Recurrent Ankle Sprains
Ankle sprains, especially of the lateral ligaments, are extremely common injuries in the athletic population. Despite the vast amount of research in this area, recurrences remain common. The recurrence rate for lateral ankle sprains has been reported to be as high as 80%.1 In one study, 75% of the ankle sprains in professional soccer players were in ankles with previous sprains or instability.2 In another study, the incidence of developing chronic ankle instability was 20-40% of those who had previously sustained an acute ankle sprain.3 Neuromuscular and proprioceptive deficits are thought to be related to chronic ankle instability, including functional and mechanical insufficiencies.4
This article focuses on recurrent sprains, with emphasis on the lateral ligaments. This article also discusses medial instability, subtalar instability, and syndesmotic instability. Conservative treatment is explored, as well as surgical options for refractory or severe cases.
For excellent patient education resources, visit eMedicine’s Sprains and Strains – First Aid and Emergency Center, Sports Injury Center, and Procedures Center. Also, see eMedicine’s patient education articles Ankle Sprain and Ankle Arthroscopy.
Related eMedicine topics:
Ankle Injury, Soft Tissue
Ankle Sprain [in the Physical Medicine and Rehabilitation section]
Related Medscape topics:
Resource Center Exercise and Sports Medicine
Resource Center Trauma
CME/CE Medical Interventions Effectively Treat Overuse Injuries in Adult Endurance Athletes
Mechanical instability (MI) relates to the laxity of the ankle joint that is caused by structural damage to the connective tissue that supports that joint. Functional instability (FI) refers to the recurrence of joint instability and the sensation of an unstable joint because of neuromuscular deficits, as opposed to structural deficits. For example, delayed activation of the peroneal muscles (everters such as the peroneus longus and brevis) that are innervated by the superficial peroneal nerve in response to sudden inversion perturbations has been hypothesized as a cause of FI following a lateral ankle sprain. Hertel and Valderrabano et al believe there is a distinct relationship between FI and MI in those patients with recurrent ankle sprains.1,3
Many studies demonstrate that MI is related to various proprioceptive changes, resulting in an accompanying FI. As a joint develops MI, proprioceptive changes may occur, resulting in alterations in those defense mechanisms that prevent injury. The result is a joint that continues to be stressed beyond its physical limitations, leading to MI and FI of the joint.1,3 Note, however, that not all patients who develop MI develop FI. These are exceptional cases.
With respect to grade III ankle sprains, the average duration of disability has been reported to range from 4.5 to 26 weeks, and only 25-60% of patients are symptom free 1-4 years after injury. Staples noted that 42% of those with grade III lateral sprains treated nonoperatively were still symptomatic at follow-up, but severe disability was uncommon.5 Others have reported a 20-40% incidence of residual FI after conservative treatment of grade III lateral sprains.
Brand et al evaluated athletes at the United States Naval Academy.6 The authors found that 10% of the incoming freshmen described functional ankle instability, and 17% of those who were studied reported a functionally unstable or “trick” ankle. In the study, FI was defined as frequent sprains, difficulty running on uneven surfaces, and difficulty cutting or jumping. Despite these findings, it was unclear from the study what proportion of symptomatic instability resulted from tibiotalar laxity versus subtalar instability.
Although no incidence studies concerning subtalar instability appear to exist in the literature, Larsen claimed that subtalar instability may occur in 10-25% of individuals who have chronic functional ankle instability.7 Chronic ankle instability in this study was defined as recurrent giving-way for at least 6 months despite adequate nonsurgical therapy.8
Isolated sprains of the medial ankle ligaments are unusual. Deltoid ligament injuries typically occur in association with lateral ligamentous or bony injury.9
Syndesmotic sprains have an estimated incidence of 10% of all ankle sprains. In a study at the United States Military Academy, Hopkinson et al reported an incidence of 1%.10 In another study, calcification of the distal tibiofibular syndesmosis was found in 32% of professional football players attending training camp, which suggests a higher incidence.11 The probable reason for the discrepancy between the 2 studies is that radiographic stress views are necessary for the diagnosis of instability, and these are not routinely performed.
The exact etiology of recurrent ankle sprains is unknown. However, many factors may play a role, such as the following:
Some believe the primary cause to be ligaments healing in a lengthened position due to scar tissue filling in the gap between separated torn ends. Furthermore, the weakness of the healed ligament may be due to the inherent weakness of the scar.
Bosien et al reported that 22% of his patients with recurrent ankle sprains had persistent peroneal weakness.12 He believed that this contributed to recurrent injury, especially in the incompletely rehabilitated ankle sprain.
An unrecognized disruption of the distal tibiofibular ligament has been cited as a potential culprit. This condition is diagnosed based on tenderness over the anterior syndesmosis and pain when the fibula is squeezed against the tibia at mid shaft, with dorsiflexion and external rotation or with excessive medial-lateral motion of the tibiotalar joint.
Hereditary hypermobility of joints has been named as a possible etiology.
Freeman et al suspected that FI that resulted in recurrent sprains was secondary to loss of proprioception of the foot.13 Mechanoreceptors and their afferent nerve fibers have been shown to exist in the ligaments and capsule of the ankle. Furthermore, disruption of the ligaments and joint capsule with grade III sprains leads to impairment of the reflex stabilization of the foot. This results in the foot giving way.14 Dysfunction of the peroneal nerve can also result in delayed muscle response, causing a delay in the activation of the peroneal muscles and leading to FI.
A sixth causative factor is impingement by the distal fascicle of the anteroinferior tibiofibular (AITF) ligament, impingement of the capsular scar tissue in the talofibular joint, or impingement by both.
Related eMedicine topics:
Peroneal Tendon Pathology
Peroneal Tendon Syndromes
In lateral sprains, the most commonly injured ligament is the anterior talofibular ligament (ATFL). The disruption typically occurs mid substance, but bony avulsions of the talus and fibula have been reported. The second most common injury is a combination rupture of the ATFL and the calcaneofibular ligament (CFL), usually mid substance. Isolated tears of the CFL are rare and may play a role in subtalar instability.9
In medial sprains, deltoid ligament rupture can occur after pronation-eversion, internal rotation, forced plantarflexion, or forced dorsiflexion. Usually, in forced abduction injuries, rupture of the superficial deltoid ligament occurs first, followed by the deep ligament. The deep deltoid ligament has been shown to have the highest load to failure compared with the lateral complex.9 (See the Relevant Anatomy section for a detailed description of the pertinent anatomy.)
In syndesmotic sprains, most clinicians agree that the most predominant causative force is external rotation. This injury can occur with abduction, but that process would be accompanied by failure of the deltoid ligament and the medial malleolus. Persistent external rotation can tear the interosseus ligament and membrane in addition to the AITF ligament. The posteroinferior tibiofibular (PITF) ligament is usually preserved.9 O’Donoghue et al suggested that, in athletes, syndesmotic sprains are the result of hyperdorsiflexion of the ankle.15 Note, however, that no study has been able to produce a purely ligamentous injury to the syndesmosis with an externally applied force.
In subtalar injuries, high-energy supination trauma to the ankle and hindfoot causes injury. The most frequently injured ligaments in these cases are the calcaneofibular, followed by the lateral talocalcaneal, then the cervical interosseus, and finally, the talocalcaneal. These injuries typically occur with lateral ankle joint instability, although isolated injuries have been reported.
Subtalar sprains have been classified into 4 types based on the mechanism of the injury and the ligaments that are damaged, as follows:
Type 1 injuries consist of a forceful supination of the hindfoot with either plantarflexion or dorsiflexion of the ankle. In these cases, the ATFL and the cervical ligament (CL) are torn.
Type 2 injuries are similar to type 1 injuries, except the interosseous talocalcaneal ligament (IOL) is also ruptured.
Type 3 injuries occur when the ankle is in dorsiflexion and the ATFL is intact.
Type 4 injuries are a combination of a severe talotibial and subtalar ligament injury. The mechanism is a forceful supination of the hindfoot while the ankle is primarily in dorsiflexion but subsequently rotated into plantarflexion.
Pisani described a mechanism that causes injuries to the IOL that was occurring in triple jumpers and basketball players.16 The injury results from a sudden impact and deceleration of the calcaneus, with inertial progression of movement of the talus.
Related eMedicine topics:
Fractures, Tibia and Fibula
Talofibular Ligament Injury
When obtaining a history, ask the patient about the mechanism of injury, as well as why, when, where, and how it occurred. Often, however, the patient’s account of the mechanism does not correlate with the structures that have been damaged. Patients often report twisting the foot. The time of onset of swelling is important. Patients may hear a pop at the time of the injury. Also, patients should be asked about their past ankle injuries, their goals regarding functional results, the level and intensity of their sports and activity, and their medical history.
Chronic medial ligament instability is uncommon, but it produces discomfort on the medial side of the ankle and is associated with slight valgus and abduction of the ankle with each step.
Patients with subtalar instability may report giving-way symptoms of the foot during activity and a history of recurrent instability, pain, swelling, and stiffness. The symptoms are often vague, and distinguishing between subtalar and tibiotalar instability is difficult. Patients may also have pain over the sinus tarsi or deep pain in the subtalar area. This sinus tarsi syndrome can be a component of subtalar instability, with tenderness to palpation over the sinus tarsi and pain upon forced inversion of the foot. Increased internal rotation of the calcaneus is also a common finding, and excessive distal displacement of the calcaneus may occur in relation to the talus compared with the normal side. Subtalar instability should be regarded as contributing to the patient’s symptoms, especially in a high-energy injury.
On physical examination, one should look for areas of tenderness and swelling. Areas of point tenderness should especially be identified so that a ligamentous correlation can be established. Ecchymosis may be present. Note, however, that blood usually settles along the medial or lateral aspects of the heels. Thus, the location of the ecchymosis may not correlate with the location of the injury. Also, active range of motion must be assessed because Achilles tendon ruptures can mimic ankle sprains. In lateral sprains, passive inversion should reproduce the symptoms. Plantarflexion should also exacerbate the symptoms because this motion stretches the ATFL to its maximum.
As with all limb injuries, the neurovascular status of the limb must be assessed. This assessment consists of palpation of the dorsalis pedis and posterior tibial arterial pulses and testing for sensation, especially over the sural nerve distribution. Sural nerve and peroneal nerve palsies, although rare, are complications of a lateral ligamentous injury. Electromyographic examinations of individuals with severe ankle sprains have shown that 80% of these patients have some degree of peroneal nerve injury.
The anterior drawer test is performed to test the stability of the ATFL. The examiner attempts to translate the foot anteriorly with respect to the leg by gripping the heel. The foot should be in 10 º of plantarflexion. This takes any slack out of the tendon being tested and removes any bony stability that would give a false-negative test result. The patient’s knee must be flexed to relax the gastrocsoleus complex, and the examiner must support the foot perpendicular to the leg.
Sometimes a dimple appears over the area of the anterior talofibular ligament on anterior translation. This is a dimple or suction sign and may appear with pain; muscle spasms are minimal. This test is not very reliable, especially if the findings are negative while the patient is not under anesthesia, because of muscle guarding by the patient. The normal amount of translation is 2 mm. Reports indicate that 4 mm of laxity in the ATFL provides a clinically apparent test result.
The inversion stress maneuver, also known as the talar tilt test, is an attempt to assess the CFL integrity. In many cases this is difficult, if not impossible, to perform secondary to patient pain and swelling. The patient should lie supine or on the side, with the foot relaxed. The gastrocnemius must also be relaxed by flexion of the knee. The talus is then tilted from side to side into adduction and abduction. The findings should be compared with the contralateral side.
The prone anterior drawer test is another test for ligamentous instability. The patient must lie prone with the feet extending over the end of the examining table. The examiner then pushes the heel steadily forward with one hand. A positive test result consists of excessive anterior movement and a dimpling of the skin on both sides of the Achilles tendon.
The Kleiger test can demonstrate the integrity of the deltoid ligament. The patient sits with the knee flexed to 90 º. The foot must be relaxed and not bearing weight. The foot is gently grasped and rotated laterally. A positive test result occurs when the patient has pain medially and laterally. The talus may displace from the medial malleolus, indicating a tear of the deltoid ligament.
In patients with suspected syndesmotic injuries, pain in the area of the syndesmosis can be elicited if the fibula is squeezed at the mid calf. Note that pain should not be felt at the site of the pressure, but rather in the lower leg. The anterior drawer and talar tilt tests should produce negative results. The most revealing test is external rotation of the affected foot while holding the leg stabilized, with the knee flexed at 90 º (also known as the Kleiger test, mentioned above). In syndesmotic injuries, this test produces pain at the syndesmosis.
See Medical therapy.
Lateral ligament anatomy and biomechanics
The lateral complex of ligaments has 3 components: the ATFL, the CFL, and the posterior talofibular ligament (PTFL) (see Image 1). When referring to the subtalar joint, the lateral complex has 5 structures: the CFL, the inferior extensor retinaculum (IER), the lateral talocalcaneal ligament (LTCL), the CL, and the interosseus talocalcaneal ligament. Note that the CFL spans both the tibiotalar and talocalcaneal joints.
In addition to the general anatomy of the ankle, note the biomechanical function of each component in stabilizing the joint. In dorsiflexion, the ATFL is loose and the CFL is taut. This is reversed in plantarflexion; the ATFL is taut and the CFL is loose. The PTFL is maximally stressed in dorsiflexion. Biomechanical studies by Attarian et al in 1985 demonstrated that the ATFL has a lower load to failure than the CFL.17 The maximum load to failure of the CFL is roughly 2-3.5 times greater than that for the ATFL.
On the other hand, the ATFL can undergo the greatest amount of deformation (strain) before failure and allows for internal rotation of the talus during plantarflexion in contrast to the CFL and PTFL. The ATFL primarily restricts internal rotation of the talus in the mortise. When in plantarflexion, the ATFL also inhibits adduction. The CFL prevents adduction and acts virtually independently in neutral and in dorsiflexed positions. The PTFL inhibits external rotation with the ankle in dorsiflexion. Note that medial ligaments are the primary restrictors of dorsiflexion and that the PTFL only assists in this function. The short fibers of the PTFL can also restrict internal rotation after the ATFL has been ruptured. After disruption of the CFL, the PTFL inhibits adduction with the ankle in dorsiflexion.
During forced dorsiflexion, the PTFL can rupture. With forced internal rotation, ATFL rupture is followed by injury to the PTFL. Extreme external rotation disrupts the deep deltoid ligament on the medial side. Adduction in neutral and dorsiflexed positions can disrupt the CFL. In plantarflexion, the ATFL can be injured.
Medial ligament anatomy and biomechanics
The deltoid ligament is divided into 2 portions: the superficial and deep deltoid ligaments (see Image 2). The superficial deltoid ligament originates from the anterior colliculus (an anterior bony prominence) of the medial malleolus. The tibionavicular portion inserts onto the tarsal navicular and is the most anterior part. The tibiocalcaneal portion begins at the anterior colliculus and inserts onto the sustentaculum tali. The final component of the superficial deltoid is the posterior tibiotalar ligament (PTTL). The deep deltoid ligament originates from the intercollicular groove and the posterior colliculus. It is shorter and thicker than the superficial portion and is contiguous with the medial capsule of the ankle joint and the medial portion of the IOL. It is divided into the anterior tibiotalar ligament and the PTTL.
Biomechanically, the deltoid ligament primarily prevents abduction. After division of both components of the deltoid ligament, anterior instability of the ankle does not increase. Once the lateral ligaments are cut, the deltoid ligament acts as a secondary restraint against anterior translation. The fibular ligament primarily inhibits lateral translation of the talus. The deep deltoid provides the greatest restraint against lateral translation. In order to tilt the talus in valgus within the mortise, both the superficial and deep deltoid ligaments must be completely ruptured.
The syndesmosis of the ankle refers to the membrane connecting the tibia to the fibula. The tibia and fibula are connected throughout their lengths by an interosseous membrane. However, 3 definable ligaments are found at the ankle: the AITF ligament, the PITF ligament, and the interosseous ligament. The AITF is the most commonly injured ligament in syndesmotic sprains. The PITF has 2 components: a deep portion (called the transverse tibiofibular ligament) and a superficial portion. The interosseous ligament is the shortest of the tibiofibular interconnections and is considered the primary bond between the tibia and fibula. Superiorly, the interosseous ligament is contiguous with the interosseous membrane, which provides some additional strength to the syndesmosis.
Biomechanically, a certain amount of motion is allowed in all planes with respect to the distal ends of the tibia and fibula. When the ankle goes from full plantarflexion to full dorsiflexion, the distance between the lateral and medial malleoli increases by approximately 1.5 mm. Rotation of the tibia on the talus can also occur while a person is walking. This rotation can be as much as 5-6°.
Ogilvie-Harris and Reed experimentally demonstrated the importance of the syndesmotic ligaments to ankle stability.18 By sectioning the ligaments, the authors concluded that the AITF ligament provides approximately 35% of ankle stability; the deep PITF, 33%; the interosseous PITF, 22%; and the superficial PITF, 9%. Rasmussen demonstrated that the ligaments of the syndesmosis play little role in the stability of the ankle as long as the other ligamentous structures are intact.19 Furthermore, no study exists in which a purely ligamentous injury to the syndesmosis has been produced through externally applied stress (namely, external rotation and abduction).
Subtalar joint and ligament anatomy and biomechanics
The subtalar joint can be divided into anterior and posterior articulations that are separated by the sinus tarsi and the tarsal canal (see Image 3). The anterior subtalar joint (talonavicular) is formed by the anterior portion of the talus, the posterior surface of the navicular, the anterior part of the calcaneus, and the calcaneonavicular ligament and the fibrous capsule. The posterior talocalcaneal portion is formed by the posterior facet of the inferior surface of the talus and the corresponding posterior facet of the calcaneus.
The primary ligaments of the talocalcaneal joint are the CFL, LTCL, CL, and the IOL. The CL is believed to be the strongest bond between the talus and calcaneus. Harper categorized the ligamentous structures of the subtalar joint in layers.20 The superficial layer consists of the lateral root of the IER, the LTCL, and the CFL. The intermediate layer consists of the intermediate root of the IER and the CL. Finally, the deep layer contains the medial root of the IER and the IOL.
From a biomechanical standpoint, the motion of the talocalcaneal joint is flexion-supination-adduction or extension-pronation-abduction. The motion occurs via talar ovoid surfaces moving over calcaneal ovoid surfaces. Sectioning studies by Kjaersgaard-Andersen et al showed that sectioning the CL resulted in a 10% increase in rotation, and sectioning of the IOL produced a 21% increase in rotation.21 In earlier studies, the same authors found a 77% increase in adduction at the talocalcaneal joint after sectioning the CFL.22 The authors’ findings emphasize the importance of the CFL in providing lateral stability to the subtalar joint. This is contrary to a study by Cass et al that demonstrated no such influence on subtalar motion.23 The discrepancy among the studies may be explained by the variability of orientation of the CFL. Trouilloud et al identified 3 primary anatomic variants, as follows24 :
Type A (35%): An LTCL blends with or reinforces the CFL.
Type B (25%): A distinct LTCL is present just anterior to the CFL.
Type C (42%): The LTCL is absent. When the CFL is injured in a type A and C anatomic variant, increased subtalar motion is expected.