- Author: Norman S Turner, MD; Chief Editor: Jason H Calhoun, MD, FACS more...
Pes cavus is a high arch of the foot that does not flatten with weight bearing. No specific radiographic definition of pes cavus exists. The deformity can be located in the forefoot, the midfoot, the hindfoot, or a combination of these sites.
The spectrum of associated deformities observed with pes cavus includes clawing of the toes, posterior hindfoot deformity (described as an increased calcaneal angle), contracture of the plantar fascia, and cock-up deformity of the great toe. This can cause increased weight-bearing for the metatarsal heads and associated metatarsalgia and calluses.
The etiology of pes cavus can be determined approximately 80% of the time. Possible causes include the following:
Malunion of calcaneal or talar fractures
Sequelae resulting from compartment syndrome
The remaining 20% of cases are idiopathic and nonprogressive. Identifying the etiology is essential to determine if the deformity is progressive, which assists in operative planning.
Neuromuscular diseases, such as muscular dystrophy, Charcot-Marie-Tooth (CMT) disease,[2, 3, 4, 5, 6, 7] spinal dysraphism, polyneuritis, intraspinal tumors, poliomyelitis, syringomyelia, Friedreich ataxia, cerebral palsy, and spinal cord tumors, can cause muscle imbalances that lead to elevated arches. A patient with a new-onset unilateral deformity but without a history of trauma must be evaluated for spinal tumors.
Multiple theories have been proposed for the pathogenesis of pes cavus. Duchenne described intrinsic muscle imbalances causing an elevated arch. Other theories include the extrinsic muscle and a combination of the intrinsic and extrinsic muscles being causes of the imbalance.
Mann described the pathogenesis of pes cavus in patients with CMT disease. An understanding of the muscles involved and the sequence of the involvement helps in understanding the deformity. An agonist-antagonist model for the muscles determines the deformity. In CMT, the anterior tibialis and the peroneus brevis develop weaknesses. Antagonist muscles, the posterior tibialis and peroneus longus, pull harder than the other muscles, causing deformity.
Specifically, the peroneus longus pulls harder than the weak anterior tibialis, causing plantarflexion of the first ray and forefoot valgus. The posterior tibialis pulls harder than the weak peroneus brevis, causing forefoot adduction. Intrinsic muscle develops contractures while the long extensor to the toes, recruited to assist in ankle dorsiflexion, causes cock-up or claw toe deformity. With the forefoot valgus and the hindfoot varus, increased stress is placed on the lateral ankle ligaments and instability can occur.
In patients with polio, the deformity is in the hindfoot and is caused by weakness of the gastrocnemius-soleus complex. This leads to a marked increase in the calcaneal pitch angle with normal forefoot alignment.
The pathophysiology of the deformity is based on the etiology (see Etiology).
The presentation for patients with pes cavus is highly variable, depending largely on the extent of the deformity. Patients can present with lateral foot pain from increased weight-bearing on the lateral foot. Metatarsalgia is a frequent symptom, as is symptomatic intractable plantar keratosis. Ankle instability can be a presenting symptom, especially in patients with hindfoot varus and weak peroneus brevis. Weakness and fatigue can be observed in patients with neuromuscular disease. Symptom severity is as variable as the symptoms themselves.
Evaluation of a patient who presents with pes cavus begins with a thorough history and complete examination to determine the etiology. Patients with a unilateral deformity frequently have a history of major trauma. Neuromuscular disorders can be identified by family history. A new-onset unilateral deformity is highly suggestive of a spinal cord tumor and necessitates an appropriate workup.
Examination begins with observation of the gait. Hindfoot positioning is evaluated through gait analysis looking for varus. During swing phase, analysis of foot positioning is carried out, looking for anterior tibialis weakness and foot drop. Cock-up toes can be observed with recruitment of the extensor hallucis longus (EHL). The shoe should also be inspected for increased lateral wear.
The range of motion of the ankle, subtalar, midfoot, and forefoot is examined. The deformity is determined to be flexible or rigid. The forefoot is observed for plantarflexion, and the hindfoot is observed for varus. Documenting the strength of the individual muscles is essential for determining surgical options. Agonist and antagonist muscle weakness must be carefully examined, especially in CMT disease.
The Coleman block test determines if the subtalar joint is flexible. The test is performed by having a patient stand with a 1-in. wood block under the heel and lateral foot. This allows the first ray to be plantarflexed off the block. If the hindfoot corrects to a neutral position, the deformity is flexible. If the hindfoot does not correct, the deformity is rigid.
A neurologic examination is required, specifically including detailed muscle strength testing. Sensory examination reveals deficits that can be observed in CMT disease.
The goal of treatment is to produce a plantigrade foot that allows even distribution of weight. Failure to maintain an asymptomatic plantar grade foot is an indication for surgery.
The relevant anatomy depends on the etiology of the deformity and the procedure performed (see Surgical therapy).
An absolute contraindication for surgery is poor vascularity. Revascularization should be performed before reconstruction if warranted. Ideally, the soft tissues around the ankle and foot should be intact, without excessive swelling or ulceration. If an ulcer is present, the wound should be healed before reconstruction in order to minimize infection risk.
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