AUTHOR INFORMATION

Section 1 of 12

Authored by Jonathan C Reeser, MD, PhD, Department of Physical Medicine and Rehabilitation, Marshfield Clinic

Jonathan C Reeser, MD, PhD, is a member of the following medical societies: Alpha Omega Alpha, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, Association of Academic Physiatrists, Phi Beta Kappa, Physiatric Association for Spine, Sports and Occupational Rehabilitation, and State Medical Society of Wisconsin

Edited by Everett C Hills, MS, MD, Medical Director, Rehabilitation Hospital, Assistant Professor of Orthopaedics and Rehabilitation, Orthopaedics and Rehabilitation, Penn State Milton S. Hershey Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Michael T Andary, MD, MS, Residency Program Director, Associate Professor, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine; Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center; and Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center

Author's Email:	Jonathan C Reeser, MD, PhD
Editor's Email:	Everett C Hills, MS, MD

eMedicine Journal, February 21 2007, VOLUME 8, Number 2

INTRODUCTION

Section 2 of 12

Background: Stress fractures are overuse injuries of bone. These fractures, which may be nascent or complete, result from repetitive subthreshold loading that, over time, exceeds the bone's intrinsic ability to repair itself. Briefhaupt originally described stress fractures in military recruits in 1855. Our present understanding of the pathophysiology of stress fractures and of bone's response to loading has been advanced by numerous studies investigating the epidemiology of stress fractures in military recruits and in athletes.

Stress fractures most commonly occur in the lower limbs as a result of the ground-reaction forces (GRFs) that must be dissipated during running, walking, marching, or jumping. Stress fractures of the vertebral arch, upper limbs, ribs, and even the scapula have also been described and are not uncommon in some sports.

Pathophysiology: Bone, like muscle, is an adaptable tissue capable of repair, regeneration, and remodeling in response to environmental (particularly mechanical) signals. Bones are exposed to both stress (ie, load) and strain (ie, deformation) with weight-bearing exercise. One measure of load is GRF, which can approach 12 times body weight during jumping and landing. Factors influencing the local skeletal response to loading include bone geometry and bone density. For example, cortical (ie, long) bones are generally more resistant to compressive forces than trabecular bones, but long bones also experience more strain in response to torsion or bending forces. In addition, a bone's strength is roughly proportional to the square of its mineral density; thus, osteopenic bone is weaker than bone of normal density.

Wolff law states that bone develops the structure most suited to resist the forces acting upon it. The ability of bone to remodel has tremendous clinical consequences. For example, an individual on prolonged bed rest quickly begins to lose bone mineral density (BMD). Conversely, an athlete who engages in a sporting discipline that requires repetitive jumping and landing is likely to have a higher BMD than a sedentary person. Such adaptation is the result of a continuous process of bone resorption and subsequent repair mediated at the cellular level by osteoclasts and osteoblasts, respectively.

Advanced cross sectional imaging has demonstrated that bone responds to repetitive loading via a continuum of stress responses that precede the onset of clinical symptoms. In their study involving a cohort of military recruits, Kiuru et al reported that only 40% of the MRI findings suggestive of a low-grade bone stress injury correlated with clinical symptoms (Kiuru, 2005). The vast majority of the radiographically detected areas of bone stress reaction remained clinically silent despite uninterrupted training, and disappeared upon follow-up imaging at the conclusion of the 5-month training program. Therefore, under normal circumstances, bone appears able to keep up with necessary repairs without manifesting clinically significant injury as it remodels in accordance with Wolff law. However, when a bone's reparative and adaptive capacity is overwhelmed by chronic overload, damage can begin to accumulate. If allowed to progress, this multifactorial process may eventually result in a stress fracture.

Animal studies have demonstrated that bone subjected to repetitive cyclical loading develops what has been termed microdamage. Furthermore, a physiological threshold appears to exist, below which such microdamage is not detectable. Increased osteoclastic activity at sites of bone stress or strain may cause transient weakening of the bone locally, predisposing the area to microdamage. Unless given appropriate time for healing and osteoblastic-mediated bone deposition, adjacent sites of microdamage are thought to coalesce, giving rise to an area of stress reaction or injury. At this stage, the individual may be minimally symptomatic and conventional radiographs are likely to appear normal. With progressive overload, the bone becomes increasingly vulnerable and the individual proceeds to develop symptoms that are thought to reflect the extent of underlying bone injury.

If uninterrupted, the process may culminate in a stress fracture. Some clinicians prefer to distinguish between stress fractures of normal bone that becomes fatigued through abnormal loading (ie, fatigue fractures) and stress fractures of pathologic bone that may fail even under comparatively normal loads (ie, insufficiency fractures). However, both processes are characterized by disrupted bone homeostasis and inadequate repair in the face of repetitive overload.

Frequency:

• In the US: Estimates of the annual incidence of stress fractures among athletes and military recruits range from 5-30%. Stress fractures are among the 5 most common injuries suffered by runners and have been reported to account for up to half of the injuries sustained by military recruits. The interaction between genetic susceptibility and other internal and external risk factors determines an individual's likelihood of sustaining a bony stress injury.

Race: Stress fractures probably occur less frequently among African Americans than among whites by virtue of the generally higher BMD found in African Americans.

Sex: Most studies suggest that females are at increased risk of developing stress fractures compared with males. The incidence of stress fractures among female military recruits and athletes has been reported to be twice that of their male counterparts. Disordered eating places females at higher risk of developing stress fractures. The clinician should be mindful that a stress fracture may herald the existence of underlying amenorrhea, disordered eating, and osteoporosis (the "female athlete's triad"). Therefore, diagnosis of a stress fracture in a female should prompt the clinician to obtain a dietary history to ensure adequate intake of both energy (calories) and calcium. Finally, in the proper clinical context, a stress fracture should alert the clinician to the possibility of osteoporosis or other underlying skeletal pathology.

Age: Stress fractures typically affect individuals who are more active, and the incidence probably increases with age due to age-related reduction in BMD. By no means, however, should the diagnosis be dismissed in children, whose bones have not reached peak density and strength.

• Interestingly, some evidence suggests that the risk of stress fracture may be lower among adult runners who have a broad athletic background that includes childhood participation in "ball sports." This finding provides additional incentive for coaches and parents to avoid promoting early sport-specialization among young athletes.

CLINICAL

Section 3 of 12

History: The most salient historical feature in the diagnosis of stress fracture is the insidious onset of activity-related pain.

• Early on, the pain typically is mild and occurs toward the end of the inciting activity.



• Subsequently, the pain may worsen and occur earlier, limiting participation in sports activities.


• • While rest may provide transient relief of symptoms in the early stages, as the stress injury progresses, the athlete's pain may persist even after cessation of activity.
  
  
  
  • Night pain is a frequent complaint.
  
  
  
  • Pain resulting from long-bone fractures is thought to be localized, while pain associated with stress injury of trabecular bone is characteristically described as more diffuse.
  
  
  
• Stress fractures, like most overuse injuries, typically are multifactorial in etiology; thus, if the diagnosis has been made or is suspected, the clinician is in the position to try to determine what risk factors precipitated or contributed to the injury.


• • Details of the athlete's training history should be noted, both in terms of volume and intensity.
  
  
  
  • Intensive sustained muscular activity may result in bone strain and overload. This type of mechanism of injury is common in rowers, who are prone to stress fractures of the ribs.
  
  
  
• Muscle fatigue, perhaps because of poor conditioning or as the result of overtraining, can attenuate the shock-absorbing capacity of the muscular system, resulting in greater transmission of GRFs to the associated parts of the skeleton.



• Structural malalignments (eg, leg-length discrepancies) or biomechanical inefficiencies (eg, excessive subtalar pronation) can result in increased stress and strain on the tibiae.



• Concurrent injury may result in subclinical biomechanical adaptations along the kinetic chain, placing atypical loads on bone and precipitating a stress injury.



• Poor bone health, whether because of hormonal, dietary, or pathological causes (eg, osteoporosis, hyperparathyroidism, skeletal involvement from malignancy), can weaken bone and make it more susceptible to injury.



• These conditions and other intrinsic and extrinsic risk factors for the development of stress fractures are summarized in Causes below.

Physical: Upon physical examination, individuals with stress fractures typically report pain upon palpation or percussion of the affected area.

• Inspection of the site may reveal localized swelling and, possibly, erythema.



• Loading the affected bone using specific maneuvers (such as the "hop test" or the "fulcrum test") may reproduce the athlete's pain. Note that no single physical examination test is sufficiently sensitive and specific to permit the unequivocal diagnosis of a stress fracture. Rather, taking the individual's history and examination into consideration, the clinician must have sufficient clinical suspicion to include the diagnosis among the different possible causes of the presenting complaints.



• Some practitioners believe that application of a vibrating tuning fork over the affected bone can provoke the athlete's pain, but Brukner et al dispute the validity of this test.



• As part of a thorough physical examination, the practitioner should assess the athlete's flexibility, lower limb alignment (including leg lengths), foot structure (eg, pes cavus vs pes planus), and motor function (eg, evaluating for strength imbalances).

Causes: Disrupted bone homoeostasis and inadequate repair in the face of repetitive overload cause stress fractures. A variety of risk factors are thought to predispose individuals to the development of stress fractures.

• Intrinsic risk factors


• • Low BMD (potentially modifiable)
  
  
  
  • Lower limb malalignment (potentially modifiable)
  
  
  
  • Foot structure (unmodifiable)
  
  
  
  • Height - Tall stature (unmodifiable)
  
  
  
  • Muscle fatigue/poor overall conditioning (modifiable)
  
  
  
  • Weakness/strength imbalance (modifiable)
  
  
  
  • Pathologic bone states (potentially unmodifiable)
  
  
  
  • Menstrual/hormonal irregularities (potentially modifiable)
  
  
  
  • Genetic predisposition (unmodifiable)
  
  
  
• Extrinsic risk factors


• • Excessive volume or intensity of training (modifiable)
  
  
  
  • Sporting discipline (modifiable): For example, runners are prone to tibial shaft stress fractures, whereas tennis players appear to be most vulnerable to navicular injuries, and volleyball players may be at a relatively increased risk of pars interarticularis injuries.
  
  
  
  • Change in training regimen - "New coach" phenomenon (potentially modifiable)
  
  
  
  • Change in training surface - Density or topography (modifiable)
  
  
  
  • Worn-out training shoes (modifiable)
  
  
  
  • Cigarette smoking (modifiable)
  
  
  
  • Inadequate nutrition - Energy (calories), calcium, vitamin D (modifiable)
  
  
  
  • Medication usage - For example, chronic steroid use (potentially modifiable)
  
  
  

DIFFERENTIALS

Section 4 of 12

Lumbar Spondylolysis and Spondylolisthesis

Other Problems to be Considered:

Strains
Sprains
Contusions
Delayed-onset muscle soreness
Tumors of bone, especially osteoid osteomas
Shin splints (ie, medial tibial stress syndrome, tibial traction periostitis)
Exertion-related compartment syndrome
Referred pain from the spine
Diskogenic low back pain
Facet-mediated low back pain
Morton neuroma
Plantar fasciitis
Subluxed cuboid

WORKUP

Section 5 of 12

Lab Studies:

• If in the course of the diagnostic workup for the stress injury the individual is discovered to have metabolic bone disease or another comorbidity (eg, inadequate nutritional status), the clinician should obtain the appropriate laboratory and imaging studies to permit definitive management of the condition (or request specialty-level consultation).

Imaging Studies:

• Imaging studies can help the physician confirm the suspected clinical diagnosis.


• • Conventional radiographic findings are often unremarkable, particularly early in the continuum that leads from stress reaction to stress fracture.
  
  
  
  • In most instances, conventional radiographic signs of a periosteal reaction are not evident within the first several weeks of symptoms.
  
  
  
  • In some cases, conventional radiography remains negative, despite clear diagnostic evidence of fracture on bone scan or cross-sectional imaging.
  
  
  
  • Other conventional radiographic findings include an area of cortical lucency (ie, the so-called thin black line) that suggests a nonhealing stress fracture.
  
  
  
• Computed tomographic (CT) scanning is a useful diagnostic imaging tool, as is magnetic resonance imaging (MRI). These cross-sectional modes of imaging may be helpful in defining the extent of the suspected fracture.



• A 3-phase bone scan (scintigraphy) may be indicated if conventional radiographic findings are negative or nondiagnostic and the clinical suspicion of stress fracture remains high. The bone scan is diagnostic of stress fracture if focal isotope uptake occurs in the area of clinical interest on the third phase of the scan.



• Scintigraphy is extremely sensitive.


• • If the scan shows no evidence of focal uptake, the diagnosis of stress fracture is quite unlikely. Note that as a result of the sensitivity of this imaging modality, focal radiotracer uptake may persist at healing stress fracture sites long after the patient has become asymptomatic. Furthermore, the bone scan may be positive even before the clinical onset of symptoms.
  
  
  
  • Drawbacks of scintigraphy include a relative lack of specificity and anatomic resolution. Nevertheless, the temporal pattern of uptake during the scan may be useful in distinguishing the etiology of the patient's symptoms. Radiotracer uptake on the third phase of the scan generally is specific to bony pathology.
  
  
  
  • For example, tibial periostitis and acute tibial stress fracture both usually demonstrate uptake on the first and second phases of the 3-phase bone scan; however, only the stress fracture results in focal uptake on the third phase.
  
  
  
  • Note that other processes besides stress fracture, including osteomyelitis and tumor, can have a similar appearance on 3-phase bone scans. Thus, for the clinician to consider the imaging study result in the context of the patient's history and physical examination findings is important.
  
  
  
• Because of the limitations inherent to scintigraphy, MRI may be a reasonable first-line imaging procedure. MRI provides greater anatomic detail of the area in question, and fat-suppressed (short TI inversion recovery [STIR]) and water-weighted (T2) signal sequences permit detection of marrow edema and/or periosteal reaction occurring during the earliest stages of stress fracture formation with a level of sensitivity that rivals bone scanning.



• In 2003, Arendt et al described a radiographic grading system that incorporates both conventional radiographic findings and those from MRI. The authors found that the grade of bone stress injury correlated with the average time to full recovery. For example, athletes with grade 1 stress injury who were treated with a standardized rehabilitation protocol returned to sporting activity in 3.3 weeks, on average, while those with grade 4 stress injury returned in 14.3 weeks.

TREATMENT

Section 6 of 12

Rehabilitation Program:

• Physical Therapy: See Deterrence/Prevention. The foundation of treatment for symptomatic stress injury is activity modification. To create an environment conducive to healing the stress injury, interrupting the cycle of repetitive overload is essential. For athletes, this typically results in time lost from competition and intensive training. For most stress fractures, the period of relative rest may be expected to last from 4-12 weeks. Factors influencing the duration of the activity restriction include the anatomic site of the stress injury, the extent of the stress injury, and the anticipated demands on the athlete upon return to play. During the period of restricted activity, the clinician should evaluate the athlete for modifiable risk factors that might have contributed to the development of the stress fracture.

  Training errors (eg, too much, too soon) are a common contributing factor to bone stress injury. One generally espoused (although inadequately validated) principle is that the athlete's training regimen (ie, volume of sport-related activity) should not increase by any more than 10% from one week to the next.

  Runners should replace their shoes every 500 km to ensure adequate midsole cushioning. Shoes should be selected with attention to the athlete's foot structure. Flexible flatter feet should be fitted with shoes that provide optimal support and motion control (possibly including orthoses), whereas rigid highly arched feet should be fitted with shoes that provide maximal cushioning.

  Rehabilitation of the individual with a stress fracture should include a program of muscle strengthening and generalized conditioning. Strong, well-conditioned muscles help to dissipate GRFs that otherwise would be transmitted to bones and joints along the kinetic chain.

  Fitness training during the rehabilitation period should include cross-training so that excessive loading of the affected bone is avoided. A brief period of restricted weight bearing may be indicated if the athlete initially experiences intolerable pain while walking. Occasionally, bracing and even casting may prove beneficial. Aquatic exercise programs are effective for maintaining the athlete's cardiorespiratory conditioning while effectively eliminating weight bearing.

  If pain persists or becomes further limiting, analgesics may be helpful. Nonsteroidal anti-inflammatory drugs (NSAIDs) are prescribed frequently, but some clinicians believe these agents should be relatively contraindicated in this setting. NSAIDs inhibit the production of prostaglandins, which are demonstrated to be involved in normal bone remodeling and fracture healing. Although animal studies have shown reasonably conclusively that NSAIDs inhibit fracture healing, the evidence from human studies is somewhat contradictory in this regard. If used at all, NSAIDs should therefore be used cautiously with a full understanding of their potential adverse effects.

  The intravenous administration of the bisphosphonate pamidronate has been reported to benefit athletes with stress fractures, and it may hold some promise as an adjunctive treatment for symptomatic bony stress injury.

  In addition to pharmacotherapy, physical therapy modalities, such as ice or interferential current, may be used to help treat symptoms. No compelling evidence exists in the literature to suggest that adjunctive therapeutic modalities (eg, electrical stimulation, pulsed ultrasonography, laser therapy) have a significant role to play in the routine treatment of bony stress injury.

  As the fracture heals and symptoms subside, advance the athlete's program accordingly to permit progressively greater loading of the affected structure. Functional progression from walking to running to sport-specific skills permits the athlete to regain fitness and confidence prior to the resumption of training and competition. Additional recommendations for treatment are included in the following brief overviews of 4 common types of stress fracture.

  Pars interarticularis stress fractures (ie, spondylolysis)

  Stress fractures of the pars interarticularis are common in athletes who participate in sports demanding repetitive lumbar hyperextension, truncal rotation, or axial loading. Once considered a congenital variation, spondylolysis is probably an acquired condition in most cases. Genetic predisposition undoubtedly plays a role in the development of spondylolysis. For example, the prevalence of spondylolysis among the Inuit population is roughly 50%, and whites appear to be at greater risk for developing pars defects than African Americans.

  Soler and Colderon found that while the prevalence of spondylolysis among a broad cross-section of elite Spanish athletes was similar to that found in the general population (8%), the highest prevalence (27%) was among athletes participating in the throwing track-and-field events (eg, javelin, discus, shot put). Roughly 17% of rowers and 14% of gymnasts were found to have spondylolysis. Approximately 13% of weightlifters were affected. The most common level of involvement was L5 (84%), followed by L4 (12%). More than one level was involved in only 3% of cases. The condition was bilateral approximately 78% of the time. Of the athletes found to have spondylolysis, 50-60% reported low back pain. Males and females appeared to be affected equally, although females were more likely to have associated spondylolisthesis than men. Other studies estimate the prevalence of spondylolysis among athletes from 15-63%, with the highest prevalence among weightlifters.

  Clinically, symptomatic individuals typically report localized axial low back pain. The pain may be provoked by lumbar extension, particularly while bearing weight on the ipsilateral lower limb. Hamstring inflexibility is a common finding among individuals with spondylolysis. Curiously, young children diagnosed with pars defects tend to be asymptomatic.

  The clinical diagnosis may be confirmed radiographically. Conventional radiography is often unrevealing, but, if present, the fracture line is usually best visualized on oblique views. Nascent or recently completed stress fractures of the pars may be detected by scintigraphy. Single-photon emission computed tomography (SPECT) is extremely sensitive and provides reasonable anatomic detail. MRI is also a justifiable first-line imaging procedure, and it offers the additional benefit of permitting concurrent evaluation of the lumbar intervertebral disks and other potential spinal pain generators. In their 2006 study, Sairyo and colleagues were able to correlate the presence of high water-weighted (T2) signal in the pedicle with the early stage of ipsilateral pars interarticularis stress injury as judged by CT, suggesting that MRI may permit early detection of stress injury and potentially enhance the outcome of treatment (Sairyo, 2006).

  Radiographically documented pars defects that are cold on bone scans probably represent remote injuries and have little chance of bony union. If symptomatic, individuals with cold defects may be treated with NSAIDs or other analgesics and should be instructed in a program of on-going home exercises to strengthen the muscle groups that provide dynamic stabilization of the lumbar spine.

  The recommended treatment for acute spondylolysis has evolved considerably over the past decade and remains somewhat controversial. As with other stress fractures, the central tenet of treatment is relative rest with appropriate activity modification. Although some clinicians recommend bracing to minimize extension and resultant shear forces across the affected segment, some evidence from biomechanical studies indicates that lumbosacral bracing may actually increase intersegmental motion at the lumbosacral junction. Therefore, the prevailing opinion appears to be that bracing should be used only for individuals who remain symptomatic despite attempting to limit their activities, or for those who require a physical/tactile reminder to avoid provocative activities.

  Once symptoms permit, the individual should begin a rehabilitation program of flexibility training and dynamic lumbar spinal stabilization. The program should emphasize pain-free functional progression. Once the athlete can perform sport-specific skills without symptoms, he or she may return to training and competition. Unilateral spondylolysis tends to have a more favorable clinical outcome than bilateral spondylolysis. For a more detailed discussion, see the article Lumbar Spondylolysis and Spondylolisthesis.

  Femoral neck stress fracture

  Stress fractures of the femoral neck can occur either on the superior or inferior aspect of the neck. Older individuals tend to develop fractures on the superior (or distraction) side of the neck, while younger people are more prone to fractures on the inferior (or compression) side of the neck. In both populations, the patient typically presents with activity-related pain in the groin, hip girdle, or anterior thigh. Physical examination may reveal pain with passive hip range of motion, particularly internal rotation. Conventional radiography and bone scanning are usually sufficient for the physician to confirm or exclude the diagnosis. However, MRI, with its sensitivity and high anatomic detail, is being used with increasing frequency.

  For patients diagnosed with early stress reaction or a nondisplaced stress fracture of the femoral neck, treatment consists of avoidance of weight bearing on the affected lower limb until symptoms resolve. Subsequently, the individual is permitted to resume partial weight bearing as tolerated, progressing over time to unprotected weight bearing, to walking, and, finally, to running. Full functional progression may take months to complete. Serial radiographs obtained periodically help confirm that healing is progressing. If the patient is found to have a significant cortical defect or if the fracture is displaced, surgical fixation is required prior to beginning a program of rehabilitation.

  Tibial stress fracture

  The tibial shaft is the most common site of stress fractures. Unfortunately, shin pain is a frequent complaint among athletes and can result from a variety of causes, including tibial periostitis (ie, shin splints) and exertional compartment syndromes (a potentially serious condition). A careful history is helpful in distinguishing these entities. Pain that occurs early in the exercise program and then improves with ongoing activity suggests periostitis. Pain precipitated by exercise that worsens progressively with continued activity may herald a stress fracture.

  Physical examination typically reveals localized tenderness over the medial aspect of the tibia. Tibial stress fractures may be more common among athletes with rigid cavus feet. Excessive subtalar pronation can also predispose an athlete to tibial stress fractures. The clinical diagnosis can be confirmed by conventional radiography, although one study suggests that this imaging modality shows evidence of stress fracture or periosteal reaction in only 10% of cases. Scintigraphy and/or MRI may be useful for confirming the suspected clinical diagnosis.

  Treatment consists of activity restriction to minimize symptoms (ie, a period of non weight bearing may be necessary) before engaging in a program of increasingly demanding strengthening and conditioning exercise, leading to an eventual return to play in 8-12 weeks. Interestingly, 3 studies have demonstrated that use of a pneumatic leg brace allowed athletes to recover more quickly than athletes treated with activity restriction alone (Anderson, 2000; Swenson, 1997; Whitelaw, 1991). It may be that compression of the leg's soft tissues helps to unload the tibia during weight-bearing activities, thereby minimizing further microdamage and facilitating bony repair.

  Cortical stress fractures of the anterior tibial midshaft should be treated with care because they tend to heal more slowly (average of 6 mo) and are prone to delayed union or nonunion. In such cases, electromagnetic stimulation may potentially be helpful in promoting healing. Some authors recommend immobilization as initial therapy. Failure of nonoperative care warrants consideration of surgical intervention. Options include reamed intramedullary nailing and internal fixation with bone grafting. Postoperative recovery time averages 6 months.

  Second metatarsal stress fracture

  The metatarsals are the second most frequent stress fracture site and are especially common among military recruits, distance runners, and ballet dancers. The second metatarsal is injured most frequently, followed in order by metatarsals 3, 1, 4, and 5. Although the idea is somewhat controversial, foot structure may contribute to an individual’s relative risk of developing lower limb overuse injuries in general and stress fractures in particular.

  One prospective study of military recruits found that flat flexible feet were associated with a significantly higher rate of metatarsal stress fractures, while individuals with cavus feet were more prone to developing tibial stress fractures. The authors reasoned that flexible feet dissipate more GRF than do rigid cavus feet, thereby subjecting the intrinsic foot structures to greater loads and transmitting less GRF proximally than would a rigid cavus foot. The relative length of the first and second rays appears to have no relationship to the development of second metatarsal stress fractures.

  The diagnosis of second metatarsal stress fracture can be made clinically, given an appropriate history of activity-related forefoot pain and the finding of focal tenderness over the second ray on palpatory examination. Treatment consists of relative rest, with return to play permitted once the individual can perform sport-specific skills without pain. Orthoses may be useful to help prevent recurrence of the injury. Custom-molded orthoses provide optimal support and may help correct biomechanical deficits, but studies have shown that over-the-counter shock absorbing insoles are equally effective in preventing lower limb stress injuries. Stress fractures at the base of the second metatarsal appear to be prone to delayed healing and may be treated best with a period of immobilization.

Surgical Intervention: In most cases, stress fractures can be managed successfully with conservative measures. High-risk displaced stress fractures, however, require surgical intervention to ensure proper healing. Surgical procedures most typically involve open-reduction internal fixation and pinning of the associated fracture sites. Postoperative recovery time averages 6 months.

Consultations: Consider consultation with an orthopedic surgeon for high-risk stress fractures. Affected female athletes who exhibit signs of eating disorders may benefit from a consultation with dietitian, psychologist/psychiatrist, or both.

MEDICATION

Section 7 of 12

The goals of pharmacotherapy are to reduce patient discomfort, minimize associated morbidity, and to prevent complications.

Drug Category: Nonsteroidal anti-inflammatory drugs -- Have analgesic, anti-inflammatory, and antipyretic activities. Mechanism of action is not known, but they may inhibit COX activity and prostaglandin synthesis. Other mechanisms may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Drug Name	Celecoxib (Celebrex) -- Inhibits primarily COX-2, which is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID-related GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek lowest dose for each patient.
Adult Dose	200 mg PO qd
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity, sulfa allergies, and renal insufficiency
Interactions	Coadministration with fluconazole may cause increase in plasma concentrations because of inhibition of metabolism; coadministration with rifampin may decrease plasma concentrations
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Some authorities believe that anti-inflammatory drugs inhibit bone remodeling and fracture healing, and therefore recommend that these agents be used with caution in individuals with healing stress fractures; may cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, and conditions predisposing to fluid retention; caution in severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction or with abnormal LFT results

Drug Name	Ibuprofen (Motrin, Excedrin IB, Advil, Ibuprin) -- DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Adult Dose	400 mg PO q4-6h, 600 mg PO q6h, or 800 mg PO q8h while symptoms persist; not to exceed 3.2 g/d
Pediatric Dose	20-70 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate; not to exceed 2.4 g/d
Contraindications	Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
Interactions	Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Pregnancy category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

Drug Name	Naproxen (Aleve, Anaprox, Naprelan, Naprosyn) -- For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of COX, which is responsible for prostaglandin synthesis. NSAIDs decrease intraglomerular pressure and decrease proteinuria.
Adult Dose	250-500 mg PO bid; may increase to 1.5 g/d for limited periods
Pediatric Dose	<2 years: Not established >2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Contraindications	Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
Interactions	Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Drug Category: Analgesics -- Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma.

Drug Name	Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin) -- May be a reasonable alternative for symptom management in individuals who cannot tolerate NSAIDs or if the practitioner is concerned that NSAIDs may interfere with bone healing.
Adult Dose	325-650 mg PO q4-6h
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; known G-6-P deficiency
Interactions	Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, or isoniazid may increase hepatotoxicity
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Hepatotoxicity possible in chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative acetaminophen doses that exceed recommended maximum dose

FOLLOW-UP

Section 8 of 12

Further Inpatient Care:

• Most stress fractures are treated successfully in an outpatient setting using conservative measures. Inpatient care is necessary only for individuals who undergo surgical intervention for the treatment of more severe displaced fractures or in an effort to treat a nonhealing fracture. If hospitalized, some patients who have been ordered to restrict weight bearing through the affected limb may benefit from consultation with a physical therapist to ensure safe ambulation. If the patient's symptoms or treatment interfere with his or her ability to independently perform aspects of daily care, a consultation with an occupational therapist may be indicated.

Further Outpatient Care:

• Treatment of stress fractures typically is performed in an outpatient setting. Patients may benefit from physical therapy to maintain overall fitness, thereby minimizing time lost from training and competition once the individual has been cleared to return to their previous activity level. The physical therapist may also assist in identifying intrinsic risk factors that might have contributed to the onset of the stress injury. See Physical Therapy.
  

Deterrence/Prevention:

• The optimal treatment for stress fractures is prevention. Ideally, coaches, athletes, trainers, and team physicians should invest themselves in a program of injury prevention that is appropriate to the sport or activity. Features common to such programs include thorough preparticipation physical examinations to screen for risk factors (see Causes); prescription of “prehabilitation” exercises designed to enhance strength, endurance, and coordination; and close monitoring of athletes for early signs that may alert the attentive clinician to an incipient overuse injury.



• Stress fractures can be largely prevented with proper conditioning and preseason training. Athletes must use proper equipment and wear appropriate shoes to avoid developing stress fractures. For certain foot structures, taping techniques or the use of orthotic inserts can prevent overloading of soft tissues and bone. Nutritional supplementation and increasing calcium intake also contribute to overall bone health and thereby decrease the likelihood of developing stress fractures.



• The cornerstone of secondary prevention of bony stress injury is a thorough assessment of potentially modifiable intrinsic and extrinsic risk factors unique to the athlete.

Complications:

• Complications of stress fracture may include avascular necrosis, nonunion, malunion, posttraumatic arthrosis, and persistent disabling pain.

Prognosis:

• The prognosis for recovery is dependent on the location and severity of the fracture and on the age and underlying condition and associated comorbidities of the affected athlete. Most stress fracture carry a favorable prognosis for full recovery when appropriate treatment has been provided.

Patient Education:

• Patient education is important in both the prevention and treatment of stress fractures. Athletes need to be educated on proper conditioning programs that decrease their chances of developing stress fractures. For example, the preseason training program should be structured to gradually increase the frequency and intensity of exercise and to avoid sudden increases in training load that might overwhelm the skeleton’s intrinsic ability to recover and repair.



• Once diagnosed with a stress fracture, the affected individual must be made to understand the importance of a period of relative rest/activity modification. Athletes should review their training history for evidence of significant training errors or overload and adjust the training program accordingly. Educating the patient in an outpatient program of progressive muscle strengthening and conditioning will enable the athlete to return safely to his or her sport once their bony stress injury has healed.



• For excellent patient education resources, visit eMedicine's Breaks, Fractures, and Dislocations Center and Sports Injury Center. Also, see eMedicine's patient education article Repetitive Motion Injuries.

MISCELLANEOUS

Section 9 of 12

Medical/Legal Pitfalls:

• Failure to complete a thorough history and physical examination of an individual with a stress fracture may result in an inaccurate diagnosis, which in turn could result in inadequate or inappropriate therapeutic intervention.

Special Concerns:

• Early diagnosis and treatment of compression fractures of the femoral neck are important. Complications of undetected displaced fractures of the femoral neck may result in avascular necrosis and nonunion.

TEST QUESTIONS

Section 10 of 12

CME Question 1: Which of the following statements concerning the etiology of stress fractures is not correct?

A: Stress injury to bone may be thought of as a continuum from subclinical stress reaction to a completed fracture with cortical disruption.
B: Intrinsic risk factors for the development of stress fractures may include low levels of physical fitness and biomechanical deficits of the lower limbs.
C: Extrinsic risk factors for the development of stress fractures may include excessive training volume and worn-out training shoes.
D: Stress fractures may be considered overuse injuries of bone.
E: Most stress fractures involve the upper limbs and thorax.

The correct answer is E: A, B, C, and D are all correct statements. E is incorrect. Most stress fractures involve the lower limbs.

CME Question 2: A 22-year-old elite female volleyball player presents with localized low back pain that worsens with trunk extension. The clinician suspects that she may have acute spondylolysis. Which of the following would not be considered a reasonable component of a comprehensive diagnostic workup and treatment plan?

A: Obtain plain films of the lumbar spine, including oblique views.
B: Obtain a 3-phase bone scan with single-photon emission computed tomography (SPECT) imaging.
C: Recommend that she modify her activities to avoid provocation of her symptoms.
D: Reassure her that her 7% body fat and history of amenorrhea are acceptable, given her athleticism, and probably are unrelated to her back pain.
E: Suggest a trial of bracing if her symptoms persist despite a period of relative rest.

The correct answer is D: A, B, C, and E are all reasonable actions. D is incorrect. The diagnosis of stress fracture in a female athlete should alert the clinician to the possibility of the female athlete`s triad (ie, amenorrhea, disordered eating, osteoporosis) and should prompt a detailed dietary and menstrual history to be taken.

Pearl Question 1 (T/F): Stress fractures of the anterior tibial cortex are prone to nonunion.

The correct answer is True: Because of this fact, some clinicians suggest casting as the preferred initial treatment for stress fractures of the anterior tibial cortex.

Pearl Question 2 (T/F): MRI is increasingly useful as an imaging modality in the diagnosis and management of stress fractures.

The correct answer is True: The stress fracture literature contains an ever-increasing number of articles that are demonstrating the use of MRI—not only for the diagnosis of stress injury to bone, but as a means of estimating the age of the stress injury (which in turn has treatment implications and may influence outcome). Many clinicians therefore consider MRI to be superior to 3-phase bone scanning for diagnosing stress fractures, particularly when considering the modality`s sensitivity and superior anatomic detail compared with scintigraphy.

Pearl Question 3 (T/F): Relative rest is the cornerstone of treatment for stress fractures.

The correct answer is True: Relative rest or avoidance of symptom-provoking activity is intended to minimize further stress on the affected bone, thereby giving it a chance to heal.

Pearl Question 4 (T/F): Nonsteroidal antiinflammatory agents should be considered the first line of pharmacologic intervention for an individual diagnosed with a stress fracture.

The correct answer is False: NSAIDs inhibit cyclooxygenase activity, which in turn inhibits the inducible synthesis of prostaglandins. Prostaglandins have been shown to play an important role in both bone turn over and fracture healing. Although animal studies are convincing, human studies are less definitive in proving an association between NSAID use and unfavorable treatment outcomes. Many clinicians recommend only short-term use of NSAIDs in the management of bony stress injury (if indeed they are used at all).

PICTURES

Section 11 of 12

Caption: Picture 1. Case 1. This image is of a 17-year-old male wrestler with a 2-month history of left-sided low back pain, worse with extension. Total body scintigraphy findings were unremarkable. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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Caption: Picture 2. Same patient as in Images 1 and 3. Single-photon emission computed tomography (SPECT) images demonstrate abnormal delayed uptake in the posterior elements of L5. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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Caption: Picture 3. Same patient as in Images 1-2. Subsequent MRI revealed an area of bright signal in the left pars interarticularis of L5 on T2-weighted images, confirming the diagnosis of acute unilateral spondylolysis. The patient was treated successfully with activity restriction and bracing with a lumbar corset for 3 months, at which point he was asymptomatic. Plain film imaging at follow-up (not shown) was unremarkable, with no evidence of spondylolysis on oblique views. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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Caption: Picture 4. Case 2. A 17-year-old female dancer with a 2-week history of left shin pain. Plain film imaging was unremarkable. Three-phase bone scanning demonstrated an area of linear uptake in the posterior medial aspect of the left tibia on blood pool images, but delayed images were considered normal. This scintigraphic pattern is consistent with medial tibial stress syndrome (shin splints), but not with stress fracture. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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Caption: Picture 5. Case 3. This is a 55-year-old female industrial worker with a 1-week history of right foot pain. Plain film imaging was unremarkable. Bone scanning revealed a stress fracture of the second metatarsal. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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Caption: Picture 6. Case 4. This image is of an 18-year-old female soccer player with a 3-week history of left leg pain, which was worse at night and with activity. Upon examination, she reported tenderness in response to palpation over the mid tibia. Bilateral pes planus was noted. Plain film radiography failed to demonstrate a fracture. Bone scanning revealed a focal area of delayed uptake on the posterior medial aspect of the proximal third of the left tibia, confirming the diagnosis of stress fracture. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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Caption: Picture 7. Case 5. A 63-year-old man with metastatic thyroid carcinoma went for a walk and awoke the following morning with left hip girdle pain. Plain film imaging revealed a subtle area of linear cortical lucency at the proximal left femoral metadiaphysis, consistent with an insufficiency fracture through pathologic bone. The patient subsequently underwent internal fixation. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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Caption: Picture 8. Enlarged image of fracture shown in Image 7, in a 63-year-old man with metastatic thyroid carcinoma who went for a walk and awoke the following morning with left hip girdle pain. Plain film imaging revealed a subtle area of linear cortical lucency at the proximal left femoral metadiaphysis, consistent with an insufficiency fracture through pathologic bone. The patient subsequently underwent internal fixation. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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Caption: Picture 9. Case 6. This case involves a 16-year-old female basketball player with a 2-year history of left foot pain refractory to casting and reduced weight bearing. Bone scanning revealed a focal area of delayed uptake lateral to the left first metatarsal phalangeal joint, which corresponded to a bipartite sesamoid on plain films. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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Caption: Picture 10. Sesamoid stress fractures are prone to nonunion, and sesamoidectomy is indicated for patients who do not respond to conservative management. Some clinicians recommend bone grafting as an alternative to complete or partial sesamoidectomy. Courtesy of Michael Spieth, MD, and Nandita Bhattacharjee, MD, MHA; Marshfield Clinic Department of Radiology.
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BIBLIOGRAPHY

Section 12 of 12

• Anderson K, Sarwark JF, Conway JJ, et al: Quantitative assessment with SPECT imaging of stress injuries of the pars interarticularis and response to bracing. J Pediatr Orthop 2000 Jan-Feb; 20(1): 28-33[Medline].
• Arendt E, Agel J, Heikes C, Griffiths H: Stress injuries to bone in college athletes: a retrospective review of experience at a single institution. Am J Sports Med 2003 Nov-Dec; 31(6): 959-68[Medline].
• Arendt EA: Stress fractures and the female athlete. Clin Orthop 2000 Mar; (372): 131-8[Medline].
• Bennell K, Matheson G, Meeuwisse W, Brukner P: Risk factors for stress fractures. Sports Med 1999 Aug; 28(2): 91-122[Medline].
• Bennell K, Brukner P: How Should You Treat a Stress Fracture? Evidence-based Sports Medicine 2002; 491-517.
• Brukner P, Bennell K, Matheson G: Stress Fractures. 1st ed. Melbourne, Australia: Blackwell Science Asia; 1999.
• Buvanendran A, Reuben SS: COX-2 inhibitors in sports medicine: utility and controversy. Br J Sports Med 2006 Nov; 40(11): 895-6[Medline].
• Callahan LR: Stress fractures in women. Clin Sports Med 2000 Apr; 19(2): 303-14[Medline].
• DiFiori JP: Stress fracture of the proximal fibula in a young soccer player: a case report and a review of the literature. Med Sci Sports Exerc 1999 Jul; 31(7): 925-8[Medline].
• Donahue SW, Sharkey NA: Strains in the metatarsals during the stance phase of gait: implications for stress fractures. J Bone Joint Surg Am 1999 Sep; 81(9): 1236-44[Medline].
• Ellerin BE, Helfet D, Parikh S, et al: Current therapy in the management of heterotopic ossification of the elbow: a review with case studies. Am J Phys Med Rehabil 1999 May-Jun; 78(3): 259-71[Medline].
• Finestone A, Giladi M, Elad H, et al: Prevention of stress fractures using custom biomechanical shoe orthoses. Clin Orthop 1999 Mar; (360): 182-90[Medline].
• Fredericson M, Ngo J, Cobb K: Effects of ball sports on future risk of stress fracture in runners. Clin J Sport Med 2005 May; 15(3): 136-41[Medline].
• Green NE, Rogers RA, Lipscomb AB: Nonunions of stress fractures of the tibia. Am J Sports Med 1985 May-Jun; 13(3): 171-6[Medline].
• Ho ML, Chang JK, Chuang LY, et al: Effects of nonsteroidal anti-inflammatory drugs and prostaglandins on osteoblastic functions. Biochem Pharmacol 1999 Sep 15; 58(6): 983-90[Medline].
• Hofmann AA, Bloebaum RD, Koller KE: Does celecoxib have an adverse effect on bone remodeling and ingrowth in humans?. Clin Orthop Relat Res 2006 Nov; 452: 200-4[Medline].
• Hoy G, Wood T, Phillips N: When physiology becomes pathology: the role of magnetic resonance imaging in evaluating bone marrow oedema in the humerus in elite tennis players with an upper limb pain syndrome. Br J Sports Med 2006 Aug; 40(8): 710-3; discussion 713[Medline].
• Ivkovic A, Bojanic I, Pecina M: Stress fractures of the femoral shaft in athletes: a new treatment algorithm. Br J Sports Med 2006 Jun; 40(6): 518-20; discussion 520[Medline].
• Johnson BA, Neylon T, Laroche R: Lesser metatarsal stress fractures. Clin Podiatr Med Surg 1999 Oct; 16(4): 631-42[Medline].
• Jones BH, Knapik JJ: Physical training and exercise-related injuries. Surveillance, research and injury prevention in military populations. Sports Med 1999 Feb; 27(2): 111-25[Medline].
• Jones BH, Thacker SB, Gilchrist J, et al: Prevention of lower extremity stress fractures in athletes and soldiers: a systematic review. Epidemiol Rev 2002; 24(2): 228-47[Medline].
• Kaufman KR, Brodine SK, Shaffer RA, et al: The effect of foot structure and range of motion on musculoskeletal overuse injuries. Am J Sports Med 1999 Sep-Oct; 27(5): 585-93[Medline].
• Kibler WB: ACSM's Handbook for the Team Physician. Baltimore, Md: Williams & Wilkins; 1996.
• Kibler WB, Herring SA, Press JM: Functional Rehabilitation of Sports and Musculoskeletal Injuries. Aspen Publishers: Gaithersburg, Md; 1998.
• Kiuru MJ, Niva M, Reponen A, Pihlajamaki HK: Bone stress injuries in asymptomatic elite recruits: a clinical and magnetic resonance imaging study. Am J Sports Med 2005 Feb; 33(2): 272-6[Medline].
• Komatsubara S, Sairyo K, Katoh S: High-grade slippage of the lumbar spine in a rat model of spondylolisthesis: effects of cyclooxygenase-2 inhibitor on its deformity. Spine 2006 Jul 15; 31(16): E528-34[Medline].
• Lauder TD, Dixit S, Pezzin LE, et al: The relation between stress fractures and bone mineral density: evidence from active-duty Army women. Arch Phys Med Rehabil 2000 Jan; 81(1): 73-9[Medline].
• Lippi G, Franchini M, Guidi GC: Non-steroidal anti-inflammatory drugs in athletes. Br J Sports Med 2006 Aug; 40(8): 661-2; discussion 662-3[Medline].
• Maquirriain J, Ghisi JP: The incidence and distribution of stress fractures in elite tennis players. Br J Sports Med 2006 May; 40(5): 454-9; discussion 459[Medline].
• Milgrom C, Simkin A, Eldad A, et al: Using bone's adaptation ability to lower the incidence of stress fractures. Am J Sports Med 2000 Mar-Apr; 28(2): 245-51[Medline].
• Miller SF, Congeni J, Swanson K: Long-term functional and anatomical follow-up of early detected spondylolysis in young athletes. Am J Sports Med 2004 Jun; 32(4): 928-33[Medline].
• Milner CE, Ferber R, Pollard CD: Biomechanical factors associated with tibial stress fracture in female runners. Med Sci Sports Exerc 2006 Feb; 38(2): 323-8[Medline].
• Murnaghan M, Li G, Marsh DR: Nonsteroidal anti-inflammatory drug-induced fracture nonunion: an inhibition of angiogenesis?. J Bone Joint Surg Am 2006 Nov; 88 Suppl 3: 140-7[Medline].
• Neal BC, Rodgers A, Clark T, et al: A systematic survey of 13 randomized trials of non-steroidal anti- inflammatory drugs for the prevention of heterotopic bone formation after major hip surgery. Acta Orthop Scand 2000 Apr; 71(2): 122-8[Medline].
• Orava S, Karpakka J, Hulkko A, et al: Diagnosis and treatment of stress fractures located at the mid-tibial shaft in athletes. Int J Sports Med 1991 Aug; 12(4): 419-22[Medline].
• Rauh MJ, Macera CA, Trone DW: Epidemiology of stress fracture and lower-extremity overuse injury in female recruits. Med Sci Sports Exerc 2006 Sep; 38(9): 1571-7[Medline].
• Rome K, Handoll HH, Ashford R: Interventions for preventing and treating stress fractures and stress reactions of bone of the lower limbs in young adults. Cochrane Database Syst Rev 2005; CD000450[Medline].
• Sairyo K, Katoh S, Takata Y: MRI signal changes of the pedicle as an indicator for early diagnosis of spondylolysis in children and adolescents: a clinical and biomechanical study. Spine 2006 Jan 15; 31(2): 206-11[Medline].
• Shaffer RA, Rauh MJ, Brodine SK: Predictors of stress fracture susceptibility in young female recruits. Am J Sports Med 2006 Jan; 34(1): 108-15[Medline].
• Shikare S, Samsi AB, Tilve GH: Bone imaging in sports medicine. J Postgrad Med 1997 Jul-Sep; 43(3): 71-2[Medline].
• Simkin A, Leichter I, Giladi M, et al: Combined effect of foot arch structure and an orthotic device on stress fractures. Foot Ankle 1989 Aug; 10(1): 25-9[Medline].
• Sinha AK, Kaeding CC, Wadley GM: Upper extremity stress fractures in athletes: clinical features of 44 cases. Clin J Sport Med 1999 Oct; 9(4): 199-202[Medline].
• Soler T, Calderon C: The prevalence of spondylolysis in the Spanish elite athlete. Am J Sports Med 2000 Jan-Feb; 28(1): 57-62[Medline].
• Standaert CJ, Herring SA: How Should You Treat Spondylolysis in the Athlete? Evidence-based Sports Medicine 2002; 239-265.
• Stasinopoulos D: Treatment of spondylolysis with external electrical stimulation in young athletes: a critical literature review. Br J Sports Med 2004 Jun; 38(3): 352-4[Medline].
• Stewart GW, Brunet ME, Manning MR, Davis FA: Treatment of stress fractures in athletes with intravenous pamidronate. Clin J Sport Med 2005 Mar; 15(2): 92-4[Medline].
• Stovitz SD, Arendt EA: NSAIDs should not be used in treatment of stress fractures. Am Fam Physician 2004 Oct 15; 70(8): 1452, 1454[Medline].
• Swenson EJ, DeHaven KE, Sebastianelli WJ, et al: The effect of a pneumatic leg brace on return to play in athletes with tibial stress fractures. Am J Sports Med 1997 May-Jun; 25(3): 322-8[Medline].
• Torstveit MK, Sundgot-Borgen J: The female athlete triad: are elite athletes at increased risk? Med Sci Sports Exerc 2005 Feb; 37(2): 184-93[Medline].
• Välimäki VV, Alfthan H, Lehmuskallio E, et al: Risk factors for clinical stress fractures in male military recruits: a prospective cohort study. Bone 2005 Aug; 37(2): 267-73[Medline].
• Van der Wall H, McLaughlin A, Bruce W, et al: Scintigraphic patterns of injury in amateur weight lifters. Clin Nucl Med 1999 Dec; 24(12): 915-20[Medline].
• Varner KE, Younas SA, Lintner DM, Marymont JV: Chronic anterior midtibial stress fractures in athletes treated with reamed intramedullary nailing. Am J Sports Med 2005 Jul; 33(7): 1071-6[Medline].
• Wheeler P, Batt ME: Do non-steroidal anti-inflammatory drugs adversely affect stress fracture healing? A short review. Br J Sports Med 2005 Feb; 39(2): 65-9[Medline].
• Whitelaw GP, Wetzler MJ, Levy AS, et al: A pneumatic leg brace for the treatment of tibial stress fractures. Clin Orthop 1991 Sep; (270): 301-5[Medline].

NOTE:

Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

eMedicine Journal, February 21 2007, VOLUME 8, Number 2
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eMedicine Journals > Physical Medicine and Rehabilitation > Lower Limb Musculoskeletal Conditions >Stress Fracture

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