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International Journal of Surgery Case Reports logoLink to International Journal of Surgery Case Reports
. 2024 Jun 22;121:109934. doi: 10.1016/j.ijscr.2024.109934

Flexor hallucis longus impingement syndrome: A case report

Ihsan Oesman a, Nurmansyah Hata Dwi Putra b, Anindyo Abshar Andar b,, Winona Andrari Mardhitiyani b
PMCID: PMC11295693  PMID: 39024995

Abstract

Introduction and importance

Long-term friction of the FHL tendon's sheath (caused by sporting activities) can result in tendinitis, which causes pain in the foot and ankle and consequently interferes with everyday life and foot function. The FHL tendon is crucial for maintaining foot stability and can be damaged by overuse. FHL tendinitis can be also caused by inflammatory tendon sheath filled. Arthroscopy can play a role in the diagnosis and treatment of this condition.

Case presentation

A 28-year-old female with left ankle pain was brought to our clinic after slipping on a train platform nine months ago. X-rays and MR imaging revealed a complete tear of the ATFL, minimal joint effusion, and a bony protrusion causing impingement. Arthroscopic surgery was performed, and the patient's pain sensation improved to 0–1 in the visual analogue scale (VAS) within three weeks. The Foot and Ankle Ability Measure (FAAM) score increased from 8 % to 100 %, and the patient was able to walk and perform daily activities normally.

Clinical discussion

The FHL tendon sheath begins at the posterior tubercles of the talus and forms a fibroosseous tunnel along the medial calcaneus, potentially leading to impingement during ankle or hallux dorsiflexion. FHL tendon impingement and tendinitis share clinical manifestations, and if conservative treatments (NSAIDs, physical therapy) fail after 6 months, arthroscopic surgery is recommended for its minimally invasive benefits. Both arthroscopic and open surgical techniques yield positive outcomes for FHL pathologies; however, they carry risks such as neurovascular complications, highlighting the necessity for surgical precision and expertise.

Conclusion

We concluded that in this case, FHL impingement was caused by the bony protrusion from Stieda process fragment. It was demonstrated that the arthroscopic surgery with loose body removal was successful and practical.

Keywords: Flexor hallucis longus, Impingement syndrome, Tendinitis, Arthroscopic surgery, Loose boby

Highlights

  • The Flexor Hallucis Longus (FHL) muscle originates from the interosseous membrane and the fibula, extending down to the great toe.

  • Overuse of the FHL tendon can lead to tendinitis, resulting in pain and reduced foot function.

  • FHL impingement syndrome is characterized by the muscle belly being too long, impacting the tendon sheath at the talus.

  • In cases where conservative methods have failed, surgical intervention has been associated with positive outcomes, notably the resolution of pain andnormal toe and ankle joint mobility, and a return to pre-injury levels of activity.

  • This case showed an FHL impingement caused by a bony protrusion from the Stieda process fragment, and arthroscopic surgery with removal of this loose body was effective in alleviating the patient's symptoms.

1. Introduction

The interosseous membrane and the back of the fibula serve as the origin of the FHL. FHL travels distally within the tendon sheath and underneath the flexor retinaculum before joining the posterior talus and calcaneus to form a fibro-osseous tunnel. The tendon is located in the groove between the medial and lateral tubercles of the talus, medial to the os trigonum. The FHL crosses dorsally to the flexor digitorum longus with a unique interconnection, the so-called Henry knot, which occurs in the midfoot at the level of the first tarsometatarsal joint. The FHL extends distally and medially to the groove on the plantar tendon of the sustentaculum tali. The tendon subsequently passes through the intersesamoid ligament and implants at the plantar aspect of the great toe's distal phalanx. The distal excursion of the FHL can be increased by up to 25 mm by dorsiflexion of the first MTP and the ankle joints, which also increases the tension on the interconnecting bands at the Henry knot [1,2].

Long-term friction of the FHL tendon's sheath (caused by sporting activities) can result in tendonitis, which causes pain in the foot and ankle and consequently interferes with everyday life and foot function. The FHL tendon is crucial for maintaining foot stability and can be damaged by overuse. Anatomical variation, os trigonum, tendon compression, overuse, excessive metatarsal flexion, and specific body positions are the main pathogenic reasons of FHL tendonitis. Nevertheless, we observed that some individuals continued to develop FHL tendinitis with the growth of a sizable inflammatory tendon sheath filled with inflammatory fluid even in the absence of the previous risk factors. Arthroscopy can play a role in the diagnosis and treatment of FHL Impingement Syndrome. During the procedure, the surgeon can directly visualize the impinged tendon, identify any accompanying pathology or structural abnormalities, and determine the extent of the impingement. This visual assessment helps guide further treatment decisions [3,4]. Fukuda et al. discovered through arthroscopy that the primary reason for FHL tendonitis was a contact between the FHL muscle belly and its tendon sheath [3,4]. Due to the limited available literature and the trend towards conservative treatment of the pathological conditions of FHL, this study aimed to present a case of arthroscopic management of FHL impingement. In addition, this study was reported according to the SCARE 2023 guideline [5].

2. Case report

We reported one case of FHL impingement syndrome. A 28 years old female was brought to our clinic due to the pain on the left ankle since 2 months ago. History of present illness revealed that patient slipped on the train platform 9 months ago, after that she couldn't walk and then mobilized with wheelchair. Patient then went to masseur for 3 sessions but the edema was increasing, then she went to Orthopaedic Clinic at regional hospital and was sent for physiotherapy session. The edema was resolved but the pain remained to persist. She was then referred to our center for further examination and treatment. On the examination, we didn't find any wound, scar, or deformity. Pain was confirmed by 2–3 visual analog scale (VAS) score, Distal sensory was normal with capillary refill time (CRT) less than two seconds. Patient had limitation for ankle dorsiflexion and plantarflexion due to pain (Fig. 1).

Fig. 1.

Fig. 1

Left ankle with limitation dorsiflexion and plantarflexion.

After the examination, patient then underwent X – Ray for the left foot (Fig. 2) which showed a loose body on the left talus without dislocation or subluxation. There was minimal gloom on Kager's fat pad. The position of the other ankle bones was in good shape. The distal tibiofibular, talotibial, talofibular, and talonavicular joints were intact. Soft tissue showed no abnormalities. Besides the appearance of the loose body posterior to the left talus, we also suspected an avulsion fracture of the posterior process of the left talus, with surrounding joint effusion.

Fig. 2.

Fig. 2

A loose body on the left talus without dislocation or subluxation.

Further examination with MRI of the right and left ankle was performed for specifying soft tissue pathologies in left ankle area. (Fig. 3) Magnetic Resonance Imaging revealed no bone marrow edema with the clearly seen trigonum bone. Fluid accumulation was seen to be slightly increased in the talocrural joint, slightly extending into the anterior-posterior recess and anterolateral gutter. The lateral ligamentous complex showed disruption of the anterior talofibular ligament (ATFL). Other ligamentous structures were intact. In the medial ligamentous complex, the deltoid ligament appeared to be intact. The plantar aponeurosis was good, with no thickening or edema. Achilles tendon structure and other tendons were still within normal limits. Sinus tarsi, anterior fat pad and Kager fat pad showed no edema. There were no major neurovascular abnormalities. Complete tear of ATFL with minimal talocrural joint effusion and a bony protrusion causing impingement were found in this MRI examination.

Fig. 3.

Fig. 3

Fig. 3

Complete tear of ATFL with minimal talocrural joint effusion.

We then diagnosed the patient with FHL impingement of left foot due to avulsion fracture of Stieda process. We performed arthroscopy of left ankle in our center. This procedure was consisted of loose body removal and flexor hallucis longus release. Incision on posteromedial and posterolateral portal was made. With the help from trocar insertion, we identified loose body from Stieda process fragment. We then performed removal of loose body and evaluate the flexor hallucis longus gliding function (Fig. 4).

Fig. 4.

Fig. 4

a. drapping and design, b. incision on posteromedial and posterolateral portal, c. trocar insertion, d. Identification of loose body (Stieda process fragment), e. loose body removal, and f. FHL gliding evaluation.

We succeeded performing the surgery and postoperatively, we observed the diminished pain sensation on of the left ankle, which was then improved to 0,1–0,3 visual analogue scale (VAS). At the 3 weeks of follow-up there was no complaint from the patient and the patient was able to walk by herself. The Foot and Ankle Ability Measure (FAAM) score exhibited a substantial improvement, escalating from 8 % to 100 %. Consequently, the patient regained the capability to resume professional duties and participate in customary activities. Furthermore, the postoperative period was devoid of notable adverse events, including surgical site infections or septic arthritis.

3. Discussion

The flexor retinaculum, which is located at the level of the posterior tubercles of the talus, is where the FHL tendon sheath begins to develop. Along the medial calcaneus and the inferior aspect of the sustentaculum tali, the tendon sheath then fuses with a fibroosseous tunnel. With ankle or hallux dorsiflexion, the muscle may be forced to penetrate the fibro-osseous tunnel, impinging the musculotendinous junction, which has a variable girth and distal extent. Additionally, tendon orientation changes linked to these anatomical regions may contribute significantly to tendon instability [6,7].

The tendon of FHL is at risk of impingement because it travels in its sheath and groove, which is covered with the retinaculum between the medial and lateral tubercles of the talus. This exposure may cause or aggravate the symptoms of FHL tenosynovitis. Impingement can occur at the flexor sheath posterior to medial malleolus, the entrance to the fibro-osseous tunnel, the knot of Henry, and the intersesamoid ligament. When significant nodular change or hypertrophy appears in the FHL tendon, the excursion can be limited because of these 3 restriction points and may causes triggering or limitation of motion of the great toe. However, when nodularity or hypertrophy part is moved proximal to the restricted fibro-osseous area by maximum plantar flexion of the ankle, dorsiflexion of the first MTP joint is restored, the so called pseudo–hallux rigidus [1].

FHL tendon impingement syndrome was distinguished form FHL tendinitis because the muscle belly of the FHL tendon is too long to impact the tendon sheath of the talus. In both cases of FHL tendon impingement syndrome and FHL tendinitis, clinical manifestations of FHL tendinitis will be present. For example, deep tenderness in the medial hind foot occurs during physical examination, the hallucis back extension test and traction test are positive, and an edema zone around the FHL tendon can be observed with magnetic resonance imaging. After 3 to 6 months of support fixation, NSAID use, cold compress use, and physical therapy for FHL tendonitis and FHL tendon impingement syndrome, clinical outcomes are typically satisfactory. After a period of six months of conservative therapy, arthroscopy is used as the primary therapeutic option if the patient shows no signs of improvement [8,9]. The similar principle was also applied to the case we presented, it was known that the patient had been experiencing pain due to a fall since 9 months ago. Several therapeutic modalities have been given to patients ranging from medication to physiotherapy. Even though the edema was reduced, the patient still felt a nagging pain, so in this case arthroscopic management was performed.

Arthroscopic surgery offers a minimally invasive approach that can be effective in treating posterior ankle impingement syndrome (PAIS) and FHL tendon disorders [8]. It allows for the treatment of various conditions such as FHL tendinopathy, osteochondral lesions, subtalar coalitions, and other ankle pathologies [10]. The literature supports hindfoot arthroscopy as a safe primary treatment for symptoms of posterior ankle impingement, including FHL tendon injuries [11]. Additionally, arthroscopic techniques can provide a thorough examination and treatment of FHL tendon problems, offering advantages in terms of visualization and access to the affected area [12]. On the other hand, open surgery, whether through a posterolateral or posteromedial approach, remains a viable option for addressing FHL impingement. Open procedures may be necessary in cases where extensive soft tissue dissection is required, especially considering the deep location of the FHL tendon [13]. Surgical techniques such as tendon transfers, including the use of the FHL tendon, have been employed in the reconstruction of chronic Achilles tendon ruptures, showcasing the versatility of open surgical approaches [14].

When considering clinical outcomes, both open and arthroscopic surgeries have shown positive results in treating FHL impingement. Surgical treatment of FHL tendon tears and other pathologic conditions has consistently yielded good outcomes [15]. Moreover, studies have highlighted the effectiveness of arthroscopic synovectomy for FHL tenosynovitis, emphasizing the benefits of arthroscopic interventions in managing FHL-related pathologies [16]. In terms of complications, both approaches have associated risks. Complications after ankle arthroscopy, including neurovascular issues, have been reported in up to 17 % of cases [17]. Similarly, risks associated with hindfoot arthroscopy, such as those related to posterior ankle impingement, have been documented, underscoring the importance of careful consideration and expertise in performing these procedures [18].

In regard to the Stieda process avulsion fracture in this patient, the mechanism of injury following trauma or falling can be attributed to specific forces acting on the lateral malleolus of the ankle. Avulsion fractures typically occur when the tensile strength of the ligament or tendon attachment site is exceeded by a sudden and forceful contraction of the associated muscle. In the case of the Stieda process, the presumed mechanism involves forced dorsiflexion, where the avulsion of the bone fragment occurs due to the pull of the ligament or tendon during this movement. This mechanism is consistent with the concept that avulsion fractures often result from indirect trauma, such as sudden and excessive tension on the attachment site.

Avulsion fractures can also be influenced by the direction and nature of the force applied to the bone. For instance, in the case of the lateral malleolus, a specific type of force like forced dorsiflexion can lead to the avulsion of the Stieda process. Additionally, avulsion fractures may occur due to high-energy trauma events like falls or accidents, where the sudden and significant impact on the bone can cause the avulsion of bony fragments.

Retrospective study from Feng et al. showed that all patients showed complete disappearance at the back of the ankle joint pain, normal great toe and ankle joint movement, return to normal gait, and full recovery to the pre-injury state at the most recent follow-up, though some patients could still experience ankle pain during vigorous jumping and running. The great toe passive traction test came back negative, and there was no pressing tenderness in the posterior FHL tendon area of the ankle joint [19]. Similar result was also observed in the case mentioned above, During the follow-up at 3 weeks, the patient presented with a Visual Analog Scale (VAS) score that had decreased to a level of 0–1. The patient's range of motion (ROM) also demonstrated normal values. The patient was able to walk well and normally without any complaints of bothersome pain sensations, numbness, or tingling. Foot and Ankle Ability Measure (FAAM) score showed marked increase from 8 % to 100 %. The patient was able to return to work and engage in normal activities. Additionally, there were no significant complications such as surgical site infections or septic arthritis following the surgical procedure.

Nevertheless, to ensure successful arthroscopic surgery for flexor hallucis longus (FHL) impingement in the ankle, surgeons should consider several tips and pitfalls. Firstly, it is crucial to accurately localize the FHL tendon to protect the nearby neurovascular bundle, which is located medially. Surgeons should be mindful of the potential pitfalls during posterior-to-anterior screw fixation, such as avoiding penetration of the subtalar joint or lateral trochlear surface, injury to the FHL tendon, and restriction of ankle plantar-flexion due to screwhead impingement. Moreover, when performing hindfoot arthroscopy, particularly for posterior ankle impingement syndrome (PAIS) and FHL tendon disorders, surgeons should pay attention to the anatomical structures and variations in the ankle and foot that may impact the surgical approach. Additionally, a systematic approach to the joint space of the posterior aspect of the ankle joint is essential, as it can sometimes be challenging to reach this area due to the shape of the talus. Furthermore, we recommended to establish a low-risk zone for temporary extra-articular calcaneo-tibial pin fixation in cases of unstable ankle or subtalar joint to prevent complications related to neurovascular structures. Surgeons should also be cautious about potential complications, such as wound erythema, which may arise postoperatively and require appropriate management.

4. Conclusion

We concluded that in this case, FHL impingement was caused by the bony protrusion from Stieda process fragment. It was demonstrated that the arthroscopic surgery with loose body removal was successful and practical. Gliding evaluation of FHL tendon was done to preserve patient mobility.

Consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Provenance and peer review

Not commissioned, externally peer-reviewed.

Ethical approval

Ethical approval for this study was not required since we only reported 1 patient and we already got patient permission to perform the procedure. In addition, we already made the manuscript into anonymous with no confidential informations of the patients was put in the manuscript. For this manuscript, we provided written and signed informed consent from patient for publishing the case report.

Funding

No funding was received in the collection, analysis and interpretation of data; in the writing of the manuscript; and in the decision to submit the manuscript for publication assist with the preparation of this manuscript. In addition, no funding was received for the publication of this manuscript.

Author contribution

IO: study concept or design, data collection, data analysis or interpretation, writing the paper

NHDP: study concept or design, analysis and interpretation, writing the paper

AAA: study concept or design, data collection, data analysis or interpretation, writing the paper

WAM: writing the paper

Guarantor

Ihsan Oesman MD accepts full responsibility for the work and/or the conduct of the study, has access to the data, and controlled the decision to publish. Ihsan Oesman MD becomes the guarantor for this work.

Research registration number

Does not need any registration.

Conflict of interest statement

The authors have no conflict interest or proprietary interests in any material discussed in this manuscript.

Acknowledgement

None.

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