Synovial Impingement in the Ankle

                     Dr. KS Dhillon

Introduction

Abnormal entrapment or contact of structures resulting in pain or restricted motion is referred to as impingement. Impingement syndromes are seen in many areas, notably subacromial impingement in the shoulder and femoroacetabular impingement in the hip. Impingement syndromes are an increasingly recognized source of pain and disability in the ankle.

Impingement syndromes in the ankle have a broad spectrum of pathology with varying etiologies, anatomic features, and presentations. There is no official classification for the impingement syndromes. These syndromes are generally defined by the particular anatomic area involved. These include anterior, anterolateral, anteromedial, posterior, posteromedial, posterolateral, and syndesmotic impingements [1,2]. These pathologies are generally grouped into anterior and posterior impingement syndromes for simplicity.

Anterior ankle impingement syndrome occurs due to compression of structures at the anterior margin of the tibiotalar joint during dorsiflexion. It has long been recognized as a cause of pain in athletes. McMurray in 1949 described the “footballer’s ankle” which is a commonly observed condition in professional soccer players. It involves anterior osteophytes of the dorsal talar neck and distal tibia. The term was later changed to “impingement exostoses” in 1957 by O’Donoghue to include other patient populations [3].

The posterior impingement syndrome is characterized by compression between the posterior tibia and calcaneus during plantar flexion. Anatomists and surgeons have long recognized structures at risk for posterior compression, such as the os trigonum. The operative treatment for posterior impingement was first described by Howse in 1982. He treated a “posterior block of the ankle joint” in a population of elite dancers [4]. The condition was later termed “talar compression syndrome” [5].

Etiology

Anterior impingement

Anterior ankle impingement occurs when there is entrapment of structures along the anterior margin of the tibiotalar joint in full dorsiflexion. It is secondary to multiple osseous and soft tissue anatomic abnormalities. 

Spurs or “exostoses” at the anterior distal tibia and dorsal talar neck have been observed in athletes with anterior ankle pain and limited motion. Talofibular lesions have also been described [6]. The morphology of anterior tibiotalar exostoses has been studied. Cadaveric dissections have found that these lesions are intra-articular within the distal tibial and dorsal talar capsular attachments [7,8]. These tibial and talar spurs often do not actually overlap and abut. CT scans have shown that talar spurs usually lie medial to the midline of the talar dome and tibial spurs are generally located laterally [9]. There is a trough in the articular talar dome that often “accepts” the tibial osteophyte during dorsiflexion. Kim et al [10] referred to the trough as a “tram-track lesion” [10], and Raikin et al [11] termed it a “divot sign” [11]. Several studies have found a high rate of corresponding talar cartilage lesions (80.7 %) and loose bodies in patients with distal tibial lesions [12].

In addition to bony impingement, anterior intra-articular soft tissues may also contribute to impingement. There is a triangular soft tissue mass composed primarily of adipose and synovial tissues in the anterior joint space. These tissues are compressed after 15° of dorsiflexion in individuals who are asymptomatic [7]. Anterior osteophytes can limit the space available for these soft tissue and that can exacerbate its entrapment, resulting in synovitis, chronic inflammation, and capsuloligamentous hypertrophy. Fibrous bands from trauma [13], thickened anterior tibiofibular ligaments [14,15], and synovial plica [16], can also cause the impingement.

The impinging anatomic lesions have been well described but their exact etiology is not well understood. Spurs are enthesophytes that are produced by traction to the anterior capsule during repetitive plantar flexion of the ankle [3]. However, studies have shown that the chondral margins and lesions are deep to the joint capsule rather than at its attachment. This disproves the traction theory [7–9]. Now it is believed that the pathology occurs due to repetitive impaction injury to the anterior chondral margin from hyper-dorsiflexion or direct impact from an external object [17,18].

It has been hypothesized that chronic lateral ankle instability also contributes to the development of both bony and soft tissue lesions associated with anterior impingement due to abnormal repetitive micromotion [14,19]. Several studies have examined the prevalence of anterior impingement lesions at the time of arthroscopy of the ankle in patients undergoing stabilization procedures for lateral ankle instability. Soft tissue lesions, such as synovitis in the anterior compartment or anterior lateral gutter, have been observed in 63–100 % of the patients. Anterior tibial osteophytes have often been found in 12–26.4 % of the patients [20–22]. In a study by Scranton et al [23], patients undergoing a Brostrom procedure had 3.37 times the incidence of bone spurs than matched asymptomatic controls.

Posterior impingement

Posterior ankle impingement occurs due to compression of structures posterior to the tibiotalar and talocalcaneal joints during full plantar flexion. This can be caused by multiple osseous and soft tissue etiologies. Posterior impingement most commonly occurs due to pathology associated with the lateral/trigonal process of the posterior talus. There are anatomic variants of this structure. An elongated tubercle is referred to as a Stieda process. An os trigonum represents the failure of fusion of a posterior secondary ossification center to the talar body. Posterior impingement related to the trigonal process can result from chronic injury due to repetitive microtrauma, acute fracture, or mechanical irritation of the surrounding soft tissues [24].

Less often, posterior impingement symptoms can result from tibiotalar or subtalar osteoarthritis due to osteophyte impingement or associated hypertrophic capsule and synovium. Symptoms can also occur from post-traumatic sequelae from fracture malunion of the posterior malleolus, talus, or calcaneus [25]. Talar osteonecrosis causing posterior impingement has also been reported [26].

There are various soft tissue structures that can cause posterior impingement symptoms. Posterior capsuloligamentous injury due to repetitive or acute hyperflexion can produce inflammation, scarring, and thickening of the capsule leading to posterior impingement. The posterior inferior tibiofibular ligament and posterior fibers of the deltoid ligament can also produce posterior impingement symptoms [27–29]. The flexor hallucis longus tendon which runs between the medial and lateral posterior processes of the talus, is commonly affected by tenosynovitis and tendinosis. The tendinopathy can result from overuse or irritation from surrounding abnormal bony anatomy. Other sources of impingement include soft tissue variants, such as the posterior intermalleolar ligament and several anomalous muscles [30–34].

Clinical Presentation

Anterior impingement

The anterior impingement syndrome presents as anterior ankle pain on full dorsiflexion. Activities such as climbing stairs, running, walking up hills, ascending ladders, and deep squatting usually exacerbate the pain. The classic association of anterior impingement with competitive soccer players has long been recognized, but the reason that this subset of athletes are commonly affected is not very clear [10,17,18]. In the later stages of anterior impingement, dorsiflexion of the ankle may be limited secondary to mechanical block or pain. This creates a cycle of progressive joint stiffness and loss of function. When there are isolated soft tissue lesions, the patient may experience subjective popping or snapping sensation.

Posterior impingement

The posterior impingement syndrome usually presents with pain deep to the Achilles tendon. Symptoms are often worsened by activities involving plantar flexion and repetitive push-off maneuvers, including downhill running and walking, descending stairs, and wearing high-heeled shoes. Posterior impingement classically presents in dancers, especially those participating in classic ballet. The impingement is due to repetitive weight bearing in the plantar-flexed en-pointe and demi-pointe positions [35–38]. In a recent systematic review by Ribbans et al [39], dancers represented 61% of patients undergoing surgery for posterior impingement. It has also been reported in fast-bowlers in cricket [40].

Physical examination

When assessing for impingement syndrome a comprehensive physical examination of the foot and ankle is carried out. The ankle and foot are inspected for joint effusion, soft tissue edema, and abnormal alignment. In patients with anterior impingement, there will be anterolateral ankle tenderness. Posterior impingement signs can be more difficult to elicit and localize since the structures are deeper. Posterolateral ankle tenderness with forced ankle plantar flexion is most likely to involve pathology associated with the trigonal process. Posteromedial ankle tenderness with resisted plantar flexion of the first metatarsophalangeal joint is most likely due to flexor hallucis longus pathology. 

The active and passive range of motion of the joints is measured. This includes plantarflexion, dorsiflexion, subtalar, and midfoot movements. On the lateral side, the peroneal tendon is assessed for tenderness, deformity, or subluxation. The sural nerve is evaluated for hypersensitivity. The Achilles tendon is assessed for fusiform enlargement or retrocalcaneal bursitis. On the medial side, the tibial nerve is evaluated for tarsal tunnel syndrome, and the posterior tibial tendon’s function is also assessed. The anterior drawer and talar tilt tests of the tibiotalar joint are performed to detect ankle instability. A straight leg raise test can be done to exclude L5 or S1 radiculopathy.

Imaging

X-rays of the ankle are done if impingement is suspected. Weight-bearing AP, lateral, and mortise view xrays are done. The lateral view x-ray can show exostoses on the distal anterior tibia and dorsal talar neck as well as posterior bony abnormalities, including a Stieda process or os trigonum.

Oblique views have been described for both anterior and posterior impingement lesions to better assess for bony abnormalities. For anteromedial lesions, the beam is aimed 45° craniocaudally with the leg externally rotated at 30° [41]. The oblique anteromedial impingement view has been confirmed to have a higher sensitivity in detecting both tibial and talar osteophytes when added to a standard lateral radiograph [42]. For lesions associated with the trigonal process, a 25° external rotation-lateral view is useful [43]. Dynamic hyper-plantar-flexed or dorsiflexed laterals can be done to demonstrate abnormal bony contact.

When the diagnosis remains inconclusive an MRI can be done. The MRI can show effusion, synovitis, bone edema, tenosynovitis, and chondral injury. In anterior soft tissue impingement there may be hypertrophic synovium or fibrosis in the anterolateral gutter. Increased marrow signal intensity at the trigonal process or os trigonum may be due to an acute injury or chronic stress fracture [44]. The efficacy of MRI in evaluating soft tissue impingement lesions is variable. The reported sensitivity is 42–89 % and specificity is 75–100 % [45–50]. Computed tomography has been used to define the morphology of bony lesions for planning surgical resections [51]. More recently, ultrasound has also gained popularity as a reliable and inexpensive modality in evaluating impingement lesions as well as for administering therapeutic injections [52,53].

Nonsurgical treatment

The anterior and posterior impingement syndromes are initially treated without surgery. Acute symptoms are treated with rest and avoidance of provocative activities. This can be supplemented with ice and NSAIDs.  For severe cases cast immobilization can be done. Heel lift orthoses to prevent dorsiflexion can be used in chronic cases. Physical therapy is done to improve ankle stability and optimize proprioception. Some authors have reported successful symptom relief with ultrasound-guided corticosteroid injections [54,55].

Surgical treatment

Surgical intervention is indicated for patients with persistent symptoms that have not responded to non-operative treatment, affected activities of daily living, or athletic performance. The surgical approach and technique will vary by the anatomic region involved and the pathology involved.

Anterior impingement

During surgery for anterior impingement, the offending pathologic lesion contributing to the symptoms is removed. This usually involves resection or debridement of bony lesions and soft tissue lesions. In earlier studies, open anterior or lateral arthrotomy was done for the surgery [3]. A lateral arthrotomy is often still used if a lateral ligamentous procedure is being performed concurrently. Now, however, most open approaches have largely been replaced by arthroscopic techniques [56–80].

Hawkins was the first in 1988 to use an arthroscope for the treatment of bony anterior ankle impingement. He stated that visualization was better and the approach was less invasive [81]. Anterolateral and anteromedial portals are utilized and may be extended with conversion to open arthrotomy if the need arises. An arthroscopic burr is used for the debridement of bony lesions. A shaver and an electrothermal device are used to debride hypertrophic or inflamed synovium and fibrotic tissue. Intraoperative fluoroscopy can be used to confirm adequate resection of the spurs. 

Zwiers et al [75] conducted a systematic review to examine the outcome of the arthroscopic treatment of anterior impingement. The review included 19 studies and 905 patients. The average age of the patients was 32.7 years. At a mean follow-up of 35.3 months, 74–100 % of patients were satisfied with the results of the procedure. AOFAS scores improved, ranging from 34–75 preoperatively and increasing to 83.5–92 postoperatively. There was a 5.1 % overall complication rate. One point two percent were considered as major complications. This is similar to a 4 % complication rate in a previous review by Simonson et al [82].

Posterior impingement

Treating posterior impingement involves resection of the anatomical structures that are causing the symptoms. Usually, relief of symptoms is obtained by excision of a painful trigonal process or os trigonum, with debridement of surrounding inflammatory or hypertrophic soft tissues.

Posterior pathology can be approached through an open lateral, open medial, or endoscopic approach. The lateral approach allows a more direct access to the trigonal process and there is less risk of injury to the medial neurovascular bundle. A medial approach allows for access to flexor hallucis longus pathology. Since 2000, posterior endoscopic approaches have gained popularity. With an endoscopic approach, there is potential for faster return to sport and lower complication rates [31,83–97]. The patient is positioned prone and the posteromedial and posterolateral hindfoot portals adjacent to the Achilles tendon provide excellent access to extra-articular posterior structures.

Ribbans et al [39] reviewed 47 papers consisting of 905 patients who were treated surgically with both open and endoscopic approaches for posterior impingement. Eighty-one percent of symptoms were due to osseous pathology. Good to excellent outcomes were seen in 67–100 % of patients. Zwiers et al [98] conducted a similar systematic review. The review included 16 studies. They found significantly lower complication rates (7.2 vs. 15.9 %) and earlier return to full activity (11.3 vs. 16 weeks) with endoscopic surgery.

Conclusions

Ankle impingement occurs due to a broad spectrum of anterior and posterior pathology that involves both osseous and soft tissue abnormalities. Anterior impingement produces symptoms with terminal dorsiflexion of the ankle. Posterior impingement is exacerbated by activities that involve hyper-plantarflexion. The diagnosis is made by taking a good history and doing a proper physical examination. Imaging studies and diagnostic injections contribute to the accurate diagnosis of the conditions. Many patients respond favorably to non-operative treatment modalities. Those not responding to non-operative treatment would need surgery. Both open and arthroscopic techniques have evolved to address chronic symptoms with successful and predictable outcomes.

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