Anatomy

Three major ligament groups provide the support for the ankle group: the superficial and deep portions of the deltoid ligament, the tibiofibular ligaments, and the lateral ligament complex. The lateral ankle ligament complex of the ankle consists of three individual ligaments: the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL) and the posterior talofibular ligament (PTFL). The other support ligaments of the lateral ankle region are the lateral talocalcaneal ligament (LTCL), the ankle syndesmosis, with its ligaments, and the subtalar joint and its ligaments. The collateral ligaments of the ankle are arranged anatomically to afford joint dorsiflexion and plantar flexion, while concomitantly not restricting subtalar joint inversion or eversion. In addition to supporting and stabilising the ankle, allowing for sagittal plane dorsiflexion and plantar flexion, they aid in proprioception.

The ATFL is the most anterior ligament of the ankle. It consists of an upper and lower band and is intracapsular and intra-articular. It lies in a transverse plane crossing from the anteroinferior surface of the fibula to the body and neck of the talus just anterior to the lateral malleolar articular facet. The medial articular surface of the talus or medial facet articulates with the opposite medial facet of the medial malleolus. The lateral articular surface of the talus or triangular lateral talar facet articulates with the analogous lateral facet of the fibular malleolus. The dorsal surface of the talus is also known as the ‘trochlear surface’, and the inferior surface of the tibia, which articulates with the trochlear surface of the talus, is referred to as the ‘tibial platform’. That space lying between the lateral articular surface of the talus and the medial articular surface of the fibular malleolus is referred to as the ‘lateral gutter’, and the opposite space between the medial malleolus and medial surface of the talus is called the ‘medial gutter’.

The ATFL is a flat quadrangular ligament that is closely developed within the joint capsule, and is the most frequently injured of the three. The ATFL runs parallel to the long axis of the talus when the ankle is in neutral or dorsiflexion, but more perpendicular to the long axis of the talus in equinus (Leonard 1949). This anatomical design leads to a very tight ligament throughout plantar flexion. The ATFL has been shown via biomechanical testing of the ankle ligaments to have the lowest yield force and ultimate load of the lateral collateral ligament complex (Siegler et al 1988). The ligaments are usually injured, with the anterior talofibular being first, followed by the CFL, and lastly the PTFL. The extent of the injury will depend on the level of plantar flexion and inversion forces, as well as the position of the ankle when the foot strikes the ground. In 20% of the population the ATFL is absent, leading to potential instability, and acute and recurrent sprains of the lateral ankle.

The CFL is a taut ligament that originates on the distal inferior surface of the fibula. It descends to an insertion on the tubercle of the lateral portion of the calcaneus. It inserts in a posteroinferior direction under the fibularis (peroneus) tendons. It lies in the sagittal plane approximately 90° inferior to the ATFL. The CFL is an extracapsular, round, cord-like structure that is finely attached to the joint capsule and to the medial surface of the fibular (peroneal) sheath. The ligament is separated from the joint capsule by a thin fatty layer. It possesses the highest elastic strength of the three collateral ligaments, having a higher yield force and ultimate load than the ATFL (Siegler et al 1988). The CFL crosses over the superior portion of the ankle as well as the subtalar joint, and lies perpendicular to the long axis of the talus when the ankle is in neutral or in dorsiflexion. The ATFL and CFL create an angle of 105° when the subtalar joint is in neutral position. The CFL has the greatest resistance to inversion, and in cases of inversion mechanism injury both the ligament and the attached fibularis (peroneus) tendon sheath will be involved.

The PTFL, the strongest of the three lateral collateral ankle ligaments, is the least commonly injured ligament. It is an intracapsular structure, is trapezoidal in shape, and originates proximally from the posterior aspect of the fibular malleolar fossa and attaches distally to the posterior surface of the talus, the lateral tubercle of the posterior process of the talus and to the os trigonum, when present. The PTL has the highest yield force and ultimate load of the three ligaments (Siegler et al 1988).

The lateral talocalcaneal ligament is a smaller ligament that crosses over the lateral aspect of the subtalar joint, and may also be torn in cases of inversion mechanism injuries of the ankle. Another important structure subject to injury is the syndesmosis, which consists of the anterior and posteroinferior tibiofibular ligaments, the interosseous ligament and the interosseous membrane. In external rotation injuries the syndesmosis is frequently injured. The syndesmosis is one of the initial structures to be damaged in either a supination eversion injury or a pronation eversion injury.

The ankle is most stable in dorsiflexion, allowing the talus to be securely locked in the ankle mortise while providing for additional stability against inversion stresses. When the ankle plantar flexes there is more anterior talar translation (drawer) and talar inversion (tilt) (Johnson & Markold 1983). Although the ATFL is the main talar stabiliser, when the ankle is in a plantar-flexed position the talus will be held less securely and will be more unstable in the ankle joint mortise. In this position the ATFL will be under greater tension and subject to higher risk of injury.

In addition to the ATFL being subject to higher loads with inversion and plantar flexion, the CFL may also be subject to injury during high loads in increased inversion. Occasionally, discrete tears in the CFL occur if the foot is forcefully dorsiflexed and inverted. The PTF rarely suffers from injury except in severe cases of total dislocation of the ankle joint. Brostrom (1964, 1966) showed that 20% of inversion ankle injuries involve both the ATFL and CFL.

Ankle ligament injuries may be classified into one of three grades according to pathology, function and instability:

Special tests can be performed to determine ankle instability (Fig. 13.24). The anterior drawer and talar tilt (inversion stress) tests are manual stress tests designed to evaluate the integrity of the ATF and CFL. The anterior drawer test is performed with the patient’s knee flexed at least to 45° to relax the gastrocnemius. When patients extend the knee, this tends to alter the resistance to movement of the talus on the tibia. The patient’s heel is grasped posteriorly and the tibia is stabilised anteriorly with the other hand. As the calcaneus is pulled forward, a posterior force is placed on the tibia. This will allow the practitioner to translate the foot forward at the tibiotalar joint. A positive anterior drawer will reveal a so-called ‘suction sign’ overlying the anterolateral aspect of the ankle (between the lateral margin of the fibula and the talar trochlea), with greater than 4 mm of anterior displacement when compared to the contralateral uninjured ankle. This reveals incompetence of the ATFL (Anderson et al 1952, Schon & Ouzounian 1991). The talar tilt test is performed by grasping the lateral aspect of the calcaneus with one hand, while the medial aspect of the tibia is stabilised with the other hand.

Figure 13.24 Inversion stress posterior tibial tendon dysfunction.

With the ankle at 0° of dorsiflexion, the examiner inverts the calcaneus to its maximum. Under normal conditions, talus inversion is limited; however, when there is excessive excursion of the talus, the ATFL is suspected of rupture. Additional lateral dimpling is indicative of CFL injury or rupture. These tests should be performed with comparison with the contralateral side to rule out ligamentous laxity of an uninjured patient. In cases of acute injury local anaesthesia may be needed to perform the test adequately while preventing involuntary guarding by the patient.

Radiographic evaluation should be performed in addition to the anterior drawer and inversion talar tilt ankle joint stress views, and should include anteroposterior, lateral and mortise views of the ankle joint (Fig. 13.25). A stress inversion of 5–10° or greater of the injured versus uninjured side is considered to be pathological. An inversion stress of 18° or greater between the two sides is indicative of a double ligamentous injury (Pearlman et al 1992).

Figure 13.25 (A) Talar tilt ankle instability; (B) talar tilt ankle instability with inversion stress applied.

Karlsson et al (1989) found that anterior translation of the talus of 10 mm and talar tilt of 9° or more reliably indicate mechanical instability. The anterior drawer and inversion stress tests afford only a value in degrees and not a clinical picture. Ankles that have ligamentous laxity, or have higher than normal numerical values may indeed be normal and not show clinical signs of instability. Therefore, the clinician should not hold these study values to be a substitute for further investigation, nor should they be an empirical determinant for surgical intervention. An injury that produces syndesmosis can be evaluated using an external rotation stress radiograph. Widening of the tibiofibular clear space on the anteroposterior and mortise views of more than 6 mm indicates diastasis (Harper & Keller 1980).

Additionally, the extensor retinaculum and periosteal structures may also be involved in lateral ankle sprains. Upon radiographic evaluation the practitioner may notice an avulsion or osteochondral fracture associated with an inversion sprain. An avulsion fracture of the posterior aspect of the distal tibia can also be a sign of an injury causing syndesmosis.

There are a number of other tests that can be performed to determine ligamentous injury and ankle instability. These include:

Initial conservative treatment for an acute lateral ankle injury, as well as chronic ankle instability, has proven to be most reliable. The focus of attention for the patient is on functional rehabilitation (range of motion, muscle strengthening and proprioceptive training). Specific areas of strengthening should include the fibular (peroneal) muscles, with stretching and flexibility of the Achilles and anterior tendon groups. Initial treatment should include rest, ice, compression and elevation (RICE), and NSAIDs. Initial conservative treatment may also include short-term cast or Cam walker immobilisation to allow the capsular and ligamentous structure to heal. On occasion, continued passive motion machine (CPM) treatment may help to restore the range of motion in the sagittal plane. High-top athletic shoes, taping before sporting events, air splints, ankle braces and orthoses may all aid in the prevention of recurrent ankle injury. Sports that involve side-to-side movement may predispose to recurrent injury, and thus may force the participant to cross-train during the rehabilitation programme (Box 13.7).

In some cases the athlete may experience residual pain and swelling for 6 weeks after the initial sprain due to injury of the ligaments and inflammation of the ankle joint. Pain on palpation may be elicited overlying the ATFL, sinus tarsi and CFL. Inversion of the subtalar joint may also elicit pain. In severe ankle sprains, ankle ligaments may not heal properly, there may be malalignment of the ankle joint, capsular tissues may heal with fibrosis and scarring, with associated hypertrophied synovitis. Chronic lateral ankle instability with recurrent sprain in the athlete is estimated to develop in approximately 20% of the injuries, regardless of the treatment (Moller-Larsen et al 1988, Rijke et al 1988). The athlete who suffers from chronic lateral ankle instability is subject to chronic pain, swelling, inflammation, recurrent injury and reduced functional stability of the ankle. Subotnick (1999c) states that this, in turn, creates a psychological fear of re-injury, impairing maximum performance as well as causing loss of training time. If, after investigative studies have been performed and exhaustive conservative care has been rendered, recurrent injury prevails and performance is hindered, surgical repair of the athlete’s unstable ankle may be required.

Surgical repair for chronic lateral ankle instability can be classified as either reparative or reconstructive. Reparative procedures involve re-establishing damaged ligamentous structures, whereas reconstructive procedures involve re-routing harvested tendons or grafts to substitute for failed ligaments (Schon & Ouzounian 1991). Reconstructive procedures can be divided according to the number of ligaments being strengthened. Single-ligament reconstruction will involve the ATFL, whereas double-ligament reconstruction (which is performed to correct anterolateral rotary instability) reconstructs the ATFL and CFL; a triple-ligament reconstruction rebuilds all three lateral collateral ligaments. Many surgical procedures have been described for repair of lateral ankle instability. The Brostrom (1965) procedure is one of the most popular, involving periosteal augmentation flaps to repair stretched out or torn ATF and CF ligaments. This repair is performed without fibularis (peroneus) tendon or other tissue harvesting, thus minimising surrounding ankle tissue damage while reconstructing the ligaments in their true physiological orientation.

Arthroscopic surgical repair of ruptured lateral collateral ankle ligaments with the use of soft-tissue anchors has been a significant advance in the treatment of chronic instability in the athlete. Although technically more difficult to perform than the open stabilisation procedures, this procedure has negated the need for tendon harvesting, minimises the disturbance of adjacent soft-tissue structures and enhances recovery by reducing recovery time. For the athlete, all these are very important factors.

This author is quite aggressive with the postoperative treatment of these delayed primary ligament repairs. Initially, a Jones compression dressing with a posterior splint is utilised to hold the foot and ankle in 0° ankle joint dorsiflexion to provide stability and control immediate postoperative oedema. Seven days postoperatively the patient returns for the first dressing change, and the splint is replaced by either a fibreglass cast or removable cast brace. The advantage of the cast brace is that it allows for gentle CPM to begin at 7–10 days postoperatively. This motion helps to prevent the occurrence of postoperative adhesions, capsulardesis and reduced ankle joint range. The Cam walker is worn for 4–6 weeks postoperatively, followed by a more aggressive physical therapy programme involving muscle strengthening, flexibility and proprioception exercises. After 2–3 months the patient is allowed to slowly return to activities. An ankle brace and orthoses are highly recommended to initially provide for additional lateral support and to help improve early restoration of proprioception.

Chronic leg pain in the athlete

Chronic sports-related leg pain is a problem that many athletes experience. In the past, chronic lower leg pain was often regarded as ‘shin splints’ and recognised as an overuse injury due to excessive training or competitive-level participation. Today, the sports medicine specialist can target the underlying aetiology behind the development of the lower leg pain and determine the precise diagnosis. The goals for the specialist are specific: early and accurate diagnosis, a proper treatment plan, a specific rehabilitation programme, and prevention of recurrent injury.

There are many origins of sports-related lower leg pain. Tissues such as bone, muscle, tendon or insertion, ligament, nerves, arteries, veins and even skin can be the source of lower leg pain. The pain can be classified as traumatic or atraumatic in origin. Atraumatic exercise-induced injuries include medial tibial stress syndrome, stress fractures, gastrocnemius–soleus muscle strains, iliotibial band friction syndrome, tendinitis; compression syndromes (e.g. chronic compartment syndrome, nerve entrapment syndromes (fibularis (peroneus), tibial, popliteal)), arterial occlusion (popliteal artery syndrome) and radiculopathies, and muscle–fascial injuries, including fascial herniations, muscle soreness and muscle cramps. A number of authors have evaluated these conditions and have shown that a significant number of sufferers are athletes, particularly runners (Clanton & Schon 1993, Jones & Jones 1987, Orava & Puranen 1979, Styf 1989).

Tibial fasciitis – shin splints

Tibial fasciitis is an overuse inflammatory condition localised to the posteromedial crest of the tibia, with occasional involvement of the anterior crest of the tibia. Among runners and other athletes. This has been shown to be the most common cause of lower leg pain among runners and other athletes (Clanton & Schon 1993).

Tibial fasciitis is commonly referred to as posterior and anterior shin splints (Siocum 1967). The syndrome has been recognised as a medial tibial stress syndrome, resulting from overuse of the soleus fascia as it inserts on the posteromedial crest of the tibia, or the periosteal tissue beneath the posterior tibial muscle. Medial tibial stress syndrome may be due to either periostitis of the tibia or insertional fasciitis of the posterior tibial or soleus muscle; however, the clinician must exclude other possible entities, such as muscle strain of those same muscles, tibial stress fracture, deep posterior compartment syndrome and direct blunt injury to the muscle or bone. Detner (1986) developed a classification and management system for medial stress syndrome, dividing the overuse injury into three categories:

Medial tibial stress syndrome (MTSS) is due to overuse or beginning an exercise programme too vigorously. There has been general agreement that certain underlying biomechanical factors contribute to the development of MTSS. Excessive pronation of the foot, as well as exercising on hard surfaces, may enhance eccentric contractions of leg muscles and contribute to the development of MTSS (Michael & Holder 1977, Richie et al 1993, Vitasalo & Kvist 1983). For runners who are excessive pronators, prolonged muscle strain and fatigue will develop. As pronation increases due to elongation of the running gait cycle, there will be a need for increased supination by the posterior tibial tendon. In the shin splint syndrome, abnormal pronation will lead to fatigue of the muscles and reduce shock absorption. With traction enthesopathy along the lower third of the tibia, pain will develop due to the periostitis at the muscle attachment. This will create increased pressure on the fascia by the tendon unit, focused on the fascia–periosteum interface along the tibial crest. Impact shock transmits with every running or jumping step that is taken. These ‘shock waves’ are transmitted along the tibia, interfering with healing of the ‘stress reaction’ along the fascia–periosteum attachment. This will lead to further injury of reparative bone cells, and prevent remodelling of damaged bone. Without adequate rest time the process continues, and can worsen to the point where a stress fracture may occur.

The duration of symptoms can be divided into:

The location of the symptoms is divided into posteromedial, anterior and combination. The severity of the symptoms uses the functional pain scale grades 1 to 4:

Participants will describe recurrent pain along the posteromedial border of the middle and distal third of the tibia, which will have a gradual onset and is exacerbated by activity and running and relieved by rest. There will be no pain or symptoms in the foot or ankle. Mild swelling may be present. Physical examination reveals pain upon palpation along the posteromedial border and to a lesser degree along the anterior margin of the tibia.

The pain can range in severity from a dull ache to severe pain, particularly with prolonged activity. Neurovascular status is unaffected by MTSS.

Radiographic findings are usually negative for MTSS, except for mild localised thickening of the cortex. On occasion, the clinician may want to order a triphasic bone scan to differentiate between a simple shin splint and a stress fracture. Bone scans normally will reveal localised periostitis. Occasionally, MRI evaluation may help to pinpoint the exact location of the injury.

Stress fracture of the tibia and fibula

Stress fractures or fatigue fractures of the tibia and fibula are frequently seen in runners (Colt & Spyropoulos 1979, McBryde 1985, Markey 1987, Shelbourne et al 1988). The tibia is the bone most commonly involved (Belken 1980, Bennell et al 1996, Morris & Blickenstaff 1967). Morris and Blickenstaff (1967) used the term fatigue fracture to describe the application of mild forces or stress with eventual alteration or disruption of a material, such as bone. Therefore, a stress fracture is not the result of a single occurrence but rather an ongoing process. A fracture may be the end result, but it is the product of continued applied forces on the bone creating a weakness by resorbing bone in advance of the laying down of new bone. Stress fractures have been described in many sports (Morris & Blickenstaff 1967, Orava 1980a, Radel et al 1992).

There have been a number of explanations for the development of stress fractures. The first hypothesis (Stanitski et al 1978) contends that stress overload causes muscle fatigue, creating a loss in shock absorption and allowing excessive forces to be transmitted to the underlying bone. The second hypothesis (Taunton et al 1981) states that stress fractures occur secondary to repeated muscular forces acting on the bone. Cortical and cancellous bone each have intrinsic properties. When a force, either compressive or tensile, is applied to the bone, stress is generated within the bone. Strain is then produced by a relative change in length. The stress–strain relationship is linear until the yield length is reached. The linear portion represents the elasticity of the bone, whereas beyond the yield strength the bone is irreversibly deformed, until it reaches the breaking point. It is at that point that the bone collapses in compression and separates in tension. A stress or fatigue fracture can occur due to repetitive small loads, or from a single large load. During these load cycles, microfractures develop that are transmitted through the bone until loads increase sufficiently to cause microstress fractures, which produce symptoms or a fracture. Compression, tension and rotation are some of the forces applied to the bones by other bones, ligaments, and muscle origins and insertions. An example of this principle was shown by Devas and Sweetnam (1956) who showed that stress fractures of the fibula are due to the contraction of the calf muscles that pull the fibula toward the tibia. In this case, the tension above the distal fibula is maximised due to a rigidly attached fibular malleolus.

Wolff’s law prescribes that bone remodels to the stress placed upon it in fairly predictable patterns. When osteoclastic activity outweighs osteoblastic activity, the bone is in a weakened state. An athlete who continues to exercise is at higher risk of developing a stress fracture until bone remodelling is complete. Complete cessation of all athletic activity is essential to allow the bone to remodel and thus be able to withstand stress that will be applied at a later time. Markey (1987) described two ‘phases’ of stress fractures. The first phase, characterised by osteoclastic activity, and radiographically noted by its rarefaction or lucency, is referred to as the fracture phase. The second phase, described as the healing phase, is shown radiographically to have increased sclerosis, cortical thickening and/or callus formation. Another term used to describe the response of bone remodelling to stress prior to stress fracture is a stress reaction (Jones et al 1989).

Stress fracture of the tibia may occur either at the medial plateau or the shaft. Approximately half of all stress fractures in athletes occur in the shaft of the tibia (Morris & Blickenstaff 1967). In ballet dancers, the middle third of the tibia is involved (Miller et al 1975) and in runners the area most frequently affected is the middle and distal thirds of the tibial shaft (Devas 1958, Devas & Sweetnam 1956). Stress fractures may also occur at the medial malleolus due to distance running or basketball or American football (Shelbourne et al 1988).

Stress fractures of the fibula generally occur in the lower third of the bone (Barrows 1940, 1948, Devas & Sweetnam 1956). Stress fractures are also seen in the proximal third of the fibula (Blair & Manley 1980), and are thought to occur as a result of the powerful muscle forces of the soleus, posterior tibial, fibular (peroneal) or flexor hallucis longus across the fibula during jumping exercise (Symeonides 1980).

Usually the athlete will describe a significant change or increase in their workout schedule. For the runner, this will be demonstrated by a sudden increase in mileage, inadequate footwear or change of shoes, downhill running, harder running surfaces or greater intensity (speed).

The athlete may have just resumed a training programme after injury, or be unprepared at the commencement of a new training programme. There is a gradual, onset of pain that develops over several weeks. The pain will usually begin after stressful activity and then recede upon rest. In runners, pain will usually be described as occurring towards the end of the run, with the intensity increasing and ultimately reaching a point where the pain becomes so severe that the athlete has to cease running. With rest, the runner will ordinarily experience relief; however, on the resumption of running the pain will reoccur, to the point where it occurs during everyday walking. The key for the clinician is to recognise the onset of a stress fracture and advise the athlete to refrain from all activity, otherwise a return to training or competition could result in a season-ending injury.

Physical examination will reveal an area of well-localised tenderness overlying the tibia or fibula. There will be pain on palpation, percussion pain, increased warmth, oedema or erythema. The patient will be unable to perform the one-legged hopping test without pain, and when treated with ultrasound the pain will be elicited.

Initially after injury, radiographs will be negative; however, after 2–3 weeks of symptoms subtle changes may be evident. These changes will include a periosteal reaction, denoted by a cortical radiolucency indicating bone resorption, followed by an increase in radiodensity, indicating cortical bone formation and thickening. A technetium-99m bone scan is most helpful when plain radiographic films are negative and the clinician suspects a stress fracture. In cases of stress fracture there will be an increased local uptake of contrast medium, which can stay positive for over a year despite the fact that healing has taken place. A triphasic or triple-phase bone scan can offer additional insight into the nature of the injury – whether it is a soft-tissue injury or a fracture, or an acute or chronic injury (Rupani et al 1985).

Treatment includes rest for at least 6–8 weeks, and if severe and chronic, 12 weeks may be necessary to allow for adequate bone healing and to prevent further injury. With rest, symptoms will resolve, and substitute cross-training activities are recommended. In the case of competitive athletes, prolonged cast immobilisation and walking with crutches may be required. On occasion, for a delayed healing fracture or malunion, pulsating electromagnetic fields (bone stimulation) may be employed to accelerate the bone-healing process (Rettig et al 1988). After a sufficient period of rest the participant can then proceed to a period of supervised rehabilitation. Again, it is essential that the clinician emphasise to the athlete the consequences of too early a return to weight-bearing activities. A slow, progressive return to full-impact activity is advised, with periods of rest or cross-training to allow for adequate recovery. The type and location of the fracture will help to determine the length of time before return to competition. For some anterior midtibia fractures an entire year of non-impact activity may be required before a return to full competition standard (Clanton & Solcher 1994). The athlete is not encouraged to return to activity until they have no symptoms of tenderness, and have achieved full range of motion and near-normal strength from their rehabilitation programme. A semirigid pneumatic-type tibial brace that allows the athlete a speedier return to competition than conventional treatment has been used, and continues to be scrutinised (Box 13.9).

The more serious anterior midshaft tibia stress fracture initially described by Burrows (1956) commonly goes on to delayed or non-union (Green et al 1985, Rettig et al 1988) and may go on to complete fracture (Brahms et al 1980). Conservative treatment for this extreme case may prove difficult and may require surgical excision, with bone grafting, as well as percutaneous drilling and/or intramedullary rodding (Barrick & Jackson 1992).

The key to success for the athlete is prevention. Recognising the aetiological factors that would lead to this type of injury is essential – for instance, biomechanical considerations (leg-length discrepancy, high tibial varum, tibial torsion, excessive pronation or cavus foot type), muscle imbalances, distorted, worn-out athletic shoes, and inappropriate training programmes should all be evaluated.

Acute and chronic compartment syndrome

Chronic compartment syndrome (CCS), less common than the acute compartment syndrome (ACS), can sometimes be confusing and make the diagnosis rather difficult. CCS is a condition that results from abnormally high intramuscular pressure during exercise or shortly afterwards. It may also be defined as a condition in which increased pressure within a limited anatomical space compromises the circulation and function of the tissues within that space, resulting in temporary or permanent damage to muscles and nerves (Matson 1975). ACS is generally secondary to trauma, although rarely it may develop due to vigorous exercise. CCS is an exercise-induced condition, with recurring symptoms when exercise is resumed and reduced symptoms when exercise is ceased. In a study by Detner (1986) of the 100 consecutive operative cases of CCS approximately 70% involved runners.

Anatomy

The leg is divided into four compartments: the anterior, lateral, deep posterior and superficial posterior (Fig. 13.26). Each compartment is separated from the others by osseous and fascial boundaries, except for the superficial posterior compartment, which has no osseous boundary and is separated only by fascia. The nerves, blood vessels and muscles are encased in compartments surrounded by non-stretch structures. The anterior compartment fascia extends from the anterior fibular (peroneal) septa and encompasses the anterior crest of the tibia. The deep posterior compartment fascia inserts into the posteromedial crest of the tibia and generally intersects the deep transverse fascia, soleus fascia and superficial posterior compartment fascia to form the intermuscular septum.

Figure 13.26 The four compartments of the leg.

Everyday activity will result in an increase in capillary filtration to supply much-needed blood to the muscles. The muscles consequently will expand by 20–25% of their normal resting volume. Anteriorly, the crural fascia can expand to permit this increase in tissue volume. Compartment syndrome is caused by an increase in tissue pressure to a critical level, resulting in compromised tissue perfusion (Ashton 1975, Matson 1975). Physiologically, circulation to the microvasculature is impeded, creating a compromised condition of the intracompartmental musculature. Intracellular and extracellular fluid accumulation within the fascial space occurs. Venous and lymphatic compromise contributes to increased tissue pressure, creating further vascular compromise.

The typical history of the athlete with CCS is one of induced pain during exercise, or immediately upon conclusion of exercise, overlying the involved compartment. Pain will dramatically decline upon rest in the early stages. An aching or cramping pain will be described, even during simple walking. In the runner, however, pain will develop after a certain distance, time or intensity. Other symptoms may include shooting pains and leg weakness, with an inability to dorsiflex the foot (foot-drop), numbness and tingling to the leg, dorsum and plantar aspect of the foot, burning of the compartmental nerve, pain upon stretching of the involved muscles or tendons, a lump formation, or muscle herniation of the leg. Four nerves, each with sensory components, are present within the four lower leg compartments. It is rare to see all four compartments affected simultaneously but it is common to see bilateral involvement. The two compartments most commonly involved are the anterior and deep posterior compartments. Rorabeck (1986) postulated that compartment syndrome of the tibialis posterior could be regarded as a fifth compartment. With signs and symptoms of compressive neuropathy of the superficial and/or deep fibular (peroneal) nerves, the clinician should pay particular attention to those compartments. Muscle herniations through fascial defects have been found at a higher rate in compartment syndrome patients (approximately 30–60%) and can be a source of chronic pain with or without related nerve entrapment or compartment syndrome (Clanton & Schon 1993).

Radiographic evaluation is helpful to rule out other conditions that may be present, such as stress fractures, periostitis, occult bone tumours or acute trauma. MRI is advantageous because it provides a non-invasive means of assessing intracompartmental pressures simultaneously in all compartments (Amendola et al 1990). Another entity that may mimic a chronic compartment syndrome is intermittent claudication, which refers to a complex of symptoms characterised by pain in the muscles of the lower extremity with exercise; therefore, vascular examination may be required to rule out arterial insufficiency to that limb.

The diagnosis of CCS is first made on clinical evidence; however, measuring the intracompartmental pressure provides reproducible, objective documentation that is needed to confirm the diagnosis of CCS. There are four requisites necessary before the diagnosis of compartment syndrome can be made:

• a limiting anatomical envelope

• an increase in tissue pressure

• compromised circulation

• neuromuscular dysfunction.

There are a number of measuring systems that can be used to record pressures at rest, before and after exercise, and during exercise. They include the needle manometer, wick catheter, Rorabeck’s slit catheter and McDermott’s solid state transducer intracompartmental (STIC) catheter (for dynamic measurement of intracompartmental pressure) (Detner et al 1985, Mibarak 1981, Pedowitz et al 1990). CCS has also been described as an exertional compartment syndrome. Mibarak (1981) and Pedowitz et al (1990) developed criteria for the diagnosis utilising the wick catheter measurement of compartment pressure as follows. Utilising a wick or slit catheter technique under sterile conditions, the catheter is inserted into the involved compartment using local anaesthesia, and compartment pressures are then monitored at rest and during exercise. The presence of the catheter creates an exercise environment that produces pain, and eventually causes the subject to stop the exercise. Three pressures are recorded: the resting pressure, the pressure during exercise and the pressure after exercise – (1) pre-exercise pressure greater than 15 mmHg, (2) 1 minute post-exercise pressure greater than 30 mmHg, (3) 5 minutes post-exercise pressure greater than 20 mmHg. After 5 minutes the pressure levels should return to their pre-exercise levels. Levels can be monitored and, if the pressure exceeds the resting value by two times during exercise, a diagnosis of recurrent compartment (ACS or CCS) syndrome can be made.

If the ACS or CCS is confirmed, the goals of the athlete must be considered. If the athlete can reduce activities to a tolerable symptom level, surgery is not indicated. Conservative measures at this point are of little benefit, and the treatment indicated is surgical decompression by means of a fasciotomy of the involved compartment. The athletic patient should be thoroughly informed that they are at risk of developing an acute exertional compartment syndrome and that surgery has its inherent risks. Adequate decompression of the involved compartment is essential, without injury to the neurovascular structures or muscles below. Surgical decompressive fasciotomy has a 90% probability of producing significant improvement in or resolution of the symptoms (Martins et al 1984, Rorabeck et al 1988, Styf 1988). After fasciotomy there can be a decrease in strength by up to 20% of the compartment’s muscles (Garfin et al 1981, Mozan & Keagy 1969). The trade-off is that muscle weakness is usually offset by the tremendous pain relief and improved performance that the athlete will later achieve.

Muscle soreness

There are a number of additional lower leg problems that are exercise-induced. They do not fit into the category of overuse injuries or claudication syndromes; however, they have just as important an effect on the athlete. They include muscle soreness or delayed-onset muscle soreness (DOMS) (Armstrong 1984). Symptoms of DOMS usually increase in intensity within the first 24 hours after exercise, and peak at 24–72 hours, and subside over the next few days. DOMS can result from an overexertion of skeletal muscles, and although many people may experience DOMS, few ever seek medical attention.

Muscle cramps

Muscle cramps may occur in both the athlete and non-athlete alike. With muscle cramps, there is pain, a tightening of the muscle group, or both. Cramp is usually due to muscle fatigue, and the accumulation of metabolites during strenuous exercise, such as marathon running, triathlon swimming, cycling or running, or any other sport that involves prolonged muscle use or intensity. In some cases muscle cramps may require further investigation regarding their cause. Limb-length discrepancies, muscle weakness and inadequate preparation are just some of the potential aetiologies of cramp.

Muscle herniations

Muscle may bulge or herniate through normal fascial openings, through congenital fascial defects or via traumatic openings. Normal openings occur at the lateral or anterior compartment and in the deep posterior compartment. Congenital and traumatic herniations occur in the anterior and lateral compartments, and rarely overlying the medial or posterior leg.

Posterior tibial tendon dysfunction in the athlete

The posterior tibial tendon (PTT) is one of the main dynamic stabilisers of the hindfoot against valgus (eversion) deformity, and as such it is subject to repetitive overuse injury such as peritendinitis and rupture (Plattner 1989). PTT dysfunction has been described frequently as a form of progressive degeneration that may develop due to biomechanical conditions, such as excessive pronation. Often, PTT dysfunction is due to an intrinsic abnormality of the tendon. In cases of PTT dysfunction in which chronic tenosynovitis is a common predisposing factor, rupture of the tendon may often be seen (Mueller 1984). This is a chronic condition ranging from early swelling and pain, to chronic inflammation, to ultimate rupture. When the condition continues and chronic peritendinitis develops, the inflammatory process can cause the tendon to degenerate, gradually elongate, develop interstitial tears, and eventually rupture (Johnson & Strom 1989, Plattner 1989).

PTT dysfunction may have its origins in overuse, secondary to biomechanical and structural weaknesses, or may result from traumatic injury. With the increased participation in exercise and sport by people of all ages, the incidence of PTT tendinopathy has increased tremendously, particularly in older participants and in sports such as tennis, aerobic dance and walk/jogging.

Anatomy

The tibialis posterior muscle arises from the interosseous membrane and the adjacent surfaces of the tibia and fibula in the proximal third of the leg. The PTT is formed in the distal third of the leg encased in its own tendon sheath by the gathering of large muscle units (Fig. 13.27). The PTT travels posterior to the medial malleolus and anterior to the flexor digitorum longus, posterior tibial artery, vein and nerve, and flexor hallucis longus tendon, beneath the flexor retinaculum.

Figure 13.27 Anatomy of the medial longitudinal arch, illustrating the course of the posterior tibial tendon.

The tibialis posterior has multiple insertion sites on the plantar–medial aspect of the foot (Fig. 13.28). The most important insertion site is into the navicular tuberosity, with additional extensions into all three cuneiform bones, as well as the bases of the second, third and fourth metatarsals. As a result of this complex anatomical design and insertional attachment, the PTT is regarded as a plantar flexor of the ankle as well as a dynamic inverter (stabiliser) of the foot. During gait, the contraction of the tibialis posterior muscle creates subtalar inversion, locking both the calcaneocuboid and talonavicular joints and creating a rigid lever for forward propulsion of the foot over the metatarsal heads.

Figure 13.28 Insertion sites of the posterior tibial tendon.

Page 350

When the tibialis posterior does not function properly, inversion of the rearfoot will be greatly diminished. This will enable the overpowering of the gastrocnemius–soleus muscle group and will act on the medial column, more specifically the talonavicular joint. With this loss of PTT function, the fibularis (peroneus) brevis muscle and tendon act independently, which then creates a dynamic abduction and eversion force. As these dynamic forces occur (the action of the gastrocnemius–soleus muscle on the talonavicular joint, and the unopposed pull of the fibular (peroneal) brevis muscle and tendon), a gradual attenuation of the medial static constraints of the longitudinal arch occurs (Mann & Thompson 1985). Disruption of the tendon can result in a loss of integrity of the secondary soft-tissue support structures, namely, the deltoid ligament, talonavicular capsule and spring ligament of the mid- and rearfoot. These secondary static and dynamic restraints then become weaker, developing less mechanical advantage than the posterior tibial tendon, which eventually fails with repeated stress. This deformity of the tendon will create an increase in the valgus deformity of the calcaneus. The progressive deformity results in a medial subluxation (plantar flexion and adduction of the talus), calcaneal valgus and Achilles tendon rotation. Eventually, as this deformity of the PTT progresses, tightening of the Achilles tendon and heel takes place, contributing to the creation of an equinus deformity. Over a period of time of PTT dysfunction, a chronic malalignment of the talonavicular joint, medial column and rearfoot will occur. This flexible deformity continues to become more rigid and fixed with time. The relative strength of the tibialis posterior muscle is a function of its large cross-sectional area, and is greater than two times the strength of its primary antagonist, the fibularis (peroneus) brevis muscle (Sutherland 1966). Because the PTT has a short excursion, elongation of just 1 cm makes the tendon ineffective as the primary dynamic restraint to the longitudinal arch (Sutherland 1966). The deformity usually progresses to a painful flatfoot deformity, with pain described along the longitudinal arch, heel, medial ankle and sinus tarsi (Ross 1997).

History, physical examination and clinical findings

The history, physical examination and clinical findings of PTT dysfunction in the athlete reveal an overuse condition that, if diagnosed early in its course, can be treated successfully without further sequelae. The athlete with PTT disruption presents with a progressive acquired deformity of the foot and will have a painful flatfoot and difficulty in running or walking normally. The majority of PTT patients describe a gradual onset of the symptoms and the deformity, with disruptions of the PTT most commonly developing in women over 40 years of age (Funk et al 1986, Johnson 1983). Although the cause of PTT dysfunction is not known absolutely, it is believed to be multifactorial, with overuse being the underlying cause, resulting in a progressive degeneration and attenuation, with eventual partial or total rupture occurring when that tensile threshold has been reached. It has been suggested that the zone of hypervascularity between the medial malleolus and the navicular tuberosity is one of the major contributing factors in the development of PTT dysfunction (Frey et al 1990). This is also regarded as the most frequent site of degeneration. An underlying biomechanical weakness can be detected, such as a hypermobile first ray, an unstable medial column and longitudinal arch, and a functional calcaneal valgus. A poor biomechanical design of the tendon, as in a flexible flatfoot, will also predispose the tendon to mechanical abrasion as it courses around the malleolar pulley. In addition, leg-length discrepancy with asymmetrical pronation creating compensation also may be another contributing factor to the development of PTT dysfunction. This condition can be seen clearly when runners who pronate excessively run on one side of the road and back on the other side, or who constantly run in one direction (e.g. clockwise) on a track. This in itself creates a compensated short limb, and with the combined pronatory effect and flexible flatfoot the ingredients for PTT overuse injury are just right. It is rare to see ruptures of the PTT in young patients; however, traumatic PTT have been reported in the young athlete (Conti 1994, Woods & Leach 1991).

A clinical picture of PTT tenosynovitis reveals diffuse swelling, tenderness, warmth and pain at the medial aspect of the ankle and along the course of the tendon, into the medial proximal calf region. Patients will notice a progressive collapse of their longitudinal arch, ambulating on their medial ankle. It is often noted that abnormal shoe wear occurs towards the medial aspect of the outer sole of the heel. The runner, or other athlete, will describe fatigue in the early part of their activity, and a reduction in their ability to withstand prolonged activity. In some cases the athlete may be unable to participate altogether due to the pain and weakness of the foot.

Pain will be elicited over the medial aspect of the ankle by active inversion of the foot against resistance. Genu valgum of the knee may be seen, which can contribute to the painful flatfoot. The symptomatic foot will be abducted and will have a prolapsed or collapsed longitudinal arch. The athlete who presents with overuse injury and degeneration of the PTT will usually complain of pain distal to the medial malleolus. Radiographs are rarely useful in the evaluation of tenosynovitis (Kettlekamp & Alexander 1969). In advanced cases of PTT dysfunction lateral recess impingement involving the calcaneofibular ligament will occur, creating possible fibularis (peroneus) tendon irritation. In addition, a sinus tarsitis can develop with PTT dysfunction simultaneously.

Approximately half the patients with PTT recall a history of localised trauma (Mann 1993). It is essential to determine the exact location of the injury. Traumatic injuries that create partial or complete ruptures of the tendon will have focal pain at the insertion of the navicular bone. A traumatic eversion injury will affect both the spring ligament and the talonavicular capsule. Avulsions of the PTT at the insertion site of the navicular are not uncommon. Frequently, symptoms are related to athletic activity, with gradual weakness, fatigue and loss of strength during the propulsive (push-off) phase of gait. As a result of the instability of the medial column, deltoid ligament or spring ligament (plantar calcaneocuboid) insufficiency may contribute to the development of PTT dysfunction.

When PTT dysfunction has reached the final stages, pes plano valgus deformity will progress, causing a lateral shift in pain due to calcaneofibular impingement. Quite often the medial foot and ankle pain will resolve (Myerson 1996). In cases where the PTT has ruptured, inflammatory symptoms may be absent, while pain may be the major presenting complaint (Banks & McGlamry 1987). This can develop into an acquired flatfoot deformity, with inversion weakness or an inability of the rearfoot to invert at all. Weakness of the PTT can be seen by having the patient attempt to invert the rearfoot against a held plantar-flexed and everted position. This test isolates the PTT and attempts to neutralise the effect of the flexor hallucis longus and anterior tibial tendons from inverting the foot. It is helpful to be able to palpate the PTT posterior to the medial malleolus and feel it contract during inversion. A palpable contraction of the tendon with an acquired flatfoot deformity usually indicates that there is no rupture of the tendon. Rather, tendinitis, a partial tear of the PTT, rupture of the deltoid ligament or rupture of the spring ligament may be present. In some cases, excessive hypermobility of the talonavicular joint may be due to attenuation of the medial capsule and spring ligament complex.

Other tests for confirming injury to the PTT are the single-heel raise test and the ‘too-many-toes sign (Kerr & Henry 1989). A classic triad of deformities on weight bearing presents on physical examination:

• valgus deflection of the heel

• loss in height of the medial longitudinal arch

• abduction of the forefoot ((too-many-toes sign).

This triad reveals a lack of supination of the foot and inversion of the heel when attempting to rise up on the toes. Thus, an inability to lift the heel off the ground is indicative of PTT dysfunction.

Other symptoms may include midlongitudinal arch pain, secondary to increased stress on the PTT, creating a weakened condition and allowing for an overpulling of the fibularis (peroneus) tendons. A significant degree of tension is produced on the surrounding ligamentous tissue, thus creating a soft-tissue shear of the talonavicular, calcaneocuboid and Lisfranc’s joints. The end result, subluxation of the lateral midtarsal joint, then occurs, creating forefoot abduction. The tibialis anterior will then become the dominant overpowering force, allowing a forefoot supinatus to develop. This increased tension on the PTT causes a change in the vascularity and a weakening of the tendon as it courses behind the distal–posterior aspect of the medial malleolus. The most hypovascular region of the tendon begins at 40 mm from its insertion to the navicular tuberosity, 1–1.5 cm distal to the medial malleolus, and extending proximally for 14 mm (Frey et al 1990, Johnson 1983, Mann & Thompson 1985).

Radiographic evidence is not a necessity before making the diagnosis of PTT dysfunction (Funk et al 1986, Mann & Thompson 1985, Rey 1953, Teasdale & Johnson 1994); however, it is important in the staging of the deformity (Teasdale & Johnson 1994). Standard anteroposterior and lateral weight-bearing radiographs of both feet, including weight-bearing radiographs of the ankle, should be performed to evaluate the athlete who has developed an acquired flatfoot deformity secondary to PTT dysfunction.

Early in the process the radiographic findings will be normal to minimal changes in the angle. As the deformity progresses, anteroposterior views will reveal a lateral subluxation of the talonavicular joint as the navicular slips laterally upon the talar head (Johnson & Strom 1989). The lateral view shows plantar flexing of the talus, decreased height of the longitudinal arch, collapse of the medial column, and prolapse of the talonavicular, naviculocuneiform and metatarsal cuneiform joints. The axial view may reveal a valgus deformity of the calcaneus. Weight-bearing anteroposterior views of the ankle are also important, particularly in the later stages of the deformity, to determine whether there are any arthritic changes or whether talar tilt is present.

Tenography, CT and MRI have been used to determine the nature of the injury and the level of pathology to the PTT (Alexander et al 1987, Beltran & Moscure 1990, Hogan 1993, Rosenberg et al 1986). Tenography has been useful in the past to evaluate the PTT, but it is an invasive procedure and has not always had positive results (Alexander et al 1987, Funk et al 1986). It can be helpful, however, when there is a rupture of the tendon and the site cannot be located, or if adhesions and fibrosis have developed. However, injection of the contrast dye into the PTT sheath can often be a difficult procedure. CT is directed more towards identifying osseous lesions and has been used to identify severe soft-tissue injuries or abnormalities of tendons.

More recently, advances in the detection of the PTT injury and dysfunction have been achieved through the use of the MRI (Conte et al 1992, Rosenberg et al 1986). Due to its superior soft-tissue contrast resolution, MRI provides a more complete view of the pathological changes than does CT (Conte et al 1992). MRI is the method of choice in the determining of pathological changes of the PTT. An additional advantage of MRI is that there is no risk to the patient from exposure to ionising radiation.

Page 352

A variety of staging and classification systems have been developed for specific paratendinous structures. Funk et al (1986) developed a classification of four types of pathology involved with PTT dysfunction:

1. avulsion from its insertion along the navicular tuberosity

2. a midsubstance tendon rupture

3. discontinuity of tendon tears without complete rupture

4. an isolated tenosynovitis of the PTT (no tear of the tendon).

Conte et al (1992) also advanced a classification system of tears (types 1 to 3) of the PTT based on MRI. The classification reflects structural features and abnormal signals within the substance of the tendon:

• in type I, the magnetic resonance image reveals one or two fine, longitudinal splits in the tendon, without patterns of degeneration

• in type II, a wider longitudinal split in the tendon is seen, with intramural degeneration

• in type III, there is more diffuse swelling and uniform degeneration of the tendon; some strands of the tendon may remain intact, or the tendon may be replaced with scar tissue formation.

Johnson and Strom (1989) devised a classification system for the staging of PTT dysfunction which has been modified by Myerson (1996). They classified PTT dysfunction abnormalities into three distinct stages, based on the presence or absence of rearfoot or transverse tarsal deformities, and the ability to achieve flexible reduction of the involved articulation.

• Stage I reveals a normal length PTT affected by inflammation and associated peritendinitis or tendinosis. There is usually chronic medial ankle pain and swelling. The single heel raise test can be performed as the tendon is intact (Fig. 13.29). Only a mild weakness and minimal deformity are present in this stage.

• Stage II is a progressive process in which inflammation and degeneration occur, resulting in an elongated, attenuated PTT. As a result, secondary deformities develop as the midfoot pronates and abducts at the transverse tarsal joint. In addition, there will be a compensatory forefoot varus deformity. The longitudinal arch begins to flatten, whereas the rearfoot articulations remain normal in the non-weight-bearing state.

• Stage III is characterised by a condition in which a rigid rearfoot and forefoot deformity develops. The rearfoot will be rigidly everted, and the forefoot abducted.

• Stage IV demonstrates a valgus angulation of the talus, with concomitant degeneration of the ankle.

Figure 13.29 Posterior tibial dysfunction – single heel raise test.

Funk et al (1986) reported that if the inflammatory process of PTT dysfunction is not interrupted by either surgical or non-surgical means, a persistent tenosynovitis (stage I) will progress to stages II and III.

In cases of acute athletic injury to the PTT, conservative non-surgical treatment is valuable in the initial stages, particularly in the presence of various underlying medical conditions that might preclude surgical intervention. Although conservative treatment may be of great benefit in the early stages, there is no guarantee that it will arrest the degenerative process. The initial treatment for PTT injury includes rest, ice, elevation, compression, NSAIDs and various types of immobilisation. In the later stages of acute PTT tenosynovitis a cast is usually indicated for several weeks or even months. The patient may be permitted to walk while wearing the cast or removable boot. However, the more practical approach is to be non-weight bearing. A comprehensive biomechanical evaluation of the lower extremity and a gait analysis should be performed in patients who have developed a flatfoot deformity. A semirigid orthosis with medial control to decrease hyperpronation and eversion of the heel and subtalar joint during the midstance phase of gait or running is prescribed. In the later stages of PTT dysfunction, an articulated ankle–foot orthosis is recommended. Physical therapy has been used as an additional treatment in reducing pain, inflammation, oedema and crepitus in the tendon sheath. On occasion, corticosteroid injections into the sheath have proved helpful in the immediate reduction of symptoms, but these injections may cause focal necrosis and lead to spontaneous rupture of the tendon, and thus their general use is contraindicated (Fadale & Wiggins 1994, Myerson 1996).

Surgical intervention is indicated only in severe cases of chronic tenosynovitis or tendon disruption that have not responded to conservative treatment. In cases of chronic tenosynovitis, characterised by changes in the sheath with degenerative changes in the tendon (as in stage I), debridement is indicated, with incising of the tendon sheath and excising of hypertrophied synovium, and decompression. This will help to decrease painful symptoms and permit improved function. The same condition is seen in attenuation of the Achilles and fibularis (peroneus) tendons. If the tendon is hypertrophied, an elliptical resection with repair can be performed. In cases in which partial tears have occurred, debridement followed by repair is required. In some cases an enlargement of the osseous groove inferior to the medial malleolus may be indicated. The objectives of the procedure are to reduce the girth size of the tendon and to provide an enlargement of the fibrous osseous groove to improve function of the tendon. Proximal Z-lengthening, tendon grafting and the Cobb procedure (taking the distal half of the anterior tibial tendon) are other procedures for direct repair of the PTT.

Postoperatively, the foot is immobilised, first in a pressure dressing followed by application of a posterior splint cast. The foot is placed in a plantar-flexed attitude to reduce stress and traction on the tendon and to allow for early passive range of motion. The patient is immobilised for a period of 3 weeks, followed by mild dorsiflexion and plantar flexion, in addition to inversion–eversion, beginning with passive range of motion and advancing to active range of motion.

In cases of chronic tenosynovitis secondary to PTT malposition, with a hypertrophied and/or accessory navicular, a modified Kidner procedure (rerouting of the tendon, with resection of the hypertrophied navicular bone and/or accessory bone) can be done using a Mitek GII or Panaloc (absorbable anchor) with Panacryl (Surgical Products, Inc., Westwood, MA) tissue anchor. The use of one or two tissue anchors to support the tendon attachment against the denuded bone helps to secure the tendon and improve the mechanical advantage of the tendon. This procedure assists in decreasing both strain and traction on the PTT in an athletic patient who does not need a tendon transfer or arthrodesis procedure, and affords a much earlier return to competitive participation (Ross 1997).

Page 353

In severe stage II cases, transfer of the flexor digitorum longus (FDL) tendon is utilised. The procedure involves excision of the incompetent tendon or ruptured remains. While positioning the foot in plantar flexion and inversion, a side-to-side anastomosis of the PTT to the FDL tendon is performed and then into the navicular, together with partial translocation of the tibialis anterior into the navicular. The pulley posterior to the malleolus is recreated by repair of the flexor retinaculum (Funk et al 1986, Sutherland 1966). The distal stump of the FDL is tenodesed to the adjacent flexor hallucis longus. Tenodesis of the more proximal segment of the FDL to the myotendinous junction of the PTT is indicated only if the posterior tibial muscle has a normal colour and good elasticity (Goldner et al 1974, Johnson 1983, Mann & Thompson 1985). Immobilisation after this procedure may vary from 8 to 12 weeks.

Although the triple arthrodesis is regarded as the procedure of choice for patients with a severe deformity of the rearfoot with associated posterior tibial tendon dysfunction, long-term studies show that the procedure can lead to degenerative joint disease of the ankle and to the distal unfused joints. This is not a procedure for the athletic or extremely demanding active individual.

Athletic patients who are properly diagnosed as having PTT dysfunction and who are treated early in the onset of the disease with aggressive conservative management have a much more favourable prognosis and are able to return to sports participation much sooner. Even in cases where surgical intervention is inevitable, conservative treatment can serve as a stopgap measure.

Fibular (peroneal) tendinitis and tenosynovitis

The fibularis (peroneus) tendons and their synovial components can develop various conditions that may result in inflammation, pain, swelling or instability of the lateral ankle and lower extremity (Hatch 1994). Some of these conditions are a result of overuse, faulty athletic shoes, inappropriate training methods or traumatic injuries from a variety of sports that involve side-to-side or torsional activity. The fibularis (peroneus) tendons lie in a common synovial sheath, inferior to the superior fibular (peroneal) retinaculum, and then distally separate into their own sheaths. A thin mesomembrane separates the two tendon sheaths in the region of the fibular (peroneal) sulcus. The floor of the common sheath shares a close anatomical relationship with the talocalcaneal and calcaneofibular ligaments. Tears of the fibular (peroneal) retinaculum can result in anterior dislocation or recurrent subluxation of the fibularis (peroneus) tendons during impact exercise.

The fibularis (peroneus) tendons act by everting and plantar flexing the foot. They are also the primary lateral stabilisers of the ankle joint. Three types of injury to the fibularis (peroneus) tendons can occur in the athlete: overuse tendinitis, chronic subluxation and acute rupture. Biomechanical considerations, such as a plantar-flexed lateral column, can develop into a chronic subluxation of the cuboid, a fibular (peroneal) cuboid syndrome, or the two together. A forced dorsiflexion–eversion mechanism injury to the foot and ankle can result in acute traumatic fibularis (peroneus) tendon subluxation. This condition is seen in medial ankle sprains and is characterised by pain, chronic fibular (peroneal) tendinitis and instability of the ankle.

Fibular (peroneal) tendinitis is related to the pulley action of the lateral malleolus on the fibularis (peroneus) tendon. Mechanical stresses acting on the fibularis (peroneus) tendons as they course through the retrofibular sulcus cause a decrease in vascularity, chronic inflammation and degenerative changes. The athlete who presents with chronic fibular (peroneal) tendinitis will have pain in the retromalleolar area in addition to oedema and tenderness overlying the course of the tendon. When the clinician attempts to evert the foot against resistance pain will be produced overlying the tendon complex and lateral ankle.

Patients with chronic fibular (peroneal) tendonitis will relate a history of postinversion ankle injury, which was not severe enough to require immediate treatment at the time of injury. In addition to pain and tenderness along the course of the tendons, there may also be synovial oedema in the region. The task for the clinician is to determine whether one or both of the tendons are involved in the postinversion fibular (peroneal) tendinitis.

Treatment of painful, tender fibular (peroneal) tendinitis includes decreased activity, NSAIDs, ice massage and physical therapy. In some more severe cases, cast immobilisation may be necessary. Biomechanical factors should be considered, with orthoses being used to correct excessive supinated heel-strike. Rearfoot varus posting with a flange along the lateral margin of the device will assist in limiting stress on the fibularis (peroneus) tendons and limiting their traction.

In cases of a subluxing cuboid or fibular (peroneal) cuboid syndrome, cuboid manipulation may be performed. When pain is elicited along the plantar aspect of the foot from the cuboid to the first metatarsal, fibular (peroneal) cuboid syndrome should be suspected. Accommodative orthoses are recommended, with a 3–6 mm heel lift and a soft pad with a dancer’s cut-out under the first metatarsal. This allows relaxation and lengthening of this short tendon, preventing repeated traction and irritation. In a more severe case of fibular (peroneal) cuboid syndrome, in addition to manipulation of the cuboid a below-knee cast is applied, followed by active physical therapy and manipulation.

MRI or sonography of the lateral ankle region can assist in diagnosing chronic fibular (peroneal) tenosynovitis, focal degeneration and attenuation of the fibularis (peroneus) tendons. Standard radiographs may show an enlarged calcaneal tubercle, which may be responsible for chronic irritation, impingement and chronic synovitis. A CT scan can help in defining the retrofibular sulcus and assist in the planning of a surgical procedure to help correct the chronic subluxation of the fibularis (peroneus) tendons.

Overuse knee injuries

Overuse knee injuries are commonly seen in the practice of sports medicine. They occur when alignment is altered and when normal synchronous movement of the foot and lower extremity are altered. Examples of the causes of injuries of this type are a change or breakdown of footwear, unrelenting hard running surfaces, training, competitive techniques, equipment and biomechanical factors.

The athlete’s knee is frequently injured as a result of both direct trauma and overuse injury. Some of the common causes of knee pain in the sport participant include meniscal tears, patellofemoral joint instability, patellofemoral maltracking, patellar tendinitis, ligamentous injury (ACL, MCL, PCL, LCL), osteochondral injury (cartilaginous), chondromalacia patellae, and degenerative joint disease in the older exerciser. Some less common conditions are apophysitis of the tibial epiphysis (Osgood–Schlatter syndrome), discoid meniscus and knee plica, and some less common sources of knee pain in the athlete include (medially) semimembranosus tendinitis, pes anserinus bursitis, tibial collateral ligament bursitis and saphenous nerve entrapment. Anteriorly, less common sources of knee pain include Hoffa’s disease (proliferation of the fat pad following injury to the knee joint) and, laterally, iliotibial band syndrome, popliteus tendinitis and instability proximally of the tibiofibular joint. As the number of participants in sports and exercise increases, the sports medicine specialist is seeing these less common entities more frequently.

Signs

Physical examination will reveal some form of biomechanical malalignment of the lower extremity and feet. Such malalignments include femoral anteversion, genu valgum or varum, tibial varum, subtalar varus, rearfoot varus or valgus, forefoot varus or valgus, and excessive pronation (Fig. 13.30). Muscle imbalance or muscle weakness can also have a bearing on overuse injury. This may also include atrophy of the quadriceps muscle group, weakened or tight hamstring muscles, or a tight gastrocnemius–soleus complex, despite the fact that there are no signs of ligamentous injury, meniscal insufficiency, internal derangement or swelling of the knee joint. Often this condition does not reveal any true pathology of the knee joint. For this reason, the clinician must obtain the proper athletic training history and observe the gait thoroughly.

Figure 13.30 Tibial varum.

The patellofemoral joint

This joint is subject to mechanical overuse injuries. The patella acts to decrease the friction of the quadriceps mechanism as it passes over the distal femoral condyles (Ficat & Hungerfred 1977); the patella acts as the sesamoid of the knee (Fig. 13.31). It works in a pulley-like groove on the femur, and serves as a fulcrum for the action of the quadriceps muscles. It guides the quadriceps complex and centralises the various actions of the four muscles of the quadriceps. These forces are then transmitted to the patellar tendon. The purpose of the patella within the extensor apparatus is to protect the tendon from friction and allow the extensor apparatus to withstand high compressive loads. The patella lengthens the extensor arm, providing a mechanical advantage for the quadriceps (Kaufer 1971).

Figure 13.31 Overuse knee injuries: patellofemoral syndrome. (A) semimembranosus/semitendonosus tendinitis, (B) patellar tendinitis, (C) tibial plateau stress fracture, (D) Osgood–Schlatter disease, (E) biceps femoris tendinitis, (F) popliteal tendinitis, (G) iliotibial band friction syndrome.

Stability of the patellofemoral joint is due to a number of factors, including patellofemoral congruency, static ligamentous stabilisers and dynamic quadriceps and hamstring muscle stabilisers (Goodfellow et al 1976, Kaufer 1971). The patellotibial and the patellofemoral medial and lateral ligaments maintain proper tracking and keep the patella in the femoral groove (Kaplan 1962). The failure of any one of these stabilising factors will cause a malalignment and allow for unfavourable patellofemoral articulation, which will subsequently lead to increased loading on the articular surfaces.

Patellofemoral problems in runners

Patellofemoral joint pain is one of the most common stress-related injuries experienced by runners. Running biomechanics will guarantee a relatively smooth tracking of the patella in the femoral groove, and therefore it is unusual for the runner to experience an acute traumatic injury to the joint.

‘Runner’s knee syndrome’ is a mild lateral subluxation of the patella, and should not be mistaken for chondromalacia patellae. Runner’s knee can often be caused by an increased Q angle, or be due to excessive pronation of the foot (Fig. 13.32). Lateral shearing forces due to a malposition of the vastus medialis will cause subluxation of the patella over a runner’s career, and consequently will establish a new position for the patella to sit, thus creating an uneven pressure on the lateral surface of the femoral condyle. The patella will change shape appropriately as stress acts on it, causing it to adapt to this new position. Excessive pronation in running causes internal rotation of the tibia, thus increasing the impact shock to the patellofemoral joint region, leading to runner’s knee pain.

Figure 13.32 The Q angle.

Runner’s knee syndrome develops because of poor running mechanics, malalignment problems, an increased Q angle, tibial varum, internal tibial torsion, a weakened quadriceps muscle group, hard running surfaces and faulty shoes. Women, due to their increased Q angle secondary to an anatomically wider pelvis, are at greater risk of suffering from this disorder. The use of prescription orthoses can help realign the foot, thus reducing the Q angle and torque, torsion and stress to the knee joint.

Chondromalacia patellae

Chondromalacia patellae has been associated with abnormalities of patellar tracking as well as changes in the contact forces of the patella. Malalignment with recurrent subluxation of the patella is probably one of the most common causes of chondromalacia (Outerbridge & Dunlop 1975). In cases where recurrent subluxation of the patella occurs, there will be damage to the patellar articular cartilage. High Q angles create greater tensile stress on the medial and, more specifically, the odd facet of the patella. Tensile fatigue has a direct effect on the medial or odd facet, contributing to the formation of an ‘open’ chondromalacic lesion. A ‘closed’ lesion of the patella is a result of a high Q angle combined with normal compressive forces producing high shear stress. A third lesion located over the lateral facet consists of a very firm, sclerotic cartilage. High compressive contact stresses act on the lateral facet in this patellar tracking disorder.

Chondromalacia is caused by a combination of factors that eventually push the patella out of its groove on the femur. These factors include: weakness of the vastus medialis muscle; an increased Q angle, creating an overpowering of the vastus lateralis muscle; and malalignment of the lower limb, creating excessive foot pronation and leading to increased tibial torsion and increased stress on the knee.

Chondromalacia is a degenerative process on the retropatellar surface. This has been classified in stages, from an early onset to an advanced stage of arthritis (Key et al 1999):

• Stage I – a softening or degeneration of the articular cartilage

• Stage II – a cleaving of the articular cartilage

• Stage III – cleaving and fronds of the articular cartilage

• Stage IV – a wearing away of the articular cartilage to subchondral bone.

On physical examination, the runner will complain of generalised, deep knee pain. In some cases, pain may be associated with the tracking areas of the patella, or the undersurfaces of the femoral condyles. The knee may be swollen, with a chronic effusion of synovial fluid. In severe cases, the clinician may elicit a positive patellofemoral grinding test. As previously mentioned, a high Q angle may be seen, as well as a patella that is malaligned. Quadriceps muscle testing will reveal a weak vastus medialis and a high insertion into the patella. The most important radiographic view is the axial or ‘skyline’ view, also known as the ‘sunrise’ or ‘sunset’ views. The infrapatellar view will consistently reveal the inferior surface of the patella in relation to the femoral condyles, without other bone projections obscuring the view. By taking views of both knees simultaneously, the clinician can determine both the morphology and the position of the patella in relation to the trochlear facets (Fig. 13.33). Radiographs may reveal osteophytic ‘spurs’.

Figure 13.33 Patella and trochlear groove.

Page 357

To make the correct diagnosis of chondromalacia patellae, several differential diagnoses should be eliminated. These include: chronic synovitis, meniscal lesions, fat pad syndrome, pre-patellar bursitis, retropatellar bursitis, infrapatellar tendon tendinitis, medial synovial plica syndrome, pes anserinus bursitis and sprain of the retinaculum.

Conservative treatment is the most prudent plan, consisting of salicylates, NSAIDs, patellar stabilising devices, icing, ultrasound, nerve stimulation, massage, and a change of running programme and running surfaces. Intra-articular steroid injections are not recommended, as collagen and protein synthesis is reduced. Quadriceps exercises and iliotibial band stretching are highly recommended, particularly if the patient is a runner. Realignment of the maltracking patella can be accomplished with the use of orthotic therapy. Steadman (1979) has stated that pronation of the foot increases the patellofemoral angle, creating pressure and symptoms in the patellofemoral joint, and that either soft or rigid orthotics can be helpful in this disorder.

Surgical intervention consists of a lateral release with a concomitant medial imbrication of the vastus medialis to achieve a proximal realignment. Arthroscopic local debridement of the articular lesion is helpful if confined to one facet or if the chondromalacia is grade II or III in severity (McCarroll et al 1983).

Knee plica

The synovial plica is an embryonic fold or septum traversing the anterior compartment of the knee, and separating the suprapatellar pouch from the main body of the knee. In the embryo, the kneecap is surrounded by a large bursa that differentiates into the prepatellar, suprapatellar and the infrapatellar bursae (Fig. 13.34). These bursae can completely resorb during adulthood and fall into folds superiorly, laterally and medially. Commonly found in runners, these lesions can be asymptomatic, or can cause a great deal of pain and discomfort. Early in the course of patellofemoral pain the clinician should examine for the presence of a synovial plica. In athletic activity, trauma, overuse or long-distance running can cause the plica to become inflamed, thickened and fibrosed. A large plica can fold under the patella and cause lateral displacement. A medially fibrous type plica may also mimic a meniscal tear. This same plica can extend transversely across the joint and can insert into the medial aspect of the infrapatellar fat pad. During running, when the knee flexes and extends, this fibrous plica will run across the medial femoral condyle and create a great deal of pain.

Figure 13.34 Bursae at the knee: (A) suprapatellar; (B) pre-patellar; (C) infrapatellar; (D) pes anserinus (lateral view).

The examiner can feel a shelf while the knee is flexed at about 30–40° and the thumb is rolled over the medial side of the patella. This test, referred to as the ‘thumb roll’, will elicit a snap or click that will be painful and strongly guarded. Arthroscopic evaluation may determine that the meniscus is normal, while a thickening of the synovial fold indicates that a synovial plica is present. This lesion may be excised arthroscopically, and the procedure has been proven to be very successful in eliminating knee pain in the athlete.

Iliotibial band friction syndrome

Iliotibial band friction syndrome is a painful, debilitating overuse injury that affects runners, particularly long-distance runners such as marathon runners and ultra-runners, and cyclists. This inflammatory disorder is an overuse injury caused by excessive friction from the iliotibial band (ITB) as it passes over the lateral femoral excrescence and possibly at Gerdy’s tubercle (Fig. 13.35). The injury develops as the knee flexes and extends during running, creating a friction ‘rub’ over the lateral femoral condyle, which is responsible for the inflammatory response. As the iliotibial tract passes distally, it remains in contact with the lateral intermuscular septum of the quadriceps muscles and inserts into a tubercle on the lateral tibial condyle. Some suggest that the ITB acts as an anterolateral stabiliser to the tibia (Kaplan 1958, Terry et al 1986). In extension, the ITB lies anterior to the lateral epicondyle of the femur, and as flexion over 30° occurs, the ITB passes over the condyle. Another underlying factor is that of significant tightness of the ITB, which is prevalent among many athletes and runners. Those runners who suddenly increase their mileage, increase intensity or include hill training in their programme are subject to developing this overuse injury. Runners who have biomechanical abnormalities such as a high degree of tibial varum, who are excessive supinators on heel strike, or who have hyperpronation after midstance are also more prone to this overuse injury. The pain will often be most intense at heel strike, while attempting to decelerate the limb (Nobel 1980). At the onset of the disorder, pain may develop after an extended run. When runners warm up adequately, painful symptoms seem to diminish. However, in more severe or chronic cases, the lateral knee will hurt even while running – the longer the distance run, the more severe the pain – with residual post-run effects. Other aetiological factors involved in the disorder include genu varum, an abnormally prominent lateral femoral epicondyle, and internal tibial torsion.

Figure 13.35 Insertion of the iliotibial band (lateral view).

The ITB is a thickening of the fascia lata that extends from the iliac crest to insert into the lateral tibial condyle. The band is developed by insertions from the tensor fascia lata and gluteus maximus muscles. The syndrome is due to the inflammation of the ITB and bursa as well as the underlying periosteum of the lateral femoral condyle. Other differential diagnoses include patellofemoral dysfunction, biceps femoris tendinitis, popliteus tendinitis, lateral plica, lateral meniscus injury, degenerative joint disease and stress fracture.

The clinical presentation of ITB friction syndrome is generally tenderness at the point where the ITB slides over the lateral excrescence or at Gerdy’s tubercle. Pain may also extend along the course of the ITB, and may radiate proximally or distally. On occasion, soft-tissue swelling may be present, and there may also be palpable crepitus present at the same site. A positive ITB test will confirm the diagnosis. The test is performed by the clinician placing a varus stress upon the knee, and then fully extending and fully flexing it. During extension the ITB slides anteriorly, and during flexion it passes posteriorly. It is this sliding over the femoral excrescence that reproduces the pain. Another way of reproducing the pain is by means of the Nobel test: the lateral femoral epicondyle is palpated by the thumb, where no pain had been elicited previously. On occasion, if needed, MRI or an ultrasound scan can be employed to confirm the diagnosis (Ekman et al 1994).

Treatment for the early stages of the condition includes adequate stretching and warm-up, with heat or topical rub before a run, followed by additional stretching and ice massage afterwards. An ITB stretching programme is highly recommended for athletes with ITB friction syndrome (Box 13.10).

In addition to the ITB stretching, rest or altering activity (e.g. shortening the duration of the training activity, avoiding hills, shortening stride length, changing directions on a circular or banked track, and running back on the same side of a crowned street) is advised, with controlling the inflammation process being the ultimate goal. Cyclists may need to change the height of their seat or their foot position on the bicycle pedal (Holmes et al 1993). When pain persists when running, alternative training programmes should be instituted, such as swimming, aqua-running and weight training. Cycling may exacerbate the ITB pain, and therefore should not be done.

Symptomatic treatment may also include iontophoresis, with a cortisone preparation. Bursal cortisone injections may also be employed in more severe cases. Again, initially ice should be used, followed by heat, whirlpool, ultrasound and NSAIDs. If the patient cannot run or exercise without pain after a course of alternative exercise and treatment, total rest for 4–6 weeks is recommended. For the most part, the great majority of athletes will respond favourably to conservative care (Box 13.11). Correction of biomechanical abnormalities may require only a simple insole or longitudinal arch support. However, in cases where there is an uncompensated inverted rearfoot, a prescription orthosis may be needed to prevent an excessive supinated heel strike, thus reducing the traction and stress on the ITB.

After 12 months of unsuccessful conservative treatment, surgical intervention may be considered. Release of the ITB at its attachment to the patella is one particular procedure that may be employed, as may a bursectomy.

Popliteus tendinitis

The popliteus muscle originates from the lateral femoral condyle and has a wide insertion on the posterior tibia above the soleal line. It passes superolaterally and anteriorly under the arcuate ligament, forming a tendon about 1 cm distal to the joint line. The tendon functions by:

This muscle will help stabilise the femur against forward displacement on the fixed tibia, particularly when running downhill.

For runners who run on a track, or a banked track, pain may be experienced on the lateral aspect of the knee, due to the internal rotation of the tibia on the femur.

Popliteus tendinitis is an overuse injury that is commonly seen in athletic individuals, particularly downhill runners and skiers, and those with excessive pronation.

Physical examination will reveal localised tenderness overlying the tendinous origin and along the lateral femoral condyle.

Treatment includes NSAIDs and restricting all downhill running, application of ice for acute symptoms, followed by whirlpool or moist heat, ultrasound, knee stretching and strengthening exercises. Alleviating stress to the popliteus is imperative. This can be accomplished by changing the side of the road or direction of running on a banked track, and by running uphill, not downhill.

Hamstring tendinitis

Injuries to the hamstring are due to a short flexor group. An athlete who does not stretch routinely or adequately is prone to a hamstring strain. Therefore, it is imperative that before engaging in any athletic activity the hamstring muscle group should be properly stretched. This is of particular importance before sprinting, running or during pre-season training. Careful attention during running to overstriding and/or oversprinting can help to prevent a hamstring injury.

Injury to the hamstring can occur at any site along its course. A strain will occur as a result of a sudden overextension of a tight hamstring, and be located either at the hip or the knee. Once a hamstring has been injured it will always be vulnerable to re-injury due to its intrinsic weakness.

On clinical examination, the hamstring will appear to be tight, and in cases where a partial or complete rupture has occurred there will be swelling, ecchymosis and/or haematoma formation. Pain will be elicited at the site of the injury, which is most commonly at the midthigh, or at the ischial tuberosity. A marathon runner who had experienced a cramp early in the race may have gone on to a partial rupture in the later stage of the race. Consequently, the runner will have pain against resistance, and may be unable to bear weight without excruciating pain.

In addition to tight hamstring muscle groups, repeated hamstring ‘pulls’ should alert the sports practitioner to the possibility of biomechanical malalignment. Examples include excessive subtalar pronation, genu valgum, internal rotation of the tibia, short limb and pelvic tilt.

In cases of internal tibial torsion, the origin of the hamstring and the insertion will be stretched and twisted, particularly in the latter stages of the propulsive phase of running. This also can be an underlying cause of injury, but will not be apparent to the untrained eye.

In cases of recurrent strain or pulls, or in chronic hamstring tendinitis, a biomechanical evaluation is essential to rule out poor foot imbalance and lower limb malalignment. In addition, muscle testing is also important to determine whether, for instance, the quadriceps muscle group is stronger than and overpowering the hamstring group. Muscle strengthening and flexibility exercises are essential to prevent recurrent injury. In some cases certain forms of sport may need to be altered or eliminated to prevent further injury. A daily stretching exercise programme to maintain flexibility and a pre-exercise warm-up should be part of the normal routine.

Groin injury/strain

A groin strain can be an extremely painful and debilitating injury, and it is commonly seen in sports such as soccer, football, tennis, rugby, and in sprinters, long-distance runners and other track and field events. The term groin strain incorporates many other conditions that cause pain in the groin region. The groin pain may occur suddenly, or be brought on by a series of traumas secondary to overuse. The structures involved in this area include the adductor muscles, inguinal ligaments, the pubis symphysis and ramus, the gracilis, the iliopsoas and the piriformis. A groin injury may be a result of a sudden violent overstretching of the leg in abduction and external rotation, particularly when there is an opposing force.

A groin injury may develop suddenly or insidiously, and the associated pain may be sharp or dull. In many cases the structure(s) involved may be difficult to identify. The injury presents in the early stages with a mild ache, following activity, which is then relieved by rest, but quickly returns during the subsequent period of activity. As the injury becomes more chronic, the pain will increase in severity, begin earlier in the activity and take longer to subside, until it reaches a point where there is a constant dull ache or pain. At this stage even walking may be painful. To test for the site of the pain, passive and active assisted motion of the patient’s hip with the leg extended in all directions, particularly abduction and external rotation, followed by careful palpation of the groin structures to pinpoint the site of injury is required.

For the most part, unless the injury was attributed to a sudden traumatic event, one should suspect a biomechanical origin. The most common aetiology for this biomechanical injury is a limb-length discrepancy, where the short limb pronates for a longer period of time than the longer limb. The hyperpronated foot creates a scenario in which increased internal rotation of the limb occurs, tilting the pelvis forward on that side. This effect on the limb, including the adductor muscle group and the iliopsoas, is to function with a twist, as the pelvis tilts downward. The adductor serves an important purpose in providing stability for the pelvis, particularly in sprinting as well as long-distance running. Functional control of the abnormality is essential to prevent recurrent or further injury.

Rest is the key to allow for healing of the groin strain or injury. Once the athlete stops all activity, pain subsides and the condition will resolve. In addition to rest, physical therapy, anti-inflammatory medication, and a well-designed and properly supervised rehabilitation programme should be part of the athlete’s post-injury care to return to a competitive level. Another goal in the treatment of groin injuries is to re-establish biomechanical control to the foot and limb. Limiting excessive pronation of the foot will assist in eliminating the twist in the leg, and in addition help to reduce some of the adverse effects of the limb-length difference. The use of orthotic devices will help to achieve this goal, while simultaneously helping to correct the pelvic tilt. The addition of a 4–7 mm heel lift to correct that imbalance or leg-length discrepancy is advised. To prevent groin injuries, the pelvis and lower extremity must be conditioned to withstand forces generated by the patient’s particular sport. Strengthening the groin muscles with exercise performed against resistance, and repetitions to build strength as well as endurance will help prevent recurrent injury. To maintain range of motion, special stretching exercises of the groin incorporating proprioceptive neuromuscular facilitation techniques should be used (Pink 1981).

Shoe manufacture

There is now a shoe for just about every sport (see also Ch. 18). Although the shoes may vary greatly in terms of their specifications, their inherent structure is basically the same throughout (Fig. 13.36).

Figure 13.36 Parts of the sports shoe: (1) last; (2) combination last construction; (3) upper – synthetic material and mesh for ventilation; (4) motion control device; (5) Achilles flex notch; (6) heel counter; (7) inner sole, removable; (8) midsole; (9) outsole.

Lasts

As with most other footwear, sports shoes are made on lasts. The process that follows may be slip lasting, where the upper of the shoe is stitched around the last with the closure being along the length of the sole. Shoes made using this process are flexible and lightweight; they do not give much control of the foot, and are usually chosen for racing.

Another process is board lasting, where the upper is stitched to a board that has the shape of the inner sole. This produces a much firmer shoe, which gives the foot much more stability and is a good base for orthotics. However, it may require some time for the shoe to be ‘worn in’.

A third form is combination lasting, in which the front part of the shoe is slip lasted and the part of the shoe from just behind the metatarsal heads to the heel is board lasted. This combination gives good stability, but because of the more flexible forepart is not so heavy and difficult to wear at first (Fig. 13.37).

Figure 13.37 Lasts: (A) fully board lasted; (B) slip lasted; (C) combination lasted.

Shape of the last

There are three basic shapes of last, the first of which is the straight or semi-straight last. This has only the slightest inflare along its medial border and is considered the most supportive; it should be chosen for overpronating low-arched and pronating feet.

Page 362

The second, and most common, shape is the semicurved last, which has a greater degree of inflare along the medial border. It offers some medial support but not quite as much as the straight last, and is used for the vast majority of the population.

The third type of last is the curved last, which is used for racing shoes and lightweight trainers, as it has the greatest amount of inflare along the medial border and provides the least amount of support. It is chosen for higher arched feet that tend to be more rigid and for mid- to forefoot strikers. The shoe is flexible and lightweight (Fig. 13.38).

Figure 13.38 Lasts: (A) semi-straight last; (B) semicurved last; (C) curved last.