Soft Tissue Injury to the Ankle: Osteochondral Injuries and Impingement

Anatomy

The anterolateral gutter of the ankle is a space bounded anteriorly by the capsule of the tibiotalar joint, the anteroinferior tibiofibular ligament, the anterior talofibular ligament, and the calcaneofibular ligament. Its lateral border is the fibula, and its medial border is the talus and tibia. The space extends inferiorly to the calcaneofibular ligament and superiorly to the tibial plafond and distal tibiofibular syndesmosis.

Pathology

Anterolateral impingement is thought to occur subsequent to relatively minor trauma involving forced ankle plantar flexion and supination. Such trauma may result in tearing of the anterolateral soft tissues and ligaments without substantial associated mechanical instability. Repeated microtrauma produces synovial scarring, inflammation, and hypertrophy in the anterolateral gutter of the ankle, with subsequent soft tissue impingement ( Fig. 34-1 ). Over time, the reactive soft tissue changes and scarring may organize into a “meniscoid” mass that causes pain and mechanical impingement. Wolin coined the term meniscoid owing to its resemblance at surgery to meniscal tissue.

Other contributing factors are hypertrophy of the inferior portion of the anteroinferior talofibular ligament and osseous spurs. First described by Bassett and colleagues, a separate distal fascicle of the anteroinferior talofibular ligament is a common variant. It becomes pathologic when a tear of the anterior talofibular ligament results in anterolateral joint laxity. With increasing joint laxity, the talus extrudes anteriorly in dorsiflexion and comes into contact with the fascicle. Constant rubbing of the fascicle against the talus thickens the fascicle, developing an impinging lesion in the anterolateral gutter. Several authors refer to this condition as syndesmotic impingement.

Clinical Presentation

Patients present with anterolateral ankle tenderness, swelling, and pain exacerbated by single-leg squatting, ankle eversion, or forced dorsiflexion. Despite a lack of true mechanical ligamentous instability, patients may report a subjective sense of ankle instability; this “functional instability” is caused by entrapment of soft tissues at the anterolateral ankle.

Imaging

Ultrasonography

Ultrasound can detect scar tissue and synovitis into the lateral gutter. There may be associated increased vascularity on Doppler imaging ( Fig. 34-2 ). Side-to-side comparison is helpful in confirming the abnormality. Posttraumatic ossicles are also well demonstrated by ultrasonography.

Computed Tomographic Arthrography and Magnetic Resonance Arthrography

CT arthrography and MR arthrography have been proven as accurate techniques for assessing the presence of soft tissue scarring in the anterolateral recess of the ankle and elucidating its extent in patients with anterolateral impingement before arthroscopy ( Fig. 34-3 ). The absence of a normal fluid-filled recess between the anterolateral soft tissues and the anterior surface of the fibula is another arthrographic finding that suggests the diagnosis of anterolateral impingement. This may be due to the presence of adhesions and scar tissue that impair the entrance of fluid into the normal recess between the fibula and joint capsule. Nevertheless, the identification of abnormal soft tissue itself does not imply the presence of clinical anterolateral impingement because anterolateral scarring and/or synovitis at CT or MR arthrography can be noted in patients without clinical features consistent with those of anterolateral impingement. Therefore, imaging features of anterolateral soft tissue abnormalities must be correlated with clinical findings.

The normal distal fascicle of the anteroinferior talofibular ligament can be readily visualized on MRI and MR arthrography. A distal fascicle causing impingement can be seen as a thickened anteroinferior talofibular ligament and hypertrophic synovial tissue in the superior aspect of the anterolateral gutter (syndesmotic impingement) ( Fig. 34-4 and see Video 34-1 ).

Differential Diagnosis

Anterolateral impingement is a diagnosis of exclusion. Lesions producing similar symptoms, including peroneal tendon tears or subluxations, sinus tarsi syndrome, stress fractures, loose bodies, osteochondral lesions, bony impingement, and degenerative joint disease, must be excluded before invasive treatment.

MRI finding of an abnormal soft tissue mass in the anterolateral ankle gutter makes it necessary to exclude conditions such as pigmented villonodular synovitis and idiopathic synovial osteochondromatosis.

Treatment

Most patients with anterolateral impingement respond to conservative therapy, including nonsteroidal anti-inflammatory drugs, rehabilitative physiotherapy, or local injection of corticosteroids.

In patients with conservative treatment failure, ankle arthroscopy may be performed for débridement of hypertrophic synovial tissue (synovitis and/or scarring) in the anterolateral gutter with good-to-excellent results (see Videos 34-2 and 34-3 ).

Pathology

The origin of anterior impingement is uncertain, and many factors are likely involved. Three different hypotheses have been proposed to explain the formation of talotibial spurs in the anterior ankle impingement syndrome.

Forced dorsiflexion results in repeated microtrauma on the tibia and talus, leading to microfractures of trabecular bone or periosteal hemorrhage, healing with new bone formation.

Another mechanism suggested is forced plantarflexion trauma, with capsular avulsion injury. However, most talotibial spurs are not located at the capsular attachment, and this hypothesis for the formation of traction spurs is therefore plausible in only a minority of cases. A recent hypothesis suggested that formation of bony spurs in the ankle is related to direct damage to the rim of the anterior ankle cartilage by repetitive kicking actions.

Once formed, forced dorsiflexion of the ankle causes impingement between reciprocating talotibial “kissing” lesions.

Clinical Presentation

Affected individuals present with pain, stiffness, swelling, and limitation of ankle dorsiflexion. Symptoms are exacerbated by athletic activity. However, these changes are very common in asymptomatic athletic populations and require no treatment.

Imaging