Chapter 100 Fractures and Dislocations of the Spine
Congenital and acquired diseases of the spine are seen frequently in small animal practice. Early diagnosis and effective treatment are crucial for success in preservation or return of normal neurologic function in these patients.
ATLANTOAXIAL INSTABILITY
Anatomy
• The atlantoaxial joint is a pivot joint that allows the head and atlas to rotate around a longitudinal axis.
• The dens is a peg-like eminence along the ventral surface of C2 (axis) that projects rostrally to lie on the floor of C1 (atlas) in the spinal canal.
• The dens is secured to the ventral arch of the atlas by the transverse atlantal ligament, to the occipital condyles by the paired alar ligaments, and to the ventral aspect of the foramen magnum by the apical ligament. The dorsal arches of the atlas and axis are stabilized by the dorsal atlantoaxial ligament.
Etiology
Atlantoaxial instability can arise from either congenital or acquired etiologies.
Clinical Signs
• Clinical signs vary from cervical pain alone to tetra-ataxia or tetraparesis and tetraplegia. The severity of clinical signs is usually dependent on the degree of atlantoaxial subluxation.
• The severity of clinical signs is also dependent on whether the patient has an intact dens. Luxation with an intact dens and luxation resulting from congenital dens malformation allows the dens to dorsally deviate into the spinal cord (Fig. 100-1). This will cause more spinal cord compression than in the patient with congenital atlantoaxial instability secondary to aplasia of the dens.
Diagnosis
• The diagnosis of atlantoaxial instability is usually made with radiography. Carefully flexed lateral radiographs of the atlantoaxial space will revealed a widened space between the dorsal arch of C1 and the dorsal spine of C2. Ventrodorsal and open-mouthed views may best outline the dens.
Surgical Procedures
Preoperative Considerations
• Be careful when manipulating the neck while under anesthesia. Do not flex the spine, which would exacerbate cord compression and cause respiratory arrest and death.
• Ventilator therapy is helpful in these patients, especially when there is concern about respiratory impairment.
Technique
Dorsal Approach (Overview)
• Dorsal approaches involve fixation of the dorsal spine of the axis to the dorsal arch of the axis using heavy-gauge suture material, orthopedic wire, or nuchal ligament grafts.
• Complications with the dorsal approach include breakage of the implant material and fracture of the dorsal arch of the atlas or dorsal spine of the axis. This can lead to acute reluxation of the atlantoaxial joint, which often causes acute neurologic decline.
• Although technically more demanding, most surgeons prefer ventral fixation of the atlantoaxial joint due to a higher success rate.
Ventral Approach
1. Place the patient in dorsal recumbency with a rolled towel positioned under the neck and the chin and chest gently taped to the table.
2. Make a skin incision on the ventral cervical midline extending from the laryngeal cartilages to the manubrium.
4. Bluntly dissect and lateralize the trachea, esophagus, and carotid sheath. Access to the ventral aspect of the atlantoaxial joint is made easier with myotomy of one of the sternothyroid muscles. Tag the cut muscle ends with suture to allow easier identification upon closure.
5. Separate and retract the paired hypaxial muscles ventral to the atlantoaxial joint using self-retaining retractors.
7. The joint may be reduced into normal position using two-point reduction forceps placed on the body of the axis.
8. When the dens is either fractured or ununited, remove it through the atlantoaxial articulation. If necessary, remove a small window of bone from the ventral arch of the atlas to assist in dens removal.
9. To perform arthrodesis of C1 to C2, remove the articular cartilage using a high-speed air drill or bone curettes, then place bone graft obtained from the greater trochanter of the humerus.
10. Several modifications of ventral fixation using K-wires, screws, and PMMA bone cement have been described. The original description of ventral stabilization involved divergent Steinmann pins, K-wires, or cortical screws placed across the atlantoaxial joint. Recent studies suggest that strongest fixation involves placement of three pairs of pins, with one set going across the atlantoaxial joint and the other two pairs fixed to C1 and C2, respectively.
11. If only two pins are going to be used for fixation, drive them from the center of the axis across the atlantoaxial joint and seat them in the atlas just medial to the alar notch. This ensures that the pins do not enter the spinal canal (Fig. 100-2).
12. For additional stability, place the second set of pins into the atlas. Direct the pins perpendicular to the long axis of the spine from ventral to dorsal into each of the pedicles of the atlas. Leave the pins long and notch them using a pin cutter. This allows better bonding with the PMMA.
13. Place the third pair of pins into the caudal body of C2. Drive the pins from the center of the body obliquely to the origin of the transverse process, taking care not to enter the spinal canal. Leave these pins long and notch them.
14. Place a small mass of PMMA ventrally to incorporate each pin, and apply cool saline flush during polymerization of the cement to dissipate heat and minimize tissue damage.
15. Close the sternothyroideus muscle if a myotomy was performed. The hypaxial muscles often cannot be reapposed due to the mass of cement.
Postoperative Care and Complications
• Restrict exercise for 4 to 6 weeks. Avoid any high-impact activity. If necessary, confine the animal to a cage.
• Obtain radiographs monthly until a complete bony fusion of the atlantoaxial joint is seen. Radiographic fusion is usually seen by 8 to 12 weeks.
CAUDAL CERVICAL SPONDYLOMYELOPATHY
Anatomy
• Relevant anatomic structures in the dorsal compartment of the cervical spine that play a role in caudal cervical spondylomyelopathy include the dorsal vertebral lamina, the articular facets and joint capsule, and the ligamentum flavum.
Etiology
• Two distinct populations of patients are seen, and their etiologies are somewhat different. Of dogs with Wobbler’s disease, 10% to 15% are young, adolescent Great Danes with osseous malformations of the cervical spine.
• The remainder are middle-aged to older patients with acquired disease that is usually secondary to cervical vertebral instability. Doberman pinschers are the largest percentage of this group of dogs (approximately 80%), although dalmatians and Labrador retrievers are also predisposed.
Pathologic Changes Associated with Wobbler’s Syndrome
Congenital Osseous Malformation
• This is seen in young Great Danes, with clinical signs occurring in the first or second year of life.
• The disease is characterized by malformation or malarticulation of the articular facets and vertebral bodies, causing dorsal and lateral stenosis of the canal.
Vertebral Tipping
• There is a malposition of the vertebral body caudal to the affected intervertebral disc. The cranial aspect of the affected vertebra dorsally displaces into the spinal canal, causing ventral compression.
Chronic Degenerative Disc Disease and Cervical Vertebral Instability
• The compression is caused by concurrent dorsal annulus and dorsal longitudinal ligament hypertrophy.
Ligamentum Flavum Hypertrophy
• This disease causes dynamic, dorsal spinal canal compression. This lesion is often associated with vertebral arch abnormalities.
Hourglass Compression
• This combination of pathologies is associated with dorsal, ventral, and lateral compression. The young Great Dane is most commonly affected.
• Compression is caused by hypertrophy of the dorsal annulus fibrosis and dorsal longitudinal ligament ventrally, hypertrophy of the ligamentum flavum dorsally, and malformation or degenerative joint disease laterally.
Clinical Signs
• Most patients have a chronic, progressive history of neck pain, hypermetria, tetra-ataxia, and tetraparesis.
• These dogs have a low-neck carriage due to the dynamic nature of the disease, and the compression worsens upon neck extension.
• Often, the clinical course is waxing and waning. Occasionally, chronically affected dogs will have an acute deterioration.
Diagnosis
Differential diagnoses include degenerative spinal cord disease, ischemic myelopathy, discospondylitis, congenital spinal cord disease, inflammatory central nervous system disease, spinal neoplasia, brachial plexus tumor, subarachnoid cysts, and trauma (see Chapter 128). Ischemic myelopathy (also called fibrocartilaginous embolization) can usually be ruled out because this process is not associated with cervical pain (see Chapter 128).
Diagnostic Imaging
• Radiographs of the cervical spine in the non-sedated or anesthetized patient are usually not helpful, unless overt bony pathology (i.e., bony neoplasia or vertebral tipping) is present.
Myelography
• Cisternal myelography is helpful in identifying the site of compression (see Chapter 4). Perform a cisternal spinal tap, and obtain cerebrospinal fluid for analysis (see Chapter 125). Inject 0.33 ml/kg of iodinated contrast material into the subarachnoid space. After injection, obtain lateral and ventrodorsal projections of the cervical spine. Traction views of the spine are helpful in differentiating dynamic from static spinal cord lesions (see Chapter 4).
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