Extract
Chronic ankle pain is common. The causes are numerous, and all ages are affected. Trauma is not necessary but is often the initiating event, so an efficient method for evaluation is beneficial. A detailed history, careful physical examination, and judicious selection of the appropriate imaging modalities are all vital to making an accurate diagnosis and providing effective treatment.
Chronic ankle pain is common. The causes are numerous, and all ages are affected. Trauma is not necessary but is often the initiating event, so an efficient method for evaluation is beneficial. A detailed history, careful physical examination, and judicious selection of the appropriate imaging modalities are all vital to making an accurate diagnosis and providing effective treatment.
Look for this and other related articles in Instructional Course Lectures, Volume 60, which will be published by the American Academy of Orthopaedic Surgeons in February 2011:
- "The ‘Not So Simple’ Ankle Fracture: Avoiding Problems and Pitfalls to Improve Patient Outcome," by David J. Hak, MD, Kenneth Egol, MD, Michael Gardner, MD, and Andrew Haskell, MD
The tarsal tunnel is bordered by the distal part of the tibia anteriorly and the posterior border of the talus and calcaneus posteriorly. The roof of the tunnel is formed by the flexor retinaculum, which begins 10 cm proximal to the medial malleolus. The contents of the tarsal tunnel include the posterior tibial artery and vein, the posterior tibial tendon, the flexor hallucis and flexor digitorum longus tendons, and the posterior tibial nerve. The posterior tibial nerve has three terminal branches: the medial plantar, lateral plantar, and medial calcaneal nerves. The three terminal nerve branches typically arise in the tarsal tunnel, although variations may occur. Recent evidence has identified separate fascial tunnels distal to the flexor retinaculum for the medial plantar nerve, the lateral plantar nerve, and the medial calcaneal nerve1. Tarsal tunnel syndrome is defined as the symptomatic entrapment of the tibial nerve and/or its branches within the confines of the tarsal tunnel or distally. Space-occupying lesions such as ganglion cysts, lipomas, varicose veins, nerve-sheath tumors, and synovitis can result in nerve compression. Similarly, a hypertrophic tarsal coalition or a nonunion of a sustentaculum tali fracture can cause compression of the neural structures within the tunnel. Pathologic hindfoot valgus can produce tension on the posterior tibial nerve and can cause symptoms of nerve irritation. Intraoperative pressure measurements have demonstrated that pronation and plantar flexion increase the pressures in the medial and lateral plantar tunnels2. Patients usually complain of a burning or tingling sensation along the plantar aspect of the foot or pain radiating proximally into the distal part of the medial aspect of the leg. Symptoms are usually exacerbated by activity such as walking or prolonged standing.
The hallmark of the physical examination is the reproduction of paresthesias with percussion over the posterior tibial nerve (i.e., Tinel sign). On physical examination, it is important to inspect for soft-tissue masses on the medial aspect of the ankle and to make note of any varicosities as well as the presence of any hindfoot malalignment. Positioning the ankle and foot in dorsiflexion and eversion may reproduce the symptoms, analogous to the Phalen sign in the hands3. Evaluation of the lumbosacral spine is important because radiculopathy can present in a similar fashion. The patient should also be questioned about other causes of neuropathy such as diabetes and alcoholism. Electrodiagnostic studies are useful for confirming the site of nerve compression and can eliminate more proximal nerve compression as a source of symptoms. Electrodiagnostic studies are accurate approximately 80% to 90% of the time, and sensory nerve conduction velocity studies are more likely to be abnormal than motor nerve conduction velocity studies. The utility of needle electromyography is uncertain in the diagnosis of tarsal tunnel syndrome4. Magnetic resonance imaging is used to exclude a mass within the tunnel.
If there is a mass within the tarsal tunnel, removal is usually recommended, but otherwise the initial treatment is rest of the foot and ankle in a removable walking boot. A local injection of a corticosteroid may be used but is associated with a risk of an injury to the posterior tibial tendon. Physical therapy modalities such as ice, heat, and ultrasound may be helpful for providing symptomatic relief. Orthotics should be prescribed for patients with biomechanical abnormalities, especially if hyperpronation is present.
The indications for surgical decompression include a failure of nonoperative treatment as described above and objective evidence of nerve compression within the tarsal tunnel. The best results of surgery are achieved in patients with positive electrodiagnostic tests, a positive Tinel sign, a space-occupying lesion, and paresthesias in the distribution of the posterior tibial nerve. The results of surgery have been reported to be successful in 50% to 90% of patients. The use of a tourniquet is optional; however, if a tourniquet is used, it should be deflated prior to closure to ensure that a hematoma does not form. Some authors have recommended distal decompression of the medial and lateral plantar tunnels1. Unsatisfactory outcomes are associated with postoperative wound complications such as infection, dehiscence, hematoma formation, incomplete release of the tarsal tunnel, and complex regional pain syndrome.
Adult-acquired flatfoot deformity begins with tenosynovitis or injury to the posterior tibial tendon, eventually resulting in tendon elongation and dysfunction. Originally, this condition was known as posterior tibial dysfunction because tendon failure occurred as a result of tendon degeneration. As the posterior tibial tendon elongates and becomes dysfunctional, unopposed peroneus brevis contraction results in hindfoot eversion, causing stretching of the unsupported medial ankle ligaments and soft tissues. The spring ligament fails, the talus plantar flexes, and the medial longitudinal arch collapses. As the forefoot abducts at the talonavicular joint, the Achilles tendon falls lateral to the midline and contributes further to hindfoot valgus.
A hypovascular zone begins 2 to 4 cm proximal to the insertion of the posterior tibial tendon, rendering this area susceptible to tenosynovitis and/or injury, with overuse being a possible cause. Patients present with posteromedial ankle pain and swelling over the posterior tibial tendon and have difficulty with stair climbing and with walking on uneven ground. In later stages, lateral pain predominates because of fibular impingement. Approximately 25% of patients have a history of a previous medial ankle sprain. On clinical examination, a pes planovalgus deformity develops as the tendon elongates and soft-tissue swelling is often observed along the course of the posterior tibial tendon. Observation of the standing patient from the rear demonstrates the "too many toes" sign (Fig. 1). The patient should be asked to do a single-leg heel rise. With the contralateral foot off the ground, a normal patient will stand on the tiptoes, and, in the process, the heel inverts. If the heel does not invert or if the patient is unable to raise the heel off the ground, there is likely dysfunction of the posterior tibial tendon.
Weight-bearing anteroposterior and lateral ankle and foot radiographs as well as an axial calcaneal radiograph should be made. Particular attention should be paid to the presence of disruption of the normal talar-first metatarsal angle on both the anteroposterior and lateral radiographs. Although not necessary for diagnosis, magnetic resonance imaging can be a useful adjunct. Axial magnetic resonance images have been reported to be 96% accurate for identifying tendon pathology.
Johnson and Strom5 described three stages of posterior tibial tendon dysfunction, and Myerson6 added a fourth (Table I). Stage I is characterized by tenosynovitis, no deformity, and preservation of posterior tibial tendon strength. Often, patients note a long history of flatfoot deformity. Stage II is characterized by tendon dysfunction and weakness in the presence of a correctable deformity. Stage II has been further subdivided on the basis of the amount of abduction that is present at the midfoot7. Stage-IIa disease is characterized by minimal abduction (<30% peritalar subluxation on a standing anteroposterior foot radiograph), whereas stage-IIb disease is characterized by uncoverage of >30% of the talar head. Stage-III deformity is characterized by a rigid deformity with lateral pain due to fibular impingement. Passive inversion of the triple joint complex is not possible past the neutral position. Stage-IV disease is characterized by ankle involvement secondary to deltoid ligament incompetence, although the foot deformity may be either flexible or rigid.
Nonoperative treatment consists of treatment in a boot, cast, or customized brace such as the Arizona brace, supplemented with nonsteroidal anti-inflammatory drugs or oral steroids. Steroid injections are not recommended because of the risk of tendon rupture. Physical therapy modalities, begun once the initial inflammation subsides, include ultrasound, iontophoresis with Decadron (dexamethasone), cryotherapy, strengthening with progressive resistance of all muscle groups about the foot and ankle, and stretching of the Achilles tendon with the subtalar joint in a neutral position. Twenty-two of thirty-two patients with stage-II posterior tibial tendon dysfunction who were managed temporarily with a double upright ankle-foot orthosis and were followed for an average of 8.6 years were able to avoid surgical intervention8. Five patients continued use of the brace, and an additional five patients underwent surgery. Alvarez et al.9 reported that forty-two of forty-seven patients with stage-I and II posterior tibial tendon dysfunction were effectively managed with an orthosis and structured exercises. A customized brace such as an articulating ankle-foot orthosis or Arizona brace is also effective for providing long-term symptomatic relief. Currently, it is unknown if these devices alter the progression of the disease.
Patients should be managed nonoperatively for at least three months. Surgical treatment of stage-I adult-acquired flatfoot deformity includes tenosynovectomy as well as possible tendon repair or flexor digitorum longus tendon transfer. If tendon transfer is performed, a medializing calcaneal osteotomy should be done concomitantly in patients with a flatfoot deformity.
The surgical treatment of stage-IIa deformity involves a transfer of the flexor digitorum longus to the midfoot and a medial displacement osteotomy of the calcaneus. An Achilles tendon lengthening or a Strayer procedure is usually necessary because the patient develops an equinus contracture. In a series of 129 surgically managed patients, Myerson et al.10 reported that 97% had pain relief, 94% had improved function, and 84% were able to wear shoes without shoe modifications or orthotics. A medial column fusion or Cotton osteotomy may be performed in order to address forefoot varus. In patients with stage-IIb deformity, a lateral column lengthening calcaneal osteotomy may be necessary to address forefoot abduction.
The surgical treatment of stage-III deformity involves a triple arthrodesis to correct the plantar flexed talus and the subluxated talonavicular joint. If excessive heel valgus remains after triple arthrodesis, a medial slide osteotomy of the calcaneus is recommended. An Achilles tendon lengthening or a Strayer procedure is usually necessary. Isolated subtalar fusion is not recommended if a rigid forefoot varus deformity is present as correction of the forefoot varus deformity can only be accomplished by including the transverse tarsal joints in the fusion. Surgical treatment for stage-IV deformity involves deltoid ligament repair or reconstruction (with use of tendon graft) to correct talar tilt. If the deformities in the hindfoot and ankle are flexible, then the same procedures utilized for a stage-II deformity can be combined with deltoid reconstruction. For rigid deformities, triple arthrodesis with reconstruction of the deltoid ligament is recommended. End-stage posterior tibial tendon dysfunction with associated ankle joint arthrosis requires either a pantalar fusion or a triple arthrodesis and total ankle replacement.
Patients with seronegative arthropathy (ankylosing spondylitis, psoriasis, and Reiter syndrome) are also at increased risk for developing a flatfoot deformity. These patients present with enthesopathy, or inflammation and maximum tenderness at the tendon insertion. Patients with rheumatoid arthritis also can develop planovalgus deformity secondary to tenosynovitis and destruction of the subtalar and talonavicular joints. When these patients have persistent tenosynovitis, they should undergo early surgical treatment to prevent tendon rupture.
Flexor hallucis longus tendinitis is differentiated from posterior ankle impingement by the presence of posteromedial pain and soft-tissue swelling along the posteromedial aspect of the ankle. The flexor hallucis longus tendon descends from the leg into the foot through a sulcus, which is bordered by the posteromedial and posterolateral tubercles of the talus. The pain may be aggravated by passive toe motion. Gymnasts, dancers, runners, and tennis players are prone to developing this condition as a result of activities that require repetitive push-off. On physical examination, crepitation over the flexor hallucis longus may be present. The Thomason test demonstrates that, in the presence of functional hallux rigidus, the patient has normal motion of the metatarsophalangeal joint with the ankle in plantar flexion, but with the ankle in dorsiflexion, passive dorsiflexion of the metatarsophalangeal joint is reduced11. In chronic cases, triggering may be present if nodules are present within the substance of the flexor hallucis longus. Radiographs may show a symptomatic os trigonum or fractures. Magnetic resonance imaging may show fluid within the tendon sheath (Fig. 2).
Nonoperative treatment begins with rest and modified training. A removable walking boot should be used as necessary. Ice, cryotherapy, ultrasound, and stretching are done next, before surgery is considered. Local steroid injections are not recommended for the treatment of flexor hallucis longus tendinitis but may be useful to exclude posterior ankle impingement due to an os trigonum. Surgery, if needed, involves a release of the flexor hallucis longus sheath through a posteromedial approach. After surgery, the patient is placed in a splint for three weeks, after which motion and strengthening exercises are begun.
The posterior process of the talus includes the posteromedial and posterolateral tubercles. The flexor hallucis longus runs between these tubercles and has a discrete osseous tunnel. In 10% of the population, an unfused posterolateral process, or os trigonum, is present12. An enlarged posterolateral tubercle is known as a Stieda process (Fig. 3). Any of these structures can cause posterior ankle pain with the ankle in plantar flexion. Most commonly, an acute plantar flexion injury will damage the os trigonum or the synchondrosis. A symptomatic Stieda process or synovitis in the flexor hallucis longus can also cause these symptoms.
The patient with posterior ankle impingement who does not have flexor hallucis longus tenosynovitis complains of posterolateral ankle pain. Activities that require repetitive plantar flexion, such as ballet dancing, downhill running, and soccer, are often associated with this impingement. The patient has posterolateral tenderness and pain on the forced plantar flexion test. The patient frequently sprains the ankle because the foot is placed in an inverted position to avoid impingement. The patient also complains of pain with motion of the great toe when flexor hallucis longus tendinitis is present. In addition to standard foot radiographs, a neutral weight-bearing lateral foot and ankle radiograph and a plantar flexion lateral foot and ankle radiograph are beneficial. A plantar flexion lateral radiograph may show an acute or old fracture of the trigonal process, the presence of an os trigonum, or dynamic impingement (Fig. 4). Computed tomography is a useful adjunct to rule out an occult fracture of the posterior process. A normal bone scan eliminates the trigonal process as a source of pathology. Magnetic resonance imaging is the study of choice to assess for bone edema and possible changes in the soft tissues, such as the flexor hallucis longus.
Icing, nonsteroidal anti-inflammatory drugs, activity modification, and strapping of the foot to minimize ankle dorsiflexion are often successful. Immobilization in a removable boot limits plantar flexion to avoid the foot position that causes pain. Injection with lidocaine and steroid may be utilized posterolaterally for both diagnostic and therapeutic purposes. After four to six weeks of this therapy, physiotherapy with stretching and strengthening exercises is prescribed.
If nonoperative treatment fails, surgical excision of the os trigonum and redundant capsule is recommended. For isolated posterior ankle impingement, a posterolateral approach is used. The patient is placed in the prone position, the sural nerve is identified and protected, and a more direct approach to the trigonal process is provided. The limiting factor in this approach is that dissection medial to the flexor hallucis longus is not advisable because of potential damage to the neurovascular structures in the vicinity. For patients with concomitant flexor hallucis longus tenosynovitis and posterior impingement, a posteromedial approach is recommended.
Arthroscopic techniques have been described for the treatment of posterior impingement. Procedures that have been performed have included excision of an os trigonum, decompression of a prominent posterior talar process, tenolysis of the flexor hallucis longus, removal of loose bodies, and debridement of posterior osteochondritis dissecans lesions. Uncontrolled case series have demonstrated earlier return to activities, less morbidity, and outcomes that compared favorably with open lateral approaches13.
Disorders of the Achilles tendon and retrocalcaneal bursa are the most common causes of posterior ankle pain. Runners are frequently affected, as are those who participate in jumping sports. The Achilles tendon arises from the gastrocnemius and soleus muscles and broadly inserts onto the calcaneal tuberosity. The tendon receives its vascular supply from proximal muscular branches and distal calcaneal branches. The tendon is protected by an external sheath, the paratenon, and has an avascular zone approximately 2 to 6 cm proximal to its calcaneal insertion due to a watershed zone of its blood supply. A retrocalcaneal bursa, located anterior to the Achilles tendon, lubricates the anterior aspect of the distal part of the Achilles tendon. Pathology of the Achilles tendon can be due to inflammation limited to the paratenon (paratenonitis), intrasubstance mucoid degeneration and tendon thickening (tendinosis), or insertional Achilles tendinosis with retrocalcaneal bursitis.
Noninsertional Achilles tendon pathology causes pain in the avascular zone (Fig. 5). Predisposing factors for noninsertional Achilles tendinitis include increased age, male sex, excessive hindfoot varus or valgus, and overuse. Patients with insertional Achilles tendinosis and retrocalcaneal bursitis present with posterosuperior heel pain that is aggravated by shoe wear and activity. Insertional Achilles tendinitis can be a presenting symptom of seronegative arthritis. Swelling, crepitus, and tenderness are characteristically present in patients with paratenonitis. Tenderness can be elicited by squeezing the tendon proximal to its insertion. Fusiform swelling is typical of degenerative tendinosis. Patients with insertional Achilles tendinitis and retrocalcaneal bursitis have tenderness at the calcaneal insertion (Fig. 6).
Medial and lateral fullness of the retrocalcaneal space is typical of retrocalcaneal bursitis. In patients with tendinitis and concomitant bursitis, tenderness is present anterior to the Achilles tendon and an enlargement of the posterior superior calcaneal process (a Haglund deformity) may be present. Standing anteroposterior and lateral radiographs of the foot and ankle should be made. Haglund deformity, if present, is seen on the lateral radiograph. Ultrasound has been reported to be sensitive and specific for confirming noninsertional Achilles tendinosis14. Magnetic resonance imaging is useful for evaluating both noninsertional and insertional Achilles tendinitis as well as paratenonitis.
Nonoperative treatment for noninsertional and insertional Achilles tendinitis is nonsteroidal anti-inflammatory drugs for pain relief, heel lifts, Achilles tendon stretching, shoes that do not put pressure on the back of the heel, and activity modification. Ice, massage, ultrasound, and iontophoresis can be used. Temporary immobilization in a removable boot or night splint or even a short-leg cast can be used if the patient has severe pain. Corticosteroid injections are not recommended because of the risk of tendon rupture. Eccentric calf-muscle strengthening has been recommended as an effective treatment for both insertional and noninsertional tendinopathy15,16. Prospective randomized studies have demonstrated that repetitive low-energy shock-wave therapy was superior to eccentric muscle training for patients with insertional and noninsertional tendinopathy17,18. In one study, kinematic evaluation of runners with noninsertional tendinopathy demonstrated an increase in eversion of the subtalar joint19. Consequently, orthotic devices that control subtalar eversion may help this group of patients. Another study evaluated the effectiveness of platelet-rich plasma in patients with noninsertional tendinopathy20. This randomized controlled trial evaluated patients who were managed with eccentric exercises and either saline solution injections (control) or platelet-rich plasma. The authors found that platelet-rich plasma did not result in significant improvements in terms of pain or function compared with the findings in the group managed with saline solution. Nonoperative treatment of acute paratenonitis is usually successful, but patients with chronic symptoms are more likely to require surgery.
Surgical treatment for Achilles tendinitis or paratenonitis is indicated for patients in whom symptoms persist despite supervised nonoperative management for six months.
Tenolysis of the paratenon and debridement of the degenerative tendon is done for patients with noninsertional disease. If >50% of the tendon is involved, augmentation with an autogenous graft is recommended. Excision of a Haglund deformity (if present) and debridement of diseased tendon is done for patients with insertional disease. If >50% of the tendon insertion is debrided, augmentation with a flexor hallucis longus transfer is recommended.
A compression dressing is applied after surgery and is kept on for one week, and then the patient is managed with a cast or a boot for six to eight weeks. The patient should use a heel lift for six more weeks and should begin to resume normal activities at three months. Maximum medical improvement may take six to twelve months, especially in patients with insertional Achilles tendinitis. Following the surgical treatment of chronic Achilles tendinopathy, 86% to 100% of patients have satisfactory results21-24.
Nine million people sustain ankle sprains each year in the United States. Most are due to a plantar flexed inversion injury that leads to compromise of the anterior talofibular ligament and/or the calcaneofibular ligament. These injuries typically heal uneventfully after short-term immobilization, ice, compression, and elevation, and early range of motion. However, a subset of patients who sustain an injury of these ligaments develop chronic lateral ankle instability and residual symptoms. They have subjective complaints of instability without radiographic abnormalities but have functional instability, complaining of the ankle "giving way." Some have measurable hypermobility and objective findings of mechanical instability.
Patients complaining of "giving way" typically have a history of a severe ankle sprain or recurrent ankle inversion injuries. Pain usually is not a predominant symptom, and, when pain is present, an associated injury should be suspected25-27. Commonly associated abnormalities are loose bodies, synovitis, osteochondral injuries, osteophytes, peroneal tendon pathology, and chondromalacia. The evaluation should include an examination for malalignment, particularly hindfoot varus, first-ray plantar flexion, and cavus deformities, which predispose to recurrent inversion injuries. Manual anterior drawer and talar tilt tests are critical for evaluating the integrity of the anterior talofibular ligament and the calcaneofibular ligament, respectively. The involved ankle should be compared with the contralateral ankle to assess for asymmetric laxity. The involved ankle should also be evaluated for peroneal tendon tenderness and subluxation.
In addition to standard radiographs, stress views can be utilized when the clinical examination is equivocal. The anterior drawer stress radiograph is the most useful. Radiographic signs of instability include >10 mm of subluxation, or 3 mm more than the contralateral side. On the talar tilt stress radiograph, >10° of varus talar tilt or a side-to-side difference of >3° raises the possibility of instability. Magnetic resonance imaging is not necessary to make the diagnosis of instability; however, it helps to identify associated intra-articular or periarticular sources of pain. Strengthening and proprioceptive training are the mainstays of physical therapy programs and can decrease the episodes of instability. Bracing and orthotics can be used, especially for patients with varus ankle malalignment.
Operative treatment is reserved for those who have had a failure of nonoperative therapy. More than eighty operative techniques have been described for the treatment of chronic lateral ankle instability. Anatomic repairs that restore normal anatomy and joint kinematics are preferred. The modified Brostrom repair, using the extensor retinaculum to reinforce the ligament repair, has a high patient satisfaction rate28-30 (Fig. 7). Patients with generalized ligamentous laxity do not do as well with the modified Brostrom technique, and nonanatomic repair techniques (e.g., the Evans tenodesis and the Chrisman-Snook procedure) are better for these patients. Nonanatomic repair procedures restore stability but sacrifice normal joint kinematics and subtalar motion in the process. Anatomic reconstruction procedures utilizing autogenous tissue (such as hamstring tendons) or allografts are also potential treatment options, without altering normal ankle kinematics. A split peroneus brevis tendon that is anchored distally at its insertion; routed through bone tunnels in the calcaneus, fibula, and talus; and then sutured back onto itself can also be used for patients with generalized laxity. Case series have indicated that 83% to 100% of patients managed with anatomic tenodesis report good or excellent outcomes31.
The peroneus longus muscle originates from the lateral condyle of the tibia and the head of the fibula. The tendon travels behind the lateral malleolus through a tunnel known as the retromalleolar groove. This groove is bordered by the fibula anteriorly and by a fibrous band known as the superior peroneal retinaculum posterolaterally. The peroneus longus tendon turns medially at the cuboid groove and inserts into the lateral part of the plantar aspect of the first metatarsal and the medial cuneiform. The function of the peroneus longus is to evert the foot and plantar flex the ankle, but it also plantar flexes the first ray and thus serves as an antagonist to the tibialis anterior muscle.
The peroneus brevis originates from the fibula in the middle third of the leg. It is located anterior and medial to the peroneus longus at the level of the ankle and inserts into the tuberosity of the fifth metatarsal and functions to evert and plantar flex the foot. Occasionally, there is a low-lying brevis muscle belly, which may become symptomatic. In most cases, however, the musculotendinous junctions of both tendons are located proximal to the superior peroneal retinaculum. The os peroneum, present in 20% of the population, is an ossified sesamoid bone, found at the level of the calcaneocuboid joint, that can become symptomatic. A peroneus quartus muscle, found in the lateral compartment in about 20% of the population, originates from the brevis muscle belly and inserts into the peroneal tubercle of the calcaneus. Patients with this muscle have a higher risk of peroneal tubercle hypertrophy and stenosing tenosynovitis.
Patients with peroneal tendon pathology have persistent swelling along the peroneal tendon sheath. Retromalleolar pain or ankle instability is the usual complaint. When the tendons are subluxating or dislocating, the patient may have a snapping sensation. In patients who have a history of an acute injury, tendon rupture should be suspected. The alignment of the hindfoot should be evaluated because a varus heel position is associated with an increased rate of peroneal tendon disorders. Eversion strength should be tested. It should be remembered that the peroneus tertius, extensor digitorum longus, and extensor hallucis longus also provide some eversion of the foot. Peroneal tendon dislocation or subluxation can be identified by rotating the ankle to see if the tendons subluxate anterior to the lateral malleolus.
Weight-bearing anteroposterior and lateral radiographs of the symptomatic ankle should be made. In addition, an axial heel radiograph will help to demonstrate the peroneal tubercle and the retromalleolar groove. Computed tomography scans are a valuable adjunct for evaluating osseous abnormalities, such as peroneal tubercle hypertrophy, os peroneum fractures, or an avulsion of the lateral malleolus. Magnetic resonance imaging has emerged as the imaging modality of choice for this condition because heterogeneity or discontinuity of the tendon, a fluid-filled tendon sheath, marrow edema along the lateral calcaneal wall, a hypertrophied peroneal tubercle, the shape of the posterior part of the fibula, and the integrity of the superior peroneal retinaculum can all be evaluated.
Nonoperative treatment of peroneal tendinitis involves nonsteroidal anti-inflammatory medications, rest, and activity modification. Mild cases of tendinitis can be treated with a lateral heel wedge. In refractory cases, a short leg cast or CAM walker can be used for six weeks. If nonoperative treatment is ineffective, an open tenosynovectomy and debridement of any region of the tendon that appears to be degenerated is recommended. The remaining portion of the tendon is subsequently repaired in a tube-like fashion with use of a running 4-0 nylon suture (Fig. 8). If the remaining portion of the tendon is of insufficient size or poor quality, a tenodesis of the diseased tendon to the adjacent peroneal tendon (i.e., peroneus brevis to longus tenodesis) should be done.
Peroneal tendon tears or ruptures are treated operatively, unless the patient is not a candidate for operative treatment because of medical comorbidities. In such cases, the patient can be managed with a lateral heel wedge. If possible, an acute tendon rupture is treated with an end-to-end repair. If this is not possible, a transfer of the flexor digitorum longus to the peroneus brevis is a viable option. Operative treatment of peroneal tendon tears is based on the amount of remaining viable tendon. Primary repair and tubularization is indicated for tears involving <50% of the tendon, and tenodesis is indicated for tears involving >50% of the tendon32. If both tendons are intact, the torn tissue is debrided and tubularized. If one tendon is torn and irreparable and the other is functional, a tenodesis can be performed with use of the myotendinous junctions of the tendons. If one tendon is torn and irreparable and the other is nonfunctional, flexor digitorum longus transfer as described above should be considered. Hindfoot varus, ankle instability, and osteophyte formation, which contribute to peroneal tendon tearing, should also be corrected. In one report, residual symptoms were reported to be present in >50% of patients and <50% of patients returned to sporting activities after operative repair33.
Peroneal tendon subluxation occurs following disruption of the superior peroneal retinaculum. Eckert and Davis described three grades of injuries to the superior peroneal retinaculum34. In grade I, the superior peroneal retinaculum is elevated from the fibula; in grade II, a fibrocartilaginous ridge is elevated from the fibula; and in grade III, a cortical fragment is avulsed with the superior peroneal retinaculum. Nonoperative treatment can be attempted for acute grade-I and III injuries with use of a short-leg cast for six weeks. If this treatment fails, the superior peroneal retinaculum is reattached surgically after the creation of an osseous trough along the posterolateral aspect of the fibula. For patients with chronic peroneal subluxation, a fibular groove-deepening procedure is indicated. This procedure involves raising an osseous flap from the posterolateral corner of the fibula and using a burr to remove the cancellous bone beneath the flap. The flap is then reduced and is tamped into place. The superior peroneal retinaculum is then repaired over the tendons, which are located in the newly-deepened groove. In a similar fashion, a bone block procedure can be performed, with a sagittal cut of the fibula, translating the more lateral portion posteriorly, and holding the displaced fibula with screws35.
Process and tubercle fractures of the hindfoot can be difficult to diagnose and treat. These injuries are often misdiagnosed as a sprain of the ankle or foot, leading to a delay in diagnosis and suboptimal outcomes36. Prompt diagnosis requires a high index of suspicion and a thorough knowledge of the anatomy of the hindfoot. Specialized radiographs as well as computed tomography and magnetic resonance imaging may be needed to confirm the diagnosis. Fractures of the anterior process of the calcaneus occur with inversion of the plantar flexed ankle and are the result of an avulsion injury of the bifurcate ligament. Tenderness is usually reproduced in an area 2 cm anterior and 1 cm inferior to the anterior talofibular ligament. This fracture is typically not visualized on standard anteroposterior radiographs of the foot and ankle. An oblique radiograph of the foot with the x-ray beam directed 10° to 25° superior and posterior to the midfoot is necessary. This projects the anterior process away from the talar neck and enables optimal visualization of the fracture. As an adjunct, multiplanar computed tomography imaging with fine 1-mm cuts can be done to provide a more accurate delineation of displacement and fragment size, which influence treatment decisions.
For fracture fragments that are <1 cm in size and are displaced by <2 mm, a below-the-knee, non-weight-bearing cast can be applied for a period of six weeks, followed by transition to a removable walking boot and progressive weight-bearing. Open reduction and internal fixation is recommended for fractures that are >1 cm in size and are displaced by >2 mm with intra-articular involvement37.
Lateral talar process fractures typically occur after a fall or motor-vehicle accident, but they also occur in association with snowboarding injuries. Approximately 2000 lateral talar process fractures occur annually in these athletes38. The lateral talar process is avulsed by the lateral talocalcaneal ligament with an inversion injury. Another mechanism is an eversion moment that is applied to a dorsiflexed, axially-loaded foot, causing compression and fracture of the lateral talar process. Careful palpation just anterior and inferior to the lateral malleolus can elicit pain, which should raise suspicion for this injury. Lateral talar process fractures usually can be visualized on routine radiographs, although subtle fragments just distal to the lateral malleolus may be difficult to appreciate (Fig. 9). The amount of displacement and the extent of articular involvement of the posterior facet of the subtalar joint are seen on a thin-cut computed tomography scan39.
Fracture fragments that are <1 cm in size and are displaced by <2 mm are treated nonoperatively. Displaced fractures are best treated with open reduction and internal fixation or primary excision, with excision favored in scenarios in which the fracture is comminuted. If open reduction and internal fixation is feasible, fixation is typically done with mini-fragment screws or Kirschner wires38.
Sinus tarsi syndrome is associated with persistent lateral ankle pain directly over the sinus tarsi. It is usually a result of an inversion injury, and the patient may complain of a feeling of instability. Several theories have been advocated to explain the source of pain, including interosseous ligament injury; hypertrophy of the synovium; or hypertrophy of the fat, resulting in impingement of the neural plexus. The diagnosis is one of exclusion and is confirmed on the basis of pain relief after an injection of local anesthetic into the sinus tarsi. Radiographs demonstrate normal findings and serve to eliminate other causes of pain, such as occult fractures or subtalar arthritis. Magnetic resonance imaging may demonstrate nonspecific inflammation in the sinus tarsi, sinus tarsi fat alterations, chronic synovitis and synovial thickening, interosseous talocalcaneal ligament tears, cervical ligament tears, or a ganglion cyst40. Nonoperative treatment is similar to that for chronic lateral ankle instability. Injections, diagnostic and therapeutic, have been reported to be successful in approximately two-thirds of patients. Open and arthroscopic debridement of the contents of the sinus tarsi have been described41.
Osteochondral lesions involving the talar dome were originally thought to be secondary to ischemia; however, most authors currently think that they are due to trauma. Various names have been used to describe osteochondral lesions involving the talar dome, including osteochondritis dissecans, transchondral fracture, and osteochondral fracture. The talus has a decreased capacity for repair because of its limited blood supply, and the sequelae of osteochondral talar injury include joint degeneration and limited range of motion at the ankle.
Osteochondral lesions of the talus are frequently associated with more obvious traumatic injuries of the foot and ankle. Diagnosis of talar dome injury is often delayed. In some series, as many as 28% of osteochondral injuries of the talus were associated with other fractures involving the foot and ankle, most frequently the malleoli. Osteochondral lesions of the talus can occur as the result of a single traumatic episode or as the result of repetitive microtrauma, such as recurrent lateral ankle sprains.
Several schemes exist for the classification of osteochondral lesions of the talus on the basis of radiographs, computed tomography, magnetic resonance imaging, and arthroscopic findings42-44 (Table II). In patients with chronic ankle pain and a history of injury, clinical suspicion for an osteochondral lesion should be high. Radiographic evaluation is the initial imaging modality of choice; however, false-negative radiographs are not uncommon. Any osteochondral lesions that are identified with use of standard radiographs should be further evaluated with use of computed tomography, which provides a more complete delineation of the integrity of the subchondral bone. Magnetic resonance imaging is a useful adjunct for patients without any radiographic abnormality (Fig. 10). The superiority of magnetic resonance imaging for visualizing the surface of the articular cartilage and edema of the talus makes it the study of choice for the evaluation of suspected stage-I osteochondral lesions. The treatment of osteochondral lesions of the talus is based on the stage of the lesion. Cast immobilization for twelve to sixteen weeks with progressive weight-bearing to full weight-bearing at the end of immobilization is recommended for stage-I or II lesions. Patients with a stage-I or II lesion that remains painful for one year and those with a stage-III or IV lesion are candidates for surgery. Surgery can involve debridement and lavage, marrow-stimulating procedures, or restorative techniques. Arthroscopic debridement of the lesion and techniques that induce healing by stimulation of underlying marrow are successful in approximately 80% of patients43. Lesions measuring >1.5 cm2 do not respond well to these techniques. Restoration of the articular surface with osteochondral autografts has been successful for the treatment of lesions measuring <1 cm2 (Fig. 11)45. The major disadvantage of using an autograft is donor-site morbidity. Osteochondral allografts have been utilized for larger lesions; however, the long-term outcomes remain uncertain. Autologous chondrocyte implantation is a promising technique and has been used for patients who remain symptomatic after previous surgery46. The location of the lesion dictates the appropriate surgical approach and may require the use of osteotomies in order to optimize visualization. Indications for performing these procedures include a lesion with a diameter of >1 cm and a depth of at least 5 mm that cannot be repaired primarily. Autologous chondrocyte implantation into the talus has demonstrated some encouraging results in preliminary studies46.
Anterior ankle impingement can be due to soft-tissue or osseous lesions and typically is related to the superior portion of the anterior talofibular ligament or the distal portion of the anteroinferior tibiofibular ligament47. Redundant injured synovial or ligamentous tissue causes joint irritation. Repetitive exaggerated ankle dorsiflexion can lead to soft-tissue impingement, and soccer and basketball players are particularly prone to developing anterior tibiotalar bone spurs, which result in osseous impingement. Patients complain of anterior pain, stiffness, and swelling. Walking uphill is painful, whereas downhill walking is more comfortable. The hallmark of the physical examination is painful limitation of passive dorsiflexion and anterior ankle tenderness. The osseous bone spurs are seen on a lateral ankle radiograph, whereas magnetic resonance imaging is useful for seeing the soft-tissue lesions (Fig. 12). Nonoperative treatment includes rest, ice, anti-inflammatory medications, and physiotherapy. An intra-articular injection of a local anesthetic and steroid can be diagnostic and therapeutic. Patients often experience symptomatic relief with a small heel lift. Patients who fail to respond to conservative treatment benefit from arthroscopic debridement of soft-tissue lesions. Osseous lesions can be treated with arthroscopic or open methods, depending on the size and location of the lesion as well as the skill of the surgeon48.
Nerve Entrapment at the Level of the Ankle
The deep peroneal nerve and the anterior tibial artery are deep to the extensor hallucis longus and the extensor digitorum brevis. Approximately 1 cm proximal to the ankle joint, the nerve branches into a medial motor branch and a lateral sensory branch. The nerve can be compressed by the superior extensor retinaculum, the inferior extensor retinaculum, and the extensor hallucis brevis muscle49. Proximal compression by the superior retinaculum causes sensory changes and clawing of the toes. Distal compression by the inferior retinaculum or the extensor hallucis brevis muscle causes isolated sensory deficits.
Patients complain of burning anterior ankle and dorsal foot pain and may have a history of trauma or recurrent ankle sprains. Paresthesias in the first dorsal web space may be present. An injection of local anesthetic 1 cm proximal to the site of nerve compression should improve or alleviate symptoms. The site of nerve compression is determined by the presence of a positive Tinel sign, which reproduces the symptoms and distal paresthesias in the distribution of the nerve. If the injection does not relieve the symptoms, nerve compression is unlikely. Radiographs may demonstrate osteophytes as the source of entrapment, and space-occupying lesions such as ganglion cysts can be seen best on magnetic resonance imaging. Electrodiagnostic testing can determine the location of the lesion, including compression more proximally in the leg or in the lumbar spine.
The superficial peroneal nerve is a pure sensory nerve that becomes superficial in the distal third of the leg, approximately 10 cm proximal to the tip of the fibula. It then continues in the subcutaneous layer and branches into the medial dorsal cutaneous nerve and the intermediate dorsal cutaneous nerve, 6 to 7 cm proximal to the malleolus. Entrapment typically occurs where the nerve becomes subcutaneous, and symptoms rarely radiate proximal to the site of nerve compression. Nerve injury or entrapment can occur in patients with inversion injury as the nerve gets tethered where its exits the fascia50. Iatrogenic entrapment can occur after open reduction and internal fixation of fibular fractures and placement of lateral ankle arthroscopic portals51,52. Occasionally, space-occupying masses such as ganglion cysts or fracture callus will entrap the nerve. Patients present with pain radiating across the ankle and the dorsum of the foot. Tenderness or a Tinel sign is typically present 10 cm proximal to the tip of the distal part of the fibula. Pain is reproduced with several provocative maneuvers, such as foot plantar flexion and inversion, which places the nerve under compression and tightens the fascia. When the foot is dorsiflexed and everted, the nerve is under tension and becomes more sensitive to percussion. The motor and reflex examination reveals normal findings. Ankle stability should be assessed, as instability can place intermittent tension on the superficial peroneal nerve. Proximal causes of nerve irritation, including compression at the fibular neck and lumbar pathology, must be considered. The differential diagnosis should also include exertional compartment syndrome, especially if the patient describes exacerbation of symptoms with activity. A diagnostic injection of local anesthetic just proximal to the site of entrapment helps to confirm the diagnosis.
The lateral sural nerve originates from the common peroneal branch of the sciatic nerve. It innervates the lateral part of the proximal third of the leg. The medial sural nerve originates from the posterior tibial branch of the sciatic nerve and is subfascial. It innervates the posterolateral part of the proximal half of the calf. These two branches meet in the lower third of the calf to form the common sural nerve, which runs along the lateral border of the Achilles tendon, next to the short saphenous vein. It then travels subcutaneously, inferior to the peroneal tendon sheath at the ankle, toward the fifth metatarsal tuberosity, and provides sensation to the lateral aspect of the fifth toe and the fourth web space. Entrapment can occur after closed and operative treatment of fractures, which cause subsequent scarring in the region of the fifth metatarsal or ankle. Space-occupying lesions can also lead to compression of the nerve.
Patients present with paresthesias in the cutaneous distribution of the sural nerve and have a history of trauma or recurrent ankle sprains. Examination of the entire course of the nerve is necessary, and local tenderness with percussion can identify any areas of impingement. More proximal causes of nerve irritation should be considered. Specifically, S1 nerve-root irritation can cause paresthesias in the lateral aspect of the foot. However, if the S1 nerve root is involved, gastrocnemius-soleus weakness and abnormal ankle reflex are typical accompanying findings. In patients with isolated sural nerve entrapment, neither of these findings should be seen.
Entrapment of the saphenous nerve over the medial aspect of the anterior part of the ankle is another source of chronic pain. Patients complain of numbness along the medial border of the foot and pain exacerbated by tight-fitting shoes, particularly with ankle straps. Iatrogenic injury can occur during placement of a medial arthroscopic portal or during open reduction and internal fixation of a medial malleolar fracture.
Radiographs reveal normal findings. Magnetic resonance imaging is useful for identifying a space-occupying lesion. Electromyography and nerve conduction velocity studies help to assess for a more proximal cause of nerve compression.
Nonoperative treatment of all nerve entrapments involves the avoidance of tight-fitting shoes, the administration of anti-inflammatory medications, and physical therapy modalities to help to modulate the pain. Supportive ankle bracing and a lateral heel wedge help to prevent inversion of the ankle. Occasionally, medications such as gabapentin or tricyclic antidepressants help to alleviate symptoms.
Surgery, consisting of neurolysis, removal of osteophytes, and excision of any soft-tissue masses, is considered if nonoperative treatment fails. The decompression should start proximally at a point where the normal anatomy of the nerve can be visualized. The release should be carried out distal to the site of the positive Tinel sign. Meticulous hemostasis should be achieved prior to closure to prevent hematoma formation and additional nerve entrapment. In recurrent cases, excision of the nerve and burying of the stump can help. The saphenous, lateral sural, medial sural, and superficial peroneal nerves do not provide sensation to the plantar aspect of the foot and can be sacrificed if necessary.
A full discourse on the diagnosis and treatment of complex regional pain syndrome is beyond the scope of this instructional course lecture. This diagnosis should be considered for patients with chronic ankle pain that is not consistent with the conditions described. Type-I complex regional pain syndrome develops after a noxious stimulating event such as a crush injury, fracture, or sprain. The symptoms typically do not follow the distribution of a single, specific nerve. Type-II complex regional pain syndrome develops after injury to a specific nerve, such as laceration. Complex regional pain syndrome is more common in females and patients who smoke, and it has been reported to occur in 1% of fractures and up to 5% of patients with peripheral nerve injuries. The stages of complex regional pain syndrome include an acute phase (zero to three months), a dystrophic phase (three to six months), and an atrophic stage. Early recognition and treatment are paramount in order to achieve successful treatment. Burning pain, cold intolerance, temperature changes, swelling, allodynia (pain from a stimulus that does not normally cause pain), and dysesthesias (unpleasant abnormal sensations) are common. Characteristic physical findings include discoloration of the skin (redness, cyanosis, mottling), altered skin temperature (hot or cold), edema, decreased range of motion, atrophy (late), abnormal sweating patterns, loss of hair, and abnormal nail growth. The kick-off sign has recently been described53. Thirty-nine patients with complex regional pain syndrome, while sitting on the examination table, held the affected extremity with the knee extended against gravity. When the leg was pushed back to a relaxed and suspended position, the thirty-nine patients eventually involuntarily resumed the extended position. This position in which the patients held the legs was termed the "kick-off" position sign. Synovial thickening and equinovarus contractures characterize the late stage of complex regional pain syndrome. Osteopenia secondary to disuse and increased blood flow is a common radiographic finding. Diffuse uptake on the delayed images of a technetium bone scan is characteristically seen, with a specificity of 75% to 98% for the diagnosis of complex regional pain syndrome54. A referral to a comprehensive pain-management team that uses a combination of medication and physical therapy is recommended. Recalcitrant cases may benefit from sympathetic blockade and spinal cord stimulation. In patients with complex regional pain syndrome who require surgery, preoperative consultation with a pain service is recommended. These patients may benefit from regional anesthesia with indwelling catheters to minimize postoperative pain.
Chronic ankle pain is a common presenting complaint in orthopaedic surgery. A careful history and physical examination are paramount in order to arrive at the correct diagnosis. Ancillary imaging testing may help confirm the diagnosis. The clinician should recognize that both intra-articular and extra-articular pain generators can be responsible for the subjective complaints.
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