Treatment of Stage 2 Posterior Tibial Tendon Dysfunction



The adult acquired flatfoot describes a clinical condition characterized by a tight heel cord, medial column breakdown, and hindfoot valgus. Posterior tibial tendon failure results from the insidious collapse of the medial longitudinal arch. Surgery is individualized to address the various components that contribute to the overall deformity. There is growing awareness and focus on medial column stabilization.


  • 1

    Biomechanical model of the adult acquired flatfoot deformity based on medial column collapse

  • 2

    Johnson classification and emerging concepts regarding arch collapse

  • 3

    Splitting: deconstructing the adult acquired flatfoot into its components and individualizing the surgical reconstruction


  • 1

    There is no generic “one size fits all” surgical solution for the flexible adult acquired flat foot deformity.

  • 2

    Equinus should be addressed by gastrocnemius lengthening.

  • 3

    Medial column instability/incompetence should be addressed by arthrodesis.

  • 4

    Hindfoot valgus should be addressed by osteotomy.

  • 5

    Essential joints should be preserved.

  • 6

    Tendon augmentation or transfer should be performed for a thickened diseased posterior tibial tendon with no excursion.


  • 1

    Undercorrection—Isolated medial column fusion or medial calcaneal slide may undercorrect a highly uncovered and plantarflexed talus.

  • 2

    Overcorrection—Lateral midfoot and hindfoot overload can result if too great a correction is made with a lateral column lengthening.

  • 3

    Technique errors—Meticulous joint preparation and rigid internal fixation are mandatory to ensure high fusion rates in arthrodesis of nonessential midfoot joints.

  • 4

    Always assess and address an equines contracture.


  • Hypermobile first ray after double osteotomy.

  • First TMT fusion with modified macBride.

  • Calcaneal osteotomy for stage 2 PTTD.


This chapter is devoted to the current state of our understanding and the surgical treatment of the flexible adult acquired flatfoot deformity. Prior to 1980, acquired flatfoot deformity was thought to be quite rare, but considerable attention has been directed to recognizing and treating the various stages of pathology of a condition now considered common. The posterior tibial tendon itself has been the focus of the majority of research and its failure is traditionally regarded as a causal factor of the adult acquired flatfoot deformity. Recently, the role of equinus as a key or primary cause has expanded. There is now greater understanding of the individual components that together contribute to the clinical appearance of the flatfoot and surgery is now individualized based on correcting each component of the larger deformity.

The concept of noninfectious tenosynovitis was first described in 1818 by Velpeau, popularized in 1895 by De Quervain, and remains today an integral component of our understanding of painful conditions of the foot and ankle. Kuwalski first described tenosynovitis (tendovaginitis) of the posterior tibial tendon in 1936. But before 1980, this condition was thought to be uncommon. Numerous authors contributed case reports or small series and a general understanding and appreciation for the condition was lacking. Johnson credited two papers in particular with key contributions. Kettelkamp and Alexander, in 1969, presented four illustrative cases and for the first time clearly defined the pathologic state of the posterior tibial tendon. They hypothesized that chronic stress on the tendon with an associated flexible planovalgus foot precipitated tenosynovitis leading to tendon degeneration and rupture. Goldner et al., in 1974, was credited by Johnson for suggesting tendon transfers as a viable reconstructive option. The credit for this contribution, though, should go to Fried et al., who in 1957 published the first paper describing a peroneus longus tendon transfer to a paralytic posterior tibial tendon. They further suggested flexor digitorum longus and flexor hallucis longus as an acceptable substitute.

In 1989, the landmark paper by Johnson and Strom solidified the general understanding of dysfunction of the posterior tibial tendon, and since then this condition remains synonymous with the adult acquired flatfoot deformity’s various stages. Basic science research has focused on the posterior tibial tendon revealing noninflammatory degenerative tendinosis (mucinous degeneration, fibroblast hypercelluarity, chondroid metaplasia, and neovascularization) in the susceptible hypovascular zone posterior and distal to the medial maleolus (1 to 1.5 cm distal to the medial maleolus extending approximately 14 mm). Despite a keen understanding of the histopathologic abnormalities, it has become apparent that stage 2 posterior tibial tendon dysfunction (PTTD) with established physical examination findings of “too many toes,” hindfoot valgus, collapsed arch, and inability to perform a single heel rise was inadequate to consistently and universally predict the varied bony and soft tissue abnormalities present resulting in the common clinical presentation.

Idiopathic failure of the posterior tibial tendon causing the flatfoot deformity remained dogma until recently. With a greater awareness and attention to the atavistic human tendency toward equinus driven collapse, the understanding of the pathomechaincs of the acquired flexible flatfoot deformity has matured. The word equinus is not mentioned once in the sentinel paper on the subject, but now it is accepted that contracture of the heel cord is an integral consideration of the overall deformity and should be addressed in most if not all reconstructions.

A mastery of anatomy and a clear understanding of the mechanics, normal and pathologic, are critical to any practitioner who undertakes surgical treatment of the acquired flatfoot deformity. In 1999, Anderson and Hansen reviewed the pathomechanics of stage 2 PTTD and included what they termed an “alternative scenario.” In this scenario, equinus drives failure of the medial column. An isolated contracture of the gastrocnemius or a combined gastrocsoleus complex contracture causes increased stress on the medial longitudinal arch. Strain is transmitted across the entire medial column: talonavicular, naviculocuneiform, and tarsometatarsal articulations. Ligamentous supports stretch, allowing the forefoot to supinate. This deformity progresses to involve the hindfoot. The compensatory heel valgus that ensues further stretches the static supports of the medial longitudinal arch including the plantar fascia, spring ligament, and the talocalcaneal interosseus ligament. The end result of the hypermobile first ray, or incompetent medial column, is hindfoot valgus. Attenuation of the ligamentous supports allows lateral or dorsolateral peritalar subluxation of the navicular. It is this cascade of events that leads to progressive PTTD due to increased demands placed on this tendon. The posterior tibial tendon must now act with a new line of pull and greater excursion requirements, normally only 1.5 to 2.0 cm. Since the force generated by the posterior tibial muscle remains constant, the work required to adduct and invert the foot increases as the lever arm is forced more laterally. Therefore, a few millimeters of lateral or dorsolateral subluxation of the navicular increases the work requirements for the PTT (work = force × distance), a condition that ultimately leads to overload and progressive failure of the tendon. The static support of the arch is attenuated and the PTT constitutes the only remaining dynamic support. Failure of the posterior tibial tendon results from the insidious collapse of the arch ( Fig. 30-1 ).


Preoperative anteroposterior and lateral weight-bearing radiographs that demonstrate one of the typical patterns of collapse of the adult acquired flatfoot deformity. The medial column breakdown primarily occurred through the naviculocuneiform articulation. This results in hindfoot valgus and dorsolateral peritalar subluxation. Postoperative radiographs show correction of the deformity by lateral column lengthening and naviculocuneiform arthrodesis. This patient required a gastrocnemius lengthening to achieve correction.

This biomechanical model remains the most cogent and likely scenario accounting for the numerous bony and soft tissue abnormalities that together contribute to the overall clinical deformity. The current challenge in surgically treating adult acquired flatfoot is to recognize the multiple components of the deformity and to individualize surgical treatment.


An exhaustive review of the nonsurgical management is beyond the scope of this chapter but does warrant mention. The theory supporting nonsurgical treatment for flexible pes planovalgus is predicated on controlling hindfoot valgus. A supple hindfoot can be placed and held in a neutral position. This will help lock the transverse tarsal joint and theoretically limit progressive forefoot abduction. The underlying pathologic process is unchanged, but tension on the posterior tibial tendon is diminished and pain can be improved. Not every patient is a candidate for this approach. Chao et al. reported 67% good to excellent results in pain relief for patients with stage 2 PTTD. Their approach used a UCBL orthosis with medial posting or a custom molded AFO. The best candidates for this treatment were nonobese patients and those with less than 10 degrees of residual forefoot varus after reducing the hindfoot to a neutral position.

Painful acquired conditions can be life altering, but the decision for elective surgery should never be taken lightly. There is a role for numerous options such as casting and custom molded braces. However, the patient must know that surgical treatment of the supple deformity may prevent the natural progression of this condition to a rigid arthritic planovalgus deformity with limited and less attractive surgical options.

The recommendation for surgery in the patient with the acquired flatfoot deformity is made based on an understanding of the diagnosis, by a surgeon capable of performing the surgery. Most important, the decision is made by the patient who understands the recommendations and has committed to the expected recuperation period.


Johnson and Strom were the first to present a classification of PTTD. The classification was based on the authors’ cumulative experience in treating this condition. Three distinct stages of dysfunction of the posterior tibial tendon were introduced, and a fourth stage was conjectured to exist.

Stage 1 dysfunction was characterized by normal tendon length. There is weakness in the posterior tibialis muscle as judged by the single heel rise test. There is minimal foot deformity with preserved forefoot to hindfoot alignment and minimal radiographic deformity. The clinical presentation described is common: medial ankle pain, weakness, and minimal deformity. However, the characteristic feature of this stage, normal tendon length, is challenged by our current biomechanical model. The more likely scenario is some degree of equinus, slight attenuation of the static ligamentous supports of the medial longitudinal arch, and early breakdown of the medial column. This cascade results in enough increase in the length of the tendon to precipitate the clinical symptoms in the susceptible patient, frequently obese.

Stage 2 dysfunction was characterized by an elongated tendon and a mobile hindfoot. There is marked weakness of the posterior tibialis and collapse of the medial longitudinal arch. Abnormal forefoot to hindfoot alignment is manifest as forefoot abduction with “too many toes” sign present. A biomechanical explanation of this stage was also presented based on a two-piece foot model—the talus and everything else. The authors postulated that the talus is fixed and dysfunction of the posterior tibial tendon allowed the calcaneus, along with the forefoot, to rotate laterally (forefoot abduction). Loss of sustentaculum tali support allows the talus to flex. This was a reasonable attempt to put together the clinical and the radiographic appearance of dorsilateral peritalar subluxation before our developing concepts of progressive equinus contracture and its effect on the medial column and the hindfoot. The authors suggested an isolated transfer of the flexor digitorum longus as treatment.

Stage 3 dysfunction is characterized by an elongated tendon and a stiff hindfoot deformity. The clinical appearance and examination are similar to stage 2, only more advanced. There is now pain in the sinus tarsi and arthritis may be present. The authors suggested a subtalar arthodesis in this stage.

A fourth and final stage of dysfunction was postulated at that time and is now commonly accepted to exist. This stage was based on their understanding of the condition and the logical conclusion that progressive hindfoot deformity will involve the ankle.

Conti et al. introduced a five-part magnetic resonance imaging (MRI) classification system, again focusing on the integrity of the posterior tibial tendon. In their series a correlation in outcome was identified in 20 patients treated by soft tissue procedures. However, the usefulness of this classification remains unclear, as there remains no consensus on the role of MRI in diagnosing the condition. An algorithmic approach was recommended in 2000 incorporating bony and soft tissue procedure. This remains a very logical approach to treating the various components of the condition.

The fundamental limitation to all adult acquired flatfoot classifications is the focus on the posterior tibial tendon. The authors introduced a comprehensive classification of foot and ankle conditions developed to more accurately represent the wide spectrum of arch collapse that occurs and the various clinical entities encountered during the process ( Table 30-1 ). Using a novel application of the empirical keying method reviewing over 1000 individual reconstructive procedures, the classification is fundamentally based on the integrity of the medial column correlated with a progressive equinus contracture ( Table 30-1 ).

Jan 26, 2019 | Posted by in ORTHOPEDIC | Comments Off on Treatment of Stage 2 Posterior Tibial Tendon Dysfunction

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