Physical Medicine and Rehabilitation for Stress Fractures

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's 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 magnetic resonance imaging (MRI) findings suggestive of a low-grade bone stress injury correlated with clinical symptoms.[11] 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's 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. An example of an insufficiency fracture is shown in the images below.

Frequency

United States

Estimates of the annual incidence of stress fractures among athletes and military recruits range from 5-30%.[12] 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.[13]

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.

Among US high school athletes, an estimated 1.54 stress fractures occur per 100,000 athlete-exposures, with the highest rates being seen in girls' and boys' cross country and in girls' gymnastics.[14]  Female sex-specific risk factors include late menarche, low body mass index, and participation in gymnastics and dance.[15]

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.

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.[16]

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).

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 are as follows:

• 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 are as follows:

• 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[17, 18] (modifiable)

• Medication usage - For example, long-term steroid use (potentially modifiable)

A literature review by Yoder et al indicated that high-prevalence risk factors for fatigue-related sacral stress fractures include dietary deficiency and a recent increase in training intensity, while high-prevalence risk factors for sacral insufficiency fractures include osteoporosis, rheumatoid arthritis, long-term corticosteroid treatment, pelvic radiation therapy, and a postmenopausal state.[19]

A study by Hughes et al, using the Total Army Injury and Health Outcomes Database, indicated that the prescription of acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs) can be linked to an increased risk of stress fracture, especially at times of increased physical activity. Soldiers who were prescribed acetaminophen or NSAIDs had a 2.1- or 2.9-fold greater risk of stress fracture, respectively, than did the overall Army population. In soldiers undergoing basic combat training, a period of particularly intense physical activity, these figures were more than four and five fold, respectively.[20]

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).

Low vitamin D levels have been associated with foot and ankle stress fractures. Assessment of the patient's vitamin D level may be beneficial.[22]

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 the acute setting, conventional radiography may only detect 15% of stress fractures.[23] 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.

CT scanning is a useful diagnostic imaging tool, as is MRI.[2] 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. MRI is considered the best imaging procedure for stress fractures.[23, 24, 25]

For example, a literature review by Wright et al indicated that MRI has the greatest sensitivity and specificity for diagnosing stress fractures of the lower extremity, when compared with conventional radiography, nuclear scintigraphy, CT scanning, and ultrasonography. According to the studies evaluated, MRI had a sensitivity of 68-99% and a specificity of 4-97%.[26]

MRI has been shown to have a 92% sensitivity in detecting stress reaction or fracture in the evaluation of spondylolysis.[27]

In 2003, Arendt et al described a radiographic grading system that incorporates both conventional radiographic findings and those from MRI.[28] 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.

Similarly, a study by Ramey et al found that in patients with femoral neck stress fractures, return-to-running time was significantly shorter for those with a grade 1 injury (mean period of 7.4 wks), as determined with MRI, than in patients with a grade 2, 3, or 4 fracture (mean periods of 13.8, 14.7, and 17.5 wks, respectively).[29]

High-resolution ultrasonography may detect bone stress injury or occult fractures before they are evident on radiographs.[10]

Physical therapy

See Deterrence. 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.[30]

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 that 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 (shown below) 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).[31] 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.[32]

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[4, 33] 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.

Snyder et al, in a review of randomized and quasi-randomized, controlled trials, found evidence that the use of insoles can reduce the incidence of femoral and tibial stress fractures in soldiers during military training.[34] It was uncertain from their investigation whether the same would be true for athletes.

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.[35, 36, 37] 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.

Long-term studies of military recruits with tibial stress fractures did not show any limitations in their physical abilities.[38]

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 (see the image below) 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.

Concern about complications is warranted when stress fractures are displaced or do not demonstrate adequate healing, despite time and appropriate interventions. Displaced stress fractures of the femoral neck, for example, have a high prevalence of complications, including avascular necrosis and pseudoarthrosis, due to the nature of the blood supply to the femoral neck. Other complications of stress fractures may include nonunion, malunion, posttraumatic arthrosis, and persistent disabling pain.[39]

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.[40] Postoperative recovery time averages 6 months.[41]

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.

The goals of pharmacotherapy are to reduce patient discomfort, minimize associated morbidity, and to prevent complications. Medications used in the management of stress fractures include the nonsteroidal anti-inflammatory drugs (NSAIDs) celecoxib, ibuprofen, and naproxen and the analgesic acetaminophen.

A study by Yoo et al suggested that in elderly patients with sacral insufficiency fractures and preexisting comorbidities, treatment with teriparatide may shorten healing time and lead to faster functional improvement and better pain reduction.[42]

Class Summary

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.

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.

Ibuprofen (Motrin, Excedrin IB, Advil, Ibuprin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

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.

Class Summary

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.

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.

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.

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.

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.

A relationship between a diminished vitamin D status and increased risk of stress fracture has been established.[17, 18, 43] A serum 25 hydroxy-vitamin D level below 75.8 nmol/L was determined to be a significant risk factor.[43, 44, 45, 46] Supplementation with 2,000 mg of calcium and 800 IU of vitamin D resulted in an approximately 20% lower incidence of stress fractures.[44]

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

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 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 patient education resources, see the Breaks, Fractures, and Dislocations Center and Sports Injury Center, as well as Repetitive Motion Injuries.