Deformity can affect all portions of the foot, including the forefoot, midfoot, and hindfoot. When associated with pain, nonsurgical treatment is always attempted. When surgical treatment is indicated, the mechanical structure and function of the foot and ankle are considered. In low-energy trauma resulting in ligamentous injuries, ankle sprains are typically treated nonsurgically at first, although midfoot sprains associated with instability may require acute surgery.

Hallux valgus (HV) deformity is defined as the lateral deviation of the proximal phalanx of the first metatarsophalangeal joint (MTP). The etiology is a combination of intrinsic factors such as genetic predisposition, or a hypermobile first tarsometatarsal joint, and extrinsic factors, predominantly related to high-heeled shoes with a narrow toe box. Other predisposing factors include rheumatoid or inflammatory arthritis, generalized ligamentous laxity, and dysmorphism of the first metatarsal (MT). The deformity is usually progressive, although the rate and degree of progression is often nonlinear. HV is most commonly seen in female patients in their fourth or fifth decades of life.

The pathoanatomy of HV involves gradual failure of the medial supportive structures (medial collateral ligament and tibial sesamoid) resulting in a varus position of the first metatarsal. Valgus deviation at the MTP joint of the proximal phalanx subsequently develops. As the deformity progresses, the alignment of the flexor and extensor hallucis longus tendons shifts laterally relative to the MTP joint, further exacerbating the deformity. The first MT varus results in a prominent first MT head medially which is the bump or “bunion” of which the patient reports. This prominent medial eminence is a common source of pain related to shoe wear. Secondary pathology and deformity can develop in the lesser toes, such as hammertoes and claw toes, which may be symptomatic.

The severity of the hallux valgus deformity and any associated pes planus can be best assessed while the patient is standing. While seated, the first MTP joint area is evaluated for signs of local irritation and bursal hypertrophy secondary to shoe wear, tenderness over
the medial eminence, and range of motion of the first MTP joint. Any pain with motion may suggest arthritis within the joint. Numbness can occur in the dorsal medial cutaneous nerve distribution because of external pressure from a shoe. The first tarsometatarsal joint is evaluated for hypermobility, which remains a diagnostic challenge with poor reproducibility.¹

Diagnostic confirmation of HV is made with the use of standard AP and lateral weight-bearing radiographs, as non-weight-bearing radiographs tend to underestimate the deformity.² Radiographs should be assessed for presence of arthritis at the first MTP joint, severity of the deformity as determined by the intermetatarsal angle between the first and second metatarsals (IMA), sesamoid subluxation, and the hallux valgus angle (HVA) (Figure 1). Radiographs are also assessed for first tarsometatarsal hypermobility (Figure 2, A and B) and congruency of the MTP joint, which is assessed by measuring the distal metatarsal articular angle (DMAA) of the first MT head (Figure 3). This metatarsal dysmorphism may be present more often in patients with juvenile onset of HV and in males.

Treatment of hallux valgus deformity should initially include wearing a wider toe-boxed shoe to accommodate the deformity. There are a number of orthotic devices including pads, spacers, arch supports, and night splints available, but none of these have been demonstrated to be successful.

The major indication for surgery following failure of the above modalities is pain; there is no indication for cosmetic surgery. More than 100 surgical procedures have been described to correct HV deformities, with no single procedure indicated for all HV varieties. Figure 4 outlines a suggested algorithm for managing patients with recalcitrant HV deformities and pain. The presence of degenerative arthritis within the first MTP joint typically requires a fusion of the first MTP joint. In the absence of arthritis, joint-sparing procedures can usually be performed using osteotomies for deformity correction. However, if hypermobility or arthritis of the first tarsometatarsal joint is present, a first tarsometatarsal fusion with correction of the intermetatarsal angle (Lapidus procedure) should be undertaken. The Lapidus procedure should always be performed together with a medial eminence resection and a distal soft-tissue rebalancing procedure at the first MTP joint (modified McBride procedure).

If there is concern about an abnormally high DMAA (usually greater than 15°), a double osteotomy is required to correct both the joint angulation and the intermetatarsal deformity which typically involves a medial closing wedge osteotomy of the distal first MT.

In the absence of the above concerns, focus of the correction is dependent on the severity of the deformity.³ In mild deformities with a normal IMA (<9°), no osteotomy is required. The medial eminence is resected, the medial capsule is reefed, and a modified McBride procedure is performed to release the contracted lateral structures preventing deformity correction. These structures include the following:

Moderate deformities (IMA 10° to 14°) may undergo a chevron osteotomy, which is a distal osteotomy of the first MT followed by translation of the metatarsal head laterally. Fixation is maintained with a temporary Kirschner wire or a bone screw.

In severe deformities characterized by an IMA greater than 14°, a proximal metatarsal osteotomy is required for a more powerful correction. There are a number of described procedures for this including the
scarf, Ludloff oblique, proximal chevron, and crescentic osteotomies. No procedure has been proven superior to another, so long as adequate correction is attained. These procedures should always be combined with a modified McBride procedure.

A variation of hallux valgus is hallux valgus interphalangeus in which the angular abnormality is between the proximal and distal phalanges of the hallux. This is corrected with a medial closing wedge osteotomy of the proximal phalanx (Akin procedure).⁴ Inadequate reduction of the sesamoids back to their anatomic position under the first MT head is the greatest predictor of procedure failure and recurrent deformity.^5,6

Lesser toe deformities develop as a result of tendinous imbalance between the toe flexors and extensors. Extrinsic forces may contribute such as high-heeled shoes, associated HV deformity, long metatarsals, cortisone injections, and inflammatory arthritic conditions.

Nonsurgical treatment includes high toe box shoe wear, inserts including metatarsal pads, Budin splints, and stiff-soled shoes. Steroid injections should be used judiciously as they may result in progression of the deformity.

Flexion contracture at the distal interphalangeal joint (DIPJ) with neutral alignment of the proximal IPJ and MTP joint is called a mallet toe (Figure 5, A). Pain can occur at the dorsum of the DIPJ as this rubs against the shoe, or at the tip of the toe which impacts the floor. In flexible deformities correction can be obtained through percutaneous release of the flexor digitorum longus tendon at the DIPJ. Fixed deformities are managed with a resection arthroplasty with or without arthrodesis of the DIPJ.

Hammer toe deformity is a flexion contracture of the proximal IPJ of the lesser toe, with a stable MTP joint (Figure 5, B). Pain and callus formation usually occurs at the dorsum of the proximal IPJ. Flexible deformities are treated with a flexor to extensor tendon transfer, whereas fixed deformities require an excision arthroplasty of the proximal IPJ with or without arthrodesis (hammer toe correction).

Chronic and severe hammer toe deformities may result in synovitis at the MTP joint leading to secondary instability of the joint. As the plantar plate gets stretched
out or tears, an extension deformity will develop at the MTP joint.⁷ In combination with the proximal IPJ flexion, the deformity is considered a claw toe (Figure 5, C). Claw toes can also develop secondary to intrinsic muscle weakness often associated with neuromuscular conditions. If concomitant pathology develops within the collateral ligaments of the MTP joint, medial or lateral deviation will occur resulting in a crossover toe deformity. These conditions are frequently associated with metatarsalgia as the plantar fat pad atrophies or displaces distally as the proximal phalanx extends. Surgical treatment for claw toes usually includes a shortening distal oblique osteotomy of the metatarsal to unload the MTP joint, combined with a hammer toe correction. The osteotomy also rebalances the metatarsal cascade in the setting of a long metatarsal. Newer procedures include repairing the plantar plate to the proximal phalanx insertion with strong nonabsorbable suture.⁸ If there is a crossover component to the deformity, the damaged collateral ligament needs to be repaired with nonabsorbable sutures to balance the coronal alignment of the toe.

Adult acquired flatfoot deformity (AAFD) is characterized by collapse of the medial longitudinal arch, hindfoot valgus, and midfoot abduction related to dysfunction of the posterior tibial tendon (PTT).

The PTT inverts the hindfoot, which locks the transverse tarsal joint, providing a stable platform for push-off during gait. When the PTT degenerates, the hindfoot falls into valgus, which stresses the medial static stabilizers of the ankle and foot, including the spring ligament. The navicular translates laterally, because of spring ligament incompetence, resulting in medial talar head uncoverage and midfoot abduction. Progressive valgus stress through the ankle may result in deltoid ligament incompetence, talar tilt, and ankle arthritis. A gastrocnemius contracture develops as the axis of pull shifts laterally, which can further exacerbate the valgus alignment. AAFD is most commonly seen in overweight, middle-aged females. Risk factors include obesity, diabetes, hypertension, trauma, and history of cortisone injections.⁹ Subtalar joint orientation may predispose some patients to developing AAFD.¹⁰

The most common classification system is based on the degree of deformity¹¹ (see Table 1). Stage I is tendinopathy of the posterior tibial tendon in the absence of significant deformity. Stage II is characterized by a flexible deformity with talar head uncoverage seen on the weight-bearing AP foot radiograph. Talar head uncoverage of greater than 30% differentiates between a stage IIa and IIb deformity. Stage III is a rigid deformity due to arthritis in the hindfoot, and stage IV indicates ankle joint involvement.

Clinically, the patients present with medial ankle pain and gait dysfunction related to deformity. With progressive disease, lateral ankle pain may develop because of subfibular impingement. On examination, there is tenderness over the PTT. Standing evaluation from behind the patient demonstrates valgus alignment. If the patient is able to perform a single-limb heel rise and the hindfoot inverts as the heel elevates, the PTT remains functional and the deformity is considered flexible. If the hindfoot does not invert, the deformity is considered rigid. The presence of a gastrocnemius contracture is assessed with the Silfverskiold test, making sure to invert the hindfoot out of valgus during examination.¹²

Weight-bearing radiographs of the foot and ankle are evaluated for degree of deformity and degenerative changes. Arch collapse is quantified by measuring Meary’s angle on the lateral view (see Figure 6, A), and percentage uncoverage of the talar head on the AP
foot radiograph is measured (see Figure 6, B). A hindfoot alignment radiograph may be useful to measure hindfoot moment arm, which can predict the amount of intraoperative deformity correction required¹³ (see Figure 6, C). Ankle radiographs should always be performed to assess for valgus talar tilt (see Figure 6, D). MRI may demonstrate degeneration in the PTT and spring ligament injury; however, it is not a requisite preoperative study in the presence of significant deformity.

Nonsurgical treatment is recommended before considering surgery. Anti-inflammatory medications, rest, and immobilization should be used initially, especially in the setting of an acute exacerbation of pain. Custom orthotics including arch support with medial heel posting may help with alignment in milder cases, together with physical therapy to work on gastrocnemius stretching and eccentric strengthening of the PTT. In the setting of more severe deformity, a custom-molded ankle-foot orthosis (AFO) or Arizona brace may help to mitigate symptoms.

Flatfoot reconstruction in the setting of a flexible deformity involves a combination of flexor digitorum longus (FDL) tendon transfers and realignment osteotomies, usually combined with a lengthening of the Achilles tendon. While exposing the PTT and FDL, the
spring ligament overlying the talar head is assessed for tear. Direct repair or reconstruction of the spring ligament may improve midfoot abduction.¹⁴ To improve hindfoot valgus, a medializing calcaneal osteotomy (MCO) is performed. Abduction can be further corrected by performing a lateral column lengthening (LCL), which involves placing bone graft or a metal wedge along the lateral aspect of the calcaneus, proximal to the calcaneocuboid (CC) joint.¹⁵ Once the hindfoot and midfoot are corrected, the forefoot is assessed for residual supination, which can be corrected with a dorsal opening wedge cuneiform osteotomy to plantarflex the first ray.¹⁶ If there is arthritis or instability through the first tarsometatarsal (TMT) joint, an arthrodesis can be performed. Rigid flatfoot deformity is treated with a realignment arthrodesis of the subtalar and talonavicular joints. The CC joint may also be fused if arthritis is present. In the setting of AAFD with talar tilt, the presence of arthritic changes in the ankle is an indication for ankle arthrodesis or arthroplasty. If there is talar tilt and preserved ankle cartilage, deltoid ligament reconstruction can be considered.¹⁷ Flatfoot reconstruction is associated with sustained improvement in functional scores and pain.¹⁸ Total recovery time may take up to 2 years, and pain relief is sustained thereafter.^18,19,20

A cavus foot is one with a high medial longitudinal arch. Approximately 10% of skeletally mature individuals have cavovarus (CV) foot alignment,²¹ with most of these individuals being asymptomatic. Unlike planovalgus deformity, which is usually degenerative in origin, many patients with a cavovarus foot deformity have underlying neurologic/neuromuscular disorder. The most common disorder is Charcot-Marie-Tooth disease (hereditary motor sensory neuropathy type I), a progressive condition which affects 50% of patients with a neuromuscular cavovarus foot. A neurologic/neuromuscular etiology should be expected when there is a family history of cavus feet, rapid onset and progression of a cavus foot deformity, marked asymmetry in foot shape, very severe deformity especially with marked clawing of the toes, focal wasting (anterior or lateral compartments) or spasticity (deep posterior compartment), or other neurologic findings. Nonneurologic causes include congenital clubfoot, posttraumatic (calcaneus or talar neck fracture with varus malunion), missed compartment syndrome, burn contractures, and idiopathic etiology.

Neuromuscular imbalance between a nonfunctioning peroneus brevis muscle and its antagonist, the posterior tibialis muscle, pulls the hindfoot into varus. Similarly, forefoot-driven varus can occur when a relatively weak anterior tibialis muscle is overpowered by its antagonist, the peroneus longus muscle, plantarflexing the first ray resulting in a cavus arch.

Clinical evaluation starts with observing the patient’s gait for subtle footdrop (anterior tibialis weakness), compensatory toe clawing, ankle instability, and peroneal weakness. The patient’s foot should be evaluated both standing and sitting, and viewed from behind and from the front of the foot. When alignment is evaluated from behind the patient, the calcaneus is seen in a varus position rather than the natural 3° to 5° of valgus. To differentiate if the hindfoot varus is secondary to forefoot varus, a Coleman block test is performed which places a block under the heel and the lateral border of the foot to “elevate” the floor. This allows the plantarflexed first ray to drop down without hitting the floor and supinating the hindfoot. If the hindfoot varus corrects, the deformity is considered forefoot-driven varus or flexible varus²² (Figure 7). The hindfoot flexibility can additionally be evaluated with the patient sitting with the physician passively manipulating the hindfoot into valgus. If the hindfoot deformity does not correct with passive manipulation or the Coleman block test, the deformity is considered hindfoot-driven varus or fixed varus. Fixed varus should not be confused with arthritic involvement and does not require a surgical fusion for correction. Fixed deformity indicates that the Chopart joints are locked in varus and that a hindfoot corrective osteotomy is required.