TITLE: Survivorship analysis of Adjacent Segment Disease
(ASD) in lumbar arthrodesis.
AUTHORS:
Dr. Esteban Calcagni, Dr. Horacio Sarramea.
It has always been considered that the segment adjacent to a
lumbar fusion suffers a mechanical overload which paves the way
to an inexorable, and most likely accelerated, disc degeneration,
given this segment does not have the physiological features
typical of a lumbosacral disc (30).
The definition of ASD, as the degenerative disc changes that
develop in spaces close to a fusion, is in general a very broad
statement, given that any abnormal process could be considered
as such (17).
As regards the etiology of the phenomenon in question, the exact
mechanism is uncertain. A variety of studies have considered the
connection between age, gender, menopause, number of fusion
levels, termination of the fusion in a healthy disc or with a certain
degree of degeneration, etc., with very variable results.
It is, however, only natural to assume that these factors play some
role in generating an ASD, as well as the individual propensity
towards disc degeneration not due solely to a fusion process.
Though biomechanical alterations caused by a lumbar fusion
probably play a significant role in generating an ASD, as far as
the prevalence and cause is concerned, there is no real consensus.
Adjacent Segment Degeneration would seem to respond to the
natural history of the disc disease and to patients’ genetic
propensity, and occurs mostly among elderly patients and women,
as does the prevalence of the degenerative disease in healthy
individuals.
This paper aims at determining clinically and/or by imaging
[radiologically] the percentage of patients developing ASD when
an arthrodesis is performed on their lumbar spine, and the
percentage of those requiring surgical treatment.
MATERIALS & METHODS
A retrospective analysis was performed on the medical histories
of 300 patients operated on between 1989 and 2008 over a total of
758 surgeries performed. Only patients displaying solid
arthrodesis with good post-operative evolution, without
significant complications have been included. All of these
displayed the adjacent disc with changes according to Pfirmann
MRI classification types 1, 2 or 3 (19).
A black disc in the MRI, without radiological evidence of lesion,
was not considered as manifest discopathy.
Sample description:
Average age of the sample population analyzed was 50 y. of age
(D.S=12 years) ranging between 21 and 75.
174/300 (i.e. 58%) were female (50.66%) and 126 (42%) were
male. Average follow-up was 8.6 years ranging between 3 and 22
years.
In all the cases under study an instrumented arthrodesis was
performed, with 75/300 (25%) patients being equipped with a
Hartshill frame and steel sublaminar wires, and 225/300 (75%)
patients equipped with titanium pedicle instrumentation.
Conditions registered as ASD in the post-operative stage were:
- Spondylolisthesis (antero or retrolysthesis)
- Pfirmann type 2 and 3 disc changes (19)
- Instability
- Disc hernia
- Canal stenosis
- Facet hypertrophy
- Osteophytosis
- Degenerative scoliosis
ASD patients have been divided into two broad groups:
Group I: Degenerative disease, 235/300 patients (78%).
Group II: Isthmic and dysplastic Spondylolisthesis, 65/300
patients (22%).
ASD existence has been assessed
a) Clinically on the basis of one or more of the following signs
and/or symptoms: severe lower back pain, lumbosciatalgia,
neurological claudication and coronal or sagittal imbalance.
b) radiologically [by imaging] using lateral and dynamic X-rays
to highlight ASD due to a reduction in the disc space exceeding
10% as compared to the pre-operative X-ray (Miyakoshi Method)
(15), the presence of antero or retrolysthesis as well as traction
osteophytes and sclerosis of the vertebral plates.
Visible changes shown by MRI involve Pfirmann type 4 and 5
disc changes, canal stenosis images, disc hernia and Modic
changes (16).
In patients operated on using a steel Hartshill frame, the MRI is
performed using open, low magnetism units, and if there is any
difficulty in the diagnosis, this is completed with a 3D CT scan
and myelotomography sections.
RESULTS:
An assessment of the data obtained in our statistics revealed that
of the total number of patients subjected to surgery who had solid
arthrodesis in the lumbar spine, 78/300 (26%) showed
radiological signs of ASD, 47/78 (26.%) displayed clinical and
radiological ASD (symptomatic patients), and 31/78 (40%) only
displayed radiological changes but were asymptomatic.
Of the 47 symptomatic patients 32 (68 %) were given
conservative treatment with very good results, or at least their
symptoms did not require further treatment at the time. The most
frequent symptoms were lower back pain, sacroiliac joint pain,
and lumbosciatalgia in third place.
15 out of 47 patients (32%) required additional surgical treatment.
Only one of them required 2 review surgeries.
In all these cases arthrodesis extension was performed with
instrumentation. The percentage of patients operated on for an
ASD was 5 % of the total number of patients under review
(n=300). All the patients operated on for ASD belonged to Group
I (degenerative).
Among patients in Group II, Spondylolisthesis, only 7 patients
were found to have Pfirmann type 1 and 2 disc changes and mild
symptoms that improved with medical treatment.
One particular case (107) is that of a female patient operated on in
2004 with Spondylolisthesis and lysis at two levels, grade 3 L4L5
and grade 2 L3L4. This patient has evolved with some change in
the sagittal contour over the last 2 years but without any
significant pain symptoms.
As to the connection between gender and ASD, of the 47 patients
30 (68.82%) were female and 17 (36.17%) were male.
Reparation surgery was required on 8/15 women (53%) and 7/15
men (47%), in all cases on the upper adjacent segment to the
fusion.
In the same proportion, 7/15 patients (47%) had had prior surgery
using frame and wires and 8/15 (53%) of them using pedicle
screws.
It is worth noting that the number of patients with a Hartshill
frame, though significantly lower, responds to the group subjected
to surgery in the earlier years of this study and reached review
surgery at an older age.
The time for appearance of pain symptoms in ASD patients was
almost invariably within the first 3 years following surgery.
Repair surgery was performed within the first 7 years in 11 of
these cases, in another 4 cases between the 11th and 12th year and
in one case 8 months after surgery. Only one patient required 2
review surgeries, performed 2 years apart, within 6 years of the
initial surgery.
The data obtained among the sample was extrapolated to the
general population using Confidence Intervals (Confidence Bands
of 95%).
DISCUSSION
Many of the publications concerning percentages of ASD
appearance are controversial and variable. Numbers range from
100% mentioned by Miyakoshi et al in a study on 45 patients (15),
where all of them were reported to have lost disc height, to
Frymoyer who reported 5.2 %. Opinions range similarly, from that
of this latter who held that “…an ASD occurring around a fusion
cannot be a significant complication” (3), to that of Hall, E B MD
(13), who in his retrospective study on adjacent disc degeneration
in lumbar fusions with instrumentation says: “adjacent segment
disc degeneration is a well-known consequence of spinal fusion”.
Other authors, in contrast to Hall’s statement, hold that the
appearance of ASD was not affected by the fusion procedure,
which is less of a cause than each individual’s genetic features or
constitutional factors which contribute to them developing an
ASD (Penta, 18) (Wai 25).
A number of publications have suggested that surgical fusion of
lumbar discs increases the load on adjacent discs, which could
lead to the likelihood of accelerating the occurrence of an ASD
(1, 4, 7, 18, 21, 23).
As to the speed of disc degeneration (acceleration) in non-fused
segments, a study by Ghiselli and Wang (5) contains an
interesting caseload broadly similar to the cases in our own study.
Out of 215 patients, 59 (27.4%) had ASD. They found 16.5% disc
degeneration after 5 years and 38% after 10 years.
To support the idea that this speed is accelerated if there has been
prior fusion, the study by Kumar (13) shows long-term follow-up
(30 years) of 56 patients operated on between 1968 and 1970,
50% of whom were subjected to a fusion (in situ posterior
arthrodesis) while the other half were treated with a simple
decompression.
On the basis of simple profile X-rays and maximum flexion and
extension profile X-rays it was found that degenerative changes
were twice as frequent in patients with fusion than in patients
only subject to decompression.
A large number of these biomechanical studies have confirmed
that fusion causes additional mechanical stress on the adjacent
disc. Intra-disc pressure increases, which means facet load is also
greater. As regards joint facets, mention should also be made of
the potential damage they could suffer in the upper pedicle screw
placement technique. Facet articulation protection is a modifiable
risk factor, which could reduce the percentage of ASD
development.
In their experience involving 65 patients with pedicle
instrumentation fusions, Hirobayashi and Aota (1) found 24.6%
of ASD, with retrolysthesis the most frequent form accounting for
over 60% of cases. Similar results are reported by Chopin D. (12)
among a caseload of 83 patients, 36% of which had ASD, among
whom retrolysthesis is once again the most frequent type.
Okuda and Morita (20) report 87 patients with lumbar arthrodesis
and classify them into 3 broad groups: Group I: patients without
any disease following surgery, 67%.
Group II: patients with ADS not involving neurological
effects, 29%.
Group III: patients with ADS, re-operated, 4%.
The data obtained in our own study is substantially similar.
A preliminary study conducted by our group in 2007 (30) on 150
patients in similar study conditions, ASD occurred in 23.33% of
cases. 77.14% received conservative treatment and 22.85% were
treated with surgery. By approximation it was therefore held at
the time that 1 out of 4 patients with an ASD could require review
surgery.
Based on the current data, among the group of symptomatic
patients, 15 of 47 (32%) required surgical treatment. The ratio
now is 1 out of 3.
The increased ratio of cases requiring surgery is probably due to
the longer follow-up time involved.
Although the exact mechanism is still uncertain, the alteration in
biomechanical tensions would seem to play a key role in ASD
development. It is significant that patients who most frequently
develop ASD are more elderly individuals with a basic
degenerative disease, i.e. group I in our study, probably due to the
impossibility of these patients’ spine to adapt to the
biomechanical changes caused by a fusion.
Other authors hold, clearly with common sense, that age is
likewise a predisposing factor in healthy individuals.
Patients suffering from isthmic or dysplastic spondylolisthesis,
group II, are younger in age (average age 40 y. of a.), with ASD
occurring in a significantly lower percentage of cases. Out of 65
patients only 7 showed mild disc variations, and symptoms that
all improved with conservative treatment.
Videbaeck (24) says that, though ASD is a long-term
complication of a fusion and neither its prevalence nor its cause
are well documented, ASD is one of the main reasons for
introducing techniques to preserve segment movement as an
alternative to fusion.
Based on this opinion, Kim et al. (9, 10) found that semi-rigid
implants led to a higher percentage of ASD than traditional ones.
In his publication on Dynesys, Kumar (29) points out that
“degeneration of the adjacent disc continues despite the use of
dynamic stabilization in connection with fused discs.”
In our own experience we have found that the largest percentage
of ASD occurred in individuals having pre-operative lumbar
lordosis described as hypolordosis or hyperlordosis.
Umehara S et al (28) studied the biomechanical effect of postoperative hypolordosis on arthrodesis, and its effect on the
adjacent disc. Experimental work on corpses shows it causes an
overload of forces on posterior structures.
As regards treatment, there is broad agreement as to the existence
of ASD symptoms not being connected to a negative prognosis
(7.48). Surgery is generally not prescribed and is viewed solely as
an option in the event conservative treatment fails. All the
surgical cases symptoms involved severe canal stenosis with
neurological deficit and segment instability.
CONCLUSIONS:
1- Patients suffering from symptomatic ASD mostly improve with
conservative treatment (in 32/47 cases - 68%).
IC95% 0.53-0.80 (between 53% and 80%).
2- We found that review surgery in a patient with ASD accounts
for 32% of cases (15/47).
IC95% 0.19-0.47 (between 19% and 47%).
3- Review surgery was performed on 15/300 of the total number
of patients included in the sample, corresponding to 5%.
IC95% 0.03-0.8 (between 3% and 8%).
Bibliography
1. Aota Y; Hirobayashi S. Post fusion instability at the adjacent
segments after rigid pedicle screw fixation for degenerative
lumbar spinal disorders. J Spinal Disord US. Dec 1995, 8 (6)
p464-73.
2. Etebar S; y col. Risk Factors for adjacent-segment failure
following lumbar fixation with rigid instrumentation for
degenerative instability. J Neurosurgery. US Apr.1999, 90 p1639.
3. Frymoyer JW, Hanley EN, Jr., Howe J, et al. A comparison of
radiographic findings in fusion and nonfusion patients ten or more
years following lumbar disc surgery. Spine 1979; 4:435–40.
4. Ghiselli G; et al. Adjacent segment degeneration in the lumbar
spine. J Bone Joint Surg AM .US.Jul 2004, 86-A (7) p1497-503.
5. Ghiselli G; Wang JC; Hsu WK; Dawson EG. L5-S1 segment
survivorship and clinical outcome analysis after L4-L5 isolated
fusion. Spine US Jun 15 2003. 28 (12) p1275-80.
6. Gillet P; y col. The fate of the adjacent motion segments after
lumbar fusion. J Spinal Disrd Tech,US. Aug 2003, 16 (4) p338-5.
7. Herkowitz HN; y col. Management of degenerative disc disease
above an L5-S1 segment requiring arthrodesis. Spine US, Jun
1999, 24 (12) p1268-70.
8. Jinkins JR; y col. Acquired degenerative changes of the
intervertebral segments at and suprajacent to the lumbosacral
junction. A radioanatomic analysis of the nondiskal structures of
the spinal column and perispinal soft tissues. Radiol Clin North
Am US, Jan 2001, 39 (1) p73-99.
9. Kim YE; y col. Effect of disc degeneration at one level on the
adjacent level in axial mode. Spine US, Mar 1991, 16 (3) p331-5.
10. Kim KT, Lee SH, Lee YH, et al. Clinical outcomes of 3 fusion
methods through the posterior approach in the lumbar spine.
Spine 2006; 31:1351–7.
11. Kulkarni V; y col. Accelerated spondylotic changes adjacent
to the fused segment following central cervical corpectomy:
magnetic resonance imaging study evidence. J Neurosurg. Spine,
US, Jan. 2004, 100 (1) p2-6.
12. Kumar MN; Chopin, D. y col. Correlation between sagittal
plane changes and adjacent segment degeneration following
lumbar spine fusion. Eur spine J. (Germany), Aug. 2001, 10(4)
p314-9.
13. Kumar MN; Jacquot F; Hall H. Long-term follow-up of
functional outcomes and radiographic changes at adjacent levels
following lumbar spine fusion for degenerative disc disease. Eur
Spine J (Germany). Aug. 2001, 10 (4) p309-13.
14. Lee CK; y col. Accelerated degeneration of the segment
adjacent to a lumbar fusion. Spine US, Mar 1988, 13 (3) p375-7.
15. Miyakoshi N, Abe E, Shimada Y, et al. Outcome of one-level
posterior lumbar interbody fusion for spondylolisthesis and
postoperative intervertebral disc degeneration adjacent to the
fusion. Spine 2000; 25:1837–42.
16. Modic MT, Steinberg PM, Ross JS, et al. Degenerative disk
disease: assessment of changes in vertebral body marrow with
MR imaging. Radiology
1988;166:193–9.
17. Paul Park, MD, Hugh J. Garton, MD, MHsc, Vishal C. Gala,
MD, Julian T. Hoff, MD, and John E. McGillicuddy, MD.
Adjacent Segment Disease after Lumbar or Lumbosacral Fusion:
Review of the Literature. Spine Vol. 29 n 17 pp 1938-1944, 2004.
18. Penta M, Sandhu A, Fraser RD. Magnetic resonance imaging
assessment of disc degeneration 10 years after anterior lumbar
interbody fusion. Spine 1995;20:743–7.
19. Pfirmann CW, Metzdorf A, Zanetti M, et al. Magnetic
resonance classification of lumbar intervertebral disc
degeneration. Spine 2001;26:1873–8.
20. Okuda S; Morita y col. Risk factors for adjacent segment
degeneration after PLIF. Spine USA, 2004, 29 (14) p1535-40.
21. Rahm MD, Hall BB y col. Adjacent-segment degeneration
after lumbar fusion with instrumentation a retrospective study. J
Spinal disord US, Oct 1996, 9 (5) p392-400.
22. Saadaki N, Hidezo Y. Y col. Long-term follow-up of posterior
Lumbar Interbody Fusion. J Spinal Disorders 1999, (12) p293-99.
23.Throckmorton TW. The impact of adjacent level disc
degeneration on health status outcomes following lumbar fusion.
J Spinal Disord Tech US. Aug 2003, 16 (4) p.418.
24. Videbaek, MD,* Niels Egund, MD, DMSc,† Finn B.
Christensen, MD.Adjacent Segment Degeneration After Lumbar
Spinal Fusion: The Impact of Anterior Column Support
A Randomized Clinical Trial With an Eight- to Thirteen-Year
Magnetic Resonance Imaging Follow-up. Spine 2010. Vol 35
n 22. pp 1955.1964.
25. Wai EK, Santos ER, Morcom RA, et al. Magnetic resonance
imaging 20years after anterior lumbar interbody fusion. Spine
2006; 31:1952–6.
26. Whitecloud TS; y col. Operative treatment of the degenerated
segment adjacent to lumbar fusion. Spine US, Mae 1 1994, 19
(19) 2244-5.
27. Wigfield C; y col. Influence of an artificial cervical joint
compared with fusion on adjacent-level motion in the treatment of
degenerative cervical disc disease. J Neurosurg Spine US Jan
2002, 96 (1)p17-21.
28. Zindick M, Umehara S. The biomecanical effect of
postoperative Hypolordosis in instrumented and adjacent spinal
segments. Spine 2000, (25) 432-37.
29. Kumar M.N . Spine Dec. 2008 vol 33 n 26.
30. Calcagni, Esteban. Buenos Aires, Argentina. Degeneración
del segmento adyacente a una fusión lumbar. [Adjacent Segment
Degeneration in lumbar fusion]. Submitted to become a Full
Member of the Argentine Spine Disease Society. August 15th
2007.