Summary of Key Points
Postoperative spinal deformity manifests as an inability of the spine to maintain an adequate load-bearing capacity or withstand dynamic forces, which may occur due to iatrogenic reasons intraoperatively (decompression, instrumentation), pseudarthrosis, or the inevitable phenomenon of rigid posterior spinal fusion (i.e., adjacent segment disease).
During spinal decompressions, prophylactic fusion should be performed after multilevel cervical laminectomy to decrease the risk of postlaminectomy kyphosis, whereas over resection of the lateral pars interarticularis and true pars in the lumbar spine should be avoided to prevent iatrogenic pars fractures and spinal instability.
To minimize the risk of creating an iatrogenic flatback after short posterior lumbar spinal fusions, a patient’s legs should be extended while positioning them to maximize lumbar lordosis and straight rods should be avoided between L4 and S1.
For long posterior spinal fusions, distal fixation should include the sacrum and iliac fixation with unilateral or bilateral iliac screws. S2 alar-iliac screws are alternatives to iliac fixation and are ideal in revision surgeries for lumbosacral pseudarthrosis or instability.
Acute complications at the junction of long posterior thoracolumbar constructs are commonly a result of a fracture at the proximal vertebrae, instrumentation pullout, or failure of the soft-tissue posterior ligamentous structures. The incidence of these may be minimized by augmenting the posterior ligamentous structures or the anterior column’s loading bearing capacity (i.e., vertebral augmentation of the last instrumented vertebra and the vertebra one level proximal to the last instrumented vertebra).
Surgical strategies to address postsurgical spinal deformity are dictated by patient age, medical comorbidities, degree of debilitation, and the unique characteristics of each deformity.
Preoperative evaluation for a patient with a postoperative spinal deformity should include a diagnostic assessment of metabolic bone disease (dual-energy x-ray absorptiometry scan, vitamin D, calcium, and parathyroid hormone levels), full-length, standing lateral and anteroposterior spinal radiographs, and advanced imaging (i.e., computed tomography, magnetic resonance imaging) as indicated.
The ideal radiographic goals of deformity correction are to bring the pelvic incidence (a fixed value) and lumbar lordosis (a dynamic value) to within 10 degrees of one another, to improve pelvic tilt to less than 20 degrees, and to achieve less than 4 cm of coronal and sagittal imbalance.
A thoughtful and integrated evaluation of spinal mobility, the deformity’s apex, previous fusion/instrumentation, and neurologic status will help shape the surgical plan for deformity correction, which may involve multilevel or three-column osteotomies.
Stability of the spine is afforded by a complex interaction between the dynamic and static structures of each spinal unit, which consists of the vertebral bodies, intervertebral disc, posterior osseous elements, facet joints, interspinous ligament, supraspinous ligament, and paravertebral muscles. Disruption or degeneration of one or multiple of these structures may result in an acute failure or a gradual loss of spinal stability. Loss of stability may occur due to several etiologies, including congenital anomalies, biologic pathologies (i.e., tumor, infection, inflammation), degeneration, or iatrogenic reasons. This chapter focuses primarily on spinal deformities that occur postoperatively. Although postsurgical spinal deformities may be a consequence of the unavoidable natural history of spinal fusion or decompression, the majority of these deformities may be prevented by a fundamental understanding of surgical techniques to preserve spinal stability intraoperatively and ensure proper alignment. Thus, surgical strategies to avoid destabilizing the spine intraoperatively as well as preventing intraoperative malalignment are also addressed in detail in this chapter.
Loss of spinal stability manifests as an inability of the spine to maintain an adequate load-bearing capacity or the ability to withstand dynamic forces. Malalignment of the spine is a common manifestation of spinal instability and the hallmark of spinal deformity. Neglected spinal malalignment often progresses to marked functional limitation. Severe sagittal imbalance may render one socially and functionally debilitated, as it compromises maintenance of horizontal gaze. Thus, performing activities of daily living, including driving, swallowing, speaking, and upkeep of personal hygiene may become more difficult with worsening kyphosis. Glassman and colleagues demonstrated that quality of life is negatively affected by mild sagittal imbalance and is significantly compromised as sagittal imbalance increases. Progressive kyphosis is better tolerated in the thoracic spine and poorly tolerated in the cervical and lumbar spine. Although coronal imbalance is better tolerated than sagittal imbalance, coronal malalignment > 4 cm is associated with worsening pain, increased disability, and worse function. In addition to pain and poor general health, postoperative spinal deformity may result in acute or progressive neurologic injury. For example, Watanabe and colleagues reported that the neurologic status of 20% of patients who sustained an acute proximal junctional fracture deteriorated from Frankel E to Frankel B. After proximal extension of the instrumentation and revision arthrodesis, these patients recovered to Frankel D. Thus, all attempts should be made intraoperatively to both avoid destabilizing the spine and avoid instrumenting and fusing the spine in a misaligned position.
Decompression-Related Postoperative Spinal Deformities
Laminectomies of the cervical, thoracic, and lumbar spine are efficacious and generally safe operations. A successful decompression hinges on removing an appropriate amount of lamina and other compressive pathology in the lateral recess. Too little bony decompression can result in persistent pain and disability, whereas over resection of the pars or facets may jeopardize spinal stability. The degree of instability depends on the extent of pars and facet resection in the cervical and lumbar spine. In the cervical spine, postoperative kyphosis has been induced by removal of as little as 25% of the facets during laminectomy, whereas removal of 50% of cervical facet capsules has been found to cause cervical instability. Because of this small margin of error, prophylactic fusion should be performed after multilevel cervical laminectomy to decrease the risk of postlaminectomy kyphosis.
In the lumbar spine, facetectomy is better tolerated than in the cervical spine. Facet integrity in the lumbar spine is particularly important for rotational and axial stability. In a finite element model, Zander and associates demonstrated that a unilateral hemifacetectomy increased intersegmental rotation during axial rotation. Lumbar facet damage also results in transfer of axial loads to the intervertebral disc’s annulus and anterior longitudinal ligament. Although wide lumbar facet joint destruction will not produce acute instability, it accelerates segmental degeneration and, therefore, should often be accompanied by fusion and posterior instrumentation. In addition to adequate facet preservation, maintaining integrity of the lateral pars interarticularis and true pars in the lumbar spine is important for spinal stability. When performing a lumbar laminectomy, the lateral pars should be exposed to determine its width so as to avoid over resection. Care should also be taken when resecting the superior edge of the distal vertebra’s lamina during decompression. An overly aggressive resection at this site can also lead to an iatrogenic pars fracture. Unlike facet destruction, pars fractures can lead to acute postoperative instability and thus require posterior instrumentation and fusion. Take for example the following clinical case ( Fig. 204-1 ).
A 59-year-old female with degenerative lumbar stenosis and spondylolisthesis at L3-4 underwent a L3-5 laminectomy with L3-5 transforaminal lumbar interbody fusions (TLIF) and posterior spinal fusion (PSF) at an outside hospital (see Fig. 204-1 ). Intraoperatively, there were no reported complications, and the initial postoperative period was uneventful. However, 2 weeks postoperatively, the patient reported worsening back and bilateral leg pain, which was then followed 2 weeks thereafter by bilateral leg weakness, numbness, and difficulty walking. Radiographs demonstrated distal junctional grade 4 spondylolisthesis at L5-S1 with bilateral pars fractures (see Fig. 204-1 ). This was presumed to be either due to removal of too much bone off the superior lateral edges of S1 bilaterally or due to an overaggressive bony resection of the lateral pars of L5 bilaterally. Of note, no pars defects were present preoperatively. She was subsequently transferred to a tertiary care center where she was taken to the operating room for deformity correction and stabilization. First, reduction of the spondylolisthesis through an anterior approach to the lumbar spine and an L5-S1 anterior lumbar interbody fusion were performed without complication. A revision L3 to ilium posterior spinal fusion was subsequently performed on the same day (see Fig. 204-1 ). As she had 30% decreased motor-evoked potentials preoperatively, an L5 laminectomy was also performed. Postoperatively, regional and global sagittal parameters were restored. At approximately 1 year postoperatively, her neurologic examination was normal and adequate alignment was maintained. Although acute destabilization of the spine is rare, this scenario exemplifies the sequelae of an over-aggressive decompression and resultant iatrogenic pars fractures.
Instrumentation-Related Postoperative Deformities
The major goal of posterior spinal instrumentation and fusion is to restore spinal stability and maintain or improve spinal alignment. Unfortunately, spinal instrumentation can easily result in iatrogenic spinal deformity, particularly iatrogenic loss of lumbar lordosis, or “flatback,” and sagittal imbalance. Distraction-based instrumentation (i.e., Harrington rods) extending into the lumbar spine or sacrum is the major historical culprit of iatrogenic flatback. Although modern posterior instrumentation improves sagittal alignment correction, it can also result in iatrogenic flatback if lumbar lordosis is not maintained or improved at the time of operation. As lumbar lordosis is significantly changed by the position of one’s hips while lying prone, proper positioning intraoperatively is critical to minimize the risk of inducing iatrogenic flatback. In the setting of a posterior lumbar fusion, patients should be placed prone with their hips extended to maximize lumbar lordosis. In several clinical studies, intraoperative hip flexion has been found to decrease lumbar lordosis by 26% to 67%. This is in contrast to hip extension, which consistently has been shown to increase lumbar lordosis. In addition to patient positioning, global and segmental angulation of the lumbar spine should be analyzed carefully. The average lumbar lordosis is approximately 60 degrees. Particular attention should be paid to the segmental angulation between L4 and S1 because these two segments account for nearly 70% of total lordosis and the apex of lumbar lordosis is located, on average, at the L4 vertebral body ( Fig. 204-2 ). As hypolordosis of instrumented L4-S1 segments results in increased loading of the posterior column of the adjacent segments, straight rods from L4-S1 should be avoided and rod contouring should focus on adequate L4-S1 lordosis (see Fig. 204-2 ).
In addition to ensuring optimal lumbar lordosis intraoperatively, providing sufficient distal fixation is also important to minimize the risk of postoperative complications and spinal decompensation. Fixation to S1 is sufficiently robust in short posterior constructs that terminate at L3 or below. However, in longer posterior lumbar fusions and instrumentations that extend proximal to L3 for adult spinal deformities, only instrumenting and fusing to S1 is not recommended because it is associated with high rates of complications, such as pseudarthrosis, sagittal deformity, and instrumentation failure. These complications are presumed to be due to inadequate bone stock of the sacrum, a large number of segments requiring arthrodesis, and unfavorable biomechanics due to a long lever arm at the lumbosacral junction. Enhancing distal fixation may be accomplished with extension to the S2 pedicle; however, McCord and colleagues demonstrated that the most biomechanically stable fixation of the lumbosacral joint included fixation of the ilium bilaterally combined with bilateral S1 fixation, as this provides 4 points of fixation of the sacrum and pelvis. Although this construct is biomechanically superior to S1-only fixation, iliac screws are not without complications. With a minimum of 5-year follow-up data, Tsuchiya and coworkers demonstrated that symptomatic iliac screw prominence and the need for screw removal is common (23 of 67 patients; 34.3%). Other potential difficulties associated with iliac screws are SI joint pain and gait abnormalities, including a short step or “waddle.” A technique designed to decrease iliac screw prominence is the S2 alar-iliac screw that has its entry site between the S1 and S2 foramen, which is 15 mm deeper than the posterior superior iliac spine entry point of traditional iliac wing screws. In addition to being low-profile, S2 alar-iliac screws provide another point for distal lumbosacral fixation, which makes them ideal in revision surgeries for lumbosacral pseudarthrosis or instability. Although iliac fixation evolves, the important fundamental concept is that sacral fixation at S1 should consistently be supplemented with either unilateral or bilateral iliac fixation for long posterior lumbar fusions. Additionally, interbody grafting of L4-L5 and L5-S1 should be used in this setting to minimize stress of the lumbosacral instrumentation. With all the aforementioned intraoperative techniques in mind, one may minimize the chances of producing an iatrogenic flatback and decrease the risk of postoperative pseudarthrosis, instrumentation failures, and significant spinal imbalance postoperatively.
Adjacent Segment Disease
The proximal and distal extents of posterior fusions are all considered “at risk” for failure as a result of increased loads and motion between the last instrumented vertebrae and unfused adjacent segment. Any pathology that occurs at the proximal or distal aspects of a posterior fusion is referred to as adjacent segment disease (ASD) and is classified based on the time at which it occurs postoperatively.
Acute complications at the junctions of a posterior construct are commonly a result of a fracture at the proximal vertebrae, instrumentation pullout, or failure of the soft-tissue posterior ligamentous structures. These primarily occur at the proximal junction of a thoracolumbar fusion extending from the pelvis into the upper lumbar or thoracic spine with spondylolisthesis occurring more commonly at the upper thoracic spine and vertebral body fractures occurring more commonly at the lower thoracic spine. Risk factors for acute proximal junctional failures include, but are not limited to, osteopenia, age greater than 55 years, obesity, and severe global sagittal imbalance. Fractures are commonly atraumatic and are the most common of the three aforementioned acute junctional complications with a reported incidence reaching 62%. Fractures result from a failure of the anterior column and occur in two forms: one at the most proximal instrumented level (UIV) and the other at the vertebra one level proximal to the most proximal instrumented level (UIV+1) ( Fig. 204-3 ). Fractures of UIV are presumed to be a result of acute concentration of mechanical stress on the UIV after correction of considerable sagittal imbalance with rigid pedicle screw constructs, whereas fractures of UIV+1 are theorized to be the result of stress concentration on unfused adjacent segments (see Fig. 204-3 ).