Chapter Objectives
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Explain the arthrokinematic considerations that influence motion in the joints of the foot and ankle.
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Explain the concentric and eccentric action of muscles in the lower leg, ankle, and foot.
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Recognize structural abnormalities in alignment of the lower leg, rearfoot, and forefoot.
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Describe key components in evaluation of injuries involving the lower leg, ankle, and foot
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Describe common athletic pathologies and rehabilitative management of lower leg, ankle, and foot injuries.
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Explain the biomechanical principles and clinical practice of orthotic therapy.
The lower leg, ankle, and foot contain 26 bones, all working as one unit to propel the body. The foot has three components: rearfoot, midfoot, and forefoot. The structure of the rearfoot and midfoot is provided by the tarsal bones. The rearfoot contains the subtalar joint, with the talus resting on top of the calcaneus. In the midfoot, the navicular and cuboid articulate with the talus and calcaneus to form the transverse tarsal joint. The three cuneiform bones are located within the midfoot. Five metatarsal and 14 phalangeal bones make up the structure of the forefoot. The shape of the joint, orientation of its axis, supporting ligaments, and subtle accessory motions at the joint surface are important determinants of normal biomechanical behavior. Treatment of pathologic hypomobility or hypermobility is predicated on a thorough understanding of these principles and their functional intimacy.
Arthrokinematic considerations
Tibiofibular Joint
The tibiofibular joint provides accessory motion to allow greater freedom of movement in the ankle. Fusion or hypomobility of this joint can restrict or impair ankle function. During ankle plantar flexion, the fibula slides caudad at the superior and inferior tibiofibular joint and the lateral malleolus rotates mediad to cause an approximation of the two malleoli. With dorsiflexion, the opposite accessory motions provide a slight spread of the malleoli and accommodate the wider portion of the anterior talus. Accessory motion of the tibiofibular joint also occurs with supination (calcaneal inversion) and pronation (calcaneal eversion). The head of the fibula slides distally and posteriorly with supination and proximally and anteriorly during pronation.
Talocrural Joint
The talocrural articulation is a synovial joint with a structurally strong mortice and supporting collateral ligaments. The concave surface of the mortice is made up of the distal tibial plafond and the tibial (medial) and fibular (lateral) malleoli. Within the mortice sits the convex surface of the talar dome. The joint derives ligamentous support from the deltoid ligament medially and the anterior talofibular, calcaneofibular, and posterior talofibular ligaments laterally.
The lateral malleolus is positioned distally and posteriorly relative to the medial malleolus, which causes the axis of motion for the ankle joint to run in a posterolateral inferior to anteromedial superior direction ( Fig. 20-1 ). This oblique orientation allows triplanar motion. Sagittal plane plantar flexion and dorsiflexion make up the primary movements of the joint and are coupled with adduction and abduction, respectively. Because the axis is nearly parallel to the transverse plane, inversion and eversion are negligible components of motion. The available range of motion is typically defined as approximately 20° of dorsiflexion (with the knee flexed) and 50° of plantar flexion.
A small amount of talocrural physiologic accessory motion also accompanies plantar flexion and dorsiflexion. As the foot plantar-flexes, the body of the talus glides anteriorly. Conversely, as the foot dorsiflexes, the direction of talar glide is posterior. Maximal stability with angular and torsional stress occurs in the close-packed position of maximal dorsiflexion, in which the talus slides posteriorly and wedges within the mortice. The resting position of the ankle joint is 10° of plantar flexion ( Table 20-1 ).
| Joint | Close-Packed Position | Resting Position | Capsular Pattern |
|---|---|---|---|
| Talocrural | Maximal dorsiflexion | 10° plantar flexion | Plantar flexion restricted more than dorsiflexion |
| Subtalar | Maximal supination | Neutral | Increasing loss of varus until fixed in valgus |
| Midtarsal | Maximal supination | STJ neutral | Limitations in adduction and inversion |
| First MTP | Maximal dorsiflexion | Slight plantar flexion | Gross limitation in extension; slight limitation in flexion |
Subtalar Joint
The talocalcaneal articulation provides the triplanar motions of pronation and supination. The medial and lateral collateral, interosseous talocalcaneal, and posterior and lateral talocalcaneal ligaments support the joint.
The joint axis runs from dorsal, medial, and distal to plantar, lateral, and proximal. It is oriented approximately 16° from the sagittal plane and 42° from the transverse plane ( Fig. 20-2 ). Because of this axis of orientation, the joint provides the triplanar motions of pronation and supination. The pronation components of motion in an open kinetic chain are calcaneal dorsiflexion, abduction, and eversion. Conversely, open kinetic chain supination consists of calcaneal plantar flexion, adduction, and inversion. Functionally, however, the subtalar joint operates as a closed kinetic chain. Closed kinetic chain motion occurs when the distal segment is fixed and the proximal segment becomes mobile, as when the foot is in contact with the ground. The distal or terminal joints meet with considerable resistance, which prohibits or restrains free motion. During the weight-bearing portion of the stance phase of gait, friction and ground reaction forces prevent the abduction-adduction and plantar flexion–dorsiflexion elements of open kinetic chain subtalar motion. To counteract these forces, the talus functions to maintain the transverse and sagittal plane motions of supination and pronation. Thus, in closed kinetic chain motion, subtalar joint pronation consists of talar plantar flexion–adduction and calcaneal eversion, whereas subtalar joint supination consists of talar dorsiflexion-abduction and calcaneal inversion ( Fig. 20-3 ). Note that the calcaneal direction of movement is unaffected by the open chain versus the closed chain type of motion ( Table 20-2 ).
| Motion of Foot | Open Chain Component (Non–Weight-Bearing Motion) | Closed Chain Component (Weight-Bearing Motion) |
|---|---|---|
| Pronation | Calcaneal eversion | Calcaneal eversion |
| Calcaneal abduction | Talar adduction | |
| Calcaneal dorsiflexion | Talar plantar flexion | |
| Supination | Calcaneal inversion | Calcaneal inversion |
| Calcaneal adduction | Talar abduction | |
| Calcaneal plantar flexion | Talar dorsiflexion |
The subtalar joint couples the function of the foot with the rest of the proximal kinetic chain. The prime function of the subtalar joint is to permit rotation of the leg in the transverse plane during gait. Rotation of the talus on the calcaneus allows the foot to become a directional transmitter and torque converter to the kinetic chain. These characteristics allow the foot to be a loose adaptor to the terrain in midstance and a rigid lever for propulsion.
Because the subtalar joint is angulated approximately 45° from the transverse plane, 1° of inversion or eversion occurs for every 1° of tibial internal or external rotation. This relationship can be observed in gait. As the subtalar joint pronates, the tibial tuberosity is seen to be rotating internally ( Fig. 20-4 ). High angles of inclination (> 45°) of the subtalar joint axis cause a relative decrease in calcaneal inversion-eversion motion and increased tibial rotation motion that leads to posture-related pathologies secondary to poor absorption of ground reaction forces. Conversely, an athlete with a low angle of inclination (< 45°) of the subtalar joint demonstrates a relative increase in calcaneal mobility that results in more foot-related overuse and fatigue problems secondary to the calcaneal hypermobility.
The physiologic accessory motions of the subtalar joint occur in the frontal plane. The convex portion of the posterior calcaneus glides laterally during inversion (supination) and medially during eversion (pronation). The close-packed position of the subtalar joint is maximal supination, whereas the resting position is the subtalar neutral position. From its neutral position the subtalar joint can supinate approximately two times as much as it can pronate. This motion is measured in the frontal plane of calcaneal inversion and eversion. Normal subtalar range of motion is approximately 30°, with two thirds of that motion being represented as calcaneal inversion and one third as calcaneal eversion. Normal gait requires at least 8° to 12° of supination and 4° to 6° of pronation.
Midtarsal Joint
The midtarsal joint consists of the talonavicular and calcaneocuboid articulations. They derive their ligamentous support from the calcaneonavicular (spring), deltoid, dorsal talonavicular, and calcaneocuboid (long and short plantar) ligaments.
The midtarsal joint has two separate axes, longitudinal and oblique. Functionally, these two axes work together to result in triplanar motion. The longitudinal axis is essentially parallel to the sagittal and transverse planes, which allows only the frontal plane motions of inversion and eversion, whereas the oblique axis is parallel to the frontal plane, which allows motion in the sagittal (plantar flexion–dorsiflexion) and transverse (adduction-abduction) planes ( Fig. 20-5 ). Because the oblique axis is angulated about equally from the sagittal and transverse planes, plantar flexion–adduction and dorsiflexion-abduction are coupled equally.
From a clinical standpoint, motion in the midtarsal joint cannot be reliably quantified. Midtarsal joint motion is dictated by the position of the subtalar joint. When the subtalar joint is pronated, the axes of the talocalcaneal and calcaneocuboid joints are parallel, which allows the midtarsal joint to unlock and become an adaptor with increased mobility. As the subtalar joint supinates, motion of the midtarsal joint decreases as the two axes diverge and “lock” the forefoot on the rearfoot in preparation for its rigid lever function during the propulsive phase of gait ( Fig. 20-6 ).
The position of the midtarsal joint is dictated by ground reaction forces during the initial contact and midstance phases of gait and by muscular activity on the joint during the propulsive phase of gait. The standard clinical index for determining midtarsal joint position is to compare the plantar plane position of the central three metatarsal heads with the plantar plane position of the neutral rearfoot when the midtarsal joint is maximally pronated about both its axes.
Physiologic accessory motions of the midtarsal joint that can be evaluated manually include dorsal and plantar glides of the navicular on the talus and the cuboid on the calcaneus. Dorsal glide of the navicular on the talus accompanies supination, and a plantar glide accompanies pronation.
Tarsometatarsal, Metatarsophalangeal, and Interphalangeal Joints
The first ray represents a functional articulation consisting of the bones of the medial column. The joint axis runs in a distolateral to proximomedial direction, almost parallel to the transverse plane. Motion occurs primarily in the sagittal (plantar flexion–dorsiflexion) and frontal (inversion-eversion) planes. The axis is angulated 45° from both these planes, so for every 1° of plantar flexion, 1° of eversion occurs ( Fig. 20-7 ).
First ray motion begins in the late stance phase of gait and continues late into propulsion. As with the midtarsal joint, first ray motion is influenced by the position of the subtalar joint. With the subtalar joint in pronation, the amount of motion of the first ray is increased. As the subtalar joint supinates, motion of the first ray decreases. The normal extent of movement is 0.5 to 1 cm (a thumb width) in the plantar and dorsal directions and is dynamically controlled by the peroneus longus.
The clinical standard for determining the neutral position of the first ray is to evaluate the position of the first metatarsal relative to the three central metatarsal heads. It should lie in the same transverse plane, neither plantar-flexed nor dorsiflexed.
The fifth ray operates about an independent axis with the same directional orientation as the subtalar joint. The central three metatarsophalangeal (MTP) joints have their axis oriented parallel to the frontal and transverse planes. Consequently, only plantar flexion–dorsiflexion motion takes place in the sagittal plane.
The first MTP joint represents the articulation between the first metatarsal and the proximal phalanx of the big toe. Minimal normal first MTP range of motion with the first ray stabilized is about 20° to 30° of hyperextension. Without stabilization, the first MTP joint should hyperextend to at least 60° to 70°. The MTP joints also have an additional vertical axis, parallel to the frontal and sagittal planes, to allow abduction and adduction of the joints.
Physiologic accessory motions of the MTP joints include plantar and dorsal glide. Plantar glide of the convex first metatarsal accompanies extension, whereas dorsal glide accompanies toe flexion.
The ideal foot is cosmetically acceptable, structurally neutral, and free of impairments. It fits comfortably into all shoes, promotes normal lower quarter biomechanics, and allows pain-free function.
Muscular function of the lower leg, ankle, and foot
The phasic action of the muscles of the lower leg and foot can be determined by examining the musculotendinous unit’s excursion from its origin to its insertion relative to the axis on which it acts ( Fig. 20-8 ). Each muscle group has specific functions that control or provide the necessary forces to create movement. The muscles of the leg and foot can be divided into subgroups or compartments. Where the tendon lies relative to the talocrural and subtalar axes dictates the motions that they create in the open chain and control in the closed chain ( Table 20-3 ; Fig. 20-9 ).
| Group | Muscle(s) | Tendon Location Relative to the STJ | STJ Motion | Location of the Tendon Location Relative to the TCJ | TCJ Motion |
|---|---|---|---|---|---|
| Anterior pretibial | Anterior tibialis | Medial | Supination | Anterior | Dorsiflexion |
| Extensor hallucis longus | On axis | — | Anterior | Dorsiflexion | |
| Extensor digitorum longus | Lateral | Pronation | Anterior | Dorsiflexion | |
| Lateral | Fibularis longus Fibularis brevis | Lateral | Pronation | Posterior | Plantar flexion |
| Superficial posterior | Gastrocnemius Soleus | Medial | Supination | Posterior | Plantar flexion |
| Deep posterior | Posterior tibialis | Medial | Supination | Posterior | Plantar flexion |
| Flexor digitorum longus | Medial | Supination | Posterior | Plantar flexion | |
| Flexor hallucis longus | Medial | Supination | Posterior | Plantar flexion | |
| Dorsal intrinsics | Extensor hallucis brevis Extensor digitorum brevis | — | — | — | — |
| Plantar intrinsics | Flexor digitorum brevis Flexor hallucis brevis Adductor hallucis Abductor hallucis Lumbricales | — | — | — | — |
Posterior Superficial Muscle Group
The posterior superficial muscle group is composed of the gastrocnemius, soleus, and plantaris muscles. These muscles originate from above and below the knee joint and have a common insertion by way of the Achilles tendon on the posterior aspect of the calcaneus. In the open kinetic chain, the triceps surae provides flexion of the knee, plantar flexion of the ankle, and supination of the subtalar joint. With closed kinetic chain function, the gastrocnemius and soleus are active throughout the stance phase of gait. Initially, at heel strike, the gastrocnemius and soleus contract eccentrically to decelerate tibial internal rotation and forward progression of the tibia over the foot. Later, during midstance and heel-off, they provide subtalar joint supination (externally rotating the tibia) and ankle plantar flexion.
Posterior Deep Muscle Group
The posterior deep muscles of the lower part of the leg include the posterior tibialis, flexor digitorum longus, and flexor hallucis longus. The posterior tibialis is a strong invertor (as a component of triplanar supination) of the subtalar joint and functions to control and reverse pronation during gait. It decelerates subtalar joint pronation and tibial internal rotation at heel strike and then reverses its function to accelerate subtalar joint supination and tibial external rotation during stance. The posterior tibialis also maintains the stability of the midtarsal joint in the direction of supination around its oblique axis during the stance phase of gait.
The flexor digitorum longus functions as a supinator of the subtalar joint and flexor of the second through fifth MTP joints in the open kinetic chain. When the foot is in contact with the ground and the digits are stable, the flexor digitorum longus actively stabilizes the foot as a weight-bearing platform for propulsion. If the flexor digitorum longus works unopposed by the action of the intrinsic muscles, clawing of the toes results.
The flexor hallucis longus has a function similar to that of the flexor digitorum longus in that it flexes the first MTP joint in the open kinetic chain. Both these long flexors help support the medial longitudinal arch.
Lateral Muscle Group
The lateral muscle group includes the peroneus longus and brevis. The peroneus longus, because of its attachment to the first metatarsal and medial cuneiform on the plantar surface, functions to pronate the subtalar joint and to plantar-flex and evert the first ray in the open kinetic chain. In the closed kinetic chain, the peroneus longus has many important functions. It provides support to the transverse and lateral longitudinal arches. During the latter portion of midstance and early heel-off, it actively stabilizes the first ray and everts the foot to transfer body weight from the lateral to the medial side of the foot.
The peroneus brevis is primarily an evertor in open kinetic chain motion. During gait it functions in concert with the peroneus longus. Its primary role is to stabilize the calcaneocuboid joint and thereby allow the peroneus longus to work efficiently over the cuboid pulley.
Anterior Muscle Group
The pretibial muscles include the anterior tibialis, extensor digitorum longus, extensor hallucis longus, and peroneus tertius. As a group they are active during the swing phase and the heel-strike to foot-flat phases of gait.
The anterior tibialis is primarily a dorsiflexor of the talocrural joint in open kinetic chain function. During gait, the anterior tibialis basically operates concentrically in the swing phase and eccentrically in the stance phase. At the end of toe-off, the anterior tibialis begins to contract concentrically to initiate dorsiflexion of the ankle and first ray, to assist in ground clearance at midswing, and then to supinate the foot slightly during late swing in preparation for heel strike. When the foot hits the ground, the anterior tibialis reverses its role to decelerate or control plantar flexion to foot flat, prevent excessive pronation, and supinate the midtarsal joint’s longitudinal axis. A weak anterior tibialis can lead to “foot slap,” or uncontrolled pronation in gait.
In non–weight-bearing function, the long extensors (extensor digitorum and hallucis longus) provide dorsiflexion of the ankle and extension of the toes. Because these tendons pass lateral to the subtalar joint axis, unlike the anterior tibialis, they provide a pronatory force at the joint. In fact, a prime responsibility of the long extensors is to hold the oblique axis of the midtarsal joint in a pronated position at heel strike and then to assist in controlled deceleration of plantar flexion to foot flat.
The action of a muscle can be determined by examining the musculotendinous unit’s excursion from origin to insertion relative to the axis on which it acts.
Intrinsic Muscle Group
Generally, the intrinsic muscles of the foot act together during most of the stance phase of gait. Their function is to stabilize the midtarsal joint and digits while keeping the toes flat on the ground until liftoff. An unstable, pronated midtarsal joint during midstance makes the intrinsic muscles work harder and longer. This phenomenon explains the common complaint of foot fatigue in athletes with a hypermobile foot.
Clinical examination
The section on clinical examination of the lower leg, ankle, and foot is presented in the online appendix of this chapter on Expert Consult @ www.expertconsult.com .
Lower leg, ankle, and foot injuries and their management
Lower Leg Injuries
Tennis Leg
Originally thought to be a tear of the plantaris muscle, tennis leg has now been proved through surgical exploration to be a musculotendinous lesion of the medial gastrocnemius head ( Fig. 20-10 ). Because this injury is more common in the fourth to sixth decades of life, the examiner will need to rule out the presence of thrombophlebitis, compartment syndrome, or intermittent claudication masking as musculoskeletal calf pain. Entrapment of the popliteal artery may need to be differentiated by diminished distal pulses and exertional calf pain during ambulation in a younger athlete. The usual mechanism of injury is sudden extension of the knee with the foot in a dorsiflexed position. This places tremendous tensile stress on the two-joint expansion of the gastrocnemius. Middle-aged athletes or those with previous degenerative changes in this anatomic area may be predisposed to this type of trauma.
The athlete feels a sudden, sharp twinge in the upper medial aspect of the calf and immediately has difficulty with full weight bearing. Typically, rapid swelling and ecchymosis occur, with point tenderness or a palpable defect found at the site of the lesion.
Acute care consists of immediate first aid measures, including analgesic medication, ice, compression, and elevation of the injured area. The ankle is placed in mild plantar flexion to alleviate stress on the area of injury. A non–weight-bearing crutch gait may initially be necessary, depending on the severity of the injury.
Gradual, gentle static stretching is initiated early in the subacute phase to align the healing scar tissue. Friction massage of the area also prevents random alignment of the collagen fibers. As the athlete progresses to full weight bearing, heel lifts can be placed in the shoe to protect against weight-bearing stress. As flexibility of the Achilles tendon improves, the height of the lifts can gradually be reduced. Instructions for maintaining calf flexibility and education regarding appropriate warm-up techniques should be provided to reduce the risk for recurrence. Table 20-4 presents further details about progression of rehabilitation for Achilles tendon–related pathology.
| Parameter | Immediate (Acute) Phase | Intermediate (Subacute) Phase | Terminal (Chronic) Phase | Return-to-Sport (Functional) Phase |
|---|---|---|---|---|
| Goal | Rest Control inflammation and pain Promote healing Create “flexible” scar | Increase pain-free ROM Restore contractile capability | Increase musculotendinous tensile strength Modify, correct, or control abnormal biomechanics | Preparation and training for specific sport or activity |
| Modalities | Ice massage NSAIDs Gentle transverse friction massage to prevent adhesion formation HVGS in the shortened position | Heat before rehabilitation Ice after rehabilitation Ultrasound (pulsed vs. continuous) Myofascial soft tissue mobilization techniques | Heat before rehabilitation Ice after rehabilitation Iontophoresis Deep transverse friction massage to improve gliding between tissue planes | Intervention sequence: Passive and active local tissue and systemic warm-up Rehabilitation activity or exercise Static stretching Cool down Cryotherapy |
| ROM/flexibility | Immobilization or pain-free ROM, depending on type and severity of pathology | Temperature-assisted, prolonged-duration, low-intensity, static stretching NWB gastroc/soleus towel stretches | Low-intensity static stretching of the involved musculotendinous unit Weight-bearing knee bent/straight wall leans Slant board stretching | Assess capability, tolerance, and response to ballistic motion and dynamic stretching of the involved tissue |
| Exercise rationale | These exercises may have to be delayed 2-6 weeks with surgically repaired ruptures Isometrics progressing from submaximal to maximal intensity in protected ROM (knee flexed and/or ankle in plantar flexion) | NWB submaximal to maximal effort isokinetics in progressively larger arcs of motion; concentric contractions at highest attainable speeds in a velocity spectrum to minimize tensile stress in this early phase | Weight-bearing concentric and eccentric isotonic exercise at increasing speeds of contraction as tolerated by the tissue’s symptomatic response | Functional rehabilitation activities—toe walking Plyometric progressions—hopping, bounding, depth jumps, and box drills Sport-specific training |
| Proprioceptive rehabilitation | BAPS board training in NWB positions if not immobilized | BAPS board training in partial weight bearing to FWB with increasing levels of ROM difficulty | BAPS board training in FWB with resistance via posterior peg overload | Balance board training |
| Alternative conditioning | Upper body ergometer | Gravity-reduced running with assistance of unloading device or floatation device in water | Gravity-reduced running Stationary cycling | Stair climber Stationary cross-country skier |
| Complementary exercise | Hip-knee-trunk strengthening and conditioning activities | Dorsiflexion, inversion, and eversion strengthening Exercise of foot intrinsic musculature | Lower extremity stretching and continuance of previous phase activities | Ensure normal plantar flexion–to-dorsiflexion strength ratios and muscle balance—3-4:1—at slow speeds of concentric contraction |
| Activity education-modification | Controlled immobilization and rest as needed Examine athletic shoes, training surface, and training regimens | Trial of low-amplitude rebounder running | Flat training surfaces only; avoid hilly and cambered terrains or muddy surfaces | Careful increases in training regimens, with program not increasing by more than 5%/wk in intensity, duration, or frequency |
| Orthotic care | Crutches as necessary; weight-bearing status dictated by severity of pathology | Viscoelastic heel lift inserts to reduce stress on the Achilles tendon and decrease ground reaction forces | Orthotic insert to control excessive or abnormal compensatory subtalar joint motion, if necessary | Orthotic and/or taping techniques |
Achilles Tendon Rupture
The Achilles tendon complex is prone to injury with a sudden and powerful eccentric contraction of the gastrocnemius-soleus muscles (considered together as the triceps surae). This mechanism is best demonstrated during jumping and landing activities in which the knee is extending while the ankle is dorsiflexing eccentrically. The tendon usually ruptures at a point just proximal to the calcaneus (see Fig. 20-10 ). Vascular impairment, nonspecific degeneration leading to tissue necrosis, and the use of injectable corticosteroids may weaken this area and predispose it to injury.
The athlete reports an audible snap and the sensation of being kicked in the leg. Plantar flexion weakness and pain, swelling, and a palpable defect are usually noted immediately. The diagnosis is confirmed by a positive Thompson test (see Fig. 7-4 ); with the athlete prone and the knee flexed and the foot relaxed, a firm squeeze of the calf should produce calcaneal plantar flexion. The test is positive if no movement of the foot occurs. This test has very high sensitivity and specificity.
Acute care consists of the application of ice with the ankle immobilized in slight plantar flexion. A non–weight-bearing crutch gait should be used until the severity of the injury has been determined. Table 20-4 provides a treatment rationale for lesions of the triceps surae mechanism.
Optimal treatment of acute Achilles tendon rupture has not been definitively established. Surgical (open or percutaneous) versus conservative (nonoperative casting or functional bracing) management decisions are based on the site and thickness of the tear in conjunction with the goals and ambitions of the patient. Both methods of management have produced acceptable results.
It is generally accepted that surgical intervention will lower the likelihood of rerupture whereas nonoperative management decreases the risk for other complications (infection, adhesions, deep vein thrombosis, and skin lesions). A metaanalysis of randomized controlled trials found that the complication rate can be reduced with percutaneous approaches. In percutaneous surgery, the surgeon makes several small incisions rather than one large one as for an open approach. Regardless of whether the issue is resolved with surgery, recent research has been quite harmonious in the endorsement of functional bracing (allowing protected mobilization) as opposed to strict cast immobilization during the first 4 to 8 weeks.
Another concept of postoperative management is the introduction of early mobilization. Protected-arc, active plantar flexion range-of-motion activities may be started as early as 2 to 4 weeks after injury. This allows collagen fibers to be laid down along the lines of stress. A 1-inch heel lift is used when weight bearing is allowed, and the height of the lift is gradually decreased as dorsiflexion range of motion improves. Multiple studies have shown that this early-motion protocol minimizes tendon elongation and improves patient satisfaction without having a negative impact on rerupture rates. Early weight bearing and functional bracing may also provide an earlier return of strength but probably do not make any significant difference in calf atrophy or long-term outcome.
Nonoperative management is still indicated for older, nonathletic patients with minimally displaced ruptures who are concerned about the potential surgical complications. However, the principles of early weight bearing and functional bracing should still be applied. For these individuals, the typical protocol is a short period of immobilization in an equinus position with slow, but progressive lowering of heel position as protected weight bearing is allowed.
Tendinopathies
Tendinous lesions of the muscles of the lower part of the leg occur frequently in athletes involved in activities of a repetitious nature. Microtraumatic damage caused by overuse, fatigue, or biomechanical abnormalities may occasionally be manifested by an inflammatory but, more commonly, a degenerative reaction of these tendons. For more on tendiopathies, see Chapter 7 .
Achilles tendinopathy
The Achilles tendon is the common tendon of the gastrocnemius and soleus muscles. It inserts into the posterosuperior aspect of the calcaneus and is a frequent site of pathology in competitive and recreational athletes. It is surrounded by the paratenon, which functions as an elastic sleeve that envelops the tendon and allows free movement against surrounding tissues. In areas in which the tendon passes over zones of potential pressure and friction, the paratenon is replaced by a synovial sheath or bursa.
The major blood supply to the Achilles tendon is provided through the paratenon. An area of reduced vascularity is found 2 to 6 cm proximal to the insertion. This region of relative avascularity may play an etiologic role in the frequent onset of symptoms at this level.
Macroscopic and microscopic histologic evaluation of Achilles disease typically shows a degenerative as opposed to an inflammatory condition. The essence of the tendinopathy is a failed healing response with haphazard collagen fibrils and an increase in noncollagenous matrix that results in a larger tendon diameter consisting of smaller, irregular, and crimped or wavy collagen fibers.
The onset of Achilles tendinopathy is usually gradual and insidious, although many precipitating factors have been implicated. These factors may include poor flexibility, prolonged subtalar joint pronation, inappropriate footwear, or the use of fluoroquinolone antibiotics, and they are usually magnified by excessive overload from an alteration or increase in the frequency, duration, or intensity of the activities. The athlete complains of a dull, aching pain during or after activity. On physical examination, slight edema or tendon thickening may be present. Point tenderness is usually elicited 2 to 3 cm proximal to the calcaneal attachment. Because this is a contractile lesion, pain usually increases with passive dorsiflexion and resisted plantar flexion. Crepitation may be noted in plantar flexion movements in the subacute and chronic stages.
Degenerative tendinopathies in middle-aged athletes are difficult to manage and often take months to fully resolve. “Weekend warriors” are the most susceptible because they often have “18-year-old ambitions in a 38-year-old body.”
Table 20-5 presents a suggested rationale for the conservative management and treatment of tendinopathies and peritendinitis. The four stages of injury define potential entry points into the treatment system. An athlete could initially be seen at any one of these stages. Progression from one stage to the next is variable and dictated by time, symptoms, and individual response.
| Parameter | Immediate (Acute) Phase | Intermediate (Subacute) Phase | Terminal (Chronic) Phase | Return-to-Sport (Functional) Phase |
|---|---|---|---|---|
| Goal | Relative rest Control inflammation and pain Promote healing | Rehabilitation of musculotendinous unit Increase ROM Maintain muscle contractile capability | Increase musculotendinous tensile, eccentric strength Modify, correct, or control abnormal biomechanics | Preparation and training for specific sport or activity |
| Modalities | Ice massage cryotherapy NSAID and acetaminophen for short-term pain relief Glyceryl trinitrate patch Gentle transverse friction massage Cold laser | Active warm-up or heat before rehabilitation activities Cool-down activities or ice after rehabilitation activities Ultrasound (pulsed vs. continuous) Myofascial soft tissue mobilization techniques | Heat before rehabilitation Ice after rehabilitation Iontophoresis/phonophoresis Deep transverse friction massage to improve gliding between tissue planes Platelet-rich plasma injections | Modality sequence: Passive-active tissue and systemic warm-up Static stretching activity or exercise Dynamic stretching Cool down Cryotherapy |
| ROM—flexibility | Pain-free ROM exercises | Temperature-assisted, prolonged-duration, low-intensity, static stretching | Low-intensity, static stretching progressing to dynamic stretching of involved musculotendinous unit | Assess capability, tolerance, and response to ballistic motion of involved tissue |
| Exercise rationale | Subsymptom threshold isometrics | Submaximal to maximal effort isotonic or isokinetic exercise in progressively larger arcs of motion | Eccentric exercise at increasing speeds of contraction as governed by symptomatic response of tissue | Functional rehabilitation activities and plyometric progressions Sport-specific training |
| Proprioceptive rehabilitation | BAPS board training in non–weight-bearing positions | BAPS board training in partial to full weight bearing with increasing levels of ROM difficulty | BAPS board training in full weight bearing with resistance overload on appropriate muscle groups | Balance board training |
| Alternative conditioning | Upper body ergometer | Stationary cycling Gravity-reduced walking/running with assistance of unloading device or floatation device in water | Progression of gravity-reduced walking/running | Ensure cross-training with alternative aerobic conditioning devices such as elliptical trainers, stair climbers, or stationary cross-country skiers |
| Complementary exercise | Hip-knee-trunk strengthening and conditioning activities | Exercise for foot intrinsic musculature such as toe curls, towel sweeps | Short-foot exercises | Ensure normal agonist-antagonist strength ratios and muscle balance |
| Activity education-modification | Controlled immobilization and rest as needed Educate regarding athletic shoes, training surface, and training regimens | Trial of low-amplitude rebounder running | Flat training surfaces only; avoid hilly and cambered terrains or muddy surfaces | Careful increases in training regimens; program not increased by more than 5%-10%/wk in intensity, duration, or frequency |
| Orthotic care | Heel lift if appropriate | Shock-attenuating inserts to decrease ground reaction forces (especially with rigid cavus feet) | Orthotic insert to control excessive or abnormal compensatory subtalar joint motion | Orthotic and/or taping techniques |
As is usually true, the best treatment of microtraumatic injuries such as Achilles tendinitis is prevention of onset. The frequency or severity of degenerative Achilles injuries may be reduced if some suggested guidelines are followed:
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Select appropriate footwear. The athletic shoe should have a firm, notched heel counter to decrease tendon irritation and control rearfoot motion. The midsole should have a moderate heel flare, provide adequate wedging, and allow flexibility in the forefoot. It is also important to maintain a relatively consistent heel height in all shoes worn during the day.
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Avoid training errors. Achilles tendon microtrauma can be magnified by errors in training. Steady, gradual increases of no more than 5% to 10% per week in training mileage and speed on appropriate terrain should be emphasized. Running on hills or inclines should be approached in a cautious manner after the symptoms have completely subsided. Use of cross-training principles may also reduce cumulative stress on the Achilles tendon.
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Ensure gastrocnemius-soleus flexibility. The talocrural joint should have 10° of dorsiflexion with the knee joint extended and 20° with the knee flexed. Normal gait requires 10° of dorsiflexion just before heel-off, during which the subtalar joint is in neutral position and the knee is extending in stance phase.
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Control pronation forces. Abnormal compensatory pronation forces can cause a whipping or bowstring effect on the medial edge of the Achilles tendon. Orthotic correction may be indicated if this abnormal pronation has a structural origin. Taping techniques to correct a convex medial tendon orientation in a compensatory pronated stance may also be beneficial.
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Restore the eccentric tensile capabilities of the triceps surae complex. Numerous studies have found that a program of progressive heel drops ( Fig. 20-11 ) accelerates recovery and improves clinical outcomes in athletes with midsubstance Achilles tendinopathy. It is important to note that a mild, temporary level of discomfort should occur during exercise. Table 20-6 provides a rationale for manipulable variables that can be used to properly prescribe and advance the heel drop program. These factors include the influence of gravity, speed of contraction, range of motion, and bilateral versus unilateral contribution to the exercise.
Figure 20-11
Eccentric heel drop progression. A, Non–weight-bearing eccentric heel drops. B, Eccentric plantar flexion with elastic tubing resistance. C, Eccentric heel drops in a gravity-eliminated position. D, Bilateral weight-bearing heel drops. E, Unilateral weight-bearing heel drops. F, Bilateral weight-bearing heel drops with the toes on an elevated surface. G, Unilateral weight-bearing heel drops with the toes on an elevated surface.
Table 20-6
Progression Variables in Eccentric Training
Position
Involvement
Arc of Motion
Speed
Resistance
Sitting
Bilateral → unilateral
Partial → full ROM
Slow → fast
Manual resistance or cuff weights
Long sitting
Unilateral
Partial → full ROM
Slow → fast
Thera-Band
Incline
Bilateral → unilateral
Partial → full ROM
Slow → fast
% of BW
Standing
Bilateral → unilateral
Partial → full ROM
Slow → fast
BW
+ 10% BW
+ 5-10 lb/wk
BW, Body weight; ROM, range of motion.
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Perform postural screening for any biomechanical malalignment to detect any abnormalities that could adversely affect the kinetic chain and increase stress on the Achilles tendon. Such conditions include leg length discrepancies, cavus foot resulting from metatarsal forefoot equinus, ankle equinus, tibial varum, and rotational influences of the femur or tibia ( Box 20-1 ).
Box 20-1
Typically a degenerative (not inflammatory) condition
Iontophoresis and/or low-level laser therapy
Heel lift and/or tape support to unload stress on the tendon
Control abnormal subtalar joint motion with tape and/or orthotics
Stretching and/or soft tissue mobilization to ensure adequate dorsiflexion range of motion
Restoration of tensile capability through a graded eccentric loading program
Gradual introduction of plyometric progression
Careful increases in training regimens, with the program not increased by more than 5% to 10% per week in intensity, duration, or frequency
Management of Achilles Tendinopathy: Key Considerations in Rehabilitation
Anterior tibialis tendinopathy
An inflammatory response of the anterior tibialis tendon occurs when it cannot absorb deceleration forces during the heel-strike phase to the foot-flat phase of gait. Uncontrolled or excessive pronation following heel strike stretches the anterior tibialis as it attempts to control the speed of forefoot loading.
Conditions that predispose the anterior tibialis to overuse usually include training errors and physical abnormalities. Frequently, the combination of excessive extrinsic force placed on intrinsic abnormalities produces stress that cannot be dissipated or tolerated by the athlete. Extrinsic factors include dramatic increases in mileage, overstriding, and excessive hill running, all of which can cause fatigue and injury. An athlete with a tight Achilles complex requires increased muscular output of the anterior tibialis to overcome the inherent posterior tautness. This condition is then magnified by uphill running, which necessitates full dorsiflexion range of motion. In downhill running, increased eccentric forces are necessary to control forefoot loading over an increased range of motion. If the anterior tibialis has undergone adaptive shortening in response to chronic hyperpronation, the musculotendinous unit cannot provide the necessary range of motion and absorption of tensile forces needed during the early stance phase.
This injury is characterized by pain and swelling over the dorsum of the foot. Crepitation along the tendon or at its point of insertion onto the navicular may be present. Examination reveals pain with stretching into the extremes of plantar flexion and pronation and pain-inhibited weakness during manual muscle testing of anterior tibialis function.
Table 20-5 summarized the treatment rationale for lower leg tendinopathies. Prime consideration should be given to correcting soft tissue imbalances, improving eccentric muscular capabilities, and selecting appropriate footwear. Shoe selection should focus on midsole materials that attenuate shock and accommodate orthotic additions. A heel lift may be used for athletes with structural equinus, or varus posting may be indicated if forefoot varus or supinatus is prolonging the pronation process.
In chronic tendinopathy conditions, the exercise rehabilitation program must gradually reintroduce tensile strain through eccentric stress and plyometric progression to restore function, reduce tendon volume, and normalize histologic neovascularization.
Peroneal tendinopathy
Degenerative lesions of the peroneal tendons or inflammation of their protective sheaths is common in athletes who for compensatory reasons overuse this musculature. The pathology is secondary to chronic lateral ankle sprains or occurs in athletes with hypermobile first rays. In both situations, the peroneal muscle tendons are worked excessively in an attempt to provide stability. Any mechanical stress caused by abnormal forefoot structures that force the foot into a valgus position can also amplify this inflammatory response.
Pain and swelling typically occur in the area just posterior to the lateral malleolus. Occasionally, symptoms are manifested at the musculotendinous junction. Tendon crepitus may be present in more chronic conditions. Pain and weakness are evident with passive overstretching of these contractile structures and when resistance is provided to plantar flexion and eversion of the first ray. When compared with peroneal longus tendinopathy, peroneal brevis tendinopathy is more affected by resistance to calcaneal eversion and ankle plantar flexion. The differential diagnosis includes peroneal subluxation, inversion ankle sprain, sural nerve entrapment, and subacute lateral compartmental syndrome, with subsequent management differing for each of these conditions.
Rehabilitation is aimed at providing relief of symptoms and identifying the causative factors. Muscular imbalances between the anterior or posterior tibialis and peroneals should be explored. A metatarsal pad with a first ray cutout or a lateral heel wedge (or both) can provide biomechanical compensation for structural abnormalities. Transverse friction massage can be used to reduce symptoms and promote healing. Table 20-5 presents further treatment considerations.
Posterior tibialis tendinopathy
Posteromedial shin pain secondary to athletic overuse can be caused by inflammatory microtrauma to the tendon of the posterior tibialis. Periosteal irritation and tibial stress reactions may also be suspected.
Medial tibial stress, whether tendinitis or periostitis, is generally the result of abnormal hyperpronation biomechanics ( Fig. 20-12 ). The muscles in the superficial posterior compartment contract in a stretched position and are overworked in an attempt to stabilize the foot during propulsion. Common predisposing factors include improper training on crowned or banked surfaces, inappropriate footwear, and any structural condition that increases the varus attitude of the lower extremity.
Pain and swelling are present over the posteromedial crest of the tibia along the origin of the posterior tibialis. Tenderness and crepitation may be found anywhere along the course of the tendon as it passes behind the medial malleolus and inserts distally on the navicular and first cuneiform. Manual resistance to plantar flexion and inversion localizes the complaint. In subacute phases, repeated unilateral heel raises, which require plantar flexion and supination of the calcaneus, can be a source of symptom aggravation.
It is important to rule out a tibial stress reaction, in which pain is present at the junction of the lower and middle thirds of the posteromedial aspect of the tibia, in the differential diagnosis. Tibial stress fractures can occur in this area if the osteoblastic activity in bone cannot keep pace with the osteoclastic stress placed on it. At approximately 2 weeks after awareness of symptoms, a fracture through the tibial cortex may become evident on radiographs. Before this finding, a bone scan reveals increased calcium uptake in the area of injury. Clinical differentiation is accomplished by detection of tenderness in areas devoid of muscle on the tibial shaft or by percussion and tuning fork vibration techniques.
Treatment is aimed at alleviating abnormal pronation by using a semirigid orthosis with a medial heel wedge. Attention should also be given to the training regimen and to finding shoes with a stable, firm, and snug heel counter.
In an older athlete, dysfunction of the tibialis posterior tendon is the most common cause of acquired adult flatfoot deformity. This pathology can arise from an acute traumatic injury, systemic disease, or chronic tendon degeneration. Like the more proximal dysfunction, it may be treated with symptom-alleviating modalities, exercise-based interventions, and control of destructive hyperpronatory forces with the use of appropriate footwear and orthotic therapy. Ice, nonsteroidal antiinflammatory medication, and rest will offer analgesic benefit, and eccentric training of the posterior tibialis may enhance the value of medially posted orthoses. Elastic tubing–resisted subtalar inversion plus foot adduction with a controlled deceleration back to the starting position is demonstrated in Figure 20-13 with a medial sweep exercise ( Box 20-2 ).
BAPS board training with anteromedial and/or posteromedial overload
Marble pick-ups with the toes and medial towel sweeps with the foot
Supro dance—arch lift and drop
Unilateral balancing activities progressing from stable to unstable surfaces
Unilateral stance with frontal plane motion in the opposite lower extremity
Bilateral progressing to unilateral stance trunk rotation with appropriate resistance and speed of motion
Flexor hallucis longus tendinopathy
An athlete (e.g., en pointe dancers) who must perform repetitive push-off maneuvers is especially prone to the development of tendinopathy in the long flexor of the great toe. Hyperpronation during propulsion also places excessive stress on the tendon as it contracts from a lengthened position. This condition is similar to posterior tibial tendinopathy and can be differentiated with selected manual muscle testing. Pain with passive extension of the first MTP joint while the ankle is dorsiflexed or with resistance to flexion of the great toe while the ankle is plantar-flexed confirms the diagnosis. The condition is managed with appropriate varus posting and tape restriction for excessive dorsiflexion of the first MTP joint. Stretching of the flexor hallucis longus (simultaneous ankle dorsiflexion and great toe extension) may prevent the development of hallux rigidus.
Flexor digitorum longus tendinopathy
The flexor digitorum longus is another musculotendinous unit in the superficial posterior compartment that is susceptible to overuse microtrauma. Pain is usually present in the posteromedial third of the leg as a result of overuse from forced, resistive dorsiflexion of the toes during propulsion. The resultant cramping sensation in the forefoot and toes can be relieved with a viscoelastic metatarsal pad, which dorsally displaces the metatarsal heads and reduces the extension angle of the lesser four MTP joints. A more rigid sole in the athletic shoe may also help prevent excessive forced hyperextension of the digits during propulsion. Exercise rehabilitation focuses on correcting any intrinsic muscular imbalances that allow toe-clawing deformities and that require the flexor digitorum longus to work harder. The intrinsic muscles of the foot can be isolated for emphasis with repetitive toe-curling exercises. Functionally, the intrinsic muscles of the foot can be trained to maintain arch integrity without toe clawing with short-foot exercise in both weigh-bearing and non–weight-bearing positions ( Fig. 20-14 ).
Strong evidence supports the off-label use of glyceryl trinitrate patches at 1.25 mg/day in individuals with chronic tendinopathy conditions to relieve pain during activities of daily living and increase tendon strength.
