Current Diagnosis and Treatment in Orthopedics, 4th Edition
Chapter 9. Foot & Ankle Surgery
BIOMECHANIC PRINCIPLES OF THE FOOT & ANKLE
The following is a limited discussion of the biomechanic principles governing the foot and ankle during the gait cycle. The physician must have a clear understanding of these principles to evaluate problems affecting the foot and ankle accurately. Once normal biomechanic function is understood, anatomic and functional abnormalities are more easily detected.
Gait is the orderly progression of the body through space while expending as little energy as possible. As the body moves through a gait cycle, forces are generated actively, by action of the body's muscles, and passively, by the effects of gravity on the body. To accommodate these forces, the foot is flexible at the time of heel strike, when it must absorb the impact of the body against the ground, and rigid at the time of toe-off, when it must assist in moving the body forward. The magnitude of the forces on the foot increases significantly as the speed of gait increases. For example, when an individual is walking, the initial force with which the foot meets the ground is approximately 80% of body weight, whereas when an individual is jogging, it is approximately 160%. The peak force against the foot during walking is approximately 110% of body weight, whereas for jogging it is approximately 240%. This marked increase probably contributes to some of the injuries seen in runners.
The Walking Cycle
The walking cycle is discussed more extensively in Chapter 1, but pertinent aspects relating to the foot are discussed here (Figure 9–1).
Observation of the patient while walking may give the clinician insight into the cause of a gait anomaly (Figure 9–2). For example, equinus deformity resulting from spasticity or contracture may cause the toe to make initial contact with the ground rather than the heel. At 7% of the gait cycle, the foot is usually flat on the ground, but spasticity or tightness of the Achilles tendon causes this to be delayed. At 12% of the cycle, the opposite foot toes off and the swing phase begins. Heel rise of the standing foot begins at 34% of the cycle as the swinging leg passes the standing limb. Heel rise may be premature in spasticity or prolonged in weakness of the gastrocsoleus muscle. Heel strike of the opposite foot occurs at 50% of the cycle, ending the period of single-limb support; this may occur sooner if there is weakness of the contralateral calf muscle. Toe-off of the opposite foot occurs at 62% of the cycle, at the beginning of the swing phase. These markers of the gait cycle should be kept in mind when observing gait, so pathologic conditions may be identified.
Motions of the Foot & Ankle
The names for various motions about the foot and ankle may be confusing and used incorrectly. The motions that occur at the ankle joint are dorsiflexion and plantar flexion. The motions of the heel medially and laterally, which occur at the subtalar joint, are inversion (varus) and eversion (valgus), respectively. The motion occurring at the transverse tarsal joint (talonavicular and calcaneocuboid) is adduction, which is movement toward the midline, and abduction, which is movement away from the midline.
Supination and pronation are terms for two different combinations of movements, but unfortunately these terms are sometimes used in the literature interchangeably. Pronation refers to dorsiflexion of the ankle joint, eversion of the subtalar joint, and abduction of the transverse tarsal joint. Supination is the opposite; namely, plantar flexion of the ankle joint, inversion of the subtalar joint, and adduction of the transverse tarsal joint.
The nomenclature may also be confusing when such terms as forefoot varus and forefoot valgus are used (Figure 9–3). Forefoot varus or valgus is an anatomic deformity that is observed when the hindfoot is placed in neutral position. Neutral position is achieved when the calcaneus is aligned with the long axis of the tibia and the head of the talus is covered with the navicular bone. Forefoot varus deformity is present when the lateral aspect of the forefoot is in greater plantar flexion than the medial aspect. With a flexible deformity, the foot lies flat on the floor during stance, but with a fixed deformity, excessive weight is borne on the lateral side of the foot. As a result, as the weight passes onto the forefoot region, the calcaneus goes into valgus position, and this may result in lateral impingement of the calcaneus against the fibula if severe. In forefoot valgus deformity, the medial side of the foot has greater plantar flexion than the lateral side and results in excessive weight bearing by the first metatarsal head. To accommodate for this deformity, the calcaneus assumes a varus position, which may result in a feeling of instability at the ankle joint.
Mechanisms of the Foot during Weight Bearing
As mentioned previously, the normal foot is flexible at the time of heel strike to absorb the impact of striking the ground. As a result, the subtalar joint literally collapses into a position of valgus, causing internal rotation of the tibia and resulting distally in unlocking of the transverse tarsal (talonavicular and calcaneocuboid) joint. Thus, the forefoot is more flexible. The only muscle group that is functioning about the foot and ankle during heel strike is the anterior compartment muscle group, which helps control the initial rapid plantar flexion following heel strike by an eccentric or lengthening contraction. The flexibility of the foot is greatest at approximately 7% of the cycle, and a series of changes is then initiated. With the foot fixed to the ground, the body passes over the foot, which lifts the heel up and forces the metatarsophalangeal joints into extension. As this occurs, the foot is converted into a rigid lever that supports the body at the time of toe-off. The mechanisms that bring about conversion of the foot from a flexible to a rigid structure are (1) the tightening of the plantar aponeurosis, the windlass mechanism, (2) the progressive external rotation of the lower extremity, which begins at the pelvis and is passed distally across the ankle joint into the subtalar joint, and (3) the stabilization of the transverse tarsal joint, which results from the progressive inversion of the subtalar joint.
Joints About the Foot & Ankle
The ankle joint consists of the articulation of the talus with the tibia and fibula, with a range of motion (ROM) of 15 degrees of dorsiflexion and 55 degrees of plantar flexion. There is also a small amount of motion in the transverse plane, approximately 15 degrees. The anterior compartment muscles of the leg, the tibialis anterior and the toe extensors, control the amount of plantar flexion of the ankle joint at the time of heel ground contact to 10% stance. In addition, these muscles provide dorsiflexion of the ankle joint during swing phase. If this muscle group does not function, a footslap is observed at the time of heel strike, and a dropfoot occurs during swing phase. The greatest force across the ankle joint during walking is calculated to be approximately 4.5 times body weight; this force is present at 40% of the walking cycle.
The subtalar joint is the articulation between the talus and the calcaneus. The primary joint surface is the posterior facet, with much smaller middle and anterior facets. The motion of this joint is inversion of approximately 30 degrees and eversion of approximately 10 degrees. The tibialis posterior causes inversion and the peroneus brevis eversion at the subtalar joint. At the time of initial ground contact, eversion is a passive mechanism and occurs because of the shape of the articulations and their ligamentous support. Inversion occurs both actively and passively at the time of toe-off. Active control is achieved by the gastrocsoleus and posterior tibial muscles, and passive inversion occurs by the action of the plantar aponeurosis, the external rotation of the lower extremity, and the oblique metatarsal break.
TALONAVICULAR JOINT AND CALCANEOCUBOID JOINT
The talonavicular and calcaneocuboid joints functionally act as a unit known as the transverse tarsal joint. Motion at the transverse tarsal joint is approximately 10 degrees of abduction and approximately 15 degrees of adduction. The head of the talus is firmly seated into the navicular at the time of toe-off, adding stability to the foot. The stability of the transverse tarsal joint is controlled by the position of the subtalar joint. When the subtalar joint is in an inverted position, the axes of these two joints are nonparallel, giving rise to increased stability of the hindfoot. When the calcaneus is in an everted position at the time of heel strike, these joints are parallel to one another, thereby giving rise to increased flexibility of these joints (Figure 9–4). The clinical implication is that when carrying out a subtalar arthrodesis, placement of the subtalar joint into a varus position locks the transverse tarsal joint, causing increased stiffness of the forefoot and, frequently, discomfort. When the hindfoot is everted into a position of 5–7 degrees of valgus, the flexibility of the transverse tarsal joint is maintained. This allows the forefoot to be more supple and makes ambulation easier.
The motion at the metatarsophalangeal joints is between 50 and 70 degrees of dorsiflexion (extension) and 15 and 25 degrees of plantar flexion (flexion). The role of the metatarsophalangeal joints during gait is discussed in the section on deformities of the first toe.
THE PLANTAR APONEUROSIS
Although the plantar aponeurosis is not an articulation per se, it probably plays the predominant role in the overall stability of the foot. The plantar aponeurosis arises from the tubercle of the calcaneus and passes distally to insert into the base of each proximal phalanx (Figure 9–5). As the metatarsophalangeal joints pass into dorsiflexion in the last half of the stance phase, the rigidity of the plantar aponeurosis forces the metatarsal heads into a plantarward direction, which raises the longitudinal arch. This is known as a windlass mechanism. It also increases the effect that a tensile force in the tendo Achilles has on the tensile force in the plantar fascia. The now-rigid foot provides support to the body for the push-off phase of gait. Secondarily, this mechanism also helps bring about inversion of the subtalar joint.
The following is a brief description of the more common gait abnormalities.
Patients with dropfoot gait lack ankle dorsiflexion, resulting in plantar flexion at the ankle joint. When walking, these patients adopt a steppage-type gait. This gait pattern is manifested by increased flexion of the hip and knee to enable the swinging leg to clear the ground. If this compensatory mechanism does not occur, the patient may catch the toes on the ground and fall.
In an equinus gait pattern, the ankle joint is fixed in plantar flexion throughout the entire gait cycle. This situation may result from a stroke or head injury, trauma to the lower extremity, or a congenital deformity, and it often is associated with tightness of the posterior capsule. This gait pattern is characterized by forefoot floor contact (no heel contact). The anterior loading of the foot results in a back knee thrust, which may, over a long period of time, result in a hyperextension deformity of the knee. A weak quadriceps muscle may accentuate this problem.
A cavus deformity is an excessive elevation of the longitudinal arch. A moderate decrease in the ROM of the foot usually accompanies this deformity. In addition, the hindfoot is often in a varus posture and the forefoot in valgus posture. This is most frequently observed in Charcot-Marie-Tooth disease but may also be seen in poliomyelitis and occasionally as a late result of calf compartment syndrome. The deformity significantly diminishes the overall surface available for weight bearing in these patients. Clawing of the toes may further reduce contact with the ground. Thus, the gait pattern in these patients is altered, with increased pressure on the heel at initial ground contact, followed by increased pressure along the lateral side of the foot and underneath the first metatarsal head as the gait cycle progresses.
Pes Planus Deformity
Usually, the patient with a pes planus deformity demonstrates just the opposite of cavus deformity; the foot is too flexible. At the time of initial ground contact, there is excessive valgus of the hindfoot and in severe cases breaking down of the longitudinal arch with an associated abduction of the forefoot. This results in an increased weight-bearing surface and often easy fatigability because of the lack of adequate support of the longitudinal arch.
DEFORMITIES OF THE FIRST TOE
The first metatarsophalangeal joint functions mainly as a weight-bearing structure and stabilizer of the medial aspect of the longitudinal arch. The static stability of the first metatarsophalangeal joint is provided by the collateral ligaments and the strong plantar plate, which consists of the plantar aponeurosis and the joint capsule. Added dynamic stability is provided by the abductor hallucis and adductor hallucis muscles, which insert along the medial and lateral sides of the metatarsal head, respectively. No muscle inserts into the metatarsal head per se, and therefore it is suspended in a sling of muscles and tendons. This allows the metatarsal head to be pushed in a medial or lateral direction, depending on the deviation of the proximal phalanx.
As previously discussed, the plantar aponeurosis forces the metatarsal heads into plantar flexion during the last third of the stance phase of the walking cycle. As a result, pressure that is present under the metatarsal heads is transferred to the toes, especially the hallux (see Figure 9–5). If this windlass mechanism for the hallux is lost as occurs in a bunion deformity, pressure is no longer transferred to the toes but remains beneath the metatarsal heads. Metatarsalgia results from this transfer of load, especially beneath the lesser metatarsal heads. The second metatarsal frequently bears the load because the weight-bearing ability of the first metatarsal is disrupted.
Any type of surgical procedure that disrupts this mechanism may result in the development of transfer lesions as well. This problem can be seen after the Keller arthroplasty, in which the base of the proximal phalanx is removed, or after prosthetic replacement of the first metatarsal joint. Metatarsal osteotomy with excessive shortening (more than 5–7 mm) or dorsiflexion of the first metatarsal may also cause this problem.
The first metatarsophalangeal joint consists of the articulating surfaces of the metatarsal head and the base of the proximal phalanx. On the plantar aspect of the foot beneath the metatarsal head are the two sesamoid bones, which are embedded in the dual tendons of the flexor hallucis brevis and lie on either side of the crista. Medially and laterally, the collateral ligaments stabilize the metatarsophalangeal joint, and toward the plantar surface, they blend with the adductor and abductor hallucis tendons along the lateral and medial sides of the joint. Further toward the plantar surface, the sesamoids are stabilized by the firm attachment of the encapsulating plantar aponeurosis, which inserts into the base of the proximal phalanx. Plantar to the sesamoids passes the flexor hallucis longus tendon. Dorsally, the extensor hallucis longus tendon is stabilized by a medial and lateral hood mechanism similar to that present in the hand, and the extensor digitorum brevis muscle inserts into the proximal phalanx along the lateral aspect of the joint. Normal motion of the metatarsophalangeal joint consists of dorsiflexion and plantar flexion.
The most common deformity of the metatarsophalangeal joint is hallux valgus or the so-called bunion deformity, which results from the lateral deviation of the proximal phalanx and the resultant medially directed pressure exerted against the metatarsal head. The medial eminence becomes prominent as the proximal phalanx drifts into a valgus position. Attenuation of the medial joint capsule and contracture of the lateral joint capsule occur. As the metatarsal head is pushed medially, the sesamoids, which are firmly anchored by the adductor hallucis tendon and transverse metatarsal ligament, slowly erode the crista. Eventually the sesamoids subluxate from underneath the first metatarsal, with the fibular sesamoid lying in the first web space. The extensor hallucis longus and flexor hallucis longus, which insert into the base of the distal phalanx, also deviate in a lateralward direction and contribute to the progressive hallux valgus deformity. As the deformity becomes more severe, both the extrinsic and intrinsic muscles lie lateral to the longitudinal axis of the first metatarsophalangeal joint, thereby further enhancing the deformity. As the deformity progresses, pronation of the great toe occurs. Attenuation of the weakest portion of the capsule (the dorsomedial aspect) allows the abductor hallucis tendon to slide beneath the metatarsal head and rotate the proximal phalanx into a position of pronation. More rapid progression of the deformity may occur in a small percentage of patients whose first metatarsocuneiform joint demonstrates a significant degree of instability.
Etiology of Hallux Valgus Deformity
Hallux valgus deformity occurs in women approximately 10 times more frequently than in men. The incidence is also significantly higher in persons who wear shoes than in those who do not. The conclusion can therefore be made that a major contributing cause of hallux valgus deformity is wearing tight pointed-toed shoes that women often wear. Other factors that may contribute to hallux valgus are congenital deformity or predisposition, severe flatfoot deformity, chronic tightness of the Achilles tendon, spasticity, hypermobility of the first metatarsocuneiform joint, and systemic disease such as rheumatoid arthritis (RA).
The clinical evaluation of hallux valgus deformity begins with a careful history to obtain the chief complaint, which may be primarily medial eminence pain, plantar first metatarsal or lesser metatarsal head pain, impingement upon the second toe, resultant deformities of the lesser toes, or the inability to wear certain shoes. The examiner should ask about factors that seem to aggravate the discomfort, the patient's occupation and level of athletic endeavors, and what type of shoe is most commonly worn.
The physical examination starts with the patient in a standing position to observe the degree of deformity of the great toe and lesser toes. The overall posture of the foot is noted. The patient's gait is observed, looking for evidence of abnormal ground contact or early heel rise, which would indicate possible tightness of the Achilles tendon. In the seated position, the ROM of the ankle, subtalar, transverse tarsal, and metatarsophalangeal joints is noted. The neurovascular status of the foot is carefully assessed, noting venous stasis changes. Doppler studies are obtained if there is any question regarding the circulatory status of the foot. The plantar aspect of the foot is examined for abnormal callus formation, particularly beneath the metatarsal head and along the medial aspect of the great toe.
The motion of the first metatarsophalangeal joint is carefully observed in its deformed position and after the toe is carefully brought back toward normal alignment. Restriction of motion gives the clinician insight into the degree of surgical correction that can be obtained at the joint without impairing motion of the joint. The first metatarsocuneiform joint is examined for hypermobility by moving it in a dorsomedial and plantolateral direction.
The radiographic evaluation consists of weight-bearing anteroposterior, lateral, and oblique radiographs. From these radiographs, the following measurements are made:
The patient should be encouraged to wear shoes of adequate size and shape. This simple form of management may relieve most symptoms.
A variety of pads are available to address symptoms that occur because of the bunion deformity. Pads may be placed in the first web space or over the median eminence to help take pressure off a painful median eminence. Pads are also available that can be placed underneath the metatarsal heads to take pressure off painful calluses or sesamoids.
If after adequate conservative management the patient continues to have discomfort, surgical intervention may be considered. Surgery is not performed for cosmetic reasons or to allow patients to wear fashionable shoes, but rather to correct a symptomatic structural deformity.
Juvenile hallux valgus deformity presents a significant problem in management, but as a general rule, conservative management should be continued until growth is completed, after which surgery may be considered. Extra care must be taken into consideration in the juvenile population where cosmetic appearance may play a greater role in the patient's or parents' desire for surgery.
Hallux valgus surgery is generally contraindicated in high-performance athletes or dancers until they are no longer able to perform at the level necessary to continue in their vocation or avocation. Premature surgery in these individuals may diminish their special abilities.
Algorithm for Surgical Treatment
If surgery is being considered, the patient's chief complaint, the physical findings, and the radiographic measurements must be correlated to enable the surgeon to select the best procedure. No single procedure succeeds for all hallux valgus deformities, and careful preoperative planning is essential.
The following factors need to be considered in the decision-making process:
The algorithm in Figure 9–8 divides hallux valgus deformities into three main groups: those with a congruent joint, those with an incongruent joint, and those associated with degenerative joint disease. The algorithm lists the operative procedure that may best correct the deformity within each classification. Although no one scheme is all inclusive, this algorithm is helpful in organizing the treatment plan.
In using this algorithm, the first question to ask is if the deformity is congruent or incongruent. A congruent metatarsophalangeal joint implies that the goal is mainly treatment of an enlarged medial eminence, and little or no correction of the stable metatarsophalangeal is required. For the congruent joint, a chevron procedure or Akin procedure with removal of the medial eminence usually results in satisfactory correction.
If the deformity is incongruent to the degree that the proximal phalanx is subluxed laterally on the metatarsal head, a procedure that moves the proximal phalanx back onto the metatarsal head is required. The procedure of choice depends on the severity of the deformity (see Figure 9–8).
If the first metatarsocuneiform joint is hypermobile, the distal soft-tissue procedure with a metatarsocuneiform arthrodesis should be considered. Generally, in the patient with severe hallux valgus deformity, greater than 45–50 degree hallux valgus angle, and degenerative joint disease, arthrodesis of the joint is indicated. If routine hallux valgus repair is attempted in the patient with advanced arthrosis, stiffness of the metatarsophalangeal joint frequently results. Use of a prosthetic replacement, as a general rule, does not produce a satisfactory long-term result, particularly in active individuals.
DISTAL SOFT-TISSUE PROCEDURE
The distal soft-tissue procedure was previously referred to as the McBride procedure, which was first modified by DuVries and subsequently modified further and given its current designation. The procedure is indicated for mild hallux valgus deformity, usually with an intermetatarsal angle of less than 12–13 degrees and a hallux valgus deformity of less than 30 degrees. Within this range of deformity, a satisfactory outcome can usually be anticipated from this procedure.
The procedure requires releasing the soft-tissue contracture on the lateral side of the metatarsophalangeal joint, including the lateral joint capsule, the adductor hallucis tendon, and the transverse metatarsal ligament (Figure 9–9). On the medial side of the metatarsophalangeal joint, the medial eminence is removed 2–3 mm medial to the sagittal sulcus and in line with the medial aspect of the metatarsal shaft. The capsule on the medial side of the joint is plicated to hold the toe in correct alignment. Postoperatively, the patient is maintained in a firm compression dressing, which is changed on a weekly basis for 8 weeks. During this period, the patient is permitted to ambulate in a postoperative shoe.
The most common complication consists of recurrence of the deformity, usually because the deformity was too severe to be corrected by the procedure. In these cases, a metatarsal osteotomy added to the distal soft-tissue procedure completes the correction.
Hallux varus deformity is a medial deviation of the proximal phalanx on the metatarsal head, a complication that may occur in approximately 5–7% of cases. This deformity is usually a result of excessive excision of the medial eminence or fibular sesamoidectomy, which causes joint instability. Occasionally, the medial joint capsule is overplicated or the lateral joint capsule fails to attain adequate strength. Mild hallux varus deformity, up to 7–10 degrees, usually is of no clinical significance unless the joint is also hyperextended.
DISTAL SOFT-TISSUE PROCEDURE WITH PROXIMAL METATARSAL OSTEOTOMY
Addition of the proximal metatarsal osteotomy to the distal soft-tissue procedure significantly expands the capability of this procedure to correct hallux valgus deformity. If the intermetatarsal angle exceeds 13 degrees, the degree of deformity between the first and second metatarsal prevents adequate correction of alignment of the metatarsophalangeal joint with the distal soft-tissue procedure alone. Realignment of the fixed bony deformity present between the first and second metatarsals permits the combined procedure to be used for deformities with up to 50 degrees of hallux valgus and a 25-degree intermetatarsal angle.
In carrying out this operative procedure, the distal soft-tissue procedure is performed as described earlier. The metatarsal osteotomy is carried out through a third incision, which is centered over the dorsal aspect of the base of the metatarsal shaft. The most commonly used osteotomy is a crescentic-shaped osteotomy whose concavity is directed proximally (Figure 9–10). This enables the surgeon to rotate the metatarsal head laterally as the metatarsocuneiform joint is pushed in a medialward direction. This usually results in approximately 2–3 mm of lateral displacement of the osteotomy site. Stabilization is carried out with a screw, which passes from distal to proximal. Other types of osteotomies are used to realign the first metatarsal, including oblique, chevron-shaped, and closing-wedge osteotomies.
Postoperatively, the treatment is the same as for the distal soft-tissue procedure, with 8 weeks of dressing changes and immobilization in a postoperative shoe. As a general rule, cast immobilization is not necessary.
The long-term postoperative results following the distal soft-tissue procedure with proximal osteotomy result in greater than 90% patient satisfaction. The addition of the osteotomy does create an increased risk of complications, but is reported to be uniformly low. Dorsiflexion of the osteotomy site may occur but is usually not of clinical significance. Nonunion of the osteotomy may develop in 1% of cases. Excessive lateral displacement of the metatarsal head can result in hallux varus deformity, which is more resistant to treatment than when osteotomy is not included.
The chevron osteotomy is usually indicated for hallux valgus deformity of less than 30 degrees, with an intermetatarsal angle of less than 12 degrees. The distal metatarsal articular angle should not be more than 12 degrees, or complete correction will not be obtained. The operative procedure is based on lateral translation of the metatarsal head, along with plication of the medial joint capsule. The joint is approached surgically through a medial incision, the capsule opened, and the medial eminence removed. A chevron-shaped cut with the apex based distally is carried out and translated laterally approximately 3–4 mm. The medial bony prominence created by the shift of the metatarsal head is excised and the medial joint capsule plicated. The osteotomy site is fixed with a pin or a screw (Figure 9–11).
Postoperatively, the foot is firmly bandaged for 6–8 weeks, and the patient is permitted to ambulate in a postoperative shoe. If a pin was used for fixation, it is removed after 4 weeks.
Uniformly good results, short and long term, are reported following a chevron procedure. In addition, more than 10-year follow-up showed consistent improvement with time. There was no difference between patients younger and older than 50 years; patients had equally positive outcomes. If it is used to correct a deformity that is too severe, the outcome may be unsuccessful. The most serious complication, occurring in 1–2% of cases, is avascular necrosis of the metatarsal head, which is probably the result of extensive stripping of the soft tissue surrounding the head. As with any type of osteotomy, the distal fragment is capable of migrating either too far laterally or medially, giving rise either to hallux varus deformity or recurrent hallux valgus deformity. Occasionally, arthrofibrosis of the joint is noted, resulting in significant joint stiffness.
The Akin procedure consists of a medial closing-wedge osteotomy at the base of the proximal phalanx. This procedure is used along with simple excision of the median eminence or with a chevron procedure to correct a hallux valgus deformity with a congruent joint. The Akin procedure is indicated for a hallux valgus deformity of less than 25 degrees, with an intermetatarsal angle of 12 degrees or less.
The operative procedure consists of a medial approach to the base of the proximal phalanx and the median eminence. After removing the median eminence in line with the metatarsal, a wedge of bone is removed from the medial aspect of the proximal phalanx. The osteotomy is closed down and stabilized internally with sutures or wires, or externally with a Kirschner wire (K-wire). Dressings are applied for 6–8 weeks postoperatively.
The Keller procedure is reserved for the older, less active patient, in a patient prone to skin problems, or in the case of an arthritic joint. This procedure is contraindicated in an active person.
The procedure consists of removal of the base of the proximal phalanx, which decompresses the metatarsophalangeal joint, and excision of the medial eminence. An attempt is made to reapproximate the intrinsic muscles that were detached by placing them into the remaining stump of bone (Figure 9–12). As a rule, a longitudinal pin is used to stabilize the operative site for approximately 4 weeks. Postoperatively, the patient is permitted to ambulate in a postoperative shoe, and dressings are changed for approximately 6 weeks.
Results in the older (more than 65 years) patient with low functional demand are satisfactory. If the procedure is used in a younger patient, a certain degree of instability and loss of weight bearing by the first metatarsophalangeal joint occurs because the base of the proximal phalanx was removed. There is significant loss of foot function, and a transfer lesion may develop beneath the second metatarsal head because the great toe no longer carries adequate weight. The metatarsophalangeal joint often becomes cocked upward and into varus.
ARTHRODESIS OF THE FIRST METATARSOPHALANGEAL JOINT
Arthrodesis of the first metatarsophalangeal joint is indicated in the patient with hallux valgus who also has advanced degenerative arthrosis of the joint, or as a salvage procedure following a previously failed surgical attempt to realign the metatarsophalangeal joint. The procedure is also indicated in the patient with advanced hallux valgus deformity that cannot be corrected by the previously described procedures. Hallux valgus deformity in which the proximal phalanx is subluxed more than 50% of the metatarsal head or one with a significant degree of stiffness about the metatarsophalangeal joint should be considered for fusion.
The arthrodesis is carried out by creating two flat surfaces or a ball-and-socket type of configuration. The arthrodesis site is stabilized with an interfragmentary screw and plate or Steinmann pins if the bone stock is poor. The position of the arthrodesis is critical. The joint should be placed in 15–20 degrees of valgus and 10–15 degrees of dorsiflexion in relation to the ground or the plantar aspect of the foot. In relation to the first metatarsal shaft, which is inclined plantarward approximately 15 degrees, it should be in approximately 30 degrees of dorsiflexion (Figure 9–13). Any pronation that is present must also be corrected at the same time.
The patient must wear a postoperative shoe until arthrodesis occurs in 10–12 weeks. The unreliable patient should be treated in a short leg walking cast until fusion occurs.
The main complication associated with arthrodesis of the first metatarsophalangeal joint is malposition. If the toe is not placed into adequate dorsiflexion or valgus, excessive stress occurs against the interphalangeal joint, which may result in a painful arthritic condition of the joint. The fusion rate is approximately 95%. Occasionally, the degree of valgus and dorsiflexion is correct but the toe is left in a pronated position, which results in pressure along the medial side of the interphalangeal joint and possible discomfort.
The patient's gait following arthrodesis of the first metatarsophalangeal joint in proper alignment is most satisfactory. These patients are able to roll over the fusion site and have little or no difficulty carrying out everyday activities. Squatting is the only activity that is difficult because the toe must be in full dorsiflexion when this activity is carried out. Patients are able to return to most types of athletic activities, although at a somewhat slower pace.
Hallux rigidus or first metatarsophalangeal joint arthritis is a relatively common problem, often affecting people at a much younger age than arthritis of other joints. Hallux rigidus is seen in patients from their 30s onward. The reason why arthritis of this joint is seen in younger patients is unclear but may be associated with an unrecognized chondral injury to the metatarsal head. It is also associated with hallux valgus interphalangeus, bilateral involvement in those with a family history, and female gender. Hallux rigidus is not associated with elevatus, first ray hypermobility, a long first metatarsal, Achilles tightness, abnormal foot posture, symptomatic hallux valgus, adolescent onset, shoe wear, or occupation.
Patients present with complaints of joint stiffness and pain with dorsiflexion of the joint. The symptoms are worse with increased physical activities. Patients also complain of a painful dorsal prominence over the metatarsal neck that makes shoe wear uncomfortable. Radiographs show varying degrees of joint space narrowing and, invariably, a large osteophyte on the dorsal aspect of the metatarsal neck.
Conservative treatment consists of nonsteroidal antiinflammatories (NSAIDs) and wearing a stiff-soled shoe with a deep toe box. In older (more than 60 years), sedentary patients, these measures are usually adequate. In more active individuals, however, surgical treatment is usually indicated.
Several surgical treatment methods are available for treating hallux rigidus. Resection of the dorsal bone spur, known as cheilectomy, is efficacious and the least intrusive surgical option. Approximately 25% of the dorsal aspect of the metatarsal head is removed along with the bone spur, and a thorough synovectomy of the joint is performed. Postoperatively, patients regain up to 50% of their dorsiflexion and have improvement of their total motion. More than 90% of patients have improvement of pain and increased physical abilities. This procedure is less likely to have a favorable outcome on joints with advanced arthritis.
A resection arthroplasty (Keller procedure) can be used on older, less active patients, but has a high rate of complications, as previously discussed. Prosthetic replacement of the arthritic first metatarsophalangeal joint can be used in older, lower demand patients but has high rates of failure in younger, more active individuals.
First metatarsophalangeal joint arthrodesis provides predictable pain relief and longevity for advanced arthritis. The drawback is that of lost motion at the joint. However, patients can remain quite active with a first metatarsophalangeal joint fusion as described previously.
The two sesamoid bones on the plantar aspect of the first metatarsophalangeal joint can become painful for a variety of reasons. Fractures, osteonecrosis, arthritis, and subluxation can affect these small bones. Often they can become painful for no clear reason, a condition referred to as sesamoiditis.
The patient with a painful sesamoid complains of discomfort on the plantar aspect of the foot, directly under the affected bone. The pain is worse with weight-bearing activities. The history may be significant for a trauma to the toe causing a fracture, but most commonly, the pain has an insidious onset.
The painful sesamoid is determined by direct palpation. Postural abnormalities of the foot that may be contributing to the condition are evaluated. For example, hallux valgus deformity may cause a subluxation of the sesamoid from its normal articulation with the plantar aspect of the metatarsal head, causing pain.
Radiographs of the foot are taken, including a skyline or sesamoid view, which is a tangential view of the sesamoid metatarsal head articulation. Abnormalities may be seen, such as subluxation of the sesamoids in the case of hallux valgus, fragmentation as seen in osteonecrosis, or joint space narrowing as seen in the case of arthritis. Displaced fractures are easy to determine, but nondisplaced fractures may be difficult to distinguish from a bipartite sesamoid that is a normal finding. A bone scan may be helpful in the case of normal radiographs to diagnose osteonecrosis or sesamoiditis.
If an acute injury has occurred and radiographs are consistent with a fracture of the sesamoid, a short leg walking cast is placed. If symptoms came on gradually, a stiff-soled shoe is used, with a soft pad placed just proximal to the sesamoids to take the pressure off the involved area. Usually the majority of symptoms resolve in a matter of weeks, although some degree of discomfort may persist for several months. If 6–12 months of conservative treatment does not relieved the symptoms, the affected sesamoid can be removed, which relieves the pain.
DEFORMITIES OF THE LESSER TOES
The most common problems involving the four lesser toes include mallet toe, hammer toe, clawtoe, and hard and soft corns. More proximally, at the metatarsophalangeal joint, subluxation or dislocation of the joint may occur. All of these conditions alter the shape of the foot and at times make wearing shoes difficult. Furthermore, in the patient with an insensitive foot, ulcerations may form over the bony prominences of these deformities.
The most common cause of clawtoe, hammer toe, and mallet toe deformities are the long-term use of tightly fitting shoe wear. These deformities may also result from intrinsic or extrinsic factors, including inflammatory arthritis, trauma, congenital abnormalities, or neuromuscular disorders. Additional predisposing factors are a wide foot or an abnormally long second ray and occasionally postural abnormalities of the foot. Identifying the etiology is important to help treat the deformity properly.
Anatomy & Pathophysiologic Findings
The metatarsophalangeal joint is stabilized on the plantar aspect by a consolidation of the plantar capsule and plantar aponeurosis (plantar plate) and medially and laterally by the collateral ligaments. Plantar flexion of the metatarsophalangeal joint is affected by the intrinsic muscles, the interossei, and lumbricals, whose lines of action pass plantarward to the axis of the metatarsophalangeal joint. The flexor digitorum brevis and flexor digitorum longus muscles produce plantar flexion of the proximal interphalangeal and distal interphalangeal joints, respectively. On the dorsal aspect of the joint, the extensor digitorum longus and brevis tendons and the extensor hood or sling constitute the extensor mechanism. This mechanism causes dorsiflexion of the metatarsophalangeal joint and can cause extension of the distal interphalangeal and proximal interphalangeal joints if the proximal phalanx is in a neutral or plantar-flexed position. When the metatarsophalangeal joint is hyperextended, the ability of the extensor hood to extend the distal interphalangeal and proximal interphalangeal joints is significantly diminished. Chronic hyperextension of the metatarsophalangeal joint eventually leads to fixed flexion deformities at the interphalangeal joints. As a general rule, a fixed deformity is significantly more bothersome to the patient than a flexible deformity.
Mallet Toe Deformity
A mallet toe is a flexion deformity of the distal interphalangeal joint. It may be a fixed or flexible deformity. In general, the deformity involves the second toe, usually because of its excessive length in relation to the adjacent toes.
SYMPTOMS AND SIGNS
A mallet toe tends to cause pain over the dorsal aspect of the distal interphalangeal joint or occasionally at the tip of the toe from striking the ground. This may result in a callus or, in cases associated with neuropathy, an ulceration. Occasionally, the nail itself is deformed if the pressure was chronic.
The initial physical examination is carried out with the patient standing to evaluate the severity of the deformity and ascertain whether deformities are present in other toes. The interphalangeal joint is then carefully palpated to determine whether the deformity is fixed or flexible. If the distal interphalangeal joint is flexible, plantar flexion of the ankle permits the joint to be straightened out completely. As the ankle joint is brought into dorsiflexion, however, the deformity recurs. In the case of a fixed deformity, ankle motion does not affect the deformity.
Radiographic evaluation confirms the clinical findings of the flexion deformity of the distal interphalangeal joint.
The patient should be encouraged to obtain a shoe with a wide enough toe box to accommodate the deformed toe. An extra-depth shoe may be necessary if the deformity is too severe. If the main complaint is pain under the tip of the toe, a small pad can be placed underneath the toe to keep it from striking the ground, or lamb's wool can be wrapped around the toe.
Surgical treatment of a flexible mallet toe deformity requires release of the flexor digitorum longus tendon, which is carried out under local anesthesia by incising the tendon on the plantar aspect of the toe at the level of the middle phalanx. This usually results in resolution of the problem.
A fixed mallet toe deformity requires a condylectomy, which is carried out through an elliptical incision made over the dorsal aspect of the distal interphalangeal joint. Along with the ellipse of skin, the extensor tendon is excised, the collateral ligaments released, and the distal portion of the middle phalanx removed. The distal phalanx is reduced and held in place either with a 0.045-in. K-wire for 4 weeks or with Telfa bolsters (Figure 9–14).
Good results may be expected following this procedure. The most common complication occurs because a contracture of the flexor digitorum longus tendon was not appreciated prior to surgery or because insufficient bone was removed from the middle phalanx to decompress the deformity adequately.
Hammer Toe Deformity
A hammer toe deformity is a plantar flexion deformity of the proximal interphalangeal joint, which may either be fixed or flexible. It is frequently associated with varying degrees of hyperextension of the metatarsophalangeal joint. A flexion deformity of the distal interphalangeal joint usually accompanies a hammer toe, but an extension deformity is occasionally observed.
SYMPTOMS AND SIGNS
Clinical evaluation is similar to that of a mallet toe deformity, with care taken to distinguish between a fixed or flexible deformity. Also, the metatarsophalangeal joints of each toe are evaluated for hyperextension deformities. Callus formation or even an ulcer may be present over the extensor surface of the proximal interphalangeal joint. Metatarsophalangeal joint correction may be necessary to alleviate the hammer toe. Similarly, a significant hallux valgus deformity that is impinging on the second toe may require treatment to make room for correction of the hammer toe.
Radiographs help in the evaluation of proximal interphalangeal flexion deformity, hyperextension deformity at the metatarsophalangeal joint, and hallux valgus deformity. It is critical that all joints be assessed when hammer toe correction is being considered.
The conservative management of hammer toe deformities is foremost that of proper shoe wear, as previously emphasized. In addition, toe sleeves are available that pad the painful callus.
Conservative management becomes more difficult if a significant fixed deformity is present, particularly if it is associated with extension of the metatarsophalangeal joint or a significant hallux valgus deformity.
Surgical decision making regarding the hammer toe hinges on whether (1) the deformity is fixed or flexible, (2) any deformity of the metatarsophalangeal joint needs to be corrected concomitantly, and (3) a space must be created for the toe by correcting the hallux valgus deformity.
Flexible Hammer Toe Deformity
A flexible hammer toe deformity is corrected with the Girdlestone flexor tendon transfer. In this procedure, the long flexor tendon is harvested from the plantar aspect of the foot, brought up on either side of the extensor hood mechanism, and sutured into the extensor hood with the toe held in approximately 5 degrees of plantar flexion and the ankle in plantar flexion (Figure 9–15). This causes the long flexor tendon to act as an extensor of the interphalangeal joints and a flexor of the metatarsophalangeal joint, thereby correcting the deformity. A soft dressing is applied and a postoperative shoe is worn for 4 weeks, after which ambulation is allowed.
Fixed Hammer Toe Deformity
The DuVries proximal phalangeal condylectomy is used for the fixed deformity. This procedure, which is identical to that described for treatment of the mallet toe deformity, involves the proximal interphalangeal joint instead of the distal interphalangeal joint (Figure 9–16). Clinical results show a majority of patients were satisfied and a low risk of recurrence of deformity.
The main complication observed with either procedure is inadequate correction of the deformity, usually because of failure to appreciate a contracture of the flexor digitorum longus tendon at the time of surgery.
Clawtoe deformity involves both the metatarsophalangeal and interphalangeal joints and may be flexible or fixed. Clawtoe deformity can be disabling, particularly in the patient with a neuromuscular disorder. This deformity is characterized by marked dorsiflexion of the metatarsophalangeal joint, which results in pain secondary to chafing over the interphalangeal joints against the shoe and pain beneath the metatarsal heads because the metatarsal heads are forced into plantar flexion. In contrast to hammer toe or mallet toe deformities, which usually involve a single toe, clawtoe deformity usually involves all of the lesser toes. An associated deformity of the great toe may occur as well.
SYMPTOMS AND SIGNS
The clinical evaluation is similar to that described for the previous lesser toe deformities. The metatarsal heads are palpated because the fat pad may be displaced distally and the skin beneath the metatarsal heads may be atrophic. Callosities may be present on the extensor surface of the proximal interphalangeal joints and on the plantar aspect of the metatarsophalangeal joints.
Radiographs demonstrate the deformity, which is present at the metatarsophalangeal and interphalangeal joints. The posture of the entire foot needs to be evaluated, looking for the presence of a cavus-type foot deformity, characterized by increased dorsiflexion pitch of the calcaneus and increased plantar flexion of the first metatarsal.
An extra-depth shoe reduces the pressure on the lesser toes, and arch supports placed under the metatarsal head area may relieve the pain. Flexible mild deformities can be treated with shoe inserts placed immediately proximal to the metatarsophalangeal joints. These can have the effect of balancing the extensors and flexors of the toes.
The type of operative intervention depends upon the nature of the deformity. Flexible deformities can be treated with the Girdlestone flexor tendon transfer. In addition, however, the extensor tendons usually must be lengthened to permit correction of the metatarsophalangeal joints to neutral plantar flexion.
A concomitant fixed contracture of the proximal interphalangeal joint requires a DuVries proximal phalangeal condylectomy as well as the Girdlestone tendon transfer procedure. Furthermore, release of the dorsal capsule, collateral ligaments, and extensor tendon is performed at the metatarsophalangeal joint. Postoperative management for the patient with clawtoe deformity is the same as discussed earlier for hammer toe deformity.
Following this surgical procedure no active motion of the toes occurs. The toes are usually well aligned in a plantigrade position. The marked deformity of the proximal interphalangeal joints is relieved so they no longer strike the top of the shoe. The main problems that can occur after surgery are (1) failure to correct a fixed hammer toe deformity adequately by use of the tendon transfer and (2) failure to release the fixed deformity adequately at the metatarsophalangeal joint, resulting in recurrence of the deformity.
Hard Corn & Soft Corn (Clavus Durum & Clavus Mollum)
A corn is a keratotic lesion that forms over a bony prominence on the lesser toes because of excessive pressure on the skin. A hard corn occurs most commonly over the dorsal and lateral aspect of the fifth toe, usually over the lateral condyle of the proximal phalanx. A soft corn represents a keratotic lesion in a web space and is so named because maceration results from moisture between the toes. The soft corn may occur anywhere along the toe where a bony excrescence is present and frequently occurs in the fourth web space between the base of the proximal phalanx of the fourth toe and the medial condyle of the head of the proximal phalanx of the fifth toe. At times, an ulceration may occur because of the extent of the maceration.
The main objective of conservative management is reducing pressure on the bony prominences. Footwear with a large toe box can relieve this pressure. Debridement or shaving of the lesion reduces pain. The procedure can frequently be carried out by younger patients without assistance but becomes increasingly difficult in older individuals because of decreasing flexibility and poor eyesight. Skin compromise, especially in the diabetic patient, must be avoided. At times, soft pads or lamb's wool can be placed around the toe to minimize pressure on the involved area, but the patient must wear a shoe with an adequate toe box to accommodate such modalities.
Surgical Treatment of the Hard Corn
The hard corn, over the fifth toe, is managed surgically by removing the distal portion of the proximal phalanx and occasionally the dorsolateral aspect of the proximal portion of the middle phalanx. The longitudinal incision is made over the dorsal aspect so the scar will not chafe against the shoe. The extensor tendon is split, the collateral ligaments cut, and the condyle exposed. With a bone cutter, the distal portion of the proximal phalanx is generously removed and the edges smoothed with a rongeur. Following closure, a compression dressing is applied for several days. The toe is taped to the adjacent fourth toe for 8 weeks. Long-term results show a high level of patient satisfaction and a low recurrence rate. Removal of excessive bone is the major complication, which causes the small toe to become too floppy, creating a nuisance for the patient.
Surgical Treatment for the Soft Corn
Soft corns are treated surgically by making an incision over the lesion and using a small rongeur to remove the underlying bony excrescence. This is a simple procedure and almost invariably results in satisfactory resolution of the problem.
Because the soft corn is caused by pressure on the skin, removal of the skin between the toes can resolve the problem. Syndactyly is a procedure by which the skin is removed between the fourth and fifth toes and the two toes are sutured together to eliminate the problem of a soft corn in the web space. Although the soft corn can usually be managed with a condylectomy, as described earlier, occasionally a great deal of maceration or ulceration precludes treating it only with a condylectomy. In these cases, syndactyly is indicated. Occasionally, a floppy fifth toe from previous surgery can be stabilized by syndactyly.
Subluxation & Dislocation of the Metatarsophalangeal Joint
Dorsal subluxation or dislocation of the metatarsophalangeal joint occurs because of weakening of the supporting plantar capsule and collateral ligament structures, which maintain the stability of the metatarsophalangeal joint. Secondary changes such as hammer toe may occur in the toe itself. Pain usually occurs either beneath the metatarsophalangeal joint or over the dorsal aspect of the toe as it strikes the top of the shoe.
The most common cause of a subluxed or dislocated joint is probably a progressive hallux valgus deformity pressing against the second toe. Over time, subluxation and eventual dislocation of the second metatarsophalangeal joint can occur.
A nonspecific synovitis, isolated to the metatarsophalangeal joint and usually involving the second metatarsophalangeal joint, is the next most common cause. The clinical picture is one of generalized swelling about the metatarsophalangeal joint that subsides over a period of 3–6 months, followed by progressive subluxation and eventual dislocation of the joint. Occasionally, subluxation or dislocation of the metatarsophalangeal joint may result from trauma.
Arthritic conditions such as rheumatoid or psoriatic arthritis can cause subluxation or dislocation at multiple joints. Advanced neuromuscular disorders may cause severe subluxation of the metatarsophalangeal joint, but dislocation is unusual.
A variant of this condition results from attenuation of collateral ligaments on one side of the metatarsophalangeal joint. The cause may be idiopathic but occasionally may follow a steroid injection into the area. The metatarsophalangeal joint, instead of subluxing in a dorsalward direction, deviates medially or occasionally laterally, crossing over the adjacent toe. This again is most common in the second metatarsophalangeal joint. When the toe deviates in a medialward direction and crosses over the great toe, the patient may have difficulty wearing shoes.
SYMPTOMS AND SIGNS
Patients complain of pain on the dorsal and plantar aspects of the affected joint. They may note swelling as well and complain of an associated hammer toe or lateral deviation of the toe if present. The degree of deformity is evaluated with the patient in a standing and sitting position. The affected metatarsophalangeal joint is palpated for active synovitis, flexibility of the joint, and degree of subluxation.
The dorsal-plantar stability of the joint is evaluated by holding the proximal phalanx between the examiner's fingers and moving it dorsally and plantarward, similar to a Lachman test of the knee. If a significant hallux valgus deformity is associated with crossover of the second toe on the first toe, the hallux valgus requires evaluation.
The radiographs of the foot reveal the extent of the subluxation or dislocation. The severity of the hallux valgus is evaluated, and changes about the articular surface of the joint are observed. In RA, multiple joint involvement is noted.
Conservative management consists of using a shoe with a wide enough toe box to accommodate the deformity and prescribing a well-molded, soft orthotic device to relieve pressure on the metatarsal head. Unfortunately, this may raise the forefoot, causing impingement on the toe box area of the shoe and some discomfort. A series of cortisone injections into the affected joint may be performed. No more than three injections are given, and at least 1 month is allowed between injections. If the patient cannot be accommodated adequately with these modalities, surgical intervention may be indicated. A significant hallux valgus deformity indicates the need for correction to make a space for second toe correction. Failure to treat both problems results in recurrence.
The subluxed metatarsophalangeal joint with a flexible hammer toe is treated by releasing the dorsal contracture of the extensor tendons and joint capsule, followed by a Girdlestone flexor tendon transfer, as previously described. This technique usually brings the toe into better alignment, although the patient loses some selective voluntary control of the toe, which is usually not of any significance. If a fixed hammer toe is present, a proximal phalanx condylectomy is added to the procedure.
The more severe complete dorsal dislocation of the metatarsophalangeal joint is a difficult surgical problem. In the past it was treated by an aggressive release of the dorsal joint capsule and collateral ligaments and a synovectomy of the metatarsophalangeal joint. The distal third of the metatarsal head is removed to decompress the joint. Accompanying hammer toe procedures are performed to correct the invariably present fixed hammer toe.
A longitudinal K-wire stabilizes the correction for 2 weeks. After pin removal, motion is started at the metatarsophalangeal joint. This procedure results in significant joint stiffness and possible resubluxation of the joint.
An osteotomy of the metatarsal neck is now used to treat dislocated or advanced subluxation of the metatarsophalangeal joint. An oblique osteotomy is performed, starting at the metatarsal neck and aimed proximally at a shallow angle to the metatarsal shaft, creating a long osteotomy site. Once the osteotomy is complete, the metatarsal head is allowed to slide proximally to the appropriate level that will allow the joint to assume a reduced position. The amount of shortening is usually between 4.0 mm and 6.0 mm. The osteotomy is fixed with a single 2.5-mm or smaller diameter cortical screw. Accompanying hammer toe procedures are then performed if necessary. Good short-term results are noted with this procedure without the complication of joint stiffness as occurs with the previously described procedures. Common complications include plantar penetrating hardware and floating-toe deformity (extension contracture of the metatarsophalangeal joint causing the toe not to touch the ground).
Repair of the medially or laterally dislocated metatarsophalangeal joint can be a technically difficult problem. Satisfactory correction can be achieved with one of two techniques. A soft-tissue release of the joint capsule can be performed on the side to which the toe deviates, allowing realignment of the toe. Alternatively, a closing-wedge osteotomy at the base of the proximal phalanx can also achieve good realignment of the toe. Severe deformities can be corrected with an oblique metatarsal neck osteotomy, previously described for treatment of dorsally subluxated metatarsophalangeal joints. The technique is identical, although some soft-tissue balancing may need to be added to the procedure.
REGIONAL ANESTHESIA FOR FOOT & ANKLE DISORDERS
Regional anesthesia is becoming more commonly used because many foot and ankle procedures are performed in the outpatient setting. Most procedures below the ankle can be performed without general anesthesia, eliminating the hazards of central nervous system depression. Pain develops gradually as the anesthesia wears off, and the analgesic requirements of the patient are thereby reduced significantly. Efficacy, safety, and high patient satisfaction are demonstrated.
Digital block is suitable for procedures used in the toes, such as treatment of nail disorders, correction of hammer toe or mallet toe, tendon releases, and some metatarsophalangeal joint procedures.
Short- and longer-term anesthesia is provided by digital block using a 1:1 mixture of 1% lidocaine hydrochloride and 0.25% bupivacaine. A short 25-gauge needle is used to inject approximately 1.5 mL on either side of the toe within the subcutaneous layer between the skin and deeper fascia. The needle is then passed toward the plantar aspect of the toe to anesthetize the digital nerves. Both sides of the toe should be anesthetized. Anesthesia should be administered before the operative site is prepared to allow approximately 15 minutes necessary for the block to take effect before starting a procedure.
Ankle block anesthesia is commonly used for operations on the forefoot and midfoot, such as bunion procedures, neuroma excision, metatarsal osteotomies, and tarsometatarsal fusions. If more than one lesser toe procedure is being performed, an ankle block is preferred to multiple digital blocks. Ankle block anesthesia is not recommended for hindfoot or ankle procedures, such as hindfoot fusions or ankle arthroscopy.
The successful ankle block must anesthetize the posterior tibial nerve, superficial branch of the deep peroneal nerve, sural nerve, saphenous nerve, and superficial peroneal nerve. The posterior tibial nerve requires a larger 3-cm, 22- or 25-gauge needle and approximately 7–10 mL of a 1:1 mixture of 1% lidocaine hydrochloride and 0.25% bupivacaine. The landmark for the posterior tibial nerve behind the malleolus is approximately two finger breadths proximal to the tip of the malleolus and along the medial border of the Achilles tendon (Figure 9–17). The needle is inserted perpendicular to the shaft of the tibia until the posterior cortex of the tibia is palpated with the tip of the needle. The needle is then withdrawn approximately 2 mm. Approximately 5 mL of anesthetic agent is injected into this area after aspiration is done to confirm that the needle is not in a vessel.
To anesthetize the deep peroneal nerve, the site of the injection is located by palpating the extensor hallucis and extensor digitorum longus tendons at the level of the navicular. The deep peroneal nerve lies just lateral to the dorsalis pedis artery. The 25-gauge needle is inserted and advanced to bone and then withdrawn 1–2 mm, aspiration is attempted, and approximately 5 mL of anesthetic is injected.
The saphenous nerve is identified one to two finger breadths proximal to the tip of the medial malleolus and just posterior to the saphenous vein. A 25-gauge needle is inserted and 5 mL of anesthetic injected.
The sural nerve is blocked approximately 1–1.5 cm distal to the tip of the lateral malleolus and can often be palpated in the subcutaneous fat. A 25-gauge needle is inserted and approximately 5 mL of anesthetic injected.
The superficial peroneal nerve branches are blocked starting two finger breadths proximal and anterior to the tip of the lateral malleolus, and the injection is carried out below the subcutaneous veins but above the long extensor tendons in a ring-type block. Approximately 5 mL of anesthetic agent is used. The anesthesia for ankle block takes effect within 15–20 minutes.
The popliteal block is used for major foot or ankle procedures. These include ankle arthrodesis, hindfoot arthrodesis, calcaneal osteotomy, tarsometatarsal arthrodesis, posterior tibial tendon reconstruction, and surgical treatment of calcaneal or ankle fractures. The popliteal block can be placed by the anesthesiologist or surgeon, and it can be used with general anesthesia, sedation, or as the sole anesthetic technique.
The patient is placed in the lateral decubitus position with a pillow between the knees. The landmarks of the popliteal fossa are identified, using the horizontal popliteal skin crease that divides the fossa into superior and inferior quadrants (Figure 9–18). Approximately 7–8 cm superior to the popliteal skin crease and 1 cm lateral to the midline is where the common peroneal branch separates from the tibial branch of the sciatic nerve. A nerve stimulator is set at 3 mA to assist in locating the nerve. When a twitch is found, the stimulator is decreased until there is loss of twitch at 0.8 to 1.0 mA (Figure 9–19). Following aspiration, 30 mL of 0.5% bupivacaine with 1:200,000 epinephrine are slowly injected. The saphenous nerve can be infiltrated with 3–5 mL of 0.5% bupivacaine proximal to the ankle.
Metatarsalgia is a general term for pain arising from the metatarsal head region. The center of pressure during normal gait is initially applied to the heel and progresses along the plantar aspect of the foot. For more than 50% of the stance time, the pressure is concentrated beneath the metatarsal head area. This extended period of pressure can cause bothersome pain. A precise diagnosis is necessary in metatarsalgia to direct treatment toward the specific cause.
Metatarsalgia encompasses a broad spectrum of conditions with various causes arising out of the anatomic structures in the area. It may be associated with abnormalities of the metatarsal head subluxation or dislocation of the metatarsophalangeal joints, systemic diseases, dermatologic lesions, soft-tissue disorders, or iatrogenic causes. Table 9–1 lists the various causes of metatarsalgia and the differential diagnoses that should be considered in evaluating these patients.
SYMPTOMS AND SIGNS
The clinical evaluation begins with a careful history directed toward delineating the precise location of the pain. The physical examination of the foot and lower extremity begins with the patient standing. Any deformities of the toes are noted, such as clawing of the toes, a long second ray, or swelling around any of the joints. The patient should be evaluated for a postural problem of the foot, such as a flat foot or cavus foot. The plantar aspect of the foot is carefully evaluated for evidence of callus formation. The metatarsal heads are palpated individually to assess for generalized plantar fat pad atrophy, a prominent fibular condyle, synovitis, or possibly a transfer lesion beneath a metatarsal head resulting from previous forefoot surgery.
The radiographic evaluation includes weight-bearing anteroposterior, lateral, and oblique views of the foot. Occasionally, the so-called skyline view of the metatarsal heads (obtained with the metatarsophalangeal joints in dorsiflexion) is helpful to evaluate their overall alignment, particularly in cases resulting from previous surgery, by demonstrating the height of the metatarsal heads. MRI can be useful in the diagnosis of metatarsalgia, such as distinguishing among a neuroma, cyst, bursa, or synovitis.
Conservative management is directed at relieving the pressure beneath the area of maximum pain. Initially, the patient must obtain a shoe of appropriate style and adequate size to allow an orthotic device to be inserted. A lace-type shoe with a soft sole material and an adequate toe box is appropriate. High-heeled shoes, loafers, or tight shoes are inappropriate because they have decreased volume for the foot and may cause increased pressure against the involved area. As a general rule, the softer the orthotic device, the more comfortable the patient. A hard acrylic orthotic device is not particularly comfortable for the patient and should usually be avoided.
The surgical management of metatarsalgia depends on the cause and is discussed in different sections of this chapter. In general, pain from a bony prominence can be relieved by a partial ostectomy or osteotomy, dermatologic lesions such as warts can often be burned off with liquid nitrogen or excised, or pain caused by a subluxated metatarsophalangeal joint can be corrected with tendon transfer. The outcome depends on the severity of the problem and the type of surgical intervention required to correct it.
KERATOTIC DISORDERS OF THE PLANTAR SKIN
Friction and pressure over bony prominences, particularly on the plantar skin, can often result in callus formation. Modest callus formation is normal, but more extensive callus formation, particularly on the plantar aspect of the foot, may become symptomatic and occasionally quite disabling.
Many of the intractable plantar keratoses arise from the bony abnormalities presented in Table 9–1.
SYMPTOMS AND SIGNS
A careful history of the problem is extremely important, especially if the patient has had multiple surgical procedures. The patient's activities, type of shoes that exacerbate or relieve the pain, how often the lesion needs to be trimmed, and the type of orthotic devices used are all important. The physical examination, however, is the most important single factor in the diagnosis of intractable plantar keratoses. First, the overall posture of the foot needs to be evaluated to determine whether the condition is the result of a postural abnormality. Specifically, a rigid plantar-flexed first metatarsal could cause a diffuse callus beneath the first metatarsal head, or a hypermobile first ray that fails to support the medial forefoot may result in generalized callus formation beneath the lesser metatarsal heads. Varus posture of the forefoot (the lateral aspect of the foot in greater plantar flexion than the medial aspect) may result in callus formation beneath the fifth metatarsal head.
The nature of the callus itself is important because it helps determine the cause of the problem. A well-localized lesion beneath the metatarsal head is often caused by a prominent fibular condyle on the second or third metatarsal. A diffuse callus is usually associated with a long metatarsal. The callus may have arisen after trauma or surgery in which an adjacent metatarsal was dorsiflexed, thereby increasing the weight-bearing load of the metatarsal. A callus on the bottom of the foot must be differentiated from a plantar wart, which can occasionally mimic a plantar callosity. Shaving the lesion reveals bleeding from end arteries in a plantar wart, whereas a keratotic lesion consists only of hyperkeratotic tissue.
Routine weight-bearing radiographs of the foot are performed and correlated with the clinical findings in evaluation of these patients.
A wide, soft lace-up shoe is recommended, often with the addition of a soft metatarsal support. The orthotic device usually consists of a soft pad (Figure 9–20). It is usually not necessary for an orthotic device to be fabricated early in the treatment of metatarsalgia because the less expensive, commercially available pads are sufficient in most cases.
The surgical management of metatarsalgia depends on the cause of the condition. The following causes of intractable plantar keratoses may respond to surgical intervention.
Localized intractable plantar keratosis beneath a metatarsal head is usually caused by a prominent fibular condyle. It occurs most frequently underneath the second metatarsal but may also be found underneath the third and fourth metatarsals. Surgical treatment is accomplished through a dorsal hockey stick incision over the metatarsophalangeal joint. The toe is plantar flexed to allow removal of 30% of the plantar condyle of the metatarsal head, thereby removing the sharp bony prominence (Figure 9–21). This procedure results in predictable pain relief of the affected toe, although 5–10% of patients develop a transfer lesion beneath the adjacent metatarsal head.
A diffuse callus beneath the second metatarsal that is the result of a dorsiflexed or hypermobile first metatarsal can be treated with dorsiflexion osteotomy done at the base of the second metatarsal. If the lesion is the result of an excessively long metatarsal, it may be shortened to the level of a line drawn between the adjacent metatarsal heads, thereby reestablishing a smooth metatarsal pattern. If the callus is a result of a dislocated metatarsophalangeal joint, the joint must be surgically reduced, using one of the techniques previously described, to alleviate the chronic downward pressure against the metatarsal head. All of these surgical procedures to eliminate a callus are fairly successful, although the possibility of a transfer lesion developing is approximately 5–10%.
Occasionally, a well-localized callus is present beneath the tibial sesamoid, which can be treated surgically by shaving the plantar third of the sesamoid. This alleviates the callus in almost all cases, with the only significant complication being caused by inadvertent disruption of the plantar medial cutaneous nerve during the surgical approach to the sesamoid.
Bunionettes are caused by prominence of the fifth metatarsal head and may lead to metatarsalgia. A diffuse callus beneath the fifth metatarsal head can be treated with a midshaft metatarsal osteotomy to bring it out of its plantar-flexed position, which usually alleviates the condition. It is unusual for a transfer lesion to occur beneath the fourth metatarsal head.
At times, the fifth metatarsal head is too prominent on the lateral aspect of the foot rather than the plantar aspect. In these cases, a chevron osteotomy of the fifth metatarsal head, displacing it in a medialward direction, alleviates the condition (Figure 9–22), sometimes with slight loss of motion of the metatarsophalangeal joint.
A subhallux sesamoid can cause a small callus beneath the interphalangeal joint of the great toe and be quite bothersome to the patient. Surgical excision of the sesamoid is indicated, with good results and little or no disability.
Approximately 22 million people in the United States are diabetic, and foot problems are the most common cause for hospitalization, accounting for 20% of all inpatient days in this population. More than half of all nontraumatic amputations are performed on diabetics. One report showed a 68% incidence of foot disorders in a large diabetic clinic, and the cost of care of these problems approaches $100 million per year. Treatment of the diabetic, who presents with foot problems, can be complex and require a team approach, involving the primary care physician, vascular surgeon, orthopedic surgeon, infectious disease specialist, orthotist, diabetic nurse specialist, and, whenever possible, the patient's family members.
Diabetes is a metabolic disorder that involves all the organ systems. Those of primary interest to the orthopedist are integumentary with the risk of ulceration, neurological with the loss of protective sensation, vascular with diminished perfusion, and immunologic with limited ability to fight infection. The most frequent problem faced by the diabetic is breakdown of the skin of the foot (Figure 9–23). The cause of foot ulcers is multifactorial but stems from diminished sensation resulting from neuropathic disease. Unappreciated local stresses are placed on the skin externally by poorly fitting shoes and internally by skeletal deformity. Autonomic neuropathy causes dry skin and cracks in the dermis, which may become portals of entry for infection. Reactive hyperemia, which normally helps clear infections, is blunted by autonomic neuropathy. Motor neuropathy affects the intrinsic muscles of the foot and may lead to clawtoe deformities with metatarsal heads and proximal interphalangeal joints becoming prominent and predisposed to ulcerations. (Figure 9–24). Hyperglycemia can impair wound healing strength as well as damage vascular endothelium, which is a precursor to atherosclerosis and leads to diminished extremity blood flow and limited healing potential. Elevated blood glucose levels over a long period also leads to glycation of the body's proteins and is commonly measured by the hemoglobin A1c. Glucose covalently binds to lycine in proteins in a reversible process. It is believed that the addition of glucose molecules changes the flexibility of tissues, especially fibrous tissue, making tissues such as skin less able to handle shear stresses. The neuropathy in diabetics is caused by the loss of myelinated and unmyelinated nerve fibers. Other factors that affect healing in diabetics include nutritional deficiencies, diminished microcirculation, and lowered resistance to infection.
When a diabetic patient presents to an orthopedist, the four areas of impact are ulcers and their prevention, amputations, Charcot arthropathy, and toenail abnormalities. With an infected foot ulceration, it is essential to obtain a history that will help delineate why the ulcer occurred and how to optimize the patient's healing potential. A past history of foot surgery is sought, previous or current antibiotic usage is detailed, and any recent trauma to the foot is noted. A history is taken about the severity of the patient's diabetes, including how long ago the diabetes was diagnosed, whether the patient is taking insulin, the recent level of control, what other organ systems are involved, and the degree of neuropathy present in the patient's feet.
Examination of the diabetic patient should begin with inspection of the shoe for internal and external wear patterns. The leg and foot are inspected for overall appearance of the skin, hair growth, perfusion, pulses, and color.
Any bony prominences are recognized as areas of potential skin breakdown. The most common prominences are located at the apex of deformities. Neurologic examination should test for the presence of protective sensation, as defined by the patient's ability to feel the 10-g Semmes-Weinstein monofilament as well as motor function. Ulcers should be carefully documented and evaluated for evidence of infection in the adjacent soft tissues. Wounds should be measured for length, width, and depth as well as documenting their location. Open wounds should be probed with a sterile cotton swab or other appropriate instrument to evaluate the extent of involvement of deeper structures, such as tendons, joints, and bone. A positive probe-to-bone test usually indicates the presence of osteomyelitis.
Vascular evaluation is essential to ensure that the patient has adequate perfusion to allow healing. The patients with palpable pedal pulses and normal capillary filling have adequate blood supply and usually do not require further vascular evaluation. For those patients with less perfusion, one method of assessing the overall potential for healing of foot lesions is the ischemic index, obtained by dividing the blood pressure measurement in the brachial artery by that in the dorsalis pedis and posterior tibial arteries, as measured by Doppler ultrasound with a calf cuff. If the index is 0.45 or greater, there is a 90% chance that a foot ulcer will heal. Lower indexes are an indication for a vascular surgery consultation. It must be kept in mind, however, that falsely elevated values of blood pressure in the foot may result from calcification of major blood vessels. Thus, apparent vascular insufficiency in the light of an adequate ischemic index also warrants a vascular surgery consultation. A laser Doppler study can also be beneficial in assessing local skin perfusion. This information can be used to help predict the patient's response to surgical intervention.
Radiographic studies should include weight-bearing radiographs of both feet and ankles as indicated. Plain radiographs can help identify bony prominences that predispose the patient to ulcer formation, and osteomyelitis or changes consistent with a neuropathic foot may be identified. Early Charcot (neuropathic) joint changes may be difficult to differentiate from osteomyelitis. The four D's of neuropathic joints are helpful in delineating more advanced cases: debris, destruction, dislocation, and densification.
The presence of bony infection may be delineated on serial radiographs as progressive osteolysis, realizing that changes on plain films are late findings and suggesting the infection was present for weeks. A technetium bone scan is sensitive in detecting early osteomyelitis but quite nonspecific. MRI can demonstrate bone and soft-tissue changes, such as edema or the extent of an abscess cavity, and can be helpful in distinguishing Charcot changes from osteomyelitis.
Classification & Treatment of Diabetic Foot Ulcers
The Rancho Los Amigos Hospital classification of diabetic foot ulcers (Figure 9–25) is based on the depth of tissue affected and extent of the foot involved. Treatment choice depends on the grade of ulcer (Figure 9–26). Table 9–2 shows treatment based on classification of foot ulcers.
As a general rule in treating infections of the foot, a balance must be struck between salvage of tissue and foot function. A healed amputation at a more proximal level is more advantageous to the patient than leaving a marginally viable area of the foot that requires constant wound care.
Large wounds heal slowly with the risk of secondary infection, and if possible, they should not be left to heal by secondary intention. Split-thickness skin grafts, especially on the sole of the foot or over an amputation site, are prone to breakdown.
SURGICAL TREATMENT FOR RELIEVING BONY PROMINENCES
As previously stated, a major goal of treatment in the ulcerated or at-risk foot is to relieve bony prominences that cause pressure on the skin. Treatment consists of measures to relieve the pressure. Many appropriate measures are available to relieve pressure on the skin from the outside. Examples include extradepth shoes for clawtoes and accommodative foot orthoses with metatarsal pads to relieve pressure under a prominent metatarsal head. If these measures fail or are inappropriate, the pressure should be relieved from the inside by correcting the bony deformity. These prominences are located at several common sites.
The hallux may have a prominence beneath the metatarsal head, on the plantar-medial aspect of the interphalangeal joint, or over the median eminence secondary to a bunion deformity (Figure 9–27). A prominence caused by the medial sesamoid can be relieved by complete or partial removal of the sesamoid. If this does not relieve the prominence adequately, a dorsiflexion osteotomy or resection of the metatarsal head can be performed. Ulcers found over the plantarmedial aspect of the interphalangeal joint can often be relieved by simple excision of the prominent medial condyles or by resection of the entire joint. A prominence over the median eminence can be addressed with a routine bunion procedure.
The diabetic patient is subject to clawtoe deformities resulting from motor neuropathy, causing prominences under the metatarsal heads and over the dorsum of the proximal interphalangeal joints. Depending on the severity, treatment varies from reduction of the metatarsophalangeal joints and proximal interphalangeal arthroplasties to resection of the metatarsal heads and interphalangeal fusions.
A collapsed longitudinal arch from Charcot changes causes the classic rocker-bottom foot with prominences along the plantar and medial aspects of the midfoot. This can be addressed with a simple exostectomy for a mild deformity, or an appropriate osteotomy and arthrodesis for a more complex deformity.
TREATMENT OF OSTEOMYELITIS
Osteomyelitis is a common complication present in a grade 3 diabetic foot ulcer. The infection is seldom eradicated without surgical debridement of the bone. Frequently, more radical treatment than simple exostectomy is required. For example, infection of a proximal phalanx is usually treated by resection of the phalanx. Osteomyelitis of the metatarsal may require ray amputation if more than just the head is involved. If multiple metatarsals are infected, a transmetatarsal amputation is often the best treatment with the reminder to always consider lengthening the tendo Achilles to decrease load on the residual forefoot.
Osteomyelitis of the midfoot is a complication of a collapsed Charcot foot. The treatment options for such an infection include wide local debridement with exostectomy or a more proximal amputation. Similarly, osteomyelitis of the calcaneus can be treated with a partial calcanectomy or a more proximal amputation.
Treatment of ulcers should make sense. A patient with a superficial wound with good blood supply, minimal infection, and protective sensation would be treated with topical wound care, a shoe to accommodate the dressing, and limited activity to control swelling. A patient with an infected deep wound with osteomyelitis and nonreconstructable dysvascularity would probably be best served with early amputation. Of course, each patient is unique and deserves an evaluation of all organ systems to develop an appropriate treatment plan.
Wound dressings should try to mimic skin. They should try to provide a healing environment that is bacteria free, warm, moist, strain free, nontoxic, and well oxygenated. There is nothing that will provide all of these. Dressings should be chosen based on the needs of the wound, possibly needing infection control and debridement in the initial phases but later only requiring protection and absorption of wound drainage. The gold standard for treating plantar ulcers is a total contact or healing cast. This protective cast provides wound protection, edema control, and a moist environment, and it decreases plantar loading to the ulcer. When the wound is draining, the cast does require frequent changing or the odor can be intolerable.
Biological wound healing products that provide wound healing factors can be helpful in the patient with marginal healing potential. Larger wounds, especially those with considerable drainage, can benefit from vacuum-assisted closure where a constant negative suction pressure is applied to a sealed wound, thereby decreasing its size and pulling away wound drainage.
A small number of patients who are marginal wound healers benefit from hyperbaric oxygen treatment. When placed at 2 atm of pure oxygen, the serum becomes supersaturated and benefits some patients who receive serial treatments.
A Charcot joint is also referred to as a neuropathic, neurotrophic, or neuroarthropathic joint. Diabetes is by far the leading cause of Charcot joints. A Charcot foot is characterized by destruction of joint surfaces, fractures often accompanied by dislocations of one or more joints in a patient with an inappropriate pain response (Figure 9–28).The requirements are an active patient who has neuropathy and adequate blood supply. The pathophysiology is not fully understood, but there are two theories. The neurotraumatic theory claims that cumulative mechanical strains in a patient with inadequate sensory protection leads to stress fractures that are progressive because the patient does not have adequate sensory feedback to limit his or her activity. The neurovascular theory suggests there is a neurally initiated vascular reflex that leads to juxtaarticular osteopenia weakening the bone in this area while glycation of the joint capsule causes stiffness. These factors when combined with mechanical stress can lead to the fracture dislocations commonly seen.
Eichenholtz defined three stages in Charcot arthropathy. Stage 1 is the acute inflammatory phase where there is swelling, redness, and increased warmth. Radiographs likely show fractures and dislocations and the involved area is unstable. The concern in this stage is to rule out infection. If the patient is neuropathic with good blood supply and has an acute, red, hot, swollen foot without an ulcer or a history of an ulcer in that area, it is probably Charcot arthropathy and not infection. Hematogenous osteomyelitis is very rare; infections in the foot are usually introduced locally through the skin. Stage 2 is the subacute phase where there are signs of healing, less swelling, warmth, and radiographic signs of new bone formation. Stage 3 is the chronic phase with consolidation and resolution of inflammation. Typical locations include the midfoot with the creation of the rocker-bottom foot deformity as the arch collapses, the hindfoot, and the ankle with the risk of collapse into varus or valgus that can lead to ulcerization.
Principles of Treatment
There are several important principles to follow in the treatment of Charcot joints. The primary goal is to limit joint destruction and preserve a stable plantigrade foot that protects the soft tissues and prevents ulceration.
Treatment of Acute Phase
For a patient who presents in the acute phase of Charcot joint, the initial treatment should be immobilization and elevation of the foot. This can best be achieved with a non–weight-bearing total contact cast for those patients who can be placed in a plantigrade position. The skin must be checked at weekly intervals initially to look for breakdown. Surgery is rarely attempted on the acute Charcot foot, unless necessitated by the inability to obtain a stable plantigrade position. Even in those patients who require acute stabilization to obtain a plantigrade foot, it is best to allow the swelling and inflammation to diminish by offloading and immobilization prior to surgical intervention. Once the acute phase subsides and the fractures heal, immobilization can be accomplished by means of an ankle-foot orthosis (AFO) or other appropriate removable support. Custom-made shoes can then be fitted to accommodate for the bony prominences.
Treatment of Subacute Phase
In this phase the foot has stabilized, and there is no ongoing bony destruction. Operations address the bony prominences that were created by Charcot destruction and collapse. Simple removal of a prominence is often all that is required, and, sometimes, fusion of one or several joints is necessary. One of the most common foot deformities is a collapsed arch and rocker-bottom deformity from subluxation of multiple joints in the midfoot. An exostectomy of the prominent bones on the plantar aspect of the midfoot usually is sufficient. Alternatively, an osteotomy and arthrodesis of the midfoot can be performed to realign the foot and reconstitute the arch in cases where a simple exostectomy is inadequate (Figure 9–29). This procedure has a high complication rate and an extended time to achieve union. In the case of Charcot involvement of the ankle joint, the goal is a stable and plantigrade foot, which often requires arthrodesis. Retrograde intramedullary nailing is successful in achieving union but also has significant complication rates.
DISORDERS OF THE TOENAILS
Toenail problems in younger (less than 20 years) patients usually involve trauma, such as stubbing the toe or, more frequently, improper nail care, which can contribute to ingrown toenails. This is usually the result of tearing off a toenail, which leaves the nail too short and predisposes it to become ingrown.
Toenail problems in the older age group are more varied, including an incurvating nail, a thickened hypertrophied nail associated with a chronic fungal infection, an ingrown nail resulting from improper nail cutting, and on rare occasions a subungual exostosis.
The anatomy of the toenail is demonstrated in Figure 9–30. The nail unit consists of four components: the proximal nail fold, the nail matrix, the nail bed, and the hyponychium. The area in which most of the problems occur is the lateral or medial nail groove, where an ingrown nail occurs at the level of the nail bed or hyponychium.
SYMPTOMS AND SIGNS
The history of most nail problems is not complex and usually quickly defines the nature of the problem.
Infection of the Toenails
Infection of the toenails usually begins slowly, with erythema and swelling along the margin of the nail, followed by increasing pain and drainage, and finally the development of granulation tissue, usually in response to the foreign body reaction of the nail itself.
In the case of the mycotic (fungal) nail, there is usually a long, slow history of development of deformation of the nail, often with medial or lateral deviation of the nail, marked hypertrophy, and increased pain when wearing shoes. At times, an incurvated nail condition develops in which one or both edges of the nail slowly curve inward, resulting in pinching of the nail plate. This may cause a localized infection, or just the sheer pressure of the nail against the skin may be the cause of the pain. Medical therapy is based on direct microscopy (KOH [potassium hydroxide]) and culture studies.
The patient who develops subungual exostosis usually notes pain evolving beneath the toenail over a long period. Erosion of the nail from below occurs because of the pressure of the exostosis against the nail itself. The patient often does not seek help until there is actual breakdown of the tissue, giving rise to a rather ugly-appearing lesion that seems much more ominous than the condition itself.
Radiographs are necessary when evaluating a toenail problem for subungual exostosis, which is clearly seen with a lateral view. In patients with long-standing infected ingrown toenails, a radiograph can be important to rule out underlying osteomyelitis.
Chronic Ingrown Toenail
For the chronic ingrown toenail, the margin of the nail is removed to relieve the pressure of the nail against the skin. This procedure, along with local care and occasionally systemic antibiotics, usually permits the condition to resolve. It is important, however, to explain to the patient the necessity of permitting the nail to grow out over the ungual labia, to depress it and prevent the ingrown nail from recurring.
Chronic Onychophosis of the Nail
Chronic onychophosis of the nail must be kept debrided. If an ingrown nail occurs, the margins must be trimmed to relieve the pressure against the skin.
Subungual exostosis that is symptomatic is treated by excision.
The surgical management of the recurrent ingrown toenail consists of the Winograd procedure, in which the medial or lateral margin of the offending nail plate is removed along with the underlying nail matrix. The nail matrix is removed as thoroughly as possible to prevent the possible growth of a nail horn, which occurs in approximately 5% of cases. The nail matrix can be removed by sharp dissection or ablated with a laser or treated with phenol to kill the nail matrix.
If chronic infections has caused severe distortion of the nail, the nail and the nail bed can be removed in their entirety. This usually results in a horny base where the nail existed, often a satisfactory outcome. The terminal Syme amputation can be carried out to eliminate the nail and matrix completely (Figure 9–31). Although results are usually satisfactory, some patients do not like the appearance of the toe or absence of the toenail because of its somewhat bulbous appearance. The terminal Syme procedure can be carried out under digital block in most patients. An elliptical incision is made over the distal end of the toe, removing the nail and its matrix in their entirety. The distal portion of the distal phalanx is removed and the edges smoothed, thus shortening the toe. The tip of the toe is defatted and loosely sutured. In this manner, the nail is completely removed and soft tissue covers the area of the former nail bed. The only significant complication associated with this procedure is the regrowth of some nail matrix beneath the healed flap, which results in an inclusion cyst that must be drained and the residual nail matrix excised.
Surgical management of subungual exostosis requires lifting the nail, identification of the exostosis, and complete removal of the exostosis and its stalk. The dissection must be carefully carried out and the entire exostosis removed to prevent recurrence. The nail bed is repaired to cover the defect.
NEUROLOGIC DISORDERS OF THE FOOT
Interdigital Neuroma (Morton Neuroma)
An interdigital neuroma is a painful affliction involving the plantar aspect of the forefoot. It usually involves the third interspace and is characterized by a well-localized area of pain on the plantar aspect of the foot that radiates into the web space. The symptoms are usually aggravated by ambulation and relieved by rest. As a rule, wearing a tight-fitting shoe aggravates the pain, and walking barefoot often relieves it.
The precise cause of interdigital neuroma is not determined. It occurs in women approximately 10 times more frequently than men, and, as a result, high-fashion shoe wear is implicated. Several studies demonstrate that the changes in the nerve appear to occur just distal to the transverse metatarsal ligament. This finding has given rise to the hypothesis that the neuroma results from the constant traction of the nerve against the ligament as the toes are brought into a dorsiflexed position, a theory that explains the higher incidence in women wearing high-heeled shoes. Although this condition is called interdigital neuroma, it is not a true neuroma. The pathologic changes involve actual degeneration of the nerve fibers associated with deposition of amorphous eosinophilic material that is felt to be consistent with an entrapment neuropathy (Figure 9–32).
SYMPTOMS AND SIGNS
Patients with an interspace neuroma usually present with a complaint of localized pain in the metatarsal head region that is increased by walking and relieved by rest and by removing the shoe. Palpation of the involved interspace produces sharp pain that often radiates into the toes. There can be a palpable mass, and squeezing the forefoot, thereby narrowing the intermetatarsal space while compressing the mass, often reproduces the patient's symptoms. If this maneuver produces a snapping sensation, it is referred to as a Mulder click. The third interspace is more frequently involved than the second, and it is extremely rare to have involvement of the first or fourth web space. Pain over the metatarsophalangeal joint itself is caused by disease involving the metatarsophalangeal joint, and pain in the interspace must be distinguished from pain associated with pathology in the metatarsophalangeal joint. The differential diagnosis of metatarsalgia includes avascular necrosis (Freiberg disease), synovitis caused by mechanical instability, synovial cysts, or even referred pain from tarsal tunnel compression or lumbar disk disease.
Radiographs are not helpful in the diagnosis of an interdigital neuroma but may reveal pathology at the metatarsophalangeal joint as the cause of the patient's symptoms. There are several reports regarding the use of ultrasound to evaluate the presence of nerve enlargement, but this is very user dependent. MRI can be used effectively but is rarely necessary.
Conservative management begins with wearing a wider soft-soled shoe to accommodate the foot without mediolateral compression and lowering the heel. A soft metatarsal support is placed in the shoe proximal to the area of the neuroma, thereby spreading the metatarsal heads and lifting them. Approximately a third of patients respond to this treatment. Steroid injection into the web space can be helpful in resolving the symptoms but is not without the hazard of local fat atrophy, which can lead to diminished padding under the metatarsal heads or local skin thinning and discoloration.
Surgical excision of the nerve is indicated if conservative treatment fails. A dorsal incision is made in the midline of the involved web space and carried down to the transverse metatarsal ligament, which is cut. The nerve is noted to lie just beneath the transverse metatarsal ligament. A quite thickened nerve is reassuring evidence that the correct diagnosis was made; however, a nerve of normal thickness should still be removed if the clinical diagnosis of neuroma was made from other evidence. The nerve is delivered into the interspace by plantar pressure and freed up distally and proximally, transected proximal to the metatarsal head, and then dissected out distally, where it is cut just past its bifurcation. Care is taken not to disrupt the surrounding fatty tissue or intrinsic muscles. A compression dressing is used for 3 weeks after routine wound closure, and ambulation is permitted in a postoperative shoe. Decreased sensation in the toes on either side of the web space is expected postoperatively. Approximately 80% of patients are totally satisfied with the results of the procedure; 20% obtain little or no relief. The precise cause of this failure rate is a bit of an enigma. Obviously in some patients, the diagnosis was made incorrectly, and the metatarsophalangeal joint was actually involved.
A recurrent neuroma is indeed a true surgical bulb neuroma that resulted following the transection of the common digital nerve on the plantar aspect of the foot. True neuritic symptoms occur in some cases in which transection was not proximal enough or the nerve became adherent and trapped beneath the metatarsal head. Careful percussion of the plantar aspect to elicit the Tinel sign can frequently localize the cut end of the nerve (bulb neuroma). If the severed nerve can be clinically well localized, reexploration for the neuroma is carried out either through a dorsal or plantar approach. The neuroma is identified and transected to a more proximal level or implanted into muscle, and symptoms are relieved in 60–70% of patients.
Tarsal Tunnel Syndrome
Tarsal tunnel syndrome is a compressive or traction neuropathy of the posterior tibial nerve as it passes behind the medial malleolus. The tarsal tunnel is formed by the fibroosseous tunnel resulting from the flexor retinaculum as it wraps around the posterior aspect of the medial malleolus (Figure 9–33). Tarsal tunnel syndrome causes poorly localized dysesthesias on the plantar aspect of the foot. The symptom complex is often aggravated by activity and relieved by rest. Some patients complain mainly of nocturnal dysesthesias.
Tarsal tunnel syndrome may arise from a space-occupying lesion within the tarsal tunnel (eg, a ganglion, synovial cyst, or lipoma) or distally against one of the two terminal branches: the medial or lateral plantar nerve. It occasionally follows severe trauma to the lower extremity, probably because of edema or scarring. Other causes are severe venous varicosities, tenosynovitis, or a tumor within the nerve. Traction neuropathy can occur in those patients who have an excessively valgus hindfoot position, especially those that are unstable. As the patient walks, the posterior tibial nerve is subjected to stretching as it courses around the convex side of the deformity. In more than half of the cases, however, the precise cause cannot be determined.
SYMPTOMS AND SIGNS
The diagnosis is entertained after obtaining a history of paresthesias or burning in the posterior tibial nerve distribution. Careful evaluation of the patient in the standing and sitting positions is necessary to check posture and increased fullness, thickening, or swelling in the involved tarsal tunnel area. Careful percussion may elicit a Tinel sign over the posterior tibial nerve in the tarsal tunnel or distally along the divisions of the posterior tibial nerve (the medial calcaneal nerve and medial and lateral plantar nerves). Muscle weakness is usually not observed, but loss of sensation and two-point discrimination may be occasionally detected.
Electrodiagnostic studies should be carried out to help confirm the diagnosis of tarsal tunnel syndrome. Nerve conduction velocities along the medial plantar nerve to the abductor hallucis muscle (latency less than 6.2 ms) and of the lateral plantar nerve to the abductor digiti quinti (latency usually less than 7 ms) should be within 1 ms of each other, otherwise indicating nerve compression in the tarsal tunnel. Motor-evoked potentials that demonstrate a decreased amplitude and increased duration are also indicative of tarsal tunnel syndrome. The most accurate study for tarsal tunnel syndrome appears to be sensory nerve conduction velocity, although this is also the least reproducible study.
The definitive diagnosis of tarsal tunnel syndrome should be based on (1) the clinical history of ill-defined burning, tingling pain in the plantar aspect of the foot, (2) positive physical findings of Tinel sign along the course of the nerve, and (3) electrodiagnostic studies. If all three factors are not positive, the diagnosis of tarsal tunnel syndrome should be suspect. MRI may be quite useful in demonstrating the presence of a space-occupying lesion.
The tarsal tunnel syndrome should be managed with NSAIDs and an occasional steroid injection into the tarsal tunnel area. Aspiration and injection of a cyst or ganglion may be attempted but is rarely successful. Immobilization in a polypropylene AFO may also be useful, especially in the patient with unstable valgus.
Surgical intervention can be considered if conservative management fails. Approximately 75% of patients operated on for tarsal tunnel syndrome are satisfied with the result. The other 25% may continue to have varying degrees of discomfort. The surgical release uses an incision behind the medial malleolus that is carried distally to about the level of the talonavicular joint. The investing retinaculum is exposed and released. The posterior tibial nerve is identified proximal to the tarsal tunnel area and carefully traced distally behind the medial malleolus. The division into its three terminal branches is identified. Because the medial calcaneal branch passes from the posterior aspect of the lateral plantar nerve, the dissection should be carried out along its dorsal aspect. There may be one or more medial calcaneal branches. The medial plantar nerve should be traced distally until it passes through the fibroosseous tunnel in the abductor hallucis muscle. The lateral plantar nerve should be traced behind the abductor hallucis muscle until it passes toward the lateral aspect of the foot. A preoperative Tinel sign distal to the tarsal tunnel area requires that the area be carefully explored to determine whether there is a ganglion or cyst within the tendon sheath as a cause of the tarsal tunnel syndrome.
Postoperatively, a compression dressing is applied and weight bearing is prohibited for 3 weeks, before progressive ambulation is permitted.
The results following tarsal tunnel release depend on the pathology found at the time of surgery. Removal of a space-occupying lesion usually relieves all of the symptoms. Involvement of a single nerve branch, such as the medial or lateral plantar nerve, also portends good results after surgery. If more diffuse pain is felt throughout the foot before surgery and no definite constriction on the nerve is found at exploration, only one half to two thirds of patients can be expected to experience pain relief. Patients with traction neuropathy caused by the unstable valgus foot are treated by correction of the instability, usually with arthrodesis, and not with soft tissue tarsal tunnel release.
Traumatic Neuromas About the Foot
A traumatic neuroma about the foot presents a difficult problem in management because footwear can cause constant irritation of the neuroma. The most frequent cause of traumatic neuroma in the foot is previous surgery. Despite caution in making incisions about the foot, many lesser and occasionally major nerve trunks can be injured. The dorsal aspect of the foot is most frequently involved (Figure 9–34).
The clinical evaluation begins with a careful history of the problem and an evaluation of the area involved to determine the precise location of the neuroma, which is essential for proper treatment. Rarely is any type of electrodiagnostic study indicated, and radiographs are not usually necessary.
Attempts to relieve pressure on the neuroma with a large shoe or a carefully designed pad may be of benefit. A cortisone injection into the area occasionally may help, particularly when a small nerve is involved. Surgical intervention is indicated if conservative measures fail.
Careful planning must be undertaken prior to the excision of a traumatic neuroma. The exact location of the neuroma and the area of sensitivity proximal to it must be determined. The incision must be made as precisely as possible to identify the neuroma and trace the nerve proximally into an area that would not be affected by pressure from shoes and boots. The neuroma is excised, leaving enough nerve to bring the cut end into an area of minimal pressure. The cut end is buried into an excavation in bone, if possible, or beneath a muscle such as the extensor digitorum brevis muscle. When carrying out a resection of the sural nerve, it is important, particularly in an individual who wears heavy work boots, that the end of the nerve is brought proximally enough so the top of the boot will not press on the nerve, resulting in continued symptoms.
The results following resection of a traumatic neuroma are quite variable. Initial relief from removing the traumatic neuroma is routine, but unless the nerve is buried where it will not be exposed to pressure, the symptoms may recur in time. It is therefore preferable to bury the end of the nerve into bone, if possible. Resection of most neuromas accentuate a sensory deficit, which is usually not a significant clinical problem.
Entrapment of the Superficial Branch of the Deep Peroneal Nerve
Osteophyte formation at the talonavicular or metatarsocuneiform joint may entrap the superficial branch of the deep peroneal nerve as it passes beneath the extensor retinaculum. Patient complaints are of dysesthesias on the foot or difficulty in wearing shoes, depending on the location of the entrapment.
The superficial branch of the deep peroneal nerve passes onto the dorsum of the foot between the extensor hallucis longus and extensor digitorum longus tendons. It continues beneath the extensor retinaculum, coursing along the dorsal surface of the talus and navicular and more distally across the metatarsocuneiform joints. Osteophyte formation at any point along the course of the nerve may cause sufficient pressure against the nerve to cause an entrapment problem.
SYMPTOMS AND SIGNS
The clinical evaluation begins with a careful history regarding the patient's complaint of dysesthesias over the dorsum of the foot. The physical examination demonstrates tingling along the course of the superficial branch of the deep peroneal nerve, which radiates into the first web space. Often the precise location of the nerve entrapment can be identified by careful palpation and by rolling the nerve across the involved bony prominence.
Radiographs usually reveal the offending osteophytes, often along the area of the talonavicular or metatarsocuneiform joints. Placing a radiographic marker at the area of maximum tenderness can help identify the offending bony prominence.
Conservative management consists of attempting to keep the pressure off the involved area, either by padding the tongue of the shoe or by trying to create a pad that will not put pressure directly on the nerve. If these measures fail, decompression of the nerve usually brings about satisfactory resolution of the condition.
Depending on the area of entrapment (talonavicular or metatarsocuneiform), a slightly curved incision is made and carried down through the retinaculum to expose the nerve. Great caution must be taken during the approach so the nerve is not inadvertently damaged. The nerve is carefully lifted off of its bed, exposing the osteophytes, which are removed with a rongeur. The bone surfaces are coated with bone wax prior to laying the nerve back on its bed. After wound closure in layers, the foot is immobilized for approximately 3 weeks in a postoperative shoe.
The results following release of the superficial portion of the deep peroneal nerve are usually satisfactory. Because the nerve itself usually is not damaged by the entrapment, a favorable outcome is expected.
The foot is involved in 90% of patients with long-standing RA, and the involvement is almost always bilateral. The forefoot is most commonly involved, and these joints are often the first joints to be affected, but deterioration of the subtalar joint is noted in approximately 35% of patients and of the ankle joint in approximately 30%.
The changes in the forefoot are caused by chronic synovitis, which destroys the supporting structures about the metatarsophalangeal joints. The joint capsules are distended and the ligaments destroyed. When these structures no longer function to provide stability for the joint, progressive dorsal subluxation and eventual dislocation of the metatarsophalangeal joints occur. As the metatarsophalangeal joints progress from subluxation to dislocation, the plantar fat pad is drawn distally, and the base of the proximal phalanx eventually comes to rest on the metatarsal head. Thus, the metatarsals are forced into a position of plantar flexion, which results in significant callus formation beneath the metatarsal heads. The changes at the metatarsophalangeal joints result in imbalance of the intrinsic muscles, and severe hammer toe and clawtoe deformities usually result.
Significant midfoot and hindfoot pathology is also found in patients with RA. A severely flattened longitudinal arch can result from long-standing subtalar joint involvement with subluxation. Pain with less severe deformity is present in isolated talonavicular involvement of the midfoot.
SYMPTOMS AND SIGNS
The clinical evaluation of the rheumatoid patient begins with a careful history of the disease and the medications the patient is taking and an attempt to ascertain whether the disease process is currently in an active or a quiescent stage. It is important to obtain some indication of the patient's wound-healing capacity in the foot or elsewhere in the body.
The vascular status of the foot and quality of the skin is noted. The feet are assessed with the patient standing, which often demonstrates marked deformities of multiple joints or localized involvement of only one or two joints. The patient is then seated and a careful evaluation of all the joints about the foot and ankle is carried out to determine precisely the degree to which they are affected. Careful palpation of the metatarsophalangeal joints often demonstrates the degree of the synovial activity as well as the degree of stability of the joints. The plantar aspect of the foot is inspected for the callus formation and past or present ulcerations. Flattening of the longitudinal arch and any hindfoot valgus are evaluated with a careful assessment of joint stability to determine the risk of deformity progression.
Radiographs help assess the number of joints involved and the degree of involvement. Bilateral involvement is frequently asymmetric. Standing radiographs are beneficial in assessing the effect of joint stability on the severity of deformity.
Conservative management includes medical management, carried out by the patient's rheumatologist. The patient with sufficient deformity should wear an extra-depth shoe with a soft accommodative liner to reduce pressure on the metatarsal heads and the toes, which may be severely contracted dorsally. Frequently, the patient is quite comfortable in this shoe and does not require further treatment. With significant hindfoot involvement, an AFO may be required to help relieve pain by providing adequate stabilization.
The main goal of surgical management of the forefoot is to create a stable foot that will alleviate the pain beneath the metatarsal head region (Figure 9–35). Arthrodesis of the first metatarsophalangeal joint is the procedure most commonly used, with the joint placed in approximately 15 degrees of dorsiflexion in relation to the floor and approximately 15 degrees of valgus position. The lesser metatarsophalangeal joints are corrected by release of the soft-tissue contracture and resection arthroplasty. The metatarsal heads are excised to decompress the metatarsophalangeal joints, and the fat pad is brought back down onto the plantar aspect of the foot by realigning and securing the plantar plates of the joints under the residual metatarsals. The hammer toes can be corrected by closed osteoclasis, which often results in satisfactory realignment. Open hammer toe procedures are also very effective in correcting residual deformities. The toes and metatarsophalangeal joint area are stabilized with longitudinal K-wires postoperatively for approximately 4 weeks.
The results of this rheumatoid forefoot repair are most gratifying in that approximately 90% of patients are satisfied with the results. There are few complications, although the blood supply to the toes is always of concern because the procedure is extensive. Occasionally, wound healing is delayed, particularly if the patient is taking high dosages of corticosteroids or the antimetabolite drugs.
Hindfoot and ankle disease is usually managed medically unless there is instability and progressive deformity. Orthotic support or bracing can be beneficial, but if the deformity is increasing and the patient's thin skin cannot tolerate further pressure, surgical stabilization with arthrodesis is necessary. If only a single joint is involved with the rheumatoid process, a less extensive procedure is carried out. For isolated talonavicular RA with no significant deformity of the arch, an isolated talonavicular fusion is adequate. If significant deformity is present because of subtalar joint subluxation, a triple arthrodesis is required. Ankle joint involvement is treated with ankle joint fusion or total ankle arthroplasty. The details of the surgical procedures are described elsewhere in this chapter.
Heel pain can be caused by several distinct entities. When evaluating the patient for heel pain, the clinician must attempt to define as precisely as possible the location and hence the cause of the pain.
Table 9–3 presents the causes of heel pain, which are quite variable and need to be carefully defined, so the proper treatment can be chosen.
SYMPTOMS AND SIGNS
The clinical evaluation begins with a careful history of the onset and location of the pain. The patient's activities and types of footwear that aggravate and relieve the pain are discussed. Specific inquiry regarding radiation of pain proximally in the lower extremity may suggest lumbar disk disease as the cause. Patients active in sports should be questioned regarding significant changes in their level of activity because heel pain often is the result of increased stress on the foot. The cause of the patient's heel pain can usually be determined by palpating the area of maximum tenderness.
Plantar fasciitis, the most common cause of plantar heel pain, usually has an area of maximum tenderness along the plantar medial aspect of the heel, which corresponds to the origin of the plantar fascia at the medial calcaneal tuberosity. In most cases the pain is most severe with the first steps upon arising. The pain is usually aggravated by dorsiflexion of the toes, the so-called windlass stretch, because this applies more tension on the damaged plantar fascia.
Achilles tendonitis/tendinosis typically occurs at one of two discrete sites: at the calcaneal insertion or centered 3–4 cm proximal to the insertion. Insertional Achilles tendinitis/tendinosis is characterized by pain and swelling that is increased by activity. There is usually tenderness in the posterior midline with local increased warmth. Noninsertional Achilles tendinitis/tendinosis is usually associated with a thickened tendon and often quite severe pain to palpation of the thickened area in the midportion of the tendon. Both of these are more degenerative than true inflammatory processes and more properly referred to as tendinosis.
Heel pain can also be caused by inflammation of the retrocalcaneal bursa, which sits between the tendo Achilles and the posterior calcaneus and is often associated with the Haglund heel deformity.
Tarsal tunnel syndrome with involvement of the medial calcaneal branches should be investigated by careful percussion of the posterior tibial nerve. Evidence of degenerative disk disease requires careful testing of motor function and sensation more proximally in the calf.
Radiographs may demonstrate calcaneal spur formation or calcification at either the insertion of the Achilles tendon or the origin of the plantar fascia. Alternatively, the posterosuperior aspect of the calcaneus may be too prominent and protrude into the Achilles tendon, a condition known as Haglund disease or Haglund deformity, with the symptoms coming from the inflamed retrocalcaneal bursa. A bone scan sometimes reveals increased activity diffusely about the calcaneus, as may be seen in systemic diseases such as Reiter syndrome or a discrete area of uptake as in a stress fracture. MRI scan may help delineate the degree of the Achilles tendon degeneration present in cases of Achilles tendinosis and can help identify rupture of the tendon if this is in question.
The conservative management of heel pain depends on the specific cause. Because many causes are related to abnormal stress on the foot, the basic principles involve reducing the stress on the involved area. Activity modification, footwear with a softer, more resilient heel, and use of a soft orthotic device under the longitudinal arch to relieve some of the pressure on the region of pain can be helpful. NSAIDs are often useful as is physical therapy to teach stretching exercises of the Achilles tendon and plantar fascia. Plantar fasciitis is treated initially with stretching exercises, soft cushioned heel shoes, NSAIDS if they are tolerated, and avoidance of strong toe-off activities such as running and jumping. The use of a night splint to help keep the Achilles tendon and plantar fascia stretched often relieves the acute pain patients experience when they first get up in the morning. Patients refractory to treatment may benefit from a steroid injection into the plantar fascia origin, although there is a risk of plantar fascia rupture. Cast immobilization also benefits these refractory patients.
In general, the treatment of heel pain is often prolonged, requiring a great deal of patience on the part of the physician and patient. It is important to explain to the patient the nature of the problem and the fact that it is often a chronic condition requiring many months to resolve.
Achilles tendinosis is treated with stretching exercises, activity modification, NSAIDS, and a heel lift. If these modalities are inadequate, bracing or casting provides more strain relief to the damaged tissue.
Patients with plantar fasciitis, in whom symptoms cannot be controlled after 9–12 months of conservative management, may become candidates for surgery. The options include orthotripsy or surgical release of the medial half of the plantar fascial origin. With surgical release, the success rate is approximately 75%. Caution must be exercised with the approach to the medial side of the heel to avoid damage to the medial calcaneal branch of the posterior tibial nerve. Disruption of this nerve causes an area of heel numbness and possibly a troublesome neuroma along the medial side of the heel. An endoscopic approach for plantar fascia release is described in patients who do not have a plantar heel spur that requires removal. Orthotripsy, although less invasive, still has conflicting literature about its effectiveness.
Surgical treatment of Achilles tendinosis is offered if 6–9 months of conservative measures do not help eliminate symptoms. Insertional Achilles tendinosis is treated with debridement of degenerative tendon and excision of bone spurs with repair of the Achilles insertion. If a Haglund deformity is present, it is also resected. Noninsertional Achilles tendinosis is treated with debridement of the degenerative tendon. In either case, if the majority of the tendon is nonviable, it must be repaired, often requiring a graft such as the flexor hallucis longus tendon.
ARTHRODESIS ABOUT THE FOOT & ANKLE
GOALS OF ARTHRODESIS
Arthrodesis is surgical fixation of a joint to obtain fusion of the joint surfaces. Arthrodesis about the foot and ankle can be effective in achieving the following goals:
PRINCIPLES OF ARTHRODESIS
An arthrodesis about the foot and ankle requires adherence to these general principles:
EFFECTS OF ARTHRODESIS ON JOINT MOTION
Following ankle arthrodesis, residual dorsiflexion and plantar flexion movement occurs within the subtalar and transverse tarsal joints, and additional, compensatory motion may develop over time. Arthritic changes in these joints may become symptomatic following ankle arthrodesis, and in time, extension of the fusion may be required.
The subtalar joint and transverse tarsal joints must be viewed as a joint complex similar to the universal joint of a car. Movement in these joints is interrelated. After subtalar arthrodesis, inversion and eversion is lost, but transverse tarsal joint motion is minimally affected. Arthrodesis of the talonavicular joint, however, eliminates most of the subtalar joint motion because rotation must occur around the head of the talus for subtalar motion to occur.
A triple arthrodesis eliminates the subtalar and transverse tarsal joint motion, causing increased stress on the ankle joint and the midtarsal joints distal to the fusion site. A small percentage of patients develop degenerative changes in the ankle joint following triple arthrodesis. It is imperative, therefore, to evaluate the ankle joint carefully prior to carrying out a triple arthrodesis.
Arthrodesis of the tarsometatarsal joints does not significantly affect motion of the foot and ankle, but a certain degree of stiffness is noted through the midtarsal area following this fusion. Fusion of the first metatarsophalangeal joint places added stress on the interphalangeal joint of the great toe, particularly with poor alignment. Although up to 40% of patients may develop degenerative changes in this joint, they are rarely of clinical significance.
DISADVANTAGES OF ARTHRODESIS
Although arthrodesis is an effective reconstructive tool, the resulting loss of motion places increased stress on the surrounding joints, making them more prone to developing arthritis or worsening preexisting degenerative changes. Thus, correction of a problem without arthrodesis is preferable whenever possible, such as with an osteotomy, tendon transfer, or both.
The main indications for ankle arthrodesis are the following:
The surgical approach preferred by the authors is a transfibular approach (Figure 9–36). The incision begins along the fibula, approximately 10 cm proximal to the tip of the fibula, and is carried distally along the shaft of the fibula and then curves toward the base of the fourth metatarsal. In this way, the incision avoids the sural nerve posteriorly and the superficial peroneal nerve dorsally. The flaps created are full thickness, to lessen the possibility of wound-healing problems. The dissection is carried across the anterior aspect of the ankle joint, to the medial malleolus and along the lateral aspect of the neck of the talus. Posteriorly, the fibula and the posterior aspect of the ankle joint are exposed; distally, the subtalar joint and sinus tarsi area are exposed. The fibula is removed approximately 2 cm proximal to the joint, after which the residual cartilage and subchondral bone are removed from the distal tibia (Figure 9–37). This cut should be made as perpendicular as possible to the long axis of the tibia and should extend to the medial malleolus but not through it. The foot is placed into a plantigrade position and a cut made in the dome of the talus parallel to the cut in the tibia, thereby creating two flat surfaces and correcting any malalignment. At this point, the ankle should be aligned in neutral position, insofar as dorsiflexion and plantar flexion are concerned, and at approximately 5 degrees of valgus. The degree of rotation should be equal to that of the opposite extremity, which is usually 5–10 degrees of external rotation. If the two joint surfaces do not easily oppose each other, it is because the medial malleolus is too long, and the malleolus should be exposed through a dorsomedial incision and the distal centimeter removed.
The two flat surfaces should now be in total apposition, with little or no pressure being exerted. Temporary fixation is obtained by inserting two 0.062 K-wires. Interfragmentary compression is gained with at least two 6.5-mm cancellous screws. These screws should be placed to gain adequate interfragmentary compression (Figure 9–38). Following insertion of the screws, there should be rigid fixation of the arthrodesis site. Because the joint surfaces are fully opposed, there is no room for bone grafting. In the immediate postoperative period, a firm compression dressing incorporating plaster splints is applied. After swelling is decreased, a short leg cast is applied and weight bearing is not allowed for 6 weeks. Weight bearing is then allowed with the short leg cast in place for another 6 weeks. Arthrodesis generally occurs following 12 weeks of immobilization.
Nonunion of the ankle joint, although uncommon, does occur. Using the surgical technique described earlier, a fusion rate of 90% can be anticipated. If nonunion occurs, bone grafting and further internal fixation may be required.
Malalignment of the ankle joint with the foot in too much internal rotation is poorly tolerated and often requires revision surgery. Excessive plantar flexion causes a back knee thrust and eventually some knee discomfort; excessive dorsiflexion causes increased stress on the heel (which can usually be treated with adequate padding); varus deformity may cause subtalar joint instability; excessive valgus causes stress on the medial aspect of the knee joint. It is extremely important not to place any pin or screw across the subtalar joint for fear of damaging the posterior facet, which may lead to arthrosis.
Avascular necrosis of the talus requires excision and tibiocalcaneal fusion or a fusion that bypasses the necrotic bone. Bone grafting may also be necessary when attempting to carry out a fusion after a severely comminuted pilon fracture because there are often defects that affect stability because of the previous crushing of cancellous bone.
Total Ankle Arthroplasty
Total ankle arthroplasty is an alternative to ankle arthrodesis for painful arthrosis of the ankle joint. Advantages include maintenance of some ankle joint motion with a more normal gait and thus less stress on adjacent joints. Unfortunately, the procedure is technically difficult with a steep learning curve, there is a higher complication rate than arthrodesis, and the long-term survival rate is unknown. The intermediate-term survival rate of the Agility total ankle reported by Saltzman suggests the outcome is durable in selected patients. Several other prostheses, including the STAR and the HINTEGRA, used primarily in Europe, have reported promising early results. The long-term results are necessary before widespread use is advocated.
The main indications for subtalar arthrodesis are the following:
The incision for subtalar arthrodesis begins at the tip of the fibula and is carried distally toward the base of the fourth metatarsal. As the incision is deepened, the sural nerve or one of its branches should be carefully noted and retracted. Small twigs of nerve may be present that unfortunately may be cut and give rise to a painful neuroma. The sinus tarsi area is exposed by reflecting the extensor digitorum brevis muscle distally. The use of a lamina spreader in the subtalar joint enhances the exposure.
The articular cartilage is removed from the joint surfaces, which include the middle and posterior facets. The bony joint surfaces are then deeply feathered or scaled using a small osteotome. These cuts through the subchondral bone greatly enhance the possibility of fusion. The area around the floor of the sinus tarsi and anterior process region can be carefully shaved to obtain local bone graft for the fusion.
The alignment of the subtalar joint is critical. It must be aligned into approximately 5–7 degrees of valgus position, producing a supple transverse tarsal joint. If it is placed in varus position, the foot is stiff and the patient must walk on the side of the foot.
Rigid fixation of the subtalar joint is achieved by using a 7-mm cannulated interfragmentary screw starting at the posterior tip of the calcaneus and passing into the body or neck of the talus. The guide pin is first placed up into the posterior facet, the subtalar joint is then manipulated into proper alignment, and the guide pin is passed into the talus. The alignment of the screw is verified on radiograph, and the screw is inserted.
Following adequate internal fixation, the local bone graft is packed into the sinus tarsi area. Additional bone may be obtained from the area of the medial malleolus, the proximal tibia, or occasionally the iliac crest, although the latter site significantly adds to the morbidity of the procedure.
Postoperatively, a firm compression dressing incorporating plaster splints is applied. A short leg cast is applied, and weight bearing is not allowed for 6 weeks. The cast is changed, and weight bearing is allowed for another 6 weeks. Twelve weeks of immobilization generally achieves an arthrodesis.
Nonunion of the subtalar joint is uncommon, although it can occur. Careful surgical technique and heavy scaling of the joint surfaces can help prevent this complication. If nonunion occurs, bone grafting and added fixation are required to attempt to achieve a solid union.
Misalignment of the subtalar joint may also be a complication. An excessive valgus deformity following subtalar fusion may result in impingement laterally against the fibula or peroneal tendons. It also causes excessive stress along the medial aspect of the midfoot and occasionally the knee joint. A varus deformity of the subtalar joint imparts rigidity to the transverse tarsal joint, resulting in stiffness of the forefoot. This also increases pressure along the lateral aspect of the foot, particularly in the area of the base of the fifth metatarsal.
The patient with RA or posttraumatic complications may have lateral subluxation of the calcaneus in relation to the talus, which usually requires CT scanning for identification. The calcaneus must be displaced medially during surgery to align it with the lateral aspect of the talus and place it under the tibia in a proper weight-bearing position. If the calcaneus is fused with significant lateral deviation, the abnormal alignment places added stress on the ankle and midfoot region.
Special attention to the peroneal tendons is necessary when a subtalar arthrodesis is done to correct an old calcaneal fracture. Protrusion of the lateral wall of the body of the calcaneus from the healed fracture results in impingement on the peroneal tendons beneath the fibula. This protrusion must be carefully excised when the subtalar fusion is carried out, so the lateral aspect of the talus and calcaneus are in line. Further, the peroneal tendon sheath should be dissected subperiosteally off the calcaneus to provide tendon sheath and protect the peroneal tendons from the raw, bony surface of the calcaneus.
Occasionally a bone block distraction arthrodesis of the subtalar joint is performed in cases of severe deformity after a calcaneus fracture. If the talus assumes a horizontal position because of flattening of Böhler's angle, it can cause limited ankle joint dorsiflexion. Placing a tricortical block of iliac crest into the posterior facet of the subtalar joint helps improve the overall alignment of the hind foot and regain ankle joint dorsiflexion.
Talonavicular arthrodesis is indicated in the following conditions:
The talonavicular joint is approached through a medial or dorsomedial incision that starts in the region of the naviculocuneiform joint and extends to the neck of the talus. The soft tissues are stripped from around the joint and the articular cartilage removed with a curet or curved osteotome. Distraction of the joint by placing a towel clip into the navicular often facilitates exposure and debridement of the joint. Correct alignment of the talonavicular joint is extremely critical because this fusion essentially eliminates motion in the subtalar joint. The fusion position of the subtalar joint is 3–5 degrees of valgus with the forefoot in a plantigrade position (Figure 9–39). After the foot is properly aligned to correspond to the opposite foot, fixation of the joint is carried out. Proper alignment of this joint is particularly critical when treating the laterally subluxed talonavicular joint in the patient with a ruptured posterior tibial tendon. The internal fixation is carried out by using interfragmentary compression with a single large screw (6.5 mm), two smaller screws (4.0 mm), or multiple staples.
Postoperatively the patient is immobilized in a non–weight-bearing cast for 6 weeks followed by a weight-bearing cast for an additional 6 weeks.
The talonavicular joint has a relatively high incidence of nonunion, which is probably the result of the difficulty in exposing the joint. If the joint is also approached medially to gain additional exposure, the surfaces can be well scaled, and the fusion rate should approach 90%.
Complications of nonunion and misalignment are similar to those discussed for subtalar joint fusion.
An isolated talonavicular joint fusion usually produces a satisfactory result, particularly in relatively sedentary patients older than 50 years. In younger, more active individuals with no other affliction (eg, RA), consideration should be given to including the calcaneocuboid joint at the same time to obtain a more stable transverse tarsal joint and enhance the fusion of the talonavicular joint through added stability.
Double Arthrodesis (Calcaneocuboid & Talonavicular Joints)
Double arthrodesis today is a procedure that provides the same degree of stability to the foot as a triple arthrodesis (Figure 9–40). By locking the transverse tarsal joint (calcaneocuboid and talonavicular), further subtalar motion is prevented because these three joints function together. This procedure is also indicated in the younger, active patient in whom an isolated talonavicular fusion is contemplated because it gives added stability to the foot.
Indications for double arthrodesis are as follows:
The talonavicular joint is approached through a medial or dorsomedial incision, as previously described, and the calcaneocuboid joint is approached through the same incision along the lateral side of the foot as described for subtalar fusion. Once these joints are exposed, the joint surfaces are denuded of articular cartilage and the subchondral bone heavily feathered.
The alignment when carrying out a double arthrodesis is extremely critical because once this fusion is achieved, the subtalar joint or the transverse tarsal joint no longer move. Therefore, the foot must be placed into a plantigrade position prior to the fixation of the arthrodesis site. The desired position is 5 degrees of valgus of the calcaneus, neutral abduction and adduction of the transverse tarsal joint, and correction of any forefoot varus that is present. This alignment creates a plantigrade foot. The fixation of the talonavicular joint is done first with the insertion of a screw (6.5 mm) or screws (4 mm) or possibly the use of multiple staples. The calcaneocuboid joint is then fixed the same way. Postoperative care is the same as for other foot fusions.
Complications of nonunion and malalignment are similar to those discussed for subtalar joint fusion.
The triple arthrodesis is a fusion of the talonavicular, calcaneocuboid, and subtalar joints (Figure 9–41). In the past, it was the procedure of choice for all hindfoot problems, before isolated fusions became more accepted. Now, this procedure is still commonly used when limited fusions are inadequate.
Indications for triple arthrodesis are as follows:
The triple arthrodesis is carried out as previously described for subtalar fusion and talonavicular fusion. The foot is fixed after manipulation back into a plantigrade position (3–5 degrees of valgus of the subtalar joint), neutral position as far as abduction and adduction of the transverse tarsal joint, and correction of forefoot varus. Postoperative care is the same as for subtalar fusion.
The main complication is failure of fusion of one of the joints, which is uncommon, because the successful fusion rate exceeds 90%. The talonavicular joint is most likely to have nonunion. Malalignment of the foot or forefoot may require revision and technically is a difficult procedure. The sural nerve may become entrapped or disrupted through the lateral approach.
Arthrodesis in the tarsometatarsal area may involve a single tarsometatarsal joint, usually the first joint, or multiple joints. The fusion mass not infrequently extends proximally to include the intertarsal bones and sometimes even the naviculocuneiform joints. A careful determination of the involved joints is important when considering a tarsometatarsal fusion for a patient with posttraumatic disorders. At times, in addition to the plain radiograph, a CT scan and bone scan may be necessary to help define the involved area precisely.
The indications for a tarsometatarsal fusion are as follows:
The surgical approach to the first metatarsocuneiform joint is through a dorsomedial longitudinal incision to expose the joint. If multiple joints are involved, the second incision is centered over the second metatarsal, through which the lateral side of the first and all of the second and third metatarsocuneiform joints can be adequately viewed (Figure 9–42). The incision must be sufficiently long to permit adequate exposure of the joints and must be extended proximally if the naviculocuneiform joints are going to be fused as well. Cautious dissection is necessary because there are numerous superficial nerves as well as the neurovascular bundle (dorsalis pedis and superficial branch of the deep peroneal nerve) passing over the area of the second metatarsocuneiform joint in this approach. If the fourth and fifth metatarsocuboid joints are to be fused, a third longitudinal incision is made over this area to enable adequate exposure. The articular cartilage is carefully removed from the tarsometatarsal and intertarsal joints, depending on the extent of the fusion mass. The bones are heavily feathered to create a good environment for healing. If a deformity is present (usually an abduction deformity of the foot or possibly dorsiflexion), it should be corrected. The first metatarsocuneiform joint is aligned and fixed using 4-mm cancellous screws or a dorsomedial plate. Interfragmentary longitudinal compression of the other joints is obtained to prevent possible nonunion. The screw pattern found to be most useful for the first metatarsocuneiform joint is one brought from the dorsal aspect of the cuneiform directed distally, and a second screw from the dorsal aspect of the metatarsal base directed proximally, crossing the metatarsocuneiform joint. Care must be taken to also correct any dorsiflexion or abduction deformity that is present.
Postoperatively, the joint is placed in a short leg, non–weight-bearing cast for 6 weeks, and then in a weight-bearing cast for another 6 weeks.
The possibility of nonunion exists, but with interfragmentary compression the risk is minimized. If nonunion occurs, bone grafting may be required as well as improved internal fixation. When multiple tarsometatarsal joints are fused, a moderate amount of swelling and tension is placed against the incisions. It is critical postoperatively to use a compression dressing to minimize the risk of swelling and prevent possible wound sloughing. If sloughing occurs, it must be treated appropriately, and, occasionally, skin grafting is required.
A tarsometatarsal fusion involving multiple joints may cause a plantar callus because one of the metatarsals was placed in a position of too much plantar flexion. Osteotomy at the base of the metatarsal may be necessary to realign the metatarsal.
Staples should be avoided as a means of internal fixation of the tarsometatarsal joints because they have a tendency to cause dorsiflexion of the metatarsals, which could result in transfer pressure problems under the uninvolved metatarsal heads.
First Metatarsophalangeal Joint Arthrodesis
See the discussion of hallux valgus at the beginning of the chapter.
Interphalangeal Joint Arthrodesis (Hallux Arthrodesis)
Interphalangeal joint arthrodesis is usually indicated for the following problems:
The interphalangeal joint is approached through a dorsal transverse incision centered over the joint. An ellipse of skin is usually removed, exposing the ends of the involved joints. Using a small power saw, the end of the distal portion of the proximal phalanx and the proximal portion of the distal phalanx are removed, placing the distal phalanx into approximately 5–7 degrees of plantar flexion and 3–4 degrees of valgus position. Internal fixation is achieved by using a longitudinal screw (4 mm) or crossed K-wires, or both. A postoperative shoe is used, with weight bearing allowed but avoiding the toe-off phase of gait until fusion occurs, usually in 8 weeks.
Nonunion of interphalangeal joint fusion is uncommon. If it does occur, it often is asymptomatic and does not require treatment. If it is symptomatic, usually the fusion needs to be revised because the area is too small for adequate bone grafting.
Congenital flatfoot is the term used to describe a flatfoot present since birth. The condition may not be apparent during the early years of life but is usually identified toward the end of the first or during the second decade. The typical asymptomatic flexible flatfoot is probably a normal variant of the longitudinal arch. This deformity must be differentiated from the symptomatic flexible or more rigid flatfoot, which usually becomes symptomatic in the early teen years and is often caused by a tarsal coalition. These individuals have a fairly flexible foot until adolescence, when the foot often becomes somewhat more rigid and symptomatic.
The patient with a tarsal coalition frequently presents with a peroneal spastic flatfoot, usually around the age of 10–12 years. The theory is that the foot is locked in a valgus position by the peroneal muscle spasm that is trying to immobilize the painful peritalar joints. A tarsal coalition is the union of two or more tarsal bones, usually occurring between the calcaneus and the navicular or between the talus and the calcaneus. This process is a congenital failure of segmentation between the bones of the hindfoot. Coalitions are usually not symptomatic until adolescence, with symptoms brought on by increasing stiffness of the hindfoot as the cartilaginous coalition begins to ossify. Flatfoot associated with an accessory navicular bone usually becomes symptomatic in the early to mid teenage years and may be unilateral or bilateral. Residual congenital deformity from conditions such as clubfoot or congenital vertical talus are present from birth and discussed in Chapter 11, Pediatric Orthopedic Surgery.
The patient with generalized dysplasia, such as Marfan syndrome or Ehlers-Danlos syndrome, may present with flatfoot. A generalized ligamentous laxity is present from the time of birth, and the diagnosis is usually already known.
SYMPTOMS AND SIGNS
The clinical evaluation begins with the patient in a standing position. In all cases of congenital flatfoot, the longitudinal arch flattens when the patient is standing. In the case of tarsal coalition with peroneal spastic flatfoot, the calcaneus is in a severe fixed valgus position. A tarsal coalition or an accessory navicular may be unilateral, as well as the residuals of a congenital deformity such as clubfoot or congenital vertical talus. The symptomatic and asymptomatic flexible flatfoot and the generalized dysplasias are present bilaterally.
The physical examination of these patients is extremely important. The asymptomatic flexible flatfoot usually demonstrates a satisfactory ROM and no contracture of the Achilles tendon. The symptomatic flexible flatfoot, however, almost invariably demonstrates an equinus contracture. To test adequately for tightness of the Achilles tendon, the head of the talus is covered with the navicular, after which the foot is brought up into dorsiflexion with the knee extended. If the foot is brought into dorsiflexion, permitting lateral subluxation of the talonavicular joint, the examiner often is fooled into thinking that dorsiflexion is adequate when indeed it is not.
The patient with tarsal coalition usually demonstrates restricted hindfoot motion secondary to peroneal spasm and to the cartilaginous or bony bar. The peroneal tendons can actually be felt to be bow strung behind the fibula, not permitting any passive or active inversion of the subtalar joint to occur. On occasion, clonus can be elicited. As a rule, stressing of these joints causes the patient increased discomfort. In flatfoot associated with an accessory navicular, pain is present over the prominence. Frequently, stressing of the posterior tibial tendon aggravates the condition. The patient with residual congenital deformity often demonstrates a certain degree of stiffness of the foot and, not infrequently, varying degrees of deformity of the remainder of the foot. The patient with generalized dysplasia demonstrates marked hypermobility of all the joints, with no contractures whatsoever.
The radiographic evaluation is useful in differentiating the various types of flatfoot. In almost all cases, the lateral view shows a lack of normal dorsiflexion pitch of the calcaneus, which is approximately 20 degrees or more. In symptomatic flexible flatfoot, the calcaneus may even be in a mild degree of equinus position. On the lateral radiograph, a line drawn through the long axis of the talus and first metatarsal demonstrates an angle of more than 30 degrees in severe flatfoot, 15–30 degrees in moderate flatfoot, and 0–15 degrees in mild flatfoot (Figure 9–43).
The calcaneonavicular coalition is best observed on an oblique radiograph and identified as a bridge from the anterior process of the calcaneus to the inferior lateral aspect of the navicular (Figure 9–44). The subtalar or talocalcaneal bar is best demonstrated on a CT scan taken in the coronal plane (Figure 9–45). Flatfoot associated with an accessory navicular demonstrates the accessory bone along the medial side of the navicular, but occasionally a medial oblique view is necessary to outline the size of the fragment (Figure 9–46). In a patient with a residual congenital deformity, such as a clubfoot or congenital vertical talus, the changes about the foot are often sufficient to make the diagnosis fairly obvious. The patient with generalized dysplasia often demonstrates complete collapse of the longitudinal arch.
Conservative management is undertaken for congenital flatfoot deformities. A longitudinal arch support may benefit the patient but is usually not necessary for the asymptomatic flexible flatfoot. For symptomatic flexible flatfoot, a semirigid longitudinal arch support and Achilles stretching exercises may be of some benefit.
The tarsal coalition can be treated conservatively with a short leg walking cast, followed by a polypropylene AFO or a University of California Biomechanics Laboratory (UCBL) insert. If adequate pain relief is achieved, further treatment is not necessary. Flatfoot with an accessory navicular may respond to modification of the shoe to relieve some of the pressure from the involved area. Occasionally, the use of a longitudinal arch support relieves the pressure.
Residual flatfoot resulting from congenital problems can be treated with an AFO or UCBL insert if symptomatic. The patient with generalized dysplasia usually does not require any treatment at all.
Surgical procedures are never appropriate for asymptomatic flatfoot. Symptomatic flexible or semiflexible flatfoot occasionally is treated surgically, particularly if equinus contracture is observed after 5 or 6 years of age. A significant equinus contracture may benefit from lengthening of the Achilles tendon. A lateral column lengthening procedure, such as an Evans calcaneal osteotomy, is indicated in cases of symptomatic flexible flatfoot that fail conservative management. This procedure helps correct heel valgus and forefoot abduction and should be done as late into growth as possible to avoid disturbing open growth centers. A triple arthrodesis should only rarely be carried out because it leaves a young patient with a very stiff foot.
A tarsal coalition that does not respond to conservative management may require resection. The surgical approach to the calcaneonavicular bar is identical to that of the subtalar joint. The bar is carefully outlined and then resected in its entirety. Talocalcaneal coalitions are resectable throughout the adolescent years, if less than 20% of the posterior facet of the subtalar joint is involved or if the coalition is confined only to the middle facet. More extensive involvement of the subtalar joint in an adolescent or any bar in an adult patient is an indication for subtalar arthrodesis. The approach is through a medial incision centered over the middle facet, and caution is taken to carefully reflect the tendons and posterior tibial nerve. The extent of the coalition is identified, and it is resected to expose the area of normal-appearing articular cartilage. Bone wax is applied to the edges or a free fat graft is inserted to prevent reformation of the bar. Flatfoot associated with an accessory navicular may require excision of the accessory navicular and plication of the posterior tibial tendon (Kidner procedure). This fairly successful operation is usually carried out during the late adolescent years.
Residual congenital deformity or generalized dysplasias usually do not require surgical management. In severe cases, a triple arthrodesis is indicated after the foot has matured.
ACQUIRED FLATFOOT DEFORMITY
Acquired flatfoot deformity is a condition affecting a foot that at one time had a normal functioning longitudinal arch. Over time, the arch progressively flattens, often causing the foot to become symptomatic. This deformity is different from congenital flatfoot deformity, present since birth. Acquired flatfoot deformity in the adult may be caused by the following conditions:
Acquired flatfoot deformities are complex deformities that affect different areas of the midfoot and hindfoot. The deformities may include dorsal subluxation of the talonavicular joint and tarsometatarsal joints, abduction of the forefoot, valgus deformity of the hindfoot, or all three. The extent of the deformity varies widely and is usually progressive. Depending on the etiology, acquired flatfoot deformity may affect a patient bilaterally.
SYMPTOMS AND SIGNS
A careful history is important to help distinguish among differing causes of acquired flatfoot deformity. Usually, no specific traumatic event is recalled by the patient who presents with dysfunction of the posterior tibial tendon. In approximately half of patients with tarsometatarsal joint arthrosis, a Lisfranc fracture-dislocation has occurred, whereas the other half has primary arthrosis. The patient with Charcot foot usually gives a relevant history of the cause of the peripheral neuropathy, such as diabetes. The patient with collapse of the talonavicular joint gives a history of prior trauma to the talus or navicular or has RA, which causes disruption of the spring ligament complex.
The physical examination begins by observing the foot with the patient standing, observing for unilateral or bilateral flattening of the longitudinal arch. Varying degrees of abduction of the forefoot and hindfoot valgus should also be evaluated.
The patient with posterior tibial tendon dysfunction demonstrates little or no active inversion strength. Usually, the posterior tibial tendon is thick and swollen and there is increased warmth and pain to palpation over the tendon sheath. When the patient is asked to stand on tiptoe, the involved calcaneus remains in valgus position rather than inverting, as normally occurs. When the patient is viewed from the posterior aspect, more toes are visible laterally on the involved foot than the uninvolved foot, commonly known as the "too many toes sign."
Arthrosis of the tarsometatarsal joints creates a deformity of abduction of the forefoot with varying degrees of dorsiflexion, giving rise to a rather prominent medial cuneiform. Not infrequently, palpable osteophytes are present on the dorsal and plantar aspect of the tarsometatarsal joints.
A Charcot foot presents with varying degrees of swelling and deformity. In the early stages, the foot demonstrates generalized swelling and increased warmth, with loss of sensation in a stocking-glove distribution. Deformity may vary from a mild flat foot to a severe rocker-bottom deformity. It is important to palpate for bony prominences on the medial and plantar aspects of the foot that make it at risk for ulcerations.
In the patient with RA, most of the changes occur within the talonavicular joint. In this case, the head of the talus is often palpable on the plantar medial aspect of the foot. When the subtalar joint is more involved, a fixed hindfoot valgus deformity is usually present as well.
The posttraumatic deformity may vary, depending on precisely which joints are involved. If trauma led to a collapse of the navicular, the longitudinal arch is flattened with little forefoot abduction, and the head of the talus is often palpable on the plantar medial aspect of the foot. There is usually little or no motion in the hindfoot and midfoot joints.
Radiographs usually differentiate the cause of the problem. In the patient with posterior tibial tendon dysfunction, there is sagging of the talonavicular joint and abduction of the navicular on the head of the talus. The patient with tarsometatarsal joint arthrosis demonstrates typical degenerative changes at the affected joints, along with varying degrees of lateral and dorsal subluxation of the joints. Patients with Charcot foot demonstrate characteristic changes seen in a neuropathic joint, including dramatic bone destruction and joint dislocations (Figure 9–47). The patient with RA demonstrates the typical destructive changes observed with this disease process, with joint space narrowing but little osteophyte formation.
Conservative management is aimed at providing support to the longitudinal arch and ankle with a polypropylene AFO. The orthosis must be shaped to accommodate any prominences that might be present. Unfortunately, these prominences present the potential for skin breakdown, particularly in the neuropathic foot. A rocker-bottom-type shoe with an adequate toe box is sometimes indicated to give the patient a smoother gait pattern.
The surgical management of these various conditions is specific for each problem. Posterior tibial tendon dysfunction with a satisfactory ROM of the joints of the hindfoot and midfoot can be treated with reconstruction of the posterior tibial tendon, using a flexor digitorum longus tendon transfer. A calcaneal osteotomy is performed as well, if a significant valgus deformity of the heel is present. Alternatively, a lateral column lengthening, consisting of a calcaneal-cuboid distraction arthrodesis, can be used to correct a flexible flat foot with significant abduction of the forefoot. When a fixed deformity is present in the hindfoot or forefoot, a triple arthrodesis is indicated.
The patient with Charcot foot is treated in a short leg cast until the acute process subsides, after which a polypropylene AFO is used. Occasionally, a bony prominence that continues to cause skin breakdown may be excised to permit the patient to use an AFO. In extreme rocker-bottom deformities, midfoot correction with an osteotomy may be required. The rheumatoid patient usually requires stabilization of the involved area with an isolated talonavicular fusion if little deformity is present, or a triple arthrodesis if there is a hindfoot or midfoot deformity.
The posttraumatic foot with involvement of the talonavicular joint requires a triple arthrodesis. The fusion may need to be extended distally to include the naviculocuneiform joints if arthrosis is present at these joints.
The patient with arthrosis of the tarsometatarsal joints responds well to surgical management by realigning the foot and carrying out arthrodesis of the involved joints.
Cavus foot deformity is characterized by an abnormal elevation of the longitudinal arch, with resulting decrease in the plantar weight-bearing area and stress concentrated on the metatarsal heads. The condition may be aggravated by clawing of the toes, further reducing the forefoot weight-bearing area. Generalized stiffness of the joints is common, causing the patient to avoid prolonged use of the foot.
The various causes of cavus foot deformity include the following:
Cavus foot deformity is extremely variable in its presentation, from mild to extremely severe degree of cavus. The types of deformities can be classified based on the localizing of the area of deformity:
Posterior Cavus Deformity
This deformity mainly involves the calcaneus, which has a dorsiflexion pitch angle of greater than 40 degrees measured on a weight-bearing lateral radiograph. Normally, the dorsiflexion pitch to the calcaneus is approximately 20 degrees. Some degree of varus deformity of the heel is usually present as well.
Anterior Cavus Deformity
In anterior cavus deformity, there is a forefoot equinus deformity with the hindfoot in a neutral position. The anterior cavus may be localized, mainly involving the first and second metatarsal, or it may be more global, with the entire forefoot in a position of plantar flexion. Some degree of adduction of the forefoot is usually present.
Combined Cavus Deformity
In a combined cavus deformity, which is the most severe, there are both anterior and posterior components.
SYMPTOMS AND SIGNS
A careful history regarding the onset of the condition and progression is important. A detailed family history should also be obtained because idiopathic cavus deformity does tend to run in families. Progression of deformity should be ascertained, particularly in the adolescent, because it may indicate a spinal cord abnormality or neoplasm. Activity level and ambulation should also be carefully evaluated as markers of progression of neural or muscular disease.
The degree of deformity of the foot must be examined with the patient in a standing position. This also reveals any evidence of atrophy of the calf muscles, as seen in Charcot-Marie-Tooth disease, clubfoot, or arthrogryposis. The active and passive ROM of the joints of the foot and ankle should be carefully measured. The muscle strength of each muscle must be carefully evaluated, especially if considering a tendon transfer. The degree of deformity and flexibility of the rearfoot, forefoot, metatarsophalangeal joints, and lesser toes must be ascertained. The presence of a tight plantar fascia should also be noted. The lateral ankle ligaments must be evaluated for integrity because they often become stretched out with long-standing varus heel deformity.
Weight-bearing radiographs of the foot and ankle are obtained to help classify the type of cavus deformity and formulate a treatment plan. Any degree of arthrosis or varus tilting of the talus in the ankle mortise is also evaluated.
Conservative care is tailored to the severity of the cavus deformity. Mild deformities may only require a softer-soled shoe. Significant clawing of the lesser toes may require an extra-depth shoe. A custom-made Plastazote liner with a built-in arch support helps decrease the stress on the metatarsal heads. A significant motor deficit may require an AFO to stabilize the ankle. Most cases of cavus foot can be managed with conservative modalities.
Surgical treatment for the cavus foot is aimed at correcting the site of the deformity. The most frequent pattern consists of plantar flexion of the first metatarsal, contracture of the plantar fascia, and varus deformity of the calcaneus. These problems respond to release of the plantar fascia, dorsiflexion osteotomy of the first and perhaps second metatarsal, and lateral closing-wedge osteotomy (Dwyer procedure) of the calcaneus to correct the varus deformity. Fusion of the joints is avoided to maintain as much flexibility of the foot as possible (Figure 9–48).
A more severe deformity involving dorsiflexion of the calcaneus can be treated with sliding osteotomy of the calcaneus (Samilson procedure), correcting any varus deformity with a lateral closing-wedge osteotomy and releasing the plantar fascia (Figure 9–49). Forefoot deformity is treated with osteotomy of the first and sometimes second metatarsal. In some patients, transfer of the peroneus longus tendon into the brevis and lengthening of the posterior tibial tendon provides dynamic muscle balance for the foot.
Severe deformities not amenable to procedures that retain joint motion require triple arthrodesis. A Siffert beak-type triple arthrodesis corrects the deformity because the navicular is mortised under the head of the talus to help reduce the elevation of the longitudinal arch (Figure 9–50). A first metatarsal osteotomy may need to be added to the procedure as well.
The lesser toes may have either fixed or flexible clawtoe deformities. Flexible deformity often responds to release of the extensor tendons and a Girdlestone flexor tendon transfer. If a fixed deformity is present, a DuVries phalangeal condylectomy corrects the hammer toe, followed by extensor tendon release and the Girdlestone procedure.
Hyperextension of the first metatarsophalangeal joint is corrected by interphalangeal arthrodesis of the hallux and transfer of the extensor hallucis longus tendon into the neck of the first metatarsal (Jones procedure) (Figure 9–51).
ORTHOTIC DEVICES FOR THE FOOT & ANKLE
Orthotic devices are used to redistribute stresses on the foot as it makes contact with the ground and to accommodate for abnormal function of defective muscles or ligaments. This is achieved by controlling the posture of the foot and padding certain areas to relieve pressure and provide increased comfort for the foot. Orthoses are also used to limit motion in arthritic joints, making them less painful. The orthotic device may be attached to the sole of the shoe, may be inserted inside the shoe as an insole, may cup the foot (UCBL insert), or may extend across the ankle to hold the entire foot and ankle in place (AFO).
Orthotic Shoe Sole Devices
A variety of heel and sole corrections are available to accommodate foot postural abnormalities. A medial or lateral heel or sole wedge (or a combination of both) can help control excessive pronation or supination from weak tendons, ligamentous instability, or fixed deformities. A wide heel is used to increase the stability of the subtalar joint. A rocker sole helps stabilize the forefoot in the case of a fracture or arthritis and also aids a patient with an ankle fusion to allow a more normal gait pattern.
Orthotic Insole Devices
Insole orthotic devices can be used for flexible deformities to alter the posture of the foot and for fixed deformities to redistribute stress. The simplest device is a soft liner for a shoe or boot made out of a high-density foam material. Other simple orthoses include a soft felt pad to relieve pressure on the metatarsal heads or a combination of materials to produce a more rigid support to help control a forefoot deformity such as forefoot varus or valgus deformity. Orthotic devices take up space in the shoe, and the patient may need a larger or deeper shoe.
University of California Biomechanics Laboratory Insert
The principle of the UCBL insert is to correct a foot deformity such as flatfoot by stabilizing the calcaneus in neutral position and molding the orthosis to block abduction of the forefoot. Posting along the medial aspect may compensate for forefoot varus. In theory, this orthotic device is excellent for controlling the rearfoot and forefoot, but two caveats apply to the use of this device. The first is that the foot must be flexible because correction of a rigid deformity is impossible. The second is that a bony prominence can chafe against the polypropylene material, resulting in pain or skin breakdown over the prominence.
An AFO is a molded polypropylene device that passes along the posterior aspect of the calf and then onto the plantar aspect of the foot to the metatarsal heads. Alterations are made in a variety of ways to accommodate the patient's problem (Figure 9–52). Ankle problems such as arthrosis or dorsiflexion weakness require adequate rigidity to eliminate ankle joint motion. An orthosis for a subtalar joint problem should have enough flexibility to provide ankle joint motion but must be rigid enough to immobilize the subtalar joint. When the problem involves the transverse tarsal joint, the AFO can be fabricated to permit some ankle joint motion but maintain immobilization of the transverse tarsal joint area, usually by blocking abduction of the forefoot. When managing tarsometatarsal arthritis, the footpiece is carried to the tips of the toes. Again, a significant fixed bony deformity results in pressure points, making fitting of the device difficult. If the patient has loss of sensation, careful construction and padding are essential to minimize the risk of ulcers forming over a bony prominence. In cases of marked instability or discomfort, an anterior shell can be added to the AFO, and the brace is extended proximally to create a patellar tendon bearing surface.
Double Upright Orthosis
The double upright orthosis with a hinged ankle may be used when individuals require stability but are engaged in physically demanding activities. The double upright orthosis is somewhat more cumbersome than the AFO but provides rigid immobilization. The hinge mechanism of the ankle joint may be changed, depending on the nature of the patient's problem. The ankle joint can be free, which allows dorsiflexion and plantar flexion to occur, or it can be fixed to prevent plantar flexion past 90 degrees. This brace can be modified with a spring load to provide dorsiflexion for the patient with dropfoot resulting from paralysis but should not be used for the patient with spasticity because it may accentuate the spasticity.
Prescriptions for Orthotic Devices
The following are typical prescriptions for orthotic devices.
METATARSALGIA OR ATROPHY OF PLANTAR FAT PAD
A full-length well-molded orthosis for metatarsal arch support is used to relieve pressure under the metatarsal heads. Soft insole material should be used.
In the treatment of metatarsalgia or atrophy of the plantar fat pad, a full-length orthosis is needed that is molded to the plantar aspect of the foot and built up just proximal to the metatarsal heads to relieve pressure on them. The material should be soft to provide extra cushioning for the foot.
RUPTURED POSTERIOR TIBIAL TENDON WITH MODERATELY SEVERE FLEXIBLE FLATFOOT DEFORMITY
AFO with trim-line cut to permit 30% ankle joint motion is molded to reestablish the longitudinal arch and built up on the lateral aspect of the footpiece to block abduction of the forefoot.
With a moderately advanced flexible flatfoot deformity, an in-shoe orthotic device alone does not provide sufficient support; the AFO is needed to provide adequate stability. Some ankle joint motion is included, which makes ambulation more comfortable for the patient. The longitudinal arch is molded to support the foot in a plantigrade position, and the lateral aspect of the AFO is built up to prevent the forefoot from moving into an abducted position. By blocking abduction, the amount of pressure needed beneath the longitudinal arch to prevent it from collapsing is decreased.
POSTERIOR TIBIAL TENDON INSUFFICIENCY WITH MILD FLATFOOT DEFORMITY AND 5 DEGREES OF FOREFOOT VARUS DEFORMITY
Use a well-molded longitudinal arch support, with a 5-degree varus post and a 3-degree medial heel lift.
Insufficiency of the posterior tibial tendon that has not produced a significant foot deformity can be treated with a well-molded longitudinal arch support. The 5-degree varus forefoot post compensates for the fixed forefoot varus, and the 3-degree heel lift likewise helps tilt the hindfoot from valgus deformity closer to neutral position.
DROPFOOT SECONDARY TO PERONEAL NERVE INJURY
An AFO with a full footpiece is molded to the longitudinal arch.
A dropfoot secondary to a peroneal nerve injury responds well to an AFO with a full footpiece. The footpiece supports the toes so they do not drop and makes it easier for the patient to put on shoes.
DIABETIC NEUROPATHY WITH CLAWFOOT DEFORMITY
An extra-depth shoe with a molded Plastazote liner is backed with a Pelite material.
The patient with clawfoot deformity requires a shoe that has extra height in the toe box. The extra-depth shoe provides enough room for the toes, so they do not chafe against the top of the shoe. The molded Plastazote liner is an excellent means of providing full contact to the plantar aspect of the foot. Plastazote has a tendency to bottom out, as it were, and by backing the material with a Pelite liner or some comparable material, the life expectancy of the Plastazote is extended significantly.
LIGAMENTOUS INJURIES ABOUT THE ANKLE JOINT
Ankle ligament injuries represent the most common musculoskeletal injury; therefore, accurate assessment and treatment of these injuries are important. The lateral collateral ligament complex is most commonly injured, but damage to other important structures around the ankle joint should not be overlooked, as discussed in this section.
The lateral collateral ligament structure of the ankle consists of three distinct ligamentous bands: the anterior and posterior talofibular ligaments (ATFL and PTFL) and the calcaneal fibular ligament (CFL).
When the ankle joint is in plantar flexion, the ATFL is positioned in line with the fibula and therefore placed under stress with an inversion injury and will be damaged. Conversely, when the ankle joint is in dorsiflexion, the CFL is positioned in line with the long axis of the fibula and is therefore subject to injury. If the applied stress is severe, both the ATFL and the CFL may be torn, no matter the position of the ankle joint. The syndesmosis ligament complex tethers the tibia and fibula together and is injured by an external rotational force to the foot. The deltoid ligament is the sole medial stabilizer of the ankle joint. An isolated deltoid ligament injury can occur with an eversion or external rotation force on the foot. The deltoid ligament can also sustain injury in conjunction with a syndesmosis ligament injury, with lateral ankle sprains, or with a concomitant fibula fracture (known as a Maisonneuve fracture).
Lateral collateral ankle ligament injuries are divided into three degrees of severity. A grade I sprain is confined to the ATFL and demonstrates no instability. A grade II sprain involves injury to both the ATFL and CFL, with mild laxity of one or both ligaments. A grade III sprain involves injury and significant laxity of both the ATFL and CFL.
SYMPTOMS AND SIGNS
A past history of injuries of the ankle and problems with chronic ankle ligament instability should be ascertained. A careful physical examination is important to evaluate the degree of involvement of each ligament and to rule out injury to any adjacent bony or soft-tissue structures. The ATFL, PTFL, CFL, and syndesmosis ligaments are palpated for tenderness. To rule out fractures, pain should be elicited in the area of the distal fibula, the anterior process of the calcaneus, the lateral process of the talus, and at the base of the fifth metatarsal. Other areas where an injury must be ruled out include the subtalar joint and the peroneal tendon sheath.
A patient with significant medial joint pain with or without lateral ligament pain should be evaluated for an injury to the deltoid ligament complex, the posterior tibial tendon, and the medial talar dome. Assessment of ankle ligament stability requires clinical and radiographic stress examinations. To perform an anterior drawer maneuver, which tests stability of the ATFL, the ankle is placed in 30 degrees of equinus, and the ankle is pulled in an anterior and slightly internally rotated direction (Figure 9–53). A feeling of subluxation is present if a significant ligament injury has occurred. A talar tilt maneuver is performed by placing an inversion stress on the heel. With the foot in plantar flexion, this tests the stability of the ATFL. With the foot in neutral or dorsiflexion, a talar tilt maneuver tests the stability of the CFL. If clinical instability is suggested by either maneuver, radiographic confirmation can be performed, with comparison to the unaffected ankle.
Deltoid ligament insufficiency may cause a feeling of instability and giving way, affecting the medial aspect of the ankle joint. Stress examination is performed by pulling the foot laterally and into valgus while stabilizing the distal tibia.
Injury to the syndesmosis ligament complex is suspected if the region between the distal anterior tibia and fibula is tender to palpation. If extensive swelling is present more than 2 cm proximal to the ankle joint, syndesmosis rupture is a strong possibility. Pain elicited by squeezing the tibia and fibula together in the midcalf is diagnostic of a syndesmosis ligament tear. A syndesmosis ligament injury is also suspected if external rotation of the foot is painful or if lateral translation of the talus in the ankle mortice occurs with direct lateral force on the foot.
Standard anteroposterior, lateral, and oblique radiographs of the ankle should be obtained to rule out a fracture of the fibula, talus, or calcaneus. If ligament laxity is suggested on clinical examination, stress radiographs should be obtained. An anteroposterior view is taken while a talar tilt maneuver is performed, and a lateral view is taken while an anterior drawer maneuver is performed. More than 10 degrees of tilt and more than 5–7 mm of anterior drawer are considered abnormal.
If a syndesmosis ligament injury is suspected, careful attention must be paid to the joint spaces to rule out widening of the ankle mortise. If instability is suspected, a stress radiograph is performed by externally rotating the foot with the tibia held still.
MRI or CT scan may be helpful in some instances if there is a high index of suspicion for an accompanying injury. Osteochondral injuries to the talus should be ruled out with an MRI scan. If a talus or calcaneus fracture is suspected, either MRI or CT scan may be of benefit.
Acute grade I ligament tears are treated with a lateral stabilizing ankle brace, ice, and avoidance of painful activities. Immediate full weight-bearing is allowed, as are non–weight-bearing physical activities, such as bicycling and swimming. The brace can be discontinued in 1 month.
Grade II ligament tears are treated with protected weight bearing and a lateral stabilizing ankle brace. The patient can begin non–weight-bearing exercise (stationary bicycle) after 7 days, along with peroneal strengthening exercises. Weight-bearing exercise (jogging) may resume after 2–4 weeks.
In a grade III ligament tear, the ankle is immobilized with a removable walking cast for 3–4 weeks. This is followed by a period of physical therapy consisting of range-of-motion (ROM) exercises, peroneal strengthening, and proprioception training using a biomechanical ankle platform system (BAPS) board.
Treatment of isolated deltoid ligament sprains depends on the severity of the injury and is similar to lateral ligament injuries. Mild injuries can be treated with immediate mobilization and rapid return to activity, whereas more severe injuries should be casted for 3–4 weeks.
Syndesmosis ligament tears, if mild, can be treated with weight bearing in a cast or brace and close follow-up to assess for widening of the ankle joint mortise. If the interosseous membrane is damaged, as evidenced by massive swelling of the leg proximal to the ankle joint, treatment depends on the radiographic appearance of the ankle. If the mortise has not widened, the patient is kept on a non–weight-bearing regime in a cast for 6 weeks, with close radiographic follow-up. If initial or follow radiographs show a widened mortise, the patient requires surgical repair of the syndesmosis ligaments with temporary screw placement until the ligaments heal.
The surgical treatment of an acute ligamentous injury is indicated only for the occasional elite athlete. Most ligamentous injuries, even grade III sprains, heal sufficiently with no significant disability if properly treated, as just described. However, even less severe ankle sprains may cause chronic pain or functional instability if left untreated.
The indication for a lateral ligament reconstruction is functional ligament instability. A patient with ligament instability complains of recurrent sprains that occur with sports activities or even with activities of daily living, despite 4–6 months of physical therapy and use of a lateral stabilizing brace. A patient with functional ligament instability also complains of difficulty walking on uneven ground. This history must be found in conjunction with physical examination findings of ligament instability.
Although many lateral ankle reconstruction procedures are described for chronic lateral ankle ligament instability, a Broström repair is generally the procedure of choice. The Broström procedure is a soft-tissue ligamentous repair in which the ATFL and CFL are plicated and reattached to their anatomic positions (Figure 9–54). The repair is reinforced by bringing up a portion of the inferior extensor retinaculum. The Broström procedure is highly effective and has lower morbidity than other procedures that harvest the peroneus brevis tendon. In patients who have severe and long-standing laxity or have failed a Broström repair, revision surgery with an allograft or autograft tendon is indicated.
Chronic lateral ankle pain following an ankle sprain may be caused by a previously undiagnosed condition rather than chronic ankle instability. The differential diagnosis for chronic ankle pain is similar to that following an acute injury and also includes subtalar joint instability, subtalar joint chondral damage or synovitis, and dislocating or torn peroneal tendons. Impingement of scar tissue in the lateral gutter between the talus and fibula may also cause chronic lateral ankle pain. In addition to a careful physical examination, an MRI or CT scan may be helpful for distinguishing among these possible causes of pain.
Surgical treatment may help relieve symptoms of chronic lateral ankle pain, once an accurate diagnosis is made. Chondral or osteochondral fractures involving the ankle or subtalar joints can be treated with arthroscopic or open debridement or pinning. Subtalar joint instability is addressed with a Broström procedure. A fracture of the anterior or lateral process of the talus is either removed if it is small or fixed if it is a large fragment. Tears or dislocations of the peroneal tendons are repaired or stabilized. Scar tissue in the lateral gutter can be treated with arthroscopic debridement.
Chronic instability of the deltoid ligament or syndesmosis ligament is uncommon but can occur after an untreated injury. Diagnosis of either condition is made with stress radiographs. Treatment usually requires a free tendon graft to reconstruct the damaged ligament, with the addition of internal fixation for chronic syndesmosis tears.
ARTHROSCOPIC EXAMINATION OF THE FOOT & ANKLE
Arthroscopy is an important tool for use in diagnosis and treatment of foot and ankle disorders. With developments in instrumentation, more ankle joint conditions can be treated arthroscopically. Arthroscopy of the subtalar joint is also now an accepted method for diagnosing and treating some subtalar joint abnormalities.
Advantages of Ankle Arthroscopy over Ankle Arthrotomy
Arthroscopy of the ankle joint offers distinct advantages over open exploration of the ankle. The entire joint can be visualized using the arthroscope, including the lateral and medial gutters and the posterior aspect of the joint. Dynamic studies can be performed to stress ligaments or identify areas of soft-tissue or bony impingement. Furthermore, the low morbidity of arthroscopy allows rapid rehabilitation.
Table 9–4 lists the indications for ankle joint arthroscopy. In addition, arthroscopic examination can be used as a diagnostic tool in some instances when the precise cause of ankle pain remains in question.
Intraarticular loose bodies are generally easy to identify and remove arthroscopically. These bony or cartilaginous fragments may occur as a result of a single incident or repetitive trauma, or they may represent a fragment of an osteochondritis dissecans lesion. They cause pain or locking symptoms of the ankle and are diagnosed on plain radiographs, CT, or MRI scan.
Ankle Joint Infection
Arthroscopic irrigation, drainage, and synovectomy is an excellent method of treating ankle joint infections.
Synovitis may be present as a result of inflammatory arthritis (RA) or neoplastic diseases (pigmented villonodular synovitis), following trauma, or for unknown reasons (idiopathic). Whether the synovitis is localized or diffuse, arthroscopic debridement of inflamed synovium often relieves symptoms. Synovectomy is more easily and thoroughly performed arthroscopically.
Repetitive trauma or early osteoarthritis can lead to osteophyte formation on the anterior lip of the tibia and the neck of the talus. These lesions can cause pain and limited ankle joint dorsiflexion and can be removed arthroscopically with a high-speed burr.
Other Lesions Within the Joint
Chondral or osteochondral lesions, whether caused by trauma or osteochondritis dissecans, can be treated arthroscopically. This may involve debridement of loose cartilage flaps, drilling of subchondral bone, or pinning of large osteochondral fragments.
Patients who present with ankle pain over the anterolateral joint line and a history of a severe ankle sprain or recurrent sprains may have impingement of scar tissue in the lateral gutter between the talus and fibula. This entity responds well to arthroscopic debridement of scar tissue from the lateral gutter.
Techniques for arthroscopically assisted ankle arthrodesis are well detailed, and several published studies discuss this method. The technique causes less morbidity and allows a shorter time to fusion than open methods of ankle fusion. But this is a technically demanding procedure and cannot be used to correct any joint deformity.
Arthroscopic debridement of the arthritic ankle joint is not beneficial for generalized arthritis but may help for localized degenerative changes accompanied by early osteophyte formation.
Arthroscopically assisted fixation of ankle fractures is described and potentially allows for more accurate realignment of the joint surfaces and identification of chondral lesions that might otherwise be missed. However, the use of arthroscopy in the treatment of most routine ankle fractures is probably not indicated.
Ankle arthroscopy can be a valuable diagnostic tool when the cause of symptoms remains unclear (Table 9–5). Chronic ankle pain or swelling that remains refractory to conservative measures and was not diagnosed by conventional imaging studies may warrant arthroscopic exploration to help make a diagnosis. Chondral damage or inflamed synovium are examples of symptomatic lesions that may not be demonstrated on imaging studies, including MRI. Patients with episodes of locking, stiffness, or instability for which a cause cannot be found may be aided by diagnostic ankle arthroscopy. Loose bodies, cartilage flaps, or arthrofibrosis may be contributing to such symptoms, all of which can be treated arthroscopically (see Table 9–5).
Technique of Ankle Arthroscopy
The patient is placed supine on the operating table with the foot positioned to allow access from all directions. This can be achieved with the foot placed off the edge of the bed or with the thigh held flexed in a well-padded thigh holder (Figure 9–55). General or spinal anesthesia is necessary for full relaxation of the extremity.
The use of distraction greatly enhances arthroscopic procedures, providing better views of the structures of the joint and allowing tools to be introduced into the joint. Noninvasive distractors with padded straps over the foot and heel are most commonly used (see Figure 9–55) Invasive distractors require placement of pins or screws through the tibia proximally and the calcaneus or talus distally. Stronger distraction forces can be obtained in this manner, but the morbidity is higher when using an invasive distractor.
Most ankle arthroscopies are performed using two anterior portals: anterolateral and anteromedial (Figure 9–56). A posterolateral portal may be helpful for use as outflow or to access the posterior aspect of the joint. Thorough knowledge of the anatomy of the tendons, nerves, and vessels is essential to prevent damage to any of these structures with portal placement. The anterolateral portal is placed just lateral to the tendon of the peroneus tertius muscle, taking care to avoid branches of the superficial peroneal nerve. The anteromedial portal is placed just medial to the anterior tibial tendon, taking care to avoid the saphenous nerve and vein. The posterolateral portal is placed just lateral to the Achilles tendon, to avoid damage to the sural nerve.
Initially, the entire joint is explored systematically, to ensure that abnormalities are not overlooked. The cartilaginous surfaces of the talus and tibia are thoroughly examined for osteochondral defects, unstable cartilage flaps, and areas of softening. The medial and lateral gutters are explored, paying special attention to tibiotalar and talofibular articulations. The synovium is inspected for inflammation. Ligamentous structures are identified, specifically the deltoid and talofibular ligaments, which are observed closely for signs of laxity while varus and valgus forces are applied. Loose bodies are carefully searched for, especially in the anterior and posterior recesses of the joint. The presence of osteophytes on the distal tibia and talar neck is also evaluated.
After a thorough diagnostic examination, surgical procedures are performed. These include synovial biopsy or synovial resection, removal of loose bodies, debridement of abnormal cartilaginous surfaces with subchondral drilling, and removal of bone spurs.
Postoperatively, a compression dressing is applied with a posterior splint for 5 to 7 days to allow the portals to heal. Weight bearing is then progressed as tolerated, and activities are advanced to normal.
Although several complications are reported, the most common is nerve damage in the form of hypesthesias or neuroma formation associated with portal placement. Postoperative joint infection, draining sinuses, arterial or tendon damage, and infections at the sites of distraction pins are all described but are very uncommon complications of ankle arthroscopy.
Subtalar Joint Arthroscopy
The subtalar joint is technically challenging for arthroscopy, given its complex shape and the difficulty distracting the joint. Subtalar joint arthroscopy is indicated for several conditions involving the subtalar joint. Talocalcaneal interosseous ligament tears, chondral lesions, synovitis, and focal degenerative changes may respond to arthroscopic debridement of the subtalar joint.
For subtalar joint arthroscopy, the patient can either be placed supine with a bump under the ipsilateral hip or in the lateral decubitus position. Two portals are used over the anterolateral subtalar joint, approximately 1.5 cm apart. The anterior and lateral portions of the posterior facet and the interosseous ligament can be visualized from these portals. A third portal is placed posterolaterally, for outflow and for visualization of the posterior aspect of the joint. The references here provide additional details about the technique of subtalar joint arthroscopy.
Tendon Injuries: Introduction
Tendon injuries about the foot and ankle are common causes of disability because large forces are acting on these tendons in a repetitive fashion during walking, running, and athletic activities. The tendons cross the ankle joint at an acute angle, which further predisposes them to injury. Injury to tendons may be caused by acute trauma, such as in Achilles tendon ruptures, or may be caused by chronic strain, such as posterior tibial tendon dysfunction.
ACHILLES TENDON INJURIES
Achilles tendon abnormalities are extremely common, especially among active men and women between 30 and 50 years of age. The primary disorders are Achilles tendinitis, either insertional or noninsertional, and Achilles tendon ruptures. Achilles tendinitis was previously discussed in the section on heel pain.
Achilles Tendon Rupture
The mechanism of injury is usually mechanical overload from an eccentric contraction of the gastrocsoleus muscle complex. This occurs as a sudden, forceful dorsiflexion of the foot as the gastrocsoleus is contracted. The tear usually occurs 3–6 cm proximal to the insertion of the Achilles tendon, at the site of its poorest blood supply (Figure 9–57). At times, a history of intermittent pain in the tendon is elicited, suggestive of a prior tendinitis. The typical patient is between 30 and 50 years of age and a recreational athlete. These factors suggest that insufficient conditioning of the musculotendon unit plays a role in many injuries. The most common sports activities leading to Achilles tendon ruptures are basketball, racket sports, soccer, and softball.
SYMPTOMS AND SIGNS
The patient describes sudden pain in the calf after attempting a pushing-off movement, often accompanied by an audible pop. Immediate weakness is noted in the affected leg. On physical examination, a palpable defect is often present in the tendon. Ankle plantar flexion is markedly weak compared with the unaffected side. A positive Thompson test, diagnostic of complete Achilles tendon rupture, is performed with the patient prone and the affected knee bent 90 degrees. Squeezing the calf causes plantar flexion of the foot if the Achilles tendon is intact or partially torn but not if there is complete rupture of the tendon.
Plain radiographs are not helpful in diagnosing Achilles tendon tear, unless there is an avulsion off the calcaneus with a fragment of bone, an uncommon condition. MRI is extremely sensitive in diagnosing this disorder and in determining if some tendon remains in continuity (Figure 9–58). However, MRI is rarely needed because physical exam is usually diagnostic of Achilles tendon rupture.
Methods for treating Achilles tendon rupture include primary repair, using open or percutaneous techniques, or cast immobilization. Surgical repair is recommended for active individuals, in the case of a rerupture, or if the injury is older than 2 weeks.
Cast treatment for Achilles tendon ruptures is recommended for more sedentary individuals, patients who are at increased risk of developing wound problems, or high-risk surgical patients. The primary risk of cast immobilization is a higher chance of rerupture. For the vast majority of patients, either treatment method results in a good outcome.
Once an acute rupture is diagnosed, the patient should be placed in a gravity equinus cast. A below-knee cast is adequate in a reliable patient. If there is a question of whether the tendon edges are properly apposed in the cast, an MRI scan be done, although this is not routine. After 4 weeks, the cast is changed, with correction of approximately half of the previous equinus. Over the next 4 weeks, the patient is brought down to neutral with serial casts. Once at neutral, the patient is given a removable walking cast for 4 weeks. Supervised strengthening activities then begin.
The surgical approach is on the medial side of the Achilles tendon sheath. The frayed edges of the tendon are debrided. The foot is positioned in equinus position equal to the resting equinus of the opposite ankle. Two heavy nonabsorbable sutures are woven through 3–4 cm of each tendon edge using a Bunnell or Kessler stitch (Figure 9–59). The repair can be reinforced with lighter, absorbable sutures at the site of the tear. If the plantaris tendon is intact, it can be harvested and used to reinforce the repair.
Postoperatively, a hard cast is used for 3 weeks, followed by a removable cast with adjustable ankle motion. Over the next 2–3 weeks, the joint should be gradually brought out of equinus. Weight bearing is then allowed, and ROM exercises are begun. The cast is discontinued at 6–8 weeks, and supervised strengthening exercises are performed.
The primary risk of surgical repair is wound healing problems, which occur in approximately 5% of patients. A percutaneous method of Achilles tendon repair is listed in the references.
TREATMENT OF CHRONIC RUPTURES OR RERUPTURES
Chronic Achilles tendon ruptures, more than 6 weeks old, or reruptures of previously treated injuries can be challenging reconstruction problems because of retraction and degeneration of the tendon ends. A number of different procedures are described to address this problem, including a variety of synthetic and interpositional grafts (Figure 9–60).
Small defects can be bridged by turning down a strip of gastrocnemius fascia, which is sutured into the distal tendon stump. Larger defects can be treated by using a V-Y lengthening of the gastrocnemius aponeurosis. If the deficit is too large for V-Y lengthening, transfer of the flexor hallucis longus tendon can be performed. The tendon of the flexor hallucis longus is transected distally in the foot, and the distal segment is tenodesed to the flexor digitorum longus to maintain flexion of the great toe. The proximal tendon is secured to the calcaneus through a drill hole or by using an absorbable anchor or screw. A central slip of the Achilles tendon is advanced to bridge the gap, and then the repair is reinforced by securing it to the flexor hallucis (Figure 9–61).
The postoperative course for these procedures includes 6 weeks of non–weight bearing and a total of 3 months protection in a cast.
POSTERIOR TIBIAL TENDON INJURIES
This topic is covered in the section on acquired flatfoot deformities.
PERONEAL TENDON INJURIES
Peroneal tendon injuries fall into the categories of peroneal tendonitis, peroneal tendon tears, and peroneal tendon subluxation or dislocation.
Inflammation of the peroneal tendons may be caused by acute trauma, inflammatory arthropathy conditions, or repetitive motion. Traumatic events that may induce tendonitis include a direct blow to the posterolateral ankle, a fracture of the calcaneus or fibula, or a severe inversion sprain of the ankle. Most tendonitis is caused by repetitive motion injury from recurrent rubbing of the peroneal tendons on the distal end of the fibula. Often there is an abnormal bony contour of the distal fibula or the peroneal tubercle. Tendonitis of the peroneus longus may be associated with abnormality of the os peroneum, a small sesamoid bone located in the tendon where it curves around the lateral border of the cuboid.
SYMPTOMS AND SIGNS
The patient complains of pain over the lateral aspect of the ankle, made worse with activity, and improved with rest and NSAIDs. The onset may be insidious, or it may be associated with an acute injury. Physical examination usually demonstrates pain located along the course of the peroneal tendons. Pain and weakness is noted with resisted eversion of the foot.
An MRI scan may help distinguish between tendonitis and a tendon tear, although small tears may not be identified on an MRI.
If symptoms are mild, the recommended treatment includes NSAIDs, activity modification, and an ankle brace. Four to 6 weeks of cast immobilization is used for more advanced symptoms or for patients who do not respond to initial treatment. Occasionally, a diagnostic injection with bupivacaine is given into the tendon sheath.
Operative intervention is recommended for patients who fail conservative treatment. The tendon sheath is explored, inflamed synovium is removed, and the tendons are carefully explored to look for tears or degenerative lesions. Postoperatively, early ROM is encouraged.
Peroneal Tendon Tears
The majority of peroneal tendon tears are attritional in nature, caused by mechanical irritation within the fibular groove. The peroneus longus tendon, which lies posterior, places pressure on the brevis tendon. Also, a sharp lateral edge of the fibula may predispose to a longitudinal split of the tendons. Laxity of the tendon sheath and subluxation of the tendons out of the fibular groove may contribute to tears as well. Acute tears of the peroneal tendons may occur with a sudden, severe stress to the ankle, but usually there is some degree of preexisting degeneration within the tendon.
Clinical presentation is similar to that of peroneal tendonitis, but with a more acute onset of pain and swelling along the tendon sheath.
Initial treatment is similar to that of peroneal tendonitis, but it is less likely to result in resolution of symptoms if a tear is present.
Surgical repair of a peroneal tendon tear is indicated when nonoperative treatment fails to relieve symptoms. At surgery, both tendons are carefully examined, the fibula is explored for sharp edges, and the tendon sheath is evaluated for laxity. Small areas of the tendon that demonstrate significant degeneration are removed. The remainder of the tendon is repaired with nylon or polypropylene suture. Postoperatively, the ankle is immobilized for 4 weeks; then weight bearing and gentle ROM is allowed.
Peroneal Tendon Subluxation and Dislocation
Peroneal tendon dislocation is caused by a sudden forceful dorsiflexion motion of the ankle combined with a simultaneous strong contraction of the peroneal musculature. This mechanism injures the superior peroneal retinaculum, which holds the peroneal tendons in place along the posterior border of the distal fibula. The retinaculum is either stripped off the fibular periosteum or avulsed with a small piece of fibular cortex. This permits the creation of a false pouch and laxity of the retinaculum, allowing the peroneal tendons to dislocate anteriorly. If this condition goes unrecognized, either the tendons remain dislocated, or they relocate with the propensity for recurrent subluxation or dislocation.
SYMPTOMS AND SIGNS
The patient usually recalls an acute episode of trauma and frequently the sensation of the tendon dislocating. Pain and swelling is localized to the peroneal tendon sheath around the tip of the fibula. With recurrent subluxation or dislocation, the tendons are felt to pop out of place. On examination, resisted eversion of the ankle elicits pain and may cause the tendons to subluxate. Unfortunately, many acute peroneal tendon dislocations go unrecognized as lateral ankle sprains.
Radiographs may show a small piece of bone lateral to the distal fibula, indicative of avulsion of the retinaculum. MRI scan usually details the injury well if careful attention is paid to this area.
Treatment of acute peroneal tendon dislocations consists of casting in plantarflexion and inversion for 4 weeks, followed by a walking cast for an additional 2 weeks. Cast treatment has at least a 50% failure rate. Once a tendon is chronically dislocated or recurrently subluxates, only surgical treatment will keep it in position.
Surgical repair is recommended for an athletic individual following an acute dislocation of the peroneal tendons. It is also recommended for patients with recurrent dislocation if their physical activities are significantly restricted. The procedure consists of repairing the superior peroneal retinaculum to the fibula, either through drill holes or with suture anchors. In the case of attenuated retinaculum caused by chronic dislocations, the repair can be reinforced with a strip of Achilles or by rerouting the calcaneofibular ligament over the tendons. At the time of surgical repair, the tendons are inspected for tears and the contour of the posterior fibular groove is evaluated. If a shallow groove is noted, a bony procedure to deepen the groove is necessary to prevent recurrent dislocations. Postoperatively, the patient is immobilized in a cast for 6 weeks.
ANTERIOR TIBIAL TENDON RUPTURE
Rupture of the anterior tibial tendon occurs infrequently, and most often in patients older than 60. The mechanism is either chronic rubbing against the inferior edge of the extensor retinaculum or rubbing against an exostosis at the first metatarsocuneiform joint. The rupture usually occurs at the distal 2–3 cm of tendon. Nondegenerative traumatic ruptures of the anterior tibial tendon are rare.
SYMPTOMS AND SIGNS
Patients with a degenerative rupture present with complaints of pain and swelling over the anterior ankle. They sense the foot slapping down, or they may be catching their toes on the ground when they walk. Patients frequently present after the symptoms have been bothersome for several months. Physical exam is notable for weakness of ankle dorsiflexion, often with a palpable mass over the anterior ankle joint.
If the diagnosis is in doubt, MRI scan can accurately determine if the tendon is ruptured.
In the case of a less active patient, nonsurgical treatment appears to give equal functional results to surgical repair. Cast immobilization is followed by long-term use of an AFO.
Acute tendon rupture in an active individual should be surgically repaired. Chronic ruptures that are symptomatic usually require reconstruction using an extensor tendon graft or tendon transfer because the distal stump is usually too degenerated to perform a primary repair.
OSTEOCHONDRAL LESIONS OF THE TALUS
Osteochondral lesions of the talus (OLTs) are defects of cartilage and subchondral bone in the talar dome. More sophisticated imaging techniques allow for precise diagnosis of OLTs, and advanced arthroscopic and open methods are available to treat this difficult problem.
OLTs, also known as osteochondritis dissecans lesions, are generally located in one of two areas on the talar dome: either posteromedial or anterolateral. The more common posteromedial lesions are usually deeper lesions involving subchondral bone. Their origin is thought to involve ischemia, often with an episode of trauma exacerbating the underlying condition. Anterolateral lesions are a result of a single traumatic episode or repetitive trauma from lateral ankle sprains. These lesions tend to be purely cartilaginous.
SYMPTOMS AND SIGNS
Patients usually present with several months of ankle pain following a routine ankle sprain. Sometimes they recount a history of recurrent sprains to the ankle. The pain is usually located over the anterior aspect of the ankle on the side of the lesion, but it may be diffuse. Occasionally, there is a sensation of locking in the ankle when a loose flap of cartilage is present. A high index of suspicion is necessary because OLTs can be misdiagnosed as a chronic ankle sprain, as discussed in the section on ligamentous injuries about the ankle joint.
Radiographs are often normal in OLTs. MRI scan is the imaging procedure of choice for determining the size, location, and extent of bony or cartilaginous involvement (Figure 9–62).
A 6-week trial of cast immobilization is warranted if the MRI scan shows no evidence of a displaced bone or cartilage fragment.
The surgical treatment method depends on the type of lesion. Acutely displaced lesions can be reduced and pinned with an absorbable pin by either open or arthroscopic methods. Purely cartilaginous lesions are curetted to a stable rim and drilled to stimulate vascular ingrowth and fibrocartilage formation. OLTs with significant bony involvement require bone grafting in addition to drilling and curettage. A medial malleolar osteotomy is required to access a posteromedial lesion. If a bony lesion has intact overlying cartilage, drilling and bone grafting can be performed under radiographic guidance through the talus, thereby sparing the overlying cartilage. Postoperatively, patients are kept non–weight bearing for 4 weeks, but early ROM is encouraged.
New techniques were developed for larger lesions or ones that fail curettage and drilling. Osteochondral autograft or allograft plugs can be used to replace bone and cartilage defects. Autograft plugs are generally harvested from the ipsilateral knee. Intermediate-term follow-up data shows good results in most patients following this technique. Autologous chondrocyte implantation is also used to a limited extent for OLTs.