Obesity, defined as a body mass index greater than 30, is associated with symptomatic low back pain, anatomical changes of the functional spinal unit, increased failure of therapeutic interventions, and increased complications related to surgical intervention.
Acute low back pain is more common than chronic, progressive low back pain that interferes with functional capacities. The latter condition is associated with risk factors that are nonmodifiable, such as age and genetic endowment, and modifiable, including tobacco use, some forms of physical activity and obesity.
Biomechanical Stress and Spinal Degeneration
The relationship between obesity and chronic, progressive low back pain is
at least in part explained by the biomechanical stresses that truncal obesity
places on the lower thoracic and lumbar spine. The weight-bearing load on
the spinal column is a function of the mass of the torso as well as of the
geometric configuration of the torso. Upright, healthy individuals carry
the weight of the torso through the spine to the pelvis, and the torso’s
center of gravity lies anterior to the spine, creating a moment arm that
multiplies the forces experienced by the spine in neutral posture. When the
weight of the torso increases and the torso expands, there is a corresponding
increase in the forces related to increased axial loading of the spine and
progressive migration of the center of gravity farther anterior to the spine.
When spinal posture is altered such that the thorax is anterior to the pelvis
or lateral to the pelvis, the spine is out of its neutral position, and the
forces experienced by the low back increase dramatically. Both the increased
weight and the abnormal geometric distribution of the weight characteristic
of truncal obesity increase the forces experienced by the spine.
In everyday life, activities such as reaching, leaning, postural adjustments and lifting are associated with the torso moving out of its neutral posture and cycling large loads through the lower spine. It is reasonable to assume that these loads cycle through the spine up to several hundred times an hour during normal routine activities of daily living. For those with truncal obesity the effects of the greater loads placed on the spine are cumulative and influenced by lifestyle activity.
Although the gross anatomical and histological changes associated with degenerative change of the lumbar spine are well known, biomolecular and cellular-level events underpinning the process are the subject of ongoing investigation. The connection remains unclear between observed pathological anatomy and the abnormal physiology in obese patients with chronic accentuated loads on the spine. In an interesting study comparing MRI findings of degenerative disc disease and occurrence of an arginine-to-tryptophan change in the COL9A3 gene (Trp 3 allele), Solovieva and colleagues demonstrated that the effect of obesity on lumbar degeneration is modified by the collagen IX gene polymorphism. In this study the incidence of MRI-defined lumbar degeneration in persistently obese people was increased in those with the Trp 3 allele.
Obesity has been demonstrated to be an independent risk factor for premature multisegmental spondylosis. Radiographic changes include phenotypic MRI markers of decreased disc space height and disc bulging into the spinal canal. In a compelling study, Sambrook and colleagues evaluated these markers in 326 pairs of twins. The heritability estimate was 74 percent, with a confidence interval of 95 percent, for lumbar degenerative disease, regardless of obesity status. However, environmental factors such as activity and obesity influenced observed variation in MRI disc signal. Whatever the biomolecular and cellular events may be that underlie these premature anatomical changes in obese people, it appears that a positive feedback cycle is initiated whereby an anatomically abnormal spine is increasingly susceptible to excessive weight loads, thus accelerating the evolution of low-back pain syndrome.
Once established, the anatomical changes associated with obesity are not thought to be spontaneously reversible. Weight reduction often will reduce discomfort in obese patients for whom diagnostic studies demonstrate degenerative spondylosis in the lumbar region. Treatments, including physical therapy, chiropractic manipulation, epidural steroids and analgesics, have a higher failure rate in obese patients compared to nonobese patients.
Surgical Complications
Spine surgery intended to relieve low back pain has been noted to have an increased
failure rate for obese patients with a BMI greater than 40. Complications
include increased likelihood of postoperative wound infection, pneumonia,
deep vein thrombosis and additional surgery for events such as recurrent
disc herniation. Patel and colleagues found a correlation between increasing
BMI and the incidence of complications in lumbar fusion surgeries. Other
case series of spine surgery in obese patients have failed to demonstrate
an increased risk of complications and report more favorable experiences.
The efficacy of lumbar surgical intervention in patients with elevated BMI
seems to vary with the type of surgery (decompression or fusion) and the
indication (radiculopathy or midline low back pain). Perioperative complications
of lumbar surgery for these patients most consistently include wound healing
disorders.
Preliminary experience describing minimally invasive surgery, MIS, in patients with elevated BMI is promising with regard to efficacy and complications. Rosen and colleagues prospectively collected data on 108 patients undergoing minimally invasive transformational lumbar interbody fusion and showed no difference in outcome between obese and normal weight patients. Park and colleagues demonstrated no difference in complications related to BMI in a series of 77 patients undergoing minimally invasive discectomy, laminectomy and fusion.
The equalizing effect of MIS on complications in obese people seems to be related to the minimization of soft tissue disruption and the small but precisely guided trajectories employed. The difficulty with intraoperative fluoroscopic imaging of morbidly obese patients reported in open surgical series is not apparent with the fluoroscopic-based docking used in MIS techniques, perhaps representing advances in equipment technology. The ability of MIS to neutralize efficacy disparities especially in fusions is difficult to explain, but may relate to rapid mobilization with diminished perioperative pain.
Patient Management
Regardless of surgical intervention, the management of obese patients who have
progressive, debilitating low back pain should include an effort to educate
them about the relationship between obesity and the etiology of disabling
low back pain. Minimal weight-bearing exercise, especially aquatic-based
activity, is fundamental in their treatment. Oftentimes, use of a lightweight
lumbar orthosis during periods of heavy activity can help avoid repetitive
cycling of loads through the low back. For some morbidly obese patients,
aggressive weight loss should be undertaken, including dietary regimens,
nutritional therapy consultations and consideration for bariatric surgery.
Ideally, obese patients will commit to lifestyle changes, including significant
weight loss, as part of an overall care plan that may include surgery.
Patrick W. McCormick MD, FACS, MBA, associate editor of the AANS Neurosurgeon, is a partner in Neurosurgical Network Inc., Toledo, Ohio. The author reported no conflicts for disclosure.
For Further Information
- Park P, Upadhyaya C, Garton HJ, Foley KT: The impact of minimally invasive spine surgery on perioperative complications in overweight or obese patients. Neurosurgery 62:693-699, 2008
- Patel N, Bagan B, Vadera S, Maltenfort MG, Deutsch H, Vaccaro AR, et al.: Obesity and spine surgery: relation to perioperative complications. J Neurosurg Spine 6:291-297, 2007
- Sambrook PN, MacGregor AJ, Spector TD: Genetic influences on cervical and lumbar disc degeneration: a magnetic resonance imaging study in twins. Arthritis Rheum 42:366-372, 1999
- Solovieva S, Lohiniva J, Leino-Arjas P, Raininko R, Luoma K, Ala-Kokko L, Riihimaki H: COL9A3 gene polymorphism and obesity in intervertebral disc degeneration of the lumbar spine: evidence of gene-environment interaction. Spine 27:2691-2696, 2002