Key Points

• Stress fractures typically occur weeks after an abrupt increase in activity level, running distance, or training frequency.

• Navicular stress fractures, anterior tibial stress fractures with a "dreaded black line," and femoral neck stress fractures are high-risk stress fractures for nonunion or progression to a complete fracture and should be referred to an orthopedic specialist.

Stress fractures result from a failure of bone to adapt successfully to repetitive loads encountered during running. Wolff's law of adaptation suggests that a bone responds to external stress by mechanical remodeling. Bone strain may become excessive as a result of increases in load magnitude, rate of loading, or number of loading cycles (Crossley et al., 1999). Advances in imaging techniques and understanding of bone pathophysiology indicate that stress injury to bone occurs on a continuum, ranging from normal bone remodeling to bone strain, to stress reaction, to stress fracture, to frank cortical fracture (Fredericson et al., 1995).

A stress fracture, or fatigue fracture, occurs when abnormal stress is applied to normal bone. In contrast, an insufficiency fracture occurs when normal or physiologic stress is applied to abnormal bone. Female athletes with premature osteoporosis, as seen in the female athlete triad, may have stress fractures resulting from abnormal stress applied to abnormal bone (Callahan, 2000).

Most stress fractures occur in the lower extremities because of impact forces produced from weight bearing during exercise. Common locations for stress fractures include the meta-tarsals, navicular, tibia, fibula, femoral shaft, femoral neck, and sacrum. The tibia is the most common site of stress fractures in running and jumping athletes and represents about 50% of all cases (Matheson et al., 1987). Less frequently, stress fractures can occur in the upper extremities, ribs, and clavicle from repetitive activity such as throwing, rowing, or weightlifting.

Lower baseline conditioning and training errors are usually involved in the development of stress fractures. A careful history will often reveal an abrupt increase in activity level, running distance, or training frequency within the 2 or 3 months before symptom onset. Many studies have analyzed bone geometry as a risk factor for stress fracture. In male military recruits and runners, studies have demonstrated that a narrower tibia in combination with a smaller tibial cross-sectional area is a risk factor for tibial stress fractures (Beck et al., 1996; Crossley et al., 1999; Giladi et al., 1987).

Female athletes with a history of eating disorders, oligo-menorrhea or amenorrhea, and delayed menarche are more likely to develop stress fractures (Arendt, 2000; Bennell et al., 1995). Inadequate caloric intake relative to energy expenditure, also known as a negative energy balance, has been implicated as the primary cause of menstrual dysfunction in young female athletes and is thought to be responsible in part for bone density changes.

Pain from a stress fracture begins with mild pain during activity that resolves with rest. As the stress fracture progresses, pain increases during activity and continues for hours afterward, usually forcing the athlete to stop exercising. With further progression, pain is present with walking and sometimes at rest. On examination, there is local tenderness at the site of the stress fracture. The hop test (asking the patient to hop on one leg) is a useful functional test for suspected lower extremity stress fractures. If a stress fracture is present, the athlete either is reluctant to hop or will have pain reproduction with hopping. Stress fractures may be seen on radiographs as an area of cortical thickening (peri-osteal reaction) and may have a linear fracture line visible. Radiographs are positive in only about 50% of cases, and an advanced imaging study such as MRI or bone scanning is often needed to confirm the diagnosis.

Stress fractures are treated with rest, activity modification, and avoidance of aggravating activities. Ambulation must be pain-free to allow for fracture healing. If the athlete cannot achieve pain-free ambulation, a period of non-weight bearing on crutches is indicated. Foot stress fractures may benefit from the use of a rigid walking boot, and tibial stress fractures may benefit from a compressive pneumatic leg brace (Swenson et al., 1997). The time for healing of a stress fracture can vary (range, 4-12 weeks), depending on the site and severity. To maintain overall conditioning, athletes can engage in nonimpact cross-training activities, such as swimming or cycling, assuming that the activity is performed without pain. Athletes with two or more stress fractures should be screened for osteopenia or osteoporosis with a bone density scan. Low bone density requires further investigation to rule out secondary causes of osteoporosis, such as vitamin D deficiency or thyroid abnormalities. Menstrual irregularities, disordered eating, and a negative energy balance in female athletes should also be corrected.

Some stress fractures are at higher risk for nonunion or progression to a complete fracture. High-risk stress fractures include navicular, anterior tibial (diagnosed by the "dreaded black line" on lateral radiograph), and femoral neck stress fractures (Fig. 29-5). Athletes with a confirmed or suspected high-risk stress fracture should be made non-weight bearing and referred to a sports medicine or orthopedic specialist.

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