FOOT AND ANKLE INJURIES IN THE ATHLETE
June 2nd, 1995
Mark S. Myerson, MD
Acute Ankle and Subtalar Sprains
Anatomy and Biomechanics
The ligamentous support of the ankle consists of three ligaments, the anterior talofibular (ATF), the calcaneofibular (CF), and the posterior talofibular. The ligaments of the subtalar joint, including the CF ligament, the lateral talocalcaneal ligament, the interosseous talocalcaneal ligament, and the cervical ligament, also have an integral role when considering ankle injury. The extensor retinaculum also contributes to the support of both the ankle and the subtalar joints, particularly the inferior extent of the extensor retinaculum where it divides into its three bundles.
The ATF ligament is short, blends with the fibers of the lateral capsule of the ankle, and inserts into the lateral aspect of the talus just anterior to the articular surface. It is relaxed when the ankle is dorsiflexed and tightens when the ankle is plantarflexed. The ATF is the first ligament to tear in a typical ankle sprain when the foot collapses into plantarflexion and inversion. The ATF has a lower load to failure than the other ankle ligaments (Siegler et al 1988; Attarian et al 1985). Patients with hindfoot varus are at significant risk for recurrent inversion sprain and gradual stretching and attenuation of both the ATF and CF ligaments (Myerson 1993). Rassmussen (Rasmussen 1985) has demonstrated that one of the primary problems with recurrent ankle sprains is not inversion but rotation of the talus. Recurrent inversion instability does not cause a simple uniplanar deformity of the talus, but a rotatory instability of the talus in the ankle mortise. The CF ligament originates from the anterior distal border of the fibula. It is generally directed posteriorly at an angle of 45o to insert on the calcaneus, just superior to the peroneal tubercle. This ligament is tight in dorsiflexion, is loose in plantarflexion, and inhibits adduction. In plantarflexion, this ligament acts with the ATF, but in dorsiflexion, when the ATF is loose, the CF ligament acts independently.
The extensor retinaculum provides major support to both the ankle and subtalar joints. The contribution of the extensor retinaculum to ankle and subtalar instability has been emphasized over the past decade since Gould et al (Gould et al 1980) published their modification of the Brostrom procedure.
The biomechanics of the subtalar joint ligamentous complex are less well understood. Many anatomic studies have attempted to reproduce subtalar instability through sequential sectioning but have failed to identify substantial rotatory instability, which occurs clinically. The cervical ligament is an extremely taut and strong ligament and with the interosseus talocalcaneal ligament supports the subtalar joint. It is likely that the cervical ligament limits inversion, but both the cervical and interosseous talocalcaneal ligaments are responsible for rotational control of the subtalar joint (Smith 1958).
Diagnosis
Clinical evaluation. Patients report a popping or tearing in the lateral aspect of the ankle associated with a plantarflexion inversion injury. Tenderness, swelling, and ecchymosis are usually present over the anterolateral aspect of the ankle. It is easy to reproduce the patient's pain by direct palpation over the affected ligaments and by gentle stress of the ankle, particularly in plantarflexion and inversion. It is important to examine the foot and ankle carefully for associated injuries that often occur secondary to plantarflexion and inversion: injury to the peroneal tendons, the subtalar joint, the anterior process of the calcaneus, the talus, and the fifth metatarsal. Each of these areas should be carefully examined with particular attention to maximum tenderness over the lateral aspect of the foot. Radiographic evaluation. Radiographic examination of an ankle sprain should include anteroposterior, lateral, and internal oblique views of the ankle and anteroposterior, lateral, and oblique views of the foot. In this manner, injuries to the anterior process to the calcaneus, the lateral process of the talus, the dome of the talus, and the base of the fifth metatarsal are less likely to be missed and can be evaluated. I am not in favor of performing stress views of the ankle after acute ligamentous injury. This examination is painful, adds no useful information, and does not affect the decision-making in treatment.
Radiographic evaluation for chronic recurrent ankle instability should focus on both the foot and ankle in the weight-bearing position, as well as with stress. Recurrent ankle instability is often associated with fixed hindfoot varus or decreased motion in the subtalar joint. For this reason, an axial view of the calcaneus and weight-bearing views of the foot should be obtained in addition to routine views of the ankle. The stress view or a talar tilt view of the ankle is an anteroposterior view of the ankle while inversion stress is applied. Although this force can be applied manually, we find that a commercially available stress device is most useful and accurate. I do not use any anesthesia to perform this stress manipulation of the ankle. When obtaining a stress view of the ankle, the opposite ankle should also be examined since significant variation in talar tilt occurs. Quite a wide range of "normal" talar tilt exists (Sedlin 1960; Berridge & Bonnin 1944; Bonnin 1949). Despite this variation in both normal and abnormal ankles, the difference in the talar tilt between both ankles should be less than 5o. The inversion stress test should be performed with the foot in a consistent position. Since laxity increases with the foot in plantarflexion, we attempt to perform this with the foot in a neutral position or in slight dorsiflexion. Since the inversion stress or talar tilt measures injury to the calcaneofibular ligament, it is highly likely that this ligament is disrupted if talar tilt is greater than 12o.
The anterior drawer test measures the integrity of the anterior talofibular ligament and is probably more reliable than the inversion or positive talar tilt test (Fig. 1). This stress test should also be performed with comparison views of the opposite ankle. There are two methods of evaluating the anterior drawer measurements, both of which are reliable (Fig. 2). I prefer to quantify the anterior subluxation according to the distance between the anterior edge of the distal tibia and the anterior dorsal surface of the talus.
Management
Although many classification systems of ankle sprains are reported (Leach & Schepsis 1990; Smith & Reischl 1988; Jackson et al 1974), these are of clinical use only if they determine the course of treatment. Since I treat all acute ankle sprains nonoperatively, it is less important to stage the severity of this injury. If bone, joint, or tendon injuries are present, then an operative approach may be used, and the ankle ligaments are repaired primarily. No study exists demonstrating the advantage of an operative approach for severe ankle sprains whether in the athletic or nonathletic population. I therefore advocate using whatever modalities are necessary to rest the ankle and commence early functional rehabilitation. Eversion strengthening with the foot in plantarflexion is emphasized, as is proprioceptive training during rehabilitation.
Although Leach and Schepsis (Leach & Schepsis 1990) have advocated operative repair of the acute ankle sprain in the athlete, 90% of all athletes will recover after a nonoperative treatment program. Of the remaining 10% who experience recurrent ankle symptoms, most are able to be treated with a rehabilitation and taping program. Certainly the concept of "down time" for the high performance athlete is a valid one, so if the athlete has to remain "off" for a specified length of time after the injury, he may as well be treated operatively. I do not advocate an operative approach for these injuries regardless of the magnitude of the tear unless it is associated with injuries that of themselves warrant surgical intervention.
Chronic Ankle Instability
Assessment
Patients with chronic ankle instability should be carefully evaluated since recurrent instability of the ankle may involve the ligamentous supports of the ankle and subtalar joints as well as the articular surfaces and surrounding tendons. Hindfoot varus, cavovarus deformity of the foot, and decreased motion in the subtalar joint all predispose to recurrent ankle instability. It is important to assess for generalized ligamentous laxity since this will have an impact on the choice of operative procedure if needed.
Conservative rehabilitation of the foot and ankle for recurrent instability is important regardless of the decision to pursue operative or nonoperative treatment. Before surgery, I stress the values of improving proprioception and eversion strengthening, including that of the foot in plantarflexion.
Surgical Correction
I use only two operative procedures for reconstructing lateral ankle instability, the Brostrom (Brostrom 1966b; Brostrom 1966a) and the Chrisman-Snook procedures (Snook et al 1985; Chrisman & Snook 1969), although numerous others are available (Evans et al 1984; Larsen 1988; Larsen & Lund 1991; Elmslie 1934; Watson-Jones 1955). The tenodesis procedures (Evans et al 1984; Larsen 1988; Larsen & Lund 1991; Elmslie 1934; Snook et al 1985; Chrisman & Snook 1969; Watson-Jones 1955) all require using all or part of the peroneus brevis tendon and routing it through various bone tunnels to reconstruct the anterior talofibular and, in some cases, the calcaneofibular ligaments. Although the reported results are satisfactory, the Watson-Jones (Watson-Jones 1955) and Evans (Evans 1953) procedures do not restore any stability to the subtalar joint.
The direct repair of the ATF and CF ligaments was originally described by Brostrom (Brostrom 1966b; Brostrom 1966a) and recently modified by Gould et al (Gould et al 1980). This method of repair is particularly important in dancers, gymnasts, and other athletes in whom the peroneal tendons are extremely important for maximum performance and function. The modified Brostrom procedure is a direct repair of both the ATF and CF ligaments. It is not as easy to repair the CF ligament with this approach; however, redundancy in this ligament is easy to identify and with experience the same surgical repair is used on the CF as with the ATF ligaments. The addition of the extensor retinaculum imbrication not only reinforces both these repairs, but importantly, contributes to stabilizing the subtalar joint.
The Chrisman-Snook procedure is particularly useful in patients who are obese, heavy football players, and those with structural deformity of the hindfoot. The Chrisman-Snook procedure is also particularly useful where ankle instability is a result of neuromuscular peroneal weakness. In these patients, the entire peroneus brevis tendon may be used instead of a split tendon procedure as is more commonly performed. It is unlikely that one can restore stability to the ankle in the presence of fixed hindfoot varus. In these patients I simultaneously perform an osteotomy of the calcaneus to stabilize the mechanical axis of the hindfoot and ankle. It is particularly important to address any malalignment of the hindfoot mechanical axis simultaneously with a calcaneal osteotomy. The calcaneal tuberosity is shifted with a triplanar osteotomy, as previously described (Saxby & Myerson 1993).
Modified Brostrom procedure. The procedure is performed on an outpatient basis under local anesthesia: 30 cc of 0.5% bupivacaine with 1:200,000 epinephrine mixed is used for the regional block. The ankle and subtalar joints are blocked as are the tibial, superficial peroneal, and sural nerves.
The incision curves over the anterior aspect of the distal fibula inferiorly toward the peroneal tendons (Fig. 3) and is deepened through subcutaneous tissue, taking care to avoid injury to the lateral cutaneous branch of the superficial nerve, which crosses just medial to this incision. The sural nerve is not visualized since it is inferior to the peroneal tendons. It is important to identify the extensor retinaculum and to mobilize this off the anterior talofibular ligament and capsule. This retinaculum varies in thickness, but is always present and easily identifiable. The incision is made through the anterior talofibular ligament and capsule without attempting to dissect the ligament off the capsule (Fig. 4). I leave a small cuff of capsule and ligament attached to the fibula approximately 3 to 4 mm in length. It is easy to recognize if the ATF ligament is redundant, in which case the incision is made directly in the substance of the ligament.
Occasionally, the ligament is avulsed off the fibula with a small bone fragment. If an avulsion off the fibula is present, then I prefer to harvest the ligament and capsule more proximally directly off the fibular and then to imbricate this up against the fibula with nonabsorbable sutures. This can be attached either with a suture anchor or through drill holes into the fibula.
More inferiorly, the CF ligament is identified lying underneath the peroneal tendons. The CF ligament blends inferiorly with the peroneal tendon sheath, which should be opened to examine the ligament. If no redundancy in the CF ligament is identified, it is left alone. Usually, however, the ligament needs to be tightened by excising a 2 mm segment. Both the ATF and CF ligaments are now repaired. The ATF ligament is imbricated in a vest-over-pants manner using nonabsorbable sutures (Fig. 5). Due to the thickness of the combined ATF ligament and ankle capsule, this imbrication is not always possible and I sometimes excise an ellipse from the tissue and do a direct end-to-end repair.
Once the repair of both the ATF and CF ligaments are complete, the ankle is taken through a full range of motion, and an anterior drawer is performed to determine stability. The extensor retinaculum is now advanced up to the fibula and attached with absorbable 2-0 sutures (Fig. 6). It is important to tie the sutures in the ATF and CF ligaments as well as the imbrication with the ankle in dorsiflexion and slight eversion. Postoperatively, patients are immobilized in a posterior splint for 10 days, after which time the dressing is changed and ambulation is begun in a short leg cast for an additional two to three weeks. Between four and six weeks, the cast is removed, a removable splint is applied to the ankle, and exercises and rehabilitation commence.
Modified Chrisman-Snook procedure. This procedure is indicated in patients with generalized ligamentous laxity, obesity, the heavy athlete, and patients with recurrent instability after prior surgical correction, where associated significant subtalar instability is present. In the presence of fixed deformity of the subtalar joint, particularly hindfoot varus, this procedure is also useful. As originally described by Chrisman and Snook (Chrisman & Snook 1969) and then by Snook et al (Snook et al 1985), half of the peroneus brevis tendon is harvested. Occasionally, tears of the peroneal tendons are present, and the split peroneus brevis tendon can be harvested through the torn portion or occasionally the entire tendon is used. This is also applicable to patient with neuromuscular deformity whose peroneal muscle is not functional, and the entire peroneus brevis tendon is used.
The procedure is performed with the patient in the lateral decubitus position using local anesthesia with 30 cc of 0.5% bupivacaine with 1:200,000 epinephrine. No tourniquet is needed. The incision is made parallel to the peroneal tendons from three inches proximal to the ankle joint and crossing distally over the peroneal tendons towards the peroneal tubercle (Fig. 7). I have not found it necessary to extend the incision more proximally into the leg, since sufficient tendon can be harvested from this limited incision. The sheath is opened and both tendons are inspected. Tears of the peroneus brevis tendon should be treated. The peroneus brevis tendon is split using the anterior half of the tendon for the transfer, leaving the posterior half attached to the muscle (Fig. 8).
During the subcutaneous dissection, it is important to identify the sural nerve, which lies immediately posterior to the incision and can be visualized with the lesser saphenous vein. The nerve is retracted with the posterior skin flap. Care needs to be taken not to cut the nerve where it crosses distally, anterior and dorsal to the peroneal tendons. A subcutaneous soft-tissue flap is elevated anteriorly and the anterior talofibular ligament and anterior capsule are identified under the extensor retinaculum. To prevent dislocation of the peroneal tendons, a small 1-cm slip of the peroneal sheath may be left intact at the tip of the fibula. I have not found this step necessary since the split peroneal transfer is brought anterior to the remaining peroneal tendons to restrain them from anterior dislocation. Although an imbrication of the anterior talofibular ligament and capsule may be performed simultaneously, I have not routinely performed this step.
The periosteum over the anterior distal fibula is elevated, leaving a small cuff to which the tendon transfer is sutured. The tendon is split just distal to the peroneal tubercle and then brought anteriorly for the transfer. A 4.5-mm drill hole is made from anterior to posterior perpendicular to the axis of the fibula (Fig. 9). The free tendon is passed from anterior to posterior through the osseous tunnel (Fig. 10). The lateral wall of the calcaneus is then prepared with subperiosteal dissection beneath the peroneus longus tendon. As originally described by Chrisman and Snook (Chrisman & Snook 1969) and then by Snook et al (Snook et al 1985), a tunnel is made in the calcaneus. However, I find this cumbersome and prefer to attach the tendon using a screw with a small spiked ligament washer as it is extremely stable and allows early range of motion post operatively.
With the tendon pulled through the fibular osseous tunnel, the ankle is held in the neutral position and two absorbable sutures are inserted in the anterior aspect of the fibula. The graft is passed over the peroneus longus and the remaining peroneus brevis tendon, and then, with the subtalar joint in the neutral position, the tendon is secured to the lateral wall of the calcaneus with a 4.0-mm partially threaded cancellous screw and a small spiked plastic ligament washer (Fig. 11). It is not necessary to use the remaining tendon to pull it up to the fibula with this technique (Fig. 12). The imbrication of the ATF and CF ligaments may then be performed. The peroneal retinaculum is closed with absorbable sutures and, after closure through subcutaneous tissue and skin, the foot is held in neutral position with a posterior plaster splint incorporated with a bandage.
The patient is allowed to commence weight bearing at 10 days in a short leg cast. In the athlete, I encourage early weight-bearing with protection in a removable ankle brace. At six weeks, function rehabilitation is encouraged in a control physical therapy program emphasizing dorsiflexion and eversion strengthening exercises.
I have been encouraged by the success of this procedure with one exception, and that is a tendency to over-tighten the repair. It is extremely important to perform the tenodesis with the ankle in neutral and not in an everted position, to prevent over-tightening of the repair, and, thereby limit inversion movement of the ankle. I would also caution the use of this procedure in patients with work-related injuries since my personal results in this group of patients have not paralleled those in the athletic population.
Subtalar Instability
Only in the past decade have we begun to recognize the contribution of the subtalar joint to acute and chronic laxity to the hindfoot and ankle. Despite this recent enthusiasm, the diagnosis and treatment of subtalar instability is still unclear. We have learned much about the functional anatomy of the subtalar joint complex, but less about methods to diagnosis instability.
Diagnosis
I find it difficult to distinguish between symptoms of ankle and subtalar instability. Patient complaints are very similar, and the location of discomfort is also in the anterolateral ankle. Pain in the sinus tarsi is more diagnostic, particularly if one is able to localize isolated pain just interior and inferior to the fibula. This becomes more confusing when one realizes that ankle and subtalar joint instability can coexist.
The diagnosis of subtalar instability is made easier if a patient with symptoms of chronic instability does not have any significant talar tilt or drawer sign on stress testing. Stress radiographs of the subtalar joint have been previously described (Clanton 1989; Clanton et al 1990; Harper 1991). On the stress lateral view of the ankle, additional forward subluxation of the calcaneus on the talus can be demonstrated with anterior gliding of the undersurface of the posterior facet. Varus instability of the subtalar joint is more difficult to demonstrate and is probably not of functional significance since subtalar instability is rotatory and not uniplanar. Nevertheless, stress Broden's views of the subtalar joint may be used to visualize the posterior facet of the subtalar joint (Fig. 13). Other methods of evaluating the joint, including stress tomography (Zollinger et al 1983) and arthrography (Meyer et al 1988; Meyer et al 1988), are less useful. I have never correctly diagnosed an acute subtalar sprain.
Treatment
In 1988, Meyer et al (Meyer et al 1988) reported on a group of acute subtalar sprains and recommended surgical management based on subtalar arthrography. I find it hard to justify this form of treatment and would recommend managing these patients in the same manner as a patient with acute ankle sprain. However, the patient with symptoms of chronic instability and pain is different. Although eversion strengthening and proprioceptive training may suffice to improve symptoms in these patients, inflammation in the sinus tarsi is often present, requiring a more directed treatment approach. Delayed reconstruction for subtalar joint instability uses a tenodesis to reconstruct the torn ligaments. Elmslie (Elmslie 1934) described a procedure in the 1930s to reconstruct the ankle joint that simultaneously addresses the components of subtalar instability. Most procedures, including those described by Elmslie (Elmslie 1934), Larsen (Larsen 1988), Larsen and Lund (Larsen & Lund 1991), Chrisman and Snook (Chrisman & Snook 1969), and Snook et al (Snook et al 1985), address both the subtalar and ankle components of instability simultaneously.
I have used the Chrisman-Snook procedure, or modifications thereof, to address subtalar instability. Schon et al (Schon et al 1991), Clanton (Clanton 1989), and Clanton et al (Clanton et al 1990) have described a reconstructive procedure that is a modification of the Chrisman-Snook procedure. I have not specifically addressed the subtalar component of instability using the modified hole in the lateral calcaneus and talus as described by Schon et al (Schon et al 1991). In my experience, the modified Chrisman-Snook procedure, as described above for ankle instability, suffices for treatment of combined ankle and subtalar instability or, in fact, subtalar instability. Certainly, the additional tunnels in the lateral calcaneus and talus are not too difficult to construct, but are probably unnecessary.
Peroneal Tendon Injury
Although dislocation of the peroneal tendons may occur voluntarily due to deficiency in the peroneal retinaculum and fibular groove and although congenital deficiencies of the fibular groove have been described (Edwards 1928), most peroneal tendon pathology, including tears and dislocations, occur after trauma. I have identified complete dislocations of peroneal tendons after trauma where no fibular groove is present at all. It is likely that the groove was not sufficient to begin with, and that with the absence of the peroneal tendons in the retrofibular region, the groove "filled in." I have identified this after open reduction and internal fixation for calcaneus fractures where the peroneal tendons are dislocated and the groove is palpated and noted to be present. If the tendons are not satisfactorily relocated, the groove may subsequently be totally deficient and absent. Retrofibular deficiency may therefore be the effect as well as the cause of peroneal tendon dislocation.
Anatomy
The peroneal tendons pass behind the fibula in a fibro-osseous tunnel. The anterior aspect of the retrofibular groove has a fibrocartilaginous rim analogous to the labrum in the shoulder. The depth of the retrofibular sulcus varies (Edwards 1928), and the height of the sulcus is increased by this fibrocartilaginous rim. In addition to the natural restraints formed by this groove, the superior peroneal retinaculum also maintains the tendons in their position behind the fibula. Division of the peroneal retinaculum, however, is not sufficient to cause dislocation of the tendons. I have seen this repeatedly after surgical correction when the tendons are relocated and the retinaculum is not yet repaired. Since these procedures are performed under local anesthesia, the patient is asked to attempt to dislocate the tendon voluntarily. The depth of the groove created is sufficient to prevent the tendons from dislocating.
Superiorly, the brevis and longus tendons pass through a single retinaculum that splits more distally, and the inferior retinaculum houses each tendon separately over the peroneal tubercle. However, the inferior peroneal retinaculum does not play a role in peroneal tendon pathology and dislocation. Although the peroneal retinaculum may be torn in the acute form of injury, some reports indicate that this tearing does not occur (Das De & Balasubramaniam 1985), a position originally supported by Eckert and Davis (Eckert & Davis, Jr. 1976). In a study of more than 70 cases of acute peroneal injury, Eckert and Davis (Eckert & Davis, Jr. 1976) showed that the peroneal retinaculum was not torn, but striped away from the edge of the fibula with or without involvement of the fibrocartilaginous rim.
Acute Dislocation
Diagnosis. Clinicians often miss the acute form of dislocation of the peroneal tendon, which occurs after resisted dorsiflexion with or without eversion. Although the injury may occur after inversion stress on the foot, it is usually associated with resistance or contraction of the peroneals. Dislocation is reportedly common in skiing injuries, where vigorous contraction of the peroneals with the foot in dorsiflexion or eversion causes the tendons to dislocate. Diagnosis of the acute injury is based on pain posterior to the fibula associated with ecchymosis. Plantarflexion and inversion is not painful, but resisted eversion is most uncomfortable. Due to swelling, it is difficult to appreciate the subluxation or dislocation of the tendons.
Treatment. Once the diagnosis of acute dislocation is made, I, as well as other clinicians (Earle et al 1972; Eckert & Davis, Jr. 1976), advocate an operative approach in preference to conservative immobilization in a cast since the latter has been associated with less than optimal results (McLennan 1980), with a high likelihood of recurrent problems, and with longer rehabilitation.
Acute repair involves direct approach to the retinaculum and fibrocartilaginous rim. The pathology is addressed directly by imbrication of the retinaculum in a vest-over-pants manner or reattachment of the fibrocartilaginous rim. I have not found it necessary to deepen the groove in these patients, although this can be performed if the groove is noted to be completely deficient. Postoperatively, the patients are allowed to ambulate after one week in a prefabricated boot or a cast for three or four weeks when functional rehabilitation commences.
Chronic Recurrent Dislocation
Diagnosis. With chronic instability of the peroneal tendons, patients report varying symptoms of discomfort associated with clicking and popping in the posterolateral aspect of the ankle (Fig. 14). This vague sense of instability is often more diagnostic of recurrent dislocation than a demonstration by the patient of the dislocation. Inability to demonstrate a dislocation does not imply that chronic dislocation is not occurring. Although I routinely obtain radiographs of the ankle to rule out a small avulsion fracture of the tip of the fibula, this finding is not often present. I have rarely resorted to computed tomography scans or magnetic resonance imagining to make the diagnosis, which by and large is a clinical one.
Treatment. Treatment for chronic instability is varied and, again, may depend on the underlying pathology. Although numerous soft-tissue and bony procedures have been described (Kelly 1920; Jones 1932; Sarmiento & Wolf 1975; Pozo & Jackson 1984), I prefer to address the problem directly by deepening the fibular groove, as reported by others (Edwards 1928; Jones 1932; Zoellner & Clancy, Jr. 1979). This procedure is simple to perform, does not involve the sacrifice of any other adjacent structures, and avoids any bone block type procedure, which in my experience is associated with potential attritional tearing of the peroneal tendons.
I perform this procedure under local anesthesia as an outpatient procedure. The patient is turned into a lateral decubitus position and 20 cc of 0.5% bupivacaine with 1:200,000 epinephrine are administered. The superficial peroneal nerve and sural nerve are infiltrated through a field block, as is the peroneal tendon sheath. More distally, the ankle and subtalar joints are infiltrated with 5 cc.
An incision, commencing 3 inches proximal to the tip of the fibula and extending 1 inch distal to the tip of the fibula, is made directly over the peroneal tendons and is usually anterior to the sural nerve, which however, needs to be identified. The incision is deepened through subcutaneous tissue, and the peroneal sheath is carefully identified. It is important at this stage to identify the underlying pathology, e.g. peroneal retinacular laxity or an avulsion of the fibrocartilaginous rim (Fig. 15). If the rim is avulsed and a small bone or cartilaginous fragment is identified, then the incision in the retinaculum is made through this defect. If the rim is still attached, then the peroneal retinaculum is divided, leaving a 3-mm cuff attached to the edge of the fibula. The retinaculum is opened and the tendons are inspected. It is not uncommon to find elements of tenosynovitis with or without tearing of the tendon, usually the peroneus brevis. The tendon tears are repaired as described below.
Since the procedure is performed under local anesthesia, it is useful to instruct the patient to attempt to actively dislocate the tendons. In this manner, one can assess the need for further deepening of the groove, which can be accomplished with a combination of gouges, curettes, chisels, and burrs.
Deepening the groove in this manner can leave a rough cancellous bone surface to which the tendons could potentially adhere. In the past, I have tried to address this potential problem by the application of bone wax, but have abandoned this method since the wax seldom remains adherent to the bone surface and can cause a foreign body reaction and further tenosynovitis. I have also attempted Zoellner and Clancey's (Zoellner & Clancy, Jr. 1979) alternative method for deepening the groove, which involves raising an osteoperiosteal flap, leaving it attached inferiorly, and following it with curettage of the underlying cancellous bone. I have discontinued using this procedure as well because the osteoperiosteal flap has often broken off. I now use a high-speed 5-mm oval burr to round of and smooth the edges. This is particularly important distally at the tip of the fibula where the tendons pass at an acute angle and may be prone to attritional wear and tear.
Once the groove is sufficiently deepened, it is extremely unlikely that the tendons will redislocate. However, I reinforce this repair by suturing the peroneal retinaculum to the under surface of the deepened groove (Fig. 16). Note that the retinaculum is sutured to the under surface of the deepened groove and not to the edge of the fibula. In this manner, a portion of the groove has a synovial layer.
Postoperatively, patients are kept non-weight-bearing for approximately 4 weeks. Early motion, however, is encouraged and commenced when the sutures are removed 5 to 7 days postoperatively. This early motion helps prevent adherence of the tendons to the rough cancellous bone surface. I have not encountered any recurrent dislocations or stenosing tenosynovitis with this method of repair. For salvage of recurrent dislocations, however, I recommend the methos described by Martens et al (Martens et al 1986), which includes a bone block transposition of the calcaneofibular ligament.
Tendinitis and Rupture
Tenosynovitis and degenerative tendinosis occur in an older patient population. Although acute rupture is rare, a recent report describes acute rupture of the peroneus longus tendon, predominantly in elderly individuals who probably had underlying predisposing degenerative tendinosis (Thompson & Patterson 1989). However, it is my belief that because this acute injury is difficult to diagnose, rupture of the peroneus longus probably occurs far more frequently than is recognized.
Complete rupture of both the longus and brevis tendons do occur, as recently highlighted by Sammarco et al (Sammarco et al 1993) and Sobel et al (Sobel et al 1990; Sobel et al 1990) in their reports on attritional tearing of the peroneus brevis tendon that commonly occurs with recurrent instability of the ankle. However, longitudinal splits and fissures of the tendon, particularly the brevis tendon, are more common (Fig. 17). The biomechanics of peroneal tendon splits have recently been highlighted, particularly in relation to recurrent ankle instability (Sobel et al 1990).
Diagnosis. The patient will present with pain, warmth, and swelling over the peroneal tendon sheath, often associated with recurrent ankle instability. In this setting, I will often inject 2 to 3 cc of 1% lidocaine into the tendon sheath for diagnostic purposes. Radiographic examination of the foot is important since the os vesalianum, which is in the substance of the peroneus longus tendon, may be seen to retract more proximally. However, the sesamoid is occasionally absent and diagnosis should not rely on retraction. Acute ruptures of the peroneus longus tendon may occur either posterior to the fibula or more distally as the tendon passes under the cuboid. Magnetic resonance imaging may be required to diagnosis this type of rupture.
Treatment. Acute tendinitis will respond to complete rest, nonsteroidal antiinflammatory medication, and immobilization in either a cast or a removable brace. I have not had much success with the conservative treatment of chronic degenerative tenosynovitis in the athlete and, for these patients, I advocate surgery. Longitudinal fissures are often present and these are debrided. If the peroneus brevis tendon is extensively involved, that portion of the tendon may be excised and a side-to-side tenodesis to the peroneus longus tendon may be performed proximal and distal to the longitudinal rupture. An end-to-end repair is rarely feasible in these patients.
Postoperatively, patients are treated with early mobilization but non-weight-bearing for 2 to 4 weeks. Peroneal rehabilitation is encouraged and is the mainstay of treatment. Athletes are usually able to return to activity 2 to 3 months after repair.
Achilles Tendon Injury
Anatomy
The Achilles tendon insertion is on the posterior inferior one-third of the calcaneal tuberosity with insertional fibers extending to the plantar aspect of the calcaneus. The insertion of the Achilles tendon is broad, and detaching the medial or lateral edge of the tendon does not functionally weaken it. The Achilles tendon is surrounded by a loose matrix of tissue, referred to as mesotenon, paratenon, and pseudosheath (Booth 1987; Bradley & Tibone 1990; Garrett, Jr. et al 1988), that functions similarly to a tendon sheath. The vascularity of the Achilles tendon has been implicated in the pathogenesis of inflammation, degeneration, and ultimate rupture. Microvascular studies have demonstrated decreased blood flow in and to the Achilles tendon 2 to 6 cm proximal to its insertion into the calcaneus (Garrett, Jr. et al 1987), which is in the same location as inflammation and rupture.
The retrocalcaneal bursa is a loose, fluid-filled sac that helps the Achilles tendon glide against the superior edge of the calcaneus. There also is a small bursal sac, referred to as the subcutaneous or precalcaneal bursa, between the skin and the Achilles tendon. Either of these bursae can become inflamed and painful.
Etiology
Achilles tendon dysfunction occurs in two separate groups of patients determined largely by their age and activity levels. The first group is composed of individuals 35 to 50 years old who are low-level competitive athletes and who typically sustain ruptures of the tendon. Of all Achilles tendon ruptures, 75% are sustained by predominantly male athletes between the ages of 30 and 40. The second group consists of a younger population of highly active athletes who develop inflammatory changes in the tendon and its lining paratenon. Athletes who participate in racquet sports and long distance running are particularly susceptible to these inflammatory changes. Approximately 15% of Achilles tendon ruptures are associated with symptoms of antecedent tendinitis. This has particular significance when treating patients with chronic retrocalcaneal pain.
Increased pronation during stance is likely to cause pathologic changes in the Achilles tendon. With functional hyperpronation, the accompanying contraction of the gastrocnemius soleus complex causes excessive stress along the medial aspect of the Achilles tendon. During the phase of gait when the foot is flat, particularly if pronation is present, there is internal rotation of the tibia, which further adds to the stress along the medial aspect of the tendon. The combination of repetitive microtrauma associated with hyperpronation and presumed poor vascularity is the cause of most forms of Achilles tendon pathology. These factors cause repetitive microtrauma to the Achilles tendon with a cumulative effect leading to inflammation, degeneration, and potentially, rupture. Achilles tendinitis may present as acute peritendinitis and a more chronic tendinosis.
Diagnosis
Peritendinitis is an inflammatory condition of the tendon pseudosheath or the paratenon, whereas tendinosis is a degeneration of the substance of the Achilles tendon itself. In acute peritendinitis, the tendon is warm and inflamed. This is easy to diagnose by squeezing the tendon between the thumb and forefinger and gliding over the tendon, which may have a feeling of crepitus. In chronic Achilles tendinosis, the tendon is often thicker, resisted plantar flexion is weak, and posterior heel pain that worsens with activity is present. Retrocalcaneal bursitis and subcutaneous bursitis are common differential diagnoses of posterior heel pain in the runner and can be caused by enlargement of the superior tuberosity of the calcaneus, improperly fitting shoes, or impingement of the Achilles tendon on the calcaneus.
Retrocalcaneal bursitis presents with heel pain but localization of the pain can be elicited by squeezing the soft tissues in a medial and lateral direction just anterior to the Achilles tendon. Plain radiographs will demonstrate soft-tissue swelling and, occasionally, calcification within the tendon.
Treatment of Achilles Tendinitis
If the tendinitis is severe and acute, a brief period of immobilization in a short leg cast is indicated and nonsteroidal antiinflammatory medication is used. Once the acute inflammation has subsided, athletic activity is increased and gastrocnemius-soleus strengthening and stretching is begun. Custom orthotic devices or heel lifts are used to control hyperpronation. Local modalities, including ice massage, ultrasound, and iontophoreses, can be beneficial. Gradual resumption of physical activity can begin with swimming, cycling, and other low-impact activities. Steroid injection to treat inflammation of the Achilles tendon is not often indicated, although a short course of tapered doses of oral steroid is occasionally warranted.
Retrocalcaneal bursitis, which has been refractory to conservative measures, is treated by debridement of all bursal tissue and aggressive resection of the superior aspect of the calcaneal tuberosity. This is usually performed in conjunction with excision of a prominent posterior lateral calcaneal tuberosity. Refractory cases of Achilles tendinitis can be managed surgically with a posteromedial longitudinal incision and debridement of the inflammatory tissue surrounding the tendon. The granular thickened paratenon is easily identified and excised (Fig. 18). After this procedure, patients are able to gradually resume athletic activities within 1 month of the tendon stripping.
This inflammatory peritendinitis is far easier to treat surgically than chronic degenerative tendinosis. Although the diseased tendon is easy to visualize both clinically and on magnetic resonance imaging as a fusiform thickening 1 to 2 inches proximal to the insertion, it is not always easy to grossly identify the diseased portions of the tendon at surgery (Fig. 19A). These longitudinal fissures or degenerative tears may be excised, but I have never been certain as to the extent of tendon debridement required. For more extensive disease with weakness, the tendon is explored for necrotic or degenerated segments and, if severe, the repair is augmented with the flexor hallucis longus muscle (Wapner et al 1993). This muscle not only strengthens the repair, but also brings in needed blood supply to the poorly perfused Achilles tendon. The Achilles tendon is exposed along its length posteromedially, and an incision is made in the foot to harvest the flexor hallucis tendon, which is then transferred proximally through a drill hole in the calcaneus (Fig. 19B).
Achilles Tendon Rupture
Etiology and diagnosis. Approximately 75% of Achilles tendon ruptures occur in athletes (Bradley & Tibone 1990; Clancy, Jr. et al 1976; Fox et al 1975; Jozsa et al 1989), predominantly in males between 30 and 40 years old (Inglis et al 1976). Injury is undoubtedly related to certain forms of activity and exercise, since the incidence of Achilles tendon rupture is more common in countries where work is generally sedentary and is markedly decreased in countries, such as China, where physical work is commonplace (Sun et al 1977). The etiology of Achilles tendon rupture is still unclear, but many theories have been proposed, including repetitive microtrauma (Soma & Mandelbaum 1994), inhibitor mechanism malfunction (Stephenson et al 1990), a correlation of rupture with blood type O (Soma & Mandelbaum 1994), hypoxic and mucoid degeneration, decreased perfusion that results in degenerative changes (Lagergren & Lindholm 1958), and systemic or locally infiltrated corticosteroids (Mahler & Fritschy 1992; Soma & Mandelbaum 1994).
A patient who sustains an acute rupture typically presents with a history of acute sharp pain and a sensation of a loud snap or pop commonly reported as being struck in the back of the leg. After rupture, patients are either completely incapacitated or can bear some weight on the extremity but lack the ability to forcibly plantar flex the foot. This ability to actively plantar flex the ankle and walk, albeit with some weakness, can be confusing and leads to errors in diagnosis. The diagnosis of acute rupture is therefore occasionally missed, and the patient may be evaluated late with a chronic rupture, persistent weakness, and difficulty with push-off. Regardless of the etiology, this injury occurs in a wide range of individuals, from the recreational/weekend sports participant to the elite athlete.
Treatment options. Treatment goals are to minimize the morbidity of this injury and to optimize the rapid return to full function. Operative options include percutaneous repair (Ma & Griffith 1977; Ma & Griffith 1981), gastrocnemius flap (Lindholm 1959), simple suture (Nistor 1981), pullout wire (Ralston & Schmidt, Jr. 1971), fascial reinforcement (Abraham & Pankovich 1975), and polylacetate implant (Clemow & Chen 1986). All treatment options, whether by nonoperative closed methods (Haggmark et al 1987; Jacobs et al 1978), open surgical procedures, or percutaneous methods of repair (Bradley & Tibone 1990; Ma & Griffith 1977; Ma & Griffith 1981), utilize a short or long leg cast as part of the recovery process.
The rationale for using a cast is that immobilization (for approximately 8 weeks) will achieve tendon healing through hematoma to collagen proliferation and maturation. Unfortunately, immobilization is associated with many complications, including muscle atrophy and long-term weakness, articular cartilage weakening and degeneration, skin necrosis, deep vein thrombosis, and joint stiffness. In addition, from a functional standpoint, cast immobilization never allows full rehabilitation of the extremity, regardless of what operative or nonoperative protocols are used. With a cast as part of the treatment, Nistor (Nistor 1981) reported at least a 10% deficit regardless of protocol use, Bradley and Tibone (Bradley & Tibone 1990) demonstrated a 13 to 20% deficit, and Inglis and coworkers (Inglis & Sculco 1981; Inglis et al 1976) described a deficit of 12 to 15% as standard. Cumulatively, these studies indicate that the there was never less than a 10% power or strength deficit with protocols utilizing immobilization. Thus, it can be concluded that immobilization, used in conjunction with reparative techniques, may cause increased morbidity.
Several studies demonstrated that mobilization is optimal for connective tissue: Booth (Booth 1982; Booth 1987) showed that muscle atrophy can be minimized, Pepels et al (Pepels et al 1983) demonstrated a decreased time of fibril polymerization to collagen, and Gelberman et al (Gelberman et al 1984) reported that mobilized extremities enhanced the orientation and organization of collagen. We have incorporated many of these concepts of early mobilization and aggressive rehabilitation into a surgical protocol for management of Achilles tendon rupture.
Although many different methods of suture repair of the Achilles tendon are available, until recently none have been strong enough to allow early range of motion of the foot and ankle. Over the past 8 years, I have been using surgical repair of Achilles tendon ruptures in athletes followed by early range of motion and aggressive rehabilitation. This protocol is based on the reports of Garrett and colleagues (Garrett, Jr. et al 1988; Taylor et al 1990; Garrett, Jr. et al 1987) of collagen's response to loading, which my colleagues and I have extrapolated to repair after Achilles tendon rupture. This treatment emphasizes early and aggressive motion and weight-bearing to enhance tendon healing and strength.
Using the technique described below, my colleagues and I have obtained a rigid and stable fixation that allows early range of motion, strengthening, and functional rehabilitation. Although the reported success rates of nonoperative treatment for Achilles tendon rupture emphasize low complication rates, I strongly recommend operative repair for Achilles tendon ruptures in active individuals and athletes. The rerupture rate is far higher with nonoperative than with operative treatment, but to the athlete, early return to maximum function is far more important and cannot be realistically attained with conservative treatment (Booth 1982).
Surgical technique. Surgery is performed with the patient in the prone position using general or local anesthesia. I find it useful to prepare both limbs, and drape both into the operative field. This allows one to examine the dynamic resting position and establish the correct tension on the repair by comparing it with the opposite limb. The incision is made medially so that the plantaris tendon, if present, may be incorporated into the repair. The rupture is identified, and the tendon ends are debrided. It is important to establish the correct length of the tendon ends before the sutures are tied. This is not always easy to accomplish, since the frayed and elongated ends of the tendon are do not meet evenly. The bulk of the tendon ends are therefore approximated before the sutures are inserted. The repair is performed with a #2 nonabsorbable polyfilament suture (Fig. 20). One or two strands of suture may be used, depending on the diameter of the tendon. When the sutures are approximated, the tendon ends should meet. It is important not to repair the tendon with any elongation since this will functionally weaken the muscle. If the plantaris tendon is present, it is cut proximally, and then it is opened up so that the tendon forms a thin sheet, which may be used to cover the repair. The peritenon is repaired using absorbable sutures of 4-0 vicryl, achieving a tight closure over the tendon. To accomplish this, a posterior release of the fascia between the superficial and deep compartments of the leg is often required. Skin closure is performed with a dermal mattress suture of 4-0 nylon, and the lower leg is immobilized with a below-the-knee posterior splint and the ankle in slight equinus.
At approximately three days after surgery, the bandages are changed to a removable posterior splint, and an early range of motion program is initiated. The patient is instructed to comfortably move the ankle passively four to five times a day through 10 to 20o of plantarflexion and dorsiflexion. The splint is worn when passive exercises are not being performed. At 2 weeks, the sutures are removed and if the wound is fully healed, early weight-bearing, coupled with range-of-motion exercises, is initiated. Patients are fitted with hinged walking boots that permit full plantar flexion but block dorsiflexion at 10o of equinus. At 4 weeks, patients may continue to use the walker boot, which is adjusted to block dorsiflexion at neutral.
Ideally, the repair is performed between 1 and 7 days after injury, depending on the amount of swelling present. If one waits more than 2 weeks, the proximal tendon retracts, and it is not always easy to approximate the ends. If this occurs, it is helpful to gently pull on the proximal tendon with the suture attached for approximately 5 to 10 minutes. This will always gain 1 to 2 cm of tendon length, particularly if the repair is performed late. If a sizeable defect is present between the tendon ends that cannot be corrected by gradual stretch, then tendon transfers using the flexor hallucis longus or peroneus brevis can be used to augment the repair. Other methods, including a turn down of the proximal central portion of the tendon and a slide of the entire musculotendinous unit, have been described.
References
Abraham E, Pankovich AM 1975 Neglected rupture of the Achilles tendon. Treatment by V-Y tendinous flap. J Bone Joint Surg 57A(2): 253-255
Attarian DE, McCrackin HJ, De Vito DP, et al 1985 Biomechanical characteristics of human ankle ligaments. 6(2): 54-58
Berridge FR, Bonnin JG 1944 The radiographic examination of the ankle joint including arthrography. Surg Gynecol Obstet 79: 383-389
Bonnin JG 1949 Radiological diagnosis of recent lesions of the lateral ligament of the ankle [comment on paper of this title by JR Hughes]. J Bone Joint Surg 31B: 478
Booth FW 1982 Effect of limb immobilization on skeletal muscle. J Appl Physiol 52(5): 1113-1118
Booth FW 1987 Physiologic and biomechanical effects of immobilization on muscle. Clin Orthop 219(Jun): 15-20
Bradley JP, Tibone JE 1990 Percutaneous and open surgical repairs of Achilles tendon ruptures. A comparative study. Am J Sports Med 18(2): 188-195
Brostrom L 1966a Sprained ankles. VI. Surgical treatment of chronic ligament ruptures. Acta Chir Scand 132: 551-565
Brostrom L 1966b Sprained ankles. V. Treatment and prognosis in recent ligament ruptures. Acta Chir Scand 132: 537-550
Chrisman OD, Snook GA 1969 Reconstruction of lateral ligament tears of the ankle. An experimental study and clinical evaluation of seven patients treated by a new modification of the Elmslie procedure. J Bone Joint Surg 51A: 904-912
Clancy WG Jr., Neidhart D, Brand RL 1976 Achilles tendonitis in runners: a report of five cases. Am J Sports Med 4(2): 46-57
Clanton TO 1989 Instability of the subtalar joint. Orthop Clin North Am 20: 583-592
Clanton TO, Schon LC, Baxter DE 1990 An overview of subtalar instability and its treatment. Perspect Orthop Surg 1: 103-113
Clemow A J T, Chen E H 1986 Induction of neo-tendons using a resorbable polymeric scaffold. Presented at the 32nd Annual Meeting of the Orthopaedic Research Society, New Orleans (LA), February 17-20.
Das De S, Balasubramaniam P 1985 A repair operation for recurrent dislocation of peroneal tendons. J Bone Joint Surg 67B: 585-587
Earle AS, Moritz JR, Tapper EM 1972 Dislocation of the peroneal tendons at the ankle: an analysis of 25 ski injuries. Northwest Med 71: 108-110
Eckert WR, Davis EA Jr. 1976 Acute rupture of the peroneal retinaculum. J Bone Joint Surg 58A: 670-672
Edwards ME 1928 The relations of the peroneal tendons to the fibula, calcaneus, and cuboideum. Am J Anat 42: 213-253
Elmslie RC 1934 Recurrent subluxation of the ankle-joint. Ann Surg 100: 364-367
Evans D 1953 Recurrent instability of the ankle -- a method of surgical treatment. Proc Roy Soc Med 46: 343
Evans GA, Hardcastle P, Frenyo AD 1984 Acute rupture of the lateral ligament of the ankle. To suture or not to suture? J Bone Joint Surg 66A(2): 209-212
Fox JM, Blazina ME, Jobe FW, et al 1975 Degeneration and rupture of the Achilles tendon. Clin Orthop 107: 221-224
Garrett WE Jr., Nikolaou PK, Ribbeck BM, et al 1988 The effect of muscle architecture on the biomechanical failure properties of skeletal muscle under passive extension. Am J Sports Med 16: 7-12
Garrett WE Jr., Safran MR, Seaber AV, et al 1987 Biomechanical comparison of stimulated and nonstimulated skeletal muscle pulled to failure. Am J Sports Med 15: 448-454
Gelberman RH, Manske PR, Vande Berg JS, et al 1984 Flexor tendon repair in vitro: a comparative histologic study of the rabbit, chicken, dog, and monkey. J Orthop Res 2(1): 39-48
Gould N, Seligson D, Gassman J 1980 Early and later repair of lateral ligament of the ankle. 1(2): 84-89
Haggmark T, Liedberg H, Eriksson E, et al 1987 Calf muscle atrophy and muscle function after non-operative vs operative treatment of Achilles tendon ruptures. 9(2): 160-164
Harper MC 1991 The lateral ligamentous support of the subtalar joint. 11: 354-358
Inglis AE, Scott WN, Sculco TP, et al 1976 Ruptures of the tendo achillis. An objective assessment of surgical and non-surgical treatment. J Bone Joint Surg 58A(7): 990-993
Inglis AE, Sculco TP 1981 Surgical repair of ruptures of the tendo Achillis. Clin Orthop 156(May): 160-169
Jackson DW, Ashley RL, Powell JW 1974 Ankle sprains in young athletes. Relation of severity and disability. Clin Orthop 101(Jun): 201-215
Jacobs D, Martens M, Van Audekercke RV, et al 1978 Comparison of conservative and operative treatment of Achilles tendon rupture. Am J Sports Med 6: 107-111
Jones E 1932 Operative treatment of chronic dislocation of the peroneal tendons. J Bone Joint Surg 14: 574-576
Jozsa L, Kvist M, Balint BJ, et al 1989 The role of recreational sport activity in Achilles tendon rupture. A clinical, pathoanatomical, and sociological study of 292 cases. Am J Sports Med 17(3): 338-343
Kelly RE 1920 An operation for the chronic dislocation of the peroneal tendons. Br J Surg 7: 502-504
Lagergren C, Lindholm A 1958 Vascular distribution in the Achilles tendon. Acta Chir Scand 116: 491-495
Larsen E 1988 Tendon transfer for lateral ankle and subtalar joint instability. Acta Orthop Scand 59(2): 168-172
Larsen E, Lund PM 1991 Peroneal muscle function in chronically unstable ankles. A prospective preoperative and postoperative electromyographic study. Clin Orthop 272: 219-226
Leach R E, Schepsis A A 1990 Acute injuries to ligaments of the ankle. In: Evarts C M (ed) Surgery of the Musculoskeletal System. Churchill Livingstone, New York. pp 3887-3913
Lindholm A 1959 A new method of operation in subcutaneous rupture of the Achilles tendon. Acta Chir Scand 117: 261-270
Ma GW, Griffith TG 1977 Percutaneous repair of acute closed ruptured achilles tendon: a new technique. Clin Orthop 128(Oct): 247-255
Ma G W C, Griffith T G 1981 Percutaneous repair of acute closed ruptured Achilles tendon: a new technique. In: Moore T M (ed) American Academy of Orthopaedic Surgeons Symposium on Trauma to the Leg and Its Sequelae. Mosby-Year Book Inc, St. Louis. pp 358-370
Mahler F, Fritschy D 1992 Partial and complete ruptures of the Achilles tendon and local corticosteroid injections. Br J Sports Med 26(1): 7-14
Martens MA, Noyez JF, Mulier JC 1986 Recurrent dislocation of the peroneal tendons. Results of rerouting the tendons under the calcaneofibular ligament. Am J Sports Med 14: 148-150
McLennan JG 1980 Treatment of acute and chronic luxations of the peroneal tendons. Am J Sports Med 8: 432-436
Meyer JM, Garcia J, Hoffmeyer P, et al 1988 The subtalar sprain. A roentgenographic study. Clin Orthop 226: 169-173
Meyer JM, Hoffmeyer P, Savoy X 1988 High resolution computed tomography in the chronically painful ankle sprain. 8: 291-296
Myerson M 1993 Cavovarus foot. In: Myerson M (ed) Current Therapy in Foot and Ankle Surgery. Mosby-Year Book Inc, St. Louis. pp 203-209
Nistor L 1981 Surgical and non-surgical treatment of Achilles tendon rupture. J Bone Joint Surg 63A(3): 394-399
Pepels WRJ, Plasmans CMT, Sloof TJJH 1983 The course of healing of tendons and ligaments. Acta Orthop Scand 54: 952
Pozo JL, Jackson AM 1984 A rerouting operation for dislocation of peroneal tendons: operative technique and case report. 5: 42-44
Ralston E L, Schmidt E R Jr 1971 Repair of the ruptured Achilles tendon. J Trauma 11(1): 15-21
Rasmussen O 1985 Stability of the ankle joint. Analysis of the function and traumatology of the ankle ligaments. Acta Orthop Scand Suppl 211: 1-75
Sammarco GJ, Chalk DE, Feibel JH 1993 Tarsal tunnel syndrome and additional nerve lesions in the same limb. 14: 71-77
Sarmiento A, Wolf M 1975 Subluxation of peroneal tendons. Case treated by rerouting tendons under calcaneofibular ligament. J Bone Joint Surg 57A: 115-116
Saxby T, Myerson M 1993 Calcaneus osteotomy. In: Myerson M (ed) Current Therapy in Foot and Ankle Surgery. Mosby-Year Book Inc, St. Louis. pp 159-162
Schon LC, Clanton TO, Baxter DE 1991 Reconstruction for subtalar instability: a review. 11(5): 319-325
Sedlin ED 1960 A device for stress inversion or eversion roentgenograms of the ankle. J Bone Joint Surg 42A: 1184-1190
Siegler S, Block J, Schneck CD 1988 The mechanical characteristics of the collateral ligaments of the human ankle joint. 8: 234-242
Smith JW 1958 The ligamentous structures in the canalis and sinus tarsi. J Anat 92: 616-620
Smith RW, Reischl S 1988 The influence of dorsiflexion in the treatment of severe ankle sprains: an anatomical study. 9: 28-33
Snook GA, Chrisman OD, Wilson TC 1985 Long-term results of the Chrisman-Snook operation for reconstruction of the lateral ligaments of the ankle. J Bone Joint Surg 67A: 1-7
Sobel M, Bohne WH, Levy ME 1990 Longitudinal attrition of the peroneus brevis tendon in the fibular groove: an anatomic study [see comments]. 11(4): 124-128
Sobel M, Warren RF, Brourman S 1990 Lateral ankle instability associated with dislocation of the peroneal tendons treated by the Chrisman-Snook procedure. A case report and literature review. Am J Sports Med 18: 539-543
Soma CA, Mandelbaum BR 1994 Achilles tendon disorders. Clin Sports Med 13: 811-823
Stephenson CA, Seibert JJ, McAndrew MP, et al 1990 Sonographic diagnosis of tenosynovitis of the posterior tibial tendon. J Clin Ultrasound 18(2): 114-116
Sun Y-S, Yen T-F, Chie LH 1977 Ruptured Achilles tendon: report of 40 cases. 57: 94-98
Taylor DC, Dalton JD Jr., Seaber AV, et al 1990 Viscoelastic properties of muscle-tendon units. The biomechanical effects of stretching. Am J Sports Med 18: 300-309
Thompson FM, Patterson AH 1989 Rupture of the peroneus longus tendon. Report of three cases. J Bone Joint Surg 71A: 293-295
Wapner KL, Pavlock GS, Hecht PJ, et al 1993 Repair of chronic Achilles tendon rupture with flexor hallucis longus tendon transfer. 14(8): 443-449
Watson-Jones R 1955 Fractures and Joint Injuries. Williams & Wilkins, Baltimore
Zoellner G, Clancy W Jr. 1979 Recurrent dislocation of the peroneal tendon. J Bone Joint Surg 61A: 292-294
Zollinger H, Meier C H, Waldis M 1983 [Diagnosis of subtalar instability utilizing stress tomography]. In: Hefte zur Unfallbeilkunde Heft 165. Springer-Verlag, Heidelberg. pp 175-177
Figure Legends
Fig. 1. Inversion (varus) stress was applied to this ankle. Eleven degrees of talar tilt was present but, to be clinically significant, should be compared with the opposite ankle.
Fig. 2. The anterior drawer test. The amount of instability may be measured using points y-y or x-x, and should be compared with the opposite ankle.
Fig. 3. The skin incision for the modified Brostrom procedure is identified by the dotted lines.
Fig. 4. The anterior talofibular ligament and capsule are incised, leaving a small cuff of tissue attached to the fibula.
Fig. 5. The anterior talofibular ligament and capsule are imbricated either by excising a segment or repairing the ligament with a "vest-over-pants" method as demonstrated here.
Fig. 6. The extensor retinalculum is advanced proximally to the anterior edge of the fibula to tighten and reinforce the repair.
Fig. 7. The incision for the modified Chrisman-Snook procedure is made parallel to the peroneal tendons, posterior to the fibula.
Fig. 8. The anterior half of the peroneus brevis is harvested, leaving the posterior half attached to the muscle.
Fig. 9. A 4.5-mm drill hole is made from anterior to posterior at the tip of the fibula.
Fig. 10. It is preferrable to pass the split peroneus brevis tendon superficial to and not deep to the two tendons, as demonstrated here.
Fig. 11. The tendon is secured to the calcaneus with a spiked ligament washer and a 4.0-mm cancellous screw.
Fig. 12. If sufficient tendon length is present, the stump may be advanced to the tip of the fibula. This step is not necessary with rigid screw fixation.
Fig. 13. Inversion stress was applied to the ankle, which remained stable. On a 40o Broden's view, the subtalar joint is noted to subluxate forward and to rotate internally.
Fig. 14. This patient reported a chronic popping behind the ankle and was able to volunatarily dislocate the peroneal tendon(s). Note the tendon(s) lying anterior to the fibula.
Fig. 15. The peroneal tendons are well located in the groove on the left but, when associated with recurrent dislocation, the fibula groove becomes shallow, and the anterior fibrocartilaginous rim is avulsed with or without a tear of the retinaculum.
Fig. 16. A groove is made posterior to the fibula, and the extensor reti, naculum is advanced deep to the groove and attached through two or three pairs of drill holes.
Fig. 17. This patient sustained an acute partial tear of the peroneus brevis tendon, which was also dislocated anteriorly. This was treated by resection of the torn portion of the tendon and repair of the peroneal retinaculum.
Fig. 18. Chronic inflammatory Achilles paratendinitis is evident with thickening of the paratenon and an acute inflammatory infiltrate over the tendon.
Fig. 19. Chronic inflammatory Achilles tendinosis is demonstrated in this 54-year-old athlete (A). This was treated with excision of the degenerated portion of the tendon and transfer of the flexor hallucis longus muscle and tendon to reinforce the repair (B).
Fig. 20. Achilles tendon repair, using locking sutures. One or more strands of suture may be used.
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