The Journal of Bone and Joint Surgery (American) 86:1793-1808 (2004)
© 2004 The Journal of Bone and Joint Surgery, Inc.
Prevention and Management of Iatrogenic Flatback Deformity
Benjamin K. Potter, MD1,
Lawrence G. Lenke, MD2 and
Timothy R. Kuklo, MD3
1 Department of Orthopaedic Surgery and Rehabilitation, Walter Reed Army Medical
Center, 6900 Georgia Avenue, Building 2, Washington, DC 20307
2 Department of Orthopaedic Surgery, Washington University School of Medicine,
One Barnes-Jewish Hospital Plaza, Suite 11300 West Pavilion, St. Louis, MO
63110
3 15619 Thistlebridge Drive, Rockville, MD 20853. E-mail address:
timothy.kuklo{at}na.amedd.army.mi
The authors did not receive grants or outside funding in support of their
research or preparation of this manuscript. They did not receive payments or
other benefits or a commitment or agreement to provide such benefits from a
commercial entity. A commercial entity (Medtronic Sofamor Danek; Restricted
Research Grant for T.R. Kuklo, Walter Reed Army Medical Center, Washington,
DC, and L.G. Lenke, Washington University School of Medicine, St. Louis, MO)
paid or directed, or agreed to pay or direct, benefits to a research fund,
foundation, educational institution, or other charitable or nonprofit
organization with which the authors are affiliated or associated.
The opinions or assertions contained herein are the private views of the
authors and are not to be construed as official or as reflecting the views of
the United States Army or the Department of Defense.
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Abstract
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The most common cause of iatrogenic flatback syndrome is Harrington
distraction instrumentation extending into the lower lumbar spine.
Other common causes and exacerbating factors include failure to enhance
regional lordosis during lumbar fusion for degenerative spondylosis,
development of pseudarthrosis or postoperative loss of correction, development
of kyphosis at the thoracolumbar junction, development of degeneration and
decompensation cephalad or caudad to a prior fusion, and hip flexion
contractures.
Prevention of flatback syndrome involves preoperative assessment of
sagittal balance, avoidance of distraction instrumentation and extension of
long fusions into the lower lumbar spine, enhancement of physiologic lordosis
during lumbar fusions, and intraoperative positioning with the hips
extended.
Treatment of flatback syndrome involves corrective pedicle subtraction or
Smith-Petersen osteotomies with segmental instrumentation.
Polysegmental osteotomies and vertebral column resection may be utilized in
cases of sloping global sagittal imbalance and related severe coronal
imbalance, respectively.
Following surgical treatment, sagittal balance is generally improved with
fair-to-good clinical outcomes, high patient satisfaction, and moderately high
perioperative complication rates.
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Introduction
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In 1973, Doherty1
described a symptomatic fixed forward inclination of the trunk due to loss of
normal lumbar lordosis following posterior spinal fusion for scoliosis, and he
treated his patient with bilateral pelvic osteotomy. Shortly thereafter, Moe
and Denis2 coined
the term "flatback syndrome" and reported their early results
after treatment of that syndrome with vertebral extension osteotomies. Grobler
et al.3 subsequently
defined the associated symptom complex and reported good short-term results
following extension osteotomy in these same patients and thirteen others.
Since then, flatback syndrome, which is also commonly known as fixed sagittal
imbalance, has become a well-recognized entity. The etiology of flatback
syndrome may be multifactorial, but the most common cause is iatrogenic loss
of lumbar lordosis secondary to Harrington distraction
instrumentation4-10.
Farcy and
Schwab11,12
described a subgroup of similar patients who had what they termed
"kyphotic decompensation syndrome" and "flat buttock
syndrome," a fixed positive sagittal imbalance due to malalignment at
the site of a spinal fusion to the sacrum performed with distraction
instrumentation for etiologies other than scoliosis. However, the clinical
presentation, root cause, and treatment of this entity are identical to those
of the previously described classic flatback syndrome. Similarly, Booth et
al.13 divided their
series of patients with flatback into a group with segmental (Type-I) loss of
lumbar lordosis or lumbar kyphosis with maintenance of normal sagittal balance
and a group with global (Type-II), or classic, flatback syndrome with a
substantial fixed positive sagittal imbalance. For the purposes of this
review, we will define flatback syndrome as a symptomatic postfusion condition
attributable to severe loss of lumbar lordosis of any etiology. Ankylosing
spondylitis, while not discussed in detail, will also be included, as many of
the techniques utilized in the operative correction of flatback syndrome were
originally described for the treatment of the progressive fixed kyphosis of
Marie-Strümpell disease.
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Etiology of Iatrogenic Flatback
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The most common cause of loss of lumbar lordosis is degenerative disc
disease due to aging. The most common reported cause of flatback syndrome is
the extension of distraction instrumentation into the lower lumbar spine or
sacrum4-10,14-16.
It has also been reported following the use of anterior thoracolumbar
compression instrumentation without structural graft support, but this is a
rare occurrence17.
The iatrogenic loss of lumbar lordosis was not a problem following fusion for
the treatment of scoliosis prior to the advent of corrective surgical
instrumentation18.
With Harrington instrumentation, the combination of a straight rod and
distractive forces causes an obligatory loss of lumbar lordosis with
subsequent anterior translation of the vertical axis and the body's center of
gravity. As the resulting imbalance is typically rigid as a result of the
fusion mass and supporting instrumentation, the patient attempts to compensate
locally by hyperextending any segments not included in the instrumentation as
well as the cervical spine and by flexing the hips and knees in order to stand
upright or see straight ahead.
The loss of lordosis correlates directly with more caudad extension of
instrumentation. In a study of ninety-six patients with scoliosis who were
treated with Harrington instrumentation, Aaro and
Ohlen4 found the
lumbar lordosis to average 38° when the implant stopped at T12 but only
21° when the fusion was to L4 and 16° when it was to L5. Other authors
have reported similar
findings8,14.
In addition, LaGrone et
al.6 noted decreased
lordosis in patients with a fusion to the sacrum and no problems in those with
instrumentation cephalad to L3. Kostuik and
Hall19 found that
twenty-two (49%) of forty-five adult patients with scoliosis who had a fusion
to the sacrum with distraction instrumentation manifested a substantial loss
of lumbar lordosis, and thirteen of the twenty-two (29% of the total number of
patients) required one or more corrective procedures. van Dam et
al.10 reviewed the
results in ninety-one adult patients treated with posterior spinal fusion with
Harrington instrumentation and noted that 43% of those with instrumentation to
L4 or L5 demonstrated marked loss of lordosis but that symptomatic sagittal
imbalance developed in only two patients. Thus, the prevalence of flatback
syndrome increases with more caudad instrumentation, and its frequency depends
on the severity of the loss of lumbar lordosis.
While distraction instrumentation is classically the primary cause of
sagittal imbalance, several other important contributing factors have been
identified (Table I). With the
increasing performance of lumbar fusions for the treatment of degenerative
spondylolisthesis, scoliosis, and stenosis with instability, a different type
of flatback with fixed sagittal imbalance is becoming more
common13,20-22.
Failure to maintain (or ideally to enhance) lumbar lordosis during a fusion of
a degenerated spine can result in an inability to compensate locally, with
accelerated adjacent degeneration and loss of sagittal
balance23-27.
As these patients lose additional lordosis as a consequence of degeneration
and aging, kyphotic decompensation may occur, presenting with fixed forward
inclination and symptoms attributable to flatback syndrome. Degenerative loss
of lumbar lordosis and flatback syndrome in the absence of prior
instrumentation or surgery, termed "lumbar degenerative kyphosis,"
has been reported to be a common problem in Asian
populations28,29.
Greater attention to sagittal alignment and enhancement of lumbar lordosis are
therefore warranted during all lumbar fusions.
Pseudarthrosis following posterior spinal fusion is also a common etiologic
factor6,7,20,30.
LaGrone et al.6
noted that pseudarthrosis contributed to the deformity in eleven of fifty-five
patients treated for symptomatic flatback syndrome. Similarly, Cummine et
al.30 found
pseudarthrosis in all five patients with loss of lumbar lordosis in their
series of fifty-nine adult patients treated with revision Harrington fusion
for adult scoliosis. Furthermore, particularly large cantilever loads are
transmitted to the lumbar and sacral instrumentation following fusion to
caudad levels, and an increased pseudarthrosis rate is noted after such
fusions9,31.
These biomechanical stresses and the risk of subsequent pseudarthrosis may be
increased with progressive loss of sagittal balance; thus, pseudarthrosis may
be both a causative factor and a complication of flatback syndrome, especially
when lordosis is not restored with operative treatment.
Progressive or fixed thoracic and lumbar kyphosis may also contribute to
iatrogenic flatback deformity. The thoracolumbar junction may be susceptible
as a result of the anatomic alignment transition from the costally supported
thoracic vertebrae to the unsupported lumbar spine, and from the regional
thoracic kyphosis to the lumbar lordosis. In addition, 80% to 90% of the
normal standing axial load in the lumbar spine is transmitted by the anterior
column32. The
magnitude and moment arm of these stresses increase with underlying fixed
positive sagittal imbalance. Thoracolumbar kyphosis may be preexisting as a
result of thoracolumbar or lumbar scoliosis or a post-traumatic etiology. In
scoliotic deformities, thoracic or thoracolumbar hyperkyphosis often develops
secondary to lumbar hyperlordosis. In such a setting, even small decreases in
lumbar lordosis may affect sagittal
balance7,21.
Alternatively, thoracolumbar kyphosis may be caused by poor contouring of the
rod6. Inadequate
lordotic compensation of any remaining mobile lumbar segments has also been
observed in patients with moderately decreased lumbar lordosis following
treatment with Harrington
instrumentation8.
Another etiologic factor contributing to the development of flatback
syndrome is decompensation by adjacent segments cephalad or caudad to a fusion
mass20,21,33.
This may occur because of a poor selection of fusion levels or increased
stresses on the adjacent segments. Similarly, patients with a fusion extending
into the upper thoracic spine are unable to compensate for decreased lumbar
lordosis with thoracic
hypokyphosis7.
Finally, hip extensor weakness and/or flexion contractures may contribute
to flatback deformity, as hip hyperextension is the physiologic method of
compensation for lumbar
hypolordosis15. Hip
extensor weakness, as seen in patients treated for postpoliomyelitic or
myelomeningocele spinal deformities, may compromise this compensatory function
and contribute to flatback
syndrome16. Hip
flexion contracture, however, is more likely the result, rather than the
cause, of flat-back syndrome, as patients must walk with both hips and knees
flexed in order to remain
upright21,34.
Nonetheless, failure of the surgeon to appreciate and address the magnitude or
severity of a hip flexion contracture or of increased pelvic tilt
preoperatively may compromise the results following an otherwise successful
operative correction of fixed sagittal
imbalance35,36.
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Clinical Presentation
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Patients with flatback syndrome typically present with painful loss of
lumbar lordosis resulting in forward inclination of the trunk with difficulty
standing erect with the knees extended
(Fig. 1). The pain is generally
associated with fatigue and may affect the cervical, upper thoracic, or lower
lumbar regions. Often, there is a history of multiple spinal operations.
Physical examination reliably demonstrates obligatory flattening of the lumbar
region and forward tilting of the trunk. In an effort to compensate for this
fixed sagittal imbalance, the patient flexes the knees and attempts to
hyperextend the cervical spine and any remaining mobile vertebral segments in
the thoracic and lumbar spine. Biomechanical studies have demonstrated that
increased paraspinal muscular forces are required to maintain an erect posture
when there is loss of normal lumbar or cervical lordosis, which may contribute
to the fatigue-related etiology of the
symptoms37,38.
Furthermore, attempts to compensate and maintain a horizontal gaze may result
in increased strain, pain, and degenerative changes within the cervical spine
or unfused lower lumbar discs, which may require operative treatment.
Degenerative cervical changes have been documented in >50% of patients with
long-term follow-up after surgery for adolescent idiopathic
scoliosis14. Pain
or tenderness in the fused lumbar region or at the thoracolumbar junction of
the spine may indicate a
pseudarthrosis7.

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Fig. 1 Lateral clinical photograph of a patient with flatback syndrome. Note the
total loss of normal lordosis and the fixed forward inclination of the
trunk.
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Hip flexion contractures are frequently apparent on examination, and pelvic
tilt may be
abnormal15,35.
The pelvic tilt is in the sagittal plane, with either anterior or posterior
pelvic inclination. Patients with increased anterior pelvic tilt may have a
less satisfactory result of operative treatment, with persistent stooping
despite the restoration of adequate lumbar
lordosis35. Sarwahi
et al.34 performed
gait analysis on twenty-one patients with flatback syndrome and found
decreased step and stride length as well as gait velocity. Cadence was
maintained compared with that of normal controls, whereas the stance phase and
hip and knee flexion were increased. Patients may have knee or quadriceps pain
and fatigue. Patients with severe progression of thoracolumbar or thoracic
kyphosis following a lumbar fusion with distraction may manifest or report
cardiopulmonary or digestive abnormalities; however, this is unusual in
patients with iatrogenic flatback syndrome. True tension signs (e.g.,
ipsilateral or crossed straight-leg raise) and radicular pain are also
unusual, but they may occur in the setting of fixed sagittal imbalance
associated with or due to spinal degeneration with stenosis or degeneration of
adjacent segments below a caudad
fusion20,35.
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Radiographic Evaluation
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Normal Sagittal Alignment
Discussion and assessment of pathologic sagittal imbalance requires a clear
understanding of normal sagittal alignment. Several investigators have
evaluated normal sagittal curvature in the thoracic and lumbar spine as well
as at the thoracolumbar junction. Reported mean values have ranged from
37° to 42° for normal thoracic kyphosis (as measured from the superior
end plate of T3 to the inferior end plate of T12 with the Cobb
method39) and
50° to 75° for normal lumbar lordosis (as measured from the superior
end plate of L1 to the superior end plate of S1 with the Cobb
method)40-43.
However, normal functional ranges vary widely, and these ranges (rather than
averages) should be considered during the radiographic evaluation of sagittal
plane deformity. It is generally accepted that normal thoracic kyphosis ranges
from 20° to 50° and normal lumbar lordosis ranges from 20° to
65° with increasing fractional lordosis in the caudad
segments40,43.
Some authors have advocated measuring lumbar lordosis from the superior end
plate of L1 to the inferior end plate of L5 because of the wide variations in
sacral inclination and the difficulties of accurately assessing the S1 end
plate radiographically, whereas other authorities have recommended measuring
from the superior end plate of T12 to
S140,41.
However, as up to 60% of the segmental lordosis occurs in the caudad two
motion segments, measurement from the sacrum is more
appropriate41. The
thoracolumbar junction should be nearly straight. Decreases in normal lumbar
lordosis of up to 20° have been recognized as a consequence of aging and
degeneration41,44.
Smaller decreases in lumbar lordosis have been observed in patients with
low-back
pain45.
More critical than absolute measurements in the assessment of sagittal
alignment is the overall sagittal balance, particularly given the wide range
of normal values for both thoracic kyphosis and lumbar lordosis. The sagittal
vertical axis is best assessed by dropping a plumb line from the center of the
C7 body to the sacrum. Normally, this axis should fall through the S1 disc
space, preferably at the posterior-superior aspect of the S1 end plate
(Fig.
2)41,45,46.
Measurements of the total sagittal vertical axis, or the sagittal plumb line,
should be performed from the posterior-superior aspect of S1. A plumb line
falling posterior to S1 is considered to represent negative sagittal balance,
whereas an anteriorly shifted line is considered to represent positive
sagittal balance. Vedantam et
al.47 demonstrated
a 4-mm posterior shift of the sagittal vertical axis with the arms raised
horizontally with the shoulders in 90° of flexion, as opposed to 30°
of forward flexion; those authors therefore recommended positioning the
shoulders at 30° of flexion to prevent this negative shift when the
sagittal vertical axis is assessed radiographically.

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Fig. 2 Schematic representation demonstrating the technique for assessing the
sagittal vertical axis in a spine with normal alignment (A) and in a patient
with fixed sagittal imbalance (B). A plumb line is dropped vertically from the
center of the C7 body, and the horizontal linear distance between the line and
the posterior-superior part of the sacral end plate is measured. A normal
value is a distance of ±3 cm.
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Flatback Syndrome
Radiographic evaluation of a patient with fixed sagittal imbalance and
suspected flatback syndrome should begin with a full-length standing lateral
radiograph of the spine made with the patient's hips and knees
extended7. Patients
may have difficulty standing upright in this position and may require support,
but failure to extend the knees may result in artificial translation of the
sagittal vertical axis. The normal sagittal vertical axis should ideally fall
within 2.5 cm of the anterior aspect of the
sacrum11,41.
Patients with flatback syndrome may be seen to have substantial flattening or
even kyphosis of the lumbar segments (Figs.
3-A and 3-B). Preoperative sagittal imbalance as great as 29.5 cm
has been reported, with averages ranging from 4.3 to 14.5 cm in patients with
flatback13,22,33,48,49.


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Figs. 3-A and 3-B Preoperative anteroposterior (Fig. 3-A) and lateral (Fig. 3-B) radiographs
of a patient with flatback syndrome due to a malaligned lumbar fusion. Note
the mild coronal imbalance on the anteroposterior radiograph and the severe
sagittal imbalance on the lateral radiograph. The deviation of the sagittal
vertical axis on the lateral radiograph measures 17 cm, demonstrating profound
imbalance.
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Flexion and extension radiographs may be helpful in the assessment of the
mobility of the remaining, unfused segments in the thoracic and lumbar spine,
but compensation through these segments is, by definition, inadequate in
patients with flatback syndrome. Supine oblique radiographs and computed
tomography may be useful for assessing and confirming the presence and
location of a pseudarthrosis as a factor contributing to the pain and
deformity. Finally, full-length standing anteroposterior radiographs of the
spine should be made to look for any associated coronal plane imbalance, so
that this can also be addressed at the time of surgery if necessary. Awareness
of the preoperative coronal status is critical, as this deformity can worsen
as a result of corrective osteotomies addressing sagittal
imbalance20.
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Prevention of Iatrogenic Flatback Syndrome
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Preoperative Planning
With complication rates after revision spinal fusion reported to be as high
as 60% (thirty-three of fifty-five patients) and with up to 47% of these
patients having residual sagittal deformity at the time of follow-up,
treatment of iatrogenic flatback must begin with prevention
(Table
II)6.
Preoperative assessment aimed at the prevention of postoperative flatback
deformity is logical and relatively straightforward. Before a patient
undergoes a long spinal fusion, he or she should have adequate and accurate
radiographic assessment of the preoperative sagittal curvature and balance as
well as of rotational and coronal plane deformities. The operation should be
planned so that the magnitude of the existing thoracic and lumbar curves is
maintained or corrected to the greatest degree possible and sagittal balance
is either maintained or restored. In short-segment fusions for treatment of
degenerative lumbar conditions, the focus should be on increasing, rather than
maintaining, lumbar lordosis in anticipation of further degeneration and loss
of regional
curvature23-26.
For patients with scoliosis, obtaining normal postoperative sagittal balance
may be more critical functionally than is restoring so-called normal thoracic
kyphosis and lumbar lordosis. Caudally, the fusion should be stopped at or
cephalad to L3 except when a more caudad level is absolutely required to
prevent curve progression or
decompensation4-8.
In addition to decreasing the risk of postoperative loss of lumbar lordosis,
saving caudad fusion segments in the lumbar spine may decrease the risks of
pseudarthrosis and late low-back pain, retrolisthesis, and degeneration of
adjacent segments caudad to the fusion
mass9,14,18,50,51.
At the time of a ten-year follow-up, Cochran et
al.14 noted
subjacent retrolisthesis in fifteen (63%) of twenty-four patients with a
fusion to L4 or L5; all fifteen had low-back pain, and eleven had degenerative
changes.
Intraoperative Positioning
Surgical positioning is critical to maintaining lumbar lordosis and
preventing flatback syndrome following long spinal fusion. If the patient is
positioned in a manner that decreases lumbar lordosis or kyphosis, it may be
difficult or impossible to restore lordosis adequately through rod contouring
or implant manipulation intraoperatively. Several authors have addressed the
effect on lumbar lordosis of positioning on various types of surgical frames
and tables. Benfanti and
Geissele52
demonstrated, in a study of thirteen anesthetized patients, that 95% of the
lordosis was maintained when the patient was positioned on a Wilson frame with
the hips in full extension and that there was a 26% decrease in the lordosis
when the hips were flexed an average of 33°. In a study of 101 patients
who had a mean preoperative standing lordosis of 45.2° before undergoing
spinal surgery, Guanciale et
al.53 found that
fifty-one patients who were positioned on an Andrews table with the hips
flexed 90° had a significant decrease in lordosis (p < 0.005), to an
average of 32.8°, whereas fifty patients who were positioned on a
four-poster frame demonstrated a mean lordosis of 47.7°, a slight increase
compared with the preoperative value.
Peterson et
al.54 compared
twenty patients who were positioned with the hips flexed 90° on a Hastings
frame with twenty others who were positioned with the hips extended on a
Jackson table. They found that hip flexion resulted in considerable decreases
(35%) in both segmental and total lumbar lordosis, whereas the prone position
with the hips extended increased segmental lordosis by 22% at the L5-S1 levels
and preserved the total lordosis and segmental lordosis at all other levels.
Finally, Stephens et
al.55 assessed the
lordosis of ten volunteers while they were standing, while they were prone on
a Jackson table with the hips in extension, and while they were positioned on
an Andrews table with the hips flexed both 60° and 90°. Positioning on
the Jackson table with the hips extended resulted in a small increase in
lumbar lordosis, whereas the position on the Andrews table produced decreases
of 67% and 47% with the hips flexed 90° and 60°, respectively.
Therefore, to preserve physiologic lumbar lordosis, positioning with the hips
in extension should be an important consideration in all lumbar fusion
surgery.
Posterior Spinal Fusion
As noted, the primary cause of the vast majority of cases of iatrogenic
flatback syndrome is loss of lumbar lordosis secondary to the use of
distraction (Harrington) instrumentation in the lumbar
spine1-10,14-16.
Following the initial recognition of this complication, there were several
attempts to modify the Harrington instrumentation, such as with the use of a
Moe squared-end rod to prevent rotation following contouring, use of
Harrington compression instrumentation on the convex side of scoliotic curves,
and the "rod-long,
fuse-short"15
technique. These modifications have been proven to be
inadequate4,5,10,15,56.
Therefore, the use of distraction instrumentation caudad to the level of L1 or
L2 is still highly inadvisable, even with the implant modifications, as a
result of the substantial risk of reducing the lumbar lordosis with variable
production of a symptomatic flatback deformity.
Fortunately, there have been substantial advancements in spinal implants in
the last two decades. Foremost among these was the advent of segmental spinal
instrumentation. As early as 1982, biomechanical analysis demonstrated that,
compared with Harrington instrumentation, Luque instrumentation with segmental
sublaminar wiring provided superior fixation, less risk of loss of lumbar
lordosis and thoracic kyphosis, and superior rotational control and resistance
against construct
failure57. In the
same year, Luque58
reported his initial results of treatment of sixty-five consecutive patients
with scoliosis and noted improved curve correction. Although Luque did not
present significant outcome data on sagittal plane correction and balance, he
hypothesized that segmental instrumentation of this type may help to improve
the magnitude of correction and the rigidity of the construct while preserving
sagittal curvature. This was subsequently confirmed by Kostuik and
Hall19 as well as
by Phillips and
DeWald59, who noted
better preservation of lumbar lordosis with Luque instrumentation.
Segmental hook instrumentation has also been shown to be highly beneficial,
and superior radiographically, in this regard. In a study of 160 patients with
scoliosis treated with Cotrel-Dubousset instrumentation, Bridwell et
al.44 noted
preservation of lumbar lordosis following fusion surgery, with preoperative
values averaging 44° and 34° and postoperative values averaging
46° and 33° for children and adults, respectively. The authors
concluded that Cotrel-Dubousset instrumentation can preserve and potentially
enhance lumbar lordosis. Similarly, Takahashi et
al.51 reported no
differences in the lumbar lordosis seen preoperatively, postoperatively, and
at the time of follow-up in thirty patients with adolescent idiopathic
scoliosis treated with segmental hook instrumentation. Finally, de Jonge et
al.60 reported the
outcomes in a large series of 306 patients with adolescent idiopathic
scoliosis who had undergone surgical correction with Cotrel-Dubousset
instrumentation. They reported that normal lumbar lordosis was preserved in
97.9% of the patients with normal preoperative lordosis and in 94.4% of those
with preoperative hypolordosis. However, it should be noted that mere
maintenance of lumbar lordosis may be inadequate; enhancement of the lumbar
lordosis may be necessary to restore sagittal balance in patients with
adolescent idiopathic scoliosis in whom thoracic hypokyphosis has also been
surgically corrected.
Anterior spinal fusion is an alternative method of preserving motion
segments and avoiding distraction across the lumbar spine to maintain
lordosis. Rodts and
DeWald61 reported
the findings on follow-up in eighteen of fifty-four patients in whom
idiopathic thoracolumbar and lumbar scoliosis had been treated with anterior
Zielke instrumentation. They noted an 18% improvement in lumbar lordosis, with
the patients with an anterior arthrodesis requiring fusion of an average of
4.7 vertebrae compared with an average of nine fused vertebrae in similar
patients who had required posterior arthrodesis. When anterior fusion
techniques are used, care must be taken to ensure appropriate structural graft
support to avoid loss of lordosis through compression and collapse of the
anterior
column46.
More recently, segmental pedicle-screw instrumentation has gained
popularity because of its potential for achieving solid three-column fixation
and improving rotational control of the scoliotic spine. In a study of
thirty-two consecutive patients with adolescent idiopathic scoliosis,
Liljenqvist et
al.62 compared the
results of treatment with mainly hook constructs with the results of treatment
with mainly screw constructs. They found improved curve correction and
sagittal alignment with the predominantly screw constructs. Moreover, Suk et
al.63 compared the
results in seventy-eight patients with adolescent idiopathic scoliosis who had
been treated with hooks, hook-patterned pedicle screws, or segmental screws.
They reported significantly greater curve correction, rotational improvement,
and sagittal alignment (all p 0.01) with the pedicle-screw constructs and
the best radiographic results with the segmental screws. In both of these
series, pediclescrew instrumentation was found to be superior to hooks and to
be safe in both the thoracic and the lumbar spine with a low prevalence of
complications.
Prevention of flatback syndrome when spinal instrumentation is placed for
long fusions extending into the lumbar spine depends on adequate preoperative
assessment and planning, appropriate positioning that maintains lordosis
through hip extension, and placement of appropriately contoured segmental
instrumentation. The evolution of posterior instrumentation has progressed
from Harrington instrumentation and modifications of that technique to Luque
segmental wiring and ultimately to Cotrel-Dubousset segmental hooks and
segmental pedicle screws. Each iteration of implant development has produced
greater curve correction, construct rigidity, and maintenance of sagittal
balance. We currently recommend placement of segmental pedicle screws in the
lumbar spine to achieve optimal lordosis and construct strength caudally and
placement of segmental screws or hooks in the thoracic spine; interbody
spacers can also be used at the caudad construct in long fusions if necessary.
Furthermore, thoracic pedicle screws are rapidly gaining popularity as a
result of their demonstrated efficacy and safety.
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Nonoperative Treatment of Flatback Syndrome
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In general, nonoperative treatment of flatback syndrome has been
disappointing. A trial of hip-extension, trunk-stabilization, and
back-extension exercises supplemented with bracing and nonsteroidal
anti-inflammatory medications may improve the functional condition of the
patient preoperatively. However, these measures have generally proven to be of
little lasting
benefit7,11,12.
Farcy and
Schwab11,12
conducted the only structured study of nonoperative treatment of flatback
syndrome of which we are aware. Of forty-eight patients with symptomatic
flatback who were initially managed with intensive physical therapy,
twenty-eight (58%) ultimately required osteotomies for operative correction of
fixed deformities and sixteen of the remaining twenty patients underwent
implant removal without decompression or operative correction because it was
suspected that the implants were causing symptoms. Only thirteen (27%) of the
forty-eight patients were ultimately considered to have had a long-term
successful result of management without operative realignment. The mean
sagittal imbalance in the twenty patients in whom operative correction with
osteotomies was not undertaken was only 3.4 cm, slightly greater than the
normal range of the sagittal vertical axis reported by Gelb et
al.41. These
patients might therefore be better classified as having symptomatic loss of
lumbar lordosis without true fixed sagittal imbalance. Alternatively, patients
with a good response to nonoperative treatment may be similar to patients with
Type-I flatback deformity, with substantial loss of segmental lordosis but
retention of sagittal balance, as described by Booth et
al.13. The
challenge when nonoperative management fails for patients with Type-I, or
segmental, flatback deformity is restoration of the normal spinal curvature
while maintaining the normal preoperative sagittal balance. Regardless, the
results of nonoperative management of flatback syndrome are frequently
disappointing, and once nonoperative treatment has failed or the deformity has
progressed, operative correction is indicated.
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Operative Treatment of Flatback Syndrome
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Preoperative Planning
The goal of corrective surgery in the treatment of flatback syndrome is to
restore physiologic lordosis and sagittal balance such that the sagittal
vertical axis intersects the posterior aspect of the sacrum. This permits
standing and walking with the hips and knees in a physiologic posture,
improves function, and reduces fatigue-associated back and neck pain.
Preexisting pseudarthrosis may compromise the results of corrective surgery
because of persistent pain or loss of correction and should be addressed
during the same procedure. For patients with a segmental-type flatback
deformity and a normal preoperative sagittal vertical axis, the challenge is
to restore lordosis and relieve pain while maintaining sagittal
balance13.
Decision-making regarding the type and location of corrective osteotomies
depends on the site of the deformity and the presence and location of the
pseudarthrosis. Although a preoperative pseudarthrosis may predispose a
patient to postoperative recurrence of deformity at the same
site20, it makes
intuitive sense to obtain correction at this site and increase the compressive
forces across it with instrumentation to enhance osseous union. In general,
corrective osteotomies should be performed at the site of maximal deformity.
In the lumbar spine, the osteotomy typically can be carried out at L2 or
caudad, where physiologic lordosis is increased, reducing the risk of conus
medullaris or spinal cord injury. For patients with preexisting thoracolumbar
kyphosis or decompensation of adjacent cephalad segments and rigid
deformities, osteotomy may be required at higher levels. However, if the
deformity is flexible, correction should be obtained caudally and the
instrumentation and fusion should be extended cephalad to achieve sagittal
balance.
Extension (Smith-Petersen) Osteotomy
In 1945, Smith-Petersen et
al.64 described and
performed the first posterior spinal osteotomy for correction of sagittal
deformity (Figs. 4-A,
4-B, and 4-C). This procedure,
which was modified by
Law65 and
others21,36,66-68,
entails resection of the posterior elements at the desired level of correction
with undercutting of the adjacent spinous processes. Sagittal correction is
then achieved through posterior compression with instrumentation, resulting in
anterior osteoclasis through the vertebral body or distraction through the
anterior longitudinal ligament and disc space. An important drawback of this
procedure is that it lengthens the anterior column and may destabilize the
spine if the instrumentation fails prior to fusion. For this reason, La
Chapelle66,
Herbert68, and
others11,12,21,67
described anterior release, discectomy, or osteotomy and structural grafting
in conjunction with posterior Smith-Petersen osteotomies. Additionally,
lengthening of the anterior column may result in traction injury of one or
more of the great vessels. Most vascular injuries associated with this
procedure have been reported in patients with ankylosing spondylitis and
presumed calcification of the great
vessels69-72.
However, vascular complications have also been reported in patients with
iatrogenic flatback deformity, and they should be given careful consideration
when corrective surgery is performed in older individuals, as they are
frequently fatal21.
Additionally, as the procedure lengthens the anterior column, superior
mesenteric artery syndrome can
result73,74.

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Figs. 4-A, 4-B, and 4-C Schematics demonstrating the bone resection pattern for a Smith-Petersen
osteotomy. Fig. 4-A The shaded area indicates the site for the
osteotomy.
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Figs. 4-B and 4-C Fig. 4-B Note the oblique nature of the bone resection following the
initial osteotomy. Following this resection, undercutting of the inferior and
superior adjacent laminae and wide foraminal decompression is performed in
order to ensure adequate space for the neural elements prior to closure of the
osteotomy. Fig. 4-C After final placement of the instrumentation and
closure of the osteotomy, the anterior column is lengthened as a result of
disc distraction, osteoclasis, or combined anterior release and osteotomy in
order to obtain sufficient correction.
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As a general rule, 1° of correction can be expected for each millimeter
of posterior bone
resection20. In
patients treated for ankylosing spondylitis, the average correction has ranged
from 33° to
40°69,70,73.
Chang67 reported an
average of 37.8° of correction in seventeen patients in whom
post-traumatic thoracolumbar kyphosis was treated with anterior discectomy and
posterior osteotomy, but he performed multiple osteotomies in twelve
patients.
Kostuik et al.21
treated fifty-four patients with flatback syndrome with single-stage anterior
opening and posterior closing osteotomies and reported a mean correction of
29°. Booth et
al.13 reported
25° and 30° of correction in five patients with segmental
decompensation and twenty-three patients with global decompensation,
respectively. The average improvement of the sagittal vertical axis was 6.4 cm
in patients with sagittal imbalance. Kostuik et al. noted that 86% of the
patients were satisfied with the procedure and that function was notably
improved in 50%. In their landmark series, LaGrone et
al.6 evaluated the
results of sixty-six Smith-Petersen-type osteotomies done through the
pseudarthroses and fusion mass in fifty-five patients with symptomatic
flatback. They noted an average initial correction of 22° in lumbar
lordosis and 9° in kyphosis at the thoracolumbar junction, with an 8.1-cm
improvement in the sagittal vertical axis. The authors also reported a high
rate of complications, including pseudarthrosis and implant failure with
substantial loss of correction at the time of follow-up. As a result, repeat
operations were required in twenty-six patients, and 47% were still leaning
forward and had inadequate correction at the time of follow-up.
Pedicle Subtraction Osteotomy
The pedicle subtraction osteotomy, or transpedicular cortical
decancellation procedure, is a three-column posterior closing wedge osteotomy
hinging on the anterior cortex that has been frequently attributed to
Thomasen75,
although an earlier variant was described by Leong et
al.76. A so-called
eggshell variation of this procedure was described by
Heinig77 and has
also been utilized by several other
authors78,79.
The operative technique involves removal of all posterior elements at the
level of the correction including the pedicles and the superior and inferior
adjacent facet joints. A posterior wedge of cancellous bone is then removed
from the vertebral body in order to allow the desired correction, with or
without (the eggshell modification) removal of the entire posterior and
lateral vertebral body walls (Figs.
5-A,
5-B, and 5-C). The osteotomy is
then closed through compression of instrumentation or by extending the
patient's position on the operative frame (Figs.
6-A,
6-B, and
6-C)80.
Care must be taken to ensure that the neural elements are not compressed, and
the exiting nerve root now shares an enlarged foramen with the superior
adjacent root. Advantages of the procedure include the sagittal correction
achievable at a single level, the ability to achieve coronal correction by
asymmetric resection of the vertebral body and cortex, preservation of the
length of the anterior column, and the excellent potential for union provided
by abundant cancellous bone contact (Figs.
7-A and 7-B). Drawbacks include the technically demanding nature
of the procedure and the substantial bleeding frequently encountered as a
result of the epidural venous plexus and the bleeding cancellous
bone20.
Contraindications to pedicle subtraction osteotomy include an anterior
pseudarthrosis (unless a separate anterior procedure is performed) or
previously placed anterior instrumentation across the correction level.

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Figs. 5-A, 5-B, and 5-C Schematics demonstrating the bone resection pattern for a pedicle
subtraction osteotomy. Fig. 5-A The shaded area indicates the site for
the osteotomy.
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Figs. 5-B and 5-C Fig. 5-B Following removal of the posterior elements, the pedicles
are isolated but the medial wall is preserved initially to protect the neural
elements and dura during the vertebral body decancellation. Fig. 5-C
After the instrumentation has been placed securely, the pedicle and vertebral
wall resections are completed and the osteotomy is closed in a controlled
fashion. Note the absence of anterior column lengthening as the correction
rotates about the middle column, hinging on the anterior cortex.
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Figs. 6-A, 6-B, and 6-C Intraoperative lateral fluoroscopic views obtained during a pedicle
subtraction osteotomy. Fig. 6-A View following bone resection.
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Figs. 6-B and 6-C Fig. 6-B View during compression of instrumentation to facilitate
closure. Fig. 6-C View after completion and closure of the
osteotomy.
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Figs. 7-A and 7-B Immediate postoperative anteroposterior (Fig. 7-A) and lateral (Fig. 7-B)
radiographs following a pedicle subtraction osteotomy at the L3 fusion mass in
a patient with flatback. Note the improved lumbar lordosis and sagittal
balance (a change in the deviation of the sagittal vertical axis from 17 cm to
0.5 cm) compared with those seen on the preoperative radiographs
(Figs. 3-A and 3-B).
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In the treatment of ankylosing spondylitis, the average achievable
correction with single-level pedicle subtraction osteotomy has ranged from
32° to
36°78,81-84.
Wu et al.85
reported a mean of 38.8° of correction in thirteen patients in whom the
operation was performed for a rigid post-traumatic kyphosis. Wu et al. noted
only 2.3° of lost correction at two years postoperatively and no cases of
pseudarthrosis. Murrey et
al.79 treated
fifty-nine patients, including thirty-seven who had rigid adult deformity,
with pedicle subtraction osteotomy. In forty-two patients followed for an
average of 4.5 years, the average postoperative correction was 26°, with
5.5° of correction lost by the time of follow-up.
Similar results of pedicle subtraction osteotomy have been documented in
patients with flatback syndrome. Noun et
al.22 reported
34° of initial correction and 31° of maintained correction at one year
after the operation in ten patients with flatback syndrome. They found no
cases of pseudarthrosis and minimal perioperative complications. Berven et
al.33 utilized
pedicle subtraction osteotomy in thirteen patients with sagittal imbalance,
including eight with flatback syndrome. They reported 30° of restored
lordosis at the time of a two-year follow-up; correction of the sagittal
vertical axis was 71% initially and 63% at the time of follow-up. However,
although the authors noted no loss of correction in three patients with
ankylosing spondylitis, four of their other ten patients lost >2 cm of
correction of the sagittal vertical axis.
Polysegmental Wedge Osteotomy
Posterior closing polysegmental wedge osteotomy was introduced by
Püschel and
Zielke86 in 1982 as
a technique to restore physiologic sagittal alignment. The technique has been
utilized in the management of fixed sagittal imbalance secondary to ankylosing
spondylitis70,87,
but we are not aware of any reports of its use in patients with flatback
deformity. Nonetheless, polysegmental wedge osteotomy deserves mention here
because of its potential utility in the management of flatback syndrome. The
technique is similar to the Smith-Petersen osteotomy, except that slightly
less bone is resected posteriorly and less correction is attempted with each
osteotomy. Advantages of the polysegmental technique include its relative
safety throughout the thoracic spine and the reduced focal anterior column
distraction, which decreases the need for concomitant anterior release,
osteotomy, or fusion. Additionally, polysegmental wedge osteotomy may allow
restoration of a physiologic, harmonious curvature across multiple vertebral
segments, making the procedure well-suited for patients with ankylosing
spondylitis or flatback with junctional or degenerative kyphosis cephalad to
instrumentation, as opposed to achieving more dramatic angular correction at a
single level.
To our knowledge, the largest published series of patients with ankylosing
spondylitis managed with polysegmental correction was reported by Hehne et
al.87. They
described the operative complications and results in 177 patients treated with
polysegmental wedge osteotomy and pedicle screw fixation. The average
correction was 9.5° per level, for a total average correction of 43°
per patient. Follow-up at eighteen and thirty-six months demonstrated losses
of correction of 15% and 18%, respectively.
Vertebral Column Resection
Vertebral column resection, or vertebrectomy, and its modifications have
been utilized for multiple indications since the original description by
MacLennan88 in
1922. Bradford et
al.48,89,90
popularized the utilization of vertebral column resection in the treatment of
fixed or progressive sagittal plane imbalance. Vertebral column resection
should not be performed for the treatment of isolated flatback syndrome, but
it can be useful in patients with fixed sagittal imbalance in addition to
degenerative or adult scoliosis with severe coronal plane deformities. As
described by
Bradford90, the
procedure consists of anterior vertebral body resection with maintenance of a
cortical and periosteal flap through a convex-sided approach; posterior
element resection is then performed in a sequential or staged fashion,
followed by correction with instrumentation, with multiple wake-up tests.
Advantages of the procedure include the dramatic correction possible at a
single level and the overall shortening of the vertebral column, which
relieves tension on anterior neurovascular structures; however, vertebral
column resection is extremely technically demanding and can be associated with
considerable perioperative morbidity.
Boachie-Adjei and
Bradford89
performed vertebral column resection in sixteen patients who had progressive
loss of coronal and sagittal balance of various etiologies. They reported
preservation of normal lumbar lordosis, when it had been present, and
physiologic alignment in the sagittal plane in all patients at the time of
follow-up, at an average of three years postoperatively. More recently,
Bradford and
Tribus48 utilized
vertebral column resection to manage twenty-four patients with progressive
rigid coronal and sagittal decompensation. They noted correction of 82% in the
coronal plane and improvement in sagittal balance of 87%. The complication
rate was 43% in the study by Boachie-Adjei and Bradford and 58% in the study
by Bradford and Tribus.
Comparison of Techniques and Complications
Each osteotomy technique for correction of sagittal deformity offers
specific advantages and disadvantages as well as potential complications
(Table III). Van Royen and De
Gast70 performed a
meta-analysis comparing the results of polysegmental, closing wedge (pedicle
subtraction), and opening wedge (Smith-Petersen) osteotomies for the treatment
of ankylosing spondylitis. Their review included sixteen studies with a total
of 523 patients. Although pedicle subtraction provided, on the average,
slightly less correction than did polysegmental and opening wedge osteotomies
(35° compared with 40°), complication rates and loss of correction
tended to be lower with pedicle subtraction osteotomy. In addition, Van Royen
and De Gast reported higher mortality rates with Smith-Petersen-type
osteotomies and more implant breakage and a greater potential for insufficient
correction with polysegmental osteotomies. Although the authors noted
insufficient presentation of data and poorly outlined surgical indications in
most reports, they concluded that pedicle subtraction osteotomy appeared to be
a safer and more reliable procedure.
Overall complication rates following operative correction of flatback
syndrome have ranged from 20% to
60%6,13,21,22,33,48,89.
Pseudarthrosis has not been reported following pedicle subtraction osteotomy,
to our knowledge, but it developed after 38% (twenty-one) of fifty-five
Smith-Petersen procedures in one
report6 and 19%
(three) of sixteen vertebral column resections in
another89. This is
suspected to be due to the large surface area of cancellous bone available for
healing following pedicle subtraction
osteotomy20. Nerve
root injuries may occur after all techniques, but they are generally
transient. Specifically, transient radiculopathies have occurred following 0%
to 13% of Smith-Petersen
procedures6,13,19
and 0% to 31% of pedicle subtraction
osteotomies22,33.
Cauda equina syndrome due to epidural hematoma formation has been reported
following pedicle subtraction
osteotomy91,92.
Vascular injuries appear to be more common after Smith-Petersen osteotomies,
particularly when a combined anterior-posterior procedure is
performed21.
In patients with iatrogenic flatback deformity, the average amounts of
operative correction maintained following Smith-Petersen and pedicle
subtraction osteotomies reportedly have been comparable, ranging from 16°
to 30° and 30° to 31°,
respectively6,13,21,22,33.
To our knowledge, the outcomes of polysegmental osteotomies for the treatment
of sagittal imbalance have been reported only for patients with ankylosing
spondylitis, and, in what we believe to be the largest series of such
patients, Hehne et
al.87 reported
correction of 9.5° per level. There are also no available data on the
results of vertebral column resection for flatback syndrome, to our knowledge.
In two series in which that procedure was performed in patients with complex
spinal deformity, Bradford et al. reported 87% correction of the sagittal
vertical axis48 and
physiologic sagittal
alignment89.
Instrumentation
The wide spectrum of preoperative deformity and variations in operative
techniques preclude a detailed analysis of the instrumentation utilized for
the correction of fixed sagittal plane deformity in patients with flatback
syndrome. However, several points deserve mention. In early series, Harrington
compression instrumentation was associated with loss of correction and
frequent implant
failure2,3,6,7.
At a minimum, segmental instrumentation should be utilized in order to
maximize stability of the construct and osteotomy sites and to achieve
bilateral compression and aid bone-healing across osteotomy sites. There
should be at least fourand preferably six, seven, or eightpoints
of fixation on each side of an osteotomy. Most modern instrumentation allows
virtually any combination of screws and hooks, as dictated by the surgeon's
preference.
Segmental pedicle screw instrumentation is often preferred in order to
achieve rigid three-column fixation and control of the deformity. Several
authors have found pedicle screws to be useful in the management of fixed
sagittal
imbalance33,67,79,85,
and use of such screws may also help to prevent loss of correction and lower
the prevalence of implant
failure71. However,
when pedicle screw placement is not feasible because the prior fusion mass
obscures landmarks, segmental hooks, particularly with a so-called claw
construct93,
provide stable fixation and excellent compression. There may be better
maintenance of restored lordosis if anterior fusion is also
performed6, although
the use of pedicle subtraction osteotomy may obviate the need for anterior
procedures.
A detailed discussion of sacropelvic fixation is beyond the scope of this
discussion. However, when a fusion is being revised because of nonunion or
when a previous lumbar fusion is extended to the sacrum in the management of
flatback syndrome, supplemental fixation should be considered. At a minimum,
bicortical or so-called tricortical screw fixation should be performed at S1,
with the screws directed medially into the sacral
promontory94.
Additionally, supplementation with iliac screws, Luque-Galveston rods, and/or
an anterior interbody fusion should be strongly considered to minimize the
substantial risks of nonunion and caudad construct
failure95-98.
 |
Overview
|
|---|
The management of iatrogenic flatback syndrome is difficult and complex,
with a high rate of operative morbidity. Thus, attention should be focused on
the prevention of this deformity through preoperative assessment and planning
of the fusion, physiologic surgical positioning, and appropriate segmental
instrumentation with maintenance or restoration of lumbar lordosis and
sagittal alignment. Once flatback syndrome is established, appropriate
operative treatment can result in excellent correction of deformity and a high
degree of patient satisfaction despite high short-term complication rates. The
exact technique of operative correction depends on the patient's pathoanatomy
and the operating surgeon's experience. However, for most patients, pedicle
subtraction osteotomy appears to be the optimal surgical technique; it
provides excellent restoration of sagittal alignment and the potential to
address coronal alignment with a decreased rate of complications, particularly
pseudarthrosis and loss of correction. The instrumentation used following
operative correction should be segmental and compressive, and pedicle screws
appear to be ideal for this task.
 |
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