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Acquired Flatfoot Deformity Following Posterior Tibial Tendon Transfer for Peroneal Nerve Injury A Case Report
Christopher J. Vertullo, MBBS, FRACS; James A. Nunley, MD
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Investigation performed at Duke University Medical Center, Durham, North Carolina

Christopher J. Vertullo, MB, BS, FRACS
James A. Nunley, MD
Division of Orthopaedic Surgery, Duke University Medical Center, Durham, NC 27710. E-mail address for J.A. Nunley: nunle001@mc.duke.edu

The authors did not receive grants or outside funding in support of their research or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

J Bone Joint Surg Am, 2002 Jul 01;84(7):1214-1217
5 Recommendations (Recommend) | 3 Comments | Saved by 3 Users Save Case

Extract

Anterior transfer of the posterior tibial tendon is a well-recognized surgical procedure that is used to restore active ankle dorsiflexion that has been lost secondary to peroneal nerve deficiency 1,2 . The many causes of peroneal nerve deficiency include knee or hip trauma, surgical misadventure, tumor, and mononeuropathy 3,4 . The tibialis posterior muscle is the primary dynamic stabilizer of the medial longitudinal arch of the foot and is the primary initiator of hindfoot inversion 5,6 . Normal toe-off during gait requires hindfoot inversion to lock the transverse tarsal joints and hence transform the supple foot into a rigid lever arm for push-off. The normal antagonist muscle to the tibialis posterior is the peroneus brevis, which everts the hindfoot. Theoretically, patients who have undergone posterior tibial tendon transfer should be at greater risk for the development of a flatfoot deformity secondary to the absence of function of the posterior tibialis muscle because of the increased stresses that are placed on the static soft-tissue supports on the medial side of the hindfoot. The plantar calcaneonavicular (spring) ligament complex appears to be the most important of these static medial soft-tissue supports. Interestingly, we are aware of no reported cases of acquired adult flatfoot deformity following transfer of the posterior tibial tendon for the correction of a peroneal nerve palsy. Some authors have speculated that this lack of flatfoot development is due to the absence of active eversion of the hindfoot because the peroneus brevis is paralytic 3 , but others have disagreed 7 . We report the case of a patient in whom a symptomatic flatfoot deformity developed after an anterior transfer of the posterior tibial tendon and the flexor hallucis longus tendon was performed to restore active dorsiflexion following a peroneal nerve injury.
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    Accreditation Statement
    These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
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    Mark S. Mizel, M.D.
    Posted on February 27, 2007
    Acquired Flat Foot Deformity
    University of Miami, Miami, FL

    To The Editor:

    I read with great interest the discussion of the acquired flat foot deformity resulting from the loss of function of the posterior tibial tendon, in the case report “Acquired Flatfoot Deformity Following Posterior Tibial Tendon Transfer for Peroneal Nerve Injury”(1) by Vertullo and Nunley. The common peroneal nerve, which was reportedly divided during excision of a Baker cyst was not recognized during the surgical procedure, and the certainty of a complete transection, cannot be absolutely relied on.

    The authors unfortunately did not obtain EMG or NCV studies to confirm a complete transection, with total loss of the evertor muscle function. As manual evaluation of muscle strength is subjective, it is possible that the clinical loss of peroneal muscle function could have been a partial loss, leaving residual peroneal muscle function. This could explain the collapse of the foot that was reported. The authors bring up interesting points, but a bettr documented example would be of assistance in confirming their thoughts.

    The author did not receive any outside funding or grants in support of his research for or preparation of this work. Neither he nor a member of his immediate family received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, division, center, clinical practice, or other charitable or nonprofit organization with which the author, or a member of his immediate family, is affiliated or associated .

    Reference:

    1. Vertullo CJ, Nunly JA. Acquired flatfoot deformity following posterior tibial tendon transfer for peroneal nerve injury: a case report. J Bone Joint Surg Am. 2002;84: 1214-1217.

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