Sports Medicine

Among children and adolescents aged 5-18 years, concussion was associated with a higher risk of mental health problems, compared with age- and sex-matched children and adolescents with an orthopedic injury, according to a cohort study published in JAMA Network Open.

While concussions are one of the most common head injuries in the pediatric population, the extent to which they increase the risk of new onset psychiatric disorders or subsequent psychopathology is unclear, lead author Andrée-Anne Ledoux, PhD, of the Children’s Hospital of Eastern Ontario Research Institute, Ottawa, and colleagues explained.

The researchers conducted a population-based retrospective cohort study to evaluate associations between concussion and risk of subsequent mental health issues, psychiatric hospitalizations, self-harm, or suicides in children and adolescents, with follow-up ranging from 1 month to 10 years.

The data were obtained from province-wide health administrative databases. Participants with concussion were included in an exposed group, while those with an orthopedic injury were included in a 1:2 age- and sex-matched comparison group.
 

Results

The study cohort comprised 448,803 participants, including 152,321 and 296,482 children and adolescents with concussion and orthopedic injury, respectively.

The incidence rates of any mental health problem were 11,141 per 100,000 person-years in the exposed group and 7,960 per 100,000 person-years in the unexposed group (difference, 3,181; 95% confidence interval, 3,073-3,291 per 100,000 person-years).

After concussion, the exposed group had a greater risk of developing a mental health issue (adjusted hazard ratio, 1.39; 95% CI, 1.37-1.40), psychiatric hospitalization (aHR, 1.47; 95% CI, 1.41-1.53), and self-harm (aHR, 1.49; 95% CI, 1.42-1.56). In addition, there was no significant difference in death by suicide between the exposed and unexposed groups (HR, 1.54; 95% CI, 0.90-2.61).

“Our results suggest that clinicians should assess for preexisting and new mental health symptoms throughout concussion recovery and treat mental health conditions or symptoms or refer the patient to a specialist in pediatric mental health,” wrote Dr. Ledoux and colleagues. “[Clinicians should also] assess suicidal ideation and self-harm behaviors during evaluation and follow-up visits for concussion.”

The researchers acknowledged that a key limitation of the study was the retrospective observational design. In addition, the identification of exposures using diagnostic billing codes could have introduced exposure or outcome misclassification.
 

Expert-recommended resources

“For more information, I’d recommend ‘Pedsconcussion,’ which are evidence-based living guidelines for pediatric concussion care,” Dr. Ledoux said in an interview. “Within domain 8, there are specific guidelines related to the management of mental health issues post concussion.”

Neuropsychology expert Talin Babikian, PhD, of the University of California, Los Angeles, commented: “Studies have shown that even a single psychoeducational session early after a concussion can minimize prolonged recoveries. Ensuring all stakeholders (family, clinicians, school, coach, peers) are on the same page and providing the same information is important to build trust and a sense of safety and agency.

“We want to provide psychoeducation early in the process to avoid unnecessary fear and avoidance. We also want to curtail misattribution of everyday symptoms or symptoms related to an unrelated condition to a brain injury, which are easier to do when caught early,” Dr. Babikian added.

This study was supported by the Institute for Clinical Evaluative Sciences, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-term Care. One author reported financial relationships with the University of Ottawa, the National Football League, Parachute Canada, and 360 Concussion Care, an interdisciplinary concussion clinic; no other conflicts of interest were reported.

Among children and adolescents aged 5-18 years, concussion was associated with a higher risk of mental health problems, compared with age- and sex-matched children and adolescents with an orthopedic injury, according to a cohort study published in JAMA Network Open.

While concussions are one of the most common head injuries in the pediatric population, the extent to which they increase the risk of new onset psychiatric disorders or subsequent psychopathology is unclear, lead author Andrée-Anne Ledoux, PhD, of the Children’s Hospital of Eastern Ontario Research Institute, Ottawa, and colleagues explained.

The researchers conducted a population-based retrospective cohort study to evaluate associations between concussion and risk of subsequent mental health issues, psychiatric hospitalizations, self-harm, or suicides in children and adolescents, with follow-up ranging from 1 month to 10 years.

The data were obtained from province-wide health administrative databases. Participants with concussion were included in an exposed group, while those with an orthopedic injury were included in a 1:2 age- and sex-matched comparison group.
 

Results

The study cohort comprised 448,803 participants, including 152,321 and 296,482 children and adolescents with concussion and orthopedic injury, respectively.

The incidence rates of any mental health problem were 11,141 per 100,000 person-years in the exposed group and 7,960 per 100,000 person-years in the unexposed group (difference, 3,181; 95% confidence interval, 3,073-3,291 per 100,000 person-years).

After concussion, the exposed group had a greater risk of developing a mental health issue (adjusted hazard ratio, 1.39; 95% CI, 1.37-1.40), psychiatric hospitalization (aHR, 1.47; 95% CI, 1.41-1.53), and self-harm (aHR, 1.49; 95% CI, 1.42-1.56). In addition, there was no significant difference in death by suicide between the exposed and unexposed groups (HR, 1.54; 95% CI, 0.90-2.61).

“Our results suggest that clinicians should assess for preexisting and new mental health symptoms throughout concussion recovery and treat mental health conditions or symptoms or refer the patient to a specialist in pediatric mental health,” wrote Dr. Ledoux and colleagues. “[Clinicians should also] assess suicidal ideation and self-harm behaviors during evaluation and follow-up visits for concussion.”

The researchers acknowledged that a key limitation of the study was the retrospective observational design. In addition, the identification of exposures using diagnostic billing codes could have introduced exposure or outcome misclassification.
 

Expert-recommended resources

“For more information, I’d recommend ‘Pedsconcussion,’ which are evidence-based living guidelines for pediatric concussion care,” Dr. Ledoux said in an interview. “Within domain 8, there are specific guidelines related to the management of mental health issues post concussion.”

Neuropsychology expert Talin Babikian, PhD, of the University of California, Los Angeles, commented: “Studies have shown that even a single psychoeducational session early after a concussion can minimize prolonged recoveries. Ensuring all stakeholders (family, clinicians, school, coach, peers) are on the same page and providing the same information is important to build trust and a sense of safety and agency.

“We want to provide psychoeducation early in the process to avoid unnecessary fear and avoidance. We also want to curtail misattribution of everyday symptoms or symptoms related to an unrelated condition to a brain injury, which are easier to do when caught early,” Dr. Babikian added.

This study was supported by the Institute for Clinical Evaluative Sciences, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-term Care. One author reported financial relationships with the University of Ottawa, the National Football League, Parachute Canada, and 360 Concussion Care, an interdisciplinary concussion clinic; no other conflicts of interest were reported.

Among children and adolescents aged 5-18 years, concussion was associated with a higher risk of mental health problems, compared with age- and sex-matched children and adolescents with an orthopedic injury, according to a cohort study published in JAMA Network Open.

While concussions are one of the most common head injuries in the pediatric population, the extent to which they increase the risk of new onset psychiatric disorders or subsequent psychopathology is unclear, lead author Andrée-Anne Ledoux, PhD, of the Children’s Hospital of Eastern Ontario Research Institute, Ottawa, and colleagues explained.

The researchers conducted a population-based retrospective cohort study to evaluate associations between concussion and risk of subsequent mental health issues, psychiatric hospitalizations, self-harm, or suicides in children and adolescents, with follow-up ranging from 1 month to 10 years.

The data were obtained from province-wide health administrative databases. Participants with concussion were included in an exposed group, while those with an orthopedic injury were included in a 1:2 age- and sex-matched comparison group.
 

Results

The study cohort comprised 448,803 participants, including 152,321 and 296,482 children and adolescents with concussion and orthopedic injury, respectively.

The incidence rates of any mental health problem were 11,141 per 100,000 person-years in the exposed group and 7,960 per 100,000 person-years in the unexposed group (difference, 3,181; 95% confidence interval, 3,073-3,291 per 100,000 person-years).

After concussion, the exposed group had a greater risk of developing a mental health issue (adjusted hazard ratio, 1.39; 95% CI, 1.37-1.40), psychiatric hospitalization (aHR, 1.47; 95% CI, 1.41-1.53), and self-harm (aHR, 1.49; 95% CI, 1.42-1.56). In addition, there was no significant difference in death by suicide between the exposed and unexposed groups (HR, 1.54; 95% CI, 0.90-2.61).

“Our results suggest that clinicians should assess for preexisting and new mental health symptoms throughout concussion recovery and treat mental health conditions or symptoms or refer the patient to a specialist in pediatric mental health,” wrote Dr. Ledoux and colleagues. “[Clinicians should also] assess suicidal ideation and self-harm behaviors during evaluation and follow-up visits for concussion.”

The researchers acknowledged that a key limitation of the study was the retrospective observational design. In addition, the identification of exposures using diagnostic billing codes could have introduced exposure or outcome misclassification.
 

Expert-recommended resources

“For more information, I’d recommend ‘Pedsconcussion,’ which are evidence-based living guidelines for pediatric concussion care,” Dr. Ledoux said in an interview. “Within domain 8, there are specific guidelines related to the management of mental health issues post concussion.”

Neuropsychology expert Talin Babikian, PhD, of the University of California, Los Angeles, commented: “Studies have shown that even a single psychoeducational session early after a concussion can minimize prolonged recoveries. Ensuring all stakeholders (family, clinicians, school, coach, peers) are on the same page and providing the same information is important to build trust and a sense of safety and agency.

“We want to provide psychoeducation early in the process to avoid unnecessary fear and avoidance. We also want to curtail misattribution of everyday symptoms or symptoms related to an unrelated condition to a brain injury, which are easier to do when caught early,” Dr. Babikian added.

This study was supported by the Institute for Clinical Evaluative Sciences, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-term Care. One author reported financial relationships with the University of Ottawa, the National Football League, Parachute Canada, and 360 Concussion Care, an interdisciplinary concussion clinic; no other conflicts of interest were reported.

The U.S. Food and Drug Administration has cleared SyncThink’s Eye-Sync technology to aid in the diagnosis of mild traumatic brain injury, the company has announced.

Eye-Sync is a virtual reality eye-tracking platform that provides objective measurements to aid in the assessment of concussion. It’s the first mobile, rapid test for concussion that has been cleared by the FDA, the company said.

As reported by this news organization, Eye-Sync received breakthrough designation from the FDA for this indication in March 2019.

The FDA initially cleared the Eye-Sync platform for recording, viewing, and analyzing eye movements to help clinicians identify visual tracking impairment.

The Eye-Sync technology uses a series of 60-second eye tracking assessments, neurocognitive batteries, symptom inventories, and standardized patient inventories to identify the type and severity of impairment after concussion.

“The platform generates customizable and interpretive reports that support clinical decision making and offers visual and vestibular therapies to remedy deficits and monitor improvement over time,” the company said.

In support of the application for use in concussion, SyncThink enrolled 1,655 children and adults into a clinical study that collected comprehensive patient and concussion-related data for over 12 months.

The company used these data to develop proprietary algorithms and deep learning models to identify a positive or negative indication of concussion.

The study showed that Eye-Sinc had sensitivity greater than 82% and specificity greater than 93%, “thereby providing clinicians with significant and actionable data when evaluating individuals with concussion,” the company said in a news release.

“The outcome of this study very clearly shows the effectiveness of our technology at detecting concussion and definitively demonstrates the clinical utility of Eye-Sinc,” SyncThink Chief Clinical Officer Scott Anderson said in the release.

“It also shows that the future of concussion diagnosis is no longer purely symptom-based but that of a technology driven multi-modal approach,” Mr. Anderson said.

A version of this article first appeared on Medscape.com.

The U.S. Food and Drug Administration has cleared SyncThink’s Eye-Sync technology to aid in the diagnosis of mild traumatic brain injury, the company has announced.

Eye-Sync is a virtual reality eye-tracking platform that provides objective measurements to aid in the assessment of concussion. It’s the first mobile, rapid test for concussion that has been cleared by the FDA, the company said.

As reported by this news organization, Eye-Sync received breakthrough designation from the FDA for this indication in March 2019.

The FDA initially cleared the Eye-Sync platform for recording, viewing, and analyzing eye movements to help clinicians identify visual tracking impairment.

The Eye-Sync technology uses a series of 60-second eye tracking assessments, neurocognitive batteries, symptom inventories, and standardized patient inventories to identify the type and severity of impairment after concussion.

“The platform generates customizable and interpretive reports that support clinical decision making and offers visual and vestibular therapies to remedy deficits and monitor improvement over time,” the company said.

In support of the application for use in concussion, SyncThink enrolled 1,655 children and adults into a clinical study that collected comprehensive patient and concussion-related data for over 12 months.

The company used these data to develop proprietary algorithms and deep learning models to identify a positive or negative indication of concussion.

The study showed that Eye-Sinc had sensitivity greater than 82% and specificity greater than 93%, “thereby providing clinicians with significant and actionable data when evaluating individuals with concussion,” the company said in a news release.

“The outcome of this study very clearly shows the effectiveness of our technology at detecting concussion and definitively demonstrates the clinical utility of Eye-Sinc,” SyncThink Chief Clinical Officer Scott Anderson said in the release.

“It also shows that the future of concussion diagnosis is no longer purely symptom-based but that of a technology driven multi-modal approach,” Mr. Anderson said.

A version of this article first appeared on Medscape.com.

The U.S. Food and Drug Administration has cleared SyncThink’s Eye-Sync technology to aid in the diagnosis of mild traumatic brain injury, the company has announced.

Eye-Sync is a virtual reality eye-tracking platform that provides objective measurements to aid in the assessment of concussion. It’s the first mobile, rapid test for concussion that has been cleared by the FDA, the company said.

As reported by this news organization, Eye-Sync received breakthrough designation from the FDA for this indication in March 2019.

The FDA initially cleared the Eye-Sync platform for recording, viewing, and analyzing eye movements to help clinicians identify visual tracking impairment.

The Eye-Sync technology uses a series of 60-second eye tracking assessments, neurocognitive batteries, symptom inventories, and standardized patient inventories to identify the type and severity of impairment after concussion.

“The platform generates customizable and interpretive reports that support clinical decision making and offers visual and vestibular therapies to remedy deficits and monitor improvement over time,” the company said.

In support of the application for use in concussion, SyncThink enrolled 1,655 children and adults into a clinical study that collected comprehensive patient and concussion-related data for over 12 months.

The company used these data to develop proprietary algorithms and deep learning models to identify a positive or negative indication of concussion.

The study showed that Eye-Sinc had sensitivity greater than 82% and specificity greater than 93%, “thereby providing clinicians with significant and actionable data when evaluating individuals with concussion,” the company said in a news release.

“The outcome of this study very clearly shows the effectiveness of our technology at detecting concussion and definitively demonstrates the clinical utility of Eye-Sinc,” SyncThink Chief Clinical Officer Scott Anderson said in the release.

“It also shows that the future of concussion diagnosis is no longer purely symptom-based but that of a technology driven multi-modal approach,” Mr. Anderson said.

A version of this article first appeared on Medscape.com.

ABSTRACT

Discoid meniscus is a rare anatomical variant with altered morphology and structure that can sometimes present symptomatically, typically in the pediatric population. The discoid meniscus is usually in the lateral compartment of the knee and is characterized by a partial or complete filling-in of central meniscal tissue, increased meniscal thickness, disorganization of longitudinal collagen fibers, and sometimes lack of peripheral attachments. These changes to both the macro- and micro-structure of the meniscus predispose affected patients to increased rates of both meniscal tears and mechanical symptoms. Surgical management of symptomatic discoid meniscus is directed toward symptom resolution while preserving sufficient functional meniscal tissue to delay or prevent the development of osteoarthritis. Modern surgical techniques consist of arthroscopic saucerization of the discoid meniscus with repair of associated meniscal tears and stabilization of peripheral attachments. Although long-term outcome data are lacking, short- and mid-term outcomes for patients treated with arthroscopic partial meniscectomy and meniscal repair and/or stabilization as needed are generally good. 

Continue to: The discoid meniscus...

The discoid meniscus is an uncommon anatomical meniscal variant that may present with pain, snapping, motion loss, swelling, and locking of the affected knee, typically during childhood or adolescence.¹ Although the etiology of discoid meniscus is not completely understood, it is considered a congenital anomaly with a possible genetic component.^{2, 3} Incidence is estimated at 0.4% to 5.2% in the Western European population but is reportedly much higher (roughly 17%) in Asian populations.^4-6, Discoid menisci, when present, are almost always in the lateral compartment, although cases of medial discoid meniscus have also been reported. The overall incidence of medial discoid meniscus has been estimated to be between 0.06% and 0.3% while that of lateral discoid meniscus, as detailed above, is significantly higher.^7-11 

ANATOMY AND MORPHOLOGY

The menisci differentiate from mesenchymal tissue early during fetal development with a clear definition by 8 weeks and a mature anatomical shape by 14 weeks in utero.¹² Interestingly, menisci never possess a discoid shape during the normal course of development.^13,14 The meniscus is fully vascularized at birth, with the central one-third becoming avascular by 9 months as the vascular supply regresses.¹⁴ By 10 years, only the peripheral one-third maintains its vascular supply, and the menisci have adult-like characteristics with tissue composed mainly of circumferential collagen fibers.^4,14-16

A normal meniscus is wedge-shaped in the coronal plane and crescent-shaped in the axial plane. The medial meniscus is shaped like the letter “C,” is connected firmly to the joint capsule, and covers approximately 50% of the medial tibial plateau. The normal lateral meniscus covers 70% of the lateral tibial plateau and has firm anterior and posterior attachments while the lateral portion is less securely tethered.¹⁷ A discoid meniscus is characterized by an atypical shape—the center being partially or completely filled in (or “disc-like”)—often associated with anomalous attachments to the tibia, femur, and surrounding joint capsule. In addition to an atypical morphology, the discoid meniscus may also be much thicker than normal, resulting in a “block-like” appearance. The increased thickness may be responsible for the pathognomonic snapping of the knee as it is brought passively into flexion or extension (hence, the term “snapping knee” was traditionally used to describe a symptomatic discoid lateral meniscus). While the discoid shape is relatively straightforward to address, the increased meniscal thickness may be quite difficult to correct surgically.^4-6,18 

In addition to the macromorphological differences characteristic of discoid menisci, histological differences have also been described, including differences in collagen density and disorganization of the circumferential collagen network.^19-21 Taken together, these differences may compromise the ability of the discoid meniscus to withstand normal forces placed across the knee and predispose it to tear. This is important because the normal meniscus plays a critical role in facilitating load distribution across the knee joint, in addition to assisting with functions including shock absorption, proprioception, and stabilization of the knee. Torn and/or unstable discoid menisci are unable to perform these functions adequately, which may ultimately result in degenerative joint disease and progress to end-stage osteoarthritis (OA). 

CLASSIFICATION

The traditional Watanabe classification of discoid meniscus consists of 3 variants: type I, a complete discoid shape; type II, an incomplete discoid shape; and type III, the Wrisberg variant.²² The Wrisberg variant is described as a more normal-appearing meniscus but lacks normal peripheral attachments.^{5, 6, 15} This classification system was expanded by Monllau and colleagues, ²³ who described a ring-type meniscus variant with normal posterior tibial attachments. Although the Watanabe classification is commonly used, its utility in assisting with clinical decision-making may be limited. 

Continue to: Several other classification schemes...

Several other classification schemes exist. Jordan and colleagues²⁴ described a classification scheme defining a meniscal type as complete or incomplete, also noting the presence of symptoms, tearing, and peripheral rim instability. They grouped stable types together, regardless of morphology, and then further classified them based on the presence of symptoms and tears. Similarly, the unstable types were grouped together and then subclassified in the same manner.^17,24 Klingele and colleagues²⁵ also described a contemporary classification scheme of discoid meniscus evaluating peripheral stability patterns that may be more clinically and surgically relevant. This classification is based on the type of discoid morphology (complete vs incomplete), the presence or absence of peripheral rim stability (stable vs unstable), and the presence or absence of a meniscal tear (torn vs untorn).^5,25 
    

EVALUATION

A stable discoid meniscus is often an incidental finding, seen either on advanced diagnostic imaging performed for another reason or at the time of arthroscopy to address another problem. Younger children with discoid meniscus tend to present with symptoms such as popping and snapping related to instability and the abnormal morphology of the discoid meniscus. Older patients tend to present with symptoms related to acute tears through the abnormal meniscal tissue. Although discoid menisci can become acutely symptomatic in the presence of a tear, the onset of symptoms may occur in the absence of a discrete traumatic event.¹ Alternatively, some patients will report a clear history of injury, often a noncontact, rotational injury mechanism related to an athletic activity. Patients with torn discoid menisci may report pain, catching, locking, and/or giving way of the knee, and on examination may have limited extension, snapping, effusion, quadriceps atrophy, and joint line tenderness. Eponymous meniscal compression tests including the McMurray, Apley, and Thessaly tests, may also be performed when meniscal tear is suspected, although this may be tricky for younger children.¹ 

Considering the high association of meniscal tears with ligamentous injuries, examination of knee stability is important. Plain radiographs of the knee should be taken, although the results will often be negative for osseous injury in the case of an isolated meniscal tear. Radiographs of a discoid knee may show subtle differences compared with radiographs of a non-discoid knee. A recent comparison of children with symptomatic lateral discoid menisci with age-matched controls found statistically significant increased lateral joint space, elevated fibular head, increased height of the lateral tibial spine, and increased obliquity of the tibial plateau.²⁶ They did not find statistically significant increased squaring of the lateral femoral condyle or cupping of the lateral tibial plateau. Radiographic signs can be subtle and may not all be present in a patient with a discoid meniscus. 

Magnetic resonance imaging (MRI) is the assessment technique of choice for the diagnosis of discoid meniscus, although MRI may not reliably identify a Wrisberg variant or incomplete discoid menisci (Figure 1).

Gans and colleagues²⁷ examined preoperative MRI and clinical examination compared with pathology found during arthroscopy. Although they found that MRI and clinical examination had excellent diagnostic accuracy of 92.7% and 95.3%, respectively, the most common missed pathology on MRI later found on diagnostic arthroscopy was the presence of a lateral discoid meniscus, which occurred in 26.7% of missed diagnoses. Adult diagnostic criteria of discoid meniscus include ≥3 contiguous 5-mm sagittal cuts showing continuity between the anterior and posterior horns of the meniscus. Other criteria include a minimal meniscal width >15 mm on the coronal view or a minimum meniscal width that is >20% of the width of the maximal tibial width.²⁸ These criteria are often applied to children as well. Additionally, if >50% of the lateral joint space is covered by meniscal tissue, a diagnosis of discoid meniscus should be considered.⁶

Continue to: TREATMENT

Management of symptomatic discoid meniscus is directed toward resolving symptoms while preserving meniscal tissue and preventing the development of OA. Incidentally found discoid menisci in asymptomatic patients should not be treated surgically and can have periodic follow-ups for detection of any functional deterioration or symptom development. Surgical treatment may be beneficial for patients with symptoms related to their discoid menisci such as pain, recurrent effusion, limited knee motion, mechanical symptoms (e.g., locking and catching), and activity restrictions.

Traditionally, surgical treatment of a symptomatic discoid meniscus consisted of subtotal (meaning nearly complete, or <3mm of peripheral rim remaining) or complete meniscectomy, often performed in an open fashion. Surgical techniques have evolved; current surgical approaches typically include diagnostic arthroscopy followed by arthroscopic saucerization (also called partial meniscectomy) of the central portion of the “disc,” leaving a peripheral rim of 6 mm to 8 mm to approximate that of the normal meniscus (Figure 2).^29,30 Saucerization removes the redundant central meniscal tissue in an attempt to create a more “normal” C-shaped morphology, although it does not address the increased thickness characteristic of many discoid menisci. It may be particularly difficult to “debulk” an abnormally thick discoid meniscus in the coronal plane, and there is little in the outcomes literature to support this approach. Following partial meniscectomy, the remaining meniscal tissue should be inspected thoroughly both for the presence of instability and for residual tears. Meniscal tears should be repaired in standard fashion; commonly, this may be a combination of all-inside sutures placed into the posterior horn, inside-out sutures placed into the midbody, and outside-in sutures placed into the anterior horn. Peripheral rim instability—identified, for example, by the ability to translate the posterior horn of the meniscus fully onto the anterior tibial plateau—should be addressed by suturing the meniscus to the adjacent capsule (Figure 2).^{25, 31} Menisci that have residual complex tears that are not amenable to repair may be treated by subtotal meniscectomy. These patients may be candidates for subsequent meniscal allograft transplantation.^32,33 

TREATMENT OUTCOMES

Performing a partial meniscectomy has consistently been shown in the laboratory to increase contact stresses proportionally to the percentage of tissue removed.³⁴ It follows logically that performing a subtotal or complete meniscectomy in a young patient would yield increased, abnormal contact stresses throughout the knee with resultant degenerative changes and progression to OA over time. While long-term outcome studies of subtotal or complete meniscectomy have shown somewhat variable results, the majority report the development of pain, instability, poor function, osteoarthritic changes and even the development of osteochondritis desiccans.^5,35 

In an early investigation of long-term outcomes associated with surgical resection of a discoid lateral meniscus, Räber and colleagues³⁶ retrospectively examined 17 knees that had undergone total meniscectomy for the lateral discoid meniscus. At a mean follow-up of 19.8 years, these authors reported that patients accounting for 10 of 17 operative knees had developed symptoms of osteoarthrosis such as pain. In addition, two-thirds of the knees that had follow-up radiographs performed (10 of 15 knees) had visible osteoarthritic changes present. 

 In 2011, Stilli and colleagues³⁷ conducted a mid-term follow-up study examining 104 knees over an average follow-up of 8.5 years, with an average age of 8 years at the time of surgery. Younger patients, 2 to 7 years, underwent subtotal meniscectomy whereas patients, 8 to 14 years, underwent arthroscopic partial meniscectomy. Patients with a Wrisberg variant underwent removal of the posterior horn. The authors of this study reported that younger patients who had undergone subtotal meniscectomy had the best outcomes (defined by self-reported questionnaire responses and clinical evaluation). However, these results should be interpreted with caution: at the time of follow-up, patients in this study would still have been in adolescence and may not yet have developed the symptomatic degenerative changes in the knee joint that are strongly associated with meniscectomy. 

Continue to: There are a few long-term...

There are few long-term outcome studies for arthroscopic saucerization. In 2014, Ahn and colleagues³⁸ examined patient-reported outcomes and radiographic changes for 48 knees in pediatric patients treated arthroscopically for a symptomatic discoid meniscus. Patients were treated with partial meniscectomy (22 knees), partial meniscectomy with meniscal repair (18 knees), or subtotal meniscectomy (8 knees). Out of 48 knees evaluated, 45 knees (94%) were rated as “excellent” or “good” at an average 10-year follow-up. However, a significant percentage of patients had evidence of degenerative changes on follow-up radiographs, specifically: 88% of the subtotal meniscectomy group, 39% of the partial meniscectomy with repair group, and 23% in the partial meniscectomy-alone group. This finding suggests that the early appearance of radiographic changes suggestive of OA does not necessarily correlate with the development of knee symptoms in this cohort, although longer-term follow-up of these patients into adulthood and middle age is clearly needed.

Recently, short-term outcomes have been reported for contemporary arthroscopic saucerization of discoid menisci with peripheral rim stabilization performed as deemed necessary at the time of surgery. In 2012, Carter and colleagues³⁹ examined 57 knees that underwent saucerization alone or saucerization with peripheral rim stabilization. At an average follow-up of 15 months, both patient populations had equivalent self-reported outcomes and clinical examination findings. The authors concluded that peripheral stabilization does not negatively affect short-term outcomes if instability is recognized and treated.

Yoo and colleagues⁴⁰ found equivalent results between patients undergoing saucerization, saucerization with rim stabilization, and subtotal meniscectomy for 100 pediatric knees with an average follow-up of 4.7 years. Subtotal meniscectomy was defined as <3 mm of peripheral rim remaining and was performed when there was severe degeneration or complex tearing of the remnant rim following arthroscopic saucerization. Taken together, these data seem to suggest that short- and mid-term outcomes for pediatric patients treated surgically are generally good in terms of reported clinical function and development of OA, although long-term follow-up studies will be essential for understanding the true impact of surgical interventions.

Shieh and colleagues^41,42 investigated risk factors for failed meniscal surgery in 324 menisci from 2008 to 2012, including in 46 discoid saucerization procedures with or without stabilization. At a mean of 40 months, 15% of the discoid saucerization cohort required a revision procedure, with increased odds of revision surgeries in patients who had undergone meniscal tear repair. The most frequent indication of revision surgery was sustaining a meniscal tear during intense physical activity in the first year after the index procedure, and patients underwent either debridement or repair for their revision procedure.

SUMMARY

Discoid meniscus is a rare anatomical meniscal variant characterized by an abnormal “O-like” shape, increased meniscal thickness, disorganization of collagen fibers, and variable absence of peripheral attachments. These morphological changes predispose patients with discoid menisci to increased rates of symptomatic meniscal instability and tearing. An MRI remains the most sensitive imaging modality for the diagnosis of a discoid meniscus, with ≥3 contiguous 5-mm sagittal cuts showing continuity between the anterior and posterior horns indicative of a discoid variant. Surgical treatment for symptomatic discoid menisci has evolved from subtotal meniscectomy to contemporary arthroscopic saucerization techniques with repair of meniscal tears and peripheral stabilization performed as needed. Long-term outcome studies for patients who undergo subtotal or complete meniscectomy reveal an association with osteoarthritic changes of the knee. Short- and mid-term outcome studies for patients who undergo arthroscopic saucerization with or without repair and/or peripheral stabilization are generally good, although reoperation rates have been estimated at 15% in the first 3 to 4 years. Longer-term follow-up, with the inclusion of validated functional outcomes measures, will be essential for understanding the true impact of various surgical interventions over time. 

ABSTRACT

Discoid meniscus is a rare anatomical variant with altered morphology and structure that can sometimes present symptomatically, typically in the pediatric population. The discoid meniscus is usually in the lateral compartment of the knee and is characterized by a partial or complete filling-in of central meniscal tissue, increased meniscal thickness, disorganization of longitudinal collagen fibers, and sometimes lack of peripheral attachments. These changes to both the macro- and micro-structure of the meniscus predispose affected patients to increased rates of both meniscal tears and mechanical symptoms. Surgical management of symptomatic discoid meniscus is directed toward symptom resolution while preserving sufficient functional meniscal tissue to delay or prevent the development of osteoarthritis. Modern surgical techniques consist of arthroscopic saucerization of the discoid meniscus with repair of associated meniscal tears and stabilization of peripheral attachments. Although long-term outcome data are lacking, short- and mid-term outcomes for patients treated with arthroscopic partial meniscectomy and meniscal repair and/or stabilization as needed are generally good. 

Continue to: The discoid meniscus...

The discoid meniscus is an uncommon anatomical meniscal variant that may present with pain, snapping, motion loss, swelling, and locking of the affected knee, typically during childhood or adolescence.¹ Although the etiology of discoid meniscus is not completely understood, it is considered a congenital anomaly with a possible genetic component.^{2, 3} Incidence is estimated at 0.4% to 5.2% in the Western European population but is reportedly much higher (roughly 17%) in Asian populations.^4-6, Discoid menisci, when present, are almost always in the lateral compartment, although cases of medial discoid meniscus have also been reported. The overall incidence of medial discoid meniscus has been estimated to be between 0.06% and 0.3% while that of lateral discoid meniscus, as detailed above, is significantly higher.^7-11 

ANATOMY AND MORPHOLOGY

The menisci differentiate from mesenchymal tissue early during fetal development with a clear definition by 8 weeks and a mature anatomical shape by 14 weeks in utero.¹² Interestingly, menisci never possess a discoid shape during the normal course of development.^13,14 The meniscus is fully vascularized at birth, with the central one-third becoming avascular by 9 months as the vascular supply regresses.¹⁴ By 10 years, only the peripheral one-third maintains its vascular supply, and the menisci have adult-like characteristics with tissue composed mainly of circumferential collagen fibers.^4,14-16

A normal meniscus is wedge-shaped in the coronal plane and crescent-shaped in the axial plane. The medial meniscus is shaped like the letter “C,” is connected firmly to the joint capsule, and covers approximately 50% of the medial tibial plateau. The normal lateral meniscus covers 70% of the lateral tibial plateau and has firm anterior and posterior attachments while the lateral portion is less securely tethered.¹⁷ A discoid meniscus is characterized by an atypical shape—the center being partially or completely filled in (or “disc-like”)—often associated with anomalous attachments to the tibia, femur, and surrounding joint capsule. In addition to an atypical morphology, the discoid meniscus may also be much thicker than normal, resulting in a “block-like” appearance. The increased thickness may be responsible for the pathognomonic snapping of the knee as it is brought passively into flexion or extension (hence, the term “snapping knee” was traditionally used to describe a symptomatic discoid lateral meniscus). While the discoid shape is relatively straightforward to address, the increased meniscal thickness may be quite difficult to correct surgically.^4-6,18 

In addition to the macromorphological differences characteristic of discoid menisci, histological differences have also been described, including differences in collagen density and disorganization of the circumferential collagen network.^19-21 Taken together, these differences may compromise the ability of the discoid meniscus to withstand normal forces placed across the knee and predispose it to tear. This is important because the normal meniscus plays a critical role in facilitating load distribution across the knee joint, in addition to assisting with functions including shock absorption, proprioception, and stabilization of the knee. Torn and/or unstable discoid menisci are unable to perform these functions adequately, which may ultimately result in degenerative joint disease and progress to end-stage osteoarthritis (OA). 

CLASSIFICATION

The traditional Watanabe classification of discoid meniscus consists of 3 variants: type I, a complete discoid shape; type II, an incomplete discoid shape; and type III, the Wrisberg variant.²² The Wrisberg variant is described as a more normal-appearing meniscus but lacks normal peripheral attachments.^{5, 6, 15} This classification system was expanded by Monllau and colleagues, ²³ who described a ring-type meniscus variant with normal posterior tibial attachments. Although the Watanabe classification is commonly used, its utility in assisting with clinical decision-making may be limited. 

Continue to: Several other classification schemes...

Several other classification schemes exist. Jordan and colleagues²⁴ described a classification scheme defining a meniscal type as complete or incomplete, also noting the presence of symptoms, tearing, and peripheral rim instability. They grouped stable types together, regardless of morphology, and then further classified them based on the presence of symptoms and tears. Similarly, the unstable types were grouped together and then subclassified in the same manner.^17,24 Klingele and colleagues²⁵ also described a contemporary classification scheme of discoid meniscus evaluating peripheral stability patterns that may be more clinically and surgically relevant. This classification is based on the type of discoid morphology (complete vs incomplete), the presence or absence of peripheral rim stability (stable vs unstable), and the presence or absence of a meniscal tear (torn vs untorn).^5,25 
    

EVALUATION

A stable discoid meniscus is often an incidental finding, seen either on advanced diagnostic imaging performed for another reason or at the time of arthroscopy to address another problem. Younger children with discoid meniscus tend to present with symptoms such as popping and snapping related to instability and the abnormal morphology of the discoid meniscus. Older patients tend to present with symptoms related to acute tears through the abnormal meniscal tissue. Although discoid menisci can become acutely symptomatic in the presence of a tear, the onset of symptoms may occur in the absence of a discrete traumatic event.¹ Alternatively, some patients will report a clear history of injury, often a noncontact, rotational injury mechanism related to an athletic activity. Patients with torn discoid menisci may report pain, catching, locking, and/or giving way of the knee, and on examination may have limited extension, snapping, effusion, quadriceps atrophy, and joint line tenderness. Eponymous meniscal compression tests including the McMurray, Apley, and Thessaly tests, may also be performed when meniscal tear is suspected, although this may be tricky for younger children.¹ 

Considering the high association of meniscal tears with ligamentous injuries, examination of knee stability is important. Plain radiographs of the knee should be taken, although the results will often be negative for osseous injury in the case of an isolated meniscal tear. Radiographs of a discoid knee may show subtle differences compared with radiographs of a non-discoid knee. A recent comparison of children with symptomatic lateral discoid menisci with age-matched controls found statistically significant increased lateral joint space, elevated fibular head, increased height of the lateral tibial spine, and increased obliquity of the tibial plateau.²⁶ They did not find statistically significant increased squaring of the lateral femoral condyle or cupping of the lateral tibial plateau. Radiographic signs can be subtle and may not all be present in a patient with a discoid meniscus. 

Magnetic resonance imaging (MRI) is the assessment technique of choice for the diagnosis of discoid meniscus, although MRI may not reliably identify a Wrisberg variant or incomplete discoid menisci (Figure 1).

Gans and colleagues²⁷ examined preoperative MRI and clinical examination compared with pathology found during arthroscopy. Although they found that MRI and clinical examination had excellent diagnostic accuracy of 92.7% and 95.3%, respectively, the most common missed pathology on MRI later found on diagnostic arthroscopy was the presence of a lateral discoid meniscus, which occurred in 26.7% of missed diagnoses. Adult diagnostic criteria of discoid meniscus include ≥3 contiguous 5-mm sagittal cuts showing continuity between the anterior and posterior horns of the meniscus. Other criteria include a minimal meniscal width >15 mm on the coronal view or a minimum meniscal width that is >20% of the width of the maximal tibial width.²⁸ These criteria are often applied to children as well. Additionally, if >50% of the lateral joint space is covered by meniscal tissue, a diagnosis of discoid meniscus should be considered.⁶

Continue to: TREATMENT

Management of symptomatic discoid meniscus is directed toward resolving symptoms while preserving meniscal tissue and preventing the development of OA. Incidentally found discoid menisci in asymptomatic patients should not be treated surgically and can have periodic follow-ups for detection of any functional deterioration or symptom development. Surgical treatment may be beneficial for patients with symptoms related to their discoid menisci such as pain, recurrent effusion, limited knee motion, mechanical symptoms (e.g., locking and catching), and activity restrictions.

Traditionally, surgical treatment of a symptomatic discoid meniscus consisted of subtotal (meaning nearly complete, or <3mm of peripheral rim remaining) or complete meniscectomy, often performed in an open fashion. Surgical techniques have evolved; current surgical approaches typically include diagnostic arthroscopy followed by arthroscopic saucerization (also called partial meniscectomy) of the central portion of the “disc,” leaving a peripheral rim of 6 mm to 8 mm to approximate that of the normal meniscus (Figure 2).^29,30 Saucerization removes the redundant central meniscal tissue in an attempt to create a more “normal” C-shaped morphology, although it does not address the increased thickness characteristic of many discoid menisci. It may be particularly difficult to “debulk” an abnormally thick discoid meniscus in the coronal plane, and there is little in the outcomes literature to support this approach. Following partial meniscectomy, the remaining meniscal tissue should be inspected thoroughly both for the presence of instability and for residual tears. Meniscal tears should be repaired in standard fashion; commonly, this may be a combination of all-inside sutures placed into the posterior horn, inside-out sutures placed into the midbody, and outside-in sutures placed into the anterior horn. Peripheral rim instability—identified, for example, by the ability to translate the posterior horn of the meniscus fully onto the anterior tibial plateau—should be addressed by suturing the meniscus to the adjacent capsule (Figure 2).^{25, 31} Menisci that have residual complex tears that are not amenable to repair may be treated by subtotal meniscectomy. These patients may be candidates for subsequent meniscal allograft transplantation.^32,33 

TREATMENT OUTCOMES

Performing a partial meniscectomy has consistently been shown in the laboratory to increase contact stresses proportionally to the percentage of tissue removed.³⁴ It follows logically that performing a subtotal or complete meniscectomy in a young patient would yield increased, abnormal contact stresses throughout the knee with resultant degenerative changes and progression to OA over time. While long-term outcome studies of subtotal or complete meniscectomy have shown somewhat variable results, the majority report the development of pain, instability, poor function, osteoarthritic changes and even the development of osteochondritis desiccans.^5,35 

In an early investigation of long-term outcomes associated with surgical resection of a discoid lateral meniscus, Räber and colleagues³⁶ retrospectively examined 17 knees that had undergone total meniscectomy for the lateral discoid meniscus. At a mean follow-up of 19.8 years, these authors reported that patients accounting for 10 of 17 operative knees had developed symptoms of osteoarthrosis such as pain. In addition, two-thirds of the knees that had follow-up radiographs performed (10 of 15 knees) had visible osteoarthritic changes present. 

 In 2011, Stilli and colleagues³⁷ conducted a mid-term follow-up study examining 104 knees over an average follow-up of 8.5 years, with an average age of 8 years at the time of surgery. Younger patients, 2 to 7 years, underwent subtotal meniscectomy whereas patients, 8 to 14 years, underwent arthroscopic partial meniscectomy. Patients with a Wrisberg variant underwent removal of the posterior horn. The authors of this study reported that younger patients who had undergone subtotal meniscectomy had the best outcomes (defined by self-reported questionnaire responses and clinical evaluation). However, these results should be interpreted with caution: at the time of follow-up, patients in this study would still have been in adolescence and may not yet have developed the symptomatic degenerative changes in the knee joint that are strongly associated with meniscectomy. 

Continue to: There are a few long-term...

There are few long-term outcome studies for arthroscopic saucerization. In 2014, Ahn and colleagues³⁸ examined patient-reported outcomes and radiographic changes for 48 knees in pediatric patients treated arthroscopically for a symptomatic discoid meniscus. Patients were treated with partial meniscectomy (22 knees), partial meniscectomy with meniscal repair (18 knees), or subtotal meniscectomy (8 knees). Out of 48 knees evaluated, 45 knees (94%) were rated as “excellent” or “good” at an average 10-year follow-up. However, a significant percentage of patients had evidence of degenerative changes on follow-up radiographs, specifically: 88% of the subtotal meniscectomy group, 39% of the partial meniscectomy with repair group, and 23% in the partial meniscectomy-alone group. This finding suggests that the early appearance of radiographic changes suggestive of OA does not necessarily correlate with the development of knee symptoms in this cohort, although longer-term follow-up of these patients into adulthood and middle age is clearly needed.

Recently, short-term outcomes have been reported for contemporary arthroscopic saucerization of discoid menisci with peripheral rim stabilization performed as deemed necessary at the time of surgery. In 2012, Carter and colleagues³⁹ examined 57 knees that underwent saucerization alone or saucerization with peripheral rim stabilization. At an average follow-up of 15 months, both patient populations had equivalent self-reported outcomes and clinical examination findings. The authors concluded that peripheral stabilization does not negatively affect short-term outcomes if instability is recognized and treated.

Yoo and colleagues⁴⁰ found equivalent results between patients undergoing saucerization, saucerization with rim stabilization, and subtotal meniscectomy for 100 pediatric knees with an average follow-up of 4.7 years. Subtotal meniscectomy was defined as <3 mm of peripheral rim remaining and was performed when there was severe degeneration or complex tearing of the remnant rim following arthroscopic saucerization. Taken together, these data seem to suggest that short- and mid-term outcomes for pediatric patients treated surgically are generally good in terms of reported clinical function and development of OA, although long-term follow-up studies will be essential for understanding the true impact of surgical interventions.

Shieh and colleagues^41,42 investigated risk factors for failed meniscal surgery in 324 menisci from 2008 to 2012, including in 46 discoid saucerization procedures with or without stabilization. At a mean of 40 months, 15% of the discoid saucerization cohort required a revision procedure, with increased odds of revision surgeries in patients who had undergone meniscal tear repair. The most frequent indication of revision surgery was sustaining a meniscal tear during intense physical activity in the first year after the index procedure, and patients underwent either debridement or repair for their revision procedure.

SUMMARY

Discoid meniscus is a rare anatomical meniscal variant characterized by an abnormal “O-like” shape, increased meniscal thickness, disorganization of collagen fibers, and variable absence of peripheral attachments. These morphological changes predispose patients with discoid menisci to increased rates of symptomatic meniscal instability and tearing. An MRI remains the most sensitive imaging modality for the diagnosis of a discoid meniscus, with ≥3 contiguous 5-mm sagittal cuts showing continuity between the anterior and posterior horns indicative of a discoid variant. Surgical treatment for symptomatic discoid menisci has evolved from subtotal meniscectomy to contemporary arthroscopic saucerization techniques with repair of meniscal tears and peripheral stabilization performed as needed. Long-term outcome studies for patients who undergo subtotal or complete meniscectomy reveal an association with osteoarthritic changes of the knee. Short- and mid-term outcome studies for patients who undergo arthroscopic saucerization with or without repair and/or peripheral stabilization are generally good, although reoperation rates have been estimated at 15% in the first 3 to 4 years. Longer-term follow-up, with the inclusion of validated functional outcomes measures, will be essential for understanding the true impact of various surgical interventions over time. 

ABSTRACT

Discoid meniscus is a rare anatomical variant with altered morphology and structure that can sometimes present symptomatically, typically in the pediatric population. The discoid meniscus is usually in the lateral compartment of the knee and is characterized by a partial or complete filling-in of central meniscal tissue, increased meniscal thickness, disorganization of longitudinal collagen fibers, and sometimes lack of peripheral attachments. These changes to both the macro- and micro-structure of the meniscus predispose affected patients to increased rates of both meniscal tears and mechanical symptoms. Surgical management of symptomatic discoid meniscus is directed toward symptom resolution while preserving sufficient functional meniscal tissue to delay or prevent the development of osteoarthritis. Modern surgical techniques consist of arthroscopic saucerization of the discoid meniscus with repair of associated meniscal tears and stabilization of peripheral attachments. Although long-term outcome data are lacking, short- and mid-term outcomes for patients treated with arthroscopic partial meniscectomy and meniscal repair and/or stabilization as needed are generally good. 

Continue to: The discoid meniscus...

The discoid meniscus is an uncommon anatomical meniscal variant that may present with pain, snapping, motion loss, swelling, and locking of the affected knee, typically during childhood or adolescence.¹ Although the etiology of discoid meniscus is not completely understood, it is considered a congenital anomaly with a possible genetic component.^{2, 3} Incidence is estimated at 0.4% to 5.2% in the Western European population but is reportedly much higher (roughly 17%) in Asian populations.^4-6, Discoid menisci, when present, are almost always in the lateral compartment, although cases of medial discoid meniscus have also been reported. The overall incidence of medial discoid meniscus has been estimated to be between 0.06% and 0.3% while that of lateral discoid meniscus, as detailed above, is significantly higher.^7-11 

ANATOMY AND MORPHOLOGY

The menisci differentiate from mesenchymal tissue early during fetal development with a clear definition by 8 weeks and a mature anatomical shape by 14 weeks in utero.¹² Interestingly, menisci never possess a discoid shape during the normal course of development.^13,14 The meniscus is fully vascularized at birth, with the central one-third becoming avascular by 9 months as the vascular supply regresses.¹⁴ By 10 years, only the peripheral one-third maintains its vascular supply, and the menisci have adult-like characteristics with tissue composed mainly of circumferential collagen fibers.^4,14-16

A normal meniscus is wedge-shaped in the coronal plane and crescent-shaped in the axial plane. The medial meniscus is shaped like the letter “C,” is connected firmly to the joint capsule, and covers approximately 50% of the medial tibial plateau. The normal lateral meniscus covers 70% of the lateral tibial plateau and has firm anterior and posterior attachments while the lateral portion is less securely tethered.¹⁷ A discoid meniscus is characterized by an atypical shape—the center being partially or completely filled in (or “disc-like”)—often associated with anomalous attachments to the tibia, femur, and surrounding joint capsule. In addition to an atypical morphology, the discoid meniscus may also be much thicker than normal, resulting in a “block-like” appearance. The increased thickness may be responsible for the pathognomonic snapping of the knee as it is brought passively into flexion or extension (hence, the term “snapping knee” was traditionally used to describe a symptomatic discoid lateral meniscus). While the discoid shape is relatively straightforward to address, the increased meniscal thickness may be quite difficult to correct surgically.^4-6,18 

In addition to the macromorphological differences characteristic of discoid menisci, histological differences have also been described, including differences in collagen density and disorganization of the circumferential collagen network.^19-21 Taken together, these differences may compromise the ability of the discoid meniscus to withstand normal forces placed across the knee and predispose it to tear. This is important because the normal meniscus plays a critical role in facilitating load distribution across the knee joint, in addition to assisting with functions including shock absorption, proprioception, and stabilization of the knee. Torn and/or unstable discoid menisci are unable to perform these functions adequately, which may ultimately result in degenerative joint disease and progress to end-stage osteoarthritis (OA). 

CLASSIFICATION

The traditional Watanabe classification of discoid meniscus consists of 3 variants: type I, a complete discoid shape; type II, an incomplete discoid shape; and type III, the Wrisberg variant.²² The Wrisberg variant is described as a more normal-appearing meniscus but lacks normal peripheral attachments.^{5, 6, 15} This classification system was expanded by Monllau and colleagues, ²³ who described a ring-type meniscus variant with normal posterior tibial attachments. Although the Watanabe classification is commonly used, its utility in assisting with clinical decision-making may be limited. 

Continue to: Several other classification schemes...

Several other classification schemes exist. Jordan and colleagues²⁴ described a classification scheme defining a meniscal type as complete or incomplete, also noting the presence of symptoms, tearing, and peripheral rim instability. They grouped stable types together, regardless of morphology, and then further classified them based on the presence of symptoms and tears. Similarly, the unstable types were grouped together and then subclassified in the same manner.^17,24 Klingele and colleagues²⁵ also described a contemporary classification scheme of discoid meniscus evaluating peripheral stability patterns that may be more clinically and surgically relevant. This classification is based on the type of discoid morphology (complete vs incomplete), the presence or absence of peripheral rim stability (stable vs unstable), and the presence or absence of a meniscal tear (torn vs untorn).^5,25 
    

EVALUATION

A stable discoid meniscus is often an incidental finding, seen either on advanced diagnostic imaging performed for another reason or at the time of arthroscopy to address another problem. Younger children with discoid meniscus tend to present with symptoms such as popping and snapping related to instability and the abnormal morphology of the discoid meniscus. Older patients tend to present with symptoms related to acute tears through the abnormal meniscal tissue. Although discoid menisci can become acutely symptomatic in the presence of a tear, the onset of symptoms may occur in the absence of a discrete traumatic event.¹ Alternatively, some patients will report a clear history of injury, often a noncontact, rotational injury mechanism related to an athletic activity. Patients with torn discoid menisci may report pain, catching, locking, and/or giving way of the knee, and on examination may have limited extension, snapping, effusion, quadriceps atrophy, and joint line tenderness. Eponymous meniscal compression tests including the McMurray, Apley, and Thessaly tests, may also be performed when meniscal tear is suspected, although this may be tricky for younger children.¹ 

Considering the high association of meniscal tears with ligamentous injuries, examination of knee stability is important. Plain radiographs of the knee should be taken, although the results will often be negative for osseous injury in the case of an isolated meniscal tear. Radiographs of a discoid knee may show subtle differences compared with radiographs of a non-discoid knee. A recent comparison of children with symptomatic lateral discoid menisci with age-matched controls found statistically significant increased lateral joint space, elevated fibular head, increased height of the lateral tibial spine, and increased obliquity of the tibial plateau.²⁶ They did not find statistically significant increased squaring of the lateral femoral condyle or cupping of the lateral tibial plateau. Radiographic signs can be subtle and may not all be present in a patient with a discoid meniscus. 

Magnetic resonance imaging (MRI) is the assessment technique of choice for the diagnosis of discoid meniscus, although MRI may not reliably identify a Wrisberg variant or incomplete discoid menisci (Figure 1).

Gans and colleagues²⁷ examined preoperative MRI and clinical examination compared with pathology found during arthroscopy. Although they found that MRI and clinical examination had excellent diagnostic accuracy of 92.7% and 95.3%, respectively, the most common missed pathology on MRI later found on diagnostic arthroscopy was the presence of a lateral discoid meniscus, which occurred in 26.7% of missed diagnoses. Adult diagnostic criteria of discoid meniscus include ≥3 contiguous 5-mm sagittal cuts showing continuity between the anterior and posterior horns of the meniscus. Other criteria include a minimal meniscal width >15 mm on the coronal view or a minimum meniscal width that is >20% of the width of the maximal tibial width.²⁸ These criteria are often applied to children as well. Additionally, if >50% of the lateral joint space is covered by meniscal tissue, a diagnosis of discoid meniscus should be considered.⁶

Continue to: TREATMENT

Management of symptomatic discoid meniscus is directed toward resolving symptoms while preserving meniscal tissue and preventing the development of OA. Incidentally found discoid menisci in asymptomatic patients should not be treated surgically and can have periodic follow-ups for detection of any functional deterioration or symptom development. Surgical treatment may be beneficial for patients with symptoms related to their discoid menisci such as pain, recurrent effusion, limited knee motion, mechanical symptoms (e.g., locking and catching), and activity restrictions.

Traditionally, surgical treatment of a symptomatic discoid meniscus consisted of subtotal (meaning nearly complete, or <3mm of peripheral rim remaining) or complete meniscectomy, often performed in an open fashion. Surgical techniques have evolved; current surgical approaches typically include diagnostic arthroscopy followed by arthroscopic saucerization (also called partial meniscectomy) of the central portion of the “disc,” leaving a peripheral rim of 6 mm to 8 mm to approximate that of the normal meniscus (Figure 2).^29,30 Saucerization removes the redundant central meniscal tissue in an attempt to create a more “normal” C-shaped morphology, although it does not address the increased thickness characteristic of many discoid menisci. It may be particularly difficult to “debulk” an abnormally thick discoid meniscus in the coronal plane, and there is little in the outcomes literature to support this approach. Following partial meniscectomy, the remaining meniscal tissue should be inspected thoroughly both for the presence of instability and for residual tears. Meniscal tears should be repaired in standard fashion; commonly, this may be a combination of all-inside sutures placed into the posterior horn, inside-out sutures placed into the midbody, and outside-in sutures placed into the anterior horn. Peripheral rim instability—identified, for example, by the ability to translate the posterior horn of the meniscus fully onto the anterior tibial plateau—should be addressed by suturing the meniscus to the adjacent capsule (Figure 2).^{25, 31} Menisci that have residual complex tears that are not amenable to repair may be treated by subtotal meniscectomy. These patients may be candidates for subsequent meniscal allograft transplantation.^32,33 

TREATMENT OUTCOMES

Performing a partial meniscectomy has consistently been shown in the laboratory to increase contact stresses proportionally to the percentage of tissue removed.³⁴ It follows logically that performing a subtotal or complete meniscectomy in a young patient would yield increased, abnormal contact stresses throughout the knee with resultant degenerative changes and progression to OA over time. While long-term outcome studies of subtotal or complete meniscectomy have shown somewhat variable results, the majority report the development of pain, instability, poor function, osteoarthritic changes and even the development of osteochondritis desiccans.^5,35 

In an early investigation of long-term outcomes associated with surgical resection of a discoid lateral meniscus, Räber and colleagues³⁶ retrospectively examined 17 knees that had undergone total meniscectomy for the lateral discoid meniscus. At a mean follow-up of 19.8 years, these authors reported that patients accounting for 10 of 17 operative knees had developed symptoms of osteoarthrosis such as pain. In addition, two-thirds of the knees that had follow-up radiographs performed (10 of 15 knees) had visible osteoarthritic changes present. 

 In 2011, Stilli and colleagues³⁷ conducted a mid-term follow-up study examining 104 knees over an average follow-up of 8.5 years, with an average age of 8 years at the time of surgery. Younger patients, 2 to 7 years, underwent subtotal meniscectomy whereas patients, 8 to 14 years, underwent arthroscopic partial meniscectomy. Patients with a Wrisberg variant underwent removal of the posterior horn. The authors of this study reported that younger patients who had undergone subtotal meniscectomy had the best outcomes (defined by self-reported questionnaire responses and clinical evaluation). However, these results should be interpreted with caution: at the time of follow-up, patients in this study would still have been in adolescence and may not yet have developed the symptomatic degenerative changes in the knee joint that are strongly associated with meniscectomy. 

Continue to: There are a few long-term...

There are few long-term outcome studies for arthroscopic saucerization. In 2014, Ahn and colleagues³⁸ examined patient-reported outcomes and radiographic changes for 48 knees in pediatric patients treated arthroscopically for a symptomatic discoid meniscus. Patients were treated with partial meniscectomy (22 knees), partial meniscectomy with meniscal repair (18 knees), or subtotal meniscectomy (8 knees). Out of 48 knees evaluated, 45 knees (94%) were rated as “excellent” or “good” at an average 10-year follow-up. However, a significant percentage of patients had evidence of degenerative changes on follow-up radiographs, specifically: 88% of the subtotal meniscectomy group, 39% of the partial meniscectomy with repair group, and 23% in the partial meniscectomy-alone group. This finding suggests that the early appearance of radiographic changes suggestive of OA does not necessarily correlate with the development of knee symptoms in this cohort, although longer-term follow-up of these patients into adulthood and middle age is clearly needed.

Recently, short-term outcomes have been reported for contemporary arthroscopic saucerization of discoid menisci with peripheral rim stabilization performed as deemed necessary at the time of surgery. In 2012, Carter and colleagues³⁹ examined 57 knees that underwent saucerization alone or saucerization with peripheral rim stabilization. At an average follow-up of 15 months, both patient populations had equivalent self-reported outcomes and clinical examination findings. The authors concluded that peripheral stabilization does not negatively affect short-term outcomes if instability is recognized and treated.

Yoo and colleagues⁴⁰ found equivalent results between patients undergoing saucerization, saucerization with rim stabilization, and subtotal meniscectomy for 100 pediatric knees with an average follow-up of 4.7 years. Subtotal meniscectomy was defined as <3 mm of peripheral rim remaining and was performed when there was severe degeneration or complex tearing of the remnant rim following arthroscopic saucerization. Taken together, these data seem to suggest that short- and mid-term outcomes for pediatric patients treated surgically are generally good in terms of reported clinical function and development of OA, although long-term follow-up studies will be essential for understanding the true impact of surgical interventions.

Shieh and colleagues^41,42 investigated risk factors for failed meniscal surgery in 324 menisci from 2008 to 2012, including in 46 discoid saucerization procedures with or without stabilization. At a mean of 40 months, 15% of the discoid saucerization cohort required a revision procedure, with increased odds of revision surgeries in patients who had undergone meniscal tear repair. The most frequent indication of revision surgery was sustaining a meniscal tear during intense physical activity in the first year after the index procedure, and patients underwent either debridement or repair for their revision procedure.

SUMMARY

Discoid meniscus is a rare anatomical meniscal variant characterized by an abnormal “O-like” shape, increased meniscal thickness, disorganization of collagen fibers, and variable absence of peripheral attachments. These morphological changes predispose patients with discoid menisci to increased rates of symptomatic meniscal instability and tearing. An MRI remains the most sensitive imaging modality for the diagnosis of a discoid meniscus, with ≥3 contiguous 5-mm sagittal cuts showing continuity between the anterior and posterior horns indicative of a discoid variant. Surgical treatment for symptomatic discoid menisci has evolved from subtotal meniscectomy to contemporary arthroscopic saucerization techniques with repair of meniscal tears and peripheral stabilization performed as needed. Long-term outcome studies for patients who undergo subtotal or complete meniscectomy reveal an association with osteoarthritic changes of the knee. Short- and mid-term outcome studies for patients who undergo arthroscopic saucerization with or without repair and/or peripheral stabilization are generally good, although reoperation rates have been estimated at 15% in the first 3 to 4 years. Longer-term follow-up, with the inclusion of validated functional outcomes measures, will be essential for understanding the true impact of various surgical interventions over time. 

ABSTRACT

Soccer players recovering from anterior cruciate ligament (ACL) injuries have better options for treatment today than they did 25 years ago. Surgical techniques have improved, and rehabilitation protocols have evolved considerably. Although the rehabilitation community is doing a better job of treating this patient population, the evidence does demonstrate that both re-injury and return- to-play (RTP) rates are still suboptimal. Most protocols focus on normalizing strength and range of motion (ROM) and achieving limb symmetry with soccer-specific movements. While these factors are certainly prerequisites for returning to the field, their inclusion does not provide a complete picture of the athlete’s presentation. An additional factor that should be prioritized with this patient population is the central nervous system (CNS). Advanced imaging has shown that peripheral deafferentation does occur with musculoskeletal injuries; this ultimately results in cortical reorganization, which makes movement planning more difficult for the player, since simpler tasks must now be processed at higher levels in the CNS. The evidence also shows that the CNS demonstrates plasticity in these cases, so that through focused neuromotor rehabilitation techniques, it is possible to bring movement planning back down to a sub-cortical level. Cognitive issues may also be a factor in preventing the player from returning. Fear of re-injury and diminished confidence can influence the way the player moves on the field, and diminish ability to demonstrate protective kinematics with all soccer-specific tasks. We believe that an approach incorporating traditional musculoskeletal rehabilitation, CNS neuro-motor training, and consideration for cognitive factors, may define an improved paradigm for treating the soccer player and assessing readiness for RTP following ACL injury.

Continue to: Although anterior cruciate ligament (ACL)...

Although anterior cruciate ligament (ACL) rehabilitation has evolved considerably over the past 2 decades, the basic paradigm has remained consistent: normalize strength and range of motion, reduce swelling and pain, achieve limb symmetry with functional tasks, and return to sport-specific activities gradually over a 6 to 12-month period. There have been some slight additions to this basic premise, such as evaluating knee and hip mechanics in the frontal plane, but the requirements here are vaguely defined and are typically only evaluated within the context of controlled clinical testing.

It is interesting to note that the typical ACL injury pattern occurs during a normal sport-specific movement, yet most rehabilitation protocols fail to recognize the potential causes of the aberrant movement pattern and how to best modify it so that the risk of repeated stress to the ACL can be minimized. It should be understood that movement occurs through the interaction of 3 discrete factors: the individual, the task being performed, and the environment in which it is performed.¹ All of these factors will play a role in how the final movement pattern is produced. For example, a soccer player (individual) may backpedal and pivot to the left 60° and accelerate to sprint after a player moving towards the touchline (task) while receiving instructions from teammates and monitoring the movements of opposing players (environment). A small variance in any 1 of these factors could significantly impact the movement pattern as the player completes the task.

In most rehabilitation programs, each of these factors may be treated in a singular, non-specific manner, but if these factors are not coordinated effectively throughout the program to produce the desired sport-specific movement, a faulty pattern may persist, leaving the player at risk for injury. Current rehabilitation programs seem to have a strong focus on creating stability, mobility, and strength, but these are trained in silos, with an internal focus of control, which only solves the biomechanical equation. Often, it is difficult for the player to coordinate good biomechanics into an efficient, protective movement pattern that is specific to the tasks performed on the field during the normal course of play. The missing link here is the central nervous system (CNS).

Limitations to the current ACL protocols may be that they rely heavily on musculoskeletal rehabilitation and that they have limited emphasis on neurological rehabilitation. As will be discussed later, the CNS has a large impact on the final movement selected by the player. In fact, cognition, perception, and action are the three factors that comprise the individual’s part of the movement paradigm,¹ yet rarely are these factors addressed in most ACL rehabilitation programs. These elements are a large part of the movement equation, so it is easy to understand how failing to address these features can lead to poor movement quality and subsequent ACL re-injury.

In addition to central neurological factors, cognitive issues may play a role in the player’s ability to return to sport. Determining optimal readiness for return to play is a difficult task for the medical community, with many variables to consider. Previous research studies have assessed the variability in return to play for various sports, including football, rugby, soccer, skiing, running, and tennis, with return-to-play rates ranging from 18% to 100%.^2,3,4-10 The risk of secondary injury may cast doubt and fear on athletes as they contemplate their successful return to play.^8,11 Although robust functional testing has become commonplace for determining athlete readiness after injury,^12-20 the assessment of psychological readiness, persistent fear, and loss of confidence are often neglected and not as commonly integrated into the return-to-play algorithm.^21-24 The purpose of this paper is to assess the various cognitive and central neural factors affecting a soccer player’s ability to recover from an ACL injury and offer suggestions for integrating treatments into the protocols to address these issues.

Continue to: CENTRAL NERVOUS SYSTEM NEUROPLASTICITY... 

 

 

CENTRAL NERVOUS SYSTEM NEUROPLASTICITY

Despite the vast amount of attention and research focused on the ACL, the re-injury rate still remains quite high. It has been reported that rehabilitation programs that employ traditional neuromotor training produce a re-injury rate as high as 30% after the athlete returns to sport.^25-28 The overall rate of sustaining a second ACL injury is 15%11 in all patient populations. For the general population <25 years of age, the re-injury rate is 21%, and for athletes <25 years of age, the re-injury rate rises to 23%.¹¹ With re-injury rates at this level, it is certainly fair to consider and be critical of the current rehabilitation methods being used with this population. One opportunity for improvement lies in the general approach used to rehabilitate ACL-injured patients. Therapy for this injury is protocol-driven, and the fact remains that most protocols prioritize restoration of peripheral systems, with minimal thought given to the cortical control necessary to manage those systems.^29,30 When neural factors are considered, it is usually within the context of increasing strength, balance, power, and biomechanical control,^31-34 which are certainly important but peripheral factors nonetheless. The missing element in many ACL protocols may be how to best manage the central neural components and cognitive factors associated with this injury.

If the CNS were to receive more consideration in ACL protocols, the opportunity for improved outcomes could be substantial because the CNS has been proven to be a very malleable system, as long as it receives the correct input. The CNS demonstrates neuroplasticity,³⁵ which means that it is capable of reorganization, based on the stimuli that it receives, whether internal or external.³⁶

This is an important consideration in ACL rehabilitation because the ACL graft, while restoring the biomechanical properties to the knee, is not fully capable of producing the same neurosensory properties of the original ACL.^37-42This is an important concept to understand because an ACL tear does indeed cause deafferentation in the ascending pathways to the brain.^37-40,42-46 This can lead to CNS reorganization and subsequent alterations in efferent output to the periphery.^37-40,42-46 Therefore, if a protocol with traditional musculoskeletal principles was used, then the mechanical function of the knee may certainly be remediated, but the neurosensory function will remain in a maladaptive state,^47-50 potentially leading to aberrant, non-protective movement strategies and a higher risk of re-injury.

The process of CNS reorganization may begin with the initial ACL injury. A peripheral musculoskeletal injury creates an inflammatory response that results in the arrival of chemical mediators such as histamine, substance P, calcitonin, and calcitonin gene-related peptide at the site of injury.⁵¹ As edema accumulates in the joint, tension is applied to the capsule, which may adversely affect proprioception from the receptors located within.⁴⁵ The interruption of consistent input from the peripheral mechanoreceptors may lead to long-term differentiation of the ascending pathways.⁵² This information is synthesized at 3 different levels of the CNS (spinal cord, brain stem, and motor cortex) to produce motor output.^53-56 Differentiation in the ascending circuitry can cause inhibition of motor neurons at the spinal cord.⁴⁵Animal research has shown that this differentiation can cause a breakdown in the cuneate nucleus of the brainstem,⁵⁷which provides sensory information from the upper body, while the gracile nucleus does the same for the lower body. These structures transfer proprioceptive input to the ventral posterior lateral nucleus in the thalamus, where it is then sent to the primary somatosensory cortex.⁵⁷ In general, the somatosensory, visual, and vestibular systems interpret afferent inputs to control movement, balance, and stability.^58,59 In a sport like soccer, where the movement tasks are dynamic and unpredictable, it is easy to see why even a slight deficit in somatosensory processing could disrupt a movement. Valeriani and colleagues^42,46 showed that somatosensory-evoked potentials were indeed altered in a cohort of ACL reconstruction (ACLR) subjects, indicating reorganization within the CNS.  Additionally, the deafferentation could not be changed by other afferent input coming from the knee or by the new ACL graft placed in the knee.^42,46The primary motor cortex has been found to have a substantial network of connectivity with the primary somatosensory cortex, which supports the theory that the motor cortex has a very strong linkage with the peripheral receptors in the joint.⁶⁰  The ligaments in the joint contain Ruffini, Pacinian, and Golgi receptors, all of which react to changes in the collagen fibers and send information regarding tension, length, speed, acceleration, position, and movement back to the CNS.^61-64 Unfortunately, the ascending pathway deafferentation can cause reorganization within the CNS, which makes the feedback provided from the periphery less effective in motor planning.

Ward and colleagues⁶⁵ have reported that reorganization within the motor cortex is the primary cause of chronic neuromuscular movement deficits in peripheral joint injuries. Researchers have used functional magnetic resonance imaging, transcranial magnetic stimulation, and electroencephalography in ACL patients to demonstrate changes in cortical activity and subsequent CNS reorganization.⁶⁵ Kapreli and colleagues⁴¹ reported that subjects with an ACL injury demonstrated higher cortical activation in the pre-supplementary motor area (pre-SMA). This is a region that is responsible for more complex motor planning.^66,67 This area becomes active before the primary motor cortex and is responsible for preparing the final movement pattern that the motor cortex executes.⁴¹ As the task becomes more complex, activity in the pre-SMA will increase.⁴¹ Additionally, they found that the posterior secondary somatosensory area and posterior inferior temporal gyrus showed increased cortical activity compared with controls.⁴¹ Visual planning is processed in the posterior inferior temporal gyrus, and so, it appears that the difficulty in processing somatosensory information due to ascending pathway deafferentation places an increased reliance on the visual system for movement planning.^68-70 This was observed while ACL-injured subjects performed a simple knee flexion-extension movement encompassing 40°, indicating the need to incorporate higher central levels of planning for a very simple movement pattern.⁴¹ Baumeister and colleagues^37,38 also showed that subjects with ACLR had higher levels of cortical activation in the areas of the brain that require attention and that process sensory input. They theorized that this occurred because of reduced efficiency of neural processing at lower levels in the CNS. Despite the higher levels of cortical activity observed, they found that subjects with an ACLR demonstrated proprioceptive testing that was deficient compared with that of controls. Heroux and Tremblay⁷¹ also demonstrated that subjects with an ACLR had increased resting motor cortex activity. They believed that this occurred as the motor cortex attempted to maintain neuromotor output to the periphery in the face of diminished afferent input.

Continue to: The reorganization that results in movement planning...

 

 

The reorganization that results in movement planning, transitioning from subcortical levels to cortical levels, is a phenomenon that researchers believe can lead to deficiencies even as the athlete has returned to sport. Grooms et al⁷²revealed in a case report that a subject with an ACLR showed higher levels of activity in the crus region of the cerebellum. This area contains corticobulbar and corticospinal tracts that transmit neural input to maintain balance and coordination.⁷³ These changes in the cerebellum, combined with increased motor cortex activity, are thought to be indicative of a global neural strategy that uses higher levels of the CNS, as opposed to subcortical processing.⁷²

The current research makes a clear and compelling argument for the importance of CNS reorganization after an ACL injury, placing increased reliance on higher cortical levels of control, as well as the visual system to coordinate balance and movement. It is thought that this reorganized method of neural transmission can then become imprinted within the CNS, if not corrected.^35,74 If this is the case, then traditional strength programs may not be sufficient to restore these connections to their pre-injury level. If the CNS has the ability to reorganize based on the aberrant input that it receives from the periphery, then it also certainly has the potential to adapt to more specific structured input via the ascending afferent pathways.^41,45 The rehabilitation program, however, needs to be structured specifically to target the reorganized regions of the brain. There needs to be an emphasis on rehabilitating not only the peripheral neuromotor structures but also the CNS.⁷⁵

CENTRAL NERVOUS SYSTEM REHABILITATION PRINCIPLES

For a neurological rehabilitation to be successful, the interventions need to be repetitive and task-specific, involve learning, employ whole and part practice, and transition from using an internal to an external focus of control.⁷⁶Movements that are repetitive, but which lack structured learning and skill, have been shown to have no effect on inducing neuroplastic changes in the primary motor cortex.^77,78 However, using neurological rehabilitation techniques that facilitate the acquisition of new motor skills by the CNS have been shown to cause neuroplastic adaptation in the motor cortex.^79-85 This occurs because neuroplasticity is determined by experience and practice.⁷⁸ The CNS operates on cues received in the ascending tracts by mechanoreceptors in the joint. If a new movement pattern is being learned by the athlete, then this new afferent input received from the periphery will start to initiate reorganization in the higher learning centers. If this occurs with optimal repetition and precision, then a positive reorganization can take place within the CNS that results in a higher percentage of motor planning and control being filtered down to a subcortical level. Essentially, the movements become instinctive, which is crucial in athletics, where attention in higher cortical areas is frequently diverted to external aspects of the competition and not solely used to focus on movement.

This is why shifting neurological rehabilitation from an internal focus of control to an external focus of control is paramount. While using an internal focus of control is required early in rehabilitation to enable the athlete to understand the specific tasks required in a composite movement, a gradual transition to an external focus of control is necessary as the athlete begins to perform tasks that are more soccer-specific. This autonomous stage of motor learning is crucial because it transfers the burden of motor planning from higher to lower levels of the CNS and frees up the pre-SMA and primary motor cortex to handle more complex patterns.^58,86-88

Continue to: ANTERIOR CRUCIATE LIGAMENT RISK POTENTIAL IN SOCCER PLAYERS...

 

 

ANTERIOR CRUCIATE LIGAMENT RISK POTENTIAL IN SOCCER PLAYERS

If a comprehensive neuromotor rehabilitation program is to be used effectively with soccer athletes, then the first priority is to define how the players should move, so that they can demonstrate protective kinematics with all soccer-specific tasks and minimize stress to the ACL. As the ideal movement pattern becomes autonomous, then it should be trained within the context of a dynamic environment; remembering that environmental changes have a large impact on the final movement pattern selected by the individual. Brophy et al⁸⁹ evaluated videos of non-contact ACL injuries in male and female soccer players and determined that 45% occurred while cutting, 25% while landing, and 16% during deceleration. These 3 patterns represent 86% of the ACL injuries observed and offer an opportunity for evaluation and treatment with specific central neuromotor rehabilitation techniques.

The foundational movement patterns for the soccer player should focus on producing leverage that minimizes stress to the ACL during the 3 primary tasks outlined above. To achieve this, it is necessary to reduce posterior ground reaction forces at the hip and knee joint during these movements. There is a high correlation between the magnitude of the posterior ground reaction force, and anterior tibial shear, and subsequent displacement.^90,91 This stress can be reduced by increasing the hip and knee flexion angles during soccer-specific movements that involve pivoting, decelerating, and landing from a jump in a unipedal stance.⁹²

This phenomenon can be explained by observing changes in the ACL elevation angle, hamstring insertion angle, and patella tendon-tibial tuberosity insertion angle. As the knee moves into flexion, the ACL takes on a more parallel orientation to the tibia, and its fibers are better able to resist elastic deformation accompanied by a posterior ground reaction force.^93,94 The quadriceps will produce less anterior translation on the tibia because the patella tendon insertion angle is reduced relative to the longitudinal axis of the tibia, and the mechanical advantage of the quadriceps is decreased.⁹⁵ Lastly, the hamstrings will be able to provide better leverage posteriorly because the resultant force trends toward a more parallel orientation to the tibial plateau, which enables the player to counter, more effectively, the posterior ground reaction force and the anterior pull directed by the quadriceps.⁹⁵

This theory is supported by the work of Li and colleagues,⁹⁶ who showed that there is an inverse relationship between knee flexion angle and ACL loading. In their study, they applied a constant quadriceps force of 200 N at 15°, 30°, and 60° angles. The anterior shear force was obviously the highest at 15° and reduced by 20% at 30° and 60% at 60°. When hamstrings co-contraction was added, there was an additional 30% reduction in anterior shear at 15° and 50% at 30° and 60°. From a more flexed position, the hamstrings can increase joint compression and reduce the anterior translation by allowing the concave medial tibial plateau to limit the anterior drawer effect and absorb the forces that occur with excessive anterior shear, internal rotation, and valgus loads.⁹⁷ As the knee flexion angle approximates 60°, the hamstring leverage is increased, and the quadriceps leverage is diminished to the point where its ability to produce anterior tibial translation is neutralized.⁹⁸ Daniel and colleagues98 referred to this as the quadriceps neutral angle.

For soccer-specific movements that are potentially injurious to the ACL, it may then be beneficial to create a default movement pattern at the knee that approximates this value. In keeping with the information presented in this paper, it will be important to have the player reproduce this angle consistently during activities that involve pivoting, decelerating, and landing from a jump within the context of match play. This will certainly require that segments located both proximal and distal to the knee are able to function within specific parameters so that a cohesive protective synergy is produced throughout the lower quarter which minimizes posterior ground reaction forces and is protective of the ACL. This is where structured neuromotor training that is able to modulate networks within the CNS may be beneficial.

Continue to: CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER...

 

 

CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER

The ultimate goal is to create a foundational movement pattern that optimizes leverage and is protective of the ACL during decelerating, pivoting, and landing in a unipedal stance from a jump. The composite segments that are necessary to achieve this include local core stability to create lumbopelvic stiffness, and global core activation to enhance posterior chain stability. This should enable the player to feel more balanced when placing the pelvis in a more posterior and inferior position while still maintaining the trunk in a position that is parallel with the tibia, as the knee is flexed to an approximate 60° angle (Figure 1). From a frontal plane perspective, the acetabulum should bisect the malleoli of the stance leg, with a neutral tibiofemoral joint alignment (Figure 1).

The neuromotor training for the composite segments of this movement can begin in the “acute postoperative phase” (Table 1).   Because the surgical repair will limit the player’s capabilities in this stage, this is a good time to break down the foundational movement pattern into its component parts and ensure that the CNS receives a high number of quality repetitions of parts. In this phase, the player may begin an isolated training for the transversus abdominis, multifidus, and pubococcygeus. This can start in a supine position using biofeedback with an isometric contraction, progress to a standing position, and incorporate deep core activation with stance-phase gait training, mini squats, and lunge variations. This phase will require an abundance of visual and verbal feedback with an internal focus of control as the player gets used to activating the deep core and quad/hip synergy during functional lower extremity movements. Even in this early phase, the player should look to minimize anterior and/or posterior pelvic tilting and maintain a stiff thoracolumbar segment that remains parallel with the tibia during all functional movements.

Table 1. Adjunct CNS Treatment Principles for ACL Reconstruction in Soccer Athletes

Phase	Goal	CNS Rehabilitation Techniques
Acute postoperative	Local core activation with weightbearing exercise. Produce trunk stiffness with lower extremity movements.	High repetitions. Verbal or tactile cues. Internal focus of control. Partial practice.
Subacute postoperative	Lumbopelvic, foot or ankle, and posterior chain segments learn to participate in movement effectively.	Requires higher levels of cortical planning. Internal focus of control. CIMT.
Static stability	Able to adopt foundational movement pattern consistently with vision eliminated.	Somatosensory vs visual processing. Partial-to-whole practice. Use internal and/or external focus of control.
Dynamic stability	Able to perform plyometrics in a single-leg position using foundational movement pattern with subcortical processing.	Increase velocity with movement challenges. Occlude or eliminate vision. Heavy reliance on an external focus of control. Prioritize movement quality.
Dynamic agility	Pivoting, decelerating, and landing are performed with hip flexion/knee flexion synergy, trunk stiffness, and posterior chain activation.	Unanticipated movement challenges. Whole practice. Ball reaction drills with vision obstructed or occluded. Contact drills with vision obstructed or occluded. Use external focus of control to include soccer-specific tasks.

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

As the player moves into the “subacute postoperative phase” (Table 1).   He or she will continue to use an internal focus of control to activate the local/global core synergy with functional movements progressing from double-leg, to single-leg positions. Partial practice, instead of whole practice, is still the predominant theme of the neural training process. In this phase, the knee and hip flexion angles can increase, and the player’s trunk and pelvic position should be critiqued in a single-leg position so that the trunk remains parallel with the tibia in the sagittal plane with a slight forward hip hinge. The pelvis should remain level throughout single-leg stance to ensure adequate activation of the lateral hip stabilizers. This is the stage where the player can learn to isolate closed kinetic chain hip rotation for pivoting, and so, single-leg hip internal and external rotation drills are useful, both with and without resistance. Skill acquisition is crucial in this phase because the patterns that the CNS adopts will form the foundation for more dynamic patterns that will occur in the later soccer-specific stages. Higher levels of cortical planning are still needed in this phase. For this reason, it is important that poor quality repetitions are recognized by the player and clinician so that he or she can learn to perform them correctly, albeit still with an internal focus of control. This is also a good time to begin to employ constraint-induced movement therapy as the player is able to replicate the desired pattern with more precision. For example, by eliminating the use of the upper extremities as a source of balance, the CNS is forced to program alternate synergies such as the lumbopelvic, and foot and ankle segments to maintain the desired alignment.

The “lower quarter static stability phase” (Table 1) marks a point where it may be useful to use direct strategies that have the capability to change CNS efferent owutput from a primary reliance on the visual processing areas in the posterior-inferior temporal gyrus back to the somatosensory area. It is critical that the player is able to make this transition in cortical reorganization and control, because ACL-injured subjects have been shown to have balance scores similar to healthy controls when they are able to use their vision, but this is reduced when vision is taken away.^99-105  Their balance will diminish even further if vision is modulated during more complex landing and pivoting maneuvers.^99-105 This may certainly explain why defending is a riskier task for ACL-injured players⁸⁹ as their visual system is focused more on tracking a player than attending to precision with movement planning.

To enhance this cortical reorganization within the context of soccer-specific movements, it is useful to start from a foundational single-leg position, with the knee approximating 60° of flexion and the trunk parallel to the tibia. In the frontal plane, the pelvis should be level, the trunk vertical, and the acetabulum bisecting the malleoli of the stance leg (Figure 1).   The player may initially work on getting into this foundational position with vision either partially obstructed using stroboscopic eyewear or completely obstructed if this equipment is unavailable.^106-108 The pattern can be progressed by constraining the upper extremities to force reliance on the lumbopelvic and foot/ankle strategies for balance. Head and/or trunk turns can be added to simulate the external focus of control that is required with movement in soccer. These should progress from slow to fast and anticipated to unanticipated as the player demonstrates competence in maintaining stability at each segment within the foundational stance position. Once this is in play, a ball should be introduced into the drills. As the player maintains the foundational position with vision diminished and upper extremities constrained, they should attempt to reach for or trap a ball from this position. If vision is completely obstructed, then the player can be instructed to open his/her eyes just as the ball arrives to induce a reactive response. Again, quality repetitions are essential for learning to occur, and subsequent skill acquisition to take place in the CNS; thus, close scrutiny should be paid to the qualitative essence of the movement patterns to ensure pristine biomechanics during this phase.

The “lower quarter dynamic stability phase” (Table 1) should continue with the same neuromotor training principles employed in the previous phase, except that the drills will now involve plyometrics. The player should ultimately progress from double-leg, to single-leg jumps and then linear to diagonal. Vision should still be obstructed and upper extremities constrained to channel the lumbopelvic region for force production and balance. Movement quality in the foundational position remains paramount with these drills to ensure that skill acquisition is occurring and injury risk is being mitigated. An external focus of control can be introduced by applying an unanticipated perturbation during a jump. Additional learning opportunities should include unanticipated head and trunk turns while landing in a unipedal stance from a jump. The task can be made more specific by having the player trap a pass while doing linear or diagonal single-leg hop progressions. In this manner, the player’s CNS can become reorganized to program the requisite synergies to maintain a protective foundational position on the stance leg, as the contralateral limb is required to perform work that is far outside the player’s base of support.

Continue to: The final segment of the CNS neuromotor rehabilitation program...

 

 

The final segment of the CNS neuromotor rehabilitation program is the “lower quarter dynamic agility phase” (Table 1), when the player will learn to perform an unanticipated directional change in a foundational position for the pivot leg. The player can begin this phase by initiating sprint-deceleration-pivot efforts, progressing at 45°, 90°, 120°, and 180° turns. This should be trained in both a forward and backpedal position. Close attention should be paid to the deceleration phase of the sprint-pivot effort, as this will set the player up to demonstrate protective kinematics during the pivot phase of the task. In this phase, the center of mass should become lower and move posteriorly, so that a deeper knee and hip flexion angle, supported by posterior chain synergies, can occur at the pivot point. This is an important skill for the player to acquire, as Cortes and colleagues⁹² have reported that female collegiate soccer players tend to perform a pivoting task with a more erect trunk position. In the same cohort, they also measured the mean knee flexion angle at initial contact during pivoting to be 24°.⁹² Movement patterns that reflect an elevated center of mass, with arms abducted away from the trunk, should be discouraged here. The drills can be progressed to have the player react to a command and perform unanticipated pivots within a 5 × 5-meter box to simulate defending. This should be progressed from eyes open and arms unconstrained, to vision disrupted and arms constrained. From here, an external focus of control can be added by playing a ball to the athlete. Vision should be withheld until the instant that the ball arrives at the player, when he/she is required to play the ball to an unanticipated spot. As is the case in all other phases of the neuromotor training, the quality of movement is the most important parameter to critique with each drill. From a qualitative standpoint, the player should demonstrate stiffness throughout the thoracolumbar region and power and control through the pelvis with each directional change. In addition, he or she should maintain a low and posteriorly oriented center of mass to optimize leverage in the hamstrings/gluteals compared with the quadriceps and reduce posterior ground reaction forces.

PSYCHOLOGICAL READINESS FOR RETURN TO PLAY

After an injury is sustained, an athlete is often subjected to a range of psychological responses in addition to the functional impairment, including stress, hesitancy, alterations in self-esteem, depression, fear of re-injury, and anxiety.^43,109-111 The aforementioned responses are often at their height in the time immediately following an injury and generally subside over time during the rehabilitation process.¹¹⁰ The rates at which athletes experience psychological distress following an injury range between 5% and 19%; the levels are comparable with patients receiving treatment for mental health illness.⁴³ However, these elements may persist, or even increase, in the later stages of the rehabilitation process as the topic of return to play is deliberated.^112,113 If these fears are left unresolved, then a significant delay can be incurred during the rehabilitation process, which might ultimately jeopardize the successful return to play.^114,115

When athletes have been cleared to return to sport, fear tends to be the most common reason for their decision to not return to play.^21,116 The persistence of fear has clinical implications and warrants close monitoring to ensure that the athlete feels adequately supported in the decision to return to sport.^117,118 Building the athlete’s confidence by addressing hesitation, lack of confidence, heightened awareness of risk or re-injury, and safe reintegration into athletic participation are important themes identified to encourage a safe return to play.⁴³ A variety of validated tools  can be integrated into an existing return-to-play decision-making algorithm (Table 2).^118-120 

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

 

Table 2. Self-Report Measurement Tools to Integrate into Return-to-Play Decision-Making Algorithm

Self-report Measurement Tools

13-item Tampa Scale for Kinesiophobia

Anterior Cruciate Ligament Return to Sport after Injury Scale (ACL-RSI)

Global Rating Scale (GRS)

International Knee Documentation Committee (IKDC) Subjective Knee Evaluation Form

Knee Injury and Osteoarthritis Outcome Score (KOOS)

Lysholm Knee Scoring Scale

Short Form-36 Health Survey (SF-36)

Subjective Patient Outcome for Return to Sport (SPORTS)

Patient Health Questionnaire-9

By integrating the necessary screening of patients for kinesiophobia and assessing patient expectations after enduring an ACL injury, clinicians may be able to identify patients who are at risk for poorer functional outcomes. A consideration of psychosocial elements such as activity avoidance, fear of movement and re-injury, loss of confidence and expectations/assumptions during the continuum of the rehabilitation process, and the decision to return to play may favorably impact the individual’s ability to safely return to sport. It is critical to address both the physical and psychosocial factors during the rehabilitation process to more optimally transition individuals back to their prior level of athleticism.

CONCLUSION

Psychosocial factors may play a role in determining a player’s readiness to return to sport, as well as a potential for re-injury. A number of tests are available for use with this patient population to identify mental deficits that may impact player performance upon return. Additionally, the CNS should be considered as a source of impairment in players with ACL injuries. Current protocols may not fully appreciate the CNS’ impact on the player’s functional outcome. Therefore, an approach that includes CNS neuromotor training with traditional musculoskeletal rehabilitation, which also incorporates cognitive and psychosocial factors, may define an improved paradigm for treating soccer athletes following an ACL injury and assessing return-to-play capability.

ABSTRACT

Soccer players recovering from anterior cruciate ligament (ACL) injuries have better options for treatment today than they did 25 years ago. Surgical techniques have improved, and rehabilitation protocols have evolved considerably. Although the rehabilitation community is doing a better job of treating this patient population, the evidence does demonstrate that both re-injury and return- to-play (RTP) rates are still suboptimal. Most protocols focus on normalizing strength and range of motion (ROM) and achieving limb symmetry with soccer-specific movements. While these factors are certainly prerequisites for returning to the field, their inclusion does not provide a complete picture of the athlete’s presentation. An additional factor that should be prioritized with this patient population is the central nervous system (CNS). Advanced imaging has shown that peripheral deafferentation does occur with musculoskeletal injuries; this ultimately results in cortical reorganization, which makes movement planning more difficult for the player, since simpler tasks must now be processed at higher levels in the CNS. The evidence also shows that the CNS demonstrates plasticity in these cases, so that through focused neuromotor rehabilitation techniques, it is possible to bring movement planning back down to a sub-cortical level. Cognitive issues may also be a factor in preventing the player from returning. Fear of re-injury and diminished confidence can influence the way the player moves on the field, and diminish ability to demonstrate protective kinematics with all soccer-specific tasks. We believe that an approach incorporating traditional musculoskeletal rehabilitation, CNS neuro-motor training, and consideration for cognitive factors, may define an improved paradigm for treating the soccer player and assessing readiness for RTP following ACL injury.

Continue to: Although anterior cruciate ligament (ACL)...

Although anterior cruciate ligament (ACL) rehabilitation has evolved considerably over the past 2 decades, the basic paradigm has remained consistent: normalize strength and range of motion, reduce swelling and pain, achieve limb symmetry with functional tasks, and return to sport-specific activities gradually over a 6 to 12-month period. There have been some slight additions to this basic premise, such as evaluating knee and hip mechanics in the frontal plane, but the requirements here are vaguely defined and are typically only evaluated within the context of controlled clinical testing.

It is interesting to note that the typical ACL injury pattern occurs during a normal sport-specific movement, yet most rehabilitation protocols fail to recognize the potential causes of the aberrant movement pattern and how to best modify it so that the risk of repeated stress to the ACL can be minimized. It should be understood that movement occurs through the interaction of 3 discrete factors: the individual, the task being performed, and the environment in which it is performed.¹ All of these factors will play a role in how the final movement pattern is produced. For example, a soccer player (individual) may backpedal and pivot to the left 60° and accelerate to sprint after a player moving towards the touchline (task) while receiving instructions from teammates and monitoring the movements of opposing players (environment). A small variance in any 1 of these factors could significantly impact the movement pattern as the player completes the task.

In most rehabilitation programs, each of these factors may be treated in a singular, non-specific manner, but if these factors are not coordinated effectively throughout the program to produce the desired sport-specific movement, a faulty pattern may persist, leaving the player at risk for injury. Current rehabilitation programs seem to have a strong focus on creating stability, mobility, and strength, but these are trained in silos, with an internal focus of control, which only solves the biomechanical equation. Often, it is difficult for the player to coordinate good biomechanics into an efficient, protective movement pattern that is specific to the tasks performed on the field during the normal course of play. The missing link here is the central nervous system (CNS).

Limitations to the current ACL protocols may be that they rely heavily on musculoskeletal rehabilitation and that they have limited emphasis on neurological rehabilitation. As will be discussed later, the CNS has a large impact on the final movement selected by the player. In fact, cognition, perception, and action are the three factors that comprise the individual’s part of the movement paradigm,¹ yet rarely are these factors addressed in most ACL rehabilitation programs. These elements are a large part of the movement equation, so it is easy to understand how failing to address these features can lead to poor movement quality and subsequent ACL re-injury.

In addition to central neurological factors, cognitive issues may play a role in the player’s ability to return to sport. Determining optimal readiness for return to play is a difficult task for the medical community, with many variables to consider. Previous research studies have assessed the variability in return to play for various sports, including football, rugby, soccer, skiing, running, and tennis, with return-to-play rates ranging from 18% to 100%.^2,3,4-10 The risk of secondary injury may cast doubt and fear on athletes as they contemplate their successful return to play.^8,11 Although robust functional testing has become commonplace for determining athlete readiness after injury,^12-20 the assessment of psychological readiness, persistent fear, and loss of confidence are often neglected and not as commonly integrated into the return-to-play algorithm.^21-24 The purpose of this paper is to assess the various cognitive and central neural factors affecting a soccer player’s ability to recover from an ACL injury and offer suggestions for integrating treatments into the protocols to address these issues.

Continue to: CENTRAL NERVOUS SYSTEM NEUROPLASTICITY... 

 

 

CENTRAL NERVOUS SYSTEM NEUROPLASTICITY

Despite the vast amount of attention and research focused on the ACL, the re-injury rate still remains quite high. It has been reported that rehabilitation programs that employ traditional neuromotor training produce a re-injury rate as high as 30% after the athlete returns to sport.^25-28 The overall rate of sustaining a second ACL injury is 15%11 in all patient populations. For the general population <25 years of age, the re-injury rate is 21%, and for athletes <25 years of age, the re-injury rate rises to 23%.¹¹ With re-injury rates at this level, it is certainly fair to consider and be critical of the current rehabilitation methods being used with this population. One opportunity for improvement lies in the general approach used to rehabilitate ACL-injured patients. Therapy for this injury is protocol-driven, and the fact remains that most protocols prioritize restoration of peripheral systems, with minimal thought given to the cortical control necessary to manage those systems.^29,30 When neural factors are considered, it is usually within the context of increasing strength, balance, power, and biomechanical control,^31-34 which are certainly important but peripheral factors nonetheless. The missing element in many ACL protocols may be how to best manage the central neural components and cognitive factors associated with this injury.

If the CNS were to receive more consideration in ACL protocols, the opportunity for improved outcomes could be substantial because the CNS has been proven to be a very malleable system, as long as it receives the correct input. The CNS demonstrates neuroplasticity,³⁵ which means that it is capable of reorganization, based on the stimuli that it receives, whether internal or external.³⁶

This is an important consideration in ACL rehabilitation because the ACL graft, while restoring the biomechanical properties to the knee, is not fully capable of producing the same neurosensory properties of the original ACL.^37-42This is an important concept to understand because an ACL tear does indeed cause deafferentation in the ascending pathways to the brain.^37-40,42-46 This can lead to CNS reorganization and subsequent alterations in efferent output to the periphery.^37-40,42-46 Therefore, if a protocol with traditional musculoskeletal principles was used, then the mechanical function of the knee may certainly be remediated, but the neurosensory function will remain in a maladaptive state,^47-50 potentially leading to aberrant, non-protective movement strategies and a higher risk of re-injury.

The process of CNS reorganization may begin with the initial ACL injury. A peripheral musculoskeletal injury creates an inflammatory response that results in the arrival of chemical mediators such as histamine, substance P, calcitonin, and calcitonin gene-related peptide at the site of injury.⁵¹ As edema accumulates in the joint, tension is applied to the capsule, which may adversely affect proprioception from the receptors located within.⁴⁵ The interruption of consistent input from the peripheral mechanoreceptors may lead to long-term differentiation of the ascending pathways.⁵² This information is synthesized at 3 different levels of the CNS (spinal cord, brain stem, and motor cortex) to produce motor output.^53-56 Differentiation in the ascending circuitry can cause inhibition of motor neurons at the spinal cord.⁴⁵Animal research has shown that this differentiation can cause a breakdown in the cuneate nucleus of the brainstem,⁵⁷which provides sensory information from the upper body, while the gracile nucleus does the same for the lower body. These structures transfer proprioceptive input to the ventral posterior lateral nucleus in the thalamus, where it is then sent to the primary somatosensory cortex.⁵⁷ In general, the somatosensory, visual, and vestibular systems interpret afferent inputs to control movement, balance, and stability.^58,59 In a sport like soccer, where the movement tasks are dynamic and unpredictable, it is easy to see why even a slight deficit in somatosensory processing could disrupt a movement. Valeriani and colleagues^42,46 showed that somatosensory-evoked potentials were indeed altered in a cohort of ACL reconstruction (ACLR) subjects, indicating reorganization within the CNS.  Additionally, the deafferentation could not be changed by other afferent input coming from the knee or by the new ACL graft placed in the knee.^42,46The primary motor cortex has been found to have a substantial network of connectivity with the primary somatosensory cortex, which supports the theory that the motor cortex has a very strong linkage with the peripheral receptors in the joint.⁶⁰  The ligaments in the joint contain Ruffini, Pacinian, and Golgi receptors, all of which react to changes in the collagen fibers and send information regarding tension, length, speed, acceleration, position, and movement back to the CNS.^61-64 Unfortunately, the ascending pathway deafferentation can cause reorganization within the CNS, which makes the feedback provided from the periphery less effective in motor planning.

Ward and colleagues⁶⁵ have reported that reorganization within the motor cortex is the primary cause of chronic neuromuscular movement deficits in peripheral joint injuries. Researchers have used functional magnetic resonance imaging, transcranial magnetic stimulation, and electroencephalography in ACL patients to demonstrate changes in cortical activity and subsequent CNS reorganization.⁶⁵ Kapreli and colleagues⁴¹ reported that subjects with an ACL injury demonstrated higher cortical activation in the pre-supplementary motor area (pre-SMA). This is a region that is responsible for more complex motor planning.^66,67 This area becomes active before the primary motor cortex and is responsible for preparing the final movement pattern that the motor cortex executes.⁴¹ As the task becomes more complex, activity in the pre-SMA will increase.⁴¹ Additionally, they found that the posterior secondary somatosensory area and posterior inferior temporal gyrus showed increased cortical activity compared with controls.⁴¹ Visual planning is processed in the posterior inferior temporal gyrus, and so, it appears that the difficulty in processing somatosensory information due to ascending pathway deafferentation places an increased reliance on the visual system for movement planning.^68-70 This was observed while ACL-injured subjects performed a simple knee flexion-extension movement encompassing 40°, indicating the need to incorporate higher central levels of planning for a very simple movement pattern.⁴¹ Baumeister and colleagues^37,38 also showed that subjects with ACLR had higher levels of cortical activation in the areas of the brain that require attention and that process sensory input. They theorized that this occurred because of reduced efficiency of neural processing at lower levels in the CNS. Despite the higher levels of cortical activity observed, they found that subjects with an ACLR demonstrated proprioceptive testing that was deficient compared with that of controls. Heroux and Tremblay⁷¹ also demonstrated that subjects with an ACLR had increased resting motor cortex activity. They believed that this occurred as the motor cortex attempted to maintain neuromotor output to the periphery in the face of diminished afferent input.

Continue to: The reorganization that results in movement planning...

 

 

The reorganization that results in movement planning, transitioning from subcortical levels to cortical levels, is a phenomenon that researchers believe can lead to deficiencies even as the athlete has returned to sport. Grooms et al⁷²revealed in a case report that a subject with an ACLR showed higher levels of activity in the crus region of the cerebellum. This area contains corticobulbar and corticospinal tracts that transmit neural input to maintain balance and coordination.⁷³ These changes in the cerebellum, combined with increased motor cortex activity, are thought to be indicative of a global neural strategy that uses higher levels of the CNS, as opposed to subcortical processing.⁷²

The current research makes a clear and compelling argument for the importance of CNS reorganization after an ACL injury, placing increased reliance on higher cortical levels of control, as well as the visual system to coordinate balance and movement. It is thought that this reorganized method of neural transmission can then become imprinted within the CNS, if not corrected.^35,74 If this is the case, then traditional strength programs may not be sufficient to restore these connections to their pre-injury level. If the CNS has the ability to reorganize based on the aberrant input that it receives from the periphery, then it also certainly has the potential to adapt to more specific structured input via the ascending afferent pathways.^41,45 The rehabilitation program, however, needs to be structured specifically to target the reorganized regions of the brain. There needs to be an emphasis on rehabilitating not only the peripheral neuromotor structures but also the CNS.⁷⁵

CENTRAL NERVOUS SYSTEM REHABILITATION PRINCIPLES

For a neurological rehabilitation to be successful, the interventions need to be repetitive and task-specific, involve learning, employ whole and part practice, and transition from using an internal to an external focus of control.⁷⁶Movements that are repetitive, but which lack structured learning and skill, have been shown to have no effect on inducing neuroplastic changes in the primary motor cortex.^77,78 However, using neurological rehabilitation techniques that facilitate the acquisition of new motor skills by the CNS have been shown to cause neuroplastic adaptation in the motor cortex.^79-85 This occurs because neuroplasticity is determined by experience and practice.⁷⁸ The CNS operates on cues received in the ascending tracts by mechanoreceptors in the joint. If a new movement pattern is being learned by the athlete, then this new afferent input received from the periphery will start to initiate reorganization in the higher learning centers. If this occurs with optimal repetition and precision, then a positive reorganization can take place within the CNS that results in a higher percentage of motor planning and control being filtered down to a subcortical level. Essentially, the movements become instinctive, which is crucial in athletics, where attention in higher cortical areas is frequently diverted to external aspects of the competition and not solely used to focus on movement.

This is why shifting neurological rehabilitation from an internal focus of control to an external focus of control is paramount. While using an internal focus of control is required early in rehabilitation to enable the athlete to understand the specific tasks required in a composite movement, a gradual transition to an external focus of control is necessary as the athlete begins to perform tasks that are more soccer-specific. This autonomous stage of motor learning is crucial because it transfers the burden of motor planning from higher to lower levels of the CNS and frees up the pre-SMA and primary motor cortex to handle more complex patterns.^58,86-88

Continue to: ANTERIOR CRUCIATE LIGAMENT RISK POTENTIAL IN SOCCER PLAYERS...

 

 

ANTERIOR CRUCIATE LIGAMENT RISK POTENTIAL IN SOCCER PLAYERS

If a comprehensive neuromotor rehabilitation program is to be used effectively with soccer athletes, then the first priority is to define how the players should move, so that they can demonstrate protective kinematics with all soccer-specific tasks and minimize stress to the ACL. As the ideal movement pattern becomes autonomous, then it should be trained within the context of a dynamic environment; remembering that environmental changes have a large impact on the final movement pattern selected by the individual. Brophy et al⁸⁹ evaluated videos of non-contact ACL injuries in male and female soccer players and determined that 45% occurred while cutting, 25% while landing, and 16% during deceleration. These 3 patterns represent 86% of the ACL injuries observed and offer an opportunity for evaluation and treatment with specific central neuromotor rehabilitation techniques.

The foundational movement patterns for the soccer player should focus on producing leverage that minimizes stress to the ACL during the 3 primary tasks outlined above. To achieve this, it is necessary to reduce posterior ground reaction forces at the hip and knee joint during these movements. There is a high correlation between the magnitude of the posterior ground reaction force, and anterior tibial shear, and subsequent displacement.^90,91 This stress can be reduced by increasing the hip and knee flexion angles during soccer-specific movements that involve pivoting, decelerating, and landing from a jump in a unipedal stance.⁹²

This phenomenon can be explained by observing changes in the ACL elevation angle, hamstring insertion angle, and patella tendon-tibial tuberosity insertion angle. As the knee moves into flexion, the ACL takes on a more parallel orientation to the tibia, and its fibers are better able to resist elastic deformation accompanied by a posterior ground reaction force.^93,94 The quadriceps will produce less anterior translation on the tibia because the patella tendon insertion angle is reduced relative to the longitudinal axis of the tibia, and the mechanical advantage of the quadriceps is decreased.⁹⁵ Lastly, the hamstrings will be able to provide better leverage posteriorly because the resultant force trends toward a more parallel orientation to the tibial plateau, which enables the player to counter, more effectively, the posterior ground reaction force and the anterior pull directed by the quadriceps.⁹⁵

This theory is supported by the work of Li and colleagues,⁹⁶ who showed that there is an inverse relationship between knee flexion angle and ACL loading. In their study, they applied a constant quadriceps force of 200 N at 15°, 30°, and 60° angles. The anterior shear force was obviously the highest at 15° and reduced by 20% at 30° and 60% at 60°. When hamstrings co-contraction was added, there was an additional 30% reduction in anterior shear at 15° and 50% at 30° and 60°. From a more flexed position, the hamstrings can increase joint compression and reduce the anterior translation by allowing the concave medial tibial plateau to limit the anterior drawer effect and absorb the forces that occur with excessive anterior shear, internal rotation, and valgus loads.⁹⁷ As the knee flexion angle approximates 60°, the hamstring leverage is increased, and the quadriceps leverage is diminished to the point where its ability to produce anterior tibial translation is neutralized.⁹⁸ Daniel and colleagues98 referred to this as the quadriceps neutral angle.

For soccer-specific movements that are potentially injurious to the ACL, it may then be beneficial to create a default movement pattern at the knee that approximates this value. In keeping with the information presented in this paper, it will be important to have the player reproduce this angle consistently during activities that involve pivoting, decelerating, and landing from a jump within the context of match play. This will certainly require that segments located both proximal and distal to the knee are able to function within specific parameters so that a cohesive protective synergy is produced throughout the lower quarter which minimizes posterior ground reaction forces and is protective of the ACL. This is where structured neuromotor training that is able to modulate networks within the CNS may be beneficial.

Continue to: CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER...

 

 

CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER

The ultimate goal is to create a foundational movement pattern that optimizes leverage and is protective of the ACL during decelerating, pivoting, and landing in a unipedal stance from a jump. The composite segments that are necessary to achieve this include local core stability to create lumbopelvic stiffness, and global core activation to enhance posterior chain stability. This should enable the player to feel more balanced when placing the pelvis in a more posterior and inferior position while still maintaining the trunk in a position that is parallel with the tibia, as the knee is flexed to an approximate 60° angle (Figure 1). From a frontal plane perspective, the acetabulum should bisect the malleoli of the stance leg, with a neutral tibiofemoral joint alignment (Figure 1).

The neuromotor training for the composite segments of this movement can begin in the “acute postoperative phase” (Table 1).   Because the surgical repair will limit the player’s capabilities in this stage, this is a good time to break down the foundational movement pattern into its component parts and ensure that the CNS receives a high number of quality repetitions of parts. In this phase, the player may begin an isolated training for the transversus abdominis, multifidus, and pubococcygeus. This can start in a supine position using biofeedback with an isometric contraction, progress to a standing position, and incorporate deep core activation with stance-phase gait training, mini squats, and lunge variations. This phase will require an abundance of visual and verbal feedback with an internal focus of control as the player gets used to activating the deep core and quad/hip synergy during functional lower extremity movements. Even in this early phase, the player should look to minimize anterior and/or posterior pelvic tilting and maintain a stiff thoracolumbar segment that remains parallel with the tibia during all functional movements.

Table 1. Adjunct CNS Treatment Principles for ACL Reconstruction in Soccer Athletes

Phase	Goal	CNS Rehabilitation Techniques
Acute postoperative	Local core activation with weightbearing exercise. Produce trunk stiffness with lower extremity movements.	High repetitions. Verbal or tactile cues. Internal focus of control. Partial practice.
Subacute postoperative	Lumbopelvic, foot or ankle, and posterior chain segments learn to participate in movement effectively.	Requires higher levels of cortical planning. Internal focus of control. CIMT.
Static stability	Able to adopt foundational movement pattern consistently with vision eliminated.	Somatosensory vs visual processing. Partial-to-whole practice. Use internal and/or external focus of control.
Dynamic stability	Able to perform plyometrics in a single-leg position using foundational movement pattern with subcortical processing.	Increase velocity with movement challenges. Occlude or eliminate vision. Heavy reliance on an external focus of control. Prioritize movement quality.
Dynamic agility	Pivoting, decelerating, and landing are performed with hip flexion/knee flexion synergy, trunk stiffness, and posterior chain activation.	Unanticipated movement challenges. Whole practice. Ball reaction drills with vision obstructed or occluded. Contact drills with vision obstructed or occluded. Use external focus of control to include soccer-specific tasks.

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

As the player moves into the “subacute postoperative phase” (Table 1).   He or she will continue to use an internal focus of control to activate the local/global core synergy with functional movements progressing from double-leg, to single-leg positions. Partial practice, instead of whole practice, is still the predominant theme of the neural training process. In this phase, the knee and hip flexion angles can increase, and the player’s trunk and pelvic position should be critiqued in a single-leg position so that the trunk remains parallel with the tibia in the sagittal plane with a slight forward hip hinge. The pelvis should remain level throughout single-leg stance to ensure adequate activation of the lateral hip stabilizers. This is the stage where the player can learn to isolate closed kinetic chain hip rotation for pivoting, and so, single-leg hip internal and external rotation drills are useful, both with and without resistance. Skill acquisition is crucial in this phase because the patterns that the CNS adopts will form the foundation for more dynamic patterns that will occur in the later soccer-specific stages. Higher levels of cortical planning are still needed in this phase. For this reason, it is important that poor quality repetitions are recognized by the player and clinician so that he or she can learn to perform them correctly, albeit still with an internal focus of control. This is also a good time to begin to employ constraint-induced movement therapy as the player is able to replicate the desired pattern with more precision. For example, by eliminating the use of the upper extremities as a source of balance, the CNS is forced to program alternate synergies such as the lumbopelvic, and foot and ankle segments to maintain the desired alignment.

The “lower quarter static stability phase” (Table 1) marks a point where it may be useful to use direct strategies that have the capability to change CNS efferent owutput from a primary reliance on the visual processing areas in the posterior-inferior temporal gyrus back to the somatosensory area. It is critical that the player is able to make this transition in cortical reorganization and control, because ACL-injured subjects have been shown to have balance scores similar to healthy controls when they are able to use their vision, but this is reduced when vision is taken away.^99-105  Their balance will diminish even further if vision is modulated during more complex landing and pivoting maneuvers.^99-105 This may certainly explain why defending is a riskier task for ACL-injured players⁸⁹ as their visual system is focused more on tracking a player than attending to precision with movement planning.

To enhance this cortical reorganization within the context of soccer-specific movements, it is useful to start from a foundational single-leg position, with the knee approximating 60° of flexion and the trunk parallel to the tibia. In the frontal plane, the pelvis should be level, the trunk vertical, and the acetabulum bisecting the malleoli of the stance leg (Figure 1).   The player may initially work on getting into this foundational position with vision either partially obstructed using stroboscopic eyewear or completely obstructed if this equipment is unavailable.^106-108 The pattern can be progressed by constraining the upper extremities to force reliance on the lumbopelvic and foot/ankle strategies for balance. Head and/or trunk turns can be added to simulate the external focus of control that is required with movement in soccer. These should progress from slow to fast and anticipated to unanticipated as the player demonstrates competence in maintaining stability at each segment within the foundational stance position. Once this is in play, a ball should be introduced into the drills. As the player maintains the foundational position with vision diminished and upper extremities constrained, they should attempt to reach for or trap a ball from this position. If vision is completely obstructed, then the player can be instructed to open his/her eyes just as the ball arrives to induce a reactive response. Again, quality repetitions are essential for learning to occur, and subsequent skill acquisition to take place in the CNS; thus, close scrutiny should be paid to the qualitative essence of the movement patterns to ensure pristine biomechanics during this phase.

The “lower quarter dynamic stability phase” (Table 1) should continue with the same neuromotor training principles employed in the previous phase, except that the drills will now involve plyometrics. The player should ultimately progress from double-leg, to single-leg jumps and then linear to diagonal. Vision should still be obstructed and upper extremities constrained to channel the lumbopelvic region for force production and balance. Movement quality in the foundational position remains paramount with these drills to ensure that skill acquisition is occurring and injury risk is being mitigated. An external focus of control can be introduced by applying an unanticipated perturbation during a jump. Additional learning opportunities should include unanticipated head and trunk turns while landing in a unipedal stance from a jump. The task can be made more specific by having the player trap a pass while doing linear or diagonal single-leg hop progressions. In this manner, the player’s CNS can become reorganized to program the requisite synergies to maintain a protective foundational position on the stance leg, as the contralateral limb is required to perform work that is far outside the player’s base of support.

Continue to: The final segment of the CNS neuromotor rehabilitation program...

 

 

The final segment of the CNS neuromotor rehabilitation program is the “lower quarter dynamic agility phase” (Table 1), when the player will learn to perform an unanticipated directional change in a foundational position for the pivot leg. The player can begin this phase by initiating sprint-deceleration-pivot efforts, progressing at 45°, 90°, 120°, and 180° turns. This should be trained in both a forward and backpedal position. Close attention should be paid to the deceleration phase of the sprint-pivot effort, as this will set the player up to demonstrate protective kinematics during the pivot phase of the task. In this phase, the center of mass should become lower and move posteriorly, so that a deeper knee and hip flexion angle, supported by posterior chain synergies, can occur at the pivot point. This is an important skill for the player to acquire, as Cortes and colleagues⁹² have reported that female collegiate soccer players tend to perform a pivoting task with a more erect trunk position. In the same cohort, they also measured the mean knee flexion angle at initial contact during pivoting to be 24°.⁹² Movement patterns that reflect an elevated center of mass, with arms abducted away from the trunk, should be discouraged here. The drills can be progressed to have the player react to a command and perform unanticipated pivots within a 5 × 5-meter box to simulate defending. This should be progressed from eyes open and arms unconstrained, to vision disrupted and arms constrained. From here, an external focus of control can be added by playing a ball to the athlete. Vision should be withheld until the instant that the ball arrives at the player, when he/she is required to play the ball to an unanticipated spot. As is the case in all other phases of the neuromotor training, the quality of movement is the most important parameter to critique with each drill. From a qualitative standpoint, the player should demonstrate stiffness throughout the thoracolumbar region and power and control through the pelvis with each directional change. In addition, he or she should maintain a low and posteriorly oriented center of mass to optimize leverage in the hamstrings/gluteals compared with the quadriceps and reduce posterior ground reaction forces.

PSYCHOLOGICAL READINESS FOR RETURN TO PLAY

After an injury is sustained, an athlete is often subjected to a range of psychological responses in addition to the functional impairment, including stress, hesitancy, alterations in self-esteem, depression, fear of re-injury, and anxiety.^43,109-111 The aforementioned responses are often at their height in the time immediately following an injury and generally subside over time during the rehabilitation process.¹¹⁰ The rates at which athletes experience psychological distress following an injury range between 5% and 19%; the levels are comparable with patients receiving treatment for mental health illness.⁴³ However, these elements may persist, or even increase, in the later stages of the rehabilitation process as the topic of return to play is deliberated.^112,113 If these fears are left unresolved, then a significant delay can be incurred during the rehabilitation process, which might ultimately jeopardize the successful return to play.^114,115

When athletes have been cleared to return to sport, fear tends to be the most common reason for their decision to not return to play.^21,116 The persistence of fear has clinical implications and warrants close monitoring to ensure that the athlete feels adequately supported in the decision to return to sport.^117,118 Building the athlete’s confidence by addressing hesitation, lack of confidence, heightened awareness of risk or re-injury, and safe reintegration into athletic participation are important themes identified to encourage a safe return to play.⁴³ A variety of validated tools  can be integrated into an existing return-to-play decision-making algorithm (Table 2).^118-120 

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

 

Table 2. Self-Report Measurement Tools to Integrate into Return-to-Play Decision-Making Algorithm

Self-report Measurement Tools

13-item Tampa Scale for Kinesiophobia

Anterior Cruciate Ligament Return to Sport after Injury Scale (ACL-RSI)

Global Rating Scale (GRS)

International Knee Documentation Committee (IKDC) Subjective Knee Evaluation Form

Knee Injury and Osteoarthritis Outcome Score (KOOS)

Lysholm Knee Scoring Scale

Short Form-36 Health Survey (SF-36)

Subjective Patient Outcome for Return to Sport (SPORTS)

Patient Health Questionnaire-9

By integrating the necessary screening of patients for kinesiophobia and assessing patient expectations after enduring an ACL injury, clinicians may be able to identify patients who are at risk for poorer functional outcomes. A consideration of psychosocial elements such as activity avoidance, fear of movement and re-injury, loss of confidence and expectations/assumptions during the continuum of the rehabilitation process, and the decision to return to play may favorably impact the individual’s ability to safely return to sport. It is critical to address both the physical and psychosocial factors during the rehabilitation process to more optimally transition individuals back to their prior level of athleticism.

CONCLUSION

Psychosocial factors may play a role in determining a player’s readiness to return to sport, as well as a potential for re-injury. A number of tests are available for use with this patient population to identify mental deficits that may impact player performance upon return. Additionally, the CNS should be considered as a source of impairment in players with ACL injuries. Current protocols may not fully appreciate the CNS’ impact on the player’s functional outcome. Therefore, an approach that includes CNS neuromotor training with traditional musculoskeletal rehabilitation, which also incorporates cognitive and psychosocial factors, may define an improved paradigm for treating soccer athletes following an ACL injury and assessing return-to-play capability.

ABSTRACT

Soccer players recovering from anterior cruciate ligament (ACL) injuries have better options for treatment today than they did 25 years ago. Surgical techniques have improved, and rehabilitation protocols have evolved considerably. Although the rehabilitation community is doing a better job of treating this patient population, the evidence does demonstrate that both re-injury and return- to-play (RTP) rates are still suboptimal. Most protocols focus on normalizing strength and range of motion (ROM) and achieving limb symmetry with soccer-specific movements. While these factors are certainly prerequisites for returning to the field, their inclusion does not provide a complete picture of the athlete’s presentation. An additional factor that should be prioritized with this patient population is the central nervous system (CNS). Advanced imaging has shown that peripheral deafferentation does occur with musculoskeletal injuries; this ultimately results in cortical reorganization, which makes movement planning more difficult for the player, since simpler tasks must now be processed at higher levels in the CNS. The evidence also shows that the CNS demonstrates plasticity in these cases, so that through focused neuromotor rehabilitation techniques, it is possible to bring movement planning back down to a sub-cortical level. Cognitive issues may also be a factor in preventing the player from returning. Fear of re-injury and diminished confidence can influence the way the player moves on the field, and diminish ability to demonstrate protective kinematics with all soccer-specific tasks. We believe that an approach incorporating traditional musculoskeletal rehabilitation, CNS neuro-motor training, and consideration for cognitive factors, may define an improved paradigm for treating the soccer player and assessing readiness for RTP following ACL injury.

Continue to: Although anterior cruciate ligament (ACL)...

Although anterior cruciate ligament (ACL) rehabilitation has evolved considerably over the past 2 decades, the basic paradigm has remained consistent: normalize strength and range of motion, reduce swelling and pain, achieve limb symmetry with functional tasks, and return to sport-specific activities gradually over a 6 to 12-month period. There have been some slight additions to this basic premise, such as evaluating knee and hip mechanics in the frontal plane, but the requirements here are vaguely defined and are typically only evaluated within the context of controlled clinical testing.

It is interesting to note that the typical ACL injury pattern occurs during a normal sport-specific movement, yet most rehabilitation protocols fail to recognize the potential causes of the aberrant movement pattern and how to best modify it so that the risk of repeated stress to the ACL can be minimized. It should be understood that movement occurs through the interaction of 3 discrete factors: the individual, the task being performed, and the environment in which it is performed.¹ All of these factors will play a role in how the final movement pattern is produced. For example, a soccer player (individual) may backpedal and pivot to the left 60° and accelerate to sprint after a player moving towards the touchline (task) while receiving instructions from teammates and monitoring the movements of opposing players (environment). A small variance in any 1 of these factors could significantly impact the movement pattern as the player completes the task.

In most rehabilitation programs, each of these factors may be treated in a singular, non-specific manner, but if these factors are not coordinated effectively throughout the program to produce the desired sport-specific movement, a faulty pattern may persist, leaving the player at risk for injury. Current rehabilitation programs seem to have a strong focus on creating stability, mobility, and strength, but these are trained in silos, with an internal focus of control, which only solves the biomechanical equation. Often, it is difficult for the player to coordinate good biomechanics into an efficient, protective movement pattern that is specific to the tasks performed on the field during the normal course of play. The missing link here is the central nervous system (CNS).

Limitations to the current ACL protocols may be that they rely heavily on musculoskeletal rehabilitation and that they have limited emphasis on neurological rehabilitation. As will be discussed later, the CNS has a large impact on the final movement selected by the player. In fact, cognition, perception, and action are the three factors that comprise the individual’s part of the movement paradigm,¹ yet rarely are these factors addressed in most ACL rehabilitation programs. These elements are a large part of the movement equation, so it is easy to understand how failing to address these features can lead to poor movement quality and subsequent ACL re-injury.

In addition to central neurological factors, cognitive issues may play a role in the player’s ability to return to sport. Determining optimal readiness for return to play is a difficult task for the medical community, with many variables to consider. Previous research studies have assessed the variability in return to play for various sports, including football, rugby, soccer, skiing, running, and tennis, with return-to-play rates ranging from 18% to 100%.^2,3,4-10 The risk of secondary injury may cast doubt and fear on athletes as they contemplate their successful return to play.^8,11 Although robust functional testing has become commonplace for determining athlete readiness after injury,^12-20 the assessment of psychological readiness, persistent fear, and loss of confidence are often neglected and not as commonly integrated into the return-to-play algorithm.^21-24 The purpose of this paper is to assess the various cognitive and central neural factors affecting a soccer player’s ability to recover from an ACL injury and offer suggestions for integrating treatments into the protocols to address these issues.

Continue to: CENTRAL NERVOUS SYSTEM NEUROPLASTICITY... 

 

 

CENTRAL NERVOUS SYSTEM NEUROPLASTICITY

Despite the vast amount of attention and research focused on the ACL, the re-injury rate still remains quite high. It has been reported that rehabilitation programs that employ traditional neuromotor training produce a re-injury rate as high as 30% after the athlete returns to sport.^25-28 The overall rate of sustaining a second ACL injury is 15%11 in all patient populations. For the general population <25 years of age, the re-injury rate is 21%, and for athletes <25 years of age, the re-injury rate rises to 23%.¹¹ With re-injury rates at this level, it is certainly fair to consider and be critical of the current rehabilitation methods being used with this population. One opportunity for improvement lies in the general approach used to rehabilitate ACL-injured patients. Therapy for this injury is protocol-driven, and the fact remains that most protocols prioritize restoration of peripheral systems, with minimal thought given to the cortical control necessary to manage those systems.^29,30 When neural factors are considered, it is usually within the context of increasing strength, balance, power, and biomechanical control,^31-34 which are certainly important but peripheral factors nonetheless. The missing element in many ACL protocols may be how to best manage the central neural components and cognitive factors associated with this injury.

If the CNS were to receive more consideration in ACL protocols, the opportunity for improved outcomes could be substantial because the CNS has been proven to be a very malleable system, as long as it receives the correct input. The CNS demonstrates neuroplasticity,³⁵ which means that it is capable of reorganization, based on the stimuli that it receives, whether internal or external.³⁶

This is an important consideration in ACL rehabilitation because the ACL graft, while restoring the biomechanical properties to the knee, is not fully capable of producing the same neurosensory properties of the original ACL.^37-42This is an important concept to understand because an ACL tear does indeed cause deafferentation in the ascending pathways to the brain.^37-40,42-46 This can lead to CNS reorganization and subsequent alterations in efferent output to the periphery.^37-40,42-46 Therefore, if a protocol with traditional musculoskeletal principles was used, then the mechanical function of the knee may certainly be remediated, but the neurosensory function will remain in a maladaptive state,^47-50 potentially leading to aberrant, non-protective movement strategies and a higher risk of re-injury.

The process of CNS reorganization may begin with the initial ACL injury. A peripheral musculoskeletal injury creates an inflammatory response that results in the arrival of chemical mediators such as histamine, substance P, calcitonin, and calcitonin gene-related peptide at the site of injury.⁵¹ As edema accumulates in the joint, tension is applied to the capsule, which may adversely affect proprioception from the receptors located within.⁴⁵ The interruption of consistent input from the peripheral mechanoreceptors may lead to long-term differentiation of the ascending pathways.⁵² This information is synthesized at 3 different levels of the CNS (spinal cord, brain stem, and motor cortex) to produce motor output.^53-56 Differentiation in the ascending circuitry can cause inhibition of motor neurons at the spinal cord.⁴⁵Animal research has shown that this differentiation can cause a breakdown in the cuneate nucleus of the brainstem,⁵⁷which provides sensory information from the upper body, while the gracile nucleus does the same for the lower body. These structures transfer proprioceptive input to the ventral posterior lateral nucleus in the thalamus, where it is then sent to the primary somatosensory cortex.⁵⁷ In general, the somatosensory, visual, and vestibular systems interpret afferent inputs to control movement, balance, and stability.^58,59 In a sport like soccer, where the movement tasks are dynamic and unpredictable, it is easy to see why even a slight deficit in somatosensory processing could disrupt a movement. Valeriani and colleagues^42,46 showed that somatosensory-evoked potentials were indeed altered in a cohort of ACL reconstruction (ACLR) subjects, indicating reorganization within the CNS.  Additionally, the deafferentation could not be changed by other afferent input coming from the knee or by the new ACL graft placed in the knee.^42,46The primary motor cortex has been found to have a substantial network of connectivity with the primary somatosensory cortex, which supports the theory that the motor cortex has a very strong linkage with the peripheral receptors in the joint.⁶⁰  The ligaments in the joint contain Ruffini, Pacinian, and Golgi receptors, all of which react to changes in the collagen fibers and send information regarding tension, length, speed, acceleration, position, and movement back to the CNS.^61-64 Unfortunately, the ascending pathway deafferentation can cause reorganization within the CNS, which makes the feedback provided from the periphery less effective in motor planning.

Ward and colleagues⁶⁵ have reported that reorganization within the motor cortex is the primary cause of chronic neuromuscular movement deficits in peripheral joint injuries. Researchers have used functional magnetic resonance imaging, transcranial magnetic stimulation, and electroencephalography in ACL patients to demonstrate changes in cortical activity and subsequent CNS reorganization.⁶⁵ Kapreli and colleagues⁴¹ reported that subjects with an ACL injury demonstrated higher cortical activation in the pre-supplementary motor area (pre-SMA). This is a region that is responsible for more complex motor planning.^66,67 This area becomes active before the primary motor cortex and is responsible for preparing the final movement pattern that the motor cortex executes.⁴¹ As the task becomes more complex, activity in the pre-SMA will increase.⁴¹ Additionally, they found that the posterior secondary somatosensory area and posterior inferior temporal gyrus showed increased cortical activity compared with controls.⁴¹ Visual planning is processed in the posterior inferior temporal gyrus, and so, it appears that the difficulty in processing somatosensory information due to ascending pathway deafferentation places an increased reliance on the visual system for movement planning.^68-70 This was observed while ACL-injured subjects performed a simple knee flexion-extension movement encompassing 40°, indicating the need to incorporate higher central levels of planning for a very simple movement pattern.⁴¹ Baumeister and colleagues^37,38 also showed that subjects with ACLR had higher levels of cortical activation in the areas of the brain that require attention and that process sensory input. They theorized that this occurred because of reduced efficiency of neural processing at lower levels in the CNS. Despite the higher levels of cortical activity observed, they found that subjects with an ACLR demonstrated proprioceptive testing that was deficient compared with that of controls. Heroux and Tremblay⁷¹ also demonstrated that subjects with an ACLR had increased resting motor cortex activity. They believed that this occurred as the motor cortex attempted to maintain neuromotor output to the periphery in the face of diminished afferent input.

Continue to: The reorganization that results in movement planning...

 

 

The reorganization that results in movement planning, transitioning from subcortical levels to cortical levels, is a phenomenon that researchers believe can lead to deficiencies even as the athlete has returned to sport. Grooms et al⁷²revealed in a case report that a subject with an ACLR showed higher levels of activity in the crus region of the cerebellum. This area contains corticobulbar and corticospinal tracts that transmit neural input to maintain balance and coordination.⁷³ These changes in the cerebellum, combined with increased motor cortex activity, are thought to be indicative of a global neural strategy that uses higher levels of the CNS, as opposed to subcortical processing.⁷²

The current research makes a clear and compelling argument for the importance of CNS reorganization after an ACL injury, placing increased reliance on higher cortical levels of control, as well as the visual system to coordinate balance and movement. It is thought that this reorganized method of neural transmission can then become imprinted within the CNS, if not corrected.^35,74 If this is the case, then traditional strength programs may not be sufficient to restore these connections to their pre-injury level. If the CNS has the ability to reorganize based on the aberrant input that it receives from the periphery, then it also certainly has the potential to adapt to more specific structured input via the ascending afferent pathways.^41,45 The rehabilitation program, however, needs to be structured specifically to target the reorganized regions of the brain. There needs to be an emphasis on rehabilitating not only the peripheral neuromotor structures but also the CNS.⁷⁵

CENTRAL NERVOUS SYSTEM REHABILITATION PRINCIPLES

For a neurological rehabilitation to be successful, the interventions need to be repetitive and task-specific, involve learning, employ whole and part practice, and transition from using an internal to an external focus of control.⁷⁶Movements that are repetitive, but which lack structured learning and skill, have been shown to have no effect on inducing neuroplastic changes in the primary motor cortex.^77,78 However, using neurological rehabilitation techniques that facilitate the acquisition of new motor skills by the CNS have been shown to cause neuroplastic adaptation in the motor cortex.^79-85 This occurs because neuroplasticity is determined by experience and practice.⁷⁸ The CNS operates on cues received in the ascending tracts by mechanoreceptors in the joint. If a new movement pattern is being learned by the athlete, then this new afferent input received from the periphery will start to initiate reorganization in the higher learning centers. If this occurs with optimal repetition and precision, then a positive reorganization can take place within the CNS that results in a higher percentage of motor planning and control being filtered down to a subcortical level. Essentially, the movements become instinctive, which is crucial in athletics, where attention in higher cortical areas is frequently diverted to external aspects of the competition and not solely used to focus on movement.

This is why shifting neurological rehabilitation from an internal focus of control to an external focus of control is paramount. While using an internal focus of control is required early in rehabilitation to enable the athlete to understand the specific tasks required in a composite movement, a gradual transition to an external focus of control is necessary as the athlete begins to perform tasks that are more soccer-specific. This autonomous stage of motor learning is crucial because it transfers the burden of motor planning from higher to lower levels of the CNS and frees up the pre-SMA and primary motor cortex to handle more complex patterns.^58,86-88

Continue to: ANTERIOR CRUCIATE LIGAMENT RISK POTENTIAL IN SOCCER PLAYERS...

 

 

ANTERIOR CRUCIATE LIGAMENT RISK POTENTIAL IN SOCCER PLAYERS

If a comprehensive neuromotor rehabilitation program is to be used effectively with soccer athletes, then the first priority is to define how the players should move, so that they can demonstrate protective kinematics with all soccer-specific tasks and minimize stress to the ACL. As the ideal movement pattern becomes autonomous, then it should be trained within the context of a dynamic environment; remembering that environmental changes have a large impact on the final movement pattern selected by the individual. Brophy et al⁸⁹ evaluated videos of non-contact ACL injuries in male and female soccer players and determined that 45% occurred while cutting, 25% while landing, and 16% during deceleration. These 3 patterns represent 86% of the ACL injuries observed and offer an opportunity for evaluation and treatment with specific central neuromotor rehabilitation techniques.

The foundational movement patterns for the soccer player should focus on producing leverage that minimizes stress to the ACL during the 3 primary tasks outlined above. To achieve this, it is necessary to reduce posterior ground reaction forces at the hip and knee joint during these movements. There is a high correlation between the magnitude of the posterior ground reaction force, and anterior tibial shear, and subsequent displacement.^90,91 This stress can be reduced by increasing the hip and knee flexion angles during soccer-specific movements that involve pivoting, decelerating, and landing from a jump in a unipedal stance.⁹²

This phenomenon can be explained by observing changes in the ACL elevation angle, hamstring insertion angle, and patella tendon-tibial tuberosity insertion angle. As the knee moves into flexion, the ACL takes on a more parallel orientation to the tibia, and its fibers are better able to resist elastic deformation accompanied by a posterior ground reaction force.^93,94 The quadriceps will produce less anterior translation on the tibia because the patella tendon insertion angle is reduced relative to the longitudinal axis of the tibia, and the mechanical advantage of the quadriceps is decreased.⁹⁵ Lastly, the hamstrings will be able to provide better leverage posteriorly because the resultant force trends toward a more parallel orientation to the tibial plateau, which enables the player to counter, more effectively, the posterior ground reaction force and the anterior pull directed by the quadriceps.⁹⁵

This theory is supported by the work of Li and colleagues,⁹⁶ who showed that there is an inverse relationship between knee flexion angle and ACL loading. In their study, they applied a constant quadriceps force of 200 N at 15°, 30°, and 60° angles. The anterior shear force was obviously the highest at 15° and reduced by 20% at 30° and 60% at 60°. When hamstrings co-contraction was added, there was an additional 30% reduction in anterior shear at 15° and 50% at 30° and 60°. From a more flexed position, the hamstrings can increase joint compression and reduce the anterior translation by allowing the concave medial tibial plateau to limit the anterior drawer effect and absorb the forces that occur with excessive anterior shear, internal rotation, and valgus loads.⁹⁷ As the knee flexion angle approximates 60°, the hamstring leverage is increased, and the quadriceps leverage is diminished to the point where its ability to produce anterior tibial translation is neutralized.⁹⁸ Daniel and colleagues98 referred to this as the quadriceps neutral angle.

For soccer-specific movements that are potentially injurious to the ACL, it may then be beneficial to create a default movement pattern at the knee that approximates this value. In keeping with the information presented in this paper, it will be important to have the player reproduce this angle consistently during activities that involve pivoting, decelerating, and landing from a jump within the context of match play. This will certainly require that segments located both proximal and distal to the knee are able to function within specific parameters so that a cohesive protective synergy is produced throughout the lower quarter which minimizes posterior ground reaction forces and is protective of the ACL. This is where structured neuromotor training that is able to modulate networks within the CNS may be beneficial.

Continue to: CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER...

 

 

CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER

The ultimate goal is to create a foundational movement pattern that optimizes leverage and is protective of the ACL during decelerating, pivoting, and landing in a unipedal stance from a jump. The composite segments that are necessary to achieve this include local core stability to create lumbopelvic stiffness, and global core activation to enhance posterior chain stability. This should enable the player to feel more balanced when placing the pelvis in a more posterior and inferior position while still maintaining the trunk in a position that is parallel with the tibia, as the knee is flexed to an approximate 60° angle (Figure 1). From a frontal plane perspective, the acetabulum should bisect the malleoli of the stance leg, with a neutral tibiofemoral joint alignment (Figure 1).

The neuromotor training for the composite segments of this movement can begin in the “acute postoperative phase” (Table 1).   Because the surgical repair will limit the player’s capabilities in this stage, this is a good time to break down the foundational movement pattern into its component parts and ensure that the CNS receives a high number of quality repetitions of parts. In this phase, the player may begin an isolated training for the transversus abdominis, multifidus, and pubococcygeus. This can start in a supine position using biofeedback with an isometric contraction, progress to a standing position, and incorporate deep core activation with stance-phase gait training, mini squats, and lunge variations. This phase will require an abundance of visual and verbal feedback with an internal focus of control as the player gets used to activating the deep core and quad/hip synergy during functional lower extremity movements. Even in this early phase, the player should look to minimize anterior and/or posterior pelvic tilting and maintain a stiff thoracolumbar segment that remains parallel with the tibia during all functional movements.

Table 1. Adjunct CNS Treatment Principles for ACL Reconstruction in Soccer Athletes

Phase	Goal	CNS Rehabilitation Techniques
Acute postoperative	Local core activation with weightbearing exercise. Produce trunk stiffness with lower extremity movements.	High repetitions. Verbal or tactile cues. Internal focus of control. Partial practice.
Subacute postoperative	Lumbopelvic, foot or ankle, and posterior chain segments learn to participate in movement effectively.	Requires higher levels of cortical planning. Internal focus of control. CIMT.
Static stability	Able to adopt foundational movement pattern consistently with vision eliminated.	Somatosensory vs visual processing. Partial-to-whole practice. Use internal and/or external focus of control.
Dynamic stability	Able to perform plyometrics in a single-leg position using foundational movement pattern with subcortical processing.	Increase velocity with movement challenges. Occlude or eliminate vision. Heavy reliance on an external focus of control. Prioritize movement quality.
Dynamic agility	Pivoting, decelerating, and landing are performed with hip flexion/knee flexion synergy, trunk stiffness, and posterior chain activation.	Unanticipated movement challenges. Whole practice. Ball reaction drills with vision obstructed or occluded. Contact drills with vision obstructed or occluded. Use external focus of control to include soccer-specific tasks.

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

As the player moves into the “subacute postoperative phase” (Table 1).   He or she will continue to use an internal focus of control to activate the local/global core synergy with functional movements progressing from double-leg, to single-leg positions. Partial practice, instead of whole practice, is still the predominant theme of the neural training process. In this phase, the knee and hip flexion angles can increase, and the player’s trunk and pelvic position should be critiqued in a single-leg position so that the trunk remains parallel with the tibia in the sagittal plane with a slight forward hip hinge. The pelvis should remain level throughout single-leg stance to ensure adequate activation of the lateral hip stabilizers. This is the stage where the player can learn to isolate closed kinetic chain hip rotation for pivoting, and so, single-leg hip internal and external rotation drills are useful, both with and without resistance. Skill acquisition is crucial in this phase because the patterns that the CNS adopts will form the foundation for more dynamic patterns that will occur in the later soccer-specific stages. Higher levels of cortical planning are still needed in this phase. For this reason, it is important that poor quality repetitions are recognized by the player and clinician so that he or she can learn to perform them correctly, albeit still with an internal focus of control. This is also a good time to begin to employ constraint-induced movement therapy as the player is able to replicate the desired pattern with more precision. For example, by eliminating the use of the upper extremities as a source of balance, the CNS is forced to program alternate synergies such as the lumbopelvic, and foot and ankle segments to maintain the desired alignment.

The “lower quarter static stability phase” (Table 1) marks a point where it may be useful to use direct strategies that have the capability to change CNS efferent owutput from a primary reliance on the visual processing areas in the posterior-inferior temporal gyrus back to the somatosensory area. It is critical that the player is able to make this transition in cortical reorganization and control, because ACL-injured subjects have been shown to have balance scores similar to healthy controls when they are able to use their vision, but this is reduced when vision is taken away.^99-105  Their balance will diminish even further if vision is modulated during more complex landing and pivoting maneuvers.^99-105 This may certainly explain why defending is a riskier task for ACL-injured players⁸⁹ as their visual system is focused more on tracking a player than attending to precision with movement planning.

To enhance this cortical reorganization within the context of soccer-specific movements, it is useful to start from a foundational single-leg position, with the knee approximating 60° of flexion and the trunk parallel to the tibia. In the frontal plane, the pelvis should be level, the trunk vertical, and the acetabulum bisecting the malleoli of the stance leg (Figure 1).   The player may initially work on getting into this foundational position with vision either partially obstructed using stroboscopic eyewear or completely obstructed if this equipment is unavailable.^106-108 The pattern can be progressed by constraining the upper extremities to force reliance on the lumbopelvic and foot/ankle strategies for balance. Head and/or trunk turns can be added to simulate the external focus of control that is required with movement in soccer. These should progress from slow to fast and anticipated to unanticipated as the player demonstrates competence in maintaining stability at each segment within the foundational stance position. Once this is in play, a ball should be introduced into the drills. As the player maintains the foundational position with vision diminished and upper extremities constrained, they should attempt to reach for or trap a ball from this position. If vision is completely obstructed, then the player can be instructed to open his/her eyes just as the ball arrives to induce a reactive response. Again, quality repetitions are essential for learning to occur, and subsequent skill acquisition to take place in the CNS; thus, close scrutiny should be paid to the qualitative essence of the movement patterns to ensure pristine biomechanics during this phase.

The “lower quarter dynamic stability phase” (Table 1) should continue with the same neuromotor training principles employed in the previous phase, except that the drills will now involve plyometrics. The player should ultimately progress from double-leg, to single-leg jumps and then linear to diagonal. Vision should still be obstructed and upper extremities constrained to channel the lumbopelvic region for force production and balance. Movement quality in the foundational position remains paramount with these drills to ensure that skill acquisition is occurring and injury risk is being mitigated. An external focus of control can be introduced by applying an unanticipated perturbation during a jump. Additional learning opportunities should include unanticipated head and trunk turns while landing in a unipedal stance from a jump. The task can be made more specific by having the player trap a pass while doing linear or diagonal single-leg hop progressions. In this manner, the player’s CNS can become reorganized to program the requisite synergies to maintain a protective foundational position on the stance leg, as the contralateral limb is required to perform work that is far outside the player’s base of support.

Continue to: The final segment of the CNS neuromotor rehabilitation program...

 

 

The final segment of the CNS neuromotor rehabilitation program is the “lower quarter dynamic agility phase” (Table 1), when the player will learn to perform an unanticipated directional change in a foundational position for the pivot leg. The player can begin this phase by initiating sprint-deceleration-pivot efforts, progressing at 45°, 90°, 120°, and 180° turns. This should be trained in both a forward and backpedal position. Close attention should be paid to the deceleration phase of the sprint-pivot effort, as this will set the player up to demonstrate protective kinematics during the pivot phase of the task. In this phase, the center of mass should become lower and move posteriorly, so that a deeper knee and hip flexion angle, supported by posterior chain synergies, can occur at the pivot point. This is an important skill for the player to acquire, as Cortes and colleagues⁹² have reported that female collegiate soccer players tend to perform a pivoting task with a more erect trunk position. In the same cohort, they also measured the mean knee flexion angle at initial contact during pivoting to be 24°.⁹² Movement patterns that reflect an elevated center of mass, with arms abducted away from the trunk, should be discouraged here. The drills can be progressed to have the player react to a command and perform unanticipated pivots within a 5 × 5-meter box to simulate defending. This should be progressed from eyes open and arms unconstrained, to vision disrupted and arms constrained. From here, an external focus of control can be added by playing a ball to the athlete. Vision should be withheld until the instant that the ball arrives at the player, when he/she is required to play the ball to an unanticipated spot. As is the case in all other phases of the neuromotor training, the quality of movement is the most important parameter to critique with each drill. From a qualitative standpoint, the player should demonstrate stiffness throughout the thoracolumbar region and power and control through the pelvis with each directional change. In addition, he or she should maintain a low and posteriorly oriented center of mass to optimize leverage in the hamstrings/gluteals compared with the quadriceps and reduce posterior ground reaction forces.

PSYCHOLOGICAL READINESS FOR RETURN TO PLAY

After an injury is sustained, an athlete is often subjected to a range of psychological responses in addition to the functional impairment, including stress, hesitancy, alterations in self-esteem, depression, fear of re-injury, and anxiety.^43,109-111 The aforementioned responses are often at their height in the time immediately following an injury and generally subside over time during the rehabilitation process.¹¹⁰ The rates at which athletes experience psychological distress following an injury range between 5% and 19%; the levels are comparable with patients receiving treatment for mental health illness.⁴³ However, these elements may persist, or even increase, in the later stages of the rehabilitation process as the topic of return to play is deliberated.^112,113 If these fears are left unresolved, then a significant delay can be incurred during the rehabilitation process, which might ultimately jeopardize the successful return to play.^114,115

When athletes have been cleared to return to sport, fear tends to be the most common reason for their decision to not return to play.^21,116 The persistence of fear has clinical implications and warrants close monitoring to ensure that the athlete feels adequately supported in the decision to return to sport.^117,118 Building the athlete’s confidence by addressing hesitation, lack of confidence, heightened awareness of risk or re-injury, and safe reintegration into athletic participation are important themes identified to encourage a safe return to play.⁴³ A variety of validated tools  can be integrated into an existing return-to-play decision-making algorithm (Table 2).^118-120 

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

 

Table 2. Self-Report Measurement Tools to Integrate into Return-to-Play Decision-Making Algorithm

Self-report Measurement Tools

13-item Tampa Scale for Kinesiophobia

Anterior Cruciate Ligament Return to Sport after Injury Scale (ACL-RSI)

Global Rating Scale (GRS)

International Knee Documentation Committee (IKDC) Subjective Knee Evaluation Form

Knee Injury and Osteoarthritis Outcome Score (KOOS)

Lysholm Knee Scoring Scale

Short Form-36 Health Survey (SF-36)

Subjective Patient Outcome for Return to Sport (SPORTS)

Patient Health Questionnaire-9

By integrating the necessary screening of patients for kinesiophobia and assessing patient expectations after enduring an ACL injury, clinicians may be able to identify patients who are at risk for poorer functional outcomes. A consideration of psychosocial elements such as activity avoidance, fear of movement and re-injury, loss of confidence and expectations/assumptions during the continuum of the rehabilitation process, and the decision to return to play may favorably impact the individual’s ability to safely return to sport. It is critical to address both the physical and psychosocial factors during the rehabilitation process to more optimally transition individuals back to their prior level of athleticism.

CONCLUSION

Psychosocial factors may play a role in determining a player’s readiness to return to sport, as well as a potential for re-injury. A number of tests are available for use with this patient population to identify mental deficits that may impact player performance upon return. Additionally, the CNS should be considered as a source of impairment in players with ACL injuries. Current protocols may not fully appreciate the CNS’ impact on the player’s functional outcome. Therefore, an approach that includes CNS neuromotor training with traditional musculoskeletal rehabilitation, which also incorporates cognitive and psychosocial factors, may define an improved paradigm for treating soccer athletes following an ACL injury and assessing return-to-play capability.

Soccer is the world’s most popular sport. As the sport has grown, so have the physical demands and the search for ways to edge out the competition with the use of sports science and nutrition. The demands, which include intense training, ≥90 minutes matches, congested fixtures, and travel, lead to increased energy and nutrient requirements, stress on the body, and risk of impaired sleep cycles. Identifying key areas to enhance a player’s performance is an ongoing effort because of individual differences. Moreover, new information is being discovered via research, and advancing technology to measure performance is always evolving. This article focuses on the core nutrition principles known to lay the foundation for a better soccer player. These principles are obvious for some; however, nutrition and hydration are often undervalued, leaving the individual player with the responsibility to eat right. This review addresses the most applicable nutrition-related recommendations for soccer players.

Technical, tactical, and physical skills are key factors in a soccer player’s performance. However, energy demands of matches and training sessions require adequate fuel and hydration to maximize those key factors. Athletes may need to manage carbohydrates, protein, and fat separately to achieve optimal body size and body composition, and to maximize performance.

Nutrition plays a vital role in keeping the player healthy, reducing risk of injuries, speeding up recovery, and enhancing training adaptations. Research has shown what we eat and when we eat can significantly impact skeletal muscle adaptation, inflammation, immune response, and energy metabolism. These are all essential nutrition considerations for soccer players.

ENERGY METABOLISM IN SOCCER

Understanding energy demands will help determine energy requirements: type, amount, and timing of macronutrients and micronutrients. Soccer utilizes both aerobic and anaerobic energy systems. Soccer is an intermittent team-based sport; thus, it contains various high-intensity movements, such as sprinting, jumping, dribbling, and frequent changing of direction performed in between numerous low-intensity slow movements. The high intense movements collectively account for about 30% of match play, whereas 70% is walking, jogging, and standing. Although sprinting and jumping are not a large part of the 90 minutes of match play, they have a huge impact on the outcome of the match. Distance covered in the last 15 minutes of match play decreases by 14% to 45% compared with the first 15 minutes of play.¹ Krustrup and colleagues² found muscles in the quadriceps to be empty or nearly empty of glycogen (stored carbohydrates) after match play. This phenomenon can help explain a significant decrease in sprinting, jumping, and intermittent movements toward the end of a match—energy demands that rely on glycogen as the primary fuel source. Being well-fueled and hydrated and having the ability to delay fatigue can place a team at a performance advantage.

ENERGY EXPENDITURE

Beyond training load or match intensity, a soccer player’s body composition, gender, age, and position can affect energy needs. Position differences in elite soccer players show that the greatest total distance covered is by central midfielders and wide midfielders (~12 km –13 km), whereas central defenders cover the least area of the field players (≤~10 km).^3,4 The environment can also play a role in energy expenditure. To further understand calorie needs, total daily energy expenditure in soccer players has been measured using doubly labeled water and estimated using heart rate, global positioning system, video match analysis, and activity records.^5,6 One study estimated that energy expended during a training day for elite male soccer players is between 3442 kcal and 3824 kcal.⁶ Another study using doubly labeled water concluded that mean energy expenditure of elite male soccer players is 3566 kcal over a 7-day period, which included 5 training days and 2 matches.⁷ In terms of energy expenditure for elite female soccer players, the mean values for match day, training days, and rest days were 2914, 2783, and 2213 calories, respectively.⁸

Continue to: FUELING THE SOCCER PLAYER

Depending on the match fixture, proper fueling can be a challenge due to the number of matches, travel time, and limited recovery time. Macronutrients will provide the mainstay of fuel for a player, specifically carbohydrates and fats. Carbohydrates are the preferred source of fuel for the majority of the calories consumed. Using body weight (kg) is a more current and accurate method of recommending the amount of each macronutrient an individual player should eat as compared to using a percentage of total daily calories.

• Carbohydrates: 5–10 g/kg/day
• Protein: 1.2–2.0 g/kg/day
• Fat: 0.8–1.5 g/kg/day

CARBOHYDRATE AND SOCCER PERFORMANCE

Carbohydrates are a limited supply of fuel compared with fat stores. They are an important fuel source for soccer players, as muscle glycogen is vital to performance during high intense training and match play (Table 1). Yet current research shows that a high carbohydrate intake is not required to be followed every day due to varied energy demands.⁹ This newer strategy is referred to as “training low,” allowing the athlete to train at a low-moderate intensity in a low glycogen state. The glycogen status of the muscle can alter the training adaptations through cellular changes in the mitochondria. Therefore, carbohydrate needs should reflect the work required or demand for optimal performance. However, on high-training load days or 24 hours pre-match, carbohydrate intake should be increased to maximize muscle glycogen stores. Soccer players need to consume up to 8-10 g/kg body weight during the 24 hours before a match.¹⁰ On low or rest days, carbohydrate intake should be reduced to reflect the decreased training load. For example, recent research has demonstrated potential training adaptations when muscle glycogen stores are not consistently high¹¹ or intentionally kept low depending on the training load. Adjusting carbohydrate intake to the physical demands of an athlete is a strategy called nutrition periodization.

However, if glycogen stores are not well supplied before a match >90 minutes, then the muscles and the brain will become fatigued and lead to poor performance. Glycogen depletion contributes to fatigue toward the end of a match.¹⁰ In the early 1970s, Saltin and colleagues¹² showed that players with high muscle glycogen stores (~400 mmol/kg dry wt) achieve higher movement intensities and cover more total distance than those players who start the match with low glycogen stores (~200 mmol/kg dry wt). Another study examined pre-match diets of male soccer players (65% vs 30% daily carbohydrate intake) to determine the effect on performance outcomes and glycogen concentrations. Results showed high-muscle glycogen concentrations in the 65% carbohydrate diet and a significantly higher amount of intense exercise bouts. More acutely, studies have shown a meal containing 200 to 300 grams of carbohydrates 2 to 4 hours before exercise prolongs endurance.^13-15 Ideally, consuming fast-digesting carbohydrate sources during or at half time will help maintain blood glucose concentrations and spare muscle glycogen reserves. The majority of literature shows a 6% to 8% solution of combined fast-digesting carbohydrates (ie, glucose, fructose, sucrose, or maltodextrin) at a rate of 30 to 60 g/h enhances at least 1 aspect of performance in soccer.^16-18 These performance benefits include increased running time, improved time to fatigue, and enhanced technical skills. Regarding recovery, soccer players should begin consuming carbohydrate-rich foods and beverages immediately after exhaustive training or a match to optimize glycogen reloading. Ingesting post-exercise carbohydrates stimulates muscle and liver glycogen synthesis up to tenfold compared with post-intake of no carbohydrates.¹⁹ This recovery period becomes vital when there are <8 hours between training sessions or another match, such as in youth tournaments. The form of carbohydrate, solid or liquid, can be based on preference and tolerance, as long as the source provides a large glycemic and insulin response.

An easy way to adjust daily carbohydrate intake is to schedule carbohydrate-rich foods at meals or snacks around important training sessions or before/during/after on match day. Anderson and colleagues¹⁰ looked at training loads for 1, 2, and 3 matches per week, recommending high carbohydrate intake match day minus 1, on match day, and match day plus 1 for 1 and 2 matches per week and lower carbohydrate intake on the other days. During a 3-match week, lowering carbohydrates any day of that week is not recommended. More research is needed to determine the best strategy for performance regarding carbohydrate periodization in soccer.

PROTEIN AND SOCCER PERFORMANCE

Protein is important to soccer players for muscle tissue repair, strength, bone health, and the immune system (Table 2). The American College of Sports Medicine, the Academy of Nutrition and Dietetics, and the Dietitians of Canada recommend 1.2 to 2.0 g/kg/day.²⁰ Most soccer players meet the daily protein requirements; however, the key to optimizing the total daily amount is focusing on the source/amino acid profile, timing, and amount per feeding. Consuming divided doses of protein (20 g to 40 g) every 3 to 4 hours gives the body a continuous flow of amino acids to support muscle synthesis and recovery. In terms of body size, the recommendation is 0.25 to 0.4 g/kg every 3 to 4 hours, which includes pre-training/match and post-training/match. Protein/amino acids consumed around strength training and high-intensity sessions can promote muscle adaptations, minimize tissue breakdown, and speed recovery. Soccer matches lead to significant muscle damage²¹ especially at 2 sessions/day or multiple matches in a week. Protein is not a priority during training or matches, as its role is not to provide energy, and the primary goal during soccer activities is energy production. Research supports an intake of 30 to 40 g of casein, which is a slow digesting protein, at night before bed when a strength-training session has been performed that day.^22,23

Continue to: FAT AND SOCCER PERFORMANCE

Fat is the primary source of energy at rest and at low-training intensities, such as walking or jogging for soccer players (Table 3). Besides providing slow, long-lasting energy, fat helps absorb vitamins A, D, E, and K; produce hormones; protect organs; and support the cell membrane structure. The dietary recommendations of total fat intake for athletes are similar to or slightly greater than those recommended for non-athletes. The total amount required depends on the training demands and the players’ goals. The recommended amount of dietary fat is between 20% and 35% of total daily energy intake.

The key to gaining performance benefits from dietary fat depends on the type of fat selected. Some fats in excess, such as omega-6 fatty acids and saturated fats, may promote inflammation, hinder recovery, and affect brain health. Other types can help reduce inflammation, enhance muscle recovery, and improve brain health. These types include polyunsaturated omega-3 fatty acids, which are essential for the health of the athlete, allowing for a balanced fatty acid profile.²³ Specific omega-3 fatty acids (EPA and DHA) have shown an improvement in the function of the mitochondria, enhancing energy cell metabolism. They also have potential to be highly anti-inflammatory, benefit rehabilitation during soft-tissue injury, and help decrease secondary damage from a concussion.

In addition, research shows that omega-3 may enhance the energy production of the mitochondria, resulting in less oxidative damage to the muscle cell.²⁵ More research is needed on the effects of performance on soccer players. Given the slow digestion and absorption of fats, fat intake must be limited leading up to or during training sessions or matches, which may risk gastrointestinal issues and displacement of carbohydrates. Low to moderate monounsaturated and polyunsaturated fats in a recovery meal have not been shown to inhibit muscle glycogen reloading or muscle protein synthesis.^26,27 In regard to fat intake post-match, fat is not a key nutrient of concern for muscle recovery, as it can be included in the next balanced meal.

MICRONUTRIENTS, VITAMINS, AND MINERALS

Exercise stresses many of the metabolic pathways where vitamins and minerals are required. High-level training demands may also increase the turnover rate of vitamins and minerals. As a result, greater dietary intakes of vitamins and minerals may be warranted. Soccer players at the greatest risk for poor vitamin and mineral levels are those who skip meals, who eliminate ≥1 of the food groups from their diet (such as vegans), or who consume unbalanced and highly processed foods. In soccer players, the micronutrients of concern include iron and vitamin D. In young female soccer players, calcium intake must be assessed along with adequate energy intake for optimal bone density. Vegetarians, vegans, and/or athletes who do not consume meat, eggs, and/or dairy in their diet are at risk for vitamin B12 deficiency. The key to obtaining all the vitamins and minerals an athlete will need is to eat a wide variety of nutrient-dense foods.

IRON

Iron deficiency, with or without anemia, may impair muscle function and limit exercise capacity. Adequate iron intake in athletes with iron deficiencies and/or anemia can improve exercise capacity. Iron depletion is 1 of the most common nutrient deficiencies observed among endurance athletes. Foot strike hemolysis can destroy red blood cells during activities such as running. Research has shown that 30% of professional male soccer players have ferritin levels <30 mcg/L at the end of a soccer season.²⁸ Thus, fatigue and poor recovery time place soccer players at risk of an iron imbalance.^29,30

Continue to: Landahl and colleagues...

Landahl and colleagues³¹ found that iron deficiency and iron deficiency anemia are common in female soccer players at the elite level. In their study of 28 female national soccer players, 57% had iron deficiency and 29% presented with iron deficiency anemia 6 months before the FIFA Women's World Cup. Testing hemoglobin alone is insufficient to detect relative anemia. Regular monitoring of hemoglobin and ferritin concentrations may be necessary to determine appropriate iron needs.

VITAMIN D

Vitamin D is required for optimal bone health, as it helps regulate calcium and phosphorus. Further research shows a link between vitamin D and non–bone-related functions, such as muscle health, immune support, and anti-inflammatory roles, which may be linked to performance. Soccer players with low levels of vitamin D (<30 ng/mL) may be more at risk for musculoskeletal injuries and stress fractures.³⁴ In other sports, vitamin D may enhance muscle strength; however, no association between vitamin D and muscle strength has been found in soccer players.^34,35 The geographic location of an athlete seems to be irrelevant to serum levels, as insufficient levels can be found at various latitudes.^34,36-38

Evidence has shown that vitamin D may improve athletic performance in vitamin D-depleted athletes, thereby improving vertical jumps, lowering risks of muscle injury/strains and stress fractures, and reducing risk of colds/flu. In 2013, researchers showed for the first time a link between vitamin D and muscle aerobic metabolism by studying the energy efficiency of the mitochondria.³² Athletes with low vitamin D levels increased their ATP production within the muscle with vitamin D supplementation over 10 weeks to 12 weeks.³³

CALCIUM

Soccer players present with stronger and denser bones than non-athletes due to running and jumping in their sport. Weight-bearing sites such as lumbar spine, hip, femoral neck, trochanter, intertrochanteric region, and both legs are sensitive to the impact of soccer movements.³⁹ Calcium and vitamin D are also important for muscle contraction.

Given the variation in genetics, sports, and gender, optimal performance requires a healthy eating plan tailored to the individual athlete. A healthy eating plan allows an athlete to train longer and harder, delay the onset of fatigue, and speed recovery. Nutrition supports optimal performance through real food, proper hydration, nutrient timing, and supplementation.

Continue to: FLUID REQUIREMENTS FOR SOCCER PLAYERS

Many athletes overlook the importance of hydration on performance, either assuming they are hydrated or they miscalculate fluid and electrolyte needs to actual sweat losses. Numerous factors play a part in optimal hydration such as sweat rate, environment, training intensity, duration, body size, and body composition. Soccer players have fewer breaks to consume fluids during a match compared with basketball, baseball, or American football players. These breaks include a 15-minute half between coming off the pitch to the locker room and back, as well as time spent with coaches reviewing strategies; this short window of time must be maximized to rehydrate. Fluids with a carbohydrate concentration of 4% to 8% at 5 to 10 ounces and breaks every 15 to 20 minutes are optimal to maximize uptake while avoiding gastric intolerance.

Studies have shown that most players do not drink sufficiently during a match to optimize hydration, replacing only ~40% to 45% of their sweat losses.^{40, 41} Maughan and colleagues measured high levels of urine osmolality in some soccer players, thereby indicating that the players started their training session dehydrated.⁴¹ Soccer players must begin training or a match well hydrated due to the limited opportunities after kick-off. The athlete should drink at least 4 hours prior to exercise; if no urine is produced or urine is dark in color, then the athlete should drink again 2 hours prior.

Changes in body mass, urine color, and thirst offer clues to the need for rehydration. Advanced hydration measurement includes testing urine specific gravity (USG) values. For example, testing pre-training or pre-match can be conducted to determine hydration status and trending changes from day to day. A USG value >1.020 is considered dehydrated in accordance with the NATA position statement.⁴² Calculating a sweat rate is a practical approach to determining individual hydration needs (see Table 4). Sweat rates will vary between soccer players based on their position and intensity of play, along with total match time.³⁹ Soccer players will lose ~1.5 to 4.5 liters during match play.^43-46 In general, athletes, including soccer players, should limit body weight loss to ≤2% to 3% to maintain performance. Studies have shown that >2% body mass loss can hinder soccer-specific performance, such as dribbling skills and intermittent high intensity sprinting.^49-51) Table 5 outlines the detrimental effects dehydration has on performance. Urine-specific gravity values between 1.021 and 1.030 may reflect 3% to 5% change in body weight.

ELECTROLYTES

Sodium is the primary electrolyte lost in sweat. Other electrolytes (potassium, magnesium, and calcium) are lost at much lower levels and typically replaced through diet. Soccer players can lose large amounts of sodium; between 700 and 1500 mg of sodium/L of sweat has been reported in several studies.^42-44 Studies of professional male soccer players have shown potassium losses in the range of 165 mg/L to 234 mg/L.^42,51,52 Sodium in a sports drink or in food aids with water uptake from the intestines and enhances the thirst mechanism in the brain, resulting in additional fluid being retained in the body.

REHYDRATION AFTER TRAINING OR COMPETITION

Within 2 hours after training or competition, the rehydration strategy should provide water to restore body fluid status, carbohydrates to replenish glycogen (fuel) stores, and electrolytes to speed rehydration (Table 6). The volume of fluids and type of fluids over the next 24 hours dictate the hydration status prior to the next day’s training session. It is a continuous cycle. Over time, an athlete increases the risk of being in a chronic dehydrated state, resulting in lack of motivation, risk of injury, and illness, fatigue, and poor performance. The current recommendation is to drink ~50% more in volume than the amount of weight lost, such as 22 to 24 ounces/pound lost.⁵²

Soccer is the world’s most popular sport. As the sport has grown, so have the physical demands and the search for ways to edge out the competition with the use of sports science and nutrition. The demands, which include intense training, ≥90 minutes matches, congested fixtures, and travel, lead to increased energy and nutrient requirements, stress on the body, and risk of impaired sleep cycles. Identifying key areas to enhance a player’s performance is an ongoing effort because of individual differences. Moreover, new information is being discovered via research, and advancing technology to measure performance is always evolving. This article focuses on the core nutrition principles known to lay the foundation for a better soccer player. These principles are obvious for some; however, nutrition and hydration are often undervalued, leaving the individual player with the responsibility to eat right. This review addresses the most applicable nutrition-related recommendations for soccer players.

Technical, tactical, and physical skills are key factors in a soccer player’s performance. However, energy demands of matches and training sessions require adequate fuel and hydration to maximize those key factors. Athletes may need to manage carbohydrates, protein, and fat separately to achieve optimal body size and body composition, and to maximize performance.

Nutrition plays a vital role in keeping the player healthy, reducing risk of injuries, speeding up recovery, and enhancing training adaptations. Research has shown what we eat and when we eat can significantly impact skeletal muscle adaptation, inflammation, immune response, and energy metabolism. These are all essential nutrition considerations for soccer players.

ENERGY METABOLISM IN SOCCER

Understanding energy demands will help determine energy requirements: type, amount, and timing of macronutrients and micronutrients. Soccer utilizes both aerobic and anaerobic energy systems. Soccer is an intermittent team-based sport; thus, it contains various high-intensity movements, such as sprinting, jumping, dribbling, and frequent changing of direction performed in between numerous low-intensity slow movements. The high intense movements collectively account for about 30% of match play, whereas 70% is walking, jogging, and standing. Although sprinting and jumping are not a large part of the 90 minutes of match play, they have a huge impact on the outcome of the match. Distance covered in the last 15 minutes of match play decreases by 14% to 45% compared with the first 15 minutes of play.¹ Krustrup and colleagues² found muscles in the quadriceps to be empty or nearly empty of glycogen (stored carbohydrates) after match play. This phenomenon can help explain a significant decrease in sprinting, jumping, and intermittent movements toward the end of a match—energy demands that rely on glycogen as the primary fuel source. Being well-fueled and hydrated and having the ability to delay fatigue can place a team at a performance advantage.

ENERGY EXPENDITURE

Beyond training load or match intensity, a soccer player’s body composition, gender, age, and position can affect energy needs. Position differences in elite soccer players show that the greatest total distance covered is by central midfielders and wide midfielders (~12 km –13 km), whereas central defenders cover the least area of the field players (≤~10 km).^3,4 The environment can also play a role in energy expenditure. To further understand calorie needs, total daily energy expenditure in soccer players has been measured using doubly labeled water and estimated using heart rate, global positioning system, video match analysis, and activity records.^5,6 One study estimated that energy expended during a training day for elite male soccer players is between 3442 kcal and 3824 kcal.⁶ Another study using doubly labeled water concluded that mean energy expenditure of elite male soccer players is 3566 kcal over a 7-day period, which included 5 training days and 2 matches.⁷ In terms of energy expenditure for elite female soccer players, the mean values for match day, training days, and rest days were 2914, 2783, and 2213 calories, respectively.⁸

Continue to: FUELING THE SOCCER PLAYER

Depending on the match fixture, proper fueling can be a challenge due to the number of matches, travel time, and limited recovery time. Macronutrients will provide the mainstay of fuel for a player, specifically carbohydrates and fats. Carbohydrates are the preferred source of fuel for the majority of the calories consumed. Using body weight (kg) is a more current and accurate method of recommending the amount of each macronutrient an individual player should eat as compared to using a percentage of total daily calories.

• Carbohydrates: 5–10 g/kg/day
• Protein: 1.2–2.0 g/kg/day
• Fat: 0.8–1.5 g/kg/day

CARBOHYDRATE AND SOCCER PERFORMANCE

Carbohydrates are a limited supply of fuel compared with fat stores. They are an important fuel source for soccer players, as muscle glycogen is vital to performance during high intense training and match play (Table 1). Yet current research shows that a high carbohydrate intake is not required to be followed every day due to varied energy demands.⁹ This newer strategy is referred to as “training low,” allowing the athlete to train at a low-moderate intensity in a low glycogen state. The glycogen status of the muscle can alter the training adaptations through cellular changes in the mitochondria. Therefore, carbohydrate needs should reflect the work required or demand for optimal performance. However, on high-training load days or 24 hours pre-match, carbohydrate intake should be increased to maximize muscle glycogen stores. Soccer players need to consume up to 8-10 g/kg body weight during the 24 hours before a match.¹⁰ On low or rest days, carbohydrate intake should be reduced to reflect the decreased training load. For example, recent research has demonstrated potential training adaptations when muscle glycogen stores are not consistently high¹¹ or intentionally kept low depending on the training load. Adjusting carbohydrate intake to the physical demands of an athlete is a strategy called nutrition periodization.

However, if glycogen stores are not well supplied before a match >90 minutes, then the muscles and the brain will become fatigued and lead to poor performance. Glycogen depletion contributes to fatigue toward the end of a match.¹⁰ In the early 1970s, Saltin and colleagues¹² showed that players with high muscle glycogen stores (~400 mmol/kg dry wt) achieve higher movement intensities and cover more total distance than those players who start the match with low glycogen stores (~200 mmol/kg dry wt). Another study examined pre-match diets of male soccer players (65% vs 30% daily carbohydrate intake) to determine the effect on performance outcomes and glycogen concentrations. Results showed high-muscle glycogen concentrations in the 65% carbohydrate diet and a significantly higher amount of intense exercise bouts. More acutely, studies have shown a meal containing 200 to 300 grams of carbohydrates 2 to 4 hours before exercise prolongs endurance.^13-15 Ideally, consuming fast-digesting carbohydrate sources during or at half time will help maintain blood glucose concentrations and spare muscle glycogen reserves. The majority of literature shows a 6% to 8% solution of combined fast-digesting carbohydrates (ie, glucose, fructose, sucrose, or maltodextrin) at a rate of 30 to 60 g/h enhances at least 1 aspect of performance in soccer.^16-18 These performance benefits include increased running time, improved time to fatigue, and enhanced technical skills. Regarding recovery, soccer players should begin consuming carbohydrate-rich foods and beverages immediately after exhaustive training or a match to optimize glycogen reloading. Ingesting post-exercise carbohydrates stimulates muscle and liver glycogen synthesis up to tenfold compared with post-intake of no carbohydrates.¹⁹ This recovery period becomes vital when there are <8 hours between training sessions or another match, such as in youth tournaments. The form of carbohydrate, solid or liquid, can be based on preference and tolerance, as long as the source provides a large glycemic and insulin response.

An easy way to adjust daily carbohydrate intake is to schedule carbohydrate-rich foods at meals or snacks around important training sessions or before/during/after on match day. Anderson and colleagues¹⁰ looked at training loads for 1, 2, and 3 matches per week, recommending high carbohydrate intake match day minus 1, on match day, and match day plus 1 for 1 and 2 matches per week and lower carbohydrate intake on the other days. During a 3-match week, lowering carbohydrates any day of that week is not recommended. More research is needed to determine the best strategy for performance regarding carbohydrate periodization in soccer.

PROTEIN AND SOCCER PERFORMANCE

Protein is important to soccer players for muscle tissue repair, strength, bone health, and the immune system (Table 2). The American College of Sports Medicine, the Academy of Nutrition and Dietetics, and the Dietitians of Canada recommend 1.2 to 2.0 g/kg/day.²⁰ Most soccer players meet the daily protein requirements; however, the key to optimizing the total daily amount is focusing on the source/amino acid profile, timing, and amount per feeding. Consuming divided doses of protein (20 g to 40 g) every 3 to 4 hours gives the body a continuous flow of amino acids to support muscle synthesis and recovery. In terms of body size, the recommendation is 0.25 to 0.4 g/kg every 3 to 4 hours, which includes pre-training/match and post-training/match. Protein/amino acids consumed around strength training and high-intensity sessions can promote muscle adaptations, minimize tissue breakdown, and speed recovery. Soccer matches lead to significant muscle damage²¹ especially at 2 sessions/day or multiple matches in a week. Protein is not a priority during training or matches, as its role is not to provide energy, and the primary goal during soccer activities is energy production. Research supports an intake of 30 to 40 g of casein, which is a slow digesting protein, at night before bed when a strength-training session has been performed that day.^22,23

Continue to: FAT AND SOCCER PERFORMANCE

Fat is the primary source of energy at rest and at low-training intensities, such as walking or jogging for soccer players (Table 3). Besides providing slow, long-lasting energy, fat helps absorb vitamins A, D, E, and K; produce hormones; protect organs; and support the cell membrane structure. The dietary recommendations of total fat intake for athletes are similar to or slightly greater than those recommended for non-athletes. The total amount required depends on the training demands and the players’ goals. The recommended amount of dietary fat is between 20% and 35% of total daily energy intake.

The key to gaining performance benefits from dietary fat depends on the type of fat selected. Some fats in excess, such as omega-6 fatty acids and saturated fats, may promote inflammation, hinder recovery, and affect brain health. Other types can help reduce inflammation, enhance muscle recovery, and improve brain health. These types include polyunsaturated omega-3 fatty acids, which are essential for the health of the athlete, allowing for a balanced fatty acid profile.²³ Specific omega-3 fatty acids (EPA and DHA) have shown an improvement in the function of the mitochondria, enhancing energy cell metabolism. They also have potential to be highly anti-inflammatory, benefit rehabilitation during soft-tissue injury, and help decrease secondary damage from a concussion.

In addition, research shows that omega-3 may enhance the energy production of the mitochondria, resulting in less oxidative damage to the muscle cell.²⁵ More research is needed on the effects of performance on soccer players. Given the slow digestion and absorption of fats, fat intake must be limited leading up to or during training sessions or matches, which may risk gastrointestinal issues and displacement of carbohydrates. Low to moderate monounsaturated and polyunsaturated fats in a recovery meal have not been shown to inhibit muscle glycogen reloading or muscle protein synthesis.^26,27 In regard to fat intake post-match, fat is not a key nutrient of concern for muscle recovery, as it can be included in the next balanced meal.

MICRONUTRIENTS, VITAMINS, AND MINERALS

Exercise stresses many of the metabolic pathways where vitamins and minerals are required. High-level training demands may also increase the turnover rate of vitamins and minerals. As a result, greater dietary intakes of vitamins and minerals may be warranted. Soccer players at the greatest risk for poor vitamin and mineral levels are those who skip meals, who eliminate ≥1 of the food groups from their diet (such as vegans), or who consume unbalanced and highly processed foods. In soccer players, the micronutrients of concern include iron and vitamin D. In young female soccer players, calcium intake must be assessed along with adequate energy intake for optimal bone density. Vegetarians, vegans, and/or athletes who do not consume meat, eggs, and/or dairy in their diet are at risk for vitamin B12 deficiency. The key to obtaining all the vitamins and minerals an athlete will need is to eat a wide variety of nutrient-dense foods.

IRON

Iron deficiency, with or without anemia, may impair muscle function and limit exercise capacity. Adequate iron intake in athletes with iron deficiencies and/or anemia can improve exercise capacity. Iron depletion is 1 of the most common nutrient deficiencies observed among endurance athletes. Foot strike hemolysis can destroy red blood cells during activities such as running. Research has shown that 30% of professional male soccer players have ferritin levels <30 mcg/L at the end of a soccer season.²⁸ Thus, fatigue and poor recovery time place soccer players at risk of an iron imbalance.^29,30

Continue to: Landahl and colleagues...

Landahl and colleagues³¹ found that iron deficiency and iron deficiency anemia are common in female soccer players at the elite level. In their study of 28 female national soccer players, 57% had iron deficiency and 29% presented with iron deficiency anemia 6 months before the FIFA Women's World Cup. Testing hemoglobin alone is insufficient to detect relative anemia. Regular monitoring of hemoglobin and ferritin concentrations may be necessary to determine appropriate iron needs.

VITAMIN D

Vitamin D is required for optimal bone health, as it helps regulate calcium and phosphorus. Further research shows a link between vitamin D and non–bone-related functions, such as muscle health, immune support, and anti-inflammatory roles, which may be linked to performance. Soccer players with low levels of vitamin D (<30 ng/mL) may be more at risk for musculoskeletal injuries and stress fractures.³⁴ In other sports, vitamin D may enhance muscle strength; however, no association between vitamin D and muscle strength has been found in soccer players.^34,35 The geographic location of an athlete seems to be irrelevant to serum levels, as insufficient levels can be found at various latitudes.^34,36-38

Evidence has shown that vitamin D may improve athletic performance in vitamin D-depleted athletes, thereby improving vertical jumps, lowering risks of muscle injury/strains and stress fractures, and reducing risk of colds/flu. In 2013, researchers showed for the first time a link between vitamin D and muscle aerobic metabolism by studying the energy efficiency of the mitochondria.³² Athletes with low vitamin D levels increased their ATP production within the muscle with vitamin D supplementation over 10 weeks to 12 weeks.³³

CALCIUM

Soccer players present with stronger and denser bones than non-athletes due to running and jumping in their sport. Weight-bearing sites such as lumbar spine, hip, femoral neck, trochanter, intertrochanteric region, and both legs are sensitive to the impact of soccer movements.³⁹ Calcium and vitamin D are also important for muscle contraction.

Given the variation in genetics, sports, and gender, optimal performance requires a healthy eating plan tailored to the individual athlete. A healthy eating plan allows an athlete to train longer and harder, delay the onset of fatigue, and speed recovery. Nutrition supports optimal performance through real food, proper hydration, nutrient timing, and supplementation.

Continue to: FLUID REQUIREMENTS FOR SOCCER PLAYERS

Many athletes overlook the importance of hydration on performance, either assuming they are hydrated or they miscalculate fluid and electrolyte needs to actual sweat losses. Numerous factors play a part in optimal hydration such as sweat rate, environment, training intensity, duration, body size, and body composition. Soccer players have fewer breaks to consume fluids during a match compared with basketball, baseball, or American football players. These breaks include a 15-minute half between coming off the pitch to the locker room and back, as well as time spent with coaches reviewing strategies; this short window of time must be maximized to rehydrate. Fluids with a carbohydrate concentration of 4% to 8% at 5 to 10 ounces and breaks every 15 to 20 minutes are optimal to maximize uptake while avoiding gastric intolerance.

Studies have shown that most players do not drink sufficiently during a match to optimize hydration, replacing only ~40% to 45% of their sweat losses.^{40, 41} Maughan and colleagues measured high levels of urine osmolality in some soccer players, thereby indicating that the players started their training session dehydrated.⁴¹ Soccer players must begin training or a match well hydrated due to the limited opportunities after kick-off. The athlete should drink at least 4 hours prior to exercise; if no urine is produced or urine is dark in color, then the athlete should drink again 2 hours prior.

Changes in body mass, urine color, and thirst offer clues to the need for rehydration. Advanced hydration measurement includes testing urine specific gravity (USG) values. For example, testing pre-training or pre-match can be conducted to determine hydration status and trending changes from day to day. A USG value >1.020 is considered dehydrated in accordance with the NATA position statement.⁴² Calculating a sweat rate is a practical approach to determining individual hydration needs (see Table 4). Sweat rates will vary between soccer players based on their position and intensity of play, along with total match time.³⁹ Soccer players will lose ~1.5 to 4.5 liters during match play.^43-46 In general, athletes, including soccer players, should limit body weight loss to ≤2% to 3% to maintain performance. Studies have shown that >2% body mass loss can hinder soccer-specific performance, such as dribbling skills and intermittent high intensity sprinting.^49-51) Table 5 outlines the detrimental effects dehydration has on performance. Urine-specific gravity values between 1.021 and 1.030 may reflect 3% to 5% change in body weight.

ELECTROLYTES

Sodium is the primary electrolyte lost in sweat. Other electrolytes (potassium, magnesium, and calcium) are lost at much lower levels and typically replaced through diet. Soccer players can lose large amounts of sodium; between 700 and 1500 mg of sodium/L of sweat has been reported in several studies.^42-44 Studies of professional male soccer players have shown potassium losses in the range of 165 mg/L to 234 mg/L.^42,51,52 Sodium in a sports drink or in food aids with water uptake from the intestines and enhances the thirst mechanism in the brain, resulting in additional fluid being retained in the body.

REHYDRATION AFTER TRAINING OR COMPETITION

Within 2 hours after training or competition, the rehydration strategy should provide water to restore body fluid status, carbohydrates to replenish glycogen (fuel) stores, and electrolytes to speed rehydration (Table 6). The volume of fluids and type of fluids over the next 24 hours dictate the hydration status prior to the next day’s training session. It is a continuous cycle. Over time, an athlete increases the risk of being in a chronic dehydrated state, resulting in lack of motivation, risk of injury, and illness, fatigue, and poor performance. The current recommendation is to drink ~50% more in volume than the amount of weight lost, such as 22 to 24 ounces/pound lost.⁵²

Soccer is the world’s most popular sport. As the sport has grown, so have the physical demands and the search for ways to edge out the competition with the use of sports science and nutrition. The demands, which include intense training, ≥90 minutes matches, congested fixtures, and travel, lead to increased energy and nutrient requirements, stress on the body, and risk of impaired sleep cycles. Identifying key areas to enhance a player’s performance is an ongoing effort because of individual differences. Moreover, new information is being discovered via research, and advancing technology to measure performance is always evolving. This article focuses on the core nutrition principles known to lay the foundation for a better soccer player. These principles are obvious for some; however, nutrition and hydration are often undervalued, leaving the individual player with the responsibility to eat right. This review addresses the most applicable nutrition-related recommendations for soccer players.

Technical, tactical, and physical skills are key factors in a soccer player’s performance. However, energy demands of matches and training sessions require adequate fuel and hydration to maximize those key factors. Athletes may need to manage carbohydrates, protein, and fat separately to achieve optimal body size and body composition, and to maximize performance.

Nutrition plays a vital role in keeping the player healthy, reducing risk of injuries, speeding up recovery, and enhancing training adaptations. Research has shown what we eat and when we eat can significantly impact skeletal muscle adaptation, inflammation, immune response, and energy metabolism. These are all essential nutrition considerations for soccer players.

ENERGY METABOLISM IN SOCCER

Understanding energy demands will help determine energy requirements: type, amount, and timing of macronutrients and micronutrients. Soccer utilizes both aerobic and anaerobic energy systems. Soccer is an intermittent team-based sport; thus, it contains various high-intensity movements, such as sprinting, jumping, dribbling, and frequent changing of direction performed in between numerous low-intensity slow movements. The high intense movements collectively account for about 30% of match play, whereas 70% is walking, jogging, and standing. Although sprinting and jumping are not a large part of the 90 minutes of match play, they have a huge impact on the outcome of the match. Distance covered in the last 15 minutes of match play decreases by 14% to 45% compared with the first 15 minutes of play.¹ Krustrup and colleagues² found muscles in the quadriceps to be empty or nearly empty of glycogen (stored carbohydrates) after match play. This phenomenon can help explain a significant decrease in sprinting, jumping, and intermittent movements toward the end of a match—energy demands that rely on glycogen as the primary fuel source. Being well-fueled and hydrated and having the ability to delay fatigue can place a team at a performance advantage.

ENERGY EXPENDITURE

Beyond training load or match intensity, a soccer player’s body composition, gender, age, and position can affect energy needs. Position differences in elite soccer players show that the greatest total distance covered is by central midfielders and wide midfielders (~12 km –13 km), whereas central defenders cover the least area of the field players (≤~10 km).^3,4 The environment can also play a role in energy expenditure. To further understand calorie needs, total daily energy expenditure in soccer players has been measured using doubly labeled water and estimated using heart rate, global positioning system, video match analysis, and activity records.^5,6 One study estimated that energy expended during a training day for elite male soccer players is between 3442 kcal and 3824 kcal.⁶ Another study using doubly labeled water concluded that mean energy expenditure of elite male soccer players is 3566 kcal over a 7-day period, which included 5 training days and 2 matches.⁷ In terms of energy expenditure for elite female soccer players, the mean values for match day, training days, and rest days were 2914, 2783, and 2213 calories, respectively.⁸

Continue to: FUELING THE SOCCER PLAYER

Depending on the match fixture, proper fueling can be a challenge due to the number of matches, travel time, and limited recovery time. Macronutrients will provide the mainstay of fuel for a player, specifically carbohydrates and fats. Carbohydrates are the preferred source of fuel for the majority of the calories consumed. Using body weight (kg) is a more current and accurate method of recommending the amount of each macronutrient an individual player should eat as compared to using a percentage of total daily calories.

• Carbohydrates: 5–10 g/kg/day
• Protein: 1.2–2.0 g/kg/day
• Fat: 0.8–1.5 g/kg/day

CARBOHYDRATE AND SOCCER PERFORMANCE

Carbohydrates are a limited supply of fuel compared with fat stores. They are an important fuel source for soccer players, as muscle glycogen is vital to performance during high intense training and match play (Table 1). Yet current research shows that a high carbohydrate intake is not required to be followed every day due to varied energy demands.⁹ This newer strategy is referred to as “training low,” allowing the athlete to train at a low-moderate intensity in a low glycogen state. The glycogen status of the muscle can alter the training adaptations through cellular changes in the mitochondria. Therefore, carbohydrate needs should reflect the work required or demand for optimal performance. However, on high-training load days or 24 hours pre-match, carbohydrate intake should be increased to maximize muscle glycogen stores. Soccer players need to consume up to 8-10 g/kg body weight during the 24 hours before a match.¹⁰ On low or rest days, carbohydrate intake should be reduced to reflect the decreased training load. For example, recent research has demonstrated potential training adaptations when muscle glycogen stores are not consistently high¹¹ or intentionally kept low depending on the training load. Adjusting carbohydrate intake to the physical demands of an athlete is a strategy called nutrition periodization.

However, if glycogen stores are not well supplied before a match >90 minutes, then the muscles and the brain will become fatigued and lead to poor performance. Glycogen depletion contributes to fatigue toward the end of a match.¹⁰ In the early 1970s, Saltin and colleagues¹² showed that players with high muscle glycogen stores (~400 mmol/kg dry wt) achieve higher movement intensities and cover more total distance than those players who start the match with low glycogen stores (~200 mmol/kg dry wt). Another study examined pre-match diets of male soccer players (65% vs 30% daily carbohydrate intake) to determine the effect on performance outcomes and glycogen concentrations. Results showed high-muscle glycogen concentrations in the 65% carbohydrate diet and a significantly higher amount of intense exercise bouts. More acutely, studies have shown a meal containing 200 to 300 grams of carbohydrates 2 to 4 hours before exercise prolongs endurance.^13-15 Ideally, consuming fast-digesting carbohydrate sources during or at half time will help maintain blood glucose concentrations and spare muscle glycogen reserves. The majority of literature shows a 6% to 8% solution of combined fast-digesting carbohydrates (ie, glucose, fructose, sucrose, or maltodextrin) at a rate of 30 to 60 g/h enhances at least 1 aspect of performance in soccer.^16-18 These performance benefits include increased running time, improved time to fatigue, and enhanced technical skills. Regarding recovery, soccer players should begin consuming carbohydrate-rich foods and beverages immediately after exhaustive training or a match to optimize glycogen reloading. Ingesting post-exercise carbohydrates stimulates muscle and liver glycogen synthesis up to tenfold compared with post-intake of no carbohydrates.¹⁹ This recovery period becomes vital when there are <8 hours between training sessions or another match, such as in youth tournaments. The form of carbohydrate, solid or liquid, can be based on preference and tolerance, as long as the source provides a large glycemic and insulin response.

An easy way to adjust daily carbohydrate intake is to schedule carbohydrate-rich foods at meals or snacks around important training sessions or before/during/after on match day. Anderson and colleagues¹⁰ looked at training loads for 1, 2, and 3 matches per week, recommending high carbohydrate intake match day minus 1, on match day, and match day plus 1 for 1 and 2 matches per week and lower carbohydrate intake on the other days. During a 3-match week, lowering carbohydrates any day of that week is not recommended. More research is needed to determine the best strategy for performance regarding carbohydrate periodization in soccer.

PROTEIN AND SOCCER PERFORMANCE

Protein is important to soccer players for muscle tissue repair, strength, bone health, and the immune system (Table 2). The American College of Sports Medicine, the Academy of Nutrition and Dietetics, and the Dietitians of Canada recommend 1.2 to 2.0 g/kg/day.²⁰ Most soccer players meet the daily protein requirements; however, the key to optimizing the total daily amount is focusing on the source/amino acid profile, timing, and amount per feeding. Consuming divided doses of protein (20 g to 40 g) every 3 to 4 hours gives the body a continuous flow of amino acids to support muscle synthesis and recovery. In terms of body size, the recommendation is 0.25 to 0.4 g/kg every 3 to 4 hours, which includes pre-training/match and post-training/match. Protein/amino acids consumed around strength training and high-intensity sessions can promote muscle adaptations, minimize tissue breakdown, and speed recovery. Soccer matches lead to significant muscle damage²¹ especially at 2 sessions/day or multiple matches in a week. Protein is not a priority during training or matches, as its role is not to provide energy, and the primary goal during soccer activities is energy production. Research supports an intake of 30 to 40 g of casein, which is a slow digesting protein, at night before bed when a strength-training session has been performed that day.^22,23

Continue to: FAT AND SOCCER PERFORMANCE

Fat is the primary source of energy at rest and at low-training intensities, such as walking or jogging for soccer players (Table 3). Besides providing slow, long-lasting energy, fat helps absorb vitamins A, D, E, and K; produce hormones; protect organs; and support the cell membrane structure. The dietary recommendations of total fat intake for athletes are similar to or slightly greater than those recommended for non-athletes. The total amount required depends on the training demands and the players’ goals. The recommended amount of dietary fat is between 20% and 35% of total daily energy intake.

The key to gaining performance benefits from dietary fat depends on the type of fat selected. Some fats in excess, such as omega-6 fatty acids and saturated fats, may promote inflammation, hinder recovery, and affect brain health. Other types can help reduce inflammation, enhance muscle recovery, and improve brain health. These types include polyunsaturated omega-3 fatty acids, which are essential for the health of the athlete, allowing for a balanced fatty acid profile.²³ Specific omega-3 fatty acids (EPA and DHA) have shown an improvement in the function of the mitochondria, enhancing energy cell metabolism. They also have potential to be highly anti-inflammatory, benefit rehabilitation during soft-tissue injury, and help decrease secondary damage from a concussion.

In addition, research shows that omega-3 may enhance the energy production of the mitochondria, resulting in less oxidative damage to the muscle cell.²⁵ More research is needed on the effects of performance on soccer players. Given the slow digestion and absorption of fats, fat intake must be limited leading up to or during training sessions or matches, which may risk gastrointestinal issues and displacement of carbohydrates. Low to moderate monounsaturated and polyunsaturated fats in a recovery meal have not been shown to inhibit muscle glycogen reloading or muscle protein synthesis.^26,27 In regard to fat intake post-match, fat is not a key nutrient of concern for muscle recovery, as it can be included in the next balanced meal.

MICRONUTRIENTS, VITAMINS, AND MINERALS

Exercise stresses many of the metabolic pathways where vitamins and minerals are required. High-level training demands may also increase the turnover rate of vitamins and minerals. As a result, greater dietary intakes of vitamins and minerals may be warranted. Soccer players at the greatest risk for poor vitamin and mineral levels are those who skip meals, who eliminate ≥1 of the food groups from their diet (such as vegans), or who consume unbalanced and highly processed foods. In soccer players, the micronutrients of concern include iron and vitamin D. In young female soccer players, calcium intake must be assessed along with adequate energy intake for optimal bone density. Vegetarians, vegans, and/or athletes who do not consume meat, eggs, and/or dairy in their diet are at risk for vitamin B12 deficiency. The key to obtaining all the vitamins and minerals an athlete will need is to eat a wide variety of nutrient-dense foods.

IRON

Iron deficiency, with or without anemia, may impair muscle function and limit exercise capacity. Adequate iron intake in athletes with iron deficiencies and/or anemia can improve exercise capacity. Iron depletion is 1 of the most common nutrient deficiencies observed among endurance athletes. Foot strike hemolysis can destroy red blood cells during activities such as running. Research has shown that 30% of professional male soccer players have ferritin levels <30 mcg/L at the end of a soccer season.²⁸ Thus, fatigue and poor recovery time place soccer players at risk of an iron imbalance.^29,30

Continue to: Landahl and colleagues...

Landahl and colleagues³¹ found that iron deficiency and iron deficiency anemia are common in female soccer players at the elite level. In their study of 28 female national soccer players, 57% had iron deficiency and 29% presented with iron deficiency anemia 6 months before the FIFA Women's World Cup. Testing hemoglobin alone is insufficient to detect relative anemia. Regular monitoring of hemoglobin and ferritin concentrations may be necessary to determine appropriate iron needs.

VITAMIN D

Vitamin D is required for optimal bone health, as it helps regulate calcium and phosphorus. Further research shows a link between vitamin D and non–bone-related functions, such as muscle health, immune support, and anti-inflammatory roles, which may be linked to performance. Soccer players with low levels of vitamin D (<30 ng/mL) may be more at risk for musculoskeletal injuries and stress fractures.³⁴ In other sports, vitamin D may enhance muscle strength; however, no association between vitamin D and muscle strength has been found in soccer players.^34,35 The geographic location of an athlete seems to be irrelevant to serum levels, as insufficient levels can be found at various latitudes.^34,36-38

Evidence has shown that vitamin D may improve athletic performance in vitamin D-depleted athletes, thereby improving vertical jumps, lowering risks of muscle injury/strains and stress fractures, and reducing risk of colds/flu. In 2013, researchers showed for the first time a link between vitamin D and muscle aerobic metabolism by studying the energy efficiency of the mitochondria.³² Athletes with low vitamin D levels increased their ATP production within the muscle with vitamin D supplementation over 10 weeks to 12 weeks.³³

CALCIUM

Soccer players present with stronger and denser bones than non-athletes due to running and jumping in their sport. Weight-bearing sites such as lumbar spine, hip, femoral neck, trochanter, intertrochanteric region, and both legs are sensitive to the impact of soccer movements.³⁹ Calcium and vitamin D are also important for muscle contraction.

Given the variation in genetics, sports, and gender, optimal performance requires a healthy eating plan tailored to the individual athlete. A healthy eating plan allows an athlete to train longer and harder, delay the onset of fatigue, and speed recovery. Nutrition supports optimal performance through real food, proper hydration, nutrient timing, and supplementation.

Continue to: FLUID REQUIREMENTS FOR SOCCER PLAYERS

Many athletes overlook the importance of hydration on performance, either assuming they are hydrated or they miscalculate fluid and electrolyte needs to actual sweat losses. Numerous factors play a part in optimal hydration such as sweat rate, environment, training intensity, duration, body size, and body composition. Soccer players have fewer breaks to consume fluids during a match compared with basketball, baseball, or American football players. These breaks include a 15-minute half between coming off the pitch to the locker room and back, as well as time spent with coaches reviewing strategies; this short window of time must be maximized to rehydrate. Fluids with a carbohydrate concentration of 4% to 8% at 5 to 10 ounces and breaks every 15 to 20 minutes are optimal to maximize uptake while avoiding gastric intolerance.

Studies have shown that most players do not drink sufficiently during a match to optimize hydration, replacing only ~40% to 45% of their sweat losses.^{40, 41} Maughan and colleagues measured high levels of urine osmolality in some soccer players, thereby indicating that the players started their training session dehydrated.⁴¹ Soccer players must begin training or a match well hydrated due to the limited opportunities after kick-off. The athlete should drink at least 4 hours prior to exercise; if no urine is produced or urine is dark in color, then the athlete should drink again 2 hours prior.

Changes in body mass, urine color, and thirst offer clues to the need for rehydration. Advanced hydration measurement includes testing urine specific gravity (USG) values. For example, testing pre-training or pre-match can be conducted to determine hydration status and trending changes from day to day. A USG value >1.020 is considered dehydrated in accordance with the NATA position statement.⁴² Calculating a sweat rate is a practical approach to determining individual hydration needs (see Table 4). Sweat rates will vary between soccer players based on their position and intensity of play, along with total match time.³⁹ Soccer players will lose ~1.5 to 4.5 liters during match play.^43-46 In general, athletes, including soccer players, should limit body weight loss to ≤2% to 3% to maintain performance. Studies have shown that >2% body mass loss can hinder soccer-specific performance, such as dribbling skills and intermittent high intensity sprinting.^49-51) Table 5 outlines the detrimental effects dehydration has on performance. Urine-specific gravity values between 1.021 and 1.030 may reflect 3% to 5% change in body weight.

ELECTROLYTES

Sodium is the primary electrolyte lost in sweat. Other electrolytes (potassium, magnesium, and calcium) are lost at much lower levels and typically replaced through diet. Soccer players can lose large amounts of sodium; between 700 and 1500 mg of sodium/L of sweat has been reported in several studies.^42-44 Studies of professional male soccer players have shown potassium losses in the range of 165 mg/L to 234 mg/L.^42,51,52 Sodium in a sports drink or in food aids with water uptake from the intestines and enhances the thirst mechanism in the brain, resulting in additional fluid being retained in the body.

REHYDRATION AFTER TRAINING OR COMPETITION

Within 2 hours after training or competition, the rehydration strategy should provide water to restore body fluid status, carbohydrates to replenish glycogen (fuel) stores, and electrolytes to speed rehydration (Table 6). The volume of fluids and type of fluids over the next 24 hours dictate the hydration status prior to the next day’s training session. It is a continuous cycle. Over time, an athlete increases the risk of being in a chronic dehydrated state, resulting in lack of motivation, risk of injury, and illness, fatigue, and poor performance. The current recommendation is to drink ~50% more in volume than the amount of weight lost, such as 22 to 24 ounces/pound lost.⁵²

ABSTRACT

Ice hockey is a fast-paced, collision sport requiring tremendous skill and finesse, yet ice hockey can be a harsh and violent game. It has one of the highest musculoskeletal injury rates in all of competitive sports. Razor sharp skates, aluminum sticks and boards made from high density polyethylene (HDPE), all contribute to the intrinsic hazards of the game. The objective of this article is to review evaluation, management, and return-to-the-rink guidelines after common lower extremity ice hockey injuries.

“Hockey is a fast body-contact game played by men with clubs in their hands and knives laced to their feet, since the skates are razor sharp, and before the evening is over it is almost a certainty that someone will be hurt and will fleck the ice with a generous contribution of gore before he is led away to be hemstitched together again.” —Paul Gallico in Farewell to Sport (1938)

Ice hockey is a collision sport with player speeds in excess of 30 miles/hour, on a sheet of ice surrounded by unforgiving boards, with a vulcanized rubber puck moving at speeds approaching 100 miles/hour.^1-3 Understanding injuries specific to this fast-paced sport is an essential part of being a team physician at any level of competitive ice hockey. We are continuing to improve our ability to correctly identify and treat injuries in ice hockey players.^2,4 On the prevention side, rule changes in hockey have been implemented, such as raising the age to allow checking and penalties for deliberate hits to the head and checking from behind, to make the game safer to play.³ Additionally, advancements in biomechanical research and 3D modeling are providing new insights into the pathoanatomy of the hip joint, which can be utilized for surgical planning in hockey players and goalies suffering from symptomatic femoroacetabular impingement (FAI) of the hip.⁵

During the 2010 Winter Olympics, more than 30% of ice hockey players were injured, which was the highest percentage amongst all competing sports.⁶ They also tallied the highest percentage of player-to-player injuries during the Olympics of any sport. Consequently, the team physician covering ice hockey should be prepared to manage upper and lower extremity musculoskeletal injuries, but also concussions, cervical spine injuries, and ocular and dental trauma.² 

One of the earliest epidemiological studies of ice hockey injuries looked at elite Danish hockey players over 2 seasons and found that head trauma accounted for 28% of all injuries, followed by lower extremity injuries at 27% with upper extremity injuries accounting for 19%.⁷ More recent epidemiological studies have shown similar rates based on body region while further defining individual diagnoses and their incidence. This should help clinicians and researchers develop prevention strategies, as well as improve treatments to optimize player outcomes and return to sport.^8,9 Our group recently reviewed the evaluation and management of common head, neck, and shoulder injuries at all competitive levels of ice hockey, and this article serves to complement the former by focusing on lower extremity injuries (Table).²

Continue to: Hip and groin...

 

 

EVALUATION AND MANAGEMENT OF COMMON LOWER EXTREMITY HOCKEY INJURIES

HIP INJURIES

Hip and groin injuries are very common amongst this group of athletes and account for approximately 9% of all ice hockey injuries.¹ Unfortunately, they are also known for their high recurrence rates, which may be in part due to delayed diagnosis, inadequate rest and rehabilitation, as well as the extreme loads that are placed on the hip during competition.^10,11 In hockey, the most commonly reported hip injuries include goaltender’s hip, FAI, sports hernia/hockey groin syndrome, adductor strains, hip pointer, and quadriceps contusions. Dalton and colleagues¹² performed the largest epidemiological study to date on hip and groin injuries amongst National Collegiate Athletic Association ice hockey players and reported that the most common injury mechanism was noncontact in nature. Contact injuries accounted for 13% (55 of 421) in men’s ice hockey players while less than 4% (4 of 114) injuries in female ice hockey players, which is likely attributed to a no checking rule in the women’s division. Some of these hip and groin injuries are difficult to diagnose so it is important for the team physician to perform a thorough history and physical examination. Advanced imaging (magnetic resonance imaging [MRI] or a computed tomography (CT) scan with 3D reconstructions) may be necessary to make the correct diagnosis. This is important for providing proper treatment as well as setting player expectations for return to sport.¹²

Table 1. Return-to-Play Guidelines for Common Lower Extremity Ice Hockey Injuries
Lower Extremity Injury	Treatment Options	Return-to-the-Rink Goal
FAI	In-season: injection, physical therapy program, NSAIDS. Off-season or unable to play: requires arthroscopic surgery	Nonoperative can take up to 6 weeks. Surgical depends on what is fixed but goal is 4 months to return to ice24,26
Sports hernia/athletic pubalgia	In-season: physical therapy program, NSAIDS Off-season or unable to play requiring surgery. Essential to make sure no other pathology (eg, FAI, osteitis pubis, adductor strain) to maximize success	Nonoperative 6-8 wk trial of physical therapy Operative: depends if concomitant FAI but in isolation goal is 3-4 mo33,54
Adductor strains	Ice, NSAIDS, physical therapy, use of Hypervolt Hyperice	Depends on position (goalie vs skater) and severity; can take up to 4-8 wk to return to ice. Want 70% strength and painless ROM to skate successfully;55 in chronic cases, may take up to 6 mo35
Quadriceps contusion	Hinged knee brace to maintain 120° of flexion, ice, compression wrap.	When player regains motion and strength, return to ice can be as fast a couple of days or as long as 3 wk8,46
MCL	Hinged knee brace, shin pad modification, ice, NSAIDs	Depends on Grade; if Grade I, 1-2 wk; Grade II, 2-4 wk; Grade III, 4-6 wk8
ACL	Surgery autograft BTB autograft soft tissue	9-10 mo41
Meniscus tear	Depends on type of tear and seasonal timing (in-season or off-season)	If surgical, 3-4 mo; if repair, 4-6 wk if partial menisectomy
High ankle sprain	Cam boot, NSAIDS, ice and physical therapy	6 wk49
Boot top laceration	Repair of cut structures, depends on depth and what is injured; best treatment is prevention with Kevlar socks	If laceration is deep and severs any medial tendons/vascular structures, return to ice can be ≥6 mo
Lace bite	Bunga pad, ice, diclofenac gel	Couple of days to up to 2 wk in recalcitrant cases3

^{Abbreviations: ACL, anterior cruciate ligament; BTB, bone-patellar tendon-bone; Cam, controlled ankle motion boot; MCL, medial collateral ligament; FAI, femoroacetabular impingement; NSAIDS, nonsteroidal anti-inflammatory drugs; ROM, range of motion.}

Throughout the hockey community, FAI is being examined as a possible source of symptomatic hip pain amongst players at all levels. A recent study, which utilized the National Hockey League (NHL) injury surveillance database, reported that FAI accounted for 5.3% of all hip and groin injuries.¹³ The etiology of FAI is thought to arise from a combination of genetic predisposition coupled with repetitive axial loading/hip flexion. This causes a bony overgrowth of the proximal femoral physes resulting in a cam deformity (Figure 1).^5,14 The abnormal bony anatomy allows for impingement between the acetabulum and proximal femur, which can injure the labrum and articular cartilage of the hip joint.

In the recent study by Ross and colleagues,¹⁵ the authors focused on symptomatic hip impingement in ice hockey goalies.¹⁵ Goaltender’s hip may be the result of the “butterfly style,” which is a technique of goaltending that emphasizes guarding the lower part of the goal. The goalie drops to his/her knees and internally rotates the hips to allow the leg pads to be parallel to the ice. This style acquired the name butterfly because of the resemblance of the spread goalie pads to a butterfly’s wings. Bedi and associates¹⁶ have evaluated hip biomechanics using 3D-generated bone models and showed in their study that arthroscopic treatment can improve hip kinematics and range of motion.

Plain radiographs showed that 90% (61 of 68) of hockey goalies had an elevated alpha angle signifying a femoral cam-type deformity.¹⁵ Goalies had a significantly lower mean lateral center-edge angle (27.3°  vs 29.6°; P = .03) and 13.2% of them were found to have acetabular dysplasia (lateral center-edge angle<20°) compared to only 3% of positional players. The CT scan measurements demonstrated that hockey goalies have a unique cam-type deformity that is located more lateral (1:00 o’clock vs 1:45 o’clock; P < .0001) along the proximal femur, an elevated maximum alpha angle (80.9° vs 68.6°; P < .0001) and loss of offset, when compared to positional players. These findings provide an anatomical basis in support of reports that goaltenders are more likely to experience intra-articular hip injuries compared to other positional players.¹³

Regardless of position, symptomatic FAI in a hockey player is generally a problem that slowly builds and is made worse with activity.¹⁷ On examination, the player may have limited hip flexion and internal rotation, as well as weakness compared to the contralateral side when testing hip flexion and abduction.^18,19 Plain radiographs plus MRI or CT allow for proper characterization and diagnosis (to include underlying chondrolabral pathology).^20,21

In the young athlete, initial management includes physical therapy, which focuses on core strengthening. Emphasis is placed on hip flexion and extension, as well as abduction and external rotation with the goal of reducing symptoms and avoiding injuries.²² A similar approach may be applied to the elite athlete, but failure of nonoperative management may necessitate surgical intervention. Hip arthroscopy continues to grow in popularity over open surgical dislocation with low complication rate and high return-to-play rate.^23-25

For the in-season athlete, attempts to continue to play can be assisted with the role of an intra-articular corticosteroid injection, which can help calm inflammation within the hip joint and mitigate pain, while rehabilitation focuses on core stabilization, postural retraining and focusing on any muscle imbalances that might be present. For positional players, ice time and shift duration can be adjusted to give the player’s hip a period of rest; meanwhile, for goaltenders, shot volumes in practice can be decreased.

Continue to: For athletes who...

 

 

For athletes who fail nonoperative care, surgical treatment varies depending on underlying hip pathology and may include femoroplasty, acetabuloplasty, and microfracture as well as labral repair or debridement. Though data are limited, Philippon and colleagues²⁶ have published promising results in a case series of 28 NHL players after surgical intervention for FAI. All players returned to sport at an average of 3.8 months and players who had surgery within 1 year of injury returned on average 1.1 months sooner than those who waited more than 1 year. Rehabilitation protocol varies between goaltenders compared to defensemen and offensive players due to the different demands required for blocking shots on goal.²⁷

One of the most challenging injuries to correctly identify in the hip area is athletic pubalgia (also referred to as sports hernia or core muscle injury) because pain in the groin may be referred from the lumbar spine, hip joint, urologic, or perineal etiologies.²⁸ Sports hernias involve dilatation of the external ring of the inguinal canal and thinning of the posterior wall. Players may report to the athletic trainer or team physician with a complaint of groin pain that is worse when pushing off with their skate or taking a slap shot.²⁹ On exam, pain can be reproduced by hip extension, contralateral torso rotation, or with a resisted sit-up with palpation of the inferolateral edge of the distal rectus abdominus.³⁰ An MRI with specific sequences centered over the pubic symphysis is usually warranted to aid in the workup of sports hernia. An MRI in these cases may also demonstrate avulsions of the rectus abdominus.³¹

Most of these injuries are managed conservatively but can warrant surgical intervention if the symptoms persist. In the study by Jakoi and colleagues,³² they identified 43 ice hockey players over an 8-year period (2001-2008) who had repairs of their sports hernias and assessed the statistics during the 2 years prior and 2 years after surgery. The authors found that 80% of these players were able to return to the ice for 2 or more full seasons. The return-to-sport rate was comparable to other sports after sports hernia repair, but players who had played in ≥7 seasons demonstrated a greater decrease in number of games played, goals, assists and time on ice compared to those who had played in ≤6 seasons prior to the time of injury. Between 1989 and 2000, 22 NHL players who failed to respond to nonoperative management of their groin injuries underwent surgical exploration.²⁹ At the time of surgical exploration, their hockey groin syndrome, consisted of small tears in the external oblique aponeurosis through which branches of the ilioinguinal or iliohypogastric could be identified. These surgical procedures were all through a standard inguinal approach and the perforating neurovascular structures were excised, while the main trunk of the ilioinguinal nerve was ablated and the external oblique aponeurosis was repaired and reinforced with Goretex (W.L. Gore & Associates Inc, Flagstaff, AZ). At follow-up, 18 of the 22 players (82%) had no pain and 19 (86%) were able to resume their careers in the NHL.²⁹ Ice hockey players with sports hernias or hockey groin syndrome often return to the sport, but it is important to identify these problems early so that surgical options can be discussed if the player fails conservative management. It is also critical to make sure that all pathology is identified, because in players with mixed sports hernia and FAI, return-to-play results improve when both issues are addressed. In a study of athletes (some of whom were ice hockey players), who had both FAI and sports hernia, and only hernia/pubalgia surgery was performed, 25% of these athletes returned to sport. If only FAI was addressed, 50% of the athletes returned to sport; however, when hernia and FAI were treated, 89% returned to play.³³

Adductor strains includes injury to the adductor muscles, pectineus, obturator externus and gracilis, and are prevalent in ice hockey players. A study of elite Swedish ice hockey players published in 1988 reported that adductor strains accounted for 10% (10 of 95) of all injuries.³⁴ Given the prevalence of these injuries, considerable research has been dedicated to understanding their mechanism and prevention.³⁵ Adductor strains within the ice hockey population have been attributed to the eccentric forces on the adductors when players attempt to decelerate the leg during a stride.³⁶ A study of NHL players revealed that a ratio <80% of adductor-to-abductor muscle is the best predictor of a groin strain.³⁷

These injuries are also well known for their recurrence rates, as was the case in an NHL study where 4 of the 9 adductor strains (44%) were recurrent injuries.³⁷ The authors attributed the recurrence to an incomplete rehabilitation program and an accelerated return to sport. This was followed by an NHL prevention program that spanned 2 seasons and analyzed 58 players whose adductor-to-abductor ratio was <80% and placed them into a 6-week intervention program during the preseason.³⁷ Only 3 players sustained an adductor strain in the 2 subsequent seasons after the intervention, compared to 11 strains in the previous 2 seasons. Thus, early identification of muscle strength imbalance coupled with an appropriate intervention program has proven to be an effective means of reducing adductor strains in this at-risk population.

Continue to: Contact injuries may...

 

 

Contact injuries may vary with checking into the boards being unique to men’s ice hockey. Hip pointers occur as a result of a direct compression injury to the iliac crest, which causes trauma to the bone but also to the overlying hip abductor musculature, and represent roughly 2.4% of ice hockey injuries.²³ The resulting contusion may cause a local hematoma formation. Early identification of the injury plus treatment with RICE (rest, ice, compression, elevation) coupled with crutches to limit weight-bearing status may minimize soft tissue trauma and swelling, and ultimately aid in pain control and return to sport.³⁸ Hip abductor strengthening, added padding over the injured area, as well as a compressive hip spica wrapping, have all been suggested to expedite return to play and help prevent recurrence of the hip pointer.⁸

KNEE INJURIES

Injury to the medial collateral ligament (MCL) is the most commonly reported knee injury (Figure 2) and second only to concussion amongst all injuries in National Collegiate Athletic Association ice hockey players.^8,39 The mechanism of injury typically involves a valgus force on the knee, which is often caused by collision into another player.³⁹ Valgus stress testing with the knee in 30° of flexion is used to grade the severity of injury (Grade I: 0-5 mm of medial opening; Grade II: 5-10 mm of medial opening; Grade III: >10 mm of medial opening).³⁹ One study that followed a single college hockey team for 8 seasons reported that 77% of injuries (10 of 13) occurred during player-to-player collision,³⁹ with 5 being Grade 1 injuries, 6 Grade 2 injuries, 1 Grade 3; information was missing for 1 player. Nonoperative management of incomplete injuries, grade 1 and 2 sprains, with RICE and early physical therapy intervention to work on knee range of motion and quadriceps strengthening typically helps the player return to sport within days for grade 1 and 2 injuries to 3 weeks for grade 2 injuries. Complete tears have been managed both operatively and nonoperatively with evidence to suggest better outcomes after surgical intervention if there is a concomitant ACL injury requiring reconstruction.^8,9

Anterior cruciate ligament (ACL) tears occur less frequently in hockey players compared to the players in other sports such as football and basketball.^38,40 Between 2006 and 2010, 47 players were identified by the NHL Injury Surveillance System as having sustained an ACL injury, which equates to an incidence of 9.4 ACL injuries per NHL season over this time span.⁴¹ The mechanism of ACL tears in ice hockey players appears to be different from other sports players based on a recent MRI study that evaluated players for concomitant injuries following ACL tear and noted significantly fewer bone bruises on the lateral femoral condyle compared to players in other sports.⁴² Early evaluation after injury with Lachman and/or pivot shift tests aids the diagnosis. Data from the NHL study identified 32 players (68%) with concomitant meniscal injuries and 32 (68%) had MCL injuries in conjunction with their ACL tears.⁴¹ Average length in the league prior to injury was 5.65 seasons. Twenty-nine of the injured players (61.7%) underwent reconstruction with a patellar tendon autograft, 13 (27.7%) had a hamstring autograft, and 5 (10.6%) had either a patellar tendon or hamstring allograft.⁴¹ Meniscus and ACL injuries were associated with a decreased length of career compared to age-matched controls and, notably, players >30 years at the time of injury had only a 67% rate of return to sport whereas those <30 years had a return-to-sport rate of 80%. Players who were able to return did so at an average of 9.8 months (range, 6-21 months) and had a significant reduction in total number of goals, assists, and points scored compared to controls. Decline in performance was typically associated with forwards and wings, while defensemen did not demonstrate the same decrease in performance following return to ice hockey.⁴¹

Meniscal tears are a well-documented concomitant injury with ruptures of the ACL, and the combination is a known pattern associated with shorter careers compared to isolated ACL tears in ice hockey players.⁴¹ The lateral meniscus is known for increased mobility compared to the medial meniscus and is more commonly injured (39% vs 8.5%) in ACL tears that occur in contact sports and downhill skiing.⁴² Ice hockey presents a scenario that is different from other contact sports because of the near frictionless interaction between the player’s ice skates and playing surface. This likely equates to a different injury mechanism and dissipation of energy after contact as well as non-contact injuries.³⁸ A recent study reviewed knee MRI findings associated with ACL tears in collegiate ice hockey players and compared to other sports known for their high rates of concomitant meniscal pathology. The authors reported a statistically significant decrease in lateral meniscus tears and bone-bruising patterns in ice hockey players with ACL injuries compared to athletes with ACL tears in other sports.⁴³ In contrast, an NHL study of ACL tears in professional ice hockey players found that 68% of players had concomitant meniscal tears (32 out of 47 players).⁴¹

Continue to: The presence of...

 

 

The presence of a meniscal tear on MRI is typically a surgical problem, especially if it occurred with an ACL injury. Meniscal repair is preferable, if possible, because there is a known association of increased cartilage contact pressures associated with meniscal debridement. Return to sport following meniscus injury hinges upon whether it is an isolated injury and how it is treated. If the meniscus injury occurs in isolation and can be treated with a debridement and partial resection alone, there is obviously a quicker return to sport as the player can be weight-bearing immediately following surgery. Return to skating after meniscal debridement and partial resection is usually 4 to 6 weeks, whereas meniscal repair protocols vary depending on surgeon; players may need 3 months to 4 months to return to the ice.

Quadriceps contusions are contact injuries that are not unique to ice hockey (Figure 3). They may result from player collision but also from direct blows from a hockey puck. A high velocity puck is known to cause immense trauma to the quadriceps muscles, which may result in localized bleeding and hematoma formation. If the player is able to anticipate the event, active contraction of the quadriceps muscle has been shown to absorb some of the energy and result in a less traumatic injury, but in a fast paced ice hockey game, the player’s anticipation is less likely than in other sports such as baseball.⁴⁴Interestingly, the degree of knee flexion after injury is predictive of injury severity with milder injuries associated with angles >90 and more severe injuries resulting in knee flexion angles <45° and typically an antalgic gait.⁴⁵ It is important to treat these injuries during the first 24 hours with the knee maintained in 120°of flexion, plus ice and compression, which can be achieved using a locked knee brace or elastic compression wrap. Quadriceps stretching and isometric strengthening should immediately follow the period of immobilization. The addition of NSAIDs may help prevent the formation of myositis ossificans. A study from West Point suggests that the average return to sport or activity ranges from 13 days (mild contusion) to 21 days (severe contusions), while others⁸ have indicated that if the injury is treated acutely and a player is able to regain motion and strength, return to ice hockey within a few days is possible.

FOOT AND ANKLE

Ice hockey has some unique injuries that can be attributed to the use of ice skates for play. One such injury is boot-top lacerations, which are fortunately rare as they can be a career-ending injury.⁴⁷ The spectrum of injury ranges from superficial abrasions to more severe soft tissue disruption, including the extensor tendons and neurovascular structures. The actual mechanism of injury involves an opponent’s skate blade cutting across the anterior ankle. One early case report described a protective method of having players place their skate tongues deep to their protective shin pads, instead of turning the tongues down.⁴⁷ Kevlar socks have also been shown to help prevent or minimize the damage from a skate blade.⁴⁸

Injury to the lateral ankle ligaments, anterior talofibular ligament or calcaneofibular ligament, are usually more common than the higher ankle sprains involving the syndesmosis. However, this is not the case in ice hockey. The rigidity of the ice skate at the level of the lateral ligaments seems to impart a protective mechanism to the lower ligaments, but this results in a higher incidence of syndesmotic injuries. These high ankle injuries are unfortunately more debilitating and often require a longer recovery period. In a study of these injuries in NHL players, syndesmotic sprains made up 74% of all ankle sprains, whereas only 18.4% of ankle sprains involved the syndesmosis in American football players..^49,50 The average number of days between injury and return to play is 45 days, and some authors believe that defensemen may have a harder time recovering because of the demands on their ankles by having to switch continuously between forward and backward skating.⁴⁹

Most patients are treated conservatively when their ankle plain radiographs show a congruent mortise and no evidence of syndesmotic widening. If the player expresses pain when squeezing the syndesmosis, it is helpful to obtain stress radiographs to further evaluate for syndesmotic injury. Nonoperative management includes RICE, immobilization in a rigid boot with crutches to protect weight-bearing with gradual advancements and eventually physical therapy to address any ankle stiffness, followed by dynamic functional activities. Treatment options for syndesmotic widening and failed conservative management includes both screw and plate options as well as suture buttons.^49,51,52

Ankle and foot fractures were historically a rare injury in ice hockey players based on radiograph evaluation; however, the recent study by Baker and colleagues⁴ demonstrated that MRI can be helpful in detecting subradiographic fractures. Most of the injuries detected after MRI were from being hit by a hockey puck; this was a novel mechanism that had not been previously reported in the literature.⁴ Of the injuries that resulted from a direct blow, 14 of 17 occurred on the medial aspect of the foot and ankle, which is believed to result another word? from a defender skating towards an offensive player and attempting to block shots on goal. In this study, all occult fractures involving the medial malleolus were eventually treated with open reduction and internal fixation and underwent routine healing.⁴ The navicular bone and base of the first metatarsal accounted for the remaining medial-sided fractures. In a recent analysis of risk factors for reoperation following operative fixation of foot fractures across the National Basketball Association, the National Football Leagues, Major League Baseball, and the National Hockey League only a total of 3 fractures involving the foot (1 navicular and 2 first metatarsal) were identified in NHL players over a 30-year period.⁵³ The study acknowledged a major limitation being a public source for identifying players with fractures.

Lace bite is another common ice hockey injury. It typically occurs at the beginning of a season or whenever a player is breaking in a new pair of skates. The cause of the lace bite is the rigid tongue in the skate that rubs against the anterior ankle. Skating causes inflammation in the area of the tibialis anterior tendon, and the player will complain of significant anterior ankle pain. First line treatment for lace bite is ice (Figure 4A), NSAID gel (eg, diclofenac 1%), and a Bunga lace-bite pad (Absolute Athletics). (Figure 4B).

SUMMARY

Lower extremity injuries are common in ice hockey players, and a covering physician should be comfortable managing these injuries from breezers to skate. Proper evaluation and work-up is critical for early diagnosis and identification of pathology, which can minimize the impact of the injury and expedite a treatment plan to return the player safely to the ice and in the game.

ABSTRACT

Ice hockey is a fast-paced, collision sport requiring tremendous skill and finesse, yet ice hockey can be a harsh and violent game. It has one of the highest musculoskeletal injury rates in all of competitive sports. Razor sharp skates, aluminum sticks and boards made from high density polyethylene (HDPE), all contribute to the intrinsic hazards of the game. The objective of this article is to review evaluation, management, and return-to-the-rink guidelines after common lower extremity ice hockey injuries.

“Hockey is a fast body-contact game played by men with clubs in their hands and knives laced to their feet, since the skates are razor sharp, and before the evening is over it is almost a certainty that someone will be hurt and will fleck the ice with a generous contribution of gore before he is led away to be hemstitched together again.” —Paul Gallico in Farewell to Sport (1938)

Ice hockey is a collision sport with player speeds in excess of 30 miles/hour, on a sheet of ice surrounded by unforgiving boards, with a vulcanized rubber puck moving at speeds approaching 100 miles/hour.^1-3 Understanding injuries specific to this fast-paced sport is an essential part of being a team physician at any level of competitive ice hockey. We are continuing to improve our ability to correctly identify and treat injuries in ice hockey players.^2,4 On the prevention side, rule changes in hockey have been implemented, such as raising the age to allow checking and penalties for deliberate hits to the head and checking from behind, to make the game safer to play.³ Additionally, advancements in biomechanical research and 3D modeling are providing new insights into the pathoanatomy of the hip joint, which can be utilized for surgical planning in hockey players and goalies suffering from symptomatic femoroacetabular impingement (FAI) of the hip.⁵

During the 2010 Winter Olympics, more than 30% of ice hockey players were injured, which was the highest percentage amongst all competing sports.⁶ They also tallied the highest percentage of player-to-player injuries during the Olympics of any sport. Consequently, the team physician covering ice hockey should be prepared to manage upper and lower extremity musculoskeletal injuries, but also concussions, cervical spine injuries, and ocular and dental trauma.² 

One of the earliest epidemiological studies of ice hockey injuries looked at elite Danish hockey players over 2 seasons and found that head trauma accounted for 28% of all injuries, followed by lower extremity injuries at 27% with upper extremity injuries accounting for 19%.⁷ More recent epidemiological studies have shown similar rates based on body region while further defining individual diagnoses and their incidence. This should help clinicians and researchers develop prevention strategies, as well as improve treatments to optimize player outcomes and return to sport.^8,9 Our group recently reviewed the evaluation and management of common head, neck, and shoulder injuries at all competitive levels of ice hockey, and this article serves to complement the former by focusing on lower extremity injuries (Table).²

Continue to: Hip and groin...

 

 

EVALUATION AND MANAGEMENT OF COMMON LOWER EXTREMITY HOCKEY INJURIES

HIP INJURIES

Hip and groin injuries are very common amongst this group of athletes and account for approximately 9% of all ice hockey injuries.¹ Unfortunately, they are also known for their high recurrence rates, which may be in part due to delayed diagnosis, inadequate rest and rehabilitation, as well as the extreme loads that are placed on the hip during competition.^10,11 In hockey, the most commonly reported hip injuries include goaltender’s hip, FAI, sports hernia/hockey groin syndrome, adductor strains, hip pointer, and quadriceps contusions. Dalton and colleagues¹² performed the largest epidemiological study to date on hip and groin injuries amongst National Collegiate Athletic Association ice hockey players and reported that the most common injury mechanism was noncontact in nature. Contact injuries accounted for 13% (55 of 421) in men’s ice hockey players while less than 4% (4 of 114) injuries in female ice hockey players, which is likely attributed to a no checking rule in the women’s division. Some of these hip and groin injuries are difficult to diagnose so it is important for the team physician to perform a thorough history and physical examination. Advanced imaging (magnetic resonance imaging [MRI] or a computed tomography (CT) scan with 3D reconstructions) may be necessary to make the correct diagnosis. This is important for providing proper treatment as well as setting player expectations for return to sport.¹²

Table 1. Return-to-Play Guidelines for Common Lower Extremity Ice Hockey Injuries
Lower Extremity Injury	Treatment Options	Return-to-the-Rink Goal
FAI	In-season: injection, physical therapy program, NSAIDS. Off-season or unable to play: requires arthroscopic surgery	Nonoperative can take up to 6 weeks. Surgical depends on what is fixed but goal is 4 months to return to ice24,26
Sports hernia/athletic pubalgia	In-season: physical therapy program, NSAIDS Off-season or unable to play requiring surgery. Essential to make sure no other pathology (eg, FAI, osteitis pubis, adductor strain) to maximize success	Nonoperative 6-8 wk trial of physical therapy Operative: depends if concomitant FAI but in isolation goal is 3-4 mo33,54
Adductor strains	Ice, NSAIDS, physical therapy, use of Hypervolt Hyperice	Depends on position (goalie vs skater) and severity; can take up to 4-8 wk to return to ice. Want 70% strength and painless ROM to skate successfully;55 in chronic cases, may take up to 6 mo35
Quadriceps contusion	Hinged knee brace to maintain 120° of flexion, ice, compression wrap.	When player regains motion and strength, return to ice can be as fast a couple of days or as long as 3 wk8,46
MCL	Hinged knee brace, shin pad modification, ice, NSAIDs	Depends on Grade; if Grade I, 1-2 wk; Grade II, 2-4 wk; Grade III, 4-6 wk8
ACL	Surgery autograft BTB autograft soft tissue	9-10 mo41
Meniscus tear	Depends on type of tear and seasonal timing (in-season or off-season)	If surgical, 3-4 mo; if repair, 4-6 wk if partial menisectomy
High ankle sprain	Cam boot, NSAIDS, ice and physical therapy	6 wk49
Boot top laceration	Repair of cut structures, depends on depth and what is injured; best treatment is prevention with Kevlar socks	If laceration is deep and severs any medial tendons/vascular structures, return to ice can be ≥6 mo
Lace bite	Bunga pad, ice, diclofenac gel	Couple of days to up to 2 wk in recalcitrant cases3

^{Abbreviations: ACL, anterior cruciate ligament; BTB, bone-patellar tendon-bone; Cam, controlled ankle motion boot; MCL, medial collateral ligament; FAI, femoroacetabular impingement; NSAIDS, nonsteroidal anti-inflammatory drugs; ROM, range of motion.}

Throughout the hockey community, FAI is being examined as a possible source of symptomatic hip pain amongst players at all levels. A recent study, which utilized the National Hockey League (NHL) injury surveillance database, reported that FAI accounted for 5.3% of all hip and groin injuries.¹³ The etiology of FAI is thought to arise from a combination of genetic predisposition coupled with repetitive axial loading/hip flexion. This causes a bony overgrowth of the proximal femoral physes resulting in a cam deformity (Figure 1).^5,14 The abnormal bony anatomy allows for impingement between the acetabulum and proximal femur, which can injure the labrum and articular cartilage of the hip joint.

In the recent study by Ross and colleagues,¹⁵ the authors focused on symptomatic hip impingement in ice hockey goalies.¹⁵ Goaltender’s hip may be the result of the “butterfly style,” which is a technique of goaltending that emphasizes guarding the lower part of the goal. The goalie drops to his/her knees and internally rotates the hips to allow the leg pads to be parallel to the ice. This style acquired the name butterfly because of the resemblance of the spread goalie pads to a butterfly’s wings. Bedi and associates¹⁶ have evaluated hip biomechanics using 3D-generated bone models and showed in their study that arthroscopic treatment can improve hip kinematics and range of motion.

Plain radiographs showed that 90% (61 of 68) of hockey goalies had an elevated alpha angle signifying a femoral cam-type deformity.¹⁵ Goalies had a significantly lower mean lateral center-edge angle (27.3°  vs 29.6°; P = .03) and 13.2% of them were found to have acetabular dysplasia (lateral center-edge angle<20°) compared to only 3% of positional players. The CT scan measurements demonstrated that hockey goalies have a unique cam-type deformity that is located more lateral (1:00 o’clock vs 1:45 o’clock; P < .0001) along the proximal femur, an elevated maximum alpha angle (80.9° vs 68.6°; P < .0001) and loss of offset, when compared to positional players. These findings provide an anatomical basis in support of reports that goaltenders are more likely to experience intra-articular hip injuries compared to other positional players.¹³

Regardless of position, symptomatic FAI in a hockey player is generally a problem that slowly builds and is made worse with activity.¹⁷ On examination, the player may have limited hip flexion and internal rotation, as well as weakness compared to the contralateral side when testing hip flexion and abduction.^18,19 Plain radiographs plus MRI or CT allow for proper characterization and diagnosis (to include underlying chondrolabral pathology).^20,21

In the young athlete, initial management includes physical therapy, which focuses on core strengthening. Emphasis is placed on hip flexion and extension, as well as abduction and external rotation with the goal of reducing symptoms and avoiding injuries.²² A similar approach may be applied to the elite athlete, but failure of nonoperative management may necessitate surgical intervention. Hip arthroscopy continues to grow in popularity over open surgical dislocation with low complication rate and high return-to-play rate.^23-25

For the in-season athlete, attempts to continue to play can be assisted with the role of an intra-articular corticosteroid injection, which can help calm inflammation within the hip joint and mitigate pain, while rehabilitation focuses on core stabilization, postural retraining and focusing on any muscle imbalances that might be present. For positional players, ice time and shift duration can be adjusted to give the player’s hip a period of rest; meanwhile, for goaltenders, shot volumes in practice can be decreased.

Continue to: For athletes who...

 

 

For athletes who fail nonoperative care, surgical treatment varies depending on underlying hip pathology and may include femoroplasty, acetabuloplasty, and microfracture as well as labral repair or debridement. Though data are limited, Philippon and colleagues²⁶ have published promising results in a case series of 28 NHL players after surgical intervention for FAI. All players returned to sport at an average of 3.8 months and players who had surgery within 1 year of injury returned on average 1.1 months sooner than those who waited more than 1 year. Rehabilitation protocol varies between goaltenders compared to defensemen and offensive players due to the different demands required for blocking shots on goal.²⁷

One of the most challenging injuries to correctly identify in the hip area is athletic pubalgia (also referred to as sports hernia or core muscle injury) because pain in the groin may be referred from the lumbar spine, hip joint, urologic, or perineal etiologies.²⁸ Sports hernias involve dilatation of the external ring of the inguinal canal and thinning of the posterior wall. Players may report to the athletic trainer or team physician with a complaint of groin pain that is worse when pushing off with their skate or taking a slap shot.²⁹ On exam, pain can be reproduced by hip extension, contralateral torso rotation, or with a resisted sit-up with palpation of the inferolateral edge of the distal rectus abdominus.³⁰ An MRI with specific sequences centered over the pubic symphysis is usually warranted to aid in the workup of sports hernia. An MRI in these cases may also demonstrate avulsions of the rectus abdominus.³¹

Most of these injuries are managed conservatively but can warrant surgical intervention if the symptoms persist. In the study by Jakoi and colleagues,³² they identified 43 ice hockey players over an 8-year period (2001-2008) who had repairs of their sports hernias and assessed the statistics during the 2 years prior and 2 years after surgery. The authors found that 80% of these players were able to return to the ice for 2 or more full seasons. The return-to-sport rate was comparable to other sports after sports hernia repair, but players who had played in ≥7 seasons demonstrated a greater decrease in number of games played, goals, assists and time on ice compared to those who had played in ≤6 seasons prior to the time of injury. Between 1989 and 2000, 22 NHL players who failed to respond to nonoperative management of their groin injuries underwent surgical exploration.²⁹ At the time of surgical exploration, their hockey groin syndrome, consisted of small tears in the external oblique aponeurosis through which branches of the ilioinguinal or iliohypogastric could be identified. These surgical procedures were all through a standard inguinal approach and the perforating neurovascular structures were excised, while the main trunk of the ilioinguinal nerve was ablated and the external oblique aponeurosis was repaired and reinforced with Goretex (W.L. Gore & Associates Inc, Flagstaff, AZ). At follow-up, 18 of the 22 players (82%) had no pain and 19 (86%) were able to resume their careers in the NHL.²⁹ Ice hockey players with sports hernias or hockey groin syndrome often return to the sport, but it is important to identify these problems early so that surgical options can be discussed if the player fails conservative management. It is also critical to make sure that all pathology is identified, because in players with mixed sports hernia and FAI, return-to-play results improve when both issues are addressed. In a study of athletes (some of whom were ice hockey players), who had both FAI and sports hernia, and only hernia/pubalgia surgery was performed, 25% of these athletes returned to sport. If only FAI was addressed, 50% of the athletes returned to sport; however, when hernia and FAI were treated, 89% returned to play.³³

Adductor strains includes injury to the adductor muscles, pectineus, obturator externus and gracilis, and are prevalent in ice hockey players. A study of elite Swedish ice hockey players published in 1988 reported that adductor strains accounted for 10% (10 of 95) of all injuries.³⁴ Given the prevalence of these injuries, considerable research has been dedicated to understanding their mechanism and prevention.³⁵ Adductor strains within the ice hockey population have been attributed to the eccentric forces on the adductors when players attempt to decelerate the leg during a stride.³⁶ A study of NHL players revealed that a ratio <80% of adductor-to-abductor muscle is the best predictor of a groin strain.³⁷

These injuries are also well known for their recurrence rates, as was the case in an NHL study where 4 of the 9 adductor strains (44%) were recurrent injuries.³⁷ The authors attributed the recurrence to an incomplete rehabilitation program and an accelerated return to sport. This was followed by an NHL prevention program that spanned 2 seasons and analyzed 58 players whose adductor-to-abductor ratio was <80% and placed them into a 6-week intervention program during the preseason.³⁷ Only 3 players sustained an adductor strain in the 2 subsequent seasons after the intervention, compared to 11 strains in the previous 2 seasons. Thus, early identification of muscle strength imbalance coupled with an appropriate intervention program has proven to be an effective means of reducing adductor strains in this at-risk population.

Continue to: Contact injuries may...

 

 

Contact injuries may vary with checking into the boards being unique to men’s ice hockey. Hip pointers occur as a result of a direct compression injury to the iliac crest, which causes trauma to the bone but also to the overlying hip abductor musculature, and represent roughly 2.4% of ice hockey injuries.²³ The resulting contusion may cause a local hematoma formation. Early identification of the injury plus treatment with RICE (rest, ice, compression, elevation) coupled with crutches to limit weight-bearing status may minimize soft tissue trauma and swelling, and ultimately aid in pain control and return to sport.³⁸ Hip abductor strengthening, added padding over the injured area, as well as a compressive hip spica wrapping, have all been suggested to expedite return to play and help prevent recurrence of the hip pointer.⁸

KNEE INJURIES

Injury to the medial collateral ligament (MCL) is the most commonly reported knee injury (Figure 2) and second only to concussion amongst all injuries in National Collegiate Athletic Association ice hockey players.^8,39 The mechanism of injury typically involves a valgus force on the knee, which is often caused by collision into another player.³⁹ Valgus stress testing with the knee in 30° of flexion is used to grade the severity of injury (Grade I: 0-5 mm of medial opening; Grade II: 5-10 mm of medial opening; Grade III: >10 mm of medial opening).³⁹ One study that followed a single college hockey team for 8 seasons reported that 77% of injuries (10 of 13) occurred during player-to-player collision,³⁹ with 5 being Grade 1 injuries, 6 Grade 2 injuries, 1 Grade 3; information was missing for 1 player. Nonoperative management of incomplete injuries, grade 1 and 2 sprains, with RICE and early physical therapy intervention to work on knee range of motion and quadriceps strengthening typically helps the player return to sport within days for grade 1 and 2 injuries to 3 weeks for grade 2 injuries. Complete tears have been managed both operatively and nonoperatively with evidence to suggest better outcomes after surgical intervention if there is a concomitant ACL injury requiring reconstruction.^8,9

Anterior cruciate ligament (ACL) tears occur less frequently in hockey players compared to the players in other sports such as football and basketball.^38,40 Between 2006 and 2010, 47 players were identified by the NHL Injury Surveillance System as having sustained an ACL injury, which equates to an incidence of 9.4 ACL injuries per NHL season over this time span.⁴¹ The mechanism of ACL tears in ice hockey players appears to be different from other sports players based on a recent MRI study that evaluated players for concomitant injuries following ACL tear and noted significantly fewer bone bruises on the lateral femoral condyle compared to players in other sports.⁴² Early evaluation after injury with Lachman and/or pivot shift tests aids the diagnosis. Data from the NHL study identified 32 players (68%) with concomitant meniscal injuries and 32 (68%) had MCL injuries in conjunction with their ACL tears.⁴¹ Average length in the league prior to injury was 5.65 seasons. Twenty-nine of the injured players (61.7%) underwent reconstruction with a patellar tendon autograft, 13 (27.7%) had a hamstring autograft, and 5 (10.6%) had either a patellar tendon or hamstring allograft.⁴¹ Meniscus and ACL injuries were associated with a decreased length of career compared to age-matched controls and, notably, players >30 years at the time of injury had only a 67% rate of return to sport whereas those <30 years had a return-to-sport rate of 80%. Players who were able to return did so at an average of 9.8 months (range, 6-21 months) and had a significant reduction in total number of goals, assists, and points scored compared to controls. Decline in performance was typically associated with forwards and wings, while defensemen did not demonstrate the same decrease in performance following return to ice hockey.⁴¹

Meniscal tears are a well-documented concomitant injury with ruptures of the ACL, and the combination is a known pattern associated with shorter careers compared to isolated ACL tears in ice hockey players.⁴¹ The lateral meniscus is known for increased mobility compared to the medial meniscus and is more commonly injured (39% vs 8.5%) in ACL tears that occur in contact sports and downhill skiing.⁴² Ice hockey presents a scenario that is different from other contact sports because of the near frictionless interaction between the player’s ice skates and playing surface. This likely equates to a different injury mechanism and dissipation of energy after contact as well as non-contact injuries.³⁸ A recent study reviewed knee MRI findings associated with ACL tears in collegiate ice hockey players and compared to other sports known for their high rates of concomitant meniscal pathology. The authors reported a statistically significant decrease in lateral meniscus tears and bone-bruising patterns in ice hockey players with ACL injuries compared to athletes with ACL tears in other sports.⁴³ In contrast, an NHL study of ACL tears in professional ice hockey players found that 68% of players had concomitant meniscal tears (32 out of 47 players).⁴¹

Continue to: The presence of...

 

 

The presence of a meniscal tear on MRI is typically a surgical problem, especially if it occurred with an ACL injury. Meniscal repair is preferable, if possible, because there is a known association of increased cartilage contact pressures associated with meniscal debridement. Return to sport following meniscus injury hinges upon whether it is an isolated injury and how it is treated. If the meniscus injury occurs in isolation and can be treated with a debridement and partial resection alone, there is obviously a quicker return to sport as the player can be weight-bearing immediately following surgery. Return to skating after meniscal debridement and partial resection is usually 4 to 6 weeks, whereas meniscal repair protocols vary depending on surgeon; players may need 3 months to 4 months to return to the ice.

Quadriceps contusions are contact injuries that are not unique to ice hockey (Figure 3). They may result from player collision but also from direct blows from a hockey puck. A high velocity puck is known to cause immense trauma to the quadriceps muscles, which may result in localized bleeding and hematoma formation. If the player is able to anticipate the event, active contraction of the quadriceps muscle has been shown to absorb some of the energy and result in a less traumatic injury, but in a fast paced ice hockey game, the player’s anticipation is less likely than in other sports such as baseball.⁴⁴Interestingly, the degree of knee flexion after injury is predictive of injury severity with milder injuries associated with angles >90 and more severe injuries resulting in knee flexion angles <45° and typically an antalgic gait.⁴⁵ It is important to treat these injuries during the first 24 hours with the knee maintained in 120°of flexion, plus ice and compression, which can be achieved using a locked knee brace or elastic compression wrap. Quadriceps stretching and isometric strengthening should immediately follow the period of immobilization. The addition of NSAIDs may help prevent the formation of myositis ossificans. A study from West Point suggests that the average return to sport or activity ranges from 13 days (mild contusion) to 21 days (severe contusions), while others⁸ have indicated that if the injury is treated acutely and a player is able to regain motion and strength, return to ice hockey within a few days is possible.

FOOT AND ANKLE

Ice hockey has some unique injuries that can be attributed to the use of ice skates for play. One such injury is boot-top lacerations, which are fortunately rare as they can be a career-ending injury.⁴⁷ The spectrum of injury ranges from superficial abrasions to more severe soft tissue disruption, including the extensor tendons and neurovascular structures. The actual mechanism of injury involves an opponent’s skate blade cutting across the anterior ankle. One early case report described a protective method of having players place their skate tongues deep to their protective shin pads, instead of turning the tongues down.⁴⁷ Kevlar socks have also been shown to help prevent or minimize the damage from a skate blade.⁴⁸

Injury to the lateral ankle ligaments, anterior talofibular ligament or calcaneofibular ligament, are usually more common than the higher ankle sprains involving the syndesmosis. However, this is not the case in ice hockey. The rigidity of the ice skate at the level of the lateral ligaments seems to impart a protective mechanism to the lower ligaments, but this results in a higher incidence of syndesmotic injuries. These high ankle injuries are unfortunately more debilitating and often require a longer recovery period. In a study of these injuries in NHL players, syndesmotic sprains made up 74% of all ankle sprains, whereas only 18.4% of ankle sprains involved the syndesmosis in American football players..^49,50 The average number of days between injury and return to play is 45 days, and some authors believe that defensemen may have a harder time recovering because of the demands on their ankles by having to switch continuously between forward and backward skating.⁴⁹

Most patients are treated conservatively when their ankle plain radiographs show a congruent mortise and no evidence of syndesmotic widening. If the player expresses pain when squeezing the syndesmosis, it is helpful to obtain stress radiographs to further evaluate for syndesmotic injury. Nonoperative management includes RICE, immobilization in a rigid boot with crutches to protect weight-bearing with gradual advancements and eventually physical therapy to address any ankle stiffness, followed by dynamic functional activities. Treatment options for syndesmotic widening and failed conservative management includes both screw and plate options as well as suture buttons.^49,51,52

Ankle and foot fractures were historically a rare injury in ice hockey players based on radiograph evaluation; however, the recent study by Baker and colleagues⁴ demonstrated that MRI can be helpful in detecting subradiographic fractures. Most of the injuries detected after MRI were from being hit by a hockey puck; this was a novel mechanism that had not been previously reported in the literature.⁴ Of the injuries that resulted from a direct blow, 14 of 17 occurred on the medial aspect of the foot and ankle, which is believed to result another word? from a defender skating towards an offensive player and attempting to block shots on goal. In this study, all occult fractures involving the medial malleolus were eventually treated with open reduction and internal fixation and underwent routine healing.⁴ The navicular bone and base of the first metatarsal accounted for the remaining medial-sided fractures. In a recent analysis of risk factors for reoperation following operative fixation of foot fractures across the National Basketball Association, the National Football Leagues, Major League Baseball, and the National Hockey League only a total of 3 fractures involving the foot (1 navicular and 2 first metatarsal) were identified in NHL players over a 30-year period.⁵³ The study acknowledged a major limitation being a public source for identifying players with fractures.

Lace bite is another common ice hockey injury. It typically occurs at the beginning of a season or whenever a player is breaking in a new pair of skates. The cause of the lace bite is the rigid tongue in the skate that rubs against the anterior ankle. Skating causes inflammation in the area of the tibialis anterior tendon, and the player will complain of significant anterior ankle pain. First line treatment for lace bite is ice (Figure 4A), NSAID gel (eg, diclofenac 1%), and a Bunga lace-bite pad (Absolute Athletics). (Figure 4B).

SUMMARY

Lower extremity injuries are common in ice hockey players, and a covering physician should be comfortable managing these injuries from breezers to skate. Proper evaluation and work-up is critical for early diagnosis and identification of pathology, which can minimize the impact of the injury and expedite a treatment plan to return the player safely to the ice and in the game.

ABSTRACT

Ice hockey is a fast-paced, collision sport requiring tremendous skill and finesse, yet ice hockey can be a harsh and violent game. It has one of the highest musculoskeletal injury rates in all of competitive sports. Razor sharp skates, aluminum sticks and boards made from high density polyethylene (HDPE), all contribute to the intrinsic hazards of the game. The objective of this article is to review evaluation, management, and return-to-the-rink guidelines after common lower extremity ice hockey injuries.

“Hockey is a fast body-contact game played by men with clubs in their hands and knives laced to their feet, since the skates are razor sharp, and before the evening is over it is almost a certainty that someone will be hurt and will fleck the ice with a generous contribution of gore before he is led away to be hemstitched together again.” —Paul Gallico in Farewell to Sport (1938)

Ice hockey is a collision sport with player speeds in excess of 30 miles/hour, on a sheet of ice surrounded by unforgiving boards, with a vulcanized rubber puck moving at speeds approaching 100 miles/hour.^1-3 Understanding injuries specific to this fast-paced sport is an essential part of being a team physician at any level of competitive ice hockey. We are continuing to improve our ability to correctly identify and treat injuries in ice hockey players.^2,4 On the prevention side, rule changes in hockey have been implemented, such as raising the age to allow checking and penalties for deliberate hits to the head and checking from behind, to make the game safer to play.³ Additionally, advancements in biomechanical research and 3D modeling are providing new insights into the pathoanatomy of the hip joint, which can be utilized for surgical planning in hockey players and goalies suffering from symptomatic femoroacetabular impingement (FAI) of the hip.⁵

During the 2010 Winter Olympics, more than 30% of ice hockey players were injured, which was the highest percentage amongst all competing sports.⁶ They also tallied the highest percentage of player-to-player injuries during the Olympics of any sport. Consequently, the team physician covering ice hockey should be prepared to manage upper and lower extremity musculoskeletal injuries, but also concussions, cervical spine injuries, and ocular and dental trauma.² 

One of the earliest epidemiological studies of ice hockey injuries looked at elite Danish hockey players over 2 seasons and found that head trauma accounted for 28% of all injuries, followed by lower extremity injuries at 27% with upper extremity injuries accounting for 19%.⁷ More recent epidemiological studies have shown similar rates based on body region while further defining individual diagnoses and their incidence. This should help clinicians and researchers develop prevention strategies, as well as improve treatments to optimize player outcomes and return to sport.^8,9 Our group recently reviewed the evaluation and management of common head, neck, and shoulder injuries at all competitive levels of ice hockey, and this article serves to complement the former by focusing on lower extremity injuries (Table).²

Continue to: Hip and groin...

 

 

EVALUATION AND MANAGEMENT OF COMMON LOWER EXTREMITY HOCKEY INJURIES

HIP INJURIES

Hip and groin injuries are very common amongst this group of athletes and account for approximately 9% of all ice hockey injuries.¹ Unfortunately, they are also known for their high recurrence rates, which may be in part due to delayed diagnosis, inadequate rest and rehabilitation, as well as the extreme loads that are placed on the hip during competition.^10,11 In hockey, the most commonly reported hip injuries include goaltender’s hip, FAI, sports hernia/hockey groin syndrome, adductor strains, hip pointer, and quadriceps contusions. Dalton and colleagues¹² performed the largest epidemiological study to date on hip and groin injuries amongst National Collegiate Athletic Association ice hockey players and reported that the most common injury mechanism was noncontact in nature. Contact injuries accounted for 13% (55 of 421) in men’s ice hockey players while less than 4% (4 of 114) injuries in female ice hockey players, which is likely attributed to a no checking rule in the women’s division. Some of these hip and groin injuries are difficult to diagnose so it is important for the team physician to perform a thorough history and physical examination. Advanced imaging (magnetic resonance imaging [MRI] or a computed tomography (CT) scan with 3D reconstructions) may be necessary to make the correct diagnosis. This is important for providing proper treatment as well as setting player expectations for return to sport.¹²

Table 1. Return-to-Play Guidelines for Common Lower Extremity Ice Hockey Injuries
Lower Extremity Injury	Treatment Options	Return-to-the-Rink Goal
FAI	In-season: injection, physical therapy program, NSAIDS. Off-season or unable to play: requires arthroscopic surgery	Nonoperative can take up to 6 weeks. Surgical depends on what is fixed but goal is 4 months to return to ice24,26
Sports hernia/athletic pubalgia	In-season: physical therapy program, NSAIDS Off-season or unable to play requiring surgery. Essential to make sure no other pathology (eg, FAI, osteitis pubis, adductor strain) to maximize success	Nonoperative 6-8 wk trial of physical therapy Operative: depends if concomitant FAI but in isolation goal is 3-4 mo33,54
Adductor strains	Ice, NSAIDS, physical therapy, use of Hypervolt Hyperice	Depends on position (goalie vs skater) and severity; can take up to 4-8 wk to return to ice. Want 70% strength and painless ROM to skate successfully;55 in chronic cases, may take up to 6 mo35
Quadriceps contusion	Hinged knee brace to maintain 120° of flexion, ice, compression wrap.	When player regains motion and strength, return to ice can be as fast a couple of days or as long as 3 wk8,46
MCL	Hinged knee brace, shin pad modification, ice, NSAIDs	Depends on Grade; if Grade I, 1-2 wk; Grade II, 2-4 wk; Grade III, 4-6 wk8
ACL	Surgery autograft BTB autograft soft tissue	9-10 mo41
Meniscus tear	Depends on type of tear and seasonal timing (in-season or off-season)	If surgical, 3-4 mo; if repair, 4-6 wk if partial menisectomy
High ankle sprain	Cam boot, NSAIDS, ice and physical therapy	6 wk49
Boot top laceration	Repair of cut structures, depends on depth and what is injured; best treatment is prevention with Kevlar socks	If laceration is deep and severs any medial tendons/vascular structures, return to ice can be ≥6 mo
Lace bite	Bunga pad, ice, diclofenac gel	Couple of days to up to 2 wk in recalcitrant cases3

^{Abbreviations: ACL, anterior cruciate ligament; BTB, bone-patellar tendon-bone; Cam, controlled ankle motion boot; MCL, medial collateral ligament; FAI, femoroacetabular impingement; NSAIDS, nonsteroidal anti-inflammatory drugs; ROM, range of motion.}

Throughout the hockey community, FAI is being examined as a possible source of symptomatic hip pain amongst players at all levels. A recent study, which utilized the National Hockey League (NHL) injury surveillance database, reported that FAI accounted for 5.3% of all hip and groin injuries.¹³ The etiology of FAI is thought to arise from a combination of genetic predisposition coupled with repetitive axial loading/hip flexion. This causes a bony overgrowth of the proximal femoral physes resulting in a cam deformity (Figure 1).^5,14 The abnormal bony anatomy allows for impingement between the acetabulum and proximal femur, which can injure the labrum and articular cartilage of the hip joint.

In the recent study by Ross and colleagues,¹⁵ the authors focused on symptomatic hip impingement in ice hockey goalies.¹⁵ Goaltender’s hip may be the result of the “butterfly style,” which is a technique of goaltending that emphasizes guarding the lower part of the goal. The goalie drops to his/her knees and internally rotates the hips to allow the leg pads to be parallel to the ice. This style acquired the name butterfly because of the resemblance of the spread goalie pads to a butterfly’s wings. Bedi and associates¹⁶ have evaluated hip biomechanics using 3D-generated bone models and showed in their study that arthroscopic treatment can improve hip kinematics and range of motion.

Plain radiographs showed that 90% (61 of 68) of hockey goalies had an elevated alpha angle signifying a femoral cam-type deformity.¹⁵ Goalies had a significantly lower mean lateral center-edge angle (27.3°  vs 29.6°; P = .03) and 13.2% of them were found to have acetabular dysplasia (lateral center-edge angle<20°) compared to only 3% of positional players. The CT scan measurements demonstrated that hockey goalies have a unique cam-type deformity that is located more lateral (1:00 o’clock vs 1:45 o’clock; P < .0001) along the proximal femur, an elevated maximum alpha angle (80.9° vs 68.6°; P < .0001) and loss of offset, when compared to positional players. These findings provide an anatomical basis in support of reports that goaltenders are more likely to experience intra-articular hip injuries compared to other positional players.¹³

Regardless of position, symptomatic FAI in a hockey player is generally a problem that slowly builds and is made worse with activity.¹⁷ On examination, the player may have limited hip flexion and internal rotation, as well as weakness compared to the contralateral side when testing hip flexion and abduction.^18,19 Plain radiographs plus MRI or CT allow for proper characterization and diagnosis (to include underlying chondrolabral pathology).^20,21

In the young athlete, initial management includes physical therapy, which focuses on core strengthening. Emphasis is placed on hip flexion and extension, as well as abduction and external rotation with the goal of reducing symptoms and avoiding injuries.²² A similar approach may be applied to the elite athlete, but failure of nonoperative management may necessitate surgical intervention. Hip arthroscopy continues to grow in popularity over open surgical dislocation with low complication rate and high return-to-play rate.^23-25

For the in-season athlete, attempts to continue to play can be assisted with the role of an intra-articular corticosteroid injection, which can help calm inflammation within the hip joint and mitigate pain, while rehabilitation focuses on core stabilization, postural retraining and focusing on any muscle imbalances that might be present. For positional players, ice time and shift duration can be adjusted to give the player’s hip a period of rest; meanwhile, for goaltenders, shot volumes in practice can be decreased.

Continue to: For athletes who...

 

 

For athletes who fail nonoperative care, surgical treatment varies depending on underlying hip pathology and may include femoroplasty, acetabuloplasty, and microfracture as well as labral repair or debridement. Though data are limited, Philippon and colleagues²⁶ have published promising results in a case series of 28 NHL players after surgical intervention for FAI. All players returned to sport at an average of 3.8 months and players who had surgery within 1 year of injury returned on average 1.1 months sooner than those who waited more than 1 year. Rehabilitation protocol varies between goaltenders compared to defensemen and offensive players due to the different demands required for blocking shots on goal.²⁷

One of the most challenging injuries to correctly identify in the hip area is athletic pubalgia (also referred to as sports hernia or core muscle injury) because pain in the groin may be referred from the lumbar spine, hip joint, urologic, or perineal etiologies.²⁸ Sports hernias involve dilatation of the external ring of the inguinal canal and thinning of the posterior wall. Players may report to the athletic trainer or team physician with a complaint of groin pain that is worse when pushing off with their skate or taking a slap shot.²⁹ On exam, pain can be reproduced by hip extension, contralateral torso rotation, or with a resisted sit-up with palpation of the inferolateral edge of the distal rectus abdominus.³⁰ An MRI with specific sequences centered over the pubic symphysis is usually warranted to aid in the workup of sports hernia. An MRI in these cases may also demonstrate avulsions of the rectus abdominus.³¹

Most of these injuries are managed conservatively but can warrant surgical intervention if the symptoms persist. In the study by Jakoi and colleagues,³² they identified 43 ice hockey players over an 8-year period (2001-2008) who had repairs of their sports hernias and assessed the statistics during the 2 years prior and 2 years after surgery. The authors found that 80% of these players were able to return to the ice for 2 or more full seasons. The return-to-sport rate was comparable to other sports after sports hernia repair, but players who had played in ≥7 seasons demonstrated a greater decrease in number of games played, goals, assists and time on ice compared to those who had played in ≤6 seasons prior to the time of injury. Between 1989 and 2000, 22 NHL players who failed to respond to nonoperative management of their groin injuries underwent surgical exploration.²⁹ At the time of surgical exploration, their hockey groin syndrome, consisted of small tears in the external oblique aponeurosis through which branches of the ilioinguinal or iliohypogastric could be identified. These surgical procedures were all through a standard inguinal approach and the perforating neurovascular structures were excised, while the main trunk of the ilioinguinal nerve was ablated and the external oblique aponeurosis was repaired and reinforced with Goretex (W.L. Gore & Associates Inc, Flagstaff, AZ). At follow-up, 18 of the 22 players (82%) had no pain and 19 (86%) were able to resume their careers in the NHL.²⁹ Ice hockey players with sports hernias or hockey groin syndrome often return to the sport, but it is important to identify these problems early so that surgical options can be discussed if the player fails conservative management. It is also critical to make sure that all pathology is identified, because in players with mixed sports hernia and FAI, return-to-play results improve when both issues are addressed. In a study of athletes (some of whom were ice hockey players), who had both FAI and sports hernia, and only hernia/pubalgia surgery was performed, 25% of these athletes returned to sport. If only FAI was addressed, 50% of the athletes returned to sport; however, when hernia and FAI were treated, 89% returned to play.³³

Adductor strains includes injury to the adductor muscles, pectineus, obturator externus and gracilis, and are prevalent in ice hockey players. A study of elite Swedish ice hockey players published in 1988 reported that adductor strains accounted for 10% (10 of 95) of all injuries.³⁴ Given the prevalence of these injuries, considerable research has been dedicated to understanding their mechanism and prevention.³⁵ Adductor strains within the ice hockey population have been attributed to the eccentric forces on the adductors when players attempt to decelerate the leg during a stride.³⁶ A study of NHL players revealed that a ratio <80% of adductor-to-abductor muscle is the best predictor of a groin strain.³⁷

These injuries are also well known for their recurrence rates, as was the case in an NHL study where 4 of the 9 adductor strains (44%) were recurrent injuries.³⁷ The authors attributed the recurrence to an incomplete rehabilitation program and an accelerated return to sport. This was followed by an NHL prevention program that spanned 2 seasons and analyzed 58 players whose adductor-to-abductor ratio was <80% and placed them into a 6-week intervention program during the preseason.³⁷ Only 3 players sustained an adductor strain in the 2 subsequent seasons after the intervention, compared to 11 strains in the previous 2 seasons. Thus, early identification of muscle strength imbalance coupled with an appropriate intervention program has proven to be an effective means of reducing adductor strains in this at-risk population.

Continue to: Contact injuries may...

 

 

Contact injuries may vary with checking into the boards being unique to men’s ice hockey. Hip pointers occur as a result of a direct compression injury to the iliac crest, which causes trauma to the bone but also to the overlying hip abductor musculature, and represent roughly 2.4% of ice hockey injuries.²³ The resulting contusion may cause a local hematoma formation. Early identification of the injury plus treatment with RICE (rest, ice, compression, elevation) coupled with crutches to limit weight-bearing status may minimize soft tissue trauma and swelling, and ultimately aid in pain control and return to sport.³⁸ Hip abductor strengthening, added padding over the injured area, as well as a compressive hip spica wrapping, have all been suggested to expedite return to play and help prevent recurrence of the hip pointer.⁸

KNEE INJURIES

Injury to the medial collateral ligament (MCL) is the most commonly reported knee injury (Figure 2) and second only to concussion amongst all injuries in National Collegiate Athletic Association ice hockey players.^8,39 The mechanism of injury typically involves a valgus force on the knee, which is often caused by collision into another player.³⁹ Valgus stress testing with the knee in 30° of flexion is used to grade the severity of injury (Grade I: 0-5 mm of medial opening; Grade II: 5-10 mm of medial opening; Grade III: >10 mm of medial opening).³⁹ One study that followed a single college hockey team for 8 seasons reported that 77% of injuries (10 of 13) occurred during player-to-player collision,³⁹ with 5 being Grade 1 injuries, 6 Grade 2 injuries, 1 Grade 3; information was missing for 1 player. Nonoperative management of incomplete injuries, grade 1 and 2 sprains, with RICE and early physical therapy intervention to work on knee range of motion and quadriceps strengthening typically helps the player return to sport within days for grade 1 and 2 injuries to 3 weeks for grade 2 injuries. Complete tears have been managed both operatively and nonoperatively with evidence to suggest better outcomes after surgical intervention if there is a concomitant ACL injury requiring reconstruction.^8,9

Anterior cruciate ligament (ACL) tears occur less frequently in hockey players compared to the players in other sports such as football and basketball.^38,40 Between 2006 and 2010, 47 players were identified by the NHL Injury Surveillance System as having sustained an ACL injury, which equates to an incidence of 9.4 ACL injuries per NHL season over this time span.⁴¹ The mechanism of ACL tears in ice hockey players appears to be different from other sports players based on a recent MRI study that evaluated players for concomitant injuries following ACL tear and noted significantly fewer bone bruises on the lateral femoral condyle compared to players in other sports.⁴² Early evaluation after injury with Lachman and/or pivot shift tests aids the diagnosis. Data from the NHL study identified 32 players (68%) with concomitant meniscal injuries and 32 (68%) had MCL injuries in conjunction with their ACL tears.⁴¹ Average length in the league prior to injury was 5.65 seasons. Twenty-nine of the injured players (61.7%) underwent reconstruction with a patellar tendon autograft, 13 (27.7%) had a hamstring autograft, and 5 (10.6%) had either a patellar tendon or hamstring allograft.⁴¹ Meniscus and ACL injuries were associated with a decreased length of career compared to age-matched controls and, notably, players >30 years at the time of injury had only a 67% rate of return to sport whereas those <30 years had a return-to-sport rate of 80%. Players who were able to return did so at an average of 9.8 months (range, 6-21 months) and had a significant reduction in total number of goals, assists, and points scored compared to controls. Decline in performance was typically associated with forwards and wings, while defensemen did not demonstrate the same decrease in performance following return to ice hockey.⁴¹

Meniscal tears are a well-documented concomitant injury with ruptures of the ACL, and the combination is a known pattern associated with shorter careers compared to isolated ACL tears in ice hockey players.⁴¹ The lateral meniscus is known for increased mobility compared to the medial meniscus and is more commonly injured (39% vs 8.5%) in ACL tears that occur in contact sports and downhill skiing.⁴² Ice hockey presents a scenario that is different from other contact sports because of the near frictionless interaction between the player’s ice skates and playing surface. This likely equates to a different injury mechanism and dissipation of energy after contact as well as non-contact injuries.³⁸ A recent study reviewed knee MRI findings associated with ACL tears in collegiate ice hockey players and compared to other sports known for their high rates of concomitant meniscal pathology. The authors reported a statistically significant decrease in lateral meniscus tears and bone-bruising patterns in ice hockey players with ACL injuries compared to athletes with ACL tears in other sports.⁴³ In contrast, an NHL study of ACL tears in professional ice hockey players found that 68% of players had concomitant meniscal tears (32 out of 47 players).⁴¹

Continue to: The presence of...

 

 

The presence of a meniscal tear on MRI is typically a surgical problem, especially if it occurred with an ACL injury. Meniscal repair is preferable, if possible, because there is a known association of increased cartilage contact pressures associated with meniscal debridement. Return to sport following meniscus injury hinges upon whether it is an isolated injury and how it is treated. If the meniscus injury occurs in isolation and can be treated with a debridement and partial resection alone, there is obviously a quicker return to sport as the player can be weight-bearing immediately following surgery. Return to skating after meniscal debridement and partial resection is usually 4 to 6 weeks, whereas meniscal repair protocols vary depending on surgeon; players may need 3 months to 4 months to return to the ice.

Quadriceps contusions are contact injuries that are not unique to ice hockey (Figure 3). They may result from player collision but also from direct blows from a hockey puck. A high velocity puck is known to cause immense trauma to the quadriceps muscles, which may result in localized bleeding and hematoma formation. If the player is able to anticipate the event, active contraction of the quadriceps muscle has been shown to absorb some of the energy and result in a less traumatic injury, but in a fast paced ice hockey game, the player’s anticipation is less likely than in other sports such as baseball.⁴⁴Interestingly, the degree of knee flexion after injury is predictive of injury severity with milder injuries associated with angles >90 and more severe injuries resulting in knee flexion angles <45° and typically an antalgic gait.⁴⁵ It is important to treat these injuries during the first 24 hours with the knee maintained in 120°of flexion, plus ice and compression, which can be achieved using a locked knee brace or elastic compression wrap. Quadriceps stretching and isometric strengthening should immediately follow the period of immobilization. The addition of NSAIDs may help prevent the formation of myositis ossificans. A study from West Point suggests that the average return to sport or activity ranges from 13 days (mild contusion) to 21 days (severe contusions), while others⁸ have indicated that if the injury is treated acutely and a player is able to regain motion and strength, return to ice hockey within a few days is possible.

FOOT AND ANKLE

Ice hockey has some unique injuries that can be attributed to the use of ice skates for play. One such injury is boot-top lacerations, which are fortunately rare as they can be a career-ending injury.⁴⁷ The spectrum of injury ranges from superficial abrasions to more severe soft tissue disruption, including the extensor tendons and neurovascular structures. The actual mechanism of injury involves an opponent’s skate blade cutting across the anterior ankle. One early case report described a protective method of having players place their skate tongues deep to their protective shin pads, instead of turning the tongues down.⁴⁷ Kevlar socks have also been shown to help prevent or minimize the damage from a skate blade.⁴⁸

Injury to the lateral ankle ligaments, anterior talofibular ligament or calcaneofibular ligament, are usually more common than the higher ankle sprains involving the syndesmosis. However, this is not the case in ice hockey. The rigidity of the ice skate at the level of the lateral ligaments seems to impart a protective mechanism to the lower ligaments, but this results in a higher incidence of syndesmotic injuries. These high ankle injuries are unfortunately more debilitating and often require a longer recovery period. In a study of these injuries in NHL players, syndesmotic sprains made up 74% of all ankle sprains, whereas only 18.4% of ankle sprains involved the syndesmosis in American football players..^49,50 The average number of days between injury and return to play is 45 days, and some authors believe that defensemen may have a harder time recovering because of the demands on their ankles by having to switch continuously between forward and backward skating.⁴⁹

Most patients are treated conservatively when their ankle plain radiographs show a congruent mortise and no evidence of syndesmotic widening. If the player expresses pain when squeezing the syndesmosis, it is helpful to obtain stress radiographs to further evaluate for syndesmotic injury. Nonoperative management includes RICE, immobilization in a rigid boot with crutches to protect weight-bearing with gradual advancements and eventually physical therapy to address any ankle stiffness, followed by dynamic functional activities. Treatment options for syndesmotic widening and failed conservative management includes both screw and plate options as well as suture buttons.^49,51,52

Ankle and foot fractures were historically a rare injury in ice hockey players based on radiograph evaluation; however, the recent study by Baker and colleagues⁴ demonstrated that MRI can be helpful in detecting subradiographic fractures. Most of the injuries detected after MRI were from being hit by a hockey puck; this was a novel mechanism that had not been previously reported in the literature.⁴ Of the injuries that resulted from a direct blow, 14 of 17 occurred on the medial aspect of the foot and ankle, which is believed to result another word? from a defender skating towards an offensive player and attempting to block shots on goal. In this study, all occult fractures involving the medial malleolus were eventually treated with open reduction and internal fixation and underwent routine healing.⁴ The navicular bone and base of the first metatarsal accounted for the remaining medial-sided fractures. In a recent analysis of risk factors for reoperation following operative fixation of foot fractures across the National Basketball Association, the National Football Leagues, Major League Baseball, and the National Hockey League only a total of 3 fractures involving the foot (1 navicular and 2 first metatarsal) were identified in NHL players over a 30-year period.⁵³ The study acknowledged a major limitation being a public source for identifying players with fractures.

Lace bite is another common ice hockey injury. It typically occurs at the beginning of a season or whenever a player is breaking in a new pair of skates. The cause of the lace bite is the rigid tongue in the skate that rubs against the anterior ankle. Skating causes inflammation in the area of the tibialis anterior tendon, and the player will complain of significant anterior ankle pain. First line treatment for lace bite is ice (Figure 4A), NSAID gel (eg, diclofenac 1%), and a Bunga lace-bite pad (Absolute Athletics). (Figure 4B).

SUMMARY

Lower extremity injuries are common in ice hockey players, and a covering physician should be comfortable managing these injuries from breezers to skate. Proper evaluation and work-up is critical for early diagnosis and identification of pathology, which can minimize the impact of the injury and expedite a treatment plan to return the player safely to the ice and in the game.

ABSTRACT

The ankle is one of the most commonly injured joints in soccer and represents a significant cost to the healthcare system. The ligaments that stabilize the ankle joint determine its biomechanics—alterations of which result from various soccer-related injuries. Acute sprains are among the most common injury in soccer players and are generally treated conservatively, with emphasis placed on secondary prevention to reduce the risk for future sprains and progression to chronic ankle instability. Repetitive ankle injuries in soccer players may cause chronic ankle instability, which includes both mechanical ligamentous laxity and functional changes. Chronic ankle pathology often requires surgery to repair ligamentous damage and remove soft-tissue or osseous impingement. Proper initial treatment, rehabilitation, and secondary prevention of ankle injuries can limit the amount of time lost from play and avoid negative long-term sequelae (eg, osteochondral lesions, arthritis). On the other hand, high ankle sprains portend a poorer prognosis and a longer recovery. These injuries will typically require surgical stabilization. Impingement-like syndromes of the ankle can undergo an initial trial of conservative treatment; when this fails, however, soccer players respond favorably to arthroscopic debridement of the lesions causing impingement. Finally, other pathologies (eg, stress fractures) are highly encouraged to be treated with surgical stabilization in elite soccer players.

Continue to: EPIDEMIOLOGY

With roughly 200,000 professional and around 240 million amateur soccer players, soccer has been recognized as the most popular sport worldwide. Nevertheless, given its rising popularity in society, one must also consider the increasing incidence of injuries as a result. Elite soccer players sustain between 10 and 35 injuries per 1000 competitive playing hours.¹ Approximately 80% are traumatic, and 20% are overuse injuries.² Soccer injuries are more frequent with increasing age of the participants, whereas the incidence of injuries in preadolescent players is low. The incidence of injuries has been found to be higher during competition when compared with practice/training sessions, with some studies showing that 59% of injuries occurred during games.² Amateur or recreational soccer players sustain fewer injuries than professional soccer players, as one would expect, given both the higher intensity of training and match schedule in professionals.

The ankle is one of the most commonly injured joints in soccer, with some studies suggesting it comprises one-fifth of all injuries sustained during soccer, which is only second to those of the knee.² Ankle sprains specifically are quite a common occurrence in soccer.^3-9 A recent study of an English premier league club showed that over a 4-season period, 20% of injuries were of the foot and ankle with a mean return to sport time of 54 days.¹⁰ Of all foot and ankle related injuries, ankle sprains are the most common, followed by bruises/contusions, and tendon lesions. Fractures are very rare (1%) in soccer, but when they do occur they impart a much more extended recovery. During the 2010 Fédération Internationale de Football Association (FIFA) World Cup, ankle sprains were among the most common injuries and approximately half lead to players missing training or competitive matches.⁵

ANATOMY

Knowledge of the biomechanics of both the foot and ankle joints is essential to understand soccer injuries. The ankle joint (talocrural articulation) consists of the distal ends of the tibia and fibula, which form the mortise, and the superior aspect of the talar dome.¹¹ As a hinge joint, the ankle provides 20° of dorsiflexion and 50° of plantar flexion,¹² with stability provided by the lateral, medial, and superior ligamentous complexes. The superior articular surface of the talus is narrower posteriorly, which creates a looser fit within the mortise during plantar flexion.¹¹ This decreased stability could help explain why the most common injury in soccer involves a plantar flexion mechanism.^13,14 Inferiorly, the talus articulates with the calcaneus to form the subtalar joint. It is at this site that the majority of both foot inversion and eversion occurs. The transverse tarsal joints (Chopart’s joints) separate the hindfoot from the midfoot. Movement of this joint depends on the relative alignment of its 2 articulations: the talonavicular and calcaneocuboid joints. During foot eversion, these 2 joints are parallel to each other allowing supple motion and aiding in shock absorption during the heel strike phase of the gait cycle. With foot inversion, the joints become nonparallel and thus lock the transverse tarsal joints providing a rigid lever needed for push-off.^11,12

LATERAL LIGAMENTS

The ankle joint is stabilized laterally by a ligament complex consisting of 3 individual ligaments, all originating from the lateral malleolus: the anterior talofibular ligament (ATFL), the posterior talofibular ligament (PTFL), and the calcaneofibular ligament (CFL) (Figure 1).^11,12,15 The ATFL is the primary restraint to inversion in plantar flexion, and it helps resist anterolateral translation of the talus in the mortise. However, it is the weakest and therefore the most frequently injured of the lateral ligaments. The PTFL plays only a supplementary role in ankle stability when the lateral ligament complex is intact. It is under the greatest strain in ankle dorsiflexion and acts to limit posterior talar displacement within the mortise as well as talar external rotation.^13,16 The CFL is the primary restraint to inversion in the neutral or dorsiflexed position. It restrains subtalar inversion, thereby limiting talar tilt within the mortise.

DELTOID LIGAMENT

The deltoid ligament complex consists of 6 continuous adjacent superficial and deep ligaments that function synergistically to resist valgus and pronation forces, as well as external rotation of the talus in the mortise.^11-13,17 The superficial layer crosses both ankle and subtalar joints. It originates from the anterior colliculus and fans out to insert into the navicular, neck of the talus, sustentaculum tali, and posteromedial talar tubercle. The tibiocalcaneal (sustentaculum tali) portion is the strongest component in the superficial layer and resists calcaneal eversion. The deep layer crosses the ankle joint only. It functions as the primary stabilizer of the medial ankle and prevents both lateral displacement and external rotation of the talus. It originates from the inferior and posterior aspects of the medial malleolus and inserts on the medial and posteromedial aspects of the talus.^12,17,18

Continue to: SYNDESMOSIS

The ankle syndesmosis, or inferior tibiofibular joint, is the distal articulation between the tibia and fibula. The syndesmosis contributes to ankle mortise integrity through its firm fixation of the lateral malleolus against the lateral surface of the talus. Ligaments comprising the ankle syndesmosis include the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the inferior transverse ligament, and the interosseous ligament (IOL).¹²

ANKLE SPRAINS

Ankle sprains are the most common pathology encountered amongst soccer players, representing from one-half to two-thirds of all ankle related injuries. Most sprains occur outside of player contact.

LATERAL ANKLE SPRAINS AND INSTABILITY

Injury to the lateral ligaments of the ankle represents 77% to 91% of all ankle sprains in soccer.^6,19 The greatest risk factor for an ankle sprain in a soccer player is a history of prior sprain.²⁰ Other risk factors include increasing age, player-to-player contact, condition of the pitch, weight-bearing status of the injured limb at the time of injury, and joint instability or laxity.^21,22

The evaluation of an ankle sprain to determine its severity is best done after the acute phase, approximately 4 to 7 days after the initial injury when both pain and swelling have subsided.²³ The anterior drawer (ATFL instability) and talar tilt (CFL instability) tests are useful in evaluating ankle instability in the delayed or chronic setting; however, both have been shown to have limited sensitivity and significant variability amongst different examiners.²⁴

Clinical examination will direct further diagnostic tests including X-rays, magnetic resonance imaging (MRI), and computed tomography (CT). The Ottawa ankle rules are generally helpful in determining whether plain X-rays are indicated in the acute setting.^25,26 (Figure 2) According to these rules, ankle radiographs should be obtained if ankle pain is reported near the malleoli and 1 or more of the following is seen during examination: inability to bear weight immediately after injury and for 4 steps in the emergency department, and bony tenderness at the posterior edge or tip of the malleolus. Stress X-rays are generally not indicated in acute injuries but may be useful in chronic ankle instability cases.²³

Continue to: Ankle sprains cover...

Ankle sprains cover a broad spectrum of injuries; therefore, a grading system was devised to aid in guiding treatment. Grade I (mild) sprains are those with minimal swelling and tenderness but have the ligaments still intact. Grade II (moderate) sprains occur when there are partial ligament tears associated with moderate pain, swelling, and tenderness. Finally, Grade III (severe) sprains are complete ligament tears with marked swelling, hemorrhage, tenderness, loss of function, and abnormal joint motion and instability.^{23, 24}

Initial treatment for all ankle sprains is nonoperative and involves the RICE (rest, ice, compression, elevation) protocol with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) during the acute phase (first 4-5 days) with a short period (no >2 weeks) of immobilization.²⁷ Most authors agree that early mobilization followed by phased rehabilitation is warranted to minimize time away from sports.^28-31 Prolonged immobilization (>2 weeks) has detrimental effects and may lead to a longer return to play.^28-31 The rehabilitation protocol is divided into stages: (1) pain and edema control, (2) range of motion (ROM) and strengthening exercises, (3) soccer specific functional training, and (4) prophylactic intervention with balance and proprioception exercises. Surgical intervention is rarely indicated for acute ankle sprains. There are exceptions, however, such as when ankle sprains are associated with other injuries that require acute intervention (eg, fracture, osteochondral lesion). Surgery is indicated in the setting of chronic, recurrent mechanical instability. Anatomical repairs (modified Brostrom) seem to produce better outcomes than non-anatomical reconstructions (eg, Chrisman-Snook). Surgical outcomes are good, and most athletes are able to return to their pre-injury level of function.³²

In athletes, prevention of recurrent sprains is key. Braces may help prevent ankle sprains and bracing has been shown to be superior to taping, as tape loses its restrictive properties within 20 to 30 minutes of initiating activity.^33,34 Application of an orthosis (lace-up ankle orthosis) has been shown to reduce the incidence of ankle re-injury in soccer players with previous ankle sprains. Several studies have found minimal, if any, effect of orthoses on athletic performance.^20,35,36 Low-profile braces for soccer have been developed which allow for minimal disruption of the player’s boot and space proximally to insert the shin guard. Another essential component of prevention is prophylactic intervention with balance and proprioceptive exercises. A study looking at first division men’s league football (soccer) players in Iran showed a significant decrease in re-injury rates with proprioceptive training.³⁷ In 2003, FIFA introduced a comprehensive warm-up program (FIFA 11+), which has since been shown in several studies to decrease the risk of injury in amateur soccer players.^38-40

MEDIAL ANKLE SPRAINS AND INSTABILITY

Soccer places an unusually high demand on both the medial foot and ankle structures when compared with other sports. For instance, striking the ball requires the player to abduct and externally rotate the foot, which preloads medial structures.⁹ Hintermann¹⁸ looked at 54 cases of medial ankle instability and found that injury commonly occurred during landing on an uneven surface, which applies to soccer players when landing after heading the ball or jumping over a tackle. Pronation with eversion and extreme rotational injuries are well known to cause deltoid ligament injury. However, complete rupture of the deltoid ligament is rare and is more often associated with ankle fractures.⁴¹ Due to its close proximity and similarly shared function in medial plantar arch stabilization with the tibiospring and spring ligaments, posterior tibialis tendon dysfunction is also frequently seen in medial ankle instability.¹⁷ After an acute injury, patients can present with a medial ankle hematoma and pain along the deltoid ligament. Although chronic insufficiency is diagnosed based on the feeling of “giving way,” pain in the medial gutter of the ankle and a valgus and pronation deformity of the foot can be corrected by activating the peroneus tertius muscle. Arthroscopy is the most specific way to confirm clinically suspected instability of the medial ankle; however, MRI can demonstrate loss of organized medial fibers (Figures 3A, 3B).¹⁸ Primary surgical repair of deltoid ligament tears yield good to excellent results and should be considered in the soccer player to prevent problems associated with chronic non-repaired tears such as instability, osteoarthritis, and impingement syndromes.¹⁸ After surgical repair, players will undergo extensive physical therapy that progresses to sport-specific exercises with the ultimate goal of returning to competitive play around 4-6 months post-operatively.

HIGH ANKLE SPRAINS (SYNDESMOSIS)

High ankle sprains are much less common than low ankle sprains; however, when they do occur they portend a lengthier rehabilitation and a poorer prognosis, especially if undiagnosed. Lubberts and colleagues⁴² studied the epidemiology of isolated syndesmotic injuries in professional football players. They pooled data from 15 consecutive seasons of European professional football between 2001 and 2016. They examined a total of 3677 players from 61 teams across 17 countries. There were 1320 ankle ligament injuries registered during 15 seasons, of which 94 (7%) were isolated syndesmotic injuries. The incidence of these injuries increased annually between 2001 and 2016. Injuries were 74% contact-related, and isolated syndesmotic injuries were followed by a mean of a 39-day absence.⁴² Moreover, football players may have an increased risk of syndesmotic sprains due to foot planting and cutting action.⁴¹

Continue to: These injuriesa are typically...

These injuries are typically identified with pain over the AITFL and interosseous membrane. Physical examination tests that help identify syndesmotic injuries include the squeeze test, external rotation test, and crossed-leg test.⁴¹ The diagnosis can be made on plain X-ray when there is clear diastasis between the distal tibia and fibula. Two critical measurements on plain films are made 1 cm above the tibial plafond and are used to evaluate the integrity of the syndesmosis: tibiofibular clear space >6 mm, and tibiofibular overlap <1 mm, which indicate disruption of the syndesmosis.⁴³ More subtle injuries can be diagnosed with better sensitivity and specificity using MRI, which can also reveal secondary findings such as bone bruises, ATFL injury, osteochondral lesions, and tibiofibular incongruity.^44,45 Arthroscopy is an invaluable diagnostic tool for syndesmotic injuries with a characteristic triad finding of PITFL scarring, disrupted interosseous ligament, and posterolateral tibial plafond chondral damage.⁴⁶

Classification of the ligaments involved can aid in the selection of appropriate treatment. Grade I injuries involve AITFL tears. Grade IIa injuries involve AITFL and IOL tears. Grade IIb injuries include AITFL, PITFL, and IOL tears. Grade III injuries involve injury to all 3 ligaments, as well as a fibular fracture. Conservative treatment is recommended for Grades I and IIa, while surgical intervention is necessary for Grades IIb and III (Figures 4A, 4B). Compared with other ankle sprains, syndesmotic injuries typically require a more prolonged recovery/rehabilitation. Some studies suggest that these injuries require twice as long to heal.⁴⁷ Hopkinson and colleagues⁴⁸ reported a mean recovery time of 55 days following syndesmotic injuries in cadets at the United States Military Academy at West Point. Some surgeons advocate surgical intervention in professional athletes with mild sprains to expedite return to play.⁴⁹

Surgery has been well established as necessary in more severe injuries where there is clear diastasis or instability of the syndesmosis. Traditionally, screws were used for surgical fixation; however, they often required a second surgery for subsequent removal. There is no general consensus on the optimal screw size, level of placement, or timing of removal.^50,51 More recently, non-absorbable suture button fixation (eg, TightRope; Arthrex) has become more popular and provides certain advantages over screw fixation, such as avoiding the need for hardware removal. TightRope has been shown to provide more accurate stabilization of the syndesmosis as compared with screw fixation.⁵² Since malreduction is the most important indicator of poor long-term functional outcome, suture button fixation should be considered in the treatment of the football player.⁵³ Finally, Colcuc and colleagues⁵⁴ reported a lower complication rate and earlier return to sports in patients treated with knotless suture button devices compared with screw fixation.

OSTEOCHONDRAL LESIONS

Osteochondral lesions (OCLs) are cartilage-bone defects that are usually located in the talus. They can be caused by an acute traumatic event or repetitive microtrauma with no apparent history of trauma (eg, ankle instability). Acute OCLs can occur in soccer secondary to an ankle sprain or ankle fracture. Symptoms of OCLs include pain, swelling, and mechanical symptoms such as catching or locking, and on physical examination, one might see an effusion. The initial imaging modality of choice is radiographing; however, in ankle sprains with continued pain and swelling MRI may be indicated to rule out an underlying OCL. Missed acute lesions have a tendency not to heal and become chronic lesions, which can cause pain and playing disability. It is well established that chronic ankle instability is an important etiologic factor for OCLs. With the normal hydrostatic pressure within the ankle joint, synovial fluid gets pushed into cartilage/bone fissures, which can then lead to cystic degeneration of the subchondral bone.^55-57

Surgical repair of an OCL is dependent on both the size and location of the lesion. Acute lesions can be managed by arthroscopic débridement, microfracture, or fixation of the lesion if enough bone remains attached to the chondral lesion. Return to play is based on development and maturation of fibrocartilage over the lesion (debridement/microfracture) or healing and incorporation of the new graft (chondral repair procedures). Meanwhile, chronic lesions can be managed in 1-stage (microfracture, osteochondral autograft transfer or 2-stage (autologous chondrocyte implantation [ACI]) procedures.^56-57 Additional biologic healing augmentation with platelet-rich plasma has been described as well.⁵⁸ Newer techniques in treating chronic talus OCLs, including ones that have failed to respond to bone marrow stimulation techniques, have been developed more recently such as the use of particulated juvenile articular cartilage allograft (DeNovo NT Natural Tissue Graft^®; Zimmer Biomet).⁵⁹ These newer techniques avoid the need for a 2-stage procedure, as is the case with ACI.

Continue to: Further studies are needed...

Further studies are needed to both investigate long-term outcomes and determine the superiority of the arthroscopic juvenile cartilage procedure compared with microfracture and other cartilage resurfacing procedures. When surgically treating OCLs, one must also restore normal ankle joint biomechanics for the lesion to heal. For instance, in the presence of ankle instability, ligament reconstruction must be performed. Also, one should also consider addressing any hindfoot malalignment with an osteotomy (calcaneus, supramalleolar). In a recent retrospective study, van Eekeren and colleagues⁶⁰ showed that approximately 76% of patients were able to return to sports at long-term follow-up after arthroscopic débridement and bone marrow stimulation of talar OCLs. However, the activity level decreased at long-term follow-up and never attained the pre-injury level.⁶⁰

ANKLE IMPINGEMENT

ANTERIOR ANKLE IMPINGEMENT (FOOTBALLER'S ANKLE)

Anterior ankle impingement is caused by anterior osteophytes on both the distal tibia and talar neck. It is thought to be related to repetitive microtrauma to the anteromedial aspect of the ankle from recurrent ball impact.⁶¹ It is very common amongst soccer players with some studies suggesting that 60% of soccer players have this syndrome. Ankle impingement is characterized by anterior pain with ankle dorsiflexion, decreased dorsiflexion, and swelling. It is primarily diagnosed with lateral ankle X-rays, which will show the osteophytes. An oblique anteromedial X-ray may increase detection of osteophytes (Figure 5). The early stages of anterior impingement can be treated successfully with injections and heel lifts. Treatment of lesions that fail to respond to conservative management involves arthroscopic or open excision of osteophytes. Most patients with no preexisting osteoarthritis treated arthroscopically will experience pain relief and return to full activity, though recurrent osteophyte formation has been noted at long-term follow-up.⁶²

Anterior ankle impingement is most often caused by acute ankle sprains with an inversion type of mechanism.⁶² The subsequent reactive inflammation can cause fibrosis leading to distal fascicle enlargement of the AITFL. Impingement in the anterolateral gutter of this enlarged fascicle can also cause both chronic reactive synovitis and chondromalacia of the lateral talar dome.⁶³ MRI can identify abnormal areas of pathology; however, 50% of cases are diagnosed based on clinical examination alone.⁶³ Patients generally present with a history of anterolateral ankle pain and swelling with an occasional popping or snapping sensation.

Soccer players commonly develop anterior bony impingement due to repetitive loading of the anterior ankle from striking the ball. This repetition can lead to osteophyte formation of the anterior distal tibia and talar neck. After the osteophytes form, decreased dorsiflexion can occur due to a mechanical stop and inflammation of the interposed capsule.

The patient will exhibit tenderness to palpation along the anterolateral aspect of the ankle, with pain elicited at extreme passive dorsiflexion.⁶² Initially, an injection with local anesthetic and corticosteroid can serve both a diagnostic and therapeutic purpose; however, patients who fail conservative treatment can be treated with arthroscopy and resection of the involved scar tissue and osteophytes. The best results are seen in those patients with no concurrent intra-articular lesions or ankle osteoarthritis (Figure 5).⁶² When treated non-operatively, a player may return to play when pain resolves; however, if treated surgically with arthroscopic debridement/resection, a player must wait until his surgical scars have healed prior to attempting return to play.

Continue to: ANTEROMEDIAL ANKLE IMPINGEMENT

Anteromedial ankle impingement is a less common ankle impingement syndrome. It is associated with eversion injuries or following medial malleolar or talar fractures.^64,65 Previous injury to the anterior tibiotalar fascicle of the deltoid complex leads to ligament thickening and subsequent impingement in the anteromedial corner of the talus. Adjacent fibrosis and synovitis are common consequences of impingement; however, osteophyte formation and chondral stripping along the anteromedial talus can also be seen. Patients typically complain of pain along the anteromedial joint line that is worse with activity, clicking or popping sensations, and painful, limited dorsiflexion. On examination, impingement can be detected through palpation over the anterior tibiotalar fascicle of the deltoid ligament and eversion or extreme passive dorsiflexion of the foot, all of which will elicit medial ankle tenderness.^17,62 Initial treatment consists of rest, physical therapy, and NSAIDs. Refractory cases may be amenable to arthroscopic or open resection of the anterior tibiotalar fascicle with débridement of any adjacent synovitis and scar tissue.⁶²

POSTERIOR ANKLE IMPINGEMENT

Posterior ankle impingement is often referred to as “os trigonum syndrome” since the posterior impingement is frequently associated with a prominent os trigonum. An os trigonum is an accessory ossicle representing the separated posterolateral tubercle of the talus. It is usually asymptomatic. However, in soccer players, pain can occur from impaction between the posterior tibial plafond and the os trigonum, or because of soft tissue compression between the 2 opposing osseous structures. The pain is due to repetitive microtrauma (ankle plantarflexion) or acute forced plantarflexion, which can present as an acute fracture of the os trigonum. Because soccer is a sport requiring both repetitive and extreme plantarflexion, it may predispose players to posterior ankle impingement (Figures 6A, 6B).^62,66

Clinically, it can be very difficult to detect and diagnose because the affected structures lie deep and it can coexist with other disease processes (eg, peroneal tendinopathy, Achilles tendinopathy).^62,66 Patients will complain of chronic deep posterior ankle pain that is worse with push-off activities (eg, jumping). On examination, patients will exhibit pain with palpation over the posterolateral process and with the crunch test. Lateral radiograph with the foot in plantar flexion will show the os trigonum impinged between the posterior tibial malleolus and the calcaneal tuberosity. An MRI will demonstrate the os trigonum as well as any associated inflammation and edema, while it can also demonstrate coexisting pathologies.

Initial treatment consists of rest, NSAIDs, and taping to prevent plantar flexion. Ultrasound-guided cortisone injection of the capsule and posterior bursa can be both therapeutic and diagnostic. A posterior injection can be used to temporize the symptoms so that the soccer player can make it through the season.

Surgical excision is saved for refractory cases, and this can be done either through an open posterolateral approach or arthroscopic techniques. Recently, Georgiannos and Bisbinas⁶⁷ showed in an athletic population that endoscopic excision had both a lower complication rate and a quicker return to sports compared with the traditional open approach. Carreira and colleagues⁶⁸ conducted a retrospective case series of 20 patients (mostly competitive athletes). They found that posterior ankle arthroscopy to address posterior impingement allowed for the maintenance or restoration of anatomic ROM of the ankle and hindfoot, ability to return to at least the previous level of activity, and improvement in objective assessment of pain relief and a higher level of function parameters.⁶⁸

Continue to: TENDON PATHOLOGY

SUPERIOR PERONEAL RETINACULUM INJURY

The superior peroneal retinaculum (SPR) forms the roof of the superior peroneal tunnel. The tunnel contains the peroneus brevis and longus tendons and is bordered by the retromalleolar groove of the fibula and the lower aspect of the posterior intramuscular septum of the leg.^69,70 The SPR originates from the posterolateral ridge of the fibula and inserts onto the lateral calcaneus, and it is the primary restraint of the peroneal tendons within the retromalleolar sulcus.

Injury to the retinaculum results from both ankle dorsiflexion and inversion, and forceful reflex contraction of the peroneal muscles, which causes subluxation or dislocation of the contained tendons.⁶⁹ A high level of suspicion is required regarding these injuries since the mechanism of injury is similar to that of a simple lateral ankle sprain. In the setting of retrofibular pain, snapping or popping sensations around the lateral malleolus, or chronic ankle instability that worsens on uneven surfaces, one must consider an injury to the SPR.⁶⁹ Radiographs are not always diagnostic; however, occasionally on an internal rotation view, one may see a cortical avulsion off the distal tip of the lateral malleolus (“fleck sign”) indicating a rim fracture from an SPR injury (Figure 7). MRI is the best imaging modality to assess the peroneal tendons, as well as an SPR injury. Recently, ultrasound has grown in popularity and may be more useful, since it allows for dynamic evaluation of subluxating/dislocating tendons.⁶⁹

Conservative management is often associated with poor outcomes, and surgery is indicated for all acute and chronic dislocations in athletes.⁷¹ Anatomic reconstruction of the SPR is the preferred surgical method.⁷² Peroneus brevis debulking and fibular groove deepening may also augment the retinaculum repair.⁷³ van Dijk and colleagues in their systematic review showed that patients treated with both groove deepening and SPR repair have higher rates of return to the sport than patients treated with SPR repair alone.⁷⁴

STRESS FRACTURES

FIFTH METATARSAL

Fifth metatarsal stress fractures usually occur secondary to lateral overload or avulsion of the peroneus brevis. The fifth metatarsal base can be susceptible to injury in a cavovarus foot. Non-operative treatment typically requires a longer period of immobilization (boot or cast) and necessitates a longer period of non–weight-bearing (anywhere between 6-12 weeks). Therefore, surgery is typically recommended in athletes or in the setting of a recurrent base of the fifth metatarsal fracture to expedite healing and return to play. Return to play is still not recommended until there is evidence of radiographic healing of the fracture. There are certain distinctions with fifth metatarsal stress fractures regarding location and healing rates that need to be taken into account.^75,76 In particular, zone 2 injuries (Jones fractures) represent a vascular watershed area, making these fractures prone to nonunion with nonunion rates as high as 15% to 30%. Occasionally, the cavovarus deformity will require correction as well as a reduction in the risk of recurrence or nonunion. Surgical fixation most commonly consists of a single screw placed in an antegrade fashion.⁷⁷ One must pay attention to screw size since smaller diameter screws (<4.5 mm) are associated with delayed union or nonunion. Moreover, screws that are too long will straighten the curved metatarsal shaft and can lead to fracture distraction or malreduction (Figures 8A, 8B).⁷⁷

Patients have returned to competitive sports within 6 weeks; however, it should be noted that causes of failure were linked to early return and return to sports before a radiographic union can lead to failure of fixation. Ekstrand and van Dijk⁷⁸ studied a large group of professional soccer players and found that out of 13,754 injuries, 0.5% (67) were fifth metatarsal fractures. Of note, they found that 45% of players had prodromal symptoms. Furthermore, after surgical treatment the fractures healed faster, compared with conservative treatment (75% vs 33%); however, there was no significant difference in lay-off days between both groups (80 vs 74 days).⁷⁸ Matsuda and colleagues⁷⁹ looked at 335 male collegiate soccer players, 29 of whom had a history of a fifth metatarsal stress fracture. They found that playing the midfield position and having an everted rearfoot and inverted forefoot alignment were associated with fifth metatarsal stress fractures.⁷⁹ Saita and colleagues⁸⁰ found that restricted hip internal rotation was associated with an increased risk of developing a Jones fracture in 162 professional football players. Finally, Fujitaka and colleagues⁸¹ looked at 273 male soccer players between 2005 and 2013. They found an association between weak toe-grip strength and fifth metatarsal fractures, suggesting that weak toe-grip may lead to an increase in the load applied onto the lateral side of the foot, resulting in a stress fracture.⁸¹

Continue to: NAVICULAR

Another common tarsal bone that sustains stress fractures is the navicular. It is not as common as calcaneal stress fractures in military recruits but can occur in the same type of population, as well as explosive athletics such as sprinters and soccer players. It commonly presents with an indistinct vague achy pain with activity that improves with rest, and pain at the dorsum of the midfoot or along the medial longitudinal arch with activity. It can easily go undiagnosed for quite some time given the difficulty in visualizing the navicular with plain radiographs. Clinically, it is difficult to make the diagnosis, and therefore advanced imaging is necessary when the injury is suspected. Both MRI and CT scans can be used to understand the extent of the injury (Figures 9A-9C). In non-displaced stress fractures, conservative non-operative treatment is the appropriate treatment modality with a brief period of immobilization and non–weight-bearing;⁸² however, operative treatment is also considered in elite athletes. In either case, return to play is discouraged until there is evidence of radiographic healing. When a displacement is noted, or there is a delay in diagnosis, then operative treatment is recommended.

CONCLUSION

Ankle injuries are very common in soccer and can result in decreased performance or significant loss of playing time. Treatment of acute injury generally follows a conservative route, with surgical intervention reserved for severe ruptures or osteochondral fracture of the ankle joint. Chronic ankle pathology resulting in mechanical or functional instability generally requires surgery to repair ligamentous damage and restore normal ankle kinematics. It is critical for the soccer player to receive appropriate rehabilitation prior to returning to play in order to reduce the risk for reinjury and further chronic instability. Prevention and early intervention of ankle injuries is key in preventing the long-term sequelae of ankle injuries, such as arthritis, in former soccer players.

ABSTRACT

The ankle is one of the most commonly injured joints in soccer and represents a significant cost to the healthcare system. The ligaments that stabilize the ankle joint determine its biomechanics—alterations of which result from various soccer-related injuries. Acute sprains are among the most common injury in soccer players and are generally treated conservatively, with emphasis placed on secondary prevention to reduce the risk for future sprains and progression to chronic ankle instability. Repetitive ankle injuries in soccer players may cause chronic ankle instability, which includes both mechanical ligamentous laxity and functional changes. Chronic ankle pathology often requires surgery to repair ligamentous damage and remove soft-tissue or osseous impingement. Proper initial treatment, rehabilitation, and secondary prevention of ankle injuries can limit the amount of time lost from play and avoid negative long-term sequelae (eg, osteochondral lesions, arthritis). On the other hand, high ankle sprains portend a poorer prognosis and a longer recovery. These injuries will typically require surgical stabilization. Impingement-like syndromes of the ankle can undergo an initial trial of conservative treatment; when this fails, however, soccer players respond favorably to arthroscopic debridement of the lesions causing impingement. Finally, other pathologies (eg, stress fractures) are highly encouraged to be treated with surgical stabilization in elite soccer players.

Continue to: EPIDEMIOLOGY

With roughly 200,000 professional and around 240 million amateur soccer players, soccer has been recognized as the most popular sport worldwide. Nevertheless, given its rising popularity in society, one must also consider the increasing incidence of injuries as a result. Elite soccer players sustain between 10 and 35 injuries per 1000 competitive playing hours.¹ Approximately 80% are traumatic, and 20% are overuse injuries.² Soccer injuries are more frequent with increasing age of the participants, whereas the incidence of injuries in preadolescent players is low. The incidence of injuries has been found to be higher during competition when compared with practice/training sessions, with some studies showing that 59% of injuries occurred during games.² Amateur or recreational soccer players sustain fewer injuries than professional soccer players, as one would expect, given both the higher intensity of training and match schedule in professionals.

The ankle is one of the most commonly injured joints in soccer, with some studies suggesting it comprises one-fifth of all injuries sustained during soccer, which is only second to those of the knee.² Ankle sprains specifically are quite a common occurrence in soccer.^3-9 A recent study of an English premier league club showed that over a 4-season period, 20% of injuries were of the foot and ankle with a mean return to sport time of 54 days.¹⁰ Of all foot and ankle related injuries, ankle sprains are the most common, followed by bruises/contusions, and tendon lesions. Fractures are very rare (1%) in soccer, but when they do occur they impart a much more extended recovery. During the 2010 Fédération Internationale de Football Association (FIFA) World Cup, ankle sprains were among the most common injuries and approximately half lead to players missing training or competitive matches.⁵

ANATOMY

Knowledge of the biomechanics of both the foot and ankle joints is essential to understand soccer injuries. The ankle joint (talocrural articulation) consists of the distal ends of the tibia and fibula, which form the mortise, and the superior aspect of the talar dome.¹¹ As a hinge joint, the ankle provides 20° of dorsiflexion and 50° of plantar flexion,¹² with stability provided by the lateral, medial, and superior ligamentous complexes. The superior articular surface of the talus is narrower posteriorly, which creates a looser fit within the mortise during plantar flexion.¹¹ This decreased stability could help explain why the most common injury in soccer involves a plantar flexion mechanism.^13,14 Inferiorly, the talus articulates with the calcaneus to form the subtalar joint. It is at this site that the majority of both foot inversion and eversion occurs. The transverse tarsal joints (Chopart’s joints) separate the hindfoot from the midfoot. Movement of this joint depends on the relative alignment of its 2 articulations: the talonavicular and calcaneocuboid joints. During foot eversion, these 2 joints are parallel to each other allowing supple motion and aiding in shock absorption during the heel strike phase of the gait cycle. With foot inversion, the joints become nonparallel and thus lock the transverse tarsal joints providing a rigid lever needed for push-off.^11,12

LATERAL LIGAMENTS

The ankle joint is stabilized laterally by a ligament complex consisting of 3 individual ligaments, all originating from the lateral malleolus: the anterior talofibular ligament (ATFL), the posterior talofibular ligament (PTFL), and the calcaneofibular ligament (CFL) (Figure 1).^11,12,15 The ATFL is the primary restraint to inversion in plantar flexion, and it helps resist anterolateral translation of the talus in the mortise. However, it is the weakest and therefore the most frequently injured of the lateral ligaments. The PTFL plays only a supplementary role in ankle stability when the lateral ligament complex is intact. It is under the greatest strain in ankle dorsiflexion and acts to limit posterior talar displacement within the mortise as well as talar external rotation.^13,16 The CFL is the primary restraint to inversion in the neutral or dorsiflexed position. It restrains subtalar inversion, thereby limiting talar tilt within the mortise.

DELTOID LIGAMENT

The deltoid ligament complex consists of 6 continuous adjacent superficial and deep ligaments that function synergistically to resist valgus and pronation forces, as well as external rotation of the talus in the mortise.^11-13,17 The superficial layer crosses both ankle and subtalar joints. It originates from the anterior colliculus and fans out to insert into the navicular, neck of the talus, sustentaculum tali, and posteromedial talar tubercle. The tibiocalcaneal (sustentaculum tali) portion is the strongest component in the superficial layer and resists calcaneal eversion. The deep layer crosses the ankle joint only. It functions as the primary stabilizer of the medial ankle and prevents both lateral displacement and external rotation of the talus. It originates from the inferior and posterior aspects of the medial malleolus and inserts on the medial and posteromedial aspects of the talus.^12,17,18

Continue to: SYNDESMOSIS

The ankle syndesmosis, or inferior tibiofibular joint, is the distal articulation between the tibia and fibula. The syndesmosis contributes to ankle mortise integrity through its firm fixation of the lateral malleolus against the lateral surface of the talus. Ligaments comprising the ankle syndesmosis include the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the inferior transverse ligament, and the interosseous ligament (IOL).¹²

ANKLE SPRAINS

Ankle sprains are the most common pathology encountered amongst soccer players, representing from one-half to two-thirds of all ankle related injuries. Most sprains occur outside of player contact.

LATERAL ANKLE SPRAINS AND INSTABILITY

Injury to the lateral ligaments of the ankle represents 77% to 91% of all ankle sprains in soccer.^6,19 The greatest risk factor for an ankle sprain in a soccer player is a history of prior sprain.²⁰ Other risk factors include increasing age, player-to-player contact, condition of the pitch, weight-bearing status of the injured limb at the time of injury, and joint instability or laxity.^21,22

The evaluation of an ankle sprain to determine its severity is best done after the acute phase, approximately 4 to 7 days after the initial injury when both pain and swelling have subsided.²³ The anterior drawer (ATFL instability) and talar tilt (CFL instability) tests are useful in evaluating ankle instability in the delayed or chronic setting; however, both have been shown to have limited sensitivity and significant variability amongst different examiners.²⁴

Clinical examination will direct further diagnostic tests including X-rays, magnetic resonance imaging (MRI), and computed tomography (CT). The Ottawa ankle rules are generally helpful in determining whether plain X-rays are indicated in the acute setting.^25,26 (Figure 2) According to these rules, ankle radiographs should be obtained if ankle pain is reported near the malleoli and 1 or more of the following is seen during examination: inability to bear weight immediately after injury and for 4 steps in the emergency department, and bony tenderness at the posterior edge or tip of the malleolus. Stress X-rays are generally not indicated in acute injuries but may be useful in chronic ankle instability cases.²³

Continue to: Ankle sprains cover...

Ankle sprains cover a broad spectrum of injuries; therefore, a grading system was devised to aid in guiding treatment. Grade I (mild) sprains are those with minimal swelling and tenderness but have the ligaments still intact. Grade II (moderate) sprains occur when there are partial ligament tears associated with moderate pain, swelling, and tenderness. Finally, Grade III (severe) sprains are complete ligament tears with marked swelling, hemorrhage, tenderness, loss of function, and abnormal joint motion and instability.^{23, 24}

Initial treatment for all ankle sprains is nonoperative and involves the RICE (rest, ice, compression, elevation) protocol with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) during the acute phase (first 4-5 days) with a short period (no >2 weeks) of immobilization.²⁷ Most authors agree that early mobilization followed by phased rehabilitation is warranted to minimize time away from sports.^28-31 Prolonged immobilization (>2 weeks) has detrimental effects and may lead to a longer return to play.^28-31 The rehabilitation protocol is divided into stages: (1) pain and edema control, (2) range of motion (ROM) and strengthening exercises, (3) soccer specific functional training, and (4) prophylactic intervention with balance and proprioception exercises. Surgical intervention is rarely indicated for acute ankle sprains. There are exceptions, however, such as when ankle sprains are associated with other injuries that require acute intervention (eg, fracture, osteochondral lesion). Surgery is indicated in the setting of chronic, recurrent mechanical instability. Anatomical repairs (modified Brostrom) seem to produce better outcomes than non-anatomical reconstructions (eg, Chrisman-Snook). Surgical outcomes are good, and most athletes are able to return to their pre-injury level of function.³²

In athletes, prevention of recurrent sprains is key. Braces may help prevent ankle sprains and bracing has been shown to be superior to taping, as tape loses its restrictive properties within 20 to 30 minutes of initiating activity.^33,34 Application of an orthosis (lace-up ankle orthosis) has been shown to reduce the incidence of ankle re-injury in soccer players with previous ankle sprains. Several studies have found minimal, if any, effect of orthoses on athletic performance.^20,35,36 Low-profile braces for soccer have been developed which allow for minimal disruption of the player’s boot and space proximally to insert the shin guard. Another essential component of prevention is prophylactic intervention with balance and proprioceptive exercises. A study looking at first division men’s league football (soccer) players in Iran showed a significant decrease in re-injury rates with proprioceptive training.³⁷ In 2003, FIFA introduced a comprehensive warm-up program (FIFA 11+), which has since been shown in several studies to decrease the risk of injury in amateur soccer players.^38-40

MEDIAL ANKLE SPRAINS AND INSTABILITY

Soccer places an unusually high demand on both the medial foot and ankle structures when compared with other sports. For instance, striking the ball requires the player to abduct and externally rotate the foot, which preloads medial structures.⁹ Hintermann¹⁸ looked at 54 cases of medial ankle instability and found that injury commonly occurred during landing on an uneven surface, which applies to soccer players when landing after heading the ball or jumping over a tackle. Pronation with eversion and extreme rotational injuries are well known to cause deltoid ligament injury. However, complete rupture of the deltoid ligament is rare and is more often associated with ankle fractures.⁴¹ Due to its close proximity and similarly shared function in medial plantar arch stabilization with the tibiospring and spring ligaments, posterior tibialis tendon dysfunction is also frequently seen in medial ankle instability.¹⁷ After an acute injury, patients can present with a medial ankle hematoma and pain along the deltoid ligament. Although chronic insufficiency is diagnosed based on the feeling of “giving way,” pain in the medial gutter of the ankle and a valgus and pronation deformity of the foot can be corrected by activating the peroneus tertius muscle. Arthroscopy is the most specific way to confirm clinically suspected instability of the medial ankle; however, MRI can demonstrate loss of organized medial fibers (Figures 3A, 3B).¹⁸ Primary surgical repair of deltoid ligament tears yield good to excellent results and should be considered in the soccer player to prevent problems associated with chronic non-repaired tears such as instability, osteoarthritis, and impingement syndromes.¹⁸ After surgical repair, players will undergo extensive physical therapy that progresses to sport-specific exercises with the ultimate goal of returning to competitive play around 4-6 months post-operatively.

HIGH ANKLE SPRAINS (SYNDESMOSIS)

High ankle sprains are much less common than low ankle sprains; however, when they do occur they portend a lengthier rehabilitation and a poorer prognosis, especially if undiagnosed. Lubberts and colleagues⁴² studied the epidemiology of isolated syndesmotic injuries in professional football players. They pooled data from 15 consecutive seasons of European professional football between 2001 and 2016. They examined a total of 3677 players from 61 teams across 17 countries. There were 1320 ankle ligament injuries registered during 15 seasons, of which 94 (7%) were isolated syndesmotic injuries. The incidence of these injuries increased annually between 2001 and 2016. Injuries were 74% contact-related, and isolated syndesmotic injuries were followed by a mean of a 39-day absence.⁴² Moreover, football players may have an increased risk of syndesmotic sprains due to foot planting and cutting action.⁴¹

Continue to: These injuriesa are typically...

These injuries are typically identified with pain over the AITFL and interosseous membrane. Physical examination tests that help identify syndesmotic injuries include the squeeze test, external rotation test, and crossed-leg test.⁴¹ The diagnosis can be made on plain X-ray when there is clear diastasis between the distal tibia and fibula. Two critical measurements on plain films are made 1 cm above the tibial plafond and are used to evaluate the integrity of the syndesmosis: tibiofibular clear space >6 mm, and tibiofibular overlap <1 mm, which indicate disruption of the syndesmosis.⁴³ More subtle injuries can be diagnosed with better sensitivity and specificity using MRI, which can also reveal secondary findings such as bone bruises, ATFL injury, osteochondral lesions, and tibiofibular incongruity.^44,45 Arthroscopy is an invaluable diagnostic tool for syndesmotic injuries with a characteristic triad finding of PITFL scarring, disrupted interosseous ligament, and posterolateral tibial plafond chondral damage.⁴⁶

Classification of the ligaments involved can aid in the selection of appropriate treatment. Grade I injuries involve AITFL tears. Grade IIa injuries involve AITFL and IOL tears. Grade IIb injuries include AITFL, PITFL, and IOL tears. Grade III injuries involve injury to all 3 ligaments, as well as a fibular fracture. Conservative treatment is recommended for Grades I and IIa, while surgical intervention is necessary for Grades IIb and III (Figures 4A, 4B). Compared with other ankle sprains, syndesmotic injuries typically require a more prolonged recovery/rehabilitation. Some studies suggest that these injuries require twice as long to heal.⁴⁷ Hopkinson and colleagues⁴⁸ reported a mean recovery time of 55 days following syndesmotic injuries in cadets at the United States Military Academy at West Point. Some surgeons advocate surgical intervention in professional athletes with mild sprains to expedite return to play.⁴⁹

Surgery has been well established as necessary in more severe injuries where there is clear diastasis or instability of the syndesmosis. Traditionally, screws were used for surgical fixation; however, they often required a second surgery for subsequent removal. There is no general consensus on the optimal screw size, level of placement, or timing of removal.^50,51 More recently, non-absorbable suture button fixation (eg, TightRope; Arthrex) has become more popular and provides certain advantages over screw fixation, such as avoiding the need for hardware removal. TightRope has been shown to provide more accurate stabilization of the syndesmosis as compared with screw fixation.⁵² Since malreduction is the most important indicator of poor long-term functional outcome, suture button fixation should be considered in the treatment of the football player.⁵³ Finally, Colcuc and colleagues⁵⁴ reported a lower complication rate and earlier return to sports in patients treated with knotless suture button devices compared with screw fixation.

OSTEOCHONDRAL LESIONS

Osteochondral lesions (OCLs) are cartilage-bone defects that are usually located in the talus. They can be caused by an acute traumatic event or repetitive microtrauma with no apparent history of trauma (eg, ankle instability). Acute OCLs can occur in soccer secondary to an ankle sprain or ankle fracture. Symptoms of OCLs include pain, swelling, and mechanical symptoms such as catching or locking, and on physical examination, one might see an effusion. The initial imaging modality of choice is radiographing; however, in ankle sprains with continued pain and swelling MRI may be indicated to rule out an underlying OCL. Missed acute lesions have a tendency not to heal and become chronic lesions, which can cause pain and playing disability. It is well established that chronic ankle instability is an important etiologic factor for OCLs. With the normal hydrostatic pressure within the ankle joint, synovial fluid gets pushed into cartilage/bone fissures, which can then lead to cystic degeneration of the subchondral bone.^55-57

Surgical repair of an OCL is dependent on both the size and location of the lesion. Acute lesions can be managed by arthroscopic débridement, microfracture, or fixation of the lesion if enough bone remains attached to the chondral lesion. Return to play is based on development and maturation of fibrocartilage over the lesion (debridement/microfracture) or healing and incorporation of the new graft (chondral repair procedures). Meanwhile, chronic lesions can be managed in 1-stage (microfracture, osteochondral autograft transfer or 2-stage (autologous chondrocyte implantation [ACI]) procedures.^56-57 Additional biologic healing augmentation with platelet-rich plasma has been described as well.⁵⁸ Newer techniques in treating chronic talus OCLs, including ones that have failed to respond to bone marrow stimulation techniques, have been developed more recently such as the use of particulated juvenile articular cartilage allograft (DeNovo NT Natural Tissue Graft^®; Zimmer Biomet).⁵⁹ These newer techniques avoid the need for a 2-stage procedure, as is the case with ACI.

Continue to: Further studies are needed...

Further studies are needed to both investigate long-term outcomes and determine the superiority of the arthroscopic juvenile cartilage procedure compared with microfracture and other cartilage resurfacing procedures. When surgically treating OCLs, one must also restore normal ankle joint biomechanics for the lesion to heal. For instance, in the presence of ankle instability, ligament reconstruction must be performed. Also, one should also consider addressing any hindfoot malalignment with an osteotomy (calcaneus, supramalleolar). In a recent retrospective study, van Eekeren and colleagues⁶⁰ showed that approximately 76% of patients were able to return to sports at long-term follow-up after arthroscopic débridement and bone marrow stimulation of talar OCLs. However, the activity level decreased at long-term follow-up and never attained the pre-injury level.⁶⁰

ANKLE IMPINGEMENT

ANTERIOR ANKLE IMPINGEMENT (FOOTBALLER'S ANKLE)

Anterior ankle impingement is caused by anterior osteophytes on both the distal tibia and talar neck. It is thought to be related to repetitive microtrauma to the anteromedial aspect of the ankle from recurrent ball impact.⁶¹ It is very common amongst soccer players with some studies suggesting that 60% of soccer players have this syndrome. Ankle impingement is characterized by anterior pain with ankle dorsiflexion, decreased dorsiflexion, and swelling. It is primarily diagnosed with lateral ankle X-rays, which will show the osteophytes. An oblique anteromedial X-ray may increase detection of osteophytes (Figure 5). The early stages of anterior impingement can be treated successfully with injections and heel lifts. Treatment of lesions that fail to respond to conservative management involves arthroscopic or open excision of osteophytes. Most patients with no preexisting osteoarthritis treated arthroscopically will experience pain relief and return to full activity, though recurrent osteophyte formation has been noted at long-term follow-up.⁶²

Anterior ankle impingement is most often caused by acute ankle sprains with an inversion type of mechanism.⁶² The subsequent reactive inflammation can cause fibrosis leading to distal fascicle enlargement of the AITFL. Impingement in the anterolateral gutter of this enlarged fascicle can also cause both chronic reactive synovitis and chondromalacia of the lateral talar dome.⁶³ MRI can identify abnormal areas of pathology; however, 50% of cases are diagnosed based on clinical examination alone.⁶³ Patients generally present with a history of anterolateral ankle pain and swelling with an occasional popping or snapping sensation.

Soccer players commonly develop anterior bony impingement due to repetitive loading of the anterior ankle from striking the ball. This repetition can lead to osteophyte formation of the anterior distal tibia and talar neck. After the osteophytes form, decreased dorsiflexion can occur due to a mechanical stop and inflammation of the interposed capsule.

The patient will exhibit tenderness to palpation along the anterolateral aspect of the ankle, with pain elicited at extreme passive dorsiflexion.⁶² Initially, an injection with local anesthetic and corticosteroid can serve both a diagnostic and therapeutic purpose; however, patients who fail conservative treatment can be treated with arthroscopy and resection of the involved scar tissue and osteophytes. The best results are seen in those patients with no concurrent intra-articular lesions or ankle osteoarthritis (Figure 5).⁶² When treated non-operatively, a player may return to play when pain resolves; however, if treated surgically with arthroscopic debridement/resection, a player must wait until his surgical scars have healed prior to attempting return to play.

Continue to: ANTEROMEDIAL ANKLE IMPINGEMENT

Anteromedial ankle impingement is a less common ankle impingement syndrome. It is associated with eversion injuries or following medial malleolar or talar fractures.^64,65 Previous injury to the anterior tibiotalar fascicle of the deltoid complex leads to ligament thickening and subsequent impingement in the anteromedial corner of the talus. Adjacent fibrosis and synovitis are common consequences of impingement; however, osteophyte formation and chondral stripping along the anteromedial talus can also be seen. Patients typically complain of pain along the anteromedial joint line that is worse with activity, clicking or popping sensations, and painful, limited dorsiflexion. On examination, impingement can be detected through palpation over the anterior tibiotalar fascicle of the deltoid ligament and eversion or extreme passive dorsiflexion of the foot, all of which will elicit medial ankle tenderness.^17,62 Initial treatment consists of rest, physical therapy, and NSAIDs. Refractory cases may be amenable to arthroscopic or open resection of the anterior tibiotalar fascicle with débridement of any adjacent synovitis and scar tissue.⁶²

POSTERIOR ANKLE IMPINGEMENT

Posterior ankle impingement is often referred to as “os trigonum syndrome” since the posterior impingement is frequently associated with a prominent os trigonum. An os trigonum is an accessory ossicle representing the separated posterolateral tubercle of the talus. It is usually asymptomatic. However, in soccer players, pain can occur from impaction between the posterior tibial plafond and the os trigonum, or because of soft tissue compression between the 2 opposing osseous structures. The pain is due to repetitive microtrauma (ankle plantarflexion) or acute forced plantarflexion, which can present as an acute fracture of the os trigonum. Because soccer is a sport requiring both repetitive and extreme plantarflexion, it may predispose players to posterior ankle impingement (Figures 6A, 6B).^62,66

Clinically, it can be very difficult to detect and diagnose because the affected structures lie deep and it can coexist with other disease processes (eg, peroneal tendinopathy, Achilles tendinopathy).^62,66 Patients will complain of chronic deep posterior ankle pain that is worse with push-off activities (eg, jumping). On examination, patients will exhibit pain with palpation over the posterolateral process and with the crunch test. Lateral radiograph with the foot in plantar flexion will show the os trigonum impinged between the posterior tibial malleolus and the calcaneal tuberosity. An MRI will demonstrate the os trigonum as well as any associated inflammation and edema, while it can also demonstrate coexisting pathologies.

Initial treatment consists of rest, NSAIDs, and taping to prevent plantar flexion. Ultrasound-guided cortisone injection of the capsule and posterior bursa can be both therapeutic and diagnostic. A posterior injection can be used to temporize the symptoms so that the soccer player can make it through the season.

Surgical excision is saved for refractory cases, and this can be done either through an open posterolateral approach or arthroscopic techniques. Recently, Georgiannos and Bisbinas⁶⁷ showed in an athletic population that endoscopic excision had both a lower complication rate and a quicker return to sports compared with the traditional open approach. Carreira and colleagues⁶⁸ conducted a retrospective case series of 20 patients (mostly competitive athletes). They found that posterior ankle arthroscopy to address posterior impingement allowed for the maintenance or restoration of anatomic ROM of the ankle and hindfoot, ability to return to at least the previous level of activity, and improvement in objective assessment of pain relief and a higher level of function parameters.⁶⁸

Continue to: TENDON PATHOLOGY

SUPERIOR PERONEAL RETINACULUM INJURY

The superior peroneal retinaculum (SPR) forms the roof of the superior peroneal tunnel. The tunnel contains the peroneus brevis and longus tendons and is bordered by the retromalleolar groove of the fibula and the lower aspect of the posterior intramuscular septum of the leg.^69,70 The SPR originates from the posterolateral ridge of the fibula and inserts onto the lateral calcaneus, and it is the primary restraint of the peroneal tendons within the retromalleolar sulcus.

Injury to the retinaculum results from both ankle dorsiflexion and inversion, and forceful reflex contraction of the peroneal muscles, which causes subluxation or dislocation of the contained tendons.⁶⁹ A high level of suspicion is required regarding these injuries since the mechanism of injury is similar to that of a simple lateral ankle sprain. In the setting of retrofibular pain, snapping or popping sensations around the lateral malleolus, or chronic ankle instability that worsens on uneven surfaces, one must consider an injury to the SPR.⁶⁹ Radiographs are not always diagnostic; however, occasionally on an internal rotation view, one may see a cortical avulsion off the distal tip of the lateral malleolus (“fleck sign”) indicating a rim fracture from an SPR injury (Figure 7). MRI is the best imaging modality to assess the peroneal tendons, as well as an SPR injury. Recently, ultrasound has grown in popularity and may be more useful, since it allows for dynamic evaluation of subluxating/dislocating tendons.⁶⁹

Conservative management is often associated with poor outcomes, and surgery is indicated for all acute and chronic dislocations in athletes.⁷¹ Anatomic reconstruction of the SPR is the preferred surgical method.⁷² Peroneus brevis debulking and fibular groove deepening may also augment the retinaculum repair.⁷³ van Dijk and colleagues in their systematic review showed that patients treated with both groove deepening and SPR repair have higher rates of return to the sport than patients treated with SPR repair alone.⁷⁴

STRESS FRACTURES

FIFTH METATARSAL

Fifth metatarsal stress fractures usually occur secondary to lateral overload or avulsion of the peroneus brevis. The fifth metatarsal base can be susceptible to injury in a cavovarus foot. Non-operative treatment typically requires a longer period of immobilization (boot or cast) and necessitates a longer period of non–weight-bearing (anywhere between 6-12 weeks). Therefore, surgery is typically recommended in athletes or in the setting of a recurrent base of the fifth metatarsal fracture to expedite healing and return to play. Return to play is still not recommended until there is evidence of radiographic healing of the fracture. There are certain distinctions with fifth metatarsal stress fractures regarding location and healing rates that need to be taken into account.^75,76 In particular, zone 2 injuries (Jones fractures) represent a vascular watershed area, making these fractures prone to nonunion with nonunion rates as high as 15% to 30%. Occasionally, the cavovarus deformity will require correction as well as a reduction in the risk of recurrence or nonunion. Surgical fixation most commonly consists of a single screw placed in an antegrade fashion.⁷⁷ One must pay attention to screw size since smaller diameter screws (<4.5 mm) are associated with delayed union or nonunion. Moreover, screws that are too long will straighten the curved metatarsal shaft and can lead to fracture distraction or malreduction (Figures 8A, 8B).⁷⁷

Patients have returned to competitive sports within 6 weeks; however, it should be noted that causes of failure were linked to early return and return to sports before a radiographic union can lead to failure of fixation. Ekstrand and van Dijk⁷⁸ studied a large group of professional soccer players and found that out of 13,754 injuries, 0.5% (67) were fifth metatarsal fractures. Of note, they found that 45% of players had prodromal symptoms. Furthermore, after surgical treatment the fractures healed faster, compared with conservative treatment (75% vs 33%); however, there was no significant difference in lay-off days between both groups (80 vs 74 days).⁷⁸ Matsuda and colleagues⁷⁹ looked at 335 male collegiate soccer players, 29 of whom had a history of a fifth metatarsal stress fracture. They found that playing the midfield position and having an everted rearfoot and inverted forefoot alignment were associated with fifth metatarsal stress fractures.⁷⁹ Saita and colleagues⁸⁰ found that restricted hip internal rotation was associated with an increased risk of developing a Jones fracture in 162 professional football players. Finally, Fujitaka and colleagues⁸¹ looked at 273 male soccer players between 2005 and 2013. They found an association between weak toe-grip strength and fifth metatarsal fractures, suggesting that weak toe-grip may lead to an increase in the load applied onto the lateral side of the foot, resulting in a stress fracture.⁸¹

Continue to: NAVICULAR

Another common tarsal bone that sustains stress fractures is the navicular. It is not as common as calcaneal stress fractures in military recruits but can occur in the same type of population, as well as explosive athletics such as sprinters and soccer players. It commonly presents with an indistinct vague achy pain with activity that improves with rest, and pain at the dorsum of the midfoot or along the medial longitudinal arch with activity. It can easily go undiagnosed for quite some time given the difficulty in visualizing the navicular with plain radiographs. Clinically, it is difficult to make the diagnosis, and therefore advanced imaging is necessary when the injury is suspected. Both MRI and CT scans can be used to understand the extent of the injury (Figures 9A-9C). In non-displaced stress fractures, conservative non-operative treatment is the appropriate treatment modality with a brief period of immobilization and non–weight-bearing;⁸² however, operative treatment is also considered in elite athletes. In either case, return to play is discouraged until there is evidence of radiographic healing. When a displacement is noted, or there is a delay in diagnosis, then operative treatment is recommended.

CONCLUSION

Ankle injuries are very common in soccer and can result in decreased performance or significant loss of playing time. Treatment of acute injury generally follows a conservative route, with surgical intervention reserved for severe ruptures or osteochondral fracture of the ankle joint. Chronic ankle pathology resulting in mechanical or functional instability generally requires surgery to repair ligamentous damage and restore normal ankle kinematics. It is critical for the soccer player to receive appropriate rehabilitation prior to returning to play in order to reduce the risk for reinjury and further chronic instability. Prevention and early intervention of ankle injuries is key in preventing the long-term sequelae of ankle injuries, such as arthritis, in former soccer players.

ABSTRACT

The ankle is one of the most commonly injured joints in soccer and represents a significant cost to the healthcare system. The ligaments that stabilize the ankle joint determine its biomechanics—alterations of which result from various soccer-related injuries. Acute sprains are among the most common injury in soccer players and are generally treated conservatively, with emphasis placed on secondary prevention to reduce the risk for future sprains and progression to chronic ankle instability. Repetitive ankle injuries in soccer players may cause chronic ankle instability, which includes both mechanical ligamentous laxity and functional changes. Chronic ankle pathology often requires surgery to repair ligamentous damage and remove soft-tissue or osseous impingement. Proper initial treatment, rehabilitation, and secondary prevention of ankle injuries can limit the amount of time lost from play and avoid negative long-term sequelae (eg, osteochondral lesions, arthritis). On the other hand, high ankle sprains portend a poorer prognosis and a longer recovery. These injuries will typically require surgical stabilization. Impingement-like syndromes of the ankle can undergo an initial trial of conservative treatment; when this fails, however, soccer players respond favorably to arthroscopic debridement of the lesions causing impingement. Finally, other pathologies (eg, stress fractures) are highly encouraged to be treated with surgical stabilization in elite soccer players.

Continue to: EPIDEMIOLOGY

With roughly 200,000 professional and around 240 million amateur soccer players, soccer has been recognized as the most popular sport worldwide. Nevertheless, given its rising popularity in society, one must also consider the increasing incidence of injuries as a result. Elite soccer players sustain between 10 and 35 injuries per 1000 competitive playing hours.¹ Approximately 80% are traumatic, and 20% are overuse injuries.² Soccer injuries are more frequent with increasing age of the participants, whereas the incidence of injuries in preadolescent players is low. The incidence of injuries has been found to be higher during competition when compared with practice/training sessions, with some studies showing that 59% of injuries occurred during games.² Amateur or recreational soccer players sustain fewer injuries than professional soccer players, as one would expect, given both the higher intensity of training and match schedule in professionals.

The ankle is one of the most commonly injured joints in soccer, with some studies suggesting it comprises one-fifth of all injuries sustained during soccer, which is only second to those of the knee.² Ankle sprains specifically are quite a common occurrence in soccer.^3-9 A recent study of an English premier league club showed that over a 4-season period, 20% of injuries were of the foot and ankle with a mean return to sport time of 54 days.¹⁰ Of all foot and ankle related injuries, ankle sprains are the most common, followed by bruises/contusions, and tendon lesions. Fractures are very rare (1%) in soccer, but when they do occur they impart a much more extended recovery. During the 2010 Fédération Internationale de Football Association (FIFA) World Cup, ankle sprains were among the most common injuries and approximately half lead to players missing training or competitive matches.⁵

ANATOMY

Knowledge of the biomechanics of both the foot and ankle joints is essential to understand soccer injuries. The ankle joint (talocrural articulation) consists of the distal ends of the tibia and fibula, which form the mortise, and the superior aspect of the talar dome.¹¹ As a hinge joint, the ankle provides 20° of dorsiflexion and 50° of plantar flexion,¹² with stability provided by the lateral, medial, and superior ligamentous complexes. The superior articular surface of the talus is narrower posteriorly, which creates a looser fit within the mortise during plantar flexion.¹¹ This decreased stability could help explain why the most common injury in soccer involves a plantar flexion mechanism.^13,14 Inferiorly, the talus articulates with the calcaneus to form the subtalar joint. It is at this site that the majority of both foot inversion and eversion occurs. The transverse tarsal joints (Chopart’s joints) separate the hindfoot from the midfoot. Movement of this joint depends on the relative alignment of its 2 articulations: the talonavicular and calcaneocuboid joints. During foot eversion, these 2 joints are parallel to each other allowing supple motion and aiding in shock absorption during the heel strike phase of the gait cycle. With foot inversion, the joints become nonparallel and thus lock the transverse tarsal joints providing a rigid lever needed for push-off.^11,12

LATERAL LIGAMENTS

The ankle joint is stabilized laterally by a ligament complex consisting of 3 individual ligaments, all originating from the lateral malleolus: the anterior talofibular ligament (ATFL), the posterior talofibular ligament (PTFL), and the calcaneofibular ligament (CFL) (Figure 1).^11,12,15 The ATFL is the primary restraint to inversion in plantar flexion, and it helps resist anterolateral translation of the talus in the mortise. However, it is the weakest and therefore the most frequently injured of the lateral ligaments. The PTFL plays only a supplementary role in ankle stability when the lateral ligament complex is intact. It is under the greatest strain in ankle dorsiflexion and acts to limit posterior talar displacement within the mortise as well as talar external rotation.^13,16 The CFL is the primary restraint to inversion in the neutral or dorsiflexed position. It restrains subtalar inversion, thereby limiting talar tilt within the mortise.

DELTOID LIGAMENT

The deltoid ligament complex consists of 6 continuous adjacent superficial and deep ligaments that function synergistically to resist valgus and pronation forces, as well as external rotation of the talus in the mortise.^11-13,17 The superficial layer crosses both ankle and subtalar joints. It originates from the anterior colliculus and fans out to insert into the navicular, neck of the talus, sustentaculum tali, and posteromedial talar tubercle. The tibiocalcaneal (sustentaculum tali) portion is the strongest component in the superficial layer and resists calcaneal eversion. The deep layer crosses the ankle joint only. It functions as the primary stabilizer of the medial ankle and prevents both lateral displacement and external rotation of the talus. It originates from the inferior and posterior aspects of the medial malleolus and inserts on the medial and posteromedial aspects of the talus.^12,17,18

Continue to: SYNDESMOSIS

The ankle syndesmosis, or inferior tibiofibular joint, is the distal articulation between the tibia and fibula. The syndesmosis contributes to ankle mortise integrity through its firm fixation of the lateral malleolus against the lateral surface of the talus. Ligaments comprising the ankle syndesmosis include the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the inferior transverse ligament, and the interosseous ligament (IOL).¹²

ANKLE SPRAINS

Ankle sprains are the most common pathology encountered amongst soccer players, representing from one-half to two-thirds of all ankle related injuries. Most sprains occur outside of player contact.

LATERAL ANKLE SPRAINS AND INSTABILITY

Injury to the lateral ligaments of the ankle represents 77% to 91% of all ankle sprains in soccer.^6,19 The greatest risk factor for an ankle sprain in a soccer player is a history of prior sprain.²⁰ Other risk factors include increasing age, player-to-player contact, condition of the pitch, weight-bearing status of the injured limb at the time of injury, and joint instability or laxity.^21,22

The evaluation of an ankle sprain to determine its severity is best done after the acute phase, approximately 4 to 7 days after the initial injury when both pain and swelling have subsided.²³ The anterior drawer (ATFL instability) and talar tilt (CFL instability) tests are useful in evaluating ankle instability in the delayed or chronic setting; however, both have been shown to have limited sensitivity and significant variability amongst different examiners.²⁴

Clinical examination will direct further diagnostic tests including X-rays, magnetic resonance imaging (MRI), and computed tomography (CT). The Ottawa ankle rules are generally helpful in determining whether plain X-rays are indicated in the acute setting.^25,26 (Figure 2) According to these rules, ankle radiographs should be obtained if ankle pain is reported near the malleoli and 1 or more of the following is seen during examination: inability to bear weight immediately after injury and for 4 steps in the emergency department, and bony tenderness at the posterior edge or tip of the malleolus. Stress X-rays are generally not indicated in acute injuries but may be useful in chronic ankle instability cases.²³

Continue to: Ankle sprains cover...

Ankle sprains cover a broad spectrum of injuries; therefore, a grading system was devised to aid in guiding treatment. Grade I (mild) sprains are those with minimal swelling and tenderness but have the ligaments still intact. Grade II (moderate) sprains occur when there are partial ligament tears associated with moderate pain, swelling, and tenderness. Finally, Grade III (severe) sprains are complete ligament tears with marked swelling, hemorrhage, tenderness, loss of function, and abnormal joint motion and instability.^{23, 24}

Initial treatment for all ankle sprains is nonoperative and involves the RICE (rest, ice, compression, elevation) protocol with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) during the acute phase (first 4-5 days) with a short period (no >2 weeks) of immobilization.²⁷ Most authors agree that early mobilization followed by phased rehabilitation is warranted to minimize time away from sports.^28-31 Prolonged immobilization (>2 weeks) has detrimental effects and may lead to a longer return to play.^28-31 The rehabilitation protocol is divided into stages: (1) pain and edema control, (2) range of motion (ROM) and strengthening exercises, (3) soccer specific functional training, and (4) prophylactic intervention with balance and proprioception exercises. Surgical intervention is rarely indicated for acute ankle sprains. There are exceptions, however, such as when ankle sprains are associated with other injuries that require acute intervention (eg, fracture, osteochondral lesion). Surgery is indicated in the setting of chronic, recurrent mechanical instability. Anatomical repairs (modified Brostrom) seem to produce better outcomes than non-anatomical reconstructions (eg, Chrisman-Snook). Surgical outcomes are good, and most athletes are able to return to their pre-injury level of function.³²

In athletes, prevention of recurrent sprains is key. Braces may help prevent ankle sprains and bracing has been shown to be superior to taping, as tape loses its restrictive properties within 20 to 30 minutes of initiating activity.^33,34 Application of an orthosis (lace-up ankle orthosis) has been shown to reduce the incidence of ankle re-injury in soccer players with previous ankle sprains. Several studies have found minimal, if any, effect of orthoses on athletic performance.^20,35,36 Low-profile braces for soccer have been developed which allow for minimal disruption of the player’s boot and space proximally to insert the shin guard. Another essential component of prevention is prophylactic intervention with balance and proprioceptive exercises. A study looking at first division men’s league football (soccer) players in Iran showed a significant decrease in re-injury rates with proprioceptive training.³⁷ In 2003, FIFA introduced a comprehensive warm-up program (FIFA 11+), which has since been shown in several studies to decrease the risk of injury in amateur soccer players.^38-40

MEDIAL ANKLE SPRAINS AND INSTABILITY

Soccer places an unusually high demand on both the medial foot and ankle structures when compared with other sports. For instance, striking the ball requires the player to abduct and externally rotate the foot, which preloads medial structures.⁹ Hintermann¹⁸ looked at 54 cases of medial ankle instability and found that injury commonly occurred during landing on an uneven surface, which applies to soccer players when landing after heading the ball or jumping over a tackle. Pronation with eversion and extreme rotational injuries are well known to cause deltoid ligament injury. However, complete rupture of the deltoid ligament is rare and is more often associated with ankle fractures.⁴¹ Due to its close proximity and similarly shared function in medial plantar arch stabilization with the tibiospring and spring ligaments, posterior tibialis tendon dysfunction is also frequently seen in medial ankle instability.¹⁷ After an acute injury, patients can present with a medial ankle hematoma and pain along the deltoid ligament. Although chronic insufficiency is diagnosed based on the feeling of “giving way,” pain in the medial gutter of the ankle and a valgus and pronation deformity of the foot can be corrected by activating the peroneus tertius muscle. Arthroscopy is the most specific way to confirm clinically suspected instability of the medial ankle; however, MRI can demonstrate loss of organized medial fibers (Figures 3A, 3B).¹⁸ Primary surgical repair of deltoid ligament tears yield good to excellent results and should be considered in the soccer player to prevent problems associated with chronic non-repaired tears such as instability, osteoarthritis, and impingement syndromes.¹⁸ After surgical repair, players will undergo extensive physical therapy that progresses to sport-specific exercises with the ultimate goal of returning to competitive play around 4-6 months post-operatively.

HIGH ANKLE SPRAINS (SYNDESMOSIS)

High ankle sprains are much less common than low ankle sprains; however, when they do occur they portend a lengthier rehabilitation and a poorer prognosis, especially if undiagnosed. Lubberts and colleagues⁴² studied the epidemiology of isolated syndesmotic injuries in professional football players. They pooled data from 15 consecutive seasons of European professional football between 2001 and 2016. They examined a total of 3677 players from 61 teams across 17 countries. There were 1320 ankle ligament injuries registered during 15 seasons, of which 94 (7%) were isolated syndesmotic injuries. The incidence of these injuries increased annually between 2001 and 2016. Injuries were 74% contact-related, and isolated syndesmotic injuries were followed by a mean of a 39-day absence.⁴² Moreover, football players may have an increased risk of syndesmotic sprains due to foot planting and cutting action.⁴¹

Continue to: These injuriesa are typically...

These injuries are typically identified with pain over the AITFL and interosseous membrane. Physical examination tests that help identify syndesmotic injuries include the squeeze test, external rotation test, and crossed-leg test.⁴¹ The diagnosis can be made on plain X-ray when there is clear diastasis between the distal tibia and fibula. Two critical measurements on plain films are made 1 cm above the tibial plafond and are used to evaluate the integrity of the syndesmosis: tibiofibular clear space >6 mm, and tibiofibular overlap <1 mm, which indicate disruption of the syndesmosis.⁴³ More subtle injuries can be diagnosed with better sensitivity and specificity using MRI, which can also reveal secondary findings such as bone bruises, ATFL injury, osteochondral lesions, and tibiofibular incongruity.^44,45 Arthroscopy is an invaluable diagnostic tool for syndesmotic injuries with a characteristic triad finding of PITFL scarring, disrupted interosseous ligament, and posterolateral tibial plafond chondral damage.⁴⁶

Classification of the ligaments involved can aid in the selection of appropriate treatment. Grade I injuries involve AITFL tears. Grade IIa injuries involve AITFL and IOL tears. Grade IIb injuries include AITFL, PITFL, and IOL tears. Grade III injuries involve injury to all 3 ligaments, as well as a fibular fracture. Conservative treatment is recommended for Grades I and IIa, while surgical intervention is necessary for Grades IIb and III (Figures 4A, 4B). Compared with other ankle sprains, syndesmotic injuries typically require a more prolonged recovery/rehabilitation. Some studies suggest that these injuries require twice as long to heal.⁴⁷ Hopkinson and colleagues⁴⁸ reported a mean recovery time of 55 days following syndesmotic injuries in cadets at the United States Military Academy at West Point. Some surgeons advocate surgical intervention in professional athletes with mild sprains to expedite return to play.⁴⁹

Surgery has been well established as necessary in more severe injuries where there is clear diastasis or instability of the syndesmosis. Traditionally, screws were used for surgical fixation; however, they often required a second surgery for subsequent removal. There is no general consensus on the optimal screw size, level of placement, or timing of removal.^50,51 More recently, non-absorbable suture button fixation (eg, TightRope; Arthrex) has become more popular and provides certain advantages over screw fixation, such as avoiding the need for hardware removal. TightRope has been shown to provide more accurate stabilization of the syndesmosis as compared with screw fixation.⁵² Since malreduction is the most important indicator of poor long-term functional outcome, suture button fixation should be considered in the treatment of the football player.⁵³ Finally, Colcuc and colleagues⁵⁴ reported a lower complication rate and earlier return to sports in patients treated with knotless suture button devices compared with screw fixation.

OSTEOCHONDRAL LESIONS

Osteochondral lesions (OCLs) are cartilage-bone defects that are usually located in the talus. They can be caused by an acute traumatic event or repetitive microtrauma with no apparent history of trauma (eg, ankle instability). Acute OCLs can occur in soccer secondary to an ankle sprain or ankle fracture. Symptoms of OCLs include pain, swelling, and mechanical symptoms such as catching or locking, and on physical examination, one might see an effusion. The initial imaging modality of choice is radiographing; however, in ankle sprains with continued pain and swelling MRI may be indicated to rule out an underlying OCL. Missed acute lesions have a tendency not to heal and become chronic lesions, which can cause pain and playing disability. It is well established that chronic ankle instability is an important etiologic factor for OCLs. With the normal hydrostatic pressure within the ankle joint, synovial fluid gets pushed into cartilage/bone fissures, which can then lead to cystic degeneration of the subchondral bone.^55-57

Surgical repair of an OCL is dependent on both the size and location of the lesion. Acute lesions can be managed by arthroscopic débridement, microfracture, or fixation of the lesion if enough bone remains attached to the chondral lesion. Return to play is based on development and maturation of fibrocartilage over the lesion (debridement/microfracture) or healing and incorporation of the new graft (chondral repair procedures). Meanwhile, chronic lesions can be managed in 1-stage (microfracture, osteochondral autograft transfer or 2-stage (autologous chondrocyte implantation [ACI]) procedures.^56-57 Additional biologic healing augmentation with platelet-rich plasma has been described as well.⁵⁸ Newer techniques in treating chronic talus OCLs, including ones that have failed to respond to bone marrow stimulation techniques, have been developed more recently such as the use of particulated juvenile articular cartilage allograft (DeNovo NT Natural Tissue Graft^®; Zimmer Biomet).⁵⁹ These newer techniques avoid the need for a 2-stage procedure, as is the case with ACI.

Continue to: Further studies are needed...

Further studies are needed to both investigate long-term outcomes and determine the superiority of the arthroscopic juvenile cartilage procedure compared with microfracture and other cartilage resurfacing procedures. When surgically treating OCLs, one must also restore normal ankle joint biomechanics for the lesion to heal. For instance, in the presence of ankle instability, ligament reconstruction must be performed. Also, one should also consider addressing any hindfoot malalignment with an osteotomy (calcaneus, supramalleolar). In a recent retrospective study, van Eekeren and colleagues⁶⁰ showed that approximately 76% of patients were able to return to sports at long-term follow-up after arthroscopic débridement and bone marrow stimulation of talar OCLs. However, the activity level decreased at long-term follow-up and never attained the pre-injury level.⁶⁰

ANKLE IMPINGEMENT

ANTERIOR ANKLE IMPINGEMENT (FOOTBALLER'S ANKLE)

Anterior ankle impingement is caused by anterior osteophytes on both the distal tibia and talar neck. It is thought to be related to repetitive microtrauma to the anteromedial aspect of the ankle from recurrent ball impact.⁶¹ It is very common amongst soccer players with some studies suggesting that 60% of soccer players have this syndrome. Ankle impingement is characterized by anterior pain with ankle dorsiflexion, decreased dorsiflexion, and swelling. It is primarily diagnosed with lateral ankle X-rays, which will show the osteophytes. An oblique anteromedial X-ray may increase detection of osteophytes (Figure 5). The early stages of anterior impingement can be treated successfully with injections and heel lifts. Treatment of lesions that fail to respond to conservative management involves arthroscopic or open excision of osteophytes. Most patients with no preexisting osteoarthritis treated arthroscopically will experience pain relief and return to full activity, though recurrent osteophyte formation has been noted at long-term follow-up.⁶²

Anterior ankle impingement is most often caused by acute ankle sprains with an inversion type of mechanism.⁶² The subsequent reactive inflammation can cause fibrosis leading to distal fascicle enlargement of the AITFL. Impingement in the anterolateral gutter of this enlarged fascicle can also cause both chronic reactive synovitis and chondromalacia of the lateral talar dome.⁶³ MRI can identify abnormal areas of pathology; however, 50% of cases are diagnosed based on clinical examination alone.⁶³ Patients generally present with a history of anterolateral ankle pain and swelling with an occasional popping or snapping sensation.

Soccer players commonly develop anterior bony impingement due to repetitive loading of the anterior ankle from striking the ball. This repetition can lead to osteophyte formation of the anterior distal tibia and talar neck. After the osteophytes form, decreased dorsiflexion can occur due to a mechanical stop and inflammation of the interposed capsule.

The patient will exhibit tenderness to palpation along the anterolateral aspect of the ankle, with pain elicited at extreme passive dorsiflexion.⁶² Initially, an injection with local anesthetic and corticosteroid can serve both a diagnostic and therapeutic purpose; however, patients who fail conservative treatment can be treated with arthroscopy and resection of the involved scar tissue and osteophytes. The best results are seen in those patients with no concurrent intra-articular lesions or ankle osteoarthritis (Figure 5).⁶² When treated non-operatively, a player may return to play when pain resolves; however, if treated surgically with arthroscopic debridement/resection, a player must wait until his surgical scars have healed prior to attempting return to play.

Continue to: ANTEROMEDIAL ANKLE IMPINGEMENT

Anteromedial ankle impingement is a less common ankle impingement syndrome. It is associated with eversion injuries or following medial malleolar or talar fractures.^64,65 Previous injury to the anterior tibiotalar fascicle of the deltoid complex leads to ligament thickening and subsequent impingement in the anteromedial corner of the talus. Adjacent fibrosis and synovitis are common consequences of impingement; however, osteophyte formation and chondral stripping along the anteromedial talus can also be seen. Patients typically complain of pain along the anteromedial joint line that is worse with activity, clicking or popping sensations, and painful, limited dorsiflexion. On examination, impingement can be detected through palpation over the anterior tibiotalar fascicle of the deltoid ligament and eversion or extreme passive dorsiflexion of the foot, all of which will elicit medial ankle tenderness.^17,62 Initial treatment consists of rest, physical therapy, and NSAIDs. Refractory cases may be amenable to arthroscopic or open resection of the anterior tibiotalar fascicle with débridement of any adjacent synovitis and scar tissue.⁶²

POSTERIOR ANKLE IMPINGEMENT

Posterior ankle impingement is often referred to as “os trigonum syndrome” since the posterior impingement is frequently associated with a prominent os trigonum. An os trigonum is an accessory ossicle representing the separated posterolateral tubercle of the talus. It is usually asymptomatic. However, in soccer players, pain can occur from impaction between the posterior tibial plafond and the os trigonum, or because of soft tissue compression between the 2 opposing osseous structures. The pain is due to repetitive microtrauma (ankle plantarflexion) or acute forced plantarflexion, which can present as an acute fracture of the os trigonum. Because soccer is a sport requiring both repetitive and extreme plantarflexion, it may predispose players to posterior ankle impingement (Figures 6A, 6B).^62,66

Clinically, it can be very difficult to detect and diagnose because the affected structures lie deep and it can coexist with other disease processes (eg, peroneal tendinopathy, Achilles tendinopathy).^62,66 Patients will complain of chronic deep posterior ankle pain that is worse with push-off activities (eg, jumping). On examination, patients will exhibit pain with palpation over the posterolateral process and with the crunch test. Lateral radiograph with the foot in plantar flexion will show the os trigonum impinged between the posterior tibial malleolus and the calcaneal tuberosity. An MRI will demonstrate the os trigonum as well as any associated inflammation and edema, while it can also demonstrate coexisting pathologies.

Initial treatment consists of rest, NSAIDs, and taping to prevent plantar flexion. Ultrasound-guided cortisone injection of the capsule and posterior bursa can be both therapeutic and diagnostic. A posterior injection can be used to temporize the symptoms so that the soccer player can make it through the season.

Surgical excision is saved for refractory cases, and this can be done either through an open posterolateral approach or arthroscopic techniques. Recently, Georgiannos and Bisbinas⁶⁷ showed in an athletic population that endoscopic excision had both a lower complication rate and a quicker return to sports compared with the traditional open approach. Carreira and colleagues⁶⁸ conducted a retrospective case series of 20 patients (mostly competitive athletes). They found that posterior ankle arthroscopy to address posterior impingement allowed for the maintenance or restoration of anatomic ROM of the ankle and hindfoot, ability to return to at least the previous level of activity, and improvement in objective assessment of pain relief and a higher level of function parameters.⁶⁸

Continue to: TENDON PATHOLOGY

SUPERIOR PERONEAL RETINACULUM INJURY

The superior peroneal retinaculum (SPR) forms the roof of the superior peroneal tunnel. The tunnel contains the peroneus brevis and longus tendons and is bordered by the retromalleolar groove of the fibula and the lower aspect of the posterior intramuscular septum of the leg.^69,70 The SPR originates from the posterolateral ridge of the fibula and inserts onto the lateral calcaneus, and it is the primary restraint of the peroneal tendons within the retromalleolar sulcus.

Injury to the retinaculum results from both ankle dorsiflexion and inversion, and forceful reflex contraction of the peroneal muscles, which causes subluxation or dislocation of the contained tendons.⁶⁹ A high level of suspicion is required regarding these injuries since the mechanism of injury is similar to that of a simple lateral ankle sprain. In the setting of retrofibular pain, snapping or popping sensations around the lateral malleolus, or chronic ankle instability that worsens on uneven surfaces, one must consider an injury to the SPR.⁶⁹ Radiographs are not always diagnostic; however, occasionally on an internal rotation view, one may see a cortical avulsion off the distal tip of the lateral malleolus (“fleck sign”) indicating a rim fracture from an SPR injury (Figure 7). MRI is the best imaging modality to assess the peroneal tendons, as well as an SPR injury. Recently, ultrasound has grown in popularity and may be more useful, since it allows for dynamic evaluation of subluxating/dislocating tendons.⁶⁹

Conservative management is often associated with poor outcomes, and surgery is indicated for all acute and chronic dislocations in athletes.⁷¹ Anatomic reconstruction of the SPR is the preferred surgical method.⁷² Peroneus brevis debulking and fibular groove deepening may also augment the retinaculum repair.⁷³ van Dijk and colleagues in their systematic review showed that patients treated with both groove deepening and SPR repair have higher rates of return to the sport than patients treated with SPR repair alone.⁷⁴

STRESS FRACTURES

FIFTH METATARSAL

Fifth metatarsal stress fractures usually occur secondary to lateral overload or avulsion of the peroneus brevis. The fifth metatarsal base can be susceptible to injury in a cavovarus foot. Non-operative treatment typically requires a longer period of immobilization (boot or cast) and necessitates a longer period of non–weight-bearing (anywhere between 6-12 weeks). Therefore, surgery is typically recommended in athletes or in the setting of a recurrent base of the fifth metatarsal fracture to expedite healing and return to play. Return to play is still not recommended until there is evidence of radiographic healing of the fracture. There are certain distinctions with fifth metatarsal stress fractures regarding location and healing rates that need to be taken into account.^75,76 In particular, zone 2 injuries (Jones fractures) represent a vascular watershed area, making these fractures prone to nonunion with nonunion rates as high as 15% to 30%. Occasionally, the cavovarus deformity will require correction as well as a reduction in the risk of recurrence or nonunion. Surgical fixation most commonly consists of a single screw placed in an antegrade fashion.⁷⁷ One must pay attention to screw size since smaller diameter screws (<4.5 mm) are associated with delayed union or nonunion. Moreover, screws that are too long will straighten the curved metatarsal shaft and can lead to fracture distraction or malreduction (Figures 8A, 8B).⁷⁷

Patients have returned to competitive sports within 6 weeks; however, it should be noted that causes of failure were linked to early return and return to sports before a radiographic union can lead to failure of fixation. Ekstrand and van Dijk⁷⁸ studied a large group of professional soccer players and found that out of 13,754 injuries, 0.5% (67) were fifth metatarsal fractures. Of note, they found that 45% of players had prodromal symptoms. Furthermore, after surgical treatment the fractures healed faster, compared with conservative treatment (75% vs 33%); however, there was no significant difference in lay-off days between both groups (80 vs 74 days).⁷⁸ Matsuda and colleagues⁷⁹ looked at 335 male collegiate soccer players, 29 of whom had a history of a fifth metatarsal stress fracture. They found that playing the midfield position and having an everted rearfoot and inverted forefoot alignment were associated with fifth metatarsal stress fractures.⁷⁹ Saita and colleagues⁸⁰ found that restricted hip internal rotation was associated with an increased risk of developing a Jones fracture in 162 professional football players. Finally, Fujitaka and colleagues⁸¹ looked at 273 male soccer players between 2005 and 2013. They found an association between weak toe-grip strength and fifth metatarsal fractures, suggesting that weak toe-grip may lead to an increase in the load applied onto the lateral side of the foot, resulting in a stress fracture.⁸¹

Continue to: NAVICULAR

Another common tarsal bone that sustains stress fractures is the navicular. It is not as common as calcaneal stress fractures in military recruits but can occur in the same type of population, as well as explosive athletics such as sprinters and soccer players. It commonly presents with an indistinct vague achy pain with activity that improves with rest, and pain at the dorsum of the midfoot or along the medial longitudinal arch with activity. It can easily go undiagnosed for quite some time given the difficulty in visualizing the navicular with plain radiographs. Clinically, it is difficult to make the diagnosis, and therefore advanced imaging is necessary when the injury is suspected. Both MRI and CT scans can be used to understand the extent of the injury (Figures 9A-9C). In non-displaced stress fractures, conservative non-operative treatment is the appropriate treatment modality with a brief period of immobilization and non–weight-bearing;⁸² however, operative treatment is also considered in elite athletes. In either case, return to play is discouraged until there is evidence of radiographic healing. When a displacement is noted, or there is a delay in diagnosis, then operative treatment is recommended.

CONCLUSION

Ankle injuries are very common in soccer and can result in decreased performance or significant loss of playing time. Treatment of acute injury generally follows a conservative route, with surgical intervention reserved for severe ruptures or osteochondral fracture of the ankle joint. Chronic ankle pathology resulting in mechanical or functional instability generally requires surgery to repair ligamentous damage and restore normal ankle kinematics. It is critical for the soccer player to receive appropriate rehabilitation prior to returning to play in order to reduce the risk for reinjury and further chronic instability. Prevention and early intervention of ankle injuries is key in preventing the long-term sequelae of ankle injuries, such as arthritis, in former soccer players.