Management of Anterior Tibialis Tendon Ruptures

Jie Chen, MD, MPH; Rishin Kadakia, MD; Craig Chike Akoh, MD; Karl Martin Schweitzer, Jr, MD

Disclosures

J Am Acad Orthop Surg. 2021;29(16):691-701. 

In This Article

Abstract and Introduction

Abstract

Anterior tibialis tendon ruptures, while relatively infrequent ruptures, are commonly identified in delayed fashion, which can lead to significant impairments in patient gait and function. Surgical treatment is typically required to restore ankle dorsiflexion function and proper gait. Depending on various patient-specific factors, tendon quality and excursion, and chronicity, a range of treatment options are available to manage these patients, from nonsurgical care to surgical treatment. Surgical options include direct repair, local tendon transfer, autograft tendon reconstruction, and allograft tendon reconstruction. Additional procedures may need to be considered. Despite the variety of described surgical procedures, limited evidence-based guidelines are available to direct surgeons in the most optimal treatment for their patients. In addition to the relevant anatomy, biomechanics, and pathoanatomy, the reconstructive armamentarium is detailed and reviewed here, along with outcomes and potential complications, to guide surgeons in the most appropriate treatment for their patients.

Introduction

First described by Dr. Brϋning in 1905, rupture of the anterior tibialis (AT) tendon is a rare rupture with several hundred cases reported in the literature.[1,2] Despite the rarity, these ruptures still represent the third most common lower extremity tendon rupture in the human body, and is one of the most common silent tendon ruptures in patients older than 70 years.[3] The primary function of the AT tendon is to dorsiflex and invert the ankle. An untreated rupture can lead to gait impairment and progressive deformity, including loss of the medial longitudinal arch, equinus contracture, and lesser toe contractures.

Traumatic injuries typically result from a direct laceration to the tendon (eg, a knife or a sharp bone fragment from a distal tibial or talus fracture) or a forcible plantar flexion moment applied to an eccentrically contracting AT muscle.[4–6] Atraumatic ruptures can have a variety of causes. Poor vascularity, underlying tendinopathy, and medical comorbidities (eg, diabetes mellitus, gout, systemic lupus erythematosus, conditions requiring long-term corticosteroid use, renal dysfunction, and inflammatory arthropathy) can contribute to attritional rupture. Local corticosteroid injections (eg, medial midfoot or ankle joint injections) and fluoroquinolone use may contribute to tendon degeneration.[7–12] Anterior ankle or dorsomedial midfoot osteophytes can impinge and produce an attritional rupture (Figure 1).

Figure 1.

Sagittal (A) and axial (B) Proton density MRI sequences demonstrating an AT tendon attritional rupture with retracted tendon stump, due to impinging, anteromedial ankle osteophytes (A and B, red arrow). An empty tendon sheath sign (B, yellow arrow) is seen near the anteromedial ankle. Intraoperative photograph (C) demonstrating the chronic anterior tibialis tendon rupture, along with the underlying ankle osteophytes seen following an ankle arthrotomy. These osteophytes will be resected to decompress the region for planned anterior tibialis allograft tendon reconstruction.

Absence of AT tendon function can be partially compensated for via recruitment of the extensor hallucis longus (EHL) and extensor digitorum longus (EDL) tendons.[13] Given the atraumatic nature and compensatory recruitment, initial symptoms may be mild, delaying diagnosis and surgical management.

Acute AT tendon ruptures can undergo primary repair if the tendon ends are robust and can be adequately reapproximated or the tendon brought to bone. Missed or neglected injuries lead to tendon attrition and contracture, formation of adhesions, and muscle degeneration. For these cases, reconstructive options include local soft-tissue rearrangement, tendon transfer, free autograft tendon, and intercalary allograft tendon. Acute ruptures can also have underlying tendon degeneration and shredding to warrant an allograft or autograft bridging procedure. Thus, an optimal treatment strategy should be based on patient-specific factors such as functional deficit and desired activity level, but also chronicity, tendon quality and quantity, AT muscle function, and rupture pattern.

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