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The Blackburn Foot and Ankle Hyperbook  
Evidence based education in foot and ankle surgery
  Ankle impingement

Impingement is a soft tissue pain syndrome that is though to be caused by soft tissue being compressed between bones, often when a joint moves to a particular position. In the ankle it may occur:

  • anteriorly, in association with ankle dorsiflexion
  • posteriorly, in association with ankle plantarflexion

Impingement-type pain may also occur lateral to the ankle in the sinus tarsi region, often in association with hindfoot valgus and injuries or arthritis in the subtalar joint.

Anterior impingement

Causes

  • The normal ankle has a triangular soft tissue component in the anterior ankle space (Tol + van Dijk 2004). This can sometimes be seen on MR scans of the ankle. When the ankle is dorsiflexed 15 deg, Tol and van Dijk found that the anterior ankle space was diminished, which could account for impingement pain, especially if the anterior soft tissues were hypertrophied after trauma.
  • The anterior inferior talofibular ligament may be torn and its inferior margin impinge in the ankle joint, causing the “meniscoid lesion”. This may be commoner in a group of people who have a particularly low attachment of the inferior leaf of the ligament
  • Damage to the inferior tibiofibular joint may cause scar tissue or synovitis to prolapse into the ankle. Schaffler et al (2003) described this condition in 70% of patients with ankle impingement compared with 49% of a control group with other proven ankle pathologies, although their selection criteria may have created bias. They also found that MR had a sensitivity of 89% and a specificity of 100% for syndesmotic impingement tissue.
  • Bony spurs, on the anterior margin of the distal tibia or the talar neck, may be found in 70% of footballers and are also found in people who play other sports or none. Berberian et al (2001) found that tibial spurs generally occur lateral to the midline of the ankle joint, while talar spurs are medial. Spurs may cause pain by direct pressure on one another or by nipping anterior soft tissue; as the spurs do not usually overlap (Berberian et al 2001) the latter seems more likely. Scranton and McDermott (1992) produced a classification of anterior ankle spurs.
The normal anterior capsular thickening is increased by synovitis and the anterior space reduced by dorsiflexion Causes of anterior ankle impingement Anterior ankle spurs. Talar spurs tend to be lateral, tibial spurs medial. They do not usually touch tip-to-tip

Spurs were thought to arise because of chronic repeated traction from the anterior ankle capsule. However, Tol and van Dijk showed that the capsule is attached 4-9mm above the ankle joint line and therefore clear of the site of formation of spurs. Indeed, this can be observed at arthroscopy. Tol and van Dijk found that the joint cartilage extended 2-3mm onto the nonweightbearing surface of the tibia and hypothesised that damage to this cartilage sets up a repair mechanism that produces a spur.

Clinical features

Patients generally complain of anterior ankle pain which may be more or less localised to the lateral or (less commonly) medial side. There is usually a history of trauma. The patient may complain of giving way, locking or catching in the ankle; sometimes these mechanical symptoms are more troublesome than the pain. Ask about previous ankle problems, problems with other joints and other medical problems.

Examination may show an effusion or synovitis. There may be tenderness in the joint line, especially anterolaterally or in the lateral gutter, but this may only be provoked by moving the ankle. Tenderness is often found over the syndesmosis or lateral ankle ligaments. Ankle dorsiflexion is often reduced, although this may be only by a few degrees compared with the other side. A few patients have both anterior and posterior symptoms.

The cardinal physical sign is the Molloy impingement test. The ankle is dorsiflexed with finger pressure in the joint line. The appearance or increase of pain under the finger is a positive test. The test may have to be repeated at different points on the joint line. Molloy (2003) found that this test had a sensitivity of 95% and a specificity of 88% to predict synovitis and hypertrophy.

An injection of lignocaine into the area of maximum tenderness will usually reduce or abolish pain.

As the primary management of ankle impingement is normally in the hands of the physiotherapist rather than the surgeon, all of our referrals with post-traumatic ankle problems, including impingement, are primarily assessed by the physio and referred to the surgical clinic only if intervention is planned.

Investigation

If there is clinical evidence of an inflammatory arthropathy this should be evaluated with the appropriate blood tests: FBC, ESR and rheumatoid factor tests are normally sufficient; in a possible spondyloarthropathy the HLA B-27 may be added.

Plain films will show spurs and loss of joint space.

MR can identify synovitis and impingement, especially with contrast or MR arthrography. Schaffler (2003) found that MR had a sensitivity of 89% and a specificity of 100% for syndesmotic impingement tissue. Huh (2003) found sensitivity of 91% and specificity of 64% for synovitis, and sensitivity of 76% and specificity of 97% for impingement.

However, impingement is largely a clinical diagnosis. In our practice imaging is mainly used for patients with intra-articular or atypical pain.

Non-surgical management

Most patients will get some benefit from local physiotherapy and an ankle rehabilitation programme to address instability and synovitis. Some struggle to complete the programme, however, due to pain on loading the ankle, and may benefit from a steroid injection before continuing. There is little information on the effectiveness of such nonsurgical treatment.

Surgery

Patients with persistent disabling pain may be offered an arthroscopic debridement. Even in the presence of mechanical instability, synovial debridement is often effective in relieving symptoms and stabilisation may not be required (Laing 2004). Usually the synovitis and adhesions are found mainly in the anterolateral joint, often with synovitis descending from the inferior tibiofibular joint. Spurs can be debrided with a burr. It is important to inspect the joint surface carefully; at least 10% have an unsuspected chondral or osteochondral lesion which can be debrided. We encourage active range of movement exercises and weightbearing as soon after surgery as possible.

At 5-8y after arthroscopic debridement, Tol (2001) reported satisfactory results in all patients without osteoarthritic changes. 77% of patients with grade-1 OA and half of those with grade-2 OA got good results. Rasmussen found 62% of patients to be pain-free at 2y irrespective of pathology, while 27% had a useful improvement in pain.

Scranton and McDermott (1992) found that patients recovered more quickly after arthroscopic than open debridement. However, Coull et al (2003) reported excellent results with open debridement – 92% of patients had little or no pain or activity limitation at 5-9y provided they had normal joint space pre-operatively.

Most spurs reform, but recurrent symptoms are not common, and published series do not report re-operations for recurrent spurs. Similarly, in the series referred to, spurs did not progress to arthritis, and early arthritis did not progress.

Posterior impingement

Causes

  • Posterior synovitis due to trauma or frequent activities in equinus, such as classical ballet. This may be associated with injuries to the posterior talofibular, posterior inferior tibiofibular, posterior intermalleolar or deep posterior tibiotalar ligaments. The latter produces the so-called posteromedial impingement (POMI) lesion.
  • The posterior talar process or its equivalent ossicle, the os trigonum, may be hypertrophic or fractured
  • Tears or tendonopathy of the flexor hallucis longus
  • Inflammatory arthritis or osteoarthritis of the ankle or subtalar joint

Clinical features

Patients mainly complain of pain posterior to the ankle on loading or in equinus. The pain sometimes radiates up the leg or down the course of the FHL tendon. Some patients complain of catching, locking or giving way. Occasionally the pain may be difficult to distinguish from that of Achilles tendonopathy.

Examination shows posterior ankle tenderness which is worse in plantar flexion. There may be some swelling or synovitis, and the range of plantarflexion is often reduced. Pain provoked by hyperextension or resisted plantarflexion of the great toe suggests FHL tendonopathy. A manoeuvre analogous to the Molloy test for anterior impingement is usually positive, although the sensitivity and specificity are not known for posterior impingement.

Investigation

If there is clinical evidence of an inflammatory arthropathy this should be evaluated with the appropriate blood tests: FBC, ESR and rheumatoid factor tests are normally sufficient; in a possible spondyloarthropathy the HLA B-27 may be added.

Plain films will show spurs and loss of joint space. A lateral film in plantarflexion may demonstrate impingement of the os trigonum or posterior talar process.

MR can identify synovitis and impingement, but has been less extensively evaluated than in the anterior ankle. It is useful to evaluate the FHL tendon, but fluid collections around this tendon are not unusual and may be due to synovial communication with the ankle.

However, impingement is largely a clinical diagnosis. In our practice imaging is mainly used for patients with intra-articular or atypical pain.

Non-surgical treatment

Local physiotherapy aiming to reduce synovitis, and an ankle rehabilitation programme, are often helpful, although possibly less than in patients with anterior symptoms. Patients whose problems are provoked by activities in equinus need a period of avoidance followed by graduated reintroduction of these activities. Local steroid injection can be used for those who fail physiotherapy or cannot follow the programme because of pain. There is little information on the effectiveness of such nonsurgical treatment.

Surgery

There are fewer reports of arthroscopic posterior debridement. In some ankles posterior debridement can be accomplished from anterior portals, but posterior portals, keeping lateral to the FHL tendon, are recognised. It is important to assess the joint surface: osteochondral lesions were present in 4/25 of Koulouris’ (2003) series. Successful results at short term follow-up have been reported in about 80% of patients.

An injured or hypertrophic os trigonum or posterior talar process can be excised through a posterior approach. Arthroscopic excision of the os trigonum has been reported (Marumotu and Ferkel 1997). Abramowitz (2003) reported a mean AOFAS hindfoot score of 87/100 at 2-6y follow-up after open surgery, although this was lower in those with symptoms for more than 2y prior to surgery. They also reported four temporary and four permanent sural nerve injuries.

Debridement and decompression of the FHL tendon has been reported, though without follow-up results.