Key Insights On Treating Early Adult-Acquired Flatfoot Deformity

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When a patient presents to the office complaining of medial ankle pain, one should consider several differential diagnoses. These include an ankle sprain, posterior tibialis or flexor digitorum longus tenosynovitis, a rupture or tarsal tunnel syndrome.

However, if the patient is middle-aged, female, mildly obese and has had medial ankle pain for several months, there should be a high index of suspicion of insufficient posterior tibialis (PT) tendon leading to adult-acquired flatfoot (AAF) syndrome. When the loss of PT tendon function due to partial or complete rupture occurs, the development of a progressive flatfoot deformity in adults is often missed.

The rupture of the PT tendon was first described in 1953. In 1969, Kettelkamp and Alexander published results of their surgical exploration of the PT tendon and reported that one cannot obtain satisfactory results in patients with delayed repair and a loss of tendon substance.¹ Mann and Thompson reported a series of 17 patients with PT tendon rupture. The duration of treatment for these patients was 43 months and in all but two of the patients, there was an incorrect initial diagnosis.²

In the adult population, researchers have reported progressive flatfoot deformity with degenerative disease of the PT tendon leading to partial rupture. The failure of the tendon is due to degeneration of the PT tendon in the middle-aged population secondary to acute angulation of the tendon as it passes posterior to the medial malleolus and the zone of hypovascularity distal to the medial malleolus.³

Currently, clinicians use the terms posterior tibial tendon dysfunction (PTTD) or AAF deformity interchangeably with a diagnosis based on the Johnson and Strom classification.4 The treatment dilemma occurs with treatment options of late Stage I or early Stage II PTTD with suspected partial rupture of the PT tendon.

An Anatomical Overview Of The PT Tendon
The PT tendon runs posterior and medial to the axis of the ankle joint, and medial to the axis of the subtalar joint. The PT tendon functions as a plantar-flexor of the ankle and an invertor of the subtalar joint complex. The PT muscle starts the process of inversion of the hindfoot during gait by bringing it into a neutral position and maximizing the mechanical advantage of the laterally positioned Achilles tendon as one rises onto the forefoot. The PT muscle drives the position of the hindfoot and determines the flexibility of the foot by its control over the transverse tarsal joints.

The loss of the force of inversion of the muscle explains why patients with PT tendon insufficiency have only a limited ability or are completely unable to rise onto their toes from a position of single leg stance. The PT muscle normally is antagonistic to the peroneus brevis muscle when there is a lack of opposition of the peroneus brevis muscle. This leads to the clinical deformities one sees in patients with rupture or dysfunction of the PT tendon.

The medial capsular and ligamentous structure of the hindfoot and midfoot plays a role in the development of flatfoot deformities. The talonavicular joint capsule, the spring ligament and deltoid ligament complexes become attenuated and they have been implicated in the progressive loss of the medial longitudinal arch of the foot and the ankle dysfunction one sees in longstanding cases of PTTD.

Recognizing the progressive nature of PTTD is very important.

What You Should Know About The Johnson And Strom Classification Of PTTD
The classification by Johnson and Strom is useful in developing algorithms for treatment of AAF deformity.⁴ However, this classification does not predict the outcome of treatment and does not consider the contracted gastrocnemius.

The Johnson and Strom classification identifies different stages of PTTD. Stage I is characterized as PT tendon dysfunction with tenosynovitis, with or without intratendinous degeneration. The tendon is not elongated and the hindfoot is not in a valgus position. The muscle strength is diminished but no noticeable foot deformity is present. The foot is in normal alignment when the patient is standing.

Early diagnosis and treatment of PTTD is important. One can make an attempt to halt the disease process in stage I, avoiding the subsequent rupture of the tendon that results in AAF deformity and preventing the development of rigid deformity. In late stage I, the patient will start to have difficulty performing single heel rise.

Stage II involves an elongated PT tendon, a mobile hindfoot and AASF deformity. The patient is unable to perform single or double heel rise.

Stage III involves an elongated PT tendon with a rigid, deformed hindfoot. Myerson later added stage IV, which involves valgus angulation of the talus and early degeneration of the ankle joint.⁵

Essential Tips On Diagnosing PTTD Secondary To Rupture Or Degeneration
The diagnosis of PTTD due to rupture or degeneration is usually based primarily on the physical examination. There is tenderness along the course of the PT tendon between the navicular and the medial malleolus. One can detect swelling or bogginess, tenderness or defects in the PT tendon. Clinicians can appreciate the swelling along the tendon sheath from a posterior view in comparison with the contralateral foot. The hindfoot alignment may be in slight valgus and the too many toes sign is positive.

Note the decreased medial arch height when the patient is weightbearing. The muscle strength test should include plantarflexing the ankle to relax the anterior tibial tendon and inverting the ankle against resistance. Evaluate PT tendon function with the single heel rise and double heel rise test. Normally, the PT tendon inverts the calcaneus to stabilize the hindfoot while the gastrocsoleus complex plantarflexes the ankle. If the patient’s heel does not invert as it rises, the PT tendon is dysfunctional. The distinguishing feature of PTTD stage I versus stage II is that stage I patients are able to perform single or double heel rise without a problem.

Radiographic evaluation includes three standard weightbearing views of ankle, foot and calcaneal axial. You may also consider ordering contralateral X-rays for a comparison in patients who have unilateral disease. Contralateral radiographs may serve as an excellent teaching tool when explaining the nature of the problem to the patient.

When it comes to patients with stage II PTTD, lateral weightbearing radiographs will show the plantar inclination of the talus in comparison to normal with collapse that one usually sees through the talonavicular joint. Anteroposterior foot radiographs demonstrate lateral peritalar subluxation of the navicular and associated abduction of the midfoot. Calcaneal axial foot radiographs will show the valgus nature of the heel.

Magnetic resonance imaging can be an excellent tool in differentiating between tenosynovitis, a partial rupture or full rupture of the PT tendon. This will also aid the practitioner in determining the treatment course.

Clinicians may utilize diagnostic ultrasound to determine the level of damage to the tendon. If there is a complete tear, ultrasound is very helpful in picking up the amount of damage. If a partial tear has occurred, you may see fluid and a split in the tendon as a hypoechoic region. One may also see tendinosis with edema and thickening with fibrosis within the tendon.

The advantage of ultrasound is its ease of use, its ability to facilitate a rapid in-office diagnosis and the ability to move the foot in real time to see the movement of the tendon. This is especially helpful for the diagnosis of impingement or stenosis of the tendon. In terms of disadvantages, there is a learning curve associated with the use of an ultrasound and it takes some time to understand the proper functional use of the machine.

Surveying The Conservative Treatment Options
Myerson recommended that the surgical procedure one chooses for PTTD should be the least invasive procedure that will decrease pain and improve function.5 The initial management of patients who present with the early stage of PT tendon insufficiency is nonoperative. Some have achieved success via immobilization of patients who have symptoms of acute tendonitis without deformity. If one suspects a partial rupture, an accommodative orthotic that is supportive of the medial longitudinal arch is usually worthwhile to try.

Although there are no published studies documenting the efficacy of orthotic devices in the treatment of the various stages of PTTD, there is certainly a population of patients who report a decreased level of symptoms associated with the use of such a device. Researchers have shown that an ankle brace (i.e. an Arizona brace or molded solid ankle foot orthosis) can help patients with PTTD.

In his case series, Alvarez reported effective treatment of patients in stage I and II PTTD with either an ankle-foot orthosis (AFO) or foot orthosis, and supervised physical therapy. In the study of over four months, 83 percent had a successful subjective and functional outcome and 89 percent were satisfied.⁶ Nonsteroidal antiinflammatory medications can decrease pain and associated swelling.

A Closer Look At Surgical Options For Addressing PT Tendon Insufficiency
Operative treatment of patients in whom conservative treatment has failed consists of either soft tissue procedures alone or a combination of soft tissue procedures with either osteotomies or arthrodesis. Patients who have late stage I PT tendon insufficiency have an inflammatory condition involving the tendon but the tendon remains competent in terms of function. One may treat these patients with debridement of the tendon and tenosynovectomy around the PT tendon.

There is only one recent follow-up study on this and the concept is that the combination of debridement and tenosynovectomy is effective in relieving pain. However, there are no published studies on this patient population that provide long-term, follow-up data.

We have used coblation therapy with the Topaz system (Arthrocare) in our institute with great success in cases of tendinosis that are unresponsive to conservative care. With this procedure, one can provide microscopic debridement of the fibrotic tissue within the tendon, increase blood supply to the tendinosis region and decrease the nerve fibers in the tendinosis region. This allows the body to help heal the damaged region with an inflammatory response.

Most ruptures in the PT tendon result from chronic degenerative processes and may result in a progressive loss of muscular function combined with atrophy, fatty degeneration and some fibrosis of the PT tendon. The PT tendon and its muscle might be in poor condition at the time of surgery. This could, in part, explain why more than 50 percent of isolated soft tissue reconstructions have failed within one year.⁷

As a result, some have advocated the flexor digitorum longus (FDL) tendon transfer in late stage I and stage II PTTD patients in order to replace the diseased PT tendon and muscle. The FDL allows for improved support of the arch and active strengthening of the pull of the PT tendon with a muscle and tendon transfer. One should also consider a gastrocnemius or percutaneous tendo-Achilles lengthening, especially in late stage I or early stage II PTTD with equinus deformity. Prior to transferring the FDL tendon, Mann recommends transecting the PT tendon by releasing the PT tendon from its insertion into the navicular and cutting proximally at the level of the medial malleolus.^2,8 This allows the tendon to retract up into the leg, completely out of the area of the operative field.

We only find this to be necessary when addressing severely degenerated tendons with no gross stability. If the tendon has any function, tightening of the tendon will help with a tenodesis support. The traditional FDL tendon transfer described by Mann involves drilling a hole in the navicular and pulling the FDL through the hole.^2,8

Another popular method of transferring the FDL tendon includes using a bioabsorbable screw to attach the FDL tendon to the navicular. A medial sliding calcaneal osteotomy is recommended in conjunction with the FDL transfer to alter the lateral mechanical axis of the Achilles tendon. The medial displacement of the calcaneus redirects the pull of the gastrocnemius muscle medial to the axis of the subtalar joint, increasing varus pull of the gastroc muscle on the hindfoot. It has been documented that the medial calcaneal displacement also lessens tension placed on the transferred FDL tendon.

In stage II PTTD, as the foot assumes a pes planovalgus deformity, usually the lateral column becomes relatively shorter in comparison to the medial column. The FDL transfer with lateral column lengthening or distraction arthrodesis of calcaneocuboid joint has been mentioned to treat stage II PTTD.

Lengthening the lateral column usually restores the medial longitudinal arch as well. Valderrabano recently reported that side to side augmentation of the repaired PT tendon to the FDL tendon can improve the strength of the reconstructed PT tendon and accordingly allow improving recovery of the muscle.⁷ Researchers performed a lateral column lengthening osteotomy (i.e. Evans calcaneal osteotomy with bone graft) to provide an improved and stable foot position, restoring the moment arm toward normal.

Final Thoughts
Adult-acquired flatfoot disorder has a broad spectrum of clinical presentations. It is crucial that one closely correlate treatment to the particular static and dynamic deformities in the patient. The classification system initially outlined by Johnson and Strom is helpful in determining the stage of disease and the treatment options available.

However, without a documented natural history of the disorder or a known timeframe for the progression from one stage to another, it remains a challenge to counsel patients regarding the optimal treatment.

Combining the joint sparing operations and limited arthrodesis with soft tissue reconstruction allow optimism for patients with late stage I or stage II PTTD, a disabling hindfoot condition. Indeed, combining these procedures may allow these patients to resume relatively normal function.

For related articles, see “A Guide To Conservative Care For Adult-Acquired Flatfoot” in the June 2007 issue of Podiatry Today.
Also check out the archives at www.podiatrytoday.com.

References:

1. Kettelkamp DB, Alexander HH. Spontaneous rupture of the posterior tibial tendon. J Bone Joint Surg [Am]. 1969;51:759–764.
2. Mann RA, Thompson FM. Rupture of the posterior tibial tendon causing flatfoot. J Bone Joint Surg 67A:556-561, 1985.
3. Kohls-Gatzoulis J, et al. Tibialis posterior dysfunction: a common and treatable cause of adult acquired flatfoot. Br Med J 329, December 2004.
4. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop 239:196-206, 1989.
5. Myerson MS. Adult acquired flatfoot deformity. J Bone and Joint Surg 1996; 78A: 780-92.
6. Alvarez RG, et. al. Stage I and II posterior tibial tendon dysfunction treated by a structured nonoperative management protocol: an orthosis and exercise program. Ft Ankle Int 27(1), January 2006.
7. Valderrabano, et al. Recovery of the posterior tibial muscle after late reconstruction following tendon rupture. Ft Ankle Int 25(2), February 2004.
8. Mann RA. Rupture of the tibialis posterior tendon. Instr Course Lect 33:302-309, 1984.

Additional References

9. Trnka HJ. Dysfunction of the tendon of tibialis posterior. J Bone Joint Surg 86-B(7), September 2004.
10. Beals, TC, Pomeroy GC, Manoli A. Posterior tibial tendon insufficiency: diagnosis and treatment. J Am Acad Ortho Surg 7(2), March/April 1999.