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

Section 3 - Anatomic Disorders in Sports

Chapter 13 - Ankle sprains, ankle instability, and syndesmosis injuries

Thomas O. Clanton







Surgical treatment









Direct ligament repair (modified Brostrom procedure)



Failed lateral ankle ligament reconstruction



Medial ankle sprains



Chronic medial ankle instability



Syndesmosis injury





Because it generally is agreed that most acute lateral ankle sprains can be treated nonoperatively while acknowledging an incidence of late problems in 10% to 20% it is no surprise that lateral ankle ligament reconstruction is commonplace.[1] This approach to the treatment of lateral ankle sprains is reasonable only if reconstructive procedures for the lateral ankle ligaments can be as successful as primary repair. Recent consensus of orthopaedic opinion supports this viewpoint. However, there is still controversy that persists regarding the best method of treatment of acute lateral ankle sprains because of the paucity of scientific studies in this field that meet the requirements for proof of method in outcomes-based research.[2]

Most patients with chronic lateral ankle sprains and instability present with either recurrent ankle sprains after an initial acute sprain or with the feeling of looseness in the ankle and the sensation of “giving way.” These patients may complain of ankle pain, but it is not a prerequisite feature of this problem, although the examination confirms the presence of a positive anterior drawer test and/or a positive inversion stress test. Tenderness may be present, but often is more indicative of associated pathology, as noted later. The examiner must be thorough enough to rule out other sources of symptoms ( Table 13-1 ) because the clinical diagnosis of chronic lateral ankle instability has been associated with the intraoperative findings of peroneal tendon pathology (tenosynovitis, tears, dislocation), anterolateral impingement lesions, ankle synovitis, intraarticular loose bodies, talar osteochondral lesions, and medial ankle tenosynovitis.[3] A comprehensive physical therapy program should be initiated first. Symptoms often will resolve with correction of the deficits in proprioception, strength, and flexibility. Regardless, therapy can improve the results in patients who ultimately require surgery. The nonoperative treatment also includes activity and/or shoe modification (e.g., lateral heel wedge), an ankle-foot orthosis, and/or orthotic devices incorporating a lateral heel wedge. Brostrom[4] found that symptoms of instability remained in 20% of his patients who were treated in a conservative fashion. Athletes may use a nonoperative approach to get through a season but rarely consider this an acceptable long-term solution unless their symptoms are minimal.

Table 13-1   -- Sources of Chronic Pain or Instability after Ankle Sprain

Articular injury


 Chondral fractures

 Anterior tibial osteophyte

 Osteochondral fractures

 Anterior inferior tibiofibular ligament

Nerve injury

Miscellaneous conditions

 Superficial peroneal

 Failure to regain normal motion (tight Achilles)

 Posterior tibial

 Proprioceptive deficits


 Tarsal coalition

 Tendon injury

 Meniscoid lesions

 Peroneal tendon (tear or dislocation)

 Accessory soleus muscle

 Posterior tibial tendon

Unrelated ongoing pathology masked by routine sprain

Other ligamentous injury

 Unsuspected rheumatologic condition


 Occult tumor


 Chronic ligamentous laxity (collagen disease)


 Neuromuscular disease (Charcot-Marie-Tooth disease)


 Neurologic disorders (L5 radiculopathy, poststroke )




Surgical Treatment

Indications for surgical treatment include young to middle-aged, active individuals who have failed a well-designed, nonoperative treatment program. I use the radiographic criteria of an anterior drawer greater than 1 cm (or a side-to-side difference of >3 mm), and a talar tilt greater than 15 degrees (or a side-to-side difference of >10 degrees) as guidelines but have found that the symptoms and signs are most critical. An in-office mini C-arm is a convenient tool to confirm the radiographic instability. Contraindications to surgery include other causes of instability (collagen diseases, tarsal coalitions, neuromuscular diseases, neurologic disorders, or functional instability), older patients with sedentary lifestyles, patients with serious medical conditions that would preclude anesthesia and major surgery, circulatory impairment, presence of ongoing infection, lateral ankle pain without documented lateral instability, history of complex regional pain syndrome, or degenerative arthritis. A relative contraindication is failure of the patient to participate in a preoperative rehabilitation program.

The goals of a reconstruction or repair procedure are correction of instability, elimination of pain, and avoidance of surgical morbidity. Anatomic repair or reconstruction is preferable in restoring normal joint kinematics. If there is associated pathology present, it must be recognized and treated simultaneously. Inadequate local tissue to stabilize the ankle may dictate the use of a tendon transfer or tendon graft. Such occasions might include patients with known collagen disease, unusually large individuals (e.g., patients larger than 250 lb), or patients with a failure of a prior anatomic repair. Avoidance of nerve injury and preservation of ankle and subtalar joint motion are major factors in preventing morbidity when performing lateral ankle stabilization.

Diagnostic and surgical arthroscopy is warranted before ankle stabilization. Chondral injury is the most common problem discovered at arthroscopy, with almost 30% of acute ankle injuries and 95% of chronic ankles having this lesion in one study of an athletic population.[5] A more recent study by Komenda and Ferkel[6] found only a 25% incidence of chondral injury in their chronic ankle instability series. Regardless, the value of ankle arthroscopy, particularly in cases of chondral fracture, loose bodies, and soft-tissue impingement has been confirmed in several studies. [0060] [0070] [0080] [0090]Hintermann and co-workers[9] concluded that essential information was obtained by performing ankle arthroscopy at the time of surgery for ankle instability.

Operations for stabilization of the lateral ankle in cases of chronic instability are numerous. When instability persists despite conservative treatment, the surgeon can choose from more than 50 methods of reconstructing the lateral ankle ligaments. Fortunately, the reported short-term success rate is greater than 80% for all these procedures, according to the literature.[10] The primary difference in the various procedures is whether or not they are designed to anatomically reconstruct the ligaments. In a manner reminiscent of the surgical history of shoulder and knee instability, more anatomic reconstructions are gaining popularity for ankle instability. This began with the introduction of the secondary repair of the previously injured ligaments by Lennart Brostrom in 1966.[11] It has taken almost four decades for the accumulation of scientific evidence to cast doubt on the tenodesis procedures described by Evans, Watson-Jones, Larsen, and Chrisman and Snook. [0120] [0140] [0150] [0160] [0170] The following discussion focuses on the anatomic procedures, whether by direct repair in the tradition of Brostrom or by the use of tissue transfer or tissue grafts done through anatomically placed bone tunnels.

Brostrom described his anatomic repair as a delayed procedure for chronic lateral ankle instability. The procedure is a straightforward division and imbrication of the anterior talofibular ligament. The calcaneofibular ligament is not addressed. Various modifications have been described, the most popular being a reinsertion into a bony trough,[17] imbrication of the calcaneofibular ligament,[18] and reinforcement with the inferior extensor retinaculum.[19] Other authors have described the use of different graft sources to rebuild the lateral ankle ligaments while emphasizing the anatomic placement of bone tunnels. Graft sources for this include the plantaris tendon, [0210] [0220] [0230] the split peroneus brevis tendon, [0240] [0250] hamstring tendons, [0260] [0270] [0280] and allograft tendons. [0290] [0300]



Results of the Brostrom anatomic reconstruction are excellent. In Brostrom's original study, 51 of 60 patients demonstrated minimal or no instability at follow-up.[11] Other reported results from the Brostrom procedure or a modification thereof include large and small series of patients from around the world, with more than 500 cases reported and results ranging from 85% to 100% successful. [0140] [0310] [0320] [0330] [0340] [0350] [0360] [0370] [0380] Lesser results are associated with heel varus, inadequate rehabilitation, nerve injury, preexisting arthritis, and significant repeat sprains.

Objective results of comparison studies that include anatomic procedures such as the Brostrom versus tenodesis procedures all favor the former procedure. In a cadaveric study comparing the Chrisman-Snook, Watson-Jones, and modified Brostrom procedures, the modified Brostrom procedure produced the least amount of talar tilt and anterior drawer translation, as well as having the greatest mechanical strength.[38] Another study, a prospective, randomized comparison of Chrisman-Snook and modified Brostrom, found that both procedures had greater than 80% good or excellent results, but there were more complications in the Chrisman-Snook group (five with wound problems, eight with sural nerve injury, and six with the feeling that the ankle was “too tight”). Brostrom complications were almost nonexistent and included no wound problems, no nerve injury, and only two with a feeling that the ankle was “too tight.”[13] In a long-term, multicenter outcome study of anatomic reconstruction versus teno-desis, Krips and associates[39] found that more patients with tenodesis procedures had positive anterior drawer signs, medial ankle degenerative changes, higher mean talar tilt, and anterior talar translation. In addition, significantly fewer patients in the tenodesis group had excellent results, and more patients had a fair or poor result. In a follow-up study, patients who underwent tenodesis procedures underwent more revision procedures, demonstrated more osteoarthritis, more instability, tenderness, chronic pain, and limited dorsiflexion. Good to excellent results were found in 80% of patients at 30-year follow-up after anatomic reconstruction, versus only 33% after Evans tenodesis.[40] Overall, it appears that tenodesis procedures fail to restore the normal anatomy, resulting in lessened mechanical stability and a decrease in patient satisfaction. Because of these well-documented inherent problems of nonanatomic tenodesis procedures, anatomic ligamentous reconstruction is the preferable treatment approach in almost all circumstances.



Neurologic damage and wound complications are not infrequent. Injury to the superficial nerves is the most common complication following operative repair of the lateral ankle ligaments. Depending on the report and the type of surgical approach used, the incidence ranges from 7% to 19%.[41] The sural nerve is at greater risk with tenodesis procedures.[42] Wound dehiscence, superficial and deep infection, loss of ankle and/or subtalar motion, and deep venous thrombosis are less-often reported complications. Wise patient selection and good surgical technique are paramount in keeping these complications to a minimum.


Direct Ligament Repair (Modified Brostrom Procedure)

For most cases of chronic lateral ankle instability in the athletic population, a modified Brostrom technique is applicable. Its advantage is that it is an anatomic repair, with no tenodesis effect and no major change in the ankle and subtalar joint biomechanics. A second advantage is that it does not sacrifice adjacent healthy tissue. Indications include those patients with chronic lateral ankle ligament instability who are unresponsive to physical therapy. Contraindications include patients with structural varus deformities, previously failed lateral ligament reconstructions, genetic collagen disorders (Marfan's and Ehlers-Danlos syndromes), or posttraumatic conditions with soft-tissue loss. Relative contraindications are obese patients (more than 250 lb) or patients whose instability exceeds 10 years duration with history of multiple severe sprains.[17] For these patients, consideration is given to use a free tendon graft (allograft or autograft) for augmentation.

My operative technique includes planned day surgery or a 23-hour hospital stay. General, spinal, or regional anesthesia may be used. The patient is positioned supine with a bolster under the ipsilateral hip. A thigh tourniquet is placed. The procedure is performed through an anterior lateral incision paralleling the border of the fibula unless a more extensile longitudinal incision is necessary to address additional pathology.




The incision begins at the level of the plafond and extends distally to the level of the peroneal tendons ( Fig. 13-1 ). The lateral branch of the superficial peroneal nerve and the sural nerve are protected.



Dissection is carried down to the capsule. To isolate the remaining portion of the anterior talofibular ligament (ATFL), it is helpful to enter the anterolateral capsule at the plafond level and carefully dissect distally to expose the ATFL fibers. If the ligaments appear stretched ( Fig. 13-2 ) and there is no obvious rupture, the capsule and ligament are divided a few millimeters from their fibular origin and imbricated.



To locate the calcaneofibular ligament (CFL), the peroneal sheath is opened and the peroneal tendons are first checked for a tear. Then the tendons are retracted exposing the CFL, and the quality of the CFL is determined. A ligament that is simply stretched can be divided and imbricated ( Fig. 13-3 ). The previously ruptured ATFL or CFL often is scarred down to capsule and tendon sheath and requires dissection to disclose their location and character. For the CFL, it is necessary to determine whether the remaining tissue can be used in the secondary repair. A distal avulsion from the calcaneus can be reattached with suture anchors. I prefer to use a bioabsorbable anchor to avoid problems from retained hardware in the event of future ankle problems that might call for a drill hole in this location. A proximal avulsion can be reattached with sutures through drill holes in the fibula (being careful to consider the anterior talofibular reconstruction) or with a suture anchor. The greatest difficulty arises with a midsubstance tear that has extensively scarred to the surrounding tissue. Careful dissection usually will define a ligamentous remnant that can be imbricated.



In the case of an ATFL avulsed from the fibula, and to be certain of sufficient tissue for the ATFL reconstruction, a periosteal flap that is continuous with the capsule and the anterior talofibular scar can be created.



Nonabsorbable or slowly absorbable sutures are placed in the ligament. A small bony trough is created above the anterior and inferior border of the distal end of the fibula, and several drill holes are made with a small drill bit or Kirschner wire ( Fig. 13-4 ). This permits imbrication of the ends of the cut ligament and capsule, as well as the anchoring of the ligament into bone. In the few cases in which the ATFL has avulsed from the fibula, it also is feasible to reattach the ATFL with suture anchors. As mentioned under number 3 previously, it is preferable to use bioabsorbable anchors here to avoid the potential problem of extricating a metal anchor that is situated in the exact location where a bone tunnel must be placed for a tendon graft reconstruction should the anatomic reconstruction fail or be disrupted in a future injury.



The sutures are tied over a bony bridge on the lateral aspect of the fibula, with the ankle held in neutral dorsiflexion and slight eversion ( Fig. 13-5 ). The surgeon must be careful to ensure that there is no anterior displacement force on the ankle while the sutures are being tied. To prevent this, a bump is placed under the distal leg to relieve any anterior directed force on the heel.



Sutures are placed in the CFL first, followed by the ATFL, and then the lateral capsule. The sutures are tagged or grouped to be tied only after all sutures are in place. Sutures are tied beginning with the CFL, then the ATFL, and concluding with the anterior capsule. The ankle is positioned in relaxed plantarflexion when the sutures in the CFL are secured and in slight dorsiflexion and eversion for tying the sutures in the ATFL.



After securing the repair, the stability is checked and further imbrication performed as needed.



Before closure, attention is directed to the inferior extensor retinaculum, which is imbricated or sutured to the periosteum over the fibula ( Fig. 13-6 ). This provides additional stability to the subtalar area and protection to the ATFL and may add some proprioceptive feedback. I believe that it is an important addition to the Brostrom technique, as noted by Gould and others. [0440] [0450] [0460]



The subcutaneous tissues are reapproximated with absorbable sutures, and the skin is closed with a subcuticular technique.



A U-shaped splint and a posterior splint or a walking boot is applied.



Figure 13-1  Anterior lateral incision paralleling the border of the fibula used for anatomic repairs and reconstructions.  Courtesy Matthew Morrey, MD.



Figure 13-2  Stretched anterior lateral ligaments found in typical chronic ankle sprains.  Courtesy Matthew Morrey, MD.



Figure 13-3  Imbrication of stretched ligaments in anatomical reconstructive procedure.  Courtesy Matthew Morrey, MD.



Figure 13-4  Bony trough used for attachment of anterior talofibular and calcaneofibular ligaments to bone.  Courtesy Matthew Morrey, MD.



Figure 13-5  Sutures tied over bony bridge on anterior lateral fibula.  Courtesy Matthew Morrey, MD.



Figure 13-6  Imbrication of inferior extensor retinaculum to periosteum of distal fibula.  Courtesy Matthew Morrey, MD.


Postoperative care

For athletes, the patient is placed in a short-leg splint with the foot in neutral dorsiflexion and slight eversion. The splint remains in place until the first postoperative visit, which usually occurs between 6 and 10 days from the day of surgery. The patient is on crutches—nonweight bearing until this visit. At the first postoperative visit, the patient is placed in a walking boot or cast and begins weight bearing as tolerated. This is continued for 3 to 4 weeks until the next office visit. During this second phase, the patient may start dorsiflexion and eversion movement if in a boot, and at 4 weeks, the patient is placed in an ankle stirrup brace. Gentle active inversion is begun at 4 weeks in association with Achilles stretching. At the same time, proprioceptive training and resistive exercises with rubber tubing are begun. The patient is allowed to progress from stationary biking to pool running to outdoor walking and straight-line running. As long as the patient shows no pain or undue swelling, rehabilitation continues as tolerated with figure-eight running in progressively smaller loops, and ultimately, cutting drills are instituted. The athlete then is allowed to resume activities specific to his or her sport, with return to competition once each task of the sport can be accomplished. For 6 months following the repair, the patient is instructed to use a protective ankle brace and/or taping to protect the repair. The typical return to competitive sport participation is 12 weeks (range 10 to 16 weeks), although it may take closer to 6 months for swelling and discomfort to resolve fully.

For nonathletes, a 10- to 12-week period of protection is warranted, the first 4 to 6 weeks with the patient being in a cast or walking boot with limited exercise and the second 6 weeks with the patient being in a removable brace or walking boot when a more aggressive rehabilitation program is begun. Resumption of vigorous exercise or recreational sports generally takes longer in this population. Although I believe in individualizing the rehabilitation program to the patient and the pathology, a table is provided as a general guideline ( Table 13-2 ).

Table 13-2   -- Rehabilitation Program for Surgically Reconstructed Lateral Ankle Ligaments

Doctor visits

Days (weeks)


Weight bearing


Surgery to first postoperative visit

0-7 (1)

Immobilized in splint or walking boot

Crutches nonweight bearing

No exercises with ankle but general conditioning as tolerated

First visit to second visit

8-28 (2-4)

Walking boot with dorsiflexion and eversion allowed

Crutches with weight bearing as tolerated, progressing to full weight and no crutches

General conditioning, stationary bike starting with stirrup brace and weight on heel, pool walking and running, light balance work

Second visit to third visit

29-42 (5-6) 43-56

Stirrup brace at all times except sleep
Stirrup brace for exercise

Full weight

Biking with increased resistance, outdoor walking and straight line running, aggressive proprioceptive education
Start figure-8 running, cutting, sports-specific drills

Third visit to return to play

57-70 up to 84 (9-12)

Brace or tape for practice


Progress drills, speed and endurance




Failed Lateral Ankle Ligament Reconstruction

Of patients who undergo a lateral ankle reconstruction, 5% to 15% may proceed to failure, requiring further intervention. Perhaps the most common cause for failure is recurrent instability. The primary surgical procedure may have been inadequate, the patient may have reinjured the ankle, or there may have been inherent factors that predisposed a patient to failure (benign joint hypermobility syndrome, Marfan's syndrome, or Ehlers-Danlos syndrome).[42] The patient often describes a loose feeling in the ankle or the sensation of “giving way” or “turning easily.” Another cause of failure in lateral ankle reconstruction is chronic pain, constant or only during activity, resulting from intra-articular pathology or postoperative stiffness.

In addition to a thorough history, it is important to obtain a record of the primary procedure, if possible. Stress tests of the lateral ligaments should demonstrate laxity. Limited range of motion of the ankle and subtalar joints can be observed in patients who were overtightened at their original reconstructive procedure. The alignment of the hindfoot should be evaluated. Varus alignment of the heel will predispose a patient to failure of a lateral ligament reconstruction.

Radiographs of the foot and ankle should be obtained to evaluate the presence of bony pathology. Stress radiographs or fluoroscopy can aid in the diagnosis of recurrent instability or an excessively tight reconstruction. Intra-articular pathology, such as osteochondral lesions, can be diagnosed with magnetic resonance imaging (MRI). Computed tomography (CT) scans are helpful in defining previous bone tunnels. Nonoperative measures may be effective in the management of recurrent instability; however, these patients typically require a second attempt at surgical stabilization.


Reconstructing the lateral ligament with a free tendon transfer using the semitendinosus or the gracilis tendon is recommended, performed in a manner similar to the method used when harvesting for an anterior cruciate ligament autologous graft. After the graft has been harvested, it is prepared by sizing it for diameter and length. Generally, the doubled semitendinosus is 9 to 11 cm in length and approximately 5 to 6 mm in diameter, whereas the gracilis is somewhat smaller. It also is possible to use an allograft tendon, and a larger tendon such as the anterior tibial tendon can be cut to the appropriate diameter for drill holes.

The lateral ankle is exposed through one of two incisions chosen on the basis of the underlying pathology. When the pathology is limited to the previously reconstructed lateral ligamentous complex, a small, curvilinear incision paralleling the anterior and distal border of the fibula is used, similar to the incision for the previously described Brostrom procedure (see Fig. 13-1 ). For cases with more extensive pathology (peroneal tendon tears or anterior osteophytes), a longitudinal incision is made over the posterior border of the fibula, curving distally to the sinus tarsi and the anterior process of the calcaneus. With both approaches, the ankle joint is exposed and the anterolateral capsule is divided, preserving as much potentially useful tissue as possible.

For proper graft placement, the insertion sites of the ATFL (talus and distal fibula) and CFL (distal fibula and calcaneus) are exposed. The surgeon then drills a 4.5- to 6.0-mm tunnel in the talus, depending on the size of the graft and the size of the interference fit screw being used. Bioabsorbable screws currently vary in size from 4 to 11 mm. I have found that the 5- to 5.5-mm screw works best in the ankle. The tendon graft is captured with a suture loop using the Arthrex Biotenodesis System and inserted into the bone tunnel to a depth of approximately 20 mm before the bioabsorbable screw is tightened against the tendon within the bone tunnel. Another option is to drill a tunnel in the talus to a depth of 25 to 30 mm and use a Beath pin to pass the sutures from the end of the tendon graft through the tunnel in the talus and out the medial side of the foot. With tension applied to the tendon through the sutures, an interference screw can be placed next to the tendon to secure the graft in the talus. Once the graft is secure in the talus, a tunnel is drilled from the anterior distal fibula at the origin of the ATFL through the distal fibula and into the area of the proximal peroneal groove. When the procedure is performed through a Brostrom-type incision, a separate 2-cm incision is made for insertion of a retractor to protect the peroneal tendons. A second fibular bone tunnel is drilled at the origin of the CFL and passed posterior to exit at the posterior fibula at the same exit site as the previously drilled fibular tunnel. Now a V-shaped channel in the distal fibula exists. A suture passer is placed through the posterior fibular tunnel, exiting anterior, and the sutures in the tendon graft are passed into the fibula, creating an ATFL graft. The suture passer next is passed posterior through the distal fibular tunnel, and the sutures in the tendon graft are passed out the distal fibula to create a CFL graft. It is important to keep a clamp around the graft at the posterior fibula to allow tensioning of the separate limbs of the graft. A tunnel is drilled in the lateral calcaneus at the site of insertion of the CFL for the tendon graft, with the depth of the tunnel being sufficient enough to pull the entire tendon graft length into the bone tunnel. A Beath pin or Keith needle then is used to pass the tendon graft sutures through the plantar medial heel.

While holding the ankle in neutral dorsiflexion and neutral inversion/eversion, the surgeon applies tension to the graft. A bioabsorbable screw is placed with an interference fit in the calcaneal bone tunnel to secure the graft ( Fig. 13-7 ). Alternatively, the Arthrex Biotenodesis System can be used to insert the tendon in the bone tunnel and fixate the graft with the bioabsorbable screw. Once the graft is secured and the tension is judged to be adequate, the ankle is tested for stability and range of motion, and stress radiographs are performed under fluoroscopy. If the ankle is still unstable, the screw in the calcaneus is removed, the graft further tensioned, and the screw replaced with the heel in slight eversion. The graft is secured to the periosteum of the fibula at the entrance and exit holes with absorbable suture. The inferior extensor retinaculum or other local tissue can be used for augmentation if further stability is required.


Figure 13-7  Bioabsorbable screws placed with an interference fit in the talar and calcaneal bone tunnels to secure the tendon graft.



Postoperatively, the ankle is protected in a splint or boot, nonweight bearing for 1 to 2 weeks. After this time period, progressive weight bearing is allowed over 2 to 3 weeks, with discontinuation of crutches by 4 weeks postoperatively. Compliant patients, under supervision, can be managed in a removable walking boot and started on active range of motion immediately. The typical ankle rehabilitation program for range of motion, strength, Achilles stretching, and proprioceptive reeducation begins at about 3 to 4 weeks and progresses as tolerated. Other pathology often dictates any alterations that must be made to this general protocol.


Medial Ankle Sprains

The medial ankle ligamentous complex is composed solely of the deltoid ligament. The overwhelming majority of deltoid ligament injuries occur in association with lateral malleolus fractures, syndesmotic disruptions, or injuries to the lateral ankle ligaments. Isolated deltoid ligament sprains account for only 2% to 3% of all ankle sprains. [0470] [0480] [0490] Chronic medial ankle instability is rarely a clinical problem, but its prevalence probably is underestimated. [0500] [0510]

Anatomy and biomechanics

The deltoid ligament is a broad, fan-shaped complex of ligaments that together serve as the medial collateral ligament of the ankle. The deltoid ligament consists of both a superficial layer and a deep layer and has enough anatomical variation that there has been some confusion in the nomenclature. [0520] [0530] [0540] [0550] Milner and Soames'[51] detailed anatomic study found six different bands, with three being consistently present (two superficial and one deep), and three bands were not found in all specimens. The constant superficial bands originate from the anterior colliculus of the medial malleolus and are divided into the tibiospring ligament (TSL) and tibionavicular ligament (TNL). The less constant portions of the superficial deltoid are the tibiocalcaneal ligament (TCL) and superficial posterior tibiotalar ligament (STTL) ( Fig. 13-8 ). By their nature, the medial ligaments blend together, forming an indistinct origin from the medial malleolus, and are characterized primarily by their distal attachment.


Figure 13-8  Superficial deltoid ligaments. (A) Tibial spring ligament. (B) Tibionavicular ligament. (C) Tibiocalcaneal ligament.



The constant band of deep deltoid ligament is the deep posterior tibiotalar ligament (PTTL). The deep anterior tibiotalar ligament (ATTL) was found in only 10% of specimens[51] ( Fig. 13-9 ). The deep bands cross only the single joint of the ankle, whereas the superficial ligaments cross two joints (ankle and either talocalcaneal or talonavicular). The deep layer of the deltoid originates from the intercollicular groove and posterior colliculus of the medial malleolus.


Figure 13-9  Deep deltoid ligaments. (A) Deep posterior tibiotalar ligament. (B) Deep anterior tibiotalar ligament.



The deltoid ligament is the primary restraint to valgus tilting of the talus within the ankle mortise.[55] Both the superficial deltoid and the deep deltoid individually resist eversion of the hindfoot. Valgus tilting of the talus does not occur if only the superficial or the deep portion of the deltoid is divided. [0560] [0570] Complete rupture of the entire deltoid complex is required to produce valgus tilting of the talus in otherwise intact ankles.[55]

The deep deltoid ligament is also a secondary restraint against both lateral talar shift and anterior talar excursion, with the fibula and lateral ankle ligaments being the primary restraint.[55] Multiple anatomic studies have shown that, with an intact deltoid, up to 3 mm of lateral talar shift is possible if the lateral malleolus has been resected. [0560] [0580] [0590] Conversely, no increase in lateral shift or anterior excursion of the talus occurs when the entire deltoid is sectioned if the lateral malleolus and ligaments are intact.[57] However, sectioning of the entire deltoid, or just the tibiospring (or tibiocalcaneal) portion of the superficial deltoid, has been shown to dramatically decrease tibiotalar contact area and increase peak ankle joint pressures up to 30%. These significant changes in contact area and peak pressures occur before radiographic evidence of medial talar tilt is present. [0600] [0610] The deltoid ligament clearly is involved in rotary stability of the talus within the mortise, but its exact function in this regard is the subject of some debate. [0570] [0620] [0630]

Mechanisms of injury

Although the deltoid ligament may be injured in conjunction with the lateral ligamentous structures by a variety of mechanisms, the classic mechanism of injury for an isolated deltoid rupture is forced abduction or eversion.[63] In these forced abduction injuries, the superficial deltoid ligament ruptures first, followed by the deep deltoid.[64] The deep deltoid has a significantly higher load to failure than the lateral collateral ankle ligaments, with its dominant mode of failure being an intrasubstance rupture near its talar insertion. [0660] [0670] Consequently, a deltoid injury requires considerably more force than the average lateral ankle sprain. Athletic injuries to the deltoid typically involve jumping sports or contact sports such as football or wrestling. A basketball player might sustain an eversion injury by landing on another player's foot after coming down from a jump, whereas a football player might sustain a forced abduction injury when an opponent falls on or steps on his lateral ankle with the foot in a pronated position. Garrick[67] noted an inordinately high frequency of ankle sprains in wrestlers, presumably resulting from their wide stance and having their feet everted to gain traction on the mat.


As stated previously, the majority of deltoid injuries occur in conjunction with lateral ankle sprains, syndesmosis injuries, or fibula fractures. Obtaining an accurate description of the patient's mechanism of injury may provide important clues to the presence of these associated injuries. Patients with acute deltoid ligament ruptures usually recall the specific injury and often feel or hear a pop on the medial side of their ankle. A history of immediate pain and swelling over the deltoid ligament is typical, along with a variable degree of difficulty with ambulation and a feeling of medial instability.

Because of the high prevalence of associated injuries, examination of an athlete with a suspected deltoid ligament injury should include evaluation of the entire lower leg. Careful palpation of the entire length of the fibula should be performed to assess for a high fibula fracture that might be seen with a Maisonneuve-type injury. An injury to the ankle syndesmosis must be ruled out by squeeze test ( Fig. 13-10 ) or external rotation test ( Fig. 13-11 ) or, if still in question, by MRI. A thorough assessment of each of the lateral ankle ligaments also must be performed. When examining the medial ankle structures, it is important to keep in mind the intimate spatial relationships of the deltoid ligament to the contents of the tarsal tunnel. Careful localization of the point of maximal tenderness and evaluation of tendon function can help to distinguish between deltoid ligament ruptures and injuries of the posterior tibial, flexor digitorum longus (FDL), or flexor hallucis longus (FHL) tendons or to the spring ligament. The patient with a deltoid injury may develop an increasingly flat foot or pronated foot deformity with weight bearing after the injury that is actively correctable with contraction of the posterior tibial muscle.[50] Finally, a brief sensory examination of the foot and ankle, including attempts to elicit a Tinel's sign, can help to identify acute traction injuries of the tibial or saphenous nerves.


Figure 13-10  Squeeze test for syndesmosis injury.




Figure 13-11  External rotation test for syndesmosis injury.



Radiologic evaluation should begin with standard views of the ankle to detect associated ankle fractures or frank diastasis of the syndesmosis. Supplemental anterior-posterior (AP) and lateral views of the leg should be obtained if the physical examination is suggestive of a high fibula fracture or proximal tibiofibular pathology. Weight-bearing AP ankle radiographs may show valgus tilt in a complete deltoid rupture.

If an isolated deltoid ligament rupture is clinically suspected, manual valgus stress radiographs should be obtained. Greater than 5 degrees of valgus talar tilt with valgus stress in neutral ankle flexion, or a side-to-side difference of greater than 2 degrees, is indicative of an isolated complete deltoid injury.[68] It should be noted that plain radiographs typically are normal in patients with ruptures of only the superficial portion of the deltoid ligament.

Although MRI is considered the gold standard for visualizing the deltoid ligament, it has been used rarely in clinical practice except in professional athletes. As with lateral ligament injuries, MRI can be helpful in the evaluation of associated ankle pathology in a patient who fails conservative management. MRI also is useful in special cases in which the diagnosis of an acute deltoid rupture must be objectively confirmed. Clinical correlation between MRI and physical examination findings is critical because MRI is highly sensitive and may demonstrate clinically insignificant changes in the deltoid ligament.[69] Schneck et al.[70] have emphasized the importance of separate dorsiflexion and plantarflexion imaging sequences to optimally visualize the individual components of the deltoid ligament. With newer high field strength magnets, updated three-dimensional imaging software, and the use of a dedicated ankle coil, foot position may be less important.[71] When ordering an MRI to evaluate the deltoid, direct consultation with the radiologist before the study helps to determine the appropriate imaging protocol for their specific equipment. Another alternative for diagnosis when nonoperative treatment fails is arthroscopy of the ankle and direct assessment of the ligamentous integrity, as described by Hintermann et al.[50] He suggests using the criteria described in Table 13-3 for grading the degree of instability by arthroscopy.

Table 13-3   -- Arthroscopic Grading and Findings in Medial Ankle Instability

Grade of instability

Opening medially (mm)

Device used



Up to 3

2-mm hook probe/2.7-mm scope

Minimal translation of talus



2-mm hook probe/2.7-mm scope

Translation discernible with probe, scarring seen in superficial deltoid



5-mm scope/4.5-mm shaver

Obvious translation with easy movement of large joint scope into medial tibiotalar space, scarring of medial ligaments or disruption both deep and superficial


More than 5

5-mm scope/4.5-mm shaver

Obvious translation with easy movement of large joint scope into medial tibiotalar space with free visualization to the posterior aspect of the ankle joint even without valgus stress applied

Modified from Hintermann B, et al: Medial ankle instability—a missed diagnosis, Presented at AAOS Annual Meeting, AOFAS Specialty Day, March 13, 2004.




In general, the treatment of acute deltoid ligament ruptures is nonoperative. However, the presence of an associated fibular fracture or syndesmotic injury most often will require operative treatment for these entities. Although it is the subject of historical controversy, most recent studies have concluded that the deltoid does not need to be surgically repaired once the lateral malleolus and/or syndesmosis have been anatomically reduced and stabilized. [0730] [0740] [0750] [0760] [0770] [0780] The anatomy of the deltoid ligament allows for maintained apposition of its torn ends if the talus is appropriately stabilized within the mortise. [0210] [0790] [0800] The main indication for deltoid ligament surgery is the infrequent case in which the deltoid or posterior tibial tendon becomes entrapped between the talus and the medial malleolus, preventing anatomic reduction of the talus within the mortise. In these cases, medial ankle arthrotomy with exploration of the posterior tibial tendon and repair of the deltoid is recommended. There are other situations that occasionally warrant repair of the deltoid in association with syndesmosis disruption, and the best determinant that I have found is stress evaluation intraoperatively following the lateral side repair.

Treatment of athletes with low-grade, isolated, deltoid ligament sprains is similar to the nonoperative treatment of acute lateral ankle sprains, but return to sports generally is more prolonged. Immediate cold therapy, antiedema measures, and the use of a functional stirrup-type brace or walking boot are begun as quickly as possible, with return to sports in 3 to 6 weeks. For high-grade sprains or complete ruptures of the deltoid, anatomic reduction must be confirmed before treatment, with 6 to 8 weeks of immobilization in a walking cast or walking boot to prevent external rotation of the talus as the deltoid heals. Although I do not routinely perform surgery on athletes with complete deltoid ligament ruptures (even in conjunction with fibular fracture or syndesmosis injury), I consider failure to achieve anatomic alignment of the medial clear space an indication for surgical repair.[80] Determining this may require examination under anesthesia and arthroscopy.

There is very little in the scientific literature regarding the acute repair of deltoid ligament injuries. Jackson et al.[81] have described the surgical repair of an isolated, complete rupture of the anterior portion of the deltoid in a high-performance football player. Jackson used a Kessler-type suture tied over drill holes in the medial malleolus and has described his post-operative protocol in detail. At 6 weeks, the patient began weight bearing in a hinged ankle brace; at 9 weeks, he was running with his ankle taped; and at 12 weeks, he was running patterns without pain or instability. One of Brostrom's[4] early reports of a series of ankle sprains included eight isolated deltoid ruptures. All patients underwent arthrography to confirm the diagnosis; three were treated operatively, one was casted, and four were treated with ankle strapping. At a mean follow-up of 3.8 years, he reported no residual symptoms in any of the deltoid ligament treatment groups. It is unclear whether surgical repair of complete deltoid ruptures offers any advantage in terms of quicker return to sports or improved outcome when compared with conservative treatment. Nevertheless, extrapolating from the findings of Hintermann et al.[50] related to chronic medial instability, examination under anesthesia, arthroscopy, and acute repair with sutures or suture anchor can be justified in the athlete with an acute injury who is suspected to have instability. Until further scientific work elucidates a clear difference between the results of operative and non-operative repair, controversy will persist in determining the best approach to the acute, severe medial ankle sprain.


Chronic Medial Ankle Instability

Chronic medial ankle instability is an uncommon but severely disabling problem. [0210] [0500] [0830] When chronic deltoid insufficiency does occur, it usually can be related to lateral ankle pathology. Deformity of the lateral malleolus from fibular fracture malunion or distal physeal arrest, as well as chronic syndesmotic diastasis, can all be contributing factors. [0160] [0830] [0840] In these cases, the lateral malleolus fails to appropriately buttress the talus within the mortise, causing the deltoid to heal in a lengthened position or to gradually attenuate. Additionally, arthroscopic findings in patients with chronic ankle instability indicate that combined medial and lateral ankle instability is more than twice as common as medial ankle instability alone.[49]

Patients with chronic medial ankle instability usually complain of recurrent episodes of giving way along with medial ankle pain. Physical examination may reveal mild pes planovalgus, tenderness over the deltoid ligament and anteromedial joint line, and a variable degree of instability to valgus stress. The ability of the patient to correct the planovalgus or pronation deformity actively while weight bearing by contracting the tibialis posterior muscle is confirmatory.[50] Manual valgus stress radiographs in neutral ankle flexion should be obtained to document the degree of valgus talar tilt. Although fibular length can be adequately evaluated by plain radiographs, a rotational malunion of the fibula or a subtle syndesmosis deformity is assessed more easily with axial CT imaging. MRI also is reasonable in these cases, because Hintermann et al.[49] have reported a high association of talar articular cartilage lesions with complete ruptures of the deltoid ligament.

Treatment of chronic medial ankle instability depends on the associated pathology. In patients with fibular malunion, derotational and/or lengthening fibular osteotomy should be performed before addressing the deltoid ligament. Similarly, chronic syndesmosis injuries first require stabilization or reconstruction of the syndesmosis. In cases of chronic medial ankle instability without associated lateral ankle pathology, patients may benefit from a period of conservative treatment. This may include any combination of supportive taping, bracing (e.g., short articulated ankle foot orthosis [AFO]), casting, functional rehabilitation, and orthoses (e.g., medial heel wedge and first metatarsal lift). If the athlete's symptoms are not reduced to a tolerable level with conservative measures, surgical reconstruction of the deltoid ligament is warranted.

Several different methods of deltoid ligament reconstruction have been described in detail. If the remaining ligamentous tissue is of adequate quality, simple imbrication using a method analogous to the lateral Brostrom procedure may be performed.[82] When possible, it seems advantageous to advance the ligament to bone using suture anchors in the talus and naviculum to accomplish this goal.[84]Alternatively, when the remaining deltoid is of poor quality, ligamentous reconstruction with a tendon graft is recommended. Wiltberger and Mallory[85] have described a method for deltoid reconstruction using the anterior half of the posterior tibialis tendon. The split tendon graft is left attached at its insertion and the free end is passed through a bone tunnel in the medial malleolus before being tied back on itself ( Fig. 13-12 ). In view of the serious potential problems created by posterior tibial tendon pathology, it seems less than ideal to take a portion of the posterior tibial tendon for use as a graft to reconstruct the deltoid ligament. More complex reconstruction of the deltoid in a patient with traumatic loss of the medial malleolus using a free tendon graft also has been described.[86] Allograft tendon or autologous hamstring tendon grafts can be used with bioabsorbable interference fit screw fixation into bone tunnels. The postoperative protocol recommended by Jackson includes 2 weeks of nonweight-bearing immobilization in a short-leg cast. This is followed by 4 weeks of weight bearing as tolerated in a walking boot, while active range-of-motion exercises are initiated. Strengthening exercises are started at 6 weeks, and the patient may begin weight bearing in a hinged ankle brace. At 9 weeks, light running is allowed, and by 12 weeks, a gradual return to the athlete's specific sport begins. Return to competition is expected at 4 to 6 months.[81]


Figure 13-12  Split posterior tibial tendon graft for deltoid ligament reconstruction.




Syndesmosis Injury

Syndesmosis injury, or the high ankle sprain, has become the injury de rigueur in the sports medicine world related to the foot and ankle. No National Football League injury report is complete, it seems, without there being some athlete who is out of action because of this entity. Although the injury clearly has been around since antiquity, it does seem to be diagnosed presently with more frequency. This probably is due not only to the larger, faster, and stronger athletes playing on surfaces with more torsional friction but also to improved diagnostic tools and physician awareness.

Anatomy and biomechanics

The stability of the distal tibiofibular complex is dependent on bony and ligamentous anatomy, and the distal tibia and fibula comprise the bony anatomy of the syndesmosis. The fibular notch ( Fig. 13-13 ), or incisura fibulare, is a vertically oriented triangular groove in the lateral tibia with which the fibula articulates. As the fibula rests in this notch, it is supported anteriorly and posteriorly by the distal tibial tubercles. The size of these tubercles correlates with the depth of the notch. Radiographically, the notch appears concave only 75% of the time, and in 16% of patients it takes on a convex appearance.[87]


Figure 13-13  Anatomy of the fibular notch.



There are three main ligaments that add stability to the distal tibiofibular syndesmosis: (1) the anterior inferior tibiofibular ligament (AITFL), (2) the posterior inferior tibiofibular ligament (PITFL), and (3) the interosseous ligament. The AITFL runs obliquely at approximately a 45-degree angle from the anterolateral tubercle of the tibia to the anterodistal fibula ( Fig. 13-14 ). It is the most often-injured ligament in syndesmosis sprains and in frank diastasis.[64] The PITFL has two components ( Fig. 13-15 ). The superficial component runs from the posterolateral tubercle on the posterior surface of the tibia to the posterior aspect of the distal part of the fibula. It covers the back of the tibiotalar joint. The deep portion of the PITFL is called the transverse tibiofibular ligament. It lies anterior to the superficial component of the PITFL and forms the most distal aspect of the tibiotalar articulation. It functions as a virtual labrum and deepens the tibiotalar articulation. The combination of strength and elasticity makes the PITFL the last syndesmotic structure to tear.[20] The interosseous ligament interconnects the tibia and fibula from 0.5 to 2 cm above the plafond. It surrounds the synovial recess that extends up approximately 1 cm from the tibiotalar joint. Although it is the shortest structure interconnecting the distal tibia and fibula, it is considered the primary bond between these two bones at the ankle. [0590] [0890] [0900] At the superior margin, the interosseous ligament blends with the interosseous membrane. The membrane itself adds very little additional strength to the stabilizing effect of the syndesmotic ligaments.


Figure 13-14  Anatomy of the anterior syndesmosis.




Figure 13-15  Anatomy of the posterior syndesmosis.



In the normal relationship between the tibia and fibula, there is motion in the frontal, transverse, and sagittal planes.[90] An increase in the intramalleolar distance of about 1.5 mm takes place from full plantarflexion to full dorsiflexion. Rotation of the ankle also is possible through the syndesmosis. A rotation of the tibia on the talus of 5 to 6 degrees occurs during dorsiflexion and normal walking.[58] In addition, the fibula migrates distally an average of 2.4 mm during the stance phase of gait.[91]

Mechanism of injury

Most clinicians agree that external rotation is the most significant force in a syndesmosis injury. [0210] [0650] [0930] [0940] The AITFL is the first to fail with an external rotation force, followed by the interosseous ligament and membrane. The PITFL usually is preserved. A syndesmosis sprain may also occur with an abduction force, requiring rupture of the deltoid ligament or fracture of the medial malleolus.

Clinical diagnosis

Patients with acute syndesmosis injuries generally have anterolateral ankle pain directly over the anterior syndesmosis. The pain and swelling may be more precisely localized than in patients with the traditional lateral ankle sprain, but this is not always the case, particularly after the first 24 hours. Uys and Rijke[94] studied the clinical association between acute lateral ankle sprain and syndesmotic ligament involvement and found that severe syndesmosis injuries were not associated with tears of the lateral ankle ligaments. Although one would expect minimal tenderness over the ATFL or CFL in syndesmosis injuries, this often is not the case, and the physical examination is notoriously unreliable in ankle sprain injuries. When the mechanism of injury is suspected to have an abduction component, a rupture of the deltoid ligament or a fracture of the medial malleolus will produce tenderness at the medial ankle. The examiner also must ensure that the fibula is palpated from distal to proximal, including the proximal tibiofibular joint, to rule out the possibility of a Maissoneuve's fracture or a proximal tibiofibular joint disruption. Delayed swelling and ecchymosis are frequent findings.

Special clinical tests

The “squeeze test,” described in 1990 by Hopkinson et al.,[93] is a method of detecting “stable” syndesmosis injuries (see Fig. 13-10 ). A recent biomechanical study confirmed separation at the origin and insertion sites of the AITFL caused by compression of the fibula and tibia proximal to the midpoint of the calf.[95] The authors further reported that the distance of separation increased as the syndesmotic ligaments were sectioned sequentially. The pain elicited during this maneuver could be caused by tension in the remaining fibers of the distal tibiofibular complex. I have not found the squeeze test to be a reliable indicator of syndesmosis injury.

When the injury is isolated to the syndesmosis, one expects the anterior drawer and talar tilt test to be negative. These tests should be performed routinely. The external rotation test is the most reliable test for syndesmosis injury, with a high interrater correlation ( Fig. 13-11 ).[96] The test is performed by stabilizing the leg with the knee flexed at 90 degrees while externally rotating the foot. Pain is produced at the syndesmosis when it is injured. The tibiofibular shuck test or Cotton test is another adjunctive test to detect instability in the distal tibiofibular articulation. [0980] [0990] [1000] The distal leg is steadied with one hand while the plantar heel is grasped with the opposite hand and the heel is moved side to side. Excessive movement when compared with the opposite ankle suggests an unstable mortise. A medial or lateral malleolus fracture should be ruled out before performing this test.

Radiographic diagnosis

Routine radiography is the next step in the evaluation of a patient with a suspected syndesmosis sprain. Careful evaluation of the distal tibiofibular relationship with regard to the medial clear space, the tibiofibular clear space, and the tibiofibular overlap is crucial ( Fig. 13-16 ). An increase in the medial clear space is defined as a widening in the space between the medial malleolus and the medial border of the talus, normally no more than 2 to 4 mm.[100] The tibiofibular clear space at the incisura fibularis tibiae and the absolute amount and percentage of overlap of the tibia and fibula at the incisura are other radiographic landmarks. A radiograph of the uninjured ankle can be used to clarify the relationship between the uninjured distal tibia and fibula. Criteria for the diagnosis of diastasis are (1) medial clear space widening, (2) increased tibiofibular clear space, and (3) less tibiofibular overlap. However, the absence of radiographic findings does not completely rule out the possibility of a significant sprain. Stress radiographs with application of an external rotation and abduction force can expose an occult diastasis ( Fig. 13-17 ). Some clinicians advocate the use of stress radiography as standard practice in the diagnosis of syndesmosis injury.[101] Other clinicians question its role. [1030] [1040]


Figure 13-16  Landmarks for radiologic diagnosis of syndesmosis injury.




Figure 13-17  External rotation and abduction stress x-ray to expose a latent diastasis.



Bone scan, CT, and MRI are other radiographic modalities used in the diagnosis of syndesmosis injury. Bone scan can be a particularly useful diagnostic tool in evaluating a patient with chronic pain after a lateral ankle sprain.[90] CT is excellent for showing bony detail of the tibiofibular syndesmosis and can be more precise in evaluating the presence of a diastasis. In one study, CT was able to detect 2- and 3-mm diastases that were not otherwise apparent on routine radiographs.[104]

MRI allows an accurate picture of ligamentous anatomy and the distal tibiofibular joint. MRI has become the preferred diagnostic study when syndesmosis injury is suspected in professional and collegiate athletes in the United States. The criteria for making an MRI diagnosis of a syndesmosis injury are (1) ligament discontinuity, (2) wavy or curved ligament contour, and (3) nonvisualization of the ligament (Fig. 13-18, A and B ). Using these criteria, Oae et al.[105] found a sensitivity of 100%, a specificity of 93%, and an accuracy of 97% in diagnosing a syndesmosis injury.



Figure 13-18  Magnetic resonance image of syndesmosis injury with tear of anterior inferior tibiofibular ligament, interosseous ligament, and avulsion of posterior inferior tibiofibular ligament. (A) Axial section. (B) Coronal section.




The treatment of syndesmosis injuries discussed here will focus on those cases in which etiology is traumatic. In the acute injury, initial management includes rest, ice, compression, and elevation (RICE). The affected extremity should be immobilized, the patient should remain nonweight bearing, and the appropriate diagnostic tests ordered. Sprains without diastasis can be treated nonsurgically. Patients may bear weight as tolerated in a walking boot or brace. Crutches are used if pain prevents weight bearing. Physical therapy can start when pain subsides and weight bearing becomes easier. These injuries take longer than most sprains to return to normal activity. One study showed that although 86% of patients reported good to excellent ankle function, stiffness and activity-related pain were persistent.[106]Patients with latent diastasis can be treated conservatively once a congruent distal tibiofibular joint is confirmed after reduction. After confirmation of the anatomical reduction by CT or MRI, the patient is immobilized in a non-weight-bearing cast or cast boot. Weight-bearing radiographs should be done at 2 to 3 weeks postinjury to confirm anatomic reduction. Gradual weight bearing can be allowed at 4 weeks, with full weight bearing by 8 weeks postinjury. In some situations, such as the elite athlete, latent diastases may do better with surgical treatment. On the other hand, frank diastasis always requires surgical management, unless there are overriding medical contraindications. Any lateral displacement of the mortise and fibula requires internal fixation.

My preferred technique for acute syndesmosis injuries with diastasis and without fracture is as follows:[90]



Make a 4- to 6-cm anterolateral incision centered over the ankle joint.



Curve the incision slightly posterior at its distal arm, beginning at the level of the plafond, to expose the AITFL insertion on the fibula.



Expose and avoid the superficial peroneal nerve by using blunt dissection through the subcutaneous layers. Be certain to warn the patient preoperatively about the probability of at least temporary numbness on the dorsal foot following the operation.



Identify the remnant of the AITFL.



A large bone-reduction forceps clamped to the medial malleolus and the fibula can be used through small percutaneous incisions to reduce the diastasis. Be certain to correct the malrotation during the reduction (usually by internal rotation pressure).



If this reduction is confirmed to be anatomic by fluoroscopic imaging, then the AITFL is repaired.



If reduction is difficult or impossible, a medial incision is made to confirm that there is no debris or infolded ligament blocking the reduction. The deltoid ligament is repaired with sutures or by using a suture anchor. The anatomic reduction is confirmed before continuing with the syndesmosis repair.



Fix the anatomically reduced fibula with a transsyndesmotic screw.



Direct the drill slightly anterior, starting at the posterolateral fibula, 2 to 3 cm above the plafond.



Four cortices are penetrated, and two 4.5-mm, fully threaded cortical screws are placed. Placing the screws across a four-hole plate provides some additional stability and protection to the fibula when the syndesmosis screws are removed. A screw across four cortices allows better purchase and provides a portion to retrieve if the screw breaks. Although this is my preference, there is no current scientific evidence to suggest that the use of one or two syndesmosis screws, the use of a plate, or the penetration of three or four cortices results in any difference in outcome.



Suture the subcutaneous tissues and skin and place in well-padded posterior and U-shaped splint or a walking boot.

At the conclusion of the procedure, the tibiofibular joint should be anatomically reduced and rigidly fixed, and the medial clear space should be reestablished to the normal range. The surgeon must pay attention to correcting rotational deformity and use anatomic landmarks, fluoroscopy, and/or routine and comparison radiographs for intraoperative confirmation of the reduction.

Postoperatively, the patient should remain nonweight bearing for 6 weeks. At the end of 6 weeks, partial weight bearing is started and progressed to full weight bearing in a cast boot by 12 weeks. At 12 weeks, the transsyndesmotic screw can be removed percutaneously in the operating room. If the patient weighs more than 220 lb, the screw may be left in longer, at the surgeon's discretion. Full activity should be reached by 6 to 8 months.

Subacute and chronic syndesmosis injuries require meticulous attention. A subacute injury (3 weeks to 3 months) usually is the result of a missed injury and is not as uncommon as it would seem, because the most difficult part of the treatment is actually making the diagnosis. Treatment is the same for this as it is for acute injuries. Autologous or allogeneic tissue may be needed to substitute for an inadequate AITFL remnant. If this fails, an iatrogenic synostosis can be created for stability. Chronic syndesmosis injuries (>3 months) are treated with the same treatment goals in mind as those for acute and subacute injuries. The difference is the presence or absence of degenerative changes in the tibiotalar joint. With degenerative changes, the outcome already may be determined, and the reliability of reconstruction is decreased. With no articular changes, syndesmosis reconstruction can proceed. A synostosis may occur with reconstruction of chronic injuries and should not be considered a poor outcome. Patients often can return to a high level of athletic performance even with a synostosis.[7]



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