AT rupture tends to occur approximately 2–6 cm above the insertion of the tendon because the blood vessel distribution and blood supply are relatively poor [14]. The main reason for the AT rupture is the degeneration of AT fibers caused by poor blood flow and mechanical factors. Obesity, local repeated block therapy, application of hormones, and oral contraceptives also have potential impacts on the occurrence of AT rupture [15, 16]. At 4 weeks after injury, highly vascularized collagen scar tissue fills the retraction gap of the ruptured AT, which is the earliest manifestation of chronic healing [17]. Therefore, it is generally accepted that the diagnosis of chronic AT rupture was defined as delayed or neglected diagnosis for more than 4 weeks after injury [18].
The nonoperative treatment of chronic AT rupture is only suitable for high-risk patients with surgical contraindications who do not have high needs for ankle function. The ankle plantar flexion can be partially strengthened with an ankle foot orthosis, however, the normal physiological gait cannot be restored. The prognosis of nonoperative treatment is poor compared to surgical options, and patient satisfaction is less than 55% [1].
Surgical repair of chronic AT rupture has been widely accepted by clinicians. Various surgical treatments have been reported in the literature, including direct suture, triceps tendon rotation flap, V-Y extension, tendon transfer, repair of scar tissue, artificial tendon transplantation, and allograft tendon transplantation [5–8, 19]. However, neither a uniform standard nor evidence-based support has been established [20–22]. Generally, a surgical plan can be constructed based on the length of the defect according to Kuwada and Myerson classifications [14, 23]. However, there are still controversies regarding the surgical methods for large defects of AT. The incidence of re-rupture after conventional surgical treatment is high. Moreover, conventional surgical treatment has disadvantages such as difficult procedure requiring skill, poor graft strength and poor blood supply particularly when the defect of AT rupture is greater than 5 cm. The reconstruction of AT with large defect using FHLT transfer was firstly reported by Hansen in 1991 [24]. This technique has been gradually recognized and continually improved over the years. Studies have shown that FHLT transfer is a safe and effective surgical approach for patients with chronic AT rupture [25–28]. However, the evidence of this technique is insufficient due to the limited number of reports and cases, and the lack of long term follow-up data.
It has been reported that the FHLT can be harvested through a single incision or double incisions. However, which incision is better and whether the distal end of the FHLT needs to be sutured to the FDLT remains controversial [29–31]. In this study, all the 18 tendons were harvested through a single posteromedial incision. According to our experience, harvesting FHLT through a single incision can be sufficiently long to prevent excessive muscle tension after transfer. The technique is simple and safe, no more incisions are need which may potentially increase the risk of infection and medial plantar nerve injury. However, note that the FHL is located on the deep side of the tarsal tunnel, posterior tibial blood vessels and nerve in the tunnel should be carefully protected when a single incision is made.
Reconstruction of AT with FHLT transfer could reduce the plantar flexion strength of the hallux, resulting in reduced balance or strength of propulsion theoretically [26, 32]. Richardson et al reported decreased distal phalangeal pressure and FHL weakness in 22 patients, but no difference was found in plantar pressure of the first or second metatarsal head [29]. We also noticed the slight weakness of hallux in all patients postoperativly, but the plantar flexion of the distal phalanx could be performed in some of the patients. The postoperative AOFAS-HM at last follow-up visit was relativly high. All patients recovered to their pre-injury daily activities and no patient complained of functional disorder or any noticeable weakness in this study. It is worth mentioning that one amateur football player returned to the pitch for football match 1 year after surgery. The reason for this phenomenon may be existence of flexor hallucis brevis and abnormal branch of other congenerous muscles. The tenodesis of FHLT to FDLT resulting in floating halluces with hyperextension and alignment problems were reported in some studies [26, 27]. Some authors do not routinely perform a tenodesis of FHLT to FDLT, they also noticed the weaker hallux postoperatively, but it was not a clinical issue for most patients [32]. However, it is uncertain whether this technique is suitable for athletes and sports participants who have a high need for movement.
At present, there is still no uniform standard for the time and angle of postoperative plaster fixation for FHLT transfer surgery. Most previous studies fixed the ankle joint in a 5°-30° plantarflexion position with a plaster for 2–6 weeks after surgery, then adjust the angle to 0°gradually or following with a weight-bearing boot for another 4–6 weeks. The time and angle of fixation differed according to the surgeons’ experience. Initially, we fixed the ankle joint in a 15°-20° plantar flexion position with a plaster within 4 weeks after surgery, and then the angle of the ankle plantar flexion is gradually adjusted to 0° under the protection of a weight-bearing brace for another 6 weeks. However, among the first 7 patients who were followed up in this study, 3 patients started to walk on their full weight without the support of a weight-bearing brace after removing of the plaster. No tendon re-rupture, ankle movement disorder, or any other discomfort could be observed after a mean follow-up of 9–12 months. Then we adjusted the rehabilitation program, the ankle joint of remaining patients were fixed in the 5–10° plantarflexion position using a plaster cast for 4 weeks. Patients were encouraged to perform exercises to improve the range of ankle motion as well as weight training under the protection of a weight-bearing brace after removing of the plaster. The brace was removed another 6 weeks later, and normal walking was gradually regained with the avoidance of strenuous exercise. None of the patients complained of tendon re-rupture, ankle movement disorder or other discomfort. The early postoperative rehabilitation exercises after FHLT transfer for reconstruction of AT may be beneficial.
The main limitations of this study are its retrospective nature with a small case series which could lead to potential sampling bias, unable to follow up all patients with a comprehensive clinical review, and the lack of a control group. The strength are that the patients of this study were followed up for a relatively longer period, averaged 43.2 months, and the preoperative and postoperative clinical evaluation were compared.