Arthroscopic and Open Approaches to Ankle Instability



Arthroscopic and Open Approaches to Ankle Instability


NIRAV SHAH

RICHARD D. FERKEL



INTRODUCTION

Ankle sprains, one of the most common injuries seen by orthopedists, are typically forced inversion injuries that disrupt the lateral ankle ligaments1 (Fig. 12-1). Usually, these injuries heal uneventfully following appropriate conservative management including rest, ice, anti-inflammatory medication, and physiotherapy. However, chronic lateral ankle instability can result in 20% to 30% of individuals despite adequate nonoperative management.2 With recurrent instability, progression may lead to increased laxity, pain, and swelling, as well as unpredictable intra-articular pathology.3 When conservative measures fail to provide symptomatic relief, surgical repair may be required to stabilize the ankle as well as address intra-articular lesions. This chapter will focus on the anatomy, diagnosis, and treatment of chronic ankle instability.




ANATOMY AND BIOMECHANICS

Stability of the ankle results from a combination of the bony architecture, ligaments, and the dynamic stability conferred from the musculature surrounding the ankle. The ankle joint is a composite of the distal tibiofibular syndesmosis and the mortise between the distal tibia and fibula and the underlying talus. The shape of the talus confers additional stability in dorsiflexion compared to plantar flexion, as the talus is wider anteriorly than posteriorly.

The ligamentous attachments provide additional stability to the inherent constraint of the bony architecture of the ankle joint.6 The ligaments include the medial deltoid ligament complex, the lateral collateral ligaments, and the syndesmotic ligaments. A detailed description of the ligaments is provided in Chapter 5. The syndesmosis is comprised of the anterior and posterior inferior tibiofibular ligaments, the transverse tibiofibular ligament, as well as the interosseous membrane (Figs. 12-2 and 12-3). The anterior portion is commonly injured after an inversion ankle sprain, but syndesmotic instability is rare. Damage to the posterior syndesmotic ligament is less common in isolated soft tissue injuries.

The deltoid ligament complex includes superficial and deep components. The superficial deltoid is a fan-like
structure sending five bundles distally from the anteroinferior aspect of the medial malleolus to the talus, navicular, and the sustentaculum tali (Fig. 12-4). The deep deltoid has two bundles and originates on the posterior aspect of the anterior colliculus and inserts on the nonarticular portion of the medial talus (Fig. 12-5). Both structures contribute equally to provide restraint against pronation and abduction of the talus.7






FIGURE 12-2. Anterolateral view of the ligaments of the ankle. (Illustration by Susan Brust.)

The lateral ligamentous complex consists of three ligaments: the anterior talofibular, the calcaneofibular, and the posterior talofibular. The calcaneofibular ligament (CFL) spans both the tibiotalar and talocalcaneal joints. It is the most prominent structure in stabilizing the subtalar joint.






FIGURE 12-3. Posterior view of the ligaments of the ankle. (Illustration by Susan Brust.)

The ATFL, which blends with the anterolateral capsule of the ankle, runs from the anterior aspect of the distal fibula and inserts on the lateral aspect of the talar body. Its fibular origin is just lateral to the articular margin 10 mm proximal to the tip of the fibula and inserts on the talus directly distal to the articular surface, on average 18 mm proximal to the subtalar joint. It can be comprised of two bands with a small central cleft, but this finding is not universal.8 The ATFL averages 24.8 mm in length and 7.2 mm in width9 (Fig. 12-6).

The CFL originates from the anterior aspect of the distal fibula, just distal to the ATFL origin, and courses inferiorly and slightly posteriorly to its insertion on the calcaneus, on average 13 mm inferior to the subtalar joint. It is an extracapsular ligament, running deep to the peroneal tendons. The CFL averages 5.3 mm in width and 35.8 mm in length, running 133° from the shaft of the fibula9 (Fig. 12-6). The posterior talofibular ligament (PTFL) originates from the posterior portion of the distal fibula and runs almost horizontally to a broad insertion on the posterior aspect of the talus. Its dimensions are highly variable based on foot position but averages 30 mm in length and 5 mm in width.

Each of the ligaments within the lateral complex has a role in stabilizing the ankle joint, depending on the position of the foot and ankle within space. Their functions are most essential in the unloaded joint, as the inherent bony stability of the mortise joint is maximized in the weight-bearing position. The ATFL is relaxed, while the CFL is taut in dorsiflexion; the reverse is true in plantar flexion.
The PTFL is relaxed in plantar flexion.9 The ATFL restricts internal rotation and anterior translation of the talus, as well as adduction when the ankle is plantar flexed.10 The CFL resists adduction primarily when the ankle is in neutral or dorsiflexed and assists the ATFL in plantar flexion. The PTFL prevents external rotation in a dorsiflexed position; it also resists adduction when the CFL has been compromised.






FIGURE 12-4. Anatomy of the superficial deltoid ligament. (Illustration by Susan Brust, copyright, Richard D. Ferkel, MD.)






FIGURE 12-5. Anatomy of the deep deltoid ligament. (Illustration by Susan Brust, copyright, Richard D. Ferkel, MD.)







FIGURE 12-6. Anatomical measurements of the lateral ankle ligaments. (From Burks RT, Morgan J. Anatomy of the lateral ankle ligaments. Am J Sports Med 1994;22:72. Illustration by Susan Brust, copyright, Richard D. Ferkel, MD.)

In biomechanical studies, Attarian et al.11 have demonstrated a lower load to failure of the ATFL compared to the CFL. The CFL has a maximum load to failure 2 to 3.5 times that of the ATFL. However, the ATFL has the capacity to undergo greater strain compared to the CFL and PTFL. Thus, although a lower load is required, the ATFL can accommodate a greater deformation prior to sustaining failure. Rasmussen10 demonstrated how the position of the unloaded ankle determines the pathology of ligamentous disruption. Adduction forces in neutral and dorsiflexion cause rupture to the CFL, while the same forces in plantar flexion disrupt the ATFL. Forced dorsiflexion causes injury to the PTFL. Internal rotation injures the ATFL and the PTFL sequentially. The lower load to failure and the common injury pattern in ankle sprains of internal rotation and adduction helps explain the greater frequency of injury to the ATFL.

The musculotendinous units that cross the ankle joint provide dynamic stabilization to the ankle joint. These include the peroneal tendons, tibialis posterior tendon, and the toe flexors. The peroneals and the superior peroneal retinaculum act in concert to provide static resistance to anterior translation of the talus. Disruption of both of these structures increases talar translation by 15% in the neutral position.12


MECHANISMS OF INJURY

Chronic lateral ankle instability begins with an initial inversion injury to the ankle. Typically, the ATFL ruptures first on a plantar-flexed ankle, followed by the CFL as the ankle moves into a position of dorsiflexion.13 Isolated ATFL injury occurs in 50% to 75% of cases, while a combination of ATFL and CFL injuries occurs in 15% to 25% of cases.12 An isolated CFL injury occurs in <1% of cases; in 60 surgical patients, Broström noted no CFL ruptures in isolation.5 Typically, ligament disruptions are midsubstance, but detachment from bony insertions or avulsion fractures can occur. Berg14 has suggested that the os subfibulare is the result of an ATFL avulsion fracture.

The majority of patients sustaining an injury to the lateral ligament complex go on to heal uneventfully. However, in 20% to 30% of patients, chronic instability develops as the injured ligaments heal in an attenuated position, thus lacking the mechanical integrity needed to resist further destabilizing stresses. Risk factors identified in chronic instability include environmental factors such as sport and position played, equipment utilized, and type of playing surface.15 Patient factors include impaired muscle strength, delayed muscle reaction time, deficient proprioception, generalized ligamentous laxity, and postural control,16 as well as anatomy producing a varus hindfoot or a posteriorly positioned fibula.17

Chronic ankle instability can be classified as either mechanical or functional instability. Mechanical instability is an objective, abnormal motion of the talus within the ankle mortise, as demonstrated on physical examination or radiographic studies. This instability is directly related to the injured lateral ankle ligaments. In addition, neuromuscular deficits can also occur following an ankle sprain due to injury to the surrounding tissues. This can manifest
as impaired balance, impaired proprioception, decreased strength, and limited ankle range of motion. Additionally, scar tissue formation after injury can lead to sinus tarsi syndrome or anterolateral impingement syndrome. This can lead to functional instability, the symptomatic feeling of repeated “giving way” episodes of the ankle and difficulty walking, especially on uneven terrain.

Other injuries are noted in association with lateral ankle sprains. These include partial or complete tears of the peroneal tendons, medial ligamentous injuries, syndesmosis injuries, and avulsion fractures of the fifth metatarsal. In addition, significant injuries within the ankle joint itself have been described, including osteochondral injuries of the talus. In one study by Komenda and Ferkel,18 intraarticular abnormalities were found at the time of surgery in 93% of ankles with chronic instability. In a similar study, intra-articular problems including soft tissue impingement, osteophytes, chondral injuries, adhesions, and loose bodies were found in 83% of ankles.19

Rates of chondral injuries in the chronically unstable ankle have been reported between 13% and 95%.18, 19, 20, 21, 22, 23 In classifying these lesions, the majority have been on the medial half of the ankle joint, with rates ranging from 62% to 86%.20, 21, 22, 23 Only the case series by Komenda and Ferkel18 described a preponderance of lesions on the lateral aspect of the talus in a 2:1 ratio. The depth of the lesion has also been characterized, with the vast majority being superficial in nature. Fibrillation and/or lesions encompassing <50% of the depth of the cartilaginous layer account for 46% to 96% of lesions, while full-thickness lesions account for <5%.21, 22, 23

Much less is known about chronic medial instability. Pronation injuries of the ankle, usually combined with forced eversion of the foot, may result in disruption of the deltoid ligament. Repeated injuries may result in chronic insufficiency of the deltoid ligament, resulting in medial instability. This usually is a result of incompetence of the superficial deltoid, while the deep deltoid sometimes remains intact. Chronic insufficiency can also be seen in other conditions such as a prolonged injury to the posterior tibial tendon with chronic hindfoot valgus deformity. As the posterior tibial tendon becomes deficient, the ability to resist valgus is lost. With worsening of the hindfoot deformity, the deltoid ligament complex is unable to resist the resultant forces placed upon it. Eventually, the deltoid ligament becomes completely incompetent and the talus tilts within the mortise, resulting in the most advanced form of disease, stage IV adult-acquired flatfoot deformity.


CLINICAL PRESENTATION

Typically, the patient presenting with chronic lateral ankle instability will complain of recurrent inversion sprains that result in lateral ankle pain and swelling. The pain and swelling will commonly abate in between episodes. A sense of instability or difficulty with uneven terrain is also occasionally noted. The inability to predict when an ankle will “give out” leads to insecurity and reluctance to rely on the ankle. Often, patients will self-limit physical activities known to cause inversion episodes. Other complaints include weakness, stiffness, tenderness, sensitivity to weather, and a sense of looseness. Persistent pain between episodes or mechanical symptoms may indicate an intra-articular process such as chondral damage or loose body formation. Chronic medial instability will present with similar complaints, but with recurrent pronation/eversion injuries.

Physical examination of the patient should include an evaluation of gait, although most patients will have a normal gait pattern. Generalized ligamentous laxity should also be noted, usually by testing the apposition of the thumb to the forearm. Lower extremity alignment should also be documented, paying close attention to any varus or valgus deformity of the hindfoot. The exam should include testing of muscle strength, especially to determine the extent, if any, of peroneal or posterior tibial weakness. Proprioceptive testing is performed by asking the patient to perform single leg balance. Local examination may reveal swelling, focal tenderness over the affected ligaments, or guarding to examination.

Stress testing of the lateral ligaments will often confirm the diagnosis of chronic lateral instability. The anterior drawer test will be positive in situations of ATFL laxity. By grasping the patient’s heel, the examiner can slide the entire foot anteriorly at the tibiotalar joint, while the opposite hand anchors the leg (Fig. 12-7). The inversion stress test is performed by stabilizing the distal tibia with one hand, while the foot is plantar flexed and inverted with the other (Fig. 12-8). Often, pain is elicited, in addition to increased translation when compared to the contralateral, unaffected side.






Sep 25, 2018 | Posted by in RHEUMATOLOGY | Comments Off on Arthroscopic and Open Approaches to Ankle Instability
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