Incidence

Stress fractures typically afflict runners, dancers, military enlistees, and anyone involved in repetitive lower-extremity activity or an exhaustive training regimen.

The most commonly studied population for the incidence of stress fracture is military recruits. The significant physical requirements, the varying training regimens, and particularly the rapid acceleration of training, makes this population at risk for stress fractures. Milgrom⁸³ studied 295 recruits in the Israeli army during an intensive physical training regimen. The alarming incidence of stress fractures in this young, active group was 31% (91 of 295). Thirty-five percent of the patients were asymptomatic, and 20% were noted to have plain radiographic findings of stress fracture. Fracture frequency by location was as follows: 51% tibial diaphysis, 5% tibial plateau, 21% femur, 13% distal femur, and a very low incidence of tarsal and metatarsal fractures.^82,83 The rates of stress fractures in soldiers in the United States has not been as significant as those found by Milgrom; some authors estimate a rate of less than 2%.⁹⁴

Pester et al⁹⁴ completed a 4-year study of U.S. military recruits at Fort Dix. The study demonstrated a significant difference in fracture rate by location between the male and female recruits. The male recruits had a predominance of metatarsal stress fractures (66%) and 20% calcaneal fractures. Only 13% of the fractures were located in the leg. The female recruits had a much higher incidence of calcaneal fractures and tibial fractures (39% and 27%, respectively). The metatarsal fracture incidence was lower (39%). The increased calcaneal fracture rate in female recruits may be the result of differences in marching techniques and training. There was no correlation with height, weight, age, or foot type. The female recruits had a two times higher incidence of bilaterality and early occurrence of fractures during their training (first week).

Greaney⁴³ has reported that 77% of stress fractures are cancellous and 23% are cortical. There is likely a natural progression from microfractures to stress reactions to frank cortical fracture. Stress fractures develop when the natural response of the skeletal system to loading is overtaxed. It is postulated that stress reactions occur by cyclic loading that does not exceed the ultimate breaking stress or limits of plastic deformation of bone. One possible cause of stress fracture is muscle fatigue, which decreases shock-absorbing capacity of the extremity, and another is repetitive force exerted by a muscle on bone. From a biomechanical standpoint, muscles increase their response to force quicker than bone does. Bone is a dynamic structure and responds to muscle activity. As stress increases, this leads to bone deformation along its elastic range, and the bone returns to its prestress state after the applied force is removed. When the elastic range is exceeded, this causes plastic deformity, which leads to microfractures. These microfractures or cracks can progress to structural failure.²⁴

Certain factors can increase the risk of stress fractures. These include such anatomic variants as cavus foot conformation, long second metatarsal (e.g., the Morton foot), and metatarsus adductus. Hormonal imbalances (amenorrhea, hyperthyroidism) and osteoporosis also play a role. Certain medications and tobacco and alcohol abuse have been implicated, as have nutritional problems and anemic disorders. Lastly, training errors, poor footwear, and improper athletic technique can increase the risk.

Clinical Presentation

The diagnosis of a stress fracture rests on a number of factors and includes a spectrum of presenting symptoms and signs. The stress reaction is a prodromal symptom and one the athlete might try to endure or run through. This phase includes a vague discomfort with activity and varying degrees of swelling. There is occasional tenderness over the involved site, which bone percussion can help localize. A one-legged hop test can also elicit pain. Eventually, a fracture occurs if loading is continued. This is because osteoclastic resorption occurs 5 to 14 days after onset, and increased vascularity occurs with endosteal and periosteal callus formation and leads to a weakened bone state. The differential diagnosis at this stage includes tendinitis, periostitis, pes bursitis, compartment syndrome, and gastrocnemius–soleus complex injury.⁷⁶

Imaging

Imaging studies confirm the diagnosis of stress-related injuries. Plain radiographs are the mainstay in conventional fracture diagnosis but are often not helpful unless there is cortical disruption. In Matheson’s⁷⁴ study of 320 stress fractures in athletes, it was noted that the period of pain onset to bony changes was weeks to months (average, 10 to 21 days) and that bone changes may be evident in only 30% to 70% of cases. A technetium-122 (⁹⁹Tc) bone scan is extremely sensitive, and uptake may be evident within 24 hours after injury. However, this test is not specific. On the other hand, MRI is sensitive and specific, particularly to location. Computed tomography (CT) is helpful only to define a fracture line and to determine whether the fracture is complete or incomplete.

The plain radiographic findings include rarefaction of bone, sclerosis, endosteal callus, cortical fissure or crack, and the occasional complete fracture.⁴⁶ Early radiographic findings include lucency without periosteal reaction or callus. The first sign is focal linear sclerosis that occurs perpendicular to the trabeculae. As this bone enters the healing phase, the appearance of thick laminar periosteal bone is noted.²⁴

Levy described two types of stress fractures.⁷² The diaphyseal stress fracture is characterized by cortical disruption, followed by dense callus. This is most common in the lesser metatarsals (second through fifth). Fractures in ends of long bones occur in cancellous bone and appear as lines perpendicular to the direction of the applied stress. This type is most common in the calcaneus and the first metatarsal.⁶⁸

Treatment

Treatment of stress-related lesions can be considered in general terms. A stress reaction—lesions with a positive bone scan or MRI without evidence of a fracture line—can be treated nonoperatively with activity modification, often for a period of 6 to 8 weeks. This does not imply a cessation of activity but rather suspending running and continuing aerobic workouts with swimming and biking. Orthotic devices and shoe modifications can be used and include a stiffer-soled shoe that avoids midfoot bend. Turf toe plates are helpful, paired with cushioned insoles. The athlete can return to sports when painfree.

The majority of true stress fractures (evidence for a fracture line on a radiograph or CT scan) can also be successfully treated nonoperatively. Initially, a boot or cast can be applied for protected weight bearing. A waterproof cast liner allows continued workouts. Weekly examinations are recommended.

Medications in the management of stress fractures are controversial and have no proven benefit to date. Currently, there are no prospective studies that evaluate their efficacy in the treatment of stress fractures of the foot and ankle. Bisphosphonates can be obtained in oral or intravenous form; both are contraindicated in premenopausal women.

Much attention recently has been give to the use of teriparatide in the treatment of osteoporosis in postmenopausal women. Teriparatide is a recombinant human parathyroid hormone analog that was approved by the Food and Drug Administration (FDA) in 2002 for the treatment of osteoporosis in women who are at high risk for insufficiency fractures. The mechanism of action is by stimulating new bone formation by favoring osteoclasts over osteoblasts. Animal studies have shown an enhanced callus formation increase in strength in healing of tibial fractures.¹⁰³ The only prospective randomized study to date in humans demonstrating accelerated fracture healing was performed in 2010. In 102 postmenopausal women with distal radial fractures, the teriparatide group had shortened time-to-fracture healing versus placebo. Current ongoing research will further discern the efficacy of this medication in the treatment of stress fractures.⁹ The use of calcitonin has also been postulated to enhance fracture healing, but current literature has not demonstrated these effects.

Nonsteroidal medications can reduce the inflammatory component but might interfere with bone production. Bone stimulation is also without proven benefit in this situation but is reasonable if it is accessible and affordable. Extracorporeal shock wave therapy has been postulated as a future treatment adjuvant. Alvarez et al³ reviewed the use of shock wave therapy in the treatment of proximal metatarsal fractures. Although this was not a comparative study, the authors demonstrated satisfactory healing rates in these fractures without any complications from this adjuvant treatment.³ Most stress fractures heal in 4 to 15 weeks. Once the fracture has healed, shoe modifications with biomechanical correction are necessary, as is the avoidance of a premature return to activity.

Nutritional and dietary factors can influence healing in stress fractures. Wentz et al,¹²³ in 2012, studied dietary and training predictors of stress fractures in female runners. Of interest, an important influence on the bone mineral density of these athletes was their milk intake during middle school. The most predictive factors for stress fractures were low bone mineral density, current calcium intake, irregular menstrual cycles, the years of running history, and training on hard surfaces.¹²³

Clinical Features

The primary clinical symptom of tibial stress fracture is pain with activity, particularly near the end of activity. The intensity typically begins as a very mild discomfort that abates with rest. This typically escalates to where the pain is reproduced with shorter distances or a lower level of activity, and the pain persists for a longer time after activity. This prodrome gradually increases over time. It is very rare to have acute-onset pain that does not resolve with short periods of rest. The pain and discomfort can progress to the point that the patient cannot participate in the activity, and training has to be discontinued.²⁷

Physical examination typically reveals tenderness at the midshaft tibial region. The tenderness can be associated with swelling, erythema, and warmth. The tenderness is more commonly located on the medial border of the tibia in this location.²⁹ Percussion can elicit specific tenderness.

Diagnosis

Radiographs are typically normal in the early stages, but they can demonstrate some periosteal reaction or cortical thickening as early as 2 to 3 weeks from the time of the earliest symptoms. The early stages can show a mild cortical lucency, which later becomes an area of increased density accompanied by a more noticeable periosteal reaction with cortical thickening. ⁹⁹Tc bone scanning or MRI is very useful in detecting stress fractures in the early or evolving stages (Fig. 31-1). The fracture line, when seen on plain radiographs, usually courses from the posteromedial cortex.²⁹ These posteromedial diaphyseal fractures typically have a more benign course and resolve with conservative measures.⁵⁶

A more infrequent location of a tibial diaphyseal stress fracture is along the anterior cortex. This is seen as an anterior cortical line, often called a “black line,” which represents a more difficult condition to treat (Fig. 31-2). This anterior stress fracture is believed to indicate or predict the development of symptomatic pseudoarthrosis.⁹⁷ Stress fracture in this location appears to be associated with jumping activities more than the posteromedial location is.^35,37

Treatment

Treatment is largely nonoperative for tibial stress fractures. Because most of these injuries are the result of training errors, all factors associated with the initial onset must be examined. The frequency, intensity, and duration of training must be studied. Particular attention to footwear and the running surface is imperative. Biomechanical imbalance caused by excessive pronation or supination can contribute to this disorder.

The initial treatment consists primarily of rest and avoidance of the instigating activity. Immobilization is not necessary but can be helpful in decreasing symptoms and reinforcing to the athlete the severity of the injury and the need for compliance with the recommended rest. The initial impact-loading activity is replaced with less intense activities, such as biking and swimming and other pool activities. Resumption of activity is based upon the presence or absence of symptoms. Training is gradually resumed and accelerated based on the absence of symptoms as well as the lack of clinical examination findings, such as swelling and tenderness. Custom-molded orthotic devices can be beneficial in resuming activities and preventing recurrent injury.

Treatment of the anterior tibial stress fracture should be undertaken with more vigilance than the typical tibial stress fracture. When an anterior cortical lucency is noted, there is a higher risk of delayed union or of progression to complete fracture.²⁷ Green⁴⁴ noted a significant nonunion rate in their athletes who had this entity (5 out of 6). Their recommendations included surgical treatment consisting of excision and bone grafting if no healing had occurred by 4 to 6 months from diagnosis. Other treatment options include intramedullary reaming and fixation, drilling of the defect, and electromagnetic bone stimulation.^27,97,105

Johansson et al⁵⁶ reviewed 11 patients with anterior tibial stress fractures. They found that in contrast to the positive results of Rettig¹⁰⁵ with conservative treatment plus electromagnetic therapy, their patients failed conservative care (which consisted of 3 months of immobilization) and ultimately required operative intervention. Even in the operative fixation and grafting group, the average time to bone union was approximately 5 months. Theories explaining the difficulty with this fracture location include the relative hypovascularity of this region.

Clinical Features

The typical presentation is a running or jumping athlete with an insidious onset of pain over the medial malleolus. It is initially poorly localized to the medial ankle, and the diagnosis may be delayed for months. Initial presentation does not typically include localized swelling to the malleolar region. This is usually a finding once symptoms have persisted. Ankle range of motion is not limited, and no instability pattern or history of inversion or eversion injury is noted.

The differential diagnosis often includes posterior tibial tendinitis with or without insufficiency, deltoid ligament sprain, medial talar dome osteochondral lesion, or other intraarticular disease. Anteromedial impingement from prominent osteophytes can have a similar presentation.

Initial limited periods of rest and mild activity restriction typically are unsuccessful in treating this entity. Symptoms usually return promptly upon resumption of the athletic activity.

Radiographs

Plain radiographs are usually normal as late as 2 months after the initial appearance of symptoms.⁹⁰ Additional useful radiographic studies are ⁹⁹Tc bone scanning, CT, and MRI. Okada⁸⁸ was the first to describe the appearance of a medial malleolar stress fracture in a case report in 1995. The T1-weighted MRI image demonstrated a vertical linear zone of decreased signal intensity at the junction of the medial malleolus and the tibial plafond. It is very difficult to determine on MRI whether the fracture line is complete or incomplete because of the extensive signal variation (Fig. 31-3). It is recommended that a CT scan with coronal and sagittal reconstructions be obtained in the event of a positive bone scan or MRI. The CT scan is useful to determine the extent of the fracture and is particularly helpful in preoperative planning to determine the fracture line location as well as the need for adjuvant bone grafting.

Treatment

The treatment of the medial malleolar stress fracture is highly variable. The level of activity of the patient, chronicity of symptoms, associated other problems, and timing of the athletic season all play into the choice of treatment. In the early stages of symptoms, immobilization, activity restriction, and rest are recommended. Restriction of weight bearing is typically not necessary. In cases where the symptoms are more chronic or the fracture line appears to be complete, the focus can turn to surgical treatment. If there is any displacement of a complete fracture on presentation, surgical fixation is recommended.

Orava,⁹⁰ in following eight patients, noted that after 2 to 3 months of conservative treatment, symptoms resumed with activity. In their series, the average time to healing was 9 months (range, 5 to 17 months) from the onset of symptoms. Three of the eight patients eventually required surgery in the form of drilling of the lesion without internal fixation.

Shabat¹¹⁰ reviewed the literature in 2002 and found 23 cases described from 1988 to 2002. The healing rates and treatment were very variable. The approximate time to return to sports activity was doubled in the nonoperatively treated group. The time to complete healing of the fractures ranged from 2 to 8 months. The surgical group averaged 4.2 months, and the conservatively treated group took 6.7 months on average. Surgical treatment ranged from drilling alone to formal fixation with bone grafting (Fig. 31-4).

Our treatment protocol includes activity restriction and immobilization with weight bearing to tolerance in the acute setting. The use of rigid immobilization in a cast limits dorsiflexion of the ankle, which prevents possible impingement of the talus on the medial malleolus. Percutaneous screw fixation of incomplete fractures can be justified, but caution is taken to avoid injury to the posterior tibial tendon. If there is evidence of a complete fracture line on plain radiographs or CT scan, surgery is typically recommended. For fracture fixation in cases with a vertical fracture line, buttress (antiglide) plating should be considered. Adjuvant bone graft should also be considered in patients with complete fracture lines. It is critical to assess the anteromedial joint line for areas of bony impingement. If present, debridement of both talar and tibial osteophytes is necessary (Fig. 31-5). In cases with an established nonunion, the authors recommend open reduction and internal fixation, take-down of the pseudarthrosis, and bone grafting. In cases that do not have complete fracture line on MRI and CT scan and that have failed initial conservative measures, fixation without formal bone grafting can be performed.

Clinical Presentation

Stress fractures of the fibula are much more common at the distal third. These are seen most often in athletes and military recruits.29,84 Pester⁹⁴ found an incidence of 1% to 5% in military recruits. The clinical presentation is typically characterized by an abrupt onset of pain, usually within 10 days of the increased activity or alteration of training. There is typically diffuse edema, generalized pain, and tenderness that is often difficult to locate.²⁹ The tenderness, when present, is usually located at the posterolateral border of the fibula approximately 4 to 7 cm from the tip of the malleolus.²⁹ If the presentation is subacute, a common clinical finding is palpable prominence from the abundant callus. Ankle range of motion is usually well preserved.¹⁷

Radiographic Findings

Radiographic findings demonstrate the fracture within 3 or 4 weeks of the initiation of symptoms. The characteristic radiographic findings include a relatively transverse fracture, low incidence of fracture displacement, and abundant callus (Fig. 31-6). Significant cortical thickening is seen both distal and proximal to the fracture site, and a less dense line is seen at the location of the initial fracture. These findings are often apparent at 12 to 16 weeks.¹⁷ Additional diagnostic studies, such as a technetium bone scan or MRI, are rarely needed (Fig. 31-7).

Etiology

There are many theories concerning the cause of these fractures. Richmond and Shafar¹⁰⁶ theorized that significant eversion of the hindfoot causing subfibular abutment opposes the pull of the tibiofibular interosseous ligament. The medial pull on the interosseous ligament plus the lateral force on the distal portion of the fibula causes significant stress concentration on the fibula just below the interosseus ligament. In a theory proposed by Devas,²⁹ the potential mechanism for development of the fracture involves the repetitive strong contraction of the plantar flexors of the ankle and the toe flexors from their origin on the fibula with running. This causes a to-and-fro movement of the fibula, ultimately resulting in failure with significant repetitive activity.

Treatment

Stress fractures of the distal fibula are most commonly treated conservatively. Rest and physical activity restriction is the hallmark of treatment. The use of a pneumatic leg brace has been described as giving excellent results, including healing within 6 weeks and resumption of activity.⁸⁴

Devas²⁹ reported on 50 athletes with fibular stress fractures. Forty fractures occurred within the lateral malleolus. These fractures were treated with elastic strapping and normal weight bearing but no athletic activity until bone tenderness was no longer noted on repeat clinical examination. The typical time to resumption of activity was 6 to 8 weeks. The authors did observe an increased incidence of these fractures with running on hard surfaces, especially in the winter. Thus further recommendations can be made on training conditions and climate.

Anatomy and Physiology

Little has been written of the sesamoids, let alone a stress fracture of these seemingly insignificant bones.4,5 The sesamoids have specific morphologic characteristics that can predispose them to a number of disorders, one being stress fracture.^22,77,122

Other than for congenital variations, there are two hallux sesamoids. The medial, or tibial, hallux sesamoid is larger, longer, and often more distally positioned. The lateral, or fibular, sesamoid, is typically smaller, rounder, and more proximal in its relation to the tibial sesamoid. As a result of these differences, the tibial sesamoid endures greater weight-bearing forces and is therefore the one more often injured.4,5,77

The blood supply to the tibial hallux sesamoid is via terminal branches of the medial plantar artery. Ossification occurs at between 9 and 11 years of age, often in multiple areas of the sesamoid. Congenital partition of the tibial sesamoid is fairly common, reportedly ranging from 10% to 33%, ten times greater than that in the fibular sesamoid. Partition is often bilateral, with a wide range of 25% to 85% reported (see Chapter 10).¹⁰⁹

The sesamoids function to dissipate forces within the hallux metatarsophalangeal (MTP) joint, elevate the metatarsal head (thereby increasing the mechanical advantage of the flexor hallucis brevis [FHB] tendon), and protect the flexor hallucis longis (FHL) tendon while maintaining its direction of pull. Quite simply, the sesamoids assist with push-off of the hallux. It has been shown that excision of the tibial sesamoid equates with a 10% loss of hallux push-off power.6,7 In addition, removal of the sesamoid can disrupt the delicate tendon balance of the hallux MTP joint, possibly resulting in malalignment. Specifically, a tibial hallux sesamoidectomy can create a disruption of the medial head of the FHB tendon, and a progressive hallux valgus can occur. For these reasons, the sesamoids should not be considered dispensable.^77,122

Diagnosis

The diagnostic evaluation of a sesamoid disorder begins with a thorough history. In general, pain is localized to the plantar hallux MTP joint and worsens with weight bearing. Most problematic for the patient is participating in sports and climbing stairs. There is often no precipitating event.

A clinical examination identifies the specific location of pain and tenderness. In the case of a symptomatic tibial sesamoid, this is plantar–medial at the hallux MTP joint, whereas the fibular sesamoid is directly plantar. There may be the swelling, warmth, or erythema. Joint motion may be restricted secondary to pain. The pain can be accentuated with direct compression of the sesamoid against the metatarsal head while dorsiflexing the joint.

Radiographic analysis includes standing anteroposterior (AP) and lateral foot views. Axial and tangential sesamoid views assist in assessing for focal arthrosis, plantar osteophytes, or bony prominences (Fig. 31-8). An oblique sesamoid view is helpful in identifying a fracture of the tibial sesamoid. It is recommended that a marker (a radiopaque BB) be placed on the skin overlying the site of tenderness to differentiate which sesamoid is indeed involved as well as confirming that it is not the flexor tendon that is the site of pain (see Chapter 10).

It is often difficult to differentiate between a fractured and bipartite sesamoid. In general, a fracture exhibits sharp irregular borders on both sides of separation. In contrast, a bipartite sesamoid has smooth cortical edges and a total size larger than that of a single sesamoid. In addition, bipartite sesamoids are often bilateral, and a radiograph of the contralateral foot can assist in the diagnosis.⁴

Other imaging studies are useful in evaluating sesamoid stress fractures. An MRI is an excellent tool to localize disease and differentiate between bone and soft tissue abnormalities. It can assess sesamoid viability, joint degeneration, and tendon continuity. A bone scan can have a high rate of false positives. A three-phase technique is helpful, with pinhole images to differentiate between the sesamoids. A CT scan can help to identify a stress fracture as well as delineating the degree of metatarsal–sesamoid arthrosis and fracture healing (Fig. 31-9).

Treatment

Surgical Treatment

Indications for surgery consist primarily of pain longer than 6 months, functional loss, and failure of nonoperative modalities. Operative treatment options include sesamoidectomy, either total or partial, and bone grafting. Tibial sesamoidectomy can result in a loss of push-off strength of up to 10%. This loss, although apparently small, may be appreciated by the running athlete. Hallux valgus and a bunion deformity can occur also after tibial hallux sesamoidectomy. If the patient has a preoperative hallux valgus deformity, then a concomitant distal metatarsal osteotomy should be considered.

In an effort to avoid tibial hallux sesamoidectomies, primarily in the athlete with stress fracture nonunions, a bone grafting procedure was described by Anderson and McBryde.5,77 Subsequent studies have shown favorable results with this technique for chronic stress fracture nonunions of the tibial sesamoid in which there was less than 2 mm of diastasis and no gross motion between the two fragments.⁵ Other contraindications include cystic fragmentation of the sesamoid, avascular necrosis, disproportionately sized fragments, and chondromalacia or frank arthritis of the sesamoid–metatarsal articulation.

Sesamoid Bone Grafting

Surgical Technique

1. A general or regional anesthetic is used.

2. Under tourniquet control, a medial–plantar medial skin incision is fashioned over the hallux metatarsophalangeal joint, extending approximately 5 cm (Figs. 31-10 and 31-11). The plantar medial digital nerve should be meticulously dissected and then protected throughout the procedure.

Figure 31-10 A medial incision along the hallux metatarsophalangeal joint is used for the bone grafting procedure.

Figure 31-11 Exposure of the medial capsule and abductor hallucis tendon.

3. A longitudinal capsulotomy is made along the superior border of the abductor hallucis tendon, allowing inspection of the joint and, in particular, the tibial hallux sesamoid (Fig. 31-12). Should the sesamoid have an intact and disease-free articular surface, bone grafting is pursued.

Figure 31-12 The capsule and abductor tendon have been longitudinally divided to allow intraarticular exposure of the sesamoid.

4. An extraarticular approach to the sesamoid is made along the plantar aspect of the joint complex, reflecting the overlying FHB tendon. A transverse fissure is identified in the waist of the sesamoid, and the fibrous union is curetted back to viable bone edges (Fig. 31-13). It is very important not to violate the articular surface or create instability between the two fragments.

Figure 31-13 Extraarticular exposure of the tibial sesamoid and identification of the fibrous nonunion. A curette is used to expose viable bone edges.

5. A cortical window is made in the medial aspect of the metatarsal head (Fig. 31-14). Cancellous bone is harvested and packed into the defect created between the proximal and distal poles of the sesamoid (Fig. 31-15).

Figure 31-14 A window is created in the medial aspect of the metatarsal head to harvest cancellous bone for grafting.

Figure 31-15 Bone graft is packed into the defect of the tibial sesamoid.

6. The overlying FHB and soft tissue is reapproximated with absorbable suture. Internal fixation has not been found necessary as long as there is no gross motion between the two fragments. If desired, cerclage suture can be placed around the sesamoid, but axial fixation should be avoided because it can comminute the fragments or lessen the surface area for osseous bridging.

Postoperative Care

The patient is placed in a plaster splint postoperatively, consisting of a toe spica extension about the hallux, maintaining slight plantar flexion. Strict non–weight bearing is recommended for 4 weeks, followed by protected weight bearing in a rigid sole boot or heel-only sandal for an additional 4 weeks. The patient may then bear weight in an accommodative shoe with a rigid sole and internal arch support.

Serial radiographs are assessed for union. A CT scan can assist with this determination (Fig. 31-16). Once healed and asymptomatic, typically at 3 months after surgery, running may commence but with the addition of a turf toe insert to minimize hallux metatarsophalangeal dorsiflexion.

Figure 31-16 Tomogram noting union across the sesamoid at 14 weeks after surgery.

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