Foot & Ankle Disorders
From first-step heel pain to the midfoot injury everyone misses
Heel and hindfoot pain
Plantar fasciitis. The most common cause of heel pain is degenerative irritation of the plantar fascia at its origin on the medial calcaneal tubercle. Obesity, prolonged standing, running, flat or high-arched feet, and a tight Achilles tendon predispose. Sharp plantar heel pain is worst with the first steps in the morning or after sitting and eases as walking continues, often returning at the end of the day. Point tenderness at the medial calcaneal tubercle, reproduced by passively dorsiflexing the great toe (windlass test), makes a clinical diagnosis without imaging.
Treatment. Plantar fascia and calf stretching, heel cups or cushioned arch supports, NSAIDs, activity modification, and night splints resolve most cases within about a year. A calcaneal spur on radiographs is common in painless feet and is incidental, never a reason for surgery. Refractory cases may receive a corticosteroid injection (risks fat pad atrophy and fascia rupture) or extracorporeal shock-wave therapy.
Tarsal tunnel syndrome. The posterior tibial nerve is compressed beneath the flexor retinaculum behind the medial malleolus by a ganglion, varicosities, flat foot, or prior trauma. Burning, tingling, and numbness of the sole worsen with standing and at night, unlike the mechanical first-step pain of plantar fasciitis. A Tinel sign behind the medial malleolus supports the diagnosis, nerve conduction studies confirm it, and treatment is orthotics, NSAIDs, or injection, with surgical release for refractory symptoms or a space-occupying lesion.
Achilles tendinopathy. Pain, morning stiffness, and tenderness sit 2–6 cm above the calcaneal insertion, the hypovascular midportion, or at the insertion itself, typically after a surge in running volume. Fluoroquinolones raise the risk of tendinopathy and rupture, especially with concurrent glucocorticoids, age over 60, or kidney or transplant disease. Relative rest, eccentric calf loading (slow heel drops), and heel lifts are first line; stop the fluoroquinolone and avoid steroid injection. A palpable gap with no plantarflexion on calf squeeze (Thompson test) indicates rupture instead.
Forefoot pain
Morton neuroma. Perineural fibrosis of a common plantar digital nerve, usually between the 3rd and 4th metatarsal heads, occurs mostly in women wearing narrow or high-heeled shoes. Burning forefoot pain radiates into the toes, feels like walking on a pebble, and eases when the shoe is removed. Squeezing the metatarsal heads while pressing the web space produces a painful click (Mulder sign). Management is wide, low-heeled shoes and a metatarsal pad placed just proximal to the metatarsal heads, then corticosteroid injection, with excision for refractory pain.
Hallux valgus. The great toe deviates laterally at the first MTP joint while the first metatarsal drifts medially, producing a medial bunion that rubs on shoes. Women, narrow or high-heeled footwear, and family history predispose, and the crowded second toe may become a hammer toe. Wide toe-box shoes, padding, and orthotics come first; osteotomy is reserved for persistent pain rather than appearance.
Metatarsal stress fracture. March fractures most often affect the 2nd metatarsal shaft, then the 3rd, after a sudden increase in activity in military recruits, runners, and dancers, or in low bone density. Pain builds gradually with point tenderness over the shaft. Radiographs are often normal for the first 2–3 weeks, so MRI (the most sensitive test) or presumptive treatment with repeat films is appropriate. Treatment is rest in a stiff-soled shoe or walking boot for about 4–6 weeks. In a young female athlete, screen for low energy availability.
Fifth metatarsal fractures
Why location matters. The proximal fifth metatarsal has a vascular watershed at the metaphyseal–diaphyseal junction, so fractures a short distance apart behave very differently. Tenderness at the base of the fifth metatarsal is one of the Ottawa foot criteria for obtaining radiographs.
| Feature | Tuberosity avulsion (pseudo-Jones) | Jones fracture |
|---|---|---|
| Location | Tuberosity (zone 1) | Metaphyseal–diaphyseal junction, about 1.5–2 cm distal (zone 2) |
| Mechanism | Inversion; peroneus brevis and lateral plantar fascia pull | Adduction force on the forefoot, pivoting athletes |
| Blood supply | Good; most common proximal fracture | Watershed; delayed union and nonunion common |
| Treatment | Walking boot or hard-soled shoe, weight bearing as tolerated; heals in about 6–8 weeks | Non-weight-bearing short-leg cast for 6–8 weeks; early intramedullary screw in athletes or nonunion |
Midfoot and ankle injuries
Lisfranc injury. The tarsometatarsal joint complex is stabilized by the Lisfranc ligament, which runs from the medial cuneiform to the base of the 2nd metatarsal. An axial load on a plantarflexed foot (a tackled football player, a missed step) or a crush disrupts it, causing midfoot pain and swelling, inability to bear weight, and plantar midfoot ecchymosis, the key clue. Non-weight-bearing films often look normal, so obtain weight-bearing or comparison views showing diastasis between the 1st and 2nd metatarsal bases or a fleck sign (avulsion fragment), with CT or MRI when equivocal. Unstable injuries need ORIF or fusion; a missed injury leads to midfoot collapse and arthritis.
Ankle fracture stability. The ankle mortise behaves as a ring: a break in one place may be stable, whereas two breaks let the talus shift. The Danis-Weber system grades lateral malleolus fractures by their level relative to the tibiofibular syndesmosis.
| Type | Fibular fracture level | Stability and management |
|---|---|---|
| Weber A | Below the syndesmosis | Stable: boot or cast, weight bearing |
| Weber B | At the syndesmosis | Stable if the medial side is intact; medial clear-space widening → ORIF |
| Weber C | Above the syndesmosis | Syndesmosis torn, unstable: ORIF |
Pitfalls. Always palpate the proximal fibula: a Maisonneuve fracture (proximal fibular fracture with medial ankle injury) signals syndesmotic disruption that needs fixation.
A dislocated ankle with tented skin or a pulseless foot is reduced and splinted immediately, before radiographs.
Charcot neuroarthropathy
Pathogenesis. Loss of protective sensation (diabetic neuropathy most often; also tabes dorsalis and leprosy) allows repetitive unperceived trauma, while autonomic hyperemia promotes bone resorption. Bones fragment and joints sublux and collapse, usually in the midfoot.
Recognition. The acute foot is unilateral, red, swollen, and warm, often more than 2 °C warmer than the other foot, yet surprisingly painless. The skin is intact, fever is absent, and the WBC is normal, but it is easily mistaken for cellulitis, gout, or DVT. Redness that fades after a few minutes of elevation favors Charcot. Early radiographs may be normal; MRI shows bone marrow edema and fragmentation. Osteomyelitis becomes the concern when there is an ulcer, especially one that probes to bone.
Treatment. Immediate offloading in a total contact cast, non-weight-bearing or protected, continues until warmth and swelling resolve and radiographs stabilize, typically several months. The disease passes through fragmentation, coalescence, and reconstruction stages, after which custom footwear or a Charcot restraint orthotic walker protects the foot. Without offloading, the midfoot collapses into a rocker-bottom deformity with plantar ulcers, osteomyelitis, and amputation.