BlueCross and BlueShield of Montana Medical Policy/Codes
Lumbar Spinal Fusion
Chapter: Surgery: Procedures
Current Effective Date: November 26, 2013
Original Effective Date: November 26, 2013
Publish Date: August 26, 2013

Back pain is one of our society’s most common medical problems—only headache is more common.  In a three-month period, about one-fourth of U.S. adults experience at least one day of back pain (NINDS, 2011).  Risk factors for low back pain (LBP) include age (more common after age 30); poor physical fitness; obesity; hereditary conditions (e.g., ankylosing spondylitis); other diseases (e.g., arthritis); occupational risks (e.g., heavy lifting); cigarette smoking (indirectly).  The causes of LBP can include:

  • Mechanical, e.g., intervertebral disc degeneration, muscle spasms or tension, ruptured or herniated intervertebral discs;
  • Injury, e.g., strains, sprains or fractures;
  • Acquired conditions, e.g., scoliosis, spondylolisthesis, spinal stenosis;
  • Infections and tumors, e.g., osteomyelitis, discitis.

The physiologic basis for low back pain is highly complex, in large part because the lumbar spine itself is an unusually complex anatomic structure.  The spine is the only organ comprised of bones, joints, ligaments, fatty tissue, multiple layers of muscles, and nerves (including peripheral nerves, nerve roots, sensory ganglia, autonomic ganglia, and the spinal cord).  Furthermore, these structures are supplied by an intricate arterial and venous system and lie in close proximity to the skin with its sensory receptors.  Diagnosis and treatment of low back pain requires an understanding of many different types of tissue, as well as knowledge of the biomechanics of complex spinal structures, the manner in which they can be injured, and the variety of biochemical manners in which each of these structures responds to trauma and to aging.  In addition, consideration should be given to certain other psychosocial factors that affect the manner in which pain is processed centrally in the brain (BCBSA TEC 2007).    

Spinal structures and tissues that possess either unmyelinated nerve innervation or documentable substance P or related peptides are assumed to have the capacity to cause pain.  Such structures include the posterior facet joints, bones and periosteum, muscles, tendons, fascia, ligaments, nerve roots, dorsal root ganglia, dura mater and the intervertebral disc (BCBSA TEC 2007).   

Intervertebral disc pain is a potential cause of low back pain.  The intervertebral disc is a circular spongy pad of cartilage tissue that provides cushioning between each vertebrae of the spine.  Each disc consists of a very firm outer ligamentous cover (annulus) and a soft jelly-like hydrated viscous “filling” (nucleus pulposus).  In childhood, the nucleus is a hydrogel consisting of 80% water.  The disc hydrogel desiccates gradually from childhood to old age, which causes the disc to lose height and resiliency, become less tense, and bulge anteriorly and posteriorly.  These changes describe degenerative disc disease (DDD), which is commonly found in the population over age 40.  As the disc narrows, osteophytes form on the margins, which is common in patients over age 60.  DDD is considered to result from the inability of the disc’s reparative capacity to keep pace with the trauma that occurs with activities of daily living.  There is no direct blood supply to the hydrogel in the nucleus pulposus; disc nutritive sources are dependent on diffusion across the vertebral endplate adjacent to the disc, which itself becomes less permeable and sclerotic, contributing to disc desiccation.  As part of this degeneration process, the annulus becomes more densely innervated by pain fibers.  As the disc narrows, increased load is placed on the facet joints.  As part of the degeneration process, synovial fluid decreases, the joint space narrows, and osteophytes and sclerosis form at the margins.  DDD can be accompanied by spinal stenosis and/or spondylolisthesis, which can cause compression of nerves and additional symptoms, such as radiculopathy and neurogenic claudication, in addition to back pain (AHRQ 2006).

There is a lack of consensus in the medical literature as to what extent the intervertebral disc is innervated.  Once believed to be inert because nerve endings could not be demonstrated in the nucleus or inner annular fibers, the intervertebral disc is now known to contain fine nerve endings in the outer one-third of the annulus.  These nerve endings are immunoreactive to a number of pain-related neuropeptides (substance P, calcitonin-gene-related peptide [CGRP], and vasoactive intestinal peptide [VIP]).  Impulses from these free nerve endings in the outer third of the disc and the adjacent longitudinal ligaments reach the spinal cord through a number of sensory nerves in the following manner:

  • the posterior and posterolateral annulus, together with the posterior longitudinal ligament and the ventral dura, is innervated by the sinu-vertebral nerves;
  • the anterior and lateral aspect of the disc, together with the periosteum of the vertebral bodies, is innervated through the gray rami communicantes.

The sinu-vertebral nerves have been shown to innervate tissues one or two layers above or below their origin, a finding that may explain the poor localization of lumbar pain. 

Evidence that the nerve endings observed in the outer one-third of the disc may be a source of low back pain is based upon several clinical observations.  First, it has been demonstrated in human volunteers that injection of 11% sodium chloride into the intervertebral disc causes, after a few seconds, very severe pain with deep aching across the back and poor localization (Hirsch et al. 1963).  There is an early case report describing a patient who had low back pain produced by pulling on a nylon suture that was looped through the intervertebral disc (Smyth and Wright 1958).  More recently, Kuslich and Ahern (1994) observed that 33–40% of patients in their large back surgery series had significant pain when the affected central or lateral annulus was stimulated.  Finally, other investigators have reported that examination of pathologic discs reveals unusually profuse innervation (Yoshizawa et al. 1980).  Grigg and colleagues (1986) suggest from evidence in animal studies that the intervertebral disc contains a relatively rich supply of what they termed “silent nociceptors”— nerve endings that are not readily excited by mechanical stress, but which, when exposed to pain-inducing substances accompanying inflammatory, degenerative, or traumatic processes, become exquisitely responsive.

Different types of disc injuries can potentially lead to pain.  These include annular tears, disc protrusions with extrusion of nucleus pulposus into radial tears in the annular fiber of the disc, and disc herniation, in which nucleus pulposus tissue escapes the confines of the annulus.  These events cause pain by stretching or tearing peripheral innervated disc fibers or by generating an irritating inflammatory reaction in adjacent spinal tissues (Swenson 1999).  Degenerative changes in the collagen fibers of the intervertebral disc may also lead to increased focal segment instability.  As the intervertebral disc ages, nuclear hydrostatic pressure is lost, leading to buckling of the annular lamellae, increased shear stress across the annular wall, and eventually annular delamination and fissuring of the annular wall.  All of these changes have been shown to alter disc mechanics, making annular disruption, a precursor of disc herniation, more likely.

Alternative Treatments for Low Back Pain Due to Degenerative Disc Disease

Acute LBP is short term, lasting a few days to a few weeks, is usually mechanical in nature, and usually requires no major treatment.  Chronic LBP is pain that persists for three months or more.  It is often progressive and the cause can be difficult to determine.  There are two categories of treatment for chronic LBP: surgical and conservative non-surgical.  The vast majority of cases of chronic LBP do not require surgery, and conservative non-surgical treatment will nearly always be tried first.  Conservative non-surgical treatment primarily includes prescription strength analgesics (including anti-inflammatory medications, if not contraindicated); participation in physical therapy (including active exercise); and evaluation and appropriate management of associated cognitive, behavioral or addiction issues when present.  Some controlled trials have shown these modalities to be effective (Cherkin et al. 2003).  However, many patients do not respond to such treatments.

Surgical arthrodesis, or fusion, has been a  surgical treatment for DDD that is not responsive to other treatments.  Elimination of motion across the disc space and reduction of loads on disc tissues theoretically result in pain relief.  Spinal fusion is an increasingly common procedure that is performed as an adjunct in the surgical management of patients with degenerative lumbar disease and instability (Resnick et al. 2005).  National survey data indicate that the number of spinal fusion operations rose 77% between 1996 and 2001, in contrast with hip replacement and knee arthroplasty, which increased 13-14% during the same period (UW Med Report 2004).  Other conditions for which spinal fusion is performed include neurologically dangerous segmental instability after trauma; unstable spondylolisthesis; chronic or complicated spinal infection; and cases of progressive neurological deficit due to a structural disorder, such as herniated disc, neoplasm, fracture, or severe stenosis.  However, treatment for lumbar disc disorders is controversial.  The relationship between an abnormal disc and neural dysfunction does not correlate statistically with the imaged pathology, and biochemical and inflammatory factors are thought to play primary roles.  Therefore, the biological influence of a disc herniation would be expected to change over time and to be altered by passive and active non-surgical interventions (Wheeler et al. 2011). 

Usually, the outcome of fusion is much more predictable in people with sciatica than in those with predominant LBP (NINDS 2011).  The AHRQ 2006 Technology Assessment states that lumbar fusion has significant short term risks, particularly in the elderly in whom mortality rates of 1-1.6% have been reported.  In addition, long term lumbar fusion reoperation rate is up to 3.7% annually, but this rate is only slightly higher than the reoperation rate for non-fusion lumbar spine operations, suggesting that the progression of degenerative disease in the spine is the major factor leading to reoperation.  Common complications of fusion include instrument failure (7%), complications at the bone donor site (11%), neural injuries (3%), and failure to achieve a solid fusion or pseudarthrosis (15%) (Deyo et al. 2004).  Fusion is thought to cause increased rate of disc degeneration in spinal segments adjacent to the fusion.   


  • Acute pain  The most common type of back pain.  Acute pain often begins suddenly—after a fall or injury, for example—and typically lasts up to 6-12 weeks.
  • Ankylosing spondylitis  A form of arthritis that affects the spine, the sacroiliac joints, and sometimes the hips and shoulders.  In severe cases, the joints of the spine fuse and the spine becomes rigid.
  • Axial back pain  Back pain that is confined to the low back, and does not radiate to other parts of the body (e.g., buttocks, legs, etc).  It is usually associated with activities, posture and/or position, may be relieved with rest, and is usually self-limiting and resolves.
  • Cauda equina syndrome  A condition in which the nerves that control the bowels and bladder are pinched as they leave the spine.  Unless treated promptly, the condition can lead to the loss of bowel or bladder function.
  • Cervical spine  The upper portion of the spine closest to the skull.  The cervical spine comprises seven vertebrae.
  • Chronic pain  The least common type of back pain.  Chronic pain may come about suddenly or gradually; it generally lasts for three months or longer.
  • Cobb angle  The measurement in degrees of side-to-side angle of the spine in scoliosis.  A Cobb angle of 10 degrees is the minimum to define scoliosis. 
  • Degenerative disc disease (DDD)  Changes of disc desiccation and disc narrowing. 
  • Disc  A circular spongy pad of cartilage tissue that provides cushioning, situated between each vertebrae of the spine.
  • Discectomy  The surgical removal of a herniated disk.  A diskectomy can be performed in a number of different ways, such as through a large incision in the spine or through newer, less invasive procedures using magnifying microscopes, x rays, small tools, and lasers.
  • Discitis  An inflammation of the vertebral disk space often related to infection.  Although an uncommon condition, discitis is often the cause of debilitating neurologic injury.
  • Facet joints  The zygapophysial joints where the vertebrae of the spine connect to one another; these joints are also involved in the degeneration process.  Facet joint degeneration can lead to degenerative spondylolisthesis.
  • Facet syndrome  Degeneration of the zygapophysial joints, and associated muscle spasms, which cause pain.
  • Fibromyalgia  A condition of widespread muscle pain, fatigue, and tender points on the body, including low back pain.
  • Flatback syndrome  Loss or flattening of the normal lumbar curve of the spine after surgery to correct scoliosis.
  • Foraminal stenosis  Narrowing of the intervertebral foramen, which are small holes through which nerves exit the spine.  The foraminal narrowing, or stenosis, can cause compression of the nerves, resulting in pain.
  • Herniated disc  A potentially painful problem in which the hard outer coating of the disk is damaged, allowing the disk’s jelly-like center to leak and cause irritation to adjacent nerves.
  • Kyphosis  Exaggerated outward curvature of the thoracic spine, resulting in a rounded upper back.
  • Laminectomy  The surgical removal of the lamina (the back of the spinal canal) and spurs inside the canal that are pressing on nerves within the canal.  The procedure is a major surgery requiring a large incision and a hospital stay.
  • Lumbar spine  The lower portion of the spine.  The lumbar spine comprises five vertebrae.
  • Lumbar degenerative stenosis  Degenerative lumbar spinal stenosis describes a condition in which there is diminished space available for the neural and vascular elements in the lumbar spine secondary to degenerative changes in the spinal canal.  When symptomatic, this causes a variable clinical syndrome of gluteal and/or lower extremity pain and/or fatigue which may occur with or without back pain.  Symptomatic lumbar spinal stenosis has certain characteristic provocative and palliative features.  Provocative features include upright exercise such as walking or positionally-induced neurogenic claudication.  Palliative features commonly include symptomatic relief with forward flexion, sitting and/or recumbency (NASS 2010).
  • Neurogenic claudication  A common symptom of lumbar spinal stenosis, or inflammation of the nerves emanating from the spinal cord.  Neurogenic (originates with a problem at a nerve) claudication (Latin for limp) is exhibited by a painful cramping or weakness in the legs that may be precipitated by walking and prolonged standing, may be relieved by a change in position or flexion of the waist, or may be painfully persistent, as in severe compression of the nerve roots.
  • Osteoarthritis  A disease in which the cartilage that cushions the ends of the bones at the joints wears away, leading to pain, stiffness, and bony overgrowths, called spurs.  It is the most common form of arthritis and becomes more likely with age.
  • Osteomyelitis  An infectious usually painful inflammatory disease of bone often of bacterial origin that may result in the death of bone tissue.
  • Osteoporosis  A condition in which the bones become porous and brittle and break easily.
  • Pseudoarthrosis  Literally mean “false joint” and refers to a nonunion, i.e., a fusion that has failed to unite.
  • Radicular pain  Neuralgia due to irritation of the sensory root or the dorsal root ganglion of a spinal nerve.
  • Radiculopathy  Objective loss of sensory and/or motor function as a result of nerve conduction blockage.  Symptoms include numbness, motor loss, wasting, weakness, and loss of reflexes.  Radiculopathy and radicular pain can occur simultaneously or independently.
  • Rheumatoid arthritis  A disease that occurs when the body’s immune system attacks the tissue that lines the joints, leading to joint pain, inflammation, instability, and misshapen joints.
  • Sacroiliac joints  The joints where the spine and pelvis attach.  The sacroiliac joints are often affected by types of arthritis referred to as spondyloarthropathies.
  • Sciatic neuralgia Pain felt in the distribution of the sciatic nerve due to pathology or the nerve itself.
  • Sciatica  Pain felt down the back and outer side of the thigh.  The usual cause is a herniated disk, which is pressing on a nerve root.
  • Scoliosis  A condition in which the spine curves to one side as a result of congenital malformations, neuromuscular disorders, injury, infection, or tumors.
  • Spinal osteotomy  A procedure in which bone, usually a wedge shape, is removed from the spine to correct a spinal misalignment.
  • Spinal stenosis  The narrowing of the spinal canal (through which the spinal cord runs), often by the overgrowth of bone caused by osteoarthritis of the spine.
  • Spondyloarthropathy  A form of arthritis that primarily affects the spine and sacroiliac joints.
  • Spondylolisthesis  A condition in which a vertebra of the lumbar (lower) spine slips out of place.
  • Vertebrae  The individual bones that make up the spinal column.

Each benefit plan, summary plan description or contract defines which services are covered, which services are excluded, and which services are subject to dollar caps or other limitations, conditions or exclusions.  Members and their providers have the responsibility for consulting the member's benefit plan, summary plan description or contract to determine if there are any exclusions or other benefit limitations applicable to this service or supply.  If there is a discrepancy between a Medical Policy and a member's benefit plan, summary plan description or contract, the benefit plan, summary plan description or contract will govern.


NOTE #1: Conservative non-surgical therapy must include, but is not limited to:

  1. Use of prescription strength analgesics (including anti-inflammatory medications, if not contraindicated); and
  2. Participation in physical therapy (including active exercise); and
  3. Evaluation and appropriate management of associated cognitive, behavioral or addiction issues when present.

NOTE #2 Significant functional impairment may include documentation of inability, or significantly decreased ability, to perform normal daily activities of work, school, or at-home duties.

NOTE #3: Persistent debilitating pain is defined as:

  1. Significant level of pain on a daily basis defined on a Visual Analog Scale (VAS) as greater than 4; and
  2. Pain on a daily basis that has a documented impact on activities of daily living in spite of optimal conservative non-surgical therapy as outlined above.

NOTE #4:  On individual consideration, conservative therapy and/or a waiting period may be waived in the presence of "red flag" symptoms or signs, e.g., severe or rapidly progressive symptoms of motor loss, neurogenic claudication, or cauda equina syndrome.

Lumbar spinal fusion surgical procedures may be considered medically necessary for any of the following conditions:

  1. Spinal fracture with instability or neural compression; or
  2. Spinal repair surgery for dislocation, tumor, or infection (including, but not limited to, abscess, osteomyelitis, discitis, or fungal infection) when debridement is necessary and the extent of the debridement to help eradicate the infection creates, or could create, an unstable spine; or
  3. Spinal stenosis, with:
    • Associated spondylolisthesis demonstrated on plain x-rays, and
    • Neurogenic claudication or radicular pain that results in significant functional impairment in a patient who has failed at least 3 months of conservative non-surgical therapy, and has documentation of central, lateral recess, or foraminal stenosis on MRI or other appropriate imaging; or
  4. Recurrent, same level, disc herniation at least 6 months after previous disc surgery in a patient who had experienced significant interval of relief of prior symptoms, and who has:
    • recurrent neurogenic symptoms (radicular pain or claudication), and
    • significant functional impairment, unresponsive to at least 3 months of conservative non-surgical therapy, and
    • neural structure compression documented by MRI or other appropriate imaging; or
  5. Adjacent segment degeneration, at least 6 months after previous fusion in a patient who had experienced significant interval of relief of prior symptoms, and who has
    • recurrent neurogenic symptoms (radicular pain or claudication), and
    • significant functional impairment, unresponsive to at least 3 months of conservative non-surgical therapy, and
    • neural structure compression documented by MRI or other appropriate imaging; or
  6. Isthmic spondylolisthesis, either congenital (Wiltse type I) or acquired pars defect (Wiltse II), that has been documented on x-ray, with persistent back pain (with or without neurogenic symptoms) and significant functional impairment in a patient who has failed at least 6 months of conservative non-surgical therapy; or
  7. Severe progressive idiopathic scoliosis (i.e., lumbar or thoracolumbar) with Cobb angle greater than 40 degrees; or
  8. Severe degenerative scoliosis with any one of the following:
    • Persistent axial (non-radiating) pain that results in significant functional impairment in a patient who has failed at least 3 months of conservative non-surgical therapy, and has documentation of progression of deformity; or
    • Persistent and significant neurogenic symptoms (claudication or radicular pain) that results in significant functional impairment in a patient who has failed at least 3 months of conservative non-surgical therapy; or
  9. Pseudoarthrosis, documented radiographically, no less than 6 months after initial fusion in a patient who had experienced significant interval of relief of prior symptoms, and who has:
    • persistent axial back pain, with or without neurogenic symptoms; and
    • significant functional impairment, or
  10. Iatrogenic or degenerative flat back syndrome with significant sagittal imbalance, when fusion is performed with spinal osteotomy; or
  11. Spinal tuberculosis.

Unless one of the above conditions is met, lumbar spinal fusion surgical procedures are considered not medically necessary if the sole indication is any one or more of the following:

  1. Disc herniation,
  2. Degenerative disc disease (DDD),
  3. Initial discectomy/laminectomy for neural structure decompression,
  4. Facet syndrome.


Outcome Assessment

Outcomes of treatments for back pain have been compared using a variety of techniques.  Most common are pain scales measured on a visual analog scale (VAS).  Various questionnaires have been developed to additionally capture measures of physical functioning.  One of the more common measurement scales in use specific to patients with back pain is the Oswestry Disability Index (ODI), originally developed in 1976.  The validity, consistency, and reproducibility of the ODI were extensively reviewed by Roland and Fairbank (2000).  An article by Meade et al. (1986), suggests that a 4-point difference in the ODI is the minimum difference carrying clinical significance.  Roland and Fairbank (2000) also cites a personal communication from the U.S. Food and Drug Administration (FDA), which states that the FDA has chosen a minimum 15-point change in spinal surgery patients as a clinically meaningful difference in the ODI.  

Spinal Fusion

A 1992 review by Turner et al. could find no randomized trials of fusion.  Combining many studies of fusion performed for many different clinical indications, they found an average of 68% of patients reported a satisfactory outcome.  A 1999 Cochrane review (Gibson et al.) concluded that at that time there was no acceptable evidence of any form of fusion for degenerative lumbar spondylosis, back pain, or “instability.”  The authors could find no randomized clinical trials (RCTs) comparing fusion to a nonsurgical alternative, only trials which compared surgical techniques of fusion to each other.

There have been two published clinical trials comparing lumbar fusion to a nonsurgical alternative treatment for patients with chronic back pain due to DDD.  Fritzell et al. (2001) conducted a multicenter RCT comparing three techniques of lumbar fusion to nonsurgical treatment.  Enrollment criteria included patients with chronic pain, severe disability, pain attributed to DDD, and no neurologic compromise due to herniated disc, spondylolisthesis, or spinal stenosis.  There was no specified nonsurgical treatment, but it was described as commonly used physical therapies.  Patients receiving fusion therapy reported mean changes from baseline in the range of 18-33% for various pain and disability scores, whereas patients in the control group had changes ranging from -21 to 8% for the same outcomes, all between-group changes being statistically significant.  In terms of patients’ overall assessment, 63% of patients receiving fusion reported being better or much better, compared to 29% of control patients.  Critics of the study have pointed to the modest effect of surgery (up to 30% mean score change), and the fact that control patients may not have received optimal nonsurgical treatment (Deyo et al. 2004).

The other randomized trial by Brox et al. (2003) assigned a specific cognitive and exercise regimen to the nonsurgical patients.  Enrollment criteria for this study were roughly similar to the other clinical trial, and outcomes were assessed at one year.  In this study, patients receiving fusion reported improvements ranging from 36 to 49% on pain and disability scales, but patients in the control arm also reported similar improvements in these scores, resulting in differences which were not statistically significant for most outcomes.  Although this trial was much smaller than the study by Fritzell et al. (2001), the point estimates of effect for each arm are very similar to each other, and confidence intervals sufficiently narrow to rule out a large clinical benefit of surgery.  The authors believe that the difference in results between the two studies is caused by the specific intervention used in the nonsurgical group, which produced improvements similar in magnitude to the surgical fusion group.

In a 2004 article, Deyo and Mirza state that it is not clear whether some patients really benefit from spinal fusion compared to rehabilitative approaches, and the complication rate is relatively high compared to other types of back surgery and to non-surgical treatment.  They also noted that spinal fusion may be overused.  Spinal fusion was initially used to treat severe scoliosis, spinal tuberculosis, and fractures.  Deyo and Mirza state that approximately 75% of spinal fusions are performed for spondylosis (spinal degenerative changes), disc disorders, and spinal stenosis exclusive of deformity.  They recommend that, although spinal fusion is effective for some conditions, efficacy for the most common indications, such as degenerative disc disease (DDD), remains unclear.  More evidence from clinical trials is needed for DDD to be an accepted indication for spinal fusion (Deyo and Mirza 2004).

In 2005, the American Association of Neurological Surgeons/Congress of Neurological Surgeons (ANNS/CNS) Joint Section on Disorders of the Spine and Peripheral Nerves published a series of “Guidelines for the Performance of Fusion Procedures for Degenerative Disease of the Lumbar Spine.”  This series addressed their methodology in forming the guidelines, assessment of functional outcomes, and spinal fusion as treatment for a variety of DDD indications, as well as diagnostic modalities and other surgical and non-surgical interventions.  The goal of the committee was to increase the objectivity in decision-making for the treatment of lumbar conditions.  Overall, the committee found that many of the published studies had flawed results due to poorly defined outcome measures, inadequate numbers of patients, and comparison of dissimilar treatment groups (Heary 2005).  Whenever Class I (well-designed RCTs) or Class II (well-designed comparative clinical studies, e.g., nonrandomized cohort studies, case-control studies, etc; less well-designed RCTs) evidence was available, the authors discarded Class III evidence (case series, case reports, opinion, flawed RCTs, etc); the result was that most published studies were not included in the review.  In most cases, the data were weak and only adequate to support recommendations for treatment options, which by their definition reflect unclear certainty.  The committee stated they could “clearly see the need for the neurosurgical community to design and complete prospective [RCTs] to answer the many lingering clinical questions with rigorous scientific power.”  (Heary 2005). 

In 2005, Fairbank et al. conducted a multicenter randomized controlled trial to assess the clinical effectiveness of surgical stabilization (spinal fusion) compared with intensive rehabilitation for patients with chronic low back pain.  The study included 349 participants aged 18-55 with chronic low back pain of at least one year's duration who were considered candidates for spinal fusion.  Subjects underwent either lumbar spine fusion or an intensive rehabilitation program based on principles of cognitive behavior therapy.  The primary outcomes were the ODI and the shuttle walking test measured at baseline and two years after randomization.  The SF-36 instrument was used as a secondary outcome measure.  Both groups reported reductions in disability during two years of follow-up, possibly unrelated to the interventions.  The statistical difference between treatment groups in one of the two primary outcome measures was marginal and only just reached the predefined minimal clinical difference, and the potential risk and additional cost of surgery also need to be considered.  No clear evidence emerged that primary spinal fusion surgery was any more beneficial than intensive rehabilitation.

In 2006, Maghout et al. conducted a retrospective population-based cohort study to evaluate the influence of lumbar intervertebral fusion devices on clinical and disability outcomes among Washington State compensated workers with chronic back pain.  Among the 1950 eligible subjects, fusion with cages increased from 3.6% in 1996 to 58.1% in 2001.  Overall disability rate at two years after fusion was 63%, reoperation rate 22.1%, and rate of other complications 11.8%.  Use of cages or instrumentation was associated with increased complication risk compared with bone-only fusions without improving disability or reoperation rates.  Legal, work-related, and psychologic factors predicted worse disability.  Discography and multilevel fusions predicted greater reoperation risk.  DDD and concurrent decompression procedures predicted lower reoperation risk.  The authors concluded that increased use of intervertebral fusion devices after their introduction in 1996 was associated with an increased complication risk, without improving disability or reoperation rates.

In 2006, the Agency for Healthcare Research and Quality (AHRQ) drafted a Technology Assessment on Spinal Fusion for Treatment of Degenerative Disease Affecting the Lumbar Spine.  The following are conclusions:

  • There is no RCT evidence that directly compares lumbar spinal fusion with non-surgical conservative treatments in populations older than 65 years of age for any indication.
  • Direct comparative trial evidence suggests that lumbar fusion may result in some benefit compared with conservative treatment in middle-aged patients with axial back pain who have severe disability (baseline ODI 41-48) or pain from disc disease.  Some studies show statistically significant benefits in ODI, but in others ODI improvements are similar for the surgical and non-surgical groups.  The average benefit is <15 point improvement in ODI; however, the relative benefit is much lower, compared to non-surgical management.  Trials are from one to two year duration.  Conservative management strategies tested in controlled trials have differed substantially from each other, and also from clinically available rehabilitation services.
  • None of the data concerns use of spinal fusion in older patients, who more often have facet disease, spondylolisthesis, stenosis and other comorbid spine and non-spine conditions with neurological symptoms far worse than axial back pain.
  • Lumbar spinal fusion has been shown to improve pain and disability in middle-aged patients with spondylolisthesis in an RCT.  Older populations have shown similar results in uncontrolled studies.
  • Instrumentation in posterolateral fusion is associated with somewhat higher rates of fusion success than the use of bone graft.  There is conflicting evidence regarding whether the increase in fusion rates result in better patient-centered outcomes such as pain or disability measures.  Perioperative complication rates may be higher for spinal fusion than for nonfusion spinal surgery for patients over 65 years of age, and may be also higher for patients under 65.  Few data are available to evaluate whether the benefit of surgery is similar for patients over 65 years of age compared with patients under age 65.  The rates and types of complications vary by surgical approach and location of fusion.  Variability in ascertaining, defining, and reporting adverse effects and complications makes systematic evaluation difficult.
  • Long term complications include late hardware failure and adjacent segment disease requiring reoperation, which occurs at up to 3.7% per year.  Whether fusion accelerates the progression of spine disease is uncertain however, because reoperation rates are similar following laminectomy and non-fusion surgery.


Due to lack of evidence of improved outcomes, spinal fusion is considered not medically necessary when the sole indication is disc herniation, DDD, facet syndrome, or initial discectomy and/or laminectomy for neural structure decompression.


Disclaimer for coding information on Medical Policies

Procedure and diagnosis codes on Medical Policy documents are included only as a general reference tool for each policy.  They may not be all-inclusive.

The presence or absence of procedure, service, supply, device or diagnosis codes in a Medical Policy document has no relevance for determination of benefit coverage for members or reimbursement for providers.  Only the written coverage position in a medical policy should be used for such determinations.

Benefit coverage determinations based on written Medical Policy coverage positions must include review of the member’s benefit contract or Summary Plan Description (SPD) for defined coverage vs. non-coverage, benefit exclusions, and benefit limitations such as dollar or duration caps. 

ICD-9 Codes

81.02-81.08, 81.23-81.38

Procedural Codes: 20930, 20931, 20936, 20937, 20938, 22533, 22534, 22558, 22585, 22612, 22614, 22630, 22632, 22633, 22634, 22800, 22802, 22804, 22808, 22810, 22812, 22840, 22841, 22842, 22843, 22844, 22845, 22846, 22847, 22848, 22851
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  2. Hirsch C, Ingelmark BE, Miller M.  The anatomical basis for low back pain.  Acta Orthop Scand 1963; 33:1-17.
  3. Yoshizawa H, O’Brien JP, Smith WT et al.  The neuropathology of intervertebral discs removed for low back pain.  J Pathol 1980; 132:95-104.
  4. Grigg P, Schaible HG, Schmidt RF.  Mechanical sensitivity of group III and IV afferents from posterior articular nerve in normal and inflamed cat knee.  J Neurophysiol 1986; 55:635-43.
  5. Kuslich DS, Ahern JW.  What tissues are responsible for low back pain and sciatica: an investigation of tissue sensitivity in humans. In: Proceedings of the Orthopedic Research Society, 40th Annual Meeting, New Orleans, LA, 1994; p. 110.
  6. Swenson R.  Differential diagnosis: a reasonable clinical approach.  Neurol Clin 1999; 17:43-63.
  7. Bratton RL.  Assessment and Management of Acute Low Back Pain.  Am Fam Physician 1999 November 15; 60(8):2299-306.
  8. Möller H, Hedlund R., et al.  Surgery versus conservative management in adult isthmic spondylolisthesis--a prospective randomized study: part 1.  Spine (Phila Pa 1976). 2000 Jul 1;25(13):1711-5.
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Lumbar Spinal Fusion