Porter & Schon: Baxter's The Foot and Ankle in Sport, 2nd ed.

Section 3 - Anatomic Disorders in Sports

Chapter 20 - Chronic leg pain

Peter H. Edwards Jr.,Peter B. Maurus


CHAPTER CONTENTS

  

 

Introduction

  

 

Medial tibial stress syndrome

  

 

Stress fractures

  

 

Chronic exertional compartment syndrome

  

 

Nerve entrapment

  

 

Popliteal artery entrapment syndrome

  

 

Operative

  

 

Summary

  

 

References

Introduction

As the general population in the United States has become more active, orthopaedists have observed an increase in the incidence of sports-related injuries. Nonspecific complaints of pain in the foot, ankle, calf, or shin are often reported, with shin pain as the most common presentation. [0010] [0020] Evaluation of leg pain not only requires knowledge of the anatomy and biomechanics of the lower extremity but also an understanding of the pathology of the injury. Conducting a thorough history and physical examination and appropriately interpreting diagnostic tests are essential to the establishment of an accurate diagnosis. In addition, specific details regarding physical activity, including training regimens, surface conditions, and shoewear must be determined, because these factors also play a significant role in the diagnosis.

Because several etiologies may present with similar characteristics, patients must be evaluated for multiple conditions.[3] The differential diagnosis of chronic leg pain includes the following conditions: bony or soft-tissue tumors, chronic exertional compartment syndrome (ECS), claudication, isolated leg trauma, medial tibial stress syndrome (MTSS), muscle strains, nerve entrapment, popliteal artery entrapment syndrome (PAES), radiculopathy, referred pain from meniscal pathology, stress fractures, and tendinitis. Despite this wide range of diagnoses, several studies demonstrate that certain conditions are more prevalent among athletes, in particular. [0010] [0040] [0050] [0060] In a retrospective review of 72 track and field athletes with athletic-related injuries, 28% of injuries were due to overuse of the leg.[4]Furthermore, chronic exertional shin pain accounts for approximately 10% to 15% of all running injuries and may be responsible for approximately 60% of all leg pain syndromes.[1] In another retrospective study of 150 patients with exercise-induced leg pain, chronic ECS was the most prevalent cause of pain, representing 33% of cases; stress fractures and MTSS accounted for 25% and 13% of cases, respectively.[6] Conversely, in our experience MTSS has been more prevalent than either chronic ECS or stress fractures. This chapter focuses on common causes of chronic leg pain in athletes, including MTSS, stress fractures, chronic ECS, nerve entrapment, and PAES. The incidence, pathology, clinical presentation, and treatment options are discussed for each condition.

 

Medial Tibial Stress Syndrome

“Shin splits” is a nonspecific diagnosis of posteromedial leg pain commonly used to describe not only MTSS but also a wide variety of other lower leg pain conditions, including chronic ECS, fascial hernia, muscle strains, periostitis, and stress fractures. [0020] [0030] [0050] [0070] [0080] [0090] One of the most common sites of overuse pain is the distal one third of the medial border of the tibia. [0090] [0100] [0110] [0120]Several terms, including medial tibial syndrome, MTSS, tibial stress syndrome, posterior tibial syndrome, soleus syndrome, and periostitis have been proposed to link this common clinical presentation to a specific condition. [0020] [0110] [0120] [0130] [0140] [0150] [0160] [0170] [0180] [0190] Medial tibial stress syndrome may be the most accurate of these terms, however, because it describes both the location and the likely pathophysiology of the syndrome. [0050] [0110] [0120] [0200]

MTSS typically is observed in runners and individuals involved in jumping activities such as basketball and volleyball. [0030] [0080] [0110] [0180] [0210] [0220] In our experience it also represents the most common cause of chronic leg pain. Both biologic and biomechanical factors have been reported as possible causes of MTSS. [0100] [0110] [0120] Although the tibialis posterior muscle historically has been implicated as the source of this condition, [0090] [0160] [0220] [0230] [0240] a recent study of 50 cadaveric legs revealed that the tibial posterior muscle was more lateral, indicating that this muscle was not a likely source of MTSS.[10] Other recent studies have identified the soleus, flexor digitorum longus (FDL), and crural fascia as sources of the pain. [0100] [0150] [0250] More specifically, a three-phase bone scan study of 10 patients with MTSS demonstrated low-grade uptake along a diffuse region of the posteromedial tibia, suggesting that the condition is related to the soleus muscle.[15]

During running, heel strike occurs in relative supination, with pronation of the foot increasing until midstance. [0110] [0170] [0260] Because the soleus is the primary plantarflexor and invertor of the foot, it has been theorized that the medial portion of this muscle contracts eccentrically as the foot pronates ( Fig. 20-1 ).[17] The repetitive eccentric contraction that occurs in hyperpronating athletes may explain the increased incidence of MTSS observed in such athletes. [0050] [0090] [0110] [0140] [0170] [0250] [0270] [0280] [0290] In addition, hyperpronation is a compensatory mechanism that occur in patients with hindfoot and forefoot varus, [0250] [0260] tibia vara,[26] tight Achilles tendon, [0260] [0280] [0290] and tight gastrocnemius and soleus muscles;[26] therefore such patients also are at increased risk for developing MTSS.

 
 

Figure 20-1  (A) During running, the medial portion of the soleus contracts eccentrically as the foot pronates. Hyperpronating athletes, in particular, are at an increased risk for developing medial tibial stress syndrome (MTSS). (B) The source of pain is at the origin of the flexor digitorum longus (FDL) and soleus fascial bridge on the posteromedial aspect of the tibia.

 

 

History

The most common complaint associated with MTSS is a recurring, dull ache localized over the distal one-third posteromedial cortex of the tibia ( Case Study 1 ). In our experience, MTSS tends to occur late in the sport season after prolonged activity, whereas stress fractures tend to occur early in an athletic season as stresses increase rapidly. Early in the development of MTSS, patients may experience pain at the beginning of a workout or run but feel a relief of symptoms with continued activity, only to be followed by a recurrence of pain either at the conclusion of the activity or some time afterward. Pain usually is alleviated with rest and generally does not occur at night. However, as this condition progresses, pain may occur throughout training or during low activity, such as walking, and possibly may continue during rest.

Case Study 1

A 16-year-old, female, cross-country runner presented for evaluation of progressive right leg pain. Over the preceding 3 weeks, training intensity had been increased in preparation for a season-ending tournament. During that time, increasing pain developed over the distal medial leg. Initially, pain was present only at the conclusion of training but progressed to include soreness on first arising in the morning and with daily activities, forcing the patient to decrease training. She denied constitutional symptoms, history of trauma, or recent shoewear change.

Physical examination was remarkable only for tenderness along the posteromedial cortex of the distal one third of the tibia. Plain radiographs were normal. On the basis of a clinical diagnosis of MTSS, conservative treatment, consisting of cessation of training for 2 weeks, NSAIDs, and ice, was recommended. At the 2-week follow-up, only minor improvement had been achieved and the patient remained in significant pain. Consequently, a range-of-motion boot was implemented and a bone scan was ordered to rule out a possible stress fracture. Because the bone scan was negative, as indicated by a diffuse uptake in the delayed phase, the patient remained in the range-of-motion boot for an additional 4 weeks. After this period, activities of daily living were conducted without pain, permitting a gradual return to training over the ensuing 6 weeks.

Physical examination

The pathognomonic physical finding in MTSS is palpable tenderness along the posteromedial edge of the distal one third of the tibia. In rare cases, erythema or localized swelling over the medial tibia also may be observed. Although studies have reported conflicting ranges of motion associated with MTSS, in theory, hypermobile pronating feet are at increased risk of MTSS. Therefore evaluation for foot pronation or subtalar varus also is recommended. Abnormal pulse, diffuse swelling, firm compartments, neurologic deficits, and vibratory pain are not associated with this syndrome.

Diagnostic studies

Roentgenograms generally are normal in patients with MTSS [0030] [0070] [0110] [0170] [0300] but are recommended to rule out abnormalities associated with other conditions such as stress fractures and tumors.[0030] [0110] [0120] A three-phase bone scan is warranted to rule out stress fractures if a conservative treatment program does not alleviate pain. This type of bone scan is a valuable diagnostic tool used to differentiate between MTSS and stress fractures, because each condition has a distinct scintigraphic pattern. [0070] [0090] [0110] [0150] [0170] [0310] [0320] A bone scan demonstrating a longitudinal and diffuse pattern in the distal one third of the tibia is indicative of MTSS ( Fig. 20-2 ). [0090] [0110] [0150] [0320] In general, only delayed images are positive in cases of MTSS, whereas both early and delayed images demonstrate uptake in cases of stress fracture. [0110] [0150] In addition, magnetic resonance imaging (MRI) is another diagnostic tool for MTSS recommended by some authors. [0110] [0310] However, we believe that MRI has a limited role in the evaluation of MTSS because of its higher cost compared with other imaging options[7] and its difficulty in delineating MTSS from stress fractures.

 
 

Figure 20-2  Classic bone scan demonstrating the increased linear uptake along the posteromedial aspect of the tibia in the delayed phase indicative of medial tibial stress syndrome (MTSS). The linear uptake is most commonly observed in the distal one third of the leg; however, in this specific case, the location is slightly more proximal.

 

 

Treatment

Conservative

The recommended management of MTSS is multimodal, consisting of rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and ice. [0030] [0120] Physical therapy modalities such as iontophoresis and ultrasound also may be used. [0030] [0120] Initially, rest or a decrease in training for 2 to 3 weeks is suggested and may be curative without further workup.[12] Cardiovascular conditioning may be maintained during this period with swimming, upper body weightlifting, and deep-water running. [0110] [0120] Stationary biking is another option but should be performed with the heel on the pedal, a precaution that will diminish muscular stress transmission to the leg. NSAIDs often are prescribed to relieve pain [0110] [0120] and to decrease possible inflammation. Ice may be used to further reduce swelling and inflammation. [0120] [0310] Addressing biomechanical abnormalities is also recommended. [0120] [0330] [0340] For example, excessive pronation may be corrected with the use of custom or off-the-shelf orthotics.[33] Physical therapy modalities, including massage, electrical stimulation, iontophoresis, and ultrasound also have been used. [0100] [0310] [0350] If pain is present with walking or at rest, range-of-motion boots and/or walkers are used. In rare cases, crutches may be necessary.

If the patient has not experienced pain during conservative treatment, a gradual return to training may be initiated. Warm-up and cool-down routines, including stretching, are advised with each workout to prevent recurrence of symptoms. If the patient remains asymptomatic, progression of training is recommended at increments of 10% to 25% for 3 to 6 weeks.[11] If symptoms return, activity should cease for at least 2 weeks before training is resumed at a lower intensity and duration.

Operative

Fasciotomies of the posterior compartments of the tibia are possible treatment options in patients with intractable MTSS. [0060] [0110] [0140] [0340] [0360] In these rare cases, fasciotomies may alleviate the pull of the soleus and deep compartment muscles on the corresponding fascial insertions. [0060] [0110] [0140] [0340] [0360] However, in our experience, conservative management alone has been successful in treating MTSS cases, eliminating the need for surgical intervention.

   Pearl

MTSS pain actually may subside during workout but will recur following cessation of activity. Conversely, pain associated with chronic ECS and PAES does not subside during activity and tends to remain until activity is completed.

Pain is localized to the distal one third of the tibia in MTSS but is usually more proximal in the typical stress fracture.

 

Stress Fractures

Repetitive loading caused by overuse or overloading of the lower leg results in microtrauma to the bone that eventually may lead to stress fracture. [0060] [0350] [0370] [0380] [0390] Stress fractures of the tibia are more frequent [0030] [0110] [0370] [0400] [0410] [0420] [0430] [0440] and more problematic to treat than those of the fibula. Fibula stress fractures tend to heal more rapidly and generally do not require adjunctive therapy. [0410] [0430] The focus of this section is on tibial stress fractures because most fibula stress fractures occur about the ankle and are covered elsewhere.

Most fractures of the tibia occur in the proximal metaphyseal or upper diaphyseal regions, [0350] [0440] [0450] whereas tibial fractures that are longitudinal in nature [0460] [0470] [0480] [0490] or occurring in the midanterior region [0090] [0350] [0370] [0380] [0500] [0510] are less prevalent. Athletes, in particular, are subject to stress fractures of the leg. Specific stress fractures also are related to certain types of activities. For example, the more common posteromedial stress fracture usually is associated with running activities. [0110] [0350] [0460] Conversely, midanterior tibial cortex stress fractures often are associated with dancers and athletes involved in cutting and jumping activities. [0350] [0380] [0500] [0510] [0520] [0530] [0540]

Risk factors for developing a stress fracture include excessive training, training errors, biomechanical variants, and menstrual irregularities with corresponding changes in bone density. [0090] [0110] [0400] [0420] [0460] [0550] [0560] Excessive training, particularly common early in the athlete's season, causes overuse or overloading, which may result in stress fracture. [0060] [0350] [0460] In addition, overlapping of sport seasons, which often occurs when teenage athletes participate in multiple sports, also may lead to an overuse scenario. Training errors, including changes in training surface, shoewear, and technique often result in overloading, which may result in stress fracture. [0060] [0350] [0370] Weather and seasonal differences affect surface conditions for many outdoor sport activities and may increase the risk of stress fracture. For example, dry conditions and the fall season are both associated with hard ground surfaces, which result in an overloading environment for soccer players. Simple measures, such as watering soccer fields when the ground is hard, may reduce the risk of stress fracture and other injuries by minimizing loading conditions. Biomechanical factors, such as cavus feet, leg-length inequality, and muscular imbalance also may increase the risk of developing a stress fracture. [0090] [0110] [0400] [0440] Finally, low body weight and menstrual abnormalities in female runners have been associated with an increased incidence of stress fractures. [0390] [0400] [0420] [0550]

The cause of stress fractures is multifactorial in nature and often results from an imbalance of natural bone formation and resorption cycle because of repetitive loading. [0370] [0440] [0510] [0560] One theory proposed to explain the mechanism of stress fracture suggests that muscle fatigue results in the transmission of excessive forces to the underlying bone, ultimately leading to stress fracture. [0200] [0370] [0440] [0510] [0550] Another hypothesis asserts that simple, repetitive weight bearing leads to a concentrated rhythmic muscle action, which causes excessive transmission of forces beyond the threshold of bone, thereby resulting in fracture. [0200] [0370] [0440] [0510] [0570] Forces from large posterior muscle groups, in particular, may cause increased tension on the anterior cortex of the tibia, possibly leading to the problematic midanterior tibial stress fracture.[51]

History

Pain associated with tibial stress fractures is more proximal than that caused by MTSS ( Case Study 2 ). Although pain typically is localized to the fracture site, diffuse pain also may occur. Stress fracture pain will develop gradually, occurring initially as a mild ache following a specific amount of exercise and then subsiding. As the condition progresses, pain may become severe and occur during earlier stages of exercise and after cessation of activity. In rare cases, night pain also is possible. Any complaints of constitutional symptoms, including fever and fatigue, should raise concern of a possible tumor or infectious process.

Case Study 2

A 16-year-old, female soccer player related a 3-week history of anterior tibial pain localized approximately 7cm below the tibial tubercle. Initially, pain was mild and occurred only with prolonged training. When the patient continued her training intensity, the pain progressed to the point at which training became difficult and persisted with daily activities; however, the patient did not seek treatment at this time. Before her final game, the patient stated that her pain was so severe she was unsure whether she should could continue to play. Despite constant pain, the patient competed in the final game and experienced a noncontact tibial fracture while running.

Roentgenograms confirmed the presence of a tibial fracture with an intact fibular that was located at the anterior tibial cortex approximately 7cm below the tibial tubercle, corresponding to the site of a presumed existing stress fracture. Conservative treatment was recommended and involved long-leg casting for 3 months. Because of minimal bone healing, determined by radiographic evaluation, long-leg casting continued and pulsed electromagnetic stimulation was added for 1 month. Following the use of the long-leg cast, a long-leg fracture brace was used with continued pulsed electromagnetic stimulation.

After 6 months of conservative treatment, aching continued at the fracture site on weight-bearing ambulation. Subsequent plain radiographs and computed tomography (CT) scan indicated small areas of spot weld healing but a largely inadequate bridging callus. Consequently, operative treatment involving reamed intermedullary nailing of the tibia without fibular osteotomy was performed. Approximately 4 months following surgery the fracture was completely healed, and, by 8 months postsurgery the patient returned to playing soccer.

In addition to obtaining a history of pain and symptoms, training and activity also should be investigated to identify possible errors that may increase the risk of stress fracture. Recent changes in activity level, such as increased quantity or intensity of training, modifications in training surface, shoewear alterations, and technique should be noted. Inquiries regarding diet also should be conducted because the presence of eating disorders increases the risk for stress fracture. Furthermore, obtaining menstrual histories of female athletes also is pertinent because oligomenorrhea and delayed menarche both increase the risk of stress fracture. Finally, a review of systems is suggested to assess general health, medications, and personal habits to identify any additional factors possibly influencing bone health.

Physical examination

On gross physical examination, the leg will appear normal. Compartments should be soft and the posteromedial aspect of the middle to distal one third of the tibia should not be tender. Joint range of motion usually is normal, but gait analysis may reveal biomechanical risk factors. Neurovascular examination typically is normal in the absence of any associated abnormalities. Palpation will reveal tenderness localized to the fracture site. In addition, erythema or localized swelling also may be noted. An ultrasound or a tuning fork will produce vibratory pain over the site of the stress fracture. In long-standing fractures, a palpable bony thickening may be present.

Diagnostic studies

A clinical diagnosis of stress fracture often may be made solely on the basis of the history and physical examination, [0370] [0560] but diagnostic imaging may confirm the diagnosis or assist in identifying the stress fracture in questionable cases. Plain roentgenograms should be performed as the first imaging step but may be negative, because radiographic abnormalities often are not observed until 2 to 3 weeks after the onset of symptoms. [0030] [0370] [0440] [0460] Radiographic abnormalities may appear as a faint periosteal reaction, a fluffy area of callus, or a cortical lucency.[39] If radiographic examination demonstrates the presence of a stress fracture, no further imaging is necessary.

A three-phase bone scan is indicated when suspicion of stress fracture remains despite negative radiographs. [0390] [0460] The specific scintigraphic pattern of a stress fracture demonstrates focal uptake in the area of fracture ( Fig. 20-3 ). [0370] [0580] MRI, another diagnostic option, differentiates among fracture, tumor, and infection and also localizes the pathology. [0310] [0440] [0460] [0560] [0590] However, because a diagnosis often may be determined by plain radiograph or bone scan, both of which are more cost effective than an MRI, we reserve MRI for special cases, including a history of allergic response to dye, an aversion to needles, or an atypical presentation. An MRI also is useful in differentiating between longitudinal stress fractures and MTSS, the more commonly observed overuse injury, because bone scans of these conditions demonstrate identical diffuse uptake in the distal one third of the tibia ( Case Study 3 ).

 
 

Figure 20-3  Bilateral bone scan demonstrating normal scintigraphy (left) versus the focal uptake pattern of a typical tibial stress fracture (right).

 

 

Case Study 3

A 47-year-old woman who regularly walks for cardiovascular fitness presented with complaints of left lower-leg pain. The patient described a “deep-aching” pain in the lower one third of her leg. Over the past 3 months, pain increased with continuation of the patient's walking program and began to occur at night, eventually resulting in limitation of activity. Her medical history was significant for osteoporosis and systemic lupus erythematosus, which was treated with multiple medications.

Neurovascular and physical examinations were grossly normal. No swelling was observed, but palpation revealed mild tenderness along the distal tibia. Plain radiographs did not reveal the presence of a fracture or periosteal reaction. An MRI was ordered to differentiate between the suspected longitudinal stress fracture and possible MTSS and subsequently demonstrated a longitudinal stress fracture in the tibial metaphysis with surrounding bone edema ( Fig. 20-5 ). Conservative treatment involving a range-of-motion boot and nonweight-bearing ambulation was recommended. Six weeks following treatment, plain radiographs demonstrated a slight callus formation, indicative of the healing process. As a result, the patient was instructed to progress from partial to full weight-bearing ambulation over a 4-week period. Full weight-bearing ambulation in a range-of-motion boot continued for an additional 4 weeks, with subsequent introduction of a regular shoe. At 4½ months, the patient resumed her walking program with a gradual increase in mileage.

In addition to its diagnostic capabilities, imaging also assists in differentiating among the various types of stress fractures. For example, radiographs depicting a small lucency or a “dreaded black line” in the midanterior cortex of the tibia are indicative of a midanterior cortex tibial stress fracture ( Fig. 20-4, A ). [0350] [0460] Because of the relatively avascular nature of this portion of the tibia, a bone scan initially may be interpreted as negative, but closer examination will depict an area of decreased uptake at the fracture site. [0460] [0540] If this type of fracture is not initially diagnosed and treated, a complete fracture may result. Conversely, plain radiographs of longitudinal tibial stress fractures often are normal, whereas bone scans will demonstrate increased uptake in the lower tibia.[60]




 

Figure 20-4  (A and B) Preoperative radiographs of a male runner who presented with a midanterior cortex tibial stress fracture, also referred to as a “dreaded black line,” which is visible in the lateral radiograph (B). (C and D) Because of the severity of the fracture, intramedullary nailing was required. As demonstrated in the 2-month postoperative radiographs, the fracture healed completely without the need for bone grafting.

 

 

Treatment

Conservative

Conservative treatment for stress fracture is focused on pain relief and protection from further injury. [0390] [0460] Improvement in muscular strength and endurance, continuation of cardiovascular fitness, and management of biomechanical factors also are important. Relative rest, possibly with weight-bearing restriction, is recommended for a minimum of 2 to 4 weeks. Mild analgesics or NSAIDs also may be prescribed in conjunction with physical therapy modalities, such as ice or cross training. [0380] [0460] Cardiovascular fitness should be maintained with cycling, swimming, deep-water running, or other nonloading activities. [0390] [0440] [0460] [0580] Upper body strength training is recommended to maintain muscle mass and is not likely to jeopardize fracture healing.[44] Bracing or casting may be required for 3 to 12 weeks to immobilize the fracture adequately in severe cases or if pain is not relieved after the initial 2- to 4-week rest period. [0330] [0610] Because prompt return to activity is a priority for elite athletes, electrical stimulation is highly recommended. Electrical stimulation also has been effective in healing nonunioned traumatic fractures. [0350] [0460] [0500] [0510]

Contributing factors, such as training errors, improper shoewear, and muscle imbalance that were identified in the history and physical examination also must be addressed. [0060] [0390] [0440] Training regimens should be individualized for each patient. Treatment plans for athletes with eating disorders or females with menstrual irregularities should involve dietary counseling and/or estrogen replacement therapy to accelerate healing and to prevent future problems. [0370] [0460] Shoes should be examined for signs of wear and inadequate support and also must be replaced every 500km. [0380] [0460] If necessary, appropriate orthotics should be implemented.

Return to activity should be gradual and individualized according to symptoms, with an emphasis on progress only when activity is accomplished without pain. [0440] [0460] It must be stressed that activity should cease if any pain occurs and should not be reattempted until the pain is alleviated. [0460] [0580] In addition, once the pain is alleviated, the patient must return to the lower loading activity and not advance until each successive activity has been accomplished without pain. A period of rest also must be implemented between activities before advancing to a higher loading activity. Although athletes may resume full training in 8 to 16 weeks, patients must be aware that a prolonged recovery period may be required for more severe stress fractures. [0510] [0540] Midanterior cortex tibial stress fractures, in particular, require a significant period of rehabilitation. [0030] [0380] [0460] [0500] [0510] [0580] Despite this prolonged rehabilitation, conservative treatment is similar to that for other tibial stress fractures and includes avoidance of activity, bracing or casting, and possible electrical stimulation. [0460] [0510] [0540]

Operative

Although most stress fractures heal successfully with conservative treatment, surgery may be warranted for severe stress fractures, such as midanterior or longitudinal tibial stress fractures, or for chronic nonunions of proximal medial stress fractures. [0380] [0500] [0510] [0540] Intramedullary nailing has yielded promising results in high-demand patients with problematic stress fractures. [0380] [0500] [0510] [0540]Our experience with intramedullary nailing also has been positive and involves the treatment of three midanterior tibial stress fractures, all of which healed completely without the need for bone grafting (Fig. 20-4, B ).

   Pearl

Vibration from a tuning fork or ultrasound will produce pain corresponding to the stress fracture site but will not elicit pain in cases of MTSS or chronic ECS.

If a stress fracture is suspected on the basis of the history and physical examination despite negative plain radiographs, additional imaging, such as a three-phase bone scan, is recommended to confirm the diagnosis.

Pain and swelling in the subcutaneous border of the tibia is indicative of a midanterior tibial stress fracture, which requires careful radiographic evaluation to confirm the presence of the subtle “dreaded black line.” If diagnosis remains questionable, a three-phase bone scan demonstrating a focal area of decreased uptake in the anterior tibial cortex will confirm the diagnosis.

 

Chronic Exertional Compartment Syndrome

Chronic ECS of the lower leg generally is induced by exercise that impairs neuromuscular function within the involved compartment and is characterized by pain and swelling. [0620] [0630] This syndrome is classified into two forms: acute, the more severe form requiring immediate surgical intervention, and chronic. [0620] [0640] [0650] [0660] [0670] [0680] [0690] [0700] [0710] [0720] Acute ECS, commonly caused by trauma, occurs when intracompartmental pressure is elevated to such a degree that immediate decompression is necessary to prevent intracompartmental necrosis. [0620] [0640] [0650] [0690] Conversely, the chronic form of ECS develops when exercise sufficiently raises intracompartmental pressure to produce small vessel compromise, which subsequently causes ischemia and pain, [0660] [0680] [0730] but not to the degree exhibited in the acute form. [0620] [0650] Athletes exhibiting chronic ECS who continue or increase training are at greater risk of developing acute ECS. [0650] [0670] [0710] Chronic ECS often presents in bilateral form in young athletes with equal incidence in males and females and typically is observed in runners or participants in sports involving ball or puck. [0030] [0080] [0630] [0740] [0750] [0760]Anterior chronic ECS is more common than the lateral and posterior forms of this syndrome ( Fig. 20-6 ). [0030] [0080] [0300] [0630] [0660] [0740] [0760] [0770] [0780] Although symptoms of chronic ECS, such as pain, muscle weakness, numbness, and swelling are general, the onset and subsidence patterns are specific to the condition. [0640] [0650] [0660] [0740] Symptoms resolve after activity is discontinued but generally return at the same interval or intensity at the next training session. [0030] [0080]

 
 

Figure 20-6  Cross-sectional view demonstrating the compartments of the lower leg and associated anatomy.

 

 

Although the etiology of chronic ECS is not as well understood as that of the acute form, raised intracompartmental pressure resulting in relative ischemia of the involved muscles is likely the pathophysiologic mechanism producing this condition. [0010] [0630] [0690] [0700] [0740] [0750] [0700] [0790] Repeated muscle contractions during exercise cause an increase in muscle volume by as much as 20% because of fiber swelling and increased intracompartmental blood volume. [0620] [0650] [0660] [0740] [0780] The resulting increase in compartmental pressures is transient and typically will normalize within 5 minutes of completing exercise in asymptomatic people. [0660] [0760] [0800] [0810] In chronic ECS, however, intracompartmental pressures may remain abnormally high for 20 minutes or longer after exercise before returning to normal. [0640] [0770] [0820]

Several theories have been proposed to explain tissue ischemia, the main symptom of chronic ECS. The first theory suggests that increased compartmental pressure during exercise causes arterial spasm, which results in decreased arterial inflow. [0740] [0830] An alternative hypothesis asserts that transmural pressure disturbances produce arteriolar or venous collapse, which subsequently leads to ischemia.[0740] [0830] [0840] [0850] Finally, and perhaps more pertinent to athletes, venous obstruction recently has been advocated as a possible cause of tissue ischemia. [0640] [0650] [0690] [0740] According to this theory, eccentric exercise results in myofiber damage, which causes release of protein-bound ions into the compartment. Such repetitive eccentric contractions therefore cause not only an increase in ion concentration within the compartment but also a subsequent increase in osmotic pressure. This resulting arteriovenous gradient, in which venous pressure is increased and arterial blood flow is decreased, consequently leads to tissue ischemia. [0640] [0650] [0690] [0740] The association between repetitive eccentric contraction in the anterior compartment of runners and the increased incidence of chronic ECS in the anterior compartment lends support to this theory. [0630] [0650] [0660] [0740] [0760] [0770] [0860] [0870]

History

Patients experiencing chronic ECS may complain of cramping, burning, or pain over the involved compartment(s) with exercise ( Case Study 4 ). Pain associated with anterior chronic ECS may not be limited to the compartment but also may radiate to the ankle and foot. The most characteristic symptom of chronic ECS is pain occurring at a fixed point in the patient activity. The pain will become progressive with continued exercise or increased intensity but often will dissipate or cease with rest, usually within 20 minutes of completion of activity. Although this pattern of pain relief is observed in the majority of athletes with chronic ECS, it is not unusual for pain to ensue for a longer period. In extreme cases, pain may be constant. In addition, patients with anterior and deep posterior compartment syndromes occasionally describe paresthesia in the dorsum of the foot or in the instep, respectively. In severe cases, transient footdrop may occur.

Case Study 4

A 15-year-old, female soccer player presented with complaints of bilateral leg pain during activity. The patient had been diagnosed with chronic ECS approximately 1 year ago and underwent bilateral fasciotomies of four compartments at another facility. After her initial postoperative rehabilitation, pain recurred on exercise. A second bilateral fasciotomy of four compartments was performed, followed by recurrence of symptoms. Presently, pain developed approximately 15 minutes after beginning soccer practice and increased until activity ceased.

The current evaluation revealed a normal examination at rest, with well-healed surgical incisions. It was noted that the medial incision was quite proximal. Compartmental pressure measurements after provocative exercise confirmed bilateral compartment syndrome, based on pre-exercise and 1-minute and 15-minute postexercise readings. The 1-minute and 15-minute postexercise measurements were greater than 21mm and 17mm Hg, respectively, in all compartments.

Edwards performed a third surgery involving bilateral fasciotomies of four compartments. Because of the proximal position of the medial incision and the suspicion that the soleus bridge previously was unreleased, a new 10-cm medial incision was created to be used in addition to the previous midleg lateral incisions. The soleus bridge subsequently was released. Recurrent scarring of the anterior and lateral fasciotomy incisions was noted, and repeat extensile releases were completed. The patient recovered fully and returned to full activity at 12 weeks postoperatively, including twice-daily soccer practice.

Physical examination

Results of physical and neurocirculatory examinations in patients exhibiting chronic ECS are normal before exercise. Because pre-exercise examinations may not yield insight into the condition, examinations also must be conducted after the patient has performed the exercise that initiates the symptoms. Following exercise, a sensation of increased fullness, swelling, tension, or increased leg girth may be produced in the involved compartments. The leg also may be tender over the involved muscles. This diffuse muscular tenderness must be distinguished from that associated with superficial nerve entrapment, which usually is focal at the site of entrapment. In cases of severe chronic ECS, muscle weakness and paresthesia to a light touch may be observed. Pulses, however, will remain normal in all cases of chronic ECS.

Diagnostic studies

In addition to physical examination, diagnostic testing, such as radiographs, bone scans, electrophysiologic testing, and MRI/magnetic resonance angiography (MRA) may assist in differentiating other possible lower leg conditions from chronic ECS. Radiographs typically are normal in cases of chronic ECS. Although rarely positive in chronic ECS, bone scans also should be obtained to eliminate MTSS and stress fracture diagnoses. Electrophysiologic testing generally is not necessary but may be beneficial in documenting the extent of motor loss in patients with footdrop. An MRI/MRA is recommended only when symptoms are accompanied by a visible or palpable mass in the leg or when clinical evidence suggests possible popliteal artery compression.

The most useful diagnostic tool to confirm chronic ECS is compartmental pressure testing. [0030] [0200] [0870] Although many authors advocate performing pressure tests before, [0200] [0650] [0810] [0880] during,[0190] [0200] [0790] [0880] [0890] [0900] [0910] [0920] and after exercise, [0200] [0650] [0880] [0930] we prefer pre-exercise and postexercise testing only and do not recommend that measurements be obtained during exercise because of technical difficulties and the unreliability of measurements. The slit-catheter technique, which we use, involves the injection of small amounts of local anesthetic into the skin using an 18-gauge needle and a hand-held compartmental measurement device ( Fig. 20-7, A ). Patients are placed in a supine position with the knee extended and the ankle in neutral dorsiflexion ( Fig. 20-7, B ). The needle tip location and depth of penetration must be controlled to obtain reliable measurements.[88] Pressure measurements are taken before exercise and at 1 minute and 5 minutes following exercise. If 5-minute measurements are borderline, 15-minute compartmental pressure measurements are obtained following exercise. We use the compartmental pressure measurement guidelines to establish a diagnosis of chronic ECS and are supported by other surgeons, as summarized in Table 20-1 . [0650] [0760] [0810] Pressures usually return to normal within 3 to 5 minutes after exercise in patients without this condition.[20] If elevated pressures continue for 5 to 10 minutes, chronic ECS is diagnosed.

 

 

Figure 20-7  (A) Hand-held compartmental pressure measurement device (Stryker Instruments, Kalamazoo, Mich.). (B) To ensure accurate compartmental pressure measurements, the patient should be placed in a supine position with the knee extended.

 

 


Table 20-1   -- Compartmental Pressure Measurement Guidelines for Establishing Chronic Exertional Compartment Syndrome

Source

Pre-exercise

1-min postexercise

5-min postexercise

15-min postexercise

Edwards PH, Myerson MS[65]

≥15mmHg

≥30mmHg

≥20mmHg

N/A

Pedowitz RA, et al.[76]

≥15mmHg

≥30mmHg

≥20mmHg

N/A

Rorabeck CH[82]

≥15mmHg

N/A

N/A

≥15mmHg

 


Treatment

Conservative

Although some authors solely advocate surgical management for the treatment of chronic ECS, we recommend beginning with nonoperative treatment to address the extrinsic and intrinsic factors that contribute to the condition.[8] Modification of extrinsic factors, including training surface, shoe design, and training intensity may decrease the symptoms of chronic ECS. Muscle imbalance, flexibility, and limb alignments are intrinsic factors that may be addressed with either strengthening and stretching exercises or orthoses. A short-leg cast used for approximately 4 weeks may cause atrophy of the leg musculature that in turn may alleviate symptoms. Biomechanical abnormalities also should be addressed and corrected, usually with an orthotic, before training is resumed. Because identifying and modifying all risk factors contributing to chronic ECS is difficult, many athletes may continue to have symptoms of chronic ECS on resumption of activity and may be unable to return to competition.[73] In such cases, an operative approach may be warranted to enable return to the previous level of intensity.

Operative

The surgical technique for treating chronic ECS involves decreasing intracompartmental pressure, as depicted in Fig. 20-8 . [0060] [0720] [0740] [0860] Fasciotomy generally is recommended if symptoms persist for at least 3 months and produces favorable results, especially in the anterior and lateral forms of the condition. [0360] [0630] [0650] [0680] [0730] [0740] [0750] [0770] [0810] [0880] [0930] [0940] [0950] Care must be taken to identify and protect the superficial peroneal nerve. In case of concomitant superficial peroneal nerve entrapment, release of any fascial tethering or compression also may be performed. To prevent postoperative fascial scarring, early passive and active range-of-motion exercises are implemented and weight-bearing ambulation as tolerated is permitted within 2 weeks following surgery. [0650] [0740] [0770] Patients may begin exercise on a stationary bicycle at 2 weeks postoperatively, followed by isokinetic strengthening exercise 3 to 4 weeks after surgery. Running may be initiated 5 to 6 weeks postoperatively, with speed and agility drills added during the eighth week. [0650] [0740] Athletes generally return to full sports participation within 8 to 12 weeks following surgery.

   Pearl

Patients are able to predict the time of symptom onset.

The physical examination typically is normal at rest.

For the most accurate diagnosis, it is imperative to perform compartmental pressure testing after activity that initiates symptoms.

 

 

 

Figure 20-8  (A) Fasciotomy technique for decompression of superficial and deep posterior compartments used for the treatment of chronic exertional compartment syndrome (ECS). i, A longitudinal incision is created on the posteromedial aspect of the leg. ii, The tibial posterior border is exposed, allowing full visibility of the saphenous vein and nerve. iii, The soleus bridge is released providing exposure of the posterior compartments. iv, The affected compartment is incised, using scissors or a fasciotome to extend the fasciotomies proximally and distally. (B) Fasciotomy technique for decompression of anterior and lateral compartments used for the treatment of chronic ECS. i, A longitudinal incision is created on the anterolateral aspect of the leg, midway between the tibia and fibula. ii, Following exposure of the fascia, a transverse incision is created. iii, The intermuscular septum is identified to assist in locating the superficial peroneal nerve. Care must be taken to avoid the superficial branch of the peroneal nerve, which crosses laterally to anteriorly approximately 10cm above the ankle. iv, The appropriate compartment is incised, using scissors or a fasciotome to extend the fasciotomies proximally and distally.

 

 

 

Nerve Entrapment

Lower extremity nerve entrapment is a mechanical irritation of a peripheral nerve caused by impingement. [0960] [0970] The common peroneal, superficial peroneal, and saphenous nerves are the most at risk for entrapment, which may produce neurogenic leg pain in the athlete ( Fig. 20-9 ). [0980] [0990] [1000] [1010] [1020] [1030] Trauma is a primary cause of all three forms of entrapment. [1000] [1030] Superficial peroneal nerve entrapment also is observed in dancers and athletes in a wide variety of sports, including bodybuilding, horse racing, running, soccer, and tennis. [0960] [0980] [1000] [1030] Common peroneal nerve entrapment often is associated with repetitive exercises involving inversion and eversion, which often occur in running and cycling. [0960] [0990] [1000] External compressive sources, such as tight plaster casts and anterior cruciate ligament (ACL) braces, and internal compressive sources, including osteophytes or proximal tibiofibular joint ganglion cysts, also may cause common peroneal nerve entrapment. [1000] [1030] [1040] Knee surgery also may cause common peroneal and saphenous nerve entrapments, [1000] [1050] the latter of which also may result from inflammatory conditions such as thrombophlebitis.[105] Superficial peroneal nerve entrapment, caused by either trauma or fascia hernias, is the most common type of nerve entrapment that we have observed.

 
 

Figure 20-9  Common sites of nerve entrapment in the lower extremity. (A) Common peroneal nerve entrapment occurs as the nerve wraps around the head of the fibula and exits the peroneal tunnel. (B) Entrapment of the superficial branch of the peroneal nerve typically occurs as it pierces the deep fascia of the lateral or anterior compartments of the leg. (C) A common site of saphenous nerve entrapment occurs where the nerve branches, approximately 15cm proximal to the medial malleolus.

 

 

Although the causes of nerve entrapment are well established, the mechanism responsible for this syndrome is unknown. [0990] [1020] Certain factors, however, predispose nerves to entrapment. Nerves coursing through soft tissues are particularly at risk for entrapment. Nerves branching near joints also are at increased risk for entrapment because joints are associated with a high volume of movement and are common sites of trauma. [0970] [1040] Additionally, nerves, as opposed to circulatory and lymphatic vessels, are susceptible to impingement because of inherent inelasticity.[97] Because nerves lack independent movement, impact or compression from either trauma or internal pressure may cause entrapment.

History

Patients suffering from nerve entrapment of the lower extremity typically present with pain that is aggravated with continued exercise. Common peroneal nerve entrapment pain is located in the region of nerve compression and is referred to the lateral leg and foot. In contrast, pain associated with superficial peroneal nerve entrapment involves the lateral calf and/or dorsum of the foot ( Case Study 5 ). Saphenous nerve entrapment often occurs just above the medial malleolus, leading to local pain and referred pain to the dorsum of the foot medially ( Case Study 6 ). Numbness, often described as a burning sensation, also may be observed with all compressive neuropathies. In addition, some patients may experience localized swelling. Diffuse swelling, on the other hand, is indicative of chronic ECS or a systemic problem. Finally, motor weakness, such as footdrop, typically is observed late in common peroneal nerve entrapment.

Case Study 5

A 30-year-old, male runner presented with complaints of lateral leg pain and foot numbness. The symptoms progressed after he began an aggressive running program during the prior year. The pain was described as sharp and tingling and typically occurred over the mid to distal aspect of his lateral leg during running. He denied a history of injury.

On physical examination, a small prominence of soft tissue was noted over the painful area. “Lightning-like” sensations and paresthesias corresponding to the superficial branch of the peroneal nerve were elicited on percussion. Gross neurovascular examination, including sensation, otherwise was normal. After conservative treatment, including failed iontophoresis, a fasciotomy was performed to release the nerve. Postoperatively, activity gradually was increased, with resumption of training at 6 weeks.

 

Case Study 6

A 52-year-old, avid golfer presented with a 3-month history of distal medial leg pain. The pain increased with activity and radiated to the dorsum of the foot. Initially, pain was mild but progressed to the point at which the patient was unable to complete a round of golf without significant pain. NSAIDs and ice were implemented without improvement. Although the patient initially denied a history of trauma, on further inquiry, he recalled that he had hit his distal tibia approximately about the medial malleolus on his daughter's bicycle 3 months before the present complaint.

Physical examination revealed full range of motion, with no swelling or cutaneous changes about the distal third of the leg. In addition, no tenderness was observed over the medial distal tibial cortex, and a vibratory test was negative. However, a positive Tinel's sign over the saphenous nerve above the medial malleolus was elicited, reproducing the distal-radiating pain. On the basis of these clinical findings and the traumatic nature of the injury, a diagnosis of posttraumatic saphenous neuritis was established. Conservative treatment comprising NSAIDs, ice, and iontophoresis was prescribed. Symptoms improved markedly at 2 weeks following treatment and completely resolved by 4 weeks, enabling the patient to return to regular activity.

Physical examination

The lower back, hips, and ankle joints should be examined to confirm that an overriding neurologic condition is not present. Fascial hernia also should be ruled out. Range of motion of all leg joints and stability of the knee and ankle should be assessed. Compression or percussion of the nerve is the hallmark test used to determine a diagnosis of nerve entrapment. A tingling sensation along the nerve or at its exit from the fascia is indicative of entrapment syndrome. Tingling typically will be elicited at the level of the fibular neck radiating distally in common peroneal nerve entrapment. Alternatively, in superficial nerve entrapment, tingling will occur 7cm to 12cm above the lateral malleolus, whereas tingling will radiate from just above the medial malleolus and more distally on the medial foot in saphenous nerve entrapment.

Diagnostic studies

Roentgenograms, MRI, compartmental pressure tests, electromyography (EMG), nerve conduction, and/or nerve block are possible diagnostic tests conducted to confirm the diagnosis of nerve entrapment.[1000] [1010] [1060] Radiographs typically are normal in nerve entrapment syndromes but assist in identifying possible compressing bony lesions and in excluding stress fractures and bone tumors. [1010] [1060]An MRI is recommended if a pressure-causing mass is suspected. Compartmental pressure tests may be conducted to distinguish between chronic ECS and nerve entrapments, [0980] [1010] [1060] because elevated compartment pressures are indicative of chronic ECS. To differentiate between common and superficial peroneal nerve entrapments and to locate the anatomic point of compression, EMG and nerve-conduction studies are recommended and should be performed before and after exercise. [1000] [1010] A nerve-conduction velocity of less than 40m/sec is considered abnormal and is indicative of nerve entrapment of the lower extremity.[107] If superficial nerve entrapment is suspected on the basis of any of the aforementioned diagnostic tests, a nerve block should be performed. The anesthetic should be injected where the Tinel's sign is the strongest or at the location corresponding to maximal pain on pressure. Immediate pain relief following injection is suggestive of nerve entrapment. [0960] [0970] [1020] [1030] [1050]

Treatment

Conservative

Conservative treatment for nerve entrapment includes modification of precipitating activity, biomechanical correction, physiotherapy, and/or soft-tissue massage. [0980] [1000] [1030] NSAIDs used in conjunction with tricyclic medications such as amitriptyline and, occasionally, gabapentin may alleviate the pain and associated swelling of all three forms of nerve entrapment.[103] Iontophoresis is another option that we prefer because of its less invasive nature in comparison with a nerve block. However, nerve blocks may be necessary if iontophoresis fails. Because constrictive clothing and/or devices, including ACL braces or patellar tendinitis straps, place additional stress on the nerves, the use of these devices is not recommended during treatment. [1000] [1030]

Operative

Although common peroneal and saphenous nerve entrapments often are successfully treated by conservative measures, superficial peroneal nerve entrapment typically requires surgical treatment. [1000] [1030] If surgery is warranted, fasciotomy is performed to expose the nerve, and, if necessary, is followed by external neurolysis. [0980] [0990] [1000] [1050] [1060] In our experience, however, fasciotomy alone typically is sufficient. In common peroneal nerve entrapment, resection of osteophytes, ganglion cysts, or other obstructions may be necessary before neurolysis is performed. [1000] [1030] In rare cases of trauma-induced saphenous nerve entrapment, neuroectomy may be required. [0100] [1020] [1050] Because of the increased risks associated with neurologic surgical procedures, including neuromas and reflex sympathetic dystrophy, surgical treatment requires a thorough knowledge of the peripheral neuroanatomy.[103] To minimize such risks, the nerve should be manipulated as little as possible and the surrounding soft tissue should be relatively undisturbed.[103] Activity may be increased gradually on wound healing.

   Pearl

A careful history and physical examination should be conducted to rule out referred pain or an overriding neurologic condition.

A positive Tinel's sign is highly suggestive of nerve entrapment.

If physical examination and all diagnostic tests, including compartmental pressure measurements, are normal, nerve compression often is the source of the pain.

The fascial exit of the superficial peroneal nerve is variable, ranging from approximately 7.5cm to 12.5cm from the tip of the lateral malleolus.

 

Popliteal Artery Entrapment Syndrome

PAES is more common in athletes than in the general population, especially as a result of increased participation in competitive sports. [0060] [1080] This condition results from an abnormal relationship between the popliteal artery and the surrounding myofascial structures ( Fig. 20-10 ), producing calf pain on exertion. [0060] [1080] [1090] [1100] [1110] PAES is progressive and, in more severe cases, may result in occlusion of the popliteal because of compression from the medial head of the gastrocnemius muscle. [0060] [1080]

 


 

Figure 20-10  Normal course of the popliteal artery versus possible aberrant pathways involving the medial head of the gastrocnemius muscle that cause popliteal artery entrapment syndrome (PAES) (popliteal artery = dark, popliteal vein = striped, tibial nerve = white). (A)Normal course of the popliteal artery in which the artery and vein course distally between the heads of the gastrocnemius muscle, over the popliteus muscle, and beneath the soleus muscle. (B) The popliteal artery deviates medially, wraps around the medial head of the gastrocnemius muscle, and then resumes the normal distal course. (C) The popliteal artery deviates medially, wraps around the medial head of the gastrocnemius muscle, and abnormally courses beneath the popliteus muscle, consequently becoming entrapped. (D) The popliteal artery courses normally but is compressed by the medial head of the gastrocnemius muscle, which is positioned laterally to its normal insertion. (E) The popliteal artery courses normally but is entrapped between the medial head and an accessory tail of the gastrocnemius muscle.  Modified from Rich NM, et al: Arch Surg 114:1377, 1979.

 



Although PAES is a possible diagnosis in any athlete with calf pain and intermittent claudication, it is predominantly observed in males under the age of 30. [0060] [1080] [1090] [1100] [1120] [1130] [1140] [1150] [1160] [1170] [1180] [1190] [1200] [1210] [1220] This condition typically occurs unilaterally [0060] [1110] [1140] [1170] [1180] [1210] [1230] but may be observed bilaterally at an incidence as high as 67%. [1080] [1090] [1140] [1160] [1230] PAES often results from high-intensity exercise with excessive dorsiflexion and plantarflexion of the ankle, which commonly occurs in football, basketball, soccer, and running. [0060] [1080] [1110]

Two forms of PAES, anatomic and functional, have been suggested to explain the mechanism of this condition. [0060] [1080] [1090] [1140] In anatomic PAES, an abnormal relationship between the popliteal artery and the surrounding myofascial structure occurs during embryonic development as the medial head of the gastrocnemius muscle migrates medially and cranially. The popliteal artery becomes entrapped during this migration and subsequently is swept medially with the gastrocnemius. Rignault et al. proposed the functional theory after observing no anatomic abnormalities within the popliteal fossa during surgical exploration. [1080] [1240] According to this theory, muscle contraction, particularly active plantarflexion of the ankle, compresses the artery between muscle and the underlying bone. This functional theory was further substantiated by Turnipseed and Pozniak,[125] who also provided an explanation for claudication by suggesting involvement of the popliteal nerve. It was hypothesized that entrapment may be due to compression of the popliteal neurovascular bundle against the lateral condyle of the femur.[125] Repetitive muscle contraction from plantarflexion causes trauma on the popliteal nerve, resulting in the subsequent neuromuscular form of claudication.[125]

History

PAES should be considered in the differential diagnosis of healthy young patients presenting with complaints of intermittent pain typically involving the foot and leg ( Case Study 7 ). Pain, described as a deep ache or cramping, generally is posterior in location and typically occurs after vigorous exercise. It is important to note, however, that claudication may be atypical early in the course of this condition, because it may occur with walking and not with prolonged leg exercise. Symptoms occurring less frequently include numbness, tingling, or coolness of the foot; these symptoms may be relieved by changing leg positions.

Case Study 7

A 19-year-old, female, competitive soccer player presented with complaints of bilateral leg pain. Pain, described as a dull ache in the posterior aspect of both legs, began during workouts. The pain continued to intensify until cessation of activity was required. However, the pain resolved after a short rest period of 5 to 10 minutes. This pattern of intense pain during activity followed by relief after rest continued without progression with every successive practice and competition.

The initial physical examination did not reveal any abnormalities, as demonstrated by soft compartments, no tenderness on palpation, and normal neurovascular findings. Radiographs and resting compartmental pressure measurements were normal. In an attempt to reproduce the patient's symptoms, the patient was instructed to exercise and subsequently returned with complaints of posterior calf pain and mild tenderness on deep palpation of the calf. During this symptomatic period, neurovascular examination and compartmental pressure measurements remained normal. A subsequent three-phase bone scan and MRI also were normal. As a result, conservative treatment consisting of rest was implemented for 1 month.

The patient returned for evaluation because of continued symptoms, but the physical examination remained normal. Compartmental pressures were reevaluated at pre-exercise and postexercise intervals and remained within normal limits. Examination of pedal pulses demonstrated normal dorsalis pedis and posterior tibial artery pulses. However, when this measurement was repeated with active plantarflexion or passive dorsiflexion with a straight leg, loss of all pulses was observed bilaterally. To confirm a diagnosis of PAES, an arteriogram with provocative maneuvers was performed and demonstrated loss of flow at both popliteal arteries ( Fig. 20-11 ). Because the patient desired to continue competitive soccer, she elected to undergo surgical release of the entrapped popliteal artery. Surgical inspection revealed a popliteal artery coursing medially to the head of the gastrocnemius muscle and anteriorly to the popliteus muscle belly ( Fig. 20-12 ). These areas of entrapment then were released. After wound healing, the patient gradually increased activity over a 6-week period and returned to competitive soccer 3 months postoperatively.

Physical examination

Physical examination often is normal at rest in PAES cases, especially if the artery is still patent. Compartments may be soft, and palpation of the bone and soft tissues may not elicit tenderness. Bilateral pulses should be examined to determine whether reduction in pulse volume exists between limbs. The pulse should be palpated with the ankle in passive dorsiflexion or active plantarflexion with the knee in extension because this maneuver places tension on the gastrocnemius muscle and will lead to extrinsic compression of the popliteal artery. On auscultation, a bruit may be heard after provocative exercise, but the significance of this observation is unclear because it also may be observed in a normal athlete.

Diagnostic studies

Doppler sonography is recommended when PAES is suspected. [0060] [1080] [1230] [1260] Pulses should be measured in a neutral position and also while the leg is maneuvered toward knee hyperextension and ankle dorsiflexion. [0060] [1110] [1190] [1260] Obliteration of the pulse or reduction in pulse pressure after exercise is suggestive of PAES. [0060] [1080] [1100] [1160] [1200] [1270] If Doppler sonography indicates PAES, arteriography is recommended to confirm the diagnosis. [1080] [1130] [1190] [1280] Often referred to as the “gold standard test” of PAES, arteriography is an invasive procedure involving radiographic imaging after injection of a radiopaque material into the suspected arterial segment. [1080] [1180] [1200] Because arteriography may be normal in PAES when the ankle is in the neutral position and the knee is extended, it is important to repeat the studies bilaterally after exercise or with the ankle in positions of provocation, because extrinsic arterial obstruction may be demonstrated with ankle plantarflexion.[0060] [1120] [1190] [1220] [1270] [1280] [1290] MRI/MRA also may be beneficial in evaluating PAES. [1280] [1290] Compartmental pressure measurement testing and three-phase bone scans are recommended to rule out chronic ECS and stress fractures, respectively.

Treatment

Conservative

Because PAES typically recurs on activity and may lead to long-term arterial damage if untreated, avoidance of activity is the only suggested form of conservative treatment. Because this is not a viable option for many athletes, a surgical approach may be warranted. [0060] [1300]

Operative

To prevent long-term arterial damage, early operative treatment is recommended if PAES recurs following resumption of activity. [1100] [1270] [1280] [1310] The principles involved in surgical treatment of PAES include releasing the entrapped nerve and restoring normal arterial flow. If the physical examination did not indicate evidence of arterial damage, a myotomy is performed with the release of the offending fibrous band. [1080] [1100] [1280] However, if the condition is more advanced and involves popliteal endofibrosis or arteriosclerosis, endarterectomy and vein-patch angioplasty is recommended.[1100] [1180] [1280] In cases of complete occlusion, a saphenous vein-bypass graft is required. [1100] [1180] [1230] [1280]

   Pearl

The knee may be warm on palpation because of increased collateral circulation.

Bilateral pulses with provocation should be examined to determine whether reduction in pulse volume between limbs exists.

If PAES is suspected on the basis of Doppler sonography, arteriography should be performed to confirm the diagnosis.

 

Summary

The most common conditions involving lower leg pain in athletes are MTSS, stress fractures, chronic ECS, nerve entrapment, and PAES. Similarities of symptoms among these conditions make diagnosis difficult. The challenge for the sports medicine specialist is to differentiate among these similarities to establish an accurate diagnosis. Although pain is the hallmark symptom in all of these conditions, subtleties exist in the location and occurrence of pain among the various conditions. Therefore determining whether the pain is generalized or localized and isolating the onset and diminishment of pain will assist in determining the appropriate diagnosis, as summarized in Table 20-2 . Keys to making an accurate diagnosis include conducting a thorough history, performing an exhaustive physical examination (Table 20-3 ), and using the appropriate diagnostic tools to distinguish further among these conditions ( Table 20-4 ). Once a diagnosis is established, the preferred treatment is conservative management, consisting of rest from activity and modification of extrinsic and intrinsic factors. Treatment should be individualized according to the patient's symptoms and involve gradual rehabilitation and return to activity. Although a conservative approach typically is successful, surgical intervention may be required for cases in which conservative treatment has failed or for diagnoses of nerve entrapment and PAES.

Table 20-2   -- Pain Locations of the Common Lower-Leg Conditions

Leg condition

Localized or generalized

Location of pain

MTSS

Generalized

Posteromedial distal 1/3

Stress fracture

Localized

Bony tenderness above distal 1/3

Chronic ECS

Generalized

Involved compartments with exercise

Nerve entrapment

Localized

Fascial exit site

PAES

Generalized

Posterior with exercise

ECS, Exertional compartment syndrome; MTSS, medial tibial stress syndrome; PAES, popliteal artery entrapment syndrome.

 

 

 


Table 20-3   -- Physical Examination Observations of Common Lower-Leg Conditions

 

MTSS

Stress fracture

Chronic ECS

Nerve entrapment

PAES

Edema/warmth

Posteromedial distal 1/3

Over site

No

No

Possible around knee

Paresthesias

No

No

Rarely

Often

Rarely

Pedal pulse

Normal

Normal

Normal

Normal

Pedal pulses with provocation

Palpation tenderness

Posteromedial distal 1/3

At site

Involved compartment(s) with exercise

Possible at site of compression

Posterior with exercise

ECS, Exertional compartment syndrome; MTSS, medial tibial stress syndrome; PAES, popliteal artery entrapment syndrome.

 

 

 


Table 20-4   -- Diagnostic Studies Useful in Distinguishing among Common Lower-Leg Conditions *

Diagnostic study

MTSS

Stress fracture

Chronic ECS

Nerve entrapment

PAES

Roentgenograms

Recommended

Recommended

Recommended

Recommended

Not recommended

Normal

Periosteal reaction/early callus after 10-14 days

Normal

Normal

N/A

Bone scan

Recommended

Recommended

Not routinely recommended

Not recommended

Not routinely recommended

Linear uptake

Focal uptake

Normal

N/A

Normal

MRI

Not routinely recommended

Not routinely recommended

Not routinely recommended

Not routinely recommended

Not recommended

Signal changes

Bone edema

Normal

Normal

N/A

MRI/MRA

Not recommended

Not recommended

Not recommended

Not recommended

Recommended

N/A

N/A

N/A

N/A

Flow with provocation

Compartmental pressure test

Not recommended

Not recommended

Recommended

Not routinely recommended

Not routinely recommended

N/A

N/A

≥15mmHg at rest; >20mmHg 5-min postexercise

Normal

Normal

Arteriography

Not recommended

Not recommended

Not recommended

Not recommended

Recommended

N/A

N/A

N/A

N/A

Obstruction with provocation

ECS, Exertional compartment syndrome; MTSS, medial tibial stress syndrome; PAES, popliteal artery entrapment syndrome.

 

*

The upper portion for each diagnostic study represents our recommendation; the lower portion indicates the results corresponding to the diagnosis.

 

 

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