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Overview of stress fractures

Author: Kevin deWeber, MD, FAAFP, FACSM
Section Editors: Patrice Eiff, MD, Chad A Asplund, MD, FACSM, MPH
Deputy Editor: Jonathan Grayzel, MD, FAAEM

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: May 2019. | This topic last updated: Dec 06, 2017.

INTRODUCTION

As defined below, stress fractures are overuse injuries to bones caused by repetitive stresses,
either tensile or compressive. Stress fractures may be the result of a small number of repetitions
with a relatively large load (eg, a military recruit marching for several miles with a heavy backpack),
a large number of repetitions with a usual load (eg, an athlete training for a long-distance race), or
a combination of increased load and increased repetitions.

An overview of the classification, risk factors, diagnosis, management, and prevention of stress
fractures is presented here. Specific stress fractures are discussed separately. (See "Stress
fractures of the tibia and fibula" and "Stress fractures of the metatarsal shaft" and "Stress fractures
of the humeral shaft" and "Proximal fifth metatarsal fractures", section on 'Stress fractures of the
proximal diaphysis'.)

DEFINITIONS

● Fracture – Fracture refers to the breaking of a bone. Complete fractures divide the affected bone
into two or more pieces, while partial (incomplete) fractures do not extend through the cortex. An
example of an incomplete fracture is the "greenstick" fracture, in which the convex side of a long
bone is disrupted, while the concave surface remains intact. These are most common in children.

● Stress fracture – A stress fracture occurs when a bone breaks after being subjected to repeated
tensile or compressive stresses, none of which would be large enough individually to cause the
 bone to fail, in a person who is not known to have an underlying disease that would be
expected to cause abnormal bone fragility.

● Insufficiency fracture – An insufficiency fracture occurs when the mechanical strength of a

bone is reduced to the point that a stress, which would not fracture a healthy bone, breaks the
weak one. The condition that causes reduced bone strength typically does so throughout the
skeleton (eg, osteoporosis, osteomalacia, or osteogenesis imperfecta) but may be more
localized (eg, demineralization in a limb due to disuse).

Insufficiency fractures due to osteoporosis, pseudofractures, and radiolucent lines seen in the
bones of patients with osteomalacia are reviewed elsewhere. (See "Clinical manifestations,
diagnosis, and evaluation of osteoporosis in postmenopausal women" and "Osteoporotic
thoracolumbar vertebral compression fractures: Clinical manifestations and treatment" and
"Epidemiology and etiology of osteomalacia".)

● Pathologic fracture – A pathologic fracture is due to a localized loss of strength in a bone from
a disease process immediately underlying the bone. Examples of pathologic fractures include
those that occur at sites of bone tumors (primary or metastatic), bone cysts, and infections.

PATHOPHYSIOLOGY

Bone remodels in response to a mechanical stress [1]. The rate and amount of remodeling depends
upon the number and frequency of loading cycles a bone is subjected to (Wolff's law). An abrupt
increase in the duration, intensity, or frequency of physical activity without adequate periods of rest
may lead to pathologic changes in bone. These pathologic changes result from an imbalance
between bone resorption and formation. During periods of intense exercise, bone formation lags
behind bone resorption. This renders the bone susceptible to microfractures. Bone responds to this
microscopic injury with a reparative response that includes edema, which can be visualized with
magnetic resonance imaging (MRI). Some of changes associated with stress fracture can appear on
MRI before symptoms develop. (See 'Imaging studies' below.)

With continued overload, microfractures may propagate (symptoms generally develop during this
process) and eventually coalesce into a discontinuity within the cortical bone (ie, a stress fracture).
Continued overload can complete the fracture and result in displacement at the fracture site. In
summary, stress fracture represents one point on a spectrum of stress-induced bone changes
referred to as stress injury.

CLINICAL CLASSIFICATION (GRADING AND RISK OF COMPLICATIONS)

No gold standard classification system has been developed for describing stress fractures [2]. Two
clinically useful systems may be used: One describes severity based upon radiographic and
clinical features; another categorizes fractures as either high-risk or low-risk based upon location.
The system involving MRI findings is described below. (See 'Magnetic resonance imaging' below.)

Stress fractures have also been classified clinically on the basis of their risk of complications,
particularly of displacement, nonunion, or fracture propagation [3]. The distinction between "low-risk"
and "high-risk" stress fractures is based primarily on the fracture site. Stress fractures at low-risk sites
are unlikely to have any of these complications and are generally amenable to conservative
management. In contrast, high-risk stress fractures are managed more aggressively, often surgically.

● Sites at LOW RISK of complications – Fractures of the second through fourth metatarsal
shafts, posteromedial tibial shaft, proximal humerus or humeral shaft, ribs, sacrum, and pubic
rami are considered low risk.

● Sites at HIGH RISK of complications:

• Spine: Pars interarticularis of the lumbar spine

• Hip and thigh: Femoral head; superior side of the femoral neck (ie, tension side)
• Knee and leg: Patella; anterior cortex of the tibia (ie, tension side)
• Ankle and foot: Medial malleolus; talus; tarsal navicular; proximal fifth and fourth
metatarsals; base of the second metatarsal; great toe sesamoids

EPIDEMIOLOGY

The incidence of stress fractures is less than 1 percent in the general population. The reported
incidence in athletic populations varies with the type of athlete. Among military recruits, the incidence
ranges from 1 to 31 percent, among runners 13 to 52 percent, and among participants in collegiate
team sports 1 to 8 percent [4]. The incidence of lower extremity stress fracture in all United States
military members between 2009 and 2012 was 5.69 per 1000 person-years [5].

RISK FACTORS

Important risk factors for developing stress fractures include a history of prior stress fracture, low
level of physical fitness, increasing volume and intensity of physical activity, female gender and
menstrual irregularity, lower body mass index (BMI), diet poor in calcium, poor bone health, and
poor biomechanics (table 1).
Prior stress fracture — A history stress fractures is a strong predictor of future stress fractures,
according to several prospective studies [6-10]. The relative risk is over sixfold in distance
runners and military recruits with a history of at least one stress fracture [6,11]. Among track
athletes, 60 percent of those who sustained a stress fracture had a history of stress fracture. The
one-year recurrence rate in these athletes was 12.6 percent [7].

Activity-related factors

● Repetitive activities – Specific repetitive activities predispose athletes to site-specific stress

fractures. As examples, throwing athletes have an increased risk of humeral and scapular
fractures, while runners are at increased risk for pelvic and lower extremity fractures, primarily
of the tibia and metatarsals [4,6,12,13]. Gymnasts have an increased risk for stress fractures of
the spine, wrist, and foot. Stress fractures of the ribs may be seen in golfers and rowers. The
following table lists the stress fractures associated with particular sports (table 2).

Weightbearing bones, primarily those of the lower extremity, are at greatest risk for stress
fracture. As an example, tibial fractures accounted for 49 percent of all stress fractures seen in
athletes, followed in frequency by fractures of the metatarsals [12]. Greater than 12 hours of
exercise per week is a risk factor for bone stress injury in women [14].

Non-athletes who abruptly increase their level of activity may also be at risk for stress fracture.
An example would be the patient whose activity was restricted by the pain of arthritis who
resumes walking after joint replacement surgery [15].

● Decreased physical fitness – Decreased muscle strength and endurance are associated with
an increased incidence of stress fractures [16,17]. Muscles play a supportive role in bone health;
when muscles are weak or fatigued, other musculoskeletal structures absorb greater impact. A
dramatic increase in physical training may overwhelm the bone's capacity to compensate with
normal remodeling. Specific factors associated with higher rates of stress fractures include >1
cm decrease in calf girth [4], less lean mass in the lower extremities [18], less than seven
months of prior strength training [19], and poor lower extremity muscle strength [20]. Rowers
with lower knee extensor to elbow extensor strength ratios also had a higher incidence of rib
stress fractures in one retrospective case control study [21].

Although muscle inflexibility has long been cited as a possible risk factor for stress fracture, its
role remains unclear [16]. Among several prospective studies looking at ankle dorsiflexion, one
found restricted flexibility to be associated with stress fractures [22], while two found no
association [18,23]. One prospective study found decreased hamstring flexibility to be associated
with tibial stress fractures in runners [24].
 ● Lower exercise levels prior to military training – Two prospective studies have reported that
lower exercise levels (which is different than fitness level) confers a higher risk of stress fracture
[10,25]. Among United States Marine recruits, those who self-classified their activity level before
basic training as "inactive" had a sixfold higher rate of stress fracture than those with "below
average" or higher activity levels [25]. The incidence among Chinese military recruits with a
history of fewer than seven hours per week of exercise before basic training was nearly twice
that of recruits with more [10].

● Worn footwear – Recruits who begin basic training using old shoes have a higher incidence
of stress fractures [25].

● Running surface – Two retrospective studies found no association between running surface
and stress fractures [26,27], but one found that running on a treadmill reduced tibial strain
compared with over-ground running [28].

Nutritional factors

● Inadequate vitamin D and calcium – Vitamin D and calcium are essential for bone health and
fracture prevention [29]. When the amounts of these nutrients are inadequate, bone is
weakened and is potentially more susceptible to fractures of any kind.

A systematic review of eight observational studies, including 761 cases of stress fracture,
reported an association between low serum 25(OH)D (hydroxy vitamin D) concentrations and
lower extremity stress fractures among military personnel [30]. A prospective, nested case-
control study in female United States Navy recruits found that women in the lowest quintile of
25OHD serum concentrations (1.5 to 19.7 ng/mL) had twice the risk of stress fracture compared
with women in the highest quintile (over 40 ng/mL) [31]. Vitamin D deficiency and insufficiency
was also seen in a high percentage (63 percent) of adolescents with pars interarticularis stress
fractures [32]. (See "Prevention of osteoporosis", section on 'Calcium and vitamin D' and
"Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment", section on
'Optimal intake to prevent deficiency'.)

Case-control studies show that lower calcium intake is associated with an increase in stress
fracture incidence in women, with a relative risk of 1.1 per 100 mg decreased intake [33,34].

● Disordered eating – Restricted caloric intake in female track and field athletes, gymnasts, and
dancers correlates with an increased incidence of stress fracture [18,35]. Disordered eating
deprives the body of the nutrients needed for bone and muscle metabolism, in addition to other
health risks. (See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis".)
Anatomic and biomechanical factors — A systematic review found that extreme foot arch
morphologies (pes planus or cavus) likely increase risk for tibial stress fractures, but no definitive
conclusions could be drawn [36].

Specific biomechanical characteristics during the ground contact phases of running may predispose
athletes to stress fractures. Preliminary retrospective studies show that increased tibial striking
torque [37], increased tibial shock and vertical load rates [38], and earlier hindfoot eversion [39] are
associated with higher tibial stress fracture rates.

One large prospective study showed that a shorter duration of foot pronation during landing was
associated with increased risk of tibial and femoral stress fractures [40]. Neither maximal pronation
angle nor pronation mean angular velocity appeared to increase risk. This suggests that how far
the foot pronates during contact with the ground is not as important as how well the subtalar joint
controls the duration of pronation. Further studies are needed to clarify these risks.

Additional risk factors

● Female gender – Females are at greater risk than males of developing stress fractures.
Relative risk ranges from 1.2 to 10 depending upon the population studied (eg, athletes versus
general population) and the fractures considered [4,5,9,13,41,42] Women have 51 times the rate
of sacral stress fractures but 3.4 times the rate of pubic ramus and proximal tibial stress
fractures [20]. Although the reasons for the gender discrepancy remain unproven, higher rates of
risk factors, such as decreased bone mineral density and disordered eating, likely contribute
[4,43]. Menstrual irregularity is an independent risk factor for stress fractures in women
[6,19,33,41,44,45]. The combination of decreased bone density, disordered eating leading to
poor energy availability, and amenorrhea comprises the "female athlete triad," which places a
woman at greatly increased risk of stress fractures (see "Functional hypothalamic amenorrhea:
Pathophysiology and clinical manifestations"). Even women without the entire syndrome but with
one or two components show a markedly increased risk for developing bone stress injuries [14].
Poor physical fitness may predispose some women to developing stress fractures. Studies of
female military recruits show that many women begin basic training at lower physical fitness
levels than their male counterparts [46,47].

● Age – The incidence of stress fractures is greatest in patients aged 17 to 26 years, but this
likely has more to do with increased activity than age, per se. Two large prospective studies of
military recruits found increased risk of stress fractures as age increased [20,42], and one
reported a bimodal distribution with increased risk in those under 20 and over 40 [5].

● Decreased bone density – Lower bone mineral density, as assessed by quantitative

ultrasonography or dual-energy x-ray absorptiometry (DEXA) scan, strongly correlates with an
 increased incidence of stress fractures in both men and women [6,18,33,48-51]. A family
history of osteopenia or osteoporosis is associated with a threefold higher risk of stress
fractures in adolescent female athletes [49]. (See "Prevention of osteoporosis".)

● Low BMI – BMI of less than about 21 increases risk in women [14,42] and men [42]. This
may seem counter-intuitive, as a higher BMI places greater mechanical stresses on weight-
bearing bones during exercise. However, low BMI is associated with lower bone density,
which is an independent risk factor.

● Other factors – Race/ethnicity other than black conferred significant risk in a large,
prospective study of basic combat training in the United States [42]. Radiographic findings of
femoroacetabular impingement may be a risk factor for femoral neck stress fractures [52].

DIAGNOSIS

Overall approach — Early diagnosis is essential to avoid complications and a prolonged delay in
return to activity. Often the history and physical examination provide sufficient information for
clinicians to diagnose and manage low-risk stress fractures. Key features include a history of
localized pain of insidious onset that increases with activity and focal tenderness limited to the stress
fracture site. Plain radiographs are recommended initially, but advanced imaging is only needed
when high-risk stress fractures are suspected, early definitive diagnosis is necessary, or patients are
not responding to usual treatment. Magnetic resonance imaging (MRI) is the best imaging technique
to make a definitive diagnosis. (See 'Clinical classification (grading and risk of complications)' above
and 'Imaging studies' below.)

The author treats clinically suspected low-risk stress fractures empirically and reserves advanced
imaging for suspected high-risk stress fracture, or low-risk fractures that are not responding after
several weeks of treatment (algorithm 1). In exceptional circumstances, such as elite athletes for
whom early definitive treatment and prognostic information are more important, obtaining advanced
imaging may be performed earlier.

History — A thorough history will often provide the diagnosis. The clinician should inquire about
likely risk factors and solicit a detailed description of the pain and any antecedent physical activity.
Particularly important are recent changes in activity level and participation in athletic activities. Often,
patients describe starting a new training program or significant changes in their training regimen (eg,
boot camp, addition of hill runs, transition to a harder training surface). The following table lists the
stress fractures associated with particular sports (table 2).
A dietary history is valuable for both men and women to exclude eating disorders and dietary
deficiency of calcium or vitamin D. A menstrual history will help to screen for potential hormonal
deficiencies.

Clinicians should look for risk factors by inquiring about the patient's general health, past and current
medical conditions, medications, alcohol and tobacco use, occupation, previous injuries, and family
history (especially of osteoporosis).

Pain description — Patients classically report the insidious onset of localized pain. The pain is
initially related to activity and increases in severity with increased activity. If the patient continues in
the inciting activity, symptoms worsen. Eventually the pain is present during less strenuous activity
and ultimately during rest. Occasionally, the patient experiences an abrupt increase in pain at the site
of milder chronic symptoms indicating that a repeatedly stressed area of bone has completely
fractured. Less frequently, a patient's initial presentation may involve the acute onset of severe pain,
resulting from a complete fracture at the site of a preexisting stress fracture. (See 'Definitions' above.)

Physical examination — Tenderness of the affected bone is the most sensitive physical finding
for diagnosing a stress fracture. Tenderness is usually limited to the site of injury, unless a
complete fracture is present, in which case the area of tenderness may be wider due to bleeding
and inflammation.

Many stress fractures are preceded by a bone stress injury of lesser severity that may be more
diffuse. As an example, shin splints often precede the development of a stress fracture of the medial
tibial border, in which case, tenderness may be present along several centimeters of the tibial shaft.
However, once a fracture develops the site of injury will likely demonstrate more focal tenderness.
(See "Overview of running injuries of the lower extremity", section on 'Medial tibial stress syndrome
(shin splints) and tibial stress fractures'.)

In areas where little soft tissue covers the injured bone, there may be subtle soft tissue swelling
over the stress fracture, and occasionally mild erythema. Bony callus may be palpable in chronic,
severe cases. Defects of the cortical surface and bony crepitus are not present.

When the fracture site is not easily palpable, maneuvers to stress the bone at the area of pain may
aid diagnosis. The fulcrum test may be useful when long bones are involved [53]. It is performed by
placing one hand under the area that is painful and applying steady pressure while the other hand
applies steady pressure at the end of the same bone. This creates a fulcrum effect that stresses the
site of suspected injury. Increased pain at the area in question during the test is consistent with a
stress fracture. The fulcrum test is neither sensitive nor specific, and imaging is needed to make a
precise diagnosis. (See 'Imaging studies' below.)
Some clinicians use the hop test to help diagnose femoral neck stress fractures [12]. This test simply
involves having the patient hop on the affected leg, which typically reproduces pain at the fracture
site. The patient should stop hopping immediately if significant pain develops around the hip or groin
while performing the test. While suggestive of injury, the hop test is nonspecific and confirmatory
imaging is necessary to make a definitive diagnosis. Some authors have expressed concern that
repeated hopping risks converting the rare tension-side femoral neck stress fracture into a complete
fracture, but we know of no actual cases where this has occurred. For patients who may have a
femoral neck stress fracture and experience pain simply bearing weight, it is prudent to prescribe
non-weightbearing status until appropriate imaging can be obtained.

The technique of placing a vibrating tuning fork directly over an area of injury to induce pain at a
stress fracture site has shown widely disparate sensitivity and specificity in two studies and therefore
cannot be recommended as a method to identify a stress fracture [54]. Therapeutic ultrasound (US)
placed in a similar manner had a pooled sensitivity of 64 percent and specificity of 63 percent for
identifying stress fractures in one systematic review of seven studies, and thus its usefulness for
diagnosis is also limited [54]. Compared to bone scan, US demonstrated a sensitivity of 43 percent
and specificity of 49 percent [55].

Biomechanical evaluation of the affected region should be done to identify factors that may have
predisposed to injury or affect healing. In general, the entire affected limb and its attachments to the
axial skeleton should be evaluated whenever a stress fracture is suspected. The examination
should assess:

● Leg length discrepancy (noted in 70 percent of patients with lower extremity stress fractures
[18])
● Joint range of motion and ligamentous stability
● Muscle strength and flexibility
● Limb alignment (eg, genu varus or valgus)
● Foot type (eg, pes cavus or planus)
● Gait analysis in shoes worn during physical activity
● Core muscle strength (eg, abdominal, back, and hip musculature)

Imaging studies

Approach to stress fracture imaging — Often history and examination provide sufficient
information for clinicians to manage low-risk stress fractures without imaging studies (algorithm 1). Plain
radiographs should be obtained initially and are helpful when positive due to their high specificity, but
they are insensitive. If plain radiographs are negative but clinical suspicion remains high and a need for
definitive diagnosis exists, MRI is recommended because it is both sensitive and
specific. Bone scan is sensitive but nonspecific. Computed tomography (CT) is used as an adjunct
if extensive bony injury is suspected because it provides greater anatomic detail of bone. Plain
radiographs, MRI, and bone scan each have an associated injury severity grading system (table 3).

A systematic review of 21 studies, nearly all of high or moderate quality, of the diagnostic accuracy of
imaging modalities for lower extremity stress fractures found MRI to be the most sensitive and most
specific [56]. Bone scan was not recommended when MRI was available due to its low specificity
(range 33 to 98 percent) and high ionizing radiation dose. CT was not recommended due to its high
false-negative rate. The value of plain radiography lay in its specificity but was limited by a high false-
negative rate.

Plain radiographs — Radiographs should be obtained but are typically normal for the first two
to three weeks after the onset of symptoms, and findings may take months to appear. Periosteal
elevation, cortical thickening, sclerosis, and a true fracture line are all examples of positive findings
(image 1 and image 2 and image 3). Severity grading based on appearance is described in the
accompanying table (table 3). Although such findings are specific, plain radiographs have poor
sensitivity in the detection of stress fractures. Of note, periosteal elevation on plain radiograph
correlates closely with high-grade stress fracture on MRI [57]. (See 'Magnetic resonance imaging'
below.)

Magnetic resonance imaging — MRI is supplanting bone scan as the imaging study of choice
for diagnosing bone stress injury. The systematic review of high and moderate quality studies
discussed above found that MRI is as sensitive as bone scan and more specific [56], and it provides
important prognostic information. (See 'Approach to stress fracture imaging' above.)

MRI appears to be useful in determining the severity along the spectrum of bone stress injury and is
better at differentiating pathologic fractures from stress fractures [58]. When an intraarticular stress
fracture is suspected, MRI better distinguishes bone injury from ligament or cartilage injury.
Additionally, MRI does not entail ionizing radiation, may be less expensive than a bone scan,
and provides information about injury to surrounding soft tissues.

Though more specific than a bone scan, MRI findings must be interpreted with caution, especially
when no clear fracture is present. Asymptomatic tibial stress reactions are seen in 43 percent of
asymptomatic runners [59]. Findings such as isolated bone marrow edema are nonspecific, and can
occur with bone tumors, avascular necrosis, and osteomyelitis [60]. Correlation of MRI findings with
the history and physical examination is critical for accurate diagnosis. MRI findings consistent with a
stress fracture range from periosteal or bone marrow edema to frank cortical fracture lines [60,61].

A system to grade bone stress injury severity based on MRI findings has been developed (table 3)
[62,63]. Grade 1 (mild) fractures show only periosteal edema, grade 2 (moderate) fractures show bone
marrow edema on T2-weighted images; grade 3 (severe) fractures show marrow edema on both
T1-and T2-weighted images; and grade 4 (severe) fractures show a cortical fracture line in addition
to edema [63]. A simplified system has been proposed in which Grades 1 and 2 fractures are
termed "low-grade" and grades 3 and 4 are termed "high-grade" [64]. The use of these grading
systems helps clinicians provide information about time to recovery. (See 'Return to activity' below.)

Bone scan — Radionuclide studies (three phase bone scan) were traditionally used for
diagnosis because they can show evidence of stress fracture within two to three days of injury and
have high sensitivity. However, the specificity of bone scan is low [56]. Approximately 40 percent of
positive findings occur at asymptomatic sites [41].

Bone scans can also be falsely positive with shin splints. Areas of increased uptake may represent
subclinical sites of bone remodeling or stress reactions. Increased uptake can also appear in the
setting of bone tumors, osteomyelitis, or avascular necrosis. Although rare, there are reports of false-
negative bone scans [60,65]. Because of these limitations, MRI is supplanting bone scan as the
diagnostic study of choice when plain radiographs are negative and confirmation of suspected stress
fracture is needed. (See 'Magnetic resonance imaging' above.)

Acute stress fractures appear as discrete, localized, sometimes linear areas of increased uptake on
all three phases (angiographic, soft tissue, and delayed phases) of a technetium-99 methylene
diphosphonate bone scan. In contrast, shin splints are typically positive only during the delayed
phase of the scan [66]. A system to grade stress fracture severity based on bone scan findings has
been developed (table 3) [67].

Computed tomography — CT is limited as a primary diagnostic imaging modality by its high false-
negative rate [56]. It can be considered if MRI is unavailable or inconclusive, but is it also useful as an
adjunct study when plain films are positive and extensive bony injury is suspected, because it provides
greater anatomic detail of bone involvement. CT can also show fracture lines in long bones. In the setting
of a negative plain radiograph and a positive bone scan, CT can differentiate between fracture and stress
reaction, or other conditions of the bone such as tumor or osteomyelitis [12].

Ultrasonography — Ultrasonography (US) continues to gain popularity as an imaging tool for

musculoskeletal conditions, particularly as image resolution improves and clinicians gain experience.
US can display several findings suggestive of stress fracture, including hematoma, periosteal
elevation, hypervascularity, and cortical defect over the area of tenderness [68-70]. A systematic
review of seven high-quality studies found US to be more sensitive than specific, signifying a low
false-negative rate but a high false-positive rate in diagnosing tibia and metatarsal stress fractures,
and concluded that it is best used (in trained hands) to rule out a stress fracture based on negative
findings [56].
DIFFERENTIAL DIAGNOSIS

Several disorders can present with localized musculoskeletal pain. Tendinopathy, muscle strains,
joint sprains, nerve entrapment syndromes, and compartment syndrome share some features with
stress fractures. Bone stress reactions probably represent precursor lesions that will progress to
stress fractures if the sites are not protected from further insults. Among runners, medial tibial stress
syndrome (ie, "shin splints") is the most common example of this phenomenon. Neoplasm and
infection represent the most worrisome diagnoses in the differential list. (See "Overview of running
injuries of the lower extremity", section on 'Medial tibial stress syndrome (shin splints) and tibial
stress fractures'.)

● Tendinopathy – Overuse syndromes frequently are due to tendinopathy, a condition

characterized by chronic pain in the affected tendon. Onset is usually insidious. Tenderness
is localized to the affected tendon, which can sometimes be difficult to distinguish from the
underlying bones. Pain may be reproduced by passive stretch and resisted contraction of the
affected tendon. (See "Overview of overuse (persistent) tendinopathy".)

● Muscle strain – Localized pain may develop acutely or insidiously as a result of isolated trauma
or repeated minor injuries to one or more muscles. Tenderness and pain with passive stretch or
resisted contraction of the involved muscle are indicative of a muscle strain. A localized
hematoma and/or palpable depression may develop at the site of a sizable muscle tear. Although
radiographs do not reveal a fracture, this is also often true with stress fractures. (See "Overview
of running injuries of the lower extremity", section on 'Labral tear'.)

● Ligament sprain – Ligamentous injuries are typically the result of a single episode of trauma,
though repeated injury may lead to a subacute or chronic disorder that could raise suspicion for
stress fracture. Tenderness with sprains is generally localized to the area of the affected
ligaments. Stressing the ligaments reproduces or exacerbates the pain, and may reveal
ligamentous laxity.

● Nerve entrapment syndromes – In addition to pain, other neurologic symptoms, particularly

paresthesia, numbness, and weakness, may be clues to the presence of a nerve entrapment
syndrome of the upper or lower extremity. (See "Overview of upper extremity peripheral nerve
syndromes" and "Overview of lower extremity peripheral nerve syndromes".)

● Exertional compartment syndrome – Compartment syndromes are caused by increased tissue

pressure within a fascial compartment that compromises local circulation and neuromuscular
function. In susceptible individuals, the compartment pressure increases with exercise, resulting in
exercise-induced pain, tightness, distal paresthesia, muscle weakness, or numbness.
 Symptoms usually resolve within several minutes of rest. There may be no symptoms or
diagnostic signs at rest; provocative testing and compartment pressure testing may be
necessary. A more detailed discussion of exertional compartment syndrome is found separately.
(See "Chronic exertional compartment syndrome".)

● Medial tibial stress syndrome (shin splints) – Shin splints are an inflammatory response of
the connective tissue of the lower leg to repetitive loading. Unlike a stress fracture, the patient
with shin splints has no discrete bone tenderness. Instead, diffuse tenderness over the middle to
distal third of the tibial border (usually medial but sometimes lateral) is typically present.
However, if overuse continues, shin splints may progress to a stress fracture without a clear
demarcation of this change, and distinguishing between the two can sometimes be difficult
clinically. Like stress fractures, shin splints develop in people who suddenly increase their level
of physical activity. The change may be in intensity, frequency, or type of exercise. The most
frequently associated exercise is running. Shin splints are discussed elsewhere. (See "Overview
of running injuries of the lower extremity", section on 'Medial tibial stress syndrome (shin splints)
and tibial stress fractures'.)

● Neoplasm – Bone pain due to neoplasm is generally characterized as being focal and constant.
Painful benign and malignant neoplasms of bone can generally be differentiated from stress
fractures by imaging studies. Lytic, blastic, and mixed lesions may be appreciated on plain
radiographs. Malignant tumors may arise primarily from bone or be metastatic. The approach to the
diagnosis of primary bone tumors and bone pain due to cancer, and the evaluation of a patient with
a complete or impending pathologic fracture, are discussed separately. (See "Bone tumors:
Diagnosis and biopsy techniques" and "Overview of cancer pain syndromes", section on 'Multifocal
bone pain' and "Evaluation and management of complete and impending pathologic fractures in
patients with metastatic bone disease, multiple myeloma, and lymphoma".)

● Infection – Osteomyelitis can cause localized bone pain and tenderness. It can occur at any
age and at different anatomic sites. Among adolescents and young adults, osteomyelitis of long
bones is most prevalent and may present in similar fashion to a stress fracture. Bone infection
that results from a contiguous soft tissue infection should be readily recognized in the
extremities, but may be more difficult to differentiate from a stress fracture in the bones of the
pelvis.

Hematogenous seeding in older children and young adults generally affects the ends of long
bones, while in skeletally mature adults the vertebrae are most often affected. Laboratory tests
and imaging studies may have some value, but it is NOT possible to exclude osteomyelitis on
the basis of noninvasive studies. The clinical features and the approach to diagnosis of
osteomyelitis are discussed elsewhere. (See "Osteomyelitis in adults: Clinical manifestations and
 diagnosis" and "Hematogenous osteomyelitis in children: Clinical features and complications",
section on 'Clinical features'.)

TREATMENT CONCEPTS

General approach — If a stress fracture is strongly suspected clinically or is confirmed with

imaging, early intervention is needed to reduce pain, promote healing, and prevent further bone
damage. The sooner treatment is begun, the quicker the patient returns to full activity [71].
Conservative management is recommended for low-risk fracture sites. Surgical consultation is
necessary for patients with fractures at high-risk sites or for whom a lengthy rehabilitation process
is untenable, such as a laborer whose livelihood depends upon a timely return to work, and some
high-level athletes.

Conservative management consists of the following:

● Acute pain control

● Protection of the fracture site with reduced weightbearing or splinting in selected stress fracture
locations
● Reduction or modification of activities such that pain is not present
● Gradual resumption of activities if pain-free
● Rehabilitative exercise to promote optimal biomechanics and fitness
● Risk factor reduction as indicated
● Proper nutrition, including additional calcium and vitamin D during treatment

Details about treatment are provided below and in reviews of specific fractures. (See "Stress
fractures of the tibia and fibula" and "Stress fractures of the metatarsal shaft" and "Stress fractures of
the humeral shaft" and "Proximal fifth metatarsal fractures", section on 'Stress fractures of the
proximal diaphysis'.)

Low-risk sites — Fractures of the second and third metatarsal shafts, posteromedial tibial shaft,
fibula, proximal humerus or humeral shaft, ribs, sacrum, and pubic rami are considered low risk for
fracture propagation or nonunion [72]. These fractures usually heal with conservative treatment.
(See 'Determining if conservative treatment is appropriate' below.)

As an example, tibia stress fractures commonly occur at the junction between the middle and distal
thirds of the diaphysis on the compression side of the bone (posterior medial). In this case, a brief
period of relative rest followed by gradual, progressive, non-painful exercise over several weeks is
appropriate therapy.
High-risk sites — Expert orthopedic or sports medicine consultation should be obtained for a stress
fracture at any site with a high risk for nonunion, complete fracture, or long-term disability. Such sites
include the pars interarticularis of the lumbar spine [73], femoral head [74], femoral neck [75],
patella, anterior cortex of the tibia (ie, tension side), medial malleolus, talus, tarsal navicular,
proximal fourth metatarsal, proximal fifth metatarsal shaft, great toe sesamoids, and base of the
second metatarsal bone [3].

Determining if conservative treatment is appropriate — Although conservative treatment is

generally preferred to surgical intervention in the management of stress fractures, each patient
should be considered individually. An elite athlete or laborer may depend upon an early return to
activity to remain competitive or earn their living. Such patients may benefit from more aggressive
rehabilitation or from orthopedic consultation earlier in their course than those whose career or
livelihood is not threatened by a longer period of rehabilitation. A patient may also require early
surgical intervention if there is evidence of nonunion (ie, cyst formation or sclerosis surrounding the
fracture) because such fractures are less likely to heal by conservative measures alone.

Elements of conservative care

Pain control — Ice (applied locally for 15 minutes every three hours as needed) and pain medication
(acetaminophen or low potency opiates) are used to control acute pain. The effect of nonsteroidal
antiinflammatory drugs (NSAIDs) on fracture healing is discussed separately. (See "Nonselective
NSAIDs: Overview of adverse effects", section on 'Possible effect on fracture healing'.)

Excessive analgesia may mask pain, making it difficult to gauge appropriate increases in physical
activity during rehabilitation [76]. It is prudent to use as little analgesic medication as possible and to
strongly discourage using analgesics as a means to increase pain-free activity.

Protection of the fracture site — The forces exerted on the injured bone must be reduced such
that pain is eliminated in order to allow for bone remodeling and healing. As examples, high-risk
femoral head and tension-side femoral neck stress fractures should be treated with crutches and
complete non-weightbearing as soon as clinically suspected and continued until orthopedic
consultation is obtained.

Other pelvic or lower extremity stress fractures should be treated with reduced weightbearing if
walking causes persistent pain. In many foot stress fractures, protection with a Controlled Ankle
Motion (CAM) boot, hard sole shoe, fracture boot, or leg splint eliminates pain with walking.

Bracing may be helpful in some instances, but studies may be limited depending on the type of stress
fracture and clinical context. Use of a calf length pneumatic brace for tibial stress fractures may reduce
the time until pain-free return to play for some patients. Bracing of the spine may be indicated
for some stress fractures of the pars interarticularis; orthopedic consultation is recommended for
such injuries. (See "Stress fractures of the tibia and fibula".)

Activity modification — Modification of activities that place stress on the affected bone is
critical to the successful treatment of stress fractures. Pain is typically used to judge the efficacy of
activity modification. Simply put, activities should be limited to those that are pain-free. Failure to do
so may prolong healing time and increase the risk of completed fracture or nonunion.

Active individuals will not tolerate long periods of inactivity. It is mentally untenable and leads to
cardiopulmonary deconditioning and muscle atrophy. Instead, patients should be encouraged to
engage in activities that closely approximate their desired activity but are pain-free. For instance,
runners may walk briskly, use elliptical machines, perform shallow-end aquatic therapy or deep
water running, or run on a reduced-weightbearing treadmill machine. Cycling and swimming are
excellent alternatives.

As healing progresses, exercises involving increasing amounts of bone stress can be added
gradually as tolerated, using pain as a guide. Should the patient experience any pain at the fracture
site, the activity should be replaced by an exercise that places less stress upon the healing bone.

Preventive measures should be considered, as discussed below, in order to reduce the risk
of recurrence. (See 'Prevention' below.)

Rehabilitative exercise — Athletes, laborers, and patients with biomechanical problems

predisposing to injury should participate in rehabilitation supervised by a knowledgeable physical
therapist, athletic trainer, or comparable professional. The key principle during rehabilitation is
protected, gradually progressive exercise that allows for adequate bone healing while promoting
cardiorespiratory fitness, muscular strength, and flexibility. If supervised rehabilitation is not possible,
education, home exercises, and close follow-up with the treating clinician are advisable.

Calcium and vitamin D — Although the evidence supporting these treatments is limited and
based primarily upon studies of fracture prevention, throughout the course of treatment for a stress
fracture, we suggest taking additional daily calcium (1500 mg) and vitamin D (800 international units)
to help ensure fracture healing. Calcium intake may be increased through dietary changes or
supplementation; vitamin D intake is typically increased with oral supplements. (See 'Nutritional
factors' above.)

Therapies of uncertain benefit

● Therapeutic ultrasound – Multiple studies suggest that US accelerates the healing of acute
fractures, but evidence for its efficacy in stress fractures is mixed. Several randomized trials have
reported no clinical benefit in stress fractures treated with low intensity pulsed US (LIPUS) [77-
 79]. However, two randomized trials, one blinded and one not, in Indian soldiers found US
treatment substantially reduced the time until return to full duty [80,81]. These protocols used 1
Watt/cm² of US energy for five minutes a day at the fracture site, in addition to usual conservative
therapy. LIPUS may be effective for particular types of stress fractures, but further analysis is
needed to determine whether this is so and what protocols may be most effective.

● Extracorporeal shock wave therapy – Reports of successful treatment of stress fracture

with ECSWT in humans is limited to case studies [82]. Controlled trials are needed before
the effectiveness of ECSWT for the treatment of stress fractures can be determined.

● Medications – A small retrospective cases series of subchondral stress fractures of the knee
showed markedly faster healing by MRI assessment at 3 and 12 months in patients treated with
the prostacyclin analogue iloprost compared to those treated with the analgesic tramadol [83].
Controlled trials are needed before the effectiveness of prostacyclin analogues for the treatment
of stress fractures can be determined.

● Electrical stimulation – Capacitatively coupled electric fields were not more effective than
placebo in healing posteromedial tibial stress fractures in a randomized controlled trial [84].

FOLLOW-UP

The clinician should reevaluate the patient every one to three weeks during the healing period. Those
with high occupational or athletic demands warrant more frequent evaluation than recreational patients.
Pain should progressively subside with treatment. If symptoms persist after several weeks, compliance
with the treatment regimen should be ascertained. Compliant patients with persistent pain may need
more restrictive activity modification, further protection of the bone, and a more gradual rehabilitation
program. Imaging is needed if there is no clinical improvement despite six additional weeks of
conservative management, including the additional measures described.

Once radiographs, MRI, bone scan, or CT confirms the diagnosis of stress fracture, the clinician
rarely needs subsequent imaging. Radiographic healing lags behind clinical healing, and both bone
scan and MRI may remain positive for up to 12 months following the original injury. Clinical response
to treatment should suffice as confirmation of healing for almost all patients. Additional imaging plays
a role only when the clinical response to treatment fails to progress appropriately. In this case, repeat
imaging will determine if the fracture has extended or developed an area of nonunion. CT images the
fracture line in long bones better than plain radiography, bone scan, or MRI. (See 'Imaging studies'
above.)
ORTHOPEDIC CONSULTATION

Prompt surgical referral (within a few days) is recommended for high-risk fracture sites, which have
higher rates of nonunion and progression to complete fracture. Orthopedic referral is appropriate for
patients who cannot tolerate a lengthy rehabilitation process, such as a laborer whose livelihood
depends upon a timely return to work or some high-level athletes. Should conservative treatment
fail, surgical consultation should be obtained, generally after repeat imaging reveals the fracture has
extended or a nonunion has developed. Of note, evidence supporting the role of surgery in the
treatment of stress fractures is limited [85]. (See 'High-risk sites' above.)

RETURN TO ACTIVITY

Athletes and laborers with a stress fracture often need to know their prognosis in terms of the time
required until they can compete or resume work. This may be difficult to determine and is based
upon several factors, including the bone affected, radiologic grade of the fracture, duration of
symptoms, compliance with the treatment plan, and underlying bone health.

Affected bone — Each stress fracture site has its own propensity to heal based on anatomic
differences such as blood supply, stability provided by surrounding structures, and amount of
weightbearing. Fractures sustained by athletes that are categorized as high-risk (femoral neck,
patella, anterior (tension side) cortex of the tibia, medial malleolus, talus, tarsal navicular, proximal
fourth metatarsal, proximal fifth metatarsal shaft, great toe sesamoids, and base of the second
metatarsal bone) take longer to heal and allow return to sport (132 days) than do low-risk fractures
(119 days) [64].

Radiologic grade of fracture — A higher fracture grade as determined by MRI findings generally
portends a longer recovery time. While retrospective study results have conflicted [62,86,87], a
prospective observational study found that MRI grade strongly correlated with recovery time in
collegiate track and field athletes [63]. Athletes with grades 1 and 2 stress (mild/moderate) injuries
returned to sport in 13.1 weeks, whereas those with grades 3 or 4 (severe) injuries took 23.6 weeks
to return. With every one-step increase in grade, return to sport increased by 48 days.

Using a simplified grading system where fractures with MRI grades 1 and 2 were categorized as
"low-grade" and grades 3 and 4 fractures as "high-grade," a retrospective study of 52 athletes with
stress fractures found that low-grade stress fractures required an average of 95 days for return to
sport, whereas high-grade fractures required 143 days (table 4) [64]. Another retrospective study of
27 femoral neck stress fractures treated conservatively reported that MRI grade 1 injuries recovered
much faster (7.4 weeks) than injuries with MRI grades 2 to 4 (about 15 weeks) [88]. However, a
prospective study of forty posteromedial tibial stress fractures found no correlation between healing
time and radiographic injury grade using plain radiographs, bone scan, CT, or MRI, although there
was trend towards a significant correlation between higher injury grade on MRI and longer recovery
time [89].

Duration of symptoms — One retrospective study found that athletes under 20 years of age who
sought treatment within three weeks of symptom onset had a markedly quicker return to activity (10.4
weeks) compared with those who delayed treatment (18.4 weeks) [71].

Underlying bone health — A prospective study of stress fractures in collegiate athletes found
that lower bone mineral density correlated strongly with prolonged return to sport [63].

PREVENTION

General guidelines — Based upon our knowledge of proven and possible risk factors, we suggest
the following guidelines for preventing stress fractures:

● Patients must be educated in proper training techniques, especially avoiding the "too much, too
soon" training errors. Athletes should increase the frequency and intensity of training in small,
incremental steps. A rough guide is no more than 10 percent increase in volume or intensity
per week.

● Prevention of osteoporosis is important. A well-balanced diet, adequate calcium and vitamin D,

muscle strength and flexibility training, and regular weightbearing exercise should be
encouraged in all patients. (See 'Nutritional factors' above.)

● Young female athletes should be assessed for menstrual irregularities and signs and symptoms of
eating disorders, and provided appropriate treatment to prevent the female athlete triad. (See
"Functional hypothalamic amenorrhea: Pathophysiology and clinical manifestations" and "Anorexia
nervosa in adults: Clinical features, course of illness, assessment, and diagnosis" and "Bulimia
nervosa in adults: Clinical features, course of illness, assessment, and diagnosis".)

Prevention in military recruits — Much of the research done on stress fracture risk factors and
prevention has been in the military recruit population, which is at particularly high risk of injury.
In addition to the above principles, the following have evidence of effectiveness:

● Physical fitness prior to enlistment ‒ Prior to basic combat training, aerobic capacity, muscle
strength, and flexibility should be optimized. Several prospective studies demonstrate that
military recruits who participate in ball sports for at least two years prior to enlistment have a
significantly lower risk of developing stress fractures during initial military service [48,90,91]. This
 implies that participation in ball sports confers some measure of increased physical fitness that
may be protective of bone health.

● Foot orthoses ‒ Either prefabricated or custom made foot orthoses are effective for preventing
lower limb stress fractures, according to a meta-analysis of four trials, with a pooled relative risk
(RR) of 0.59 (95% CI 0.45 to 0.76) [92]. Quality varied among studies. The RR was lowest for
metatarsal stress fractures (RR 0.25; 95% CI 0.09 to 0.69), but the intervention was also
effective for tibial shaft (RR 0.65; 95% CI 0.43 to 0.96) and femoral neck (RR 0.53; 95% CI 0.35
to 0.80) stress fractures. Separate analyses of prefabricated orthoses and of custom made
orthoses showed that both types were similarly effective. The estimated number needed to treat
(NNT) to prevent one stress fracture was 20 people.

● Physical training modifications ‒ Traditionally, military physical training has emphasized

middle distance running, but modifications to this approach have reduced stress fractures in
military populations. Several observational studies report substantial reductions in lower
extremity stress fracture rates among recruits and soldiers who follow modified physical training
programs [93-95]. Modifications have included reduced running mileage, greater variety of
exercises (eg, multiaxial movements, agility training), progressive and periodized training, and
consuming nutrients soon after high-intensity exercise.

The incidence of pelvic stress fractures in female military recruits was reduced from 11.2 to 0.6
percent by lowering march speed from 7.5 to 5 km/hour, running on softer surfaces,
encouraging individual step length and running speed rather than marching or running in step,
and using interval training (eg, alternating sprints and jogging) instead of traditional middle-
distance runs [96].

● Vitamin D and calcium supplementation ‒ Daily vitamin D (800 international units) and
calcium (2000 mg) supplementation decreased stress fracture rates in a randomized trial of
female United States Navy recruits and in several other prospective observational studies
[29,97]. (See 'Additional risk factors' above and "Vitamin D deficiency in adults: Definition,
clinical manifestations, and treatment", section on 'Optimal intake to prevent deficiency'.)

Interventions for which research has shown borderline or no significant benefit in military recruits
include:

● Oral contraceptive (OC) use in female distance runners led to a nonsignificant decrease in
stress fracture incidence compared with those who did not take OCs, according to one
randomized trial [34]. The study was under-powered due to medication noncompliance, and
women with oligomenorrhea or amenorrhea who took OCs had a significant increase in their
bone mineral density.
 ● A meta-analysis of seven studies found that flat-contour, shock-absorbing insoles were not
effective in preventing stress fractures or other lower extremity injuries [92]. The participants in
one study were non-military soccer referees.

● Rest from running for one week during the middle of an eight-week basic military training
regimen did not reduce stress fracture rates [98].

● Treatment with risedronate for 12 weeks in military recruits deemed to be at high risk for stress
fracture did not reduce injury rates [99].

PREVENTION IN THOSE WITH PRIOR STRESS FRACTURE

(SECONDARY PREVENTION)

Underlying causes and risk factors for stress fractures must be addressed to optimize healing and
prevent recurrent injury. Referral to a clinician with sports medicine training or experience
managing stress fractures may be beneficial.

Disordered eating — Disordered eating must be addressed. A careful history and examination can
identify patients whose eating habits predispose to injury. Those with the "female athlete triad"
(disordered eating, amenorrhea, and decreased bone density) are at particularly high risk and should
have treatment by a multidisciplinary team consisting of a mental health professional, nutritionist, and
primary care clinician [100]. (See "Eating disorders: Overview of prevention and treatment".)

Evaluate for decreased bone density — Consideration of performing bone density testing using dual-
energy x-ray absorptiometry (DEXA scanning) should be made in patients with any of the following:

● Stress fractures unexplained by excessive activity

● Recurrent stress fractures
● Family history of osteoporosis
● Regular use of glucocorticoids
● Disordered eating

Those with low bone density values should be treated with weightbearing exercise (as part of a
graded treatment plan), calcium, vitamin D, and other indicated medications. Additional laboratory
testing may be needed. Secondary osteopenia and osteoporosis are discussed in detail
separately. (See "Evaluation and treatment of premenopausal osteoporosis".)

Dietary habits that promote higher bone mineral density may decrease the risk of stress fractures in
susceptible individuals. In a prospective observational study of 17 female runners, higher intake of
calcium, skim milk and dairy products was associated with lower rates of stress fracture and
increased bone mineral density [101].

Improve physical fitness — An assessment of past physical activity, the activity that led to the
stress fracture (frequency, intensity, exercise selection), and future activity needs can help patients
develop a fitness plan that promotes health and fitness, but avoids recurrence of stress fractures.
Consultation with a knowledgeable fitness specialist may be helpful. (See "The benefits and risks
of aerobic exercise".)

Evaluate for anatomical and biomechanical factors — Biomechanical evaluation for factors,
such as leg length discrepancy, muscle inflexibility, excessive foot pronation during running, and
pes cavus (high arch) or pes planus (flatfoot), should be performed. Runners should be counseled
to replace running shoes before the tread becomes worn or cushioning is lost (approximately every
350 to 500 miles). Gait analysis in runners can help identify problems and assist in the selection of
appropriate running shoes. Orthotic prescription may help in some patients. Consultation with a
sports medicine specialist can be helpful. Running injuries are discussed in detail separately. (See
"Overview of running injuries of the lower extremity".)

SUMMARY AND RECOMMENDATIONS

● A stress fracture occurs when a bone breaks after being subjected to repeated tensile or
compressive stresses, none of which would be large enough individually to cause the bone to
fail, in a person who is not known to have an underlying disease that would be expected to cause
abnormal bone fragility. Stress fracture is part of a spectrum of bone stress injury. (See
'Definitions' above.)

● High-risk stress fractures are those at greater risk for displacement, nonunion, or fracture
propagation. (See 'Clinical classification (grading and risk of complications)' above.)

• High-risk sites for stress fractures include the pars interarticularis of the lumbar spine,
femoral head, superior side of the femoral neck (ie, tension side), patella, anterior cortex of
the tibia (ie, tension side), medial malleolus, talus, tarsal navicular, proximal fourth and fifth
metatarsals, great toe sesamoids, and the base of the second metatarsal.

• Low-risk sites include the second through fourth metatarsal shafts, posteromedial tibial
shaft, proximal humerus or humeral shaft, ribs, sacrum, and pubic rami.

● Important risk factors for stress fractures include a history of prior stress fracture, low level of
physical fitness, a sudden increase in the volume and intensity of physical activity, female gender
and menstrual irregularity, a diet poor in calcium and vitamin D, low bone mineral density,
 disordered eating, increasing age, and poor biomechanics (table 1 and table 2). (See
'Risk factors' above.)

● Early diagnosis of stress fractures is essential to avoid complications. In most cases, the history
and physical examination provide sufficient information to diagnose and manage low-risk stress
fractures without imaging studies (algorithm 1). (See 'Diagnosis' above.)

● Many patients with stress fractures describe the insidious onset of localized pain within days to
weeks of beginning a strenuous physical activity. Examination generally reveals focal
tenderness at the fracture site. (See 'History' above and 'Pain description' above and 'Physical
examination' above.)

● Radiographic imaging is needed when high-risk stress fractures are suspected or a definitive
diagnosis is necessary. Plain radiographs should be obtained initially and are helpful when
positive due to their high specificity, but they are insensitive. Magnetic resonance imaging is
recommended if plain radiographs are negative, but clinical suspicion remains high, and a
need for definitive diagnosis exists. (See 'Imaging studies' above.)

● The differential diagnosis for stress fracture includes tendinopathy, muscle strain, joint sprain,
nerve entrapment, exertional compartment syndrome, neoplasm, and infection. (See
'Differential diagnosis' above.)

● Stress fractures at low-risk sites are managed conservatively with the following interventions
(see 'Low-risk sites' above):

• Acute pain control as needed using ice, and acetaminophen and/or low-potency opioids

• Protection of the fracture site with reduced weightbearing or splinting in selected stress
fracture locations

• Reduction or modification of activities such that pain is not present

• Gradual resumption of activities if pain-free

• Rehabilitative exercise to promote optimal biomechanics

• Risk factor reduction as indicated

• Proper nutrition, including additional calcium and vitamin D (see 'Treatment concepts'
above)

● Orthopedic consultation is necessary for patients with fractures at high-risk sites or for whom a
lengthy rehabilitation process is untenable, such as a laborer whose livelihood depends upon a
 timely return to work, and some high-level athletes. (See 'High-risk sites' above.)

● We suggest the following general guidelines for preventing stress fractures (see 'Risk
factors' above and 'Prevention' above and 'Prevention in those with prior stress fracture
(secondary prevention)' above):

• Educate athletes about proper training. Increase training in small, incremental steps. A
rough guide is no more than 10 percent increase in volume or intensity per week.

• Encourage a well-balanced diet, including adequate calcium and vitamin D, muscle strength
and flexibility training, and regular weightbearing exercise in all patients, particularly those at
risk for osteoporosis. (See 'Nutritional factors' above.)

• Assess young female athletes for menstrual irregularities and signs and symptoms of eating
disorders, and provide appropriate treatment to prevent the female athlete triad. (See
"Functional hypothalamic amenorrhea: Pathophysiology and clinical manifestations" and
"Anorexia nervosa in adults: Clinical features, course of illness, assessment, and diagnosis"
and "Bulimia nervosa in adults: Clinical features, course of illness, assessment, and
diagnosis".)

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Topic 255 Version 31.0

GRAPHICS

Risk factors for stress fractures

Established risk factors

Prior stress fracture

Poor bone health (osteopenia and osteoporosis)

Substantial increase in intensity or volume of activity (eg, military boot camp)

Decreased physical fitness (poor muscle strength or endurance)

Dietary disorders (eg, insufficient calcium intake, vitamin D deficiency, eating disorders)

Family history of osteopenia or osteoporosis

Poor running biomechanics

Female gender

Menstrual irregularity in females

Low body mass index

Prolonged glucocorticoid use

Older age

Factors of uncertain risk

Shoe type; Worn-out shoes

Running surface

Foot anatomy (eg, extreme high arch)

Muscle inflexibility

Graphic 79279 Version 2.0

Stress fractures associated with particular sports

Sport High risk fracture Low risk fracture

Baseball (pitchers) Humerus, scapula

Basketball Fifth metatarsal Tibia

Cheerleading Pars interarticularis Clavicle, radius, scaphoid

Dance Pars interarticularis; sesamoids Tibia, fibula, navicular, metatarsals

(American) football Pars interarticularis; fifth metatarsal Tibia

Gymnastics Pars interarticularis; navicular Radius, scaphoid, midfoot

Rowing Clavicle, rib

Running & track Metatarsals, fibula, tibia

Skating Navicular Tibia, fibula, metatarsals

Skiing (cross-country) Sesamoids Tibia

Soccer (football) Femoral neck Tibia, tarsals, metatarsals

Softball (fast-pitch) Rib, ulna, humerus, metacarpals

Tennis Pars interarticularis Rib, tibia

Volleyball Pars interarticularis Metatarsals, tibia

Adapted from: Netter's Sports Medicine. Madden C, Putukian M, Young C, McCarty E (Eds), Philadelphia: Elsevier,

2010. Graphic 93236 Version 2.0

Overview of imaging and assessment of stress fracture

MRI: magnetic resonance imaging; CT: computed tomography.

Graphic 114447 Version 1.0

Stress fracture imaging findings and severity classification

[1] [2]
Grade Plain radiographs Bone scan MRI
1 Normal Small ill-defined cortical area of mildly increased Positive STIR image
activity

2 Normal Larger well-defined elongated cortical area of Positive STIR and T2-weighted images
moderately increased activity

3 ± Periosteal reaction Wide, fusiform cortico-medullary area of highly Positive T1- and T2-weighted images, no
increased activity cortical fracture line

4 Periosteal reaction, ± Extensive trans-cortical area of intensely increased Cortical fracture line; positive T1- and T2-
fracture line activity weighted images

STIR: short-tau inversion sequence.

1. Zwas, TS, Elkanovitch, R, Frank, G. Interpretation and classification of bone scintigraphic findings in stress fractures. J Nucl Med 1987;28(4):452.
2. Fredericson, M, Bergman, AG, Hoffman, KL, Dillingman, MS. Tibial stress reaction in runners: Correlation of clinical symptoms and
scintigraphy with a new magnetic resonance imaging grading system. Am J Sports Med 1995;23:472.

Graphic 58048 Version 2.0

Stress fracture of distal tibia

Periosteal reaction is evident at the site of this stress fracture (arrow).

Courtesy of Karl B Fields, MD.

Graphic 62977 Version 3.0

Periosteal thickening of tibial stress fracture

Cortical thickening and sclerosis are evident at the site of this stress fracture. However, it is
important to remember that most plain films taken during the first few weeks following injury
will be negative.

Courtesy of Karl B Fields, MD.

Graphic 69856 Version 4.0

Stress fracture of the anterior tibial cortex

The so-called "dreaded anterior black line" associated with this tibial stress fracture is
clearly visible (arrow). Also note the thickened cortex around the fracture line.

Courtesy of Karl B Fields, MD.

Graphic 73240 Version 3.0

Time to return to sport by stress fracture radiographic findings

Stress fracture type Recovery time

Metatarsals (not proximal second/fourth/fifth) 3 to 12 weeks

Tibia (posteromedial) 2 to 7 weeks (average 3.5)

Fibula 10 to 13 weeks

Femoral neck (compression-side, non-surgical treatment) 4 to 32 weeks (average 7.4 weeks if MRI grade 1; average 15 weeks
if MRI grade 2 to 4)
¶
Low-risk site* and low-grade severity on MRI/bone scan 8.7 weeks
High-risk site and low-grade severity on MRI/bone scan 19.3 weeks
◊
Low-risk site and high-grade severity on MRI/bone scan 21.8 weeks
High-risk site and high-grade severity on MRI/bone scan 18.7 days

MRI: magnetic resonance imaging.

* Low-risk sites: Metatarsal shafts 2,3,4; posterior tibial cortex, fibula, tarsals other than talus or navicular, pelvis, femoral shaft.
¶ Low-grade severity: Grades 1 or 2 on MRI or bone scan.
High-risk sites: Base of second metatarsal, fifth metatarsal, tarsal navicular, talus, femoral neck, patella, medial malleolus, great toe
sesamoids.
◊ High-grade severity: Grades 3 or 4 on MRI or bone scan.

References:
1. Beck BR, Matheson GO, Bergman G, et al. Do capacitively coupled electric fields accelerate tibial stress fracture healing? A
randomized controlled trial. Am J Sports Med 2008; 36:545.
2. Henningsen A, Hinz P, Lüdde R, et al. [Retrospective analysis of march fractures in the german armed forces in the years 1998 to
2000]. Z Orthop Ihre Grenzgeb 2006; 144:502.
3. Heaslet MW, Kanda-Mehtani SL. Return-to-activity levels in 96 athletes with stress fractures of the foot, ankle, and leg: a
retrospective analysis. J Am Podiatr Med Assoc 2007; 97:81.
4. Dobrindt O, Hoffmeyer B, Seidensticker M et al. Estimation of return-to-sports-time for athletes with stress fractures - an
approach combining risk level of fracture site with severity based on imaging. BMC Musculoskeletal Disorders 2012; 13:139.
5. Ramey LN, McInnis KC, Palmer WE. Femoral neck stress fracture: can MRI grade help predict return-to-running time? Am J Sports
Med 2016; 44:2122.
Courtesy of Kevin deWeber, MD.

Graphic 114376 Version 1.0

Contributor Disclosures
Kevin deWeber, MD, FAAFP, FACSM Nothing to disclose Patrice Eiff, MD Nothing to disclose Chad A
Asplund, MD, FACSM, MPH Nothing to disclose Jonathan Grayzel, MD, FAAEM Nothing to disclose

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