Introduction
Evidence & Methods
Additional compression fractures following vertebroplasty or kyphoplasty commonly occur. Some of these may be treated with vertebral augmentation. This article assesses possible risk factors that may predict augmentation procedures.
The authors found that 22% of patients had additional compression fractures that were treated with kyphoplasty. Steroid use was found to be a risk, but other common sources of osteoporosis were not.
The fact that nearly a quarter of the patients had additional procedures is an important benchmark. Other questions remain: how many patients had additional fractures that were not treated with kyphoplasty? Would a baseline bone mineral density assessment have been the greatest determinant of risk? Was the study underpowered to detect minor predictors? And what impact did surgical decision making (choosing or being told to undergo kyphoplasty) have on the observed future events?
—The Editors
Vertebral compression fractures (VCFs) are estimated to affect 44 million Americans each year with an annual health-care cost of 440 million dollars [1], [2]. The morbidity of VCFs is well documented and includes back pain, decreased ambulation, prolonged bed rest, decreased pulmonary function, and decreased ability to live independently [2], [3]. Risk factors for VCFs include steroid use, prior VCF, smoking, female gender, and local kyphosis [4], [5], [6].
Several reports have shown that patients with symptomatic VCFs can benefit with respect to pain relief and functional improvement with minimally invasive procedures such as kyphoplasty [7], [8]. However, up to 50% of patients can experience further VCFs, usually at levels adjacent to prior fractures [9], [10].
To date, no study has adequately evaluated the prevalence of additional symptomatic VCFs in a large cohort of patients after kyphoplasty procedures. Furthermore, there is limited documentation about important risk factors, such as the specific vertebral levels involved or correlation with the sagittal spinal alignment in patients who develop additional VCFs after kyphoplasty.
Our hypothesis is that medications that decrease the strength of the vertebral body or residual sagittal spinal malalignment (thoracic kyphosis and/or loss of lumbar lordosis) would predispose patients to additional symptomatic VCFs. Other factors, such as bisphosphonate use, are hypothesized to be negative risk factors for additional symptomatic VCFs. This study sought to assess the impact of these predictive factors on the rate of additional VCFs in a large population of patients undergoing kyphoplasty for their initial fracture.