Veterinary Spinal Surgery
David Holmberg Canada
It is not the function of these notes to act as a comprehensive review of neuro-surgical techniques; these can be gleaned from any one of several textbooks. Rather, this is a summary of my own bias and the philosophy used in the treatment of spinal injury on my surgical service.
Stability between the vertebral bodies is maintained by the articular facets, intervertebral disks, ligaments and tendon attachments of the surrounding musculature. The articular facets are true joints composed of joint capsules and articular cartilage. The intervertebral disk (IVD) is composed of an outer fibrous shell (annulus fibrosus) and gelatinous center (nucleus pulposus). The main function of the IVD is that of a shock absorber between the vertebral end plates but it is also an important contributor to the rotational stability of the vertebral column.
The neurologic structures encountered during spinal surgery include the spinal cord, which is divided into the inner gray matter and outer white matter. The ascending sensory tracts are situated dorso-laterally and the descending motor tracts ventrolaterally. The dorsal and ventral nerve roots and dorsal root ganglia appear as a single lateral structure within their dural covering. The cervical intumescence, which contains the cell bodies for the nerves of the brachial plexus (spinal segments C6 to T2), is located in the area of vertebral bodies C5 to T1. The lumbar intumescence (spinal segments L4 to S3) and termination of the spinal cord varies between breeds and is located from vertebral bodies L3 to L6.
PATHOPHYSIOLOGY OF SPINAL CORD INJURY
Regardless of the etiology, the form of spinal cord injury can be divided into four components: Concussion, ischemic reaction, inflammation, and mass effect.
Removal of the mass effect is, in my opinion, the major benefit of surgical intervention. There is no question that a mass causing compression of spinal tissue results in loss of function. Compression of neural tissue interferes with its local blood supply, impedes transmission of impulses through axons and can cause demyelination. Some time after the onset of compression, the axons will no longer function or the nerve cells will die. At what point the damage will be irreversible has not been documented but after the fifth day, some permanent neural damage should be expected. The extent of recovery is influenced by the severity and duration of the compression.
RADIOGRAPHIC DIAGNOSIS AND LOCALIZATION OF SPINAL CORD INJURY
Survey radiographs and myelographic evaluation are the diagnostic modalities most commonly used to help localize the site of the lesion.
Abnormalities commonly found on survey radiographs include:
Lysis of the vertebral bodies suggestive of a neoplastic process.
Sclerosis and proliferation of bony endplates consistent with diskospondylitis.
Malalignment of the vertebral bodies indicating trauma or congenital malformation.
Calcification of the intervertebral disks associated with degeneration of the disks.
Narrowing of the disk space and wedging of the vertebral endplates.
Narrowing or increased density within the intervertebral foramen.
Narrowing of the facet articulation.
Myelographic findings will depend on the type of lesion and can generally be classified as:
Extradural (tapering of the dye column towards the cord) caused by compression from outside the dural tube, usually the result of disk prolapse or tumors of the vertebral bodies.
Intradural/extramedullary lesions obstruct dye flow within the dural tube but are outside the spinal cord (“golf tee” configuration). These are associated with tumors such as meningiomas.
Intramedullary lesions cause enlargement of the cord's silhouette and result in the dye column tapering away from the central canal. Mild intramedullary swelling can be associated with fibrocartilagenous emboli but significant enlargments are almost pathognomonic for tumors within the spinal cord. The diagnosis of an intramedullary lesion requires the symmetrical swelling of the cord be visible on both the lateral and ventrodorsal view.
SURGICAL TREATMENT OF SPINAL CORD COMPRESSION
Decompression of the spinal cord, in most clinical patients, is achieved by removal of the “mass effect” or correcting the abnormal anatomy that is putting pressure on the neural tissue. In such cases, the benefit of removing the surrounding bony lamina or splitting of the dural tube to allow the injured cord to swell is, in my opinion, of minimal benefit and adds excessive trauma to the surgical procedure. The surgical approach that causes the least iatrogenic damage to the cord and facilitates the easy removal of an offending mass in the thoracolumbar area, is the pediculectomy. Using this technique, laterally positioned disk material or tumors are interposed between the bone being removed and the spinal cord. Ventrally located masses can be seen directly and removed without undue manipulation of the cord. Pediculectomy results in minimal destabilization of the vertebral column and the lateral approach permits easy fenestration of all remaining disks. In the cervical area the ventral approach and slotting of the vertebral bodies adjacent to the lesion is used almost exclusively for disk prolapse. These approaches require precise, preoperative localization of the lesion. The limited exposure they provide makes them inappropriate when the diagnosis is in doubt. Hopefully, following thorough physical and neurological examination, and radiographic study, extensive laminectomies or general exploration of the spinal cord will seldom be needed.
Prophylactic fenestration of the intervertebral disks is somewhat controversial. Many authors claim a significant reduction in the recurrence rate of disk prolapse following fenestration. Some experimental studies have shown that creation of a defect in the annulus fibrosus results in an on-going inflammation and destruction of the remaining nucleus pulposus. It is also speculated that normal body movements cause the remaining nucleus to be extruded through the fenestration defect. Other studies (my own included) indicate that the residual nucleus stays unchanged within the disk and the annulus defect heals over by fibrosis, preventing the escape of additional material. Incising the ventral portion of the annulus fibrosus with a scalpel blade is adequate for evacuation of cervical disk spaces. Complete removal of the nucleus from thoracolumbar disks can be difficult in any dog and nearly impossible in dogs with spondylosis. The use of a high-speed burr to create the fenestration has resulted in reduced operating time and more complete removal of the nucleus from thoracolumbar disks.
Stabilization of the vertebral bodies is not necessary following routine decompressive surgery for disk prolapse or tumor removal. Traumatic fracture/luxations or congenital malformations may necessitate some internal fixation of the affected vetebral bodies. In the cervical area, fixation may involve placing pins or screws across the facet articulations, plating or pinning the vertebral bodies ventrally with or without the addition of methylmethacrylate bone cement. The thoracic area is innately more stable then the cervical or lumbar areas because of the support of the ribs and associated musculature. Rigid bone plates can be used on the lateral aspect of the thoracolumbar vertebrae. Flexible (Lubra7) plates or a combination of pins and wires attached to the dorsal processes will give some stability to vertebrae L1 to L5. In the lower lumbar and sacral areas, the dorsal processes are quite short and the use of cross pins with methylmethacrylate cement or pins in combination with flexible plates may be needed.
SPECIFIC SURGICAL DISEASES OTHER THAN DISK HERNIATION
Traction injuries of the sacral plexus can occur if dogs and cats get their tails caught in doors or gates when they are passing through them at full flight. Separation of the sacrococcygeal vertebrae may occur causing significant neural damage. The nerves roots at the site of the traction are usually destroyed resulting in an anesthetic and paralyzed tail. More importantly, the nerve roots of the sacral plexus may be avulsed at their foramina. This injury will cause a loss of function to the urinary bladder and anus.
It is often difficult to determine whether the animal will recover adequate neural function for voluntary urine and fecal control based on the initial examination. Clipping the hair from the perineal area and mapping the limits of cutaneous sensation with an indelible marker, facilitates following the patient's progress. As a rule, anal tone and control of the urinary bladder will be regained if cutaneous sensation returns to the anal area. Those patients that show no progression of the sensory level for two weeks should not be expected to regain bladder or bowel control.
Cauda Equina Syndrome
Because the spinal cord stops mid-lumbar and the nerves of the cauda equina continue into the lower lumbar and sacral region, this area is quite resistant to injury. Presenting histories range from a stiff gait to a reluctance of the animal to climb stairs or jump. Physical exam findings may include a shortened stride, proprioceptive deficits in the hind limbs, poor withdrawal reflexes, lumbosacral hyperesthesia, and extreme pain on elevation of the tail or extension of the hips. Survey radiographs may show lumbosacral spondylosis, but are often normal. Epidurography, MRI, CT and intraosseous venography have been used to demonstrate compression of either the cauda equina or one of the nerve roots exiting at the lumbosacral junction. Electromyography may also suggest denervation of one or more of the nerve roots. It has been my experience that often all diagnostic tests are normal and the animal is surgically explored based on the historical and physical findings alone. Abnormal findings may not be apparent during surgery, but patients often experience resolution of their clinical signs postoperatively.
A dorsal approach is used, dorsal lamina is removed from L7-S1 and the articular facets exposed. If manipulation of the vertebrae results in significant motion between the articular facets, the articular cartilage is burred off and K-wires or screws are placed transarticularly. Spreading the nerve roots away from the midline may reveal prolapsed disk material. If survey radiographs are suggestive of disko-spondylitis, the disk space can be fenestrated dorsally and cultured. The intervertebral foramina are explored by palpation with a probe and explored dorsally if the nerve root is entrapped by bony or fibrous proliferation. A fat graft taken from the local subcutaneous tissue is placed to minimize scarring.
The etiology of this condition is traumatic with or without predisposing congenital agenesis of the dens. Both dorsal and ventral approaches have been reported for surgical stabilization. The dorsal approach is slightly easier, but the weakness of the dorsal lamina of the cervical vertebrae makes fixation tenuous. The ventral approach with cross pinning of the articular facets is more reliable in my hands. Long-term prognosis remains guarded due to the potential for implant failure and migration.
Postoperative care of spinal surgery patients is the same as that used for the conservative treatment of disk prolapse. Good nursing care with physiotherapy and intense monitoring of bladder and bowel function are required. Adequate padding of the kennel is needed to prevent pressure sores and the use of synthetic ‘fleece’ material is recommended. Swimming and hydrotherapy not only helps keep the patient clean, but also stimulates circulation to the skin. The potential for gastric ulceration and colonic perforation in neurologically impaired patients is well documented and the use of gastroprotectants is recommended. Evidence of gastrointestinal bleeding is a contraindication to the use of corticosteroids. Similarly, non-steroidal anti-inflammatory drugs have little or no place in the treatment of spinal injury.
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