CLASSIFICATION OF THE FLATFOOT DEFORMITY

Stage I: Tenosynovitis Without Deformity

In stage I disease, the tendon is inflamed or partially ruptured and may or may not be accompanied by systemic inflammatory disease. In either case, deformity is absent or minimal and the overall continuity of the tendon is maintained. Tendon continuity is confirmed on physical examination with an intact single-leg heel raise and good resisted foot inversion strength with the foot plantar flexed. Stage I is subdivided into three categories:

A. Inflammatory disease: Posterior tibial tendon (PTT) rupture that results from a systemic disease such as rheumatoid arthritis and the other inflammatory arthritides is recognized as a separate entity. In stage IA, hindfoot anatomy is maintained and the foot alignment is normal. Surgical treatment consists of tenosynovectomy.

B. Partial PTT tear with normal hindfoot anatomy: Care for this stage typically begins with a conservative treatment consisting of anti-inflammatory medications and immobilization in a cast, walking boot, or custom brace.

C. Partial PTT tear with hindfoot valgus: Presence of a slight (deviation of 5 degrees or less) deformity distinguishes stage IC from stage II disease. Although care begins with conservative treatment, this stage may represent a more incipient rupture, and the foot should be monitored closely. Surgical treatment consists of a tenosynovectomy and a medial translational osteotomy of the calcaneus.

Stage II: Ruptured Partial Tibial Tendon and Flexible Flatfoot

Stage II disease is defined by presence of PTT tendon rupture, as evidenced on physical examination by a clinically apparent flatfoot, weakness with inversion of the plantar-flexed foot, and inability to perform a single-leg heel raise. Stage II disease is subdivided into five categories on the basis of the most salient feature present. Because some patients exhibit several of the following features, some degree of overlap may exist.

A. Hindfoot valgus: In stage IIA, once the heel is reduced from valgus to neutral, there is a varying degree of residual forefoot supination. Treatment options include a flexor digitorum longus (FDL) tendon–to–PTT transfer combined with either a subtalar arthroereisis implant to limit subtalar eversion or a medial displacement calcaneal osteotomy (“calcaneal slide”) to reduce hindfoot valgus.

B. Flexible forefoot supination: In stage IIB, reducing the hindfoot from valgus to neutral results in forefoot supination because of gastrocnemius muscle contracture (Figure 18-3). However, the forefoot deformity is flexible; if the ankle is plantar flexed to relax the gastrocnemius muscle, the forefoot supination is corrected (Figure 18-4). Recommendations for this stage would be similar to those for stage IIA, but with the addition of an Achilles tendon lengthening or a gastrocnemius muscle recession, depending on the cause of equinus.

C. Fixed forefoot supination: In stage IIC, as a consequence of long-standing hindfoot valgus, adaptive changes have occurred in the frontal plane of the forefoot. Thus, although the hindfoot deformity is supple and reducible to neutral, the forefoot deformity becomes fixed once the heel is held in a reduced position. In other words, when the ankle is plantar flexed while the hindfoot is held in reduction, the forefoot remains supinated. The operative treatment recommendation for stage IIC is to angulate the medial ray plantarward to rectify the fixed forefoot supination and restore a plantigrade foot (in addition to the treatment for stage IIA or IIB disease). Correction typically is accomplished with a dorsal opening wedge osteotomy of the medial cuneiform with insertion of an allograft bone wedge.

D. Forefoot abduction: This may occur at the transverse tarsal joint (most commonly) or at the first tarsometatarsal (TMT) joint. The first TMT joint instability can be either a primary deformity or a result of TMT joint arthritis. The simplest way to make this distinction is through examination of the lateral view radiograph for a gap at the plantar joint surface, which is present with primary deformity. Primary deformity of the first TMT joint also may result in secondary hindfoot deformity, including rupture of the PTT. Surgical treatment consists of an FDL tendon transfer combined with a lateral column lengthening procedure such as a modified Evans procedure. This is accomplished with a lateral opening wedge osteotomy of the calcaneus 1.5 cm posterior to the calcaneocuboid joint with insertion of allograft bone.

E. Medial ray instability: As in stage IIC (fixed forefoot supination), the stage IIE foot retains forefoot supination with reduction of the valgus heel to neutral. This supination persists even with ankle plantar flexion, as a result of instability of the medial column, and may arise from any component structure of the medial column. It may occur at the talonavicular, naviculocuneiform, or medial cuneiform–first metatarsal joint, or a combination thereof. This situation is similar to that in stage IIA; after the heel is corrected to neutral, however, the unstable medial ray will tend to dorsiflex; this dorsiflexion causes the foot to collapse to pronation, leading to painful subtalar joint impingement. Generally, the treatment used is the same as for stage IID disease. The addition of medial column arthrodesis (naviculocuneiform or TMT) could be considered. This arthrodesis usually is unnecessary for most patients, however, because medial column stability commonly is restored after lateral column lengthening with the addition of an opening wedge osteotomy of the medial cuneiform.

Figure 18-3 A, The hindfoot is in valgus, with moderate abduction of the forefoot at rest. B, The foot is very flexible and can be completely restored to a neutral position by holding the heel in neutral.

Figure 18-4 A, In this case, slight forefoot supination is apparent with the heel reduced to neutral. B, This forefoot supination disappears when the forefoot is held in equinus, thereby ruling out an effect of the Achilles tendon or the gastrocnemius muscle in producing contracture in the foot.

Stage III: Rigid Hindfoot Valgus

Stage III disease generally is associated with a more advanced course of tendon rupture and deformity and typically is characterized by rigid hindfoot valgus. Forefoot deformity also may be present and usually consists of rigid forefoot abduction.

A. Hindfoot valgus: Treatment usually consists of triple arthrodesis.

B. Forefoot abduction: Treatment also consists of triple arthrodesis, but in certain cases lateral column lengthening with a bone block arthrodesis of the calcaneocuboid joint also may be required to fully adduct the forefoot back to neutral.

Stage IV: Ankle Valgus

Stage IV disease occurs after chronic tendon rupture and is associated with deltoid ligament rupture and medial ankle instability, leading to ankle (tibiotalar) joint valgus deformity. It can occur in the setting of previous triple arthrodesis. Several variants of this condition have been seen. It may or may not be associated with ankle instability and arthritis and a flexible or rigid hindfoot.

A. Flexible ankle valgus: In this setting, reconstructing ankle deformity with medial-sided ankle procedures is appropriate. This condition is relatively rare.

B. Rigid ankle valgus: This is the more common presentation of stage IV disease. In stage IVA, the ankle valgus deformity is mostly rigid and is almost irreducible. Nonoperative treatment consists of use of an ankle orthosis such as a custom Baldwin or Arizona brace, and operative treatment is with ankle arthrodesis (in the setting of previous triple arthrodesis), pan-talar arthrodesis, tibiotalocalcaneal arthrodesis, or talectomy with tibiocalcaneal arthrodesis.

SURGICAL PROCEDURES FOR CORRECTION OF FLATFOOT

Tenosynovectomy

A tenosynovectomy is indicated in patients who have inflammatory changes in the PTT but do not have deformity. Usually tenosynovectomy is necessary early in the course of the disease process as the tendon is beginning to tear. In some patients, however, an inflammatory tenosynovitis may be associated with a seronegative spondyloarthropathy. I am more inclined to perform earlier surgery in these patients, because infiltrative tenosynovitis will eventually cause rupture of the tendon (Figure 18-5). A tenosynovectomy is indicated after failure of nonoperative care, whatever that happens to consist of. The nonoperative regimen generally consists of a period of immobilization in either a boot or a cast, followed by use of some sort of brace or orthosis. In addition, a decision has to be made whether to correct any (mild) deformity of the hindfoot along with the tenosynovectomy.

Figure 18-5 Inflammatory changes in the tendon in a patient who had psoriasis with multiple additional symptoms, including pain of 2 months duration in the posteromedial ankle.

If, as is probable, tenosynovitis represents the early stage of rupture of the PTT, then some hindfoot deformity also is likely to be present. This deformity usually consists of valgus of the heel, slight pronation at the midfoot, and contracture of the gastrocnemius-soleus muscle. In patients with such deformity, therefore, the performance of a medial translational osteotomy of the calcaneus, along with the tenosynovectomy, may be prudent. Certainly, adding this procedure would be a good idea if minor fissuring indicative of early rupture was present in association with the tenosynovitis. This additional surgery usually is not necessary, however, when the tenosynovitis is associated with a seronegative inflammatory disorder. In patients with such disorders, the tenosynovitis develops as part of a spondyloarthropathy and enthesopathy, and deformity occurs much later, after complete rupture of the tendon. The goals of the tenosynovectomy are to decrease pain and to remove any of the inflammatory tissue that may hasten the rupture. Then the foot should be rested until healing takes place.

To begin the tenosynovectomy, an incision is made posteromedially along the length of the tendon, and the retinaculum is opened completely (Figure 18-6). Occasionally, the tenosynovitis is a result of a stricture or stenosis of the retinaculum immediately behind the medial malleolus. This stricture creates an hourglass shape to the tendon, with obvious deformity and inflammatory change visible in the tendon. Once the retinaculum has been opened, the tendon is inspected. The inflammatory change is not always that obvious and frequently is on the posterior surface of the tendon and tendon sheath. The tendon must then be rotated to inspect the posterior surface. I find that skin hooks are the easiest way to do this, by flipping the tendon around to inspect the posterior surface. The inflammatory tissue is then removed from the tendon sheath and the tendon itself; either dissection scissors or a knife blade is used in this procedure. Rubbing the tendon vigorously with a sponge also facilitates removal of this inflammatory tissue. Finally, the tendon should be inspected for any tears, which, as stated, usually are on the posterior surface (Figure 18-7). If a tear is identified, it is repaired with a running suture of monofilament absorbable suture. I use a 2-0 suture and bury the knot and then run the suture along the length of the tendon, imbricating the tendon along the way as the repair is performed. I do not repair the flexor retinaculum, because the tendon will not subluxate provided that the foot is immobilized for a few weeks after surgery. It is always a good idea to support the tendon if there is a tear, which is simultaneously repaired; in such instances, either an arthroereisis or a calcaneus osteotomy can be performed. Weight bearing can be started as tolerated in a boot, and gentle passive range-of-motion exercises can start after 2 weeks, followed by non–weight-bearing exercise, including swimming and cycling.

Figure 18-6 A, The incision is made along the course of the posterior ankle. B, The tendon sheath is then opened. C, Note the extensive tenosynovitis along the length of the tendon, evident in B. Involved tissue was removed by sharp dissection.

Figure 18-7 A 44-year-old athletic patient presented with posteromedial ankle pain of 6 month duration. A, Opening the tendon sheath revealed hypertrophic and proliferative tenosynovitis. B, On further exploration, the tendon was noted to be torn longitudinally and was repaired. No associated deformity whatsoever was present. In order to protect the tendon during the healing process, a medial translational osteotomy of the calcaneus was performed simultaneously.

Medial Translational Osteotomy of the Calcaneus

Correction of the flexible flatfoot deformity, with or without an associated tear of the PTT, begins with the lateral approach, including calcaneus osteotomy. Once the osteotomy has been completed, the incision is closed, and the patient is turned from the lateral to the supine position for the tendon transfer and PTT correction.

This osteotomy is an extremely utilitarian procedure, and I use the medial translation osteotomy for correction of multiple types of deformities whenever hindfoot valgus is present and when the medial aspect of the foot needs to be supported. Restructuring the medial column of the foot, leaving the hindfoot in valgus, does not correct the hindfoot deformity. The rationale for the medial translation is not only the movement of the calcaneal tuberosity medially, with corresponding improvement of the mechanical tripod of the heel with respect to the forefoot, but also the medialization of the insertion of the Achilles tendon relative to the axis of the subtalar joint.

Many clinical and biomechanical studies have supported this osteotomy, with its positive impact on both the foot and the ankle. The osteotomy can be used to improve the mechanics of the tibiotalar joint because medial translation will increase the contact pressure on the medial aspect of the tibiotalar joint when valgus deformity is present in the ankle. The osteotomy also can be added to a triple arthrodesis to improve the mechanical support of the ankle in a stage IV rupture of the PTT in conjunction with reconstruction of the deltoid ligament. This is an extremely reliable operation, and nonunion is not a problem. With internal fixation, the tuberosity can be shifted at least 12 mm without any concern for instability or nonunion. Overcorrection into slight varus can occur, albeit rarely.

An incision is made two fingerbreadths below the tip of the fibula in line with the peroneal tendon (Figure 18-8). The incision is deepened into subcutaneous tissue, and immediately the sural nerve and lesser saphenous vein must be identified and retracted. A retractor is inserted into the tissue, and then once the nerve is retracted, the incision is deepened onto periosteum, which is reflected to expose the calcaneus. I try to perform the osteotomy as close as possible to the axis of the subtalar joint. After subperiosteal dissection, two curved soft tissue retractors are inserted on the dorsal and inferior aspect of the tuberosity. The inferior retractor is pushed between the calcaneus and the plantar fascia and serves as a retractor of the soft tissues during the osteotomy. The cut is made perpendicular to the axis of the tuberosity at a 45-degree angle with respect to the calcaneal pitch angle. An osteotome should not be used, because more control is afforded by the use of a wide saw blade. A punching action of the saw is used for the osteotomy, to permit the perforation through the medial aspect of the tuberosity to be felt. A smooth laminar spreader with no teeth is inserted into the osteotomy site to distract the calcaneus, and the medial periosteum is separated. The medial translation is then facilitated, but cephalic translation is avoided. Once the calcaneus is held in the desired position, which is approximately 10 to 12 mm of medial shift, it is fixed with one 6.5-mm cannulated screw introduced from inferolateral to anteromedial to enter the harder sustentacular bone. Compressing the overhanging lateral ledge of bone is important because presence of a ridge can cause irritation on the soft tissues and sural nerve. This is a stable osteotomy, and weight bearing can start after 10 days, either in a cast or in a boot, depending on the additional procedures performed.