Introduction
Sports injuries of the foot and ankle are a frequent reason for office visits to the orthopedic surgeon or non-operative sports medicine physician. No matter what the sporting event is or whether an individual is a professional athlete or a weekend warrior, the foot and ankle is likely needed in some capacity to participate and is therefore at risk of injury. This area of the body is extremely complex due to its unique biomechanics and 3D anatomy, with 28 bones, 33 joints, 107 ligaments, and 19 muscles and tendons. As these structures are all in close proximity, the various injuries can present with similar signs and symptoms, so understanding of the anatomy is essential. In this chapter our discussion is limited to injuries involving the lateral ankle ligamentous complex, the syndesmosis, the peroneal tendons, anterior and posterior ankle impingement syndromes, and turf toe.
Lateral Ankle Ligamentous Complex Injuries
Acute ankle sprains are among the most common musculoskeletal injuries1–2. The vast majority involve the lateral ankle ligament complex, which consists of the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL). Fifteen to 20% of all sports injuries involve the lateral ankle ligament complex3–4. Nevertheless, despite their frequency, the injury is often considered an insignificant one with about 55% of individuals not even seeking treatment5. Therefore the true incidence is likely much higher. When diagnosed and treated in an appropriate manner, long-term sequelae are rare. The problem with this injury occurs when either the diagnosis is missed or the injury is undertreated. This often leads to chronic pain, muscular weakness, and instability.
Lateral ankle sprains most commonly occur following excessive inversion and internal rotation of the hindfoot while the leg is externally rotated. This puts the lateral ankle ligament complex under maximal tension2, 6. The ATFL, the weakest of the three lateral ankle ligaments, is involved in nearly all lateral ankle sprains, either alone, or in combination with the CFL in 50 to 75% of such injuries. The PTFL is involved in only 10% of injuries7. The PTFL is not commonly injured because of the large amount of dorsiflexion and force that is required to put the ligament under significant tension. Increasing dorsiflexion in fact stabilizes the ankle, which further decreases the likelihood of a PTFL injury8.
A patient with an acute lateral ankle ligament sprain will most often complain of pain and a sense of decreased stability. Assessment of the patient should begin with a thorough history and physical examination based on the Ottawa ankle rules for diagnosing a possible ankle fracture. When warranted, standard ankle radiographs must be obtained. Examination often reveals diffuse swelling, ecchymosis on the lateral side of the ankle, and heel and tenderness over the ATFL and CFL. Anterior talofibular ligament laxity is evaluated clinically by assessing the amount of anterior displacement of the talus from the ankle mortise using the anterior drawer test9. Here the hindfoot is held with the ankle in 15 to 20° of plantar flexion and the distal tibia is immobilized with the other hand. The hindfoot is then drawn anteriorly with slight internal rotation, and the amount of anterior translation and character of the endpoint are noted10. The talar-tilt test assesses the integrity of the CFL and is performed by inverting the hindfoot on the tibia, with the foot held in neutral dorsiflexion/plantar flexion. Again the amount of movement and character of the endpoint are estimated11. Both of these tests are subsequently compared to the contralateral, uninjured side and differences noted. Clinical examination is reasonably accurate in diagnosing a lateral ligament complex injury, but may be subject to false negatives2. It is important to note that in an acute injury the anterior drawer or talar-tilt test is painful, making it difficult to accurately assess the stability of the joint, as the patient may guard against examination. Once the swelling and tenderness subside, it is possible to perform a more accurate assessment of the joint. A local anesthetic ankle block an is option if an acute evaluation is necessary.
Lateral ankle ligament injuries are graded from I to III12.
Grade I: The ATFL is stretched with some tearing of the fibers, but no disruption. Clinically, the patient presents with mild swelling, ATFL tenderness, and no or mild restriction of active range of motion. Difficulty full weight bearing is sometimes seen. There is no laxity on examination.
Grade II: A moderate injury, frequently with a complete tear of the ATFL and a partial tear of the CFL. Examination reveals a restricted range of motion with localized swelling, ecchymosis, and tenderness of the anterolateral aspect of the ankle. The ankle may be mildly lax or stable. A grade II injury may present with swelling and functional loss, making it indistinguishable acutely from a grade III injury.
Grade III: Injury implies complete disruption of both the ATFL and CFL. A capsular or PTFL tear may also be present.
Malliaropoulos further subclassified grade III injuries into IIIA and IIIB, based on anterior drawer stress radiographs. According to Milliaropoulos’ classification, grade III injuries lack more than 10° of movement and have more than 2 cm of measurable edema compared to the uninjured side. In a grade IIIA injury the stress radiographs are normal, as opposed to a grade IIIB injury where there is a 3 mm, or greater, measurable distance between the posterior articular surface of the tibia and the nearest point of the talus when compared to the normal side13.
Although stress views are not required to establish the diagnosis of instability, they can be a helpful adjunct when the clinical presentation is unclear or to assess the severity of the injury. The standard stress views evaluate anterior draw of the talus beneath the tibia and a varus tilt of the talus within the mortise (Figures 11.1 and 11.2). There is no absolute value that confirms instability, so comparison views with the opposite side can be very helpful and should be considered. In a stable ankle, the anterior drawer translation should measure less than 10 mm, or within 3 to 5 mm of the opposite side11. Normal talar-tilt values can range widely from 5 to 20°, although an absolute value of more than 10°, or a difference of greater than 3 to 5° compared to the uninjured side, is consistent with laxity11. Nevertheless laxity is common and often non-pathological, thus the numerical value of stress radiographs alone should never dictate your treatment.
Figure 11.1 Positive anterior drawer stress radiograph as illustrated by the anterior translation of the talus on the tibial plafond due to anterior talofibular ligament incompetency.
Figure 11.2 Positive varus tilt stress radiograph with significant instability of the lateral ankle ligament complex due to calcaneofibular ligament injury.
MRI scanning has been shown to be an ineffective diagnostic modality for acute injuries and is of no value as a static test to determine dynamic instability2, 11. Furthermore up to 60% of patients undergoing MRI scans for pathology other than instability have an ATFL tear as an incidental finding. Nevertheless, bearing in mind these limitations, MRI can be very useful in the subacute or chronic ankle sprain where pain persists and is unresponsive to conservative measures. The MRI can demonstrate other causes of ankle pain, such as osteochondral lesions of the talus or tibial plafond, occult fractures, tendon tears, degeneration, and impingement lesions.
In the patient with an acute lateral ankle ligament complex sprain, the primary goals are to manage pain, control inflammation, and protect the joint. This involves early mobilization with an external support and a protocol of rest, ice, compression, elevation (RICE), and non-steroidal anti-inflammatory medication (NSAID) therapy. This is followed by a rehabilitation program, which consists of range-of-motion exercises, peroneal tendon strengthening, proprioception, and activity-specific training. Proprioception training is particularly important for the recovery of balance. In addition to providing mechanical stability, external supports provide additional proprioceptive feedback and aid rehabilitation2, 4–5.
Ardèvol conducted a randomized controlled trial comparing cast immobilization with functional rehabilitation14. Functional management allowed an earlier return to sport, with fewer symptoms at three and six months post injury. There was also a greater reduction in radiographic laxity, although there was no difference in the re-injury rates between the two groups. A meta-analysis of randomized controlled trials comparing immobilization and functional rehabilitation of acute lateral ankle ligament injuries has demonstrated that functional management allows a higher proportion of patients to return to sport15. The functionally rehabilitated patients also demonstrated a higher rate of satisfaction, returned to work earlier, had less swelling, and their range of motion was improved when compared to those who were treated with cast immobilization15. Finally, in a systematic review of acute ankle ligament injuries, Kerkhoffs concluded that lace-up supports were most effective, while taping was found to be no better than semi-rigid supports. Of note, elastic bandages were the least effective form of treatement16.
Treatment of the acute sprain is dependent on how quickly the patient wishes to return to athletic activity. In the elite athlete, an acute, severe sprain in an ankle, which is stable to clinical testing, can be treated symptomatically. An unstable ankle with a positive anterior drawer or talar tilt by clinical examination is further evaluated with stress radiographs2, 4–5, 9, 12. If the stress radiographs are negative, then functional treatment is instituted. If they are positive, then surgical repair can be considered. It is important to understand that non-operative treatment is acceptable in the athlete and continues to demonstrate good results in approximately 90% of cases2, 4–5. If non-operative treatment is unsuccessful, late reconstruction of the ligaments gives a good outcome12. In the non-elite athlete, non-operative treatment is pursued in the vast majority of cases. Acute operative intervention should be considered when an unstable ankle occurs in association with an osteochondral fracture, there is evidence of a syndesmotic injury, or in the presence of other associated injuries that would require surgical treatment, such as peroneal tendon injuries.
Chronically the main indication for surgery is failure of non-surgical management, with persistent, symptomatic ankle instability. Two subtypes of chronic instability have been described – mechanical and functional9. Patients with mechanical instability complain of giving way and have reproducible hypermobility of the tibiotalar joint on physical examination. Individuals with functional instability present with a complaint of ankle instability but a lack of any objective signs of instability. Patients with mechanical instability are more likely to benefit from surgery than patients with functional instability.
Many surgical techniques are described for chronic lateral ankle instability; however, they fall into two basic categories: anatomic repair and tenodesis.
Anatomic repair: The goals of anatomic repair are to restore the normal anatomy and joint mechanics. Anatomical repairs are based upon the “Broström procedure,”2, 9 although the exact technique varies from surgeon to surgeon. Broström originally described a midsubstance imbrication of the lateral ligaments with sutures17. Gould subsequently augmented this with the posterior portion of the extensor retinaculum – the “Gould modification”18. In most procedures today the “Broström procedure” has been modified such that suture anchors are used to reattach the shortened and retensioned ATFL to its fibular insertion point. This is then reinforced with the Gould modification reefing the extensor retinaculum.
Tenodesis stabilization: Where the lateral ligaments are irreparable tendon grafts can be used to reconstruct the ankle ligaments. The three classic reconstructions, all of which use the peroneus brevis tendon, are the Evans, Watson-Jones, and Chrisman–Snook procedures (Figure 11.3). All are well documented with both the short- and long-term results reported12, 19–21. One of the major drawbacks of all of the above procedures is that they are non-anatomic reconstructions and sacrifice normal structures. This is particularly concerning when utilizing the peroneus brevis tendon as it is the primary dynamic stabilizer of the ankle joint. Transfer of the peroneus brevis may in turn result in altered ankle kinematics, which could ultimately lead to degenerative changes of the ankle or subtalar joints.
The Watson-Jones procedure reconstructs the ATFL, but not the CFL, by using a split peroneus brevis tendon transfer21. Several good short-term results have been reported, but long-term follow-up studies showed disappointing results12.
The Evans tenodesis is the least technically demanding, but biomechanically it does not reconstruct either the ATFL or the CFL, as the tendon graft is positioned in between these two ligaments20. Several investigators reported good short-term results after this reconstruction, but the long-term results have varied12.
The Chrisman–Snook procedure attempts to restore both the ATFL and CFL by routing the tendon through a complex system of bone tunnels, and probably is the most widely used tenodesis to reconstruct the ligaments12. In one study, satisfactory results were reported in 94% of patients with stress testing showing less residual laxity2.
Semitendinosis tendon allograft in a more recent study showed promising results where the ligament reconstructions were carried out with a near-anatomically placed graft to reconstruct the ATFL and CFL. Preservation of the peroneal tendons avoided loss of eversion strength and the reconstruction provided good ankle stability without sacrificing subtalar motion. There was also a decreased predisposition to subtalar arthritis in short-term follow-up22.
Coexistent pathology should also be addressed at the same time as the ligament reconstruction. This is principally in two areas.
In the cavovarus foot, correction of the deformity with a calcaneal or first-ray osteotomy, as dictated by the Coleman block test, should be considered at primary surgery to prevent recurrence.
The patient with an underlying connective tissue disorder and global hypermobility also needs identifying. These patients are better treated with an augmented reconstruction. We use a semitendinosus allograft or autograft.
Studies show that wound problems, nerve injury, recurrent instability, and stiffness are not uncommon following surgery2, 23.
Wound complications tend to be superficial in nature, while nerve injuries can range in severity from mild disturbances in sensibility to neuroma formation. Both tend to occur less commonly in the anatomic repairs. This has been attributed to the more extensive dissection required for the tenodesis procedures2, 12, 23.
Instability after surgical reconstruction can occur early or late. Several factors have been shown to predispose patients to operative failure, which include longstanding instability, high functional demand, reduced muscle strength, and slow muscle reaction time.
The patient with recurrent instability needs to be carefully examined for a cavovarus deformity and hypermobility – these factors should ideally be assessed at the time of primary surgery as outlined above.
Patients with recurrent instability should initially be treated with a proprioceptive-based physical therapy program. It has to be recognized that persistent functional instability in the setting of a structurally sound repair unfortunately can be very difficult and frustrating to treat. The outcome of revision surgery has been shown to be very unpredictable2, 9, 12.
The literature has consistently reported that patients with a previous history of lateral ankle sprain who wear ankle braces or tape have a lower incidence of re-injury than those who do not2, 5, 12. This reduction may be due to the mechanical support and enhanced proprioception that the brace offers.
Stiffness is common after both anatomic and non-anatomic lateral ankle reconstruction procedures, although it occurs more frequently after tenodesis procedures as a result of overtightening the graft. Generally such stiffness is well tolerated2, 23 and considered to be an acceptable trade-off. Unfortunately, it can ultimately lead to impingement-type pain.
Major complications, including deep venous thrombosis, pulmonary embolism, septic arthritis, and osteomyelitis, have been reported following the operative treatment of lateral ligamentous complex injuries2, 5, 9, 23. They are fortunately rare.
Figure 11.3 Three, largely historical, tenodesis procedures to reconstruct the lateral ankle ligaments: (a) Watson-Jones procedure; (b) Evans procedure; (c) Chrisman–Snook procedure.
Syndesmosis Injuries
An injury to the ankle syndesmosis, also referred to as a “high ankle sprain,” is a significant injury, especially in the athlete. Literature dating back to 1773 has emphasized the importance of this ligamentous complex24. The diagnosis unfortunately is not always an easy one and requires a high index of suspicion as it constitutes a wide spectrum of injuries, ranging from a simple ligamentous sprain to frank diastasis with a concomitant osteochondral and medial ligament injury. Isolated syndesmotic sprains are reported to account for about 1% of all ankle sprains25, although the prevalence may be much higher, as the injury is frequently misdiagnosed or missed completely. In one study 32% of professional football players were noted to have late calcification of the syndesmosis, signifying previous injury25–26. Mismanaged injuries can ultimately lead to chronic ankle pain, disability, and eventually arthritic change.
The ankle syndesmosis ligament complex consists of four main structures4, 24, 27 (Figure 11.4).
The anteroinferior tibiofibular ligament (AITFL) is the most frequently injured. It is often multifascicular, with the most inferior fascicle sometimes described as a separate structure entirely – Bassett’s ligament. Bassett’s ligament is a cause of anterior ankle impingement, and can impinge on the lateral talar dome28.
The interosseous ligament (IOL) connects the tibia and fibula from 0.5 cm to 2 cm above the plafond and surrounds the synovial recess, which extends upward from the ankle. At its superior margin, the IOL blends with the interosseous membrane (IOM). The IOM adds very little in terms of strength.
Posteriorly there are two ligaments. The inferior transverse ligament (ITL) has a fibrocartilaginous appearance and functions, similarly to the glenoid labrum, to deepen the tibiotalar articulation. This is often continuous with the posterior tibiofibular ligament (PITFL). The ITL will be considered a part of the PITFL for the purposes of this chapter. Without these ligamentous restraints, the syndesmosis widens (Figure 11.5).
As a result of the unique shape of the talus, the fibula externally rotates and translates proximally and laterally during ankle dorsiflexion. It moves in the opposite direction with plantar flexion29. The syndesmotic ligaments, which accommodate this dynamic process, are most commonly injured in the setting of forceful external rotation and hyperdorsiflexion of the talus29–31. The talus external rotates against the fibula and in turn tensions the AITFL, which ultimately fails first (Figure 11.6). If the force is continued, disruption of the IOL and IOM occurs (Figure 11.7), followed by the PITFL. Isolated, complete ruptures of the syndesmosis were traditionally considered to be a rarity, with syndesmosis injuries thought to more usually occur in conjunction with a distal fibula fracture. However, with increasing awareness and more sophisticated imaging isolated syndesmotic injuries are increasingly being recognized26, 32.
Figure 11.4 The four principal components forming the syndesmotic ligament complex. For abbreviations see text.
Figure 11.5 Ankle syndesmosis injury. Note the increased medial and tibiofibular clear spaces, as well as the decreased tibiofibular overlap.
Figure 11.6 T2 weighted MRI demonstrating an AITFL tear.
Figure 11.7 T2 weighted MRI in a patient with a Maisonneuve fracture variant and subsequent injury to the interosseous membrane. Note the substantial amount of soft tissue edema, demonstrating the severity of the injury.
Numerous cadaveric studies have been performed to evaluate the relative contributions of each structure to ankle stability. Ogilvie-Harris determined that the AITFL contributes about 35%, the PITFL 40%, and the IOL 22% to overall stability. Injuring two of these structures decreases the syndesmotic resistance to lateral displacement by nearly 50%33. Xenos performed serial sectioning studies and found that cutting the AITFL alone resulted in an average 2.3 mm diastasis. Sectioning the distal 8 cm of the IOM/IOL resulted in an additional 2.2 mm, and sectioning the PITFL a further 2.8 mm. This equates to a total displacement of 7.3 mm34. These are large displacements as there is a 42% reduction in contact area, and consequent increase in pressure, with lateral translation of the talus of 1 to 2 mm, fibular shortening of 2 mm, and external rotation of 5° of the distal fibula with deltoid ligament strain29–31. This pathologic redistribution of pressures can result in the accelerated development of post-traumatic arthritis.
It is important to maintain a high index of suspicion as pain and difficulty with ambulation are common to both syndesmotic and lateral ankle ligament injuries. The physical examination of both injuries usually reveals ecchymosis and swelling over the anterolateral aspect of the ankle. The classic finding in acute syndesmotic, as opposed to a lateral ligament injury, is localized tenderness anteriorly over the syndesmosis, which is aggravated with forced dorsiflexion. The distance over which this tenderness extends proximally has been referred to as the “tenderness length.” This is shown to correlate strongly with the degree of injury and time of return to sports activity35. It is also important to palpate the entire length of the fibula and both malleoli to rule out an associated bony or ligamentous injury36.
A number of provocative stress tests have been described. The “squeeze test” is performed by compressing the tibia and fibula above the midpoint of the calf; this is positive if it induces pain at the level of the syndesmosis37. Although commonly used, studies have shown that the squeeze test is not reliable enough to confirm the diagnosis25. A far more reliable test is the “external rotation test”25, 30, 33. The patient sits with the knee flexed to 90° and the foot held in a neutral position. The foot is gently externally rotated. If this causes pain over the anterolateral ankle, proximal to the joint line, the test is considered positive. The “external rotation test” has been shown to have the best inter-observer reliability and sensitivity. A functional “stabilization test” has also been described. It is mainly used in athletes26, 38. Athletic tape is tightly applied circumferentially above the ankle joint. If toe raises, walking, or jumping are less painful upon taping the test is considered positive.
Standing anteroposterior (AP), lateral, and mortise radiographs of the ankle should always be obtained. In patients who have proximal leg tenderness, additional AP and lateral views of the entire fibula should be obtained to rule out a Maisonneuve injury. It is important remember that up to 50% of all syndesmotic injuries may present with a bony avulsion of the distal anterior or posterior tibia. In chronic injuries, calcification of the syndesmosis, or even a synostosis, may be seen39.
Three major radiological criteria define an unstable syndesmosis on radiographs (Figure 11.8).
1. The medial clear space is normally less than 4 mm, and is the space between the medial malleolus and medial border of the talus, 1 cm below the joint line. An increase in this space signifies an associated deltoid ligament injury29, 31, 39. Bonnin suggested that it is variable and should be used with caution40.
2. The tibiofibular clear space is regarded as the most accurate parameter and is defined as the distance between the lateral cortex of the tibia and the medial cortex of the fibula, 1 cm above the joint line. In a cadaveric study, specimens without a syndesmotic injury consistently displayed a clear space of less than 6 mm30. A further cadaveric study noted sex-specific differences with a clear space of less than 5.2 mm in female patients and 6.5 mm in male patients41.
3. The tibiofibular overlap is the overlap of the posterior tibia on fibula at the level of the incisura. It can be calculated either as an absolute amount or percentage of fibular width. Cadaveric studies have shown that tibiofibular overlap should be more than 6 mm, or 42% of the fibular width30. In sex-specific cadaveric studies the overlap should be greater than 2.1 mm in female and 5.7 mm in male patients, or 24% of the fibular width41. Although these numbers are widely accepted, it is important to remember that a radiograph of the uninjured ankle is instrumental in defining what is normal for a specific patient.
If a syndesmosis injury remains a concern, despite normal radiographs, external-rotation stress radiographs may help. While many advocate their use, the reliability of stress radiographs has been questioned. This stems from a study by Xenos who showed that there was only slight widening of the mortise when an external-rotation torque was applied to an ankle, despite sectioning all of the ligaments34. Negative-stress radiographs have also been obtained in patients who subsequently had an arthroscopically confirmed syndesmosis injury42. Therefore additional imaging studies in the form of a CT scan or MRI may be required to establish the diagnosis.
Figure 11.8 The tibiofibular clear space and overlap, which are used for detecting syndesmotic injury.
Ebraheim demonstrated in a cadaver model the superiority of CT scanning over plain radiographs. The CT shows fibular shift, rotation, shortening, and bony avulsions43. Routine radiographs did not show small 1 or 2 mm diastases, whereas all were detected on CT. Routine radiographs even failed to diagnose a syndesmotic injury in 50% of patients who had 3 mm diastases. It is important to evaluate the fibular rotation and tibiofibular distance at exactly the same level, if bilateral scans are obtained, to avoid misdiagnosis. An MRI gives the most detail about the integrity of the ligamentous complex and has become the standard of care in evaluating athletes suspected of having a syndesmosis injury. This stems from studies conducted by Takao who found the sensitivity, specificity, and accuracy of an MRI in identifying a syndesmotic injury to be 100%, 93.1%, and 96.2% for a tear of the AITFL and 100%, 100%, and 100% for a tear of the PITFL44. The sensitivity (90%) and specificity (95%) in identifying a chronic syndesmosis injury are also high39. Although both CT and MRI give the clinician a significant amount of information, it is important to remember that the images are non-weightbearing or unstressed. If subtle instability exists, an injury can still be missed. Lui showed that ankle arthroscopy was more sensitive than intraoperative stress radiographs in detecting syndesmotic injury45. Some have even advocated routine ankle arthroscopy with this in mind, especially in view of the fact that multiple studies have shown significant functional improvement with arthroscopy29–31.
Numerous classification systems have been described for ankle syndesmosis injuries, but none clearly define the degree of injury, provide a clear therapeutic algorithm, or predict prognosis. Treatment decisions should thus be based on the patient’s signs and symptoms, their level of activity, injury severity on imaging, and whether the injury is acute, subacute, or chronic.
Sprains without diastasis or instability can be managed non-operatively. The first phase is directed at protecting the ankle and limiting pain with RICE and anti-inflammatory medication. It has been also recommended that the ankle should be immobilized with a protective boot or brace, with weightbearing status determined by the patient’s symptoms. The second phase begins when the acute pain has subsided and involves joint mobilization, strengthening, and neuromuscular training. In the third phase, the athlete progresses to an advanced proprioception-training program with sports-specific drills. Overall, the results of non-operative management show good to excellent results ranging from 86 to 100%29–31.
Those with instability but no diastasis on stress testing have also been treated successfully non-operatively29. These patients need to be managed with a non-weightbearing cast for at least four weeks. Obtaining a repeat weightbearing radiograph is recommended at two weeks in order to confirm that reduction is maintained. After the initial four weeks, progressive weight bearing in a protective boot or walking cast may be started so that the patient is fully weight bearing at eight weeks post injury. Some authors have recommended that high-performance athletes with this degree of injury should be treated more aggressively with surgery32. However, this approach has yet to be justified by the literature. Ultimately, it is important to inform the patient that the recovery from syndesmosis injuries is much longer than that from a lateral ankle ligament injury, with several studies illustrating a doubling of the amount of time before being able to return to full, unrestricted activity29, 32.
Patients with frank diastasis of the syndesmosis require operative treatment, and extreme care needs to be taken to accurately reduce the fibula within the incisura. Traditionally it was recommended that the ankle needed to be held in dorsiflexion at the time of fixation, to ensure that the widest part of the talus is within the ankle mortise during fixation to avoid overtightening of the joint. This was challenged by Tornetta who demonstrated that it is anatomic reduction of the fibula into the sigmoid notch that is the most important factor in successful syndesmosis fixation46. Fixation should be performed though an open lateral incision, exposing the incisura and ensuring an anatomic reduction prior to fixation. If an anatomic reduction is not possible a medial arthrotomy, to address medial pathology, should be undertaken. Historically the syndesmosis has been fixed rigidly with screws. McBryde determined that the screws should be placed 2.0 cm proximal to the tibiotalar joint, as this provides better stability than placing the screws more proximally47. Even with good quality intraoperative fluoroscopic imaging, postoperative CT scans have demonstrated that malreduction of the syndesmosis occurs in up to 24% of cases39, although it has been shown that the malreduced fibula usually self-reduces anatomically after screw removal48. The number of screws, their size, and number of cortices fixed continues to be debated. Screws are kept in place for a minimum of six to eight weeks, while some investigators recommend that they are not removed for three months. Where the screws are left in situ, breakage and osteolysis around the screw is likely, although the patients have been shown to do well49–50.
Bioabsorbable screws have also increased in popularity, as they do not need to be removed and provide excellent stability. An additional advantage is that although the length of time the screws take to dissolve remains unknown, if the fibula is malreduced it may reduce as the screws dissolve. The clinical results of bioabsorbable screws appear to be equivalent to those of metal screws. The main drawback is that they may create a local inflammatory reaction, which can manifest as a sterile abscess or cyst51.
Semi-rigid fixation with polyester/polyethylene sutures secured with buttons tensioned across the syndesmosis have the theoretical advantage of maintaining movement (Figure 11.9). Thornes compared these with syndesmosis screw fixation and found that the semi-rigid fixation was at least as good as screws52. Seitz found a suture to be comparable to a 4.5 mm screw fixed across four cortices53. The semi-rigid suture technique is also associated with a shorter rehabilitation, faster return to work, and lack of complications29, 54. In contrast, a cadaveric biomechanical study reported the failure of the suture to maintain adequate syndesmotic reduction when compared with a metallic screw, particularly with rotational forces55.
Figure 11.9 Suture endobutton syndesmotic fixation.
The salvage procedure of choice for arthritis, secondary to chronic instability of the syndesmosis, is syndesmotic arthrodesis, which has been shown to produce good long-term pain relief.
In addition to chronic instability and arthritis, the most commonly cited complication following a syndesmotic injury is heterotopic ossification26, 31, 39. The presence of pain with heterotopic ossification is inconsistent26, 31, 39. Hopkinson and colleagues described nine cases of heterotopic ossification all of which were asymptomatic26. On the other hand, McMaster and Scranton found radiographic evidence of tibiofibular synostosis in several patients who had persistent pain three to 11 months after injury26. Veltri and colleagues reported two cases of symptomatic tibiofibular synostosis in collegiate and professional football players. Both returned to full activity after resection56. In general, it is accepted that when a painful synostosis occurs, it should be resected and sealed with bone wax to prevent recurrence.
Peroneal Tendon Injuries
Lateral ankle sprains are the most common traumatic injury of the ankle, and other causes of lateral ankle pain are frequently overlooked. Once considered to be rare, peroneal tendon injuries in athletes have been recognized as a common cause of non-resolving pain after a “typical” ankle sprain57. Thus a high index of suspicion is required.
The peroneal musculature makes up the entire lateral compartment of the leg. At the level of the ankle, the tendon of the peroneus brevis (PB) lies against the retromalleolar groove of the distal fibula. The peroneus longus (PL) tendon lies behind that of the PB, compressing it in the groove. At this level both tendons are contained within a shared fibro-osseous tunnel, the fibular groove, which is deepened by a cartilaginous ridge. The tunnel is completed posteriorly and laterally by the superior peroneal retinaculum (SPR). The muscle belly of PB is more distal than that of PL, and can overstuff the tunnel and in turn predispose to injury57. Additional differences in the anatomy of the groove may also predispose some individuals to peroneal instability. Edwards noted that a fibular sulcus, or groove, was present in 82% of individuals, the bone was flat in 11%, and in 7% it was convex58. Ozbag found that 68% had a concave fibular groove, whereas the remaining specimens had a flat or convex area on the distal fibula59.
Both tendons pass distal to the fibula and turn toward the peroneal tubercle, where the common tendon sheath bifurcates and passes under the inferior peroneal retinaculum. The PL then enters a second tunnel under the cuboid where the os peroneum, a sesamoid bone present in 10 to 20% of individuals, is located60. The PL ultimately inserts into the plantar aspect of the base of the first metatarsal and medial cuneiform. The PB courses over the calcaneofibular ligament, above the peroneal tubercle, and inserts into the base of the fifth metatarsal. Both tendons are relatively weak ankle plantar flexors, but do contribute significantly to hindfoot eversion57, 61. The PL also plantar flexes the first ray. The PB is the strongest abductor of the forefoot. Both work together to dynamically stabilize the lateral ankle ligament complex.
An accessory muscle, the peroneus quartus (PQ), is present in 13 to 22% of the population62. It most commonly originates from the PB and inserts distally on the peroneal tubercle of the calcaneus. The presence of the PQ has been associated with peroneal tears, instability, and stenosing tenosynovitis by virtue of its bulk in the restricted space under the SPR60, 63. Unfortunately, even with MRI scanning the diagnosis can be difficult to make as the accessory tendon can appear similar to a split in the PL57.
Traditionally patients with inflamed and painful peroneal tendons are said to be suffering with “peroneal tendinitis.” However, when surgical specimens of the peroneal tendon are examined histologically, very few inflammatory cells are present64. Instead, a much more degenerative pattern is seen, where the collagen matrix is organized in a random fashion with numerous fibroblasts64. Therefore the condition is better described as a “tendinosis,” a description that also applies to the tendo Achillis. An acute inflammatory process of the well-vascularized tenosynovium can result in an effusion within the peroneal sheath64. Stenosing tenosynovitis of the peroneal tendons has been described in chronic cases, in which thickening of the tendon sheath constricts the tendons. This usually occurs in one of three areas, namely the retromalleolar sulcus, the peroneal tubercle, or the cuboid tunnel.
Typical symptoms of peroneal tendon pathology include weakness, pain, and swelling along the lateral aspect of the ankle, particularly posterior to the lateral malleolus. Pain is exacerbated by passive plantar flexion and inversion of the ankle, or by active, resisted dorsiflexion and eversion of the foot. The actual strength of the peroneal musculature is usually good, despite the pain. Circumduction of the foot and ankle is important at the time of examination as it may provoke subluxation or dislocation of the tendons. The presence of such instability alters the treatment61, 63. A tight gastrocnemius–soleus complex, with increased calcaneal varus, should also be noted, as the presence of significant varus can ultimately result in re-injury if it is not corrected.
Radiographic examination is usually normal, and is only necessary to exclude other sources of pain and to assess the foot alignment. Rarely an acute avulsed flake of bone may be seen from the lateral tip of the fibula, where the SPR has been avulsed, and the tendons consequently dislocated. Another rare abnormality is a proximally migrated fractured os peroneum with a PL tear65. Tenography has been described, but is rarely used with the advent of MRI and USS. An MRI scan demonstrates fluid within the tendon sheath, although it is important to bear in mind that with the alteration in direction of the peroneal tendons at the inframalleolar region, and the flat morphology of the PB, false positive findings of tendinosis or split tears may be seen on MRI scanning as a result of the “magic angle phenomenon”66. A USS is more operator dependent, but can be helpful in reaching a diagnosis, as well as guiding diagnostic or therapeutic injections. It is generally recommended that injections are kept to a minimum to avoid soft-tissue atrophy and tendon rupture. One of the biggest advantages of US is the ability to dynamically assess the tendons in cases of suspected peroneal subluxation or dislocation67–68.
The recommended non-operative management of acute peroneal tenosynovitis is RICE. Use of NSAIDs and a period of immobilization using a cast, boot, or orthosis for four to six weeks can be helpful. After symptoms subside, the patient should be mobilized as soon as possible with a course of physical therapy concentrating on proprioception, flexibility, and strengthening. Taping of the ankle or the use of an ankle brace during vigorous activity can be tried. It is extremely rare for tenosynovitis to progress to the point where surgery is required. If surgery is necessary, a tenosynovectomy and resection of any impinging bony prominences is undertaken. This, along with the correction of any associated biomechanical disorder, such as hindfoot varus, usually gives excellent results62.
In cadaver studies, PB tears are found in 11 to 37% of specimens69–70. Although PL tears are less common, when they do occur they are associated with a varus hindfoot71. The varus position increases the force on the tendons and the peroneal tubercle. The tubercle in turn hypertrophies, further damaging the tendons. PB and PL tears usually take the form of longitudinal splits, although complete ruptures do occur leading to weakness and functional ankle instability.
Acute peroneal tears (Figure 11.10) are often the result of a sporting injury. The mechanism is usually subluxation of the PB over the posterolateral edge of the fibula as a result of injury to the SPR. Repetitive compression of the PB by the PL against the posterior fibula in the fibular groove may also cause a tear of the PB. Other contributing factors include tenosynovitis, distal insertion of the peroneus brevis muscle belly, and the presence of a PQ72. These last two factors lead to overcrowding of the fibular groove and predispose to tendon subluxation or dislocation. It is thought that flat or convex fibular groove morphology predisposes to tendon instability57, 61, 63.
Figure 11.10 Intraoperative photograph illustrating a split tear in the peroneus brevis tendon as it courses around the distal fibula within the retromalleolar groove.
Conservative management is as described above for tenosynovitis, with the possible addition of an orthosis with lateral posting of the hind- and forefoot. If non-operative treatment fails, operative treatment may be needed. Krause and Brodsky described a simple classification system to help guide the surgical treatment of PB tears. This can also be applied to PL tears73. After an extensive tenosynovectomy and debridement, the remaining tendon is graded based on the amount of tendon still remaining. In grade 1 tears, 50% or more of the tendon is in continuity and viable after debridement. This 50% can be repaired with tubularization. In grade 2 tears less than 50% of the tendon remains viable after debridement. The abnormal tendon is excised and the stumps are tenodesed to the intact, uninvolved peroneal tendon, both proximally and distally.
Subluxation and dislocation of the peroneal tendons from the retromalleolar groove to the lateral aspect of the fibula (Figure 11.11) can cause lateral ankle pain, clicking, and instability. Frequently these injuries are misdiagnosed acutely as a routine ankle sprain. Acute peroneal tendon dislocations most commonly result from a sudden, forceful, passive dorsiflexion of an everted foot with a sudden, strong contraction of the peroneal muscles74. However, this injury has also been described with the foot held inverted75. This vigorous contraction causes the superior peroneal retinaculum to strip off the fibula at its periosteal attachment. The peroneals subsequently dislocate anteriorly. With chronic, recurrent dislocation, the patient presents with a snapping sensation over the distal fibula, which is usually painful.
Figure 11.11 MRI demonstrating significant peroneal tendon instability with disruption of the superior peroneal retinaculum and complete dislocation of the peroneal tendons.
Eckert and Davis (Figure 11.12) described three types of injury patterns76. In grade 1, the retinaculum and its attachment to the periosteum are stripped from the distal fibula. The peroneal tendons dislocate anteriorly into the pouch formed between the lateral border of the fibula and the periosteum/retinaculum. In grade 2 injuries, the fibrocartilagenous ridge is stripped, remaining attached to the retinaculum/periosteum. In a grade 3 injury the periosteum avulses where the cartilaginous rim attaches, giving a characteristic radiological appearance. In 1987, Oden described a grade 4 injury where the peroneal tendons dislocate through a tear in the peroneal retinaculum74.
