Physical Medicine and Rehabilitation for Stress Fractures Clinical Presentation

Updated: Sep 10, 2019
  • Author: Stephen Kishner, MD, MHA; Chief Editor: Consuelo T Lorenzo, MD  more...
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The most salient historical feature in the diagnosis of stress fracture is the insidious onset of activity-related pain.

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

Subsequently, the pain may worsen and occur earlier, limiting participation in sports activities. While rest may provide transient relief of symptoms in the early stages, as the stress injury progresses, the athlete's pain may persist even after cessation of activity. Night pain is a frequent complaint. Pain resulting from long-bone fractures is thought to be localized, while pain associated with stress injury of trabecular bone is characteristically described as more diffuse.

Stress fractures, like most overuse injuries, typically are multifactorial in etiology; thus, if the diagnosis has been made or is suspected, the clinician is in the position to try to determine what risk factors precipitated or contributed to the injury. Details of the athlete's training history should be noted, both in terms of volume and intensity. Intensive sustained muscular activity may result in bone strain and overload. This type of mechanism of injury is common in rowers, who are prone to stress fractures of the ribs.

Muscle fatigue, perhaps because of poor conditioning or as the result of overtraining, can attenuate the shock-absorbing capacity of the muscular system, resulting in greater transmission of GRFs to the associated parts of the skeleton.

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

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

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

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



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

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

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

Some practitioners believe that application of a vibrating tuning fork over the affected bone can provoke the athlete's pain, but Brukner et al dispute the validity of this test. [16]

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



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

Intrinsic risk factors are as follows:

  • Low BMD (potentially modifiable)

  • Lower limb malalignment (potentially modifiable)

  • Foot structure (unmodifiable)

  • Height - Tall stature (unmodifiable)

  • Muscle fatigue/poor overall conditioning (modifiable)

  • Weakness/strength imbalance (modifiable)

  • Pathologic bone states (potentially unmodifiable)

  • Menstrual/hormonal irregularities (potentially modifiable)

  • Genetic predisposition (unmodifiable)

Extrinsic risk factors are as follows:

  • Excessive volume or intensity of training (modifiable)

  • Sporting discipline (modifiable) - For example, runners are prone to tibial shaft stress fractures, whereas tennis players appear to be most vulnerable to navicular injuries, and volleyball players may be at a relatively increased risk of pars interarticularis injuries.

  • Change in training regimen - "New coach" phenomenon (potentially modifiable)

  • Change in training surface - Density or topography (modifiable)

  • Worn-out training shoes (modifiable)

  • Cigarette smoking (modifiable)

  • Inadequate nutrition - Energy (calories), calcium, vitamin D [17, 18] (modifiable)

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

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

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