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Heel pain results in 1 million medical visits per year and comprises 1% of all visits to orthopaedic surgeons.
The majority of patients with heel pain will be treated successfully nonoperatively.
Heel pain can be plantar (subcalcaneal) or posterior.
Posterior pain is often due to insertional Achilles tendinopathy &/or retrocalcaneal bursitis.
Etiologies of heel pain include:
Plantar fasciitis, most common by far
Plantar nerve impingement/entrapment
Calcaneal stress fracture
Fat pad atrophy
Cavus or calcaneus deformity
Inflammatory enthesopathy
Plantar fasciitis is thought to be due to irritation of the proximal plantar fascia.
Plantar fasciitis has been associated with a tight gastrocnemius and hamstrings.
Specialized imaging studies are typically not needed in the diagnosis and treatment of plantar fasciitis.
Initial treatments for plantar fasciitis include rest, antiinflammatories, heel cups, full orthotics, corticosteroid injections, stretching exercises, and immobilization (night splint or cast).
Because most patients with plantar fasciitis have a tight gastrocnemius, stretching is a logical treatment choice.
Treatments for recalcitrant plantar fasciitis include extracorporeal shock wave therapy, radiofrequency ablation, low-level laser therapy, platelet-rich plasma, botulinum toxin injections.
If plantar fasciitis symptoms have persisted more than 6 months despite appropriate treatment, surgery can be considered. There are several surgical options.
The Achilles tendon inserts on the posterior calcaneus.
Fibers continue plantarward to merge with the origin of the plantar fascia.
Between the Achilles tendon and the posterosuperior calcaneal tuberosity lies the retrocalcaneal bursa.
This bursa is deep to the Achilles tendon.
The plantar fascia runs from its origin on the plantar calcaneus to spread out into the plantar aponeurosis.
The plantar aponeurosis consists of 3 segments:
The medial and lateral segments cover the abductor hallucis and abductor digiti quinti.
The central portion of the plantar aponeurosis originates from the medial tuberosity of the calcaneus and is referred to as the plantar fascia.
The central portion inserts into the plantar plate of the proximal phalanges and through the sesamoids into the great toe.
Hyperextension of the toes and metatarsophalangeal joints tenses the plantar fascia, raises the longitudinal arch of the foot, inverts the hindfoot, and externally rotates the leg.
This apparatus is referred to as the windlass mechanism.
The windlass effect provides a passive mechanism for increased foot stability.
The subcutaneous tissue under the calcaneus is the plantar fat pad.
Fibrous septa enclose small “cells” of adipose, giving the entire structure the ability to absorb shock during gait.
The tibial nerve branches just at or above the medial malleolus into the medial and lateral plantar nerves.
The medial calcaneal nerve comes off the medial plantar nerve at this level to supply sensation to the medial, posterior, and inferior heel.
When making a posteromedial ankle incision, this nerve can be injured if the incision is carried too far distally.
The 1st branch of the lateral plantar nerve runs under the inferomedial calcaneus and deep to the fascia of the abductor hallucis.
It provides motor function to the abductor digiti minimi and the flexor digiti brevis as well as innervation to some calcaneal periosteum.
Heel spurs were originally thought to be an etiology of heel pain.
Epidemiologic studies, however, have improved our understanding of their origin.
Heel spurs are present in ~ 50% of patients with subcalcaneal pain syndrome and in ~ 15% of the general population.
Less than 5% of patients with spurs have pain.
Spurs were assumed to originate in the plantar aponeurosis but are actually located in the origin of the flexor hallucis brevis.
This too casts doubt on the spur’s role in the etiology of heel pain.
Spurs are probably caused by chronic inflammation and are not the primary etiology of heel pain.
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