Posterior tibial tendon dysfunction (PTTD) insufficiency is the most common cause of adult acquired flatfoot deformity. Failure of the tendon affects surrounding ligamentous structures and will eventually lead to bony involvement and deformity. The extent this disease progression will be explained in this review. PTTD is a progressive and debilitating disorder, which can be detrimental to patients due to limitations in mobility, significant pain, and weakness.[1] Risk factors for the disease have been studied and may include hypertension, obesity, diabetes, previous trauma, or steroid exposure.[2]
Researchers have proposed numerous mechanisms for the degeneration of the posterior tibial tendon (PTT). The most commonly the cause for PTT degeneration is credited to a repetitive loading causing microtrauma and progressive failure. A retromalleolar, hypovascular region does exist and may also contribute to the disease. In a study by Manske et al., cadaver specimens showed a region of decreased blood supply from 2.2 +/- 0.8cm proximal to the medial malleolus to a region 0.6 +/- 0.6cm proximal to the medial malleolus.[3]
The anatomic course of the posterior tibial tendon also likely contributes as the tendon does make an acute turn around the medial malleolus. This location puts a significant amount of tension on the tendon in the region distal and posterior to the medial malleolus. The adjacent tendons, namely the flexor hallucis longus and the flexor digitorum longus, do not take this sharp turn.[4]
Other potential culprits include constriction beneath the flexor retinaculum,[5] abnormal anatomy of the talus,[6] degenerative changes associated with osteoarthritis,[7] and preexisting pes planus.[8]
Although no significant large-scale studies have been performed about the overall incidence of this disease, it is believed that the prevalence is anywhere from 3.3 to 10%, depending on the sex and age of the patient. This disorder is associated with adult-acquired flatfoot deficiency which can cause it to be misdiagnosed, meaning the actual prevalence may be much higher than shown in the literature. The underreporting may also be due to early, asymptomatic stages of PTTD. The classic PTTD patient is an obese woman in her sixth decade of life.[9]
The normal posterior tibial tendon should be comprised of linear collagen bundles, normal fibroblast cellularity, and low proportion of vascular density. In posterior tibial tendon dysfunction, the tendon undergoes microtrauma and subsequent tendinitis characterized by increased mucin contentment, neovascularization, and fibroblast hypercellularity.[7]
The majority of posterior tibial tendon dysfunction patients will demonstrate medial ankle and foot pain, especially in the early stages of the disease. At later stages, lateral pain can be seen as well, due to sub-fibular impingement or peroneal tendon injury.[10] A thorough physical examination can help to determine the grading and severity of the disease. Attention should first be turned to the gross inspection of the feet while standing. A weight-bearing examination is of importance as a flexible deformity may present normally, while the patient is non-weight bearing. The medial longitudinal arch collapse leads to pes planus, an easily visualized condition. While inspecting the patient, one will also commonly see a “too many toes” sign, which is visible when looking from behind the patient. Due to the valgus alignment of the foot, you will see flaring out of more than two toes from the lateral hindfoot. Equinus contracture is also a common finding, which can limit ankle dorsiflexion.
Single-limb heel raise is an important clinical test that can differentiate stage 1 disease from stage 2 and higher. A patient in stage 1 disease should be able to perform this test without pain. In stage 2 disease, patients may be able to perform the test but will likely have pain. In later stages, the rigid deformity may prevent the patient from completing the test. The flexibility of the foot also requires evaluation on an exam.[10]
Imaging is critical in determining the severity of disease and subsequent treatment. Anteroposterior (AP) and lateral radiographs are necessary. Increased talonavicular uncoverage and increased talo-first metatarsal angle (or Simmons angle) will present on the AP foot radiograph. The normal talo-first metatarsal angle is around 7 degrees, and angles over 16 degrees indicate flatfoot deformity.[11] The talonavicular coverage expresses itself as the amount of the talus that is not in contact with the navicular medially, with values over 30 to 40% typically indicated forefoot abduction seen in stage II-IV PTTD.[9] On the weight-bearing lateral radiograph, one should evaluate for increased talo-first metatarsal angle (or Meary angle) which normally measures 0 degrees +/- 4 degrees but typically measures over 20 degrees in flatfoot deformity.[10]
Treatment for posterior tibial tendon dysfunction is a complicated subject, so this review will attempt to simplify by each stage for the reader:
Although posterior tibial tendon dysfunction is the most common cause of adult acquired flatfoot deformity, there are many other related conditions. Diagnoses listed below can present very similarly to PTTD and should merit consideration during evaluation [18]:
Stage 1:
Stage 2A:
Stage 2B[19]:
Stage 3:
Stage 4 [19]:
Posterior tibial tendon dysfunction is a progressive disorder that will continue to deteriorate without treatment. Early detection and intervention will help to slow progression. Patients provided with custom orthotics and rehabilitation have been shown to have significant improvement. In a recent study by Alvarez et al., about 89% of their patients with stage I and II PTTD responded to orthotics and PT. Nearly all of these patients were back to full strength by 4 months.[20] According to analyses of outcomes of surgical treatment, results are much less predictable, and a return to the pre-disease state should not be guaranteed. Patients may continue to have some residual effects after reconstructive surgeries.[21]
General complications include thromboembolic events, infection, wound dehiscence, neurologic injury, and/or painful hardware. Reports exist of wound healing complications in up to one-third of patients undergoing flatfoot reconstruction, so proper wound care is paramount.[22]
Postoperative care is crucial to the success of the procedures. Typically, patients will receive a type of non-weight bearing cast or splint for around 6 to 8 weeks. Followup should be between 10 to 14 days for suture removal evaluation. Physical therapy may be necessary for certain patients.
Patient education and emphasis of conservative approach can help patient outcomes:
The importance of finding posterior tibial tendon dysfunction at early stages may prevent rapid deterioration with conservative measures. Primary care physicians and nurse practitioners may be able to refer patients to sub-specialists, such as foot and ankle orthopedic surgeons for a more thorough workup/evaluation, which can lead to significantly better patient outcomes.
PTTD requires an interprofessional team approach, including physicians, specialists, specialty-trained nurses, and pharmacists, all collaborating across disciplines to achieve optimal patient results. [Level V]
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