NB This page is from the 2005 Hyperbook.
Last evidence check February 2007 but no substantial revision since Feb 2005.
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:
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.
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| 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.
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.
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.
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.
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.
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.
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.
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.
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.