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Congenital Spinal Malformation in a French Bulldog

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					Congenital Spinal Malformation in a French Bulldog

Cassandra E. Wishon Dr. Stuart Bliss Senior Seminar Paper Cornell University College of Veterinary Medicine October 31st, 2007

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Abstract: Vertebral malformations, observed most commonly in screw tailed breeds, can result in spinal cord compression and hind limb paresis and ataxia. Treatment of the condition may involve conservative cage rest or surgical decompression with stabilization, possibly accompanied by correction of the malangulation. Postoperative recovery is often lengthy and complex, with weeks of intensive supportive care and months of physical therapy. Long term outcome is variable and can be influenced by the degree of compression as well as the speed of onset and duration of neurological injury.

Introduction: Vertebral malformations, specifically those referred to as wedge vertebrae or hemivertebrae, are the product of a localized failure of vascularization in the developing vertebrae resulting in a defect in ossification of the developing central cartilage4. These malformations are common in brachycephalic, “screw-tailed” breeds as they produce the characteristic curved tail and can cause kyphosis, scoliosis, or lordosis of the vertebral column with possible stenosis of the spinal canal.1 While these abnormalities are often subclinical, neurologic deficits, when present, are most commonly seen in skeletally immature animals, usually those less than nine months of age.2,3 In a few cases, clinical signs may develop in adult, mature animals and are thought to occur due to slowly progressive degenerative changes of the discs, longitudinal or interarcuate ligaments, or joint capsules of the articular facets, with fibrosis and ligaentous or capsular proliferation causing gradual compression of the spinal cord. It is theorized that a critical threshold of neurological dysfunction is eventually reached, beyond which the spinal cord is no longer

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able to compensate for the degree of compression, resulting in neurologic deficits. A second theory involves minor trauma, most likely unobserved by the owner, but significant enough to cause a vascular insult, and result in neurologic deficits.

Case History: An eight year old male castrated French Bulldog presented to his referring veterinarian initially with acute spinal pain and an abnormal gate. Plain radiographs revealed a severe kyphotic vertebral malformation with spondylosis deformans; radiographic evidence of hip dysplasia was also noted. Tramadol (2.4mg/kg) and prednisone (4mg/kg) were prescribed with minimal improvement noted. The dog continued to progress with paraparesis and ataxia noted in the hindlimbs two weeks later, prompting referral to Cornell University School of Veterinary Medicine.

Clinical Findings: Physical examination by the emergency service at Cornell at the time of initial presentation revealed atrophy of the epaxial muscles from thoracic vertebrae six to lumbar vertebrae three as well as of the hind limb musculature bilaterally. An upper airway stertor with clear lungs sounds of both fields and mild seborrhea sicca was also noted. Upon further neurologic assessment, an abscent panniculus bilaterally with conscious proprioceptive deficits of both hind limbs was noted. Possible cervical pain was also observed, but difficult to discern definitively due to the patient’s limited cervical range of motion. Cranial nerves and thoracic limbs were within normal limits.

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Problem List: After initial assessment had been completed clinical signs were classified into two primary problems, a T3-L3 myelopathy and an upper airway stertor. Different diagnosis for the myelopathy includedintervertebral disc disease, neoplasia, diskospondilitis, fibrocartilaginous embolic myelopathy, and congenital spinal malformations or trauma resulting in compression of the thoracic spinal cord. The upper airway stertor was thought to be caused by one or a combination of components of brachycephalic syndrome; stenotic nares, elongation of the soft palate, eversion of the laryngeal ventricles, or hypoplasia of the trachea common in brachycephalic breeds.

Diagnostic Plan: A complete blood count and serum chemistry were performed at the time of initial assessment and were within normal limits save for a moderate elevation in alanine transferase (334U/L) and alkaline phosphatase (183U/L) which were thought to be due to exogenous steroid administration prior to presentation. The absence of an inflammatory or infectious white blood cell response decreased the likely hood of diskospondylitis as the cause of the patient’s neurologic deficits. Radiographs were then taken of the vertebral column followed by a myelogram, allowing evaluation of the entire spinal cord to further characterize the malformation of the thoracic vertebrae and to identify other possible areas of compression which could affect the prognosis and treatment method. Initial imaging revealed a wedge vertebrae at T6 with a misshapen vertebrae at T5 and T7, narrowing of the spinal canal at T5-7, and curvature of the dorsal spinous processes of T4-6. Block vertebrae of C3-4, ankylosis of

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the caudal vertebrae and thinning of ribs 6-9 bilaterally with decreased mineral opacity were also noted. After thorough review of the imaging with no other areas of compression noted, it was then theorized the vertebral malformation at T6 caused T5 and 7 to be misshapen as a result of compensation for the primary abnormality during skeletal growth. These irregularities produced a severe kyphosis with a mild scoliosis of the thoracic vertebral column causing compression of the spinal cord and the resultant upper motor neuron signs of the hind limbs. The specific structure causing compression was still unknown, although theorized to be a herniated intervertebral disc due to the abnormal confirmation, a neoplastic mass, or a stenosis of the bony canal. A computed tomographic evaluation was then performed, and a reconstructed model created. No evidence of disc material or neoplasia was noted on examination; however, narrowing of the spinal canal was clearly visible at the site of the malformation.

Theraputic Plan: Treatment options for correction of the neurologic deficits consisted of cage rest, dorsal or hemilaminectomy with dorsal stabilization, or correction of the malangulation with stabilization. Cage rest is typically used in young, skeletally immature animals with mild, non-progressive neurologic disease, and was not an option in this case as the animal was skeletally mature and had been cage rested for seven days with continued progression of neurologic signs. Surgical correction typically performed in veterinary medicine consists of dorsal or hemilaminectomy and stabilization dorsally with a combination of polymethylmethacrylate, kirschner wires, positively threaded pins, and suture without

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correction of the malangulation1,3. Surgical correction commonly employed in human medicine, often in children with scoliosis or other vertebral malformations, is aimed at correction of the malangulation with stabilization of both the anterior and posterior compartments of the vertebral comumn. . Surgical intervention was determined to be the most appropriate course of action as the patient had continue to deteriorate, with only deep pain remaining in the hind limbs prior to surgery. The dog was placed in sternal recumbency, and a dorsal approach to the mid-thoracic vertebral column was performed with extension of the approach along the left dorsolateral thoracic wall. Ribs six through eight were then disarticulated from the vertebral column and a three to four centimeter section of each rib removed proximally allowing greater access to the malformed vertebrae. The left hemilamina and the majority of the vertebral body of T6 were removed using a high speed burr, resulting in the release the tethering effect of the ventral longitudinal ligament. The spinal canal was then enlarged by removing the inner cortex of the remaining lamina in the area of greatest compression, a process known as undercutting. A Steinmann pin, bent into a narrow “U” shape was placed along the dorsum of the vertebral column, with the curved end between the spinous processes of C7 and T1 and the long ends extending toward the thoracolumbar junction. Orthopedic wire was then looped around the rib heads cranial and caudal to the lesion bilaterally, the loose ends threaded through the interspinous ligaments, tightened and secured to the Steinmann pin in a cerclage fashion on the contralateral side. The implant provided stabilization and a 17 degree correction of the malangulation (128 degrees pre-operatively, 145 degrees post-operatively). The incision was closed using a standard technique and a

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thoracostomy tube placed for correction of the pneumothorax and removal of pleural fluid post-operatively. This was later removed when it was noted to be nonfunctional. Radiographs were taken, a urinary catheter and two nasal oxygen canulas placed. The patient recovered from surgery and anesthesia with minimal complications, but was given supplemental oxygen due to the breed’s propensity for respiratory difficulty. Fentanyl, meditomidine and hydromorphone were administered for analgesia, and fluid therapy, blood products, antibiotics, prednisone, and gastroprotectants initiated. During the immediate post-operative period, blood volume, electrolytes, cardiac function, and oxygenation were monitored, with two thoracocentesises preformed to remove excessive pleural fluid accumulation noted on ultrasound. Three days following surgery, with the patient stabilized, and supportive therapy decreasing, a body splint was created using fiberglass casting material to immobilize the spine, preventing strain on the implants during healing. The splint was modified, padded and lengthened prior to discharge one week after surgery, at which time the patient was without deep pain to the hind limbs. The splint remained in place for ten weeks and the dog was restricted to strict cage rest observed except for physical therapy which occurred two or three times daily and involved weight bearing, range of motion, and swimming exercises after removal of the sutures. At the first recheck two weeks post operatively, the patient was noted to have weak motor in both hind limbs, the right greater than the left, voluntary micturition, and no inflammation or irritation noted from the splint. Physical therapy was continued with withdrawal exercises added and swimming discontinued due to the patient’s strong aversion to water.

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Two months following surgery motor function had dramatically improved in the pelvic limbs and the patient was able to ambulate on all four limbs when walking on nonslippery surfaces. Although still weak in the hind limbs and back, the progressive muscle atrophy had stabilized with a small amount of body weight regained. Radiographs were taken with mild cranial movement of the implant noted and a lack of callous formation at the surgical site observed. It should be noted that radiographic evidence of fusion does not often occur, even if the surgical site has undergone complete mechanical fusion (I think the reason we do not see much callus with healing of vertebral fractures, especially across a disc space, is that there is usually a great deal of movement at the site – probably most never truly ossify, but become strong fibrous or fibrocartilaginous pseudoarthoses). Four months post surgery the patient presented for his final recheck, with significant improvement in ambulation and strength. The muscle mass of the hind limbs had noticeably increased and a return to a normal quality of life had been achieved. Use of the splint was discontinued, and to date the patient has remained stable and healthy.

References: 1) Aikawa T, Shinichi K, Yoshigae Y, et al. Verterbral Stabilization Using Positively Threaded Profile Pins and Polymethylmethacrylate, with or without Laminectomy, for Spinal Canal Stenosis and Vertebral Instability Caused by Congenital Thoracic Vertebral Anomalies. Veterinary Surgery 2007:36:5:432-441 2) Bailey CS, Morgan JP. Congenital Spinal Malformations. Veterinary Clinics of North America: Small Animal Practice 1992:22:4:985-990 3) Gossot P, Scotti S, Klein A, et al. Thoracic Hemivertebra Surgical Treatment with Realignment and Stabilization: Radiographic Study and Four Cases of Treated Dogs. Presentation Abstracts at 16th Annual Scientific European College of Veterinary Surgeons 2007:6

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4) Jeffery N, Smith P, Talbot C. Imaging Findings and Surgical Treatment of Hemivertebrae in Three Dogs. Journal of the American Veterinary Medical Association 2007:230:4:532-536

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