Introduction
Degenerative lumbosacral stenosis (DLSS) is a common syndrome affecting mainly large
breed dogs.[1]
[2] Degenerative lumbosacral stenosis is a multifactorial degenerative disorder characterized
by intervertebral disc degeneration/herniation and bony and soft tissue proliferations
that contribute to spinal stenosis and cauda equina compression leading to pain, lameness
and neurological signs.[3] Clinical suspicion of DLSS based on low back pain and findings on neurological examination
is confirmed by findings on computed tomography (CT) and magnetic resonance imaging
(MRI), with MRI giving the most detailed information on bony and soft tissue changes.
MRI findings may include intervertebral disc degeneration and herniation, compression
of the dural sac and/or nerve roots, focal cauda equina neuritis, foraminal stenosis
and bony changes like end plate sclerosis and spondylosis.[3]
[4]
[5] Conservative medical and surgical treatment have been suggested in veterinary literature,
but at this time evidence-based recommendations are lacking.[6] Surgical treatment consists of dorsal laminectomy, dorsal fenestration (or annulectomy)
and nuclear pulpectomy.[2]
[3] In case of foraminal stenosis and nerve root compression, the surgery can be expanded
to include foraminotomy or distraction with, for instance, pedicle screw and rod fixation
(PSRF).[7]
[8]
[9]
[10] Pedicle screw and rod fixation has initially been used to treat pre-existent lumbosacral
instability and to prevent further subluxation of the sacrum[3]
[11] the safe corridors for the pedicle screws have been described in detail.[3]
[11]
[12] When PSRF is combined with distraction, it also restores the intervertebral disc
and foraminal width which is beneficial in case of severe DLSS and foraminal stenosis.[9]
[10] Other techniques of fixation at the lumbosacral level include transarticular fixation
of the facet joints using pins or transarticular positional screws.[13]
[14]
[15]
[16] Distraction can be further biomechanically supported by the insertion of an intervertebral
spacer like a cage which may also promote vertebral fusion which is not achieved by
PSRF alone.[9]
[10] Vertebral fusion through the cage has been demonstrated in dogs with caudal cervical
spondylomyelopathy who were treated with an instrumented intervertebral cage, [17] but has not been reported previously for the lumbosacral segment.
The aim of the present case report was to describe and evaluate a distraction–stabilization
technique using an intervertebral titanium cage and PSRF in a dog with severe DLSS.
Outcome was assessed during long-term follow-up, and vertebral fusion was examined
using radiography, CT, micro-CT and histopathology.
Case Description
Animal and Clinical Examination
A 4-year-old male neutered Leonberger was presented with complaints of difficulty
rising, sitting and lying down. On clinical examination, low back pain was evoked
when pressure was applied at the lumbosacral junction. On neurologic examination,
sciatic and tibial cranial hyporeflexia and pseudo hyperreflexia of the patellar reflex
were present, consistent with a lumbosacral lesion localization.
Diagnostic Imaging
Magnetic resonance imaging (Philips scanner 2013, type Ingenia 1.5T Omega, The Netherlands)
showed severe DLSS with signs of chronic pre-existent discospondylitis at the level
of L7–S1, characterized by severe intervertebral disc degeneration (Pfirrmann grade
V,[18]), Hansen type 2 disc protrusion, signal intensity changes of the end plates and
vertebral bodies indicating oedema (Modic changes [MC]) type 1, and sclerosis (MC
type 3[19]), L7–S1 foraminal stenosis, central and lateralized compression of neural structures
and spondylosis ([Fig. 1]). Pre-existing chronic discospondylitis was added as co-existing disease considered
likely, based on the severity of the signal intensity changes of the end plates and
vertebral bodies.
Fig. 1 Sagittal T2-weighted magnetic resonance imaging (T2W MRI) in neutral position. At
the level of the white arrow (L7–S1), signal intensity is absent. There is a large
amount of hypointense extradural material noted at the ventral aspect of the spinal
canal at the level of L7–S1, causing severe compression of the cauda equina at this
level. The end plates of L7–S1 are ill-defined and along the caudal half of L7 and
the cranial half of S1, diffuse hypointense signal is noted (*). Also, heterogenous
T2W hypointense signal is noted ventrally to L7–S1. MRI findings are compatible with
chronic pre-existent discospondylitis and degenerative lumbosacral stenosis (DLSS).
Surgical Technique
The dog was initially treated conservatively, including a limited exercise regime
and medication, but clinical signs recurred, and surgical treatment was indicated.
Medical treatment consisted of a non-steroidal anti-inflammatory drug for dogs given
for the patient's weight (Novacam for dogs 1.5mg/ml, AST Farma, Oudewater, The Netherlands)
with a starting dose of 0.2 mg/kg and continued as 0.1 mg/kg once daily. In addition,
the dog was treated with amoxicillin/clavulanic acid in a dose of 12.5mg/kg twice
daily (Synulox, Zoetis, Cappele a/d IJssel, the Netherlands). Surgical treatment consisted
of dorsal laminectomy at the level of L7–S1 according to the technique described by
Danielsson and Sjöström.[20] Briefly, the dorsal spinous process and caudal half of the dorsal lamina of L7 and
the dorsal lamina and dorsal spinous process of S1 were removed leaving the juxta-epiphyseal
joints intact. The dorsal spinal process was removed using a Ruskin bone rongeur and
the dorsal lamina was removed using a 5 mm fluted burr (Stryker, Amsterdam, The Netherlands).
Bone was collected from the dorsal spinal process and the cancellous bone and cortical
bone chips were mixed and saved to be used later as autologous bone graft. Partial
discectomy included the dorsal annulus fibrosis and the nucleus pulposus followed
by curettage using a 2-mm spoon bone curette. Disc material from the nucleus pulposus
cavity was sampled for aerobic and anaerobic microbiological culture. Decompression
was followed by instrumented insertion of an intervertebral body spacer. First, two
titanium monoaxial pedicle screws (DePuy Synthes, Johnson-Johnson, Oberdorf, Switzerland)
were inserted on the right side in S1 and L7 using previously determined safe entry
points.[12] Second, an intervertebral spacer was inserted identical to the one used in patients
with cervical spondylomyelopathy.[17] Distraction with a cervical vertebral body distractor was applied to the pedicle
screws which opened the intervertebral disc space. Limited osteostixis of the sclerotic
vertebral end plates was performed with a 2.0 mm drill. A trial cage was inserted
with a custom-made implant holder (DePuy Synthes) and when fit was confirmed, the
definitive titanium cage (SynCage-C Short, curved, DePuy Synthes) was inserted and
seated just below the dorsal vertebral cortex ([Fig. 2]). The cauda equina was carefully deflected laterally, without severe traction, using
neurosurgical non-traumatic nerve retractors. Before insertion the cage was filled
with the prepared, mixed, cancellous-cortical, autologous bone graft. Third, two monoaxial
pedicle screws were inserted on the left side in the same manner as on the right,
and L7 and S1 pedicle screws were connected with a 5 cm long titanium bar (diameter
6-mm) and both bars were firmly tightened to the pedicle screws ([Fig. 2]). Finally, a free autogenous fat graft was harvested and placed in the laminectomy
defect.
Fig. 2 Left-right lateral radiographs before and after treatment by distraction–fixation
using an intervertebral spacer and pedicle screw and rod fixation (PSRF). Preoperative
(A), postoperative (B), 12 months postoperative (C) and 26 months (post-mortem) postoperative (D) radiographs. The cage was impacted just ventral to the dorsal surface of the vertebral
bodies of L7–S1.
Postoperative Management
Immediate postoperative care included monitoring of the neurologic status, urinary
bladder function, antibiotic therapy and analgesia. The dog went home on carprofen
(Carporal, AST Farma, Oudewater, The Netherlands, 2 mg/kg orally) twice daily for
14 days, tramadol (Tramadol, AST Farma, Oudewater, The Netherlands 5 mg/kg) three
times daily for 14 days and amoxicillin–clavulanic acid (Synulox, Zoetis, Capelle
a.d IJssel, The Netherlands, 13.5 mg/kg) twice daily for 10 days, with 6 weeks of
leash walks only and slowly increasing the amount of exercise. The amoxicillin–clavulanic
acid was stopped when aerobic and anaerobic bacterial culture of the swab returned
negative.
Clinical Follow-up
The dog returned for clinical check-ups at 6 weeks, 6, 7.5, 9 and 12 months after
surgery. Low back pain resolved, and at 7.5 months a slight proprioceptive deficit
of the left hindlimb was noted, but at the same time a left cranial cruciate ligament
rupture was diagnosed. At 1 year after surgery the dog was presented with bilateral
cranial cruciate rupture and medial coronoid disease and at 26 months after surgery
the dog passed away due to a gastric dilation and volvulus. With the owner's consent,
the lumbosacral spine segment was harvested for further examination.
Follow-up Imaging
Follow-up imaging included radiography (Digital RAD TH, 2008, Philips, The Netherlands)
directly postoperatively, and at 6 weeks, and 12 and 26 months after surgery, and
CT (Siemens scanner 2014, type Somatom Definition AS 64, The Netherlands) at 9 months
after surgery and at 26 months (post-mortem). Radiographs were assessed for implant
location, structure of the surrounding bone and vertebral fusion. The criteria for
the assessment of radiographic fusion were adapted from McAfee and colleagues. Fusion
was considered successful if there was evidence of continuous bony bridging between
the vertebral bodies and no peri-implant lucency or evidence of implant loosening.
Postoperative radiographs and CT imaging were assessed for implant position and adjacent
segment pathology, based on disc space narrowing and degenerative changes at the end
plates of adjacent vertebral bodies.[21]
The immediate postoperative radiographic view ([Fig. 2B]) showed that the lumbosacral spinal unit was fixated in a slight lordotic position
correcting the step lesion that was evident on the preoperative radiograph ([Fig. 2A]). The lordotic position and the cage positioned in the dorsal half of the vertebral
body of L7 and S1 increased the foraminal aperture. In comparison with the postoperative
radiograph ([Fig. 2B]), at 1 year follow-up there was a slight (4 mm) dorsal displacement of the cage
and minimal subsidence in the end plate of L7 ([Fig. 2C]). These findings were also evident at CT at 9 months postoperatively ([Fig. 3A]), but on all other follow-up imaging the presentation of the implants remained stable
([Fig. 2D] and [Fig. 3B]). The cage remained level to the dorsal surface of the vertebral bodies and spondylosis
at the level of L7–S1 increased over time ([Fig. 3]). On CT at 9 months after surgery, the pedicle screws appeared in the correct corridors
of L7 and S1 on the transverse images. There was some degree of adjacent segment pathology
visible 9 months after surgery at L6–L7 characterized by disc protrusion.
Fig. 3 Sagittal computed tomography (CT) (A, B), sagittal micro-CT (C) and coronal micro-CT (D) reconstruction images of the lumbosacral junction at 9 (A) and 26 (B, C, D) months after treatment by distraction–fixation using an intervertebral spacer and
pedicle screw and rod fixation (PSRF). There is prominent bone ingrowth in the largest
hole of the cage (arrows).
Vertebral Fusion, Post-mortem Imaging, and Histopathology
The post-mortem lumbosacral spine segment was fixed and stored in a neutral-buffered
4% formaldehyde solution for CT, micro-CT and histopathology.
The data of CT and micro-CT were used to measure bone ingrowth through the largest
hole in the cage as has been described previously.[17] In short, the obtained DICOM files were transferred to an image analysis programme
(Mimics Medical, v19, Materialise, Leuven, Belgium) and subjected to multi-planar
reconstruction to position the largest hole of the cage in line with the normal (craniocaudal)
geometrical axis of the cage. A cylinder was fit into the inner volume of the cage
(5.0 mm diameter × 4.5 mm length) and isolated using the Boolean subtraction method
as the region of interest. Micro-CT (Quantum FX, Perkin Elmer, Waltham, Massachusetts,
United States) was performed under tube voltage of 90 kV, tube current of 180 μA,
scan time of 3 minutes and resolution of 42 μm. Automated threshold values for compact
bone (Hounsfield unit [HU]: 662–1988) and all bone (HU: 266–1988) were used to segment
the bone in the area of interest. The threshold volume percentage out of the total
volume of the region of interest was calculated to determine the amount of bone ingrowth
in the largest hole of the cage. On CT there was clear evidence of bone fusion through
the largest hole of the cage ([Fig. 3]). There was an increase in all bone ingrowth (85% to 91%) and compact bone ingrowth
(55% to 76%), respectively, at 9 months after surgery and in the post-mortem specimen
at 26 months after surgery, indicating progression of fusion ([Table 1]). Vertebral fusion was also evident on micro-CT at 26 months ([Fig. 3]) and measurements were 93% for all bone and 81% for compact bone ([Table 1]).
Table 1
All bone and compact bone percentages of bone ingrowth through the largest hole of
the cage at 9 and 26 months postoperatively
|
Follow-up (months after surgery)
|
Modality
|
% All bone threshold: HU 266–1988
|
% Compact bone threshold: HU 662–1988
|
CT settings
|
Titanium scattering
|
|
9
|
CT
|
84.90
|
54.61
|
Slice: 1 mm
kV: 100
MAS: 341
|
Cage
4 PS
2 rods
|
|
26
|
CT
|
91.04
|
76.12
|
Slice: 1 mm
kV: 100
MAS: 111
|
Cage
4 PS
2 rods
|
|
26
|
Micro CT
|
92.79
|
80.75
|
Slice: 42 µm
kV: 90
MAS: NA
|
Cage
4 parts of PS
|
Abbreviations: CT, computed tomography; HU, Hounsfield unit; kV, Kilovolt; mAs, Milliampere-seconds;
PS, pedicle screws.
The lumbosacral spine specimen, including the cage, was processed for histological
examination. After dehydration of the sample, using benzoyl peroxide, the material
was first embedded in methyl methacrylate before the sample was sawed into histological
slides of ∼350-µm using a diamond saw (Leica SP1600, Leica Microsystems, Germany).
Histological evaluation of the intervertebral lumbosacral spinal unit showed the presence
of well-differentiated trabeculae of lamellar bone and some fibrous tissue within
the cage ([Fig. 4]). The trabecular bone within the boundaries of the cage appears to be continuous
with the bone of both adjacent vertebral bodies. The less organized mixture of bone
and fibrous tissue in the central region of the cage probably reflects the mixed cancellous—cortical
autologous bone graft that was inserted in the centre of the cage before it was placed
in the intervertebral disc.
Fig. 4 Histopathology (methylene blue, basic fuchsine staining) of the lumbosacral spinal
unit. Bone tissue is stained red-pink, and the titanium cage is stained black. The
centre of the cage is largely filled with bone (arrow) and complete fusion of the
vertebral body is established. Bar: 5 mm.
Discussion and Conclusion
This case study showed that distraction–fixation using an intervertebral cage and
PSRF resulted in good clinical outcome for low back pain in a dog with severe DLSS.
Clinical follow-up was at 12 months postoperatively, survival was 26 months and the
owner's questionnaire reflecting the state of the dog just prior to passing away of
the patient. Also, post-mortem examination at more than 2 years after surgery revealed
evidence of vertebral fusion, both on CT, micro-CT and histological evaluation.
A limitation to this study is that the assessment of bone fusion through the cage
is hampered by titanium scattering. However, bone growth was visible on histology
and therefore we can assume that at least to some degree the bone growth through the
cage has been correctly identified by the measurements on CT and micro-CT. Dorsal
migration of the cage and minimal subsidence occurred in the first 9 months postoperatively,
and then remained stable. Minimal movement in the first months may have led to delayed
bone ingrowth and bone remodelling in the cage, possibly explaining why at 26 months
there is still some disorganized bone tissue in some central parts of the cage.
In this patient, it remains unclear why the patient showed proprioceptive deficits
of the left hindlimb during clinical follow-up. Dorsal migration of the cage or adjacent
segment pathology (ASP) identified at the level of L6–L7 may be responsible for these
signs in this patient due to nerve root impingement. After lumbar or lumbosacral fusion
in humans ASP was seen in 5.2 to 100% of patients in several studies; whereas the
higher range was seen using only the radiographic criteria. The interval of occurrence
of ASP was shorter after instrumented fusion than non-instrumented fusion. However,
the actual significance of ASP after fusion remains uncertain.[22]
The SynCage was developed for the human cervical spine and is indicated in cervical
myelopathy to restore disc width and achieve stabilization through vertebral fusion
(DePuy Synthes, Surgical Guide, Johnson and Johnson). Multiple sizes are available
for humans; however, for this dog the smallest size (4.5 mm) was chosen, due to the
comparable width of the L7–S1 intervertebral disc in a large breed dog.
It remains to be investigated what the effect is of insertion of the intervertebral
cage on the volume of the intervertebral foramen and decompression of the L7 nerves.
However, a recent canine cadaveric study in the lumbosacral spine using the same cage
showed that intervertebral distraction significantly expanded the L7–S1 intervertebral
foramen.[23]
Also, the question arises whether the cage can be used as a stand-alone device or
should always be used in an instrumented fashion. In a biomechanical study using the
same cage, it was shown that insertion of a stand-alone intervertebral cage (after
dorsal laminectomy) restored the vertebral stability, the intervertebral height and
the intervertebral foraminal apertures to a state similar to the native (unmodified)
spine. Therefore, from a biomechanical standpoint, the use of a stand-alone intervertebral
cage seems to be a promising alternative.[10]
In conclusion, this case study showed that there was trabecular bone ingrowth and
bone filling of the cage and vertebral spinal fusion achieved by distraction–fixation
with an intervertebral spacer (SynCage) and PSRF in a dog with severe DLSS and foraminal
stenosis. Whether this is a treatment of first choice in dogs with DLSS needs to be
investigated in larger prospective case-studies.
