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Chronic Leg Pain in Athletes M. Tyrrell Burrus, Brian C. Werner, Jim S. Starman, F. Winston Gwathmey, Eric W. Carson, Robert P. Wilder and David R. Diduch Am J Sports Med published online August 25, 2014 DOI: 10.1177/0363546514545859 The online version of this article can be found at: http://ajs.sagepub.com/content/early/2014/08/25/0363546514545859

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Clinical Sports Medicine Update

Chronic Leg Pain in Athletes M. Tyrrell Burrus,* MD, Brian C. Werner,* MD, Jim S. Starman,* MD, F. Winston Gwathmey,* MD, Eric W. Carson,* MD, Robert P. Wilder,y MD, and David R. Diduch,*z MD Investigation performed at the University of Virginia Health System, Charlottesville, Virginia, USA Chronic leg pain is commonly treated by orthopaedic surgeons who take care of athletes. The sources are varied and include the more commonly encountered medial tibial stress syndrome, chronic exertional compartment syndrome, stress fracture, popliteal artery entrapment syndrome, nerve entrapment, Achilles tightness, deep vein thrombosis, and complex regional pain syndrome. Owing to overlapping physical examination findings, an assortment of imaging and other diagnostic modalities are employed to distinguish among the diagnoses to guide the appropriate management. Although most of these chronic problems are treated nonsurgically, some patients require operative intervention. For each condition listed above, the pathophysiology, diagnosis, management option, and outcomes are discussed in turn. Keywords: leg pain; athletes; medial tibial stress syndrome; compartment syndrome; stress fracture; popliteal artery; nerve entrapment; Achilles; thrombosis

For orthopaedic surgeons taking care of athletes, chronic leg pain is a very common complaint.25,38,75 Between 12.8% and 82.4% of athletes will be seen at least once for such an issue, and properly diagnosing and treating their ailment can be challenging.77 Many of the responsible conditions have overlapping symptoms and require a meticulous workup to tease out seemingly minor distinctions. The lifestyle of these patients predisposes them to these conditions and, likewise, can make their successful treatment difficult. The differential diagnosis includes medial tibial stress syndrome (MTSS), chronic exertional compartment syndrome (CECS), stress fracture, popliteal artery entrapment syndrome (PAES), nerve entrapment, Achilles tightness and tendinopathy, deep vein thrombosis (DVT), and complex regional pain syndrome (CRPS). While this list is not exhaustive, it does include the more common diagnoses.15,94 In this review article, we discuss the clinical presentation, physical examination, diagnostic modalities, treatment options, and outcomes of the above conditions.

MEDIAL TIBIAL STRESS SYNDROME Of all the conditions causing exercise-induced leg pain, MTSS, or true shin splints, is by far the most common, as it accounts for about 5% of all athletic injuries.94 Described as exercise-induced pain along the middle to distal posteromedial aspect of the tibia, the estimated incidence is between 13% and 22% of injuries in runners and dancers and 35% in naval recruits.107,108 There remains disagreement about the origin and pathophysiology of MTSS. Until recently, inflammation of the periosteum due to excessive traction by the tibialis posterior or soleus was theorized as the most likely cause of MTSS.79 Johnell et al49 first proposed the bone stress reaction theory (rather than originating from the periosteum) based on their findings of osseous metabolic changes and no evidence of inflammation in limbs with MTSS. Additional evidence against the traction theory is that the musculature of the superficial and deep compartments do not insert on the tibia where the pain is most commonly located.91 More recent studies have supported the theory that MTSS is a bony overload injury, whereas the tibia bends during weightbearing activities causing strain.31,36 This strain normally causes microdamages within the bone, leading to bony adaptation processes to strengthen the bone in an effort resist bending. When this strain exceeds a certain threshold, the osteoclast activity may outpace osteoblast activity, leading to local tibial osteopenia.34

z Address correspondence to David R. Diduch, MD, Department of Orthopaedic Surgery, University of Virginia Health System, Box 800159, 400 Ray C. Hunt Drive, Suite 330, Charlottesville, VA 22908, USA (e-mail: [email protected]). *Department of Orthopaedic Surgery, University of Virginia Health System, Charlottesville, Virginia, USA. y Physical Medicine and Rehabilitation Department, University of Virginia Health System, Charlottesville, Virginia, USA. The authors declared that they have no conflicts of interest in the authorship and publication of this contribution.

Diagnosis The most commonly accepted definition of MTSS is that proposed by Yates and White108: ‘‘pain along the posteromedial border of the tibia that occurs due to exercise,’’ which is reproduced ‘‘by palpation of the posteromedial border of the tibia’’ and ‘‘is present over a length of five

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or more consecutive centimeters.’’ Physical examination of the patient with MTSS focuses on several important aspects. The exact location of the pain should be sought out, as posteromedial bony pain, rather than soft tissue tenderness, is imperative for the diagnosis. The patient may have a mild exacerbation of the pain with resisted ankle plantar flexion, although this is not a requirement. Dynamic foot hyperpronation has been associated with MTSS, as has been pitting edema over the area of maximal tenderness.70,79 Any neurovascular changes (eg, paresthesias, diminished pulses) do not commonly accompany MTSS and should point the practitioner toward other diagnoses, such as exertional compartment syndrome or PAES. While imaging studies are not typically indicated in the initial evaluation of patients with suspected MTSS, magnetic resonance imaging (MRI), high-resolution computed tomography scans, or bone scintigraphy may aid in the diagnosis.36 Plain radiographs do not have significant utility in the diagnosis of MTSS, except to rule out other causes of leg pain, including stress fractures.25 Other plain radiographic findings, such as periosteal reaction on the posteromedial aspect of the tibia or callus formation, are infrequently present and are neither sensitive nor specific in the diagnosis of MTSS.9 High-resolution computed tomography has been found to have a sensitivity of 42% to 100% and a specificity of 88.2% to 100% in the diagnosis of MTSS.35,36 Magnetic resonance imaging readily shows periosteal reaction and bony edema, offering a sensitivity of 78% to 89% and a specificity of 33% to 100% for the diagnosis of MTSS.9,35 On the basis of data from available studies, MRI is the most accurate study in symptomatic patients to help differentiate between MTSS and advanced stress fracture.79

Management Nonoperative Treatment Options. The initial management for all patients with MTSS should be nonoperative, including modalities such as rest, cryotherapy, compression, elevation, stretching, physical therapy, and pneumatic leg bracing. Most studies support rest or cessation of offending activities as the most important treatment in early phases of MTSS.37,56 In a recent review of the literature on nonoperative treatment options for MTSS, Galbraith and Lavallee37 concluded that most studies support rest, ice, and analgesics in the acute phase of MTSS. Many experts also recommend modifying training routines, stretching and strengthening the lower extremity, wearing appropriate footwear, using orthotics and manual therapy to correct biomechanical abnormalities, and gradually returning to activity. A classic study by Andrish et al4 conducted a randomized controlled evaluation of 97 marine recruits who had MTSS. Patients were divided into 5 groups with varying combinations of nonoperative therapies, including rest, cryotherapy, stretching, and casting. The mean recovery time averaged over all groups was 8.6 days (range, 6.410.8 days) with no significant difference among groups. Additional nonoperative options in the management of MTSS refractory to common nonoperative intervention include custom made orthotics, alterations of training routines, extracorporeal shock wave therapy (ESWT), and

injections. A controlled study of 94 consecutive patients with chronic recalcitrant MTSS evaluated the effectiveness of low-energy ESWT. Half the patients underwent home training and ESWT; the remaining half served as a control group, with home training alone. Success rates in the ESWT group were statistically greater than the controls at 1 month, 4 months, and 15 months from baseline, with a 76% final success rate.82 Operative Treatment Options. The majority of MTSS patients treated with nonoperative management will have significant improvement, with surgical intervention only reserved for severe, recalcitrant cases. In such situations, most authors describe a posterior fasciotomy through a variety of surgical approaches.43,47,102 Overall, these studies report generally positive outcomes with good to excellent results in 69% to 92%. Return to preinjury level of activities is less favorable, varying between 31% and 93%.22,47 Yates et al107 reported outcomes of 46 patients who underwent posterior fasciotomy for MTSS after failing nonoperative management. The authors reported that surgery significantly reduced pain levels by an average of 72%. An excellent result was achieved in 35% of the limbs; a good result in 34%; a fair result in 22%; and a poor result in 9%. Despite the success with regard to pain reduction, only 41% of the athletes fully returned to their presymptom sports activity.

CHRONIC EXERTIONAL COMPARTMENT SYNDROME Exercised-induced anterior leg pain is caused by CECS in 27% of cases, but in spite of this, there is an average of 22 to 28 months from presentation to correct diagnosis.21,33,92 Patients are an average age of 20 to 24 years old, with approximately equal incidence between women and men and bilateral disease in 60% to 80% of patients.21,98 Anterior and lateral leg pain predominates because of involvement of these 2 compartments reported in up to 95% of cases. Other studies, however, have identified the deep posterior compartment in up to 40% of cases.98 A recent military epidemiology study uncovered a higher incidence in females, patients of increasing age, and white patients.104 The pathophysiology of CECS is not completely understood or universally accepted.98 During exercise, muscle volume can increase by 20%, resulting in increased intracompartmental pressures as the surrounding fascia does not proportionally expand.18 However, evidence exists that this does not necessarily result in tissue hypoperfusion and ischemic muscle pain.3,12,95 Based on singlephoton emission computed tomography and MRI imaging, no significant relative perfusion decrease was seen between patients and controls.3,95 Stretch of fascial pain receptors and/or pressure fibers and inadequate myocyte response to increased metabolism are additional theories.3,12,95

Diagnosis The clinical presentation of CECS is characteristic and should immediately clue the physician to consider its

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diagnosis. Patients have predictable leg pain that begins at the same time, distance, or intensity during the workout and resolves with rest. Later in the disease process, leg pain may be present with everyday ambulation or even at rest.98 Weak ankle dorsiflexors may result in the foot ‘‘slapping’’ the ground during ambulation with associated dermatomal paresthesias.21,98 As with acute compartment syndrome, swelling is a pertinent finding but, since it is activity related, may not be present during a clinic visit. Tenderness over the compartments, pain with passive digit and ankle motion, and palpable muscle herniation through fascial defects are commonly encountered.98 Measurement of intracompartmental pressure is routinely performed during the evaluation of CECS, as it is considered the diagnostic gold standard.98 Intracompartmental needle manometry is performed in all 4 compartments before exercise and at 1 and 5 minutes after exercise. According to Pedowitz et al,74 values of 15, 30, and 20 mm Hg, respectively, are diagnostic of CECS. As a comparison, preexercise compartment pressures in control subjects range from 5.7 to 12 mm Hg.6 Despite the reliance on these values, a recent metaanalysis suggested that only the values after 1 minute of exercise are accurate for the diagnosis.6 Currently, imaging plays more of a role in ruling out other causes of leg pain than it does in diagnosing CECS. Plain radiographs will show no abnormalities and have no utility unless other diagnoses are being considered. After-exercise T2-weighted MRI findings of muscular edema correspond to increased intracompartmental pressures and are 87% sensitive and 62% specific for CECS.14,16,71,81 Infrared spectroscopy, which measures levels of oxygenated and deoxygenated blood, is sensitive for CECS when the postexercise ratio of deoxygenated to oxygenated blood remains elevated.14 Thus, these 2 imaging modalities may be considered for noninvasive screening options, although neither is routinely obtained.

Management Nonoperative Treatment Options. Due to the often delayed diagnosis of CECS and unwillingness of patients to modify their activity levels, nonoperative management has a high failure rate.32,71,72 Options include ice, nonsteroidal anti-inflammatory drugs, massage, stretching, ultrasound, shoe modifications, and, more recently, gait modifications; however, activity modification or cessation of the offending activity has the greatest efficacy.18,23,60,98 Injection of botulinum toxin A was shown to reduce postexercise anterior and lateral intracompartmental pressures by .50% for up to 9 months, and 15 of 16 patients (94%) experienced complete resolution of exertional leg pain.23,45 Operative Treatment Options. Patients with failed nonoperative management who are unwilling to modify their activity levels should be offered surgical release of the involved compartments. Surgical options include the traditional single incision (open) technique, the more minimally invasive (subcutaneous) 1- or 2-incision techniques with or without endoscopic assistance, and the additional step of removing a strip of fascia53,54,60,98,106 (Figure 1). These

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Figure 1. Intraoperative image of the 2-incision technique for anterior and lateral compartment fasciotomies. Incisions are planned halfway between the anterior tibial cortex and the palpable edge of the fibula.

minimally invasive options and endoscopic assistance have been developed to reduce the morbidity of the larger open incisions. Attention should be paid to the superficial peroneal nerve as it exits the lateral compartment approximately 10 cm proximal to the lateral malleolus, although there is significant variation as to its location.27 Dissecting out the nerve and performing a neurolysis of any adhesions or fascial bands creating compression is a crucial step, as residual nerve entrapment has been noted as a cause of treatment failure.103 Although their study was underpowered, Raikin et al76 showed that simultaneous bilateral fasciotomies returned patients back to sports participation sooner (10.7 weeks) compared with staged procedures (22.7 months). Postoperatively, a brief period of immobilization is followed by a gradual return to activity. Complication rates of 11% to 16% include infection, nerve or vascular injury, DVT, wound dehiscence, CRPS, scar hypersensitivity, and seroma/hematoma formation.14,103 Recurrences are thought to be due to incomplete release, incorrect diagnosis, excessive scarring, or inappropriate rehabilitation.18,99 Early reports showed higher recurrence rates and complications for subcutaneous or minimally invasive versus open fasciotomies, although recent literature appears to refute this.7,27,32,106 In a recent retrospective review of 754 fasciotomy outcomes in military personnel by Waterman et al,103 44.7% experienced a recurrence of symptoms, and 5.9% underwent revision surgery, with only 14% of those having complete resolution of symptoms. Their overall surgical failure rate was 21.8%, which is slightly worse than previously published success rates of 80% to 100% for anterior and lateral fasciotomies.15,72,93 Interestingly, posterior compartment releases have success rate of only around 50% and are thus rarely performed.14

STRESS FRACTURES Another potential source of chronic leg pain in athletes is a stress fracture, which results from repetitive microtrauma to the bony architecture.11,19 The majority of lower extremity stress fractures are seen in the tibia and may

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occur in different locations on the bone depending on the type of activity or sport.11,56,90 They are typically seen in the upper diaphyseal or proximal metaphyseal regions in volleyball and basketball players. However, in runners, stress fractures are more commonly observed in the distal one-third of the tibia.25

Diagnosis The clinician should have a high index of suspicion for a stress fracture when evaluating patients with a history of eating disorders, menstrual irregularities, or a previous stress fracture or in athletes participating in sports where lower body weights are emphasized.11,17,90 History should specifically include any recent changes to workout regimens, training intensity or frequency, running surfaces, alterations of training equipment (eg, footwear), and, when evaluating females, a specific set of screening questions for the so-called female athlete triad.57,97 Many universities use a standardized questionnaire as part of the annual preparticipation evaluation that includes questions regarding the patient’s perception of one’s own weight, eating in secret, feelings of losing control over one’s diet, the initial onset of and current regularity of one’s menstrual cycle, and whether there is a history of a previous stress fracture.65 Patients will typically describe an insidious onset of pain in a specific area of the bone, reproduced and worsened with weightbearing activities and relieved by rest.17,101 As the stress fracture progresses, pain may persist even after cessation of activity and, in rare cases, include night pain.17 On examination, direct palpation at the site will reproduce pain with local swelling and erythema, although frequently the leg will visually appear normal.25 The presence of vibratory pain, elicited by a tuning fork or ultrasound, is 75% sensitive and 67% specific and so cannot be used to definitely rule in or out the disease.59 Examination should include an assessment of limb and foot alignment, muscle tone, and limb length discrepancy, as these have been associated with an increased risk for stress fracture.75 Although stress fractures may often be diagnosed with history and physical examination alone, they are typically confirmed with one or more forms of imaging. With plain radiographs as a diagnostic tool, a classic finding is the ‘‘dreaded black line,’’ defined as a cortical lucency of the midanterior cortex of the tibia (Figure 2A). Other subtle changes, such as a faint periosteal reaction or focal callus formation, may be seen, and in many cases, particularly early on, the bone may appear normal.17,90 In cases of a normal radiograph but high clinical suspicion, the diagnosis can be confirmed with MRI with characteristic edema or a bone scan with focal uptake11,17,66,75 (Figure 2B).

Management The mainstay of treatment of tibial stress fractures is nonoperative and focuses on rest, pain relief, and modification of identifiable risk factors, such as shoewear, running surface, training regimens, and nutritional deficiencies.17 After diagnosis, the athlete should limit weightbearing

Figure 2. (A) Lateral plain radiograph showing the ‘‘dreaded black line’’ highlighted with the square. (B) Coronal T1weighted magnetic resonance image showing bony edema and fracture line in the same patient. (C) After failing nonoperative management, the patient underwent tibial intramedullary nailing with evidence of healing the stress fracture. for 2 to 6 weeks with mild analgesics for pain. Weightbearing and activity should be reduced to the level that relieves all pain. That is, if pain is experienced with walking, then restrict to partial weightbearing; if pain with partial weightbearing, then back off to no weight; if pain with rest, consideration may be given to bracing or casting or a longer period of nonweightbearing.39 Nonsteroidal antiinflammatories are considered a reasonable choice for pain control, despite theoretical concerns about their effects on bone healing that have prompted many clinicians to restrict their use at least in the first few weeks of treatment.25 Some authors have also advocated electrical stimulation as a treatment modality; however, evidence to support its efficacy is limited.83 Progression of activity back to normal levels is guided primarily by pain, and the athlete should be counseled to avoid any activities that cause recurrence of pain. A general rule of thumb is to increase running mileage an average of 10% per week to return to full training levels. Typically, recovery to full activity level takes place over an 8- to 16-week period; however, in more severe cases, it may take longer.17,66,80 In such cases that show delayed healing or recurrence, operative treatment with intramedullary nailing may actually allow for a faster recovery, and this has been increasingly advocated for high-level athletes with tibial stress fractures19,40,80,101 (Figure 2C). As a caveat to this treatment algorithm, the clinician should differentiate between medial tibial stress fractures, which resolve with 6 weeks

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of weightbearing rest (with or without leg brace) during which cross-training is permitted, and anterior tibial stress fractures, which are associated with greater periods of healing and are treated as described above. In some cases, it may be appropriate to refer the patient for further evaluation and management by a dietician, nutritionist, or gynecologist.17,90 Without restoration of regular menstrual cycles and adequate nutrition, the chances of successful treatment diminish considerably. Evaluation of serum 25-hydroxy vitamin D3 levels is an important part of ensuring adequate nutritional status. Supplementation to achieve ‘‘high normal’’ serum levels in the range of 50 ng/mL of 25(OH)D3 has been recommended to improve healing, and .75% of the white and 90% of the African American population are likely deficient.86

POPLITEAL ARTERY ENTRAPMENT SYNDROME Popliteal artery entrapment syndrome, the most common arterial cause of leg pain in athletes, involves dynamic compression of the popliteal artery as it passes through or around the 2 heads of the gastrocnemius causing intermittent claudication. Furthermore, the popliteal artery may aberrantly course medial to the medial head of the gastrocnemius or to a slip of the muscle. Rarely, the popliteus muscle or a posterior knee fibrous band can cause compression.42 If untreated, transient arterial stenosis can evolve into permanent vascular damage with aneurysmal dilatation and thrombosis with distal emboli.

Diagnosis A common population for this disease includes young athletes and military recruits who have well-developed ankle plantar flexors. This muscle hypertrophy creates relatively less space for an at-risk artery and can accentuate the compression caused by underlying atypical anatomy. Complaints of leg cramping and pain with strenuous exercise are consistent with intermittent claudication, and mild leg swelling may be noted. Critical limb ischemia and risk factors for peripheral vascular disease are not commonly present. A recent study found palpable pulses in 9 of 11 patients, and 10 of 11 patients had a normal ankle brachial index.2 Bilateral complaints are seen in 38% of patients, and paresthesias are not consistently noted.89 If clinical suspicion exists, a vascular surgery consultation is obtained and accompanied by imaging studies, such as a duplex ultrasound, digital subtraction arteriography, computed tomography angiography, or magnetic resonance angiography. Ultrasound testing is performed with the patient’s ankle in neutral and then repeated in maximal active plantar flexion. Peak systolic velocity .200% of the proximal segment or occlusion distally is diagnostic of PAES, although improper technique can result in a high rate of false positives.2 Computed tomography angiography or magnetic resonance angiography provides additional information regarding the local anatomy as well as the arterial structure and, when performed with provocative maneuvers (passive dorsiflexion or active plantar flexion),

Figure 3. Coronal magnetic resonance angiography sequences of the right leg in the same patient showing (A) no stenosis of the popliteal artery with the ankle in a neutral position and (B) .80% focal stenosis with active ankle plantar flexion. The patient underwent subsequent surgical release of the medial head of the gastrocnemius with resolution of symptoms. is 100% and 94% sensitive, respectively89 (Figure 3). There have been no studies directly comparing the diagnostic accuracy of the two, although magnetic resonance angiography is becoming the test of choice, owing to its soft tissue definition and ability to direct surgical releases.89

Management If surgery is indicated, the posterior or medial approach to the knee permits a myotomy of the affected head of the gastrocnemius.2 Saphenous vein grafting is reserved for aneurysmal or embolic disease. Endoluminal stenting with or without thrombectomy appears to have unacceptable failure rates and is not preferred to open release.64 A recent systematic review showed a 70% to 100% rate of successful resolution of symptoms after surgical release, although high-quality long-term outcome studies do not exist.89

LOWER EXTREMITY NERVE ENTRAPMENT The saphenous, common peroneal, superficial peroneal, and sural nerves are most commonly implicated in lower extremity nerve entrapment syndromes leading to leg pain in athletes.30,62,63 Initial presentation of nerve

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compression syndromes may be masked by acute injuries and may be appreciated only when functional limitation persists beyond the expected time course of recovery from the initial injury. Interestingly, trauma is the primary cause of all forms of entrapment, although the exact origin varies by the involved nerve.63 Common peroneal nerve entrapment is commonly associated with exercises involving repetitive inversion and eversion, including running and cycling.5,25,62,63 Superficial peroneal nerve entrapment more commonly occurs in dancers, body builders, soccer players, tennis players, and jockeys in addition to runners.63 This may also be associated with a focal muscle hernia. Saphenous nerve injury is most commonly seen in cyclists and rowers, where the presumed mechanism relates to repetitive knee flexion, although it can be an unfortunate iatrogenic injury at the time of arthroscopic knee surgery.63,69 Sural nerve entrapment is the least common of these syndromes and occurs as a result of the crural fascia acting as a compression or a fixation point for the nerve during activities, such as running or track sports. Extrinsic compression from tight ski boots and casts may similarly induce this problem in the athletic population.63

Nonoperative interventions are typically less successful in the management of superficial peroneal nerve entrapment, although an initial trial of nonoperative management is not unreasonable. Operative Treatment Options. Surgical management is indicated in patients with a confirmed diagnosis of nerve entrapment who have failed nonoperative measures. The general goal of surgical decompression is to release the site (or sites) of compression and prevent recurrence. In common peroneal nerve entrapment, the compression is most commonly seen around the fibular neck, related to pressure from the overlying muscle and fascia, particularly in the area where the nerve travels under the sharp fibrous edge of the peroneus longus origin.63 Decompression of the superficial peroneal nerve may be combined with an anterior compartment fasciotomy if there is concern for concomitant exertional compartment syndrome or in the presence of a focal muscle hernia. Sural nerve decompression can be accomplished with a longitudinal incision usually just posterior and lateral to the musculotendinous junction of the Achilles tendon.28 Decompression of the saphenous nerve requires an incision approximately 8 to 10 cm proximal to the patella, just anterior to the sartorius muscle.63

Diagnosis Most athletes with nerve entrapment syndromes have activity-induced leg pain that is exacerbated by continuing the offending exercise.15,25,63 Pain is typically located at the site of nerve compression and referred in the distribution of the affected nerve. Paresthesias or burning along the distribution of the affected nerve is also commonly reported.30,63 The diagnosis of nerve entrapment is typically accomplished with a thorough physical examination. Percussion or compression of the nerve is the standard diagnostic test used to evaluate for nerve entrapment. A tingling sensation or pain along the course of the nerve or at its site of exit from the fascia is indicative of an irritated nerve due to entrapment.25,63 Once a nerve entrapment syndrome is suspected, confirmatory tests should be sought, such as nerve conduction studies or electromyography.63 Although there is limited evidence in the literature to mandate postexercise electrodiagnostic studies, given the frequent relationship of symptoms to exercise, consideration should be given to pre- and postexercise electromyographic studies.58 The main role of radiologic imaging modalities, such as radiograph, MRI, bone scanning, and ultrasound, is to detect bone and soft tissue lesions rather than neurologic disease.8,24,61 In most cases of nerve entrapment, radiographic findings are normal but are suggested to rule out possible compressing bony lesions, stress fractures, and bone tumors.25,30

Management Nonoperative Treatment Options. The initial management for patients with nerve entrapment syndromes is nonoperative, including modification of the offending activities, physiotherapy, stretching, or massage.5,25,69 Some authors have reported success with iontophoresis and nerve blocks in the management of these disorders.25

ACHILLES TIGHTNESS A less commonly recognized cause of chronic leg pain in athletes is intrinsic tightness of the Achilles tendon, which can result in posterior calf pain and tendinopathy. The Achilles tendon may absorb as much as 12.5 times the athlete’s body weight during running activities.55 In athletes, overuse and lack of flexibility in the overtight tendon predispose the Achilles tendon to injury through microtears and degenerative changes.38 Jumping athletes with reduced dorsiflexion appear to overload their plantar flexors, which may, if left untreated, contribute to subsequent tendinopathy.105 Additionally, underlying abnormalities in limb alignment and gait pattern may result in abnormal loading of the Achilles tendon complex, which can further exacerbate the condition.38

Diagnosis The history is similar to many of the associated diagnoses of lower extremity leg pain, with activity-associated pain of insidious onset most commonly reported. Pain is more likely to be located in a posterior location along the Achilles tendon and calf but may be vague and difficult to reproduce on examination. In chronic cases, the pain may migrate more distally and may actually be described as heel pain.96 A high index of suspicion must therefore remain for excluding other possible causes before making the diagnosis. The Silfverskio¨ld test, which measures passive ankle dorsiflexion with the knee flexed to 90° and then in extension, will determine whether the source of tightness is isolated to the gastrocnemius or combined with the soleus. Radiographs and other imaging studies may be utilized to exclude other possible causes of pain but are otherwise unnecessary for this diagnosis.

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Management For cases of mild Achilles tightness, a trial of rest, physical therapy, and stretching may be successful, with nonsteroidal anti-inflammatories prescribed for pain control.87 Shoe modifications may be helpful in athletes with associated gait or foot abnormalities.84 In patients with moderate to severe tightness or when nonoperative treatment has failed, surgical lengthening of the gastrocnemius-soleus complex may be indicated. In cases of isolated gastrocnemius tightness, proximal division of the fascia of the muscle may be successful, as seen in the Strayer, or gastrocnemius recession, procedure.88 However, in cases of combined tightness, procedures involving lengthening of the more distal Achilles tendon itself are utilized. There has been a transition from traditional open Achilles tendon lengthening to more percutaneous procedures because of concerns over wound complications, but most of the research in this arena has been focused on diabetic pedal ulcerations and pediatric and spastic equinus deformities.41,46 There have been no high-quality trials in athletes assessing the outcomes of these various procedures, likely because of the high success rate in nonoperative treatment in this patient population.

DEEP VEIN THROMBOSIS Although normally thought of as an entity seen in sedentary individuals, the presence of a DVT should be considered even in the younger athletic population. A DVT is a rare diagnosis in athletes, with potentially devastating consequences if not treated appropriately. A pulmonary embolism occurs in up to 50% of individuals with an untreated DVT, and of 243 high school and college football deaths, pulmonary embolism was the cause of 5 (2.1%).10 A more common complication of the disease, postthrombotic syndrome, manifests as chronic leg pain, heaviness, swelling, and cramping. The classic risk factors for developing a DVT are defined by Virchow’s triad of venous stasis, endothelial damage, and hypercoagulability. Fortunately, athletic participation and exercise do confer some protection from these elements, as evidenced by increased blood volumes and velocities during exercise and increased collateral vessels. Venous stasis, as seen during bus rides and plane flights, may confer a 4-times greater risk over the next 2 months after exposure for developing a DVT.52 Training in high altitude, anabolic steroids, and dehydration are thought to be a risk factor for venous stasis secondary to hemoconcentration.48,67 Endothelial damage occurs during repetitive microtrauma, as seen during endurance sports, and can also be caused by frequent collisions during contact sports.67 Endothelial damage from surgery and postoperative immobilization combine to increase the risk of DVT in athletes. Hypercoagulability in athletes is most commonly associated with genetic mutations, such factor V Leiden, prothrombin 20210A, antithrombin III, homocysteine, and proteins C and S.67 Additionally, females on oral

Figure 4. Color Doppler ultrasound study showing a nonocclusive deep vein thrombus (DVT) in the superficial femoral vein. PFA, profunda femoris artery; PFV, profunda femoris vein; SFA, superficial femoral artery; SFV, superficial femoral vein. contraceptives have a 5-times increased risk of developing a DVT.100 In a prospective study, Parker et al73 uncovered that Boston marathon runners flying for more than 4 hours incited an acute hypercoaguable state compared with those who traveled less than 2 hours. However, there is no definitive evidence that vigorous exercise encourages blood coagulation via activation of clotting factors.

Diagnosis When a deep vein thrombus is diagnosed, the clinical examination exhibits low sensitivity (11%) and predictive value (25%) but high specificity (76%-85%).29 Physical examination findings include unilateral diffuse swelling, calf tenderness, increased extremity warmth, and a lowgrade fever.26,51 A positive Homan sign, evidenced by calf pain with forced ankle dorsiflexion, is 60% to 88% sensitive and 30% to 72% specific for a DVT and should not be used to exclude the diagnosis.50 Duplex ultrasound is the screening test of choice as it is 93% to 97% sensitive, 98% specific, relatively cheap, and noninvasive68 (Figure 4). However, a negative study with a high clinical suspicion or an elevated serum D-dimer level should encourage advanced imaging such as a magnetic resonance venography.

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Management

Management

Questions regarding treatment of DVTs in athletes always involve 2 issues: appropriate medication and duration and when can the athlete return to play. In most cases, therapeutic weight-based low molecular weight heparin is instituted, immediately followed by a transition to warfarin with a goal of an international normalized ratio of 2 to 3.29,85 Newer oral medications on the market do not require international normalized ratio monitoring. Per the American College of Chest Physician recommendations, anticoagulation should be continued for 3 months for a provoked DVT, and then the risk-to-benefit ratio should be evaluated for longer-term therapy for a spontaneous DVT.51 Placement of an inferior vena cava filter should be considered if there is a contraindication to anticoagulation, recurrent pulmonary emboli while adequately anticoagulated, or if there is a concern for anticoagulation medication compliance.78 There is no consensus regarding whether athletes should undergo genetic hypercoagulable testing after their first DVT; however, after 3 separate diagnoses of a DVT, the patient should be placed on lifelong anticoagulation.85 Athletes who play contact sports may return to play only when off of anticoagulation, but there is no consensus as to how long to restrict noncontact physical activity. Historically, patients were placed on bed rest for 7 to 10 days, but the trend now is early mobilization with gradual return to sports participation.1,51,67

Treatment of CRPS is typically nonoperative, with a combination of medications and goal-directed physical therapy. Specific therapy modalities include transcutaneous electrical nerve stimulation, progressive weightbearing, tactile desensitization, massage, and contrast bath therapy.20 A full discussion of medications for CRPS treatment is beyond the scope of this article but may include antidepressants, anti-inflammatories, steroids, GABA analogs, and alpha- or beta-adrenergic blocking agents.13,44

CONCLUSION Chronic leg pain in athletes is a not uncommon office visit or training room complaint. The differential of the common diagnoses includes MTSS, CECS, tibial stress fracture, PAES, nerve entrapment, Achilles tightness, DVT, and CRPS. They have overlapping symptoms but with differing treatment algorithms and thus need to be distinguished. We recommend a methodical evaluation of these patients, including an extensive history, thorough physical examination, and the appropriate imaging and referrals, when necessary. When managed properly, most of these diagnoses have favorable outcomes and will allow athletes a meaningful return to competition.

REFERENCES

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Diagnosis In the evaluation of chronic lower extremity pain in athletes, CRPS is primarily a diagnosis of exclusion; however, it is an important consideration when other diagnostic evaluations are negative and symptoms persist. History may include a mild or moderate inciting injury before the onset of symptoms, with progression of pain despite a grossly normal appearing extremity. On physical examination, changes may be seen in skin color and temperature, and sweating may be abnormal. Allodynia or hyperalgesia may be noted with light touch or pinprick. There is no gold standard diagnostic test to confirm CRPS; however EMG, thermography, sweat testing, and nerve blocks can build the diagnostic picture and help distinguish between CRPS types I and II.13,44

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