INTRAOPERATIVE PATHOLOGY OF THE POSTERIOR TIBIAL TENDON
March 6th, 1997
Jeffrey N. Kann, MD and Mark S. Myerson, MD
Introduction
Dysfunction of the posterior tibial tendon (PTT) is a common clinical problem. The pathological findings vary according to the underlying etiology of the tendon disorder, which varies, ranging from inflammatory synovitis to degenerative rupture, and occasionally acute trauma. The gross intraoperative pathology generally correlates with the systemic disorder, however patients with severe unilateral flatfoot occasionally can have a grossly normal tendon and a rupture of the spring or deltoid ligaments, or the talonavicular capsule.
In this paper we will demonstrate a variety of gross pathological PTTs, and describe their underlying etiology.
Case Presentations
Case 1: A 26 year old with seronegative spondyloarthropathy, and the findings of severe tenosynovitis.
Seronegative disorders are a group of acute and chronic rheumatic diseases that are clinically, genetically, and pathologically related to conditions such as ankylosing spondylitis, psoriasis, and Reiter’s syndrome.2 The surgical findings include attenuation of the tendon sheath, with the synovium adhering to and infiltrating the substance of the tendon (Fig. 1). The tendon itself is attenuated and frequently contains longitudinal fissures coursing through damaged areas (Fig. 2). Myerson et al5 presented the manifestations of seronegative inflammatory disease, and described the clinical and laboratory features associated with PTT dysfunction in this patient population. Unlike tenosynovitis in other groups of patients this is an aggressive and rapidly worsening infiltrative condition. Tenosynovitis in a younger male should always raise the question of an underlying seronegative disorder.
Case 2: A 39 year old with rheumatoid arthritis.
The patient with rheumatoid arthritis will invariably have involvement of the foot, with the midtarsal and subtalar joints involved 67% of the time.9 These patients frequently have a proliferative synovitis with laxity of the involved joints of the foot particularly involving the talonavicular joint, leading to a painful planovalgus deformity which is progressive. Tenosynovitis of the PTT leading to a flatfoot deformity is uncommon in the rheumatoid population,9 but if present and symptomatic, should be addressed (Fig. 3), since tenosynovectomy of the PTT sheath can be quite helpful in relieving pain and preventing worsening deformity.1,4
Case 3: A 56 year old otherwise healthy male with infiltrative tenosynovitis and rupture of the PTT.
A non-specific tenosynovitis, unrelated to any known systemic inflammatory disorder, of long-standing duration can also be the cause of ruptures of the PTT . The aggressive synovium infiltrates the tendon leading to longitudinal fissures, stretching and possibly frank rupture of the tendon (Fig. 4). Patients with tenosynovitis who do not respond to an adequate trial of conservative care ( in our practice, 6 to 8 weeks of adequate immobilization) should undergo a tenosynovectomy.
Case 4: A 52 year old with an early degenerative rupture of the PTT.
This case represents the more classic degenerative rupture of the PTT. The tendon sheath tends to be edematous and thickened. There are fibrous adhesions present which tend to extend posteriorly from the medial aspect of the tendon. These tears are commonly located 2 cm distal to the medial malleolus (Fig. 5).6 If the tendon looks grossly normal, one should inspect the posterior surface of the PTT, which often reveals the pathology clearly.
Case 5: A 57 year old with a progressive flatfoot deformity.
This case represents a Stage II degenerative tendon. In these patients, weakness is present; they are unable to stand on tiptoe on the affected side, and the subtalar joint remains fairly flexible. The midfoot is pronated and the forefoot is abducted.6 The PTT may be frankly ruptured or stretched so that it is no longer functioning (Fig. 6). The normal excursion of the PTT is 1 to 1.5 cm and with degenerative fissuring and elongation, the tendon may not be functioning.
Case 6: A 61 year old with a long standing flatfoot deformity.
This represents a Stage III dysfunction of the PTT which is characterized by all of the changes seen in Stage II, with the exception that the flatfoot deformity is more severe and the hindfoot is rigid. These patients tend to have a complete rupture of the PTT. The proximal stump will have a thickened, bulbous end and tend to be fibrosed to the tendon sheath (Fig. 7).
Case 7: A 40 year old athlete with medial foot pain and minimal clinical deformity.
Occasionally the clinical and radiographic deformity does not correlate with the findings at surgery. In this case, a complete rupture of the PTT and a tear of the talonavicular capsule was present. At the time of reconstruction the talonavicular capsule should be repaired. We routinely plicate the talonavicular capsule which is usually attenuated although a complete tear as demonstrated is not uncommon.
Case 8: A 48 year old with medial foot pain and a clinical flatfoot deformity.
This is another example of a patient with the clinical picture of a flatfoot deformity but the intraoperative findings of more than just PTT pathology. This patient had a complete talonavicular capsular tear in addition to stage two tendon pathology (Fig. 9). It is important to recognize and treat these capsular tears by imbricating the capsule, or using a pants-over-vest-type repair.
Case 9: A 51 year old who noted a sharp pain in the medial aspect of the foot while hiking.
A rare finding in a patient with a unilateral flatfoot deformity is the complete tear of the spring ligament (Fig. 10). This entity may be associated with a normal PTT. The spring ligament is a main stabilizer of the medial longitudinal arch,3 and the inferior calcaneonavicular ligament is the most important aspect of the spring ligament for stability of the talonavicular joint.8 Deland et al3 have demonstrated experimentally that the superomedial calcaneonavicular ligament is the main stabilizer of the talonavicular joint. This ligament should be repaired with nonabsorbable suture or augmented with a tendon transfer, and the foot should then be immobilized for 4-6 weeks to allow ligament healing.
Case 10: A 57 year old with a unilateral flatfoot and medial ankle joint pain.
Patients with a progressive flatfoot deformity will eventually develop secondary changes on both the medial and lateral sides of the ankle. The distal deltoid ligament blends with the fibers of the talonavicular capsule and spring ligament.7 As the flatfoot progresses, the deltoid can be stretched and attenuated, or may even rupture (Fig. 11). This must be addressed with either an imbrication or, if ruptured, reattachment to the medial malleolus using bone anchors.
Discussion
The adult acquired flatfoot deformity is a common problem seen by the Orthopaedic surgeon. The etiology of the dysfunction of the PTT is quite varied. The destruction of the tendon is inherently related to the patient’s underlying systemic disorder. It is important to recognize that the PTT is just one anatomical structure which helps to maintain the medial longitudinal arch. As we have clearly shown, there are a variety of associated pathological entities (spring ligament, deltoid, talonavicular capsule) that must be looked for and addressed at the time of reconstruction.
References
1. Bouysset M, Tavernier T, Tebib J, et al: CT and MRI evaluation of tenosynovitis of the rheumatoid hindfoot. Clin Rheumatol 14:303, 1995
2. Capen D, Scheck M: Seronegative inflammations of the ankle and foot: diagnostic challenges. Clin Orthop 155:147, 1981
3. Deland JT, Arnoczky SP, Thompson FM: Adult acquired flatfoot deformity at the talonavicular joint: reconstruction of the spring ligament in an in vitro model. Foot Ankle 13:327, 1992
4. Michelson J, Easley M, Wigley FM, et al: Posterior tibial tendon dysfunction in rheumatoid arthritis. Foot Ankle Int 16:156, 1995
5. Myerson M, Solomon G, Shereff M: Posterior tibial tendon dysfunction: its association with seronegative inflammatory disease. Foot Ankle 9:219, 1989
6. Myerson MS: Adult acquired flatfoot deformity. Treatment of dysfunction of the posterior tibial tendon. J Bone Joint Surg 78A:780, 1996
7. Resnick RB, Jahss MH, Choueka J, et al: Deltoid ligament forces after tibialis posterior tendon rupture: effects of triple arthrodesis and calcaneal displacement osteotomies. Foot Ankle Int 16:14, 1995
8. Sarrafian SK: Anatomy of the Foot and Ankle. Descriptive, Topographic, Functional, ed. 2. Philadelphia, JB Lippincott Co, 1993
9. Vainio K: The rheumatoid foot: a clinical study with pathological and roentgenological comments. Ann Clin Gynaecol 45:1, 1956
Figure Legends
Fig. 1. This patient had an inflammatory infiltrate eroding the substance of the PTT. This finding is typical of ruptures in patients with seronegative inflammatory disease.
Fig. 2. A 22 year old with psoriasis and the operative findings of severe tenosynovitis. The tendon itself was attenuated and had longitudinal tears.
Fig. 3. A patient with PTT tenosynovitis who underwent debridement with relief of pain and swelling.
Fig. 4. An example of a frank rupture of the PTT as a result of a long standing non-specific tenosynovitis.
Fig. 5. A classic rupture of the PTT, with longitudinal attritional tearing and a thickened edemous tendon sheath.
Fig. 6. These three pictures represent a stretched out tendon. Note the constriction of the tendon at the level of the medial malleolus and the dilation (thickening) distal to this thinned out area.
Fig. 7. A complete rupture of the PTT with the bulbous proximal stump. The flexor digitorum longus is under the retractor.
Fig. 8. This is an example of a complete rupture of the PTT (note distal stump attached to naviculum), and a tear of the talonavicular capsule.
Fig. 9. This is an example of stage two tendon pathology with longitudinal fissuring and tenosynovitis. The talonavicular capsule has a complete tear which was repaired at the time of the reconstruction.
Fig. 10. This patient has a relatively healthy PTT but a complete tear of the spring ligament. This was repaired using nonabsorbable suture.
Fig. 11. An example of Stage II PTT pathology with a complete tear of the deltoid ligament. This must be addressed during reconstruction.
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