Risk of aorta injury in patients treated by accomplishing an anterior

advertisement
Aorta injury in opening wedge osteotomy
Risk of aorta injury in patients treated by accomplishing an anterior open wedge
and lengthening of anterior column for sagittal imbalance or kyphosis
Kao-Wha Chang, MD, Hung-Chang Chen, MD, Ku-I Chang, MD, Tsung-Chein Chen,
MD
Taiwan Spine Center and Department of Orthopaedic Surgery
Armed Forces Taichung General Hospital, Taiwan, Republic of China
Address all correspondence and reprint requests to: Kao-Wha Chang, MD
Taiwan Spine Center and Department of Orthopaedic Surgery,
Armed Forces Taichung General Hospital, Taiwan.
No.348, Sec.2, Chung-Shan Rd
Taiping City, Taichung Hsein, Taiwan, Republic of China.
TEL:(8864)23935823; FAX: (8864)23920136
E-Mail: kao-wha@803.org.tw
Aorta injury in opening wedge osteotomy
ABSTRACT
Study Design: Retrospective
Objectives: To inspect the suspected dominant roles of aorta injury including aorta
elongation at the level of osteotomy in patients with athromatous calcification and
propose a probable mechanism of aorta injury associated with treatment for sagittal
imbalance.
Summary of Background Data: Fatal aortic rupture has previously been reported in
four patients, all associated with opening wedge osteotomy.
Methods: Consecutive patients (n=354) with kyphotic deformity or sagittal
imbalance achieved an anterior open wedge and lengthening of anterior column by
opening wedge osteotomy (Group A, n=141), apical lordosating osteotomy (Group B,
n=79), and closing-opening wedge osteotomy (Group C, n=134) without aortic injury.
Radiographic analysis of the four suspected dominant roles was performed.
Results: No aorta-anterior longitudinal ligament adhesion was found any patient. The
mean lengthening of aorta with athromatous calcification at the level of osteotomy
was 2.8 cm (range 1.7–3.5). Sagittal translation of vertebral column occurred with
frequencies of 31% (Group A), 7% (Group B), and 21% (Group C). Spike formation
at the edges of an anterior open wedge occurred only in Group A (7%).
Conclusion: Aortic tolerance of lengthening at a single level is exceptional, even with
Aorta injury in opening wedge osteotomy
athromatous calcification. For a calcific aorta, spike formation at the edges of an
anterior open wedge combined with or without sagittal translation of vertebral column
probably was the major mechanism of aorta injury during the corrective procedures
for sagittal imbalance or kyphosis.
Key words: aorta injury, apical lordosating osteotomy, closing-opening wedge
osteotomy, opening wedge osteotomy
Aorta injury in opening wedge osteotomy
Key Points

Aortic tolerance of lengthening at a single level was exceptional, even with
athromatous calcification.

Spike formation at the edges of the anterior open wedge combined with or
without sagittal translation of cephalad or caudad vertebral column probably was
the major mechanism of aorta injury in ankylosing spondylitis patients with
calcific aorta treated with opening wedge osteotomy.

No aorta injury occurred in patients treated with apical lordosating osteotomy or
closing-opening wedge osteotomy, likely because of the absence of spike
formation at the edges of the anterior open wedge.
Aorta injury in opening wedge osteotomy
Mini Abstract
Consecutive patients (n=354) with kyphotic deformity or sagittal imbalance achieved
an anterior open wedge and lengthening of anterior column without aortic injury.
Aortic tolerance of lengthening at a single level was exceptional, even with
athromatous calcification. Spike formation at the edges of the anterior open wedge
combined with or without sagittal translation of vertebral column probably was the
major mechanism of aorta injury.
Aorta injury in opening wedge osteotomy
INTRODUCTION
In elderly patients, anterior column lengthening at a single level carries the potentially
catastrophic risk of elongation of the tethered aorta or calcific nondistensible aorta1-3.
We have conducted opening wedge osteotomy4 (OWO), closing-opening wedge
osteotomy5 (COWO) and apical lordosating osteotomy6 (ALO) (Fig 1A-C) for
correction of sagittal imbalance in 354 patients. The absence of aortic injury
associated with anterior open wedge and lengthening of anterior column at a single
level was an encouraging prelude to the present study. Herein we report on our
investigation of suspected dominant roles of aorta injury including aorta elongation at
the level of osteotomy in patients with advanced athermatous degeneration and
marked calcification seen roentgenographically in the aorta, sagittal translation of
vertebral column, spike formation at the edges of the anterior open wedge, and
adhesion between aorta and anterior longitudinal ligament. Furthermore, we propose a
probable mechanism of aorta injury associated with anterior column lengthening at a
single level by OWO.
MATERIALS AND METHODS
Patients
We retrospectively reviewed the medical records of 354 consecutive patients who
underwent OWO for kyphotic deformity (n=141, group A), apical lordosating
Aorta injury in opening wedge osteotomy
osteotomy in cord territory for thoracic or thoracolumbar kyphotic deformity (n=79,
group B), cauda equina COWO for sagittal imbalance or kyphotic deformity (n=134,
group C). All patients were managed by one surgeon at Armed Forces Taichung
General Hospital from 1990–2005. Group A was comprised of 129 men and 12
women (mean age 32.1 years, range 16–49) diagnosed with ankylosing spondylitis
with kyphotic deformity. Group B was comprised of 18 men and 61 women (mean
age 70.3 years, range 58–78) diagnosed with thoracic or thoracolumbar osteoporotic
kyphosis as a result of single or multiple vertebral compression fracture. Group C was
comprised of 51 men and 83 women (mean age 68.1 years, range 52–78) diagnosed
with flatback syndrome with instrumented lumbar fusion (n=16), degenerative
kyphosis (n=28), degenerative kyphoscoliosis (n=43), posttraumatic kyphosis (n=15),
iatrogenic kyphosis (n=13), and ankylosing spondylitis (n=19). All these surgical
procedures involved an anterior open wedge and lengthening of the anterior column at
a single level. No aorta injury occurred in any patient. Of the 354 patients in groups
A–C, 101 displayed athermatous deposits and calcification in the abdominal aorta that
were discerned by plain radiographs. Among these patients, 49 displayed athromatous
calcification marks exactly opposite the level of osteotomy seen roentgenographically
in the aorta. The 49 patients (35 females and 14 males, mean age 67.5 years, age
range 59.1–76.3) comprised group D. Group D treatment for correction of sagittal
Aorta injury in opening wedge osteotomy
imbalance or kyphotic deformity included ALO at L1 (n=4) and COWO at L2 or L3
(n=45). Preoperative diagnosis in the group D patients was flatback syndrome with
instrumented lumbar fusion (n=7), ankylosing spondylitis (n=7), degenerative
kyphosis (n=9), degenerative kyphoscoliosis (n=11), traumatic kyphosis (n=8), and
iatrogenic kyphosis (n=7).
Radiographic analysis
Four suspected dominant roles of aorta injury were inspected roentgenographically at
the level of osteotomy.
Anterior column and aortic lengthening
Anterior column lengthening at the level of osteotomy was measured by comparing
the pre- and postoperative length difference between the distance between the
cephalad and caudad endplates of the osteomized vertebrae. The aorta lengthening at
the level of osteotomy was measured by comparing the pre- and postoperative length
difference between the distance between the arthromatous calcification marks exactly
opposite the osteotomized vertebrae (Fig. 2). Only group D patients could undergo
this radiographic analysis according to pre-and postoperative radiographs, because the
aorta lengthening could not be measured in patients without calcified marks exactly
opposite the osteotomized vertebra.
Sagittal translation of vertebral column
Aorta injury in opening wedge osteotomy
Sagittal translation in group A patients was any measurable displacement more than 2
mm between the posterior inferior edge of the cephalad vertebral body and the
posterior superior edge of the caudad vertebral body at the OWO level (Figs. 3A and
3B). Sagittal translation in group B, C, and D patients was any measurable
displacement more than 2 mm between the posterior inferior edge of the cephalad
portion of the osteotomized vertebral body and the posterior superior edge of the
caudad portion of the osteotomized vertebral body (Fig. 3C).
Spike formation at the edges of the anterior opening wedge
The edges of the anterior opening wedge of all patients were inspected with
magnifying glass to search for spikes (Fig. 4).
Adhesion between aorta and anterior longitudinal ligament
A gap between the posterior wall of aorta and anterior longitudinal ligament at the
level of osteotomy identified preoperatively by plain radiographs, computed
tomography, or magnetic resonance imaging was indicative of a lack of adhesion
between the two structures (Fig. 5).
RESULTS
The mean anterior column lengthening at the level of osteotomy of the 49 group D
patients was 2.4 cm. The aorta lengthening averaged 2.8 cm (range 1.7–3.5). Aorta
and anterior column lengthening at the level of osteotomy were comparable (Fig. 2).
Aorta injury in opening wedge osteotomy
Sagittal translation occurred in 44 of the 141 group A patients (31%), seven of
the 79 group B patients (9%), 28 of the 134 group C patients (21%), and eight of the
49 group D patients (16%) (Fig 3).
All the edges of the anterior open wedges were smooth and without spike
formation in patients of groups B, C, and D. Ten of the 141 patients of group A (7%)
developed spikes at the edges of the anterior open wedge after OWO (Fig 4).
In all patients with or without athermatous calcification seen
roentgenographically in the aorta, the posterior wall of the aorta and anterior
longitudinal ligament at the level of osteotomy displayed roentgenographic evidence
of separation (Fig. 5A), with the exception of 18 group D patients who presented with
a large anteriorly protruding degenerative osteophyte. In the latter, a gap could not be
identified preoperative between the two structures (Fig. 5B). In eight of these 18
patients, migration of the athermatous calcification mark in the aorta wall located
caudad to the osteophyte preoperatively to a location cephalad to the osteophyte
postoperatively, or visa-versa, was evident upon comparison of the calcification mark
on the pre-and post-operative radiographs (Fig. 5C), which was evidence of a lack of
adhesion between the aorta and the osteophyte.
DISCUSSION
Fatal aortic rupture associated with the creation of an anterior open wedge and
Aorta injury in opening wedge osteotomy
anterior lengthening of the lumbar spine has been reported in four patients1–3. Of
particular concern, two patient had preoperative x-ray therapy that produced
adherence between the aorta and the underlying anterior longitudinal ligament and
resulted in a complete transverse tear in the posterior wall of the aorta after manual
osteoclasis and non-surgical or surgical correction1,2. Presently, none of the
retrospectively studied patients had preoperative x-ray therapy. Moreover, we found
nothing in the pathologies of the etiologies that raised concern of an aorta-anterior
longitudinal ligament adhesion. With the exception of the patients with large
anteriorly protruding, degenerative osteophytes at the osteotomized vertebra,
preoperative imaging revealed a gap between the two structures at the level of
osteotomy. Observations of postoperative migration in some group D patients
indicates that degenerative osteophytes do not produce adherence between the two
structures. Nonetheless, patients who have had preoperative X-ray therapy or an
operation between aorta and anterior longitudinal ligament that can produce
adherence between the two structures may be at risk of aortic injury following an
anterior open wedge and lengthening of anterior column for correction kyphosis, if
not accompanied by the freeing of the attached, relatively fixed aorta by a two-stage
procedure.
The other two vascular injuries evident in the literature3 include a tear in the wall
Aorta injury in opening wedge osteotomy
of aorta and dissection of media. These were related to one-level OWO for the three
ankylosing spondylitis patients with athromatous calcification of their abdominal
aorta. Stretching of calcific and nondistensible aorta may have created internal and
media tears, leading to rupture and aneurysm. However, presently we observed no
occurrence of aortic injury in 101 patients with athromatous calcification of their
abdominal aorta in whom sagittal correction was accomplished by an anterior open
wedge and lengthening of anterior column. Our findings concerning measurements of
aortic lengthening support the view that the aorta tolerates stretching and lengthening
exceptionally well, even with athermatous calcification. Our findings run counter to
the conventionally-held view.
In the operations described for the aforementioned two patients3, the spine was
osteotomized through the posterior element and corrected by direct pressure on the
osteotomy site (L2-3). The upper body and legs were extended to form a hollow
cavity between the patient’s ventral trunk and the surgical table, and the pressure
caused the ossified anterior vertebral column to fracture. If occurring with a sudden
snap,
avulsion of a bone fragment from the vertebral body can form a spike (Fig 4),
which can injure the aorta while the anterior wedge is opened. Before 1993, 39 of the
141 group A patients underwent manual osteoclasis and OWO with a similar
maneuver. Ten of the 39 patients developed spikes at the edges of the open wedges.
Aorta injury in opening wedge osteotomy
Fortunately, our patient criteria for OWO were an age of less than 50 years and the
absence of athromatous calcification of aorta4. So, despite spike formation, no
vascular injury occurred in these 10 patients, likely owing to a sufficiently flexible
aorta. After 1993, if osteoclasis occurred at the intervertebral disc at the level of
osteotomy during performed posterior osteotomy by gravity of the patient’s trunk or
by light pressure on the osteotomy site after osteotomy, we consistently observed that
the edges of the anterior open wedge were smooth and without spike formation. If the
ossified anterior vertebral column was too hard to be fractured by light pressure, a
fluoroscopically guided osteotome was placed through the intervertebral disc at the
level of the osteotomy. Then, osteoclasis was formed by gentle manipulation. In this
way, that osteoclasis that forms occurs at the anterior disc space. Correction should
not be started without assured osteoclasis and is accomplished by a slow and finely
controlled closure of the osteotomy. As the posterior wedge is closed, correction
occurs in the anterior vertebral column by opening of the anterior disc space with
smooth edges.
Unlike OWO, in which the whole anterior an middle vertebral columns can be
fractured by manual osteoclasis, potentially resulting in spike formation, the thin
anterior cortex of the osteotomized vertebral body fractures in a greenstick manner,
and opens with smooth edges and without spike formation during the corrective
Aorta injury in opening wedge osteotomy
procedures of COWO and ALO. Accordingly, no spike was found in patients of
groups B, C, and D.
Previously, we have demonstrated that sagittal translation is one of the basic
mechanisms for correction of sagittal imbalance in ankylosing spondylitis by OWO
(Figs. 3A and 3B)7. Similar to OWO, the ALO, and COWO procedures involve
three-column release and unrestricted movement of the hinge of correction, which can
produce sagittal translation (Fig. 3C). Sagittal translation subjects the aorta to an
anteriorly directed force in addition to stretch. In the presence of sagittal translation,
spike formation at the anterior edges of the open wedge might result in a stabbing
injury of the tensed aorta or internal media tears due to stress concentration effect.
While the absence of X-ray and postmortem information makes confirmation
impossible, we believe spike formation combined with or without sagittal translation
very probably was the main mechanism responsible for the aorta injury in the three
cases.
Aorta injury in opening wedge osteotomy
References
1. Lichtblau PO, Wilson PD. Possible mechanism of aorta rupture in orthopaedic
correction of rheumatoid spondylitis. J Bone Joint Surg Am 1956;38:123-7.
2. Klems VH, Friedebold G. Ruptur der Aorta abdominalis nach
Aufrichtungsoperation bei Spondylitis ankylopoetica. Z Orthop 1971;108:554-63.
3. Weatherly C, Jaffary D, Terry A. Vascular complications associated with osteotomy
in ankylosing spondylitis: a report of two cases. Spine 1988;13:43-6.
4. Chang KW, Chen YY, Lin CC, et al. Closing wedge osteotomy versus opening
wedge osteotomy in ankylosing spondylitis with thoracolumbar kyphotic deformity.
Spine 2005;30:1584-93.
5. Chang KW, Chen HC, Chang KI, et al. Closing-opening wedge osteotomy for the
treatment of sagittal imbalance. Spine 2007, submitted.
6. Chang KW, Chen YY, Lin CC, et al. Apical lordosating osteotomy and minimal
segment fixation for the treatment of thoracic or thoracolumbar osteoporotic
kyphosis. Spine 2005;30:1674-81.
7. Chang KW, Chen HC, Chen YY, et al. Sagittal translation in opening wedge
osteotomy for the correction of thoracolumbar kyphotic deformity in ankylosing
spondylitis. Spine 2006;31:1137-42.
Aorta injury in opening wedge osteotomy
FIGURE LEGENDS
Figure 1. Diagrams of opening wedge osteotomy (A and B), apical lordosating
osteotomy (C and D), and closing-opening wedge osteotomy (E and F). A. Lateral
view outlining the bone block to be resected. Total pediculectomy avoided nerve root
compression by the remaining pedicle. B. Postoperative lateral view depicting the
correction achieved by vertebral body posterior border hinging, of vertebral body,
closure of the posterior osteotomy, and creation of an anterior column open wedge. C.
Lateral view depicting the bone block to be resected. D. Postoperative lateral view
depicting the correction achieved by lordotic cage hinging and creation of an
opening wedge of the anterior column. The lordotic cages were used to maintain the
height of middle column, preventing cord kinking after correction. E. Lateral view
depicting the bone block to be resected. F. Postoperative view depicting the correction
achieved by hinging on the closed middle column, closing the intravertebral
osteotomy, and creating an open wedge of the anterior column.
Figure 2. Data from a 67-year-old Group D patient with iatrogenic kyphosis
treated with closing-opening wedge osteotomy at L2. A. Presurgical image
showing 75o kyphosis, 15 cm sagittal balance, 61o T12–S1 lordosis, and athromatous
calcification marks exactly opposite L2. Final values were -30o (kyphosis), 3 cm
Aorta injury in opening wedge osteotomy
(sagittal balance), and -55o (T12–S1 lordosis). B. Anterior column lengthening (2.2
cm) determined by measuring the difference in length between black arrows pre- and
postoperatively. Aorta lengthening was 2.4 cm by measuring the difference in length
between white arrows pre- and postoperatively. The black arrows indicate the same
points of the cephalad and caudad endplate of the osteotomized vertebra before and
after operation. The white arrows indicate the same athromatous calcified marks
exactly opposite to osteotomized vertebra before and after operation. Aorta and
anterior column lengthening were comparable.
Figure 3. Sagittal translation data. A. Cephalad vertebral column sagittal translation
in OWO. B. Caudad vertebral column sagittal translation in OWO. C. Sagittal
translation in COWO.
Figure 4. Spike formation in OWO for ankylosing spondylitis kyphosis.
Figure 5. Imaging of posterior wall of aorta. A. A gap between the posterior wall of
aorta and anterior longitudinal ligament could be identified by plain radiographs. B. A
gap between posterior wall of aorta and the large anteriorly protruding degenerative
osteophyte could not be identified by plain radiographs and magnetic resonance
Aorta injury in opening wedge osteotomy
imaging. C. The athromatous calcification mark in the aorta (black arrow) located
caudad to the osteophyte preoperatively migrated to a location cephalad to the
osteophyte postoperatively demonstrated no adhesion between the two structures.
Aorta injury in opening wedge osteotomy
Aorta injury in opening wedge osteotomy
Aorta injury in opening wedge osteotomy
Aorta injury in opening wedge osteotomy
Aorta injury in opening wedge osteotomy
Aorta injury in opening wedge osteotomy
Aorta injury in opening wedge osteotomy
Aorta injury in opening wedge osteotomy
Aorta injury in opening wedge osteotomy
Download