The causes of cavovarus foot can broadly be classified into neurological, post-traumatic, residual clubfoot and idiopathic. The common final pathway involves imbalance of the muscles around the foot and ankle, often with weakness of tibialis anterior and peroneus brevis and relatively stronger tibialis posterior and peroneus longus.
The commonest cause of bilateral deformity is Charcot-Marie-Tooth disease. Unilateral pathology may be a result of spinal pathology. Neurological causes can involve any structures from the motor cortex to peripheral nerves. The deformities can vary from subtle and flexible to severe and fixed. The spectrum of pathology involves plantarflexed first ray, forefoot pronation and adduction, and hindfoot varus or high calcaneal pitch.
It is the most common inherited progressive sensory motor neuropathy. It results from defects in the genetic code for the protein of the peripheral myelin sheath and is classified into subtypes varying in progression.
Type I CMT is a demyelinating condition that slows nerve conduction velocity. It is autosomal dominant, presents in first or second decade of life and most commonly leads to cavus foot.
Type II is a result of direct axonal death caused by Wallerian degeneration. It is usually less disabling than Type I, presents in second decade of life or later and most commonly leads to flaccid foot. CMT IA is the most common type. In most cases, the disease process is progressive rather than static; therefore, the deformities worsen and surgical treatment must be considered to prevent the progression to a fixed and symptomatic deformity.
Primary or idiopathic cavovarus foot is diagnosed by elimination in more than half the cases and it is generally believed that it is the consequence of a latent neurological disorder. Therefore, neurological disorders must be looked for in the family histor clinical assessment and electrophysiological evaluation.
The deformity can be divided into posterior, anterior or mixed. Both intrinsic and extrinsic muscle imbalance may play a role in the final deformity. Manoli et al. consider the primary deforming force to be the plantarflexed first metatarsal, which is thought to be a result of peroneus longus overaction.
Relative weakness of the peroneus brevis and tibialis anterior muscles with strong tibialis posterior and peroneus longus muscles cause plantar flexion of the first metatarsal and varus of the hindfoot. Recruiting EHL and EDL as secondary ankle dorsiflexors will lead to ‘cock-up’ deformity of the hallux and clawtoe deformity of the lesser toes. To allow the toe pulp to touch the ground, the flexor muscles of the toes contract, producing clawing of the toes, which is also aggravated by a deficiency of the interosseous muscles.
Clawing of the toes accentuates the slope of the metatarsals due to the exaggerated pressure on the metatarsal heads, which in turn increases the tension in the plantar aponeurosis. Additional contracture of the plantar fascia will accentuate the windlass mechanism and further depress the metatarsal heads.
Clinical examination must include a full neurological assessment of the lower limbs. In addition to the detailed foot and ankle examination, Coleman block test should be performed. If the hindfoot varus persists, then the deformity is fixed. If the hindfoot corrects to physiologic valgus, then the deformity is flexible and driven by the forefoot.
Frequently, the hindfoot varus partially corrects, and it is important to see the magnitude of the heel correction beyond neutral or a varus position.
Weight-bearing plain radiographs are important in lateral, frontal and dorsoplantar projections. EMG studies are important to identify or exclude neurological causes.
Coleman Block Test
Hindfoot varus is described as being forefoot or hindfoot driven. In forefoot-driven varus, excessive plantarflexion of the first metatarsal and supination of the midfoot leads to the hindfoot moving into varus, whereas hindfoot-varus-driven is related to simple varus malalignment of the heel. Coleman block test is used to evaluate flexibility of hindfoot. Flexible hindfoot will correct to neutral when block placed under lateral aspect of foot and a rigid hindfoot will not correct into neutral. Hindfoot varus predisposes to chronic lateral instability, rupture of peroneal tendons, development of varus arthritis, tightness of medial gastrocnemius and increased plantar fascia.
Coleman Block test
Majority of patients with mild symptoms associated can be treated by conservative means. The aim is to re-align the hindfoot correctly to offload the lateral border of the foot and to overcome the gastrocnemius tightness. In most cases, a flexible deformity can be corrected using a custom orthosis.
The type of orthotic depends on the Coleman ‘block test’. In a forefoot-driven cavus with a supple hindfoot, correction of the plantarflexed first ray will allow the hindfoot varus to correct and a first ray recess associated with a metatarsal bar and lateral forefoot post are frequent enough. In front of a hindfoot-driven cavus, the appropriate orthosis includes a lateral hindfoot-to midfoot heel wedge with a first metatarsal recess and minimal or absent medial arch support.
High lacing shoes that provide ankle support aid stability and a wide toe box will better accommodate the foot. To treat equinus, a gastrocnemius-stretching programme should be initiated and the heel may be slightly elevated.The ankle instability is treated with proprioception training and an ankle support brace worn during exercise.
Surgery is considered in carefully selected patients if conservative treatments fail. The aim of surgery is to achieve a plantigrade, mobile and pain-free foot. A wide variety of procedures have been described including soft tissue release or lengthening and tendon transfers, hindfoot or midfoot osteotomy, or arthrodesis.
Various soft-tissue procedures are preferred while the deformity is flexible and corrective arthrodesis or osteotomy must be used when the deformity becomes rigid. Soft-tissue release alone is no longer applicable in fixed deformities in adults.
In subtle cavovarus foot, the equinus deformity and fixed forefoot deformity are addressed first and a valgus osteotomy should be performed if required.
The Achilles tendon must be carefully assessed. If a global gastroc-soleus contracture is present, an Achilles tendon lengthening using a triple hemisection is performed. In some cases, an isolated gastrocnemius tightness is addressed by using a gastrocnemius recession.
Achilles tendon lengthening is justified when the heel is in varus, but if the heel is in a neutral position, the increased calcaneal pitch is secondary to Achilles weakness and tendon lengthening should be avoided. To the extent that plantar fascia retraction contributes to the high medial arch, the need for a plantar fascia release is debatable. A subcutaneous plantar fascia release may benefit patients with minimal deformity. In severe fixed pes cavus a complete release is recommended.
Tendon transfers can be used for flexible deformities or in conjunction with bony correction for preventing recurrence of the deformity and should be done within the same surgery. Most authors recommend using peroneus longus to brevis to correct forefoot pronation, reduce the first ray plantarflexion and re-inforce the weak eversion of the hindfoot. Tibialis posterior transfer is more commonly used to weaken the deforming power and strengthen deficient functions of the tibialis anterior.
Dorsal wedge osteotomy of the first metatarsal is an effective way to decrease the medial forefoot plantarflexion. A dorsal wedge is excised around 2 cm from the TMTJ. For severe first ray deformity with poor correctability, a first TMTJ dorsiflexion arthrodesis is preferred, which produces a higher degree of forefoot cavus correction than metatarsal osteotomy.
If the Meary’s angle is markedly increased with poor passive correctability, this dorsal metatarsal osteotomy will be insufficient and a midfoot dorsal wedge osteotomy should be considered. Anterior tarsectomy, described by Cole and Meary, is centred on the naviculo-cuneiform space and the cuboid and consists of a dorsomedial closing-wedge osteotomy that predominantly affects the medial rays. This allows correction in the frontal, sagittal and coronal planes without compromising the tarsal inversion/eversion and dorsoplantar motion of the foot.
When the hindfoot varus is reducible and forefoot-driven, a valgus calcaneal osteotomy is not required. Conversely, if the hindfoot varus is flexible or if there is residual varus after midfoot surgery, a calcaneal osteotomy must be considered. In case of any doubt, an overcorrection is better than an undercorrection.
A varus deformity of the distal tibia can be corrected with a supra-malleolar osteotomy held with internal fixation or in the case of large deformities by using external fixation to achieve gradual correction to protect the medial neurovascular structures.
In cases of rigid cavovarus deformity, the management is challenging and fusions and osteotomies represent the mainstay of treatment once the foot has lost its reducibility. Severe rigid cavus foot requires complex midfoot osteotomies to correct three dimensional multiplanar deformity.
Results of a plantigrade foot obtained by an arthrodesis are better than joint-sparing surgery leading to an inadequate correction. However, many authors consider that it is preferable to fuse the minimum number of joints possible in order to maintain as much function as possible.
In many cases, a triple arthrodesis is indicated but soft-tissue balancing, by means of tendon transfers, must frequently be included in the correction to maintain a successful result over time.
There is a paucity of good quality evidence of treatment of the cavovarus foot. The majority of published studies are of small series of patients. Given the diversity of aetiologies and surgical techniques reported, useful comparisons are difficult. For patients with a mobile hindfoot short to mid-term results following osteotomy of the first ray, calcaneus or both combined with soft tissue release and tendon transfers appear satisfactory.
For patients undergoing fusion there is little reported on long term outcomes. Wukich et al. found good objective outcomes in only 32% of patients at average 12 year follow up following triple arthrodesis for cavovarus due to CMT. Wetmore and Drennan reported similar results with only 24% of patients reporting good or excellent results following triple arthrodesis at a mean follow up of 21 years.
C Maynou, C Szymanski, A Thiounn, Instructional Lecture, EFORT open reviews, EOR volume 2, MAY 2017; DOI: 10.1302/2058-5241.2.160077.
Joo SY, Choi BO, Kim DY, et al. Foot deformity in charcot marie tooth disease according to disease severity. Ann Rehabil Med 2011;35:499-506.
Berciano J, Gallardo E, García A, et al. New insights into the pathophysiology of pes cavus in Charcot-Marie-Tooth disease type 1A duplication. J Neurol 2011;258: 1594-1602.
Rosenbaum AJ, Lisella J, Patel N, Phillips N. The cavus foot. Med Clin North Am 2014;98:301-312.
Coleman SS, Chesnut WJ. A simple test for hindfoot flexibility in the cavovarus foot. Clin Orthop Relat Res 1977;123:60-62.
Ortiz C, Wagner E, Keller A. Cavovarus foot reconstruction. Foot Ankle Clin 2009;14:471-487.
O rtiz C, Wagner E. Tendon transfers in cavovarus foot. Foot Ankle Clin 2014;19:
Leeuwesteijn AE, de Visser E, Louwerens JW. Flexible cavovarus feet in Charcot-Marie-Tooth disease treated with first ray proximal dorsiflexion osteotomy combined with soft tissue surgery: a short-term to mid-term outcome study. Foot Ankle Surg
F aldini C, Traina F, Nanni M, et al. Surgical treatment of cavus foot in Charcot-Marie-tooth disease: a review of twenty-four cases: AAOS exhibit selection. J Bone Joint Surg [Am] 2015;97:e30.
Malerba F, De Marchi F. Calcaneal osteotomies. Foot Ankle Clin 2005;10:523-540, vii.