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

Section 4 - Unique Problems in Sport and Dance

Chapter 22 - An international perspective on the foot and ankle in sports




Personal perspective on foot and ankle sports conditions



Ankle instability



Osteochondral lesions of the talar dome



Achilles tendon lesions



Plantar fasciitis



Lisfranc sprains






Further reading



Treatment of Achilles tendon ruptures





















Foot and ankle injuries in United Arab Emirates sports



Nerve injuries complicating inversion ankle sprains






Clinical picture









Further reading



Foot and ankle injuries caused by traditional Japanese martial arts












Foot and ankle problems caused by some traditional Chinese habits and sports



Foot and ankle sports injuries in Korea






Ssireum (Korean traditional wrestling)



Taekwon-do (Korean martial arts)



Basketball, soccer, rugby, and baseball



Accessory navicular syndrome



Australian foot and ankle conditions in sport



Foot/ankle injuries in surf lifesaving






Further reading



Soccer: hallux osteochondral lesion and rupture of the Achilles tendon



Hallux osteochondral lesion in beach soccer players



Neglected rupture of the Achilles tendon






Footballer's (soccer) ankle in Venezuela



Clinical evaluation



Additional studies












The biologic perspective of sports disorders affecting foot and ankle









Principles of tendinopathy management



Surgical management










A A. Personal perspective on foot and ankle sports conditions

  1. Giannini,
    F. Vannini

Ankle Instability

The lateral ligamentous complex of the ankle may be the most commonly damaged structure in sport injuries. [0010] [0020] Garrik[3] reported a frequency of 45% in basketball practice, 31% in soccer, and 25% in volleyball.

Primary repair of the ligaments was previously recommended; nonoperative treatment also has been recently recommended. [0020] [0050] However, despite adequate primary functional treatment, some patients develop chronic instability. In 20% of the cases, ligamentous reconstruction is required.[5] Indications for ligament reconstruction are mechanical and functional instability and failure of rehabilitative treatment. The goal of surgical treatment is to improve stability and proprioceptive sensation maintaining complete range of motion (ROM).

Ankle instability surgery has been divided into an anatomic repair consisting of imbrications of the local tissue of the lateral ligamentous complex and an ankle-ligament reconstruction involving tendon grafts. A nonanatomic tenodesis results in stiffness of the operated ankle, prolonging recovery and decreasing sport[6] because of the incorrect orientation of the reconstructed ligaments.

Because of these considerations, our choice technique is a modified Brostrom with a reinforced flap when the local tissues are strong enough. Otherwise an “anatomic reconstruction” is performed with a tendon graft using the plantaris. When no plantaris is available, a tibialis posterior hemisection harvested from a cadaver is used.

Surgical technique 1

The anatomic reconstruction has been described previously by Brostrom[4] and consists of the direct suture of the stumps of residual tissue. In our experience, to reinforce the reconstructed ligaments a periosteal flap should be harvested from the anterolateral aspect of the fibula and turned down and sutured as talofibular ligament or split in two and used also to reinforce the calcaneofibular ligament ( Fig. 22A-1 ).


Figure 22A-1  To reinforce the reconstructed ligaments, a periosteal flap should be harvested from the anterolateral aspect of the fibula and turned down and sutured as talofibular ligament or split in two and used also to reinforce the calcaneofibular ligament.



Surgical technique 2

When the residual tissues are not strong enough to permit direct suture or after failure, we perform a reconstruction of the talofibular and calcaneofibular ligaments using the plantaris, if present, or a cadaveric tibialis posterior graft. The tendon is fixed through a transosseous tunnel or with an anchor on the neck of the talus. A tunnel is created through the anterior aspect of the lateral malleolus where the talofibular is inserted and the tendon is passed in and sutured to the periosteum. In case of an associated calcaneofibular lesion, the tendon will be passed through the apex of the lateral malleolus and be sutured on the lateral wall of the calcaneus ( Fig. 22A-2 ). We pay particular attention to reconstruct the ligament with a proper length, direction, and tightness similar to those of the healthy anatomic complex to obtain an isometry of the new ligaments permitting a physiologic ROM and avoiding stiffness.[7]



Figure 22A-2  (A) A tunnel is performed through the anterior aspect of the lateral malleolus where the talofibular is inserted. The tendon is passed and sutured to the periosteum. In case of an associated calcaneofibular lesion, the tendon will be passed through the apex of the lateral malleolus and be sutured on the lateral wall of the calcaneus. (B) A bone procedure such as a dorsiflexion metatarsal osteotomy may be performed to correct the associated cavus deformity of the foot.



In a 1983 study, Giannini et al.[8] concluded that 67% of ankle sprains in sports activity were in athletes with cavus foot. Because of this observation, in cases with a cavus foot associated with a varus of the calcaneus, evaluated as reducible according to the Coleman test,[9] a mini-invasive dorsiflexion metatarsal osteotomy (see Fig. 22A-2 ) associated with the ligamentous reconstruction is indicated. This procedure will rebalance the foot, helping to prevent further sprains and improving function.

Osteochondral Lesions of the Talar Dome

Osteochondral lesions of the talar dome are very common in sports activity as a consequence of ankle sprains. [0110] [0120] Procedures for the treatment of osteochondral lesions of the talus including debridement of the joint, shaving of fibrillated cartilage, and resection or perforation of subchondral bone in the last decade have been performed arthroscopically with low morbidity. These surgeries are not effective in lesions larger than 1.5cm[2] and have not been histologically effective in restoring the hyaline cartilage. [0130] [0140] [0150] [0160] [0170] [0180] [0190] [0200] [0210]


Figure 22A-3  Immunohistochemical staining for collagen type II.




Figure 22A-4  Immunohistochemical staining for proteoglycans.




Figure 22A-5  Alcian blue staining for proteoglycans detection.



Autologous chondrocyte transplantation (ACT) has proved to be capable of restoring the articular hyaline cartilage surface, including defects larger than 2cm[2] (Figs. 22A-3, 22A-4, and 22A-5 [0030] [0040] [0050]).[17] In the past, this practice required a medial or lateral malleolar osteotomy, and, although there were good clinical and histologic results, the technique was quite invasive and technically demanding.[17] Recently, advancement in tissue engineering permitted the development of absorbable synthetic scaffolds, permitting a completely arthroscopic technique through the traditional anteromedial and anterolateral approaches. Because of this improvement, it appears to be reasonable, mostly in the young athletes, to extend the indications of ACT even in smaller lesions traditionally treated with microfractures.

Surgical technique

The first step requires ankle arthroscopy with cartilage harvesting for cell culture, performed directly from the affected joint using the osteochondral fragment. After 30 days, a second step ankle arthroscopy through traditional anteromedial and anterolateral accesses is performed. The focus of the lesion is carefully shaved, and care is taken to reach the healthy cartilage.

The Hyalograft-C scaffold, made of hyaluronic acid, is sized and prepared in the right shape and placed on the positioner (Fig. 22A-6 [0060] [0070]).

Through an appropriate cannula, the self-adhesive scaffold is positioned to cover the lesion (Fig. 22A-7 [0060] [0070]).


Figure 22A-6  The Hyalograft-C (FIDIA s.r.l. Abano PD, Italy) scaffold, made of hyaluronic acid, is sized and prepared in the right shape and placed on the positioner.




Figure 22A-7  Arthroscopic view showing the self-adhesive scaffold positioned to cover the lesion.



Immediate daily continuous passive motion (CPM) for 6 to 8 hours begins after surgery and continues for a period of 6 weeks. Touchdown (20%-30%) crutch walking is permitted for 6 weeks. After 6 weeks, progressive increased weight bearing and active ROM are permitted. Full weight bearing will be allowed at 8 weeks. Return to cutting, turning, or jumping sport is permitted only after 1 year.

Achilles Tendon Lesions

Achilles tendon lesions in soccer are 31% to 34% of all traumas, according to Lanzetta et al.[21] The Achilles tendon rupture usually is caused in soccer by direct or indirect trauma during jumping, cutting, or turning.[22] Predisposing factors in the soccer player are due to an overuse of the calcaneal-Achilles-plantar system, possibility of preexisting tendinopathy, or corticosteroid injections.

The clinical presentation is variable. Pain may be mild for the preexisting degeneration of the tendon because functionality may be performed by the retromalleolar pronator and supinator muscles with different percentages, making the clinical evidence less clear. Rerupture occurs in 10% to 30% of high-performance active patients with nonoperative treatment; [0240] [0250] [0260] therefore surgery generally is recommended. Because formal open procedures have been associated with a high rate of complications related to poor wound healing, deep infection, adhesion of scar tissue, and disturbance of sensation,[0240] [0250] our choice is surgical repair with a mini-invasive technique. The advantages of mini-invasive surgery are less surgical trauma, better quality of reparative scar tissue, avoidance of damage to the local vascularity, faster recovery, and return to sport activity. Indications for the mini-invasive treatment are lesions from 6 to 8cm from the calcaneal insertion and no more than 6 days after the rupture.

Surgical technique

The Achilles tendon repair system ( Fig. 22A-8 ) permits a suture of the tendon through a 1.5-cm incision. Both stumps of the ruptured tendon are identified. The instrument is introduced in the closed position, under the paratenon, in a proximal direction. When the tendon lies between the two branches of the instrument, the sutures are passed, and the end of each is held with a small clamp to keep the sutures separate from each other. When the instrument is withdrawn, the sutures slide to a peritendinous position. Afterward, the same sequence is performed on the distal stump, and the tendon reduction is performed under visual control.


Figure 22A-8  The Achilles tendon repair system permitting a suture of the tendon through a 1.5-cm incision.



Postoperative treatment consists of a boot worn for 8 weeks. Mobilization is permitted only in plantarflexion from the first to the sixth week, after which complete ROM is achieved.

Partial weight bearing (15kg) is permitted with the boot in plantarflexion for 3 weeks. Partial weight bearing (15kg) is permitted with the boot at 90 degrees for 3 weeks. Total weight bearing is permitted with boot ROM from 10 degrees plantarflexion to 10 degrees dorsiflexion for 2 weeks.

Plantar Fasciitis

Plantar fasciitis is common in high-performance athletes, mostly runners and basketball and volleyball players because of the high stress concentrated at the fascia insertion in running and jumping.[26]

Commonly cited risk factors for plantar fasciitis are the flat or cavus foot, a tight Achilles tendon, the type of training shoes worn, and errors in the training routine.[27]

Anti-inflammatory medications may be helpful in providing symptomatic relief. Some improvement is possible with the use of a shoe insert providing 1cm height at the hindfoot and daily stretching exercises of the Achilles tendon-plantar fascia complex.

A safe and effective nonoperative treatment that we feel should be considered before surgery is the application of low-energy shock waves at the fascia insertion (three applications of 2100 impulses of low-energy shock waves), usually providing good results.[28] If the fasciitis does not respond to the nonoperative treatment, in a minimum of 4 months for a professional athlete, surgical treatment should be attempted.

Because the open technique has a high failure rate, with 15.5% of the patients reporting dissatisfaction,[29] we prefer the use of a percutaneous fasciotomy. It is important to note that this technique does require surgical experience and may be associated with complications.

Surgical technique

A 14-mm K-wire is inserted manually in the medial aspect of the foot to identify the level of the insertion of the fascia. The fasciotomy is performed with a tenotomy blade while the foot is maintained in dorsiflexion and the fascia is probed externally with a finger ( Fig. 22A-9 ).


Figure 22A-9  The fasciotomy is performed with a tenotomy, maintaining the foot in dorsal hyperflexion and probing the fascia with a finger.



This method reduces the formation of scars and provides for a fast recovery at a low cost. Surgery should be followed by early ROM, stretching exercises, and ankle dorsiflexion. An orthosis that maintains the foot and ankle in 10 degrees of ankle dorsiflexion should be worn during the night for the first 3 weeks.

Lisfranc Sprains

Injuries to the Lisfranc ligament complex in the general population are uncommon and typically occur as a result of high-velocity and indirect trauma that causes an obvious displacement and disruption of the tarsometatarsal anatomy.[30] Low-velocity Lisfranc sprains also can occur after an indirect trauma when the foot is plantarflexed and slightly rotated. This is a frequent condition in soccer players.

Lisfranc sprains represent a spectrum of injuries to the Lisfranc ligament complex, from partial sprains with no displacement to complete tears with frank diastasis[31] ( Fig. 22A-10 ). Although the nondisplaced injuries often heal uneventfully, patients with displacement should undergo a closed reduction and internal fixation with cannulated screws.


Figure 22A-10  Lisfranc sprains resulting in a frank diastasis.



Surgical technique

A percutaneously placed large bone clamp is used to assist the reduction. Under C-arm control, percutaneous guidewires are inserted, followed by placement of cannulated screws ( Fig. 22A-11 ).


Figure 22A-11  Under C-arm control, percutaneous guidewires and cannulated screw are used to maintain the reduction.



Postoperatively, a nonweight-bearing boot is maintained for 4 weeks, followed by 4 weeks of boot with progressive weight bearing. Screw removal occurs from 14 to 24 weeks.

Return to sport activity should be permitted after a functional rehabilitation program, usually after 4 months.


  1. Burks RT, Morgan J: Anatomy of the lateral ankle ligaments.  Am J Sports Med1994; 22:72.
  2. Kannus P, Renstom P: Current concepts review. Treatment for acute tears of lateral ligaments of the ankle: operation, cast or early controlled mobilization.  J Bone Joint Surg Am1991; 73:305.
  3. Garrick JM: The frequency of injuries, mechanism of injury and epidemiology of ankle sprains.  Am J Sports Med1977; 5:241.
  4. Brostrom VI: Sprained ankles: surgical treatment of chronic ligament ruptures.  Acta Chir Scand1966; 243:551.
  5. Renstrom PA: Persistently painful sprained ankle.  J Am Acad Orthop Surg1994; 2:270.
  6. Baumhauer JF, O'Brien T: Surgical considerations in the treatment of ankle instability.  J Athl Train2002; 37:458.
  7. Leardini A, et al: A geometric model of the human ankle joint.  J Biomech1999; 32:585.
  8. Giannini S, et al: Nostri orientamenti sul trattamento degli esiti delle fratture-lussazioni della Lisfranc.  Chir del piede1983; 17:169.
  9. Coleman SS, Chestnut WJ: A simple test for hindfoot flexibility in the cavus varus foot.  Clin Orthop1977; 123:60.
  10. Schenck R, Goodnight JM: Osteochondritis dissecans: current concepts review.  J Bone Joint Surg1996; 78A:439.
  11. Tol JL, et al: Treatment strategies in osteochondral defects of the talar dome: a systematic review.  Foot Ankle Int2000; 21:119.
  12. Alexander AH, Lichtman DM: Surgical treatment of transchondral talar-dome fractures (osteochondritis dissecans).  J Bone Joint Surg1980; 62A:646.
  13. Altman RD, et al: Preliminary observations of chondral abrasion in a canine model.  Ann Rheum Dis1992; 51:1056.
  14. Brittberg M, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation.  N Engl J Med1994; 331:889.
  15. Buckwalter JA, Lohmander S: Operative treatment of osteoarthrosis: current concepts review.  J Bone Joint Surg1994; 76A:1405.
  16. Buckwalter JA, Mow VC, Ratcliffe A: Restoration of injured or degenerated articular cartilage.  J Am Acad Orthop Surg1994; 2:192.
  17. Giannini S, et al: Autologous chondrocyte transplantation in osteochondral lesions of the ankle joint.  Foot Ankle2001; 22:513.
  18. Hangody L, et al: Mosaicplasty for the treatment of osteochondritis dissecans of the talus: two to seven year results in 36 patients.  Foot Ankle2001; 22:552.
  19. Homminga GN, et al: Perichondral grafting for cartilage lesions of the knee.  J Bone Joint Surg1989; 72B:1003.
  20. Kumai T, et al: Arthroscopic drilling for the treatment of osteochondral lesions of the talus.  J Bone Joint Surg1999; 81A:1229.
  21. Lanzetta A, Meani E, Tinti G: Le lesioni dell'Achilleo nella pratica sportiva: considerazioni etiopatogenetiche e indicazioni terapeutiche.  Ital J Sport Traumatol1989; 3:113.
  22. Hattrup SJ, Johnson KA: A review of ruptures of the Achilles tendon.  Foot Ankle1985; 6:34.
  23. Carden DG, et al: Rupture of the calcaneal tendon. The early and late management.  J Bone Joint Surg Br1987; 69:416.
  24. Cetti R, et al: Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature.  Am J Sports Med1993; 21:791.
  25. Roberts C, et al: Dynamised cast management of Achilles tendon ruptures.  Injury2001; 32:423.
  26. Snider MP, Clancy WG, Mc Beath AA: Plantar fascia release for chronic plantar fasciitis in runners.  Am J Sports Med1983; 11:215.
  27. Warren BL: Plantar fasciitis in runners. Treatment and prevention.  Sports Med1990; 10:338.
  28. Rompe JD, et al: Shock wave application for chronic plantar fasciitis in running athletes. A prospective, randomized, placebo-controlled trial.  Am J Sports Med2003; 31:268.
  29. Clanton TO, DeLee JC: Osteochondritis dissecans: history, pathophysiology and current treatment concepts.  Clin Orthop1982; 167:51.
  30. Mantas JP, Burks RT: Lisfranc injuries in the athlete.  Clin Sports Med1994; 13:719.
  31. Nunley JA, Vertullo CJ: Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the athlete.  Am J Sports Med2002; 30:871.


Further Reading

Davies MS, Weiss GA, Saxaby TS: Plantar fasciitis: how successful is surgical intervention?.  Foot Ankle Int  1999; 20(12):803-807.


B B. Treatment of Achilles tendon ruptures

Hajo Thermann,Christoph Becher


The rapidly growing trend for participation in recreational and competitive sport is accompanied by an increase of overuse syndromes. In the foot and ankle, the incidence of Achilles tendon rupture and subsequent problems has increased significantly in recent decades. [0340] [0350] [0360] In Germany the incidence of acute Achilles tendon rupture is estimated to be 15,000 cases/year.[3] The rupture usually does not occur at the time of top-level sporting activities. Most studies show a peak between the ages of 30 and 45 years. [0370] [0380] [0390] [0400] [0410] [0420] The patient collective has a remarkably large portion of leisure-time athletes and patients with sedentary occupations.[10] The portion of injuries in track-and-fields athletics is cited as only 10%. These are mostly young patients who sustained a tendon rupture as a result of an incompletely treated achillodynia or an enormous training workload.[9] In the future, an increasing number of older patients (older than 50 years) will sustain Achilles tendon rupture as strenuous sports activities become more and more common in this age group. Of all the tendons of the human body, the Achilles tendon seems to be the most susceptible to degenerative changes. The male-to-female ratio of persons with Achilles tendon rupture ranges between 5:1 and 10:1 in most studies, and on average the men are older. [0420] [0440] According to the literature and our experience, Achilles tendon ruptures occur most often (in 80% to 90% of cases) 2 to 6cm proximal to the calcaneal insertion.[9] The incidence of proximal ruptures distal to the musculotendineal transition is 10% to 15% and is caused by degenerative changes. Ruptures near the calcaneal insertion are rare and mostly are found in hyperpronators with a heel spur (Haglund's heel). In contrast to impulsive injury mechanism in tendinous ruptures, bony avulsions usually are caused by continuously increasing tension and strength or direct impact.[9] The rupture mechanism usually is a consequence of an indirect loading and traction mechanism, such as a push-off with the foot in plantarflexion and simultaneous knee extension or a sudden, unexpected dorsiflexion of the ankle with powerful contraction of the calf muscles.[9] Direct impact, such as a kick or hit on the tensed tendon, accounts for only 1% to 10% of ruptures. [0440] [0450] The degenerative and the mechanical theory of etiopathogenesis of Achilles tendon rupture face each other. Aseptic inflammations (tendinitis, paratendinosis) and reduced vascular supply lead to degenerative changes with cell loss and disorders of mucopolysaccharide content, even to fatty, mucoid, or calcifying degeneration.[13] Repetitive or single stresses result in minor microtrauma. Low temperature and fatigue of athletes (lactic acid) lead to decreased maximal load resistance.[9] If regenerative healing processes cannot keep pace, the sum of microtrauma leads to rupture.


The typical characteristic of a tendon rupture is a hit or whiplash-like sudden pain. Ruptures happening in contact sports often are perceived as a hit by an ax or a bar. A crack or a popping sound often is heard. A palpable gap and a positive Thompson test are the first clinical signs of an acute Achilles tendon rupture. Because of hematoma, these signs are not always visible but usually are palpable. The strength of plantarflexion typically is decreased or completely lost, resulting in an inability of heel rise and weak rolling of the foot with stalking landing of the leg and an externally rotated foot. A remaining plantarflexion does not indicate an intact tendon because extrinsic flexors such as the plantaris muscle also are able to produce this movement.

Although most Achilles tendon ruptures can be diagnosed clinically, evaluation by ultrasonography and magnetic resonance imaging (MRI) enables a definitive diagnosis and is decisive for the choice of treatment (Figs. 22B-1 and 22B-2 [0120] [0130]). Ultrasonographic appearance of acute Achilles tendon rupture shows broad variations. The most common signs are interruption of continuity and demarked tendon stumps. Hypoechogenic accumulations of liquid at the rupture site and loss of the typical parallel hyperechogenic reflex patterns are depicted regularly by experienced examiners. Because some ruptures do not show a visible diastase of the stumps from the hematoma, dynamic examination in dorsiflexion and plantarflexion is essential. Even if there is no visible gap, a spreading of fine parallel echoes, corresponding to a loss of cross-wise network of elastic fibers, reveals a rupture. Inflammatory tendinosis with edematous dissolution of the structures must be differentiated. Disrupted or retracted soleus fibers, which are detected mostly in top-level athletes, are significant for the choice of treatment and especially for the surgical technique. Although this can be detected by ultrasonography, MRI shows a better validity.[9] The soleus muscle must be examined with sagittal and axial scans. Furthermore the differentiation of rupture area and tendon ends enables an exact determination of the diastase and distance to the calcaneal insertion.


Figure 22B-1  T1-weighted magnetic resonance imaging (MRI) sagittal. Complete rupture of the Achilles tendon with diastase of the tendon stumps.




Figure 22B-2  Ultrasonography of an acute Achilles tendon rupture. Interrupted continuity and demarked tendon stumps (arrows).




Conservative treatment

Primary conservative immobilizing treatment and postoperative aftercare in a cast are not justified concerning the disadvantages of muscle atrophy and loss of coordination and proprioception. The concept of primary functional treatment considers the ultrasound or MRI morphology as a basis for treatment strategy. The ultrasonographic or MRI depiction of complete adaptation of tendon ends in 20-degrees plantarflexion is required. The validity of this method, compared with operative treatment, could be proven in a series of more than 550 patients using a high-shaft shoe, comparable to a modified boxer boot (Variostabil, Orthotech, Germany) * [14] ( Fig. 22B-3 ). Indication for primary functional treatment independent of the ultrasonographic or MRI findings should be preferred in the elder nonactive patient or in patients with altered operative risk or reduced capacity for tissue regeneration (e.g., after organ transplantation surgery, systemic corticosteroid treatment, diabetes).[15]


Figure 22B-3  The Variostabil boot (Orthotech GmbH, 82131 Gauting, Germany; www.orthotech-gmbh.de).



*  Available from Orthotech GmbH, 82131 Gauting, Germany (www.orthotech-gmbh.de).

Operative treatment

Issues that comprise the decision for operative treatment include the following:



Patients with dubious compliance for primary functional treatment.



Patients who insist on or feel safer with a surgical procedure.



Patients in whom no adaptation of the tendon stumps was found sonographically or on MRI.



Patients with a demonstrable disruption of the soleus muscle.



Patients such as top athletes for whom surgery is intended to prevent medial gastrocnemius atrophy.



Patients with distal ruptures (≤2cm) near the calcaneal insertion.

It generally is possible to appose the tendon stumps within 3 weeks of rupture. In older ruptures the tendon ends usually are retracted and need reconstructive modalities.


In acute Achilles tendon ruptures, simple end-to-end or three-bundle sutures have been the methods of choice to date ( Fig. 22B-4 ). In recent years in the United States the suture technique by Krackow (Fig. 22B-5 ) has become popular because it provides strong mechanical stability that allows early functional rehabilitation. [0490] [0500] A biomechanical study by Watson et al.,[17] however, proved the weak stability of the suture realized by the different open techniques and questioned the advantages of the open surgical treatment.


Figure 22B-4  End-to-end suture technique according to Bunnel-Mason.




Figure 22B-5  The suture technique according to Krackow.



The combination of the advantages of the biology of tendon healing from the primary functional treatment along with minimally invasive surgery to stabilize the tendon stumps adaptation for the first healing period is addressed by the percutaneous technique described by Buchgraber and Pässler[18] ( Fig. 22B-6 ). Using only five small incisions, a 1.3-mm polydioxanone suture (PDS) is guided percutaneously by means of an awl. It connects the proximal tendon with the calcaneal insertion and crosses the rupture site, thereby acting as an internal fixator. To tighten the cord into the tendon, multiple dorsiflexions of the foot are performed. Another advantage of this technique is the remaining integrity of the paratendon, which is important for the healing process. To prevent the potential risk of injuring the sural nerve, an endoscopically assisted percutaneous technique with a 2.8-mm arthroscope can be used.[9]


Figure 22B-6  The percutaneous technique described by Buchgraber and Pässler.



The lace technique by Segesser pays special attention to the rotation of radiating tendon bundles, as described by Cummins. With his technique he provides an adequate reinsertion of the medial gastrocnemius and soleus fibers, which often are disrupted or retracted in Achilles tendon ruptures in top-level athletes ( Fig. 22B-7 ).


Figure 22B-7  The lace technique by Segesser.



For rehabilitation, functional aftertreatment in the Variostabil boot is an essential part of an optimal outcome.

Treatment of reruptures

In the treatment of reruptures there are two options. If an adaptation of the tendon stumps is seen in plantarflexion either sonographically or by MRI, a simple percutaneous suture can be performed.

In cases with a tendon gapping, a shortening of the gastroc-soleus-Achilles complex with adhesions is probable. This happens in the majority of delayed cases. In these circumstances, a small medial incision (4–5cm) at the former incision is made. Then the gastro-soleus complex is released distally ( Fig. 22B-8 ). A normal subcutaneous suture is performed and serves as an “internal fixator” of the ruptures tendon. In addition, classic Krakow sutures are applied for the tendon stumps ( Fig. 22B-9 ).


Figure 22B-8  Digital distal release of the gastro-soleus complex.




Figure 22B-9  Subcutaneous suture in addition to Krackow's technique in the treatment of reruptures.



The aftertreatment has the same protocol with the Variostabil boot.

Treatment of chronic ruptures

The problem of chronic rupture is retraction of the tendon stumps with the lack of an efficient regenerate. Sometimes a primary reconstruction is possible, but in most cases reconstructive techniques are indispensable. The decision for the correct reconstructive technique depends on the amount of insufficient tissue. Therefore evaluation by MRI is mandatory. Defects of 2 to 5cm are the indication for reconstruction with a modified “two flaps technique,” first described by Thermann in the year 2000. For reconstruction, two flaps of the aponeurosis of the triceps surae muscle are used. In the first step, the muscle is released proximal by a medial incision, followed by the preparation of the two flaps from the medial and lateral part of the aponeurosis. Essential for the modification is the turning down and 180-degree rotation of the medial flap approximately 1.5cm proximal to the corresponding lateral part. This offset considerably facilitates the skin closure later. After fixing the flaps medially and laterally at the distal stump, suturing is performed continuously with a 3.0-mm PDS cord in a “tubulation technique,” thus creating a “neotendon” as a consequence ( Fig. 22B-10 ). The neotendon should be stretched in a manner that forces a slight plantarflexion. For wound healing, a cleaved cast is applied, followed by rehabilitation in the Variostabil boot for 8 weeks according to primary functional treatment. [0420] [0520]


Figure 22B-10  The modified “two flaps technique.”



Reconstruction of larger defects requires a transfer of the flexor hallucis longus tendon[20] or the peroneus brevis tendon.[21] In both techniques the distal and proximal stump are sewn together with the transferred tendon. Also, the neotendon should be adequately stretched to put the foot in an equine position ( Fig. 22B-11 ). Because the peroneal tendon is not “in phase,” there are only very limited indications for this procedure. Rehabilitation protocol corresponds to the “two flaps technique.”


Figure 22B-11  The transfer of the flexor hallucis longus tendon or the peroneus brevis tendon. In both techniques, the distal and proximal stumps are sewn together with the transferred tendon.




The Variostabil boot plays a major role in rehabilitation and regaining of functional performance. The general concept is to prevent stress at the rupture site while having axial loading, which promotes a safe and powerful tendon healing.

This boot has a plastic tongue to prevent dorsiflexion; the lateral shaft-stabilization reduces torsion, and the reducible heel pad allows a gradual adjustment of 20 degrees from plantarflexion to neutral position. Its functional potential regarding gastrocnemius activities was proved by electromyography, which showed comparable amplitudes to the uninjured side after 3 months.[15] With the fitted boot the patient is allowed to perform full weight bearing and to continue the previously begun isometric exercises. The patient wears the boot for 6 weeks, day and night (or alternatively uses a night splint to protect the tendon) and for the following 2 weeks only during the daytime. After 3 weeks the patient is allowed to exercise on a stationary bike, but only with little application of power. In ambitious patients, a physiotherapeutic treatment with well-dosed strengthening exercises (isometric exercises, isokinetic bicycle), proprioceptive neuromuscular facilitation (PNF), and coordination exercises in the boot is allowed after 4 weeks. In addition, ultrasound application (1Hz) and cryotherapy are performed to enhance tendon regeneration. From the sixth week on, leg-press training is begun in the boot. After 8 weeks, an ultrasonographic control evaluates the restoration of continuity and tendon regeneration. After an appropriate tendon regeneration has been achieved (8 to 12 weeks MRI or sonography control), the treatment in the boot is discontinued. A small heel lift in the normal shoe is recommended for a further 6 to 8 weeks. Jogging is allowed after 3 months if coordination and muscle power are appropriate.


The goal of treatment today is not only the restoration of the tendon continuity but also the regaining of the former activity level at the earliest possible time. This is achievable by the appropriate surgical technique and also depends on the adequate aftertreatment and rehabilitation protocol.


  1. Christensen J: Rupture of Achilles’ tendon.  Acta Chir Scand1953; 106:50.
  2. Schönbauer HR: Diseases of the Achilles’ tendon.  Wien Klin Wochenschr1986; 14(suppl 1):23.
  3. Thermann H: Treatment of Achilles’ tendon ruptures.  Foot Ankle Clin1999; 4:773.
  4. Cetti R, et al: Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature.  Am J Sports Med1993; 21:791.
  5. Inglis AE, Sculco TP: Surgical repair of ruptures of the tendo Achillis.  Clin Orthop1981; 156:160.
  6. Jakobs D, et al: Comparison of conservative and operative treatment of Achilles’ tendon rupture.  Am J Sports Med1978; 3:107.
  7. Lo IK, et al: Operative versus nonoperative treatment of acute Achilles tendon ruptures: a quantitative review.  Clin J Sport Med1997; 7:207.
  8. Nistor L: Surgical and non-surgical treatment of Achilles tendon rupture. A prospective randomized study.  J Bone Joint Surg Am1981; 63:394.
  9. Thermann H: [Treatment of Achilles tendon rupture].  Unfallchirurg1998; 101:299.
  10. Jozsa L, et al: The role of recreational sport activity in Achilles tendon rupture. A clinical, pathoanatomical, and sociological study of 292 cases.  Am J Sports Med1989; 17:338.
  11. Riede D: Therapy and late results of subcutaneous Achilles’ tendon rupture.  Beitr Orthop Traumatol1972; 6:328.
  12. Arner O, Lindholm A: Subcutaneous rupture of the Achilles tendon; a study of 92 cases.  Acta Chir Scand1959; 116(suppl 239):1.
  13. Kannus P, Jozsa L: Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891 patients.  J Bone Joint Surg Am1991; 73:1507.
  14. Thermann H, Zwipp H, Tscherne H: [Functional treatment concept of acute rupture of the Achilles tendon. 2 years results of a prospective randomized study].  Unfallchirurg1995; 98:21.
  15. Thermann H: [Rupture of the Achilles tendon–conservative functional treatment].  Z Orthop Ihre Grenzgeb1998; 136:20.
  16. Mandelbaum BR, Myerson MS, Forster R: Achilles tendon ruptures. A new method of repair, early range of motion, and functional rehabilitation.  Am J Sports Med1995; 23:392.
  17. Watson TW, et al: The strength of Achilles tendon repair: an in vitro study of the biomechanical behavior in human cadaver tendons.  Foot Ankle Int1995; 16:191.
  18. Buchgraber A, Pässler HH: Percutaneous repair of Achilles tendon rupture. Immobilization versus functional postoperative treatment.  Clin Orthop1997; 341:113.
  19. Lindholm A: A new method of operation in subcutaneous rupture of the Achilles tendon.  Acta Chir Scand1959; 117:261.
  20. Monroe MT, et al: Plantarflexion torque following reconstruction of Achilles tendinosis or rupture with flexor hallucis longus augmentation.  Foot Ankle Int2000; 21:324.
  21. Trillat A, et al: [Treatment of former rupture of the Achilles tendon (transfer-plasty of the lateral peroneus brevis)].  Lyon Chir1967; 63:603.


C C. Foot and ankle injuries in United Arab Emirates sports

  1. Kazim

The United Arab Emirates (UAE) has a desert climate and is situated directly on the Persian Gulf. This unique geography lends itself to a truly wide variety of sporting activities among the residents. Water sports such as water skiing, wakeboarding, and kite surfing are hugely popular. Other sports such as soccer, rugby, tennis, and squash are commonplace. In the desert, sand boarding and motor sports command the winter months. Most of the common injuries seen elsewhere are encountered but with some unique scenarios.

Certain niche sports are found in the UAE. For example, falcons are trained to hunt prey. This involves long periods of bonding and progressive conditioning of the predator bird. To accomplish this, the owner often has to run rapidly to tend to his falcon, and in the soft sand this is better accomplished barefoot. Sandals typically are worn ( Fig. 22C-1 ) to keep the foot high off the ground to prevent entry of pebbles but are discarded when running in soft sand. Still, minor stub and barb injuries are common. Because the terrain underfoot is soft, the barbs or other objects have little force for any penetration. When training the falcons on the harder desert plain, one wears enclosed shoes (Figs. 22C-2 and 22C-3 [0240] [0250]) to prevent the entry of foreign objects. Also, ankle sprains (mostly lateral) tend to be relatively minor on the sand because the surface is not firm and thus is very forgiving during inversion.


Figure 22C-1  A unique sport in the UAE is hunting prey with falcons. The sandals keep the foot high off the ground to prevent entry of pebbles. They are discarded when running in soft sand.





Figure 22C-2  On the harder desert plain, the hunter seen here with the falcon (A) uses enclosed shoes (B).




Figure 22C-3  Another example of the falcon trainer (A) with typical shoewear (B) used for hard desert terrain (C).



Arabs have a long tradition with horses. In the UAE, horse racing (speed and marathon) and polo are two sports in which injuries are relatively common. Most tend to be in the upper extremities from falls, but foot and ankle injuries also occur. The prolonged “heel down” position in the saddle can lead to impingement syndromes of the anterior chamber of the ankle, requiring removal of any kissing osteophytes or soft tissues. Because these are mostly symptomatic early in their development, arthroscopic debridement is very successful, with arthrotomy rarely being required. Minor crush injuries of the foot and ankle occur as the horses collide during play, but serious crush injuries from hooves are surprisingly uncommon in the UAE. This could possibly be from the combination of a high standard of horsemanship and well-trained thoroughbreds that are used in the sport.

Motocross has its share of injuries because dirt bikes are ridden in the sand at high speeds. Riders are required to wear body armor and protective footwear ( Fig. 22C-4 ). However, unlike hard dirt terrain that causes a violent plantarflexion force of short duration, sand produces a more moderate force of longer duration. This leads to sprains of the anterior structures, with relatively frequent anterior capsular tears. Conservative care with walker-type removable braces allows rapid return to riding. Occasionally, more severe problems such as Lisfranc injuries and subluxations or dislocations of the talocrural joint occur. When surgical reconstruction is warranted, rigid internal fixation is used, possibly including the repair of a deltoid ligament avulsion and concomitant syndesmosis stabilization ( Fig. 22C-5 ).



Figure 22C-4  A popular winter sport is motocross. The rider wears body armor and protective footwear to minimize injury. (A) The rider here is preparing to land on a dune following a jump. (B) The rider cuts across the soft and at times unstable sand and is susceptible to ankle and leg trauma.





Figure 22C-5  (A) This syndesmotic injury was noted on a stress view of the ankle. (B) Two syndesmotic screws close the tibiofibular space and suture anchors stabilize the deltoid tear.



Long-distance bike riding is now becoming popular in the UAE. A relatively common problem seen in these cyclists is Morton's neuroma. This happens despite appropriate shoewear and possibly results from a combination of the high heat and humidity causing edema of the foot. Conservative care with metatarsal pads and a wider toe box to accommodate the forefoot is very successful.

In the UAE, we emphasize rapid rehabilitation and return to sports. Fast-track programs and hydrotherapy for management of foot and ankle injuries provide an early start to the recovery process, with weight bearing as soon as safely possible. Rapid progression to strengthening and proprioceptive feedback exercises has been beneficial to returning the player quickly to his or her sport.


D D. Nerve injuries complicating inversion ankle sprains

  1. Melamed,C. Zinman

Inversion, plantarflexion, and twisting forces put the ankle ligaments and bones under tension and strain that eventually may cause them to fail, culminating in ankle sprain and fractures. Diagnostic workup in the athlete usually is directed to rule out fractures, assess the severity of the ankle ligaments injury, and tailor treatment and rehabilitation to ensure healing of the ligaments in the desired length and strength. The proprioceptive mechanism and peroneal muscle strength also must be addressed to ensure safe return to sporting activities.

Inversion injury imposes stretch and stress also on the more superficial structures, the nerves and integument. Skin swelling and hematoma formation are caused by injury to the skin and its lymphatics, small venules, and capillaries (in addition to bleeding from the torn ligaments) and is a sin qua non of ankle sprain. It usually resolves with time and is not a reason for concern to the treating physician or coach. However, there often is less awareness of the existence and importance of stretch to the nerves.[1]

Overall, the superficial peroneal nerve (SPN) is the most commonly injured nerve in ankle sprain as well as ankle fractures. The spectrum of injury to the SPN runs from mild (hardly noticeable stretch resulting in mild numbness, dysesthesia, or transient burning sensation in the distribution of that nerve) to severe allodynia, sudomotor changes, severe spontaneous pain, and paresis involving whole or large parts of the foot and ankle. These changes may evolve rapidly into a florid pain syndrome, reflex sympathetic dystrophy (RSD) by the older nomenclature or complex regional pain syndrome (CRPS) type 2 by the new one.

In this section we briefly review the anatomy of the SPN, the pathomechanics and pathology of its stretch injury, and the myriad of symptomatology, focusing on early diagnosis of injury to the nerve. We equip the reader with some useful tips regarding early institution of therapy for these individuals by the primary care sport physician or orthopaedist. We review the algorithm and treatment options for the more severe cases.


The peroneal branch of the sciatic nerve separates from the tibial one at the popliteal fossa, where it takes a more lateral course. It emerges from underneath the biceps tendon near its insertion to fibula head and courses around the neck of the fibula, where it divides to the SPN and deep peroneal nerves (DPN). The SPN travels in the lateral compartment underneath the peroneus longus and exits the crural fascia to become subcutaneous about 10 to 15cm proximal to the tip of the lateral malleolus in most cases. [0560] [0570] There are variations, however, in the exit mode, some of which carry special clinical relevance. The nerve can have a low exit point (5cm from the tip in 2% and 7.5cm in 5%).[4] It also may penetrate into the anterior compartment first and then through the crural fascia. The SPN bifurcates to main two branches, the intermediate dorsal cutaneous nerve, supplying the dorsolateral aspect of the foot, and the dorsomedial cutaneous branch, which innervates the skin on the medial aspect of the dorsal forefoot and the hallux. Occasionally it also supplies the second toe and some cross innervation with the DPN in the first webspace.[3]

Pathoanatomy of nerve injury with ankle sprain

Normal excursion of the peroneal nerve during ankle inversion is about 4cm.[5] This excursion is transferred and shared by the whole nerve up to the level of the common peroneal nerve through several gliding mechanisms. Severe ankle inversion may stretch the nerve beyond its physiologic capability to withstand stretch and gliding.[6] Anatomic variations and preexisting conditions may hamper the gliding mechanisms and predispose to more severe injury.[7] The exit level is important because if there is impedance to nerve gliding through the fascial hiatus and the exit is low, the same stretch is imposed on a shorter nerve segment. Even with a normal exit, overstretching because of severe inversion-plantarflexion may result in nerve damage. Typically a combination of the two will result in a more severe injury. Nerves that penetrate to the anterior compartment before emerging through the fascia cruris also are prone to stretch injury.[8]

We postulate other possible mechanisms that may contribute to gliding impedance and that have not been studied. The “acute on chronic entrapment” means that because of chronic entrapment there is fibrosis, thickening, or other changes in the fascial opening that impede gliding. In the case of severe sprain and extreme nerve stretch, the excursion of the nerve is relatively slow in the canal. The excessive stretch is loaded mainly on the distal part of the nerve.

We assume that muscle swelling and increased intracompartmental pressure created during rigorous athletic activity[9] presses the nerve against the fascia cruris and impedes nerve gliding through the hiatus. Another hypothesis is the “intraperoneal entrapment.” During acute inversion the nerve glides distally. At the same time, rigorous contraction of the peroneal muscles may compress and entrap the SPN, which courses between them. The contracting muscles pull the nerve proximally, in the opposite direction, thus increasing the stretch on the nerve.

There may be damage to the subcutaneous tissue because of shearing and ruptures of subcutaneous fat, small blood vessels, and lymphatics. Scarring will ensue, and the areolar tissue, which allows the nerve to glide smoothly, will lose its pliability. The clinical relevance of this phenomenon per se may be the experience of pain on inversion (sometimes even at night because of the plantarflexed-inversion position of the foot at sleep) and/or chronic, occasional subclinical entrapment, which may manifest itself only in a future sprain episode. Quite often the picture is mixed, with intraneural, perineural, and nerve bed changes.

Histologically, in the severe cases stretching injury to nerve will result in perineural tears, which may lead to intraneural and perineural fibrosis. [0640] [0650] In cases in which we had to resect the nerve following inversion ankle injury, we saw on histology laceration and discontinuation of nerve fibers. In one extreme case we observed fatty degeneration with marked thickening of the nerve. Macroscopically the picture varies from a nerve that appears normal to a thickened one. The fascial exit site may show frank cicatrization. Extensive scarring may be seen at the nerve bed at the dorsum of the foot, which interferes with nerve gliding ( Fig. 22D-1 ).


Figure 22D-1  A 22-year-old sustained an ankle sprain 3 years before surgery. She developed pain in the distribution of the superficial peroneal nerve (SPN) that worsened with walking and at night. SPN block relived 80% of her pain. She was not improved with nonsurgical therapy. At surgery to release the nerve, dense scarring was found along the course of the nerve (A-C). A stepwise release was carried out (B and C). Nerve release and dissection must continue proximally to the exit point of the nerve from the peroneal muscle compartment (C). The nerve is freed distally until unscarred nerve can be seen (in this case far beyond the bifurcation to its two main branches. At completion of release, the fascia has been opened and the nerve can be seen emerging freely from the muscular compartment(D). The patient felt complete relief immediately after surgery, but over the course of the next year worsened to some extent. Two years after surgery she has mild pain on daily activities but does not take pain medications. She can perform limited sport activities.



New evidence sheds light on the role of inflammation in the pathology and perpetuation of nerve pain with the development of pain syndromes. [0660] [0670] [0680] Although the importance of the inflammatory mechanism is not completely clear, and the research was focused on patients with CRPS, the available data suffice to justify the addition of anti-inflammatory agents to the treatment protocol.

Clinical Picture

Symptoms related to nerve injury in association with ankle sprain or inversion injury vary according to the severity of nerve damage. They often are masked by the associated mechanical derangement. The clinician may tend to ascribe the symptoms and pain to the mechanical ligamentous or bony injury and miss the opportunity to initiate early treatment, which in the severe cases may prevent deterioration to florid pain syndrome.

In general, we divide the clinical presentation of nerve injuries after ankle sprain to three groups on the basis of their myriad of symptoms and severity. Group 1 represents those with mild traction neuritis. They typically have mild numbness and/or allodynia. Their pain level is moderate (visual analogue score [VAS] score usually 4–7). The nerve is tender to palpation, percussion, and inversion. These patients usually heal well within 1 to 2 months.

Patients in group 2 have significant symptoms and signs of neuritis. Pathologically there is perineural fibrosis, scarring, or intraneural microscopic changes. They may well have entrapment of the nerve in the fascial hiatus. They either have constant pain (usually burning, tingling, or electric shooters), which exacerbates with activities, or they may have only provoked pain. The nerve may look and feel thickened. Plantarflexion of the foot and fourth toe causes the nerve to be more prominent, and usually there is tenderness to percussion along the course of the nerve. Further plantarflexion and inversion is unpleasant and aggravates the athlete's symptoms. Occasionally the tenderness will be confined to the exit site of the nerve from the fascia at the distal anterolateral aspect of the leg. In such cases entrapment is the probable diagnosis and the prognosis is favorable after surgical decompression.

Group 3 was composed of patients with neuropathic pain whose pain and symptoms are beyond the distribution of the injured SPN. These patients suffer from increased general activity of the pain system and actually may have CRPS type 2.[15] Their pain score is high (VAS 7–10). They have spontaneous and provoked pain in which pain often is worse at night. It is characterized by a burning quality, deep ache, or electric shooters. There often is diffuse swelling from the toes to the distal leg, transient color and temperature (vasomotor) changes, and sudomotor disturbances, which may manifest as edema and hyperhydrosis or dry skin. The skin often is swollen and shiny. Allodynia (pain in response to nonpainful stimuli, e.g., light touch) is common. Sensation typically is disturbed beyond the territory of the injured nerve. Weight bearing is limited and often impossible. The prognosis for these patients typically is grave. We assume that early intervention with pain treatment may halt the progression to florid pain syndrome in many of these patients. The role of early surgical intervention has not been established yet, but certainly in some of the cases it is justified.


Nonsurgical treatment

As a routine, nonsurgical treatment should be used first. In some of the cases, however, nonoperative modalities will not be effective, and occasionally, delaying surgery has its own risks. For example, traction injury to the SPN, which flares out the adjacent nerves and the pain system with evolving CRPS, may be treated best with early nerve release or transection. In such cases, a short course of aggressive medical treatment may need to be followed by early surgery.

Nonsurgical means include oral medications, topical applications, repeated nerve blocks, physical therapy, and pain modalities. More complicated pharmaceutic interventions, sympathetic or epidural blocks, or spinal cord stimulation can be performed by physiatrists and pain specialists.

Oral medications

We prescribe pain medications, which affect the various modalities of the altered pain pathways. Such treatment may include a combination of acetaminophen (or dipyrone), nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., celecoxib, rofecoxib, etodolac, diclofenac), nerve pain medication that is usually either antidepressants or antiepileptics, and tramadol (Ultram; Ortho-McNeil, Inc., Raritan, NJ) and/or narcotic medications. [0700] [0710]

The selection of treatment modality is determined mainly according to the severity and intensity of symptoms. The relationship between the type of pain and specific drug selection is not so clear. In the mild to moderate cases an ascending prescription attitude can be adapted. In this approach either a new or additional medication or higher dose of a given one is added gradually as needed. Simple pain medication (e.g., acetaminophen or dipyrone) is sufficient in group 1 or mild group 2 cases. (Dipyrone is an antianalgesic and antipyretic but not an anti-inflammatory medication; it is approved for use in many parts of the world but not in United States because of the rare incidence of agranulocytosis). An NSAID is prescribed concomitantly or subsequently. If pain is refractory to these medications, or in the presence of neuropathic symptoms (allodynia, burning sensation), nerve pain medication is added. Nerve pain medications usually are either antidepressants or antiepileptics. Their role is to decrease the spontaneous nerve activity and reset the correct pain threshold. Typically, the dose is increased gradually. The next step is a more potent pain medication. Tramadol is a weak μ receptor agonist and N-methyl-D-aspartate (NMDA) receptor inhibitor. Although it is not regulated as a narcotic medication, it resembles narcotics in its affinity to μ receptors and in having (uncommon) addictive potential. Narcotics can be prescribed for severe or refractory cases. In common use is oxycodone, which is available in a controlled-release preparation (daily every 8–12 hours) or in combination with aspirin (Percodan; Endo Pharmaceuticals, Chadds Ford, PA) or acetaminophen (Percocet; Endo Pharmaceuticals, Chadds Ford, PA). OxyContin (sustained-release oxycodone; Purdue Pharma L.P., Stamford, CT) usually is prescribed at 10mg twice a day initially, and the dose can be increased to 20mg twice a day. If a higher dose is needed, we recommend urgent referral to pain clinic.

It is worthwhile for the orthopaedist or sport physician to have in his or her armamentarium two or three nerve pain medications.

Our first choice drug is amitriptyline (Elavil; AstraZeneca Pharmaceuticals LP, Wilmington, DE), which is a tricyclic antidepressant, 10mg daily at night. The goal and treatment rationale should be discussed with the patient; otherwise he or she may not comply. The patients typically will read on the package that this is an antidepressant therapy and are reluctant to take the medicine, unless they had received the needed explanation. The dose may be increased in weekly intervals to 20 (two 10-mg pills), 25, 35, and 50mg. The main side effect is sedation, which may be beneficial in case of night pain. The patient should be warned against driving or performing tasks that mandate alertness. Other common side effects are dry mouth, blurred vision, and constipation. Because of the relative low doses (in comparison with that required for depression) the side effects usually are not severe, and approximately three quarters of patients can tolerate the drug.

Carbamazepine (Tegretol; Novartis Pharmaceuticals, East Hanover, NJ) is an antiepileptic medication with known antineuralgic effect. For many physicians this is the drug of choice for neuralgic pain. The dose for that indication usually is 400 to 800mg/day. The initial dose is 100mg twice a day, and it can be increased in 200-mg daily increments. Timonil (carbamazepine sustained release; Desitin Pharmaceuticals, Hamburg, Germany) is a prolonged-release version, manufactured in 300-mg tablets that can be divided to quarters. One quarter of a tablet daily is taken initially and the dose is increased by another quarter every week. Drowsiness, dizziness, and blurred vision are the main side effects. Discontinuation should be implemented gradually.

Gabapentin (Neurontin; Pfizer, New York, NY), also an antiepileptic drug, may be the most effective medication available for neuropathic pain, with fewer side effects and good tolerability. Its main limitation is high cost, and in many countries it is not approved yet for peripheral neuritic pain. The initial dose is 300mg once a day, increased every 3 days by 300mg to 300mg four times a day (e.g., change from once to twice to three and four times a day, with every change made after 3 days of getting used to the new dosage). Higher doses may be required, but we recommend in such cases that the patient be seen by a pain specialist or a physiatrist.

Topical preparations

Few topical preparations are available.

Capsaicin (Zostrix; Rodlen Laboratories, Health Care Products, Amityville, NY) is an active ingredient of red pepper that causes substance P depletion, thus interrupting nerve transmission at the peripheral level. It is applied on the tender regions (or along the course of the nerve if it is tender) three or four times daily. The main side effect is burning sensation at the site of application. If severe, this sensation can be relieved by preventive lidocaine application (EMLA cream) before applying Zostrix. It may take a few days to 1month before Zostrix exerts its analgesic effect. Once the burning sensation has decreased, one can change from the low to the higher potency (0.075%).

Another alternative is the lidocaine patch (Lidoderm; Endo Pharmaceuticals, Chadds Ford, PA), which is applied once daily and releases the local anesthetic in a controlled mode.

Topical NSAID preparations may have a role in mild cases but we have not seen great benefit in cases of neuropathic pain. In the United States, Custom Meds (Inverness, FL) a custom compounding company, formulates nearly all of the previously mentioned medications into an absorbable, topically applied gel. The formulations, combinations of various doses of medications, can be applied to the affected area with good results.

Nerve blocks

Nerve block with local anesthetic often is essential to confirm the diagnosis. In some patients the block has a therapeutic effect with symptomatic improvement that outlasts the pharmacologic effect of the local anesthetic. The physiologic basis for this phenomenon is not completely clear. There is cessation of bombardment of the central nervous system with painful impulses that may affect the central sensitization of the pain system. We combine a short-acting local anesthetic (e.g., lidocaine) with a longer-acting one. Bupivacaine is a long-acting local anesthetic with average effect of 6 to 12 hours. The main hazard is inadvertent intravenous injection, which may cause lethal arrhythmia (ventricular fibrillation). Alternatively, the addition of adrenaline may double its duration. Ropivacaine (Naropin; AstraZeneca Pharmaceuticals LP, Wilmington, DE) has a local anesthetic effect for nearly 24-hours and has the benefit of a good safety profile. Its main disadvantage is high cost. When performing a nerve block we generally use a 25-gauge needle to minimize the additional risk of inadvertent damage to the nerve.

We estimate that up to one third of patients will respond favorably to repeated nerve block. If the patient experiences a beneficial effect that lasts several days, there is a role for repeated nerve blocks.

Surgical treatment

If nonsurgical means fail to achieve the desired effect, surgery may be contemplated. In general, entrapment of the SPN at its exit site from the compartment will respond favorably to surgical release of the fascia. The surgical findings will dictate whether fascial release will be sufficient and will help to establish the prognosis. In cases in which adhesions are found, release of the nerve should provide immediate relief. If there is a thick scar bed, the risk that new adhesions will form is significant. In the case of intrasubstance damage to the nerve, a nerve release probably is not going to help. In addition, it is important to consider and to inform the patient that there is an element of unpredictability in the response of nerve to surgery (and insult). This is particularly true if resection of a diseased nerve is indicated. In this case, there is considerable risk for temporary and even permanent pain exacerbation, often in adjacent nerves.

Type of surgery selected

As a rule, the choice of surgery follows Schon's algorithm of surgical treatment for nerve pain.[18] The common surgeries are nerve release, revision nerve release (with or without containment), nerve resection (usually with burial of the nerve stump), and peripheral nerve stimulation (PNS).

Neurolysis of the nerve often is successful in the case of entrapment. The crural fascia is opened 3 to 5cm from the original exit site. Smooth excursion of the nerve is checked intraoperatively. The surgeon observes that there also is free movement of the nerve in the fatty tissue more distally. If the fat and nerve seem normal, there is no need to extend the surgical incision distally. In case of adhesion bands, the nerve is freed as far distally as needed, usually beyond the division to its two main branches ( Fig. 22D-1 ).

Scar tissue may be formed around the nerve. Dense adhesions imply damage to the nerve bed and increase the likelihood of rescarring. The typical result will be temporary relief with worsening of symptoms beginning after 6 weeks. In the milder cases, new adhesions may be formed up to 1 or 2 years from surgery.

If there is no relief after surgery, either an incomplete release or an intrasubstance nerve lesion is the cause. The nerve may have looked normal or grossly disturbed. If there are no adhesions or entrapment, intranerve damage is the probable cause. The surgeon then should consider whether to resect the nerve. If the symptoms are severe (VAS score 8–10), the nerve probably should be resected. We bury the stump in the fibula and have not experienced stump tenderness.[19] Loss of sensation on the dorsum of the foot usually is unpleasant but tolerable. If there is a flare-up of the pain in adjacent nerves and the patient shows signs of CRPS, then more aggressive management is indicated.

If nerve resection fails to relieve pain and the pain is confined to the specific nerve distribution, PNS is the next step. [0740] [0750] In this procedure an electrode is implanted on the nerve and is connected to an internal pacemaker that can stimulate the nerve. Stimulation of the nerve generates nonpainful stimuli that “close the gate” to painful impulses and thus relieve the pain. The surgery involves a wake-up test after the nerve is isolated and the wound anesthetized. During this portion of the implantation, the patient is reversed from anesthesia and the 4-electrode lead is placed in various locations around the nerve until pain relief is achieved. If the test is favorable, the patient is placed under anesthesia to permit tunneling of the wires and insertion of the pacemaker device in the thigh. In severe cases, some surgeons advocate considering the combination of concomitant nerve resection and PNS. In a long-term follow-up study (3–16 years), good results (more then 50% relief of pain with abstinence from analgesic medications) were reported by 36 out of 46 patients (78%).[20]


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  14. Weber M, et al: Facilitated neurogenic inflammation in complex regional pain syndrome.  Pain2001; 91:251.
  15. Stanton-Hicks M, et al: Reflex sympathetic dystrophy: changing concepts and taxonomy.  Pain1995; 63:127.
  16. McQuay HJ, et al: A systematic review of antidepressants in neuropathic pain.  Pain1996; 68:217.
  17. Monfared H, Sferra JJ, Mekhail N: The medical management of chronic pain.  Foot Ankle Clin North Am2004; 9:373.
  18. Schon CL, Easley ME: Chronic pain.   In: Myerson MS, ed. Foot and ankle disorders, vol 2. Philadelphia: WB Saunders; 2000.
  19. Melamed EA, Schon LC: Deep burial of resected nerve in bone—a simple technique.  Foot Ankle Int2002; 23:952.
  20. Eisenberg E, Waisbrod H, Gebershagen HU: long term peripheral nerve stimulation for painful nerve injuries.  Clin J Pain2004; 20:143.
  21. Schon LC, et al: Prelimunary results of peripheral nerve stimulation for intractable, lower extremity nerve pain.  Pain Med2000; 1:195.


Further reading

Schon LC, Easley ME: Chronic Pain.   In: Myerson MS, ed. Foot and ankle disorders,  London, England: WB Saunders; 2000.

Styf J: Entrapment of the superficial perineal nerve.  J Bone Joint Surg  1989; 71B:131.


E E. Foot and ankle injuries caused by traditional Japanese martial arts

Yasuhito Tanaka

In Japan, there are many forms of traditional martial arts that are still actively practiced today. This chapter explains in detail foot and ankle injuries associated with the three most popular martial arts: judo, sumo, and kendo. Although the origin of these martial arts is not known, the earliest known mention of their basic forms is found in Japanese documents written during the eighth century. In the last half of the nineteenth century, the modern rules for these martial arts were established, and people began to practice them as sports. Because these martial arts are practiced barefoot, there is a high incidence of ankle and foot injuries among their practitioners. However, because playing surfaces and styles of competition differ markedly among these three martial arts, they are associated with different foot injuries.


Because judo is an Olympic sport, the number of people who practice judo is increasing worldwide. A judo contest is a fight between two contestants who wear judo suits and fight on tatami (straw) mats. The first contestant to score a full point (“ippon”) wins. A contestant can score a full point by throwing the opponent on his or her back, holding the opponent for 30 seconds, or making the opponent concede. Injuries almost always are caused by throwing moves. Many judo injuries occur in the lower extremities, particularly at the knees, ankles, and feet. Because mild foot injuries are so common, those who sustain them rarely seek treatment at a medical institution.

The most common foot injury is ankle sprain; about half of all judo practitioners suffer an ankle sprain at some point ( Fig. 22E-1 ). Severe inversion sprains typically are accompanied by osteochondral fracture of the talar dome. Also, ankle instability persists in many cases, and many people who practice judo for a long period develop osteoarthritis of the ankle. Also, when a strong external force is applied, a malleolar fracture occurs, but plafond fractures and talar fractures are rare.


Figure 22E-1  Many judo injuries occur in the lower extremities. During “Ohsoto-gari,” a throwing technique, the foot and ankle assume an equinovarus position. Inversion sprain can occur in the foot of a defense (arrow).



The incidence of toe injury is high among judo practitioners. Turf-toe is a well-known injury associated with sports played on turf, such as American football. Most cases of turf-toe are caused by excessive dorsiflexion of the great toe. When a foot sweep is attempted in judo, the sweeping foot is in the equinovarus position and is swung horizontally. If the sweeping foot gets caught in the seams of the tatami mats or on the opponent's foot, the metatarsophalangeal joint of the great toe is excessively plantarflexed ( Fig. 22E-2 ). Although this generally causes sprain without a fracture, severe bending can cause a chip fracture. This type of toe injury is sufficiently unique to judo to merit its own name (perhaps “tatami toe”). If accompanied by osteochondral damage to the metatarsophalangeal joint of the great toe, osteoarthritis can lead to hallux rigidus. Although toe injuries most often affect the great toe, sometimes they can affect the lesser toe.


Figure 22E-2  The great toe is easily plantarflexed (arrow) (“tatami toe”). Tatami (straw) mats typically are used as a floor covering in judo.




Sumo is a sport in which two wrestlers fight on a round ring that is made of packed earth and has a diameter of about 4m. Sumo wrestlers wear nothing but a loincloth belt. In each bout, two wrestlers initially face each other from behind two parallel lines at the center of the ring. Once the bout begins, they collide violently, like guards and tackles in American football. The loser is the first wrestler to touch the ring with any part of the body other than the bottom of the feet or the first wrestler to go out of the ring. Sumo wrestlers try to push each other out of the ring, and heavy body weight confers an advantage in this pushing. Consequently, sumo wrestlers intentionally try to achieve and maintain a heavy body weight. Although the most common clinical problem associated with sumo is lumbar pain, injuries in the lower extremities account for more than half of all injuries associated with sumo.

Ankle and foot injuries account for about 15% of all sumo-related injuries. It might seem that this is a low percentage for a sport that is practiced barefoot. The reason for this low percentage is the manner in which sumo wrestlers move, by shuffling their feet instead of lifting their feet off the ground ( Fig. 22E-3 ). In sumo, the friction between the ground and the soles of the feet is important in keeping a wrestler in position. If either foot comes off the ground for even a short time, the wrestler easily can be pushed out of the ring. Thus shuffling helps to prevent a wrestler from being pushed out of the ring. During shuffling, the knees are bent in the valgus position, the lower legs are abducted, and the feet are pronated. As a result, sumo training strengthens the peroneal muscles, thus lowering the incidence of inversion sprain. Furthermore, even if a sprain occurs, it usually does not cause persistent ankle instability.


Figure 22E-3  Exercise of shuffling. Keeping the feet on the ground improves stability in this sport, which evolves around collisions and pushing. The knees are bent in the valgus position, the lower legs are abducted, and the feet are pronated. The playing surface is packed earth. Sumo wrestlers tape their toes and wear “tabi” to prevent lacerations on the soles of their feet.



Foot shuffling and squatting with knees spread apart are the basic movements of sumo, and during these movements the ankles are dorsally flexed. Thus in competition, the ankle often is dorsally flexed (Fig. 22E-4 ). Furthermore, when a wrestler braces against being pushed out of the ring, the ankles are in excessive dorsiflexion. On the anterior surface of the ankle, the tibia often collides with the neck of the talus, causing impingement exostosis. Because this condition exists in most sumo wrestlers, and not many sumo wrestlers have ankle instability, its onset must involve collision.


Figure 22E-4  The ankles often are dorsally flexed in a bout. The incidence of anterior ankle impingement exostoses is high in sumo wrestlers.



Because sumo wrestlers are heavy and collisions are violent, there is a high incidence of bone fracture around the ankle. Pronation-external rotation-type malleolar fracture is common because the lower leg is abducted and the foot is pronated, unlike the case in sports that are played with a ball. However, despite their severity, rehabilitation of such injuries is faster than for soft-tissue injury.

Severe toe injuries are less common than severe ankle injuries. Unlike judo, sumo does not involve many moves in which a foot in the equinovarus position is swept sideways. However, lacerations of the skin on the plantar side of the first metatarsophalangeal joint are very common. Some sumo wrestlers prevent such lacerations by taping their toes or wearing Japanese thick-soled socks (“tabi”) ( Fig. 22E-3).


Japanese swords are the symbol of the Samurai culture. Unlike Western swords, Japanese swords are held using both hands. Kendo is a sport modeled after samurai sword fighting, using bamboo swords resembling Samurai swords. Practitioners wear protective pads on the face (“men”), belly (“do”), and forearm (“kote”). A point is scored when a bamboo sword cleanly hits one of the protective pads. A kendo practitioner holds a bamboo sword using both hands, with the right hand in front of the left hand, somewhat like a right-handed baseball player holding a bat. The two competitors face each other so that the tips of their bamboo swords are lightly touching ( Fig. 22E-5 ). Right- and left-handed practitioners take the same stance. The right foot is placed in front, while the left foot stays back. Competitors put their weight on the front half of each foot and slightly lift the heels so that they can move very quickly.


Figure 22E-5  A starting posture of kendo is demonstrated. Note that the sport is practiced barefoot on a wooden floor. The right leg is in front of the left. Weight is kept on the forefoot.



Kendo is generally a safe sport, with a low incidence of fracture, but mild toe injuries are quite common. Beginners often complain of heel pain. Because kendo is practiced barefoot on a wooden floor, there is great impact on the feet during kendo moves. About 40% of kendo practitioners develop hemoglobinuria because red blood cells in the skin and subcutaneous tissue of the sole are destroyed by the impact of the heel hitting the floor. Some kendo practitioners develop a condition called “black heel,” which is characterized by ecchymosis on the sole of the feet. Usually, heel pads are used to treat this condition.

In kendo, the most common severe injury is rupture of the Achilles tendon. This injury almost always occurs in the left leg, because of the positions of the legs in the kendo stance ( Fig. 22E-6 ). During kendo moves, a great amount of force is applied to the left leg. When the body pushes forward, the triceps muscle of the calf is tensed, and the Achilles tendon can rupture if there is a delay in plantarflexion of the ankle. In most sports, rupture of the Achilles tendon is rare among young people, but among kendo practitioners, this injury is somewhat common in high school students. This supports the theory that a great amount of force is applied to the Achilles tendon in the left leg when the body pushes forward in kendo. Rupture of the Achilles tendon is rare among beginners but is more common among skilled practitioners. Most of those who sustain this injury chose to undergo surgery, and rehabilitation takes 6 to 12 months.


Figure 22E-6  An offense hit on a face guard (“men”). The right leg goes forward during a lunge. Excessive force is loaded on the left Achilles tendon during the sport. The incidence of Achilles tendon injuries is high relative to the other martial arts.



Further Reading

Nitz AJ, Dobner JJ, Kersey D: Nerve injuries and grade II and III ankle sprains.  Am J Sports Med  1985; 13:177.


F F. Foot and ankle problems caused by some traditional Chinese habits and sports

Xu Xiangyang,Zhu Yuan

There are some traditional sports that are still popular in China, such as shuttlecock kicking, rope skipping, and Chinese “wushu,” often called kung fu. Although Chinese wushu is changing to be more competitive, most of the time traditional Chinese sports are pursued for health purposes and personal fulfillment. Thus there are infrequent opportunities for competitive athletics among the general public. Still it is not unusual to see foot and ankle injuries caused by these traditional Chinese sports in clinic, usually a soft-tissue injury without a major fracture ( Fig. 22F-1 ).

The frequent reasons for foot and ankle injury stem from the players performing a trick when they kick the shuttlecock and/or skip rope. Coupled with uneven ground, this is a typical setup for an accident. Although some players did this well when they were young, their mental capabilities may be greater than their physical competence in their later years. Furthermore, injury may occur as a result of increasing body weight, decreasing strength of their ligaments, or declining general fitness. Chronic injury is seen in Chinese wushu when the player continues to practice wushu exercises for decades after a primary injury that occurred when he or she was younger.


Figure 22F-2  “Wushu,” a popular traditional sport.




Figure 22F-3  “Wushu,” a popular traditional sport.




Figure 22F-4  Shuttlecock kicking.



There are many different kinds of foot and ankle injuries caused by these traditional Chinese sports. They include ankle sprain, fifth metatarsal base avulsion fracture, medial and lateral malleolus fracture, Achilles tendon rupture, diastasis of syndesmosis, metatarsophalangeal joint capsular injury, and instability of the ankle.

Most of the time we manage these kinds of injuries with traditional Chinese medicine unless we find the injury unstable or prone to sequelae. There are some special, traditional treatments for soft-tissue injuries of the ankle joint in China that have a long history. These include acupuncture needles, Chinese herb ointment, fomentation, and foot massage.

Ice, Chinese herb ointment, and sometimes a splint are the usual management for soft- tissue injury in the early stage of trauma. Chinese herb ointment can effectively decrease the swelling and dissipate the sludge (edema, etc.) quickly. Fomentation, needles, and massage, accompanied by functional exercises, are the treatments for subacute injury.


Figure 22F-5  Rope skipping.




Figure 22F-6  Chinese herb ointments and their original materials.



Needles and massage are important components of restoring balance to the person's vital energy channels, which form the basis behind traditional Chinese medicine. The channels are a system of conduits throughout the body that carry and distribute Qi, or vital energy. Disease is present when the flow of vital energy through the channels is disrupted. This may occur when the integrity of the channels themselves is damaged by a sprain or strain. The Chinese describe this as a disease of “Bi,” or pain, caused by a localized disruption to the flow of Qi.

The traditional Chinese explanation for soft-tissue injury is that the channel running through the damaged tissue has been physically disrupted, resulting in local pain, a disease of Bi. To treat the pain, the integrity of the channel and the flow of vital energy through the channel must be restored. This can be achieved by the selective use of points on the damaged channel, thereby restoring the flow of Qi and relieves the pain.

The foot plantar surface is an important place for the body because there are many points of channels, which represent many internal organs. Therefore foot massage not only treats the injury of foot but also can treat diseases anywhere in the body. In China, foot massage hygiene is looked on as a good method for preventing and treating diseases and is popular throughout the whole country.


Figure 22F-7  Foot massage.




Figure 22F-8  Foot massage.



Foot massage is used to stimulate the points of the channels that can activate the gates of the body, which are opened and closed to adjust circulation in the channels. Foot massage has four functions: (1) it can enhance the blood circulation, so as to accelerate the metabolism of the body; (2) it can regulate the nervous system; because there are many nerves endings in the foot, one can stimulate the reflex zone of the foot to regulate the corresponding tissues and organs; (3) it can mobilize Qi, moisture, and blood and invigorate proper function of the muscles, nerves, vessels, glands, and organs; and (4) it brings the efficacy of release and relaxation.

Generally, foot and ankle soft-tissue injury can be cured with Chinese traditional medicine in 2 to 3 weeks. Even if there is instability of the ankle, most patients can get good results after these treatments. Only a few patients need surgery for ligament repair. Certainly, if there is a relatively severe fracture of the ankle and foot, surgery or casting is necessary. In general, foot massage is the mainstay of treatment and is used for healthy care as well.


Figure 22F-1  “Wushu,” a popular traditional sport.



Further Reading

Blair JM, Botte MJ: Surgical anatomy of the superficial peroneal nerve in the ankle and foot.  Clin Orthop  1994; 305:229.


G G. Foot and ankle sports injuries in Korea

Hong-Geun Jung,Kyung-Tai Lee,
Yong-Wook Park


Overall, foot and ankle sports injuries in Korea are similar to those in the rest of the world, because most of the sports that are played at present, such as soccer, basketball, and baseball originated in non-Asian countries. Distinct sports injuries occurring during some of popular Korean traditional sports and martial arts, such as ssireum and taekwon-do, are reviewed. Furthermore, we present some specific injuries that seem to show a higher incidence in Korea.

Ssireum (Korean Traditional Wrestling)

Ssireum is a contest of physical strength and technique in which two contestants compete in direct contact against one another. It is a form of traditional wrestling found in Korea. There also are some sports similar to Korean ssireum in other countries, such as sumo in Japan. buh in Mongolia. sambo in Russia, and kara kuçak or yağli gureš in Turkey.

Ssireum involves two contestants grasping, pulling, lifting, twisting, pushing, and tumbling as each competitor attempts to throw the opponent to the ground ( Fig. 22G-1 ). If a competitor can force any part of the opponent's body above the knee to touch the ground, the competitor wins the bout. There are hundreds of techniques, categorized into hand techniques (throwing the opponent to the ground by using the hands), leg techniques, and trunk techniques (using the back).



Figure 22G-1  The ankle often is injured when the two ssireum contestants forcefully try to tumble the opponent down on the uneven ground.



Studies have shown that rupture of the Achilles tendon, ankle sprains, acute dislocation of the peroneal tendon, chronic lateral ankle instability, osteoarthritis of the ankle, and osteochondral lesion of the talus are not infrequently experienced during ssireum.

Acute ankle sprains and chronic lateral ankle instability are the most commonly experienced injuries in ssireum because of the repeated turnings and the difficulty in maintaining balance against force in the sand. Two frequent mechanisms occur when the opponent pushes the trunk while the foot is stuck in the sand, causing ankle twisting injury, and when the opponent lets the player down on the sand, abruptly causing ankle imbalance and ligament injury. Osteochondral lesions of the talus are also experienced because of the weight of the players and the frequency of injuries of the ankle. Similarly the high body weight, poor balancing, and repetitive lifting of the large opponents on the sand are factors that contribute to the rupture of the Achilles tendon. In addition, fracture of the base of the fifth metatarsal, ankle fractures, and big toe fracture or sprain have been observed and are due partly to the uneven ground surface made of sands.

Taekwon-Do (Korean Martial Arts)

Taekwon-do is a well-known Korean martial art that is established as an international sport and is also being accepted for the Olympic Games. It is the martial art that mainly uses the lower extremities for hitting the opponent in the match. The various dazzling kicking techniques such as front kick, side kick, and roundhouse kick (the most commonly used kick in sparring) are the key weapons in winning the game. These maneuvers ( Fig. 22G-2 ) subject the participants to injuries around the foot and ankle.


Figure 22G-2  A taekwon-do expert attacks the opponent in the head with roundhouse kick; the forefoot or midfoot often gets injured during these kicks.



The most common injury occurs on the dorsal lateral aspect of the midfoot when the player hits the opponent with this part of the foot with the ankle at maximum plantarflexion. Typically, the foot strikes the opponent's elbow, dorsal foot, or even pelvis, leading to Lisfranc joint trauma or metatarsal fractures. Likewise, the anterior aspect of the ankle and shin often are bruised under the same circumstances as they strike against the guarding elbow. Fortunately these impacts rarely require surgical treatments.

Big toes at the metatarsophalangeal (MTP) and interphalangeal (IP) joints are the second most common sites of foot and ankle injuries, often because of incorrect kicking and unbalanced landing on the floor. These are mainly ligamentous traumas that sometimes result in MTP or IP dislocations and rarely involve fractures. Front kick injuries can cause toe sprains, dislocations, or fractures, as well as acute and chronic posterior ankle impingement. Sever's disease, calcaneal apophysitis, also can occur in children who engage in the sport.

Ankle sprains often occur while kicking the opponent or while landing on the mattress or floor after the kick. Chronic lateral ankle instability is quite common because of repeated inversion injuries. Approximately 40% of a college taekwon-do team experienced at least three ankle sprains in a year, and 60% experienced ankle pain during the match.

Basketball, Soccer, Rugby, and Baseball

Survey of the foot and ankle injuries in Korean college basketball, soccer, rugby, and baseball teams was performed. Ankle sprains (100%) and chronic lateral instability (50%) were very common among basketball players because of frequent jumping and landing in the limited space. This also led to second and fifth metatarsal and navicular stress fractures.

Soccer players often experienced ankle sprains (100%, 23/23) on the artificial lawn after jumps and tackles. Ankle and toe fractures, as well as tibial and metatarsal stress fractures, also were noted. Approximately 26% (6/23) of the players also experienced posterior impingement of the ankle.

Rugby players often experienced ankle sprains (97%) during stumbling, feint motions, or tackles. Thirty-five percent (11/31) experienced Achilles tendinitis, and 55% (17/31) experienced tibial stress fractures. Most of the baseball players sustained ankle sprains (95%, 19/20), which often happened while catching side-passing balls during defense plays.

Accessory Navicular Syndrome

Although the overall incidence of accessory navicular syndrome (ANS) in Korea is similar to that in other countries (4%-12%), type-2 symptomatic ANS seems to show relatively high incidence in Korean athletes.

One foot and ankle institution in Korea experienced more than 200 cases of type 2 ANS, most of them symptomatic. They were treated with bony ossicle excision and posterior tibialis tendon (PTT) reattachment. Rehabilitation started at 4 weeks after operation and players returned to sports at about 3 months postoperatively. In a retrospective review of 84 operated ANS patients, 70% were professional or amateur athletes involved in activities such as football, basketball, or marathons. The follow-up period averaged 17 months. Ninety-four percent (79/84) of the patients showed excellent or good results postoperatively and returned to previous sports activity within 3 months after operation. Poor results came from one heavyweight volleyball player and other patients who had associated PTT insufficiency greater than grade 2.

Further Reading

Saraffian SK: Anatomy of the foot and ankle: descriptive, topographic, functional,  ed 2. Philadelphia: Lippincott; 1993.


H H. Australian foot and ankle conditions in sport

Terence S. Saxby,Jonathan C. Dick

Australia is a very isolated country. The population is approximately 20 million people and the landmass of the country is approximately the size of the United States of America.

Sport is extremely important to the Australian way of life. Almost every sport would be played to some extent in Australia.

Games originating in North America, including baseball, basketball, and even American football are played in Australia. However, because of its historical links with Great Britain and Europe, sports played in these countries predominate. Rugby union, netball, hockey, and soccer are extremely popular sports in this country. Foot and ankle injuries sustained by participants in such sports are much the same the world over.

Because of its isolation and historical independence, Australia has produced its own novel sports including Australian football, which is a combination of Gaelic football, soccer, and rugby. This is an extremely popular sport with a large following in certain states of Australia. It is a fast-flowing game played on a large field requiring athleticism rather than brawn. A profile of Australian Football League (AFL) injuries presenting to sports medicine clinics found that foot and ankle injuries accounted for 14.2% of all injuries.[1] These are most often sprains of the lateral ligament complex of the ankle and therefore not unique to Australian sport.

Australia is an island continent; therefore water sports, including surf lifesaving and other water-based recreational activities, are extremely popular.

Because of the large variety of sports and recreational activities carried out in Australia by a large number of individuals, sporting injuries are quite common. Injury profiles for the majority of these activities reflect patterns of injuries seen overseas. However, there is one particular injury to the foot/ankle complex that is unique to Australian sport.

Foot/Ankle Injuries in Surf Lifesaving

Surf lifesaving is an intrinsic part of Australian culture. Australians love to participate in activities based around the surf beach. Australian beaches can be extremely dangerous for swimmers. Therefore the volunteer Surf Life Saving Association was developed to reduce the risk of participation in this activity. Inflatable rescue boats (IRBs) are used to a large extent by the Surf Lifesaving Association ( Fig. 22H-1 ). These inflatable vessels are now the primary rescue aid used by surf lifesavers in Australia. The use of IRBs has resulted in a number of serious foot and ankle injuries to the boat crew, as demonstrated by recent studies. [0780] [0790]


Figure 22H-1  Inflatable rescue boat.



IRBs have been designed essentially for inshore search and rescue but also are used in training and competitions.[2] They are powered by a 25-horsepower outboard motor and structurally are composed of two rigid, nylon mesh pontoons with a removable lightweight laminate floor to prevent craft deformation. They are manned by a driver and a crewman. The driver sits at the rear left side of the boat and the crewman at the forward right side. The crew requires foot straps, one for the driver and two for the crewman, to give them some anchor to the boat in the often-trying conditions ( Fig. 22H-2 ). These foot straps are not adjustable to foot size or stance position and do not allow any rotation. As a result, these foot straps have been blamed recently for some of the unique injuries sustained by Australian lifesavers.[3]



Figure 22H-2  Inflatable rescue boat showing foot straps.



Bigby[2] reported on the workers compensation claims made by Surf Lifesaving members in Queensland (northeastern state) for a 12-month period from July 1997 to assess the incidence of serious injuries sustained from IRBs and to describe their nature.[2] In Queensland alone there are 2819 rescues per year, and in 731(26%) an IRB was used. For the year there were 37 insurance claims to the workers compensation board specifically from IRB injuries. Incidence of claim for injury annually is 1.2% in IRB crewmen. Sixty-eight percent of claims involved injury to the lower limbs. Fifty percent were associated with fracture or fracture dislocations. The crewman (81%) rather than the driver was injured more often. The right side (79%) was more commonly injured. Bigby concluded that the crewman was more likely to be injured because the crewman is unable to brace himself or herself, with two foot straps being the only fixed support.

Ashton reviewed 12 significant foot and ankle injuries sustained while riding in an IRB that were admitted to his regional hospital emergency department.[3] Ten of these injuries required operative surgery as the initial form of treatment. They consisted of six Lisfranc injuries (dislocation of the midfoot), four ankle fractures, one tibia and fibula fracture, and one traumatic dislocation of peroneal tendons. These injuries were sustained on three occasions when the IRB overturned, four on landing after going over a wave, and four from hitting a broken wave. One occurred when a crewman alighted from the boat as it approached the beach at speed. Eleven of the 12 injuries were to the crewman. The crewman takes the initial impact of the wave and has no control of the boat's direction. This contributes to his or her being less stable than the driver and therefore at more risk of injury[3] ( Fig. 22H-3 ).



Figure 22H-3  Inflatable rescue boats at work.




The tarsometatarsal joints are inherently stable because of their joint congruency and ligamentous supporting structures. There is little range of motion (ROM) at these joints, the first and fifth being most mobile. The bony configuration, with the base of the second metatarsal being recessed and the bone being shaped trapezoidally, provides economical load-bearing characteristics. The Lisfranc ligament is a large, strong, short ligament connecting the base of the second metatarsal to the medial cuneiform. No ligament connecting the base of the first and second metatarsals has yet been described. This leaves a relative weakness inherent at this level. The dorsalis pedis artery crosses over this area, and a branch dives down between the bases of the first and second metatarsal to join the plantar supply. Also the deep sensory branch of the common peroneal nerve is medial to the artery at this level. These structures may be damaged when open reduction and internal fixation are performed.

Lisfranc injuries

The mechanism of Lisfranc injuries sustained by IRB crew is thought to be due to abduction injuries because the feet are constrained by hard foot straps. This generally causes a homolateral type of injury.

Lisfranc dislocations have since been classified by several authors, but none of the classification systems provide a helpful system that aids in treatment methods. The simplest classification, by Quenu and Kuss (1909)[4], divided these injuries into three groups ( Fig. 22H-4 ):












Figure 22H-4  Lisfranc classification.



This by no means is a comprehensive classification system but is useful when describing this injury.


Investigation of these injuries initially is by plain x-ray. To assess normal anatomy, the continuous line along the medial border of the second metatarsal and medial cuneiform and medial border of the fourth metatarsal and medial cuboid should be present on both anterior-posterior (AP) and oblique views. If there is any doubt about the diagnosis or further investigation is warranted, a computed tomography (CT) scan is helpful and often aids in making decisions and determining options for treatment.


Treatment of displaced Lisfranc injuries usually requires open reduction and internal fixation with either small fragment/cannulated screws and K-wires. Outcome from these injuries is variable with a guarded prognosis, although there is an abundance of literature that supports the practice of anatomic reduction's leading to optimal conditions for a reasonable outcome.


  1. Gabbe B, Finch C: A profile of Australian football injuries presenting to sports medicine clinics.  J Sci Med Sport2001; 4:386.
  2. Bigby J, McClure R, Green A: The incidence of inflatable rescue boat injuries in Queensland surf lifesaver.  Med J Aust2000; 172:485.
  3. Ashton A, Grujic L: Foot and ankle injuries occurring in inflatable rescue boats (IRB) during surf life saving.  J Orthop Surg2001; 9:39.
  4. Quenu E, Kuss G: Étude sur les luxations du metatarse.  Rev Chir1909; 39:1.


Further reading

Hardcastle P, et al: Injuries to the tarsometatarsal joint incidence, classification and treatment.  J Bone Joint Surg  1982; 64-B:349.

Arntz CT, Veith RG, Hansen ST: Fractures and dislocations of the tarsometatarsal joint.  J Bone Joint Surg  1988; 70-A:173.

Adelaar R: The treatment of tarsometatarsal fracture-dislocation.  Instruct Course Lect  1990; 39:141.


I I. Soccer: hallux osteochondral lesion and rupture of the Achilles tendon

Verônica Vianna,Sergio Vianna,
Abrão Altman

Soccer is one of the most popular sports in the world, played by more than 60 million people in more than 150 countries, according to the Fédération Internationale de Football Association (FIFA).[1] In Brazil soccer represents a true passion among all ages and social levels. It is practiced all over (schools, streets, soccer fields, beaches, backyards, and public squares), and on diverse terrain (grass, dirt, and sand). Therefore Brazilian sports specialists see a great number of foot and ankle lesions that affect all levels of athletes, not only professional players. Among these are two lesions that we feel are of particular interest regarding diagnosis and treatment.

Hallux Osteochondral Lesion in Beach Soccer Players

Beach soccer is a popular soccer modality practiced barefoot along the Brazilian coast. During the game, the hallux is subjected to trauma—direct trauma against the ball, the ground, or another player and indirect trauma because of the forces from running over the sand.[2] Furthermore, the hallux metatarsophalangeal (MTP) and interphalangeal (IP) joints are stressed in a repetitive mode, particularly in dorsiflexion with pivoting and running. Unlike the aforementioned stresses, kicking will induce lesions that tend to be on the dominant side, the side used to kick the ball. Milani et al.[3] described 19 patients with hallux osteochondral lesions. All were males between the ages of 14 and 67 who practice beach soccer for a mean of 12.8 years. The lesions were located at the IP joint with the distribution shown in Fig. 22I-1 . In all cases the lesion involved the dominant foot (the one used to kick the ball).


Figure 22I-1  Distribution of the hallux osteochondral lesion.



Typically the pain and swelling during the acute phase does not stop the patient from practicing soccer. By the time the orthopaedic surgeon sees the athlete, the symptoms are more dramatic and there often is a “tumor” noted at the dorsomedial aspect of the IP joint of the hallux. Many will develop a callus over the lesion that can be particularly symptomatic in shoes during daily activity.

The radiographic study shows an osteolytic, punched lesion with a sclerotic border ( Fig. 22I-2 ).


Figure 22I-2  Radiographic aspect of a typical hallux osteochondral lesion.



Altman classified these lesions as types I to V, according to the anatomic location ( Fig. 22I-3 ). Type I, lesion at the lateral border of the distal phalanx articular facet, is responsible for 40% of the lesions.


Figure 22I-3  Altman's classification for the hallux osteochondral lesions.



Conservative treatment may be successful when performed during the acute phase. It consists of anti-inflammatory medication and immobilization of the hallux with taping for pain relief. In general, if the patient stops playing soccer, the pain is not a big issue.


Surgical treatment consists of resection of the osteochondral fragment and articular debridement. The results are uniformly good and the patients are able to resume playing soccer approximately 1month after surgery. A gauze-and-tape compression dressing is applied at the conclusion of surgery and is changed the following day, when passive motion starts. Two weeks after surgery, the patient resumes walking barefoot on the sand at the beach. The athlete can start running and kicking barefoot 1month after surgery.

Neglected Rupture of the Achilles Tendon

“Weekend athletes” typically are older soccer enthusiasts who used to play soccer routinely but now participate only on weekends. They are particularly vulnerable to injury and will not uncommonly sustain a rupture of the Achilles tendon. Unfortunately the diagnosis often is missed in the acute phase, probably because of inadequate initial care. It is a problem not only in our practice but throughout Brazil both in private and public practice. Therefore it is not uncommon that Brazilian specialists encounter these chronic lesions of the Achilles tendon.

Our approach has been to use the flexor hallucis longus (FHL)[4] as a substitute for the ruptured tendon. Hansen[5] was the first to describe the use of the FHL for chronic Achilles rupture. This is the strongest tendon after the Achilles, and it contracts in phase with the gastrocnemius-soleus complex. In addition, the force axis of the transferred FHL reproduces the one of the Achilles tendon. Its position facilitates its use during the surgical procedure without injuring the neurovascular bundle and preserves the muscle balance around the ankle joint.

The role of the FHL during gait, running, and jumping is yet to be determined. Frenette and Jackson,[6] studying complete tears of the FHL in athletes, concluded that its integrity is not essential for push-off and balance during gait. Motivated by a chronic laceration of the FHL in an 11-year-old runner, the authors studied nine cases of lacerations of the FHL in athletically inclined patients. All of them returned to their activities, even those patients who had no appreciable active IP joint flexion after surgery. In these cases the lack of active flexion was felt most likely to be due to adherence of the repaired tendon in the scar tissue. Perhaps the return to function despite the lack of IP flexion relates to the tendon's role during gait, running, and jumping. MacConaill and Basmajian[7] reported that the FHL shows its greatest electromyographic activity during midstance, whereas during heel-off there is negligible activity in normal subjects. In our series of FHL transfers for chronic Achilles tendon ruptures, all 37 patients had normal passive IP flexion, and despite no active IP flexion there was no limitation to daily activities or to the return to sports. Our patients have returned to the practice of sports, including soccer, modern dance, and capoeira (an Afro-Brazilian dance form that incorporates self-defense maneuvers). Preliminary studies of the gait analysis in our series have not shown discrepancies between the operated and the nonoperated side on the parameters of the gait. Perhaps if we had treated ballet dancers or sprinters, who stress their FHL more aggressively, there would have been some limitation.


We position the patient prone on the surgical table and drape out the affected side. The FHL is harvested in the medial aspect of the foot while the knee is flexed to 90 degrees during identification of the tendon[8] ( Fig. 22I-4 ). A longitudinal incision is made along the medial border of the midfoot just above the level of the abductor muscle, from the navicular to the neck of the first metatarsal. The abductor muscle is reflected dorsalward, and the FHL and the flexor digitorum longus are identified within the substance of the midfoot. The FHL is divided as far distally as possible, and the distal stump is retained to be sutured to the flexor digitorum longus. The tendons must be dissected from one another, detaching any decussating tendons at the knot of Henry to allow the FHL to be withdrawn through the posterior incision.


Figure 22I-4  Identification of the flexor hallucis longus in the medial aspect of the foot.



We prefer to transfer the tendon through a hole in the calcaneus tuberosity despite the level of the lesion in the Achilles tendon ( Fig. 22I-5 ). With the foot held in approximately 10 to 15 degrees of plantarflexion, the tendon of the FHL is passed through the hole from medial to lateral and sutured to itself with absorbable suture. The FHL and the gastrocnemius-soleus complex are sutured together proximally.


Figure 22I-5  Tendon transfer through the calcaneus.



Postoperative protocol

Full recovery takes an average of 6 months. At this time the patient may resume all sport activities, including soccer. After surgery, compressive dressings and plaster are applied to maintain 15 degrees of ankle plantarflexion. Before discharge, the patient is placed in a short-leg, nonweight-bearing cast at 15 degrees of equinus for 2 weeks. At that time the sutures are removed and the wound inspected. Then, another short-leg, nonweight-bearing cast at 15 degrees of equines is placed for 2 more weeks. Following that period, the ankle is positioned into neutral for an additional 4 weeks of a short-leg walking cast, and weight bearing is allowed. A rehabilitation program for strengthening and range of motion is begun 8 weeks postoperatively. Running, jumping, and impact sports such as soccer and volleyball are restricted for 6 months after surgery.


  1. Cohen M, et al: Lesões ortopédicas no futebol.  Rev Bras Ortop1997; 32:940.
  2. Nery C: Tornozelo e Pé–Diagnóstico e Tratamento.   In: Cohen M, ed. Lesões nos Esportes, São Paulo,  Revinter; 2003.
  3. Milani C, et al: Lesione osteocondrale dell'alluce in giocatori di cálcio sulla spiaggia.   In: Turra S, ed. Ortopedia e Traumatologia delo Sport in Etá Evolutiva,  Pisa: SIOT; 1994.
  4. Wapner KL, et al: Repair of chronic Achilles tendon rupture with flexor hallucis longus tendon transfer.  Foot Ankle1993; 14:443.
  5. Hansen ST: Trauma to the heel cord.   In: Jahss MH, ed. Disorders of the foot and ankle,  ed 2. Philadelphia: WB Saunders; 1991.
  6. Frenette JP, Jackson DW: Lacerations of the flexor hallucis longus in the young athlete.  J Bone Joint Surg1977; 59-A:673.
  7. MacConaill MA, Basmajian JV: Muscles and movements.  A basis for human kinesiology,  Baltimore, William & Wilkins, 1969.
  8. Vianna V, Vianna S: Ruptura Crônica do tendão de Aquiles: reparo com tendão flexor longo do hálux.  Ver Brás Ortop1996; 31:542.



J J. Footballer's (soccer) ankle in Venezuela

Gabriel Khazen,Cesar Khazen

Football (soccer) is the most popular sport worldwide, and even though Venezuela does not have a strong reputation for its national team, football is the favorite sport among young people in our country. Although baseball has a better organization and infrastructure, particularly for teenagers and professionals, football can be played anywhere by any number of players and needs only a ball made of any material. For these reasons it is particularly popular with people of all socioeconomic means.

The special characteristics of this sport make its athletes prone to acute and overuse injuries.[1] Footballer's ankle is characterized by chronic anterior ankle impinging tibial and/or talar osteophytes, resulting in painful limited range of motion, mainly in dorsiflexion. It was first described by Morris in 1943; McMurray[2] in 1950 named it footballer's ankle and suggested osteophyte excision as treatment. It has been reported that this pathology can affect 50% or 60% of the professional football players, but it has been described in many other activities, such as running and dancing.

The exact etiology of this syndrome is still unknown, although there are many hypotheses that have attempted to explain it. The first and traditionally accepted is McMurray's hypothesis that recurrent traction on the joint capsule during forced ankle plantarflexion when kicking the ball was the cause of these osteophytes. However, recent studies have shown that the capsule attaches on average 6mm proximal to the anterior cartilage rim in the tibia and 3mm distal to the cartilage border of the talus, where the osteophytes form.[3] Other hypotheses suggest that direct trauma to the rim of the anterior ankle cartilage in combination with recurrent microtrauma caused by the soccer ball impact, will induce inflammation and scar tissue, which calcifies and forms the osteophytes[4] ( Fig. 22J-1 ).

Massada[5] described the morphologic adaptation of the talus in football players to compensate for overuse and overstress; these changes produced in the talus by the impingement of the anterior articular distal epiphysis of the tibia can be similar to the “squatting facet” found in certain societies in which this crouched position is common. In these situations, the exostoses would be without important clinical significance in the majority of cases.

Ankle instability seems to be an important issue in this pathology; Cannon and Hackney[6] described osteophyte formation and recurrence when lateral ankle instability was not addressed at the time of resection of the impinging lesions. Conversely, there was no osteophyte recurrence following resection when anatomic lateral ligament reconstruction was performed in the presence of lateral ankle instability. This may be the key to the high incidence of footballer's ankle in Venezuela; most of the patients with this syndrome on whom we have had to operate needed simultaneous anatomic lateral ankle ligament reconstruction. Perhaps in our country two factors are responsible for this. First, because most of the football grounds are uneven and sandy, there is a higher incidence of ankle sprain and subsequent instability. Second, the majority of the population cannot afford appropriate footwear and equipment, leaving them more vulnerable to injury when an accident occurs (Figs. 22J-2 and 22J-3 [0470] [0480]).


Figure 22J-1  Forced ankle plantarflexion and direct trauma when kicking the ball.




Figure 22J-2  The majority of football grounds are uneven and sandy in Venezuela.




Figure 22J-3  There is a higher risk of ankle sprain in uneven grounds.



Clinical Evaluation

The main symptom of footballer's ankle is anterior ankle pain. Patients complain of joint stiffness and pain, exacerbated by activities that force ankle dorsiflexion such as walking uphill or squatting. McMurray in 1950 pointed out that the footballer manifested stronger pain when kicking a “dead ball.” Physical examination should be performed carefully to establish a diagnosis and eliminate other causes of ankle pain and impingement. Palpation of the anterior distal tibia and dorsal talus causes tenderness and discomfort; and range of motion is limited and painful, mostly in ankle dorsiflexion. Pain might be caused by synovial impingement between the osteophytes and the distal tibia or talar bone surface. It is important to note that 45% of football players with anterior ankle osteophytes are asymptomatic. In advanced cases, osteophytes can be palpated, and generalized synovitis may cause important swelling.

Joint stability should be examined carefully. We like to perform an ankle anterior drawer test to assess anterior talofibular ligament. Subtalar forced inversion with 15-degrees ankle dorsiflexion is used to test the calcaneofibular ligament.

Other causes of anterior ankle pain should be ruled out, including talar or tibial osteochondral defects; loose bodies; tendinitis; rheumatoid, posttraumatic, or crystalline arthropathies; and pigmented villonodular synovitis.

Additional Studies

Ankle anterior-posterior (AP), lateral, and mortise view radiographs should be performed routinely. Anterior tibial and talar neck osteophytes can be seen in lateral views and are described as “kissing” osteophytes.[7] Recently, an oblique anteromedial view has been suggested, with the radiographic beam tilted in a 45-degree craniocaudal direction with the leg in 30-degrees external rotation to detect medially located tibial and talar osteophytes[8] (Figs. 22J-4 and 22J-5 [0490] [0500]).


Figure 22J-4  X-ray showing characteristic anterior tibial and talar osteophytes in footballer's ankle.




Figure 22J-5  X-ray showing characteristic medial tibial and medial talar osteophytes in footballer's ankle.



Anterior and lateral stress radiographs under sedation or general anesthesia should be performed if lateral ankle stability is suspected. Although the efficacy of this study is hotly debated, we think it is helpful. Most of the studies that found this procedure unreliable were done in vitro; the few studies made in vivo show good correlation between lateral stress radiographs and instability.

Computed tomography (CT) scan is a helpful in determining the precise size and location of osteophytes. Berberian et al.[9] showed that talar spurs on average lie medial to the midline of the talus and that tibial spurs are wider and lie lateral to the midline. Thus overlapping spurs are less likely.

Magnetic resonance imaging (MRI) should be ordered if the diagnosis is not clear or concomitant soft-tissue lesions must be identified.


The treatment of the footballer's ankle depends on the duration and severity of symptoms as well as the ankle joint condition. Conservative treatment should be attempt first, with rest, braces, nonsteroidal anti-inflammatory medication, and physical therapy.

If conservative treatment fails to diminish pain and restore joint function in the absence of advanced joint osteoarthritis, osteophyte removal is the treatment of choice. This procedure can be performed arthroscopically or by small arthrotomy. Arthroscopy has the advantage of being a minimally invasive procedure and provides a magnified and extensive ankle view, with a low risk of complications. [1010] [1020] [1030]

We like to place the patient supine on the operating table, with the ipsilateral hip and knee flexed 45 degrees and supported by a leg holder. A tourniquet is applied and, after draping, the ankle is placed in a noninvasive distractor and force is applied. The ankle joint, tibialis anterior tendon, and superficial peroneal nerve are delineated in the skin as landmarks to safe and correct portals placement. We create the anterolateral portal through a 1-cm longitudinal skin incision, 1cm lateral to the superficial peroneal nerve at the ankle joint level that has been identified previously with an 18-gauge needle. Careful dissection of the joint is performed with a hemostat and a 3.5-mm arthroscope is inserted (we use this arthroscope size because it gives a larger ankle view). The anteromedial portal is identified under direct vision (from the anterolateral portal) and a needle inserted 0.5cm medial to the tibialis anterior tendon, following the same steps for the anterolateral portal.

First we perform a joint evaluation, examining the medial gutter and deltoid ligament and looking for the presence of tibial or talar chondral defects. The lateral gutter, anterior inferior tibiofibular ligament, anterior talofibular ligament, calcaneofibular ligament, and joint synovium are visualized.

Shaving of synovitis, scar tissue, and any ligament thickening is performed first, to improve joint space and osteophyte visualization.

Anterior tibial and talar osteophytes can be reached without joint distraction; extensive distal tibia and talus evaluation is performed, switching portals to identify the position and extent of the osteophytes, which are debrided aggressively with a powered 4.0 burr. Intraoperative ankle fluoroscopy or radiographs can be used to assess osteophyte resection (Figs. 22J-6, 22J-7, and 22J-8 [0510] [0520] [0530]).


Figure 22J-6  Anterior tibial osteophyte arthroscopic image.




Figure 22J-7  Anterior tibial osteophyte arthroscopic debridement with a powered 4.0-mm burr.




Figure 22J-8  Anterior distal tibia after arthroscopic osteophyte debridement.



If mechanical lateral ankle instability is present, it should be addressed in the same procedure by anatomic lateral ankle ligament reconstruction; we like to perform the Brostrom-Gould technique. As stated earlier, we believe that ankle instability and anterior ankle osteophytes are causally related, and thus combined surgery for both conditions may reduce the recurrence of exostosis as well as improve the outcome.

In the presence of large or abundant osteophytes, open resection can be performed by extending the arthroscopy portals. In case lateral ligament reconstruction is necessary, the osteophytes can be removed by direct vision, slightly extending the incision.

After the procedure, we recommend that our patients avoid weight bearing on the operated ankle for 8 days and start active and passive ankle motion on the third postoperative day; a week later physiotherapy is begun to improve ankle range of motion, tendon strengthening, and proprioception.

If the patient requires lateral ankle ligament reconstruction, we immobilize the ankle in a cast for 4 weeks and then put the patient in a sport Aircast (DJO, San Diego, CA) brace to be worn day and night for 4 weeks and then only during the night for another 2 weeks. We start passive physiotherapy at 4 weeks postoperatively in these patients and active physiotherapy at 6 weeks postoperatively.

Good results have been reported widely for arthroscopic resection of anterior bony ankle impingement. Olesen reported that dorsiflexion improved in 59% of the patients, 70% had less pain, and 59% returned to sports, but 23% had given up because of the symptoms. [1010] [1020]

Tol et al.[13] reported a mean 6.5-year follow-up for arthroscopic excision of soft-tissue overgrowth and osteophytes. They found that patients without osteoarthritis all had excellent or good results; patients with grade I osteoarthritis had 77% good or excellent results, despite two thirds of the patients developing partial or complete recurrence of osteophytes. Fifty-three percent of the patients with grade II osteoarthritis had excellent or good results without joint narrowing progression.

Between 1999 and 2002 we operated on 36 footballers with anterior ankle osteophytes who had not achieved symptomatic improvement with conservative treatment. Seventeen were high-level footballers, and the rest played for local leagues. The age of the patients ranged between 23 and 48 years. Fourteen patients needed anatomic lateral ankle ligament reconstruction because of mechanical lateral ankle instability. Using the Scranton McDermott classification, 21 patients were classified as either type I or II (type I: tibial spurs 3mm or less; type II: tibial spurs larger than 3mm without talar spurs); 9 patients were type III (tibial and talar osteophytes), and 6 patients were classified as type IV (tibial and talar osteophytes with ankle joint osteoarthritis signs).

Seventeen of 21 patients with type I or II underwent follow-up examination. Fifteen reported less pain in the ankle after the surgery (visual analog scale [VAS]); 12 patients experience improvement in their range of the ankle dorsiflexion by 5 degrees or more; 15 patients returned to play at the same level; and only 3 patients experienced recurrence of tibial osteophyte.

Eight of 9 patients with type III ankle osteophytes were available for follow-up. Because of the size of the osteophytes, 4 of these patients needed a small arthrotomy for the resection; 5 of the patients reported less ankle pain after the procedure (visual analog scale [VAS]); 4 experienced improvement in the range of ankle dorsiflexion by 5 degrees or more; 5 players returned to play at the same level and 3 experienced recurrence of ankle osteophytes.

Of the four patients with type IV ankle osteophytes, three needed open resection of the osteophytes; two reported less pain after the procedure (VAS); and none experienced improvement in ankle dorsiflexion. All of the patients played in the veterans’ football division; one patient could return to play at the same level, and one patient needed subsequent ankle arthrodesis.


The incidence of complications after this procedure is low. The main complication can be neurovascular damage related to the portal placement, infection, and formation of scar tissue.

Osteophyte recurrence is the main chronic complication and, although the incidence has been discussed earlier in this chapter, it is clear that an aggressive and efficacious osteophyte resection and a stable ankle joint leads to a satisfactory result and the least incidence of osteophyte recurrence.


  1. Lees A, Nolan L: The biomechanics of soccer: a review.  J Sports Sci1998; 16:211.
  2. McMurray TP: Footballer's ankle.  J Bone Joint Surg1950; 32B:68.
  3. Tol JL, van Dijk C: Etiology of the anterior ankle impingement syndrome: a descriptive anatomical study.  Foot Ankle Int2004; 25:382.
  4. Tol JL, Slim E, van Dijk CN: The relationship of the kicking action in soccer and the anterior ankle impingement syndrome. A biomechanical analysis.  Am J Sports Med2001; 1:1.
  5. Massada JL: Ankle overuse injuries in soccer players. Morphological adaptation of the talus in the anterior impingement.  J Sports Med Phys Fitness1991; 31:447.
  6. Cannon LB, Hackney RG: Anterior tibiotalar impingement associated with chronic ankle instability.  J Foot Ankle Surg2000; 39:383.
  7. Robinson P, White LM: Soft-tissue and osseous impingement syndromes of the ankle: role of imaging in diagnosis and management.  Radiographics2002; 22:1457.
  8. Van Dijk CN, et al: Oblique radiograph for the detection of bone spurs in anterior ankle impingement.  Skeletal Radiol2002; 31:214.
  9. Berberian W, et al: Morphology of tibiotalar osteophytes in anterior ankle impingement.  Foot Ankle Int2001; 22:313.
  10. Ogilvie-Harris DJ, Mahomed N, Demaziere A: Anterior impingement of the ankle treated by arthroscopic removal of bony spurs.  J Bone Joint Surg1993; 75-B:437.
  11. Olesen S, Breddam M, Nielsen AB: “Footballer's ankle.” Results of arthroscopic treatment of anterior talocrural “impingement,”.  Ugeskr Laeger2001; 163:3360.
  12. Rasmussen S, Hjort Jensen C: Arthroscopic treatment of impingement of the ankle reduces pain and enhances function.  Scand J Med Sci Sports2002; 12:69.
  13. Tol JL, Verheyen CP, van Dijk CN: Arthroscopic treatment of anterior impingement in the ankle.  J Bone Joint Surg2001; 83-B:9.



K K. The biologic perspective of sports disorders affecting foot and ankle

Mohammad Zafar,Ansar Mahmood,
Nicola Maffulli


Achilles tendinopathy is common among athletes. Its prevalence is approximately 11% in runners, 9% in dancers, and less than 2% in tennis players.



The etiology of tendinopathy remains unclear, and many factors have been implicated. Tendon injuries can be acute or chronic and are caused by intrinsic or extrinsic factors, either alone or in combination. Overuse injuries generally have a multifactorial origin. Tendon vascularity, gastrocnemius-soleus dysfunction, age, gender, body weight and height, pes cavus, and lateral ankle instability are common intrinsic factors. Excessive motion of the hindfoot in the frontal plane, especially a lateral heel strike with excessive compensatory pronation, is thought to cause a“whipping action” on the Achilles tendon and predispose it to tendinopathy.

Changes in training pattern, poor technique, excessive loading, previous injuries, footwear, and environmental factors such as training on hard, slippery, or slanting surfaces are common extrinsic factors. In acute trauma, extrinsic factors predominate.

Free radical damage occurring on reperfusion after ischemia, hypoxia, hyperthermia, impaired tenocyte apoptosis, cytokines, prostaglandins, and fluoroquinolones have all been linked with tendinopathy.


Histologically, tendinopathy is characterized by an absence of inflammatory cells and a failed healing response, with noninflammatory intratendinous collagen degeneration, fiber disorientation and thinning, hypercellularity, scattered vascular in-growth, and increased interfibrillar glycosaminoglycans. Frank inflammatory lesions and granulation tissue are infrequent and are associated mostly with tendon ruptures.

Hence the term tendinopathy should be used as a generic descriptor of the clinical conditions in and around tendons arising from overuse, and the terms tendinosis and tendinitis should be used only after histopathologic examination. Various types of degeneration may be seen in tendons, but in the Achilles tendon mucoid or lipoid degeneration is usually found.


Tendon healing occurs in three overlapping phases. The initial inflammatory phase comprises recruitment of inflammatory cells, phagocytosis of necrotic materials, release of vasoactive factors, initiation of angiogenesis, and stimulation of tenocyte proliferation.

After a few days, the proliferative phase begins. Synthesis of type III collagen peaks during this stage, which lasts for a few weeks.

After approximately 6 weeks, the remodeling phase commences, with decreased cellularity and decreased collagen and glycosaminoglycan synthesis, and the repair tissue changes from cellular to fibrous. A higher proportion of type I collagen is synthesized during this stage.

After 10 weeks, the maturation stage occurs, with gradual change of fibrous tissue to scar-like tendon tissue over the course of 1 year. During the latter half of this stage, tenocyte metabolism and tendon vascularity decline.

Role of metalloproteases and growth factors

Matrix metalloproteases (MMPs), a family of zinc and calcium-dependent endopeptidases active at a neutral pH, are important regulators of extracellular matrix remodelling via their broad proteolytic capability, and their levels are altered during tendinopathy. Twenty-three human MMPs have been identified, with a wide range of extracellular substrates. MMPs can be subdivided into four main groups: collagenases, gelatinases, stromelysins, and membrane-type MMPs. Some of the studies suggest that MMP-9 and MMP-13 participate only in collagen degradation, whereas MMP-2, MMP-3 and MMP-14 participate in both collagen degradation and collagen remodelling. Wounding and inflammation also provoke release of growth factors and cytokines from platelets, polymorphonuclear leukocytes, macrophages, and other inflammatory cells. These growth factors induce neovascularization and chemotaxis of fibroblasts and tenocytes and stimulate proliferation of fibroblast and tenocytes, as well as synthesis of collagen.

Insulin-like growth factor (IGF) is expressed in avian flexor tendons and induces tenocyte migration, division, and matrix expression. IGF-I and II increase collagen synthesis in a dose-dependent manner in animal models and also increase proteoglycan synthesis

IGF-I acts synergistically with platelet-derived growth factor BB (PDGF) to stimulate tenocyte migration. Intratendinous injection of IGF-1 has been evaluated in a rat Achilles tendon transection model. Rats in the IGF-1–treated group had higher Achilles functional index scores and accelerated recovery compared with control groups

Vascular endothelial growth factor (VEGF) is an endothelial mitogen that promotes angiogenesis and increases capillary permeability. It is expressed in ruptured and fetal human Achilles tendons but not in normal adult Achilles tendons. VEGF plays a key role in tendon healing by inducing vasodilatation results partly through stimulation of nitric oxide synthase in endothelial cells.

VEGF treatment at the time of surgical repair of transected rat Achilles tendons resulted in significantly improved tensile strength at 2 weeks. However, no significant difference was present by 4 weeks.[1]

Increased levels of transforming growth factor b2 (TGF-b2) have been reported in tendinopathic human Achilles tendons and in rabbit flexor tendons after injury. TGF-b induces increased collagen production in rabbit tenocytes, and upregulation of TGF-b receptors occurs following flexor tendon injury and in tendinopathic human Achilles tendons.

Cartilage-derived morphogenetic proteins (CDMPs), the human analogs of growth and differentiation factors, are members of the TGF- superfamily and are related to bone morphogenetic proteins. Injection of CDMP-1, CDMP-2, and CDMP-3 into lacerated rat Achilles tendons results in a significant dose-related increase in strength and stiffness.

Not all cytokines prove beneficial for tendon healing. The ideal cytokine or combinations of cytokines that will improve tendon healing are still to be determined. Cytokine effects often are dose dependent, and optimal dosage regimes must be established. The ideal form of administration also remains to be determined. Options include direct injection at the injury site or gene therapy. Further research will help to resolve these issues.

Tissue engineering/stem cells

Mesenchymal stem cells (MSCs) prevalent in bone marrow, muscle, fat, skin, and around blood vessels are capable of undergoing differentiation into a variety of specialized mesenchymal tissues, including bone, tendon, cartilage, muscle, ligament, fat, and marrow stroma.

MSCs can be applied directly to the site of injury or can be delivered on a suitable carrier matrix, which functions as a scaffold while tissue repair takes place.

Tissue engineering also may prove useful for managing tendon ruptures. A 1-cm-long gap injury model in rabbit Achilles tendons was used to compare suture alone versus a cell-collagen gel composite contracted onto a pretensioned suture. Evaluation at 4, 8, and 12 weeks following surgery revealed that structural and material properties of the cell-treated implants typically were approximately twice the value of controls. Cell-treated repairs were larger in cross section and histologically better organized than suture alone repairs.

Polyglycolic acid scaffolds seeded with tenocytes were implanted into hen flexor tendon defects. Twelve weeks after surgery, tenocytes and collagen fibers became longitudinally aligned. At 14 weeks, engineered tendons displayed a typical tendon structure, with a breaking strength of 83% of normal.[2]

At present, tissue engineering is an emerging field, and many difficulties must be overcome before it becomes a real option in the management of tendon disorders. It is important to determine whether effective vascularization and innervation of implanted tissue-engineered constructs takes place. Vascularization is important for the viability of the construct. Innervation is required for proprioception and to maintain reflexes, mediated by Golgi tendon organs, to protect tendons from excessive forces.

Gene therapy

Gene therapy delivers genetic material to cells to alter protein synthesis and cell function and can be achieved via viral vectors or liposomes. Liposome constructs have been used to deliver galactosidase to rat patellar tendons. Animal studies have demonstrated that gene therapy can be used to alter the healing environment of tendons. Adenoviral transfection of focal adhesion kinase into partially lacerated chicken flexor tendons resulted in an expected increase in adhesion formation. Although this study reports an adverse outcome, it proves the feasibility of gene therapy as a management modality.[3]

Complementary deoxyribonucleic acid (cDNA) for PDGF–B was transfected into rat patellar tendons using liposomes, resulting in an early increase in angiogenesis, and collagen deposition and matrix synthesis were greater at 4 weeks. However, there were no differences between the treated and control groups by 8 weeks.

Gene therapy can be used to manipulate the healing environment for up to 8-10 weeks. This may be long enough to be clinically significant. Many genes may prove beneficial to tendon healing, and further research is required to establish the most advantageous genes to transfer.

Principles of Tendinopathy Management

Conservative management

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Although tendinopathy is a noninflammatory condition, NSAIDs are widely used in attempts at treatment. There is no biologic basis for NSAID effectiveness in treating this condition, and no evidence of any benefit particularly in athletes. NSAIDs appear to be effective, to some extent, only for pain control. This causes patients to ignore early symptoms and thus may lead to further damage of the tendon and delay definitive healing. Theoretically NSAIDs could benefit patients with tendinopathy by increasing the tensile strength of tendons via accelerated formation of cross linkages between collagen fibers. COX-2 inhibitors should be avoided in the early period following tendon injury because of their deleterious effect on tensile strength. During remodelling, on the other hand, inflammation has a negative influence, and NSAIDs such as COX-2 inhibitors might be valuable for the final outcome.


In recent years, aprotinin has been used in the management of chronic tendinopathy. Aprotinin is a broad spectrum serine protease inhibitor derived from bovine lungs. It acts on trypsin, plasmin, and kallikrein, blocks matrix metalloproteinases, and may specifically act as a collagenase inhibitor in tendinopathy.

Until recently, evidence for aprotinin use in the management of Achilles tendinopathy was based on uncontrolled studies, reporting success rates of approximately 80%. In the only randomized controlled trial to examine the role of aprotinin in Achilles tendinopathy, the authors concluded that there was no statistical significant improvement in outcome. However, this study was underpowered.[4]

The main reported side effect of aprotinin is that of allergic reactions. The risk of hypersensitivity/anaphylactic reaction with aprotinin is less than 0.1% on first exposure but rises to 2.7% with re-exposure.

Maffulli has used aprotinin since 1988 for the management of chronic tendinopathy in more than 1200 patients. To his knowledge, only two cases of systemic allergic reactions have been reported, both in middle-aged active but nonathletic women.

Eccentric exercise

Limited levels of evidence exist to suggest that Eccentric Exercise (EE) has a positive effect on clinical outcomes such as pain, function, and patient satisfaction/return to work when compared with concentric exercise, stretching, splinting frictions, and ultrasound. EEs are low cost, relatively easy to perform and noninvasive. The results can be seen after 12 weeks of daily EE training.[5]

Laser therapy

Laser therapy also has been studied in tendon healing. Using a placebo-controlled, double-blind prospective study model in 25 patients with 41 digital flexor tendon repairs, laser therapy reduced postoperative edema but provided no improvement in pain, grip strength, or functional evaluation compared with controls.[6] Further well-controlled clinical studies should be performed using different laser types and dosages to delineate the role of laser phototherapy in the management of tendon injuries.

Radiofrequency coblation

This is a new application of bipolar radiofrequency energy used for volumetric tissue removal. Under appropriate conditions, a small vapor layer forms on the active electrode of the device. The electrical field of on the energized electrode causes electrical breakdown of the vapor, producing a highly reactive plasma that is able to break down most of the bonds found in soft-tissue molecules. Rapid pain relief has been reported in a preliminary prospective, nonrandomized, single-center, single-surgeon study of 20 patients with tendinopathy of the Achilles tendon, patellar tendon, and of the common extensor origin. Six months after the procedure, magnetic resonance imaging (MRI) showed complete or nearly complete resolution of the tendinopathy lesion in 10 of the 20 patients enrolled in the study.[7]

Sclerosing injections

Using ultrasonography and color Doppler during eccentric calf-muscle contraction, we found that the flow in the neovessels disappeared when the ankle was dorsiflexed. These observations raised the question of whether the good clinical effects demonstrated with eccentric training could be due to action on the neovessels, and whether the neovessels and accompanying nerves were the main source of pain. In a recent study, ultrasound and color Doppler follow-up showed that most patients with good clinical results had no residual neovessels. Patients with a poor result showed residual neovascularization. These findings indicate that the area with neovessels may be important to the pain suffered during Achilles tendon loading activity.[8]

In a further noncontrolled pilot study, a sclerosing agent (Polidocanol) was injected into the area with neovessels on the ventral side of the tendon. The short-term (6 months) results were promising, but no real benefit was achieved in long term.[9] For this reason we do not use sclerosing injections in our center. However, the results of a randomized controlled study comparing the effects of injections of a sclerosing substance with injections of a nonsclerosing substance are presently under evaluation.

Shock wave therapy

Several studies evaluated the application of electrical and magnetic fields to tendons. Pulsed magnetic fields with a frequency of 17Hz resulted in improved collagen fiber alignment in a rat Achilles tendinopathy model.[10] Extracorporeal shock wave therapy applied to rabbit Achilles tendons at a rate of 500 impulses of 14kV in 20 minutes resulted in neovascularization and an increase in the angiogenesis-related markers endothelial nitric oxide synthase and vascular endothelial growth factor. Extracorporeal shock wave therapy also promotes healing of Achilles tendinopathy in rats. The authors proposed that improvement in healing resulted from an increase in growth factor levels, because they noted elevated levels of TGF-1 in the early stage and persistently elevated levels of IGF-1.[11]However, caution should be exercised when using extracorporeal shock wave therapy because dose-dependent tendon damage, including fibrinoid necrosis, fibrosis, and inflammation, has been reported in rabbits.

Glyceryl trinitrate

Review of literature showed that tropical Glyceryl trinitrate (GTN) is a well-tested medication with no irreversible side effects and that use of this therapy is warranted to treat chronic tendinopathies. However, further investigations are required to define the mechanism of action of GTN in tendinopathy and to delineate the most effective dosage regime to maximize effect and limit side effects.

Mobilization and mechanical loading

Animal experiments have demonstrated that training results in improved tensile strength, elastic stiffness, along with increase in weight, and cross-sectional area of tendons. These effects in the tendon can be explained by an increase in collagen and extracellular matrix synthesis by tenocytes. Little data exist on the effect of exercise on human tendons, although intensively trained athletes are reported to have thicker Achilles tendons than control subjects.

Early resumption of activity promotes restoration of function, and motion therapy strategies aim to facilitate healing, reduce adhesion formation, and increase range of motion. Many studies have shown the benefit of early mobilization following tendon repair, and several postoperative mobilization protocols have been advocated. Repetitive motion results in increased DNA content and protein synthesis in human tenocytes. Even 15 minutes of cyclic biaxial mechanical strain applied to human tenocytes results in cellular proliferation.

The precise mechanism by which cells respond to load remains to be elucidated. However, cells must respond to mechanical and chemical signals in a coordinated fashion. Intercellular communication to mount mitogenic and matrigenic responses is achieved via gap junctions ex vivo. Tissue-engineered tendons must allow for this intercellular communication. Mechanical loading of cells in monolayer or three-dimensional constructs can result in increased cell proliferation and collagen synthesis.

Surgical Management


Surgery is recommended for patients in whom nonoperative management has proved ineffective for at least 6 months. Twenty-four percent to 45.5% of the patients with Achilles tendon problem fail to respond to conservative treatment and eventually require surgical intervention. Paavola et al., in a prospective long-term follow-up study, showed that the prognosis of patients with acute to subchronic Achilles tendinopathy managed nonoperatively is favorable.[12]

Principles of surgery

There are minor variations in surgical technique for tendinopathy. Nevertheless, the objective is to excise fibrotic adhesions, remove degenerated nodules, and make multiple longitudinal incisions in the tendon to detect intratendinous lesions and to restore vascularity, and possibly to stimulate the remaining viable cells to initiate cell matrix response and healing. Most authors report excellent or good result in up to 85% of cases. [9130] [9140]

Management of paratendinopathy includes releasing the crural fascia on both sides of the tendon. Adhesions around the tendon are then trimmed and the hypertrophied adherent portions of the paratenon are excised. In tenolysis, classically longitudinal tenotomies are made along the longitudinal axis of the tendon in the abnormal tendon tissues, excising areas of mucinoid degeneration. Reconstruction procedure may be required if large lesions are excised.

Preoperative planning

Each patient should be managed on an individual basis, and appropriate workup for theatre should be instituted. Diagnosis is made on the basis of history of burning pain in the posterior aspect of the calf and ankle, often worse at the beginning of a training session and after exercise. Some patients have difficulty taking the first few steps in the morning. Pain during activities of daily living include prolonged walking and stairs.

Clinically, diagnosis is made mostly on the basis of palpation and on the use of the painful arc sign. In paratendinopathy, the area of tenderness and thickening remains fixed in relation to the malleoli when the ankle is moved from full dorsiflexion into plantarflexion. If the lesion lies within the tendon, the point of tenderness and any swelling associated with it move with the tendon as the ankle is brought from full dorsiflexion into plantarflexion. In mixed lesions, both motion and fixation of the swelling and of the tenderness can be detected in relation to the malleoli.

Ultrasound scan is a diagnostic aid to the surgeon. Ideally, a real time U.S. machine equipped with at least a 10-MHz sectorial transducer should be used. Commercially available soft polymer echo-free material can be used to provide adequate contact between the skin and the probe and to improve the image quality by placing the tendon in the optimal focal zone of the transducer. The variables considered in the evaluation of the tendon and of the peritendinous tissues are tendon size and borders, intratendinous and peritendinous ultrasonographic pattern, and possible surgical sequelae. An ultrasonographic diagnosis of tendinopathy can be made when the tendon presents altered intratendinous structure, at times with a well-defined focus. An ultrasonographic diagnosis of paratendinopathy is made when the peritenon is thickened or shows altered echogenicity.

Any relevant comorbidity should be highlighted and managed. Although the techniques reported in this article are performed under local anesthesia, there is a small chance that general anesthesia may be necessary, and therefore baseline investigations such as blood tests, electrocardiogram and chest radiographs should be undertaken if deemed necessary. Patients should have deep vein thrombosis prophylaxis. Valid informed consent should be achieved before the operation, and the patient should be aware of risks of infection, bleeding, wound and scar problems, and operation failure, and that further surgery may be required.

Surgical technique

When an open surgical approach is necessary, we use a longitudinal curved incision, with the concave part toward the tendon and centered over the abnormal part of the tendon. Placing the incision medially avoids injury to the sural nerve and short saphenous vein, and the curvature of the incision prevents direct exposure of the tendon in case of skin breakdown.

The paratenon and crural fascia are incised and dissected from the underlying tendon. If necessary, the tendon is freed from adhesions on the posterior, medial, and lateral aspects. The paratenon should be excised obliquely because transverse excision may produce a constriction ring, which may require further surgery. Areas of thickened, fibrotic, and inflamed tendon are excised. The pathology is identified by the change in texture and color of the tendon. The lesions then are excised, and the defect can either be sutured in a side-to-side fashion or left open. Open procedures on the Achilles tendon may lead to difficulty with wound healing because of the tenuous blood supply and increased chance of wound breakdown and infection. Hemostasis is important because the reduction of postoperative bleeding speeds up recovery, diminishes the chance of wound infection, and diminishes any possible fibrotic inflammatory reaction.

In patients with isolated Achilles tendinopathy with no paratendinous involvement and a well-defined nodular lesion less than 2.5cm long, multiple percutaneous longitudinal tenotomies can be used when conservative management has failed. An ultrasound scan can be used to confirm the precise location of the area of tendinopathy.

Postoperative management

On admission, patients are taught to perform isometric contractions of their triceps surae. Patients are instructed to perform the isometric strength training at three different angles, namely at maximal dorsiflexion, maximal plantarflexion, and at a point midway between the two.

The foot is kept elevated on the first postoperative day, and nonsteroidal anti-inflammatory medications are given for pain control. Early active dorsiflexion and plantarflexion of the foot are encouraged. On the second postoperative day, patients are allowed to walk using elbow crutches, weight bearing as able. Full weight bearing is allowed after 2 or 3 days, when the bandage is reduced to a simple adhesive plaster over the wounds. Stationary bicycling and isometric, concentric, and eccentric strengthening of the calf muscles are started under physiotherapy guidance after 4 weeks. Swimming and water running are encouraged from the second week. Gentle running is started 4-6 weeks after the procedure, with mileage gradually increased. Hill workouts or interval training are allowed after a further 6 weeks, when return to normal training is allowed. Patients normally discontinue physiotherapy by the sixth postoperative month. For open surgery, the cast is applied for 2 weeks and the whole rehabilitation process described above is started later.




Subcutaneous hematoma



Superficial infection



Hypersensitivity of the stab wounds



Hypertrophic painful scar


The management of Achilles tendinopathy aims to return the patient to a level of activity similar to that before acquisition of tendinopathy in the shortest possible time and without significant residual pain. Physiotherapy and conservative treatment should be the first form of management.

If conservative measures fail, multiple percutaneous longitudinal tenotomy is simple, requires only local anesthesia, and can be performed without a tourniquet. If postoperative mobilization is carried out early, preventing the formation of adhesions, this will allow the return to high levels of activity in the majority of patients.

Current concepts and research/the future

Current management strategies, such as nonsteroidal anti-inflammatory drugs or corticosteroids, offer symptomatic relief but do not result in definitive disease resolution. Surgery may be appropriate for certain patients, but recovery may be protracted and is associated with pain and discomfort. The ideal management should accomplish its goal in a relatively short period of time with little discomfort or disability to the patient. Novel management methods should aim to stimulate a healing response to restore the normal biomechanical properties of tendon.

Adhesion prevention

The most important factor implicated in adhesion formation is trauma. Many attempts have been made to reduce adhesion formation using materials acting as mechanical barriers such as polyethylene or silicone, or using pharmacologic agents such as indomethacin and ibuprofen, but no simple method is widely used.

Hyaluronate, a high molecular weight polysaccharide found in synovial fluid around tendon sheaths, decreased adhesion formation in rabbit flexor tendons. However, no statistically significant difference in adhesion formation was found in a rat Achilles tendon model.[15] The absence of a synovial membrane around the Achilles tendon may explain this difference. 5-Fluorouracil, an antimetabolite with anti-inflammatory properties, effectively preserves tendon gliding in experimentally lacerated chicken flexor tendons.[16]

Physical modalities also have been used to try to limit adhesion formation. Direct current applied to rabbit tendons in vitro results in increased collagen type I production and reduced adhesion formation. However, pulsed electromagnetic field stimulation resulted in no difference in adhesion formation in rabbit flexor tendons after 4 weeks.[17]

Despite many efforts, adhesion formation after trauma to tendons still remains a clinical problem, and no ideal method of prevention exists. Most studies of adhesion formation focus on flexor tendons. Further research is required to determine whether the results also are applicable to extrasynovial tendons.


Tendon injuries give rise to significant morbidity, and at present only limited scientifically proven management modalities exist. A better understanding of tendon function and healing will allow specific management strategies to be developed. Many interesting techniques are being pioneered. The optimization strategies discussed in this article are currently at an early stage of development. Although these emerging technologies may develop into substantial clinical management options, their full impact must be critically evaluated in a scientific fashion.


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