Etiology

Osteophytes are protrusions of bone and cartilage around the joint space. Osteophytic formations occur with weight-bearing articular cartilage damage, such as osteoarthritis of the hip and knee, and occur without weight-bearing articular cartilage damage, such as bony impingement lesions.⁸

Controversy exists about the cause of bony osteophytes around the ankle with normal articular cartilage. Adjacent or articulating bones that are repetitively in contact can stimulate the cambium layer, the deep layer of periosteum that has osteogenic potential, to form osteophytes. The osteophytic prominence causes bony impingement, often increases in size, and eventually may break off, forming a loose body. After the spur is formed, it may alter normal mechanics or motion of the ankle. Morris⁶ and McMurray⁷ described osseous exostoses of the anterior rim of the tibia and the sulcus of the talus, and they believed these to result from a traction injury of the joint capsule of the anterior aspect of the ankle that occurred when the foot was in extreme plantar flexion (i.e., capsule-ligament traction). However, the capsule of the ankle attaches above the location of the tibial osteophytes and distal to the talar ones. In later studies, anatomic observations during arthroscopic surgery confirmed that tibial osteophytes were located at the joint level and talar osteophytes were found proximal to the talar neck notch, away from the capsular attachment sites (Fig. 5-1); the osteophytes were intra-articular.^9,10 O’Donoghue¹¹ attributed these exostoses to direct osseous impingement during forced dorsiflexion or to post-traumatic calcification. Van Dijk and colleagues¹² attributed the osteophytes to medial impingement from inversion of the talus onto the medial tibia and thought they might be related to instability (Fig. 5-2). The osteophytes were related to direct trauma associated with the impingement of the anterior articular border of the tibia in the talar neck during forced dorsiflexion of the ankle joint.

FIGURE 5-1 Talar osteophyte lies away from the capsular attachment.

FIGURE 5-2 Anteromedial osteophytes of the tibia and the talus.

Classification

In 1992, Scranton and McDermott⁸ classified four types of anterior ankle impingement by the radiographic appearance of bony spurs (Table 5-1). The classification system grades the degree of spur formation and assists in predicting the length of recovery time. Van Dijk’s 1997 radiographic classification (Table 5-2) was based on osteoarthrosis of the ankle on plain radiographs (Fig. 5-3).¹⁰ The degree of osteoarthritic change is a better prognostic indicator for the outcome of arthroscopic surgery for anterior ankle impingement than size and location of spurs.

TABLE 5-1 Classification of Anterior Ankle Impingement

From Scranton PE Jr, McDermott JE. Anterior tibiotalar spurs: a comparison of open versus arthroscopic débridement. Foot Ankle. 1992;13:125-139.

TABLE 5-2 Classification of Osteoarthritic Changes of the Ankle Joint

From van Dijk CN, Tol JL, Verheyen CC. A prospective study of prognostic factors concerning the outcome of arthroscopic surgery for anterior ankle impingement. Am J Sports Med. 1997;25:737-745.

FIGURE 5-3 A, Osteophytes without joint space narrowing (Scranton type III, Van Dijk grade I). B, Joint space narrowing with osteophytes (Scranton type IV, Van Dijk grade II).

Anatomy

The talus articulates with the os calcis so that the axis of the talus is roughly in line with the first web space of the foot and the axis of the os calcis is in line with the fourth web space. In dorsiflexion, bony impingement occurs anteromedially between the neck of the talus and the anterior lip of the tibia. In plantar flexion, bony impingement occurs posterolaterally between the os calcis and the posterior lip of the tibia. The impingement can be found in all quadrants around the ankle: anterior, lateral, posterior, and medial. Bony impingement most often occurs anteromedially and posterolaterally, whereas soft tissue impingement occurs anterolaterally and posteromedially.

The Anterior Ankle

Anterior impingement syndrome of the ankle is the most common cause of anterior ankle pain in many sports participants. Repetitive forced dorsiflexion also can result in impaction-related microtrauma of the anterior chondral margin of the tibiotalar joint. Over time, attempted repair with resultant fibrosis and fibrocartilage proliferation leads to the formation of osteophytes.⁷ When osteophytes form, they limit dorsiflexion, facilitate further impingement, and result in more periosteal stimulation, creating a repetitive cycle. Careful inspection of the pathologic anatomy shows that osteophytes do not form in the capsular insertion but instead where bones come together.¹¹ Osteophytes can break off and become loose bodies (Fig. 5-4).

FIGURE 5-4 A, Loose body in a female basketball player with recurrent ankle sprains. B, Articular grooving from the loose body.

In supination injury, damage to the anterior non–weight-bearing cartilage rim occurs.¹² The cartilage proliferation, scar tissue formation, and calcification that may result from attempted repair depend on the degree of initial damage and on chondral and bone cell stimulation. Recurrent forced dorsiflexion of the ankle is the main factor in the development of spurs.^13,14 Another factor is recurrent microtrauma, and it has been demonstrated that spur formation is related to recurrent ball impacts in soccer players.¹⁵ The entire process of spur formation and hypertrophied synovium or fibrosis is exacerbated by recurrent ankle sprains and persistent ankle instability. Synovial changes may result from chronic inflammation of the soft tissue (e.g., synovial fold, subsynovial fat, collagen tissue) that was crushed during forced dorsiflexion movements between spurs.¹⁶

The common history of patients with anterior ankle impingement is recurrent inversion sprain. The typical patient is a young athlete presenting with chronic anterior ankle pain.¹⁷ Pain likely results from entrapment of hypertrophied synovial tissue between the talus and the anterior tibia, which is exacerbated by the presence of anterior spurs. Patient usually present with swelling after activity and with limited ankle dorsiflexion movement.

Physical examination reveals anterior tenderness and thickening of the synovium, often with an effusion, palpable osteophytes with the ankle in slight plantar flexion, limited dorsiflexion when compared with the opposite ankle, and a positive dorsiflexion impingement sign (i.e., pain with forced dorsiflexion of the ankle when the knee is flexed).

Standard lateral radiographs of the ankle usually show spurs. The weight-bearing lateral view with the ankle in maximal dorsiflexion (i.e., plié view) demonstrates anterior impingement, and this view commonly is used in evaluating dancers. Conventional magnetic resonance imaging (MRI) accurately detects and localizes anterior tibiotalar spurs, adjacent reactive synovitis and fibrosis, subchondral bone edema, and other coexisting lesions, such as collateral ligament complex injury, osteochondral lesions of the talus, or intra-articular bodies. There is little or no additional information gained through indirect magnetic resonance (MR) arthrography for evaluating anteromedial impingement compared with conventional MRI.¹⁸

Several conditions can mimic the anterior impingement syndrome, including osteochondritis dissecans of the talus, a “high” ankle sprain involving the anterior tibiofibular ligament,¹⁹ impingement by Bassett’s ligament,¹ an aberrant distal insertion of the anterior tibiofibular ligament that can cause persistent symptoms, Ferkel’s disease,¹⁶ an accumulation of debris and synovitis in the anterolateral gutter, degenerative joint disease of the tibiotalar or talonavicular joints (especially in the early phases when the radiographic findings are subtle), and a stress fracture or an osteoid osteoma in the tarsal navicular.

Conservative treatment with rest, physical therapy, shoe modification, or local injection constitutes first-line therapy for most cases of anterior ankle impingement. If all modalities of conservative treatment are unsuccessful, operative treatment may be indicated. The goal of surgery is removal the osteophytes to restore the anterior space and to reduce the chance of symptoms recurring. Numerous investigators have reported good results with open arthrotomy, but it can be complicated by cutaneous nerve entrapment, wound dehiscence, damage of the long extensor tendons, and formation of hypertrophic scar tissue.^7,11,17 In recent years, the arthroscopic treatment of anterior ankle impingement has had a high success rate. The first series reported by Biedert³ had a success rate of approximately 67%. Ferkel and colleagues¹⁶ reported a success rate of approximately 84% for 31 patients with soft tissue impingement of the ankle. Ogilvie-Harris and colleagues²⁰ described an average of 39 months’ follow-up for patients who were treated for anterior ankle impingement by arthroscopic removal of bony spurs. The good and excellent results were obtained for 88% of 17 patients.²⁰ In a prospective study, Amendola and coworkers²¹ treated 79 cases of ankle impingement by arthroscopic débridement. Fifteen cases of soft tissue impingement and 14 cases of anterior bony impingement were included in the study. There were statistically significant decreases in subjective analog scores. Eighty percent of the soft tissue impingement lesions and 86% of the bony impingement lesions benefited from the procedure. Eighteen percent of patients had neurologic complications, including partial deep peroneal nerve neurapraxia and superficial peroneal nerve irritation.²¹

Scranton and colleagues⁸ reported the comparative open and arthroscopic treatment of ankle impingement. The recovery time of the arthroscopic treatment patients was approximately one half of the time of open treatment patients. The patients treated arthroscopically returned to full athletic training 1 month faster than the other group.⁸

Tol and associates⁹ described the results for 5 to 8 years of follow-up for the arthroscopic treatment of anterior impingement in the ankle. Excellent or good results were obtained for 100% of patients without osteoarthritis, 77% of patients with grade I disease, and 53% of patients with grade II diseases according to the classification for osteoarthritis of the ankle (see Table 5-2).²² Osteophytes recurred in two thirds of the ankles with grade I osteoarthritis, but the recurrence of osteophytes did not correlate statistically with the return of symptoms. Narrowing of the joint space increased in 47% of patients with grade II osteoarthritis.⁹

Anteromedial Ankle Impingement

Anteromedial ankle pain is caused by impingement of the anterior portion of the medial malleolus on a spur on the medial shoulder of the talus. Spurs often occur on both sides of the joint. They result from injury to the deltoid ligament complex, leading to scar formation and synovitis along the anteromedial joint line. Patients complain of pain along the anteromedial joint line that is aggravated by walking or sporting activities. Patients often report a clicking sensation and painful limited dorsiflexion of the ankle. On physical examination, the anteromedial aspect of the ankle appears swollen and is tender to palpation over the anterior tibiotalar fascicle of the deltoid ligament. The anteromedial spur often can be palpated on physical examination but usually cannot be visualized on standard anteroposterior and lateral radiographs of the ankle. In a cadaver study, Tol and colleagues¹⁵ described medially located talar osteophytes and anteromedial tibial osteophytes that were up to 7.3 mm in diameter, originated from the anteromedial border, and could remain undetected due to overprojection or superposition of the lateral part of the talar neck and body and the prominent anterolateral border of the distal tibia, respectively.¹⁵

These osteophytes are easy to miss (i.e., “hidden spurs”). A special oblique anteromedial impingement view (Fig. 5-5) has been developed to aid in the detection of anteromedial spurs, and it is obtained with the beam tilted in a 45-degree craniocaudal direction with the leg in 30 degrees of external rotation and the foot in plantar flexion in relation to the standard lateral radiograph position.²³ The sensitivity of lateral radiographs for detecting anterior tibial and talar osteophytes is 40% and 32%, and their specificity is 70% and 82%, respectively. The combination of lateral and oblique anteromedial impingement radiographs of the ankle increase the sensitivity to 85% for tibial osteophytes and 73% for talar osteophytes.²⁴

FIGURE 5-5 A special oblique anteromedial impingement view.

Conventional MRI has not been useful in detecting anteromedial impingement syndrome. Robinson and associates²⁵ demonstrated that the cross-sectional MR arthrography could confirm anteromedial ankle impingement. Their findings included capsular and synovial soft tissue thickening anterior to the tibiotalar ligaments and associated osseous abnormalities such as anteromedial osteophytes.²⁵ The impingement is thought to be soft tissue entrapment associated with previous injury to the anterior tibiotalar fascicle of the deltoid ligament complex. A thickened anterior tibiotalar ligament can impinge on the anteromedial corner of the talus, often resulting in adjacent fibrosis or a meniscoid lesion and synovitis that may lead to adjacent spur formation.

The Lateral Ankle

The lateral ankle can be a complex site of pain and discomfort, and an accurate diagnosis can be difficult. Symptoms often begin after ankle sprains.

The “meniscoid” of the ankle is the soft tissue trapped between the lateral shoulder of the talus and the lateral malleolus. McCarroll and associates³⁶ described this lesion in four soccer players who had a history of frequent ankle sprains, and after failing conservative treatment, they underwent arthroscopic débridement of the lesion. After appropriate rehabilitation, all four returned to competition with cessation of the symptoms; only one player rarely had pain.

Fracture of the lateral process of the talus³⁷ causes impingement beneath the lateral malleolus. Snow-boarder’s fracture is a synonym for this fracture because of the increased incidence in this patient population. The fracture is often misdiagnosed as an ankle sprain, and routine plain radiographs often are read as normal. CT is the investigation of choice. Treatment is surgical excision or open reduction and internal fixation.³⁸

The os subfibulare is an accessory ossicle that may be asymptomatic. It can be loosened by injury and become symptomatic.

An avulsion fracture of the tip of fibula can remain mobile or become trapped in or under the lateral ankle joint and become symptomatic. It also can occur in the insertion of the calcaneofibular ligament. Treatment depends on the size of the avulsion fragment. If it is small, it should be excised, and the stump of the ligament should be sutured into the tip of the lateral malleolus.

The pain of chronic, healed os calcis fractures may be difficult to differentiate from subtalar joint impingement pain. A small injection of local anesthetic beneath the tip of the lateral malleolus can help to differentiate impingement from an os calcis fracture.

The Medial Ankle

Medial ankle pain usually is not caused by bony impingement. Medial ankle sprains are rare because the medial structures are strong and rigid compared with lateral sprains, but after medial ankle instability occurs, medial osteophytes may cause bony medial impingement (Fig. 5-6). The medial ankle pain common in athletes typically is caused by posterior tibial tendonitis. Flexor hallucis longus (FHL) tendonitis often is found in dancers (i.e., dancer’s tendonitis), and it causes posteromedial pain. In dancers, the most common cause of pain around the medial malleolus comes from “rolling in” (i.e., pronating) to obtain proper turnout. This is one of many overuse syndromes causing chronic strain on the deltoid ligament. The lesion results from the chronic strain on the deep posterior fibers of the deltoid ligament complex between the medial talus and the medial malleolus. Injury leads to the formation of scar tissue and fibrosis located along the posteromedial joint line that becomes entrapped between the posterior talus and medial malleolus, resulting in persistent medial ankle pain. This lesion may be isolated, but it most often coexists with symptoms of anterolateral ankle pain and instability. If the lesion remains unrecognized and untreated, medial ankle impingement may result in persistent pain after lateral ankle reconstruction.^39,40

FIGURE 5-6 Osteophytes are causing medial ankle impingement.

The Posterior Ankle

Posterior ankle impingement, or talar compression syndrome,¹³ is natural result of full weight bearing in maximal plantar flexion of the ankle in full pointe position. It is also referred to as os trigonum syndrome, posterior triangle pain, and posterior tibiofibular impingement. Posterior ankle pain is common in athletes, dancers, gymnasts, swimmers, divers, figure skaters, and soccer players who require repetitive and extreme plantar flexion.

The key structures involved in posterior ankle impingement syndrome can be divided into osseous and soft tissue components. The osseous components include the posterior tibia and talus and the superior calcaneum. Posterior talar anatomy variations are the principal predisposing osseous factors in posterior ankle impingement syndrome. The posterior aspect of the talus has two tubercles: the medial tubercle and lateral tubercle. The lateral tubercle is the origin of the posterior tibiofibular ligament. If it is large, it is referred to as the posterior process of the talus, or Stieda’s process. The os trigonum is the ununited lateral tubercle on the posterior aspect of the talus. It is present in 7% to 14% of people, and it is often bilateral.^41,42 The os trigonum is the second most common accessory bone in the foot; the accessory navicular is the most common.

The key soft tissue structures involved in posterior ankle impingement syndrome include the FHL tendon, the posterior ankle ligaments, and the joint capsule and synovium. The FHL tendon forms a groove on the posterior tibial plafond before passing between the medial and lateral tubercles. This groove is converted into a fibro-osseous tunnel by condensations of fibrous connective tissue between two tubercles. The FHL tendon runs from its origin on the fibula laterally to its insertion in the distal phalanx of the hallux medially. The posterior talofibular ligament (PTFL) passes horizontally from the posteroinferior tip of the fibular malleolus to the lateral tubercle of the posterior process of the talus. The tibial slip connects the PTFL to the medial malleolus and is located just inferior to the intermalleolar (transverse tibiofibular) ligament, which runs from the medial posterior tibial plafond to the posteroinferior tip of the fibular malleolus. If the intermalleolar ligament is thickened, it may be caused by posterior ankle impingement syndrome.

Pain may result from osseous structures of the posterior ankle impacting one another or from compression of the soft tissue between the two opposing osseous structures. FHL tendon irritation is often caused by the adjacent impingement. Pain also can result from acute trauma to the posterolateral talar process or as a result of chronic repetitive microtrauma, causing direct injury to Stieda’s process or the os trigonum.⁴³

Clinical diagnosis of posterior impingement can be difficult compared with anterior impingement. It is much less common, and the affected structures of the posterior ankle are much deeper, with numerous overlying soft tissue support structures that may be the source of posterior ankle pain, such as the Achilles tendon, FHL tendon, tarsal tunnel, and retrocalcaneal bursa. A lateral radiograph of the ankle may demonstrate a prominent Stieda process or os trigonum, but radiographs usually are unremarkable in patients who have posterior ankle impingement. An underexposed 25-degree lateral rotation radiograph usually reveals more calcified deposits than does the conventional view.

Conventional MRI is the most beneficial investigation for suspected posterior ankle impingement because of various types of ankle impingement. MRI can delineate the anatomic site of the abnormality accurately and demonstrate evidence of posterior ankle impingement and coexisting pathology. The MRI features can be divided into osseous and soft tissue abnormalities. Positive MRI findings include edema within or surrounding the os trigonum or posterolateral tubercle of the talus, FHL tenosynovitis, posterior capsular synovitis, and thickening or tears of the PTFL, posteroinferior tibiofibular ligament, and intermalleolar ligament. Hindfoot CT scans are extremely useful and are superior to MRI for demonstrating the lesion’s location and size in osteochondral ankle pathology. The differential diagnoses of posterior ankle impingement are talar or calcaneal stress fractures and osteochondral injuries.

Most patients with posterior ankle impingement respond to conservative treatment, such as rest, shoe modification, and physical therapy. Image-guided steroid and local anesthetic injection into areas of focal inflammation provides diagnostic confirmation and long-lasting symptomatic relief in most patients, and this approach avoids the need for surgery.⁴⁴

Posterolateral Ankle Impingement

Posterolateral ankle impingement manifests as posterolateral pain in the back of the ankle when the posterior lip of the tibia closes against the superior border of the os calcis. Posterolateral ankle impingement is the natural result of full weight bearing in maximal plantar flexion of the ankle in the demi-pointe or full pointe position (Fig. 5-7).

FIGURE 5-7 The demi-pointe position of the ankle is causing posterior ankle pain.

Posterolateral ankle impingement is often associated with an os trigonum or trigonal process in the back of the ankle. It is rare in most athletes. Chronic repetitive microtrauma can lead to inflammation of the os trigonum. Sometimes, acute trauma in plantar flexion may result in a contusion, compression, or fracture of the posterior process of the talus. People who have an os trigonum may or may not be symptomatic, and the degree of symptoms is not always related to its size. Occasionally, symptoms can be caused by soft tissue entrapment between the posterior lip of the talus and the os calcis. Entrapment manifests as posterior lateral pain of the ankle when the posterior lip of the tibia closes against the superior border of the os calcis. It can be confirmed on physical examination by tenderness behind the peroneal tendons in the back of the lateral malleolus (often mistaken for peroneal tendinitis) and pain with forced passive hyper-plantar flexion of the ankle (i.e., plantar flexion sign), causing the posterior talar process or the os trigonum to be compressed between the posterior rim of the tibia and the calcaneus. The examiner can apply a rotational movement on the point of maximal plantar flexion, thereby “grinding” the posterior talar process or os trigonum between tibia and calcaneus. A negative test result can rule out a posterior ankle impingement. A positive test result in combination with pain on posterolateral palpation indicates posterior ankle impingement.

Posterior ankle impingement is seen best on a lateral view of the ankle en pointe or in full plantar flexion. The MRI findings include bone marrow edema located within the posterior talus or within the posterolateral talar process or os trigonum, a prominent posterior calcaneal process, and the posterior tibia a with downward sloping signal. Common soft tissue abnormalities include posterior capsule thickening, a fluid-distended posterior joint space, increased T2-weighted signal, or postcontrast enhancement along the posterior margin of the ankle that indicates synovitis and FHL tenosynovitis.^45–47

The combined presence of bone marrow edema and posterior ankle synovitis may suggest the diagnosis of posterolateral ankle impingement (Fig. 5-8). The diagnosis can be confirmed by injection of 0.5 mL of a local anesthetic into the posterior soft tissue behind the peroneal tendon. If the pain is relieved by this small injection, the diagnosis is almost certain. The most common cause of posterolateral ankle pain is os trigonum syndrome. The differential diagnosis includes acute ankle injury causes, such as PTFL avulsion, fracture of the trigonal process (i.e., Shepherd’s fracture), and acute disruption of the os trigonum synchondrosis, and chronic injury causes, such as posterior capsule and adjacent soft tissue thickening, peroneal tendonitis, loose avulsion fragments of the posterolateral ankle ligament, and loose bodies. The talus is relatively plantar flexed and adducted, which causes further stress on the trigonal process by means of tension in the posterior talocalcaneal ligament in the pes planus foot. In cavus foot, the talus is supinated, moving the posterior surface medially and inferiorly and causing stress on the trigonal process by means of a tense PTFL.

FIGURE 5-8 Magnetic resonance imaging shows bone marrow edema and posterior ankle synovitis.

Best and colleagues⁴⁸ reported anomalous muscles caused posterolateral impingement. The peroneus quartus, which originated on the fibula separate from the peroneal muscles, extended distal to the level of the ankle joint and inserted onto the peroneal tubercle of the calcaneus. The peroneocalcaneus internus muscles arose from the posterolateral aspect of the FHL muscle, coursing along the lateral margin of the FHL tendon within the tendon sheath and inserting onto the distal aspect of the medial margin of the sustentaculum tali.⁴⁸

Treatment should follow an orderly sequence. The first step, similar to the treatment for tendonitis, is activity modification (i.e., following the injunction to first do no harm), avoidance of an equinus position, physical therapy (not to force the foot into equinus to achieve further plantar flexion), and nonsteroidal anti-inflammatory drugs (NSAIDs). Symptoms usually subside without further intervention. If this approach fails or the symptoms recur, an injection of 0.25 to 0.5 mL of a mixture of a long-acting and a short-acting corticosteroid often can give dramatic and permanent relief of symptoms.

When local anesthesia does not relieve symptoms, the lesion should be treated by surgical excision. It should be stressed that the presence of an os trigonum usually is not a surgical problem; most athletes with os trigonum do not need to have them removed surgically. Surgical excision is indicated only after failure of conservative treatment. Abramowitz and colleagues⁴⁹ reported the outcomes for resection of a symptomatic os trigonum with an open posterolateral approach. The postoperative American Orthopaedic Foot and Ankle Society (AOFAS) score averaged 87.6 points. Complications included a 19% rate of sural nerve sensory loss, which was temporary in four and permanent in four patients; a 2% rate of the superficial wound infection; and a 2% rate of reflex sympathetic dystrophy.⁴⁹ The two posterior portal techniques provide excellent visualization of the posterior ankle structures, and the views obtained are superior to those in open procedures. The os trigonum may be separated and removed from the posterior talar process. Loose bodies and fragments of bone may be removed easily. The FHL tendon sheath may be released (Fig. 5-9).⁵⁰

FIGURE 5-9 The os trigonum is causing posterior ankle impingement.

Posteromedial Ankle Impingement

Bony impingement does not commonly occur at the posteromedial aspect of the ankle because the tibia and talus do not come together in this location. Most posteromedial ankle impingement is caused by soft tissues. The key soft tissue structures are the posteromedial flexor tendons, joint capsule, and posterior fibers of the tibiotalar ligament (PTTL). The osseous structures affecting posteromedial ankle impingement include the posteromedial talar process, the posterior aspect of the medial malleolus, and an isolated accessory ossicle.

Tendonitis of the FHL tendon behind the medial malleolus of the ankle is common in dancers (i.e., dancer’s tendonitis), but it also occurs in sports participants. It is often misdiagnosed as posterior tibial or Achilles tendonitis. The FHL passes through a fibro-osseous tunnel behind the talus between the medial and lateral tubercles to the level of the sustentaculum tali like a rope through a pulley. As it passes through this pulley, it is easily strained. The positions of en pointe and demi-pointe in ballet require the FHL tendon to function through an extreme range of motion while passing through its fibro-osseous tunnel.¹³

Frequent, prolonged repetitive motion of dance movements can lead to irritation and swelling of the FHL tendon. Chronic inflammation and hypertrophy of the musculotendinous unit within this tunnel can lead to painful stenosing tenosynovitis, analogous to de Quervain disease in the wrist. If a nodule or partial tear is present, triggering of the big toe may occur. This condition is known as hallux saltans. In severe case, the tendon may become completely frozen in the sheath, causing pseudohallux rigidus.

Physical examination findings include localized tenderness and swelling over the FHL sheath behind and lateral to the medial malleolus. Palpation of the sheath during active and passive motion of the hallux elicits the patient’s symptoms. Dorsiflexion of the first metatarsophalangeal joint can be reduced or absent when the ankle is in maximum dorsiflexion and the muscle fibers of the FHL are drawn into the FHL tunnel, producing a functional hallux rigidus (i.e., Thomasen’s sign) (Fig. 5-10). This finding is not always pathologic, and it may be present in asymptomatic patients. Usually, there is no pain with forced plantar flexion of the ankle. The differential diagnoses of posteromedial ankle pain are FHL tendonitis, soleus syndrome, posterior tibial tendonitis, and posteromedial fibrous tarsal coalition (Table 5-3). The muscles that adhere to the neurovascular bundles behind the medial malleolus arise from the gastrocnemius-soleus complex and insert onto the quadrates plantae muscle.⁴⁸

FIGURE 5-10 Tendonitis of the flexor hallucis longus tendon in a young girl. Excursion often causes impingement of the muscle belly within the fibro-osseous tunnel. A, Before release. B, Metatarsophalangeal joint dorsiflexion. C, After release.

TABLE 5-3 Differentiating Posterior Impingement Syndrome from Flexor Hallucis Longus Tendonitis

Posterior Impingement Syndrome	Flexor Hallucis Longus Tendonitis
Posterior lateral	Posterior medial
Tenderness behind fibula	Tenderness over flexor hallucis longus tendon
Pain with plantar flexion of the ankle	Pain or triggering with motion of the hallux
Positive plantar flexion sign	Positive Thomasen’s sign
Mistaken for peroneal tendonitis	Mistaken for posterior tibial tendonitis

From Hamilton WG, Chao W. Posterior ankle pain in athletes and dancers. Foot Ankle Clin. 1999;4:811-832.

Nonoperative treatment is typically useful for posteromedial ankle impingement. Rest and modified activities (e.g., no pointe work) are important components of therapy to break the chronic cycle of repetitive trauma, and NSAIDs can help. Steroid injections into the sheath of the tendon may be done infrequently but usually should be avoided. Injection of an anesthetic to confirm the diagnosis is easy to perform but is usually not needed. Operative release of the fibro-osseous tunnel is indicated when conservative treatment has failed.

The insidious onset of posteromedial ankle pain 4 to 6 weeks after a supination injury and tenderness in the posteromedial ankle in forced plantar flexion and inversion are diagnostic of posteromedial ankle impingement. The MRI findings include posteromedial capsular thickening, loss of striation of the PTTL, and posteromedial synovitis (Fig. 5-11).⁵¹ Injection of a steroid and long-acting anesthetic along with dry needling of the capsular abnormality allows most patients return to activity rapidly. Surgical resection of capsular thickening is successful in resistant cases.⁵²

FIGURE 5-11 Magnetic resonance imaging shows posteromedial synovitis and flexor hallucis longus tendonitis.

Posterior ankle impingement can be treated by open or arthroscopic techniques. The open technique has a success rate of 73% to 90% and mean time to return to sporting activities or dancing of 3 to 6 months, but it has a complication rate of 12% to 24%.^49,53 Arthroscopic treatment improves the success rate (good or excellent results for 80% of cases) and has a shortened recovery time (return to sport activities at 9 weeks) and a decreased complication rate (1% to 9%).^54,55 The overall results for bony impingement appear to be better than those for soft tissue impingement.

Van Dijk and associates⁵⁶ described the two-portal posterior endoscopic approach to the hindfoot with the patient in the prone position. It offered excellent access to the posterior compartment of the ankle joint, the posterior subtalar joint, the FHL tendon, and the os trigonum. It caused less morbidity and facilitated a quick recovery.⁵⁶ Lijoi and coworkers⁵⁷ verified the safety of a posteromedial portal in the arthroscopic treatment of the hindfoot.⁵⁷ Phisitkul and colleagues⁵⁸ showed the potential to increase the arthroscopic working area in the posterior subtalar joint. Horibe and associates⁵⁹ described the posterolateral portal for arthroscopic visualization and the accessory posterolateral portal for insertion of instruments to excise a symptomatic os trigonum without any complications. Willits and coworkers reported the short-term clinical outcome for posterior ankle arthroscopy in the treatment of posterior ankle impingement. The excellent or good results were obtained for 93% of patients. The mean score on the AOFAS Ankle and Hindfoot Scale was 91, and the score on the AOFAS Lower Extremity Functional Scale was 75. Complications included temporary numbness in the region of the scar and temporary ankle stiffness.⁵⁰

Sinus Tarsi Syndrome

Sinus tarsi syndrome (STS) was first described by Denis O’Connor. STS is a rare condition characterized by pain in the sinus tarsi that usually occurs after a sprain.⁶⁰ STS has been associated with previous trauma, most commonly inversion ankle sprains.⁶¹ Clinically, it manifests as pain or tenderness over the sinus tarsi laterally. The diagnosis is confirmed by complete relief of pain by injection of a local anesthetic in the sinus tarsi. Subtalar pain often is present, and some investigators have confirmed a high incidence of STS on imaging studies.⁶²

Several theories have been proposed to explain the cause of STS, including interosseous talocalcaneal ligament scarring or injury, synovial inflammation with impingement, and sensory nerve traction injury, but the true cause is not clear. Different diagnostic techniques have been proposed for the evaluation of STS, including arthrography, MRI, and local injection of anesthetic.^63,64 However, the anatomy of the sinus tarsi, inconsistent inflammatory tissue and fibrosis, and chronicity of the problem make the diagnosis difficult.

Arthroscopy of the subtalar joint and sinus tarsi has provided another method of evaluation and treatment of this difficult problem. Investigators have described the results of arthroscopic débridement of the sinus tarsi for chronic pain in this area. Frey and colleagues⁶⁵ reviewed subtalar arthroscopies, and of the 14 feet that had a preoperative diagnosis of STS, all the diagnoses were changed at the time of arthroscopy. The postoperative diagnoses included 10 cases of interosseous ligament tears, 2 cases of arthrofibrosis, and 2 cases of degenerative joints. The investigators thought that STS was an inaccurate term that should be replaced with a specific diagnosis.⁶⁵

Lee and coworkers⁶⁶ reported a rate of 88% for good or excellent results with arthroscopic treatment for STS. The mean score on the AOFAS Ankle and Hindfoot Scale improved from 43 preoperatively to 86 points postoperatively.⁶⁶

Lateral Bony Impingement of the Subtalar Joint

The accessory anterolateral facet was first described in a study of the astragalus by Sewell.⁶⁷ The accessory anterolateral facet is associated with painful talocalcaneal impingement in cases of flatfoot deformity. The accessory anterolateral talar facet causes lateral bony impingement of the subtalar joint, as reported by Martus and colleagues.⁶⁸ Sarrafian reported that a large accessory talar facet was found in 4% of 100 tali specimens. An accessory anterolateral talar facet was present in 34% of the specimens in a pediatric bone study.⁶⁸ It was associated with male sex, a smaller angle of Gissane, and dorsal talar beaking. When subtalar eversion is removed, narrowing of the sinus tarsi is accentuated by the presence of a large accessory facet.⁶⁸ Malicky and associates⁶⁹ described CT imaging performed with the foot positioned in frames that simulated weight bearing in 19 patients with lateral talocalcaneal impingement. Impingement occurred between the lateral talar process and the calcaneal neck (Fig. 5-12).

FIGURE 5-12 The accessory facet is causing lateral bony impingement of the subtalar joint.

Injection of an anesthetic to confirm the diagnosis is useful and easily performed. Arthroscopic resection is indicated when conservative treatment has failed (Fig. 5-13).

FIGURE 5-13 Arthroscopic resection of the accessory facet of the talus.