Stress Reaction and Fractures

Etiology

Mechanism of Stress Fractures

Stress fractures are partial or complete bone fractures resulting from submaximal loading. This injury is often compared analogously to fatigue fractures found in engineering materials, eg, bridges and buildings, although some would argue that the mechanisms are different. Normally, submaximal forces do not result in the fracture; however, with repetitive loading and inadequate time for healing and recovery, stress fractures can potentially occur. The debate continues whether the cause is contractile muscle forces acting on a bone or increased fatigue of supporting structures; both likely contribute.[5][6]

Stress fractures are categorized as high-risk or low-risk based on the likelihood of progression to displacement or nonunion, which may necessitate surgical intervention. High-risk fractures occur in areas like the femoral neck, talar neck, tarsal navicular, and anterior tibial cortex, while low-risk injuries include fractures of the fibula, posteromedial tibial shaft, and second through fourth metatarsal shafts.[7]

Types of Activities Associated with Stress Fractures

Specific sports and activities are associated with distinct types of stress fractures. Runners often experience tibial and metatarsal fractures, with female runners also prone to pelvic fractures. Hurdlers have an increased risk of patella fractures, while gymnasts, female soccer players, and weightlifters are at risk for spondylolysis—a stress fracture caused by repeated spinal hyperextension.[8] March fractures, or metatarsal stress fractures, occur predominantly in the second and third metatarsals due to repetitive weight-bearing stress. The second metatarsal is particularly susceptible due to its limited mobility and structural constraints.

Stress reactions and fractures result from repetitive microtrauma rather than acute injuries.[9] Stress fractures are common among runners and military recruits, often associated with changes in training intensity, footwear, or surfaces. Rapid changes in training programs, including increased distance, pace, volume, or cross-training without adequate time for adaptation, can contribute. Failure to follow intense training days with easy ones for recovery can also contribute to injury.[10] Therefore, prevention strategies focus on gradual activity increases, proper footwear, and sufficient recovery time.

Additionally, weekly distances exceeding 32 km (20 miles) significantly increase stress fracture risk for runners. These injuries typically arise during basic training or increased running and marching among military recruits. Female athletes and those with a prior history of stress fractures are at higher risk, especially when subjected to the same training regimens as male counterparts.[11][12] The higher incidence in females may reflect hormonal influences, lower bone density, or anatomical differences.[13]

Biomechanical and Nutritional Factors of Stress Fractures

Biomechanical factors also influence stress fracture risk. Narrow tibial width and increased external rotation were identified as risk factors among military recruits, while female runners with stress fractures exhibited smaller calf girths and less lean muscle mass in the lower limb. Contrary to earlier beliefs, ground reaction forces have limited evidence as a contributing factor; however, the vertical loading rate during heel strikes correlates positively with stress fracture risk.[14] Diagnostic imaging has revealed that athletes with stress fractures often have smaller tibial cross-sectional areas, suggesting a role for bone geometry in injury development.

Another factor influencing stress fracture development is overtraining, or a more current name would be relative energy deficiency syndrome. This is commonly seen as part of the female athlete triad. The athlete's training volume is too high, and calorie intake is too restricted, impairing recovery. This leads to disordered menstruation and hormonal imbalances, with estrogen levels falling, leading to osteoporosis with a stress fracture as a result. A phenomenon in male endurance athletes with similar high training volumes and restricted calorie intake has been noted. This will result in lower testosterone levels, resulting in osteoporosis and stress fracture development.[15]

Vitamin D is another potential factor influencing the development of stress fractures. In a prospective trial of Finnish military recruits, those who sustained a stress fracture had a lower average vitamin D concentration than those who did not. A randomized trial of female military recruits showed vitamin D supplementation might have prevented a significant percentage of trainees from developing a stress fracture.[15]

Risk Factors for Stress Reaction and Fractures

The most common risk factor is a sudden increase in activity levels, with longitudinal studies showing that higher pretraining activity levels may confer some protection. Other risk factors for stress fractures include the following intrinsic and extrinsic elements:

• Intrinsic factors:
  • Poor physical conditioning
  • Female sex
  • Hormonal imbalances
  • Menstrual disorders
  • Low bone density
  • Reduced muscle mass
  • Anatomical variations, such as genu valgum or a short leg [13][10][2]
• Extrinsic factors:
  • High-impact activities (eg, running, jumping)
  • Abrupt increases in physical activity levels
  • Inadequate footwear
  • Irregular or angled training surfaces
  • Nutritional deficiencies, particularly low vitamin D and calcium
  • Smoking
  • Poorly conditioned muscles [13][10][2]

Epidemiology

Stress injuries account for up to 20% of all sports medicine clinic visits and are particularly common among athletes and military recruits.[16][17] In high school sports, 0.8% of all injuries are stress fractures, with an incidence rate of 1.54 per 100,000 athlete exposures, the highest among cross-country runners.[18] The lower leg (40.3%) and foot (34.9%) represent the majority of stress injuries in this group. Elite soccer players experience a lower incidence of 0.04 injuries per 1,000 hours, with 78% affecting the fifth metatarsal.[19] Among United States Army recruits, the rate of stress fractures is significantly higher, with 19.3 cases per 1,000 male recruits and 79.9 cases per 1,000 female recruits, reflecting the higher overall incidence of stress fractures in females compared to males under similar training conditions.

Stress fractures are predominantly seen in weight-bearing limbs, with the tibia, metatarsals, and fibula being the most frequently affected sites. Medial tibial stress syndrome, or shin splints, is the earliest manifestation of stress injuries and represents a spectrum of medial tibial pain that may progress to a fracture if not addressed. The specific location of stress fractures often varies by sport. For example, navicular, tibia, and metatarsal fractures are common in track athletes, while tibia and fibula fractures are prevalent among distance runners. Dancers predominantly suffer from metatarsal fractures, and military recruits often experience fractures in the calcaneus and metatarsals. The ulna is the most frequently affected upper extremity bone.

Stress fractures account for nearly 16% of all injuries in runners, with those averaging more than 25 miles per week at significantly higher risk. The most common stress fractures, in decreasing order of occurrence, include the tibia (23.6%), tarsal navicular (17.6%), metatarsals (16.2%), femur (6.6%), and pelvis (1.6%).[20] Among military members, repetitive training activities led to a stress fracture rate of 5.69 per 1,000 person-years between 2009 and 2012. Metatarsal stress fractures are prevalent, representing 25% of all stress fractures and 20% of sports medicine visits, with the second metatarsal being the most frequently affected due to its limited motion and structural characteristics.

Stress fractures are notably recurrent, with 60% of individuals experiencing a second fracture after a previous one.[21] Women are disproportionately affected, not only in incidence rates but also in march fractures, which are more common in females than males. Overall, 40% of athletes will sustain a stress fracture at some point in their careers, emphasizing the importance of prevention, early diagnosis, and appropriate management to mitigate risks and recurrence.[22]

Pathophysiology

Understanding the intricate balance of bone remodeling, mechanical stress, and extrinsic factors is essential in preventing and managing stress injuries. These insights into the pathophysiology of stress reaction and fractures guide tailored interventions to mitigate risk, promote recovery, and ensure long-term bone health.

Bone Remodeling Pathophysiologic Mechanisms

Stress injuries occur when a mismatch between the bone's innate strength and the mechanical load it endures is present, leading to a gradual weakening of the bone structure. This mismatch can result from 2 primary mechanisms: fatigue fractures, where abnormal stress is applied to healthy bone, and insufficiency fractures, where normal stress is exerted on a compromised bone, specifically at muscle insertion points where repetitive load and stress are highest.[9] Insufficiency fractures may sometimes be referred to as pathological fractures, though this term traditionally describes fractures arising from focal bony abnormalities.

In normal, healthy bone, osteoblastic activity repairs microdamage caused by regular physical activity. However, when the recovery period is insufficient, osteoclastic resorption outpaces osteoblastic bone formation, weakening bone structure. Over time, repetitive mechanical loading leads to stress reactions, which can progress to complete stress fractures if training or activity is not adjusted. Advanced imaging studies often reveal microfractures in trabecular bone caused by this repetitive stress. Wolff's law highlights the bone's ability to adapt and strengthen under mechanical forces, but excessive cyclic loading can disrupt the signaling processes of osteocytes—the cells that regulate osteoblast and osteoclast activity.[17]

When osteocyte signaling is compromised, bone repair mechanisms falter, allowing osteoclastic activity to dominate. This imbalance leads to stress fractures, with the normal bone remodeling cycle of 3 to 4 months becoming insufficient under chronic excessive stress.[23] Stress fractures tend to occur either from bone fatigue—when healthy bone cannot withstand excessive mechanical demand—or bone insufficiency, where underlying abnormalities weaken the bone's structure.[9][24]

Biomechanic Pathophysiologic Mechanisms

Biomechanical factors also influence stress fracture development. Compression stress fractures, typically less common, occur on the concave side of the bone and run parallel to its axis, while tensile stress fractures develop on the convex side and are perpendicular to the bone axis.[25] Foot biomechanics, with longer or more plantarflexed metatarsals bearing a disproportionate load, can significantly impact fracture risk. Certain foot types, such as cavovarus, increase stress on the lateral column and predispose individuals to fractures of the fourth and fifth metatarsals.[26][27] External factors, including training type, intensity, environmental conditions, footwear, and even shoe age, further contribute to stress fracture risk.

Histopathology

Objective information on stress fracture healing is negligible as biopsies are rarely taken as part of routine treatment.[28] However, histology studies of stress fractures demonstrate that repetitive stress response leads to increased osteoclastic activity, surpassing the rate of osteoblastic activity and new bone formation. Subsequently, the bone weakens. 

Furthermore, research is limited to animal studies and often focuses on forearm stress fractures. Animal studies have found that at the cellular level, stress fractures are characterized by irregular bone changes. At 2 weeks, this irregular woven bone develops islands of cartilage and active resorption cavities along the periosteal margin. At 4 weeks, the woven bone is remodeled, starting from the periosteal surface and progressing along the fracture plane and into the medullary cavity.[29] A hallmark sign of healing is the formation of periosteal hard callous.[28] Slow healing rates and recurrent stress fractures may be explained by the failure or slow healing of the most central portions of a stress fracture.[29]

History and Physical

Clinical History

A thorough clinical history is pivotal in diagnosing stress reactions and fractures. A high index of suspicion, coupled with careful consideration of training history, biomechanics, and risk factors, is essential for accurate diagnosis and management of stress injuries. Key historical elements include recent increases in activity intensity, duration, or frequency over the last 6 to 8 weeks, changes in terrain or footwear as these may elucidate changes in force distributions through the foot, and the onset of pain that improves transiently with rest but worsens with activity.[30] Pain is often described as dull and aching, exacerbated by weight-bearing activities.[31]

A detailed medical history should assess intrinsic risk factors, eg, age, body composition, bone mineral density, endocrine disorders, and previous stress fractures.[22] Advanced age, low body mass index (particularly in women), and conditions like the female athlete triad—characterized by amenorrhea, osteoporosis, and disordered eating—are significant risk factors.[22] Medications (eg, glucocorticoids and bisphosphonates) can also increase fracture risk.[32] Extrinsic factors include dietary habits, medication regimens, and biomechanical influences, including foot structure or gait abnormalities.

Patients with stress reactions and fractures typically report an insidious onset of pain without any specific traumatic event. Their history often includes significant volumes of a specific exercise (eg, running) or recent training intensity, volume, or surface changes. Initially, pain occurs only during training but can progress to discomfort during daily activities. Symptoms tend to improve with rest and cessation of activity, but if training continues, the pain may worsen and persist, even upon waking.

Physical Examination

On physical examination, focal tenderness over the affected area is common, often accompanied by soft tissue swelling. Differentiating between muscle injury, early stress reactions, and stress fractures is critical. Soft tissue tenderness usually indicates muscle strain or early stress reactions, while bony tenderness strongly suggests a stress fracture. Certain anatomical sites, like the pelvis and sacrum, can present diagnostic challenges due to subtle symptoms, requiring a high degree of clinical suspicion based on the patient's history.

Several clinical tests aid in diagnosis. The "one-leg hop test" helps distinguish medial tibial stress syndrome from tibial stress fractures; patients with stress fractures are unable to hop without pain, particularly upon landing. For femoral shaft stress fractures, the "fulcrum test" involves using the examiner's arm as a fulcrum under the thigh while applying pressure to the knee, with pain or apprehension indicating a positive result.[21] Lumbar extension or single-leg hyperextension (Stork test), in which the patient flexes 1 leg and extends the lower back, is commonly used to assess for spondylolysis. However, these tests have limited sensitivity and specificity.[33][8][33] Spondylolysis, often asymptomatic, may be found incidentally on imaging, while spondylolisthesis involves anterior migration of the vertebral body due to an unhealed pars defect.

Furthermore, physical examination should include a biomechanical evaluation, with special attention to foot type and weight distribution. A more supinated foot, for example, increases the risk of second metatarsal stress fractures due to greater forefoot loading. Palpation can help localize the pain, and joint motion near the fracture site may exacerbate symptoms. Patients may exhibit a limping gait with weight-bearing, and joint involvement can further aggravate discomfort.[34]

Diagnostic tools and techniques have limitations. For instance, reproducing pain with a tuning fork or low-pulsed ultrasound has moderate sensitivity and specificity.[35] Imaging is often required for confirmation, particularly when clinical findings are inconclusive.

Evaluation

Plain Radiographs

The diagnostic evaluation of suspected stress injuries begins with radiographic imaging of the affected area. Plain radiographs, while readily available, cost-effective, and low in radiation exposure, often yield normal results in the initial stages of a stress injury, limiting their sensitivity.[11] Early radiographic findings, if present, may include subtle changes such as periosteal elevation, cortical thickening, sclerosis, or a fracture line. A distinctive "dreaded black line" may be seen in high-risk stress fractures such as those of the tibia or femur. However, these findings typically take 2 to 3 weeks to manifest on x-rays, necessitating additional imaging modalities when suspicion remains high despite normal radiographs.[36][37] Plain films in spondylolysis are challenging. To best visualize the par, 5 views are needed.[33] However, they can miss early changes; therefore, additional modalities should be considered if the plain films are negative and the diagnosis is suspected.

Computed Tomography and Magnetic Resonance Imaging

Computed tomography (CT) can offer detailed imaging of stress injuries, showing sclerosis, new bone formation, periosteal reactions, or fracture lines. CT scans are beneficial for evaluating occult fractures and distinguishing between healing bone and fibrous unions, but they involve higher radiation exposure and lower sensitivity compared to magnetic resonance imaging (MRI). Bone scintigraphy, which uses radioactive tracers to identify areas of high bone turnover, is moderately sensitive and can detect stress injuries within days of symptom onset. However, its low specificity means it may identify other conditions, eg, cancer or osteomyelitis, which may increase bone turnover.

MRI is the most sensitive and specific imaging modality for stress injuries, with sensitivity ranging from 80% to 100% and specificity at 100%.[38] MRI findings may include periosteal and bone marrow edema, fracture lines extending into the medullary canal, and surrounding soft tissue involvement (see Image. Stress Fracture on MRI). MRI is especially advantageous as it can also evaluate concurrent muscle, ligament, and cartilage injuries while avoiding radiation exposure. This modality is increasingly considered the gold standard for diagnosing stress injuries.[39][40]

Special attention should be given to metatarsal stress fractures, commonly referred to as "march fractures." Early on, plain radiographs may be falsely negative, with subtle periosteal reactions or cortical blurring being the only indicators. The "gray cortex" sign—a poorly defined cortical lucency—suggests an early stress fracture.[41] As the fracture matures, findings such as callus formation or cortical lucency of an incomplete, nondisplaced fracture may become evident.[42] When plain radiographs fail to identify fractures, advanced imaging such as MRI or CT is essential for definitive diagnosis.

Additional Imaging Studies

Other imaging techniques, such as single-photon emission computed tomography (SPECT) and 3-phase bone scans with technetium-99, are also used to detect early stress reactions not visible on plain radiographs (see Image. Bone Scan).[2] Bone scintigraphy is moderately sensitive at 74%. These scans are highly sensitive but less specific, often showing increased uptake in areas of high bone turnover. Conditions like avascular necrosis, infections, or malignancies can also produce similar findings, limiting their diagnostic utility in certain cases. These modalities are not typically used for follow-up imaging due to their lower specificity.

Laboratory Studies

Laboratory studies generally do not play a significant role in diagnosing stress fractures unless the injuries are recurrent or frequent. Vitamin D deficiency has been associated with an increased risk of stress fractures, with serum levels below 20 ng/mL linked to higher incidence rates.[39] Further evaluations may be warranted for patients with recurrent fractures, including tests for thyroid-stimulating hormone, parathyroid hormone, and bone mineral density, to uncover underlying risk factors.[17] 

Classification Systems 

Stress fractures can be divided into 2 broad categories: high-risk and low-risk injuries. Metatarsal stress fractures are considered low-risk fractures because they are common and tend to heal well with activity modification while weight-bearing.[24] Furthermore, various classification systems are used to categorize imaging findings of stress fractures to help define the extent of the injury and estimate prognosis.

Radiographic grading system

The following 5-tiered grading system for stress fracture developed by Kaeding and Miller is associated with specific radiographic findings:

1. Asymptomatic radiographic findings
2. Pain with no fracture on imaging
3. Nondisplaced fracture on imaging
4. Displaced fracture on imaging
5. Sclerotic nonunion on imaging [43]

Magnetic resonance imaging grading system

Nattiv et al developed a classification for stress fractures in athletes, similar to the grading system suggested by Fredericson et al, involving the evaluation of bone marrow edema and periosteal reaction in bone stress injuries on MRI (see Image. T1 and T2 Images of Stress Fracture).[44] The following findings are associated with each grade:

• Grade 1: mild marrow edema or periosteal edema on fat-suppressed T2WI (but not on T1WI) 
• Grade 2: moderate marrow edema or periosteal edema on fat-suppressed T2WI (but not on T1WI) 
• Grade 3: severe marrow edema or periosteal edema on both fat-suppressed T2WI and T1WI, without a fracture line on T1WI or T2WI
• Grade 4: severe marrow edema or periosteal edema on both fat-suppressed T2WI and T1WI, with a fracture line on T1WI or T2WI (see Image. Grade 4 Stress Fracture) [20]

Treatment / Management

The treatment of stress injuries varies depending on whether the injury is a stress reaction or stress fracture, its location, and its suitability for rehabilitation. Clinicians should recognize which fractures are at risk for delayed union, nonunion, displacement, or intra-articular involvement. General management principles include relative rest or nonweight bearing for 2 to 6 weeks, followed by gradual reintroduction of activity. Recognizing the injury early is essential, as early intervention is associated with more rapid healing and recovery. 

Low-Risk Fracture Management

Stress injuries that are low-risk sites are typically managed conservatively with a 2-phase protocol. A low-risk stress fracture can be seen in the posterior tibia, 2nd to 4th metatarsals, femur, inferior and superior pubic rami, sacrum, and fibula. Phase 1 includes analgesia, modified weight bearing, and activity modification, including discontinuing the offending activities. If the patient cannot ambulate without pain, temporary immobilization is indicated. Examples of activity modification include water fitness, cycling, and elliptical to maintain strength and fitness.[21][9][39]

Phase 2 begins after a period of pain-free rest and involves a gradual return to activity over the subsequent weeks, including continued physical therapy. For example, a runner may initially start running at half pace and distance every other day. Over the ensuing weeks, patients can gradually increase their distance, frequency, and intensity with the goal of returning to their baseline.

The length of each phase can vary. A good rule of thumb is however long an injury takes to become pain-free, the same amount of additional time is needed to perform a graduated return to activity. When adding in the time required for rehabilitation training to achieve prior physical fitness levels, loss of training time can be as long as 19 weeks.

High-Risk Fracture Management

High-risk stress fractures are seen in areas with challenging blood supply, frequently occurring in areas of maximal tensile load, and are at high risk for nonunion.[20][45] They can be difficult to diagnose and require a high index of suspicion. High-risk stress fractures include the femoral neck, anterior tibia, tarsal navicular, talus, sesamoid bones, and 1st and 5th metatarsal bones. High-risk stress fractures and tension-sided stress fractures are the highest risk because of the tendency to displace secondary summative forces, causing distraction caused by an imbalance between gravity and muscular attachments. High-risk stress fractures may be managed conservatively or surgically depending on the occupation and sport of choice of the individual. However, these stress fractures generally do not respond to conservative management and often result in significant morbidity.[45] 

Femoral neck stress fractures can be an exception. Obtaining magnetic resonance imaging is recommended when a stress fracture is suspected since plain radiographs are unreliable in this particular injury. Femoral neck stress fractures can be thought of as 2 separate injuries. If the imaging shows tension (superior side) stress fractures, these should be referred for surgical consultation. If the imaging shows a compression (inferior side) stress fracture, and if a fracture line is present, it should be less than 50% of the width of the bone. These can be managed nonoperatively but need close follow-up. If the pain increases or the fracture increases in size, then a surgical consult should be obtained. If the fracture becomes displaced, it should be treated rapidly as there is a high risk of avascular necrosis to the femoral head.[46]

Athletes with overly pronated or supinated feet may benefit from orthotics. Inadequate shock absorption may also be ameliorated by changing or addressing footwear. Running shoes should be changed every 300 to 350 miles of use depending on the type of shoe, surface, and athlete.[47] Characteristics of a proper running shoe include heel width and support, firm midsole, and a straight last. Clinicians with expertise in running may be able to perform gait analyses and recommend form changes that will reduce their risk of reinjury.

Spondylolysis Management

Spondylolysis is a unique stress fracture. Few large clinical trials on treatment exist, so recovery and return to play can be challenging to manage.[8] Experts recommend treating this conservatively with activity modification, core strengthening, and bracing. Resting from activity can be from 2 weeks to as long as 6 months. The key is waiting for the athlete to become pain-free. Bracing can be helpful, but its use is controversial. The brace should limit lumbar extension and be worn 23 hours daily for up to 6 months.[33] Some limited studies using a rigid lumbosacral orthosis had >80% pain-free return to sport.[48] Finally, physical therapy rehabilitation focuses on core strength and spine stabilization, followed by a gradual return to play program with the athlete remaining pain-free. Those refractory cases can be considered for surgical management, and several techniques have been described.[33](A1)

Nutritional Supplementation

Patients may also benefit from calcium and vitamin D supplementation, though studies do not demonstrate a clear benefit or quicker healing. In one study of female United States Navy recruits, giving 2000 mg of calcium and 800 IU of vitamin D resulted in a 20% reduction in stress fractures during training.[49] Some difficulties are generalizing the findings to the population at large or females attending boot camps of the other military branches. However, another study by Tenforde et al found female athletes using a calcium supplement had a 3 times higher risk of stress fractures.[12] (A1)

Female runners with late menarche, fewer menses, and lower bone mineral density are at an increased risk of stress fracture. A bone mineral density test and endocrine workup should be considered if history reveals these risk factors. Routine vitamin D and calcium supplementation is not typically indicated unless dietary inadequacy exists. Testing vitamin D and calcium levels and subsequent supplementation in deficient individuals is recommended in athletes with repeated stress fractures. Athletes with eating disorders should be evaluated, and psychiatric testing and nutritional counseling should be recommended when indicated. Bisphosphonates, which work by inhibiting osteoclastic activity and increasing bone mineral density, have shown early promise in individuals with stress fractures, although more research is required.

Bone Specific Management 

Recommendations for the management of specific types of stress fracture include:

• Rib: Rib stress injuries are managed nonoperatively with rest, analgesia, and cessation of the offending activity. Correction in training errors and faulty mechanics may be helpful as well.
• Pelvis: Pelvic stress injuries are managed conservatively with rest, crutches (if required), and a gradual return to sport.
• Femoral neck: Compression side femoral neck stress injuries can be managed conservatively with nonweight bearing using crutches and activity restriction if the fatigue line is <50% of the femoral width. Tension-side stress injuries or a compression fracture with a fatigue line of >50% of the femoral neck width typically require open reduction and internal fixation (ORIF) with percutaneous screw fixation.
• Femoral shaft: Most femoral shaft stress injuries can be managed conservatively, including rest, activity modification, and protected weight bearing. If the patient has low bone mineral density, is older than 60, or has fracture completion or displacement, ORIF with an intramedullary nail is indicated.
• Patella: Patellar stress injuries can be managed conservatively with immobilization and a gradual return to activity.
• Tibia: Most tibial shaft stress injuries can be managed conservatively. This includes activity restriction and protected weight-bearing. If the “dreaded black line” is present and violates the anterior cortex, ORIF with intramedullary tibial nailing or plating may be indicated. This depends on the duration of conservative treatment, the patient’s occupation, and the sport in which the patient participates. Medial tibial plateau stress fractures can be managed conservatively. Medial malleolus stress fractures can typically be managed conservatively but should be discussed with the orthopedic surgeon.
• Fibula: Fibular stress injuries can be managed conservatively with rest, immobilization, activity modification, and a gradual return to play.
• Tarsals: Calcaneal stress injuries respond well to conservative management with rapid healing and return to activity. Navicular stress injuries are at high risk of nonunion. They can be managed conservatively, including remaining nonweight bearing for up to 12 weeks with close follow-up before beginning return to play. If a completed fracture line is present, ORIF with screw fixation is typically performed. Medial cuneiform and some talus stress injuries can also be managed conservatively.
• Metatarsals: Most metatarsal fractures can be managed conservatively, including adding metatarsal padding as needed. Dancer fractures at the base of the second metatarsal should be made nonweight-bearing. Fifth metatarsal stress fractures are at high risk for nonunion and should be nonweight bearing with immobilization and close follow-up as they may require surgical intervention. Sesamoid stress fractures require rest from offending activity and immobilization and offloading of the sesamoids.

Differential Diagnosis

The differential diagnosis for stress reactions and fractures is broad but may be narrowed to the affected area, including:

• Cellulitis
• Osteomyelitis
• Tendonitis
• Tendinopathy
• Exertional compartment syndrome
• Tumors (benign or malignant)
• Nerve entrapment
• Arterial entrapment
• Coagulation disorders
• Compartment syndrome
• Neuropathic pain
• Complex regional pain syndrome
• Bursitis
• Degenerative changes
• Arthropathy
• Radiculopathy
• Bone contusion
• Avascular necrosis
• Infection (osteomyelitis)

Where anatomically appropriate, nonmusculoskeletal causes could include dermatologic, vascular, neurologic, genitourinary, reproductive, or gastrointestinal etiologies. For example, a stress injury of the pelvis and proximal femur could present as the pelvis, hip, thigh, or groin pain, and the differential should be focused on this region. Stress fractures of the fibula will present as leg pain, and the clinician will need to consider the appropriate anatomy. The differential diagnosis of tibial stress injuries includes periostitis or completed stress fracture, chronic exertional compartment syndrome (CECS), and popliteal artery entrapment syndrome.

On advanced imaging, stress fractures may present similarly to several other differential diagnoses, including malignancies with an osteoid matrix or periosteal reaction (osteosarcoma, Ewing sarcoma, metastasis) or relatively more benign presentations of bone marrow edema or hyperintense signal changes (chronic osteomyelitis, osteoid osteoma). MRI has a reported 93% to 98% accuracy in differentiating between a stress fracture and a pathologic fracture.[24]

Prognosis

Most athletes will return to play with minimal pain and normal function if provided appropriate relative rest and rehabilitation. However, if they return too soon or are inadequately rehabilitated, their pain may lead to chronic injury, and the patient may experience residual pain. Adequate rest, immobilization, nonweight bearing when appropriate, and a gradual return to activity typically result in a return to the preinjury level of play. The primary issue with stress injuries is missed playing time.

High-risk stress fractures carry considerably higher risks. They are more likely to progress toward nonunion and thus require surgical treatment.[15] High-risk stress fractures are more likely to necessitate a change in the sport for an athlete and may result in more significant postrecovery pain

Complications

Acute complications from stress injuries include pain, swelling, and missed playing time. Individuals with full cortical break may require surgery and all the risks associated with surgical intervention. Chronic complications include chronic pain, inability to return to the initial level of play, and repeat or recurrent stress fractures.

If pain and advanced imaging show no improvement of the stress fracture at 6 to 8 weeks, patients should be referred to a subspecialist (eg, foot and ankle surgeon). Nonunion is a complication of March fractures with symptoms of chronic pain, swelling, or instability in 20% to 67% of patients.[39] Surgical options such as medullary curettage, autologous bone grafting, bridge plating, or intramedullary nailing may be warranted.[39][50][51] Postoperatively, healing can be arduous, sometimes taking months to years. Other treatment options include bone stimulation, shockwave, or ultrasound. Injectable bone cement options (calcium sulfate hydroxyapatite) have not had favorable outcomes as a stand-alone treatment.[52] Although pulsed ultrasound may be noninvasive, it has not significantly decreased overall healing time.[53] Shockwave has shown some promising outcomes secondary to increased bone turnover, osteoblast stimulation, and neovascularization and offers a noninvasive adjunct to treatment.[54]