9.5 Tendon and ligament disorders of the foot and ankle

Tibialis posterior dysfunction is the most common cause of acquired flat-foot deformity in the adult.

The tibialis posterior muscle lies in the deep posterior compartment of the calf and is innervated by the tibial nerve (L4, L5). The musculotendinous junction is 4cm above the medial malleolus and the tendon passes behind the medial malleolus in its own sheath. It attaches mainly to the tuberosity of the navicula by three bands: anterior, middle, and posterior. The anterior is the largest (65%) attaching to the navicular tuberosity and inferior medial cuneiform. The middle band extends to the more lateral cuneiforms, cuboid, and metatarsal bases of the second, third, and fourth rays. The posterior band contributes to the soft tissue components of the acetabulum pedis.

The posterior tibial tendon plays an important role in function of the foot and ankle. During gait the foot fulfils two purposes. As the foot contacts the ground it is flexible and acts as a shock absorber. By the end of the stance phase, the foot has changed into a rigid lever to maximize push-off strength. As a flexible shock-absorbing foot, the transverse tarsal (talonavicular and calcaneocuboid) joints are parallel and move in concert. With activity of tibialis posterior the heel inverts, the orientation of the transverse tarsal joints changes and flexibility is abolished.

Where tibialis posterior is dysfunctional the transition from flexible shock absorber into rigid lever does not occur. This places excess strain upon the medial column of the foot (the spring ligament in particular) and eventually leads to planovalgus deformity.

Posterior tibial tendon dysfunction (PTTD) is a progressive disorder. Johnson and Strom proposed a staging system that was later modified by Myerson (Table 9.5.1).

Most patients with early PTTD go unrecognized. It occurs mostly in people with pre-existing low arches. Posteromedial ankle pain and swelling occur first, but it is the ‘collapse’ of the medial longitudinal arch that usually prompts referral.

Once deformity becomes marked, fibular impingement develops.

Walking aids, orthotics, and shoes are inspected for wear.

The medial longitudinal arch and the inclination of the heel are observed from behind. The ‘too many toes’ sign is a marker of forefoot abduction but not pathognomonic of PTTD (Figure 9.5.1).

The patient is asked to rise onto tiptoes. Normally both heels will invert. Failure of inversion indicates PTTD (Figure 9.5.2) but subtalar joint stiffness may cause the same appearance.

If double-stance heel rise is normal then single-stance heel rise is performed.

This may be: impossible; more difficult than on the unaffected side; or fatigue easily with repetition—according to the severity of the PTTD.

It is important to consider the more proximal parts of the lower limb.

The leg must be exposed to allow knee alignment to be assessed as valgus deformity of the knee may be associated with an acquired flat-foot deformity.

To assess contracture of the gastrocnemius, the patient is asked to stand on their heels only, with the toes clear off the ground (forefoot ground clearance).

The pulses and sensation are checked.

Ankle and triple joint flexibility is assessed, and joint line tenderness noted. Silfverskiold’s test demonstrates the severity of an associated gastrocnemius contracture by assessing the difference in ankle equinus observed when the knee is flexed compared to when the knee is extended fully (Figure 9.5.3).

The forefoot to hindfoot alignment is observed after reducing and holding the heel into neutral position beneath the tibia, then observing the relative position of the sole of the forefoot to the heel.

Where the first ray is elevated in relation to the fifth ray, the deformity is known as forefoot varus (Figure 9.5.4).

Acquired flat foot in adulthood is most commonly caused by PTTD. Tarsometatarsal osteoarthritis, spring ligament injury, and subtalar joint inflammatory arthropathy are important differential diagnoses.

Plain weight-bearing anteroposterior (AP) radiographs show dorsolateral peritalar subluxation. Bilateral films allow comparison of the degree of uncovering of the talar head. A weight-bearing lateral film may demonstrate alignment of first tarsometatarsal and naviculocuneiform joints (Figure 9.5.5). These films and an oblique view should be studied for evidence of degenerative joint disease.

In advanced PTTD, an AP weight-bearing radiograph of the ankle may show ankle arthritis.

Ultrasound of the posterior tibial tendon is a useful means of confirming tenosynovitis, thickening, or rupture of the tendon but is operator dependent so may be less useful to the treating surgeon than a magnetic resonance imaging (MRI) scan (Figure 9.5.6).

Physiotherapy and orthotic management are the mainstays of treatment. Physiotherapy addresses the gastrocnemius contracture and strengthens the tibialis posterior tendon and toe flexors.

Orthotics may be corrective or accommodative. Functional foot orthoses (FFOs) extend only across the foot. More extensive devices (e.g. ankle–foot orthosis, AFO) are reserved for advanced stages of PTTD.

Details of specific orthotics are contained in (chapter 9.4)

Surgery for PTTD should achieve a stable, painless, and plantigrade foot.

Corrective knee surgery must be undertaken before the foot and ankle are addressed.

The stage of PTTD is a useful guide to treatment (Box 9.5.1)

If non-operative treatments for stage 1 PTTD do not work, tenosynovectomy may prevent progression of the tendinopathy and relieve the pain and swelling in about three-quarters of patients. In selected cases this may now be performed arthroscopically.

In stage 2, joint-preserving surgery with tendon transfer and osteotomy is preferable to arthrodesis. It is most successful where the forefoot varus is correctable.

The most widely used tendon is the flexor digitorum longus (FDL). This fails in isolation, so it is combined with medializing calcaneal osteotomy. The osteotomy protects the tendon transfer by correcting heel valgus and medializing the insertion of the Achilles tendon. Plication of the spring ligament and short plantar ligaments are also performed to restore static restraint.

In patients with medial column joint laxity, midfoot osteoarthritis, or hallux valgus, appropriate midfoot fusions and/or correction of the hallux valgus may be required to restore structure.

Surgical correction of associated gastrocnemius contracture should be performed if tight.

Alternative techniques to FDL transfer and calcaneal osteotomy include lateral column lengthening.

Where the hindfoot is stiff or there is significant degenerative joint disease (stage 3), corrective fusion is preferred. Traditionally, triple arthrodesis has been used, but produces considerable hindfoot stiffness.

Subtalar fusion may be used if there is no fixed midfoot deformity, with cuneiform osteotomy, midfoot fusion, or talonavicular fusion also sometimes required to correct the forefoot–hindfoot relationship.

Where the talonavicular joint is unstable, isolated talonavicular fusion may be considered.

In severe cases, where there is ankle degenerative joint disease, pantalar fusion or corrective triple arthrodesis followed by an ankle replacement are considered (Figure 9.5.7).

Surgical treatment of stage 2 PTTD gives satisfaction rates of 90% after 2 or 3 months’ cast immobilization. It takes another 6–9 months for swelling to resolve and strength to improve.

Selective or triple joint fusion for stage 3 PTTD also has good results, as long as plantigrade position is achieved.

Ankle injuries make up 10% of attendances to Emergency Departments. The majority are inversion injuries resulting in localized pain, swelling, and bruising maximal over the anterolateral aspect of the ankle from damage to the anterior talofibular ligament (ATFL) and joint capsule.

Most are treated initially with rest, ice, compression, and elevation (RICE) followed by early weight bearing with an ankle brace. Physiotherapy concentrates on proprioceptive training and peroneal tendon strengthening.

Approximately 20–30% of patients suffer ongoing problems with their ankle. Table 9.5.2 shows the possible differential diagnoses.

Varus ankle, tarsal coalition, cavovarus foot posture (e.g. Charcot–Marie–Tooth), and generalized joint laxity predispose to ankle sprain.

There are three groups of ligaments each of which has three elements (Table 9.5.3).

Ankle sprains most commonly injure the ATFL. The calcaneofibular ligament (CFL) is involved in more severe cases.

Examination aims to define which ligaments are torn and to exclude fracture. Watson Jones described passive inversion of the ankle to test for ligament insufficiency. Test the ATFL by inversion with the foot plantarflexed and the CFL with the foot dorsiflexion).

Early functional treatment is recommended initially for all grades of injury.

There is no evidence for surgery after an uncomplicated acute injury. RICE is supplemented by early weight bearing, physiotherapy, and bracing. Return to sport is gradual.

The syndesmosis is injured in 18% of ankle sprains. The mechanism of injury is external rotation with a dorsiflexion component. These injuries cause more disability than isolated injury to the lateral ligament complex.

Tenderness is maximal at the distal tibiofibular articulation. The ‘squeeze test’ compresses the tibia and fibula together thereby stressing the syndesmosis. If this provokes pain then the test is positive. External rotation of the foot with the ankle dorsiflexed will also stress the inferior tibiofibular articulation. If the patient twists their body while standing on the affected leg only (sometimes called the Jive test) discomfort is produced in cases of subtle syndesmosis injury.

Plain radiographs and axial computed tomography (CT) of both ankles allows asymmetry of the tibiofibular joint to be detected. MRI can demonstrate injury to the component ligaments of the joint complex. Fluoroscopic examination under anaesthesia may show instability.

Stable injuries are treated symptomatically.

A removable boot allows a graduated approach to rehabilitation. Recovery takes considerably longer for syndesmosis injuries than for sprain of the lateral ligament complex. There should be a low threshold for exposing the interior tibio-fibular joint through an anterolateral incision to ensure proper reduction.

An acute unstable syndesmosis injury should be treated surgically. The goals of surgery are anatomical reduction and stabilization.

When closed reduction is difficult, open or arthroscopic clearance of soft tissue from the medial side of the joint is performed. Stabilization of the tibiofibular joint is then performed with a diastasis screw. The screw is used as a position screw, and not in lag mode. More recently, suture devices passed across fibula and tibia have become popular.

Screw removal should be scheduled for no earlier than 12 weeks from surgery. Weight bearing may be permitted prior to screw removal, but screw breakage is a possibility, especially where the screw engages the far medial cortex of the tibia (four-cortex technique).

In chronic cases the medial side of the ankle and the distal tibiofibular joint should always be explored. The syndesmosis is debrided and the ligament repaired or reconstructed.

Recurrent giving way of the ankle may be due to mechanical instability or functional insecurity.

Mechanical instability is where recurrent giving way of the ankle occurs in association with an abnormal displacement of the talus.

It is usually due to ligamentous disruption, osteochondral injuries or loose bodies, and peroneal tendon pathology can all contribute.

By contrast, functional insecurity is present when a patient complains of recurrent giving way, yet physical examination and radiological tests reveal a stable joint. Synovial impingement, peroneal muscle weakness, and poor proprioception are common causes of functional instability.

Synovial impingement may be caused by, or give rise to, recurrent painful episodes of giving way.

Synovial impingement may occur with or without joint laxity. The synovial impingement sign is a useful physical sign. It relies upon the examiner’s thumb pushing inflamed hypertrophic synovium into the tibiotalar joint as the ankle is moved from plantar flexion into dorsiflexion, trapping the synovium and producing pain (Figure 9.5.8). The test is highly sensitive but not specific for isolated synovitis.

Patients with synovial impingement syndrome enjoy excellent results with examination under anaesthetic, arthroscopic assessment, and debridement of the joint.

Where clinical assessment reveals both synovitis and true ligamentous instability then the decision to simply debride the joint or to proceed to lateral ligament reconstruction at the same time is difficult.

Debridement of synovitis in isolation carries a quicker recovery time and requires no cast immobilization—advantages which must be weighed against the small chance of requiring a second procedure to reconstruct the ligament if addressing the synovial impingement alone provides insufficient improvement.

Osteochondral lesion of the talar dome (OLT) is now the preferred term for this condition—although other terms such as osteochondral disease, osteochondral defect, and osteochondral fracture are also used.

A high index of suspicion is required for the diagnosis of OLT since symptoms may be vague and plain radiographs unrevealing. MRI scan is often required and will tend to underdiagnose the cartilage component and overdiagnose bony oedema.

Unstable cartilage on the dome of the talus may cause insecurity of the joint, an ill-defined ‘deep’ pain, acute pain, and clicking or just aching. OLT of the talus is treated by arthroscopic debridement of the unstable surface and underlying necrotic bone. In over 80% of patients the resultant fibrocartilagenous healing affords excellent symptom relief. For the 15 percent where debridement and microfracture fail repeating this procedure affords a further 80 percent success rate.

Occasionally, cases relapse and then treatment by cartilage graft, cartilage substitution, or, in the presence of major and/or increasing joint damage, even arthrodesis may be indicated.

Physiotherapy is important and focuses upon peroneal tendon strengthening and proprioception.

Activity modification, ankle support bracing, footwear modification, and orthotics are useful means of avoiding giving way.

Surgical treatment is reserved for ankles that have failed non-operative management.

In cases requiring surgical stabilization, anatomical repair is preferred to non-anatomic reconstructions. This is because of the high incidence of degenerative change seen in follow-up after non-anatomic reconstruction (up to 60%), due to altered biomechanics. Non-anatomic reconstruction also has a high incidence of sural nerve damage and lengthy recovery time. It is therefore reserved for recurrent cases or very heavy patients, and robust sports.

Brostrom, in 1966, described anatomic repair of the attenuated ligaments. The most popular modification is that described by Gould who advocated advancing the extensor retinaculum across the repair (Figures 9.5.9). As well as reinforcing the repair, this increases subtalar stability.

Non-anatomic reconstructions use peroneus brevis to stabilize the joint.

Where lateral ligament insufficiency is consequent upon a cavus foot, consideration must be given to a dorsiflexion first metatarsal osteotomy and peroneus longus to brevis transfer.

Aftercare for either requires 4–6 weeks’ immobilization in cast or brace, followed by rehabilitation with an emphasis on proprioceptive re-education.

Injury to the tarsometatarsal joint is frequently overlooked, especially as the patient often has multiple injures. It is a potent cause of late disability.

Purely ligamentous injuries to the tarsometatarsal joint complex result from more minor accidents and again often cause long-term symptoms.

Lisfranc was one of Napoleon’s surgeons who observed injuries in cavalry officers falling from their mounts while one foot remained in a stirrup.

The anatomy of the midfoot is complex. Stability depends upon bony and ligamentous anatomy, as well as dynamic (musculotendinous) stabilizers.

The wedge-shaped cuneiforms and metatarsal bases form a transverse arch. The second metatarsal base is considered to form the ‘keystone’ of the tarsometatarsal joint as it is the apex of the transverse arch and is recessed between the medial and the lateral cuneiforms providing lateral stability. In addition there are three groups of ligaments: dorsal, interosseous, and plantar (Figure 9.5.10). Without these ligaments the tarsometatarsal joint complex is inherently unstable.

Severe fracture or dislocation of the tarsometatarsal joint will be obvious, with gross swelling and deformity. The plantar ecchymosis sign, with a bruise under the foot at tarsometatarsal joint level, is seen. Tenderness is maximal over the second tarsometatarsal joint.

In contrast, a seemingly innocuous injury to the foot that presents late, once swelling and bruising have improved, is easily missed and requires careful examination and a high index of suspicion.

Most cases of tarsometatarsal joint injury are presumed to be a ‘sprained foot’. It is safer to assume that ‘there is no such thing as a sprain of the midfoot’.

In severe injuries, fracture and/or dislocation are usually obvious.

In contrast, in pure ligamentous injury, they may show no abnormality, particularly if taken non-weight bearing.

Positive radiographic features are the ‘fleck sign’ (a small avulsion of bone from the base of the second metatarsal) and an increase in the gap between the bases of the first and second metatarsal. The medial edge of the base of the second metatarsal should be aligned with the medial edge of the intermediate cuneiform. This is best assessed on an AP radiograph of both feet taken with the patient bearing weight (Figure 9.5.11A). Where plain radiographs are normal CT, MRI, or bone scan can be helpful (Figure 9.5.11B).

Targeted joint injection of local anaesthetic may be useful to confirm that pain is from the second tarsometatarsal articulation in chronic cases.

Untreated, the ligamentous Lisfranc injury often results in a chronically painful foot with planovalgus deformity and tarsometatarsal joint arthrosis from which late salvage surgery in the form of corrective midfoot fusion gives unpredictable results.

Non-operative treatment is only successful when no displacement is present, so a normal CT scan is a prerequisite.

Treatment comprises cast immobilization for 12 weeks with no weight bearing for the first half of this time period. Physiotherapy is required afterwards, as is prolonged support with a rigid FFO.

When displacement is present, open reduction is preferred to give accurate reduction. Historically, K-wire stabilization was recommended. Screws across the tarsometatarsal articulation provide more stability but damage an already disrupted joint, so bridging plates are preferred by many surgeons.

In selected cases, primary fusion may be considered (Figure 9.5.12) to avoid repeated surgery and a protracted recovery.

Trauma to the Lisfranc joint is a potentially devastating injury. Even with good treatment, pain, stiffness and swelling lead to difficulty with sporting activities and shoe fitting in many patients. Patients should be warned that the foot is unlikely to return to full function, and may require long-term orthotic support.

The Achilles tendon is the largest tendon in the body. In orthopaedic foot and ankle surgery, disorders of the Achilles relate to pain and swelling with resultant disability or to rupture.

The microscopic appearances of tendons that have ruptured are similar to the findings in specimens sent from tendons with tendinopathy without rupture, suggesting a pre-existing abnormality, prior to acute tearing.

However, many patients who sustain an acute rupture have never had symptoms while patients who endure chronic pain and swelling of the tendon rarely rupture.

The Achilles tendon is the combined tendon of the three components of the triceps surae muscle. The gastrocnemii pass across both the knee joint and the ankle joint. Soleus does not extend above the knee. This distinction is important when stretching programmes are considered as part of a treatment programme, as the gastrocnemius cannot be properly stretched unless the knee is held in full extension.

The fibres of the Achilles tendon rotate through 90 degrees as they pass distally. The medial fibres proximally become the posterior fibres distally. Thus valgus collapse of the ankle tends to increase the twist and therefore tightness of the tendon.

The tendon inserts onto the middle one-third of the posterior surface of the tuberosity of the calcaneum. Structurally the insertion changes by way of transitional zone: fibrocartilage, mineralized fibrocartilage, and finally bone. This allows effective force dissipation.

The tendon immediately proximal to the site of insertion is related to the superior one-third of the posterior surface of the os calcis. This surface is covered by fibrocartilage and the tendon is protected by the retrocalcaneal bursa. Another bursa lies between the Achilles tendon and the skin.

The blood supply in the non-insertional region of the Achilles tendon is poor. This is important in the pathophysiology of tendinopathy and rupture.

Posterior heel pain most commonly arises from the Achilles tendon. Pathology may arise from the insertion of the tendon or from the non-insertional region. This distinction is helpful.

Non-insertional Achilles tendon pathology is more common and is due to degenerative changes within the tendon, thickening of the paratenon, or a combination of the two.

Retrocalcaneal bursitis with insertional tendinopathy accounts for approximately 20% of all Achilles tendinopathies. Pure insertional tendinopathy makes up only 5%.

Maffulli has clarified the nomenclature. The triad of pain, swelling, and impaired function should be referred to as Achilles tendinopathy.

Achilles tendinopathy is common, but there are no reliable epidemiological data. An association with athletic training supports the theory that overuse is the principal cause, although it can trouble sedentary individuals as well. It is more common in older athletes.

An enlarged posterosuperior border of the tuberosity of the os calcis is called the bursal projection (Haglund deformity), and may impinge against the tendon resulting in retrocalcaneal bursitis or degenerative change in the tendon. With retrocalcaneal bursitis the heel is swollen and maximally tender posteromedially or, more commonly, posterolaterally. It may also cause the heel counter of shoes to rub. This results in local swelling and tenderness.

Insertional heel pain may also be due to changes within the transitional zone of the tendon, to retrocalcaneal bursitis, or to both.

Patients with insertional tendinopathy complain of posterior heel pain that is maximal in the midline and inferiorly, at the insertion of the tendon.

A careful history determines the relationship of symptoms to: activity; new training regimens; poor warm-up technique; or to specific shoes. Atypical features in the history, such as night pain, should prompt investigations for enthesopathy or rare neoplastic causes.

Examination will reveal the site of maximal tenderness. The tendon is tender and swollen in non-insertional tendinopathy. Midline tenderness suggests insertional tendinopathy whereas maximal tenderness to the lateral (or less commonly medial) side of the tendon is due to bursitis.

Increased calcaneal pitch with heel varus makes the bursal projection of the calcaneum excessively prominent. Heel valgus with a low medial longitudinal arch and forefoot varus causes overpronation of the foot, tightening of the tendon, and secondary Achilles tendinopathy.

If a systemic inflammatory cause is suspected, general examination is performed and supplemented with blood tests.

Plain radiographs may show deformity, bony lumps, and ectopic calcification (Figure 9.5.14A).

Ultrasound scan and MRI both provide useful information. MRI provides a permanent image (Figure 9.5.14B), but ultrasound allows dynamic assessment.

Patients must be informed of the natural history of non-insertional tendinopathy because the majority of patients improve and are only left with a palpable non-tender lump in the Achilles tendon in the long term.

Stretching regimens for non-insertional tendinopathy are effective, with 90% of patients responding. The patient and physiotherapist must understand that the knee has to be fully extended during the stretch for the gastrocnemius contracture to be improved. If the hamstrings are tight then stretches for this muscle group should be added to the regimen.

Steroid injection should be avoided except in proven cases of pure paratendinitis or bursitis, because of the risk of rupture. Sclerosant injection therapy is successful in the treatment of non-insertional tendinopathy. Extracorporeal shock wave lithotripsy is under evaluation.

Patients with ‘pump bumps’ respond to education, modification of shoes, and occasionally an orthotic to lift the affected part, or a silicone lined sock. To avoid recurrence it is important that the patient understands that they must continue to be careful with shoes even after the symptoms resolve.

Retrocalcaneal bursitis can be managed in the same way. Corrective orthotics for planovalgus deformity can be helpful, but over correction is poorly tolerated, especially in running athletes. There may be some benefit from anti-inflammatory medication or gel, but steroid injection should only be considered if an MRI or ultrasound scan shows normal tendon.

Non-operative treatments are successful in about 90% of cases, so surgery is rarely required—especially as recovery times are often very long.

Surgery is rarely required. Available procedures include decompression—performed open or percutaneously by multiple incisions and paratenon stripping. In severe cases, surgeons increasingly perform supplementary transfer of the flexor hallucis longus (FHL) tendon, to augment the Achilles tendon.

Excision of the bursal projection is performed through a medial incision for osteotomy of the posteromedial and/or lateral bony prominence, minimizing risk to the sural nerve. At least 50% of the attachment of the tendon can be released without the need for suture anchor repair and without cast immobilization.

Combined excision of bursa and bony prominence results in 50% of patients being symptom free and a further 20% improved. In patients operated on within a year, 92% are cured or improved.

In rare cases where surgery is required for isolated insertional tendinitis, a posterior midline tendon splitting approach is used (Figure 9.5.15). The tendon is debrided, and may be completely detached and reattached. The success rates for pain relief are good, but the eventual outcome is often limited and not all patients improve sufficiently to resume sports.

The incidence of wound problems after surgery in the region of the Achilles tendon is small but troublesome. Minimally invasive surgical techniques for debridement to the retrocalcaneal bursa and bursal projection may offer reduced surgical morbidity.

Enthusiasts report no complications and a rapid return to normal function. The recovery time is equal in both methods, but the endoscopic group have fewer wound infections, fewer sensitive scars, and a lower incidence of altered sensation.

Management of the patient with rupture of the Achilles tendon is controversial. Operative repair offers advantages of predictability, but at the expense of surgical risk.

Rehabilitation protocols have significantly changed with emphasis now on early weight bearing and movement.

Patients usually sustain a rupture of their Achilles tendon while engaged in athletic activity. The risk of rupture is greatest in unaccustomed activity.

Racquet sports (especially squash and badminton) have a reputation for injury, and anecdotally patients typically believe that their opponent has struck the back of their heel.

Sudden pain is a constant feature of the presentation, often with an audible tearing or snapping sound, though the pain may not last long.

Sadly even patients with classical presentations are misdiagnosed as having a sprained ankle, pulled calf muscle, or ‘partial tear’ of the Achilles tendon.

Clinicians may be deceived by the patient’s ability to plantar-flex using the muscles of the deep posterior compartment of the calf.

In the acute setting, soft tissue swelling and tenderness may mean that the gap between the tendon ends cannot be palpated. The only reliable way to diagnose rupture is to use the clinical test of Simmonds and Thompson. The patient lies on a couch or kneels on a chair with the feet and ankles hanging free. The examiner notes the resting posture of the ankles. The affected side will lie in a less plantar-flexed position, through loss of the pull of the gastrosoleus complex (Matle’s test). The examiner then squeezes the normal calf and this action shortens the gastrosoleus muscle causing the foot to plantar-flex. When the manoeuvre is repeated on the affected limb there is no such movement at the ankle because there is no continuity of the tendon. To avoid confusion, the test should not be referred to as positive or negative—which is ambiguous—but as normal or abnormal.

Sudden onset of posterior heel pain should be assumed to be due to a (complete) rupture of the Achilles tendon, until proven otherwise.

Imaging is seldom required. Ultrasound or MRI (Figure 9.5.16) may be useful as an adjunct to clinical assessment where the presentation has been delayed or where there is a suspicion that the rupture is high, at the musculocutaneous junction—but may be misleading if clot or scar fills the gap.

Achilles tendon rupture may be managed non-operatively or by surgical repair.

The benefits of surgical repair include a lower incidence of re-rupture and the opportunity to achieve adequate tension in the tendon. Most surgeons specializing in foot and ankle surgery are proponents of repair. A review of the Cochrane database concluded that surgery is advantageous as long as compli-cations can be avoided. Wound infection and/or breakdown, in an area with a thin soft tissue envelope, is the most important complication.

The decision to surgically repair a ruptured Achilles tendon is made after considering:

At one extreme, the older patient who has poor skin, smokes, and presents immediately after an injury may be managed non-operatively—avoiding high risks of wound problems, but mindful of an increased rate of re-rupture.

A sportsman with a few days’ delay in presentation should undergo surgical repair, as this allows the haematoma between the tendon ends to be evacuated and both length and tension of the tendon restored.

Conservative treatment should be active and is not ‘treatment by neglect’. Equinus cast or functional immobilization should be monitored by ultrasound scans to confirm apposition of tendon ends at intervals during healing. After immobilization or functional treatment for 6 weeks, a heel raise allows the patient to gradually stretch out the repaired tendon during rehabilitation.

Open surgery allows direct visualization and robust repair but at the expense of possible wound complications. In an effort to avoid this, percutaneous repair has evolved. The incidence of painful sural nerve injury has been problematic.

The Achillon^® device (Figure 9.5.17) facilitates percutaneous repair and has a very low incidence of nerve injury. Functional results after percutaneous repair are equal to those after open repair, but for those not familiar with its use, open procedures are more applicable.

Whether the tendon is repaired or treated conservatively, the rehabilitation protocol should allow the patient to bear weight from an early stage. This has been shown to improve collagen remodelling. With rapid rehabilitation it is often possible for the patient to be to bearing weight almost immediately and free from support by 6 weeks from the injury.

When a patient presents with a delayed Achilles tendon rupture a variety of terms may be used. Neglected may mean that the patient did not seek medical attention at the time of injury; Missed implies that the doctor, physiotherapist, or nurse failed to make the diagnosis.

When the rupture is not treated the natural history is for the tendon to heal, but at a length that prevents proper function of the triceps surae.

The patient may give a clear history of acute tendoachilles rupture that was not treated or of a minor exacerbation of chronic symptoms that was not appreciated to be a rupture. In either case, the presenting complaints are weakness, poor balance, difficulty with stairs, or inability to stand on tiptoes, with swelling of the ankle and pain.

On examination the ankle can be passively dorsiflexed further than the normal side; single-stance heel-rise is weak or impossible; the tendon is often thin at the site of rupture, if elongated healing has occurred; or deficient with a palpable gap.

Plain films (lateral weight bearing of the foot and ankle) may show alterations of the normal soft tissue shadows, and may show features of insertional tendinopathy (calcification, Haglund deformity) which raises the possibility of distal rupture.

Ultrasound and MRI may confirm the diagnosis but also give information about the level of the rupture, the extent of retraction of the proximal stump, and the length of intervening scar tissue (Figure 9.5.18), but both may be deceptive and fail to differentiate between clot, scar, and tendon.

This may be chosen when the patient reports minimal symptoms or if surgery is contraindicated. Physiotherapy strengthens the calf muscles and minimizes symptoms. Improvement may continue for more than 2 years.

Surgical treatment aims to restore plantar-flexion power to the ankle. There is a wide range of surgical techniques from which to choose. The choice is made according to the gap between the proximal and distal stump after debridement of scar tissue.

Available techniques include direct repair and indirect methods, and the more controversial autograft, synthetic graft, or allograft reconstructions.

End-to-end repair is unlikely to be successful if treatment is delayed for more than a few weeks. Advancement of the proximal stump can be achieved by means of V–Y-plasty or a ‘turn-down’ procedure. This produces a bulky repair with risk of wound problems and is less popular since the introduction of tendon transfer techniques.

Tendon transfer techniques may use peroneus brevis, FDL or (most commonly) FHL.

Reports of FHL transfer are good to excellent with negligible weakness of hallux flexion.

Synthetic graft should only be used in exceptional circumstances.

Plantar heel pain is common, disabling, and usually due to plantar fasciitis at the point of insertion onto the heel.

Patients are often middle aged or elderly and present with severe heel pain, especially start-up pain that is most troublesome upon rising in the morning and improves, only to deteriorate again with prolonged standing or walking.

Atypical presentation in younger patients may be associated with stress fractures, enthesopathy, arthritis, tarsal tunnel syndrome, or lumbar radiculopathy.

Patients should be examined for signs of a calcaneal stress fracture (calcaneal squeeze test) and for tarsal tunnel syndrome (Tinel sign over tibial nerve; altered sensation in sole of foot). Plantar fasciitis is classically maximally tender over the medial calcaneal tuberosity (Figure 9.5.19).

The majority of patients with plantar fasciitis have isolated shortening of the gastrocnemius, identified using Silfverskiold’s test (Figure 9.5.3).

Conservative treatment includes orthotics, physiotherapy (including ultrasound and stretching), night splints and lithotripsy. Patients who present early recover more quickly than those presenting late with established symptoms. The majority of cases respond, but in refractory cases, injection (preferably ultrasound guided) can be helpful. Rupture of the fascia is, however, a potential and serious complication (Figure 9.5.19B).

Open or endoscopic release of the plantar fascia insertion is sometimes performed, but the risk of provoking prolonged severe pain in association with acute flat foot and nerve damage means that it has not been adopted widely in the United Kingdom.

The peroneus longus and brevis tendons cause ankle symptoms either because of acute injury or because of chronic tendinopathy.

Peroneus brevis lies anterior to longus as they course behind the lateral malleolus. Both are supplied by the superficial peroneal nerve (L5, S1 roots).

Proximal to the malleolus the tendons are invested in a synovial sheath. This extends beneath the peroneal retinaculum. After rounding the tip of the lateral malleolus, the tendons diverge, passing either side of the peroneal tubercle on the lateral wall of the os calcis. They pass beneath the inferior extensor retinaculum before following different courses. The brevis tendon passes to the styloid process of the fifth metatasal base. Peroneus longus passes beneath the cuboid and across the sole of the foot to insert on the plantar aspect of the base of the first metatarsal. At the point that the tendon changes direction it is strengthened by a sesamoid bone, the os perineum, which is often cartilaginous.

Inversion injuries of the ankle may result in acute inflammation of the peroneal tendons leading to signs of: local tenderness; pain on passive stretch; and pain on active resisted movement. Swelling behind the fibula is characteristic.

The position of peroneus brevis, between the longus tendon and the fibula, makes it vulnerable to injury. It may also be trapped beneath the fibula when there is valgus deformity of the heel.

Plain radiographs will not show the tendons but in the case of peroneus longus rupture may show proximal migration of a fracture through the os peroneum.

Ultrasound or MRI is more useful to show the structure of the tendons.

Non-operative treatments include activity modification and orthotic provision to address any cavovarus deformity or valgus collapse. Corticosteroid injection should usually be avoided.

Synovectomy can be performed arthroscopically. Open surgical exploration, with tenosynovectomy and repair or tendon debulking with tubularization of split/thickened tendons is indicated in severe cases with tendinosis/chronic rupture.

The peroneal tendons dislocate from behind the fibula as a result of a twisting injury. In the normal ankle the peroneal retinaculum prevents this.

At the time of injury the tendons strip the retinaculum away from the bone of the fibula—a ‘Bankart’ lesion of the ankle.

Only occasionally does an avulsion fracture from the fibula make the injury apparent on plain radiographs. Neither MRI nor ultrasound is 100% sensitive.

A high index of suspicion is required to make the diagnosis in the acute setting.

After the acute symptoms have resolved, recurrent snapping of the tendons over the malleolus may be demonstrated by the patient.

After an acute injury cast immobilization may allow satisfactory healing. Surgery aims to repair the ‘Bankart’ lesion anatomically

In recurrent situations after failed surgery, various techniques have been described to augment the repair. The ‘groove’ behind the fibula can be deepened with an osteotomy or using a burr. A strip of tendon from the lateral portion of the Achilles tendon may be used to fashion a new retinaculum. Alternatively, the calcaneofibular ligament may be transposed into a position superficial to the tendons.

Results of repair are good, but 6–8 weeks of protection in a cast are required, and a lengthy rehabilitation period follows this.