Acute Tarsal Tunnel Syndrome After Total Ankle Arthroplasty With Varus Deformity

Abstract

Background

A 54-year-old woman presented with varus ankle arthritis, which was corrected with total ankle arthroplasty (TAA). Immediately postoperatively, she was insensate throughout the plantar foot. After seven weeks, she underwent tarsal tunnel release, and the tibial nerve was found to be intact. Plantar sensation improved by one week after exploration with neurolysis and was completely intact at one year.

Conclusion

Loss of plantar sensation can occur following TAA for varus arthritic deformity. One potential cause is tibial nerve compression from tightening the laciniate ligament, resulting in acute tarsal tunnel syndrome. The condition can be remedied with early recognition and tarsal tunnel release.

Level of Evidence: V

Introduction

Tarsal tunnel syndrome (TTS) is an uncommon entrapment neuropathy resulting from compression of the tibial nerve or its branches in the fibro-osseous space posterior and inferior to the medial malleolus. Risk factors include both intrinsic causes (e.g., ganglion cysts, tenosynovitis, tumors) and extrinsic causes (e.g., systemic inflammatory diseases, trauma, anatomic abnormalities). Diagnosis can be difficult as symptoms can be vague or inconsistent across presentations. After failing conservative management, surgical treatment involves ligamentous release and/ or removal of the space-occupying lesion.

Total ankle arthroplasty (TAA) is used to treat tibiotalar osteoarthritis and can concurrently correct for coronal plane deformity with or without the use of associated osteotomies.¹ Previously reported neurological injures following TAA usually involve the deep peroneal, superficial peroneal, or common peroneal nerves,^2-5 but there have been few reports of tibial nerve complications.^6-8 In particular, we are aware of only three publications describing acute tarsal tunnel syndrome following TAA.^6,7,9

The following describes a case of acute TTS following TAA performed for varus arthritic deformity. Associated literature is subsequently reviewed. The patient consented to publication of her case.

Case Report

A 54-year-old female presented for evaluation of progressively worsening left ankle pain. She reported a previous ankle injury that involved a misstep during ambulation, as well as an associated ankle arthroscopy and debridement a year later with little improvement. At presentation to our clinic 11 years after the initial injury, she had worsening ankle pain and a hindfoot varus deformity. She had ankle dorsiflexion to neutral, plantar flexion to 15 degrees, and limited inversion and eversion. She was neurovascularly intact with good strength throughout and had normal sensation in the tibial, sural, saphenous and superficial/ deep peroneal nerve distributions. Radiographs and CT of the left ankle (Figs. 1 and 2, respectively) demonstrated end-stage tibiotalar arthritis with a 15° varus tibiotalar deformity and a relatively preserved subtalar joint.

Figure 1A to 1D.

Preoperative radiographs of the left ankle in AP (1A), oblique mortise (1B), lateral (1C), and Saltzman (1D) weightbearing views.

Figures 2A to 2D.

Preoperative CT scan of the left ankle in coronal (2A), axial (2B), and sagittal (2C) planes, as well as 3D reconstruction (2D).

The patient consented to a left TAA, Achilles tendon lengthening, and possible Malerba valgus-producing osteotomy. She ultimately underwent left TAA with intra-articular deformity correction and Achilles triplehemi-section; the Malerba osteotomy was deferred secondary to neutral hindfoot correction via the ankle replacement (Fig. 3). No intraoperative complications were noted. At her one-week postoperative visit, she was noted to be insensate throughout the full distribution of the tibial nerve distal to the tibiotalar joint line. After extensive discussion, early operative intervention for this neurologic deficit was deferred in favor of watchful waiting. At her three-week postoperative visit, her numbness was unchanged, and she was prescribed gabapentin and a short course of steroids, again choosing watchful waiting as part of a shared decision-making process. At her third postoperative visit, her numbness remained unchanged, with no sensation to light touch or painful stimuli. She also demonstrated toe clawing and diminished toe abduction strength at this point. Electromyography revealed left distal tibial neuropathy. At this point, operative intervention with tarsal tunnel release and possible nerve repair and/ or grafting was offered to the patient, to which she consented.

Figure 3A to 3C.

Six-week postoperative radiographs in AP (3A), oblique mortise (3B), and lateral (3C) touchdown films.

The patient returned to the operating room with the assistance of a hand surgeon trained in microsurgery to be available for any requisite neurologic reconstruction. The tibial nerve was approached through an incision beginning 4cm proximal to the medial malleolus and curving around the medial malleolus into the plantarmedial midfoot, stopping at the level of the talonavicular joint overlying the midportion of the abductor hallucis muscle. The proximal portion of the laciniate ligament (flexor retinaculum) was identified and opened into the sheath containing the tibial nerve. The nerve was identified and followed distally with release of the laciniate ligament, exposing its three distal branches within the tarsal tunnel. The medial plantar nerve was identified and traced distally around the malleolus, following beneath the abductor hallucis to the talonavicular joint level, with complete release of its fibro-osseous tunnel. The lateral plantar nerve was also traced distally and released, including the abductor hallucis deep fascia. Finally, the first branch of the lateral plantar nerve was identified and similarly released. The tibial nerve and its branches were noted to be in continuity, with no evidence of complete or partial transection; however, the nerve did have a boggy, edematous appearance within the tarsal tunnel (Fig. 4). The tibial nerve was not taut and had satisfactory excursion, and the laciniate ligament was not repaired during closure.

Figure 4.

Intraoperative photograph of the isolated tibial nerve of the left ankle during the tarsal tunnel decompression.

One week after tarsal tunnel release, the patient demonstrated partial return of sensation in the plantar midfoot arch. Three weeks postoperatively, the patient had sensation plantarly from the heel to midfoot but was insensate at the plantar forefoot. Toe abduction remained weak. She started formal physical therapy and transitioned to weightbearing in a supportive shoe. Five months postoperatively, she reported normal heel and midfoot sensation but persistent lack of plantar forefoot sensation. At one-year postoperatively, the patient was sensate throughout the plantar aspect with only minor occasional subjective paresthesias in the forefoot. At that time, 5.07 monofilament testing was intact throughout. Her toe clawing had resolved, and toe abduction strength approached that of her contralateral side.

Discussion

Complete loss of plantar sensation is an uncommon complication following TAA and suggests acute tibial nerve injury.¹ Complete or partial transection of the nerve during tibiotalar joint preparation is a possibility and can be difficult to distinguish from severe neuropraxia. We were prepared to address transection with microsurgical reconstruction during the secondary procedure. However, no evidence of transection was found.

A compression neuropraxia is another potential cause of acute complete loss of plantar sensation. Compression of the tibial nerve can occur in the tarsal tunnel and is referred to as TTS. Few TTS cases have been described after TAA in the literature, but this phenomenon can occur when the procedure involves correction of varus or valgus deformity.^6,7 The mechanism is increased pressure within the tarsal tunnel due to constraint by the laciniate ligament.^6,7 However, complete plantar sensation loss is a rare manifestation of TTS. More commonly, patients complain chiefly of shooting pain along the tarsal tunnel and into the plantar foot, sometimes associated with burning, tingling, and other paresthesias.

The diagnosis of TTS in this case is supported by a number of factors. First, there is an anatomic and physiologic explanation: varus deformity correction lengthened the medial side of the ankle putting tension on its surrounding retinaculum. Moreover, improved ankle dorsiflexion with the change from stiff and varus to valgus may have put more tension on the nerve.¹⁰ Second, release of the tarsal tunnel appeared to create space around a compressed nerve that appeared boggy and dysvascular. Third, tarsal tunnel release resulted in rapid improvement in plantar sensation and eventual complete deficit resolution.

Diagnosis of TTS following TAA can be challenging due to variability in inciting factors and clinical presentation. For example, Bejjanki et al. reported on a TAA patient who developed acute TTS secondary to a displaced posteromedial osteophyte. This patient presented with heel pain, medial foot hypersensitivity, and abductor hallucis muscle wasting. The decision to remove the osteophyte only occurred after she was also found to have significant abductor hallucis denervation on nerve conduction studies.⁹ Removal resulted in signs of improvement by six weeks postoperatively, but the authors noted a five-month delay between symptom onset and surgery. Similarly, Primadi conducted a retrospective study of 150 TAA patients and found that tibial nerve complications occurred in nine (6%).⁶ Three of these patients were found to have TTS—of note, all three underwent coronal plane deformity corrections (two valgus, one varus). The presentation in each case was partial plantar numbness and pain/paresthesias. Two patients did not develop symptoms until three and six months after TAA, respectively, while the third patient experienced symptoms within the first month. All patients underwent tarsal tunnel release, with one patient experiencing complete symptom resolution and two experiencing partial resolution.⁷

Tarsal tunnel syndrome has also been reported following lateralizing calcaneal osteotomy (LCO) in the correction of hindfoot varus.^11-14 Krause et al. reported on two such cases in patients with Charcot-Marie-Tooth. Both patients developed numbness in the medial and lateral plantar nerve distributions, and one underwent tarsal tunnel release, resulting in complete symptom resolution.¹³ Bruce et al. later demonstrated that LCO produced a significant reduction in tarsal tunnel size, providing some rationale for prophylactic tarsal tunnel release in patients planning for LCO.¹⁵ While VanValkenburg found a tibial nerve injury rate of 33.8% in their 80 LCO cases, they found no difference in this rate between patients with and without prophylactic tarsal tunnel release.¹⁴ Hence, the role of prophylactic tarsal tunnel release prior to LCO remains unclear.

In conclusion, coronal plane deformity correction as part of TAA can rarely result in acute TTS. While this typically manifests as tarsal tunnel pain radiating into the plantar foot, we present here a case in which it resulted in complete plantar numbness, presenting more similarly to a complete or partial tibial nerve transection. Physical exam can also show toe abduction weakness and clawing, and electromyography is a helpful confirmatory study. Definitive treatment involves release of the tibial nerve and its branches as they pass through and exit the tarsal tunnel into the plantar foot. Timely and complete release can result in resolution of both sensory and motor symptoms.