Summary of Key Points
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Ankylosing spondylitis (AS) is a chronic, inflammatory rheumatic disease characterized by inflammatory back pain and potential progression to disability and deformity.
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Clinical characteristics of inflammatory back pain can be distinguished from other causes of chronic back pain.
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It is important to be aware of the bony disease complications of AS, such as early osteoporosis, in assessing and managing patients.
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Spine corrective surgery in AS patients is generally reserved for those with severe disabling deformity.
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The goal of deformity surgery in AS is the restoration of sagittal balance and improvement of horizontal gaze.
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Understanding the surgical treatment indications, options, and potential complications are critical in treating this challenging disease process.
Ankylosing spondylitis (AS) is a chronic, inflammatory rheumatic disease 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 under intense scrutiny, with efforts underway to determine the exact roles of the mixture of genetic susceptibility, chronic inflammation, bone-forming pathways, and environmental contributions.
Guidelines from the Assessments in Ankylosing Spondylitis International Society and European League against Rheumatism (ASAS/EULAR) recommend spine corrective surgery in patients with severe disabling deformity. This chapter details the presentation and sequelae of AS and focuses on considerations and options in the 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. The prevalence of AS is between 0.5% and 1.3% and varies due to definition of the cases (pure AS versus 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 from chronic inflammatory sacroiliitis is low back pain. The pain may be unilateral or bilateral and may include radicular symptoms in late stages of AS due to compressive or active lesions. Inflammatory back pain typically exhibits at least four of the five features: insidious onset, age of onset < 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.
Ankylosing spondylitic 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.
Complications of Ankylosing Spondylitis
It is important to be aware of osteoporosis in AS. Initially thought of as a late finding, osteoporosis is now considered an early event, found even in AS without peripheral osteoporosis. Bone loss is secondary mainly to inflammation. Syndesmophyte formation may also correlate with lower bone mineral density of the spine. Paradoxically, dual-energy x-ray absorptiometry (DEXA) scans in advanced AS may overestimate bone mineral density due to the increased mineral concentration in syndesmophytes, which provide no real functional support. Computed tomography (CT) can help correlate osteoporosis and disease duration. The clinical consequences of this osteoporosis are profound. Patients with early AS and mild osteoporosis have a fracture prevalence five times greater than in the normal population.
The combination of inflammation and osteoporosis promotes AS fractures and is paradoxically related to ossification. Ossification of the disc space occurs centripetally through the anulus fibrosus, and only rarely is the center of the disc involved. This incomplete ossification leads to formation of polysegments in the spine, with resulting long lever arms of force. The combined stress concentration from loss of polysegmental spinal motion and secondary osteopenia predisposes patients to spinal fracture and nonunion. Aseptic spondylodiscitis, presenting as focal pain with coexisting erosive sclerotic changes in adjacent vertebral bodies, is noted at these sites. It is uncertain whether aseptic spondylodiscitis is a primary inflammatory process or the result of trauma. Radiographically, the appearances of spondylodiscitis, pseudarthrosis, and discitis are similar.
Acute traumatic fractures, particularly in the cervical spine, are also widely reported. Again, osteoporosis and stress forces due to long, stiff lever arms enhance the susceptibility of the AS patients to acute spinal fracture. The lifetime incidence of acute traumatic fractures is believed to be approximately 14%. It is reported that 75% of fractures occur in the cervical or cervicothoracic junction, 14% in the thoracic spine, and 5% in the lumbar spine. Cervical fractures commonly involve both anterior and posterior columns, leading to higher rates of mortality and neurologic complications in AS than in non-AS patients. Even minor trauma such as a simple slip and fall can cause a major spinal fracture and neurologic injury, with the rate of neurologic deficit ranging from 53% to 83%. There should be a high index of suspicion in any AS patient with acute onset of new focal pain or deformity, including any newly observed loss of height. Occult fractures must be suspected any time an abrupt change occurs in the patient’s condition, and CT is often required to fully evaluate the symptomatic areas. Undiagnosed or poorly managed spinal fractures can contribute to worsening kyphosis and deformity, particularly if the fractures heal in flexion.
Spinal deformity leads to disability and subsequent mortality. Chin-on-chest deformity seen with fixed cervical flexion significantly hinders forward vision, swallowing, hygiene, and self-esteem. The combination of debilitating disease, deformity, and limited treatment options makes managing these deformities difficult. Although the surgical management of AS deformity is technically challenging and not without risks, the psychological and functional impairment of progressive deformity warrants surgical correction and stabilization when conservative options have been exhausted.
Surgical Management
General Principles
Because AS can lead to severe flexion deformities of the spine, the goal in treatment of these patients is early recognition and adequate medical therapy in an attempt to control the disease progress and prevent associated deformities. However, patients may still become grossly deformed and functionally disabled. Spinal osteotomy may be indicated to correct the deformity and achieve upright posture.
The initial evaluation of the AS patient with deformity involves identifying the primary area in need of correction. Physical examination involves assessing the patient while seated, supine, and upright with hips fully extended. A primary cervical deformity demonstrates cervical flexion while the patient is supine. In contrast, a hip or thoracic/lumbar deformity corrects while the patient is sitting or supine.
Accurate measurement of the deformity is required for surgical planning. Simmons has advocated the chin-brow to vertical (CBV) angle as the most effective and reproducible measurement of deformity. The CBV is a clinical measurement of sagittal deformity of the spine and its effect on horizontal gaze. The CBV can be evaluated on photographs and is the angle created by (1) the vertical axis of the patient standing with hips and knees extended and (2) the line drawn from the chin to the brow. A greater CBV angle correlates with greater compromise of horizontal gaze and is a critical marker for the degree of deformity ( Figs. 154-1A and B ). Normal CBV is 0 degrees but can exceed 90 degrees in severe chin-on-chest deformity. A final corrected angle of approximately 10 degrees of flexion is generally recommended.

Radiographic studies should include a plain 36-inch standing anteroposterior and lateral radiograph with the knees in full extension to allow complete evaluation of sagittal and coronal balance. In addition, the pelvis should be clearly visualized in lateral studies to assess the pelvic parameters. A plumb line should be drawn for the C7 vertebral body to the level of S1. The horizontal distance from the plumb line to the posterior corner of S1 is the sagittal vertical axis (SVA), with a normal range of ± 5 cm. Osseous anatomy for instrumentation, existing stenosis requiring decompression, and evaluation of soft tissue or vascular structures like the vertebral arteries can be better delineated on the CT and magnetic resonance imaging (MRI) studies necessary for preoperative planning. Flexion and extension radiographs can evaluate for instability (particularly atlantoaxial instability) sometimes present in AS.
The technique and location of the osteotomy depends on the region of the spinal deformity that maximally influences sagittal alignment. Overall spinal balance as well as balance of the hips must be evaluated to delineate the primary site of deformity. In some patients, more than one site may contribute to the deformity. The common sites of deformity include the cervicothoracic junction, midthoracic spine, thoracolumbar spine, and hip joints. Assuming equal deformity at these levels, lumbar correction surgery should be considered prior to cervical correction surgery because of the lower rate of complications.
The site of correction depends on the site of deformity. Deformities isolated to the lumbar spine are corrected by a lumbar osteotomy procedure. The osteotomy is preferred below the level of the conus medullaris and is usually performed at L3 to avoid acute angular correction at the cord level. Most thoracolumbar kyphotic deformities can be addressed through a single lumbar osteotomy. The correction should be planned so that the plumb line from C7 falls within the body of S1. Even in cases in which the thoracic kyphosis is greater than normal, a compensatory lumbar osteotomy may correct sagittal plane malalignment and allow the patient to have forward gaze with the hips and knees fully extended. In cases of severe thoracic kyphosis, where the lumbar and cervical lordosis have been at least partially maintained, thoracic osteotomy by a combined ventral and dorsal approach may be indicated. It is important to note that due to fixed cervical deformity, overcorrection of the gaze angle can cause significant gait difficulty. When the primary deformity is at the cervicothoracic junction with a chin-on-chest deformity, an osteotomy of the cervical spine is indicated. The C7-T1 junction is the preferred location because it places the osteotomy below the entrance of the vertebral arteries into the transverse processes at C6 and uses the relatively large spinal canal-to-cord area ratio to safely obtain correction.
The influence of severe hip flexion contractures, with or without associated hip joint disease, is critical in the preoperative assessment. Soft tissue release about the hips or, more commonly, total hip joint arthroplasty may be sufficient to allow the patient to stand reasonably upright and see straight ahead, irrespective of the spinal deformity. These procedures should be performed prior to any larger surgical correction of spinal deformity.
Diligent presurgical screening is paramount, because AS patients frequently have multiple comorbidities. Preoperatively, patients with a fixed thoracic deformity should be screened for cardiac and pulmonary abnormalities that can be associated with extra-articular manifestations of AS. Although pulmonary function abnormalities secondary to decreased thoracic expansion have not carried anesthetic risk for most patients, 10% will have cardiac pathology, generally either aortic stenosis or conduction abnormalities. Nonsteroidal anti-inflammatory agents may need to be halted prior to surgery to reduce the risk of pseudarthrosis and nonunion. Nutrition should be optimized, sometimes with tube feeding or parenteral nutrition in extreme cases, especially with postoperative risks of swallowing difficulty.
Surgical Correction
The major categories of osteotomies for AS deformity include the Smith-Petersen osteotomy (SPO), polysegmental wedge osteotomy (PWO), and pedicle subtraction osteotomy (PSO).
Smith-Petersen Osteotomy
Smith-Petersen and Larson first proposed their osteotomy for the correction of flexion deformity for rheumatoid arthritis in the lumbar spine on six patients in 1945. Since that time, the Smith-Petersen osteotomy (SPO), also known as the opening wedge osteotomy and extension osteotomy, has been used extensively and optimized for AS. It has been reported primarily in the lumbar and cervical spine.
Smith-Petersen originally performed a V-shaped wedge resection osteotomy at the L1, L2, and L3 levels ( Fig. 154-2 ). In the original operation, the L2 spinous process was removed completely along with the articular processes of L1, L2, and L3. Each level provided about 7 degrees of correction. This dorsal osteotomy wedge was then closed and the deformity corrected via forceful manual manipulation through hyperextension. This maneuver used the middle column (e.g., the posterior longitudinal ligament) as a fulcrum and caused disruption of the anterior longitudinal ligament with a monosegmental opening wedge and extension of the anterior column. Local bone grafts were placed across the osteotomy sites, and the patient was immobilized in a postoperative cast for 2 months followed by a back brace for 1 year. Detailed results were not described.

In 1973, McMaster and Coventry reported on 17 patients with an SPO of the lumbar spine using a plaster case with a turnbuckle and hip spica immobilization for postoperative correction (no instrumentation was used). They reported an impressive 39-degree correction average, which other authors have replicated. Twelve of the 17 patients had complications, including 2 deaths and 5 neurologic deficits.
The SPO has also been commonly employed in the cervical spine. In 1953, Mason and colleagues reported successful correction of flexion deformity of the cervicothoracic spine in a patient with AS. They performed the osteotomy distal to C7 to avoid damage to the vertebral arteries. In 1958, Urist reported a successful osteotomy at the cervicothoracic junction in a patient awake under local anesthesia. However, it was Simmons who elaborated on the SPO in the first large case series of 42 patients in 1977.
The Simmons SPO modification involved a wide laminectomy from C6 to T1, with osteotomy at the C7-T1 space ( Fig. 154-3 ). Simmons resected the entire dorsal arch of C7, the inferior half of C6, and the upper half of T1. The laminae were undercut and foraminotomies performed to prevent impingement of the C8 nerve root. Following bony decompression, Simmons extended the neck and “cracked” the anterior column. Simmons performed the procedure under local anesthesia with halo control and then fixed the halo to a body cast that was worn for 4 months. There were no mortalities, and C8 weakness was the primary morbidity, occurring in 18 patients, with five permanent deficits.

Some authors have performed an initial ventral release prior to a cervical SPO. Mummaneni and associates described a staged ventral-dorsal-ventral procedure for cervical osteotomy. This consists of a ventral release (C5-6 discectomy and partial wedge resection of C5 and C6 vertebral bodies), followed by a dorsal SPO with controlled correction supplemented by a screw-rod construct, and finally a ventral placement of iliac autograft in the opening wedge defect with a cervical plate and screws. Ventral release and osteotomy have the advantages of allowing a controlled correction with neck extension without the abrupt fracture from an SPO. The osteotomy is controlled to a specific site, whereas correction of SPO can lead to a fracture at a random, undesired level. Finally, ventral exposure allows for placement of a structural graft. It should be noted that ventral exposure in AS may be inappropriate in certain cases because an ankylosed, osteoporotic spine will often fracture without excessive force. Chin-on-chest deformity may limit the exposure and operative corridor with a ventral approach. Finally, syndesmophyte formation limits a surgeon’s ability to distinguish normal from abnormal anatomic landmarks of the disc spaces. The added risk of patient repositioning and extended anesthesia must also be considered. Finally, the use of standard dorsal screw-rod instrumentation provides greater mechanical stability than ventral constructs.
Several adjustments of the original SPO technique have since become standard. General anesthetic is now frequently used with controlled halo correction, followed by either an intraoperative wakeup test or spinal cord monitoring. Lateral mass screws are used in the cervical spine, with pedicle screws the method of choice elsewhere for internal fixation. Indeed, modern instrumentation is now ubiquitous in deformity surgery. Halo and vest supplementation may or may not be used. Neurologic compression is now minimized by adequate decompression and undercutting of the lamina prior to closure of the osteotomy site and rigid stabilization. Despite these modifications, subluxation caused by rupture of the posterior longitudinal ligament has been associated with nonunion, high neurologic complications, and mortality. Although the SPO remains in common use, some surgeons prefer other alternatives.
Polysegmental Wedge Osteotomy
In 1949, Wilson and Turkell reported the first polysegmental wedge osteotomy (PWO) on a patient with thoracolumbar kyphotic deformity attributed to AS. Correction was achieved by multiple closing wedges of dorsal lumbar osteotomies including the interlaminar space and by trimming the facet processes. In contrast to the SPO, a PWO leaves the anterior longitudinal ligament (ALL) intact and generates a more gradual multisegment curvature. In the 1980s, Zielke and coworkers advocated polysegmental lumbar dorsal wedge osteotomies with internal fixation. They first used Harrington rods and laminar hooks then later used transpedicular screws.
Several authors have demonstrated good results with the PWO. van Royen and colleagues reported a mean correction of 36.3 degrees overall (9.5 degrees per level) in 21 patients treated with PWOs in the thoracic and lumbar spine. At the last follow-up, however, there was a mean loss of 10.7 degrees, with a significant rate of pedicle fractures, deep wound infections, and pseudarthrosis. Hehne and Zielke described 177 patients with AS and 44-degree overall correction (9.5 degrees per segment) without resulting pseudarthrosis and no loss of correction over the long term. Chen reported an average correction of 25.8 degrees overall (5 degrees per level) with a 25% pseudarthrosis rate. These results suggest that PWOs are reasonable when gradual correction is necessary over multiple levels. There may be concern for insufficient correction, however, especially if the intervertebral discs are calcified.
PWOs are relevant in thoracic osteotomies. Note that thoracic osteotomies are rarely required in patients with AS. As stated previously, if the thoracic kyphosis is mild or moderate and associated with a flat or kyphotic lumbar spine, the deformity can be addressed with a lumbar spine osteotomy. The rare patient has severe thoracic kyphosis with minimal loss of lumbar or cervical lordosis. This is the patient in whom a thoracic osteotomy may be indicated.
Smith-Petersen pointed out in 1945 that single-stage dorsal thoracic osteotomy correction is compromised by stiffness of the costovertebral joints. An alternative involves a two-stage procedure that consists of a first-stage transthoracic approach creating osteotomies through the ossified thoracic disc spaces. Ventral interbody fusion is performed with an autogenous cancellous bone graft. This is followed at the same sitting or 1 week later by PWOs with segmental instrumentation. Dural adhesions to the lamina that formed during the inflammatory phase of the disease can be encountered during dorsal osteotomy and likewise may make passage of sublaminar wires used in the Luque technique more difficult. Hook-rod or screw-rod compression instrumentations are alternatives commonly used today. The approach is similar to that used for severe juvenile kyphosis.
Pedicle Subtraction Osteotomy
The pedicle subtraction osteotomy (PSO), also known as the decancellization procedure, eggshell osteotomy, or closing wedge osteotomy, has been well described in the literature. Today, the PSO is primarily performed at the upper lumbar and in the cervicothoracic junction. The PSO is a mainstay in correcting deformity due to iatrogenic kyphosis, traumatic kyphosis, rheumatoid arthritis, and AS.
A PSO involves first removing a wedge of the dorsal elements and bilateral pedicles, followed by resection of the dorsal vertebral cortex as well as the cancellous bone of the vertebral body ( Fig. 154-4 ). The ALL and ventral cortex of the vertebral body are left intact. In contrast to the SPO, the ALL is the fulcrum for closure and results in three-column bone-on-bone closure. Closure effectively shortens the spinal canal and achieves angular correction at a single level. Moreover, removal of the pedicle creates a “superforamen,” which transmits the nerve roots from the adjacent segments and decreases the chance for root compression. Generous undercutting and decompression of the supra- and subadjacent laminar edges are performed to ensure adequate space for the redundant dura that may be produced during closure of the osteotomy. Segmental spinal fixation using screw-rod or hook-rod constructs is used to allow for immediate patient mobilization. The surgical table is carefully extended, closing the osteotomy. If necessary, closure can be augmented by pressure on the patient’s shoulders or legs and by compression between the pedicle screws once the rods are placed. A wake-up test or neuromonitoring is routinely performed to assess neurologic function. Finally, a local bone graft is applied and augmented with iliac crest autograft or banked bone, as needed.
