Stage IV Posterior Tibial Tendon Rupture

Foot Ankle Clin N Am 12 (2007) 341–362

Stage IV Posterior Tibial Tendon Rupture Eric M. Bluman, MD, PhDa,b,*, Mark S. Myerson, MDc a

Division of Orthopaedics, Orthopaedic Foot and Ankle Service, Madigan Army Medical Center, 9040A Fitzsimmons Avenue, Tacoma, WA 98431, USA b Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA c The Institute for Foot and Ankle Reconstruction, Mercy Medical Center, Baltimore, MD 21202, USA

Historical perspective and definition of the condition Adult acquired flat foot deformity is known to advance through well defined stages. Numerous investigators have proposed systems for staging the condition and its associated deformities [1–4]. All of these systems recognize the central role of the posterior tibial tendon in maintaining proper hindfoot alignment. A decade ago Myerson [5] modified Johnson and Strom’s classification system with the addition of a fourth, more advanced stage of the disease. This fourth stage describes the involvement of the tibiotalar joint in addition to the hindfoot malalignment seen in stages II and III. This most advanced stage of adult acquired flatfoot deformity is comprised of a hindfoot valgus deformity, resulting from degeneration of the posterior tibial tendon, with associated valgus tilting of the talus within the mortise (Fig. 1). The deformity at the tibiotalar joint may or may not be rigid in nature. Natural history and pathogenesis The active and dynamic stabilizers of the arch are affected in patients who have the advanced stages of posterior tibial tendon rupture (PTTR). The posterior tibialis is the most powerful invertor of the foot [6] and has a significant role in maintenance of the medial longitudinal arch of the foot [7]. * Corresponding author. Orthopaedic Foot and Ankle Service, Madigan Army Medical Center, 9040A Fitzsimmons Avenue, Tacoma, WA 98431. E-mail address: [email protected] (E.M. Bluman). 1083-7515/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.fcl.2007.03.004 foot.theclinics.com

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Fig. 1. Stage IV PTTR. Significant tibiotalar valgus angulation seen in conjunction with posterior tibial tendon rupture. (A) Lateral view of the foot. (B) Anteroposterior view of the ankle demonstrating the tibiotalar joint valgus angulation associated with the flatfoot deformity.

When functioning normally the posterior tibial musculotendinous complex acts as the individual moves from midstance to heel rise. In doing this it prevents abduction of the midfoot on the hindfoot and brings the hindfoot through neutral to a varus position. This locks the foot and allows the triceps surae to propel the body forward. As the hindfoot valgus deformity advances in PTTR there is progressive insufficiency of the posterior tibialis. The posterior tibial tendon in patients who have stage IV disease is ruptured. The site of rupture may be along the hypovascular zone [8] or distal to this area [9]. The peroneals, tibialis anterior, and triceps surae all have functions that antagonize the posterior tibialis. The hindfoot valgus in PTTR often allows a triceps surae contracture to develop, which in turn can exacerbate the deformity. To arrive at stage IV PTTR most patients have progressed through stage III; however, there are rare instances in which a patient develops tibiotalar valgus without a rigid flatfoot deformity. It seems that in these rare instances patients have progressed from stage II directly to stage IV. Static stabilization is provided by the spring ligament, plantar fascia, and deltoid ligament complex. The spring ligament complex (made up of the tibiospring and calcaneonavicuar ligaments) provides a hammock-like structure to prevent medial and plantar movement of the talar head relative to the navicular. This complex is often ruptured or insufficient in patients who have advanced PTTR [2,10–13]. With continued progression, insufficiency of the talonavicular capsule, spring ligament complex, and long plantar ligament become more severe. The deltoid ligament complex is a multiunit structure that provides support and restraint for the tibiotalar joint, subtalar joint, spring ligament, and talonavicular joint. As the mechanical axis of the leg is shifted medially (relative to the foot) and hindfoot deformity becomes more severe, tension is progressively increased on the soft tissues of the medial ankle. The medial collateral

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complex becomes unable to resist the loads placed on it, resulting in eventual insufficiency and lengthening.

Deltoid ligament anatomy and function Although there have been several studies investigating the anatomy of the deltoid ligament complex there has not been complete agreement as to the number and nomenclature of its components. Most investigators agree that there are superficial and deep components to the complex. Descriptions of the superficial layer of this complex have varied, however. This most likely is caused by the lack of individual ligament demarcation along its wide fan-shaped insertion, the arc of which extends from the navicular to the posterior tibiotalar capsule. There is general agreement that the deep portion of the complex originates from the intercollicular groove and posterior colliculus of the medial malleolus and inserts on the medial face of the talar body near the medial center of rotation of the tibiotalar joint. This deep portion is intra-articular but extrasynovial [14]. Although some investigators limited their descriptions to superficial and deep components without further subdivision [15,16], most have further characterized individual ligaments within the superficial and deep layers [14,17–20]. Perhaps the first detailed description of the modern era was put forth by Pankovich and Shivaram [14]. In their study they delineated tibionavicular, tibiocalcaneal, and tibiotalar ligaments as making up the superficial component and anterior and posterior tibiotalar ligaments comprising the deep component of the deltoid. They found that the tibiocalcaneal ligament was the strongest of the three within the superficial layer. Despite this detailed work they stated that it may be difficult to separate these fascicles from one another within the deep and superficial components. Rasmussen and colleagues [19] also performed detailed anatomic and functional studies on the medial collateral complex. This group described the superficial part as consisting of the tibiocalcaneal ligament and a deep complex comprised of the tibionavicular, anterior tibiotalar, intermediate tibiotalar, and posterior tibiotalar ligaments. From their sequential sectioning studies they determined that the tibiocalcaneal and the anterior tibiotalar ligaments provided the most resistance to tibiotalar tilt. Milner and Soames [17] agreed with the anatomy described by Pankovich and Shivaram [14] but reported an additional component, the tibiospring ligament, as being part of the superficial complex. This component was uniformly present in all cadavers they studied. The tibiocalcaneal ligament that several groups have described as being the largest or strongest of the superficial bands [14,20–22] was present in less than 20% of the cadavers that Milner and Soames dissected. In contrast, Boss and Hintermann [20] found that in addition to the tibiospring ligament they were able to demonstrate a tibiocalcaneal ligament in all of their specimens.

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Although there is no doubt some variation in the anatomy of the superficial ligaments, it is curious that one group of investigators [14] reports the most robust portion of the superficial layer to be the tibiocalcaneal ligament, whereas another reports that this same component is absent in more than 80% of individuals [17]. These inconsistencies raise the question of whether all researchers are identifying components of the superficial layer in a similar manner. Indeed, Milner and Soames [17] allow that the tibioclcaneal ligament seen by other investigators may be equivalent to the tibiospring ligament that was ubiquitous in their studies. Although the nuances of the anatomic organization of the superficial layer need further resolution, the contribution of the deep and superficial layers to maintenance of ankle alignment in the coronal plane seems clearer. From biomechanical studies, Harper reported that the deltoid was the primary restraint against valgus tibiotalar tilt. Sequential sectioning of the medial collateral components showed that the superficial and deep components were effective in restraining tibiotalar tilt. He also found that the capsular structures on the medial side of the ankle contribute to stability in this regard. Most germane to the subject at hand is that the superficial and deep components needed to be incompetent before any significant valgus tibiotalar tilt would occur [16]. The findings of Earll and colleagues [23] concur with these results. So it seems that individuals who have substantial amounts of valgus tibiotalar tilt must have not only insufficiency of the deep and superficial components of the deltoid ligament complex but also attenuation of the medial capsular structures.

Diagnosis Clinical diagnosis Many of the physical examination findings in stage IV are similar to those seen in stage III disease. As with less severe stages of PTTR, the patient who has stage IV disease reports a history of medial-sided foot or ankle pain. This is often associated with weakness and signs of inflammation. Some patients may relate an early onset of medial-sided foot and ankle pain that subsides and then returns. This pattern represents the paratenonitis of early disease that subsides after frank rupture of the PTT and recurrence of medial-sided pain as the medial ligamentous and capsular structures become more severely involved. Pain may also be reported laterally. Symptoms of neuropathy within the tarsal tunnel may be present because of the medial stretch caused by valgus deformity [24,25]. Patients frequently provide a history of progressive deformity, shoewear modification, orthotics, or brace wear. The hindfoot has a large degree of valgus deformity. Although substantial, the severity of hindfoot deformity does not necessarily correlate with the degree of ankle involvement. In rare instances individuals may progress

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through stage II directly to stage IV. The authors have observed patients who had tibiotalar valgus associated with a flexible flatfoot. This makes obtaining ankle films essential, even when evaluating patients who have earlier stages of PTTR. Evaluation of gait reveals an antalgic pattern with decreased stride length. The patient is not able to come to a heel rise on the affected side. The status of the skin overlying the medial malleolus should be determined. Abrasions or attenuation may be noted not only from stretching caused by the valgus deformity but also pressure from shoes or orthosis wear. Careful examination over the lateral foot and ankle should be performed to discern pathology. Lateral pain may represent sinus tarsi or subfibular impingement, lateral ankle joint arthritis, or in severe cases distal fibular stress fracture (Fig. 2). Pain in the sinus tarsi is frequently unrecognized or underappreciated before palpation by the clinician. Selective intra-articular blocks often help the clinician localize the exact source of pain. Callosity and pain below the talar head may be present if substantial dorsolateral peritalar subluxation has caused a prominence in the medial plantar midfoot. Because of the decreased working length of the triceps surae resulting from chronic hindfoot valgus, there is contracture of these muscles. Residual forefoot varus is often severe. Its presence requires preoperative evaluation. Complete evaluation of the transverse tarsal, midtarsal, and tarsometatarsal joints should be performed to allow appropriate planning for intraoperative correction. Because of the chronic nature of the disease process, strength is greatly diminished and likely absent because of rupture. The patient is neither able to resist hindfoot eversion nor actively bring the forefoot across midline.

Fig. 2. Fibular stress fracture associated with stage IV PTTR. With the longstanding valgus malalignment, the calcaneus eventually impinges on the distal fibula causing a stress fracture.

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Evaluation of ankle range of motion should be undertaken, although several factors may make this task difficult. Because of the fixed hindfoot deformity a falsely optimistic impression of tibiotalar dorsiflexion may be obtained. Re-establishment of ankle and hindfoot alignment without an appropriate lengthening of the heel cord creates or exacerbates an equinus deformity. Severe ankle arthritis may also limit ankle range of movement (ROM). The surgeon must also evaluate for the presence of ipsilateral knee valgus [26]. If this is significant, consideration should be given to correction of the proximal deformity before the foot and ankle surgery. Correction of the leg– ankle–foot axis without attention to knee deformity may not adequately relieve valgus stress through the reconstructed lower limb and may result in recurrence of deformity. Radiographic evaluation Radiographic evaluation requires at minimum three weightbearing images of the foot and weightbearing views of the ankle. Comparison views should also be considered. Adjunctive studies such as cross-sectional imaging or scintigraphy are generally not indicated. Dorsolateral peritalar subluxation, increased talo-first metatarsal angle (on the anteroposterior and lateral views of the foot), decreased calcaneal pitch, and loss of talar head coverage by the navicular may all be seen on plain films. Anteroposterior weightbearing ankle films in patients who have stage IV disease demonstrate increased tibiotalar tilt. Tibiotalar valgus angulation is measured according to the method used by Karlsson and colleagues [27,28]. Measurement of the angle subtended by a line joining the superior articular surfaces of the medial and lateral talar shoulders and the corresponding articular surfaces on the tibial plafond is performed. The upper limit of normal for tibiotalar valgus angulation has been reported to be 2 [29,30]. In the authors’ practice, patients who have tibiotalar valgus angulation of 3 or greater on standing anteroposterior radiographs are considered to have substantial ankle pathology. These patients are evaluated for the presence and magnitude of tibiotalar arthritis. Once there is recognition of abnormal tibiotalar valgus angulation in conjunction with PTTR, it needs to be tested for correctability. Evaluation of the ability to passively correct tibiotalar deformity is done by manual application of a varus force to the joint under fluoroscopy (Fig. 3). The ability to correct deformity through the tibiotalar joint is central to surgical decision making for patients who have stage IV PTTR (Fig. 4). In addition to medial-sided instability, the competency of the lateral ankle ligament complex must also be evaluated. Because of the sometimes severe hindfoot valgus in patients presenting with stage IV of the disease, rupture of the lateral ankle ligaments (the calcaneofibular ligament in particular) may occur. This results from the erosive effects between the lateral

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Fig. 3. Intraoperative fluoroscopic image showing the ability to correct stage IV tibiotalar valgus tilt in the patient illustrated in Fig. 1.

calcaneus and the fibula. Evaluation for this possibility should be done clinically and radiographically. The authors choose to perform varus stress testing manually in conjunction with fluoroscopy or conventional radiographs. For the patient in whom medial and lateral collateral ligament complexes are incompetent, reconstruction on the medial and lateral sides needs to be performed.

Frequency and subclassification of stage IV posterior tibial tendon rupture With greater awareness of stage IV PTTR and perhaps increasing numbers of these patients presenting to orthopedists, it has become clear that this late stage of the disease is inhomogeneous. Within stage IV two groups can be differentiated with respect to the ability to correct tibiotalar angulation. The authors have divided stage IV into passively correctable (IV-A) and rigid (IV-B) with respect to the ankle joint deformity [31]. Other investigators have reported that it is more common to see fixed rather than flexible tibiotalar deformity in stage IV disease [32]. The ratio of stage IV-A patients relative to IV-B patients observed may vary because of several factors. Patients who are diagnosed just after they have advanced into stage IV disease are more likely to have a correctable tibiotalar deformity. Earlier presentation may be caused by referral patterns from primary care providers or general orthopedists. Although unlikely, regional variations in patient population may also affect the observed IV-A:IV-B ratio. Alternatively, increased vigilance on the part of the clinician may lead to recognition of

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Recognition of Native Tibiotalar Joint Pathology in Conjunction with PTTR

Assess Ability to Passively Correct Tibiotalar Joint & Severity of Tibiotalar Arthritis Rigid Deformity Passively Correctible Deformity with Substantial Arthrits

Passively Correctible Deformity with Mild Arthrits

Pantalar or Tibiotalocalcaneal Fusion Present

Evaluate for Multiplanar Tibiotalar Instability

Evaluate for Multiplanar Tibiotalar Instability Present

Absent

Reestablishment of Plantigrade Foot, Total Ankle Arthroplasty & Deltoid Reconstruction

Absent

Address Lateral Ankle Ligament Deficiency at Time of Foot and Deltoid Ligament Reconstruction

Reconstruction of Deltoid Ligament with Reconstruction of Foot

Fig. 4. Algorithm for clinical decision making in the patient who has stage IV PTTR.

greater numbers of early ankle involvement (stage IV-A) in a population similar to those presenting to other orthopedic foot and ankle specialists. The authors have attempted to gauge the frequency of presentation in the senior author’s (MSM) practice. Over a period of 11 years (1993–2003), 19 patients (19 feet) were treated surgically for stage IV-A PTTR. During the same period of time, an additional 830 patients were treated for stages I to III PTTR. For this time period, patients who presented with stage IVA disease represented 2.3% of those treated for PTTR. The authors suspect that the number of patients presenting with this advanced stage of disease will increase as the population ages and simultaneously becomes more obese [33–35]. The clinician needs to be careful not to apply the classification of PTTR IV in the wrong setting. This classification should only be used in patients who have deformity resulting from disease of the posterior tibial tendon. There are patients who develop valgus tilting at the tibiotalar joint without having deficiency of the posterior tibial tendon or muscle. For example, a patient may present with valgus deformity present through the prosthetic joint after a total ankle arthroplasty has been performed. This frequently is caused not by secondary or unrecognized posterior tibial tendon dysfunction, but rather is caused iatrogenically by inadvertent intraoperative laceration of the deltoid ligament complex or fracture of the medial malleolus [36]. These conditions

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should not be grouped with PTTR or staged with PTTR systems, because the pathogenesis is not related to the posterior tibial tendon. It has been reported that patients who have improperly positioned triple arthrodeses with residual hindfoot valgus experience greater strain on the deltoid ligament [37]. This greater strain can lead to incompetence of the deltoid complex and resultant valgus tibiotalar tilt [30,38]. This represents a specialized case of stage IV disease, the treatment of which is described below.

Treatment Nonsurgical Although some investigators have reported good results with nonoperative treatment of PTTR [39,40], many have advocated surgical treatment even in the earlier stages [41,42]. Previous investigators have downplayed nonoperative options in the spectrum of management for patients who have PTTR IV [30,32,43]. We believe that nonoperative care has a limited role in patients who have stage IV disease. All but those patients who have medical comorbidities contraindicating surgery should undergo surgical reconstruction. Conservative therapy may still be needed to relieve pain and temporize deformity while related orthopedic conditions are corrected. Bracing may halt the progression of tibiotalar valgus angulation but is of questionable value in preventing the development of tibiotalar arthritis once stage IV has been reached. Pain may be reduced with custom molded orthoses, such as an Arizona or Baldwin brace. The increased contact pressures present within the mortise with tibiotalar valgus angulation, however, are frequently not corrected with these types of accommodative orthoses and continue to contribute to erosive, degenerative changes within the joint. Surgical Historically the presence of stage IV disease did not present much of a diagnostic or therapeutic dilemma. If there was involvement of the ankle, fusion would be required. The procedure would involve fusion of the tibiotalar joint in conjunction with the reconstructive procedures needed to re-establish a plantigrade foot. Because most patients would also require hindfoot fusions, the question evolved into whether a tibiotalocalcaneal fusion would be sufficient or whether a pantalar fusion would be required. One requirement central to the success of any surgical procedure performed for correction of stage IV PTTR is restoration of the foot to a plantigrade position. In recent years the treatment of stage IV PTTR involves more options. As mentioned earlier, the authors have refined Myerson’s modification of the Johnson and Strom staging system. This refinement is functional and descriptive as it aids in surgical decision-making. Part of the refined classification is subdivision of stage IV into two groups. Stage IV-A involves a tibiotalar

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deformity that is passively correctable, whereas that of stage IV-B is rigid and not passively correctable. Before surgical treatment is decided on, a determination must be made as to which of these subclasses the patient who has stage IV disease falls into (Fig. 4). Patients who have stage IV-A disease have the potential to undergo tibiotalar sparing reconstructive surgery, whereas those who have stage IV-B should have either a tibiotalocalcaneal or pantalar fusion [31]. Tibiotalocalcaneal and pantalar fusions have been well described in the literature. Although these arthrodesis procedures may be successful in establishing a stable plantigrade foot [44–46], they are not without morbidity. Previous investigators have demonstrated that despite a high level of satisfaction with tibiotalocalcaneal arthrodesis, a large percentage of patients who underwent these procedures complained of residual pain [45,46]. Papa and Myerson [46] reported that even after successful re-establishment of tibiotalar stability with arthrodesis, energy expenditure of ambulation was increased exponentially, whereas functionality and satisfaction were decreased. Despite these drawbacks, the authors consider tibiotalocalcaneal or pantalar fusion in patients who have stage IV-B disease to be the lesser of two evils (Fig. 5). Attempting tibiotalar joint sparing surgery in stage IVB disease results in recurrence of deformity and worsening of tibiotalar arthritis. Nonoperative therapy is not a reasonable option in most patients, because it results in continued pain and the potential for increasing deformity and eventual medial soft-tissue breakdown. Joint-sparing procedures Tibiotalar joint sparing procedures should only be attempted in patients who have stage IV-A disease. Although frequently more extensive and more technically demanding, joint-sparing procedures avoid the debility encountered when the ankle and subtalar joints are fused. Before commencement of a joint-sparing procedure, evaluation for multidirectional instability is repeated with the patient under anesthesia. This is performed to assess the magnitude of the deformity unhindered by muscular splinting that may have been present in the office. Here again the authors prefer to incorporate fluoroscopy into the intraoperative evaluation. If lateral ankle ligament instability is present, then lateral ankle ligament reconstruction should be incorporated into the treatment plan. The cases of stage IV-A PTTR that the authors have observed with concomitant lateral ankle ligament incompetence have been caused by severe hindfoot valgus and resultant subfibular impingement. It is questionable whether an imbrication or reefing of the calcaneofibular ligament would ultimately be successful in restoring ligamentous restraint. In cases of stage IV PTTR with lateral ankle ligament insufficiency, the authors use a modification of the method of Coughlin and colleagues [47] for reconstruction. In most cases in which tibiotalar sparing reconstructions are performed, the authors have found it easier to perform the necessary hind- and midfoot

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Fig. 5. Reconstruction of rigid stage IV deformity using tibiotalocalcaneal fusion. (A) Preoperative weightbearing lateral roentgenogram of the foot showing loss of medial column height and severe tibiotalar arthritis. (B) Anteroposterior radiograph of right ankle demonstrating severe tibiotalar valgus angulation and arthritis. The left is included for comparison. (C) Lateral postoperative view of the ankle after tibiotalocalcaneal fusion using retrograde intramedullary fixation. (D) Restoration of the leg–ankle–foot axis is demonstrated on anteroposterior view of the ankle after tibiotalocalcaneal fusion.

realignments and follow these with the ligament reconstructions. Bony procedures may consist of any combination of appropriate osteotomies and fusions as previously described [48]. Whatever components make up the reconstruction they must re-establish a stable plantigrade foot and ankle. Inadequate correction of coronal plane deformity ultimately overstresses any ligament reconstruction and results in eventual failure of the reconstruction. Contracture of the heel cord may necessitate release or lengthening for prevention of a postoperative equinus deformity. The patient who has tibiotalar tilt resulting from an improperly positioned hindfoot arthrodesis presents a specialized case (Fig. 6). These patients may fall into stage IV-A or IV-B. If the patient falls into the latter category the malalignment should be corrected at the time that the tibiotalar fusion occurs. Patients who have stage IV-A deformity should undergo a revision triple arthrodesis as described by Haddad and colleagues [49] with subsequent reconstruction of their medial ankle ligaments. As in previously

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Fig. 6. Tibiotalar valgus in a patient with previously-performed hindfoot arthrodesis. Weightbearing (A) lateral foot and (B) anteroposterior ankle views are shown. The tibiotalar deformity was caused by substantial hindfoot valgus that was residual from an improperly performed fusion. The deltoid ligament eventually becomes insufficient, allowing tilting of the talus within the mortise.

untreated disease, attempts to address the problem with isolated reconstruction of the deltoid ligament without realignment of the deformity of the foot are doomed to result in recurrence no matter how strong the reconstruction. In the clinical literature, previous investigators have also suggested that ankle joint-sparing procedures may be considered in selected patients [30,32,43]. Because of the rarity of this condition there has been a paucity of literature on clinical outcomes after joint-sparing procedures and as a result many questions remain unanswered. Whatever method is used, the goal is to re-establish tibiotalar congruity perpendicular to the mechanical axis of the leg over a plantigrade foot. In an effort to avoid ankle arthrodesis while imparting stability to the tibiotalar joint, several investigators have proposed deltoid ligament reconstruction procedures [50–56]. Methods of medial ligament reconstruction fall into three groups: repair of host tissue, advancement of host tissue, and allografting to substitute for portions of the deficient ligamentous complex. The authors have undergone an evolution in theory and in practice for reconstruction of the insufficient deltoid ligament complex. The authors’ initial focus was on advancement or reefing of native tissue for retightening of the medial collateral complex [54]. This technique as described uses suture anchors to restore soft-tissue tension to the superficial fibers of the deltoid complex (Fig. 7). Other surgeons have used a vertically-oriented wafer osteotomy of the medial portion of the medial malleolus with proximal displacement and fixation as attributed to Manoli (Fig. 8) [32]. Imbrication of the attenuated ligament fascicles may also be performed to aid in re-establishment of medial soft-tissue tension [57]. Hintermann and colleagues [58] has performed repairs of the anterior portion of the deltoid complex. These reconstructions were done for sprains that left patients with medial instability, not for stage IV PTTR. These

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Fig. 7. Advancement and fixation of superficial deltoid ligament with suture anchor placed into the medial malleolus. (A) Line drawing depicting placement of suture anchor in the medial malleolus with reefing of the superficial deltoid fibers Used with permission from Raikin SM, Myerson MS. Surgical repair of ankle injuries to the deltoid ligament. Foot Ankle Clin 1999;4(4):745–53.) (B) Intraoperative placement of suture anchor within the medial malleolus. The arrowhead points to the superficial deltoid fibers that have yet to be secured back to the medial malleolus. (C) Postoperative weightbearing view of the same patient demonstrating late failure of deltoid advancement and recurrence of tibiotalar valgus deformity despite congruent intraoperative reduction.

patients included patients who had valgus tibiotalar tilt. Although the tissues were sutured with restoration of tibiotalar congruence, injured tissues were used for the repairs. Good early results were reported with repair of just the anterior components of the superficial layer. The long-term results of his group’s work are not yet available. When these methods are used for repair and advancement, the tissue used is frequently not physiologically sound and as a result is not structurally sound. A histologic study published by Brostrom and Sundelin [59] in 1966 reported that in chronic sprains there was ‘‘parallel arrangement of the collagen bundles reminiscent of the structure of normal ligament.’’ However, more recent work has demonstrated that the functional and histologic changes that

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Fig. 8. Medial malleolar wafer osteotomy that has been advanced proximally to restore soft-tissue tension to the superficial deltoid ligament. (A) Preoperative view demonstrating magnitude of tibiotalar valgus deformity. (B) Postoperative view shows long-term failure of this advancement procedure with recurrence of valgus deformity.

occur with significant ligamentous injury are not restored to normality. Hurschler and colleagues [60] performed electron microscopic studies demonstrating histology consistent with persistent ligamentous laxity after gross healing of complete lesions that had been directly repaired. Even with partial injuries there is evidence that functional healing does not return to preinjury levels. Using a rat model, Provenzano and colleagues [61] evaluated ligamentous strength after creating an in situ grade II injury. Mechanical data showed that immature animals recovered their strength after a grade II sprain at a faster rate than mature animals. Ligament laxity was still present in both groups 2 weeks after the injury, however, and was not completely removed by growth in the immature group. Clinically, in the authors’ hands, these concerns regarding tissue integrity were borne out. It became evident that reconstructions using host tissues that previously were insufficient were not durable. Eventual recurrence of the deformity occurred. Such cases necessitated revision procedures to re-establish tibiotalar congruency and effected a change in our approach to using healthy allograft tissue for medial ligamentous reconstructions (Figs. 7C and 8B). Other investigators have also recognized the value of healthy tissue in reconstructions [50,52]. One of the procedures that has been described is allograft reconstruction of the tibionavicular component of the superficial deltoid ligament [50]. This method places a figure-of-eight allograft tendon between the medial malleolus and the medial cuneiform or talus. Although this construct showed favorable biomechanical properties in cadaveric testing of simulated acquired flatfoot deformity, its described purpose was to aid in restoration of the medial longitudinal arch and not in maintenance of

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tibiotalar congruence. The use of healthy allograft or autograft tissue avoids the strength and durability issues that may be encountered with attenuated host tissue. This graft, however, is not aligned in an optimal orientation to resist the coronal plane forces resulting in the tibiotalar valgus deformity. Recently Deland’s group [52] described an anatomic repair of the medial ligamentous structures. Their technique uses autograft peroneus longus tendon. After transection proximally the tendon is led through talar and medial malleolar tunnels to reconstruct the deep deltoid fibers. The free end of the tendon is fastened to a screw or stapled to the lateral tibia while the distal insertion is maintained. Although this repair anatomically recreates the deep deltoid fibers it does not reconstruct any of the superficial fibers that some investigators believe provide the predominant restraint to valgus forces [19,62,63]. In performing this reconstruction the peroneus longus must be sacrificed. In addition, the described technique uses a large extensile (16–18 cm) incision over the lateral leg to harvest the tendon and obtain fixation to the lateral tibial shaft. The authors’ initial method of medial allograft ligament reconstructions used screw and washer constructs in conjunction with tendon allograft (Fig. 9). These proved to be more durable but also required larger exposures

Fig. 9. Allograft reconstruction of deltoid ligament using a soft-tissue washer. (A) Allograft tendon being secured to medial talus using screw and washer construct. (B) Completed allograft reconstruction after tendon secured to the medial malleolus (C) Repair of the native superficial soft tissues over the allograft reconstruction.

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and hardware with a fairly large footprint that sometimes hindered anatomic placement of the grafts. The authors have recently described improved allograft techniques to allow for a more anatomic, more easily performed, and minimally invasive reconstruction of the deltoid ligament [64,65]. Our initial method uses a forked allograft tendon in conjunction with soft-tissue interference screws to reconstruct the deep tibiotalar ligaments and the superficial calcaneofibular fibers. Briefly, the graft is anchored in a tibial tunnel that is created parallel to the joint surface at the level of the distal tibial physeal scar. Krackow sutures are placed in the distal tendon ends and these are then passed through a subcutaneous tunnel running over the medial malleolus. The deep deltoid fibers are reconstructed first. A talar tunnel is created, the path of which passes through the talus starting at the medial center of tibiotalar rotation and exits at the lateral junction of the talar dome and neck. One end of the sutured tendon is then passed through the tunnel from medial to lateral and is anchored at an appropriate tension using an interference screw placed into the medial terminus of the talar tunnel. The calcaneotibial ligament is then reconstructed. A calcaneal tunnel is created along an axis from the sustentaculum tali to a point approximately 1 cm superior to the peroneal tubercle on the lateral side of the calcaneus. The free end of the remaining limb of the tendon graft is passed through the calcaneal tunnel. Tensioning is done manually. Tibiotalar joint position is checked under fluoroscopy. When appropriate tension is achieved a soft-tissue interference screw is inserted from medial to lateral into the calcaneal tunnel. The appearance of the final construct is illustrated in the line drawing shown in Fig. 10. This reconstruction has the advantages of requiring a short incision length, respecting the tibiotalar axis of rotation, and being aligned to maximally resist deforming forces in the coronal plane. The authors have used this technique in several patients and the short-term results have been favorable (Fig. 11). The surgeon needs to be vigilant for over-correction of the medial collateral ligament complex irrespective of the technique used. This has been noted in a small number of patients whom the authors have treated with joint-sparing procedures. Over-tightening of the medial ligament reconstruction may accelerate medial joint degeneration over time. Although we are not aware of any objective measures to avoid over-tightening of the deltoid ligament, the authors use intraoperative fluoroscopy to aid in achieving the appropriate tension. One question that remains unanswered is how much arthritis is acceptable when attempting to reconstruct stage IV deformity. This arthritis is frequently asymmetric with the lateral side of the joint affected earlier and more severely than the medial side. Re-establishment of hindfoot and mortise alignment in patients who have moderate to severe arthrosis lessens pressure and relieves pain over the lateral joint line [66–69] but may overload the medial side. An argument may be made to do a fusion at the index procedure to avoid potential deterioration of the medial tibiotalar articular

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Fig. 10. Line drawing depicting minimally invasive allograft deltoid ligament reconstruction. (A) Lateral and (B) posteroanterior views after insertion of the forked graft to reconstruct the superficial and the deep deltoid ligaments. The blue represents the talar limb reconstructing the deep deltoid fibers and the green represents the calcaneal limb reconstructing the superficial deltoid fibers.

cartilage that may occur with joint-sparing reconstruction of the deformity. Another line of reasoning is to realign the weightbearing axis with a hindfoot fusion and perform a total ankle arthroplasty if there is substantial progression of the tibiotalar arthritis [43]. Although this treatment plan seems to provide a good option for patients who have stage IV disease associated with moderate to severe arthritis, it should be entered into carefully. In

Fig. 11. Reconstruction of stage IV-A PTTR of patient depicted in Figs. 1 and 3 using triple arthrodesis and minimally invasive allograft deltoid ligament technique. (A) Weightbearing lateral view of foot showing improvement of calcaneal pitch and lateral talo-first metatarsal line. (B) Anteroposterior weightbearing view of the ankle demonstrating restoration of tibiotalar congruence.

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a small cohort of patients, Sangeorzan’s group recently reported that 50% of the stage IV patients treated with triple arthrodeses and total ankle arthroplasty developed persistent valgus malalignment [70]. That deltoid reconstructions were not performed in these patients calls into question the advisability of this plan without medial ligamentous reconstruction. In the immediate postoperative period following joint-sparing reconstruction of PTTR stage IV disease a plaster splint is applied in neutral position. Postoperatively physiotherapy starts after the incisions have healed, usually approximately 2 weeks postoperatively. Therapy in the case of joint-sparing procedures consists of passive and active mobilization of the ankle joint and intrinsic muscle exercises. Weight-bearing is started progressively but is not full until 12 weeks postoperatively. Gait training is instituted as needed after weight-bearing is commenced. Long-term results of joint-sparing therapies for stage IV PTTR are not available. As a greater number of patients in this late stage of PTTR are treated, outcomes need to be compared and evaluated. It is hoped that further development of therapies that include deltoid ligament reconstruction and total ankle arthroplasty will reduce the number of patients requiring ankle arthrodesis. Summary Stage IV posterior tibial tendon rupture is comprised of a hindfoot valgus deformity resulting from degeneration of the posterior tibial tendon with associated valgus tilting of the talus within the mortise. Deltoid ligament insufficiency is central to the pathoetiology of this form of the disease. Although rare, increasing numbers of patients who have this advanced form of the disease are being recognized. It is expected that the trend for increasing incidence will continue. Experience with this advanced stage has led to recognition that it may be subclassified further to reflect the ability to correct the tibiotalar component of the deformity. Although historically patients who had stage IV disease were relegated to procedures involving tibiotalar fusion, the recognition of a subclass of patients in whom the ankle deformity is correctable and without substantial degenerative changes has led to efforts at tibiotalar joint-sparing surgical therapies. Whether tibiotalar joint-sparing or fusing procedures are decided on, proper realignment of the foot and ankle is of paramount importance. Those patients who have nonsalvageable tibiotalar joints should undergo a procedure that involves tibiotalar fusion or arthroplasty. The goal in patients undergoing tibiotalar joint-sparing surgeries should be re-establishment of a congruent ankle joint perpendicular to the mechanical axis of the leg above a plantigrade foot. When performed, deltoid ligament reconstruction should use healthy allograft tissues. A novel technique by which deep and superficial fibers of the deltoid ligament may be reconstructed in a minimally invasive manner has shown excellent early results. In addition to the deltoid ligaments the lateral ankle ligament complex should also be evaluated in

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this patient population to determine whether multidirectional instability is present. Patients who have multidirectional instability need this problem addressed with other reconstructive procedures. Postoperative rehabilitation of these patients should include early nonweightbearing ROM exercises. References [1] Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop 1989;239: 196–206. [2] Deland J. The acquired flatfoot and spring ligament complex. Foot Ankle Clin 2001;6: 129–35. [3] Sizensky J, Marks R. Medial sided bony procedures in patients with adult acquired flatfoot deformity. Foot Ankle Clin 2003;8:539–62. [4] Schon L. Posterior tibial tendon dysfunction. Presented at The International Foot and Ankle Congress. Toronto (Canada), May 11–14, 2005. [5] Myerson MS. Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon. Instr Course Lect 1997;46:393–405. [6] Mann R, Inman VT. Phasic activity of intrinsic muscles of the foot. J Bone Joint Surg [Am] 1964;46:469–81. [7] Kitaoka HB, Luo ZP, An KN. Effect of the posterior tibial tendon on the arch of the foot during simulated weightbearing: biomechanical analysis. Foot Ankle Int 1997; 18(1):43–6. [8] Goncalves-Neto J, Witzel SS, Teodoro WR, et al. Changes in collagen matrix composition in human posterior tibial tendon dysfunction. Joint Bone Spine 2002;69(2):189–94. [9] Funk DA, Cass JR, Johnson KA. Acquired adult flat foot secondary to posterior tibial-tendon pathology. J Bone Joint Surg [Am] 1986;68(1):95–102. [10] Deland JT, de Asla RJ, Sung IH, et al. Posterior tibial tendon insufficiency: which ligaments are involved? Foot Ankle Int 2005;26(6):427–35. [11] Balen PF, Helms CA. Association of posterior tibial tendon injury with spring ligament injury, sinus tarsi abnormality, and plantar fasciitis on MR imaging. AJR Am J Roentgenol 2001;176(5):1137–43. [12] Yao L, Gentili A, Cracchiolo A. MR imaging findings in spring ligament insufficiency. Skeletal Radiol 1999;28(5):245–50. [13] Gazdag AR, Cracchiolo A 3rd. Rupture of the posterior tibial tendon. Evaluation of injury of the spring ligament and clinical assessment of tendon transfer and ligament repair. J Bone Joint Surg [Am] 1997;79(5):675–81. [14] Pankovich AM, Shivaram MS. Anatomical basis of variability in injuries of the medial malleolus and the deltoid ligament. I. Anatomical studies. Acta Orthop Scand 1979;50(2): 217–23. [15] Grath GB. Widening of the ankle mortise. A clinical and experimental study. Acta Chir Scand Suppl 1960;(Suppl 263):1–88. [16] Harper MC. Deltoid ligament: an anatomical evaluation of function. Foot Ankle 1987;8(1): 19–22. [17] Milner CE, Soames RW. The medial collateral ligaments of the human ankle joint: anatomical variations. Foot Ankle Int 1998;19(5):289–92. [18] Siegler S, Block J, Schneck CD. The mechanical characteristics of the collateral ligaments of the human ankle joint. Foot Ankle 1988;8(5):234–42. [19] Rasmussen O, Kromann-Andersen C, Boe S. Deltoid ligament. Functional analysis of the medial collateral ligamentous apparatus of the ankle joint. Acta Orthop Scand 1983;54(1): 36–44. [20] Boss AP, Hintermann B. Anatomical study of the medial ankle ligament complex. Foot Ankle Int 2002;23(6):547–53.

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