Sunday, July 19, 2009
I've been fortunate enough to spend time with a great triathlete and good friend, Kate Bevilaqua the past few months. Fortunate for those of us in Boise, she chose to spend the Northern Hemisphere summer training here. The past several months have been filled with some unfortunate injuries, the most recent a inferior pubic rami stress fracture. With her permission, I've loaded her most recent x-ray on the bottom (right side, bottom of the "O ring" in the pelvis). Recently, I was forwarded another pro triathletes x-ray with a femoral neck stress fracture (upper xray...note the lucency in the superior part of the bone between the ball and the hip). I thought it might be worthwhile discussing the basics of stress fractures. In upcoming posts I will delve a bit further into more detail in the training aspects when returning from healing fractures. The bulk of this article was recently posted on Endurance Corner's Feature article at www.xtri.com.
Stress fractures are the result of repetitive biomechanical stress to bones which do not recover from that stress. Anyone may develop a stress fracture so long as the involved level of activity produces stress greater than the bone’s ability to resist it. The fracture occurs when repetitive activities produce nonpainful microfractures of bone trabeculi. If the collective stresses remains below a specific threshold (different for each individual) or if the athlete rests between episodes of stress, the microfractures will heal. On the other hand, if the athlete continues the offending activity the microfractures will increase to the point that pain will occur with activity. This is the first symptom of a stress fracture in most individuals, although some athletes may limp without complaining of pain. If the athlete heeds the pain and reduces the stress at this point, the fracture should heal without other treatment. If the athlete continues with the activity, the stress fracture will become more evident clinically and radiographically.
There are conditions that mimic stress fractures. Some conditions are the result of overuse, such as tendinitis or periostitis (inflammation of the periosteum surrounding the bone) and cause similar symptoms. In fact, these condition are likely an earlier finding along the continuum of overuse injury that leads to a stress fracture. Stress reactions, the term used to distinguish the earliest such findings, are accelerated remodeling with bone marrow or soft tissue inflammatory changes.
Rarely bone lesions can cause similar pain. The most common of these rare lesions is benign condition called an osteoid osteoma. The pain of an osteoid osteoma usually does not increase with activity, however. It will cause pain at times of both activity and inactivity, especially at night. Both lesions will produce periosteal reactive bone and cortical thickening. Even more rarely, certain malignant lesions can cause bone pain. Also rare, an area of subacute or chronic bone infection may simulate a stress fracture.
The diagnosis of a stress fracture can generally be made by the history of progressive pain following increasing training loads, accompanied by point tenderness of the affected bone at the point of the stress fracture. Stress fractures may present for diagnosis and treatment before the plain x-rays are abnormal, because radiographic changes frequently lag behind clinical symptoms by weeks. In individuals with symptoms of a stress fracture with normal radiographs, a bone scan or MRI will confirm the diagnosis. The longer the patient is symptomatic, the more evident the fracture becomes.
Some people more prone to the development of a stress fracture than others. Since stress fractures are the result of excessive stress, and abnormally angulated bones or extremities result in increased stresses delivered to bone, abnormal limb alignment increases the chance of development of a stress fracture. For example, an athlete with a varus deformity of the hindfoot (opposite of a flat foot) will place more stress than normal on the base of the fifth metatarsal, which may result in the development of a stress fracture of the proximal diaphysis of the fifth metatarsal (Jones fracture). Limb length discrepancies are likely risk factors as well. Hormonal abnormalities, specifically in females, increase the risk of stress fractures as well. Though beyond the scope of this article, new information suggests that ammenorrhea, when coupled with chronic energy deficit as the result of inadequate caloric intake and increased exercise, result in an increased combined risk of fracture.
Stress fractures in running athletes occur most commonly in the bones of the lower leg and foot. Their most common location is in the posterior medial aspect of the proximal tibia, but the 2nd metatarsal is also frequently seen. However, fractures of the spine, pelvis, hip, femur, tibia and foot have been reported. Though not well-documented, the location of stress fractures in triathletes is similar to runners, albeit, it seems to occur with a lower incidence.
The treatment of stress fractures is based upon by classifying them as either high-risk or low-risk for complicated outcomes. High-risk stress fractures occur in the superolateral femoral neck, anterior tibial shaft, tarsal navicular, proximal fifth metatarsal, and talar neck. These require immediate attention and often surgery.
Examples of low-risk stress fractures occur in the lateral malleolus, calcaneus, 2nd through 4th metatarsals, and the femoral shaft. The reason to differentiate the two is that the undertreatment of high-risk stress fractures can lead to completion of the fractures with disastrous outcomes. On the other hand, overtreatment of low-risk stress fractures can result in unnecessary deconditioning, prolonged immobilization, and subsequent increased fracture risk.
Daily supplementation with 2,000 Mg of calcium and 800 IU of vitamin D has been shown to decrease the risk of new stress fractures. This should certainly be entertained by those new to the sport or anticipating an increase in training load. If ammenorrheic, your physician will likely recommend an oral contraceptive to normalize hormone levels.
The return to regular training is highly individualized to both athlete and fracture location, but commonly takes 8-12 weeks at minimum. This return to activity should be closely monitored by a physician familiar with endurance sports medicine.
Best of luck with your summer training,