Emerging Concepts In Posterior Tibial Tendon Repair

The multifactorial etiology of posterior tibial tendon dysfunction (PTTD) can make it challenging to select the best course of treatment. Accordingly, these authors review the pathomechanics of the condition and offer essential diagnostic insights. They also discuss conservative care options, provide an algorithm for surgical procedure selection and weigh in on emerging modalities that may be beneficial.

Posterior tibial tendon dysfunction (PTTD) is a well defined clinical entity of the lower extremity that various researchers have reported in the podiatric literature. The etiology of posterior tibial tendon dysfunction is multifactorial and is attributed mainly to causes such as traumatic events, inflammatory neuropathies, steroid use, diabetes and faulty foot and ankle biomechanics.

   Studies have shown that potential causes of PTTD include direct and indirect traumatic injuries such as puncture wounds, lacerations, ankle fractures as well as injuries to the tendon and its supportive tissues.1 Authors have also shown that severe ankle sprains and fractures, which are mainly associated with the pronation external rotation mechanism, may be direct causes of PTTD secondary to tendon rupture.2

   Schaffer and colleagues have reported acute tendon ruptures following ankle inversion injury secondary to tight binding of the tendon by the flexor retinaculum.3 Repetitive microtrauma to the tendon with increased tendon loading will ultimately result in microtears within the tendon itself, leading to inflammation, elongation and long-term tendon dysfunction.

   Most of the cases of PTTD that physicians encounter in the clinical setting can be attributed to degenerative and chronic conditions. A systemic inflammatory disease state such as rheumatoid arthritis can manifest itself overall as chronic inflammation of the tendon and its supportive soft tissues. This is also known as tenosynovitis, which ultimately leads to degenerative changes in the tendon with reduced tendon strength and tendon rupture.

   Research by Downey and colleagues has demonstrated that the chronic inflammatory mediators noted with rheumatoid arthritis predispose the patient to the formation of tenosynovitis within early stages of tendon dysfunction.4 Michelson and co-workers supported the aforementioned finding by reporting similar results in their study.5

   Seronegative spondyloarthropathies such as Reiter’s syndrome, psoriasis and ankylosing spondylitis have been associated with PTTD as well. Jahss was the first to suggest a relationship between seronegative spondyloarthropathies and tendon dysfunction in 1982.6 A study by Myerson and co-workers had demonstrated a direct correlation between seronegative spondyloarthropathies and PT tenosynovitis with associated ensethopathy in two-thirds of the studied patient population.7 Patients will typically present with a loss of the longitudinal arch, pain along the course of the posterior tibial tendon and the inability to perform a single heel rise test, as well as multiple sites of ensethopathy. As the chronic inflammatory condition progresses over time, the physician could appreciate forefoot abduction while performing a routine clinical examination.

   Hypovascularity of the tendon is yet another factor that has been associated with tendon dysfunction. The posterior tibial tendon has a relative zone of hypovascularity in the mid-portion of the tendon itself, just distal to the medial malleolus. The zone of hypovascularity represents a common site of tendon rupture secondary to chronic degenerative changes in the tendon that develop over time.

   Age related, decreased vascular supply to the tendon may result in overall tendon ischemia and loss of tendon function. Frey and Shereff have reported a zone of relative avascularity at the level of the medial malleolus while utilizing the Spalteholz technique.8 The authors also reported hypovascularity of the synovial sheath and absence of the mesotenon.

   Biomechanical abnormalities contributing to tendon overuse with subsequent inflammation, weakening and rupture have been associated with PT tendon dysfunction. Conditions such as obesity, equinus, a preexisting pes valgus condition as well as excessive pronation of both the subtalar joint (STJ) and metatarsophalangeal joint (MPJ) associated with repetitive mechanical torque on the tendon ultimately lead to tendon strain, degeneration and possible rupture.

   Researchers have reported iatrogenic causes of posterior tibial tendon dysfunction such as long-term oral intake of steroids, multiple local steroid injections, intraoperative posterior tibial nerve damage as well as inadvertent transection of the tendon itself associated with medial ankle surgery. Gonclaves and colleagues have reported overall changes in the composition of the tendon collagen matrix in dysfunctional PT tendons.9 The study showed an overall increase in type III and V collagen and a decreased proportion of the type I collagen component in the diseased tendons associated with decreased tendon elasticity and diameter.

Understanding The Pathomechanics And Function Of The Posterior Tibial Tendon

The posterior tibial tendon, also known as the dynamic supporter of the medial longitudinal arch, plays a dominant role in providing stability to the foot during the phases of the gait cycle. In order to truly appreciate the function of the posterior tibial tendon, one should have familiarity with the anatomic position and course of the tendon on the medial side of the ankle joint.

   The posterior tibial muscle arises from the tibia as well as the fibula and its associated interosseous membrane. The posterior tibial tendon lies in the deep posterior compartment of the leg and is the most medial tendinous structure that crosses the ankle joint in relation to the medial malleolus. The medial malleolus itself acts as a pulley through which the tendon exerts its force as it acutely changes direction in comparison to the other long flexors of the deep posterior muscle compartment of the leg.

   The tendon passes through the relatively shallow groove while being tightly bound down by the flexor retinaculum. The tendon passes medially to the STJ axis. This provides the PT tendon with the greatest inversion moment arm of all tendons and establishes the tendon as the most powerful and efficient supinator of the foot. The tendon itself is unique in that it has multiple insertional points but primarily inserts at the navicular tuberosity, which permits further stabilization and supination of the talonavicular joint.

   The posterior tibial tendon plays an important role in supporting the medial longitudinal arch during the gait cycle through several mechanisms, including deceleration of internal rotation of the leg, acceleration of external rotation of the leg as well as acceleration of the MPJ and STJ supination during the gait cycle. Following the heel contact phase of the gait cycle, eccentric contraction of the PT tendon serves as a decelerator of STJ pronation as well as internal rotation of the leg, which ultimately serves as a shock absorption during the contact phase of the gait cycle. During midstance, eccentric contraction of the tendon acts in concert with the peroneus longus tendon to adduct the transverse tarsal joint, leading to supination of both the MPJ and STJ all at once.

   The tendon acts in concert with the peroneus brevis muscle as well to stabilize the lesser tarsal area, which will ultimately allow the foot to act as a rigid lever during the gait cycle. Dysfunction of the muscle and the tendon component will ultimately result in collapse of the medial longitudinal arch, leading to pes valgus deformity. The overall loss of internal foot deceleration as well as talus support will permit excessive pronation as well as pathologic adduction and plantarflexion of the talus on the calcaneus. As the collapsing forces and deformity continue during the midstance phase, talonavicular congruency ceases and unroofing of the talar head occurs.

   The ligamentous structures are under excessive tension as well. This results in laxity with an overall decreased stability and hypermobility of the first ray. As the first ray becomes hypermobile, it elevates those ligamentous structures and increases the overall pes planus deformity. Due to the dysfunction of the tendon itself, the peroneus brevis tendon remains unopposed and gains a mechanical advantage with unlocking of the transverse tarsal joints and excessive rearfoot pronation.

   With a severely pronated STJ, the gastroc soleus complex exerts an overall pronatory force on the insertion of the Achilles tendon, which shifts lateral to the STJ axis. As the pathologic condition continues, transverse plane deviation of the forefoot on the rearfoot occurs with possible lateral talar tilting secondary to elongation of the medial structures, particularly in the deltoid ligament.

How Planal Dominance Can Influence Treatment Selection

A thorough understanding of the planal dominance or the primary plane of dysfunction associated with posterior tibial tendon tear is paramount in order to choose the correct surgical procedure in every case.

   The average STJ axis is located approximately 42 degrees from the transverse plane and 16 degrees from the sagittal plane. If the axis were oriented more parallel to the transverse plane, then most of the motion across the STJ would occur in the frontal plane in the form of inversion and eversion with no transverse plane motion. On the other hand, if the axis were parallel to the frontal plane, transverse plane motion in the form of abduction and adduction would occur with no associated frontal plane motion. The more vertical the STJ axis is, the more motion occurs in the transverse plane. The more horizontal the STJ axis is, the more motion occurs in the frontal plane. In regard to the sagittal plane, the more parallel the STJ axis is to the sagittal plane, the more frontal plane motion will occur. On the contrary, the more parallel the STJ axis is to the frontal plane, the greater the sagittal plane motion.

   It is important to estimate the primary plane of motion of the STJ in order to predict the correct surgical procedure needed to control the pathologic STJ motion along the plane of dominance. It is equally important to determine the planal dominance of the MPJ, via observation of the forefoot motion, as the planal dominance of both the STJ and MPJ determine the primary plane of compensation of the foot.

What You Should Know About The Clinical And Radiographic Findings

Patients who suffer from the dysfunction of the posterior tibial tendon will present in the clinical setting with complaints of pain and swelling along the course of the posterior tibial tendon. The history may reveal an overall increase in strenuous physical activity and/or trauma. Such a history has resulted in overall progressive loss in the height of the medial longitudinal arch, fallen arches and an overall fatigue with prolonged standing or physical activity.

   The patient may also report of symptoms of plantar fasciitis and the formation of bunion and hammertoe deformities. Lateral foot and ankle pain, especially over the sinus tarsi, is a common finding in severe cases.

   The clinical examination reveals an overall more abducted or pronated foot type. The talar head appears prominent on the medial side with an overall decrease in arch height. In severe and chronic PTTD, transverse plane subluxation of the forefoot on the talus itself occurs. Arthritic changes in the subtalar and midtarsal joints are common findings with a longstanding deformity. Palpation along the course of the PT tendon reveals pain, warmth and edema. Manual muscle testing reveals overall muscle weakness with inversion against resistance.

   When it comes to the weightbearing examination, the heel rests in a valgus position while the talar head is severely adducted and prominent on the medial side of the ankle joint. While the patient is performing the single heel rise test, the heel of the affected extremity fails to invert as well. The patient has a slow antalgic gait with overall shortened stride length as well.

   Radiographic findings include an overall increase in the talocalcaneal angle, forefoot abduction and increased cuboid abduction on the calcaneus. The talar head appears uncovered with an overall increased talar declination angle. Medial column sag/fault occurs with the apex at the talonavicular, naviculocuneiform, first metatarsocuneiform or combination of the aforementioned joints. Magnetic resonance imaging (MRI) findings may include an overall increased tendon girth with associated fluid accumulation around the tendon as one will note on T2 weighted images. Longitudinal tears and tendon degeneration are common findings as well.

Key Insights On Conservative Treatment

Conservative treatment for posterior tibial tendon dysfunction appears to be suitable in patients with mild PTTD who have no degenerative changes within the tendon itself. Classic conservative treatments include arch supports, orthopedic shoes, non-steroidal anti-inflammatory drugs (NSAIDs) and bracing.

   The goals of conservative management include reduction of the symptomatology, arrest of the deforming forces and prevention of future arthritic changes. Reduction of all pathologic forces acting on the tendon and its associated supportive tissues is indicated in acute or mild cases. Immobilization may be required in certain cases and patients can achieve this with the use of a cast, a controlled ankle motion (CAM) walker or bracing. One may find it useful to immobilize the affected extremity in a slight plantarflexion and adduction position in order to reduce tension on the tendon itself.

   Initiate physical therapy in the treatment protocol to restore overall muscle and tendon strength and function, and reduce scar tissue formation. Physicians often prescribe modalities such as massage, ultrasound and electrical stimulation. Orthotic therapy is yet another modality clinicians employ mainly for chronic conditions. The goal here is to remove any pathologic stress from the affected tendon by controlling abnormal osseous relationships and abnormal/ excessive motion. The use of braces in the treatment of PTTD is indicated in late stage/severe cases in patients who are poor surgical candidates and have fixed deformities that orthotic therapy cannot control.

Choosing An Appropriate Surgical Procedure

Surgical management of posterior tibial tendon dysfunction is dependent on the plane of deformity. In a majority of cases, one can combine soft tissue and osseous procedures to correct the foot deformity. Procedure selection is categorized by the level of deformity and stage of dysfunction. The surgeon must consider the level of arch collapse, the valgus position of the heel, the lateral deviation of the midtarsal joints and forefoot varus. Soft tissue considerations include the level of equinus deforming the foot and the limited to nonfunctional quality of the posterior tibial tendon.

   Our institute has spent considerable time attempting to present an algorithm for procedure selection in the treatment of PTTD. Here are our suggestions for appropriate procedures based on our clinical experience.

Soft tissue
• Minor PT tear with no arch collapse or equinus — PT repair
• PT tear with weakness of tendon — PT repair with flexor digitorum longus (FDL) transfer
• Ligamentous tear — spring ligament and deltoid repair
• Equinus deformity — Achilles lengthening or gastrocnemius recession

Osseous procedures (supple foot)
• deformity — Evans/calcaneocuboid fusion
• Valgus heel — calcaneal slide
• Naviculocuneiform sag — naviculocuneiform fusion
• Forefoot varus with no hypermobility — Cotton procedure
• Forefoot varus with bunion or hypermobility — Lapidus procedure

Osseous procedures (rigid foot)
• Ankle — ankle fusion
• Hindfoot — subtalar joint/talonavicular/calcaneocuboid fusion (combine as necessary)
• Midfoot — TN/NC fusion
• Forefoot — Lapidus

   Through the combination of the aforementioned procedures and proper procedure selection, surgeons may treat any level of deformity causing posterior tibial tendon dysfunction.

Can New Modalities Play A Role?

There are several exciting new trends in the treatment of posterior tibial tendon dysfunction. Many of these involve combining new modalities with more tried and true procedures to accelerate healing and decrease downtime.

   Biologics are beginning to play a more significant part in soft tissue therapy. Both platelet rich plasma (PRP) and stem cell aspirate therapy (SCAT) are beginning to find their place in the treatment of posterior tibial tendon dysfunction.

   In early stage PT tears or synovitis, we have been using PRP therapy to treat patients who are not responding to conservative care. It is fairly well understood that after a period of initial inflammation, the PT tendon will begin to scar and lose its healing capacity. This is due to the body decreasing the healing inflammatory response to the site of chronic repeated trauma. Platelet rich plasma can fool the body into responding to the chronic injury site of the PT tendon by causing a large and specific inflammatory response, resulting in a cascade of healing response from the patient’s own body. One can perform this procedure in the office and the patient wears a protective device to allow the tendon time to heal.

   In more severe cases of tears that require surgical treatment, SCAT has allowed bone aspiration and the formation of a gel wrap for tendon repair augmentation. The technician draws a bone aspirate from any bone in the body and spins it down in order to remove the white and red blood cells. One subsequently combines the stem cell material with PRP and thrombin to form a gel concentrate that clinicians can mold into any shape or size. The surgeon can then wrap this material around the repaired or augmented posterior tibial tendon in order to speed up and assist in tissue healing.

   Tissue augmentation through the use of multiple soft tissue augmentation materials has also been an emerging trend in the treatment of soft tissue problems. We have extensively used soft tissue augmentation materials for both ligamentous and tendon repair procedures. In most cases, a xenograft soft tissue material increases the strength of the tendon repair either to bone or about the tendon itself. The augmentation material can incorporate into the body’s soft tissue over time and decrease the stress on the repair region during healing. Tissue augmentation has also been very helpful in ligamentous repairs. For example, in cases of spring ligament tear that may be difficult to repair primarily, augmentation tissue may bridge the ligamentous gap and act as a latticework for tissue ingrowth.

   One of the main problems with soft tissue correction of posterior tibial tendon issues has been the treatment of an overstretched or torn deltoid ligament. Unlike the lateral ankle, which does very well with primary repair of the collateral ligaments, the deltoid ligament is difficult to repair primarily and the results of primary repair have been mixed.

   A new treatment involves the use of allograft tendon and bio-tenodesis technology for secondary repair and augmentation of the deltoid ligament. One drills the allograft tendon into the medial malleolus and secures it with a Biotenodesis screw (Arthrex). The surgeon then routes the tendon into the talus for one point of fixation and then into the calcaneal medial sustentaculum region for a second point of fixation. Alternatively, one makes the tendon into an upside down “v” and secures it into the tibia with two points secured anteriorly and posteriorly into the talus for additional stability.

   The addition of rigid fixation of tendon to bone through the use of bio-tenodesis technology has also been an excellent option for tendon repair of the PT. Not only can the surgeon pull the PT tendon distally and repair the tendon to the navicular, one can properly tension a flexor tendon transfer to the navicular and attach it to the navicular. Through the use of bio-tenodesis technology, early range of motion and strengthening can start to allow rapid recovery and decrease downtime.

   Little has changed in the way that surgeons perform osseous procedures for PTTD. However, new fixation techniques allow for early range of motion and limited non-weightbearing time. The advent of locking plates and compression screw fixation has become standard in bone reconstruction and advanced the level of stability and positioning options.

   Biologics in bone healing have also been a great advancement as far as increased rates of union and decreased healing time. One incorporates stem cell bone aspirate material into a gel plug that the surgeon can put into fusion sites or permeate into allogenic bone graft material to speed up healing. We have noted a two to three week decrease in healing time with the use of this technology.

In Conclusion

The most important treatment parameter in PTTD is proper procedure selection. It is essential to treat the foot as a unit and deal with all the regions of deformity, both soft tissue and bone. Ankle valgus will lead to failure of any foot procedure and is commonly due to a weak or torn deltoid ligament. Hindfoot realignment requires a neutral heel position and limited to no lateral midtarsal position. The treatment of forefoot varus and naviculocuneiform sag is essential to stability of the forefoot and arch region. If this is not treated, the foot functions as a three-legged table with one leg, the midfoot and first ray, being wobbly and resulting in a poor outcome.

   One of the main issues that is not commonly treated and a source of many problems in failed PTTD reconstruction is equinus. By decreasing the load on the arch associated with an equinus deformity, there is less strain and pressure transferred to the midfoot and posterior tibial tendon repair region, and the foot is on the ground in a stable position for a greater amount of time during the gait cycle. This ultimately leads to better function and less stress on the PT repair.

   Finally, ligamentous weakness of the spring ligament and deltoid are essential to consider. Tissue augmentation procedures have allowed improved soft tissue reconstruction options and allow surgeons to perform difficult ligament repairs with excellent outcomes.

   Dr. Baravarian is an Assistant Clinical Professor at the UCLA School of Medicine. He is the Chief of Foot and Ankle Surgery at the Santa Monica UCLA Medical Center and Orthopedic Hospital, and is the Director of the University Foot and Ankle Institute in Los Angeles.

   Dr. Nazarian is a Fellow at the University Foot and Ankle Institute in Los Angeles.

References:

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