Secondary Logo

Journal Logo

Predicting the Risk of Adjacent Segment Pathology After Lumbar Fusion: A Systematic Review

Lawrence, Brandon D., MD*; Wang, Jeff, MD; Arnold, Paul M., MD, FACS; Hermsmeyer, Jeff, BS§; Norvell, Daniel C., PhD§; Brodke, Darrel S., MD*

doi: 10.1097/BRS.0b013e31826d60d8
Adjacent Segment Pathology of the Thoracolumbar Spine
Free
SDC

Study Design. Systematic review.

Objective. To perform a systematic review to define the incidence of clinical adjacent segment pathology (CASP) after lumbar fusion surgery and define potential risk factors for the development of CASP.

Summary of Background Data. Concerns for the longevity of current arthrodesis constructs and the effects of arthrodesis on adjacent segments have received increasing attention during the past decade. There is a lack of precision regarding the terminology used to describe the pathologies of adjacent segment disease. The term ASP is proposed as an umbrella term to refer to the breadth of clinical and/or radiographical changes at adjacent motion segments that developed subsequent to a previous spinal intervention.

Methods. A systematic search was performed in Medline and the Cochrane Collaboration Library for literature published through January 2012. Level of evidence ratings were assigned to each article independently by 2 reviewers. Extracted were the percentage risks of CASP during 5- and 10-year time periods, risk factors, the effect estimates (relative risks and odds ratios), and corresponding confidence intervals reported from each study's multivariate analyses. Forest plots of odds ratios or relative risks with their 95% confidence intervals evaluating patient, disease, and surical risk factors were constructed using the data provided by the individual studies.

Results. We identified 162 total citations from our literature search. Of these, 31 full- text articles were evaluated for meeting inclusion criteria. From these 31 studies, 5 studies met inclusion criteria. The mean patient ages ranged from 50 to 64 years. The mean annual incidence of CASP ranged from 0.6% to 3.9%. With respect to patient factors, age more than 60 years was associated with an increased risk of developing CASP. Other factors that may increase the risk of developing CASP are pre-existing facet degeneration, degenerative disc disease, performing a multilevel fusion, stopping a construct at L5, performing a laminectomy adjacent to a fusion, and excessive disc height distraction during posterior interbody fusion.

Conclusion. This systematic review was limited to higher-quality studies that evaluated risk factors using multivariate analyses. Identified were key patient, disease, surgical, and radiographical factors that may be considered when counseling and treating patients with degenerative conditions. Further high-quality studies are required before any concrete conclusions can be made about this controversial topic.

Consensus Statements 
  1. The risk of developing CASP after lumbar fusion occurs at a mean annual incidence of 0.6% to 3.9%.
  2. Strength of Statement: Strong
  3. Patients older than 60 years or who have pre-existing facet/disc degeneration may have an increased risk of developing CASP.
  4. Strength of Statement: Strong
  5. The risk of developing CASP may be greater after multilevel fusions and fusions adjacent to but not including the L5–S1 level, and may increase when performing a laminectomy adjacent to a fusion.
  6. Strength of Statement: Strong

A systematic review was performed focusing on clinical adjacent segment pathology (CASP) with 5 articles meeting inclusion criteria. The most important factor predisposing a patient to the development of CASP is age more than 60 years. Other possible factors include pre-existing facet degeneration and/or degenerative disc disease, multilevel fusion, stopping a construct at L5, performing a laminectomy adjacent to a fusion, and excessive disc height distraction during posterior interbody fusion.

*Department of Orthopaedics, University of Utah, Salt Lake City, UT

Department of Orthopaedics, University of California, Los Angeles, School of Medicine

Department of Neurosurgery, University of Kansas, Kansas City, KS

§Spectrum Research, Inc, Tacoma, WA.

Address correspondence and reprint requests to Brandon D. Lawrence, MD, Department of Orthopaedics, University of Utah, 590 Wakara Way, Salt Lake City, UT 84108; E-mail: Brandon.lawrence@hsc.utah.edu

Acknowledgment date: April 30, 2012. First revision date: June 18, 2012. Second revision date: August 1, 2012. Acceptance date: August 2, 2012.

The device(s)/drug(s) is/are FDA-approved or approved by corresponding national agency for this indication.

Supported by AOSpine North America, Inc. Analytic support for this work was provided by Spectrum Research, Inc., with funding from the AOSpine North America.

One or more of the author(s) has/have received or will receive benefits for personal or professional use from a commercial party related directly or indirectly to the subject of this manuscript: for example, honoraria, gifts, consultancies, royalties, stocks, stock options, decision making position.

The concept of spinal arthrodesis was first introduced 100 years ago for the treatment of Pott disease.1 Since that time, fusion technologies have dramatically advanced, and indications for vertebral fusion in the cervical, thoracic, and lumbosacral spine have been expanded. Given the early reported success rates of spinal arthrodesis, the implications on adjacent segments were largely ignored. During the past the last several decades, the indications for spinal arthrodesis have expanded and with that trend some of the outcomes and success rates after spinal arthrodesis have been questioned. Specifically, utilizing spinal arthrodesis for treatment of degenerative disc disease in patients with axially based symptoms alone has been called into question by some. As spinal fusion techniques and indications have evolved, alternatives to spinal arthrodesis have been developed (total disc arthroplasty, facet replacement, etc.); in parallel, the concerns for the longevity of current arthrodesis constructs have arisen and the concern of adjacent level degeneration have come to the fore.

There is a lack of precision regarding the terminology used to describe the pathologies of adjacent segment degeneration. The term adjacent segment pathology (ASP) is proposed as an umbrella term to refer to the breadth of clinical and/or radiographical changes at adjacent motion segments that developed subsequent to a previous spinal intervention. Under this umbrella, radiographical ASP (RASP) and clinical ASP (CASP) are then used to categorize radiographical features (e.g., degenerative changes on imaging studies) and clinical manifestations (e.g., pain, radiculopathy and/or myelopathy), respectively, that were formerly referred to as adjacent segment degeneration and adjacent segment disease. For the purposes of this review, we will evaluate CASP only.

Several review articles and level III or IV studies have been published reporting the risk and risk factors for ASP.327 Park et al22 summarized 22 individual studies that reported the risk of both RASP and CASP after lumbar fusion. They reported the risk of RASP and CASP ranging from 8% to 100% and 5.2% to 18.5%, respectively. Potential risk factors included posterior lumbar interbody fusion, injury to the adjacent facet joint, fusion length, sagittal alignment, pre-existing adjacent degenerative discs, lumbar stenosis, age, osteoporosis, female sex, and postmenopausal state. However, there were no effect estimates reported, which limits the reader's ability to estimate the relative magnitude of having a specific risk factor (e.g., >60 yr of age) versus not having the risk factor (e.g., ≤60 yr of age). The authors appropriately state that the actual significance of these risk factors remains uncertain due to the retrospective nature of the studies, differences in methodologies, patient populations, and definitions of ASP. Furthermore, these studies did not control for multiple risk factors. There are in fact several potential factors that may seem significant in a one-to-one correlation with ASP (bivariate analysis); however, when included in a multivariate model with other significant factors, they may no longer be significant. The primary reason that prognostic studies fail to achieve a level I or II classification is the lack of control of other factors that may also be associated with the outcome. That is, since these articles are typically observational studies (rather than randomized trials), bivariate associations that do not control for other important factors can lead to confounding. Confounding bias may mislead the clinician to think a patient may be at greater risk of a poor outcome due to the existence of a factor that is spurious. Levels I and II prognostic studies account for other factors through multiple regression or other appropriate statistical techniques.

For the purposes of this review, we will focus on CASP and attempt to elucidate factors that may play a role in CASP development after short lumbar fusion (≤4 levels) in prognostic studies that provide effect estimates (e.g., relative risks [RRs]) and control for multiple risk factors. The development of ASP after longer thoracolumbar fusions including both proximal and distal pathologies is discussed in a separate article in this focus issue. By focusing on spinal arthrodesis, the most commonly reported treatment in the literature associated with ASP, we effectively control for treatment while estimating the effects of each important risk factor. This systematic review will attempt to break down potential prognostic risk factors for CASP into 4 different categories: patient, disease, surgical, and radiographical factors. The primary goal of this review is to perform an evidence synthesis of the levels I and II prognostic literature to identify risk factors for the development of CASP after lumbar fusion. The following key questions will be addressed: (1) What is the estimated risk of CASP after lumbar fusion over a 5- and 10-year period?; and (2) Among patients undergoing lumbar fusion, are there patient, disease, surgical, and radiographical factors associated with an increased risk of CASP? If so, what is the increased risk?

Back to Top | Article Outline

MATERIALS AND METHODS

We conducted a systematic search in Medline and the Cochrane Collaboration Library for literature published through January 2012. The search results were limited to human studies published in the English language. Reference lists of key articles were also systematically checked to identify additional eligible articles. We included studies evaluating adult patients who have had lumbar fusion surgery of 4 or fewer levels for degenerative disc disease, degenerative lumbar scoliosis, degenerative spondylolisthesis, kyphosis, and lumbar radiculopathy (Table 1). Our goal was to identify level I or II prognostic studies. Specifically, we wanted to include studies that were of the highest quality, including prospective studies (or well-designed retrospective studies), with high follow-up rates, a long-enough follow-up to establish ASP risk, and multivariate methods such as logistic or Cox regression to account for multiple risk factors and provide effect estimates (e.g., RRs and odds ratios [ORs]). If we were able to identify an adequate number of studies evaluating clinically important prognostic factors, we stopped because these methods set this review apart from previous reviews. If level I or II studies were not available, we sought to include level III studies published since the review by Park et al22 that included a multivariate analysis. We were interested in the following prognostic categories: patient, disease, surgical, and radiographical factors (Table 1). We were interested only in studies reporting on CASP. Exclusion criteria from our study included pediatric patients and those patients with infection, tumor, or trauma. We also excluded studies that did not report ASP as an outcome, but reported outcomes such as range of motion, kinematic measures, disc height, and lordosis/angle changes at adjacent levels. If studies were therapeutic only or consisted of an N < 10, they were also excluded. Other studies excluded were animal, cadaver, and biomechanical studies.

TABLE 1

TABLE 1

Back to Top | Article Outline

Data Extraction

From the included articles, the following data were extracted: study design and study purpose; patient demographics; inclusion and exclusion criteria; follow-up duration and the rate of follow-up for each treatment group; treatment interventions; and definition of ASP. We reported the risks (%) of CASP during 5- and 10-year time periods from those studies that performed an analysis using person time in the denominator (e.g., survival analysis). We also reported the effect estimates (RRs and ORs) and corresponding confidence intervals (CIs) reported from each study's multivariate analyses.

Back to Top | Article Outline

Study Quality and Overall Strength of Body of Literature

Level-of-evidence ratings were assigned to each article independently by two reviewers (J.T.H, D.C.N.) using criteria set by the Journal of Bone & Joint Surgery, American Volume,8 for therapeutic studies, and modified to delineate criteria associated with methodological quality described elsewhere.28 (See Supplemental Digital Material, Supplemental Digital Content 1, available at http://links.lww.com/BRS/A705, for individual study ratings.)

The overall body of evidence with respect to each key question was determined on the basis of precepts outlined by the Grades of Recommendation Assessment, Development, and Evaluation working group10 and recommendations made by the Agency for Healthcare Research and Quality.11 Risk of bias was evaluated during the individual study evaluation described earlier in the section “Study Quality.” This system, which derives a strength-of-evidence grade of “High,” “Moderate,” “Low,” or “Insufficient” for each outcome or key question, is described in further detail in the methodology article in this focus issue.28 A detailed description of how we arrived at the strength of evidence for each key question can be found in the Supplemental Digital Material29–32 (Supplemental Digital Content 1, available at http://links.lww.com/BRS/A705).

Back to Top | Article Outline

Data Analysis

Where the data were available, we reported incidence of CASP from an analysis that included person-time-at-risk in the denominator. For the incidence, we recorded either the annual incidence rate or the risk (cumulative incidence) of developing CASP. The annual incidence rate was defined as the proportion of patients who had been disease free at the start of a given year and had subsequent development of new CASP during that year. Prevalence was defined as the proportion of patients who had been disease free at the time of the index fusion and had subsequent development of new disease at final follow-up, and when CASP was defined in a way that one could recover from the disease (e.g., when CASP was defined as a new radiculopathy or myelopathy). Data were not pooled because we did not have the raw data generating the effect estimates from individual study multivariate analyses. We reported the results of each study's multivariate analysis including RRs, ORs, 95% CIs, and P values for these estimates. When authors reported RRs or ORs less than 1.0, we standardized the reporting of effect sizes so that all ratios were more than 1.0 by taking the inverse of the RR or OR, and reversing the categories or description of the results to keep conclusions consistent. Forest plots for ORs or RRs with their 95% CIs were constructed using the data provided by the individual studies to provide a graphical display illustrating the relative effect of each risk factor. Forest plots were created using Review Manager (Rev-Man, The Nordic Cochrane Centre, The Cochrane Collaboration, Copenhagen, Denmark).

Back to Top | Article Outline

Clinical Recommendations and Consensus Statements

Clinical recommendations or consensus statements were made through a modified Delphi approach by applying the Grades of Recommendation Assessment, Development, and Evaluation/Agency for Healthcare Research and Quality criteria that imparts a deliberate separation between the strength of the evidence (i.e., high, moderate, low, or insufficient) from the strength of the recommendation. When appropriate, recommendations or statements “for” or “against” were given “strong” or “weak” designations based on the quality of the evidence, the balance of benefits/harms, and values and patient preferences. In some instances, costs may have been considered. A thorough description of this process can be found in the methodology article in this focus issue.28

Back to Top | Article Outline

RESULTS

Study Selection

We identified 162 total citations from our literature search. Of these, 131 were excluded by the title/abstract and 31 full-text articles were evaluated for meeting inclusion criteria. From these 31 studies, 26 were excluded that were level of evidence III or IV. None of them provided effect estimates controlling for multiple risk factors. Details of the excluded articles can be found in the Supplemental Digital Material (see Supplemental Digital Content 1, available at http://links.lww.com/BRS/A705). The remaining 5 studies met our inclusion criteria and are summarized in this report (Figure 1). There were 4 retrospective cohorts3336 and 1 case-control study.37 The 4 cohort studies were level of evidence II and the case-control study was level of evidence III; which, however, was a well-conducted case-control study that controlled for multiple risk factors and provided multivariate effect estimates.

Figure 1

Figure 1

The primary diagnoses of the 4 cohort study populations were spondylolisthesis, spinal stenosis, and scoliosis. The patient ages in the 4 studies ranged from 50 to 64 years with male subjects making up 33% to 45% of the study population. Follow-up time ranged from 3 to 10 years. Inclusion criteria were similar across studies. Patients had to be available for final follow-up at least 2 years after index surgery. The majority of patients underwent posterior fusion. All studies included lumbar fusions and the study by Ahn et al33 also included thoracolumbar fusions. ASP was evaluated by using radiographs in the studies by Kaito et al35 and Ahn et al.33 Specifically, Kaito et al35 defined ASP as the appearance of antero- or retrolisthesis more than 3 mm or decrease in disc height more than 3 mm. The studies by Kaito et al35 and Ahn et al33 also monitored neurological impairment. Sears et al36 simply defined ASP as the progressive degeneration of disease to the adjacent levels after fusion. Revision surgeries were performed in the studies by Ahn et al,33 Sears et al,36 and Ghiselli et al34 if there was a presence of RASP or CASP and the patients consented to additional surgery.

In the case-control study by Lee et al,37 the primary diagnoses were spinal stenosis, isthmic and degenerative spondylolisthesis, and lumbar degenerative kyphosis. The mean patient age was 58 years with male subjects making up 36% of the study population. Inclusion criteria included patients older than 35 years with any type of fusion to the lumbar or lumbosacral region. ASP was defined as a condition in which a patient showed the relief of symptoms for at least 6 months after the index operation, the newly developed symptoms were compatible with the lesions in adjacent segments demonstrated in radiological images, and the patient had revision surgery for that problem.

Back to Top | Article Outline

What Is the Risk of CASP After Lumbar Fusion?

Three of the five studies were designed to estimate the annual, 5- and 10-year incidence of CASP after fusion using survival analysis. The study by Ahn et al33 was a retrospective cohort study designed to examine the risk and risk factors of CASP after thoracolumbar fusion. The study included 3188 patients with a mean age of 57 years and various degenerative conditions. Of the 3188 patients, 107 (3.5%) underwent a second procedure for CASP. Using the Kaplan-Meier method, the 5-and 10-year ASP failure rate of adjacent segments was 3% and 6%, respectively. The survival curve was linear suggesting a 0.6% rate of CASP with each year.

The study by Sears et al36 was a retrospective cohort study designed to examine risk factors of CASP after posterior lumbar fusion and to determine the annual incidence and prevalence of further surgery. The study included 1000 procedures in 912 patients, with a mean age of 63 years and various degenerative conditions. Of the 1000 procedures, 130 (13%) underwent a second procedure for CASP. Using the Kaplan-Meier method, the mean annual incidence of CASP during the first 10 years in all patients was 2.5%, with prevalence of CASP failure of 13.6% and 22.2% at 5 and 10 years, respectively.

The study by Ghiselli et al34 was a retrospective cohort study designed to determine the rates of degeneration and survival of the motion segments adjacent to the site of a posterior lumbar fusion. The study included 215 patients with a mean age of 50 years and various degenerative conditions. Of the 215 patients, 59 (27.4%) underwent a second procedure of decompression or fusion for CASP. Postoperatively, new disease at an adjacent level developed at a relatively constant rate of 3.9% per year. Using the Kaplan-Meier method, the 5- and 10-year CASP failure rate of adjacent segments was 16.5% and 26.1%, respectively.

Back to Top | Article Outline

Are There Factors Associated With an Increased Risk of CASP?

Two studies33,36 reported “patient risk factors” from a multivariate model for CASP among patients who had undergone fusion. Results from the multivariate Cox regression revealed age, degenerative disease, multilevel fusion, and sex to be significantly associated with the risk of CASP. Patients older than 61 years were nearly 4 times as likely (OR, 3.9; 95% CI, 2.6–6.0) to develop CASP than those younger than or equal to 60 years during the 10-year period (Table 2 and Figure 2). Sears et al36 reported similar findings to include an increased risk with increasing age categories. Patients were 4 times as likely (OR, 4.0; 95% CI, 1.6–10.0) to develop CASP when comparing those older than 60 years with those younger than 45 years and nearly 2 times as likely (OR, 1.8; 95% CI, 1.1–2.9) when compared with those 45 to 60 years of age during a mean 5-year period (Table 2 and Figure 3). The Ahn et al33 study also found that men were nearly 2 times as likely (OR, 1.8; 95% CI, 1.2–2.6) to develop CASP than women over a 10-year period (Table 2 and Figure 2).

TABLE 2

TABLE 2

Figure 2

Figure 2

Figure 3

Figure 3

Three studies33,35,37 reported “disease risk factors” from a multivariate model for CASP among patients who had undergone fusion. The study by Ahn et al33 reported that patients with degenerative disease (in the superior vertebral body) were nearly 3 times as likely to develop CASP over a 10-year period (Table 2 and Figure 2). The study by Lee et al37 reported patients with disc degeneration in the proximal or distal adjacent segment at the time of index operation were twice as likely (OR, 2.1; P = 0.17); however, this was not statistically significant (Table 2 and Figure 3). In the study by Lee et al,37 the only significant risk factor from the multivariate analysis was the presence of facet degeneration (in the superior vertebral body). Patients were 100 times as likely to experience CASP; however, the confidence interval was very wide (Table 2 and Figure 3). The study by Kaito et al35 also evaluated facet degeneration but did not report a significant association. Lee et al37 and Kaito et al35 used the criteria of Weishaupt to diagnose facet degeneration and Ahn et al33 did not report the method of diagnosis.

Three studies33,34,36 reported surgical risk factors from a multivariate model for CASP among patients who had undergone fusion. Sears et al36 reported 4 independent factors from their Cox regression multivariate model that were associated with CASP (Table 2 and Figure 4). Patients who had a laminectomy in addition to the fusion were more than 2 times as likely (OR, 2.4; 95% CI, 1.1–5.2) to develop CASP during a mean 5-year period. For fusions of the same length, patients with fusion stopping at L5 were nearly 2 times as likely (OR, 1.7; 95% CI, 1.2–2.4) to develop CASP compared with those with fusion to S1. The study by Sears et al36 and the study by Ahn et al33 reported similar results with respect to multilevel fusion, while Ghiselli et al34 reported conflicting results. Sears et al36 reported patients with 3 or 4 levels fused to be 3 times as likely (OR, 3.0; 95% CI, 1.9–4.9) to develop CASP as those with 1 level fused. Those with 2 levels fused were more than twice as likely (OR, 2.1; 95% CI, 1.4–3.3). Ahn et al33 reported those with multilevel fusion to be nearly twice as likely (OR, 1.9; 95% CI, 1.3–2.8) to develop CASP compared with those with single-level fusion. In contrast, Ghiselli et al34 reported segments adjacent to single-level fusions were more than 3 times as likely (OR, 3.4; 95% CI, 1.8–6.2) to develop CASP after a mean of 6.7 years compared with those adjacent to multilevel fusions. The authors indicated that this was contrary to their hypothesis and suggested that this may be explained by the fact that a patient who has a single-level fusion has more levels at risk than a patient who has a long fusion segment.

Figure 4

Figure 4

Two studies35,37 reported “radiographical risk factors” from a multivariate model for CASP among patients who had undergone fusion. Among these, only the study by Kaito et al35 reported a significant factor among the 12 radiological factors evaluated. The distracted distance of the L4–L5 disc space by cage insertion was 3.1 ± 2.2 mm in the group without CASP, 4.4 ± 1.7 mm in the group with L3–L4 CASP, and 6.2 ± 2.6 mm in the group with CASP. No other radiographical factors were found to be significant from the multivariate models of these studies and these are listed in Table 2.

Back to Top | Article Outline

Evidence Summary

The final overall strength of the body of literature expresses our confidence in the estimate of effect and the impact that further research may have on the results. A summary of these finding and the method of arriving at each strength of evidence can be found in Table 3. With respect to the risk of CASP, the mean annual incidence of CASP ranges from 0.6% to 3.9% after lumbar fusion. The estimates of risk for CASP after fusion among studies performing survival analysis are broad ranging from 3% to 16.5% at 5 years and 6% to 26.1% at 10 years. Two of the three studies estimated higher rates suggesting the risk may be greater than 10% and 20% at 5 and 10 years, respectively; however, because of the inconsistency, the strength of evidence is Low to arrive at a definitive estimate. That is, we have low confidence that the evidence reflects the true effect, and further research is likely to change the confidence in the estimates of effect and likely to change the estimates.

TABLE 3

TABLE 3

With respect to patient factors, patients who are older than 60 years are at a significantly increased risk of developing CASP 5 to 10 years after fusion. This risk ranges from 2 to 4 times that of patients younger than 60 years. The strength of evidence is High, that is, we have high confidence that the evidence reflects the true effect. Further research is very unlikely to change our confidence in the estimate of effect. Men are at greater risk of developing CASP compared with women; however, this is based on only 1 study; therefore, the strength of evidence is Low.

With respect to disease factors, patients with facet degeneration adjacent to the index level of fusion seem to have an increased risk of developing CASP. Findings from studies are imprecise; therefore, the overall strength is Low. Patients with degenerative disc disease adjacent to the index level of amputation are more likely to develop CASP. One study reported statistically significant results, whereas the results of another were not significant; therefore, the overall strength is Low.

With respect to surgical factors, patients with multilevel fusion seem to be at greater risk of developing CASP, and it seems the risk goes up with additional fusion segments; however, 1 study found single-level fusion to be associated with a greater risk so the strength of evidence was downgraded to Moderate, meaning we have moderate confidence that the evidence reflects the true effect, and further research may change our confidence in the estimate of effect and may change the estimate. Patients with fusion to L5 compared with fusion to S1 are at greater risk of developing CASP; however, this is based on only 1 study. Patients with laminectomy in addition to fusion are more than 2 times as likely to develop CASP; however, this is based on only 1 study. Therefore, the strength of evidence for these 2 factors was graded as Low.

With respect to radiographical factors, patients with excessive disc height distraction are at greater risk of developing CASP; however, this is based on only 1 study. Therefore, the strength of evidence for these factors is Low. A multitude of other radiographical factors were not found to be associated with an increased risk of developing CASP.

Back to Top | Article Outline

DISCUSSION

There have been several studies published on the development of ASP after lumbar spinal arthrodesis.3,4,6,10,11,13,14,16,18,20,21,27 The vast majority of these are level III or IV studies that do not control for other factors, which can be problematic given that ASP is part of a larger disease process that is potentially associated with a multitude of factors including natural history. A previous systematic review by Park et al22 found that the risk of RASP and CASP ranges from 8% to 100% and 5.2% to 18.5%, respectively. Potential risk factors were posterior lumbar interbody fusion, injury to the adjacent facet joint, fusion length, sagittal alignment, pre-existing adjacent degenerative discs, lumbar stenosis, age, osteoporosis, female sex, and postmenopausal state. We sought to answer similar questions but restricted our inclusion criteria to level I or II prognostic studies that controlled for other potential confounding factors through multivariate analyses. We identified 4 level II studies and included 1 level III study that was a well-designed case-control study that controlled for a multitude of other risk factors. Studies performing survival analysis that calculated the annual incidence of CASP range from 0.6% to as high as almost 4% per year. The 5- and 10-year estimates of risk for developing CASP after fusion were broad, ranging from 3% to 16.5% and 6% to 26.1%, respectively; however, 2 of the 3 studies estimated rates on the higher end suggesting the risk may be greater than 10% and 20%, respectively.

Risk factors identified through multivariate analyses included age more than 60 years, male sex, facet degeneration, and degenerative disc disease adjacent to the fused segment, multilevel fusion, fusion to L5 (vs. S1), an additional laminectomy, and excessive disc height distraction. Among these, age was the only significant factor and there seemed to be a dose-response effect as the RR increased significantly as age more than 60 years was compared with lower age categories. Multilevel fusion was associated with moderate evidence as 2 studies reported increased risks including a dose response with a greater risk associated with more levels fused; however, 1 study reported an increased risk of CASP in segments adjacent to single-level fusion compared with those adjacent to multilevel fusion. The authors suggested that this may be explained by the fact that a patient who has a single-level fusion has more levels at risk than a patient who has a long fusion segment.

The other patient, disease, surgical, and radiographical factors were associated with low evidence, primarily due to only 1 study supporting the findings. Specifically, multilevel fusions, not including the L5–S1 level, and performing a laminectomy adjacent to a fusion may increase the risk of CASP. Unfortunately these risk factors are contradictory to one another. Performing a single-level fusion seems to be the most ideal; but if the L5–S1 foundational level has advanced degenerative changes and is adjacent to the index procedure, then it may be beneficial to include it to decrease CASP. Clearly, more studies evaluating a large number of patients and risk factors while controlling for all pertinent patient, disease, surgical, and radiographical factors are necessary to improve the quality of the evidence in this area.

Back to Top | Article Outline

CONSENSUS STATEMENTS

  1. The risk of developing CASP after lumbar fusion occurs at a mean annual incidence of 0.6% to 3.9%.
  2. Strength of Statement: Strong
  3. Patients older than 60 years or who have pre-existing facet/disc degeneration may have an increased risk of developing CASP.
  4. Strength of Statement: Strong
  5. The risk of developing CASP may be greater after multilevel fusions and fusions adjacent to but not including the L5–S1 level, and may increase when performing a laminectomy adjacent to a fusion.
  6. Strength of Statement: Strong
Back to Top | Article Outline

Key Points

  • CASP occurs at a mean annual incidence of 0.6% to 3.9%.
  • Age more than 60 years is significantly associated with the development of CASP.
  • Other factors that may predispose a patient to the development of CASP include the following:
    • Pre-existing facet degeneration
    • Pre-existing degenerative disc disease
    • Multilevel fusion
    • Stopping a construct at L5
    • Performing a laminectomy adjacent to a fusion
    • Excessive disc height distraction during posterior interbody fusion
Back to Top | Article Outline

Acknowledgments

The authors thank Ms. Nancy Holmes, RN, and Chi Lam, MS, for their administrative assistance. Analytic support for this work was provided by Spectrum Research, Inc. Authors B.D.L., J.W., P.M.A., and D.S.B contributed to study concept, interpretation, manuscript preparation, and manuscript revision; J.T.H. and D.C.N.: data analysis and interpretation, and manuscript preparation and revision.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.spinejournal.com).

Back to Top | Article Outline

References

1. Albee FH. Transplantation of a portion of the tibia into the spine for Pott's disease: a preliminary report 1911. Clin Orthop Relat Res 2007;460:14–6.
2. Hilibrand AS, Robbins M. Adjacent segment degeneration and adjacent segment disease: the consequences of spinal fusion? Spine J 2004;4(suppl):190S–4S.
    3. Aiki H, Ohwada O, Kobayashi H, et al. Adjacent segment stenosis after lumbar fusion requiring second operation. J Orthop Sci 2005;10:490–5.
    4. Bae JS, Lee SH, Kim JS, et al. Adjacent segment degeneration after lumbar interbody fusion with percutaneous pedicle screw fixation for adult low-grade isthmic spondylolisthesis: minimum 3 years of follow-up. Neurosurgery 2010;67:1600–7; discussion 1607–8.
    5. Brantigan JW, Neidre A, Toohey JS. The lumbar I/F cage for posterior lumbar interbody fusion with the variable screw placement system: 10-year results of a Food and Drug Administration clinical trial. Spine J 2004;4:681–8.
      6. Cheh G, Bridwell KH, Lenke LG, et al. Adjacent segment disease following lumbar/thoracolumbar fusion with pedicle screw instrumentation: a minimum 5-year follow-up. Spine 2007;32:2253–7.
      7. Cho KJ, Suk SI, Park SR, et al. Complications in posterior fusion and instrumentation for degenerative lumbar scoliosis. Spine 2007;32:2232–7.
      8. Cho KJ, Suk SI, Park SR, et al. Short fusion versus long fusion for degenerative lumbar scoliosis. Eur Spine J 2008;17:650–6.
      9. Chou WY, Hsu CJ, Chang WN, et al. Adjacent segment degeneration after lumbar spinal posterolateral fusion with instrumentation in elderly patients. Arch Orthop Trauma Surg 2002;122:39–43.
      10. Disch AC, Schmoelz W, Matziolis G, et al. Higher risk of adjacent segment degeneration after floating fusions: long-term outcome after low lumbar spine fusions. J Spinal Disord Tech 2008;21:79–85.
      11. Djurasovic MO, Carreon LY, Glassman SD, et al. Sagittal alignment as a risk factor for adjacent level degeneration: a case-control study. Orthopedics 2008;31:546.
      12. Ha KY, Lee JS, Kim KW. Degeneration of sacroiliac joint after instrumented lumbar or lumbosacral fusion: a prospective cohort study over five-year follow-up. Spine 2008;33:1192–8.
        13. Hayashi T, Arizono T, Fujimoto T, et al. Degenerative change in the adjacent segments to the fusion site after posterolateral lumbar fusion with pedicle screw instrumentation—a minimum 4-year follow-up. Fukuoka Igaku Zasshi 2008;99:107–13.
        14. Kumar MN, Baklanov A, Chopin D. Correlation between sagittal plane changes and adjacent segment degeneration following lumbar spine fusion. Eur Spine J 2001;10:314–9.
        15. Lee DY, Jung TG, Lee SH. Single-level instrumented mini-open transforaminal lumbar interbody fusion in elderly patients. J Neurosurg Spine 2008;9:137–44.
        16. Liao JC, Chen WJ, Chen LH, Niu CC, Keorochana G, et al. Surgical outcomes of degenerative spondylolisthesis with L5-S1 disc degeneration: comparison between lumbar floating fusion and lumbosacral fusion at a minimum 5-year follow-up. Spine 2011;36:1600–7.
        17. Lund T, Oxland TR. Adjacent level disk disease—is it really a fusion disease? Orthop Clin North Am 2011;42:529–41.
          18. Min JH, Jang JS, Jung B, et al. The clinical characteristics and risk factors for the adjacent segment degeneration in instrumented lumbar fusion. J Spinal Disord Tech 2008;21:305–9.
          19. Okuda S, Iwasaki M, Miyauchi A, et al. Risk factors for adjacent segment degeneration after PLIF. Spine 2004;29:1535–40.
          20. Okuda S, Oda T, Miyauchi A, et al. Lamina horizontalization and facet tropism as the risk factors for adjacent segment degeneration after PLIF. Spine 2008;33:2754–8.
          21. Park JY, Cho YE, Kuh SU, et al. New prognostic factors for adjacent-segment degeneration after one-stage 360 degrees fixation for spondylolytic spondylolisthesis: special reference to the usefulness of pelvic incidence angle. J Neurosurg Spine 2007;7:139–44.
          22. Park P, Garton HJ, Gala VC, et al. Adjacent segment disease after lumbar or lumbosacral fusion: review of the literature. Spine 2004;29:1938–44.
          23. Pellise F, Hernandez A, Vidal X, et al. Radiologic assessment of all unfused lumbar segments 7.5 years after instrumented posterior spinal fusion. Spine 2007;32:574–9.
          24. Rahm MD, Hall BB. Adjacent-segment degeneration after lumbar fusion with instrumentation: a retrospective study. J Spinal Disord 1996;9:392–400.
          25. Schoenfeld AJ. Adjacent segment degeneration after lumbar spinal fusion: risk factors and implications for clinical practice. Spine J 2011;11:21–3.
          26. Schulte TL, Leistra F, Bullmann V, et al. Disc height reduction in adjacent segments and clinical outcome 10 years after lumbar 360 degrees fusion. Eur Spine J 2007;16:2152–8.
          27. Yang JY, Lee JK, Song HS. The impact of adjacent segment degeneration on the clinical outcome after lumbar spinal fusion. Spine 2008;33:503–7.
          28. Norvell DC, Dettori JR, Skelly AC, et al. Methodology for the systematic reviews on adjacent segment pathology. Spine 2012;37:S10–7.
          29. Wright JG, Swiontkowski MF, Heckman JD. Introducing levels of evidence to the journal. J Bone Joint Surg Am 2003;85-A:1–3.
          30. Norvell DC, Dettori JR, Fehlings MG, et al. Methodology for the systematic reviews on an evidence based approach for the management of chronic LBP. Spine 2011;36:S10–8.
          31. Atkins D, Best D, Briss PA, et al. Grading quality of evidence and strength of recommendations. BMJ 2004;328:1490.
          32. West S, King V, Carey TS, et al. Systems to Rate the Strength of Scientific Evidence. Evidence Report/Technology Assessment No. 47. Prepared by the Research Triangle Institute-University of North Carolina Evidence-based Practice Center, Contract No. 290-97-0011). Rockville, MD: Agency for Healthcare Research and Quality; 2002.
            33. Ahn DK, Park HS, Choi DJ, et al. Survival and prognostic analysis of adjacent segments after spinal fusion. Clin Orthop Surg 2010;2:140–7.
            34. Ghiselli G, Wang JC, Bhatia NN, et al. Adjacent segment degeneration in the lumbar spine. J Bone Joint Surg Am 2004;86-A:1497–503.
            35. Kaito T, Hosono N, Mukai Y, et al. Induction of early degeneration of the adjacent segment after posterior lumbar interbody fusion by excessive distraction of lumbar disc space. J Neurosurg Spine 2010;12:671–9.
            36. Sears WR, Sergides IG, Kazemi N, et al. Incidence and prevalence of surgery at segments adjacent to a previous posterior lumbar arthrodesis. Spine J 2011;11:11–20.
            37. Lee CS, Hwang CJ, Lee SW, et al. Risk factors for adjacent segment disease after lumbar fusion. Eur Spine J 2009;18:1637–43.
            Keywords:

            adjacent segment degeneration; adjacent segment disease; adjacent segment pathology; degenerative disc disease; posterior fusion; interbody fusion; lumbar spondylosis

            Supplemental Digital Content

            Back to Top | Article Outline
            © 2012 Lippincott Williams & Wilkins, Inc.