What Is the Evidence?

James L. Cook Comparative Orthopaedic Laboratory, College of Veterinary Medicine, University of Missouri, Columbia, MO 65211.

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Cristi R. Cook Comparative Orthopaedic Laboratory, College of Veterinary Medicine, University of Missouri, Columbia, MO 65211.

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A 4-year-old male German Shepherd Dog weighing 33.2 kg (73 lb) was evaluated at the University of Missouri Veterinary Medical Teaching Hospital for a 3-month history of decreased ability to perform athletically. The dog trained for and competed in agility events, and the owner had observed that the dog would refuse or not successfully complete jumps and A-frames during training and competition. According to the owner, the dog also had signs of mild, intermittent lameness of the right hind limb. When the owner first noticed the problem, the dog was evaluated by a veterinarian who diagnosed a possible hamstring (semimembranosus, semitendinosus, and biceps femoris muscles) injury and recommended physical rehabilitation and NSAID medications. The owner also sought treatment from a veterinarian practicing chiropractic manipulations. This treatment regimen was undertaken for 6 weeks with no improvement observed.

At the hospital, physical and orthopedic examinations revealed the dog was in good body condition (score of 5 on a 9-point scale) but had apparent atrophy of the gluteal and thigh musculature bilaterally. The dog had a consistent shortening of the stride in the right hind limb. No evidence of pain or musculoskeletal abnormality was detected during palpation and manipulation of either forelimb and the hip, stifle, and tibiotarsal joints. Marked signs of pain in the dog were observed to be associated with pelvic lordosis and direct palpation over the lumbosacral joint. Neurologic examination revealed normal cranial nerve and thoracic limb neurologic function. Slightly delayed conscious proprioception responses were evident in the hind limbs. A slightly exaggerated patellar reflex with slightly depressed sciatic and cranial tibial reflexes was detected in the right hind limb. The neurologic abnormalities were localized to the L4 through S3 spinal cord segments.

The dog was sedated with medetomidine to allow for palpation and radiography. While the dog was sedated, palpation and radiography of the hip and stifle regions as well as palpation of the tarsal joints revealed no abnormalities. Radiographic views of the lumbosacral vertebral column were obtained, including a ventrodorsal view and lateral views with the vertebral column in a neutral position, flexed at the lumbosacral joint, and extended at the lumbosacral joint. Assessment of the radiographs revealed sclerosis of the endplate of S1, bony remodeling of the caudal articular facets of L7 as well as the cranial articular facets of S1, and subluxation of the facet joints at L7-S1 and stairstepping of the L7 and S1 vertebral bodies and lamina in the flexed and extended views. A presumptive diagnosis of dynamic lumbosacral stenosis and lumbosacral instability (LSI) was made, and computed tomography (CT) with the possibility for subsequent surgery was recommended to the owner.

The following day, the dog was anesthetized and CT imaging was performed with the vertebral column in a neutral position, flexed at the lumbosacral joint, and extended at the lumbosacral joint. Three-millimeter contiguous transverse slices were obtained from L3 through S3, and the transverse images as well as multiplanar reformatted images revealed bony remodeling of the caudal articular facets of L7 and cranial articular facets of S1, subluxation of the L7-S1 facet joints, malalignment of the L7 and S1 vertebral bodies on sagittal reformatted views in the flexed and extended positions, protrusion and telescoping of the lamina of the sacrum into the vertebral canal with nerve root impingement in the extended position, and slight hypertrophy and protrusion of the L7-S1 dorsal annulus fibrosis. Additional diagnostic procedures such as electrodiagnostic testing of neuromuscular function and magnetic resonance imaging (MRI) were not believed likely to provide information critical to decision making for treatment options or determining prognosis.

The owner was advised of the diagnosis of LSI and subsequently expressed a desire to pursue treatment for the dog with a primary goal of return to agility training and competition. The owner was not limited by financial costs.

Formulation of the Clinical Question

The problems identified were pain and neurologic dysfunction of the hind limbs caused by a lumbosacral abnormality. The treatment options considered in this situation included epidural corticosteroid infiltration with activity restriction followed by additional physical rehabilitation, surgical decompression, or surgical decompression-stabilization.

Clinical Question

Which treatment option is most likely to allow for return to athletic function in dogs with LSI?

Evidentiary Search Strategy

A targeted literature search for the most recent and pertinent reports on the subject of lumbosacral disease in dogs was performed. The PubMed electronic database of medical literature published between 1948 and January 2010 was searched with the keywords canine and lumbosacral. This initial search identified 405 reports; therefore, treatment and clinical were added to the keywords for a subsequent search. In that search, 75 reports were identified, which were then individually assessed for usefulness in addressing the clinical question on the basis of the title and review of the abstract.

After initial assessment of the reports, 20 were identified as having potential relevance to the case scenario. Eleven of the reports were retrospective or observational case series. There were 3 literature reviews, an experimental in vivo study in which 2 cohorts of clinically sound dogs were evaluated, an ex vivo biomechanical study, a retrospective cohort study, a prospective case-control study, and 2 prospective case series. A more broad or more narrow search as well as use of other keywords could have provided more evidence for review on this topic. However, the search strategy used was believed to be most likely to retrieve reports that would provide the current best evidence for practical and efficient clinical decision making.

Review of the Evidence

The evidentiary value of retrieved reports was evaluated by use of a hierarchy-of-quality pyramid1 based on type of study design. Most reports used were of lower hierarchical levels (case series, case reports, animal research, in vitro research, and opinions) offering relatively weak evidence for broad application to the clinical scenario. Whereas several of the reports were considered to provide higher-level evidence (cohort and case-control studies), none were considered of highest evidentiary value (systematic reviews and randomized, controlled, prospective clinical studies) and none were of studies that directly addressed the clinical question of interest by comparing outcomes among the primary treatment options with respect to return to athletic function in dogs with LSI. Therefore, extrapolation of data from the peer-reviewed literature and the previous clinical experiences of the supervising clinician were blended to guide decision making and owner communication for this case.

Evidence gathered from the literature suggested that there is a spectrum of disease associated with lumbosacral disorders (including LSI) and that CT or MRI, or potentially both of these advanced imaging modalities, can be helpful for fully characterizing the nature and extent of the disease. Results of the ex vivo biomechanical study2 suggested that LSI can be effectively stabilized with internal fixation. With respect to clinical treatment, epidural infiltration with methylprednisolone acetate was associated with resolution of clinical signs in 53% of affected dogs and improvement in clinical signs in 79% of dogs for 5 to 66 months after treatment.3 Decompression surgery was associated with clinical improvement in signs of pain and lameness in up to 93% of affected dogs, with 41% to 67% of working dogs returning to full intended function.4,5

Recurrence of clinical signs may occur in 17% to 55% of dogs undergoing decompression surgery alone.4 Factors that may be associated with poorer outcomes in dogs with lumbosacral disease include older age at the time of surgery, radiographic evidence of foraminal narrowing, severe preoperative neurologic dysfunction (particularly urinary incontinence, fecal incontinence, or both), and hypertrophic or remodeled articular facets and interarcuate ligament.

Given the aforementioned evidence, what decision would you make?

Clinical Decision and Outcome

Nonsurgical management or decompression surgery cannot be expected to consistently result in return to full function for working dogs with lumbosacral disease. In the authors' opinion and experience, expedient surgical intervention in the form of a decompression-stabilization procedure of the lumbosacral spinal column was determined to be associated with the best prognosis for return to the athletic level of function desired with a diagnosis of LSI in a young working dog. The success rates, recurrence rates, and complications reported in the literature as well as the supervising clinician's recommendations based on his opinion and experiences were communicated to the owner, who opted to pursue this course of treatment. The dog underwent surgery immediately following completion of the CT scan and communication with the owner.

For surgery, the dog was positioned in sternal recumbency, with the vertebral column and pelvis secured in a weight-bearing position with the aid of vacuum-activated surgical positioning bags. A dorsal approach over the sixth lumbar to second caudal vertebrae was performed, and the dorsal aspects of L7 and the sacrum were exposed. The interarcuate ligament and joint capsules of the L7-S1 facets were noticeably thickened. After excision of the dorsal portion of the joint capsules, irregular bony remodeling and hypertrophy, articular cartilage lesions, and osteophytosis at the dorsal margins of the facets were noticed. Articular cartilage of the L7 and S1 facets was debrided. The interarcuate ligament was excised. Dorsal laminectomy of the caudal portion of L7, S1, and S2 was performed, and care was taken to preserve the base of the facets. Facet joint capsule and hypertrophied bone that impinged into the vertebral canal, lateral recesses, or foramina were carefully removed. The nerve roots were examined to ensure their integrity and freedom from impingement and then retracted carefully to examine L7-S1. Mild hypertrophy and protrusion of the dorsal annulus fibrosis were evident, but no fiber separation or disk extrusion was apparent.

A fat graft was placed over the laminectomy site. One 3.5-mm stainless steel positional screw was placed through the L7-S1 facets and into the ilium from cranio-medial to caudolateral on each side. The lateral aspects of the dorsal laminae of L7 and S1 were scarified by use of a pneumatic-driven burr. An autogenous cancellous bone graft from the right iliac crest was placed over the lateral aspects and facets of L7–S1 on both sides of the laminectomy site. The surgical site was closed routinely. Examination of postoperative ventrodorsal and lateral radiographic views of the lumbosacral vertebral column confirmed appropriate implant placement.

The dog was monitored and treated with IV-administered analgesics in the intensive care unit for approximately 12 hours after surgery and then transferred to the surgical ward. Two days after surgery, the dog was discharged from the hospital with instructions to the owner for routine incision care and directions to take the dog for short-leash walks outdoors for urination and defecation only and to confine it when unobserved for the first 6 weeks following surgery.

The dog was reexamined by the supervising clinician 6 weeks after surgery. At that time, the dog was ambulating well at a walk with no evidence of pain, gait abnormalities, or neurologic dysfunction. Examination of ventrodorsal and lateral radiographic views revealed no evidence of complications related to the surgery, and smooth, bridging new bone formation was apparent on the dorsal aspect of the lumbosacral vertebral column at the location of the bone grafts. On the basis of clinical and radiographic findings, the owner was instructed to allow the dog to return to full pet-level function by progressively increasing the duration, frequency, and intensity of activity over the subsequent 6 weeks. Full pet-level function was achieved at the 12-week postoperative point, so the owner was then instructed to reinstitute training for agility work. The dog successfully completed training and returned to agility competitions within 5 months after surgery. The dog continued to train and compete at preinjury levels more than 2 years after surgery with no signs of recurrence or related problems.


The current best evidence for clinical decision making for this dog with LSI consisted of reports of lower evidentiary value and the clinical experiences of the supervising clinician. The supervising clinician believed there were 2 major factors influencing the approach to this case. The first was the owner's desire to maximize the chances for return to full intended function; the second was the nature of the disease.

On the basis of signalment, history, clinical signs, and examination and imaging findings, a diagnosis was made of clinically important LSI causing consistent and repetitive compressive injury to the cauda equina nerve roots. Therefore, review of the evidence, clinical decision making, and owner communication needed to be undertaken with the goal of returning a young working dog with evidence of instability in the lumbosacral vertebral column to training and competition in agility events. Given the available literature, the supervising clinician's experience, and consultation with another surgeon with extensive experience in this area,a nonsurgical therapy or decompression surgery was deemed not to be associated with a high success rate for return to the level of function desired. Whereas successful return to work has been reported for up to 67% of military working dogs after decompression surgery alone, much lower success rates (≤ 41%) and very high recurrence rates have also been reported.

It is plausible that unsuccessfully treated dogs with LSI comprise a different subset of disease (eg, instability) with associated risk factors for unsatisfactory outcomes. The risk factors reported to negatively influence outcome4 were all believed to be relevant for the dog of this report and influenced the decision for expedient decompression-stabilization surgery. This approach was successful in achieving the desired outcome in this dog and other similar dogs examined and treated by the authors. As such, the diagnostic and therapeutic protocols described are considered our current standard-of-care recommendations for cases of suspected LSI in dogs. However, these recommendations are currently based only on our experiences and opinions, which must be considered of very low evidentiary value.

The possible dangers associated with our diagnostic and therapeutic approach include the potential for not addressing intervertebral disk disease and pain, the potential for implant failure or fracture, and the potential for compromise of adjacent intervertebral disks because of the biomechanical alterations to the vertebral column. None of these critical points can be directly addressed given the paucity of studies of high evidentiary value at this point in time. As such, this present case scenario and discussion highlight the need for prospective clinical studies to investigate diagnostic and therapeutic approaches for lumbosacral disorders in dogs. Standardized and validated outcomes measures need to be applied to examine and compare cohorts of dogs so that high-level, relevant evidence is available for clinicians to optimally advise owners and treat patients in the clinical setting.


Carpenter LG, Veterinary Surgical Service, Sturgis, SD: Personal communication, 2010.


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