Flatfoot

The spring ligament is an important stabilizer of the medial arch. It consists of 2 parts.

• The superomedial calcaneonavicular (SMCN) ligament arises from the sustentaculum tali and fans out to insert on the edge of the medial navicular facet.

• The inferior calcaneonavicular ligament runs from the anterior sustentaculum tali and inserts on the plantar aspect of the midnavicular cortex.

The superficial deltoid originates on the medial malleolus and inserts on the dorsal edge of the SMCN ligament.

• Its function is to serve as a check rein for the entire complex.

The plantar fascia also contributes to arch integrity.

• In biomechanical testing, it fails under load at 1.7-3.4 times body weight. (Hintermann 1995).

• Division of the plantar fascia results in depression of the longitudinal arch and elongation of the medial length of the foot (Sharkey et al 1998).

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    Arch stiffness decreases by 25% (Huang et al 1993).

The long plantar ligament runs from the anterior tuberosity of the inferior surface of the calcaneus.

• The majority of fibers insert on the cuboid, and the more superficial fibers insert on the 2nd-5th metatarsals.

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    It is thought to be of secondary importance in arch support.

The posterior tibial tendon (PTT) is a powerful inverter and plantar flexor of the foot.

• It locks the transverse tarsal joints [talonavicular (TN) and calcaneocuboid joints].

• Biomechanical and electromyographic studies suggest that the tendon acts as an arch supporter during gait and loading situations.

An imbalance between the PTT and its antagonists (tibialis anterior, peroneal longus and brevis, and triceps surae) may lead to arch collapse.

• This occurs in muscle imbalance disorders, such as cerebral palsy.

Extrinsic and intrinsic toe flexors also contribute to arch support but have a secondary role.

• The flexor tendons fail under repetitive stress without a functional PTT.

Hindfoot motion locks and unlocks the transverse tarsal joints.

• With subtalar eversion, the transverse tarsal joints are flexible, which keep the forefoot supple to accommodate uneven surfaces.

• When the PTT fires just prior to the heel rise portion of gait, the axes of the TN joint and calcaneocuboid joint are divergent, locking the transverse tarsal joints.

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    This creates a rigid medial column and long lever arm for forceful push-off during gait.

In the normal gait cycle, firing of the PTT just prior to heel rise inverts the heel, bringing the Achilles vector medial to the subtalar joint.

• Achilles contraction then supports the arch and encourages locking of the transverse tarsal joints.

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    This stabilizes the arch for push-off.

Although arch collapse is traditionally noted in the TN joint, deformity can occur with any combination of TN, naviculocuneiform (NC), &/or 1st tarsometatarsal (TMT) subluxation/collapse.

Using the “tripod” model of foot structure, loss of the medial post of the tripod through collapse of any of these joints allows the hindfoot to collapse into valgus.

Acquired flatfoot is a 3D deformity of hindfoot valgus, longitudinal arch collapse, and forefoot abduction.

The talus becomes plantar flexed, the calcaneus everts, and the navicular and cuboid move to a more everted location.

With increasing hindfoot valgus, the forefoot assumes a compensatory forefoot supination.

The lateral column is effectively shortened as the deformity progresses.

The talus slides anteriorly relative to the calcaneus.

Hindfoot valgus occurs as a result of rotation through the subtalar and TN joints.

Achilles contracture is a deforming force that can both cause and exacerbate arch failure.

• When the heel is in valgus, the Achilles insertion lies lateral to the axis of the subtalar joint so that Achilles contraction promotes subtalar eversion and, thus, arch collapse.

When the PTT fails to invert the hindfoot prior to heel rise, the calcaneal insertion of the Achilles remains lateral to the axis of the subtalar joint.

• Achilles contraction then leads to hindfoot eversion.

• The transverse tarsal joints are unlocked, and the arch can sag.

Recurrent cycles of this dysfunctional gait can break down the static support of the arch.

In some situations, Achilles contracture may precede any other pathology.

• With Achilles contracture, the talus and calcaneus are plantar flexed.

• Weight bearing places a dorsiflexion force on the forefoot.

• Because of the oblique axis of the subtalar joint, subtalar eversion also produces some dorsiflexion.

• In a foot with a tight Achilles tendon, subtalar eversion is necessary to produce a plantigrade foot.

• With subtalar eversion, the PTT can become secondarily strained and eventually injured.

Many patients with active PTT tendonitis will have a tight gastrocnemius and a low arch on the “normal” foot.

A flatfoot deformity exacerbates Achilles contracture by maintaining the foot in hindfoot valgus and equinus.

The Achilles may become more contracted, which further antagonizes PTT function and arch integrity with a progressive deformity.

So, an acquired flatfoot can be caused by tightness of the Achilles (especially the gastrocnemius component) and can also result in a contracted Achilles tendon.

In the deformity, hindfoot and midfoot joint degeneration may develop secondary to increases in joint reactive pressures.

• With a flatfoot deformity, the subtalar joint facets sublux, so that only 1/2 of the articular surface is in contact.

• The decrease in contact area leads to increased contact pressures (Ananthakrisnan et al 1999).

The pes planovalgus deformity alters joint mechanics as well as foot and ankle alignment.

Pain can occur in the foot, ankle, or even more proximal locations.

• The lower back and hip may be sore from limping or from altered gait mechanics.

• Continued valgus stress on the knee from a valgus foot can lead to medial compartment disease.

• Valgus foot alignment can also lead to a valgus ankle deformity with painful joint degeneration.

• In the foot, pain may be felt medially or laterally and may arise from inflammation, tendinitis, arthritis, &/or impingement.

In cases of PTT tendinitis, patients may feel pain only in the medial hindfoot from tenosynovitis or from a complete or longitudinal tear within the tendon.

In an advanced flatfoot of any etiology, pain may occur over the medial malleolus and deltoid ligament, as the deltoid fibers are tensioned to oppose the worsening hindfoot valgus.

With hindfoot valgus, lateral hindfoot pain can occur as a result of the calcaneus impinging on the distal tip of the fibula or lateral process of the talus.

Cyst formation &/or sclerosis in this region, either on plain film or computed tomography (CT), should create suspicion of impingement.

A CT imaging study compared control subjects with patients with severe deformity under 75 N of axial loading (Malicky et al 2002).

• It determined that the prevalence of sinus tarsi impingement was 92%, and the prevalence of calcaneofibular impingement was 66% in the flatfoot group vs. 0% and 5%, respectively, in the control group.

• The study patients who had calcaneofibular impingement also had sinus tarsi impingement.

Arthritis may be the causative agent or the end result of a chronic severe deformity.

Alteration of joint reaction forces causes abnormal loading of the subtalar, tibiotalar, transverse tarsal, and Lisfranc joints and may result in painful arthritic conditions.

If the normal balance of arch support is disturbed (such as with fracture malunion, PTT injury, or Achilles tightness), persistent abnormally directed weight-bearing forces will tax the remaining support of the arch (such as the PTT or spring ligament), leading to progressive arch collapse.

Once the deformity is established, it may be difficult to determine which came first, the Achilles contracture, PTT dysfunction, or spring ligament rupture.

Perhaps the most important treatment for an acquired flatfoot is prevention.

• If the “at-risk” foot could be identified, early intervention might prevent the deformity.

• Once the deformity is established, it is often self-perpetuating and progressive.

• An “at-risk” foot would be one with a very tight Achilles and normal PTT function or one with severe flatfoot deformity but still normal PTT function.

The muscle arises from the posterior tibia as a large muscle in the deep posterior compartment of the calf.

The tendon travels in the medial malleolar groove and inserts broadly into the medial foot.

• It primarily inserts onto the navicular tuberosity, but multiple slips fan out to insert into the 2nd-4th metatarsals, into the plantar surface of the cuneiforms, and on the cuboid on the lateral foot.

• On the plantar surface, it attaches to the deep fascia, peroneal longus tendon, and long and short toe flexors.

A zone of hypovascularity exists 40 mm proximal to the navicular tuberosity and extends proximally over 14 mm of tendon.

• There is no mesotendon in this region, and surrounding synovial tissue is also hypovascular.

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    This area is subject to mechanical wear.

It is possible that a transient ischemia creates tendon insufficiency and sets up the cascade of dynamic instability.

• A diseased PTT has high relative concentrations of type 3 collagen (it is the main collagen in early tendon healing).

• It has decreased tensile strength, which can cause tendon insufficiency and dysfunction with recurrent use.

In an evaluation of spontaneously ruptured tendons and controls in an over-35 population, degenerative pathologic changes, such as hypoxic degeneration, mucoid degeneration, tendolipomatosis, and calcifying tendinopathy, were identified (Kannus and Jozsa 1991).

• Of note, these changes were observed in 34% of control tendon specimens.

• Normal tendon structure was not identified in any of the ruptured tendon specimens.

• These findings suggest that degenerative tendinopathy is common after age 35.

It is more often seen in women between 45-65 years of age.

It occurs with increased frequency in obese and ­diabetic patients.

About 1/2 of patients will relate a traumatic event to the initiation of symptoms.

As previously mentioned, with PTT dysfunction, the transverse tarsal joint will not lock during heel rise. Weight-bearing forces across these unlocked joints lead to fatigue failure of the ligaments. In these cases, PTT dysfunction precedes arch collapse.

• Weight-bearing forces across these unlocked joints lead to fatigue failure of the ligaments.

• In these cases, PTT dysfunction precedes arch collapse.

Arch-flattening forces, such as a tight gastrocnemius and obesity, may contribute to a flatfoot, as the repetitive forces of weight bearing cause the deformity to progress.

• This may worsen PTT dysfunction.

In some cases, static deformities can cause PTT dysfunction (the arch fails first).

• The position of forefoot pronation and valgus (arch ­collapse) will lead to PTT failure and worsening ­deformity.

• If the talocalcaneonavicular complex loses stiffness, the PTT insertion sites are in a valgus position.

• Lengthening of the tendon even 1 cm reduces its efficiency as the primary dynamic stabilizer of the arch.