Overview

Flat back syndrome, otherwise known as fixed sagittal imbalance, describes a clinical entity that results in a symptomatic and fixed loss of physiologic lumbar lordosis, causing an overall spinal malalignment. Doherty first described the condition in the early 1970s, after he observed a decrease of lumbar lordosis in a patient with scoliosis treated by posterior spinal fusion to the sacrum. Subsequent descriptions by Moe and Denis and later Grobler and colleagues introduced the term “flat back syndrome” as well as providing descriptions of surgical management and follow-up on the condition. Today, flat back syndrome has become a well-recognized condition, most commonly resulting from Harrington rod distraction and instrumentation for scoliosis into the lower lumbar spine and sacrum. The terms kyphotic decompensation syndrome and flat buttock syndrome have since been introduced in patients with fixed sagittal imbalance who were treated for conditions other than scoliosis. Clinically, radiographically, and prognostically, these terms are synonymous with flat back syndrome and differ only in etiology.

Fixed sagittal imbalance is generally classified into two broad categories: type 1 imbalance includes segmental hypolordosis or kyphosis across a fused section of vertebrae; in a type 2 imbalance, the C7 vertebrae remains centered over the sacrum, and the patient is able to compensate by hyperextension of the remaining mobile segments to maintain overall sagittal alignment of the spine. Type 2 imbalance describes the more classic “flat back,” in which the hypolordotic malalignment is global and causes the cervical spine and thorax to be shifted anteriorly relative to the sacrum.

Patients with flat back syndrome come to medical attention with a clinically evident decrease in normal lumbar lordosis that results in pain, fatigue, and difficulty standing upright with the knees fully extended. Although nonoperative treatment is the first line of defense, it is largely unsuccessful in moderate to severe malalignment cases; this leaves surgical correction as the only viable option for patients with significant symptoms. Surgery involves corrective osteotomies, such as Smith-Peterson and pedicle subtraction osteotomies and combined anterior–posterior approaches used to restore normal lumbar lordosis and sagittal alignment. Complication rates are high in surgically corrected flat back patients, and a large percentage experience residual pain. However, the majority of patients report subjective improvement following surgery, therefore strict adherence to surgical principles and proper planning are essential to maximizing patient outcomes with this challenging condition.

This chapter will highlight the etiologies and workup for patients with flat back syndrome. The surgical management of this disorder will be outlined to include the most commonly performed corrective surgeries: the Smith-Peterson osteotomy (SPO) and the pedicle subtraction osteotomy (PSO; Fig. 62-1 ).

Clinical photo of patient with flat back deformity.

Etiology

The etiology of flat back syndrome is often multifactorial. However, by and large, the most common cause is posterior distraction of Harrington rod instrumentation into the lower lumbar spine and sacrum. The majority of lordosis in the lumbar spine occurs within the two most caudal spinal segments, and as a result, the loss of lordosis following posterior spinal fusion is directly related to how far caudally the fusion extends. Aaro and Ohen found in their series that lumbar lordosis averaged 38 degrees when posterior fusion was stopped at T12; when stopped at L4, it averaged 21 degrees, and it averaged only 16 degrees when L5 was included in the fusion. This observation was later reinforced in Lagrone’s series of flat back patients: no patient treated had a fusion cephalad to L3, and all patients in the cohort who underwent corrective surgery had fusions that extended into the lower lumbar spine and sacrum.

In addition to the caudal extent of the fusion, flat back syndrome is further related to the type of instrumentation used for fusion. With straight Harrington rod instrumentation followed by a distractive corrective maneuver, the lumbar lordosis is forced straight and later reinforced and made rigid by successful fusion, thus leading to a flat back. Prior to the use of Harrington rod distraction, and today with modern segmental instrumentation technology, flat back syndrome following posterior spinal fusion for scoliosis is much less common ( Fig. 62-2 ).

Harrington rod distraction instrumentation into the lower lumbar spine increases the risk of subsequent flat back deformity.

Several other causative factors have been identified as etiologies of flat back syndrome, and with an increasing number of lumbar fusions being performed for clinical conditions other than scoliosis—such as degenerative lumbar spondylosis, spondylolisthesis, posttraumatic kyphosis, and lumbar stenosis with instability—their prevalence as factors in the development of flat back syndrome is rising. In the series by Lagrone, thoracolumbar kyphosis was identified as the second most common cause of symptomatic flat back, behind Harrington rod distraction and instrumentation. Fusions with a cephalad extent at the thoracolumbar junction or an unrecognized preexisting kyphosis in the thoracolumbar junction and thoracic spine may contribute to flat back. Furthermore, to maintain sagittal balance, patients with thoracolumbar kyphosis compensate by increasing lumbar lordosis, thus even small decreases in lumbar lordosis may significantly alter overall sagittal alignment. Pseudoarthrosis is another accepted cause and, at times, a complication of flat back syndrome. After fusion into the lower lumbar spine, pseudarthrosis occurs at a higher rate secondary to the higher cantilever forces to which this region of the spine are subjected. Pseudarthrosis results in eventual implant failure and progressive loss of sagittal alignment, therefore it plays a role in the pathogenesis of flat back syndrome, which was present in 20% of patients in the series by Lagrone.

In addition to degeneration of cephalad and caudal intervertebral disks next to the fusion mass, fractures of vertebral bodies in the thoracolumbar spine are also recognized causes of flat back syndrome. Both adjacent segment degeneration and vertebral body fractures result in loss of structural support and subsequent loss of height of the anterior column, leading to progressive kyphosis or straightening of the lumbar spine. If the rest of the spine is unable to compensate for the loss of lordosis, a flat back syndrome may occur. Finally, other less common causes include hip flexion contractures, ankylosing spondylosis, and anterior lumbar compression instrumentation.

Clinical Presentation

The most common clinical presentation of patient with flat back syndrome is the inability to stand upright without flexing the knees and hips. Patients often complain of frequent stumbling or difficulty walking on uneven ground. These symptoms, coupled with a history of multiple spine surgeries, should clue the clinician in to the diagnosis. In an attempt to maintain horizontal gaze and upright posture, the patient will flex the knees and hips and extend the thoracic and cervical spine through the remaining mobile spinal segments; maintaining this posture results in fatigue and pain.

Although pain is a common initial complaint, it is not a distinguishing symptom of flat back syndrome. Pain may be related to increased strain on the paraspinal muscles, adjacent disk degeneration, and possible pseudarthrosis. The pain is poorly localized to the low and mid back and typically worsens with prolonged activity or standing. Radicular pain is rare, although the patient should be examined for the presence of true tension signs. Pain can occasionally extend into the thoracic and cervical spine, as these remaining mobile segments are hyperextended to preserve horizontal gaze. The fatigue caused by flat back syndrome is secondary to the increased strain on the paraspinal muscles from the straightening of the lumbar spine, and it is also the result of the increased amount of work required by these muscles, as the patient struggles to maintain an upright posture.

Physical exam reveals an obvious loss of normal lordotic contour to the lumbar spine with forward tilting of the trunk. The loss of lordosis is typically rigid and therefore does not correct with bending or manipulation maneuvers. The patient should be evaluated for hip flexion contractures, because their presence may be a contributing factor of the flat back syndrome and must be taken into account during the preoperative planning and positioning process. Other joint contractures, pelvic obliquity, and the flexibility of the thoracic and cervical spine should be evaluated.

Clinical Presentation

The most common clinical presentation of patient with flat back syndrome is the inability to stand upright without flexing the knees and hips. Patients often complain of frequent stumbling or difficulty walking on uneven ground. These symptoms, coupled with a history of multiple spine surgeries, should clue the clinician in to the diagnosis. In an attempt to maintain horizontal gaze and upright posture, the patient will flex the knees and hips and extend the thoracic and cervical spine through the remaining mobile spinal segments; maintaining this posture results in fatigue and pain.

Although pain is a common initial complaint, it is not a distinguishing symptom of flat back syndrome. Pain may be related to increased strain on the paraspinal muscles, adjacent disk degeneration, and possible pseudarthrosis. The pain is poorly localized to the low and mid back and typically worsens with prolonged activity or standing. Radicular pain is rare, although the patient should be examined for the presence of true tension signs. Pain can occasionally extend into the thoracic and cervical spine, as these remaining mobile segments are hyperextended to preserve horizontal gaze. The fatigue caused by flat back syndrome is secondary to the increased strain on the paraspinal muscles from the straightening of the lumbar spine, and it is also the result of the increased amount of work required by these muscles, as the patient struggles to maintain an upright posture.

Physical exam reveals an obvious loss of normal lordotic contour to the lumbar spine with forward tilting of the trunk. The loss of lordosis is typically rigid and therefore does not correct with bending or manipulation maneuvers. The patient should be evaluated for hip flexion contractures, because their presence may be a contributing factor of the flat back syndrome and must be taken into account during the preoperative planning and positioning process. Other joint contractures, pelvic obliquity, and the flexibility of the thoracic and cervical spine should be evaluated.

Radiographic Workup and Evaluation

Radiographic evaluation begins with standing anteroposterior (AP) and lateral 36-inch cassette plain films to assess the overall alignment of the spine. If needed, flexion and extension views or an extension prone view can be obtained to accurately define the rigidity of the deformity. Although difficult for some patients, effort must be made to ensure that the hips and knees are fully extended during standing radiographs. Flexion through these joints will mask potential sagittal imbalance and skew the overall measured alignment. Scoliotic deformity in the sagittal and coronal plane should be measured using the Cobb method. Although flat back syndrome is primarily a disorder of the sagittal plane, the spine surgeon must also evaluate for the presence of deformity in the coronal plane ( Figs. 62-3 and 62-4 ).

Standing lateral 36-inch film indicates positive sagittal balance as seen using the sagittal vertical axis ( red line ).

Standing anteroposterior 36-inch film depicts lumbar scoliosis and coronal imbalance.

If not accounted for, coronal plane deformities can be worsened during surgical correction designed for pure sagittal imbalance, as with the SPO. The normal curvature of the spine varies among patients and is typically reported as a range of values. In general, normal ranges are 20 to 50 degrees for thoracic kyphosis and 20 to 65 degrees for normal lumbar lordosis; the thoracolumbar junction should be within a few degrees of straight. As alluded to earlier, lumbar lordosis increases in more caudal levels of the lumbar spine. Approximately 67% of the lordosis in the lumbar spine occurs from L4 to the sacrum. However, more important than the exact degree of deformity measured, and whether it falls within the accepted ranges, is the overall sagittal alignment of the spine; thus the diagnosis of a global flat back cannot be made based only on the degree of lordotic curve on a static plain film.

Determination of the sagittal balance of the spine is accomplished through the use of a plumb line, otherwise known as the sagittal vertical axis. This axis is a vertical line drawn from the center of the C7 body to the sacrum on the standing lateral film. In a spine with a normal sagittal alignment, the plumb line should cross the posterior superior end plate of S1. Spines that have a negative sagittal balance will have a plumb line that falls posterior to S1, and spines with a positive balance, as in flat back syndrome, will have a plumb line anterior to S1. Normal spines have a plumb line that falls within 2 to 3 cm of the anterior aspect of the sacrum or 5 to 6 cm from the posterior superior aspect of S1. Positive sagittal balance occurs when the plumb line falls more than 4 to 5 cm anterior to the sacrum promontory. Patients with flat back syndrome have positive sagittal balances that range from 4.3 to 25 cm ( Fig. 62-5 ).

Severe positive sagittal imbalance measuring approximately 20 and 21 cm is revealed on 36-inch films.

Advanced imaging, such as computed tomography (CT) and magnetic resonance imaging (MRI), can be helpful during the workup. CT is used to evaluate for the presence of a potential pseudarthrosis and to better define bony anatomy. MRI is utilized in the occasional patient who does exhibit neurologic symptoms to assess for the presence of nerve root impingement or spinal stenosis.