PRESENT's Surgical Editor, Harold Schoenhaus, DPM, FACFAS.

Dr. Schoenhaus is currently in private practice in Philadelphia, PA and a full professor at the Temple University School of Podiatric Medicine and also a member of the Board of Governors.  He brings 39 years of experience and relationships to further enhance surgical education. He is an attending Podiatric Surgeon at Presbyterian Medical Center, which is part of the University of Pennsylvania Health System, and also has privileges at Chestnut Hill Hospital, Temple University and Cooper Hospital in New Jersey.  Dr. Schoenhaus' career in Podiatric medicine and surgery began in 1971, following his studies at the Pa College of Podiatric Medicine and serving a Foot & Ankle surgical residency at Parkview Hospital in Philadelphia.

In this week's issue of Residency Insight, Dr. Schoenhaus examines Posterior Tibial Dysfunction.

     —John Steinberg, DPM, PRESENT Editor

Harold Schoenhaus, DPM, FACFAS PRESENT Surgical Editor

Posterior Tibial Dysfunction

Sometimes described as adult acquired flatfoot, it remains an enigma as to its true etiology.  The posterior tibial tendon/muscle complex is the strongest supinator of the foot, having the peroneus brevis as its primary antagonist.  Their phasic activity demonstrates activity primarily during contact phase and into mid-stance.  The foot demonstrates exaggerated re-supination with heel off and does not require posterior tibial activity to achieve this phenomenon.

The function of the tibialis posterior and the peroneus brevis is to stabilize the sub-talar and mid-tarsal joints, to prevent excessive pronation or supination, but not to initiate either activity.  At the end of contact phase, pronation achieves its maximum effect and re-supination of the weight bearing limb is the result of external rotation of the leg, as the opposite leg begins to swing forward.

It is important to recognize that if the posterior tibial tendon is dysfunctional, it loses its stabilizing capability and the arch collapses.  When this occurs, the peroneus brevis gains mechanical advantage, thus the transverse plane domination with the talar escape medially and loss of the longitudinal arch.

In pediatric uncontrollable hypermobile flatfoot, a healthy tibialis posterior cannot overcome the deforming forces of primary equinus or internal torque forces.  Reactive forces of gravity contribute to collapse of the foot, and the foot cannot be stabilized by the posterior tibial tendon.

It is interesting to note that most of the breakdown of the tendon in adult acquired flatfoot occurs between the medial malleolus and the tuberosity of the navicular.  The disease state of PTTD usually peaks in the 5th or 6th decade of life, when weight gain has truly taken its effect. 

In my experience, other than acute trauma, the deformation continues, aggravated by weight gain.  It appears the continuous pulling of insertion to origin of the tendon cause significant inflammation of the tendon and its surrounding structures, to cause the clinical findings of tenosynovitis, swelling, fluid accumulation, tendon weakness and pain.  The watershed area of the posterior tibial tendon is located between the medial malleolus and the tuberosity of the navicular, thus the association of tendon breakdown and tearing in the area of decreased circulation during the 40's - 60's age group.  Similar to the achilles, the Posterior Tibial tendon watershed area is susceptible to trauma.

Tears in the tendon develop in line with the tendon and are often referred to as a longitudinal tear.  This is most easily visible on an MRI.  The MRI can also identify the length and breadth of the tear.

Treatment of PTTD is often predicated on the staging of the disease.  Conservative treatment including - orthoses, NSAIDS, and immobilization are most effective in early disease prior to advanced tears and the development of DJD of the sub-talar and mid-tarsal joints.

Surgical decisions are also predicated on staging with various soft tissue or osseous procedures recommended or motion blocking procedures such as arthroeresis.  Repair of the tendon is important, unless fusions of the rear foot are employed, such as talo-navicular fusion or triple arthrodesis. Patients with PTTD should be treated aggressively, considering these patients often develop postural symptoms such as genu valgum.  Post operatively, orthoses and bracing are important to support extra-articular procedures and allow for restoration of posterior tibial tendon function.  Post-operative physical therapy can also be utilized to promote healthy tendon function.

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	The Diabetic Charcot Foot: Principles and Management by Robert G. Frykberg DPM, MPH, Editor
	This text provides the reader with the most current information available on the pathogenesis, natural history, and management of the diabetic Charcot foot. Many of the world's experts have come together to present their unique perspectives on this disorder. It is our hope that this work can become a valuable resource for those less familiar with the peculiarities of this often misunderstood complication of peripheral neuropathy. I am indebted to each author for the contribution of their time, efforts and expertise.
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