Porter & Schon: Baxter's The Foot and Ankle in Sport, 2nd ed.

Section 2 - Sport Syndromes

Chapter 6 - Injuries to the tibialis anterior, peroneal tendons, and long flexors of the toes

Vincent James Sammarco,G. James Sammarco

  

 

Introduction

  

 

Flexor hallucis longus

  

 

Flexor digitorum longus

  

 

Tibialis anterior

  

 

Peroneal tendons

  

 

References

Introduction

The extrinsic muscles of the anterior, lateral, and deep posterior compartments of the leg play an important part in both static and dynamic body support. Actions of these muscles serve to stabilize the body during stance, as well as provide power and stability during all lower-extremity motion. They are of particular importance because they provide balance and power during push-off, as well as decelerating the body while stopping, turning, and cutting. They also stabilize the foot on both even and uneven surfaces. The muscles of the anterior compartment, the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius, are important because of their location, functioning to dorsiflex the ankle and toes and to control the forefoot during the swing phase of gait. Injuries to nerve, muscle, or tendon may lead to pain, weakness, and dropfoot. Muscles of the lateral compartment include the peroneus longus, an important lateral foot stabilizer that also controls pressure beneath the first metatarsal head, which is so important in jumping activities, cutting, and turning as in skiing. The peroneus brevis is the strongest abductor of the foot, and both peroneal muscles act as accessory flexors of the ankle and foot. Muscles of the deep posterior compartment of the leg, the posterior tibialis, flexor digitorum longus, and flexor hallucis longus, likewise serve important functions by stabilizing the longitudinal arch of the foot. They also provide additional power during running, cutting, turning, and stopping. The flexor digitorum longus and flexor hallucis longus are of particular importance because of their attachments to other muscles and tendons within the foot itself. Injury to these muscles and tendons, whether partial or complete, can compromise a sports career. This is particularly true with respect to the flexor hallucis longus in the classical ballet dancer. Injury to the nerves that innervate the deep flexors of the leg result in weak push-off and decreased stability. This chapter deals with injuries to muscles and tendons in the anterior compartment, the tibialis anterior, extensor hallucis, and extensor digitorum longus, as well as those in the lateral compartment, the peroneus brevis, and peroneus longus, and the deep posterior compartment, the flexor hallucis longus and flexor digitorum longus. Conditions of the tibialis posterior and Achilles tendons are presented elsewhere. Early diagnosis is emphasized. Special diagnostic studies, including magnetic resonance imaging (MRI) computed tomography (CT), and electrodiagnostic testing, are useful, special diagnostic studies that help to confirm a diagnosis. Surgical intervention often is necessary to correct these problems, and rehabilitation ultimately is required to return the athlete to preinjury status.

 

Flexor hallucis longus

The flexor hallucis longus muscle arises in the deep posterior compartment of the calf. From its attachment on the interosseus membrane, lower two thirds of the fibula and intermuscular septa, it passes from the deep compartment into its own tunnel at the posterior aspect of the talus, lateral to the flexor digitorum longus tendon and deep to the posterior tibial artery and nerve. It then passes beneath the sustentaculum tali of the calcaneus in a fibro-osseous tunnel from the posterior talus to the master knot of Henry, where it lies beneath the flexor digitorum longus tendon. Here it gives a slip of tendon that inserts on the medial fibers of the flexor digitorum longus tendon. It then passes beneath the first metatarsal between the sesamoids to insert onto the distal phalanx of the hallux. A sesamoid may be present within the tendon at the metatarsophalangeal joint. Like all polyarthrodial muscles, the extrinsic muscles of the foot in the anterior, lateral, and posterior compartments of the leg have a complex function. The flexor hallucis longus muscle functions as a flexor of the distal and proximal phalanges of the hallux; aids in flexion of the midtarsal joints and supination of the foot, as well as plantarflexion of the ankle; and also supports the longitudinal arch during ambulation, particularly in the latter part of the stance phase of gait.

Tendinitis

Acute tendinitis occurs most commonly at the posterior ankle.[1] This injury is common in dancers and has been termed “dancer's tendinitis.” [0020] [0030] [0040] It is less common than Achilles tendinitis and occurs in inexperienced dancers and in athletes who are not conditioned. Tendinitis also develops when athletes change sports without proper conditioning for the new activity. Symptoms begin within a few days following a change of technique or at the beginning of the season. When the dancer rises on the ball of the foot, pain occurs in the posterior aspect of the ankle. The pain initially is vague and occurs with flexion of the ankle and foot. Passive dorsiflexion of the ankle with deep palpation 1cm anterior and medial to the Achilles tendon at the ankle joint elicits tenderness and crepitus.[2]

Radiographs exclude bony abnormalities such as os trigonum and posterior talar fracture. Treatment includes improving dance technique or reducing running in the athlete. Noninflammatory medication is prescribed, and a program of flexibility and power-building exercises is instituted.

Chronic tendinitis produces symptoms of tenderness in the same region with active flexion and also on deep palpation of the tendon during flexion and extension.[5] Crepitus is present over the tendon. Radiographs differentiate this from os trigonum syndrome and arthritis of the subtalar joint. Symptoms of os trigonum syndrome include pain in the posterior ankle when the patient actively rises on the ball of the foot. The provocative test is reproduction of pain with passive forced plantarflexion of the foot and ankle. The differential diagnosis includes pseudocyst of the flexor hallucis longus tendon, symptomatic subtalar cyst, posterior impingement syndrome, and insertional Achilles tendinitis. MRI helps to rule out a mass but may show a “dumbbell”-shaped configuration of fluid in the tendon sheath around the ankle, narrowing beneath the sustentaculum and enlarged distal to the sustentaculum tali ( Fig. 6-1 ).

 
 

Figure 6-1  Magnetic resonance imaging (T2-weighted sagittal cut) of a patient with symptomatic tendinitis of the flexor hallucis longus tendon. There is significant swelling of the tendon sheath (arrows) starting at the musculotendinous junction above the ankle joint, narrowing as the tendon sheath is compressed beneath the sustentaculum, and then ballooning out again as the tendon passes into the midfoot, “dumbbell sign.”

 

 

In the well-conditioned athlete, the muscles of the calf are hypertrophied. Because of the low insertion of the fibers of the flexor hallucis longus muscle onto its tendon, dorsiflexion of the ankle draws the enlarged lower muscle fibers into the fibro-osseous tunnel through which the tendon passes behind the ankle. This causes inflammation at the musculotendinous junction, the stopper bottle sign, and symptoms of posterior ankle pain. Treatment includes anti-inflammatory medication and a flexibility program including gentle stretching.[6] If symptoms do not abate, surgical intervention with release of the pulley and tenosynovectomy may be necessary. In cases in which significant hypertrophy of the muscle is present, a myoplasty, excision of impinging muscle fibers, may be necessary. The tendon is debrided, and fibrosed muscle fibers that attach on the tendon just above the pulley also are excised to permit smooth passage of the tendon in the tunnel throughout its full excursion.

Other areas of chronic tenosynovitis of the tendon include the midfoot and metatarsophalangeal joint.[7] Symptoms of pain with tenderness usually occur in the specific area of stenosis. To relieve symptoms, the pulleys in either of these areas are released surgically, and a tenosynovectomy is performed. Injections of corticosteroids should be avoided because inadvertent injection directly into the tendon may cause it to rupture.[2]

   Pearl

Flexor Hallucis Longus Tendinitis

(1) Crepitus on deep palpation of the tendon behind the medial malleolus during active plantarflexion and dorsiflexion of the ankle and foot. (2) Pain posterior to the ankle when rising on toes or on dorsiflexion of the ankle against resistance. (3) No pain with passive plantarflexion of the ankle.

Trigger toe

Partial rupture of the flexor hallucis longus tendon consists of a longitudinal tear in the tendon and a fusiform thickening at the distal end of the tendon tear beneath the sustentaculum tali. [0040] [0080] [0090]

Occasionally the tendon may be trapped in a fracture. [0100] [0110] [0120] When the nodule on the tendon lies distal to the sustentaculum, the narrow tunnel through which the tendon passes restricts motion in a manner similar to that of the flexor pulley of trigger finger. The result is triggering of the great toe. The condition occurs commonly in ballet dancers and is more common in females in their second to fourth decades. As the dancer begins to rise (relevé) on the ball of the foot (demi-pointe), the great toe dorsiflexes and remains in contact with the floor ( Fig. 6-2 : photos of toe flexed and extended). The flexor hallucis longus contracts, but the tendon excursion is limited by the nodule's position at the distal end of the tarsal canal. Once the dancer has achieved demi-pointe, pain may occur in the posterior ankle. As the dancer further rises onto her toes (sur les pointes), the great toe plantarflexes from 90 degrees dorsiflexion to neutral position to support the body. The pull of the flexor hallucis longus muscle is strong enough to force the nodule proximally through the stenotic tunnel, triggering the great toe into flexion. While the dancer is en pointe, the nodule lies proximal to the tunnel. As the dancer returns from pointe to flat foot, the tendon is passively pulled distal, and the fuseform thickening in the tendon snaps forward distally through the stenotic tunnel again. As the great toe snaps straight, it produces pain and may alter the dancer's appearance in the dance step. The longitudinal tendon tear usually is single, but it may be multiple, and measures from 3 to 5cm in length.

 
 

Figure 6-2  Left and right, Clinical appearance of the trigger toe sign. Left, With ankle and foot actively flexed, the interphalangeal joint of the hallux snaps into flexion. Right, When the ankle and foot are actively extended, the interphalangeal joint of the Hallux remains locked in flexion (left) or snaps straight.

 

 

Radiographs exclude bony abnormalities. MRI reveals a tear with degeneration of the tendon. A pseudocyst of the tendon may be present.[13] The differential diagnosis includes a posterior impingement syndrome of the ankle, os trigonum syndrome, retrocalcaneal bursitis, and Achilles tendinitis. Conservative therapy consisting of gentle stretching exercises, and anti-inflammatory medication to reduce swelling may be effective. Patients with compromised performance who fail to respond to conservative measures are surgical candidates.

Surgical approach consists of a 5-cm incision on the posteromedial aspect of the ankle. The posterior tibial neurovascular structures are retracted medially. The tendon is delivered through the wound with a tendon hook, and the pulley is released at its lateral attachment to the talus and calcaneus distally. The nodular swelling present at the distal end of the tear is trimmed to conform to the uniform diameter of the tendon throughout its length ( Fig. 6-3 ). The tear is repaired with a running 4-0 braided nonabsorbable suture. The tendon must be trimmed to slide easily in the canal throughout full flexion and extension. Following closure, a splint is applied until two weeks postoperatively. A gentle active range of motion (ROM) program is begun 3 weeks following surgery. The foot and ankle are protected for 3 additional weeks in a splint, and the patient then is transitioned to an ankle stirrup brace. Dancing en pointe may take up to 4 months, whereas return to full athletic routine usually occurs by 3 months. Full recovery may take 6 months.

 
 

Figure 6-3  Left, Operative photograph of a ballet dancer with trigger toe. The flexor hallucis longus tendon is exposed and delivered into the wound. A longitudinal tear is visible distally (at the right). The thickening of the tendon seen in the region of the tear is causing triggering as the ankle and foot are flexed and extended. Right, The tendon is repaired using a 4‐0 nonabsorbable Dacron running suture.

 

 

   Pearl

Trigger Toe

(1) A snap noted on palpation of the tendon behind the medial malleolus with active flexion, and extension of the ankle and hallux with patient in sitting position. (2) Toe snaps backward and forward with flexion and extension of the ankle and hallux. (3) Dancer complains of pain in the posterior ankle region and a snapping sensation of the great toe when rising up (relevé) or landing from a leap. (4) Occurs most commonly in female, classical ballet dancers who dance on their pointes.

Case Study 1  

A 28-year-old, female, classical ballet dancer noticed increasing pain in her posterior ankle following dance class for 2 months. She then developed a snapping of her great toe when rising from thedemi-pointe position (on the ball of the foot) to en pointe position (on her toes). A triggering sensation was felt behind the ankle. When descending from en pointe position to a flat foot, the great toe snapped again as the toe dorsiflexed. Pain was felt behind the ankle. The snapping of the foot was visible and became unaesthetic as well as disabling. Physical examination revealed a palpable popping sensation felt posteriorly at the ankle as the foot, ankle, and great toe were moved repeatedly from dorsiflexion to plantarflexion. At surgery, a 5-cm incision was made at the posteromedial aspect of the ankle, and the flexor hallucis longus muscle and tendon were identified. Traction with a tendon hook revealed a 5-cm longitudinal tear in the tendon beginning at the musculotendinous junction and extending distally (see Fig. 6-3, A and B ). The fibro-osseous canal through which the tendon passed was noted to be tight. A fusiform thickening of the tendon was present at the distal end of the tear. The thickened tendon was trimmed sharply so that the width of the tendon was uniform throughout, and the tendon sheath was carefully released, allowing the tendon to slide its length unimpeded through a full ROM of the ankle and foot. The tear was repaired with 4-0 braided Ethibond suture. A splint was applied for 3 weeks, followed by gentle active ROM and a supervised physical therapy program. Three months later, the dancer was able to resume dance. She returned to dancing sur les pointes 4 months after surgery. Six months following surgery, she was asymptomatic.

Complete rupture

Complete rupture of the flexor hallucis longus is uncommon but can occur in several areas. Iatrogenic surgical laceration has been described.[14] Avulsion fracture from the hallux distal phalanx is caused by great resistance to flexion on the distal phalanx as the foot is forcibly plantarflexed. If the avulsed tendon contains a fragment of bone, anatomic open reduction is recommended. Tear of the tendon at its insertion without a bony fragment permits the tendon to retract proximally, allowing the great toe to dorsiflex. Surgical repair is performed through a medial incision along the proximal phalanx of the hallux above the neurocirculatory bundle. The tendon sheath is exposed at or just proximal to the metatarsophalangeal joint with a direct repair of the tendon to the distal phalanx.

Tendon rupture also can result following corticosteroid injection into the tendon at the metatarsophalangeal joint ( Fig. 6-4 ). Symptoms include pain, sudden loss of active flexion at the interphalangeal joint, and weakness in flexion at the metatarsophalangeal joint. This is accompanied by a dramatic change in athletic performance. Chronic, complete, spontaneous rupture also has been reported in basketball players and aerobic walkers at the sustentaculum tali. Symptoms occur over a 6-week period.

 
 

Figure 6-4  An operative photograph taken through a medial incision at the level of the metatarsophalangeal joint. The two ends of the ruptured flexor hallucis longus tendon are visible held by two Adson forceps. The athlete received several injections of corticosteroids beneath the first metatarsal head for “metatarsalgia.” Following debridement the tendon was reconstructed using a plantaris tendon graft.

 

 

Treatment in the high-performance athlete consists of surgical repair. If the tendon has retracted proximally and cannot be reapproximated, a tendon graft using plantaris tendon may be necessary to reestablish continuity. Reconstruction returns strength to flexion of the metatarsophalangeal joint, although a flexion lag at the interphalangeal joint commonly results. [0020] [0040]

Complete rupture of the flexor hallucis longus tendon within the tarsal tunnel and beneath the sustentaculum tali may be treated by transfer of the flexor digitorum longus to the stump of the flexor hallucis longus. [0150] [0160] Resection of the degenerated portion of the flexor hallucis longus tendon also is performed. The flexor digitorum longus tendon lies adjacent to the flexor hallucis longus beneath the sustentaculum tali. Suturing of the flexor hallucis longus tendon stump to the flexor digitorum longus tendon proximal to the master knot of Henry permits good function, if not complete return of strength.

An alternative method of treatment for complete rupture is to use a tendon graft. The graft is sutured proximally and distally following resection of the diseased portion of the flexor hallucis longus tendon. The foot and ankle are immobilized for 6 weeks.[17] Both methods provide good function of the flexor hallucis longus but do not necessarily return normal flexion to the hallux interphalangeal joint. In some patients with low demands on the foot, complaints of a hyperextended distal phalanx rubbing on top of the shoe persist. Arthrodesis of the hallux interphalangeal joint in 20 degrees of flexion provides relief of symptoms without altering performance.

Tumor masses

The most common mass of the flexor hallucis longus tendon is a pseudocyst located at the posterior ankle. It may extend distally into the foot along the tendon sheath and is associated with degeneration or tears of the tendon. Symptoms of fullness and achiness along with decreased performance are common. Symptoms of tarsal tunnel syndrome also have been reported. An MRI reveals a cystic mass, often bilobed, with one end at the posterior ankle and the other end distal to the tarsal tunnel in the midfoot ( Fig. 6-1 ). If symptoms warrant, excision of the cyst and tenosynovectomy are performed through a posteromedial ankle incision. Associated tendon tears are repaired as described previously. Postoperatively, the ankle is protected in a splint for 3 weeks, followed by initiation of a flexibility and power-building program. Return to play is permitted when postoperative pain subsides and foot function approaches the level of the normal, contralateral side.

 

Flexor Digitorum Longus

Isolated injury to the flexor digitorum longus tendon is uncommon. This muscle takes origin deep in the posterior calf on the tibia and distal one-third of the fibula and passes medial to the flexor hallucis longus tendon posterior to the ankle in its own tunnel. It lies close to the tibialis posterior tendon at the sustentaculum tali, then crosses superficially to the flexor hallucis longus at the master knot of Henry distally. The tendon receives the insertion of the quadratus plantae muscle as it divides into four slips, one to each of the toes. A slip of the flexor hallucis longus tendon also inserts on its medial fibers. Each of the four lumbricals originates on the individual tendon slips. The lumbricals pass forward to insert on the extensor hoods of their respective toes. The tendon then passes through the distal split in the flexor digitorum brevis of each of the toes to insert on its respective distal phalanx. This muscle functions primarily to flex the toes. Accessory functions include foot and ankle flexion, as well as a stabilization of the foot during the stance phase of gait.

Tendinitis

Tendinitis often is associated with tendinitis of associated flexor tendons, including the flexor hallucis longus and posterior tibialis. Isolated lesions of the tendon are rare and are associated with penetrating injuries, most commonly in the forefoot. Generalized disease such as gout can result in tophus deposition within the tendon at the ankle. Small longitudinal rents have been noted. Symptoms consist of tenderness deep beneath the medial malleolus of the ankle in the region of the sustentaculum tali. An MRI reveals fluid in the sheath about the tendon. Treatment primarily is nonoperative and consists of anti-inflammatory medication and stretching exercises. In recalcitrant cases that compromise athletic performance, surgical debridement and repair are recommended.

 

Tibialis Anterior

Anatomy

The tibialis anterior muscle lies in the anterior compartment of the leg and originates from the proximal lateral tibial metaphysis and proximal two thirds of the tibial shaft and interosseous membrane. The tendon twists and crosses the extensor hallucis longus tendon at the level of the ankle at which it enters a synovial tendon sheath. The tendon courses dorsomedially across the foot and rotates 90 degrees from the myotendinous junction to the broad insertion.[18] The majority of tendons insert at the plantar medial border of the first metatarsal and medial cuneiform. Approximately 10% of tendons have variations to the insertion, the most common being a bifid insertion to the cuneiform and first metatarsal, or insertions reaching proximally or distally along the medial column of the foot. [0190] [0200]Accessory tibialis anterior tendons have been reported, but are rare and have not been reported to cause pathology.

The tibialis anterior is bounded proximally to the ankle by the superior extensor retinaculum, and variably may enter a synovial tendon sheath within the retinacular fibers at this level. More distally, the tibialis anterior tendon predictably enters a synovial sheath as it passes into the inferior extensor retinaculum complex. An early study using a modified Spaltehoz technique failed to reveal any zones of hypovascularity within the tendon,[21] but a later study using immunohistochemical methods suggests that such a zone exists within the inferior retinacular system where tendon rupture is most likely to occur. [0220] [0230]

The tibialis anterior acts primarily in dorsiflexion of the ankle and also as a strong inverter of the subtalar joint. It is active during the first phase of gait and contracts eccentrically from heel strike to toe-off. Its primary function is to decelerate the foot during the initial plantarflexion that occurs immediately following heel strike, and to clear the foot during toe-off. Absence of this muscle in active individuals is poorly tolerated, causing a slapping of the foot during heel strike and a steppage gait, with difficulty clearing the foot during swing.

Tibialis anterior tendinitis

Tendinitis of the tibialis anterior is an uncommon entity that may be caused by overuse of the tendon or poor conditioning. It is seen most commonly in runners and usually accompanies a rapid increase in mileage or change in training techniques. Both uphill and downhill running significantly increase demands on the tibialis anterior, as does the practice of running stairs. A tight gastrocsoleus muscle also contributes to increased strain in the myotendinous unit. Symptoms include anterior ankle pain with activity that often continues for a few hours after exercise. Other diagnoses that must be considered are exertional compartment syndrome, tibial stress fracture, intra-articular ankle pathology, and tibial periostitis.

The diagnosis is readily appreciated on physical examination. Physical findings include pain with palpation of the tendon and pain with resisted dorsiflexion. The tendon may be tender, particularly as it passes under the superior extensor retinaculum. Palpable synovitis, swelling, and crepitance are variably present. In cases in which weakness in dorsiflexion is present, or when swelling and tenderness exist more distally within the inferior extensor retinaculum or at the tendon insertion, a more aggressive workup is required to rule out intrasubstance degeneration or impending rupture. In these instances, MRI or ultrasound are useful tools for evaluating tendon continuity and tendonosis [0240] [0250] [0260] ( Fig. 6-5 ).

 

 

Figure 6-5  Magnetic resonance imaging demonstrating distal avulsion of tibialis anterior tendon. (A) The tendon usually retracts proximally to the level of the inferior extensor retinaculum. (B) Axial cuts demonstrate intrasubstance degeneration of the tendon.

 

 

In younger, athletic individuals, the area of inflammation usually involves the superior extensor retinaculum and responds well to conservative management. A three-phase rehabilitation protocol is used to resolve the tendinitis. [0060] [0270] Phase I involves limiting the extent of injury and diminishing inflammation. An oral anti-inflammatory is initiated, and the area may be iced and wrapped with an ACE bandage to diminish pain and swelling. Immobilization is rarely indicated, but discontinuation of the exacerbating activity is required for 10 to 14 days. Phase II is started after pain and swelling have diminished and involves guided rehabilitation. Equinus contracture must be addressed with frequent stretching exercises. Resistive exercises with elastic tubing can isolate the tibialis anterior for pliability and strengthening. Therapeutic modalities also can be helpful because of the subcutaneous positioning of the tendon. Phase III involves return to activity. Running should be initiated on a flat surface such as a track or treadmill, with gradual advance of mileage and hilly terrain as tolerated. We avoid the use of steroid injections around the tendon sheath because of the risk of rupture. [0280] [0290] Rarely, proximal degeneration of the tendon occurs that does not resolve with appropriate rehabilitation techniques. In these recalcitrant cases, surgical exploration and tenosynovectomy may be required to resolve symptoms. Pain and swelling of the tendon at or near its insertion represents a different disease process and may represent significant degeneration and impending rupture, as discussed in the next section.

   Pearl

Tibialis Anterior Tendinitis

Tenderness and often crepitus on palpation over the tendon at the superior extensor retinaculum, a “leather bottle sign.”

Tibialis anterior rupture and laceration

The tibialis anterior tendon is vulnerable to laceration because of its subcutaneous position over the anterior aspect of the foot and ankle.[30] The tendon may be cut in a “boot top” laceration when a sharp object such as a skate, ski edge, or sharp cleat cuts the skin and underlying structures. [0310] [0320] Dropping a sharp object onto the dorsum of the foot also can result in laceration. A high index of suspicion is required to make the diagnosis because these lacerations typically look benign, with minimal bleeding or pain. Dorsiflexion of the ankle will be weakened and lack full extension but will be intact because of the secondary action of the extensor hallucis longus (EHL) and extensor digitorum longus (EDL). Routine exploration of all dorsal foot and ankle lacerations should be performed if there is suspicion of partial or complete tendon laceration. These structures heal well and have minimal dysfunction when repaired acutely. Traumatic rupture may occur because of higher energy blunt trauma and is associated with anterior compartment syndrome. [0330] [0340] [0350] [0360] [0370] [0380]

Spontaneous rupture of the tendon at or near its insertion is the more common presentation of tibialis anterior deficiency. It typically occurs in middle-aged athletes and often accompanies other comorbid conditions, such as diabetes, inflammatory arthritis, gout, obesity, and steroid use. [0240] [0390] [0400] [0410] [0420] The tendon in this location may demonstrate a zone of relative hypovascularity near its insertion that may predispose it to tendinosis and rupture in this area. A prodrome of pain and swelling along the medial arch variably precedes rupture. Pain and tenderness at the insertion of the tibialis anterior tendon should be treated as an impending rupture. The patient is immobilized in an ROM boot unlocked in dorsiflexion but locked at 0 degrees of plantarflexion. This allows active tendon remodeling and motion while protecting the tendon from further degeneration. Physical therapy is initiated with the goals of decreasing inflammation and encouraging tendon remodeling through therapeutic exercises and modalities. The ROM boot is unlocked gradually to allow more plantarflexion as symptoms permit. The boot may be discontinued after 4 to 6 weeks. In recalcitrant cases or elderly individuals, a hinged ankle foot orthosis (AFO) with a plantarflexion stop may be necessary to control symptoms and prevent tendon rupture.

Rupture of the tibialis anterior in the middle-aged athlete often is the result of a minor trauma. The mechanism of injury involves a strong contraction of the muscle with the ankle in plantarflexion. The rupture may be painless, but dysfunction is noted immediately by the patient, who develops a slapping gait and experiences tripping on his or her toes. Medical attention may not be sought for weeks, and the diagnosis often is missed at the initial evaluation. [0050] [0430] The diagnosis can mimic peroneal nerve or L5 nerve root dysfunction. [0400] [0440] [0450] Diagnosis may be made by physical examination and presents as the classic triad of ankle dorsiflexion by hyperextension of the toes, a slapping gait, and a mass over the anterior ankle (pseudotumor) ( Fig. 6-6 ). Weakness in ankle dorsiflexion occurs because the tibialis anterior function is lost, but ankle dorsiflexion is still present because of the secondary function of the digital extensors. The patient complains of a slapping gait and has notable difficulty clearing his or her toes during swing phase. The mass over the anterior ankle, or pseudotumor, is the avulsed tibialis anterior tendon stump, which becomes entrapped at the inferior border of the superior extensor retinaculum.

 

 

Figure 6-6  Physical findings with tibialis anterior avulsion. (A) Absence of the usually pronounced tibialis anterior tendon is appreciated with compared active dorsiflexion of both ankles. (B) The affected ankle demonstrates a pseudotumor, which represents the proximally migrated tendon stump at the level of the ankle. Ankle dorsiflexion is incomplete and weak and occurs by hyperextension of the hallux and lesser digits.

 

 

Repair may be performed early or late, but the results of surgery are better if repair is performed within the first 3 to 6 weeks. Nonoperative treatment is acceptable for elderly, inactive patients, but primary or delayed repair is preferred for active individuals regardless of age. [0460] [0470] [0480] [0490]

   Pearl

Tibialis Anterior Rupture and Laceration

The triad of (1) pseudotumor anterior to the ankle; (2) loss of normal anatomy of the tibialis anterior tendon at the medial aspect of the ankle and foot when compared with the contralateral normal side; and (3) the use of accessory dorsiflexors, extensor digitorum longus, and extensor hallucis longus, to dorsiflex in the ankle. A less consistent finding is a slapping gait on the affected side.

Surgical treatment of tibialis anterior tendon rupture

In rupture of the tibialis anterior tendon, the ruptured tendon end often becomes caught at one of the extensor retinacular layers and easily may be palpated beneath the skin. The skin incision is made in line with the axis of the tendon from 1 to 2cm proximal to the palpable tendon end and carried distally to the terminal insertion at the plantar medial aspect of the first tarsometatarsal joint ( Fig. 6-7 ). Deeper dissection involves incision of the inferior extensor retinacular sheath for the tibialis anterior tendon, which usually is well defined. If the delay to surgery has been greater than 3 or 4 weeks, the tendon sheath will have filled with fibrous tissue, which must be excised sharply or removed with a small rongeur. In more acute cases, the sheath may be filled with fluid or hematoma. Atraumatic tendon rupture usually occurs by partial avulsion from the insertion and elongation of the degenerative tendon within the inferior extensor retinaculum. Twenty percent to 30% of the distal tendon stump may remain in continuity with the anatomic insertion and, if present, should be preserved for use in the repair. In exposing the proximal tendon stump, consideration should be given to the superior extensor retinaculum. When possible, the superior extensor retinaculum should be left intact during exposure of the tendon. The retinaculum at the level of the ankle often is thin, and repair can be difficult. Adhesions of the repaired tendon to the retinaculum are common and difficult to avoid because of the immobilization required in the postoperative protocol. In patients with comorbid conditions, the retinaculum may not be repairable, possibly leading to subcutaneous adhesions, bowstringing of the tendon, and wound healing problems. Often retraction of the tendon will stop at the inferior margin of the superior extensor retinaculum, either because the tendon end has formed a pseudotumor that becomes entrapped here or because some of the more proximally inserting fibers are still in continuity.




 

Figure 6-7  Surgical technique of repair of the tibialis anterior. (A) The tendon end usually can be teased distally without violating the inferior edge of the superior extensor retinaculum. Avoiding incision of the latter helps to prevent tendon adhesions and wound problems.(B) Once the tendon is pulled distally, it can be grasped with a Krackow-style suture and pulled to full excursion. Adhesions are disrupted to free the tendon by gently passing a freer around the tendon and muscle belly. (C) Repair is accomplished by pulling the tendon distally to its insertion. One or two suture anchors usually are needed to secure the repair.

 

 

If the tendon is at the inferior edge of the retinaculum or just under it, it can be grasped with an Alice clamp and teased distally, then secured with a Krackow-type, locking suture. Once the tendon has been secured, tension is applied, and a blunt elevator such as a small Cobb or Freer is passed proximally within the retinaculum and used to break up adhesions and gain excursion of the tendon. In delayed cases in which adequate tendon excursion cannot be gained by blunt dissection, or when more significant tendon retraction has occurred, the superior retinaculum must be divided for exposure.

Once the tendon end has been recovered and adequate excursion obtained, the tendon end must be debulked of fibrous material and degenerative tendon. Dissection of the scarred end usually will reveal intact tendon fibrils mixed with degenerative tendon and a mass of scar tissue. Degenerative tendon and scar tissue must be excised before repair, but maximal length of the tendon must be maintained.

Lacerated tendons may be sutured primarily if repaired within 2 or 3 days using a Krackow, Kessler, or Bunnell suturing method. In cases of delayed treatment, reattachment of the tendon to its anatomic insertion is ideal but not always possible. For cases in which the repair is under tension, we reconstruct the insertion of the tendon and augment fixation with one or more suture anchors. The distal tendon tract overlying the medial cuneiform is incised before repair, and a curette is used to roughen the underlying medial cuneiform to encourage attachment of the tendon. The tendon is pulled distally, using the previously applied suture, and is sewn to the distal tendon stump or attached to a suture anchor at the insertion. An anchor also is applied dorsally along the course of the tendon, usually in the medial cuneiform, and is used to suture the tendon tightly down to the curetted tendon tract. In cases in which repair is delayed more than 6 weeks, successful results can still be achieved but may require a free tendon graft, either as a reinforcement of the primary repair or as an intercalated graft if adequate length cannot be obtained.[50] The extensor hallucis longus tendon also may be used as a transfer in chronic cases because it is easily accessible.

After the tendon has been repaired or reconstructed, the overlying extensor retinaculum is repaired with absorbable suture. Meticulous repair of the retinaculum is important to prevent tendon adhesions, bowstringing or wound dehiscence. If 5 to 10 degrees of ankle dorsiflexion is not present with the patient under anesthetic, we perform a gastroc-soleus recession to lengthen the tendo-Achilles complex. Layered closure of the skin and subcutaneous tissue is performed, and the extremity is splinted in neutral dorsiflexion. This is changed to a shortleg walking cast at 10 days. Cast immobilization is discontinued at 3 to 4 weeks, depending on the quality of the tendon repair, at which time an ROM boot is applied. This device is left unlocked in dorsiflexion and locked to prevent plantarflexion beyond 0 degrees, thereby allowing active motion of the tendon during walking but protecting the repair. Physical therapy is initiated after casting is discontinued and begins with gentle, passive ankle dorsiflexion and plantarflexion. Active strengthening may be started at 6 weeks with elastic tubing. The ROM boot is discontinued at 6 to 8 weeks. Activities are progressed as tolerated.

 

Peroneal Tendons

Anatomy

The lateral or peroneal compartment of the leg houses the peroneus longus and brevis tendons. The peroneus longus originates in the head of the fibula and the proximal two thirds of the shaft and interosseous membrane. The peroneus brevis originates more distally from the lateral shaft of the fibula and intermuscular septum. The superficial peroneal nerve innervates the lateral compartment, and its sensory branches exit the compartment proximal to the ankle and divide to become the medial and lateral dorsal cutaneus nerves of the foot.

The peroneus longus and brevis become synovial tendons at the level of the ankle joint, with the longus becoming completely tendinous 2 to 3cm proximal to the ankle and the brevis usually retaining some muscle fibers to the level of the ankle joint. Both tendons enter a series of fibro-osseous tunnels as they approach their insertion points. The retromalleolar tunnel is bounded anteriorly by the fibula, which usually has a natural concavity to hold the tendons, and posterolaterally by the superior peroneal retinaculum. The peroneus brevis sits anterior to the longus as the muscles enters the retromalleolar tunnel, and at this level is flat or cupped around the longus tendon. Both tendons course around the distal fibula, passing superficial to the calcaneofibular ligament, and enter separate tunnels along the anterior process of the calcaneus. These tunnels are parallel and divided by the peroneal tubercle, with the peroneus brevis passing dorsal to the tubercle and the longus tendon passing plantar to the tubercle. The peroneus brevis proceeds over the cuboid and then fans out to its broad insertion on the lateral styloid of the fifth metatarsal. The peroneus longus tendon continues plantarly and enters an osseous groove at the lateral cuboid, where it is redirected medially across the midfoot to its main insertion at the plantar lateral tubercle of the first metatarsal. Variable lesser insertions usually are present at the medial cuneiform, second metatarsal base, and fibrous septae of the medial interossei. An osseous (approximately 20%) or fibrocartilaginous sesamoid is present as the peroneus longus tendon changes directions at the cuboid laterally. [0200] [0510] Stenosing tenosynovitis can occur at any of the fibro-osseous tunnels in either or both tendons.[52]

Accessory muscles and tendons are common, particularly tendinous slips from the peroneus brevis to the fifth toe.[20] Complete accessory muscles may originate from the distal fibula, the lateral calcaneus, or the peroneal muscles and tendons themselves. [0530] [0540] Well-developed accessory muscles can cause impingement, particularly if the muscle enters the fibro-osseous tunnel system distal to the fibula.

The peroneus brevis tendon is the primary everter of the subtalar joint and acts to balance the forces of the foot against inversion during weight acceptance and to stabilize the subtalar joint during stance phase and push-off. The peroneus longus tendon acts to plantarflex the first metatarsal and aids in eversion of the subtalar joint. Loss of function of either of these tendons may result in varus of the hindfoot because of loss of opposition to the posterior tibialis, and loss of the peroneus longus may cause cavus of the midfoot because of lack of opposition to the tibialis anterior and posterior.

Tendinitis

Tendon injury occurs through one of three mechanisms. Direct injury occurs primarily with laceration. Indirect injury occurs when a musculotendinous unit is loaded beyond its ultimate strength and fails primarily. This occurs most often as an avulsion fracture at the tendon insertion or as a tear at the myotendinous junction. The peroneus longus tendon may avulse from its insertion at the base of the first metatarsal,[55] or the os peroneum may fracture and be pulled proximally. [0560] [0570] Acute injuries usually are incomplete, but if the myotendinous unit loses continuity, prompt surgical repair is recommended.

Tendon overuse and entrapment is seen more commonly. Repetitive microtrauma may lead to small tears of the collagen fibrils. Localized hemorrhage and infiltration of inflammatory cells result in pain and edema. If the condition becomes chronic, the paratenon and synovial lining will hypertrophy and scar. Hypertrophy of the synovium causes further entrapment of the tendon at the fibro-osseous tunnels, further impairing healing by compromising blood flow. As microtears develop in the tendon, the resultant load on the remaining intact fibrils increases, potentially causing further tears and elongation of the structure. Calcification of the peroneus longus tendon is associated with chronic tendinitis and may complicate treatment. [0580] [0590]

Tendinitis of the peroneal tendons is encountered most commonly as an overuse phenomenon and typically responds well to conservative treatment.[6] Lateral ankle pain after vigorous exercise is the usual presenting complaint and often occurs early in the athlete's season or during a period of increased intensity in training. Downhill skiing, basketball, skating sports, ballet, running, and soccer are the sports at highest risk. Poorly fitting footwear, particularly ski boots and hockey skates, often is an inciting factor. Tendinitis may be present at the myotendinous junction or in the fibro-osseous tunnel system beginning at the distal fibula. Tendinitis in the synovial sheath may progress to the stenosing condition that often requires surgery. Pain proximal to the myotendinous junction that worsens with exercise may represent an exertional compartment syndrome or superficial peroneal nerve entrapment and warrants investigation. [0600] [0610] [0620] A stress fracture of the fibula, particularly in dancers, also may create pain at the distal one-third of the fibula and can be difficult to differentiate from tendinitis. Varus alignment of the hindfoot predisposes to both lateral ankle instability and peroneal tendon pathology.[0560] [0570] [0630] [0640] [0650] [0660]

Initiation of a nonsteroidal anti-inflammatory drug (NSAID), a brief period of immobilization, and avoidance of exacerbating activities usually are effective in diminishing acute pain and inflammation. Cross training with swimming, biking, a cushioned treadmill, or other low-impact activities can be used to maintain aerobic conditioning. A stirrup ankle brace usually is effective in diminishing tendon demands and may diminish pain and inflammation, although if subluxation at the distal fibula is present, the pressure from the brace may worsen the symptoms. If boggy synovitis, crepitance, or significant weakness is present, a short period of immobilization in a ROM boot is indicated. Weight bearing is allowed as tolerated, and active ranges of motion exercises are initiated. Active eversion uses both the peroneus longus and brevis muscles. The muscles are isolated best when eversion exercises are performed in plantarflexion. Stretching of the peroneal tendons occurs as the ankle is brought into maximal inversion and dorsiflexion. Graduated peroneal strengthening and open-chain exercises are advanced as tolerated. Therapeutic ultrasound is helpful and may improve the quality of the tendon as it remodels. Cryotherapy, particularly ice massage, is effective for the peroneal tendons because of their subcutaneous position. Underlying hindfoot varus should be addressed with a laterally posted orthotic. Shoewear must be examined because the heel counter may impinge directly on the tendons, or a laterally worn running shoe may cause a slight varus thrust at heel strike.

Chronic or recurrent tenosynovitis reflects a more difficult entity to treat. Once secondary changes in the tendon occur, surgery often is required to resolve symptoms. Attritional tears of the peroneus brevis tendon; stenosing tenosynovitis or peroneal entrapment; chronic or acute peroneal dislocation; accessory peroneal muscles; traumatic rupture; or posttraumatic sequelae represent the spectrum of entities that may require surgical intervention.

Peroneus brevis entrapment and attritional tendinitis

The peroneus brevis tendon is subject to both tension and significant compression during standing and the weight-bearing portion of gait. As it passes around the distal fibula, it lies between the peroneus longus tendon and the fibula and takes on a flattened or semilunar shape. The tendon is tightly constrained at this level, and similarly as it passes superior to the lateral process of the calcaneus. Entrapment can occur because of synovial swelling with overuse or inflammatory conditions. It has been theorized that hypovascularity may occur in pathologic states and may be responsible for impaired tendon repair, although there does not appear to be a distinct hypovascular zone.[67] Certain anatomic features, such as low-lying muscle fibers on the peroneus brevis, anomalous tendons or muscles, or bony irregularities can initiate and exacerbate entrapment. In an anatomic study, Sobel noted an 11.3% incidence of attritional tears of the peroneus brevis tendon in cadavers.[68] Histologic examination of the attritional tears showed minimal inflammatory response, suggesting that these tears are mechanical in nature.[69] The peroneus longus muscle acts as a wedge against the tendon, and even small tears are propagated proximally and distally as the ankle moves in dorsiflexion and plantarflexion. Hypertrophy of the synovium may stretch the peroneal retinaculum, allowing subluxation over the lateral fibula, and this may initiate and propagate tears ( Fig. 6-8 ). Complete rupture of the tendon is unusual in the athletic population but can occur, particularly in the middle-aged athlete.

 

 

Figure 6-8  Peroneal tendinitis with synovitis at the superior retinaculum. (A) Physical examination demonstrates tenderness and a boggy synovitis posterior to the fibula. (B) Surgical exploration shows the stretched tendon sheath. (C) Hypertrophied synovium requiring excision. (D) Attritional tears of the brevis tendon at the level of the fibula. Excision of the degenerative tendon and side-to-side repair is performed.

 

 

More distally, the peroneus brevis can become entrapped along the lateral border of the anterior process of the calcaneus. An accessory muscle can act as a space-occupying lesion in this area, causing entrapment. The peroneus brevis tendon passes superior to the peroneal tubercle, where it can become entrapped and undergo degeneration. A large, peroneal tubercle may predispose to entrapment at this level.[70] As the tendon courses distally, anomalous slips of the tendon passing distally to the fifth digit are common and can be a source of pain and entrapment, particularly if a muscle belly arises in this area ( Fig. 6-9 ).

 

 

Figure 6-9  Accessory peroneal tendons. (A) Most commonly, these exist as an accessory muscle that lies within the peroneal compartment. Mass effect can cause tendinitis and impingement as the tendons enter the superior peroneal retinaculum. (B) Distally, accessory tendon slips may branch from the brevis and extend to various insertions along the fifth metatarsal or toe. In this instance, a large accessory muscle was present beneath the inferior extensor retinaculum, causing pain and impingement.

 

 

Diagnosis can be determined on the basis of history and physical examination. Lateral ankle pain, weakness, and episodes of giving way are typical complaints. Pain, tenderness, and swelling posterior to the distal fibula or pain with palpation of the tendon during resisted eversion are diagnostic. Swelling and palpable synovitis of the sheath often are present once secondary changes begin to occur. Weakness and pain with resisted eversion are present. An MRI can be helpful in defining the extent of involvement and the presence of accessory muscles.

We prefer not to inject corticosteroids into the tendon sheath because this may impair the recovery process and can lead to tendon rupture. Injection of local anesthetic into the peroneal tendon sheath has been described as a method of verifying the diagnosis, although communication of the tendon sheaths with the ankle or subtalar joint may make it less specific.[71] Early in the disease course, oral anti-inflammatory medication, a short period of immobilization with a boot walker, or bracing with a stirrup ankle brace can help to diminish acute inflammation. Functional rehabilitation as outlined above should be initiated. Once secondary changes occur in the tendon, conservative treatment usually is ineffective. If symptoms are not controlled after 4 to 6 weeks, surgical exploration, debridement, and repair should be considered to prevent further progression and possible tendon rupture.

   Pearl

Peroneus Brevis Tendon Tear

(1) Tenderness over the peroneus brevis tendon behind and inferior to the lateral malleolus. (2) Pain in the same area on active flexion and abduction of the foot and ankle against resistance.

Peroneus longus entrapment and tendinitis

The peroneus longus tendon also is subject to a combination of tensile and compressive forces as it enters the fibro-osseous tunnels of the ankle and foot. Like the peroneus brevis tendon, the peroneus longus can become entrapped as it enters the synovial sheath posterior to the fibula, although pathology of the peroneus brevis is much more common at this level. The tendon courses inferior to the peroneal tubercle and can develop stenosing tenosynovitis at this level, particularly in the presence of a large peroneal tubercle. [0560] [0700] [0720] [0730] The most common site of pathology in the peroneus longus tendon is at the osseous groove beneath the cuboid. It is here that the tendon sharply changes direction, resulting in a combination of tensile and compressive forces within the tendon fibers. A bony sesamoid or cartilaginous thickening is variably present at this level and often is the site of rupture in advanced cases. [0550] [0570] [0740] More distal avulsion from the medial cuneiform may occur, but this is rare because of the multiple attachments in the plantar midfoot. Rupture can occur as the result of a sudden inversion injury and usually occurs at the level of the cuboid. [0520] [0570] [0750] [0760] [0770] Fracture of the os peroneum also can occur and will result in proximal migration of part or all of the ossicle. [0780] [0790] [0800] [0810] [0820]

Stenosing tendinitis occurs with chronic overuse in athletes. Calcification of the peroneus longus tendon and its synovium is associated with inflammatory arthropathy, and if present it warrants rheumatologic workup. [0580] [0590] [0830] [0840] Diagnosis of the condition is similar to peroneus brevis tendinitis. Pain, swelling, and tenderness along the course of the tendon and pain with resisted eversion are the hallmarks of diagnosis. Sammarco noted that 8 of 14 cases had no prodrome before peroneus longus rupture, whereas 6 of 14 patients had a prodrome of increasing pain and discomfort during activity.[57] In this series, diagnosis was delayed more than 6 months in all cases but one. Brandes and Smith noted a cavovarus position of the foot in 82% of patients, although it is not clear whether this was secondary to chronic tendon insufficiency or the inciting event in tendonopathy.[56] Plain x-rays of the foot may demonstrate a fractured os peroneus. If the tendon is no longer in continuity, the proximal fragment will migrate proximally and become entrapped just distal to the peroneal tubercle, where it can be palpated and is typically exquisitely tender. Unusually, the tendon will avulse from its insertion at the medial cuneiform and first metatarsal base and present with longitudinal arch pain with progressive cavus of the midfoot. Early MRI is useful in the diagnosis and may demonstrate attritional tears or complete rupture.[85]

Tendon rupture is poorly tolerated and results in muscular imbalance of the foot and development of pes cavovarus. [0560] [0860] Early repair results in better outcome; therefore a high index of suspicion is necessary, and early diagnostic studies are indicated. Fracture of the os peroneum with even a small separation of the fragments should be treated as a complete rupture and warrants exploration and repair. As noted previously, early tenosynovitis can be treated conservatively, but once attritional changes in the tendon occur, surgery often is necessary to alleviate symptoms and restore function.

   Pearl

Peroneus Longus Tendinitis

(1) Tenderness over the peroneus longus tendon at the inferior calcaneus laterally and distally and at the calcaneocuboid joint inferiorly. (2) Pain in the same area on active ankle flexion and with depression of the first metatarsal head.

   Pearl

Peroneus Longus Entrapment and Rupture

(1) Tenderness over the peroneus longus tendon along the lateral distal calcaneus. (2) A mass may be present on the lateral calcaneus. Palpable os perineum noted on the lateral calcaneus with complete rupture and proximal migration of the sesamoid. Lateral x-ray of the foot reveals proximal migration of the os perineum (when ossified).

Surgical treatment of stenosing tenosynovitis, attritional tendinitis, rupture, and laceration

In addressing pathology of the peroneal tendons, it is helpful to divide the course of the tendons into anatomic zones. Brandes and Smith divided the areas of pathology into three zones for the peroneus longus tendon, but this same system can be useful in evaluating the peroneus brevis tendon, as well[56] ( Fig. 6-10 ). Zone A includes the superior peroneal retinaculum and distal fibula. Zone B is the inferior peroneal retinaculum at the level of the peroneal tubercle of the calcaneus. Zone C is the cuboid notch where the peroneus longus turns and enters the osseous groove. We have added an additional zone D to this classification that involves avulsion of the tendons from their insertion at the respective metatarsal base. If the tendons are diffusely involved, the entire tendon sheath may need to be explored; however, if the pathology is limited to one or two zones, surgery often can be limited to the affected zone.

 

 

Figure 6-10  Zones of entrapment of the peroneal tendons. (A) Zones A, B, and C. (B) Zone D: Rarely, avulsion may occur at the insertion of the peroneus brevis at the base of the fifth metatarsal or the peroneus longus distal to the os peroneus.  A, modified and reprinted from Brandes CB, Smith RW: Foot Ankle Int 21:462, 2000.

 



Attritional tears of the peroneus brevis tendon are most commonly affected in zone A, although both tendons often have an associated hypertrophic synovitis. During exploration, it is important to evaluate the stability of the tendons, and, if instability is present, this should be addressed. Attritional tears of the brevis typically are longitudinal, and complete rupture is infrequent. After the retinaculum is incised, the tendons are inspected, and any redundant synovium is excised. If an accessory peroneal muscle or tendon is present, this also is excised. Degenerative and frayed tendon edges are debrided. If a thickening of the tendon is present, this represents an area of intrasubstance tendinopathy, and an incision is made in the tendon overlying the affected area in line with its fibers. Any central fibrosed or degenerative tendon is sharply excised, taking care not to transect the normal peripheral tendon fascicles. A side-to-side repair of the tear then is performed with 2-O nonabsorbable suture. Deepening of the fibular groove and repair of the superficial peroneal retinaculum should be performed if necessary, as discussed in the section on tendon dislocation.

Tendon pathology in zone B may involve both the longus and brevis tendons. The primary site of entrapment is the peroneal tubercle, where the inferior peroneal retinaculum attaches to the peroneal tubercle and divides the peroneal tendons into two separate tendon sheaths. The peroneus brevis tendon courses superior to the tubercle and the longus inferiorly. Entrapment of the longus or brevis tendons can result from a large or hypertrophic peroneal tubercle or, alternatively, from an accessory muscle or tendon ( Fig. 6-11 ). Chronic tenosynovitis can result in fusiform swelling of the tendon that worsens the entrapment phenomenon and may result in longitudinal tears. The surgical incision for lesions isolated to zone B is directly over the peroneal tubercle, in line with the axis of the tendons. Care must be taken to identify and protect the sural nerve in this area, because it usually lies directly in the surgical field and may have branches that cross dorsally over the tendons. The tendon sheath must be incised in a way that it can be closed without tension over the tendons. The retinaculum is incised just inferior to the tubercle and split from proximal to distal over the peroneus longus tendon. The superior portion of the sheath then is elevated subperiosteally from its insertion on the lateral wall of the calcaneus and peroneal tubercle, and the central coalescence of fibers that insert on the tubercle then can be split to add length to the retinaculum ( Fig. 6-12 ). The entire peroneal tubercle should be excised with an osteotome or chisel so that the area is flush with the lateral wall of the calcaneus. The longus and brevis tendons are inspected for intrasubstance degeneration or gross attritional tears, debrided, and repaired side to side as described previously. Any anomalous muscles or tendons or hypertrophic synovium should be excised. The peroneal sheath then is closed, and the surgeon must make certain that there is adequate room for the tendons to glide. If not enough length has been gained during the approach for a loose closure of the retinaculum, a Z-lengthening of the inferior retinaculum can be performed.




 

Figure 6-11  Case Study: Entrapment of the peroneus longus at the peroneal tubercle. A 13-year-old girl with pain over the lateral ankle and peroneal tubercle. (A) Anteroposterior ankle radiograph demonstrating enlarged peroneal tubercle. (B) Peroneal tubercle is best visualized with oblique foot film, which demonstrates the tubercle in profile. (C) Coronal magnetic resonance imaging demonstrates synovitis of peroneus longus and brevis and the large peroneal tubercle. (D) Operative findings: The peroneus longus tendon was subluxing over the enlarged tubercle. Excision of the tubercle, localized tenosynovectomy, and reconstruction of the inferior peroneal retinaculum resolved the patient's symptoms.

 

 



 

Figure 6-12  Excision of the peroneal tubercle and reconstruction of the inferior peroneal retinaculum. (A) The peroneal tubercle lies between the peroneus brevis and longus tendons and can be a source of impingement. (1) The tubercle is approached through the longus sheath, inferior to the coalescence of fibers that insert onto the tubercle. (B) (2) The dorsal portion of the inferior retinaculum is elevated subperiosteally, exposing the peroneal process. (3) A sharp chisel is used to excise the process. (C) (4) The bony process is removed flush with the lateral wall of the calcaneus. (5) The retinaculum is carefully split with a sharp scalpel to add length, and (6) repaired with suture.

 

 

Zone C involves the peroneus longus tendon where it changes course abruptly to enter the osseous groove on the plantar surface of the cuboid. Tendon pathology at this level often presents as complete rupture of the peroneus longus tendon. Fracture of the os peroneus may be complete with retraction of the proximal fragment or incomplete with some separation of the fragments ( Fig. 6-13 ). Complete or partial rupture of the tendon requires repair. An incision is made overlying the peroneus longus tendon, and dissection is carried distally, extending from the peroneal tubercle to the osseous groove of the cuboid. If the tendon is ruptured, the proximal end must be sought, and dissection proximal to the fibula may be required. An os peroneum that has fractured or avulsed may require excision of the fragment, and direct repair of the tendon should be accomplished with at least a four-strand repair of 2-O nonabsorbable braided suture. If the fragments are large or the tendon has avulsed from the proximal pole, direct repair may be accomplished, retaining the os peroneum by freshening the osseous surface, drilling through the ossicle with a K-wire, and locking the suture into the adjacent tendon.

 

 

Figure 6-13  (A) A fractured os peroneus following inversion injury in a 35-year-old man. This was treated with casting. (B) Repeat radiographs 2 weeks later revealed proximal migration of the fragment to the peroneal tubercle. Surgical repair was accomplished with good functional results.

 

 

Zone D injuries involve avulsion of the insertion of the tendon. Peroneus brevis tendon avulsion usually is traumatic and incomplete. Avulsion may accompany a fracture of the metaphyseal area of the fifth metatarsal and usually carries a small piece of bone. Most avulsions heal with a short period of immobilization and limited weight bearing. Chronic avulsions can be painful and may require surgical repair by fixation and bone grafting of the avulsed fragment or by excision of smaller fragments with direct repair to the metatarsal. Avulsion of the distal insertion of the peroneus longus tendon is rare because of its multipenate insertion. Clinical diagnosis is difficult, and early diagnosis is required if reattachment is to be successful. Surgical repair may be accomplished using medial and lateral incisions, avoiding incision of the plantar aspect of the foot. If diagnosis or treatment is delayed, transfer of the longus to the brevis at the lateral ankle is preferred over delayed reconstruction because the tendon tract will obliterate with fibrous tissue.

Laceration of the peroneal tendons may occur in sport because of sharp penetration by cleats or skates or by direct injury from a fixed object, such as the metal supports of gymnastic equipment. Any laceration directly overlying the course of the tendons must be treated with a high index of suspicion because substitution by the uninvolved peroneal may mask injury. Surgical repair usually is successful with limited morbidity. Absence of either of the peroneals is poorly tolerated. Surgical repair is always indicated.[30]

Delayed diagnosis of rupture or laceration of the peroneal tendons presents a challenging problem. The resultant muscular imbalance may cause varying degrees of midfoot cavus and hindfoot varus deformity. Most neglected ruptures still can be repaired if they are treated within 4 to 6 months, although surgical results are not as good as those repaired primarily.[57] Typically, the entire tendinous portion must be exposed laterally, and the lateral muscular compartment of the leg also must be entered so the muscular unit can be freed up. The proximal portion of the tendon is grasped with a running locked suture, and tension is pulled distally while a medium-sized Cobb or other blunt elevator is used to free the muscle belly from any surrounding adhesions. Approximately 3 to 4cm of excursion is necessary for delayed repair to be successful. If the muscle is fibrosed and no meaningful excursion can be regained, transfer of the distal stump of the tendon to the uninvolved tendon should be performed. If good excursion can be obtained but primary repair of the tendon ends still cannot be accomplished, a bridging tendon graft can be harvested from the Achilles or the plantaris. Longer standing cases tend to develop inflexible deformity that may require calcaneal and metatarsal osteotomies or arthrodesis to achieve a plantigrade foot.[64]

Peroneal tendon dislocation

Acute dislocation of the peroneal tendons is an uncommon injury that results from forceful contraction of the peroneal tendons with the ankle in a position of risk. The exact mechanism has not been demonstrated; however, it has been our experience that traumatic dislocation can accompany both eversion and inversion sprains. Fracture of the calcaneus also is associated with dislocation of the tendons. Dislocation occurs at the level of the fibula and is accompanied by avulsion of the superficial peroneal retinaculum; this in turn may avulse the distal lateral rim of the peroneal groove in the fibula. The anatomy of the distal fibula has been inferred to predispose some individuals to dislocation. Edwards described anatomic variations of the distal fibula in relation to the peroneal tendons ( Fig. 6-14 ).[87] In an anatomic study of 178 fibulas, 82% of specimens had a definite sulcus posteriorly, whereas 11% were flat and 7% were convex. At the posterolateral edge of the fibula, a bony or cartilaginous flange[88]often is present that helps to contain the peroneal tendons. Absence of a lateral bony ridge was noted to be 30% in Edwards' series. The presence of a distinct sulcus and lateral ridge give bony support to the peroneal tendons and is protective for dislocation. Absence of these anatomic features may predispose to acute dislocation and often accompanies chronic subluxation, which can lead to tendon degeneration. [0650] [0890] [0900] [0910]



 

Figure 6-14  Edward's anatomic observations of the distal fibula. (A) In 82% there is a distinct concave groove for peroneal containment. (B) In 11% the posterior fibula is flat with no groove. (C) In 11% the posterior fibula is convex, which predisposes the tendons to subluxation and dislocation.

 

 

Classification of these injuries was first proposed by Eckert and Davis[88] and modified by Oden.[92] In Type 1, the osseous attachments of the retinaculum to the fibula are disrupted, whereas the attachment to the periosteal sleeve remains intact. The tendons dislocate to a subperiosteal location at the lateral fibula, and the periosteal sleeve remains intact with the superficial peroneal retinaculum. Type 2 represents a rupture of the retinaculum at the fibular insertion. Type 3 represents an avulsion fracture of the posterolateral fibula at the insertion of the retinaculum, and type 4 represents an avulsion of the retinaculum from the posterior origin at the Achilles fascia ( Fig. 6-15 ).




 

Figure 6-15  Classification of peroneal tendon dislocation. I, Superior peroneal retinaculum remains in continuity with fibular periosteum. II, Avulsion of retinaculum from fibula. III, Avulsion fracture of distal fibula. IV, Avulsion of the retinaculum from posterior origin. Retinaculum becomes interposed between tendons and osseous groove in fibula.

 

 

Diagnosis of acute peroneal tendon dislocation often is delayed because the tendons often spontaneously relocate following the injury. Pain and tenderness at the insertion of the peroneal retinaculum is the hallmark of the injury. Swelling and ecchymosis over the lateral fibula often is present. If the tendons remain dislocated, more commonly in type 3 and type 4 injuries, they can be palpated along the lateral edge of the fibula. Resisted eversion with the ankle in plantarflexion may cause the tendons to redislocate or sublux. Ankle radiographs may reveal an avulsion fracture in type 3 injuries but usually are not diagnostic.[93] If the diagnosis is in question, CT or MRI can be helpful and may demonstrate dislocated tendons, avulsion of the retinaculum, or a fluid collection laterally over the fibula. [0730] [0940] [0950] [0960]

Treatment is controversial. Some authors recommend treatment for 6 weeks in a short leg cast with the ankle in slight plantarflexion if the tendons are reducible and stable. [0880] [0920] Recurrent dislocation can be problematic with nonoperative treatment even if reduction is accomplished in a timely manner. Recurrent tendon instability following closed treatment of acute tendon dislocation may be as high as 50%. [0910] [0970] [0980] [0990] A high recurrence rate and the extended cast immobilization required for nonoperative treatment has led to the recommendation for surgical repair as the primary treatment recommendation in active and athletic individuals. [0520] [0970] [0990] [1000] [1010] [1020] Type III dislocations represent a disruption of the osseous fibular groove and are inherently unstable. These injuries are best treated surgically. In type IV dislocations, the peroneal retinaculum itself may become entrapped behind the tendons, preventing reduction and necessitating surgery.[92]

Chronic subluxation of the peroneal tendons is a common cause of lateral ankle pain and peroneal tendinitis. Recurrent sprains and chronic ankle instability are associated with chronic subluxation of the tendons because of progressive incompetence of the peroneal retinaculum.[66] As discussed previously, some individuals without an adequate osseous groove at the posterior fibula are anatomically predisposed to tendon subluxation even without trauma. Conservative treatment is rarely effective in the presence of gross instability, and surgical reconstruction should be considered in symptomatic individuals to prevent progressive degeneration of the tendons. [0520] [0890] [0900] [0990] [1020] [1030] [1040] [1050] [1060]

   Pearl

Acute Peroneal Tendon Dislocation

(1) Tenderness and swelling at the lateral malleolus with the tendons easily subluxing on flexion of the ankle with rotation of the foot internally and/or externally. (2) AP and oblique x-rays of the ankle may reveal a “flake” fracture at the lateral malleolus.

   Pearl

Chronic Peroneal Tendon Dislocation

(1) The tendons are palpable lateral or anterior to the lateral malleolus at the ankle. (2) Weakness is noted with gait and tenderness over the dislocated tendons.

Surgical management of peroneal tendon subluxation and dislocation

The surgical approach to acute and chronic dislocation of the peroneal tendons is similar. The goals of surgery are to repair the injured structures, which may include tears of the peroneal tendons, avulsion of the retinaculum, and fracture of the fibula. It also is important to address any anatomic features that increase the risk of dislocation or subluxation.

An incision is made posterior to the fibula directly over the peroneal tendon sheath and extends proximal to the tip of the fibula 4 or 5cm. This approach lies distinctly between the sural nerve and superficial peroneal nerve. Care must be taken during the dissection to avoid aberrant branches that may lie in the field of dissection because injury to a branch may lead to painful neuroma formation.

Inspection of the sheath at this point will determine the deeper approach. Incision of the retinaculum is dependent on the pathology at hand and is extremely important for successful reconstruction. For type 1 dislocations, in which the retinaculum remains in continuity with the periosteum, it is helpful to incise anterior to the fibular border and harvest 3 or 4mm of periosteum in continuity with the retinacular sleeve. This will ensure that enough tissue is present for adequate repair of the retinaculum during closure. Chronic or congenital subluxation mimics the anatomy of a type 1 dislocation, in which the retinaculum is in continuity with avulsed periosteum, and incision of the retinaculum should similarly harvest a slip of contiguous periosteum for aid in later repair. In types 2 and 3 dislocations, the retinaculum is avulsed from the fibula, either with or without a small piece of bone. The tendons overlie the fibula in the subcutaneous tissue, and the peroneal retinaculum must be dissected posteriorly so that it can be repaired later. Large avulsion fractures should be left in continuity with the retinaculum and repaired directly to the fibula, whereas the typical small fleck fracture should be excised. It is important to recognize type 4 dislocations because the retinaculum should not be incised. The retinaculum is avulsed from the deep posterior tissues, and this torn edge must be identified with the anterior retinaculum left intact. In the type 4 dislocations, the avulsed retinaculum may lie within the peroneal groove posterior to the fibula holding the tendons displaced.

Direct inspection of the tendons is performed after adequate exposure has been obtained. Traumatic dislocations are associated with tendon pathology infrequently, whereas chronic subluxation or acute or chronic dislocation often are associated with attritional tears of the peroneus brevis. Redundant synovium should be excised. Attritional tears are debrided and repaired side to side with 2–0 or 3–0 nonabsorbable suture. If the peroneus brevis muscle belly extends distal to the tip of the fibula, the muscle fibers should be excised to diminish impingement within the fibro-osseous tunnel. Similarly, accessory muscles may cause impingement and lend to instability because of mass effect and should be excised.

It is important to assess the anatomy of the distal fibula because a flat or convex fibula lends to instability of the tendons that must be addressed at the time of repair. Multiple procedures have been described to assess this problem. [0980] [1000] We have found that deepening of the fibular groove is highly effective in preventing recurrent subluxation or dislocation. [0520] [0890] [1070] The peroneal tendons are pulled anteriorly with a tendon hook, and the distal fibula inspected. A shallow or absent sulcus necessitates deepening of the groove. We do not recommend deepening the groove by burring or rasping a trough in the posterior aspect of the fibula because this removes the cortical bone and cartilaginous surface necessary for the smooth tendon glide. If the posterior surface is simply burred or rasped, adhesions between the tendon and rough cancellous surface may impede recovery, particularly if the ankle is immobilized for a significant period of time (>2 weeks). We prefer a modification of the method described by Zoellner and Clancy.[107] The posterolateral edge of the fibula is incised with a sharp chisel or thin oscillating saw from the inferior tip of the fibula 3 or 4cm proximally. The medial cortex is left intact, and the posterior fibular cortex, with its cartilaginous lining, is hinged open to expose the cancellous bone of the distal fibula. Three or 4mm of the underlying cancellous bone are removed with a curette or burr, and the cortical flap in hinged back into place, then impacted into the defect with a bone tamp to create an osseous groove. This effectively deepens the groove and creates a lateral ridge of fibular cortex, preventing recurrence of the subluxation. The tendons are allowed to relocate, and the ankle and subtalar joints are brought through a full ROM. The tendons should remain reduced in all positions, even without repair of the superior peroneal retinaculum. The avulsed retinaculum then can be repaired directly to the lateral cortical ridge with nonabsorbable suture during closure.

In acute dislocations, direct repair of the retinaculum is accomplished with multiple nonabsorbable sutures that are passed and tied directly through drill holes in the lateral fibula. If a large piece of bone is avulsed, this may be reduced and sutured into place or fixed with 3.0-mm compression screws. In type 4 dislocations, the tendons are reduced, and the posterior torn edge of the peroneal retinaculum must be sutured to its posterior insertion. Proximally, this is the deep posterior compartment fascia overlying the distal aponeurosis of the Achilles tendon, and distally the retinaculum is repaired to the periosteum of the lateral calcaneus.[20]

In chronic dislocations, the superficial peroneal retinaculum often is attenuated, if not entirely absent. This is particularly problematic when the dislocation was unrecognized following surgical treatment of severe ankle trauma or following closed or open treatment of calcaneus fracture. In these instances, secondary reconstruction can be accomplished with a tendon graft [1040] [1080] [1090] [1100] or in conjunction with reconstruction of the calcaneofibular ligament. [1020] [1070] [1110] [1120] [1130] If ankle instability is not an issue, the retinaculum can be reconstructed with a split graft from the peroneus brevis or Achilles tendon, or with an accessory tendon if one is present. A 5-cm slip of tendon is harvested as a free graft and sutured to the deep fascia overlying the Achilles complex. The graft then is attached to the fibula 3cm proximal to the tip of the fibula either by suturing it to the periosteum of the fibula or attaching it directly to bone. The graft then is attached distally to the tip of the fibula in a similar fashion and sutured to the calcaneofibular ligament near its calcaneal insertion or attached directly to the calcaneus with a suture anchor. If lateral ankle instability is surgically addressed in conjunction with the repair, the retinaculum can be reconstructed successfully by passing the tendons deep to the calcaneofibular ligament during its reconstruction.

Postoperatively, the patient is placed in a well-padded splint with the ankle in neutral dorsiflexion. The splint is discontinued at 8 to 10 days following suture removal, and the patient is allowed to bear weight in a ROM boot. Passive and active motion exercises of the ankle and subtalar joint are permitted in a controlled setting. Peroneal strengthening exercises with an elastic band can be initiated at 3 or 4 weeks, depending on the quality of the reconstruction. Weight-bearing, proprioceptive exercises are allowed after 5 to 6 weeks, and activities are advanced as tolerated.

 

References

  1. Burman M: Stenosing tenosynovitis of the foot and ankle.  Arch Surg1953; 67:686.
  2. Sammarco GJ, Cooper P: Flexor hallucis longus tendon injury in dancers and nondancers.  Foot Ankle1998; 19:356.
  3. Sammarco GJ, Miller EH: Forefoot conditions in dancers. Part I & Part II.  Foot Ankle1982; 3(2):85.
  4. Sammarco GJ, Miller EH: Partial rupture of the flexor hallucis longus tendon in classical ballet dancers.  J Bone Joint Surg1979; 61A:149.
  5. Crosby LA, Fitzgibbons TC: Unrecognized laceration of tibialis anterior tendon: a case report.  Foot Ankle1988; 9:143.
  6. Sammarco V: Principles and techniques in rehabilitation of the athlete's foot: part II—rehabilitation of tendon injuries.  Tech Foot Ankle Surg2003; 2:51.
  7. Sanhudo JAV, Lompa PA: Checkrein deformity—flexor hallucis tethering: two case reports.  Foot Ankle2002; 23:799.
  8. McCarroll JR, Ritter MS, Becker TE: Triggering of the great toe: a case report.  Clin Orthop1983; 184:
  9. Thompson FM, Snow SW, Hershon SJ: Spontaneous atraumatic rupture of the flexor hallucis longus tendon under the sustentaculum tali: case report, review of the literature and treatment options.  Foot Ankle1993; 14:414.
  10. Carr JB: Complications of calcaneus fractures: entrapment of the flexor hallucis longus: report of two cases.  J Orthop Trauma1990; 4:166.
  11. Carranza-Benzaco A, Gomez-Arroyo JA, Fernandez-Torres JJ: Hallux flexus deformity due to entrapment of the flexor hallucis longus tendon after an open fracture of the tibia and fibula.  Foot Ankle Surg2000; 6:133.
  12. Rosenberg GA, Sferra JJ: Checkrein deformity—an unusual complication associated with a closed Salter-Harris type II ankle fracture: a case report.  Foot Ankle1999; 20:591.
  13. Romash MM: Fracture of the calcaneus: an unusual fracture pattern with subtalar joint interposition of the flexor hallux longus. A report of two cases.  Foot Ankle1992; 12:32.
  14. Brand Jr JC, Smith RW: Rupture of the flexor hallucis longus after hallux valgus surgery: case report and comments on technique for abductor release [comment in Foot Ankle 12:132, 1991].  Foot Ankle1991; 11:407.
  15. Krakow KA: Acute traumatic rupture of a flexor hallucis longus tendon: a case report.  Clin Orthop1980; 261:
  16. Rasmussen RB, Thyssen EP: Rupture of the flexor hallucis longus tendon: a case report.  Foot Ankle1990; 10:288.
  17. Stark HH, et al: Bridge flexor tendon grafts.  Clin Orthop1989; 242:51.
  18. Fennell CW, Phillips 3rd P: Redefining the anatomy of the anterior tibialis tendon.  Foot Ankle Int1994; 15:396.
  19. Luchansky E, Paz Z: Variations in the insertion of tibialis anterior muscle.  Anat Anz1986; 162:129.
  20. Sarrafian SK: Anatomy of the foot and ankle: descriptive, topographic, functional,  ed 2. Philadelphia, JB Lippincott, 1993.
  21. Geppert MJ, Sobel M, Hannafin JA: Microvasculature of the tibialis anterior tendon.  Foot Ankle1993; 14:261-264.
  22. Petersen W, Stein V, Bobka T: Structure of the human tibialis anterior tendon.  J Anat2000; 197(Pt 4):617.
  23. Petersen W, Stein V, Tillmann B: Blood supply of the tibialis anterior tendon.  Arch Orthop Trauma Surg1999; 119:371.
  24. Aydingoz U, Aydingoz O: Spontaneous rupture of the tibialis anterior tendon in a patient with psoriasis.  Clin Imaging2002; 26:209.
  25. Bianchi S, et al: Evaluation of tibialis anterior tendon rupture by ultrasonography.  J Clin Ultrasound1994; 22:564.
  26. Otte S, et al: Operative treatment in case of a closed rupture of the anterior tibial tendon.  Arch Orthop Trauma Surg2002; 122:188.
  27. Sammarco V, Sammarco G: Principles and techniques in rehabilitation of the athlete's foot: part I—introduction of concepts and Achilles tendon rehabilitation.  Tech Foot Ankle Surg2003; 2:50.
  28. Richter R, Schlitt R: [Subcutaneous rupture of the tibialis anterior-tendon. (Report of 3 cases) (author's transl)].  Z Orthop Ihre Grenzgeb1975; 113:271.
  29. Velan GJ, Hendel D: Degenerative tear of the tibialis anterior tendon after corticosteroid injection—augmentation with the extensor hallucis longus tendon, case report.  Acta Orthop Scand1997; 68:308.
  30. Myerson MS, Sammarco VJ: Penetrating and lacerating injuries of the foot.  Foot Ankle Clin1999; 4:647.
  31. Griffiths JC: Tendon injuries around the ankle.  J Bone Joint Surg Br1965; 47:686.
  32. Stuart MJ: Traumatic disruption of the anterior tibial tendon while cross-country skiing. A case report.  Clin Orthop1992;193.
  33. Church JS, Radford WJ: Isolated compartment syndrome of the tibialis anterior muscle.  Injury2001; 32:170.
  34. Din R, Therkilsden L: Rupture of tibialis anterior associated with a closed midshaft tibial fracture.  J Accid Emerg Med1999; 16:459.
  35. Freundlich BD, Dashiff JE: Avulsion of tibialis anticus and peronei muscles resulting in acute anterior and lateral compartment syndrome.  J Trauma1987; 27:453.
  36. Hovelius L, Palmgren H: Laceration of tibial tendons and vessels in ice hockey players. Three case histories of a skate boot top injury.  Am J Sports Med1979; 7:297.
  37. Machani B, Narayan B, Casserly HB: Closed avulsion of the tibialis anterior: an unusual cause of compartment syndrome.  Injury2000; 31:738.
  38. Simonet WT, Sim L: Boot-top tendon lacerations in ice hockey.  J Trauma1995; 38:30.
  39. Bernstein RM: Spontaneous rupture of the tibialis anterior tendon.  Am J Orthop1995; 24:354.
  40. Kashyap S, Prince R: Spontaneous rupture of the tibialis anterior tendon. A case report.  Clin Orthop1987;159.
  41. Kausch T, Rutt J: Subcutaneous rupture of the tibialis anterior tendon: review of the literature and a case report.  Arch Orthop Trauma Surg1998; 117:290.
  42. Patten A, Pun WK: Spontaneous rupture of the tibialis anterior tendon: a case report and literature review.  Foot Ankle Int2000; 21:697.
  43. Dooley BJ, Kudelka P, Menelaus MB: Subcutaneous rupture of the tendon of tibialis anterior.  J Bone Joint Surg Br1980; 62-B:471.
  44. Meyn Jr MA: Closed rupture of the anterior tibial tendon. A case report and review of the literature.  Clin Orthop1975;154.
  45. Moskowitz E: Rupture of the tibialis anterior tendon simulating peroneal nerve palsy.  Arch Phys Med Rehabil1971; 52:431.
  46. Markarian GG, et al: Anterior tibialis tendon ruptures: an outcome analysis of operative versus nonoperative treatment.  Foot Ankle Int1998; 19:792.
  47. Ouzounian TJ, Anderson R: Anterior tibial tendon rupture.  Foot Ankle Int1995; 16:406.
  48. Rimoldi RL, et al: Acute rupture of the tibialis anterior tendon: a case report.  Foot Ankle1991; 12:176.
  49. Weissinger M, Landsiedl F: [Bilateral subcutaneous rupture of the tendon of the anterior tibial muscle and its differential diagnosis].  Z Orthop Ihre Grenzgeb1984; 122:659.
  50. Forst R, Forst J, Heller KD: Ipsilateral peroneus brevis tendon grafting in a complicated case of traumatic rupture of tibialis anterior tendon.  Foot Ankle Int1995; 16:440.
  51. Le Minor JM: Comparative anatomy and significance of the sesamoid bone of the peroneus longus muscle (os peroneum).  J Anat1987; 151:85.
  52. Sammarco GJ: Peroneal tendon injuries.  Orthop Clin North Am1994; 25:135.
  53. Sobel M, Bohne WH, O'Brien SJ: Peroneal tendon subluxation in a case of anomalous peroneus brevis muscle.  Acta Orthop Scand1992; 63:682.
  54. Sobel M, Levy ME, Bohne WH: Congenital variations of the peroneus quartus muscle: an anatomic study.  Foot Ankle1990; 11:81.
  55. Cooper ME, Selesnick FH, Murphy BJ: Partial peroneus longus tendon rupture in professional basketball players: a report of 2 cases.  Am J Orthop2002; 31:691.
  56. Brandes CB, Smith RW: Characterization of patients with primary peroneus longus tendinopathy: a review of twenty-two cases.  Foot Ankle Int2000; 21:462.
  57. Sammarco GJ: Peroneus longus tendon tears: acute and chronic.  Foot Ankle Int1995; 16:245.
  58. Cox D, Paterson FW: Acute calcific tendinitis of peroneus longus.  J Bone Joint Surg Br1991; 73:342.
  59. Roggatz J, Urban A: The calcareous peritendinitis of the long peroneal tendon.  Arch Orthop Trauma Surg1980; 96:161.
  60. Eisele SA, Sammarco GJ: Chronic exertional compartment syndrome.  Instr Course Lect1993; 42:213.
  61. Fronek J, et al: Management of chronic exertional anterior compartment syndrome of the lower extremity.  Clin Orthop1987;217.
  62. Rorabeck CH, Bourne RB, Fowler PJ: The surgical treatment of exertional compartment syndrome in athletes.  J Bone Joint Surg Am1983; 65:1245.
  63. Harris N, Stevens M: A cavovarus foot is a predisposing factor for rather than a result of peroneus longus tendinopathy.  Foot Ankle Int2001; 22:525.
  64. Sammarco GJ, Taylor R: Cavovarus foot treated with combined calcaneus and metatarsal osteotomies.  Foot Ankle Int2001; 22:19.
  65. Sobel M, et al: The dynamics of peroneus brevis tendon splits: a proposed mechanism, technique of diagnosis, and classification of injury.  Foot Ankle1992; 13:413.
  66. Sobel M, Geppert MJ, Warren RF: Chronic ankle instability as a cause of peroneal tendon injury.  Clin Orthop1993;187.
  67. Sobel M, et al: Microvascular anatomy of the peroneal tendons.  Foot Ankle1992; 13:469.
  68. Sobel M, Bohne WH, Levy ME: Longitudinal attrition of the peroneus brevis tendon in the fibular groove: an anatomic study.  Foot Ankle1990; 11:124.
  69. Sobel M, et al: Longitudinal splitting of the peroneus brevis tendon: an anatomic and histologic study of cadaveric material.  Foot Ankle1991; 12:165.
  70. Boles MA, et al: Enlarged peroneal process with peroneus longus tendon entrapment.  Skeletal Radiol1997; 26:313.
  71. Mizel MS, Michelson JD, Newberg A: Peroneal tendon bupivacaine injection: utility of concomitant injection of contrast material.  Foot Ankle Int1996; 17:566.
  72. Pierson JL, Inglis AE: Stenosing tenosynovitis of the peroneus longus tendon associated with hypertrophy of the peroneal tubercle and an os peroneum. A case report.  J Bone Joint Surg Am1992; 74:440.
  73. Rademaker J, et al: Tear of the peroneus longus tendon: MR imaging features in nine patients.  Radiology2000; 214:700.
  74. Evans JD: Subcutaneous rupture of the tendon of peroneus longus. Report of a case.  J Bone Joint Surg Br1966; 48:507.
  75. Ross G, et al: Rupture of the peroneus longus tendon in a military athlete.  Am J Orthop1999; 28:657.
  76. Thompson FM, Patterson AH: Rupture of the peroneus longus tendon. Report of three cases.  J Bone Joint Surg Am1989; 71:293.
  77. Wind WM, Rohrbacher BJ: Peroneus longus and brevis rupture in a collegiate athlete.  Foot Ankle Int2001; 22:140.
  78. Bianchi S, Abdelwahab IF, Tegaldo G: Fracture and posterior dislocation of the os peroneum associated with rupture of the peroneus longus tendon.  Can Assoc Radiol J1991; 42:340.
  79. Kilkelly FX, McHale KA: Acute rupture of the peroneal longus tendon in a runner: a case report and review of the literature.  Foot Ankle Int1994; 15:567.
  80. Peacock KC, Resnick EJ, Thoder JJ: Fracture of the os peroneum with rupture of the peroneus longus tendon. A case report and review of the literature.  Clin Orthop1986;223.
  81. Peterson JJ, Bancroft LW: Os peroneal fracture with associated peroneus longus tendinopathy.  AJR Am J Roentgenol2001; 177:257.
  82. Tehranzadeh J, Stoll DA, Gabriele OM: Case report 271. Posterior migration of the os peroneum of the left foot, indicating a tear of the peroneal tendon.  Skeletal Radiol1984; 12:44.
  83. Geppert MJ, Sobel M, Thompson FM: Peroneus longus tendon calcification.  J Bone Joint Surg Br1992; 74:163.
  84. Malhotra CM, Lally EV, Buckley WM: Ossification of the plantar fascia and peroneus longus tendons in diffuse idiopathic skeletal hyperostosis (DISH).  J Rheumatol1986; 13:215.
  85. Khoury NJ, et al: Peroneus longus and brevis tendon tears: MR imaging evaluation.  Radiology1996; 200:833.
  86. DeLuca PA, Banta JV: Pes cavovarus as a late consequence of peroneus longus tendon laceration.  J Pediatr Orthop1985; 5:582.
  87. Edwards M: The relations of the peroneal tendons to the fibula, calcaneum and cuboideum.  Am J Anat1928; 42:213.
  88. Eckert WR, Davis Jr EA: Acute rupture of the peroneal retinaculum.  J Bone Joint Surg Am1976; 58:670.
  89. Kollias SL, Ferkel RD: Fibular grooving for recurrent peroneal tendon subluxation.  Am J Sports Med1997; 25:329.
  90. Krause JO, Brodsky JW: Peroneus brevis tendon tears: pathophysiology, surgical reconstruction, and clinical results.  Foot Ankle Int1998; 19:271.
  91. Stover DN, Bryan DR: Traumatic dislocation of the peroneal tendons.  Am J Surg1962; 103:108.
  92. Oden RR: Tendon injuries about the ankle resulting from skiing.  Clin Orthop1987;63.
  93. Church CC: Radiographic diagnosis of acute peroneal tendon dislocation.  AJR Am J Roentgenol1977; 129:1065.
  94. Rosenberg ZS, et al: MR features of longitudinal tears of the peroneus brevis tendon.  AJR Am J Roentgenol1997; 168:141.
  95. Rosenberg ZS, Feldman F, Singson RD: Peroneal tendon injuries: CT analysis.  Radiology1986; 161:743.
  96. Rosenberg ZS, et al: Peroneus brevis tendon in normal subjects: MR morphology and its relationship to longitudinal tears.  J Comput Assist Tomogr1998; 22:262.
  97. Alanen J, et al: Peroneal tendon injuries. Report of thirty-eight operated cases.  Ann Chir Gynaecol2001; 90:43.
  98. Clarke HD, Kitaoka HB, Ehman RL: Peroneal tendon injuries.  Foot Ankle Int1998; 19:280.
  99. Safran MR, O'Malley Jr D, Fu FH: Peroneal tendon subluxation in athletes: new exam technique, case reports, and review.  Med Sci Sports Exerc1999; 31:S487.
  100. Mason RB, Henderson JP: Traumatic peroneal tendon instability.  Am J Sports Med1996; 24:652.
  101. McLennan JG: Treatment of acute and chronic luxations of the peroneal tendons.  Am J Sports Med1980; 8:432.
  102. Steinbock G, Pinsger M: Treatment of peroneal tendon dislocation by transposition under the calcaneofibular ligament.  Foot Ankle Int1994; 15:107.
  103. Hammerschlag WA, Goldner JL: Chronic peroneal tendon subluxation produced by an anomalous peroneus brevis: case report and literature review.  Foot Ankle1989; 10:45.
  104. Hansen BH: Reconstruction of the peroneal retinaculum using the plantaris tendon: a case report.  Scand J Med Sci Sports1996; 6:355.
  105. Karlsson J, et al: Surgical treatment of concomitant chronic ankle instability and longitudinal rupture of the peroneus brevis tendon.  Scand J Med Sci Sports1998; 8:42.
  106. Sammarco GJ, Diraimondo CV: Chronic peroneus brevis tendon lesions.  Foot Ankle1989; 9:163.
  107. Zoellner G, Clancy Jr W: Recurrent dislocation of the peroneal tendon.  J Bone Joint Surg Am1979; 61:292.
  108. Jones E: Operative treatment of chronic dislocation of the peroneal tendons.  J Bone Joint Surg Am1932; 14:574.
  109. Mick CA, Lynch F: Reconstruction of the peroneal retinaculum using the peroneus quartus. A case report.  J Bone Joint Surg Am1987; 69:296.
  110. Stein RE: Reconstruction of the superior peroneal retinaculum using a portion of the peroneus brevis tendon. A case report.  J Bone Joint Surg Am1987; 69:298.
  111. Acevedo JI, Myerson MS: Modification of the Chrisman-Snook technique.  Foot Ankle Int2000; 21:154.
  112. Platzgummer H: [On a simple procedure for the operative therapy of habitual peroneal tendon luxation].  Arch Orthop Unfallchir1967; 61:144.
  113. Sobel M, Geppert MJ: Repair of concomitant lateral ankle ligament instability and peroneus brevis splits through a posteriorly modified Brostrom Gould.  Foot Ankle1992; 13:224.