section epub:type=”chapter” role=”doc-chapter”> Noel Fitzpatrick Degenerative lumbosacral stenosis (DLSS) is a common cause of caudal spinal pain in medium‐ and large‐breed dogs. It is seen less commonly in small dogs and cats. DLSS results in a narrowing of the vertebral canal and intervertebral foramina at the level of the lumbosacral junction. The narrowing results in compressive radiculopathy of the L7 nerve roots and the nerve roots of the cauda equina. Compression of the nerve roots is a multifactorial process. Direct compression of the nerve roots can be caused by prolapse of the annulus fibrosus, hypertrophy of the joint capsule of the L7‐S1 (LS) articular facets and hypertrophy of the interarcuate ligament. Osteophytosis / spondylosis at the level of the intervertebral foramena may also cause direct compression of the L7 nerve roots abaxially. The compressive process may also have a dynamic component whereby compression of the nerve roots is exacerbated or relieved depending on degree of flexion or extension at the LS junction. This is the result of further disc protrusion, motion of the spondylotic new bone on the caudal aspect of L7 and the cranial aspect of S1, ventral migration of the dorsal lamina of the sacrum relative to L7 and relative motion of the inflamed articular facets. It is well established that the intervertebral foramen undergoes narrowing when the LS junction is placed into extension [1, 2]. Though direct consequences of compression of the L7 and cauda equina nerve roots can be observed with neurogenic deficits producing paresis, muscle weakness and urinary issues, the most commonly encountered clinical signs are related to pain, both acute and chronic, and lameness, both profound and subtle. In the author’s experience, pain only or pain and lameness are often the only signs manifested. Because muscle spasms can be associated with persistent or intermittent claudication of the L7 nerve roots, the condition is commonly confused with other scenarios such as iliopsoas muscle strain‐sprain or sacroiliac pain. In dogs affected by DLSS, pain may often be elicited during physical examination by application of direct pressure over the lumbo‐sacral junction dorsally, but one must be careful to neutralize the coxofemoral joints so as not to confuse hip pain. Simultaneous hyperextension of the LS spine may also produce a painful response. Along the sciatic nerve pathway, pain may be evoked on deep digital pressure application, either externally by placing the thumb in the caudal thigh recess between the biceps femoris and the semitendinosus‐membranosus (Holsworth Test) or per rectum using a gloved index finger where the sciatic nerve can be palpated on the axial aspect of the lesser ischiatic notch (Fitzpatrick Test). Clinical signs are caused by direct compression of the cauda equina and impingement of the ganglia of the spinal nerve roots as they exit through the intervertebral foramena [3]. Figure 26.1 Typical MRI findings in DLSS. T2 weighted (a–c) and STIR (d) MRI scans of a typical presentation of degenerative lumbosacral stenosis (DLSS). (a) Sagittal plane demonstrating marked compression of the cauda equina dorsal to L7‐S1 intervertebral space. Nucleus pulposus signal is reduced and irregular. (b) Transverse plane through L7‐S1 disc with dramatically reduced nucleus pulposus signal and obliteration of both the spinal canal and the L7 neuroforamina, which normally manifest nerve roots within fat signal. (c) Parasagittal plane manifesting hypointensity of lateralized disc protrusion within the neuroforamen when compared with more cranial segments. (d) Dorsal plane demonstrating near‐complete discontinuation of nerve root and fat signal at junction of conus medullaris and cauda equina. The patient is positioned in ventral recumbency and supported in the midline with positioning aids to maintain patient stability. The hind limbs are drawn forward with the metatarsal bones parallel to the top of the surgical table to flex the lumbosacral spine and open the L7‐S1 space. A standard dorsal approach to the L7‐S1 junction is adopted [7] with dorsal laminectomy involving approximately one‐third of the cranial to caudal width of the L7 lamina and two‐thirds of the cranial extent of the sacral lamina. Meticulous hemostasis is important to maintain a clear surgical field during implant positioning, but this can be very challenging because frequently in chronic cases there is significant bleeding associated with chronic inflammation, and bleeding from the ventral venous sinuses can be considerable. Muscular dissection is extended cranially to allow access for screw placement on either side of the L7 vertebral body. Surgical management of LS disease involves either decompression alone, stabilization alone, or distraction‐stabilization, with dorsal facet and /or ventral vertebral body fusion being preferable for any stabilization technique. Decompression without surgical stabilization may provide immediate symptomatic relief for some patients, and this may be maintained indefinitely, although analysis of long‐term outcomes is required to validate this approach [8]. However, laminectomy alone can only be successful for central protrusion or extrusion, and this accounts for a very small proportion of clinical cases of DLSS in the author’s practice. Decompression via dorsal laminectomy alone does not address lateralized neuroforaminal impingement and it can be difficult to achieve adequate decompression of all of the entry, middle, and exit zones by foraminotomy techniques alone. The possibility for iatrogenic damage of the L7 nerve roots must also be considered and impairment of visibility produced by hemorrhage potentially compromises optimal removal of osseous and soft tissue compressive elements. Dorsal laminectomy and dorsal disc annulectomy destabilize the L7‐S1 spinal segment and increase the range of motion in flexion and extension [9–11]. Extension of the mobile L7‐S1 junction that ensues may decrease the foraminal aperture and exacerbate the effect of foraminal stenosis on nerve root impingement [12], even when foraminotomy has been performed. Foraminotomy may be a successful intervention for lateralized L7 compression but fails to address the dynamic compressive effect of spinal motion on foraminal occlusion. Ongoing lumbosacral instability can accelerate the progression of lumbosacral disease and may exacerbate clinical signs associated with nerve root occlusion [1, 12]. Additionally, even if satisfactory decompression is achieved at the time of foraminotomy, bone and scar tissue may grow back such that longer‐term success of decompression might not be maintained. Transarticular fixation of the facet joints with screws following decompression seeks to preserve relative vertebral position and to maintain foraminal aperture (Figure 26.2a), but it has been observed that such stabilization may not significantly alter long‐term outcomes versus decompression alone [13, 14]. Furthermore, the author has observed fracture of the L7‐S1 facets following screw stabilization after both dorsal laminectomy and foraminotomy, separately or combined. Additionally, facet screws do not result in distraction and therefore may not adequately resolve clinical signs because of residual static impingement. Figure 26.2 Fixation modalities in lumbosacral fusion. (a) Facet screw fixation. (b) Noncustomized pedicle screw with fixed‐angle connecting rod and clamp. (c) Contoured SOP plate with fixed‐angle pedicle screws. (d) Multi‐angled pins secured with PMMA. Stabilization of the L7‐S1 junction has been achieved using a variety of methods. Pins or screws and polymethylmethacrylate cement deployed either in neutral or flexed lumbo‐sacral positions have been deployed most commonly (Figure 26.2d). Custom locking plates have purportedly been employed but not yet reported. The string‐of‐pearls (SOP™, Orthomed, Huddersfield, UK) locking plate applied dorsally has been reported (Figure 26.2c) but found to have no biomechanical benefit over pins and PMMA cement [15]. It is challenging to effectively deploy fixed‐angle locking systems in the lumbosacral area as the anatomy makes it difficult to obtain sufficient bone stock and plates can be challenging to contour. Variable angle locking systems may be more suitable for use, however these systems often lack the angular freedom needed for successful deployment.
26
Lumbosacral Stabilization
26.1 Introduction
26.2 Clinical Examination
26.3 Decision‐Making
26.3.1 Radiography
26.3.2 CT Scan
26.3.3 MRI
26.4 Surgical Planning: Patient Positioning and Surgical Approach
26.5 Surgical Techniques
26.5.1 Decompression Alone – Dorsal Laminectomy and Foraminotomy
26.5.2 Decompression + Dorsal Fixation
26.5.2.1Dorsal Fixation with Facet Screws
26.5.2.2Dorsal Fixation with Screws + Plates or Screws /Pins + Cement
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