Tibialis Posterior Anatomy

Tibialis posterior is the deepest and most central muscle of the deep posterior compartment of the leg, and the only leg muscle to take origin from the tibia, the fibula and the interosseous membrane between them. Its tendon runs behind the medial malleolus, turns sharply forward beneath the sustentaculum tali, and fans out onto almost every bone of the midfoot.

It is far more than an invertor. During stance it is the dynamic locker of the transverse tarsal joint, converting the flexible midfoot into a rigid lever against which the gastrocsoleus can push. Its loss produces the single most common acquired deformity of the adult foot.

The transverse tarsal lock. The transverse tarsal (Chopart) joint comprises the talonavicular and calcaneocuboid joints. With the hindfoot in valgus their axes are parallel and the midfoot is unlocked and flexible, which is useful at heel strike for shock absorption and for accommodating uneven ground. With the hindfoot in varus the axes are divergent and the midfoot is locked and rigid, which is essential at heel rise so that the triceps surae can transmit force to the forefoot through a stiff lever.

Tibialis posterior converts one state into the other. It inverts the calcaneus at the start of heel rise and locks the midfoot, and only then can the gastrocsoleus generate an efficient push-off.

When it fails. The heel stays in valgus, the transverse tarsal joint never locks, the gastrocsoleus pushes against a flexible midfoot, and the arch collapses through the talonavicular joint. The forefoot abducts and the talus plantarflexes and adducts. The deformity then perpetuates itself, because the Achilles vector now lies lateral to the subtalar axis and itself becomes an evertor.

The Achilles as a deforming force. In a valgus hindfoot the Achilles is a deforming force, not merely a tight one. That is the reason a contracted gastrocnemius must be lengthened during flatfoot reconstruction.

Actions by plane. Inversion is the dominant and defining one:

• Inversion (supination) of the subtalar and transverse tarsal joints, in the frontal plane. It is the strongest invertor of the foot, roughly twice as strong as its direct antagonist, peroneus brevis
• Weak ankle plantarflexion: the tendon passes posterior to the ankle axis, but its moment arm is small
• Forefoot adduction in the transverse plane, resisting the abduction that characterises the collapsing flatfoot
• Elevation and dynamic support of the medial longitudinal arch through its broad plantar insertion, a dynamic sling under the talonavicular joint augmenting the static spring ligament

Timing in gait. It is active from just after heel strike through to heel rise, an early and mid-stance muscle. Early in stance it works eccentrically, decelerating the physiological pronation that follows heel strike and controlling the rate of arch flattening; at heel rise it contracts concentrically to invert the calcaneus and hand the foot over to the gastrocsoleus as a rigid lever. It is essentially silent in swing, which makes it a poor donor for a swing-phase role such as dorsiflexion without phase conversion.

Excursion and strength. The working excursion is only about 1 to 1.5 cm, the shortest useful excursion of any of the major tendons about the hindfoot. Flexor digitorum longus has roughly 2 to 3 cm of excursion, and its strength is only around one-third that of tibialis posterior, so it is not a strength-matched substitute.

What that means for the FDL transfer. The transfer does not replace lost inversion power. It acts as a tenodesis and a proprioceptive checkrein and supplements a bony realignment, which is exactly why it must be combined with a medial displacement calcaneal osteotomy: the osteotomy does the mechanical work, and the transfer holds the correction and provides some dynamic support.

Why the tendon alone is never the whole story. A dynamic stabiliser cannot fail in isolation and produce a fixed deformity; that requires the static restraints to fail as well. In progressive collapsing foot deformity the sequence is:

1. Tendon tenosynovitis and elongation (dynamic failure), while the foot still looks normal
2. Repetitive overload of the spring ligament and the talonavicular capsule (static failure): the talar head drops medially and plantarwards, the forefoot abducts, and the deformity becomes visible
3. Attenuation of the deltoid ligament, with valgus talar tilt in the mortise (stage IV)

Simply repairing or reconstructing the tendon therefore does not correct an established deformity. Modern reconstruction always includes a bony realignment (medial displacement calcaneal osteotomy, lateral column lengthening, or a medial column procedure) and often a spring ligament repair.

Palpation. The tendon is palpable immediately behind and inferior to the medial malleolus, running forward to the prominent navicular tuberosity, which sits roughly 2.5 to 3 cm distal and anterior to the malleolar tip. Swelling and tenderness along its course, with a boggy fullness behind the malleolus, is the earliest physical sign of stage I disease.

Isolating the muscle. Test resisted inversion with the foot in plantarflexion, which relaxes tibialis anterior. No other manoeuvre isolates tibialis posterior as well.

Reading the single heel raise. The test asks two questions: can the patient rise, and does the heel invert as they rise? A patient may rise onto the toes on the gastrocsoleus alone while the heel remains in valgus, and that is a positive test indicating tibialis posterior insufficiency. Fingertip balance support is permitted; without it, balance failure produces false positives.

The fatigue variant. Ask for ten repetitions. Early dysfunction shows as progressive loss of height and loss of heel inversion with repetition, when a single attempt looked normal.

Before surgery. Five further assessments are required:

• Hindfoot flexibility - stage II versus stage III, the single most important determinant of treatment
• Forefoot varus (supination) - with the hindfoot corrected to neutral, look at the plane of the forefoot. A fixed forefoot varus of more than about 10 to 15 degrees needs a medial column procedure (Cotton opening wedge medial cuneiform osteotomy, or a naviculocuneiform or first tarsometatarsal fusion), otherwise the corrected hindfoot will simply fall back into valgus to get the first ray to the ground
• Forefoot abduction - talonavicular uncoverage on a weightbearing anteroposterior radiograph, which decides whether lateral column lengthening is needed (stage IIB, below)
• Gastrocnemius contracture - a Silfverskiold test in every case
• Ankle valgus - a weightbearing ankle radiograph or weightbearing CT to exclude stage IV

Imaging. What each study shows:

• Weightbearing lateral - the Meary line (talus-first metatarsal angle) breaks plantarwards at the talonavicular or naviculocuneiform level, the calcaneal pitch falls below about 18 degrees, and the lateral talocalcaneal angle increases
• Weightbearing anteroposterior - increased talonavicular uncoverage, increased talus-first metatarsal angle, forefoot abduction
• Hindfoot alignment (Saltzman) view - quantifies valgus of the calcaneus relative to the tibial axis
• Weightbearing CT - increasingly demonstrates peritalar subluxation, sinus tarsi and subfibular impingement, and middle facet subluxation, which correlates strongly with the clinical deformity
• MRI - tenosynovial fluid, tendon thickening or attenuation, longitudinal split tears, and the integrity of the spring ligament and deltoid

Posterior tibial tendon dysfunction. The condition is now widely termed progressive collapsing foot deformity (PCFD), to acknowledge that the tendon is one component of a multiplanar deformity. The Johnson and Strom staging with the Myerson modification remains the language of the exam.

Stage II is subdivided in common practice. Stage IIA has minimal forefoot abduction and is treated with medial displacement calcaneal osteotomy and FDL transfer. Stage IIB has significant forefoot abduction, with more than about 40 per cent talonavicular uncoverage, and requires lateral column lengthening in addition.

Who gets it. The risk factors are female sex, age over 40, obesity, hypertension, diabetes, seronegative and inflammatory arthropathy, prior local steroid injection, and pre-existing pes planus.

The pain moves. Early disease causes medial hindfoot pain and swelling. As the deformity progresses the pain often migrates laterally to the sinus tarsi and the subfibular region as the calcaneus impinges beneath the fibula. A patient describing lateral hindfoot pain with a flat foot has advanced disease, not a new problem.

Acute rupture. Acute traumatic rupture is uncommon. It follows a forced eversion injury or a medial malleolar fracture with entrapment, and it is often missed in the trauma setting.

Entrapment. Tendon entrapment or incarceration within a medial malleolar fracture or a subtalar dislocation prevents reduction. Tibialis posterior is the classic block to reduction of a lateral subtalar dislocation, while the peroneals block a medial dislocation. Look specifically for the tendon in any medial malleolar fracture that will not reduce, and in any open reduction of a pilon or plafond injury approached medially.

Tarsal tunnel syndrome. The tibial nerve is compressed beneath the flexor retinaculum (laciniate ligament) between the medial malleolus and the calcaneus. The causes are:

• Space-occupying lesions: ganglion, lipoma, varicosities, or an accessory muscle such as an accessory flexor digitorum accessorius longus
• Post-traumatic scarring and malunion
• Tenosynovitis of the adjacent flexor tendons
• Hindfoot valgus, which stretches the nerve

Tarsal tunnel findings. It presents with burning plantar pain, a positive Tinel sign over the tunnel, and sensory disturbance in the medial or lateral plantar territory. The dorsiflexion-eversion test is positive when sustained maximal dorsiflexion and eversion with toe extension for 5 to 10 seconds reproduces symptoms. Heel sensation is often spared, because the medial calcaneal branch may arise proximal to the retinaculum.

The link to the tendon. A valgus hindfoot from tibialis posterior dysfunction can itself produce a traction tarsal tunnel syndrome, and correcting the deformity may relieve the neuropathy.

Deep posterior compartment syndrome. The compartment contains tibialis posterior, flexor digitorum longus, flexor hallucis longus, the tibial nerve and the posterior tibial and peroneal vessels. The signs are pain on passive toe extension and passive foot eversion, deep calf tenderness that is hard to appreciate because the compartment is covered by soleus, and plantar sensory disturbance.

The compartment most often missed. The deep transverse fascia separating the deep from the superficial posterior compartment must be divided in a posteromedial fasciotomy, and failing to open it is a classic cause of a missed compartment syndrome. The late consequence is a fibrotic, contracted deep compartment with claw toes, a cavovarus foot and plantar sensory loss.

Accessory navicular. A symptomatic type II accessory navicular causes medial midfoot pain over a prominent bony bump, worse in stiff footwear and with activity, typically in an adolescent. Non-operative management with activity modification, orthoses and immobilisation succeeds in the majority.

The Kidner procedure. When non-operative care fails, the accessory ossicle is excised and the tibialis posterior tendon advanced and re-attached plantarwards onto the navicular, which modern practice usually does with a suture anchor. Debate persists as to whether simple excision without formal advancement gives equivalent results.

The medial hindfoot approach. The incision is curved, centred 1 cm posterior to the medial malleolus and curving distally toward the navicular tuberosity, and roughly 8 to 10 cm long. This single exposure gives access to the tibialis posterior tendon, flexor digitorum longus, the spring ligament and the navicular.

At risk in the medial wound. The saphenous vein and nerve lie anteriorly, the posterior tibial neurovascular bundle posteriorly, and the medial calcaneal branches of the tibial nerve cross the distal part of the wound.

The safe plane. Flexor digitorum longus lies directly posterior to tibialis posterior and anterior to the neurovascular bundle, which lies immediately deep and posterior to it. FDL is therefore harvested in the plane between the two tendons, staying strictly anterior to the bundle throughout.

FDL transfer with medial displacement calcaneal osteotomy. This is the operation to know.

Transfer for foot drop. This is the classic use of tibialis posterior as a donor. The tendon is transferred anteriorly through the interosseous membrane to the dorsum of the foot, usually the lateral cuneiform or split between the cuneiforms, to restore dorsiflexion in a common peroneal nerve palsy, in leprosy, or in post-polio paralysis.

Routing. The interosseous route requires a generous window in the membrane, at least 3 to 4 cm, to prevent the tendon binding, and the anterior tibial neurovascular bundle must be protected. Circumtibial routing, subcutaneously around the medial border of the tibia, is an alternative but gives a less direct line of pull and a poorer vector.

What the transfer can do. Dorsiflexion requires an excursion of about 3 cm against the muscle's 1 to 1.5 cm, and it is a stance-phase muscle asked to do a swing-phase job. Results are best regarded as a dynamic tenodesis rather than true active dorsiflexion, and most patients are converted from a flail foot to a plantigrade one rather than to normal. Warn that harvesting tibialis posterior in a foot with any pre-existing planovalgus tendency will accelerate arch collapse.

Split posterior tibial tendon transfer (SPOTT). It is used for spastic equinovarus in which tibialis posterior is the deforming muscle. Half the tendon is passed behind the tibia and fibula and attached to peroneus brevis.

Terminology and consensus

• An international consensus group has recommended replacing the term adult-acquired flatfoot deformity with progressive collapsing foot deformity (PCFD), and has proposed a classification describing the deformity by its components - hindfoot valgus, midfoot and forefoot abduction, forefoot varus, peritalar subluxation and ankle instability - rather than by a single linear stage. Both systems are examinable; the Johnson and Strom stages with the Myerson modification remain the common clinical language, and a candidate should be able to speak both.
• Weightbearing CT has changed the assessment of peritalar and middle facet subluxation, and is increasingly regarded as the reference standard for quantifying three-dimensional deformity where available.

Anatomical variation across populations

• Accessory navicular is present in roughly 10 to 15 per cent of feet across most populations, with reported prevalence varying by imaging modality and by population, and is bilateral in the majority.
• The number and distribution of the plantar insertional slips varies considerably; the navicular slip is universal, the cuneiform and metatarsal slips vary.
• Flexible flatfoot is far more common than symptomatic PCFD and, in the absence of a tight Achilles or a tarsal coalition, is a normal variant in children that requires reassurance, not treatment.

Side-by-side guidance

Resource-dependent practice

• Well-resourced settings: weightbearing CT, MRI, custom orthoses, arthroereisis implants and total ankle replacement for stage IV.
• Limited-resource settings: the diagnosis of PCFD is entirely clinical - too-many-toes, single heel raise, passive correctability - and weightbearing radiographs suffice for planning. Medial displacement calcaneal osteotomy with FDL transfer requires only a saw, two screws and basic instruments, and is entirely deliverable at district hospital level. Where implants are limited, a well-executed triple arthrodesis remains a reliable and durable operation for rigid deformity.
• Tibialis posterior transfer for drop foot is one of the highest-value operations in leprosy and post-polio programmes worldwide, and is performed in enormous numbers in South Asia and sub-Saharan Africa.

Registry and outcome signals

• There is no dedicated international registry for flatfoot reconstruction. Institutional cohorts consistently show durable improvement after combined tendon transfer and bony realignment for flexible stage II deformity, with the principal causes of failure being under-correction, an unaddressed gastrocnemius contracture, and unrecognised fixed forefoot varus.
• Total ankle replacement registries show that pre-operative coronal-plane deformity greater than about 10 to 15 degrees is associated with higher failure rates, which is why hindfoot realignment must precede or accompany arthroplasty in stage IV disease.

The condition this tendon causes when it fails: Adult Flatfoot Deformity, with Flexible Flatfoot and Rigid Flatfoot as the two ends of the correctability question the hindfoot examination is actually asking.

The structures that fail alongside it - and the reason a tendon transfer alone does not hold: Spring Ligament Insufficiency and Deltoid Ligament Injuries. The deltoid is what separates stage III from stage IV.

The contracture that must be looked for at every reconstruction: Gastrocnemius Equinus Contracture and Gastrocnemius Anatomy - the Silfverskiold test is only interpretable if the hindfoot is held neutral.

Conditions that present as the same painful medial foot and are not tendon dysfunction: Accessory Navicular, Navicular Stress Fracture, Talonavicular Arthritis, Subtalar Arthritis and Tarsal Coalition - a stiff hindfoot in a young adult is a coalition until proven otherwise, not a stage III deformity.

The opposite deformity, and the neurological cause that produces it: Cavovarus Foot and Charcot-Marie-Tooth Disease. Charcot Neuroarthropathy is the collapse that must never be mistaken for a failing tendon.