Session VI - Geriatric Trauma

Accelerated Bone Mineral Loss following a Hip Fracture: A Prospective Longitudinal Study

Douglas R. Dirschl, MD, Richard C. Henderson, MD, PhD, Ward C. Oakley, MD

University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA

Purpose: One risk factor for sustaining a hip fracture is a history of a previous fracture; the risk of sustaining a contralateral hip fracture has been estimated to be 20 times that of the first fracture. It is often assumed that immobility following the initial hip fracture will result in additional loss of bone mineral, contributing to the increased risk of subsequent fractures. Thus, it is a basic tenet to mobilize the elderly patient following treatment of a hip fracture, in part to preserve bone mineral. The purpose of this prospective study was to monitor the bone mineral density (BMD) of the lumbar spine and contralateral femoral neck in the first year following an osteoporosis-related fracture of the hip and to correlate the rate of loss of BMD with ambulatory ability, as well as other pre- and post-injury variables. A major goal of the study is to identify those patients most at risk for accelerated bone loss following a hip fracture.

Methods: Eighty-three elderly patients (mean age 77 years) who had sustained a hip fracture had determination of BMD made at the time of fracture; forty-nine of these patients were available for repeat assessment of BMD 1 year later. BMD was assessed using dual energy x-ray absorptiometry (DEXA). A detailed clinical and laboratory assessment was performed at the time of fracture and at one year following fracture. Data collected included level of physical/ ambulatory activity, mental status, average daily dietary calcium intake, serum levels of 25-hydroxy and 1,25-dihydroxy vitamin D, and routine serum chemistries. Sixteen patient died during the study period, a mortality rate of 19%, and 18 patients did not complete the follow-up assessment at one year after fracture. The change in BMD in the year following a hip fracture was calculated both as percentage loss and absolute loss (gm/sq cm), and was correlated with the pre- and post-injury variables.

Results: In the year following a hip fracture, BMD decreased a mean of 5.4 ± 1.5% (mean ± SE) in the contralateral femoral neck and 2.4 ± 0.7% in the lumbar spine. These losses were independent of age and sex. Calcium intake correlated with the loss of BMD from the femoral neck (p=0.015), but not the lumbar spine. Patients with daily calcium intakes of less than 500 mg/d (32% of patients) had a more than 10% decrease in femoral neck BMD in the year following their hip fracture. Serum 1,25-dihydroxy vitamin D level correlated with loss of BMD from the lumbar spine (p=0.001), but not from the femoral neck. Loss of BMD from either site showed no correlation with 25-hydroxy vitamin D level. The patients' ambulatory ability did not correlate with loss of bone mineral from either the femoral neck or lumbar spine. The mean change in BMD at the femoral neck in community ambulators was -4.6%, while it was -4.9% in nonambulators. There was no correlation between the loss of bone mineral from either measurement site and the patients' mental status. There was no difference in results when change in BMD was expressed as percentage loss or as absolute loss.

Discussion: The results of this study can be compared to numerous investigations which used DEXA to examine loss of bone mineral from the proximal femur in ambulatory postmenopausal women who had not sustained a hip fracture. The reported rates of loss in those studies ranged from 0.7- 1.0% per year, less than one-fifth that found in the present study of patients who had sustained a hip fracture. The rate of loss of bone mineral in patients returning to full community ambulation was no different than in patients who remained nonambulatory following fracture. This finding has not been previously reported, but seems to indicate that aggressive efforts at and large expenditures of money for rehabilitation, although effective in reducing some post-fracture complications, are not effective in blunting the accelerated rate of loss of bone mineral following a hip fracture. Dietary calcium intake is strongly correlated with the rate of loss of bone mineral from the femoral neck; this finding supports previous investigations of the effects of dietary calcium intake on BMD in the elderly and underscores the importance of adequate dietary intake of calcium in this population. The importance of adequate levels of 1,25-dihydroxy vitamin D to the maintenance of BMD is well known, and the results of this study are consistent with those of previous investigations.

Conclusions: The results of this study indicate that there is an accelerated rate of loss of bone mineral in the year following a hip fracture, particularly from the contralateral proximal femur, and that this loss is independent of the patients ability to return to full community ambulation. The loss of BMD from the femoral neck in the year following a hip fracture is more that 5 times that reported in the non-fractured elderly population. The potential clinical significance of this finding is tremendous in an osteopenic population that can ill afford further loss of bone mineral. Accelerated loss of bone mineral in the year following a hip fracture is likely to contribute to the high incidence of a second hip fracture. Pharmacologic agents, such as the bisphosphonates, are available which have the potential to diminish bone mineral loss after a hip fracture. Prospective, randomized trials to assess interventions targeted at this critical time period are certainly warranted.