Estenose Lombossacra em Cães: Reconhecer e Tratar

Definition

The term "cauda equina" is defined as the leash of nerve roots derived from the terminal spinal cord segments from L7 caudally (Cd1-Cd5) that travels through the vertebral canal in the lumbosacral area. It means that there are only nerves from peripheral nervous system in this area.¹

The "cauda equina syndrome" is the set of signals produced by a variety of conditions that affect the nerve roots of the cauda equina as: Degenerative (mainly LSDS), inflammatory, infiltrative, anomalies, trauma and vascular.

Lumbosacral (LS) degenerative stenosis (LSDS) is a degenerative disease which may consist of some or more of the following aspects: LS spondylosis, endplate sclerosis, disc protrusion or herniation, hypertrophy of the interarcuate ligament, facet joint hypertrophy and sometimes varying degrees of vertebral body misalignments. Is frequently encountered in middle-aged, medium to large breeds of working dogs, and more often in males.²

Pathogenesis

Normally, LSDS promotes an acquired narrowing of the vertebral canal and/or intervertebral foraminae resulting in compressive radiculopathy of the cauda equina.

The LS joint of large-breed dogs is prone to degenerative change. One or more nerves of the cauda equina become compressed by alterations of the soft and bony tissues associated with the spine, coupled with or caused by suspected instability of the L7-S1 intervertebral motion segment.

Presumably, the degenerative process that leads to LSDS starts in the intervertebral disc as the result of prolonged stress associated with activity and age, and by changes which occur from strain beyond normal physiological limits. The degenerating disc develops fibrous metaplasia (Type II degeneration) and cannot absorb and distribute loading, and the resultant tearing of Sharpey's fibers leads to circumferential formation of osteophytes around the LS joint.³

In German shepherd dogs, as well as other large-breed dogs, the presence of transitional vertebrae at the lumbosacral junction has been associated with the development of LSDS. In one study, dogs with transitional lumbosacral vertebrae were eight times more likely to develop degenerative lumbosacral stenosis than dogs without such anomalous vertebrae.¹

In some circumstances, alterations as: ventral subluxation of S1; proliferation of the soft tissues surrounding the cauda equine (e.g., hypertrophy of the interarcuate ligament [ligamentum flavum], the joint capsule, and epidural fibrosis) can coexist with degenerative changes and worsen the process.³

The intervertebral disc space is narrowed as the disc protrudes dorsally, and this loss of spacing affects the size of the foramen. Protrusion of disc material in a dorsolateral direction can affect the entrance and middle zones of the foramen, while impingement of the exit zone can be the result of narrowing of the intervertebral disc space, osteophytosis or hypertrophy of soft tissue in the region of the facets.³

Clinical Signs

The clinical signs of LSDS in dogs have been well documented. Generally, clinical signs are directly related to the physical compression of the cauda equina.

Hyperesthesia may arise from compression and/or inflammation of meninges and nerve roots of the cauda equina, from the bony components of the lumbosacral area, from the L7-S1 disc, and from L7-S1 articular facet joint capsules. The affected dog shows reluctance to jump, climb and rise. Sometimes the animal stands in a kyphotic pelvic position.⁴

Lumbar hyperaesthesia can be induced by extension of one or both hindlimbs, inducing low lumbar lordosis. In more severe cases, neurological deficits can be observed. These may be proprioceptive deficit, decreased hock flexion with a reduced Achilles tendon reflex, urinary or faecal incontinence, and root signature signs such as stamping, lifting of a hindlimb, and lower back flea-biting behavior.⁴

Pelvic limb weakness may be apparent with damage to sciatic nerve contributions, and decreased to absent tail tone and movement may occur with damage to caudal segments and/or nerve roots. In some cases, the patient may be observed to exhibit an abnormally low tail carriage or a tail deviated to one of the sides.¹

Diagnostic Imaging

The diagnosis of LSDS in dogs is based on the history, clinical signs, orthopedic and neurological examinations. Imaging techniques of the lumbosacral region are needed to further assess the patient with suspected lumbosacral stenosis.⁵

Conventional radiography, stress radiography, myelography, epidurography, discography, computed tomography (CT), and magnetic resonance imaging (MRI) have been used for evaluating LSDS in dogs.⁵

Computed tomography has been established as a sensitive, noninvasive technique for evaluating the anatomy of the canine lumbosacral spine and for identifying the locations of compressive tissues in dogs with lumbosacral stenosis.⁵

Changes observed in CT scans include a loss of epidural fat, disc margin bulging, bone proliferation, nerve tissue displacement, degenerative articular process joint disease, vertebral subluxation, and idiopathic/developmental stenosis. Degenerative process appears in CT images as joint space narrowing or irregular margination, subchondral sclerosis, periarticular osteophytes, subchondral cystic lesions, and/or articular process.⁵

MRI provides visualization of the intervertebral disc, ligaments, nerve roots and pathologic changes of the lumbosacral region. The advantage of MRI over CT is providing better soft tissue resolution, the ability to acquire sagittal and dorsal plane images without degradation of the image due to reformatting, and detection of disc degeneration. The MRI findings in dogs with LSDS may include intervertebral disc protrusion, dural sac and/or nerve root displacement, disc degeneration and loss of epidural fat.⁵

Electromyography of the coccygeal and anal musculature is another reasonably valuable diagnostic method for detection of nerve root compression.²

Despite of diagnostic imaging findings, it is proposed that the diagnosis of LSDS or the decision to carry out decompressive surgery should not be made without reference to the clinical signs.

Treatment

Treatment of LSDS may consist of conservative therapy or surgical methods. Although conservative treatment has been suggested for dogs with mild-to-moderate clinical signs without neurologic deficits, little is known about the clinical signs and outcome of dogs treated conservatively for LSDS. Conservative treatment can be achieved with body weight reduction in case of obesity, and restricted activity during a period of 4–6 weeks associated with gabapentine (10 mg/kg q 12 h) and NSAIDs (carprofen 2.0 mg/kg q 12 h).^1,4,5

A study published in 2009 demonstrated that three epidural infiltrations of 1.0 mg/kg methylprednisolone acetate was a safe and well-accepted treatment that seems to achieve clinical results comparable to those of decompressive surgery. Unfortunately, the paper was based only in questionnaries and clinical findings.⁴

Surgical treatment of LSDS is indicated in cases with moderate-to-severe caudal lumbar pain unresponsive to conservative treatment, and in case of neurological deficits. The aim of the surgery is to decompress the cauda equine and free nerve roots that may be entrapped by connective tissue. The surgical procedures may include dorsal laminectomy that can be combined either with dorsal fenestration, partial discectomy, facetectomy, and/or foraminotomy. When subluxation of the lumbosacral joint is present, stabilization by fixation and fusion may be needed.

Several stabilization techniques in dogs have been reported, including cross pin fixation, vertebral body fixation with a lag screw, as well as fixation and fusion using screws in the pedicles fixed with a bone cement bridge or titanium pedicle screw-rod fixation that promotes vertebral distraction and reduction of the nerve root impingement.⁵

References

1.  Dewey CW, Da Costa RC, editors. Practical Guide to Canine and Feline Neurology. 3rd edition. Ames, IA: Willey Blackwell; 2016.

2.  Janssens LAA, Moens Y, Coppens P, et al. Lumbosacral degenerative stenosis in dogs: the results of dorsal decompression with dorsal anulectomy and nucleotomy. Vet Comp Orthop Traumatol. 2000;13:97–103.

3.  Worth A. Degenerative lumbosacral stenosis in dogs: current concepts of diagnosis and treatment. In: Proceedings of the 3rd AVA/NZVA Pan Pacific Veterinary Conference, Brisbane, 2010.

4.  Janssens L, Beosier Y, Daems. Lumbosacral degenerative stenosis. The results of epidural infiltration with methylprednisolone acetate: a retrospective study. Vet Comp Orthop Traumatol. 2009;6:486–491.

5.  Suwankong N, Meij BP, Voorhout G, et al. Review and retrospective analysis in 156 dogs with degenerative lumbosacral stenosis treated by dorsal laminectomy. Vet Comp Orthop Traumatol. 2008;3:285–293.

6.  Smolders LA, Voorhout G, Van de Ven R, et al. Pedicle screw-rod fixation of the canine lumbosacral junction. Vet Surg. 2012;41:720–732.