PubMed · 11301765
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J Murtagh. 2001. A technique for ankle dysfunction.. https://pubmed.ncbi.nlm.nih.gov/11301765/
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In a patient with a high a priori risk of peripheral vascular disease, the positive predictive value of an abnormal physical diagnostic examination is high. In patients with a low prior probability of peripheral vascular disease, the physical examination makes little contribution to the diagnosis or exclusion of arterial insufficiency. For this purpose the ankle-brachial systolic pressure index is preferable. Peripheral arterial disease is unlikely when this index is normal. However, a low ankle-brachial index necessitates further investigations to determine possible arterial insufficiency in the lower extremities.
The posterior tibial tendon muscle plays a critical role in the function of the foot. It is, with the exception of the triceps surae, the largest of the extrinsic foot muscles. It is called upon to provide a critical posturing and stabilizing function to the foot during gait. This review discusses the anatomy, physiology, functional characteristics, and measurement of the strength of this muscle.
PTT tenosynovitis is a recognized entity no longer confused with an ankle sprain. Three possible causes are (1) overuse or age related (mechanical in cause, true stage I disease), (2) seronegative spondyloarthropathies (clinical suspicion, hematologic analysis), and (3) rheumatoid arthritis (deformity may be owing to ligamentous or capsular destruction). The PTT has a hypovascular zone 40 mm proximal to the insertion of the tendon and 14 mm in length. Pain often is localized to this portion of the tendon (primarily in stage I disease). Ultrasound is an inexpensive and accurate method to assist in the diagnosis of this condition and may replace MR imaging as more experienced ultrasonographers appear. The initial management of PTT tenosynovitis includes tendon rest and nonsteroidal anti-inflammatory medication and physical therapy. Surgical synovial débridement is performed early (6 weeks) in patients with enthesopathies (seronegative disease). This procedure may be delayed 3 months in patients with true stage I disease. At surgery, the undersurface of the tendon must be inspected for longitudinal split tears, and these must be repaired with nonabsorbable suture, burying the knots. The excursion of the tendon should be checked intraoperatively. Patients with stage I disease should be evaluated carefully for preoperative structural deformity to choose the appropriate surgical procedure and prevent failure of isolated tenosynovectomy.