Disorders of Tendons

The treatment of disruption of extensor tendons varies depending on whether a laceration or rupture has occurred. The first step in the treatment is an accurate diagnosis based on a careful physical examination. With an isolated rupture, typically only one tendon is involved. On the other hand, with a penetrating wound or laceration, several structures may be damaged. It is important to routinely assess the function of individual tendons and to evaluate the neurovascular status of the anterior ankle and dorsal foot. Knowledge of tendon anatomy, particularly the courses and insertions, is useful in determining the nature and extent of the pathologic process.

Anzel et al ³ evaluated 1014 cases of tendon injuries at the Mayo Clinic and noted that 21 injuries were to the extensors to the toes, a 2% incidence. They did not differentiate between injuries to the extensor hallucis longus (EHL) and extensor digitorum longus (EDL).

Extensor Digitorum Longus

Bell and Schon ⁴ have noted that the EDL proper can only be lacerated between the ankle and the midfoot because individual tendons are found below this level. Above the ankle, the EDL tendons are in a more centralized location, but their slips are separate, making multiple EDL lacerations possible. Obliquity of the lacerations that occur above the ankle are indicative of a common mechanism, that being the falling of a sharp object against the leg or ankle (Fig. 24-1). One may be deceived when looking at these injuries because the superficial laceration may reveal intact tendon below, only to have the deeper tendon laceration occur more distally below intact skin. The EDL is relatively superficial and easily lacerated with trauma (Fig. 24-2). Because the main function of the EDL is extension of the metatarsophalangeal (MTP) joint and the proximal and distal interphalangeal (PIP and DIP) joints of the lesser toes, when it is transected and not repaired, a claw toe deformity can develop. Patients with chronic extensor tendon lacerations report difficulty controlling the toes when attempting to put on socks or slide into shoes. During these activities, the toe tends to catch on the fabric or insole and passively flex underneath the foot. Often, because of the proximity of the anterior tibial tendon to the extensor hallucis longus and the neurovascular bundle, injury to these structures can occur simultaneously.

Figure 24-1 Extensor digitorum longus laceration. A, Oblique laceration of the lower leg. B, Laceration has led to transection of both the extensor digitorum longus and the extensor hallucis longus, leaving an inability to extend any of the toes. Weakness of ankle dorsiflexion is commonly observed as well. C, After acute repair. D, After repair, note identical dorsiflexion of all the toes.

Figure 24-2 A, Dorsal toe laceration with distal disruption of extensor hallucis longus. After resection of the margins of the wounds, the tendon was repaired. B, Dorsal lateral foot laceration with disruption of the extensor tendons and preservation of the extensor hallucis longus tendon. After wound debridement, longitudinal proximal and distal extensions of the wounds permitted repair of the tendons.

Anatomy

The EDL originates on the lateral tibial condyle, the anterior crest of the fibula, and the interosseous membrane, and it inserts on the base of the terminal phalanges of the four lesser toes. Innervated by the deep peroneal nerve, the EDL functions to extend the toes at the DIP joint and to dorsiflex and evert the foot.

The EDL divides into two separate tendons beneath the superior retinaculum and then further divides into two lateral tendons to the fourth and fifth toes and two medial tendons to the second and third toes (Fig. 24-3). The individual tendon of the EDL to each toe is joined on the lateral aspect by the tendon of the extensor digitorum brevis. These individual tendons are anchored at the level of the MTP joint by a fibroaponeurotic dorsal digital expansion.²⁴

Figure 24-3 The extensor digitorum longus tendon divides into two separate tendons beneath the extensor retinaculum and then further divides into separate tendons to the four lesser toes.

Physical Examination

On physical examination, an absence of extension of the lesser toes at the MTP joint is demonstrated after disruption of the EDL. Weakness of extension of the toes can also be appreciated at the PIP and DIP joints. Furthermore, because the EDL affects eversion and dorsiflexion of the foot, significant weakness of this function can be noted after tendon disruption. On palpation, a gap may be noted at the area of tendon injury. An interruption of the EDL may be diagnosed by an inability to palpate this tendon in the forefoot or ankle region as well as by weakness of lesser toe extension. The status of the superficial peroneal and deep peroneal nerves should be evaluated as well as the function of the extensor digitorum brevis.

On physical examination, difficulty can surround the diagnosis because of the ability of one tendon to substitute function for another. For example, the extensor digitorum brevis (EDB) can substitute for the EDL. On the plantar aspect of the foot, the flexor digitorum longus (FDL) can substitute for the flexor hallucis longus (FHL) because of a crossover connection between the two flexor tendons. Comparison with unaffected contralateral toes can be useful. It is also useful to passively hold the ankle in both maximum dorsiflexion and plantar flexion and observe the positioning of the toes. In plantar flexion, the resting tension on the toes should permit them to lie in a neutral position or dorsiflexion when the tendons are intact. There should be a springiness to the toes with intact tendons that is appreciated when pushing them into plantar flexion while holding the ankle in plantar flexion. In dorsiflexion of the ankle, the toes should drop into a plantar-flexed position versus the ankle plantar-flexion position, when they should dorsiflex. Careful assessment is important to delineate a specific tendon injury.

Surgical Treatment

Bell and Schon ⁴ recommend that the EDL be primarily repaired using a modified Kessler suture technique. Alternatives include a modified Bunnell or Krackow technique (Fig. 24-4). Postoperatively, the foot is protected for 3 to 4 weeks with the foot and ankle in neutral position, with subsequent gradual initiation of passive range-of-motion exercises. The authors suggest night splinting after cast immobilization is discontinued.

Figure 24-4 Technique of tendon repair. A, Modified Bunnell technique. B, Kessler technique. C, Krackow technique.

At surgical exploration after a laceration, careful and comprehensive management is important with an open wound. All wounds should be thoroughly explored, debrided, and copiously irrigated. Any foreign bodies or materials should be removed. Inspection of adjacent neurovascular structures is important, and they should be repaired or ligated as appropriate. Parenteral antibiotics, tetanus prophylaxis, and immobilization should be used depending on the specific tissue injury. A second-look operation 24 to 72 hours later should be considered for wounds with greater contamination. Postoperatively, the patient should be instructed in passive dorsiflexion of the ankle and toes, to maintain tendon gliding without straining the repair. After the wound is healed, active assistive dorsiflexion can be instituted. Resistive exercises should be avoided for 6 to 8 weeks depending upon the repair. The patient should sleep in a protective night splint to maintain neutral position. Full weight bearing in a CAM-boot can be started after the incision has healed because the boot, when standing and walking, helps maintain the tendons in a position with minimal tension.

Rooks ²³ reviewed reports of EDL injuries^{9,10,16,28,33} and noted 26 cases of EDL disruption. A preponderance of satisfactory results occurred after surgical repair. Lipscomb and Kelly¹⁶ reported on six lacerations of the EDL in combination with other tendon injuries and reported 50% good results. Floyd et al⁹ reported on eight EDL disruptions, seven of which were primarily repaired. The one tendon that was not repaired had a poor result. Other reports note generally good results with surgical intervention.^10,28,33 Wicks et al³³ reported on four lacerations of the EDL and concluded that those not repaired did not have a significant problem. Floyd et al⁹ reported a high incidence of painful dorsal scars after laceration of the dorsum of the foot. Rooks²³ advised surgical repair of a disrupted EDL if it could be accomplished with minimal extension of the wound. He advised careful attention to associated nerve injuries as well.

Akhtar and Levine ¹ reported a case of spontaneous dislocation of the EDL after a rupture of the inferior extensor retinaculum. They repaired the retinaculum and relocated the tendon successfully.

In general, injuries to the EDL tendon occur with lacerations to the dorsum of the foot or anterior ankle. In the course of surgical exploration, appropriate treatment of nerve and vessel injuries should be carried out, and repair of the disrupted EDL tendons should be done when feasible.

Extensor Digitorum Brevis

The EDB tendon originates on the distal lateral and superior surface of the calcaneus and inserts on the lateral aspect of the extensor digitorum longus tendon and also on the base of the proximal phalanx of the second through fourth toes. It is innervated by the deep peroneal nerve and provides extension at the MTP joint. The muscle is the only intrinsic muscle on the dorsum of the foot. There is no EDB tendon to the fifth toe.

The EDB is located on the lateral aspect of the forefoot and covers the lateral aspect of the subtalar joint. The tendons are quite small and are often injured after a laceration on the dorsolateral aspect of the foot. Bell and Schon ⁴ suggest that if the tendons are easily identified at the time of an EDL repair, an EDB repair should be performed as well. If the EDB is not repairable, EDL repair alone is adequate. No series have been reported on repairs of the EDB.

Kriza and Mushlin ¹³ reported an avulsion fracture of the EDB from its origin on the calcaneus. It was treated nonsurgically with a successful result. An avulsion fracture of the EDB should be distinguished from an os peroneum, a fracture of the anterior process of the calcaneus, the peroneal trochlea, a fracture of the cuboid, or a rupture of the calcaneofibular ligament.

Extensor Hallucis Longus

Anatomy

The EHL originates on the midportion of the anterior fibula and the interosseous membrane and inserts onto the base of the distal phalanx of the hallux. Innervated by the deep peroneal nerve, it extends the hallux and everts the foot. The EHL receives its motor supply much farther distally than the anterior tibial muscle and the EDL. The motor branch to the EHL travels in close proximity to the fibula for about 10 cm before penetrating the muscle belly.²⁵ The EHL is connected to the base of the proximal phalanx by the extensor aponeurosis, which receives contributions from the abductor and adductor hallucis. At the level of the ankle joint, the EHL becomes tendinous as it enters three successive soft tissue tunnels beneath the superior extensor retinaculum and inferior extensor retinaculum and within the extensor hood of the hallux (Fig. 24-5). These three areas play a role in a tendon entrapment or in preventing proximal retraction of the EHL tendon after injury.¹²

Figure 24-5 At the level of the ankle joint, the extensor hallucis longus becomes tendinous as it courses between superior and inferior extensor retinaculum. The six zones of laceration of the extensor hallucis longus are illustrated.

Lipscomb and Kelly ¹⁶ noted that as the EHL passes beneath the extensor retinacular ligaments, it is enveloped in a separate sheath, providing a gliding mechanism on the anterior aspect of the tibia and ankle.

History and Physical Examination

Attritional ruptures can occur at or around the level of the ankle joint.¹⁹ Spontaneous ruptures of the EHL tendon occur, but lacerations are more common.^2,6 On occasion, calcification can occur with associated tendinopathy.³¹

Surgical transection of the EHL can occur during any exposure adjacent to its course, but more commonly, it can be traumatized during osteotomies when not completely protected. During cheilectomy of the first metatarsal head through a dorsal approach, the saw blade can inadvertently lacerate the EHL. Similarly, during a metatarsal osteotomy from the medial apporach, the EHL can be cut. A partial laceration can occur that may make the tendon vulnerable to late “spontaneous” rupture. An EHL rupture at the interphalangeal (IP) joint can occur in association with a violent passive plantar flexion of the IP joint with a concurrent eccentric contraction of the EHL. This can happen during soccer as the player is kicking and is blocked by another player or an object.

The patient might experience a sudden pop with a subcutaneous rupture of the EHL. Development of ecchymosis in the area of the tendon and tenderness to palpation are coupled with an inability to dorsiflex the great toe (Fig. 24-6). Tearing of the skin over the hallux IP joint may occur in association with the EHL ruptures that occur after severe IP plantar-flexion injuries. The tendon typically is not painful after rupture. An obvious defect may be present in the region of the anterior ankle with disruption of the EHL, and a gap may be noted. The tendon might not be palpable. EHB substitution can allow weak extension of the IP joint of the hallux.²⁸ Patients having difficulty pulling on socks and shoes because of the weakened extension of the hallux readily experience the toe getting caught in the toe box or sock. Walking barefoot can be problematic because the patient can stub the hallux on the floor. In this situation, the toe tip has friction against the ground that, because of the forward motion and the lack of a full lift-off, results in a disruption of normal gait, making the patient vulnerable to tripping and/or falling. Depending on the location of the tendon disruption, some function might remain. Lacerations over the dorsum of the foot and the anterior ankle may be accompanied by injury to the anterior tibial or dorsalis pedis artery, deep and superficial peroneal nerves, and the anterior tibial tendon (Fig. 24-7).

Figure 24-6 Technique of push-up test to examine function of the extensor hallucis longus (EHL). A thumb or finger is pressed on the plantar aspect of the first metatarsophalangeal joint. With unopposed function of the flexor hallucis longus, the interphalangeal joint flexes, demonstrating discontinuity or dysfunction of the EHL.

Figure 24-7 Magnetic resonance images demonstrating normal tendons on the left and injured extensor hallucis longus and anterior tibial tendon on the right after an anterior ankle deep laceration. The solid arrows indicate the anterior tibial tendon, and the open arrows indicate the extensor hallucis longus.

Al-Qattan ² classified the zones of injury of the extensor hallucis tendon lacerations into six areas:

Zone 1: at the insertion site on the distal phalanx

Zone 2: the area between zones 1 and 3

Zone 3: over the first metatarsophalangeal joint

Zone 4: on the dorsum of the foot between zones 3 and 5

Zone 5: laceration of the tendon beneath the extensor retinaculum

Zone 6: in the lower leg proximal to the extensor retinaculum (see Fig. 24-5).

Surgical Treatment

Extension of any laceration should be performed in a longitudinal direction to assess an injury to the EHL. Evaluation of the anterior tibial tendon, deep peroneal nerve, or other elements of the neurovascular bundle is important. The tendon is approximated and repaired with a 2-0 nonabsorbable suture with a modified Kessler or Krackow technique (Fig. 24-8; see Fig. 24-4).

Figure 24-8 Distal laceration of extensor hallucis longus (EHL; zone 3). A, Laceration closed in emergency room without repair of tendon. B, Note extensor lag of the hallux. C, Exploration defining intact extensor hallucis brevis and complete laceration of extensor hallucis longus. D, After primary repair of EHL. E, Note extension of the hallux after the repair.

If the tendon is retracted, a more proximal incision or an extension of the exposure may be necessary in the area of the anterior ankle (Fig. 24-9), and a tendon graft may be necessary to bridge a substantial defect in the case of a delayed repair (Fig. 24-10).^8,30,32 The tendon may become caught beneath the more proximal extensor retinaculum. It is also very helpful to dorsiflex the ankle and the toes to passively deliver the tendon ends into the wound. Once the ends are found, the surgeon can insert a long 25-gauge needle perpendicularly to skewer the tendon, and this keeps it from retracting. This is a relatively atraumatic way to hold the tendon during repair.

Figure 24-9 Laceration of extensor hallucis longus (zone 4). A, Distal laceration of extensor hallucis longus (tendon found at edge of extensor retinaculum). B, Preparation for transfer of tendon distally. C, Krakow suture placed at end of both tendons ends. D, After repair of tendon laceration.

Figure 24-10 Delayed reconstruction of extensor hallucis longus (EHL) tendon with gracilis tendon allograft. A, The gracilis tendon is harvested from the ipsilateral knee. B, Tenolysis of the EHL is performed, and then a gracilis autograft is sutured to the proximal EHL stump with a Pulvertaft weave technique. Arrow illustrates the proliferative scar tissue attached to the distal stump of tendon that, when resected, leaves a 3-cm gap. C, The tendon graft has been sutured to the distal stump but also secured through a transverse drill hole in the proximal phalanx. An interphalangeal joint arthrodesis has been performed. The arrow denotes that the 3-cm defect has been spanned with the gracilis tendon autograft. D, Anteroposterior standing radiograph demonstrates the interphalangeal joint arthrodesis. E, Active extension of the hallux metatarsophalangeal (MTP) joint is demonstrated 6 months after reconstruction. F, The hallux MTP joint demonstrates 60 degrees of passive motion postoperatively. (A and F, Courtesy B. Smith, MD. B-E, From Smith B, Coughlin M: Reconstruction of a chronic extensor hallucis longus tendon laceration with a gracilis tendon autograft, Orthopedics 31:pii:orthosupersite.com/view.asp?rID=31525, 2008. Used with permission.)

After a primary repair, a posterior splint, brace, or cast is used for 4 weeks. Once the wound is stable, early passive and active assistive dorsiflexion of the MTP joint exercises can be initiated. Poggi and Hall ²² recommend a below-knee cast with the ankle positioned at a 90-degree angle and further plantar flexion blocked. A removable boot brace is best used in compliant patients because it permits controlled passive and active assistive dorsiflexion but not active dorsiflexion of the toe and ankle, to minimize adhesions. One should avoid passive or active plantar flexion or active dorsiflexion until 4 to 8 weeks after the repair.

Results and Complications

At the time of an EHL injury, the foot often is in a dorsiflexed position, with the EHL under tension. Significant retraction can develop depending on the level of the laceration. Laceration of the digit distal to the extensor expansion may be evidenced by no significant tendon retraction because the extensor expansion prevents proximal migration.7,20 Scaduto and Cracchiolo²⁶ reviewed the world literature and noted only 43 reported cases of extensor hallucis longus tendon lacerations. Undoubtedly, there are many more cases, but experience may be diluted by the small number of cases repaired at any one institution. Al-Qattan² reported a large series of 15 patients treated with surgical repair of the EHL over a 12-year period. These included distal injuries as well as lacerations in zone 4 (over the dorsum of the foot). The author advocated temporary Kirschner wire fixation of both the interphalangeal and metatarsophalangeal joints for 6 weeks during the acute healing phase after the primary tendon repair. He reported a high level of satisfactory results. Duke and Greenberg⁷ recommend nonsurgical treatment after a distal injury. Noonan et al²⁰ reported on three patients who sustained lacerations of the base of the nail with Salter fractures and concluded that these could be treated conservatively.

More proximal EHL injuries have been reported by a number of authors.9,10,16,27–29,33 Floyd et al⁹ reported on 13 EHL lacerations, of which 11 underwent a primary repair. One was not repaired, and one had a secondary repair. Using a modified Kessler suture technique or a modified Bunnell technique, they reported seven good and six fair results. They concluded that a primary repair of the disrupted EHL is indicated. Wicks et al³³ reported on 11 lacerations of the EHL, with 7 of 9 showing good results. They suggested that patients with a late, unrepaired tendon disruption may be better cared for by conservative treatment. Simonet and Sim²⁸ reported on 5 lacerations of the anterior ankle treated with a primary repair with satisfactory results.

Griffiths ¹⁰ reported on six cases of EHL disruption in younger patients (ages 4, 19, 21, 22, 23, and 25), five of which were repaired acutely. Based on the one patient who did not have a surgical repair, the author concluded that “formal repair of the extensor hallucis longus seems unnecessary. Its natural tendency for spontaneous repair after tenotomy is well known.” Although this suggests that the EHL does not need to be repaired, Floyd et al⁹ noted that the sole justification for not repairing this tendon appears to be Griffiths’s one patient, who recovered spontaneously. Indeed, Griffiths did not even note the actual location of the injury.

Kass et al ¹² observed that after an isolated tenotomy with the foot in a plantar-flexed position, minimal retraction occurs. On the other hand, with the EHL under tension, significant retraction can occur, and a significant gap can develop that precludes later tendon healing. Floyd et al⁹ did note significant proximal retraction of the EHL in two cases. Kass et al¹² and Floyd et al⁹ concluded that tenotomies are quite different from lacerations of the EHL.

Duke and Greenberg ⁷ reported on 75 distal tenotomies of the EHL and found no evidence of weakness of the great toe in 16 patients seen in follow-up. Bell and Schon⁴ noted that the EHL, according to the literature, if left unrepaired, suffers no sequelae. They concluded, however, that these notions are based on the experience of Griffiths and thought it was imprudent to extrapolate that spontaneous recovery of EHL function routinely occurs and that EHL repair is not warranted. Since the time of that article, the authors have seen several minor chronic sequelae from a neglected laceration. The primary problems observed are clumsiness donning shoes or boots and plantar-flexion deformity of the hallux. In general, based on our clinical observations, efforts to repair the tendon should be undertaken when possible.

Isolated rupture of the EHL occurs infrequently. Menz and Nettle ¹⁸ described a case with rupture at the musculotendinous junction. Poggi and Hall²² reported on a closed rupture of the EHL at the level of the MTP joint that occurred several years after a cheilectomy.

Another example is that of a ruptured EHL tendon at the IP joint of the hallux seen in a professional soccer player with a history of a trauma during a game. The player reported a hyperdorsiflexion injury of the MTP joint in conjunction with severe plantar flexion of the IP joint. The patient reported significant pain, an inability to play and had difficulty walking for several months. On exam, he was noted to have a 1-cm healed scar from the superficial tearing of the skin and weakness of dorsiflexion of the IP joint. A bone contusion was seen on magnetic resonance imaging (MRI) of the proximal phalangeal base and dorsal metatarsal head and a medial plantar plate injury of the MTP joint. At the time of surgery, a defect was noted in the EHL tendon and dorsal capsule at the IP joint, with discontinuity of the tendon. The EHL was repaired, the MTP joint debrided, and the plantar plate repaired medially. The athlete returned to full function for several succeeding seasons without difficulty.

Sim and Deweerd ²⁷ reported on a spontaneous rupture of the EHL on the anterior aspect of the ankle in a skier. Spontaneous ruptures have also been reported after a hyper–plantar-flexion injury in a taekwondo athlete¹⁵ and from chronic impingement because of a dorsal talar osteophyte.⁸ One case of delayed rupture after injury from radiofrequency ablation during arthroscopic surgery has also been reported.³²

McMaster ¹⁷ stated that spontaneous rupture of a tendon rarely occurs without predisposing factors such as chronic disease. Successful surgical treatment centers on early diagnosis and prompt surgical intervention. Sim and Deweerd²⁷ and Skoff²⁹ repaired the tendon primarily, Langenberg¹⁴ used a free tendon graft, and Menz and Nettle¹⁸ transferred the peroneus tertius tendon to reconstruct the EHL. All had excellent results.

With delayed treatment of an old EHL rupture, Berens ⁵ noted that on initial exploration the proximal portion of the tendon could not be identified. Therefore the extensor hallucis brevis tendon was transferred into the distal stump of the extensor hallucis brevis. Menz and Nettle¹⁸ noted that a primary repair was not possible and used the tendon of the peroneus brevis that was mobilized and sutured it directly to the EHL. Hoelzer and Kalish¹¹ also reported an EHL tendon disruption and noted at exploration 4 months after injury that the proximal end had retracted. The tendon of the EDL to the second toe was split and anastomosed to the distal stump of the EHL. Allografts and autografts have also been reported as a means to bridge significant defects with delayed treatment of EHL injuries with satisfactory results^{8,21,30,32,34}

Postoperative scarring and adhesion formation can lead to diminished postoperative motion ²⁹ and may be a source of pain, but this is uncommon. Floyd et al⁹ reported that 38% of those injured had a painful scar.

Conclusion

With only one reported exception, the results of surgical repair of acute disruption of the EHL tendons have been good.

The actual site of injury is an important factor in developing a plan for treatment of a disruption of the EHL. If the injury is distal to the extensor expansion, nonsurgical treatment is considered, as long as the hallux can be maintained in a neutral position with tendon apposition. An injury proximal to the extensor expansion may be treated with a primary repair. Treatment of EHL injuries 6 weeks or later after injury is often associated with an inability to reapproximate the tendon ends. A tendon transfer or tendon graft may be necessary to bridge the interval gap (Fig. 24-11 and Video Clip 114). In these cases, one should assess the amount of tendon loss by placing moderate tension on the tendon ends and placing the ankle and hallux in neutral position. When the tendon ends cannot be opposed without excessive tension, a tendon slide, using healthy proximal EHL tendon for defects up to 4 to 5 cm, may be attempted. For anything greater than a 5-cm gap, a tendon transfer may be performed. Although in the past a common reported transfer was the peroneus tertius,¹⁸ a split of the extensor to the second toe for use in lacerations distal to the ankle joint¹¹ is a good alternative. Allograft and autograph tendon transfers have become more popular to bridge obvious tendon gaps.^{8,21,30,32,34}

Figure 24-11 Delayed repair of extensor hallucis longus laceration, 1 year after injury (zone 4 injury). A, Lateral radiograph shows clips at ends of distal stump and proximal stump with retraction beneath the extensor retinaculum. B, Interphalangeal joint fusion completed. C, Krakow-type suture placed in proximal end of distal stump. Distal end of proximal stump grasped with clamp (3-4 cm gap in tendon). D, Allograft weaved through proximal stump. E and F, Allograft is pulled distally beneath skin bridge. G and H, Pulvertaft weave of tendon graft through the distal stump. I, Completed delayed extensor hallucis longus reconstruction.

Aggressive surgical treatment of open lacerations about the foot is most important. Adequate exploration and debridement and anatomic restoration of tendons are usually appropriate. Although Griffiths ¹⁰ noted that the EHL tendon might heal spontaneously and that formal repair is not indicated, review of the literature does not support the notion that conservative management is warranted. Surgical repair of the EHL is important when feasible. On the other hand, with significant soft tissue loss, an EHL repair might not be feasible, but secondary tendon grafting can be considered if there is a distal stump, pliable tissues without extensive fibrosis along the tendon path, and no evidence of infection.

Anterior Tibial Tendon Rupture

Subcutaneous rupture of the anterior tibial tendon has received little attention in the literature, and relatively few ruptures have been reported. Anagnostakos et al ³⁶ reviewed the literature and noted 110 published cases of anterior tibial tendon disruption; in only four series were there more than four cases, the remaining being case reports or very small series.^3,16,68,77 In one of the largest series reported to date, Markarian et al⁶⁸ described 16 anterior tibial tendon disruptions, including 10 ruptures and 6 lacerations. At this time, less than 150 cases (case reports or series) of anterior tibial tendon rupture have been reported in the literature.

Anatomy

The anterior tibial tendon functions as the major dorsiflexor of the ankle,⁴⁸ primarily during the swing phase, heel strike, and early stance phase of the walking cycle.^41,81 It originates from the proximal half of the anterior tibia, the lower lateral tibial condyle, lateral tibia, and the interosseous membrane and inserts on the plantar medial aspect of the first cuneiform and the plantar base of the first metatarsal (Fig. 24-12). At the level of the lower and middle thirds of the tibia, it becomes tendinous and is surrounded by a synovial sheath. Anagnostakos et al³⁶ reported on the dissection of 53 cadaveric specimens and reported three different patterns of insertion of the anterior tibial tendon into the medial midfoot. In 36 cases (68%), the tendon inserted into the medial cuneiform and base of the first metatarsal, and in 13 cases (25%), it inserted only into the medial aspect of the first cuneiform. In four feet (7%), the tendon inserted into both the cuneiform and the metatarsal, but there was an additional accessory tendon that inserted onto the base of the first metatarsal.

Figure 24-12 The anterior tibial tendon courses beneath the transverse crural ligament and cruciate crural ligament before inserting on the plantar medial aspect of the first cuneiform and plantar base of the first metatarsal.

Innervated by the deep peroneal nerve, the anterior tibial tendon functions to dorsiflex and invert the foot and provides controlled plantar flexion at heel strike. The tendon is active in heel-strike phase in an eccentric mode because it allows the ankle to slowly plantar flex until foot flat. It is active again in the swing phase in a concentric mode, dorsiflexing the ankle and keeping the forefoot from dragging. Congenital absence of an anterior tibial muscle and tendon is a rare occurrence ⁴² and may be associated with clawing of the toes because of recruitment of the EHL and EDL to assist in dorsiflexion of the foot and ankle.

The tendon passes beneath the superior extensor retinaculum and the upper and lower limbs of the inferior extensor retinaculum. Petersen et al ⁷⁸ investigated the structure and vascular pattern of the tibialis anterior tendon by using injection techniques, light and transmission electron microscopy, and immunohistochemistry. They found a well-vascularized peritenon, with blood vessels penetrating the tendon and anastomosing with a longitudinally oriented intratendinous network. Despite a well-vascularized posterior surface of the tendon, they found an avascular zone where the tendon runs under the superior and inferior retinacula. This results in an area 1 to 2 cm from the insertion that is at risk for rupture.

Not only is the tendon vulnerable to spontaneous rupture here but, as the tendon passes beneath these retinacular structures, it also lies on the distal surface of the tibia and is at risk for injury with fracture of the tibia or a laceration.⁶⁹ Lipscomb and Kelly¹⁶ stated that the tendon had 6 to 7 cm of excursion at this level.

An acute disruption of the anterior tibial tendon can occur with trauma at any age from fracture of the tibia or laceration.43,45,65,68,69 Three quarters of these disruptions occur in male patients. A spontaneous rupture can occur from an underlying degenerative process.^50,51,66 Inflammatory arthritis,^49,62 gout,⁵⁸ rheumatoid arthritis,^46,68,77 impingement from an underlying exostosis, a local steroid injection,* and diabetes^† have all been cited as contributing factors in anterior tibial tendon rupture. A ganglion in the region of the anterior ankle can masquerade as a rupture of the anterior tibial tendon, with the formation of an enlarged mass (Fig. 24-13).⁸²

Figure 24-13 Ganglion of the anterior ankle region eroding the anterior tibial tendon, masquerading as a tendon rupture. A, Lateral radiograph with dorsal talar spur. B, Magnetic resonance image demonstrating a mass anterior to the anterior tibial tendon. C, Mass at surgery. D, After resection, the anterior tibial tendon is intact. The joint is exposed to remove the osteophytes.

Ruptures occur near the anterior tibial tendon’s insertion, most often close to or within 2 to 3 cm of the insertion (Fig. 24-14). They can be caused by chronic wear from an exostosis at the talonavicular, naviculocuneiform, or metatarsocuneiform joints or by attrition from rubbing against the edge of the inferior extensor retinaculum.⁵⁴ McMaster¹⁷ noted that ruptures occur in the presence of an abnormal tendon structure. This correlates well with the deficiency in the tendon’s vascular supply.

Figure 24-14 Spontaneous rupture of anterior tibial tendon (arrows) typically occurs in distal 3 cm of tendon.

Markarian et al ⁶⁸ have described “acute on chronic” tears manifesting as a degenerative tear in the anterior tibial tendon. These ruptures usually occur in men between the fifth and seventh decades of life and most often are reported in the seventh decade.^38,44 They appear to develop as an age-related phenomenon. A prodromal phase is unusual, and patients do not routinely complain of pain before tendon rupture. Patients may notice an enlarged nodule on the degenerative tendon before rupture.

Anterior tibial tendon ruptures occur with forced or excessive plantar flexion against a contracted anterior tibial muscle.38,64,71,81 An acute rupture is usually one of two different clinical presentations. With acute trauma in a younger patient who is involved with a higher functional level of activity, the rupture is associated with the acute onset of pain but infrequently with severe trauma. Walking down a ramp or slope can trigger eccentric contracture of the anterior tibial muscle, which may precipitate a tendon rupture. Decreased dorsiflexion strength is noted at the time of injury, which usually prompts the patient to seek medical evaluation and treatment soon after injury. On the other hand, an older patient typically has no history of antecedent trauma and often presents several months after the incident with a complaint of a painless footdrop.⁷⁹ Frequently, a patient does not remember a precipitating event,⁸¹ and the older patient often is unaware of the condition.⁴⁴ Markarian et al⁶⁸ reported an average 10-week delay in diagnosis in their series of 16 anterior tibial tendon disruptions. Late diagnosis is common, and permanent disability is rare.

The patient often experiences a snapping sensation that is associated with a brief episode of sharp pain over the anterior aspect of the ankle and is accompanied by swelling. Ambulation may be difficult in the initial few hours after rupture, but the pain subsides rapidly. A patient might note lack of coordination, a slapping gait, or an inability to clear the toes with ambulation. In time, the anterior tibial muscle atrophies. Both Frigg et al ⁵⁰ and George et al⁵¹ have reported cases of simultaneous degeneration of the anterior tibial and posterior tibial tendons that required hindfoot arthrodeses and anterior tibial tendon reconstructions.

The anterior tibial tendon, on occasion, may be involved with tendinopathy (tendinitis or tendinosis), as described by Burman,³⁹ Goldman,⁵³ and Hamilton.⁵⁶ Beischer et al³⁷ has described a series of 29 cases of tendinosis that were characterized by swelling over the insertion, nocturnal pain, and, on examination, point tenderness over the insertion of the anterior tibial tendon. Beischer et al observed longitudinal split tears in the distal tendon in 19 of 29 cases and typical tendinosis on those that were explored. They found a much higher incidence of involvement in females in this series and speculated that this may be a different clinical entity than the typical patient (typically elderly males) who sustains a spontaneous rupture of the tendon. Beischer et al suggested a provocative “stretch” test to assess tendinosis, which included forced ankle plantar flexion, midfoot eversion, and abduction with a pronation force applied to the foot in an attempt to acutely passively stretch the anterior tibial tendon. A positive test was characterized by aggravation of the typical pain the patient had previously experienced. In a follow-up study on the operated patients in this series, Grundy et al⁵⁴ reviewed the results of 12 cases, mostly women, who were explored for tendinosis and longitudinal tears of the distal anterior tibial tendon. Although there was evidence of macroscopic tendinosis in all cases, those with less than 50% degeneration were treated with a debridement while those with greater than 50% degeneration were treated with debridement and an EHL tendon augmentation. Later rupture in those who only had a debridement, led the authors to recommend more aggressive reconstruction and use of the EHL augmentation on a routine basis.

Insertional tendinopathy can occur after prolonged walking or running. Besides the localized pain, patients may complain of pain in the anterior ankle and lower leg. At times, it will manifest as anterior “shin splints” or even chronic exertional compartment syndrome. The repetitive eccentric load at the bone tendon interface of the contracted anterior tibial tendon musculotendinous unit during impact on heel strike induces microtears that generate a localized inflammatory response. The condition can be exacerbated while descending slopes or inclines, when the sudden jarring at the insertion of the anterior tibial tendon at the cuneiform is maximized. Avoiding these stresses and wearing cushioned heeled shoes can help the tendon to recover. For more intractable cases, patients will benefit from a CAM-boot or an ankle–foot orthosis (AFO). Platelet-rich plasma derived from peripheral blood, or bone marrow injected at the tendon insertion can be helpful in conjunction with immobilization when bracing alone is unsuccessful.⁵⁹ Steroid injections at this location should be avoided to minimize the risk of tendon rupture (Fig. 24-15).