Stress Fractures


Stress fractures are relatively common overuse injuries occurring in individuals participating in a variety of physical activities. They have been reported to account for up to 20% of all injuries seen in sports medicine clinics. As an overuse injury, stress fractures occur by the accumulation of repetitive forces, which are lower than the force required to cause a fracture with a single load. Compression, tension, bending, torsion, or shear forces applied to the bone result in a deformation of the bone. When the force exceeds the bone’s elastic range, damage (e.g., microfracture) occurs. Repeated stress of bone causes a disruption in the equilibrium between osteoclastic and osteoblastic activity. This results in an increased risk of microfractures to the bone as the repetitive mechanical loads result in a shift toward osteoclastic activity and thus overall bone resorption. Over time, osteoblasts are unable to keep up with bone remodeling demands and microfractures accumulate, which can lead to a disruption in the integrity of the bone and ultimately a fracture in the cortical bone.

There are two types of stress fractures: fatigue and insufficiency fractures. An insufficiency fracture occurs when the bone quality is not able to withstand normal forces that are placed upon it. In these cases, compromised bone structure allows injury at otherwise normal physiologic strain levels. This can occur when a bone is weakened most commonly from osteoporosis, but it can also be attributed to various medications or other abnormal metabolic processes such as rheumatoid arthritis, fibromuscular dysplasia, Paget disease, osteogenesis imperfecta, osteomalacia, hyperparathyroidism, metastatic disease, or areas that have received radiotherapy. In contrast, a fatigue fracture occurs as a result of repetitive forces on normal bone. In this situation, the subsequent frequency and/or intensity of the strain exceeds the bone’s ability to adequately repair itself. When the bone fails to sufficiently keep up with the remodeling process required because of the excessive strain, microscopic fractures occur. If the frequency and/or intensity of loading of the bone is not diminished, the microfractures propagate and can result in a stress injury.

It is often a combination of several risk factors that lead to the development of a stress fracture. Risk factors are often described as either intrinsic or extrinsic ( Table 23.1 ). Muscle fatigue has been described as a possible risk factor for developing stress fractures. During activity, muscles absorb, counteract, and redirect forces experienced by the bone. When the bone experiences a bending force, one side is subjected to a compressive force and the opposite side is subjected to a tensile force. An eccentric contraction of muscle on the tensile side serves to decrease the tensile force applied to the bone. As muscle becomes fatigue, this protective mechanism is weakened and as a result the bone is subjected to higher repetitive forces leading to bone fatigue. Muscle fatigue can result in the muscle’s inability to decrease shear force seen in some individuals with poor gait mechanics. That section of bone is now subjected to higher levels of force resulting in increased microdamage. Leg length discrepancies, pes planus, and pes cavus have been shown to play a role in increasing the risk of developing stress fractures. Multiple studies have demonstrated that a decreased bone cross-sectional area increases the risk of developing stress fractures. , The importance of calcium and vitamin D in the role of bone health has been extensively described in the literature. Studies regarding the role of calcium and vitamin D in the prevention of stress fractures have shown mixed results.

Table 23.1

Risk Factors for Stress Fractures.

Intrinsic Extrinsic
Decreased bone density Muscle fatigue
Female gender Poor footwear
Anatomic variants Training surface
Medical conditions affecting metabolic/nutrition status Impact sport/activity
Disruption of menstrual cycle Low vitamin D levels
Bone cross-sectional area Poor calcium intake
Previous history of stress fracture Excessive or rapid change in activity level
Poor biomechanics

Females demonstrate an increased propensity of developing stress fractures compared with males. Studies attribute this to hormonal, nutritional, biomechanical, and anatomic differences. , Females manifesting one or all of the components of the female athlete triad (or relative energy deficiency in sports) are at particularly high risk for developing stress fractures. The female athlete triad consists of low energy availability with or without concomitant eating disorder, menstrual disturbances, and altered bone mineral density. The combination of decreased calorie intake and increased calorie expenditure from activity results in a low-energy or negative-energy state. This can result in estrogen deficiency and deficiency in other hormones that play a role in overall bone health. Estrogen has the effect of protecting bone from resorption, and estrogen receptors have even been found on osteoblastlike cells. When coupled with increased bone resorption from repetitive stresses, fracture risk further increases. Females experiencing oligomenorrhea or amenorrhea appear to have an increased risk of developing a stress fracture. Prepubescent females participating in high-intensity physical activity have been shown to be at increased risk of primary or secondary amenorrhea, stress, fractures, and nonhealing fractures.


Diagnosis of stress fractures includes a thorough history including risk factor assessment, comprehensive physical examination, and imaging studies. Important factors in the patient’s health history include exercise regimen (e.g., change in type, intensity, and duration), dietary intake, history of prior stress fractures, past medical history, and menstrual cycle. Patients typically report an insidious onset of pain without an inciting event or trauma. They often describe symptoms with activity that are relieved with rest. Physical examination should involve the affected limb or body part, contralateral limb if applicable, as well as the joint above and below the involved body part. Palpation may reveal bony tenderness; however, owing to the depth of the overlying soft tissue, bony palpation may be difficult at certain anatomic locations. Tuning fork test, therapeutic ultrasound, percussion test, fulcrum test, and functional tests (e.g., hop test) may be performed to assist in the diagnosis. , , ,

The clinical scenario, along with a thorough history and physical examination, should provide information to formulate and narrow the working differential. Additionally, appropriate diagnostic tests, when determined to be clinically necessary, assist in finalizing the diagnosis. The broad differential diagnoses to be considered when evaluating patients with a suspected stress fracture may include the following: bone contusion, surrounding soft tissue pathology (bursitis, tendinitis, muscle strain, ligament strain), infection, neoplasm, compartment syndrome, avascular necrosis (AVN), insufficiency fracture, contusion, nerve entrapment, vascular entrapment, arthritis, and sickle cell disease.

Imaging Studies

Imaging studies are readily used in the diagnosis of stress fractures. Plain radiography is typically the first study performed when evaluating for a suspected stress fracture. In the early stages of the disease process, radiographs will often appear negative, thus resulting in an initial high false-negative result rate. Radiographic findings are highly dependent on the timing between onset of symptoms and obtaining the imaging study, as well as if the patient continued with the contributing activity. In the early stages, radiographic findings vary depending on the type of bone and may include a lucency through the cortex without periosteal reaction or callus in long bones or a focal linear area of sclerosis perpendicular to the trabeculae in cancellous bone. A periosteal thickening occurs as bone heals and ultimately, if previously seen, the fracture line disappears. Obtaining serial radiographs over several weeks may not manifest characteristic evidence of fracture healing or new bony callus formation. Therefore when clinical suspicion remains despite negative radiographs, more advanced imaging techniques are required to confirm or rule out the diagnosis.

Nuclear medicine scintigraphy (bone scans) are highly sensitive and may aid in the early diagnosis of stress fractures. A diagnostic bone scan will demonstrate radiotracer uptake in an area of bony remodeling, trabecular microfracture, periosteal reaction, or callus formation. Nuclear scintigraphy is sensitive to early bony remodeling changes and can detect stress fractures or reactions within 72 h after the initial injury. Although bone scans are very sensitive for bone turnover and remodeling, they are not always specific for stress fractures. Any condition producing increased bone turnover, such as osteogenic tumors, infection, trauma, or inflammation, will result in increased radiotracer uptake. Conversely, a negative bone scan allows for the exclusion of a stress fracture. A bone scan involves radiation exposure approximately 44 times that of a standard chest radiography, which should be considered when choosing an imaging study.

Magnetic resonance imaging (MRI) can detect early bone marrow changes and bone remodeling related to stress reaction and fractures. MRI also offers more intricate detail of surrounding soft tissue, which could potentially be the source of the patient’s pain. Use of water-sensitive pulse sequence (e.g., fat suppression) allows for the detection of endosteal bone marrow edema, which is one of the earliest changes seen in stress fractures. When compared to nuclear scintigraphy, MRI allows for a more precise location of fractures, allows for a comprehensive evaluation of the surrounding structures including soft tissue, and does not have radiation exposure. Given that MRI is sensitive for bone marrow edema, MRI findings must be correlated with the patient’s clinical presentation, as bone marrow edema may be detected on asymptomatic patients/athletes and it may persist after diagnosis and treatment of stress fractures, even as cortical healing continues.

Computed tomographic (CT) imaging is not as commonly used to diagnose stress fractures and is used primarily when the patient is unable to undergo an MRI or to further delineate a fracture line. CT does not have the ability to show bone marrow edema and lacks the precision to determine the acute or chronic nature of the lesion. Diagnostic musculoskeletal ultrasound is another emerging diagnostic tool in the evaluation of stress fractures. Cortical buckling and hypoechogenic callous formation have been seen in superficial bones such as the distal tibia and metatarsals. The usefulness of ultrasound remains limited and has not been recommended as a stand-alone diagnostic tool.


Education and prevention are the cornerstones for management and prevention of stress fractures. Proper identification and education of patients at risk of developing stress fractures can assist in the prompt diagnosis of stress fractures once they occur, thus typically resulting in improved outcomes as well as avoidance of complications and recurrence.

Fortunately, nonoperative management often yields excellent outcomes. , Initially, the goal of treatment should be aimed at pain control, which can typically be achieved through medication, cryotherapy, elevation, and most importantly rest from the aggravating activity. In addition to activity modification, rest involves off-loading the involved bone/extremity. Medications often include acetaminophen, nonsteroidal antiinflammatory drugs (NSAIDs), and rarely narcotics. There is some controversy regarding the risk of delayed healing or developing a nonunion with the use of NSAIDs ; therefore the treating physician should take into account the current evidence when considering the use of NSAIDs. Additionally, use of medication may decrease the patient’s symptoms, thus prompting the patient to increase the use of the involved body part prior to sufficient healing.

Stress fractures typically heal over a period of 4–8 weeks, depending on the severity, the location, and the age of the patient; however, in some cases, healing may take up to 12 weeks. , Some stress fractures require strict non-weight-bearing (NWB) status or immobilization with a cast, splint, or controlled ankle motion (CAM) boot, whereas others may require only restriction of activity. Although typically not indicated, except in the case of nonunions, low-intensity pulsed ultrasound could be considered as a tool to increase bone healing; however, the literature has been mixed with its use in treating stress fractures. , Planned follow-up including repeat clinical examinations and, when deemed necessary by the treating physician, repeat imaging studies may be important to ensure appropriate healing of the stress fracture.

Patients may benefit from a structured multidisciplinary program guided and overseen by their treating physician as the stress fracture heals and activity is reinitiated. This medical team typically includes the treating physician, a physical therapist, and/or a certified athletic trainer. During the initiation of increased activity, careful attention should be paid to the patient’s symptoms as they progress to higher levels of activity. In the setting of pain, the patient should not be allowed to progress to the next phase, as the presence of pain indicates that additional time is required for adequate healing. Provided the athlete is pain free, conditioning exercises that do not stress the involved bone are permitted. During the rehabilitation stage, biomechanical errors or other predisposing factors leading to the development of the stress fracture should be identified and corrected in order to effectively manage and prevent the recurrence of stress fractures. Some physicians prescribe over-the-counter or custom orthotics to improve biomechanics and provide shock absorption, which may play a role in the prevention of stress fractures. A review of the individual’s prior training regimen, along with functional testing and a gait analysis, may guide the rehabilitation and return-to-play program. Once the stress fracture is healed and the functional deficits are addressed, an emphasis should be placed on gradual return to full activity. Female athletes diagnosed with one or more stress fractures should be screened for the female athlete triad. The screening should be part of the history taking and should include a menstrual history, dietary assessment, and, when appropriate, consideration of obtaining bone density testing. , Treatment of the female athlete triad requires a multidisciplinary approach.

Although most stress fractures can be treated nonoperatively, surgical intervention may be required in the setting of high-risk stress fractures or stress fractures that have failed conservative management. High-risk stress fractures are more likely to progress to complete fracture, result in delayed union or nonunion, and/or are on the tensile side of the natural biomechanical axis ( Table 23.2 ). , ,

Table 23.2

High-Risk Stress Fractures.

Tension-side femoral neck
Anterior tibia
Medial malleolus
Tarsal navicular
Jones fracture (proximal fifth metatarsal)
Talar neck
Base of the second metatarsal
Great toe sesamoid

Specific Stress Fractures

Femoral Stress Fractures

Stress fractures of the femur are the fourth most common type of stress fracture. Military recruits, dancers, distance runners, jumpers, female athletes, and older athletes are at higher risk of developing a femoral stress fracture. , Determining the true incidence of femoral stress fractures is difficult, and these fractures are thought to be underdiagnosed. It is estimated that up to 75% of femoral stress fractures are missed or misdiagnosed on initial evaluation. Patients often present with vague, nonspecific complaints. A high index of suspicion combined with a thorough history, comprehensive physical examination, and obtaining the appropriate imaging studies can confirm the diagnosis. Arriving at a prompt diagnosis may result in improved patient outcomes with a decreased risk of complications.

Femoral stress fractures are often classified based on their anatomic location. Although they can occur at any location along the femur, they are most commonly seen at the femoral neck. Stress fractures involving the femoral neck are of particular importance, given the risk of serious complication including fracture displacement. With regard to the femur, the mechanical axis falls medial to the majority of the femur, thus the compression side is the medial aspect of the femoral neck and the lateral side is considered the tensile side. Compression-sided femoral neck stress fractures ( Fig. 23.1 ) are typically treated nonoperatively with a period of rest, which initially includes a limited weight-bearing status followed by a gradual progression of activity. If the patient fails conservative measures, he/she may require referral for surgical consultation. Although there have been some studies demonstrating successful conservative management of tension-sided femoral neck stress fractures with extensive periods of protected weight-bearing, early surgical intervention continues to be favored due to the risk of displacement. A displaced femoral neck stress fracture is at risk of progression to nonunion or osteonecrosis of the femoral head and is therefore considered a surgical emergency.

Fig. 23.1

Femoral compression-side stress injury.

Magnetic resonance T2 coronal image showing edema along the medial aspect of the right femoral neck compression-side stress reaction without discrete fracture line.

Stress fractures of the subtrochanteric region and shaft are less common and occur most often along the medial or posteromedial cortex. When diagnosed early, they can be managed nonoperatively. In cases of displacement or continued pain despite conservative measures, operative fixation is indicated. The long-term use of bisphosphonates has been identified as a risk factor for developing an atypical subtrochanteric femur fractures. The risk and benefits of these medications in the treatment of osteoporosis should be weighed before initiating treatment. Stress fractures of the femoral shaft ( Fig. 23.2 ) have been described more frequently in military recruits and athletes and often involve the posteromedial aspect of the proximal third of the femur. Distal femur stress fractures are even more rare; however, this should remain in the physician’s differential diagnoses when the patient presents with a concerning history and physical examination finding.

Fig. 23.2

Femoral shaft.

Magnetic resonance T2 coronal image showing edema midshaft consistent with stress injury.

The patient’s history often involves an insidious onset of gradually worsening leg, thigh, or hip pain that may worsen with activity. Athletes with femoral neck stress fractures may report symptoms as early as 2 weeks after increasing exercise intensity and typically report pain in the groin. Patients with femoral shaft stress fractures often report activity-related pain in the thigh or ipsilateral knee but typically lack tenderness or swelling. Pain may limit athletes from participation in athletic activities and sometimes may be associated with night pain.

The general location of the pain may guide physical examination, although the clinical presentation can be variable. Typically, muscle tone and bulk are normal. Due to the overlying soft tissue, the point of maximal tenderness may be difficult to elicit with proximal femur and femoral shaft stress fractures, although some distal femoral stress fractures may demonstrate tenderness to palpation. Pain at the end range of passive hip motion or straight leg raise as well as a positive log roll test result may be present in patients with femoral neck stress fractures. A positive hop test result has been strongly associated with femoral stress fracture. The fulcrum test has proven to be beneficial in the diagnosis of femoral shaft stress fractures. Both the hop and fulcrum tests should be performed with caution so as to not complete a fracture.

When a femoral stress fracture is clinically suspected based on history and physical examination, imaging begins with plain radiography. In the early stages of the disease process, radiographs are often negative, and in fact, radiographic evidence of femoral stress fracture is present in only 10% of cases within the first week. New periosteal bone formation may be noted approximately 10 days after the injury begins, with peak formation at 6 weeks. , When suspicion of a femoral stress fracture remains despite negative serial radiographs, additional imaging becomes necessary. MRI is often the test of choice, although CT or nuclear scintigraphy may be considered. MRI provides a more precise location of the fracture and allows evaluation of the surrounding tissue pathology. It should be noted that MRI may show persistent bone marrow edema at the site of the femoral stress fracture for up to 6 months after injury.

In summary, the mainstays of conservative care consist of rest and activity modification. Displaced or high-risk fractures typically require surgical intervention. Depending on the location and severity of the femoral stress fracture, the degree of rest and unloading varies from weight-bearing as tolerated to strict NWB. , The healing process primarily occurs over a period of 6–8 weeks but may take up to 12 weeks. ,

Tibial Stress Fractures

Stress fractures occur most commonly at the tibia, accounting for 25.9%–49.1% of all stress fractures. Developing as a result of recurrent high load-bearing activities, tibial stress fractures have an incidence as high as 10%–20% in distance runners. Stress fractures of the tibia are typically transverse. Longitudinal fractures, although more rare, are at an increased risk of delayed union or nonunion. , The majority of tibial stress fractures ( Fig. 23.3 ) occur at the diaphysis and are often broken up into two groups based on location and risk classification. , The majority of tibial stress fractures occur posteromedially and are considered low risk, while stress fractures located anteriorly are classified as high risk. With regard to the tibia, the tension side is anterior and the compression side is posterior. Runners are at an increased risk of developing posterior tibial stress fractures, while the anterior tibial stress fractures are seen more frequently in athletes who participate in jumping/landing activities. Smaller tibial cross-sectional dimensions have been associated with an increased risk of developing a tibial stress fracture. Although treatment for both begins with a trial of nonoperative management, the clinical course and outcomes for anterior and posterior tibial stress fractures vary significantly. Posterior tibial stress fractures demonstrate significantly shorter return-to-sport times compared with anterior tibial stress fractures, which may ultimately require surgical intervention and can be career threatening. ,

Fig. 23.3

Right tibial stress fracture.

Magnetic resonance coronal short tau inversion recovery image showing diffuse endosteal and periosteal marrow edema in the lower tibia extends proximally to mid-one-third diaphysis. Posterior tibial cortex is discretely disrupted with elevated cortical ridges suggesting cortical fracture. Mild intermuscular edema noted between tibialis anterior and tibialis posterior.

Patients typically present with an insidious onset of pain, which initially occurs only during the inciting activity, but may progress to daily weight-bearing activity. Pertinent physical examination findings include focal tenderness over the involved bony area. Swelling may be noted and percussion away from the fracture site may elicit pain. Special tests including the hop test and fulcrum test may be performed, but they should be conducted with caution. A lower limb alignment assessment should be performed to evaluate for possible contributing factors, including mechanical overload.

Early recognition of tibial stress fractures is important to minimize the patient’s recovery time as well as avoid potentially devastating complications. When there is clinical suspicion for a tibial stress fracture, radiographs should be ordered. Although early in the process they demonstrate a low sensitivity of 10%, they may confirm the diagnosis. , Although often of limited utility, radiographs may demonstrate the “dreaded black line” indicating the presence of a high-risk anterior cortex tibial stress fracture. It may take 3 weeks for periosteal reaction and cortical irregularities to be visualized under radiography, and thus additional imaging is recommended when clinical suspicion remains high despite negative radiographs. , MRI is considered the imaging modality of choice given its high sensitivity (86%–100%) and specificity (100%). , MRI also has the benefit of evaluating the surrounding soft tissue, which can assist in confirming other diagnoses such as medial tibial stress syndrome if no stress fracture is identified. Bone scans are also capable of identifying tibial stress fractures early; however, they lack the specificity of MRI. CT scans may be useful, but are not as sensitive as MRI.

Conservative management (e.g., rest, pneumatic bracing) of posterior tibial stress fractures demonstrates excellent outcomes with return rates of 100%. Multiple studies have shown evidence of significant clinical benefit including earlier return to participation with the use of low-intensity pulsed ultrasound. , These fractures typically heal in 4–8 weeks. Aerobic fitness, especially low- or no-impact activities (e.g., cycling or swimming), should be encouraged during the treatment.

Management of low-grade anterior cortex tibial stress fractures typically resolve without surgery with a period of relative rest, immobilization, and modified weight-bearing. However, higher grade stress fractures may require early surgical intervention. Treatment recommendations should be based on the fracture site, grade, and level of sport participation. Return to activity is only considered when complete healing of the fracture has been confirmed to avoid progression to a complete fracture. , Anterior tibial cortex stress fractures are associated with lower rates of return to activity. Of those who are able to return to full participation, the mean time of return to activity varies in the literature from 5 to 7 months. , Once the patient no longer demonstrates tenderness to palpation, experiences no pain with normal ambulation, has normalized joint range of motion, and has addressed strength deficits, the patient may initiate a guided return to running program. The sports medicine physician should monitor for any recurrence of pain as the athlete gradually increases to preinjury activity levels.

Foot and Ankle Stress Fractures

Stress fractures in the foot and ankle can be categorized as either low-risk or high-risk stress fractures ( Table 23.3 ). High-risk fractures are typically located on the tension side of the bone, develop in locations with limited vascularity, have a tendency to have delayed union or nonunion, and may require surgical intervention.

Aug 21, 2021 | Posted by in SPORT MEDICINE | Comments Off on Stress Fractures

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