Monday, 4 March 2019

Acquired Spondylosis following spinal fusion

             Acquired Spondylosis following spinal fusion 

                                         Dr KS Dhillon



Intervertebral Disc and spondylosis

The intervertebral discs are fibrocartilaginous, cylindrical structures which connect adjacent vertebral bodies. The disc consists of a central nucleus pulposus which is surrounded by the annulus fibrosus. The intervertebral discs undergo changes with age leading to degenerative disc disease (DDD) of the spine. The discs loses hydration and elasticity with age.

For the diagnosis of DDD, magnetic resonance imaging (MRI) is the most commonly used imaging modality. The degenerative changes in the disc on MRI imaging can be graded using the Pfirrmann grading system [1]. MRI T2 spin-echo weighted images are used for grading. There are 5 grades of changes in disc degeneration:


  • Grade I, where the disc is homogeneous with bright hyperintense white signal intensity and normal disk height.
  • Grade II, where the disc is inhomogeneous, but the hyperintense white signal nucleus and annulus are clearly differentiated. A gray horizontal band could be present. The disc height is preserved.
  • Grade III, where the disc is inhomogeneous with intermittent gray signal intensity. The distinction between nucleus and annulus is not clear. The disc height is normal or slightly decreased. 
  • Grade IV, where the disc is inhomogeneous with a hypointense dark gray signal intensity. There is no distinction between the nucleus and annulus. The disc height is slightly or moderately decreased.
  • Grade V, where the disc is inhomogeneous with a hypointense black signal intensity. There is no distinction between the nucleus and the annulus. The disc space is markedly narrow.

As the disc space narrows the facets override and this increases motion at that spinal segment and further hastens the damage to the disc. Annular fissures and herniation can occur and facet joints undergo hypertrophy.

Marginal osteophytes begin to develop. These osteophytes stabilize the vertebral bodies adjacent to the level of the degenerating disc and increase the weight-bearing surface of the vertebral endplates. Degeneration of the joint surfaces and hypertrophy of ligaments decreases motion and this acts as a limiting mechanism against further deterioration. Degeneration of the disc and facet joints, hypertrophy of ligaments and formation of osteophytes defines the spectra of spinal spondylosis.

Acquired spondylolysis after spinal fusion

Spinal fusion, also know as spondylodesis or spondylosyndesis, is a surgical procedure where two or more vertebral segments are joined together or fused so that no movement occurs between the fused segments.

Spinal fusion is usually carried out for spinal instability. The spine can be divided into three columns namely anterior, middle, and posterior columns [2]. Generally, two of three columns must be anatomically intact for functional stability. Instrumentation is usually necessary if more than one column of the spine is disrupted.The instability may be from birth as in spondylolisthesis or acquired due to trauma or from tuberculosis, metabolic, degenerative or neoplastic disorders of the spine and sometimes from iatrogenic causes.

Most spinal segmental fusions are carried out using instrumentation such as plates for anterior spinal fusions and pedicular screws with rods for posterior fusions. The instrumentation immobilizes the segments allowing for bony growth and a successful fusion.

The long-term sequelae of spinal fusion, despite its frequent success, is that there is a loss of mobility at the fused segments and this places increased stresses on adjacent segments of the vertebral column. There is an increase in motion in the adjacent segment after spinal fusion or spinal instrumentation as compared to the normal state and the increase is more in two level fusion as compared to a one level fusion [3]. These increased stresses can increase the likelihood of degenerative changes, ligamentous instability, and even stress fracture at the mobile adjacent segments.

The adjacent segment pathology or abnormality has been classified into two categories by Hilibrand and Robbins [4], the first being "adjacent segment degeneration" and other "adjacent segment disease". Radiographic changes in the adjacent segment to the fusion without symptoms is called "adjacent segment degeneration" and radiographic changes with clinical symptoms is known as "adjacent segment disease".

Some are of the opinion that the term "adjacent segment degeneration or disease" is ambiguous and Riew et al. [5] proposed the term "adjacent segment pathology" (ASP), which includes any change that occurs adjacent to a previously operated level. They further subdivided ASP into asymptomatic "radiographic ASP" (RASP) and symptomatic "clinical ASP" (CASP). Adjacent segment changes may be seen at one or even two level.

Park et al [6] did a literature review to study the definition, etiology, incidence, and risk factors associated with adjacent segment disease. They found that the most common abnormal finding at the adjacent segment was  disc degeneration. Increased intradiscal pressure, increased facet loading, and increased mobility at the adjacent segment after fusion leads to biochemical changes which cause adjacent segment disease. Age is also a major contributor to progressive spinal degeneration. At a follow up ranging from 36 to 369 months after fusion the incidence of radiographic changes at the adjacent disc varies from 5.2% to 100%. The incidence of symptomatic adjacent segment disease, however, is much lower, ranging from 5.2 to 18.5% at 44.8 to 164 months follow-up. They also found that the incidence of symptomatic disease was higher in patients with transpedicular instrumentation (range between 12.2-18.5%) as compared to other forms of instrumentation or with no instrumentation (range between 5.2-5.6%). They found that the potential risk factors were the type of instrumentation used, the fusion length, sagittal malalignment, facet injury during surgery, age, and pre-existing degenerative changes.

Radiographic asymptomatic adjacent segment disease though common, it however, does not correlate with functional outcomes.

Harrop et al [7] in a review of 27 studies found that the incidence of RASP ranged from 8% to 100% and the incidence of CASP ranged from 0% to 27.5%. This result suggests that radiographic degenerative changes at adjacent segments are common; however, clinical symptoms are less likely to be manifested. The incidence of revision surgery for ASP is low at between 0.74% to 15% [7,8].
Booth et al. [9] on the other hand reported that although radiological degenerative change were common 5 years after lumbar vertebral fusion;  there were no cases with symptom. Several other authors also noted that there was no correlation between radiological change and clinical symptoms [ 10,11,12,13].

Soh et al [14] found that on more than 5 years follow up of patients with   pedicle screw fixation and fusion, the patients’ gender, age, residential area, fusion method, the number of fusion segments, and the degree of preoperative adjacent disc degeneration on MRI showed no significant relationship with the postoperative degenerative change at the adjacent segments. They, however, found that there was a significantly positive correlation between the fusion segment lordotic angle per level and the postoperative degenerative change. Restoration of the fusion segment lordotic angle per level to >15° reduced the incidence of degenerative change at the adjacent segments.

Conclusion

The long-term sequelae of spinal fusion is that there is a loss of mobility at the fused segments and this places increased stresses on adjacent segments of the vertebral column. This increased stresses lead to degenerative changes in the adjacent mobile segments. These changes are usually known as adjacent segment pathology (ASP). If the patient is asymptomatic it is referred to as radiographic ASP (RASP) and if symptomatic it is known as clinical ASP (CASP).

The incidence of RASP ranges from 8% to 100% and the incidence of CASP ranges from 0% to 27.5%. Some authors report that there is no correlation between radiographic changes and clinical symptoms. The incidence of revision surgery for ASP is low at between 0.74% to 15%.
There are conflicting reports regarding the risk factors for ASP. Adjacent segment degeneration can also occur due to aging irrespective of the presence or absence of spinal fusion.


References


  1. Pfirrmann CW, Metzdorf A, Zanetti M et-al. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine. 2001;26 (17): 1873-8.
  2. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine 1983;8:817– 831.
  3. Brooker et al. Segmental biomechanics after single and multi-level lumbar spine fusion. 27th Annual Scientific Meeting of the Spine Society of Australia, 8-10 April 2016, Melbourne, Vic.
  4. Hilibrand AS, Robbins M. Adjacent segment degeneration and adjacent segment disease: the consequences of spinal fusion? Spine J. 2004;4(6 Suppl):190S–194S.
  5. Riew KD, Norvell DC, Chapman JR, Skelly AC, Dettori JR. Introduction/Summary statement: adjacent segment pathology. Spine (Phila Pa 1976) 2012;37(22 Suppl):S1–S7.
  6. Park P, Garton HJ, Gala VC, Hoff JT, McGillicuddy JE. Adjacent segment disease after lumbar or lumbosacral fusion: review of the literature. Spine (Phila Pa 1976). 2004 Sep 1;29(17):1938-44.
  7. Lee JC, Kim Y, Soh JW, Shin BJ. Risk factors of adjacent segment disease requiring surgery after lumbar spinal fusion: comparison of posterior lumbar interbody fusion and posterolateral fusion. Spine (Phila Pa 1976) 2014;39:E339–E345.
  8. Liang J, Dong Y, Zhao H. Risk factors for predicting symptomatic adjacent segment degeneration requiring surgery in patients after posterior lumbar fusion. J Orthop Surg Res. 2014;9:97. Published 2014 Oct 12. doi:10.1186/s13018-014-0097-0
  9. Booth KC, Bridwell KH, Eisenberg BA, Baldus CR, Lenke LG. Minimum 5-year results of degenerative spondylolisthesis treated with decompression and instrumented posterior fusion. Spine (Phila Pa 1976) 1999;24:1721–1727.
  10. Rahm MD, Hall BB. Adjacent-segment degeneration after lumbar fusion with instrumentation: a retrospective study. J Spinal Disord. 1996;9:392–400.
  11. Etebar S, Cahill DW. Risk factors for adjacent-segment failure following lumbar fixation with rigid instrumentation for degenerative instability. J Neurosurg. 1999;90:163–169.
  12. Cho JL, Park YS, Han JH, Lee CH, Roh WI. The changes of adjacent segments after spinal fusion: follow-up more than three years after spinal fusion. J Korean Soc Spine Surg. 1998;5:239–246.
  13. Ghiselli G, Wang JC, Bhatia NN, Hsu WK, Dawson EG. Adjacent segment degeneration in the lumbar spine. J Bone Joint Surg Am. 2004;86:1497–1503.
  14. Soh J, Lee JC, Shin BJ. Analysis of risk factors for adjacent segment degeneration occurring more than 5 years after fusion with pedicle screw fixation for degenerative lumbar spine. Asian Spine J. 2013;7(4):273-81.


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