Accessory Navicular Bone

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Definition/Description

Also known as Prehallux, Os Tibiale Externum and Navicular Secundum.

An accessory navicular bone is a bone of the foot that develops abnormally causing a  plantar medial
enlargement of the navicular. The accessory navicular bone presents as a sesamoid in the posterior
tibial tendon, in articulation with the navicular [1] or as an enlargement of the navicular itself.

The Geist classification divides these into three types:

Type I: is a sesamoid bone in the posterior tibialis tendon. There is a small gap of approximately 3mm
or less between the sesamoid and the navicular.
Type II: consists of an accessory bone, up to 1.2cm in diameter, where synchondrosis develops
between it and the navicular.
Type III: is the fused accessory navicular resulting in a large cornuate shaped navicular.

Clinically Relevant Anatomy

The navicular is an intermediate tarsal bone on the medial side of the foot [2], which articulates
proximally with the talus. Distally it articulates with the three cuneiform bones. In some individuals it
also articulates laterally with the cuboid. The tibialis posterior tendon inserts into the navicular bone [3].
Tibialis posterior is an inverter of the foot, assists in the plantar flexion of the foot at the ankle and also
has a major role in supporting the medial arch of the foot.  [4] This can be compromised where there
 exists an abnormal insertion of the tendon into the accessory navicular bone [5] [6] and result in a loss of
suspension of the tibialis posterior tendon, possibly causing peroneal spastic pes planus or simple pes
planus. However, the cause and effect relationship between the accessory navicular and pes planus is
speculative as there is no clear proof of that relationship. [7]

The presence of a type I or II accessory navicular is also a cause of Posterior Tibial tendinopathy as the
insertion of the Tibialus Posterior tendon onto the accessory navicular is more proximal (dashed line).
Leverage of the malleolus on the Tibialus Posterior tendon is reduced increasing stress on the
tendon. [8]

The calcaneal pitch angle is also reduced in patients with a symptomatic accessory navicular than in
normal subjects. [9]

Epidemiology /Etiology

The foot and ankle have numerous accessory ossification areas, with the most common being the
accessory tarsal navicular bone which occurs in 4-14% of the population. [1][10][2]

 An accessory navicular bone is present in ~10% of the population

 It first appears in adolescence, with incidence of 4-21% in children. [8] 
 It is more common in females [1]
 Reported prevalence bilaterally is ~70% (range 50-90%)
 People who have an accessory navicular are often unaware of the condition as it causes no symptoms.
Some individuals, however, will develop accessory navicular syndrome, a painful condition where the
bone and/or posterior tibial tendon become aggravated. This can result from any of the following:

 Trauma, such as a foot or ankle sprain

 Chronic irritation from shoes or other footwear rubbing against the accessory bone
 High levels of activity or overuse

Characteristics/Clinical Presentation

 Typically seen in young females (10-20 years of age) complaining of mid food/arch pain which
may be insidious or post trauma
 Difficulty getting comfortable footwear
 Prominent navicular
 Tenderness over the prominence
 Pain over the posterior tibialis tendon and reduced mobility in the Achilles tendon in chronic
cases
 pes planus is often present
 Inflamed bursa

Differential Diagnosis

 Stress fracture
 Tendinopathy
 Medial tuberosity fracture [4]
 Bone Tumor
 Kohler’s disease [5]

Diagnostic Procedures

 X-Ray: An accessory navicular is often clear to see in standing AP and lateral views, but in
some cases an oblique view is also required in order to fully diagnose the extent of the navicular
abnormality. Bilateral investigations are often done as there is a high incidence of symmetrical
abnormalities.
 When examining the lateral weight bearing X-ray, alignment of the talonavicular cuneiform and
first metatarsal dorsal should be carefully examined as well. “Sag” at this joint indicates structural
integrity of the area.
 In rare cases, an MRI or CT is indicated in order to exclude a tumor, fracture of the medial
tuberosity, or bone marrow edema.

AP View
 Lateral View

Oblique View

Outcome Measures

Examination
 Patients with an accessory navicular may present with complex pain patterns requiring a thorough
examination. [6] The examination should include key assessments:

 Differentiation of the navicular prominence from the talar head prominence in flat foot
deformities by inverting and everting through the subtalar joint with a thumb over the bony
prominence. [7]
 Assessing for any loss of structural integrity of the longitudinal arch is important as this
component of the deformity will not be corrected by surgical treatment where surgery is required.  [8]
 Thorough gait examination.

Medical Management

Conservative:

1. Physical therapy
2. Medications. Oral nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, may be
prescribed. In some cases, oral or injected steroid medications may be used in combination with
immobilisation to reduce pain and inflammation. [8]

Surgical: Depending upon the severity of symptoms, non-operative or conservative treatment should

be maintained for at least 4- 6 months before any surgical intervention.

There are 2 surgeries that can be performed depending upon the condition and symptoms

 A simple surgical excision to remove the accessory navicular along with its prominence. In this
procedure, the incision is made dorsally to the prominence of the accessory navicular. Symptoms are
relieved in 90% of cases. [11]
 The 2nd procedure excising the boney prominence in conjunction with reattachment of the
posterior tibial tendon. . [5][6] The posterior tibial tendon is split and is reattached further up the medial
side of foot to provide increased support to the longitudinal arch.

After surgery the lower leg is put into a cast for 4 weeks, which is moulded into the shape of the arch,
with the foot maintained in a plantigrade position. Partial weight bearing is indicated for 8 weeks after
which full weight bearing is permitted. [6][8]. Once the cast is removed, a strength and conditioning
programme is highly recommended. [7]
 Occasionally, a limited fusion of the cuneiform metatarsal or talonavicular joints is also recommended.
The rationale and efficacy of this operation have been questioned however.

Arthrodesis may be a reasonable treatment option in selected cases of patients with symptomatic
recalcitrant Type II accessory naviculars that are large enough to accept small fragment screws. [1]

Physical Therapy Management

If the accessory navicular bone becomes problematic, physical therapy may be prescribed.

This includes use of therapeutic modalities to relieve pain, increase strength and stability in the foot.
An accessory navicular bone is often linked to posterior tibial dysfunction and pes planus. In some
cases orthotics may be indicated.

 Well padded shoe orthotics should be worn for arch support. This decreases direct pressure over
the navicular.
 Strength and conditioning exercises for the peroneal and posterior tibialis muscles.
 Strengthening of the intrinsic foot muscles and the lateral rotators of the pelvis. [8]
 Activity modification in the initial stages, such as limiting or stopping any strenuous activities
which may cause the accessory navicular bone to become symptomatic. [8]
 Gait re-training and stability exercises.

Some examples of functional posterior tibialis strengthening:

[12]

[13]

[14]
[15]

Clinical Bottom Line

A type I accessory navicular is rarely symptomatic. Where symptoms do appear, type I usually
responds well to conservative management. Patients with Type II have an increased risk of injury and
onset is usually insidious or as a result of trauma. It fails to respond to conservative treatment when
severe and fusion of the accessory navicular to the navicular may successfully relieve pain without
disrupting the tibialis posterior tendon insertion. [10] With Type III, excising the accessory navicular is
indicated over excising the navicular prominence. [8]

Related articles

Tibialis posterior rupture - PhysiopediaSearch Strategy Databases Searched: Pubmed, ADB, web of
knowledge, PEDro, The Journal of Joint and Bone Surgery, Dynamed, PhysioAdvisor Keyword
Searches: tibialis posterior tendon (TPT) , tibialis posterior rupture (TPR), tibialis posterior tendon
rupture (TPTR), TPTR treatment, TPTR postoperative treatment, flatfoot, pes planovalgus, tendinitis  
Definition/Description Whenever the tibialis posterior muscle contracts or is stretched, tension is
placed through the tibialis posterior tendon. If this tension is excessive due to too much force or
repetition, damage to the tibialis posterior tendon may occur. This can range from minor tearing of the
tendon with subsequent inflammation to a complete tibialis posterior tendon rupture. Early diagnosis
and surgical repair will restore full normal function. [1] A rupture of the posterior tibial tendon can be
easily missed because the symptoms of this injury resemble the symptoms of a normal ankle sprain.
Some physicians may feel that posterior tibial tendon rupture is a rare condition, one that they have
never seen. Clinically Relevant Anatomy   Epidemiology /Etiology Posterior tibialis tendon ruptures
occur predominantly in the late middle-aged population (average age 57 years). For posterior tibialis
dysfunction, the patient is typically a female over the age of 40 who exhibits ligamentous laxity in
multiple joints and has an occupation that requires extended periods of standing. They usually do not
recall any acute traumatic event. There is another subset of the populations in which posterior tibial
tendon insufficiency occurs and that consists of the 20- to 40-year old athletes. They usually recall a
traumatic event, usually a direct blow to the medial malleolus. Or, they present with years of
involvement in athletics with a pronated foot.[1]  Characteristics/Clinical Presentation[1] • Swelling
along the medial aspect of the foot and ankle • Absence of the classical sudden severe pain of a tendon
rupture • Tenderness along the posterior tibialis tendon • Progressive loss of longitudinal arch → pes
planus and heel valgus • Palpable pain between medial malleolus and navicular • Pain in the plantar
medial arch Differential Diagnosis[2] • Attenuation or rupture of the calcaneonavicular (spring)
ligament complex • Degenerative arthritis of the ankle joint with valgus talar • Arthritis of the
talonavicular joint • Posttraumatic tarsometatarsal (Lisfranc) joint arthritis • Inflammatory arthritis of
the hindfoot, usually secondary to rheumatoid disease   Diagnostic Procedures add text here related to
medical diagnostic procedures Outcome Measures add links to outcome measures here (also see
Outcome Measures Database) Examination Observation:[3] Posterior tibialis tendon rupture is strongly
suspected in patients presenting a complex of findings. These include: • Eversion ankle injury •
Generalized medial ankle pain • Medial ankle swelling • Flexible, asymmetric pes planus and forefoot
pronation • Gait disturbance secondary to deformity • Talonavicular sag in lateral standing radiograph
The first four findings are nondiagnostic, however, seen together they are helpful in identifying
patients with posterior tibialis tendon pathology. Manual testing of the posteroir tibialis tendon should
be performed in the presence of these findings to confirm the tendon's functional status. Tests:[4] •
Palpation from area between malleolus medialis and os naviculare • “Too many toes” sign secondary to
an increase in forefoot abduction and heel eversion • Nonfunctional posterior tibialis tendon on manual
testing • Motion of the ankle and subtalar joints • Positive first metatarsal rise sign test • Positive
single-limb heel rise-test • Ottawa ankle rules test to exclude fractures within the first week after an
ankle injury Medical Management [1] Postoperative rehabilitation for tendon transfer procedure:
Complications: • With attenuation or rupture of the posterior tibial tendon, the medial longitudinal arch
of the foot collapses and there is a relative internal rotation of the tibia and talus • The subtalar joint
everts, causing the heel to assume a valgus position and the foot to abduct at the talonavicular joint. A
compensatory forefoot varus deformity ensues • As the heel assumes an increased valgus alignment,
the Achilles tendon becomes positioned lateral to the axis of rotation of the subtalar joint. Over time,
the shortened position of the hindfoot results in an Achilles tendon contracture • As the deformity
progresses, the fibula abuts against the lateral wall of the calcaneus, causing pain in the lateral hindfoot
Physical Therapy Management [5] Furthermore, Woods and Leach (1991) pointed out that "the key" to
successful treatment is early diagnosis23. (Randall E. Marcus, 1993) Phase I: • Ice • Non steroidal anti
inflammatory drugs • massage Phase II: • Passive ROM exercice for eversion and dorsiflexion such as
manual mobilisation ankle Phase III: • Closed kinetic chain activities and eccentric strengthening
exercises such as single leg standing toe raises with controlled lowering eccentric loads Phase III
excercices:  without moving your leg, pull theraband away lateral with your foot without moving your
straight leg, invert your feet of your bended leg without moving your leg, pull theraband away from
you to the ground place towel on the floor, keep the heel on the floor, use toes to pull towel towards
you Key Research add links and reviews of high quality evidence here (case studies should be added on
new pages using the case study template) Resources add appropriate resources here Clinical Bottom
Line add text herePosterior Tibial Tendon Dysfunction - PhysiopediaIntroduction Posterior tibial
tendon dysfunction (PTTD) insufficiency is the most common cause of adult-acquired flatfoot
deformity. Failure of the tendon affects surrounding ligamentous structures and will eventually lead to
bony involvement and deformity. PTTD is a progressive and debilitating disorder, which can be
detrimental to patients due to limitations in mobility, significant pain, and weakness.   Tendon
degeneration begins far before clinical disease is apparent. Early detection of PTTD may prevent
operative means of repair; if left to progress, surgical reconstruction with osteotomy and arthrodesis
becomes necessary[1] Risk factors for the disease include hypertension, obesity, diabetes, previous
trauma, or steroid exposure.[2] Posterior tibial tendon dysfunction (PTTD) is a progressive condition
that can be classified into four stages[3]. In the early stages, there may be pain, the area may be red,
warm and swollen.  There are not usually symptoms during gait but symptoms may be present in
running. Later as the arch begins to flatten, there may still be pain on the inside of the foot and ankle
but at this point, the foot and toes begin to turn outward and the ankle rolls inward. As PTTD becomes
more advanced, the arch flattens even more and the pain often shifts to the outside of the foot, below
the ankle. The tendon has deteriorated considerably and arthritis often develops in the foot. In more
severe cases, arthritis may also develop in the ankle. [4] Clinically Relevant Anatomy Tibialis posterior
originates from the posterolateral tibia, posteromedial fibula and interosseous membrane. It runs
through the deep posterior compartment of the leg and its tendon passes behind the medial malleolus.
Blood supply to the tendon is poorest in this area and is the most common site for rupture. Close to its
insertion site the tendon splits into a main, plantar and recurrent components, with the main component
inserting onto the navicular tuberosity, the plantar portion onto the second, third, fourth metatarsals,
second and third cuneiforms and cuboid. The recurrent component attaches to the sustentaculum tali of
the calcaneus. Tibialis posterior acts as the primary dynamic stabilizer of the medial longitudinal arch
and main inverter of the midfoot. Its contraction also elevates the medial longitudinal arch, causing the
hindfoot and midfoot to become a rigid structure. This allows the gastrocnemius to act with greater
efficiency during the gait cycle[1] If compromised, a resulting pes planus foot may develop and place
greater stress on the surrounding ligaments and soft tissue[5] Etiology Researchers have proposed
numerous mechanisms for the degeneration of the posterior tibial tendon (PTT). The most commonly
the cause for PTT degeneration is credited to a repetitive loading causing microtrauma and progressive
failure. A retromalleolar, hypovascular region does exist and may also contribute to the disease. The
anatomic course of the posterior tibial tendon also likely contributes as the tendon does make an acute
turn around the medial malleolus, putting a significant amount of tension on the tendon in the region
distal and posterior to the medial malleolus (the adjacent tendons the flexor hallucis longus and the
flexor digitorum longus, do not take this sharp turn). Other proposed causes are - constriction beneath
the flexor retinaculum, abnormal anatomy of the talus, degenerative changes associated with
osteoarthritis, and preexisting pes planus.[2] Epidemiology The overall incidence of this disease, it is
believed that the prevalence is anywhere from 3.3 to 10%, depending on the sex and age of the patient.
PTTD is associated with adult-acquired flatfoot deficiency which can cause it to be misdiagnosed,
meaning the actual prevalence may be much higher than shown in the literature.[2] Conditions such as
- diabetes, hypertension, obesity, previous surgery, foot/ankle trauma and steroid use is found in up to
60% of patients. Though many of these risk factors are generalized medical conditions, only one side is
typically affected; bilateral disease is rare[1] Risk factors to get PTTD are: Elderly: especially middle
aged women [6][7],with up to 10% prevalence in this group. Young athletes [6] Hypertension [6][7]
Obesity [6][7] Diabetes mellitus [6][7] Seronegative arthropathies [6] Accessory navicular bone [6]
Ligamentous laxity [7] Pes planus (flatfeet) [7] Steroid therapy [6][7] Accesory navicular: may
interfere with posterior tibial tendon function [6] Overuse [4] [8] Previous trauma (certain types of
ankle fracture)  [9] Steroid injections[9] Psoriatic arthritis / Rheumatoid arthritis Characteristics /
Clinical Presentation Most patients report a slow, insidious onset of unilateral flatfoot deformity. A
history of trauma may be present in up to 50% of cases. Patients will describe the pain and swelling
along the medial aspect of the foot and ankle, which may be exacerbated with activity. Standing on
their toes may be painful and difficult, as may walk up or down stairs or on uneven surfaces. patients
may complain of an exacerbation of a preexisting limp. As the medial longitudinal arch collapses, the
deformity of the foot increases; in this instance patients may describe abnormal wear on their shoes. In
severe cases of deformity the distal fibula will come into contact with the calcaneus, and pain will
move to the lateral aspect of the foot; patients at this stage may describe the feeling of walking on the
medial ankle.[1] Change in static/dynamic foot ( pes planus) Impaired balance Impaired MMT PF/IV
Difficulty/inability to perform unilateral heel raise. Limited calcaneal inversion upon ascent Impaired
subtalar mobility  The Posterior Tibial Tendon During Gait The functions of a healthy tendon are
plantar flexion of the ankle, inversion of the foot and elevating the medial longitudinal arch of the foot
(it appears as the primary stabilizer of this arch). This elevating of the medial longitudinal arch causes
a locked entire of the mid-tarsal bones, so the midfoot and hindfoot are stiff. This allows the muscle
gastrocnemius to act more efficiently during gait. With PTTD the other joint capsules and ligaments
become weak. The subtalar joint everts, foot abducts (talonavicular joint) and heel is in valgus
position. A flattened arch develops what can cause an adult   acquired flatfoot. Gastrocnemius is unable
to act without the posterior tibial tendon what results in affected balance and gait. In below figure,
shows different intramuscular EMG activity in tibial posterior activation during walking between acute
stage II PTTD to unaffected people. Differences in muscle activation: Participants with PTTD shows a
significantly greater tibialis posterior EMG amplitude during the second half of stance phase. They
walk with a pronated foot and exhibit an increased tibialis posterior activity compared to the
participants without PTTD. [10]  Differential Diagnosis Although posterior tibial tendon dysfunction is
the most common cause of adult-acquired flatfoot deformity, there are many other related conditions.
Diagnoses listed below can present very similarly to PTTD and should merit consideration during
evaluation : Tarsal coalition Inflammatory arthritis Charcot arthropathy Neuromuscular disease
Traumatic disruption of midfoot ligaments[2] Diagnostic Procedures Besides the clinical diagnosis,
radiographic evaluation can be used to asses deformity and the possible presence of degenerative
arthritis or other causes of pes planus. MRI has the highest sensitivity, specificity and accuracy, but
ultrasound is less expensive and almost as sensitive and specific as MRI. Clinical tests for PTTD (more
information in Examination)[11]: Too many toes sign [12] Single leg heel raise First metatarsal rise
sign[13] Plantar flexion and inversion of the foot against resistance Mobility of TN and CC joints
Weightbearing X-Rays Stages of PTTD As per Johnson and Strom[4][8][12] [12]: Stage I: Posterior
tibial tendon intact and inflamed, no deformity, mild swelling Stage II: Posterior tibial tendon
dysfunctional, acquired pes planus but passively correctable, commonly unable to perform a heel raise
Stage III: Degenerative changes in the subtalar joint and the deformity is fixed Stage IV ( Myerson):
Valgus tilt of talus leading to lateral tibiotalar degeneration Stage I Deformity: tenosynovitis Physical
exam: single-leg toe raise test (+) Radiography: normal Stage IIA Deformity: Flatfoot deformity,
flexible hindfoot, normal forefoot Physical exam: single-leg heel raise (-), mild sinus tarsi pain
Radiography: arch collapse deformity Stage IIB Deformity: Flatfoot deformity, flexible
hindfoot/rearfoot, forefoot abduction Physical exam: Same stage IIA Radiography: same stage IIA
Stage III Deformity in stage II becomes fixed, rigid or inflexible Deformity: flatfoot deformity, rigid
forefoot abduction, rigid hindfoot/rearfoot valgus Physical exam: sever sinus tarsi pain, single-leg heel
raise test (-) Radiography: arch collapse deformity (subtalar arthritis) Stage IV Deformity: flatfoot
deformity, rigid forefoot abduction, rigid hindfoot/rearfoot valgus, deltoid ligament compromise
Physical exam: single-leg heel raise test (-), severe sinus tarsi pain, ankle pain Radiography, arch
collapse deformity, subtalar arthritis, talar tilt ankle mortise Examination The diagnosis of posterior
tibial tendon dysfunction can be made clinically based on history and objective testing. Subjective
Before a clinical examination is performed, the patient should be asked a series of questions to rule out
other disorders. It is essential to diagnose posterior tibial tendon dysfunction (PTTD) in an early phase
to prevent permanent deformities of the foot/ankle, a physical examination is therefore essential  [6].
Objective The physiotherapist can palpate the posterior tibial tendon from above the medial malleolus
to its insertion, to control the integrity and assess possible pain and swelling that are common for the
first stages of PTTD. In the later stages, the deformity can progress and pes planus may be visible. It is
important to examine the whole lower body and not just the foot, as valgus in the knees can accentuate
the appearance of pes planus. A healthy person has a 5° valgus in his hindfoot, in patients with PTTD
the valgus is increased and the abduction in the forefoot is also more pronounced[14] The
physiotherapist can determine the severity of the pes planus by checking how many fingers can be
passed underneath the midfoot[6]. Special tests for PTTD/AAFD include:[15]   The too many toes sign:
the foot should be inspected from behind and above. The too many toes sign is a manner of inspection
from behind. At this manner they can establish if there is abduction of the forefoot and a valgus
angulation of the hindfoot. It is based on how many toes you can see from behind. By an affected foot,
it will be more than one and a half to two toes see also Foot Posture Index Double leg heel rise: to go
with both feet from a flatfoot stance to standing on the toes. Patients in stage I dysfunction can do this,
but it's painful. Patients with stage II, III or IV dysfunction are unable to do a heel raise. When a
patient stands on tiptoes the heel of the affected foot will not bend inwards;  the normal foot will stay
into inversion while the affected hindfoot will stay in valgus. A single-leg heel raise: patients can't do a
single heel raise with the affected foot;  The first metatarsal rise sign[13]: the patient stands on both
feet, the shin of the affected foot is taken with a hand and rotated externally. When the patient has
PTTD, the head of metatarsal I is lifted, while normal metatarsal I stays on the ground; Plantarflexion
and inversion of the foot against resistance: to test the power of the tibialis posterior. Outcome
Measures Foot Function Index (FFI)[11] 5-Minute Walk Test [11] Instruments to record kinematics
from tibia, calcaneus and first metatarsal: e.g. Milwaukee Foot Model [11][16] Medical Management
Treatment for posterior tibial tendon dysfunction is a complicated subject, to decide whether patients
need operative or non-operative treatment, different variables have to be taken into account by the
attending physician. [17] Non-invasive therapy, such as orthosis and physical therapy [18] are
preferable for they do not damage healthy surrounding tissue, but only when non-operative treatment
fails, surgical treatment is required. [17] [19] Clear evidence exists that suggests that the quality of life
for patients with posterior tibial tendon dysfunction is significantly affected. Evidence suggests that
early conservative intervention can significantly improve quality of life regarding disability, function,
and pain[20]. Treatment for posterior tibial tendon dysfunction is a complicated subject, to decide
whether patients need operative or non-operative treatment, different variables have to be taken into
account by the attending physician. [17] All Stages initially: Conservative management with NSAIDs
and activity modification. Also meant for non-surgical candidates or low demand, elderly patients.
Stage 1: Conservative management through immobilization in a walking boot or cast for up to 3 to 4
weeks to allow for healing of the posterior tibial tendon followed eccentric strengthening with physical
therapy. If immobilization and physical therapy are successful, transitioning into custom-molded
orthotics or AFO is appropriate to maintain relief. Emphasis on medial forefoot posting is critical.
Conservative therapy should be for 3 to 4 months, and if it fails, then surgical intervention may be
warranted. A tenosynovectomy, with tubularization, may be indicated Stage 2A: Conservative
immobilization and physical therapy with orthotics or ankle-foot orthosis (AFO) as recommended in
stage 1 Surgical treatment involves medial calcaneal osteotomy with posterior tendon debridement and
repair. Ancillary procedures may include any/all of the following: flexor digitorum tendon (FDL)
transfer, spring ligament reconstruction, or Achilles tendon lengthening. Stage 2B: All of the
previously listed procedures in Stage 2A +/- lateral column lengthening, or isolated subtalar joint
arthrodesis Stage 3: Conservative therapies, as mentioned above. Surgical treatment is often warranted
as it involves rearfoot arthritic changes and a medial double arthrodesis or triple arthrodesis common
(subtalar, calcaneocuboid, and talonavicular arthrodesis) is indicated with or without deltoid ligament
repair. Stage 4 Conservative therapies, as mentioned above. Surgical treatment is often necessary as it
involves arthritic changes in the ankle, as well as rearfoot. Tibiotalocalcaneal (TTC) arthrodesis for
rigid hindfoot with significant valgus alignment of the talus within the ankle mortise.[2] Physical
Therapy Management The key to a successful outcome is early detection of the dysfunction and
conservative management to prevent chronicity.   The goals of nonoperative treatment include the
Elimination of clinical symptoms, Improvement of hindfoot alignment, and the Prevention of
progressive foot deformity. Patient education re: Activity restriction and modification Providing relief
through prescriptions for medial arch support insoles or custom orthotics (necessary in many cases).
Conservative management with physiotherapy and orthotics for Stage I and II is the first option. [21].
Options include: Orthotic devices or bracing: to support the arch. A walking cast or CAM boot can be
used to immobilize the foot. If this brings relief, the patient can have shoe inserts or modifications,
orthotics or an ankle-foot orthosis (AFO) fitted. Achilles tendon stretching and tibialis posterior
strengthening, concentric/eccentric training of the posterior tibialis. along with nonsteroidal anti-
inflammatories[1] Immobilization: a short-leg cast or boot, it allows the tendon to heal, or avoid all
weight-bearing. Medications: non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, help
reduce the pain and inflammation. Shoe modifications: advise changes such as special inserts designed
to improve arch support. [4] Toe Pick-Ups:The exercise consists of picking up small objects such as
pebbles, marbles or tiny toys with your toes and depositing them in a bucket or other container. Arch
Strengthening Caterpillar: the arch strengthening caterpillar exercise begins by lying on your back with
your knees bent and your feet flat on the floor about two feet from your butt. Lift both foot arches and
pull your toes back toward your heels. Relax your arches and slide your feet slightly back toward your
butt. Repeat the process, allowing your feet to inch closer and closer to your glutes in a caterpillar
motion. Once your feet are nearly touching your butt, repeat the sequence in reverse, slowly moving
your feet away from your butt in the same caterpillar motion. Arch Raises: Sit in a chair with your back
straight, your knees bent in a 90-degree angle and your feet flat on the floor. Raise the arch of one foot
off the floor without curling your toes or lifting your heel. (It’s much harder than it sounds!) When
done properly, you should feel muscle strain in your foot, lower leg and thigh. Alphabet Writing: You
can strengthen your entire foot by imagining a pencil in between your toes, pointing the toes outward
and “writing” the alphabet in the air in front of you[22]. Up to 4 months of nonoperative treatment
should be trialled; if there is no improvement after this period, a tendon synovectomy or debridement
may be indicated.[1] Orthotics: Optimisation of foot loading management by means of foot orthoses
and adequate footwear is the most important aspect in therapy. Depending on the progression of the
pathology, this can be progressively managed with over-the-counter non-individualised foot orthoses,
then with individualised foot orthoses and finally with semi-rigid ankle-foot orthoses[21].  For stage I
disease, nonsurgical treatment should be tried for at least 3 to 4 months. A short walking cast or
removable cast boot immobilization is indicated for patients with acute tenosynovitis. If symptoms are
improved after immobilization, then a custom orthotic or ankle-foot orthosis (AFO) may be fitted to
the patient. The orthotic should be a full-length, semirigid, total contact insert with medial posting. The
primary function of the orthotic is to provide arch support and correct the flexible component of the
deformity. Treatment options per stages of PTTD are determined on the basis of whether there is an
acute inflammation and whether the foot deformity is fixed or flexible: Stage I: Acute: 4-8 weeks
immobilisation, RICE; Chronic: flat footwear and corrective orthosis or ankle-foot orthosis, lace-up
Stage II: Acute 4-8 weeks immobilisation, RICE; Chronic: lace-up, corrective orthosis and flat
footwear Stage III: Lace-up, customised footwear or semirigid shoes and accommodative orthosis
Stage IV: Lace-up, customised footwear or semirigid shoes and accommodative orthosis Prognosis
Posterior tibial tendon dysfunction is a progressive disorder that will continue to deteriorate without
treatment. Early detection and intervention will help to slow progression. Patients provided with
custom orthotics and rehabilitation have been shown to have significant improvement. In a recent study
by Alvarez et al., about 89% of their patients with stage I and II PTTD responded to orthotics and PT.
Nearly all of these patients were back to full strength by 4 months. Outcomes of surgical treatment are
much less predictable, and a return to the pre-disease state should not be guaranteed. Patients may
continue to have some residual effects after reconstructive surgeries[1] Clinical Bottom Line PTTD
requires an interprofessional team approach, including physicians, specialists, physiotherapists, and
pharmacists, all collaborating across disciplines to achieve optimal patient results.[2] Posterior tibial
tendon dysfunction characteristically is a slow onset condition mainly affecting middle-aged, obese
women. Risk factors include obesity, hypertension, diabetes, steroid use and seronegative
arthropathies. Patients may complain of pain and swelling around the medial ankle, difficulty
mobilizing or exacerbation of an existing limp. Examination may show tenderness along the course of
the tendon, difficulty performing a single heel raise or “too many toes” when feet are viewed standing
from behind. X-ray and MRI can confirm diagnosis, help stage disease and assist in preoperative
planning. The disease as an entity is under-recognized, and early stages of the disease can be
misdiagnosed, but prompt treatment can prevent deformity and need for surgery.[1] Pes Planus -
PhysiopediaDefinition/Description Pes planus also known as flat foot is the loss of the medial
longitudinal arch of the foot, heel valgus deformity, and medial talar prominence.[1] In lay terms, it is
a fallen arch of the foot that caused the whole foot to make contact with the surface the individual is
standing on. The deformity is usually asymptomatic and resolves spontaneously in the first decade of
life, or occasionally progresses into a painful rigid form which causes significant disability. All at birth
has flat feet and noticeable foot arch are seen at around the age of 3years.[2] It is of two forms; flexible
flat foot and rigid flat foot. When the arch of the foot is intact on heel elevation and non-bearing but
disappears on full standing on the foot, it is termed flexible flat foot while rigid flat foot is when the
arch is not present in both heel elevation and weight bearing.[3] Prevalence Previous studies[4][5][6]
indicate the prevalence of flatfoot between < 1% and 28% at certain age groups. Pes planus is more
prevalent in children and females are more predisposed to this condition than their male counterparts in
adulthood.[1] There are about 20-30% of children with some form of flat feet.[2] Pita-Fernandez et
al[7] reported a prevalence of 26.62% in random sample. Also, older individuals and high BMI are
found to have a significant influence on having flat feet. Etiology/Causes[8] The etiology of flatfoot
has several factors implicated. depending on etiology pes planus can be divided into types, namely
congenital and acquired. These factors are: Talipes equinovarus deformity, ligamentous laxity, foot
equinus deformity, tibial torsional deformity, presence of the accessory navicular bone,[9] congenital
vertical talus, and tarsal coalition. Diabetes[10] and obesity[11] are also probable factors related to pes
planus.[12][13][2] Foot and ankle injury such as rupture or dysfunction of the posterior tibial tendon
Genetic malformation such as Down syndrome and Marfan syndrome[3] Familial factors[14] Arches
weakness due to overuse and certain forms of foot condition or injuries Some medical conditions such
as arthritis, spina bifida, cerebral palsy, Arthrogyroposis, and muscular dystrophy.[15] Flat feet can
also occur as a result of pregnancy.[16][17] Iatrogenic factors such as posterior tibialis tendon (PTT)
transfer.[15][18] [19] [20] Pathophysiology[8] The calcaneus, navicular, talus, first three cuneiforms,
and the first three metatarsals make up the medial longitudinal arch. This arch is supported by posterior
tibial tendon, plantar calcanea navicular ligament, deltoid ligament, plantar aponeurosis, and flexor
hallucis longus and brevis muscles. Dysfunction or injury to any of these structures may cause acquired
pes planus. Also, excessive tension in the triceps surae, obesity, Achilles tendon or calf muscle
tightness, ligamentous laxity in the spring ligament, plantar fascia, or other supporting plantar
ligaments may result in acquired flat foot. Rigid pes planus is rare but usually starts from childhood;
tarsal coalition, accessory navicular bone, congenital vertical talus, or other forms of congenital
hindfoot pathology. are usually the underlying factors Characteristics/Clinical Presentation The major
symptom of flat feet is foot pain due to strained muscles and connecting tissues; Pain along the course
of the posterior tibial tendon (PTT) and inability or pain upon attempts to perform a single-leg heel rise
Some individuals with flat feet have an inwards turned ankles with most of the weight bearing on the
foot deviated medially. The detorted weight bearing could result in abnormal lower limbs
biomechanics thus, may predispose the arch of the foot, calf, knee, hip, lower back and lower legs to
pain Possible oedema at the medial side of the foot Stiffness of one or both arches of the feet.
Contractures of feet and ankle muscles att the lateral compartment Uneven distribution of body weight
with resultant one-sided wear of shoes leading to further injuries. Difficulty in walking[15] Associated
Co-morbidities Co-morbidities include but not limited to neurological conditions such as cerebral
palsy; genetics e.g downs syndrome, Marfan syndrome or Ehlers Danos; charcot joint; tibialis posterior
dysfunction; Obesity; arthropathies;[21] Shprintzen-Goldberg syndrome.[22] Medical Management
Treatment is based on etiology and NSAIDS are sufficient for pain. Surgery is required in rigid pes
planus and in cases resistant to therapy to reduce symptoms.[23] Most surgical methods aim at
realigning foot shape and mechanics. These surgeries could be tendon transfers, realignment
osteotomies, arthrodesis and where other surgeries fail, triple arthrodesis is performed[24] Physical
Therapy Management[25][26][8][24] The aim of Physical therapy is to minimize pain, increase foot
flexibility, strengthen weak muscles, train proprioception, and patient education and reassurance. Pain
management includes rest, activity modification, cryotherapy, massage, and nonsteroidal anti-
inflammatory medication. Ultrasound and pulsed electrical stimulation can also be used for pain relief.
Electric stimulation will aid blood circulation, promoting healing processes and diminishing discomfort
and oedema. Flexibility exercises are passive ROM exercise of the ankle and all foot joints; Stretching
of gastrocnemius soleus complex and peroneus brevis muscles to facilitate varus and foot adduction;
Heel-cord stretch for the Achilles tendon and calf muscles to relief tight heel cord.[27] Strengthening
Exercises: Strengthening exercises are given to anterior and posterior tibialis muscles and the flexor
hallucis longus, Intrinsic, interosseus plantaris muscles, and the abductor hallucis to prevent valgus and
flattening of the anterior arch. Arch muscle strengthening exercise with theraband Global activation of
the muscles known to support the medial longitudinal arch and the varus with and without resistance.
Single leg weight bearing Toe walking For Proprioception, Toe and heel walking, Single leg weight
bearing, and Descending an inclined surface are exercises that could be prescribed. Also, Toe clawing
of towel and pebbles, forefoot standing on a stair, toe extension and toe fanning/spreading, and heel
walking are all good exercises to maintain viable foot arches. Counselling on proper footwear,
recommendation on motion control shoes, orthotics and braces are also needed. Foot orthotics such as
shoe inserts are used to support the arch for foot pain secondary to pes  planus alone or combination
with leg, knee, and back pain. Obese and overweight individuals should be counseled on weight loss
through exercise and dieting; Possibly refer to a dietician for appropriate insight. Other co-morbidities
amenable to physiotherapy can also be treated following a proper examination and treatment plan. [28]
Resources Allen J, Solan S. Physiotherapy management of paediatric flat feet. Available from:
https://www.peacocks.net/_filecache/316/436/892-physiotherapy-management-of-paediatric-flat-
feet.pdf  Halimah bt. Hashim. Physiotherapy Management For Flat Foot (Pes Planus). Health Online
Unit, Ministry of Health Malaysia, 2019. Available from:
http://www.myhealth.gov.my/en/physiotherapy-management-for-flat-foot-pes-planus/ Raj MA, Tafti D,
Kiel J. Pes Planus (Flat Feet). StatPearl-NCBI Bookshelf, 2020. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK430802/ Pes valgus - PhysiopediaDefinition/Description
This text describes pes valgus in children. It is a problem commonly encountered in paediatric
orthopaedics and is generally considered as caused by the collapse of the medial longitudinal arch in
the foot. It was found that 42% of children between 3 and 6 years which normal weight develop pes
valgus. Age, gender, obesity, cerebral palsy, syndrome of Down, … are known risk factors for the
development of growth and musculoskeletal changes. Almost 20% of the adult population has pes
valgus.[1][2][3][4][5]; Epidemiology/Etiology The medial longitudinal arch of the foot normally
develops by the age of 5 or 6 as the fat pad in babies is gradually absorbed and balance improves as
skilled movements are acquired. In some children however, the arch fails to develop which may be a
result of tightness in the calf muscles, laxity in the Achilles tendon or poor core stability in other areas
such as around the hips.[3][6]Over time it may lead to an altered walking pattern, clumsiness, limping
after long walks, and pain in the foot, knees or hips. Beside the aforementioned causes for pes valgus,
tarsal coalitions, peroneal spasm and vertical talus are common aetiologies during the childhood. It is
therefore important that appropriate treatment starts at an early age.[7] Middle aged women are most
commonly affected, and the prevalence is known to increase with age. Pes planus, hypertension,
diabetes mellitus, steroid injection around the tendon, high impact sports, Obesity, and seronegative
arthropathies have all been identified as risk factors.[2][6] Anatomical Causes There are 4 groups of
anatomical peculiarities which predispose to flat foot. The inheritance of many of these peculiarities
explains the frequent familial incidence of the disorder. The lower limb may be wrongly ‘set’ on the
trunk. The entire limb may be externally rotated or the leg only may be rotated from the knee
downwards. In either case, the line of body weight falls too far medially. As a result, when the body
moves forward in walking the force of the body weight imposes considerable strain upon the apex of
the arch and tends to topple over it. The leg may be wrongly ‘set’ on the thigh, for example in knock-
knees. Here, too, as in external rotation, the line of the body weight falls to medially. The combination
of knock-knees and flat foot is common in children aged 2 – 6 years. The foot may be wrongly ‘set’ on
the leg. A short calf muscle or Achilles tendon prevents adequate dorsiflexion of the ankle (unless the
knee is bent). In walking, the knee is straight and, as the front leg swings forward, the back leg must
dorsiflex considerably at the ankle. If adequate dorsiflexion is hindered by a tight calf the Achilles
tendon bowstrings across the outer side; this is accompanied by a topple of the arch to the medial side.
The forefoot may be wrongly ‘set’ on the hind foot. The forefoot may be varus, with the soles of the
feet tending to face each other; this is sometimes due to a relatively short tibialis anticus muscle, and
sometimes to a short or elevated first metatarsal. Whatever the cause, as the weight comes on the
forefoot in walking the first metatarsal is forced down from its elevated position on to the ground; the
apex of the arch is pushed downwards and inwards and flatfoot results. There has been emphasised the
varus forefoot is commoner than generally supposed, but the deformity may not be recognised unless
the foot is correctly examined with the heel held square. Once weight is on the foot the obvious
deformity is the valgus heel. Physiological causes The bony arch of the foot is potentially unstable. It
is bound together by ligaments, but these are capable of resisting short term stress only; indeed, their
main function is to act as sensory end organs, and when they are stretched appropriate muscles are
reflexly brought into action. Even the most anatomically perfect foot will become rapidly and grossly
flat unless it has muscles of good bulk and tone to support it. The psychological fault may lie in the
muscle itself or in its nervous control. Inadequate nervous control We are not here concerned with the
gross and obvious inadequacies which result from poliomyelitis or spina bifida, for in these conditions
flat foot is overshadowed by other disabilities. An example of inadequate nervous control is infantile
flat foot. A baby has to learn to balance first its head, then its trunk and eventually to balance the whole
body on the feet. The difficult art is not required during the early months of life; but sometimes the
balancing reflexes fail to develop even after the child has begun to walk. In that event the arch
inevitably collapses with body weight. Myelination of the pyramidal fibers to the foot is incomplete at
birth and the plantar responses in babies is extensor. If the infantile flat foot persists into early
childhood the extensor responses may persist too, and it is tempting to assume that balancing cannot be
easily learned until myelination is complete. Inadequate muscles After illness or enforced recumbence
the muscles may temporarily be weak and the arch consequently falls when walking is resumed. A
more lasting form of muscle weakness accompanies a generally poor posture. The child (often a pre-
adolescent girl) presents a familiar flabby contour with head stuck forward, mouth open, chest flat,
back rounded and abdomen protuberant. The gluteal muscles are concerned largely with posture (Wiles
1949). They help to straighten the hip and knee, and to twist the limb outwards. This twist can not be
imparted to the foot which is anchored to the ground, and so the rest of the limb turns outwards relative
to the foot. As a result, the arch is lifted and the line of weight corrected only when the glutei work
properly. Relative inadequacy of muscle is well illustrated by when extra strain is put upon the arch,
for example in overweight individuals. Prolonged standing is more harmful to the feet than walking
because, during walking, the muscles supporting the arch alternately contract and relax which is the
best training for a muscle.[2][6] Clinically Relevant Anatomy The classification of the pes valgus is
based on three aspects: Arch height[1][8] The best parameter to characterize medial longitudinal arch
structure was found to be a ratio of navicular height to foot length. It is accepted that the flatness of
normal children’s feet and their age are inversely proportioned. Heel eversion angle[7][1] Heel
eversion or hindfoot valgus is generally accepted as a normal finding in young, newly walking children
and is expected to reduce with age. The eversion of the heel has been repeatedly used for determining
the posture of the child’s foot. Resting calcaneal stance position is a more recent method. It has guided
clinicians in assessment of the child’s foot posture and calcaneal eversion has been suggested to reduce
by a degree every 12 months to a vertical position by age 7 years. A vertical heel is optimal for foot
function. The average rear foot angle for children from 6 to16 years is 4° (raging from 0 to 9° valgus).
Whether the flat foot structure is rigid or flexible (cf. Jack’s test[6]) Rigid pes valgus, also called
congenital pes planovalgus (convex)[3], is often a result of tarsal coalition, which is typically
characterized as a painful unilateral or bilateral deformity.  In flexible pas valgus, also called congenital
pes cancaneovalgus[8], the foot lies against the lower leg, or can be extended without resistance until it
impinges against the leg. In contrast to the congenital pes planovalgus, the foot can be restored to a
normal position without great resistance. Plantar flexion is occasionally is reduced. The skeletal
framework of each foot is formed by 28 bones: 7 tarsals, 5 metatarsals, 14 phalanges and 2 sesamoid
bones. From the functional point of view, the feet can be divided in three parts: the hind foot, formed
by talus and calcaneus, the midfoot, consisting of navicular, cuboid and three cuneiform bones, and the
fore- foot, formed by metatarsals and phalanges. The talus, calcaneus, cuboid, navicular and three
cuneiform bones form the tarsus, comprising the hind-foot and mid-foot. The hind foot extends from
the calcaneal tuberosity to the transverse tarsal joint (Chopart’s joint); the latter consists of the
talonavicular part of talocalcaneonavicular joint and the calcaneocuboid joint. The anterior limit can be
traced on the surface along the S-shaped line (medially convex and laterally concave) connecting the
tuberosity of the navicular bone (palpable infero-anteriorly to the tip of the medial malleolus) with the
point located half-way between the lateral malleolus and the tuberosity at the basis of the 5th
metatarsal. The movements of the mid-foot on the hind foot at the transverse tarsal joint augment the
inversion (turning the sole towards the median plane) and eversion (turning the sole laterally),
occurring mostly at the subtalar joint. The anterior limit of the mid-foot follows the tarsometatarsal
joints (Lisfranc’s joint), traced on the surface by the slightly convex line between the tuberosity of the
1st and the prominent tuberosity of the 5th metatarsal bone. These joints allow only slight movement of
sliding. The shape of the tarsal and metatarsal bones accounts for the presence of longitudinal and
transverse arches of the foot. The medial longitudinal arch extends between the calcaneus and talus
(posterior pillar), and first three metatarsal and three cuneiform bones (anterior pillar). The keystone,
corresponding to the talar head, is 15-18 mm above the ground. The lateral longitudinal arch is much
flatter and rests on the ground in the weight bearing feet. It is composed of the calcaneus (posterior
pillar), the lateral two metatarsals (anterior pillar) and the cuboid bone (keystone), which may be 3-5
mm from the ground in the non-weight bearing feet. The transverse arch runs from side to side at the
tarsometatarsal joint level. Its medial pillar is represented by the medial cuneiform and the basis of the
1st metatarsal bone, the lateral pillar is formed by the lateral cuneiform, cuboid and the bases of the
3rd-5th metatarsals; the keystone corresponds to the intermediate cuneiform, which can be 18-20 mm
above the ground. The arches are passively maintained by plantar aponeurosis and ligaments (long and
short plantar ligament, plantar calcaneonavicular ligament) and dynamically supported by tendons of
extrinsic muscles (tibialis anterior, flexor hallucis longus and brevis, flexor digitorum longus and
brevis for the longitudinal arch; peroneus longus, tibialis posterior for the transverse arch) and by
intrinsic muscles that run between the pillars of the arches. These structures act together as a unit to
support and distribute appropriately the body weight during walking.[7] Diagnostic Procedures
Footprints[7] It is still controversial if footprints reflect the real morphology of the medial longitudinal
arch. Recent development found an initial correlation between dynamic pressure patterns and static
foot-prints. X-rays[7][1] X-rays are used to categorise the feet as having normal, slightly flat and
moderate arches. Foot-posture index (FPI-6)[6] It is based on six specific criteria: Talar head palpation
Curves above and below lateral malleolus Inversion/eversion of the calcaneus Bulge in the region of
the talonavicular joint (TNJ) Congruence of medial longitudinal arch Abduction/adduction of the
forefoot en rear foot Supination resistance test [6][7] This test is used to estimate the magnitude of
pronatory moments. The foot is manually supinated. The higher the force required, the greater the
supination resistance and the stronger the pronatory forces. This test is subjective. Jack’s test and Feiss
angle (are related) [6] Performing the Jack’s test. The hallux is manually dorsiflexed while the child is
standing. If the medial longitudinal arch rises due to dorsiflexion of the hallux, the foot is considered a
flexible flat foot. If the medial longitudinal arch remains unchanged, the test designates a rigid flat
foot. The purpose of this test is to check the foot flexibility and the onset of the windlass mechanism
by tensioning the plantar fascia trough the extension of the first metatarsophalangeal joint. The Feiss
line is the line interconnecting malleolus medialis, navicular and first metatarsal head. The inclination
of this line with the ground increases when the first metatarsophalangeal joint is dorsiflexed (Jack’s
test). This dorsiflexion activates forefoot supination and raises the arch height (140°± 6°). Ankle range
[6][7] Children’s ankle range assessment is generally an unreliable measure, as typically assessed when
the child is non-weight-bearing. So it is suggested that therapists look at a child’s ability to squat, heel
walk and increase stride length.[6] Physical Therapy Management In congenital pes valgus, surgery is
most recommended, but conservative treatment is also available. For children with pes valgus it usually
consists of: [3][4] Advice on appropriate footwear. [1][6] Advice on appropriate insoles to improve
foot position and referral to an podiatrist and an orthotist: in-shoe wedging, foot splints, night stretch
splints and cast orthoses. The primary action splint therapy is aimed at stabilising the rear foot and
midfoot but not blocking the forefoot. Age-expected foot position, stance and gait are dynamic
considerations and need to be well understood. [6] Reducing pain and risk of secondary joint problems.
[1][3][7] Providing advice on exercise to help stretch tight muscles and strengthen weak areas to aid
development of correct foot posture. [6]  Acquired pes valgus because of a tibialis posterior
dysfunction is treated according to different stages of this pathology. In stage 1 and 2 the foot is still
flexible, while in stage 3 and 4 the foot becomes more rigid. Stage 1 and 2 Possible inflammation
surrounding the sheath of the tibialis posterior tendon should be dealt with before the chronic aspect is
treated. As therapy it is recommended to be immobilised during 4 to 8 weeks in a plaster cast below the
knee or removable boot as to control accompanying inflammation. In conjunction Rice and anti-
inflammatories can be used. Footwear has an important role, and patients should be encouraged to wear
flat lace-up shoes or lace-up boots, which accommodate orthoses. Stage 1 patients may be able to
manage with an off the shelf orthotic or may try first a laced canvas ankle brace. The various casted
and semirigid orthoses support the medial longitudinal arch of the foot and either hold the heel in a
neutral alignment in a stage 1 patient. In stage 2 it corrects the outward bent heel to a neutral
alignment. This therapy has several functions, those are to alleviate stress on the tibialis posterior, to
make gait more efficient by holding the hindfoot fixed and to prevent progression of the deformity.
Stage 3 and 4 In this stage the inflammation is a less common feature. The treatment revolves around
accommodating the deformity, rather than attempting to correct it, with a customised moulded rigid
orthoses, used in conjunction with appropriate footwear.[1] Characteristics/Clinical Presentation
Patients may complain of medial ankle pain caused by posterior tibial tenosynovitis and/or
tendinosis. Further in the deformity progress, patients commonly experience lateral foot pain, arising at
the angle of Gissane from talocalcaneal impingement or in more rare cases from fibular abutment
against the calcaneus. They may also experience pain on palpation of arthritic joints.[6] Differential
Diagnosis Chronic ankle sprain Tarsometatarsal osteoarthritis Charcot arthropathy Inflammatory
arthritis  Unrecognized tarsal coalition Neuromuscular disease[2][5]  Examination During gait, it must
be noted whether the heel touches the ground and what degree normal toe-off is possible. The position
of the heel is examined from behind, patient having heel down as far as possible. If pain occurs that
must be noted. Also the joint motion and position of the subtalar joint must be evaluated with the heel
in everted and inverted position. The affected heel will stand in a valgus position, and flattening of the
medial longitudinal arch, forefoot abduction is visible. The tightness of the Achilles tendon is assessed
with forced dorsiflexion, this way we can evaluate tightness and the flexibility of the foot. Also the
area posterior to the medial malleolus should be examined for swelling and palpation along the distal
portion of the posterior tibial tendon (PTT) is highly suggestive of PTT degeneration. The inability to
perform a single heel rise is suggestive of PTT insufficiency.[2][6]   Medical Management Researchers
define different possibilities of surgery depending on the type of pes valgus. Congenital pes valgus is
usually treated at a young age, while acquired pes valgus is being treated later on when diagnosed.[1]
[2][3][4]  For the congenital pes valgus treatment, researchers have defined the best possible treatments
depending on the age of the person/child. In a child younger than 2 years they recommend an extensive
release with lengthening of the Achilles tendon and fixation procedure. It is less invasive than other
techniques, because there is no tendon transfer or bony procedures needed. The explanation could be
because of the greater adaptability of the cartilaginous structures. In a child with neural tube defect,
younger than 2 years of age they recommend an extensive release with tendon transfer procedure. A
neuromuscular imbalance between a weak tibialis posterior tendon and a strong evertor of the foot
could be responsible for this condition. Good results are found for this operation which aims to correct
this imbalance. In a child older than 2 years of age they recommend an extensive release with tendon
transfer procedure. Surgical correction becomes increasingly difficult in older children because of
secondary changes of the bone. This procedure resulted as the best for children whose walking and
standing potential has been established. In case of failure of precedent procedures, a bony procedure
may be considered. There are good results for children of 4 years and older with these procedures.
Only in extreme cases and when the child is older than 4 years of age a subtalar or triple arthrodesis
may be considered.[3][4] In acquired pes valgus they only apply surgery if all conservative therapies
are inefficient, in certain cases they define different stages. Every stage has a different surgical
therapy. Stage 1 A calcaneal osteotomy is performed with the aim to correct the underlying foot
deformity and to attempt to preserve the foot’s function in conjunction with either debridement of the
tendon or tendon transfer. Stage 2 This treatment entails a tendon transfer in combination with
corrective osteotomy. The rationale behind this surgery is that osteotomy is required to correct the
bony architecture of the foot in order to optimise the biomechanics of the reconstructed tibialis
posterior tendon. Various osteotomies of the calcaneus can correct the bony alignment and may
augment with a lengthening of the tibialis anterior tendon. The tendons used to reconstruct the tibialis
posterior are either a split tibialis anterior tendon or a flexor digitorum longus. Stage 3 The goal of
surgical treatment is to correct the deformity and alleviate pain trough a triple arthrodesis of the
subtalar, calcaneocuboid, and talonavicular articulations. Stage 4 In this stage there are additional
degenerative changes present in the ankle joint. Surgery consists usually of a salvage treatment with a
pantalar arthrodesis of the ankle (the subtalar, calcaneocuboid and talonavicular articulations). Every
surgery is usually followed by a plaster cast for two to three months. The recovery after surgery takes
about 6 months to 1 year to heal completely and to recover completely on a functional level.[1][2]
[4] The Os Trigonum Syndrome - PhysiopediaDefinition/Description Sagittal T1-weighted MR image
in plantar flexion showing the “nutcracker-phenomenon”. The os trigonum together with surrounding
soft tissues are wedged between talus, calcaneus and tibia. The Os Trigonum Syndrome refers to pain
posterior of the ankle and reduced plantarflexion caused by “the nutcracker-phenomenon”. When an os
trigonum is present, this accessory ossicle together with surrounding soft tissues can become wedged
between the tibia, talus and calcaneus. This can lead to inflammation of the involved structures. [1][2]
[3] The os trigonum syndrome can also be named the symptomatic os trigonum, the talar compression
syndrome or posterior tibial talar impingement syndrome.[4] Clinically Relevant Anatomy
Embryologically, the body of the talus and the posterior talar process are separate ossification centers.
Between the 7th and the 13th year of life, the posterior talar process appears as a separate ossicle: the
os trigonum. Normally, within a year of its appearance, it fuses with the talus, but about 7% of the
adult population has still this os trigonum. It can be present unilaterally or bilaterally, with smooth or
serrated margins. The os trigonum is usually seen as an individual bone, but can also exist of two or
more pieces. It is less than 1cm in size, but this can vary. [3][5] [4] Superior view of talus The os
trigonum is usually triangular with an anterior, inferior and posterior surface. The anterior surface
connects with the lateral tubercle by cartilaginous synchondrosis. The inferior side may articulate with
the calcaneus. The posterior surface is nonarticular, but is used as a point of attachment for
capsuloligamentous structures. The os trigonum may also be round or oval. [4] The flexor hallucis
longus tendon is situated medial to the os trigonum, in the sulcus between the medial and lateral
tubercle.[4]   Epidemiology /Etiology There are three mechanisms for the development of an os
trigonum: fusion failure of an ossification center fracture of the posterior margin of the tibia fracture of
the posterior process of the talus.[6] The presence of an os trigonum isn’t sufficient to create the
syndrome. It must be combined with a traumatic event. [3] The os trigonum syndrome can be caused
by overuse or trauma. When it’s due to overuse, it’s mostly found by ballet dancers and runners. The
forceful plantar flexion that happens during an “en pointe” or “demi-pointe” position, as well as by
running downhill, produces compression on the posterior aspect of the ankle joint. In cause of a
trauma, the os trigonum can be displaced by forced plantarflexion. [3] Soft tissue structures, including
the ankle joint capsule and surrounding ligaments, may react by forming a hypertrophic mass. [4][2]
Characteristics/Clinical Presentation A load-dependent, persistent pain between the Achilles tendon
and the peroneal tendons is the first indicator of the syndrome. Stiffness, weakness and swelling can
also be observed in this zone. The second main symptom is a decrease in plantarflexion compared with
the unaffected ankle. In some cases the bony prominence may be palpable.[5][6][1][7] Eversion or
inversion movements may cause discomfort. Pain at the posterior aspect of the ankle will be
experienced by plantarflexion of the foot or dorsiflexion of the great toe.[4][8] Differential Diagnosis
The following diagnosis must be considered: Tendinitis flexor hallucis longus[3];*Tarsal tunnel
syndrome[3];*Subtalar pathology[3];*Achilles tendinopathy[5];*Peroneal tendinopathy[5];*Achilles
tendon bursitis[5];*Osteochondritis dissecans of the talus. [5] Diagnostic Procedures Lateral X-ray[8],
possibly weight-bearing, with the foot in full plantarflexion.[6] CT-scan[8][5] MRI is the preferable
technique[4] for establishing the presence[9] and the size of the ossicle[8],  coexisting pathologies and
soft tissue and bone damage.[6] Flexion/extension MRI gives information about the mobility of the os
trigonum.[4] Technetium bone scan[6][5][9] shows increased uptake in the region of the os trigonum.
lateral x-ray of foot showing os trigonum Technetium bone scan Examination   On posterolateral
palpation, between the Achilles tendon and peroneal tendons, pain and swelling may be noticed.[5][7]
[3] The passive forced plantarflexion test: It should be executed with repetitive quick and passive
hyperplantarflexion movements in a neutral position, possibly with exo- or endorotation movement on
the point of maximal plantarflexion. Thereby grinds the ossicle between tibia and calcaneus.[3]
Medical Management Nonsteroidal anti-inflammatory medication or corticosteroid injections are used
to reduce soft tissue inflammation.[8][1][3] In case of fracture, a below-knee cast is used for 4-6weeks.
[8] If symptoms persist, surgery is applied. (high evidence, all studies mention good results.) This
involves the removal of the os trigonum. Postoperatively we apply a plaster cast for 5days. Hereafter
physiotherapy is started for 4-8 weeks. Afterwards full sports activities can be resumed. It will take up
to 6 months until full recovery.[1][3] Physical Therapy Management Rest, ice, massage and ultrasound
treatment will reduce inflammation.[5][8][3] Isometric and eccentric exercises to strengthen and stretch
the lower-leg muscles are used in a physiotherapeutic treatment.[6] Also exercises to improve deep
muscle action during plantarflexion are designated. The deep muscles of the lower leg, such as tibialis
posterior, flexor digitorum longus, flexor hallucis longus and the peroneals are the opposites of the
M.gastrocnemius. By using the deep muscles, the talus is shifted forward during plantarflexion, what
will reduce the impact of the os trigonum on the posterior tibia, contrary to using the M.gastrocnemius,
which results in lifting the calcaneus and compression of the os trigonum.[6] Fig. 5: Strengthening of
the deep muscles. Performing demipointe (2) and en pointe (3) while holding the calcaneus in place
with the hands. Knee flexion at 90° to prevent contraction of the M.gastrocnemius.[6] Also
proprioceptive exercises on a tilt board are applied to correct malalignments of the lower limb.[6] All
of these exercises were found in only one study of 11 dancers with a posterior ankle impingement
including 6 cases with an os trigonum. Nine of them had good results with these exercises, the other
two ones underwent surgical excision.[6]
 References

1. ↑ Jump up to:1.0 1.1 1.2 1.3

       Raymond T., Morrissy and Stuart L.Weinstein .Lovell, Winter’s Padiatric
Orthopaedics. United States: Lippincot William’s Wilkin Publication, 2005.
2. ↑ Jump up to:2.0 2.1
   D.Richard, V.Wayne, M. Adam, Gray’s Anatomy for Students. Spain: Elsevier
Publishers, 2005
3. Jump up↑ Golano P., ‘The anatomy of the navicular and periarticular structures.’ Foot Ankle
Clinics, 2004, March, vol. 9, p. 1-23.
4. ↑ Jump up to:4.0 4.1
   Kiter E., Erdan N., Karatosun V., Gunall I., ‘Tibialis posterior tendon
abnormalities in feet with accessory navicular bone and flatfoot’. Acta orthopaedica Scandinavia, 1999,
December, vol. 70, p. 618-621
5. ↑ Jump up to:5.0 5.1 5.2
     Kulkarni. G.S. Textbook of orthopedics and trauma.India: Jaypee Brother
Publication, 1999
6. ↑ Jump up to:6.0 6.1 6.2 6.3 Kidner FC. The prehallux (accessory scaphoid) in its relation to flat-foot. J
Bone Joint Surg 1929 : II : 831
7. ↑ Jump up to:7.0 7.1 7.2 Kidner FC. Pre-hallux in relation to flatfoot. JAMA 1933; 101: 1539-42.
8. ↑ Jump up to:8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7
               A. Bernaerts, F.M. Vanhoenacker, S. Van de Perre, A.M. De
Schepper, P.M. Parizel1 Accessory navicular bone: Not Such a normal variant. JBR–BTR, 2004, 87 (5)
page 250-252
9. Jump up↑ Prichausuk S, Sinphurmsukskul O: Kinder Procedure for symptomatic accessory
navicular and its relation to pes planus, Foot Ankle 16:500,1995
10. ↑ Jump up to:10.0 10.1
   Shands AR Jr, Wentz IJ. Congenital anomalies, accessory bones and
osteochondritis in the feet of 850 children. Surg.Clin.North Am 1953:97:1643-1666
11. Jump up↑ Kulkarni. G.S. Textbook of orthopedics and trauma.India: Jaypee Brother
Publication, 1999.&lt;/ref&gt;&lt;ref name="p7"&gt;Kidner FC. The prehallux (accessory scaphoid) in
its relation to flat-foot. J Bone Joint Surg 1929 : II : 831
12. Jump up↑ ShaychiITA. Tibialis Posterior Basic Strengthening. Available
from: http://www.youtube.com/watch?v=zmh1FisBeeM  [last accessed 24/11/12]
13. Jump up↑ ShaychiITA. Tibialis Posterior Basic Multiplanar Strengthening. Available
from: http://www.youtube.com/watch?v=qv76eBxGQXI  [last accessed 01/12/12]
14. Jump up↑ ShaychiITA. Tibialis Posterior Functional Strengthening: Full Body Weight
Maintaining Supination. Available from: http://www.youtube.com/watch?v=1C_C5N9reB8 [last
accessed 01/12/12]|}
15. Jump up↑ ShaychiITA. Tibialis Posterior Functional Strengthening: Maintain Arch with
Compass Squats. Available from: http://www.youtube.com/watch?v=TdHgyFZbOPk [last accessed
24/11/12]|}