Deformity Surgery for Ankylosing Spondylitis

Summary of Key Points

Ankylosing spondylitis (AS) is a chronic, inflammatory rheumatic disease characterized by inflammatory back pain and potential progression to disability and deformity.
Clinical characteristics of inflammatory back pain can be distinguished from other causes of chronic back pain.
It is important to be aware of the bony disease complications of AS, such as early osteoporosis and occult fractures, in assessing and managing patients.
Advancements in the medical management of AS have been made in regard to biologic therapy. Consideration of preoperative optimization and consultation with a rheumatologist are recommended before surgical intervention.
Spine corrective surgery in AS patients is generally reserved for those with severe disabling deformity.
The goal of deformity surgery in AS is the restoration of sagittal balance and improvement of horizontal gaze.
Understanding the operative treatment indications, optimizing surgical tools, and reducing potential complications are critical in treating this challenging disease process.

Acknowledgment

The authors wish to acknowledge Helen Cambron, RN, FNP-C, for her illustrative contribution to this chapter.

Ankylosing spondylitis (AS) is a part of a family of chronic, inflammatory rheumatic diseases called spondyloarthropathies. It is characterized by inflammatory back pain and formation of syndesmophytes leading to ankylosis, with potential progression to disability and deformity. ^, AS is characterized by a strong heritability factor, with most of the risk for susceptibility being connected to the presence of certain genes. The pathogenesis is thought to be immune-mediated joint erosion and bone proliferation that primarily affects the axial skeleton, including ligaments and articulations of the pelvis and spinal column. Inflammation of the vertebral joints and intervertebral disc spaces leads to ossification and fusion of the spine characterized by syndesmophyte formation, ankylosis, and the classic hallmark appearance of “bamboo spine.” Concomitant osteoporosis causes the spine to become brittle and susceptible to fracture and progressive spinal deformity. The etiopathogenesis of AS is unclear, with efforts underway to determine the exact roles of the mixture of genetic susceptibility, chronic inflammation, bone-forming pathways, and environmental contributions. ^,

The newest guidelines (2016) from the Assessments in Ankylosing Spondylitis International Society and European League against Rheumatism recommend that spinal corrective osteotomy in specialized centers be considered in patients with severe disabling deformity. The purpose of this chapter is to review the clinical presentation and surgical management of AS deformity.

Clinical Presentation

AS is a chronic lifelong disease that affects men two to three times more frequently than women and manifests clinically between the ages of 20 and 30 years. The prevalence of AS is between 0.5% and 1.3% and varies because of definition of the cases (pure AS vs. spondylarthritis), screening criteria, ethnicity, and presence of the major histocompatibility complex class I molecule human leukocyte antigen B27 (HLA-B27). Although there is a strong correlation between the prevalence of HLA-B27 and AS, it is suspected, but has not been proved, that several non–HLA-B27 genes are related to the disease progression.

The primary clinical axial spine symptom of AS is low back pain, which is derived from chronic inflammatory sacroiliitis. The pain may be unilateral or bilateral and may include radicular symptoms in late stages of AS because of compressive or active lesions. Inflammatory back pain typically exhibits at least four of the following five features: insidious onset, age of onset younger than 40 years, improvement with exercise, no improvement with rest, and pain at night (with improvement upon arising). Several of the features of AS distinguish inflammatory back pain from other causes of chronic back pain. In addition, pain may involve the hips or buttocks.

AS spinal deformity results from progressive flexion and kyphosis of the lumbar, thoracic, and cervical spine as patients attempt to unload stress from painful spondylitic facet joints. Autofusion in kyphosis results in a fixed flexion deformity and global sagittal imbalance, with ventral displacement of the patient’s center of gravity. Compensatory flexion contractures of the hips and knees may develop as the patient attempts to maintain an erect posture and adequate field of vision. These strains lead to osseous remodeling, further kyphosis, and progressive deformity.

Inflammation and new bone formation drive vertebral column remodeling in AS. Indeed, the first two spinal lesions in AS, described by Andersson and Romanus and Yden, are inflammatory in nature. Andersson lesions appear as a spondylodiscitis that destroys the central portion of the intervertebral disc and adjacent vertebral body. Romanus lesions are erosive changes at the ventral and dorsal vertebral end plates that appear on radiographs as “shiny corners.” In late disease, these Romanus lesions lead to destruction and rebuilding of the cortex, resulting in squaring of the vertebral bodies.

Other inflammatory lesions are also characteristic of AS. Enthesopathy, or inflammation of the ligamentous insertion points, characterizes AS throughout the axial spine. Indeed, enthesitis is the cause of both Andersson and Romanus lesions. Synovitis occurs at zygapophyseal, costovertebral, and costotransverse joints. Inflammation then promotes ectopic bone formation within affected ligaments, resulting in ossification of spinal ligaments and within intervertebral discs, end plates, and apophyseal structures. Formation of new ectopic bone leads to formation of syndesmophytes (bridging the ossified nucleus pulposus at each disc level) or enthesophytes (osseous outgrowths that do not bridge structures). Therefore, advanced AS is characterized by universal syndesmophytosis and squared vertebral bodies with kyphotic deformity that is aptly termed bamboo spine. It is this propensity of AS patients to make new bone that may not be affected by newer biologic agents that provide remarkable symptom relief. This is the challenge to our understanding of the fundamental nature of this disease.

Clinical Management

The principles of managing AS include physical and lifestyle interventions, nonsteroidal antiinflammatory drugs (NSAIDs), biologics, and possibly small molecule oral agents. A review of 11 trials with 763 participants concluded that individual home-based or supervised exercise programs are better than no exercise, and supervised group physical therapy is superior to home exercise. It is recently recommended that all patients with AS, in addition to those with a suspicion of axial spondyloarthritis, be seen and evaluated by a rheumatologist. This recommendation is the result of a set of deliberations by an international society of experts in the field of spondyloarthritis where key areas for quality improvement in the management of AS were identified, discussed, rated, and agreed upon.

Principles of Medication Management for Ankylosing Spondylitis Patients

The use of NSAIDs is recommended over no treatment, and their continuous use is superior to intermittent use. No particular agent has been shown to be superior to others. There is also some evidence that continuous use may slow radiographic progression. Methotrexate and sulfasalazine have little to no effect upon axial AS and are not useful unless peripheral arthritis is present. There is no evidence that adding it to an anti–tumor necrosis factor (TNF) inhibitor is helpful.

Biologics for AS have traditionally included initial use of TNF inhibition. There is compelling evidence of their ability to treat inflammation and slow radiographic progression, and this is most profound with etanercept and adalimumab. Patients who have elevated C-reactive protein or sedimentation rate, inflammation noted on magnetic resonance imaging (MRI), and shorter duration of symptoms have the best response. Unfortunately, 30% to 40% of AS patients continue with active disease despite NSAID and anti-TNF therapy. Anti-TNFs are especially useful over other options if the patient has coexisting inflammatory bowel disease or uveitis. When used for AS, anti-TNFs have had an excellent safety profile. There appears to be only a slight increase in infections, occasional injection site reactions or rashes, and no evidence for increased malignancies if used as monotherapy. Work over the last decade has demonstrated that the IL-17/IL-23 pathway plays an important role in pathogenesis of AS. Secukinumab and ixekizumab are superior to changing to a different anti-TNF if one agent fails, are approved for AS, and decrease radiographic progression. Anti-TNF therapy also has an excellent safety profile and works well if there are rashes as well (e.g., psoriatic spondylitis). Small molecule oral agents have recently been studied for AS. None have been approved for AS, but promising results have been reported with tofacitinib, filgotinib, and upadacitinib. These agents should only be used if anti-TNFs, secukinumab, or ixekizumab are contraindicated or are not successful, until there is more real-world experience.

Surgical interventions for severe kyphosis, advanced osteoporosis, or advanced hip arthritis are reviewed in this chapter. Discontinuing or tapering the disease-modifying regimen is commonly done; however, newer emerging guidelines have advised against discontinuation.

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