Christian Lattermann MD
Derek Armfield MD
Dane K. Wukich MD
Lower Leg Pain
Athletes performing any sport expose themselves to a particular subset of sports-specific injuries including injury to the foot and ankle. Approximately 25% of all sports injuries involve the foot and ankle and about 45% of these are simple lateral ankle sprains. In cutting sports such as football, baseball, volleyball, and soccer these injuries account for up to 25% of lost playing time. Some sports have a low incidence of foot injuries. Swimming, for example, has a very low incidence of ankle injuries. Basketball and figure skating have the highest incidence. With respect to foot injuries, football and weight lifting are the lowest risk sports. Hiking and high-speed motor sports have a higher incidence (>50%).
Overall, every sport poses a specific threat to the athletes' foot and ankle as a result of the activity and the equipment that is used. These injuries may not be benign. Approximately 40% of all simple ankle sprains lead to chronic disabilities that may end the athlete's career.
In this chapter the diagnosis and treatment of common injuries and conditions of the lower leg and foot that frequently occur in athletes will be discussed. Anatomic, biomechanical, and functional principles of the foot and ankle will be described. We will discuss conservative as well as operative treatments.
Muscle Strains
Essentials of Diagnosis
Pathogenesis
Muscle strains of the gastrocsoleus complex are the most frequent injuries in athletes who jump or sprint. Muscle injuries account for up to 30% of all injuries sustained in sports events. These injuries pose a significant challenge to every sports medicine clinician. The majority of these muscle injuries are caused by contusion or excessive strain of the muscle and they can sideline athletes for a long time.
Athletes with a prior history of muscle strains have increased risk of further injury. The closer the reinjury is to the previous calf strain the higher the risk for recurrence. There also seems to be a relationship with age, with older athletes predisposed to a higher risk for calf strains.
Prevention
Fatigue may play a key role in the incidence of calf strains since muscle strain injuries seem to occur late in either training sessions or competitive settings. It was shown that the energy absorbed before failure was significantly less in fatigued than in control muscles. Therefore, proper conditioning to reduce or delay fatigue should be part of the prevention strategy.
Calf stretching and warm-up should be an integral part of the athletes' preparation. The musculotendinous unit has specific viscoelastic properties that can be influenced by warm-up and cyclic stretching. Cyclic stretching up to 50% of the maximum stretch to failure has a beneficial effect on the amount of energy that a muscle can absorb before failure. Stretching past 50% of the maximum stretch reduces the maximal amount of energy that the muscle can absorb. Therefore, the recommendation is to perform light stretching exercises before sports activities. Viscoelasticity is temperature dependent. Therefore, the warm-up exercises help to increase the viscoelastic properties of the musculotendinous unit before athletic activity.
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Clinical Findings
Calf muscle strains can occur in cutting and jumping sports such as basketball, football, soccer, tennis, and racquetball. The athlete is usually not able to return to play after a significant calf muscle strain. It is important to know if the athlete had a prior, recent, minor injury to the affected calf because a muscle reinjury is likely to be more severe. Patients report immediate pain in the back of their calf. They may have felt a sudden pop or snap. Feeling “as if someone hit them in back of the calf” is often mentioned.
It is important to do a thorough physical examination to determine if the injury is in the muscular portion of the medial or lateral head of the gastrocnemius or at the musculotendinous junction of the gastrocsoleus complex. A muscle strain may be palpable as a swelling of the calf. Alternatively, if a disruption of the muscle fibers has occurred a gap may be felt by physical examination before swelling occurred or after it subsided. The gap and swelling are usually felt in the muscle substance. A rupture of the medial head of the gastrocnemius is more frequent than a rupture of the lateral head. The gap is therefore palpable medial or lateral to the midline. The most important differential diagnosis of a calf strain is the rupture of the Achilles tendon. Therefore, if the gap is palpable directly in the midline and distal to the musculotendinous junction, a rupture of the Achilles tendon rather than a muscle strain should be suspected. The Thompson test or calf squeeze test is helpful in making the differential diagnosis. To perform the Thompson test the patient is positioned prone with the foot hanging over the edge of a table. The examiner squeezes the calf muscle and watches for plantar flexion of the foot. If there is plantar flexion the test is negative and identifies an intact musculotendon complex. If there is no plantar flexion, either the gastrocsoleus complex is torn at the myotendinous junction or the Achilles tendon is torn.
The need for imaging of the calf after a calf muscle strain depends on the severity of the injury. If the physical examination suggests a large or complete tear of the medial or lateral gastrocnemius, magnetic resonance imaging (MRI) may be used to evaluate the extent of the injury. This also aids in surgical planning. MRI may also be used to monitor the healing of a muscle strain (Figure 4-1).
Calf muscle strains can also occur in combination with other injuries such as ankle sprains, fractures of the fibula, or neurovascular injuries, in which case the associated injuries dictate the need for imaging modalities.
Treatment
Treatment for calf muscle strains begins immediately at the sideline according to the RICE (rest, ice, compression, elevation) principle. This initial treatment regimen is designed to avoid the formation of a large hematoma, which may affect the size of the scar tissue formed during the recovery. Initial treatment can continue for 24–48 hours.
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Figure 4-1. T2-weighted MRI showing edema in the medial gastrocnemius (white arrow). This edema is the response to the muscle strain. |
After the initial treatment the subacute treatment protocol calls for rehabilitation as well pain control with nonsteroidal antiinflammatory drugs (NSAIDs). NSAIDs do not adversely affect healing in the initial phase of recovery from muscle strain; however, they should not be given long term (more than 7–10 days) as they may interfere with muscle healing at a later stage. A mainstay for the treatment of muscle strains is rehabilitation. Light stretching and strengthening as well as ultrasound therapy provide significant pain relief and begin to recondition the muscle fibers and help the scar tissue heal. The key is not to disrupt healing of the soft tissue. Treatment should be started after a few days of rest. Light stretching exercises such as towel stretches, standing calf stretches, and progressive
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resistive exercises can be performed very early. The exercise should be performed within the pain-free range of motion (ROM). After 7–10 days, light strengthening exercises can be performed using standing heel raises, single leg exercises such as hops, and gradual return to sports-specific exercises involving running, cutting, and jumping.
Surgical Treatment
Injury resulting in tears of the entire muscle mass are more frequent in the abdominal, hamstring, or rectus muscles but also occur in the calf. These injuries usually involve a very large palpable gap and result in significant loss of function. Conservative treatment of massive muscle tears results in very large amounts of scar tissue that may preclude return to sport. Primary muscle repair in complete disruptions of the muscle belly may lead to smaller scar formation and better functional recovery.
Return to Play
Generally, the severity of the muscle strain will determine the time to return to play. It is important to keep in mind that a previous calf strain predisposes the athlete to a more severe calf strain. It may therefore be prudent to let the strain heal fully before the athlete returns to play. Depending on the severity of the strain recovery time may range from 1 to 4 weeks. An important criterion for return to play is an isometric muscle strength that is within 90% of the opposite side or the preinjury value. The athlete has to be able to perform all of the cutting and specialty maneuvers required for the sport without having pain.
Leadbetter WB: Soft tissue athletic injury. In: Sports Injuries: Mechanism, Prevention, Treatment. Fu FH, Stone DA (editors). Lippincott Williams & Wilkins, 2001.
Noonan TJ, Garrett WE Jr: Muscle strain injury: diagnosis and treatment. J Am Acad Orthop Surg 1999;7(4):262.
Stress Fractures & Stress Reaction
Essentials of Diagnosis
Pathogenesis
Stress fractures of the tibia can commonly be seen in dancers and runners. There is a higher occurrence of tibial stress fractures in female athletes. Stress fractures around the foot and ankle most often occur in the metatarsal bones. The second or third metatarsals are the most common locations followed by the fifth metatarsal and the navicular. Other sites for stress fractures are the calcaneus and the cuboid.
In general, stress fractures are the result of chronic overload. This chronic overload can be due to anatomic predisposition (eg, anterior bow of the tibia in dancers) or to participation in sports that elicit extreme deceleration or chronic deceleration forces in the tibia such as the bravura technique in ballet dancers. Stress fractures in the foot are often due to overly heavy gear (eg, third metatarsal “marching fracture”), faulty training routines, or atypical foot alignment (eg, short first ray), which may predispose the metatarsals to overload. Alterations in footwear, previous injuries and fractures, as well as underlying health problems such as osteopenia, osteoporosis, and metabolic disorders can lead to the occurrence of stress fractures around the foot. As preventive measures, the athlete should not overtrain and should use appropriate training techniques. In ballet dancers the “Balanchine” technique, which requires more fluid motion and very few jumps into “pose,” puts the dancer at much less risk than the “bravura” technique.
The best footwear for the sporting activity should be used and may need to be customized in case of anatomic variation (eg, high arch, flat foot, short first ray). In case of suspected osteopenia or osteoporosis, a bone densitometry analysis should be performed.
Clinical Findings
Athletes will have pain at the site of the stress fracture after exercise. Most commonly this is at the junction of the middle and distal third of the tibia on its medial side. If the stress fracture is in the foot, the athlete may notice swelling after exercise and some local point tenderness. For example, for a navicular stress fracture the “N” spot should be palpated. The pain typically appears during exercise. Often athletes will not experience tenderness after initial activity but after a certain amount of exercise, the pain will set in. In fact, the pain may occur after a repeatable distance or time after exercise begins. Athletes are often able to continue with their activity, although with pain at the site of fracture.
Signs
It is crucial to do a full physical examination of the tibia and the foot. The tender spots need to be palpated to define the anatomic location of the injury. Navicular
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stress fractures, for example, typically hurt in the midportion of the navicular very close to the insertion of the tibialis anterior. To differentiate tibialis anterior tendinitis from a navicular stress fracture it is important to examine the tibialis tendon and its function and to directly palpate the outline of the navicular. For metatarsal stress fractures, it is important to inspect the plantar aspect of the foot for plantar calluses that may provide a clue about improper force distribution in the forefoot.
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Figure 4-2. T2-weighted MRI image showing edema in the tibia. The coronal section shows the typical medial location of the stress fracture (left arrow). The axial cut shows the marrow edema that accompanies the fracture and healing response (right arrow). |
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Figure 4-3. T1- and T2-weighted MRI image of the midfoot showing a stress fracture of the anterior process of the calcaneus and the cuboid. The left image is the T1-weighted image that shows some blood and cortical irregularity in the anterior calcaneus (arrow). The right image shows the typical edema that accompanies stress fractures in the anterior calcaneus and the cuboid. |
A stress fracture is usually diagnosed based upon clinical suspicion. Very often, the initial radiographs are negative. A stress fracture will be detectable on radiographs once the healing response and sclerosis at the fracture site have begun. This usually occurs 2–3 weeks after the onset of the symptoms. Radiographic changes are very subtle and consist of cortical thickening, trabecular sclerosis, and possibly cortical defects. In the tibia the dreaded “black line” can be identified at a later stage, once the stress fracture has essentially become a nonunion. For further imaging, usually an MRI or a bone scan is required. We believe that a bone scan is the most sensitive test. It will show a hot spot right at the fracture site. The advantage is that it will also assess surrounding bones and indicate other bones that are in danger. An MRI scan is an excellent tool with which to evaluate the surrounding soft tissues as well as the involved bone. Typically, a stress fracture leads to edema at the fracture site, which can easily be visualized by MRI (Figure 4-2). Edema typically shows up as a very low signal on the T1 sequences and as a high-density area on the T2 sequences. Inversion recovery images can be utilized to display more subtle stress reactions in smaller bones such as the anterior process of the calcaneus or the navicular (Figures 4-3 and 4-4).
Complications
The most serious complications of a stress fracture result from ignoring the telltale signs and not being responsive to the athlete's complaint. Nonoperative treatment has certain risks that are associated with the casting treatment including deep vein thrombosis and skin injuries. It is important to arrange periodic follow-up after cast treatment to inspect the soft tissues. Operative treatment has surgical risks and may result in painful hardware that may have to be removed once the fracture is healed.
Treatment
The treatment of stress fractures around the foot is largely nonoperative. Stress fractures generally require immobilization in a hard-soled shoe or cast for 6–8 weeks. Stress fractures of the forefoot (ie, metatarsal fractures) can be treated in a hard soled shoe (eg, cast shoe) or a removable boot with a rocking sole. Stress fractures of the tarsal bones usually need to be protected or non-weight bearing for 6–8 weeks. Once the fracture has healed, a gradual return to activities can be allowed. Precautions should be taken to avoid the training errors or activities that led to the initial stress fracture. Very rarely a stress fracture will advance to a nonunion, the most notorious involving the base of the fifth metatarsal fracture, known as the “Jones fracture.” This stress fracture occurs in athletes who jump a lot such as basketball, football, or volleyball players. In high-level athletes with fifth metatarsal stress fractures, an intramedullary screw allows faster return to play. In the average recreational athlete, however, the treatment of choice is modification of activity and cast or boot treatment for 4–6 weeks.
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Figure 4-4. Inversion recovery MRI image of a navicular stress fracture. This may be a subtle finding on a T2-weighted image so special MRI techniques such as inversion recovery may be required. |
For a stress fracture that proceeds to become a nonunion or a malunion the same rules apply as for acute fractures. Any rotational misalignment needs to be corrected. A painful nonunion needs to be taken
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down operatively and bone grafted. Rigid fixation with an intramedullary nail, screws, or plates is then necessary.
Verma RB, Sherman O: Athletic stress fractures: part II. The lower body. Part III. The upper body with a section on the female athlete. Am J Orthop 2001;30(12):848.
Wilder RP, Sethi S: Overuse injuries: tendinopathies, stress fractures, compartment syndrome, and shin splints. Clin Sports Med 2004;23(1):55.
Exertional Compartment Syndrome
Essentials of Diagnosis
Pathogenesis
Although athletes, and especially runners, are predisposed to overuse injuries, exertional compartment syndrome must be differentiated from two other conditions. The first of these and the most common is the medial tibial stress syndrome. Typically, the athlete has distinct pain along the posteromedial border of the middle to distal third tibia. There are no sensory, motor, or vascular anomalies. The distal one-third of the tibia is tender posteromedially and the pain can be elicited with a forced plantar flexion against resistance. This syndrome was previously referred to as classic “shin splints.” Prevention of and therapy for this problem involve careful cross-training, light stretching, and a combination of initial rest and subsequent careful strengthening of the weak muscle groups.
The second condition that needs to be ruled out before a diagnosis of exertional compartment syndrome is made is a muscle strain in the medial gastrosoleus. Discussed earlier in this chapter, it may present in a fashion similar to the medial tibial stress syndrome.
Exertional compartment syndrome results from overcompression of the calf muscles during strenuous physical exercise. There are four major muscle compartments within the calf: anterior, lateral, posterior, and deep posterior. Others separate the calf into as many as seven compartments. During exercise, the muscle compartment can undergo a normal volume increase of up to 20%. Most often, the involved compartment is the anterior compartment followed in frequency by the deep posterior compartment. Fascial membranes make up the compartment and provide the anatomic casing for the muscles lying within its confines. As the muscle volume increases with exercise, it expands against the fascia, yet the fascia does not yield. Henceforth the intramuscular (intracompartmental) pressure will rise. As long as this pressure remains below a threshold that will not compromise blood flow and soft tissue integrity, the muscle functions within its physio-logic capabilities and can recover. If the pressure rises above this physiologic threshold, the soft tissues are compromised. There is no preventive program.
Clinical Findings
Exertional compartment syndrome typically presents as a dull ache or pain in the involved compartment. Patients usually indicate that the onset follows a very specific duration or type of exercise. This onset is so reproducible that it has been given the eponym “third lap syndrome.” In 75–90% of patients, symptoms are bilateral, usually with one leg being worse than the other. The dull ache and discomfort typically remain for a certain duration after the exercise (minutes to hours) and then dissipate. In some patients, this may be accompanied by weakness, numbness, or paresthesias.
Immediately after exercise, the affected compartment may be tender or may feel significantly swollen. This, however, is usually helpful only if just one side is affected. In some patients muscle herniations can occur and be palpated. The presence of these herniations, although frequently found in patients with compartment syndrome, is usually incidental and has no diagnostic value.
Imaging modalities can aid in ruling out the diagnoses of medial tibial stress syndrome, medial gastrocnemius rupture, and stress fracture of the tibia. Radiographs in two orthogonal planes (ie, anteroposterior and lateral) will usually show the periosteal stress reaction in posteromedial stress syndrome. It may or may not show a stress fracture. MRI scanning is very sensitive in evaluating edema around the calf. In case of a muscle injury, it will show a significant signal change with a high intensity in the T2-weighted image. A chronic compartment syndrome may show chronic scarring in the affected compartment. A bone scan cannot be used to diagnose chronic exertional compartment syndrome but it may rule out a stress reaction or stress fracture.
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The most helpful tool for the diagnosis of chronic exertional compartment syndrome is the direct measurement of compartment pressures immediately after exercise in combination with the clinical findings. There are multiple different techniques to measure compartment pressures ranging from a handheld pressure measurement device to the utilization of an arterial line and arterial pressure monitor.
Chronic exertional compartment syndrome is diagnosed if any one of the following three criteria are met:
These measurements are not affected by age but may be affected by position. The correct position during the test involves having the patient supine and the foot vertical.
Treatment
Conservative treatment of a chronic exertional compartment syndrome is generally unsatisfactory. Attempts can be made with the use of NSAIDs and rest, but usually the symptoms will improve only if the athlete is willing to completely stop the activity that brings on the symptoms. If the athlete wishes to continue the activity, operative intervention is the treatment of choice.
All involved compartments need to be surgically released with great care and adequate homeostasis. Multiple different techniques have been described from a single incision to a two-incision technique. Care must be taken to identify the peroneal and saphenous nerves as well as the saphenous vein.
The results of operative compartment release have been consistently good; 90% of patients have a complete recovery with no residual symptoms.
Correctly diagnosing exertional compartment syndrome in an athlete with lower leg pain can be difficult. Successful treatment, of course, depends on the correct diagnosis. Failure of treatment largely results from excessive scarring or incomplete compartment release, especially of the deep compartment. This may happen when the surgeon, for cosmetic reasons, makes the skin incisions too small. Patients must realize that this is not a cosmetically pleasant procedure and it cannot be done through small incisions. Five to 10% of patients have residual symptoms after surgery. Failure can also result in infection, scarring, nerve and vessel damage, as well as recurrence of symptoms despite adequate compartment release.
Return to Play
After surgical treatment, the patient can start gradual strengthening and aerobic training as soon as the incisions have healed. The athlete should be able to return to a full exercise program 8–12 weeks after surgery.
Linz JC et al: Foot and ankle injuries. In: Sports Injuries: Mechanism, Prevention, Treatment. Fu FH, Stone DA (editors). Lippincott Williams & Wilkins, 2001.
Shah SN et al: Chronic exertional compartment syndrome. Am J Orthop 2004;33(7):335.
Ankle Pain
Ankle injuries are among the most common injuries in athletes. Soft tissue sprains and strains as well as ligament ruptures make up the vast majority of all ankle injuries. Ankle sprains and ligament tears can usually be treated successfully with nonoperative management and athletes recover quickly from these injuries. Some pathologic conditions, however, can lead to chronic irritation and inflammation of the ankle and pose substantial problems over a prolonged period.
Posterior Tibial Tendonitis
Essentials of Diagnosis
Pathogenesis
Posterior tibial tendinitis is a very rare occurrence in athletes under the age of 30 years. The majority of posterior tibial tendon problems occur in middle-aged athletes and particularly in women. Posterior tibial tendon injuries rarely develop acutely. There is usually a precipitating
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incident and subsequent slowly developing pain along the course of the posterior tibial tendon. This makes the tendinitis and subsequent rupture of the posterior tibial tendon a chronic disease process. Although it is a rather rare problem for athletes it is devastating should the tendon rupture since the therapeutic options are not ideal and usually lead to a dysfunction.
The posterior tibial tendon is predisposed to injury due to its critical zone of local hypovascularity combined with great mechanical stress acting on the tendon. The large distance between the posterior tibial tendon insertion and the axis of the subtalar joint provides a large lever arm that magnifies the stress on the tendon. Rapid changes in direction (ie, cutting) and jumping activities place the greatest stress on the tendon. Sports such as basketball, tennis, ice hockey, and soccer predispose the athlete to posterior tibial tendon injuries.
Clinical Findings
Athletes complain of medial-sided ankle pain, worse with activity. Night or morning pain indicates more severe injury.
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Figure 4-5. T1-weighted MRI images of the hindfoot. The left image shows a normal hindfoot with the posterior tibial tendon (PTT), the flexor digitorum longus (FDL), and the flexor hallucis longus (FHL). The tendons appear dark and do not show fraying or degeneration. On the right, there is significant fraying and even a tear in the posterior tibial tendon (arrow). The FDL and FHL look normal but there is some fatty degeneration inside the tendon sheaths (white areas within the tendon sheath). |
Physical examination reveals medial-sided point tenderness just inferior and posterior to the medial malleolus. This pain is usually exacerbated by forced inversion or eversion against resistance. A single leg toe raise is usually not possible. Commonly, the athlete will have a flat foot. Athletes usually show up early in the course of this disease because it is debilitating and usually not well tolerated for longer periods of athletic activity.
Imaging Studies
Posterior tibial tendinitis is a clinical diagnosis and does not require imaging. However, it is useful to obtain an MRI for the purpose of documentation and to evaluate the integrity of the tendon and the success of treatment (Figure 4-5). X-Rays of the foot and ankle are utilized to rule out other pathologic entities such as an accessory navicular stress fracture, degenerative joint disease, or anterior tibiotalar impingement.
Ultrasonography is equally accurate in diagnosing tendinitis as well as a rupture of the tibialis posterior tendon and can be easily done in an office setting.
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Treatment
Nonoperative treatment is successful in the majority of patients with posterior tibial tendinitis. The initial treatment follows the earlier described RICE principle. A reduction in the current training program combined with NSAIDs is usually successful. In some athletes, a medial arch support may be helpful, particularly if they have a pronounced flat foot deformity. This treatment should be tried for 6 weeks. If this is not successful then immobilization in a cast or cast-boot should be tried for 4–6 weeks.
If no improvement of symptoms is obtained by 4–6 months surgical treatment options should to be considered.
Surgical Treatment
Operative treatment for posterior tibial tendinitis includes tendon inspection and a tenosynovectomy. The adjacent structures such as the anterior deltoid ligament and the immediately adjacent spring ligament need to be inspected for fraying and tears. If torn, they should be repaired. For more severe injuries, a tendon reconstruction using the flexor hallicus longus or the flexor digitorum longus tendons may be necessary. For severe and chronic injuries with a flexible hind foot, a medial slide osteotomy of the calcaneus may be needed in addition to tendon reconstruction to rebuild the medial arch; however, this is rare in athletes.
Return to Play
Return to play after nonoperative treatment is guided by the absence of pain. The process usually takes 2–4 months before full athletic activity can be resumed. Postoperatively a full ROM needs to be achieved and the return to 80% or more inversion strength and toe raise strength should be obtained before return to full activities. This takes between 4 and 12 months depending on the magnitude of surgery done.
Anterior Tibiotalar Impingement
Essentials of Diagnosis
Pathogenesis
True anterior tibiotalar impingement was first described in 1943 as the “athlete's ankle” and was subsequently described as the “footballer's ankle” in 1950 and as “impingement exostosis of the tibia and talus” in 1954. Athletes who perform sports requiring repetitive forced dorsiflexion of the ankle (ie, soccer, football, dance, and gymnastics) report repetitive small sprains to the anterior ankle that they sustain in full dorsiflexion of their foot. These repetitive injuries lead to chronic sprains of the anterior ankle capsule and microtrauma to the anterior cartilage cap of the distal tibia. These microinjuries lead to a continuous cycle of microtrauma, inflammation, scarring of the capsule, subsequent calcification, and finally formation of bone spurs. Once the bone spurs grow large, they can directly impinge on each other and cause limited dorsiflexion. They may also fracture resulting in the formation of loose bodies in the ankle.
Prevention
Both anterior and anterolateral tibiotalar impingement are chronic conditions that are the result of repetitive microtrauma and therefore are very difficult to prevent. Anterior shin guards extending over the span of the ankle have been tried on soccer players; however, acceptance has been very low since these guards tend to interfere with the soft touch that these athletes require while handling the ball. Taping the ankle against maximally forced dorsiflexion as well as stretching and strengthening exercises should be routine measures for any competitive athlete. The athlete may use local antiinflammatory measures such as cryotherapy if the ankle is sore or after a minor ankle sprain. This may prevent the vicious cycle of chronic inflammation and scar formation early in the process.
Clinical Findings
Patients most often present with a history of anterior ankle or midfoot pain radiating toward the lateral aspect of the ankle joint or the fibula. Initially this pain occurs after vigorous activity and dissipates soon after the activity is stopped. Gradually these symptoms may appear with light or even daily activity and may not dissipate after the activity is stopped. Patients typically report difficulties with climbing stairs and squatting as well as stiffness of the ankle.
Physical examination may reveal marked tenderness over the anterior border of the tibia and sometimes over the dorsum of the talus when the foot is plantar flexed. A ridge may be palpable over the dorsum of the talus. Patients usually display reduced dorsiflexion and a tight
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heel chord. A ligamentous examination of the ankle is usually within normal limits and does not show ligamentous injury.
Radiographs of the ankle show that the anterior margin of the tibia has lost its round contour. Sometimes a bone spur can be seen on the dorsal surface of the neck of the talus. These spurs may be fragmented and can be a source of loose bodies.
Treatment
The initial treatment is nonoperative and involves rest and the use of NSAIDs. If this fails immobilization in a cast or cast-boot for 4–6 weeks should be tried. If the symptoms do not dissipate with modified activities and conservative treatment then an operative procedure should be considered.
Operative treatment addresses the bone spurs and involves removing the anterior osteophyte on the tibia as well as the dorsal bone spur on the neck of the talus. This can be done with an arthroscopic or a miniopen technique. The arthroscopic technique may result in a faster return to activities and enables the surgeon to inspect the ankle joint and thus recognize concomitant pathologies such as osteochondral defects, loose bodies, or formation of scar tissue. For anterolateral impingement the arthroscopic technique is preferred.
Postsurgical rehabilitation aims at restoration of motion and muscle strengthening. Once the surgical incisions have healed a gradual return to activities can be started.
Return to Play
Full ROM of the ankle and 80–100% of inversion/ eversion and plantar flexion dorsiflexion strengths should be regained before return to competitive athletic activity.
Anterolateral Tibiotalar Impingement
Pathogenesis
Anterolateral tibiotalar impingement has a different underlying pathology. Diagnosed much less frequently, it follows repetitive ankle sprains or chronic overuse in sports that involve pivoting. Anterolateral tibiotalar impingement can also follow nondisplaced fibula fractures or ligamentous avulsions of the fibula. The underlying pathology is believed to be a chronic synovitis and thickening of the distal most portion of the anterior inferior tibiofibular ligament complex (eg, anterior syndesmotic band) as a result of repetitive inversion injuries to the ankle. This scar formation was first described as a “meniscoid band” in 1950. Subsequently, a separate band was described as being within the distal aspect of the anteroinferior tibiofibular ligament that is separated, through a fatty-fibrous layer, from the rest of the ligament and can impinge on the talar dome in maximal dorsiflexion of the ankle.
Prevention
Prevention of anterolateral tibiotalar impingement should follow the general principles of preventing ankle sprains, particularly inversion trauma to the ankle. Taping as well as off-the-shelf or custom lace-up braces to provide restraints against forced inversion of the ankle as well as proper strengthening and stretching exercises are the best preventive measures for chronic ankle sprains. High-top athletic shoe-wear, particularly for basketball players, is another means of trying to protect the ankle against inversion injury.
Clinical Findings
Anterolateral tibiotalar impingement is a chronic condition that needs to be considered in patients who have severe anterolateral point tenderness and soreness for a prolonged period of time. Most importantly, it needs to be differentiated from symptoms of chronic instability. It is usually a diagnosis of exclusion and should not be made before all nonoperative treatment options such as NSAIDs, rest, ice, rehabilitation, and modalities have been exhausted.
Patients typically have anterolateral pain with dorsiflexion and sometimes clicking with motion of the ankle. Anterolateral impingement does not cause ankle instability.
Radiographs need to be obtained to rule out stress fractures or fracture of the lateral process of the talus. An MRI can be helpful in identifying the thickened synovial band in the anterolateral recess of the ankle joint. MRI can be helpful in differentiating anterolateral impingement from chronic ruptures of the anterior talofibular ligament (ATFL). The “gold standard” for this diagnosis is ankle arthroscopy, characterized by a thickening of the anterolateral inferior band of the syndesmosis and a synovial fold in the anterolateral recess. Sometimes a small meniscus can cause the symptoms.
Treatment
The initial nonoperative treatment is identical to the treatment of anterior tibiotalar impingement. Operative treatment is an arthroscopic debridement of the synovial
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fold and the inferior anterior band of the syndesmosis. Once this is resected patients usually have a substantial reduction in pain.
Return to Play
Ambulation should be allowed immediately after surgery. Most importantly these patients need to undergo a vigorous rehabilitation program to regain their ROM. Because many of these patients have been deconditioned for a long period of time the coordination and strength of the ankle flexors and extendors as well as pronators and supinators need to be regained and proprioceptive exercises should be part of the rehabilitation process. Return to play should be possible after a 6-week rehabilitation period.
Mosier SM et al: Pathoanatomy and etiology of posterior tibial tendon dysfunction. Clin Orthop Relat Res 1999;(365):12.
Urguden M et al: Arthroscopic treatment of anterolateral soft tissue impingement of the ankle: evaluation of factors affecting outcome. Arthroscopy 2005;21(3):317.
Ankle Instability
Injuries to the ankle are among the most common lower extremity injuries in sports. Overall there are as many as 23,000 ankle sprains in the United States each day. Women have a slightly higher risk of suffering a grade 1 ankle sprain than men on a collegiate level. The recurrence rate after a lateral ankle sprain is high. In high-demand sports such as basketball, the rate of recurrence may be as high as 70%.
Pathogenesis
Lateral ankle sprains most commonly occur due to excessive supination of the rear foot about an externally rotated lower leg soon after initial contact of the rear foot during gait or landing from a jump. Excessive inversion and internal rotation of the rear foot, coupled with external rotation of the lower leg, result in strain to the lateral ankle ligaments. If the strain in any of the ligaments exceeds the tensile strength of the tissues, ligamentous damage occurs. Increased plantar flexion at initial contact appears to increase the likelihood of suffering a lateral ankle sprain.
The ATFL is the first ligament to be damaged during a lateral ankle sprain, followed most often by the calcanofibular ligament (CFL). After the ATFL is ruptured, the amount of transverse-plane motion (internal rotation) of the rear foot increases substantially, thus further stressing the remaining intact ligaments. This phenomenon, described as “rotational instability” of the ankle, is often overlooked when considering laxity patterns in the sprained ankle. Concurrent damage to the talocrural joint capsule and the ligamentous stabilizers of the subtalar joint is also common with lateral ankle sprains. The incidence of subtalar joint injury may be as high as 80% among patients suffering acute lateral ankle sprains.
The cause of lateral ankle sprain may be an increased supination moment at the subtalar joint. An increased supination moment about the ankle moment could thus cause excessive inversion and internal rotation of the rear foot in the closed kinetic chain and potentially lead to injury of the lateral ligaments. Individuals with a rigid supinated foot would be expected to have a more laterally deviated subtalar axis of rotation and a calcaneal varus (inverted rear foot) malalignment, which could predispose those with a rigid supinated foot to lateral ankle sprains.
Whether the peroneal muscles are able to respond quickly enough to protect the lateral ligaments from being injured once the ankle begins rapid inversion has been questioned. The peroneal muscles are active before initial foot contact during stair descent and when landing after a jump. This preparatory activity, along with similar activity in the other muscle groups that cross the ankle, is likely to create stiffness in tendons before initial foot contact with the ground. If the peroneal muscles are to protect against unexpected inversion of the rear foot, preparatory muscle activation before foot contact with the ground is necessary.
Structural predispositions to first-time ankle sprains include increased tibial varum and nonpathologic talar tilt, whereas functional predispositions include poor postural-control performance, impaired proprioception, and higher eversion-to-inversion and plantar flexion-to-dorsiflexion strength ratios. Further research into prevention programs based on these predisposing factors is clearly warranted.
Clinical Findings
Typically an inversion injury has occurred that can be associated with an audible “pop” or a click. The ankle typically becomes swollen, tender, and painful with movement and full weight bearing.
The examiner must delineate the extent of the injury to determine if the patient injured one or multiple ligaments, tendons, bone, or even nerves. Systematically the examiner should palpate the ATFL, the CFL, and the posterior tibiofibular ligament (PTFL). The syndesmosis needs to be examined as well as the medial aspect of the ankle, the deltoid ligament, and the medial malleolus. The lateral malleolus should be palpated at its posterior border and tested for tenderness. Peroneal tendons and the base of the fifth metatarsal also need to
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be palpated. The clinician should stress the ATFL by performing an anterior drawer test. This may or may not be possible in the acute setting depending on the level of pain. The test is performed with the patient sitting and the lower leg hanging freely. The examiner holds the heel and positions the foot in slight plantar flexion. Then the heel is directed anterior while the other hand pushes the tibia posterior. This test is compared to results from the uninjured side. A difference is positive and is considered pathologic. The ankle inversion test can be used to differentiate between the ATFL and the CFL. A forced ankle inversion is performed and any difference from the opposite side is recorded. The inversion tested in plantar flexion evaluates the ATFL. The CFL is tested in dorsiflexion.
To examine the syndesmosis either the Hopkinson's syndesmotic squeeze test or a forced external rotation of the tibia can be performed. Pain when squeezing the fibula and tibia together approximately 10 cm above the joint and pain with forced external rotation of the tibia versus the talus (Keigler test) is suspicious. Tenderness at the inferior syndesmotic band in any of these tests is to be regarded as evidence of a syndesmotic injury until proven otherwise.
Radiographs are used to rule out a fibular fracture, anterior process of the calcaneus fracture, lateral or posterior process of the talus fractures, midtarsal fractures, osteochondral lesions of the talus, and disruptions of the ankle mortise indicating a syndesmotic injury (“high ankle sprain”). MRI can be useful in determining the presence of bone contusions and ligament injuries (Figure 4-6).
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Figure 4-6. Inversion recovery MRI image of the anterior talofibular ligament (ATFL). On the left, the ATFL (arrow A) is intact. It is visible as a strong dark band. On the right (arrow B), it is disrupted, disorganized, and not visible as a collagenous dark structure. |
Treatment
The initial treatment of an ankle sprain consists of the RICE principle. Additional modalities such as electrical stimulation or iontophoresis may be helpful adjuncts to reduce pain and swelling. Provided the injury does not involve the syndesmosis and there is no fracture, rehabilitation of the ankle sprain should be started as soon as pain control has been achieved. The rehabilitation process has to address ROM, strength, and proprioception. Once this phase has been completed and the athlete is pain free with exercises the third phase, designed to bring the athlete back to sports-specific drills and maneuvers such as cutting, jumping, and running, can begin. When the patient returns to athletic activities a protective, lace-up ankle brace should be worn to reduce recurrence of the injury.
If patients report recurrent sprains, continue to experience pain for a long period of time, and continue to have swelling and instability, surgical treatment options may need to be considered.
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A myriad of different techniques have been described for the repair of the ATFL and CFL. The most common operative technique today is probably the Gould modification of the Brostrom technique. This technique essentially repairs the ATFL and CFL directly and imbricates the extensor retinaculum over the top of the direct ligament repair thus serving as a reinforcement of the ATFL and CFL repair. This technique has led to excellent results in high-level athletes and dancers. Using this technique there is no need to harvest any other tendon around the ankle as is required for many of the other ATFL and CFL reconstruction techniques. After a modified Brostrom procedure the athlete must wear a cast or cast-boot for about 6 weeks followed by ROM exercises and the formal rehabilitation program outlined above.
If a syndesmotic injury is suspected, it is imperative that the integrity of the syndesmosis (ie, ankle mortise) is scrutinized. Any increase in medial joint space, disruption of the mortise, or widened gap between the fibula and the tibia may indicate a syndesmotic injury. These “high” ankle sprains are not uncommon. Up to 10% of all ankle sprains also involve the syndesmosis. They occur more frequently in high-energy collision sports such as ice hockey, football, and soccer.
If the athlete suffered a syndesmotic sprain the initial treatment is a cast or cast-boot for a minimum of 2–4 weeks followed by a reexamination. If the tenderness at the anterior syndesmotic band persists, the cast treatment needs to be continued for an additional 2 weeks. Once the anterior syndesmotic tenderness has subsided, the rehabilitation protocol can begin. It is important to know that athletes with a “high” ankle sprain will be sidelined significantly longer than athletes with a simple ankle sprain. If the syndesmosis is disrupted surgical repair with insertion of a syndesmotic screw needs to be performed. This will require wearing a cast and cast-boot for 6–9 weeks followed by rehabilitation.
Return to Play
Patients with simple ankle sprains can be treated with RICE and can return to play as soon as they experience no pain with their sports-specific activities. Those with ATFL tears should undergo formal rehabilitation and can return to play after the third phase of the rehabilitation has been concluded successfully. This usually takes 3–6 weeks. Patients with “high” ankle sprains will be sidelined for 4–12 weeks depending on the treatment necessary.
Osborne MD, Rizzo TD Jr: Prevention and treatment of ankle sprain in athletes. Sports Med 2003;33(15):1145.
Zoch C et al: Rehabilitation of ligamentous ankle injuries: a review of recent studies. Br J Sports Med 2003;37(4):291.
Foot Pain
Achilles Tendonitis
Essentials of Diagnosis
Pathogenesis
There are three different inflammatory entities of the TA that are closely related and require the same initial treatment regime:
A predominantly sedentary life-style followed by a sudden increase in physical activity involving walking, jogging, and running in the mid ages (40–60 years of age) in combination with tight heel chords and decreased ROM of the ankle leads to TA injury. As a general precaution stretching of the TA combined with a gradual increase in activity for elder athletes helps to avoid TA injury. Achilles tendinitis in high-level athletes is usually a sign of faulty training, improper running techniques, or overuse.
Clinical Findings
Most patients complain of a gradual onset of pain in the posterior calf approximately 2–6 cm above the insertion of the TA. Often this pain is accompanied by swelling. Initially the pain will appear after physical activity. This
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can change and the athlete may experience pain during physical activity, usually indicating a worsening of the pathology. Insertional TA tendinitis presents similarly with the exception that it often appears as night pain when the athlete rests the foot on the back of the heel while sleeping.
The diagnosis of Achilles peritendinitis versus tendinosis can theoretically be made by evaluating the location of the point of maximal tenderness. In peritendinitis the entire paratenon is inflamed and therefore will not be affected by ankle ROM during the examination. TA tendinosis is a localized inflammation, in which case ROM will lead to a migration of the point of maximal tenderness throughout the examination. It is important to rule out a tear of the Achilles tendon, which can be done with the Thompson test as described in the section on muscle strains.
Standard radiographs of the ankle may show some calcification along the TA. There may be a thickened soft tissue shadow visible. In case of an insertional tendinitis there may be calcifications anterior to the insertion of the TA (Figure 4-7). An MRI may be helpful in differentiating tendinitis from tendinosis. In tendinitis there is significant fluid retention within the tendon without hypertrophy of the tendinous tissue. This is an acute finding and can usually be successfully treated with antiinflammatory medication and RICE. Significant hypertrophy of the tendon indicates replacement of tendon tissue with a fibrous scar (Figure 4-8). This tendinosis can predispose the patient to a rupture of the TA.
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Figure 4-7. The left image shows a plain radiograph with an increased widened soft tissue shadow along the tendo Achilles (TA) (fat arrow). In addition, this patient has calcifications on the TA insertion (dotted arrow) and a Haglund's deformity (dashed arrow). On the T1-weighted axial MRI image there is an easily appreciated very thick inhomogeneous TA (arrow). |
Treatment
All three injuries of the Achilles tendon initially receive the same treatment. This consists of nonoperative management including NSAIDs and rehabilitation exercises such as stretching and strengthening of the TA and strengthening of the gastrocsoleus complex. If the patient has significant hindfoot varus or valgus a correcting orthosis may need to be issued. Modalities such as iontophoresis and electrotherapy do not have proven
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efficacy but may be employed if pain relief can be obtained. It is usually not necessary to treat patients immobilized in a cast, although in rare cases this may be necessary for recalcitrant pain.
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Figure 4-8. This T1-weighted image of the ankle shows a sagittal view of Achilles tendonopathy. The arrow marks the area of hypertrophic scarring. |
Steroid injections should not be given into the tendon or the tendon insertion as these can lead to an early rupture of the tendon making a primary repair difficult, if not impossible, secondary to the degeneration that the tendon undergoes in response to the steroid injection.
Surgical Treatment
Recalcitrant cases that have not responded to treatment in over 6 months may require surgical debridement of the paratenon and the tendinosis. Using a slightly medially based skin incision the paratenon is incised and debrided and the thickened tendon is thoroughly debrided. If more than 50% of the tendon is involved the plantaris tendon may be woven into the defect to strengthen the repair. The tendon is repaired as well as the paratenon. To ensure that the paratenon is not tightened too much, it can be released carefully on its anterior aspect thus allowing posterior closure without undue tension. A lateral approach is used for insertional tendinitis and the calcaneal bursa is excised. In some cases there is a prominent bony ridge of the posterior calcaneus (ie, “Haglund's deformity”) that may abut the tendon insertion. This bony ridge needs to be removed with an osteotome. Postoperatively the patient is put into a cast or cast-boot for 4–6 weeks. Weight bearing is usually allowed between 2 and 4 weeks and is followed by rehabilitation for 6 weeks.
Return to Play
Once the symptoms have subsided a gradual return to former activities can be allowed. If symptoms return, the eliciting activity should be stopped immediately and a more gradual return should be tried. After operative treatment the rehabilitation protocol is similar after the initial postoperative casting period.
Linz JC et al: Foot and ankle injuries. In: Sports Injuries: Mechanism, Prevention, Treatment. Fu FH, Stone DA (editors). Lippincott Williams & Wilkins, 2001.
Mizel MS et al: Evaluation and treatment of chronic ankle pain. Instr Course Lect 2004;53:311.
Heel Pain
Essentials of Diagnosis
Pathogenesis
Plantar heel pain has many medical names such as plantar fasciitis, runner's heel, policemen's heel, calcaneodynia, and heel pain syndrome. It is one of the commonest problems experienced by athletes. The differential diagnosis of plantar heel pain is often difficult and has to address various different anatomic sites. The spectrum ranges from systemic conditions such as Reiter's syndrome, ankylosing spondylitis, or rheumatoid arthritis to medial plantar nerve entrapment or plantar fibromatosis. Most commonly, however, it is the running athlete who presents with complaints about plantar heel pain. A higher intensity of training sessions, weight gain, and return of overweight athletes to previous training schedules can be reasons. Furthermore, there are certain
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risk factors, such as high-impact aerobics or prolonged daily walking on hard surfaces (ie, construction workers, orthopedic residents). To understand the underlying pathology it is necessary to understand the anatomy and function of the plantar fascia.
The plantar fascia is a strong collagenous structure that originates on the anteromedial aspect of the calcaneus and inserts at the base of each proximal phalanx. The fascia is divided such that the flexor tendons can perforate the fascia to reach the toes. This results in 10 individual insertions of the plantar fascia. Overlying the plantar fascia is the plantar fad pad, which is approximately 2–3 cm thick.
The biomechanical function of the plantar fascia is a continuation of the Achilles tendon around the calcaneus resulting in the “windlass” mechanism. This mechanism enables the foot to stabilize itself in midstance due to a tightening of the longitudinal foot arch.
The tibial nerve splits into its final branches at the level of the medial malleolus. In particular, the first branch of the lateral plantar nerve, the posterior branch or “Baxter's nerve,” can be a source of pain if it becomes trapped between the abductor hallucis and the quadratus planti muscle.
Clinical Findings
Patients report that they have sharp stabbing pain with the first steps in the morning. The pain eases during the day and toward the evening the entire heel is sore.
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Figure 4-9. These MRI images show a sagittal view of a T1-weighted image of a normal foot on the left (A). The T1-weighted image in the middle (B) shows a calcification inside the plantar fascia (arrow). The T2-weighted image on the right (C) shows that these calcifications are inside a zone of edema in the plantar fascia signifying plantar fasciitis. |
Physical examination has to address the underlying pathology and starts with an evaluation of the gastrocsoleus and TA complex. Almost all patients with plantar fasciitis have a tight heel chord and lack dorsiflexion up to, or past, neutral. Furthermore, the forefoot needs to be evaluated. A pronated or plantar flexed first ray can lead to plantar fasciitis in itself. Typically patients have palpable pain directly anteromedially on the plantar surface of the tuber calcanei. If a nerve entrapment is suspected there should be a positive Tinel's sign over the medial aspect of the heel just beneath the medial malleolus. Furthermore, a careful palpation of the plantar fascia should be performed to rule out single or multiple plantar fibromata.
Radiographs do not usually show the pathology. There may be a “bone spur” along the anterior aspect of the calcaneus, however, this bone spur actually arises within the aponeurosis of the flexor digitorum brevis and is not involved in the development of plantar fasciitis. An MRI scan can be helpful in detecting abnormalities of the plantar fascia. It will show increased fluid uptake in the T2-weighted images along the anteromedial border of the plantar fascia (Figure 4-9). It may also show a plantar fibroma or a neuroma of Baxter's nerve. An MRI scan may also indicate occult stress fractures that could be the cause of plantar foot pain such as an anterior process of the calcaneus fracture.
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Treatment
The treatment for plantar fasciitis is focused on addressing the underlying disorder. Patients need to be counseled so that they understand that this condition is self-limiting and that successful treatment can take up to a year. The chronic tightness of the plantar fascia leads to a contracture of the fascia during sleep. The first steps in the morning stretch this contracted fascia and cause microtears that subsequently scar during the next rest period until the plantar fascia has eventually elongated to a point at which no more microtears occur. To break this cycle the first line treatment is stretching of the plantar fascia and the TA. A short heel chord leads to overuse of the windlass mechanism and consequently results in overtightening of the plantar fascia. Patients therefore should be instructed to stretch the TA multiple times during the day. In addition, they can be provided with night splints that prevent the contraction of the plantar fascia and keep the foot in neutral dorsiflexion during sleep. Furthermore, heel cups help to cushion the hard impact on the heel. There is some debate about the usefulness of full arch supports. It has been shown that they work as well as simple heel cups as long as they are utilized in conjunction with stretching exercises. In severe cases of plantar fasciitis it may be helpful to treat the patient with a cast or cast-boot for a few weeks to rest the plantar fascia before a rigorous stretching program is started.
We discourage steroid injections into the plantar fascia. Although the literature provides conflicting data on the success of steroid injections, there is clear evidence that use of steroid injections is associated with a high risk of a tear of the plantar fascia, which results in a catastrophic flat foot deformity that is essentially not correctible.
If the source of pain is entrapment of Baxter's nerve an electromyogram (EMG) should be obtained. If the EMG and nerve conduction studies suggest a nerve entrapment the first line of treatment is orthotics that correct any present foot deformity (overpronation, pes planus, pes planovalgus etc).
Surgical Treatment
Surgical release of the plantar fascia is reserved for very rare severe cases of plantar fasciitis in which there is intractable pain for 1 or more years. Various techniques have been used to release the plantar fascia. It is important that this is done under direct visualization. The medial aspect of the plantar fascia needs to be partially excised. A complete release will result in a deficiency of the plantar fascia and an uncorrectable flatfoot deformity. If a release of a plantar fascia is performed it is prudent to include a release of Baxter's nerve. This is important for two reasons. First, the nerve needs to be visualized so as not to cut it and second, there may be an element of both pathologies that can easily be addressed through one approach.
Return to Play
Athletes who are pain free can return to their previous exercise program. Running athletes are advised to maintain the stretching program in their warm-up routine.
Linz JC et al: Foot and ankle injuries. In: Sports Injuries: Mechanism, Prevention, Treatment. Fu FHg, Stone DA (editors). Lippincott Williams & Wilkins, 2001.
Williams SK, Brage M: Heel pain-plantar fasciitis and Achilles enthesopathy. Clin Sports Med 2004;23(1):123.
Turf Toe
Essentials of Diagnosis
Pathogenesis
Sprains of the first MTP joint have been described as “turf toe” injuries since it was noted that athletic competition on artificial turf resulted in an increased incidence of soft tissue injuries to the great toe. Injuries to the first MTP joint occur in football and soccer but can happen during any athletic activity that forces the first MTP joint into hyperplantar or hyperdorsiflexion. Injuries to the first MTP joint are by no means benign and carry a significant short- and long-term morbidity. Despite the usual perception that this is a “trivial” injury, overall estimates of loss of playing time rank MTP joint injuries first, at the same level as ankle sprains even though they occur far less frequently.
The mechanism of injury is a hyperdorsiflexion injury that usually happens when the foot is planted and the first MTP joint is maximally dorsiflexed. The dorsal edge of the proximal phalanx is cocked against the articular surface of the metatarsal head. The capsuloligamentous structures are maximally stretched in this position. Forcing the first MTP joint into greater hyperdorsiflexion will lead to a structural failure of either the volar capsule or the collateral ligament or a fracture of either the dorsal phalanx or the metatarsal head. Classically this situation occurs when an offensive lineman plants his foot for maximal traction and another player falls onto his heel forcing his forefoot into greater hyperdorsiflexion. It also occurs when the foot, in maximal plantar
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flexion with the first toe pointed, is struck from behind, driving the first MTP joint into greater hyperplantar flexion.
To prevent these injuries the first MTP joint can be taped to limit dorsiflexion and plantar flexion. The variability in ROM of the first MTP joint is great. Normal ROM can range from 3–43 degrees of dorsiflexion to 40–100 degrees of plantar flexion. Individuals with a naturally limited ROM are at increased risk for “turf toe” injuries and should be taped. There is some evidence that the use of an orthotic (eg, Morton extension) or a 0.51-mm spring steel insert may help prevent these types of injuries.
Clinical Findings
Injuries to the first MTP joint vary widely. The spectrum of injury ranges from a simple sprain to complete avulsions of the dorsal or volar plate with or without associated fractures of the metacarpal head or base of the phalanx. In addition, the sesamoid bones can be involved in the injury if the flexor tendons are part of the injury.
The trainer or physician on the sideline must keep a close eye on players who come off the field with a limp. Turf toe injuries are often treated as a minor injury by players. This leads to prolonged recovery and problems later on. Patients complain of first MTP joint pain and difficulty pushing off the injured foot.
A physical examination of the first MTP joint should include a study of active and passive ROM. The results of the examination have to be compared to the results from the opposite side and it needs to be noted if either active or passive ROM is painful. The normal examination should be painless. Pain at the extremes of ROM may indicate whether the injury is volar or dorsal. Strengths of the flexor hallucis longus as well as the extensor hallicus longus need to be tested to rule out an avulsion injury. Stability of then first MTP joint in valgus and varus stress also needs to be evaluated to rule out collateral ligament damage.
A classification system has been designed that is helpful in assessing the severity of the damage.
Grade 1 sprains represent stretch injuries:
Grade 2 sprains represent a partial tear of the capsuloligamentous complex:
Grade 3 sprains are complete disruptions of the capsuloligamentous complex with or without bony avulsions and osteochondral fractures:
Once the clinical diagnosis of a turf toe injury is made further diagnostic tools may be needed to clearly delineate the severity of the injury. We believe that any turf toe injury that is significant enough to cause pain with ROM should be evaluated with radiographs. Further diagnostic tools should be used if it is suspected that the severity of the injury is greater.
Radiographs reveal avulsion fractures, osteochondral incongruencies in the metatarsal head or base of the phalanx, migration of the sesamoids, widening of the bipartite sesamoids, or subchondral bone resorption that can be seen with chondral injuries. If a collateral ligament or a purely ligamentous volar/dorsal plate injury is suspected, stress radiographs should be performed in valgus or maximal plantar/dorsiflexion of the MTP joint. If a stress fracture of a sesamoid is suspected, a bone scan can be obtained. An MRI can be used for diagnosis of ligament avulsions, particularly of the volar plate (Figure 4-10)
Treatment
Treatment of turf toe injuries is primarily nonsurgical. The initial treatment protocol adheres to the RICE principle followed by cryotherapy during the first 48 hours after the injury. The most important factor for rehabilitation following these injuries is rest until painless ROM is obtained. For simple grade 1 sprains without any structural damage the athlete can usually return to light stretching and functional rehabilitation within the painless ROM. Taping and toe spacers can be used to counter the initial injury mechanism.
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Figure 4-10. These T1- and T2-weighted MRI images of a turf toe injury show the disruption of the plantar plate at the first matatarsophalangeal joint (arrows). |
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For more severe grade 2 sprains athletes may miss between 5 and 14 days of training and game time. The treatment follows the same rules as for grade 1.
For grade 3 sprains the treatment depends on the anatomy of the injury. The initial treatment is the same as for grade 1 and 2 sprains. Athletes often require crutches for a few days to immobilize the toe.
In grade 3 injuries, surgical treatment may be necessary. Although capsular avulsions and collateral ligament injuries usually heal with nonoperative treatment, fractures, osteochondral avulsions, and nonreducible dislocations need to be addressed surgically. Late sequelae such as osteochondral nonunions, sesamoid nonunions, loose bodies, or late acquired deformities such as hallux varus or rigidus almost always require surgical intervention if conservative measures have failed.
Return to Play
For simple grade 1 sprains, once the athlete is pain free return to play is possible. For grade 2 sprains, it is imperative that the athlete is pain free before return to play. After a grade 3 injury, an athlete may need between 4 and 8 weeks to return to play. These injuries can be career ending, so it is not desirable to push a return to play until the athlete is completely pain free throughout all required drills.
Katcherian DA: Pathology of the first ray. In: Orthopaedic Knowledge Update (OKU)2. Mizel M et al (editors). American Academy of Orthopaedic Surgeons, 1998.
Mullen JE, O'Malley MJ: Sprains: residual instability of subtalar, Lisfranc joints, and turf toe. Clin Sports Med 2004;23(1):97.
Watson TS et al: Periarticular injuries to the hallux metatarsophalangeal joint in athletes. Foot Ankle Clin 2000;5(3):687.