A cavus foot is defined as dropping or equinus of the forefoot. This usually produces a high arched foot and, this is often used as the definition. In most people's mind, cavus foot is associated with dorsiflexion or clawing of the toes: it is sometimes referred to as claw foot (Fig. 1) 2615. Cavus foot represents one of the most complex foot deformities, both aetiologically and in terms of treatment. Various heel positions may be associated with the forefoot equinus: these produce either a calcaneocavus foot, or a cavovarus foot.

Cavus foot is most frequently associated with an underlying neurological problem. This may be derived from the brain, secondary to spasticity associated with cerebral palsy or a space-occupying lesion such as a neoplasm. Patients with Friedreich's ataxia also characteristically display a cavus foot, usually during the spastic phase. Lesions in the spinal cord are the most common cause of cavus foot: such lesions include poliomyelitis, tethered spinal cord, epidural lipoma, spinal cord neoplasm, and myelodysplasia. Peripheral neuropathies, most typically Charcot-Marie-Tooth disease, may present with a cavus foot, as may isolated nerve injuries, such as trauma to the peroneal nerve. Cavus foot may occur following compartment syndrome with contracted muscle, and may also occur as compensation for a poorly corrected club foot. Some patients have no neurological or myopathic disorders, but have relative equinus of the forefoot which develops into cavus foot.

Teleological consideration of this condition makes treatment more logical. The patient always tries to put his foot relatively flat on the floor. Therefore if the heel is in calcaneus position and the forefoot is up in the air, either gravity or relative tightness of the flexor muscles will pull the forefoot down and give a calcaneocavus foot. If the hindfoot is in varus, for example, in a patient with an uncorrected club foot, the first metatarsal drops to share in the weightbearing, producing a cavovarus foot.

Good medical care, and especially good orthopaedic care, dictates that the underlying aetiology should be determined before treatment begins. Muscle transfers for the correction of a cavus foot in a growing child with an undiagnosed epidural lipoma will fail as progressive nerve damage and muscle weakness ensue. Investigation starts with a history, looking for abnormalities at birth such as low birthweight or prematurity, or delayed milestones suggestive of spasticity or cerebral palsy. CNS symptoms such as ataxia or headaches may be elicited. Family history may reveal the presence of conditions such as Friedreich's ataxia or Charcot-Marie-Tooth disease. A history of progressive clumsiness suggests either ataxia or peripheral muscle weakness. Other suggestions of sensory problems include dysaesthesias in those with Charcot-Marie-Tooth disease. Spinal cord problems such as tethering or lipoma are often associated with symptoms such as bedwetting or incontinence. Travel or residence in a foreign country could suggest poliomyelitis. Finally, injuries which would suggest peripheral nerve damage or compartment syndrome should be sought. Questions should also be asked about previous treatment for club foot or other foot deformities.

A thorough neurological examination should be undertaken, including examination of the spine for superficial lesions and determination of sensation of the lower sacral roots. Undergrowth of an extremity in length or muscle atrophy is often indicative of a chronic problem. All muscle groups in the feet should be carefully tested, as should sensation, whether the heel is in varus, and how rigid or flexible this component is. The plantar fascia should be checked for contracture and tightness. The block test, described by Coleman, is a helpful part of the examination. If the first metatarsal is plantar flexed and rigid, the heel assumes a position of varus as a necessity. To eliminate this factor, Coleman had the patient stand with his heel elevated on a block to eliminate the forefoot factor and to demonstrate true heel varus.

Radiographs are essential in making the diagnosis of cavus foot. They should include non-weight-bearing, active dorsiflexion lateral, and weight-bearing lateral views. This series will give an indication of the flexibility of the arch (Fig. 2) 2616. Weight-bearing axial views will describe the position of the heel—varus or valgus. Lumbar spine films are mandatory. It is prudent to obtain electromyographic studies of the lower extremity and possibly an MRI or myelogram if there is any suggestion of spinal abnormality.

Treatment is dictated by the nature of the muscle imbalance, the type of disease, the age of the patient, and the rigidity of the deformity. An immature and growing child with no fixed bony deformity requires soft tissue balancing. A child with a mature bony deformity needs osteotomies and/or fusion, possibly combined with balancing of the muscles. The important rule is that a bony procedure performed in a growing child without balancing muscles is associated with recurrence. Similarly, balancing muscles will not usually correct a fixed bony deformity. The final important principle is to try and avoid fusion in an insensate foot. The same part of the foot hits the ground with each step and, unless the fusion is perfect in terms of plantigrade positioning, malposition leads to severe ulceration and even to osteomyelitis.

Muscle balancing is performed to match the disease process and deficiency. The most common condition producing dropping of the forefoot involves isolated weakness of the anterior tibial muscle (Fig. 1) 2615. This usually occurs in poliomyelitis; it may also be idiopathic or associated with the forme fruste of Charcot-Marie-Tooth disease. If the toe extensors are normal, they are transferred to the dorsum of the metatarsal necks. If the first metatarsal is depressed and relatively rigid, a midshaft osteotomy to dorsiflex the toe can be performed at the same procedure. This repair is accompanied by release of the plantar fascia as well as a closing lateral wedge osteotomy of the calcaneus.

The bony procedures and plantar fascia release are undertaken initially. Six weeks later the toe extensors are transferred. The plantar fascia is released through a medial incision, starting at the medial malleolus and ending at the medial border of the plantar surface. The vessels are followed down, all muscles superficial to them being released. The calcaneal osteotomy requires a lateral incision extending from the insertion of the tendon Achilles to the front of the calcaneus. The peroneal tendons and the sural nerve are retracted and a wedge of about 1 cm is removed from the calcaneus. The first metatarsal osteotomy and toe extensor transfers are performed through two longitudinal incisions, the first between the first and second metatarsal, the other usually over the fourth metatarsal (Fig. 3) 2617. The metatarsal osteotomy cannot be performed proximally if the growth plate is still open. We construct a dome or V osteotomy and dorsiflex the metatarsal head and neck so that the apex is posterior. Fixation is accomplished with crossed K-wires. For tendon transfer, the foot is dorsiflexed so that the proximal tendon is not slack in the dorsiflexed position, nor under too much tension. The tendon is cut, placed in a small hole in the metatarsal neck, and is sutured to itself. The operative repair is followed by cast immobilization for 6 weeks.

In other patients, the anterior tibialis muscle, the toe extensors, and the peroneal muscles are weak. This is most typical of Charcot-Marie-Tooth disease. In this case, the transfer uses the posterior tibial muscle, with transfer of its tendon through the interosseous membrane to a new insertion site on the dorsum of the foot. Traditionally, all of these patients ultimately required triple arthrodesis because they lacked lateral stabilizers of the foot. However, several such transfers have now been undertaken without triple arthrodeses with good results. In some of these cases, a midtarsal osteotomy, with removal of a dorsal wedge, is applicable. This procedure flattens the foot, but still retains subtalar motion (Figs 2, 4) 2616,2618. When the posterior tibialis muscle is transferred, the traditional approach is to bring it through the interosseous membrane and under the retinaculum, attaching it to the lateral or intermediate cuneiform. However, the forefoot still appears to drop. We now lengthen the posterior tibial tendon with a graft made from one-third of the tendon Achilles. While some textbooks suggest making the transfer opposite the second metatarsal, we move it to the neck of the third metatarsal.

In some forms of cavus foot, the tibialis anterior muscle is not primarily weak, but is relatively weak secondary to spasticity of the gastrocnemius and soleus. This obviously occurs in patients with spasticity. The feet are usually completely in equinus and do not look like a cavus foot. However, in many patients the heel cord is lengthened, bringing the heel back into neutral. The tibialis anterior muscle, which has been overly stretched, is still very weak, allowing the forefoot to drop. The toe extensors then try to bring up the forefoot, leading to clawing. In this case the tibialis anterior muscle is reinforced by moving the toe extensors to the metatarsal necks. Lengthening of the heel cord is required if this is tight. As always, a tight plantar facia may require release; if bony deformities accompany the equinus posture, a first metatarsal osteotomy may be helpful.

The calcaneocavus foot, in which there is no gastrocnemius or soleus, clearly needs different treatment. This is typically seen in cases of poliomyelitis, but may also be associated with myelodysplasia or tethering of the spinal cord. In these instances the lower roots of the spinal cord cease to function, while the higher ones are intact. Two options exist for the treatment of an L-5 lesion, with strong tibialis anterior and toe extensors, present but weak peroneal and tibialis posterior muscles, and no functioning gastrocnemius or soleus. The preferable procedure is to move the tibialis anterior posteriorly through the interosseous membrane to act as a plantar flexor of the foot. The toe extensors can then be moved to the metatarsal necks to act as a foot extensor. The alternative is to move the peroneal and tibialis posterior muscles to the tendo Achilles. Since muscles typically lose one grade of strength when transferred, an already weakened muscle may not function effectively.

Other types of muscle imbalance are seen in the forefoot. Isolated plantar contracture, may require plantar release. If there is also intrinsic loss, transfer of the long toe flexor to the dorsal hood over the proximal phalanx may be effective, if the clawing is not rigid. Dorsal tenotomy of the extensor tendon may also be required.

Non-operative treatment of the cavus foot involves unweighting the metatarsal heads. This can often be accomplished with shoe inserts, alleviating painful cavus foot. Metatarsal pads and rocker bars are viable options; however, the best solution is a moulded longitudinal arch, composed of soft and flexible material, such as cork or leather. These inserts usually have raised pads behind the metatarsal heads with depressions to accompany the prominent head.

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