The biomechanical interactions between the foot and ankle joints are fundamental to maintaining normal function and preventing degeneration and pain. These interactions can be influenced by the presence of both congenital and posttraumatic conditions and deformity. Nonsurgical treatments are typically attempted initially; however, if these fail, there are surgical options to allow patients to return to higher activity levels.

Hallux valgus is the most common deformity of the metatarsophalangeal (MTP) joint and can result from both intrinsic and extrinsic factors. These include genetic predisposition, ligamentous laxity, and systemic diseases such as cerebral palsy, rheumatoid arthritis, or inflammatory arthritis.¹ Hallux valgus also can result from extrinsic factors such as wearing high-heeled shoes and shoes with a narrow, pointed toe box. The progression of hallux valgus deformity is a gradual failure of the medial capsule of the MTP joint, leading to varus of the metatarsal.² As a result, the flexor hallucis longus and extensor hallucis longus are laterally deviated relative to the MTP joint axis, and the pull of the adductor hallucis provides a valgus and pronating force on the proximal phalanx. Ultimately the crista of the sesamoids erodes, resulting in lateral subluxation of the sesamoids and further progression of the deformity.

Patients often report pain over the medial eminence (the prominent medial portion of the metatarsal head) and numbness extending into the hallux caused by the stretch of the dorsal medial cutaneous nerve (a branch of the superficial peroneal nerve). Other conditions, including metatarsalgia, hammer toes, and claw toes, may accompany these changes. Patients should be carefully examined for the underlying ligamentous laxity and evidence of MTP joint arthritis because this can influence surgical management. Weight-bearing foot radiographs should be evaluated for the hallux valgus angle (HVA, normal > 15°), intermetatarsal angle (IMA, normal < 9°), and distal metatarsal articular angle
(normal < 10°; Figure 1). Plantar gapping of the first tarsometatarsal (TMT) joint can indicate hypermobility.³ Initial treatment for hallux valgus includes footwear modification, bunion pads, night splints, or special orthotics; however, these have not been shown to be effective for preventing progression of the deformity.

Surgical correction is considered when nonsurgical methods have failed to relieve pain and function. An MTP fusion should be considered in severe bunions or if there is evidence of MTP joint arthritis because deformity correction will not improve arthritic pain. Bunions can be managed surgically by a number of different methods, and the decision is primarily based on characteristics observed on radiographs.¹,⁴ In general, mild bunions (defined as IMA < 12° and HVA < 20°) are often managed with a distal metatarsal osteotomy, whereas moderate bunions (IMA < 15° and HVA < 40°) are best managed with a proximal metatarsal osteotomy. Severe bunions (IMA < 15° and HVA < 40°) may require proximal and distal osteotomies. In addition, if there is evidence of TMT instability, a Lapidus (TMT joint fusion with distal soft-tissue correction) should be performed.³ All osteotomies should be accompanied by a medial eminence resection and a modified McBride procedure (a distal soft-tissue rebalancing procedure involving a lateral capsular release, medial capsule imbrication, and an adductor hallucis release). In addition, if there is evidence of an angular deformity of the proximal phalanx (hallux valgus interphalangeus), a medial-wedge closing osteotomy (Akin) can be performed.¹ Figure 2 provides
a surgical treatment algorithm for hallux valgus correction. Radiographic evaluation of the sesamoids can assist with determining the degree of correction.⁵

Morton neuroma is an entrapment neuropathy involving the transverse metatarsal ligament that most often occurs in the third web space at the location of the confluence of the medial and lateral plantar nerves.⁶ Patients often present with burning plantar foot pain radiating to the toes that worsens with activity, and may note sensation alterations in the toes. Imaging is not required; however, as described in a 2019 study, ultrasonography can be used to visualize a neuroma, whereas MRI and radiographs are best used to rule out other pathologies.⁷ Ethanol or lidocaine injections can be performed for diagnostic or therapeutic purposes.⁶ Nonsurgical treatment for Morton neuroma involves wearing shoes with a wide toe box, metatarsal bars, NSAIDs, and calf stretches. If nonsurgical methods fail, surgical excision can improve symptoms. The most common postoperative complication is either inadequate resection or a stump neuroma.

Lesser toes function with a delicate balance of intrinsic muscles and extensor and flexor tendons. When this balance is disrupted, lesser toe deformities can occur.⁸ Hammer toes (either flexible or fixed) occur when there is a contracture of the proximal interphalangeal joint with extension of the MTP and distal interphalangeal joints. Claw toes occur when the intrinsic muscles overpower the flexor and extensor tendons in the toe, resulting in a flexed deformity of the proximal interphalangeal and distal interphalangeal joints. Because this process is driven by the foot intrinsic muscles, it is often seen with traumatic and neurologic etiologies. Finally, mallet toes are fixed at the distal interphalangeal joint. Treatments include silicone sleeves or Budin splints. For flexible deformities, surgical management involves the tendons (eg, flexor digitorum longus tenotomy with or without extensor digitorum longus repair at the distal interphalangeal joint), whereas fixed deformities involve interphalangeal joint resection or arthrodesis⁹ (Table 1).

A bunionette is the deviation of the fifth metatarsal, causing pain on the lateral aspect of the foot.¹⁰ A type I bunionette is an overgrowth of the lateral condyle of the metatarsal head, whereas a type II presents as a curved metatarsal. A type III bunionette presents as a widened IMA of the fourth and fifth metatarsals. Treatment of bunionettes is primarily nonsurgical, including shoe modifications and orthotics. Surgical treatment of a type I bunionette includes ostectomy of the metatarsal head; types II and III require metatarsal osteotomies to correct alignment.¹⁰,¹¹

Turf toe is a disruption of the plantar capsuloligamentous complex of the great toe caused by an axial load with the foot in equinus. This results in hyperextension of the first MTP joint.¹² The injuries range from a stretching of the capsuloligamentous complex (grade 1) to a complete tear of the capsuloligamentous complex (grade 3). Patients often present with pain and swelling at the MTP joint and pain with extension of the great toe. Weight-bearing radiographs of both feet can
be used to evaluate for proximal migration of the sesamoids, which suggests a tear of the capsuloligamentous complex. If there is clinical suspicion of this injury, MRI can be used to determine the degree of ligamentous and articular injury.

Treatment of grade 1 and 2 turf toe includes symptomatic management with stiff insoles or a Morton extension foot plate or a short period of immobilization in a controlled ankle movement boot or a toe spica in mild plantar flexion. Cortisone should not be used because it can weaken the capsule. Surgical intervention can be considered in the setting of a traumatic bunion, a loose body, or grade 3 injury with significant sesamoid retraction or a large capsular tear.¹³ Surgical intervention involves repair of the plantar capsuloligamentous complex and can result in good outcomes in cases of a grade 3 turf toe injury.¹²,¹⁴

Plantar plate injuries to the lesser toes can be a result of acute or chronic trauma and can occur with inflammatory arthritis, neuromuscular disease, or from multiple steroid injections. The plantar plate stabilizes the MTP joint; therefore, when disrupted the toe dorsiflexes at the MTP joint because the extensor digitorum longus tendon overpowers the intrinsic muscles.¹⁵ Plantar plate injuries often are associated with hammer toes.¹⁶ Nonsurgical treatment options include orthotics with a metatarsal bar, crossover toe taping, a gel toe sleeve, or a Budin splint. Surgical treatment involves a release of the MTP joint and capsule and repair.¹⁷ This procedure often is done in conjunction with a distal metatarsal osteotomy to allow for proper reduction of the joint and to maintain forefoot balance.¹⁶

Progressive collapsing foot deformity (PCFD), previously termed adult acquired flatfoot deformity or posterior tibial tendon dysfunction, is a syndrome resulting from a series of alterations in the architecture of the foot.¹⁸ It often begins as dysfunction of the posterior tibial tendon and the thinning and stretching of the calcaneonavicular (spring) ligament.¹⁹,²⁰ This results in the collapse of the midfoot and valgus tilt of the calcaneus. The rotation of the calcaneus results in uncoverage of the talar head and lateral translation of the navicular on the talus. Although previous classifications were based on deformity and physical examination, there has been recent emphasis on development of a new classification system that better encompasses this pathology associated with PCFD.¹⁸ The new classification is split into flexible (stage I) and rigid (stage II) deformities and is separated into five anatomic locations of deformity labeled A through E (Table 2). For each deformity location, an indication of whether it is flexible or fixed is indicated as well. For example, a patient with a flexible hindfoot valgus and forefoot varus without additional deformity would be classified as 1AC, whereas a patient with a fixed hindfoot valgus with a flexible forefoot varus would be classified as 2A1C. This better represents the spectrum of disease and better classifies the range of deformities in the syndrome. Often initially, patients present with medial pain from posterior tibial tendinitis, and as the deformity worsens the pain shifts to the lateral ankle as a result of subfibular impingement on the calcaneus. Physical examination demonstrates hindfoot valgus and loss of medial arch. When viewed from behind, the “too many toes” sign is evident on the affected foot, and there is failure of inversion when performing a heel raise.

Imaging in patients undergoing evaluation for PCFD should include weight-bearing foot and ankle radiographs to evaluate for the lateral talar/first TMT angle and uncovering of the talar head. Hindfoot alignment views can be helpful as well for surgical planning. Although not required for diagnosis, advanced imaging modalities such as CT or MRI can be performed to identify the presence of subtalar osteoarthritis and to evaluate the posterior tibial tendon integrity. Initial treatments for PCFD include NSAIDs, ice, medial heel post orthotics, and physical therapy focusing on posterior tibial tendon strengthening. If the deformity changes extend into the ankle, an Arizona brace can be prescribed. If nonsurgical measures have failed, surgical treatment is based on the degree and locations of deformity.

Surgical treatment of patients with PCFD is based on the location and flexibility of deformities. In most cases if a deformity is flexible, osteotomies are performed to improve alignment, whereas fusions are performed in the setting of a rigid deformity. For example, a patient with an isolated hindfoot valgus with adequate talonavicular coverage and without forefoot varus can be treated with an isolated bony procedure such as medializing calcaneal osteotomy. This is often performed in the setting of additional soft-tissue procedures such as a spring ligament reconstruction and/or flexor digitorum longus transfer that often occurs with a gastrocnemius recession.²¹ If there is evidence of talar head uncoverage greater than 50%, a lateral column lengthening is considered and there does not appear to be a difference in outcomes in patients older than 65 years compared with younger patients who undergo the same procedures.²²,²³ For patients with fixed deformities, a double or triple arthrodesis is performed (the subtalar, talonavicular, and calcaneocuboid joints). Once the hindfoot and midfoot procedures are completed, the forefoot should be evaluated for a residual varus deformity, which can develop over time as compensation for the hindfoot valgus. If present, a dorsal opening wedge osteotomy of the medial cuneiform (Cotton) should be performed to prevent lateral foot overload.²⁴ However, if there is evidence of TMT joint arthritis, a first TMT joint plantar flexion fusion should be performed instead of a Cotton osteotomy. Finally, if the deformity extends to the ankle, treatment is based on whether there is evidence of ankle arthritis.¹⁹,²⁰ If cartilage loss is less than 50% on the lateral aspect of the joint and the deformity is flexible, ligament rebalancing through procedures such as a deltoid reconstruction can be performed to restore talar tilt. However, if ankle arthritis is evident, either an ankle fusion or ankle arthroplasty can be considered in conjunction with the foot procedures.

Cavus foot is defined as a plantarflexed first ray, which results in a high medial longitudinal arch. This often occurs in conjunction with a varus deformity of the heel.²⁵ Cavovarus is often bilateral and, for many patients, asymptomatic. Often the development of cavovarus disorder is related to neurologic conditions including cerebrovascular accident, traumatic nerve injuries, or cerebral palsy or can be a result of a posttraumatic deformity from a talar or calcaneal fracture.²⁶,²⁷ One of the most common neurologic conditions resulting in a cavovarus foot deformity is Charcot-Marie-Tooth disease, an autosomal dominant motor sensory neuropathy that presents in two types: type 1, which has an underlying myelin disorder; and type 2, which demonstrates abnormal axonal function, resulting in a later presentation than type 1.²⁵ The neuropathy progresses from distal to proximal, resulting in early dysfunction of the intrinsic muscles in the feet and progressing to the anterior tibialis muscle and then the peroneus brevis. As a result, there is an overpowering by the posterior tibialis muscle and the peroneus longus muscle, pulling the hindfoot into varus and ultimately resulting in plantar flexion of the first ray and a cavus-appearing arch.

These patients can also present with claw toes, metatarsalgia, and subtle foot drop and will describe a history of recurrent ankle sprains or a history of fifth metatarsal fractures in conjunction with ankle sprains, and peroneal tendinopathy.²⁸ Physical examination will reveal an Achilles tendon or gastrocnemius muscle contracture and lateral callosities and a varus hindfoot (peek-a-boo heel sign in which the medial heel pad is visible from the front); however, it is important to evaluate the etiology of the hindfoot varus by the use of the Coleman block test.²⁵,²⁶,²⁷ A block is placed under the heel and the lateral half of the foot, and if the hindfoot varus is corrected, then the varus is considered flexible, or forefoot driven.