Musculoskeletal Soft Tissue
Andrew D. Posner
Kyle Angelicola-Richardson
INTRODUCTION
Repetitive muscle and tendon injuries in the foot and ankle are frequent causes of patient pain and disability. These injuries are common and affect both young athletes in sports participation as well as older sedentary populations. While some condition may originate in an insidiously manner, they have the potential to progress to chronic debilitating injuries. In this chapter, the authors present pain pathologies of the foot and ankle, which are related to tendon injury, muscular dysfunction, or instability. A thorough understanding of these common injuries will allow for a logical approach to diagnosis and treatment.
PERONEAL TENDON DISORDERS
Peroneal tendon pathology is a relatively common, yet frequently misdiagnosed source of lateral foot and ankle pain. These basic pathologies include peroneal tendinopathy, subluxation/dislocation, and tendon tears.1
The peroneal tendons are the primary evertors of the foot and include the peroneus longus, peroneus brevis, and peroneus tertius. The longus and brevis are located in the lateral compartment of the leg, while the peroneus tertius lies in the anterior compartment. Proximally, the brevis and longus tendons share a common synovial sheath that spans the last 4 cm of the fibula and 1 cm distally. The peroneus brevis originates from the distal two-thirds of the fibula and the intermuscular septum, and then inserts at the base of the fifth metatarsal (MT). It becomes tendinous 2 to 3 cm proximal to the distal tip of the fibula, at which point it becomes flat in shape and passes posterior to the fibula. The peroneus longus originates from the proximal two-thirds of the fibula, the intermuscular septum, and the lateral condyle of the tibia. Its tendinous portion is more rounded and overlies the brevis as it traverses posterior to the fibula. It eventually crosses the plantar aspect of the foot and inserts on the plantar aspect of the medial cuneiform (MC) and the base of the first MT. The distal fibers of the longus contain a sesamoid bone called the os peroneum. The tendons pass posterior to the fibula through the retromalleolar groove, a fibro-osseous tunnel created by the superior peroneal retinaculum (SPR), the posterior talofibular ligament (PTFL), the calcaneofibular ligament (CFL), and the posterior inferior tibiofibular ligament.
The longus and brevis hug the lateral wall of the calcaneus in individual sheaths and pass on either side of the peroneal tubercle before the brevis inserts on the fifth MT and the longus enters the fibro-osseous cuboid tunnel. The cuboid tunnel is formed by the long plantar ligament and the cuboid groove. It continues across the plantar aspect of the foot to insert on the MC and first MT as previously mentioned. The superior and inferior retinacula overlay the tendons spanning from the distal 2 cm of the fibula to the Achilles tendon and to the lateral calcaneus, respectively.
The peroneus tertius originates from the distal third of the anterior tibia, terosseous membrane, and the intermuscular septum. It inserts at the dorsal aspect of the fifth MT.1,2
Peroneal Tendinosis
Peroneal tendinosis is characterized by posterolateral ankle pain with swelling and tenderness over the peroneal tendons. There is thickening, nodularity, and focal tendon degeneration most often in the inframalleolar portion. Definitive diagnosis can be made with magnetic resonance imaging (MRI) or ultrasound. Pain is worsened with activity and usually resolves with rest. Treatment of mild cases consists mainly of rest, activity modification, nonsteroidal anti-inflammatory drugs (NSAIDs), and lateral forefoot posting orthosis. Some cases may require a CAM walker boot or short leg cast. For cases of refractory to nonoperative treatment, open synovectomy is the operation of choice.1,2
Peroneal Tendon Instability
Acute and chronic peroneal tendon instability can be differentiated by whether the instability is directly related to an acute injury. Many chronic cases are likely the sequelae of misdiagnosed injuries. The SPR is the primary constraint to dislocation/subluxation of the peroneal tendons. Acute injuries are commonly found in athletes after forced contraction of the peroneal tendons within the groove causing disruption of the SPR through its periosteal insertion on the fibula or subperiosteal elevation.2 It is hypothesized that lateral ankle instability is a risk factor for peroneal instability due to the finding that the CFL is strained in the dorsiflexed and inverted position limiting the space in the retromalleolar groove, a common mechanism increasing stress to the SPR.
Nonoperative management for peroneal tendon instability consists of immobilization and strapping techniques, but success is limited, leading many patients to require operative treatment.1,3 Cast immobilization for more than 6 weeks can be an alternative treatment for patients who are not operative candidates. Surgical treatment includes SPR repair, SPR reconstruction, rerouting procedures, bone block procedures, and groove deepening procedures. Each of these procedures has shown satisfactory outcomes, but each has its own complications. Bone block procedures in particular have a high rate of reoperation.1,4
Peroneal Tendon Tears
Peroneal tendon tears cause lateral ankle pain with activity and walking, tenderness to palpation over peroneal tendons, and lateral ankle edema. Acute tears tend to be less common than chronic tears, and like other peroneal tendon pathologies, they require a high index of suspicion for early diagnosis. Both acute and chronic tears are beginning to be recognized as more common than previously known, especially in combination with other lateral ankle pathology. Acute tears are most often found after ankle inversion injuries. Studies have shown a high incidence of peroneal tendon pathology in patients undergoing operative management of lateral ankle instability. In patients treated surgically for peroneal tendon pathology, up to 88% have peroneus brevis tears, 13% have tears of peroneus longus, and 38% have tears of both.2
A low-lying peroneus brevis muscle belly, a peroneus quartus tendon, or a bifid brevis tendon can “overcrowd” the retrofibular region and can cause tendon tears. This overcrowding can also be caused by tenosynovitis or hypertrophy. There are 3 specific areas in which longus tendons occur: the lateral malleolus, the peroneal tubercle, and the cuboid groove. The brevis tends to tear at the lateral malleolus where a sharp posterior fibular ridge can cause irrigation. A brevis split tear is thought to be caused by subluxation or compression between the longus and the fibula during forced contraction. Tears of both tendons are frequently seen in association with cavovarus foot and occur at the cuboid notch.5 Surgery is the mainstay of treatment for peroneal tears. The literature thus far has shown favorable outcomes for properly indicated surgical techniques.6
Peroneal Tenosynovitis
Peroneal tenosynovitis is caused by repetitive or prolonged trauma to the tendons. It can result from stenosis of the sheath due to
aforementioned causes of “overstuffing” the retrofibular space including a hypertrophied peroneal tubercle that was found to be associated with this condition. The pathology usually develops where the tendons change direction, similar to where the tendons are seen to tear. Nonoperative treatment is typically successful with a regimen that may include activity modification, ankle bracing or lateral wedge orthosis, physical therapy, and NSAIDs. Immobilization can be used for persistent cases. Cases refractory to nonoperative treatment can be successfully treated with synovectomy, débridement, and removal of any space-occupying structures.1,7
aforementioned causes of “overstuffing” the retrofibular space including a hypertrophied peroneal tubercle that was found to be associated with this condition. The pathology usually develops where the tendons change direction, similar to where the tendons are seen to tear. Nonoperative treatment is typically successful with a regimen that may include activity modification, ankle bracing or lateral wedge orthosis, physical therapy, and NSAIDs. Immobilization can be used for persistent cases. Cases refractory to nonoperative treatment can be successfully treated with synovectomy, débridement, and removal of any space-occupying structures.1,7
ACHILLES TENDON DISORDERS
Pathology of the Achilles tendon can be the source of significant functional morbidity and pain. Disorders of the Achilles tendon include tendonitis, tendinopathy, and tendon rupture. The Achilles tendon is formed by the 2 heads of the gastrocnemius and soleus muscles and inserts slightly medial to midline on the posterior aspect of the calcaneus. It acts primarily to plantarflex the foot but also imparts some inversion force. The tendon is surrounded by the paratenon, which is a highly vascular membrane continuous with the fascia and surrounding muscle that supplies blood to the tendon.
Achilles Tendon Rupture
Despite being the thickest, strongest tendon in the body, the Achilles is one of the most commonly ruptured tendons. A tear can be acute if diagnosed without 6 weeks of the injury or chronic if diagnosed greater than 6 weeks following the injury. The patient often presents with pain, swelling, and tenderness to palpation over the heel and Achilles tendon. There is often a palpable defect proximal to the calcaneus. Chronic tears can present with maintained plantar flexion without a palpable defect. These patients, however, can have calf weakness and ambulate with a limp.8
Ruptures commonly occur in middle-aged men during recreational activities, but can also occur in sedentary individuals. During explosive plyometric contractions, the Achilles tendon can experience forces 6 to 12 times the total body weight. Overloading of the tendon leads to degeneration and eventual rupture. An area 2 to 6 cm proximal to the calcaneal insertion is the most susceptible to tear due to its hypovascularity, smaller diameter, and large eccentric loads. Alterations in distal and proximal joint alignment alter Achilles mechanics, leading to shear stresses and increased eccentric load on the tendon. Blood flow and tensile strength decrease with age, increasing the risk of rupture.9
Treatment of Achilles tendon rupture is primarily surgical. For acute tear, surgical options include open or percutaneous tendon repairs. For chronic ruptures with tendon defects, reconstruction with VY advancement or flexor hallucis longus (FHL) transfer may be required.8
Achilles Tendinopathy
Achilles tendinopathy is a chronic, noninflammatory degenerative condition. It is classified as insertional or noninsertional. Noninsertional is further organized as peritendinitis, peritendinitis with tendinosis, or tendinosis. Patients may present with pain along the course of the tendon and weakness of plantar flexion. Poor vascularity, repetitive microtrauma, and age lead to chronic degeneration of the Achilles tendon. Other risk factors include diabetes, obesity, hypertension, steroid use, and estrogen exposure. Younger, more active patients more commonly develop peritendinitis, while older patients have peritendinitis with tendinosis.
Nonoperative treatment of Achilles tendinopathy is effective in up to 75% of cases. The mainstay of treatment is NSAIDs, activity modification, and eccentric strengthening. Cast immobilization can be used as well, if necessary. Surgical treatment is indicated after failure to improve with nonoperative therapy for 6 months. Surgical management may include Achilles tendon débridement and removal of the diseased tendon (sometimes necessitating augmentation with an FHL transfer), paratenon release, percutaneous tenotomy, or gastrocnemius lengthening.10,11
TIBIALIS ANTERIOR TENDON DISORDERS
Tibialis anterior (TA) tendon pathologies include both tendinosis and tendon ruptures.12 The TA originates from the anterolateral tibia. Distally, the TA tendon passes underneath the superior and inferior extensor retinaculum and inserts on the medial aspect of the base of the first MT and medial cuneiform. It is innervated by the deep peroneal nerve. The blood supply to the tendon is provided by the anterior tibial artery proximally and by branches of the medial tarsal artery distally. The TA functions as the primary dorsiflexor of the ankle. During the late swing phase of gait, the muscle dorsiflexes the ankle to allow clearance of the foot. At heel strike, the tendon contracts eccentrically to control and slow progression to the foot flat position. In addition, the anterior tibial tendon functions to assist with hindfoot inversion. The most commonly encountered TA tendon pathologies are tendinosis or tendon ruptures, which can be either traumatic lacerations or closed ruptures.12
TA Tendinosis
Tendinosis of the TA typically presents in 2 patient populations: it can present as medial foot pain in overweight women or as anterior ankle pain in athletes following an increase in activity.13 For the athletic population, tendinosis of the anterior tibial tendon is an overuse injury. On examination, these patients will have swelling and tenderness distinctly at the insertion of the tendon and their pain will be reproduced with resisted ankle dorsiflexion. A provocative maneuver is the TA passive stretch test, which has sensitivity of 90% and specificity of 95% for diagnosis of TA tendinosis.13 In this test, pain is elicited with ankle plantar flexion, hindfoot eversion, midfoot abduction, and an applied pronation force. There are also several key diagnostic physical examination findings that can differentiate tendinosis from TA tendon rupture. These include the preservation of ankle dorsiflexion strength, the absence of a drop foot gait, and the absence of a palpable defect in the tendon.12
MRI can confirm the diagnosis of tendinosis. Classic MRI findings are a thickened tendon with peritendinous edema, synovitis, and possibility longitudinal tears.14 Treatment is conservative and focuses on symptomatic management and ankle immobilization. Ankle foot orthoses (AFOs) are used to keep the ankle in a plantigrade position. Most patients improve with nonoperative treatment; however, for the few resistant cases, surgical management can be considered. Failure of conservative management may be related to the presence of longitudinal tears and loss of fibrillary structure in the tendon.12 Operative strategies in these cases includes tendon débridement or tendon repair with suture anchor fixation.15 In cases where greater than 50% of the tendon is involved, tendon augmentation with adjacent tendon transfer can be considered.15
