7 days maximum followed immediately with the initiation of passive hallux plantarflexion to keep the sesamoids moving. Active hallux plantarflexion is started at 4 weeks after surgery with active dorsiflexion from 6 to 8 weeks. Patients are transitioned to an accommodative shoe with stiff hallux insert 8 weeks postoperative with continued therapy focusing on hallux ROM. Running is initiated at 12 weeks and return to play (RTP) is typically allowed 4 months after surgery.

 

 

Jones Fractures

Jones fractures are fractures of the 5th metatarsal at the metaphyseal-diaphyseal junction, where there is a watershed area of decreased vascularity between the intramedullary nutrient and metaphyseal arteries. Current thought is that the rising rate of Jones fractures among football players is partially caused by the use of flexible, narrow cleats that do not provide enough stiffness and lateral support for the 5th metatarsal during running and cutting. Additionally, lateral overload from a baseline cavovarus foot posture with or without metatarsus adductus and/or skewfoot is thought to contribute to Jones fractures.10 Preoperative radiographs should be evaluated for fracture location, orientation, amount of cortical thickening, and overall geometry of the foot and 5th metatarsal. In elite athletes, the threshold for surgical intervention is decreasing in order to expedite healing and recovery and decrease re-fracture risk. This rationale is based on delayed union rates of 25% to 66%, nonunion rates of 7% to 28%,11 and re-fracture rates of up to 33% associated with nonoperative treatment.12 Nonoperative management is usually not feasible in the competitive athlete, as it typically involves a period of protected weight-bearing in a tall controlled ankle motion (CAM) boot for 6 to 8 weeks with serial radiographs to evaluate healing.

Our preference for surgical intervention involves percutaneous screw fixation with a “high and inside” starting point on fluoroscopy (Figures 2A-2D).

Figures 2A-2D
The guidewire is inserted percutaneously through the skin 2 cm proximal to the base of the 5th metatarsal. Incorrect starting point can lead to a prominent screw head laterally or perforation of the medial cortex. A 1-cm incision is made around the guidewire entry point and intramedullary cannulated drilling enters the proximal third of the metatarsal, removing any thickened lateral cortex. Due to the natural curve of the 5th metatarsal, cannulated drilling is not continued distally but can be safely completed with a 3.2-mm solid drill bit. Proper tap sizing should generate enough torque to begin to rotate the entire foot as the tap is advanced (Figures W4A-W4F).
Figures W4A-W4F
The largest solid screw with a low-profile head that “comfortably” fits the intramedullary canal of the 5th metatarsal should be inserted (Carolina Jones Fracture System, Wright Medical Technology).13 In elite athletes, we will typically use a 5.5-mm or 6.5-mm screw that is 45 to 55 mm in length. Screw threads should pass just across the fracture site, avoiding “straightening” of the curved 5th metatarsal that will create a lateral gap and increase the rate of nonunion. We do not recommend headless tapered screws due to inconsistent compression and difficulty with later removal if re-fracture or nonunion occurs.

In career athletes, we augment the fracture site using a mixture of bone marrow aspirate concentrate (BMA) (Magellan, Arteriocyte Medical Systems) and demineralized bone matrix (DBM) (Mini Ignite, Wright Medical Technology) injected percutaneously in and around the fracture site under fluoroscopic guidance. Using this technique in a cohort of 25 NFL players treated operatively for Jones fractures, we found that 100% of athletes were able to RTP in the NFL in an average of 9.5 weeks.14 Two patients (7.5%) suffered re-fractures requiring revision surgery with iliac crest bone graft and repeat screw placement with a RTP after 15 weeks. We did not find an association between RTP and re-fracture rate.

The appropriate rehabilitation protocol for Jones fractures after surgery remains controversial and dependent on individual needs and abilities.15,16 For athletes in-season, we recommend a brief period of NWB for 1 to 2 weeks followed by toe-touch weight-bearing in a tall CAM boot for 2 to 4 weeks. After 4 weeks, patients begin gentle exercises on a stationary bike and pool therapy to reduce impact on the fracture site. Low-intensity pulsed ultrasound bone stimulators (Exogen, Bioventus) are frequently used directly over fracture site throughout the postoperative protocol as an adjuvant therapy. If clinically nontender over the fracture site, patients are allowed to begin running in modified protective shoe wear 4 weeks after surgery with an average RTP of 6 to 8 weeks. RTP is determined clinically, as radiographic union may not be evident for 12 to 16 weeks. Useful custom orthoses include turf toe plates with a cushioned lateral column and lateral heel wedge if hindfoot varus is present preoperatively.10 The solid intramedullary screw is left in place permanently.

In our experience, we have found the average re-fracture and nonunion rate to be approximately 8% across all athletes. Our observation that union rates do not appear to be related to RTP times suggests that underlying biology such as Vitamin D deficiency may play a larger role in union rates than previously thought. We have found that most Jones re-fractures occur in the first year after the initial injury, but can occur up to 2.5 years afterwards as well.14 For the management of symptomatic re-fractures and nonunions, the previous screw must be first removed. This can be difficult if the screw is bent or broken, and may require a lateral corticotomy of the metatarsal.

After hardware removal, we advocate open bone grafting of the fracture site using bone from the iliac crest retrieved with a small, percutaneous trephine. Re-fixation should be achieved using a larger, solid screw and postoperative adjuvants may include bone stimulators, Vitamin D and calcium supplemention, and possible teriparatide use (Forteo, Eli Lilly), depending on individual patient profile. In a cohort of 21 elite athletes treated for Jones fracture revision surgery with screw exchange and bone grafting, we found that 100% of patients had computed tomography (CT) evidence of union, with an average RTP of 12.3 weeks.17

 

 

Lisfranc Injuries

Lisfranc injuries include any bony or ligamentous damage that involves the tarsometatarsal (TMT) joints. While axial loading of a fixed, plantarflexed foot has traditionally been thought of as the most common mechanism of Lisfranc injury, we have found that noncontact twisting injuries leading to Lisfranc disruption are actually more common among NFL players. This mechanism is similar to noncontact turf toe and results in a purely ligamentous injury. We have found this to be particularly true in the case of defensive ends engaged with offensive linemen in which no axial loading or contact of the foot occurs. Clinically, patients often have painful weight-bearing, inability to perform a single limb heel rise, plantar ecchymosis, and swelling and point tenderness across the bases of the 1st and 2nd metatarsals.

It is critical to obtain comparison weight-bearing radiographs of both feet during initial work-up to look for evidence of instability. Subtle radiographic findings of Lisfranc injury include a bony “fleck” sign, compression fracture of the cuboid, and diastasis between the base of the 1st and 2nd metatarsals and/or medial and middle cuneiforms (Figures 3A, 3B).

Figures 3A, 3B
Stress testing involves pronation and adduction of the foot under live fluoroscopy to evaluate for diastasis. MRI can be helpful in cases of vague pain with negative radiographs and subtle displacement. Nonoperative treatment for cases of no instability or displacement involved protected weight-bearing for 4 weeks followed by progressive increase in activities, with RTP 6 to 8 weeks after injury.

The goal of surgical intervention is to obtain and maintain anatomic reduction of all unstable joints in order to restore a normal foot posture. One of the difficulties with Lisfranc injuries is that there are no exact diastasis parameters and individuals should be treated based on symptoms, functional needs, and degree of instability. It has been shown that 5 mm of displacement can have good long-term clinical results in select cases without surgery.18 For surgery, we recommend open reduction to remove interposed soft tissue debris and directly assess the articular surfaces (Figures 4A-4D).
Figures 4A-4D
A freer can be placed in the individual joints to assess for areas of instability. We prefer solid screw fixation (Charlotte Lisfranc Reconstruction System, Wright Medical Technology) to decrease the risk of later screw breakage. A homerun screw from the proximal aspect of the medial cuneiform to the distal-lateral aspect of the 2nd metatarsal base should be placed first. Bridge plates can be used over the 1st and 2nd TMT joints to avoid articular cartilage damage without a loss of rigidity.19

Proximal-medial column Lisfranc injury variants are increasingly common among football players.20 In these injuries, the force of injury extends through the intercuneiform joint and exits out the naviculocuneiform joint, thus causing instability at multiple joints and an unstable 1st ray. Patients often have minimal clinical findings and normal radiographs and stress radiographs. MRI of the foot often reveals edema at the naviculocuneiform joint. Often patients fail to improve with nonoperative immobilization with continued inability to push off from the hallux. Unrecognized or untreated instability will lead to rapid deterioration of the naviculocuneiform joint. Surgical intervention requires a homerun screw and intercuneiform screw. We do not recommend primary arthrodesis in athletes due to significant risk of malunion and nonunion unless severe articular damage is present.

Patients are typically kept NWB in a splint for 2 weeks after surgery followed by NWB in a tall CAM from 3 to 4 weeks postoperative. Progressive weight-bearing and ROM exercises are initiated from 4 to 8 weeks, followed by return to accommodative shoe wear from 10 to 12 weeks. Hardware removal is performed 4 to 6 months after surgery, typically in the off-season to allow for 6 to 8 weeks or protected recovery afterwards. Premature hardware removal can lead to loss of reduction, particularly at the intercuneiform joints. All hardware crossing the TMT joints should be removed, while the homerun screw can be left in place in addition to the intercuneiform screw. RTP in football typically occurs 6 to 7 months after surgery. Final functional outcome is related to the adequacy of initial reduction and severity of the initial injury.21

Syndesmotic Disruption

Syndesmotic injuries comprise 1% to 18% of ankle sprains in the general population, but occur at much higher rates in football due to the increased rotation forces placed on the ankle during cutting and tackling. RTP after syndesmotic injury often takes twice as long when compared to isolated lateral ankle ligamentous injury.22 Missed injuries are common and if not treated properly can lead to chronic ankle instability and posttraumatic ankle arthritis.23 Syndesmotic injury can occur in isolation or with concomitant adjacent bony, cartilaginous, or ligamentous injuries. Therefore, clinical examination and imaging work-up are critical to successful management.

 

 

Syndesmotic injuries often result from an external rotation force applied to a hyperdorsiflexed ankle while the foot is planted. This mechanism causes the fibula to externally rotate while translating posteriorly and laterally, resulting in rupture of the anterior inferior tibiofibular ligament (AITFL) first, followed by the deep deltoid ligament, interosseous ligament (IOL), and lastly posterior talofibular ligament.24 Most syndesmotic injuries involve rupture of only the AITFL and IOL.25 Multiple clinical stress tests have been designed to assess syndesmotic stability, including the squeeze test, external rotation stress test, crossed-leg test, and fibula-translation test.26-29 However, no physical examination maneuver has been shown to reliably predict the presence or degree of syndesmotic injury and therefore imaging studies are necessary.30

Initial imaging should include standing radiographs of the affected ankle. An increase in the medial clear space between the medial malleolus and talus can occur with a combined syndesmotic and deltoid disruption. In the case of subtle syndesmotic injuries, contralateral comparison weight-bearing radiographs are recommended. CT and MRI can provide additional information, but these static imaging tests cannot identify instability. Fluoroscopic stress evaluation is beneficial but has a high false-negative rate in low-grade injuries and may not detect partial rupture of the AITFL and IOL.31 It has been shown that malrotation of as much as 30° of external rotation can occur if relying on intraoperative fluoroscopy alone.32 It has been our practice to recommend surgical reduction and stabilization for any syndesmotic injury with documented diastasis or instability seen on imaging and/or arthroscopy.

Nonoperative treatment is indicated for truly stable grade I syndesmotic injuries. This involves rest and immobilization followed by a progressive rehabilitation program consisting of stretching, strengthening, and proprioceptive exercises.33 After 1 week of protected weight-bearing in a cast or tall CAM boot, progression to full weight-bearing should occur over the following week. Active-assisted ankle ROM exercises and light proprioceptive training should then be initiated followed by sport-specific exercises 2 to 3 weeks after injury.

Arthroscopy can be a valuable diagnostic tool in the setting of subtle syndesmotic injury with negative radiographs, positive MRI for edema, and a protracted recovery course with vague pain (Figures W5A-W5E).

Figures W5A-W5E
In these situations, an examination under anesthesia is performed, the syndesmosis is probed under direct arthroscopic visualization, and distal tibiofibular instability is evaluated while performing an external rotation stress test. For surgical intervention of these subtle varieties or any athlete with documented instability, we prefer the use of dynamic stabilization with a knotless suture-button construct (TightRope, Arthrex) or hybrid fixation with screws (3.5/4.5 mm) and suture-buttons. Advantages of a knotless suture-button construct include more physiologic motion at the syndesmosis and decreased hardware irritation and implant removal.

Implants are placed above the true syndesmotic joint (at least 15 mm above the tibial plafond) angled 30° posterior to anterior to follow the normal relationship of the fibula to the distal tibia in the incisura. Typically 2 suture-buttons are used, with the devices placed in a divergent fashion. We highly recommend the use of a fibular buttress plate with button placement in individuals returning to contact activity. This construct increases surface area distribution while preventing stress risers and the risk of fibula fractures. In a cadaver model with deliberate syndesmotic malreduction, suture-button stabilization resulted in decreased postoperative displacement as opposed to conventional screw fixation.34 Therefore, dynamic syndesmotic fixation may help to decrease the negative sequelae of iatrogenic clamp malreduction. 
Postoperative rehabilitation involves NWB in a cast or tall CAM boot for 4 weeks followed by ankle ROM exercises and progressive weight-bearing and physical therapy. Patients are transitioned to a lace-up ankle brace and athletic shoe from 6 to 12 weeks postoperative with increasing activity. Running and jumping is permitted 4 months after surgery with RTP typically at 6 to 7 months. Athletes who have had surgical stabilization for documented instability without any diastasis may engage in a more rapid recovery and RTP as symptoms and function allow.

Deltoid Complex Avulsion

Missed or neglected deltoid ligament injuries can lead to progressive chondral injury and joint degeneration. These injuries are often subtle and difficult to diagnose. An inability to perform a single limb heel rise, persistent pain with activity, and lack of normal functional improvement despite appropriate care are indicators of subtle ligament instability. These injuries often require an examination under anesthesia with combined ankle arthroscopy. Valgus stress testing of the ankle while directly visualizing the deltoid ligament from the anterolateral portal can reveal medial laxity in addition to potential osteochondral lesions along the anterolateral talar dome.

In American football players, we have observed that infolding and retraction of an avulsed superficial deltoid ligament complex after an ankle fracture, Maisonneuve injury, or severe high ankle sprain can be a source of persistent increased medial clear space, malreduction, and postoperative pain and medial instability. We have found that there is often complete avulsion of the superficial deltoid complex off the proximal aspect of the medial malleolus during high-energy ankle fractures in football players that is amenable to direct repair to bone (Figures W6A-W6E).

Figures W6A-W6E
In a cohort of 14 NFL players who underwent ankle fracture fixation with ankle arthroscopy and debridement, fibula fixation with plate and screws, syndesmotic fixation with suture-button devices, and open deltoid complex repair with suture anchors, all athletes were able to return to running and cutting maneuvers by 6 months after surgery.35 There were no intraoperative or postoperative complications noted, and no players had clinical evidence of medial pain or instability at final follow-up with radiographic maintenance of anatomic mortise alignment.

During surgical repair, an incision is made along the anterior aspect of the medial malleolus and the superficial deltoid ligament complex can often be found flipped and interposed in the medial gutter. A rongeur is used to create a bleeding cancellous bone surface for soft-tissue healing and 1 to 2 suture anchors are used to repair and imbricate the deltoid ligament complex back to the medial malleolus. The goal of these sutures is to repair the tibionavicular and tibial spring ligaments back to the medial malleolus. We believe that superficial deltoid complex avulsion during high-energy ankle fractures is a distinct injury pattern that should be recognized and may benefit from primary open repair.

We currently open explore every deltoid ligament complex in athletes with unstable syndesmotic injuries, as we believe that deltoid avulsion injuries are underrecognized and do not heal in an anatomic fashion if left alone. Postoperative recovery follows the same immobilization, progressive weight-bearing, and physical therapy protocol as that for syndesmotic disruption.

 

 

Achilles Ruptures

Acute midsubstance Achilles tendon ruptures are an increasingly common injury in patients 30 to 50 years of age, with more than 50% of all injuries occurring during basketball.36,37 Among NFL players, we have found that Achilles ruptures tend to occur at a higher rate during training camp, when athletes are deconditioned and quickly returning to explosive push-off activities. Physical examination should include a Thompson test, palpation of a gap within the tendon, and evaluation of resting ankle dorsiflexion in the affected extremity in the prone position with the knees bent. Lateral radiographs should be analyzed for the presence of a bony avulsion fragment indicative of an insertional avulsion injury or midsubstance calcium deposition reflecting chronic Achilles tendinosis, as both of these conditions will change surgical management. MRI is not recommended with acute midsubstance ruptures but may be helpful in the case of chronic ruptures or more proximal tears of the musculotendinous junction.

The management of acute midsubstance Achilles tendon ruptures is controversial, with no general consensus in the literature regarding nonoperative treatment, surgical repair, and ideal repair technique.36,38-42 American Academy of Orthopaedic Surgeons clinical practice guidelines report moderate evidence that nonoperative treatment of Achilles tendon ruptures has lower wound healing complications but higher rates of re-rupture.38,39 Additionally, limited incision approaches have been found to have fewer overall complications compared with traditional open repair. In an effort to reduce the incidence of postoperative wound complications while improving functional recovery, modern repair techniques focus on a limited incision repair using percutaneous suture insertion and management (PARS Achilles Jig System, Arthrex).36 The limited incision technique utilizes a 2-cm transverse incision and non-disposable jig with divergent needle passes and locking suture fixation options to secure and fixate both tendon ends with minimal dissection of skin, subcutaneous tissue, and paratenon. Limited incision repair is ideally performed within 2 weeks of the injury to ensure that both tendon ends are easy to identify, mobilize, and repair. An open repair is generally recommended for midsubstance ruptures more than 4 weeks old and cases of insertional rupture and Achilles tendinopathy.

In a cohort of 9 NFL players treated for midsubstance Achilles ruptures using the PARS technique, we found no re-ruptures, no wound complications, and no sural nerve issues after surgery.43 A comparative review of 270 cases of operatively treated Achilles tendon ruptures (101 PARS, 169 traditional open repair) showed that the PARS group had significantly shorter operative times and a higher number of patients able to return to baseline physical activities by 5 months compared to open repair.36 Although not statistically significant, the overall PARS complication rate was 5% while the open complication rate was 11%. The PARS group had no cases of sural neuritis or deep infection requiring reoperation. We currently use a limited incision technique for all acute midsubstance Achilles ruptures in athletes regardless of sport, patient size, or position played.

During surgery, a 2-cm transverse incision is made over the gap in the Achilles tendon and dissection is carried down to the rupture site with minimal manipulation of the skin (Figures 5A-5F).

Figures 5A-5F
A transverse incision is made through the paratenon and typically a hematoma is expressed. An Allis clamp is inserted and the proximal tendon stump is grabbed securely and pulled through the wound approximately 1 to 2 cm. The PARS jig is inserted around the proximal tendon and centered so that the needle and sutures will pass through tendon. Needles and sutures are passed in a stepwise fashion and then the entire jig is removed from the wound. Sutures are passed to create 2 non-locking and 1 locking suture. The jig and suture passing process is repeated for the distal tendon stump. Then, each pair of sutures is tied together with the ankle in maximum plantarflexion to obtain a secure end-to-end repair. The knots are cut short and tucked into tendon so that they do not protrude and cause subcutaneous tissue irritation. Absorbable sutures are used to close the paratenon, followed by closure of subcutaneous tissues and skin followed by placement of a short leg posterior mold NWB splint with the ankle in resting plantar flexion.

A key aspect of postoperative recovery is avoiding excessive ankle dorsiflexion while the tendon is healing during the first 4 weeks after surgery, as this can lead to an elongated tendon with loss of push-off strength. Patients are kept in a plantarflexion splint NWB for 2 weeks after surgery. If the incision is healed at 2 weeks, sutures are removed and patients are transitioned into a NWB tall CAM boot for 2 weeks with gentle ankle ROM exercises. If there is any concern regarding wound healing status, sutures are maintained for an additional 1 to 2 weeks.

From 4 to 8 weeks after surgery, progressive weight-bearing with continued ankle ROM exercises is initiated with peel-away heel lifts (~2 cm thick total, 3 layers). Each layer of the heel lift is gradually removed as pain allows every 2 to 3 days with the goal of being full weight-bearing with the foot flat at 6 weeks postoperative. Physical therapy focusing on ankle ROM and gentle Achilles stretching and strengthening is also started 6 weeks after surgery. From 8 to 12 weeks postoperative, patients are transitioned out of the tall CAM boot into normal, accommodative shoe wear with full weight-bearing. We avoid ankle dorsiflexion past neutral until 12 weeks after surgery, as overlengthening of the Achilles complex and the subsequent loss of push-off power can be devastating to running athletes. Activity levels are increased as tolerated, with no running or jumping from 12 to 16 weeks with full release to all activities after 16 weeks. RTP often takes 5 to 6 months after surgery, depending on the position played.

Am J Orthop. 2016;45(6):358-367. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. Canale ST, Cantler ED Jr, Sisk TD, Freeman BL 3rd. A chronicle of injuries of an American intercollegiate football team. Am J Sports Med. 1981;9(6):384-389.2. Robey JM, Blyth CS, Mueller FO. Athletic injuries. Application of epidemiologic methods. JAMA. 1971;217(2):184-189.

3. Saal JA. Common American football injuries. Sports Med. 1991;12(2):132-147.

4. Thompson N, Halpern B, Curl WW, et al. High school football injuries: evaluation. Am J Sports Med. 1987;15(2):117-124.

5. Kaplan LD, Jost PW, Honkamp N, Norwig J, West R, Bradley JP. Incidence and variance of foot and ankle injuries in elite college football players. Am J Orthop. 2011;40(1):40-44.

6. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.

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

8. Bowers KD Jr, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8(2):81-83.

9. McCormick JJ, Anderson RB. Turf toe: anatomy, diagnosis, and treatment. Sports Health. 2010;2(6):487-494.

10. Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367-1372.

11. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete. Orthop Clin North Am. 2002;33(3):587-598.

12. Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am. 1995;26(2):353-361.

13. Nunley JA, Glisson RR. A new option for intramedullary fixation of Jones fractures: the Charlotte Carolina Jones Fracture System. Foot Ankle Int. 2008;29(12):1216-1221.

14. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8-16.

15. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones fractures. Analysis of failure. Am J Sports Med. 2002;30(1):55-60.

16. Portland G, Kelikian A, Kodros S. Acute surgical management of Jones’ fractures. Foot Ankle Int. 2003;24(11):829-833.

17. Hunt KJ, Anderson RB. Treatment of Jones fracture nonunions and refractures in the elite athlete: outcomes of intramedullary screw fixation with bone grafting. Am J Sports Med. 2011;39(9):1948-1954.

18. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871-878.

19. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw fixation. Foot Ankle Int. 2005;26(6):462-473.

20. Ardoin GT, Anderson RB. Subtle Lisfranc injury. Tech Foot Ankle Surg. 2010;9(3):100-106.

21. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A(11):1609-1618.

22. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.

23. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35(7):1197-1207.

24. Beumer A, Valstar ER, Garling EH, et al. Effects of ligament sectioning on the kinematics of the distal tibiofibular syndesmosis: a radiostereometric study of 10 cadaveric specimens based on presumed trauma mechanisms with suggestions for treatment. Acta Orthop. 2006;77(3):531-540.

25. McCollum GA, van den Bekerom MP, Kerkhoffs GM, Calder JD, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1328-1337.

26. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.

27. Nussbaum ED, Hosea TM, Sieler SD, Incremona BR, Kessler DE. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med. 2001;29(1):31-35.

28. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle syndesmosis injuries. Foot Ankle Int. 2005;26(2):187-188.

29. Beumer A, van Hemert WL, Swierstra BA, Jasper LE, Belkoff SM. A biomechanical evaluation of clinical stress tests for syndesmotic ankle instability. Foot Ankle Int. 2003;24(4):358-363.

30. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14(4):232-236.

31. Beumer A, Valstar ER, Garling EH, et al. External rotation stress imaging in syndesmotic injuries of the ankle: comparison of lateral radiography and radiostereometry in a cadaveric model. Acta Orthop Scand. 2003;74(2):201-205.

32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.

33. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2(6):460-470.

34. Westermann RW, Rungprai C, Goetz JE, Femino J, Amendola A, Phisitkul P. The effect of suture-button fixation on simulated syndesmotic malreduction: a cadaveric study. J Bone Joint Surg Am. 2014;96(20):1732-1738.

35. Hsu AR, Lareau CR, Anderson RB. Repair of acute superficial deltoid complex avulsion during ankle fracture fixation in National Football League players. Foot Ankle Int. 2015;36(11):1272-1278.

36. Hsu AR, Jones CP, Cohen BE, Davis WH, Ellington JK, Anderson RB. Clinical outcomes and complications of percutaneous Achilles repair system versus open technique for acute achilles tendon ruptures. Foot Ankle Int. 2015;36(11):1279-1286.

37. Raikin SM, Garras DN, Krapchev PV. Achilles tendon injuries in a United States population. Foot Ankle Int. 2013;34(4):475-480.

38. Chiodo CP, Glazebrook M, Bluman EM, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on treatment of achilles tendon rupture. J Bone Joint Surg Am. 2010;92(14):2466-2468.

39. Chiodo CP, Glazebrook M, Bluman EM, et al. Diagnosis and treatment of acute achilles tendon rupture. J Am Acad Orthop Surg. 2010;18(8):503-510.

40. Khan RJ, Fick D, Keogh A, Crawford J, Brammar T, Parker M. Treatment of acute achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2005;87(10):2202-2210.

41. Renninger CH, Kuhn K, Fellars T, Youngblood S, Bellamy J. Operative and nonoperative management of achilles tendon ruptures in active duty military population. Foot Ankle Int. 2016;37(3):269-273.

42. Khan RJ, Carey Smith RL. Surgical interventions for treating acute achilles tendon ruptures. Cochrane Database Syst Rev. 2010;(9):CD003674.

43. McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv. 2014;23(4):179-183.

References

1. Canale ST, Cantler ED Jr, Sisk TD, Freeman BL 3rd. A chronicle of injuries of an American intercollegiate football team. Am J Sports Med. 1981;9(6):384-389.2. Robey JM, Blyth CS, Mueller FO. Athletic injuries. Application of epidemiologic methods. JAMA. 1971;217(2):184-189.

3. Saal JA. Common American football injuries. Sports Med. 1991;12(2):132-147.

4. Thompson N, Halpern B, Curl WW, et al. High school football injuries: evaluation. Am J Sports Med. 1987;15(2):117-124.

5. Kaplan LD, Jost PW, Honkamp N, Norwig J, West R, Bradley JP. Incidence and variance of foot and ankle injuries in elite college football players. Am J Orthop. 2011;40(1):40-44.

6. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.

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

8. Bowers KD Jr, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8(2):81-83.

9. McCormick JJ, Anderson RB. Turf toe: anatomy, diagnosis, and treatment. Sports Health. 2010;2(6):487-494.

10. Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367-1372.

11. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete. Orthop Clin North Am. 2002;33(3):587-598.

12. Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am. 1995;26(2):353-361.

13. Nunley JA, Glisson RR. A new option for intramedullary fixation of Jones fractures: the Charlotte Carolina Jones Fracture System. Foot Ankle Int. 2008;29(12):1216-1221.

14. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8-16.

15. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones fractures. Analysis of failure. Am J Sports Med. 2002;30(1):55-60.

16. Portland G, Kelikian A, Kodros S. Acute surgical management of Jones’ fractures. Foot Ankle Int. 2003;24(11):829-833.

17. Hunt KJ, Anderson RB. Treatment of Jones fracture nonunions and refractures in the elite athlete: outcomes of intramedullary screw fixation with bone grafting. Am J Sports Med. 2011;39(9):1948-1954.

18. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871-878.

19. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw fixation. Foot Ankle Int. 2005;26(6):462-473.

20. Ardoin GT, Anderson RB. Subtle Lisfranc injury. Tech Foot Ankle Surg. 2010;9(3):100-106.

21. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A(11):1609-1618.

22. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.

23. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35(7):1197-1207.

24. Beumer A, Valstar ER, Garling EH, et al. Effects of ligament sectioning on the kinematics of the distal tibiofibular syndesmosis: a radiostereometric study of 10 cadaveric specimens based on presumed trauma mechanisms with suggestions for treatment. Acta Orthop. 2006;77(3):531-540.

25. McCollum GA, van den Bekerom MP, Kerkhoffs GM, Calder JD, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1328-1337.

26. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.

27. Nussbaum ED, Hosea TM, Sieler SD, Incremona BR, Kessler DE. Prospective evaluation of syndesmotic ankle sprains without diastasis. Am J Sports Med. 2001;29(1):31-35.

28. Kiter E, Bozkurt M. The crossed-leg test for examination of ankle syndesmosis injuries. Foot Ankle Int. 2005;26(2):187-188.

29. Beumer A, van Hemert WL, Swierstra BA, Jasper LE, Belkoff SM. A biomechanical evaluation of clinical stress tests for syndesmotic ankle instability. Foot Ankle Int. 2003;24(4):358-363.

30. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14(4):232-236.

31. Beumer A, Valstar ER, Garling EH, et al. External rotation stress imaging in syndesmotic injuries of the ankle: comparison of lateral radiography and radiostereometry in a cadaveric model. Acta Orthop Scand. 2003;74(2):201-205.

32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.

33. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2(6):460-470.

34. Westermann RW, Rungprai C, Goetz JE, Femino J, Amendola A, Phisitkul P. The effect of suture-button fixation on simulated syndesmotic malreduction: a cadaveric study. J Bone Joint Surg Am. 2014;96(20):1732-1738.

35. Hsu AR, Lareau CR, Anderson RB. Repair of acute superficial deltoid complex avulsion during ankle fracture fixation in National Football League players. Foot Ankle Int. 2015;36(11):1272-1278.

36. Hsu AR, Jones CP, Cohen BE, Davis WH, Ellington JK, Anderson RB. Clinical outcomes and complications of percutaneous Achilles repair system versus open technique for acute achilles tendon ruptures. Foot Ankle Int. 2015;36(11):1279-1286.

37. Raikin SM, Garras DN, Krapchev PV. Achilles tendon injuries in a United States population. Foot Ankle Int. 2013;34(4):475-480.

38. Chiodo CP, Glazebrook M, Bluman EM, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on treatment of achilles tendon rupture. J Bone Joint Surg Am. 2010;92(14):2466-2468.

39. Chiodo CP, Glazebrook M, Bluman EM, et al. Diagnosis and treatment of acute achilles tendon rupture. J Am Acad Orthop Surg. 2010;18(8):503-510.

40. Khan RJ, Fick D, Keogh A, Crawford J, Brammar T, Parker M. Treatment of acute achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2005;87(10):2202-2210.

41. Renninger CH, Kuhn K, Fellars T, Youngblood S, Bellamy J. Operative and nonoperative management of achilles tendon ruptures in active duty military population. Foot Ankle Int. 2016;37(3):269-273.

42. Khan RJ, Carey Smith RL. Surgical interventions for treating acute achilles tendon ruptures. Cochrane Database Syst Rev. 2010;(9):CD003674.

43. McCullough KA, Shaw CM, Anderson RB. Mini-open repair of achilles rupture in the national football league. J Surg Orthop Adv. 2014;23(4):179-183.

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The American Journal of Orthopedics - 45(6)
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The American Journal of Orthopedics - 45(6)
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