Spinal Cord Trauma
Robert J. MacKay • Lisle W. George
Vertebral trauma is a relatively common cause of spinal cord dysfunction in both livestock and horses. The spinal cord is normally protected by a complex of bones and ligaments that can be conceptualized in biomechanical terms as two columns: dorsal and ventral.1 The ventral column consists of the vertebral bodies, intervertebral disks, and dorsal and ventral longitudinal ligaments, whereas the dorsal column consists of alternating bony complexes (arches, articular processes, and dorsal spinous processes) and ligamentous complexes (supraspinous ligament, interspinous ligaments, ligamenta flava, and joint capsules).
According to biomechanical models that have been used for assessment of spinal trauma in humans and small animals, acute spinal instability occurs when there is disruption of both of these columns by external mechanical forces. The corollary is that a single intact column provides stability. This two-column system has not been validated for large animals. Fractures of vertebral transverse processes and dorsal and ventral spinous processes and partial fractures of vertebral bodies or arches (i.e., stress fractures) do not cause spinal instability or neurologic signs.2Most, but not all, traumatic spinal cord injuries are accompanied by vertebral fracture, subluxation, or dislocation.3 Conversely, many spinal injuries are associated with pain, reduced mobility, and abnormal neck position but do not cause acute neurologic signs. In large animals, cervical spinal cord trauma is usually caused by hyperextension or hyperflexion of the spine in the sagittal plane with superimposed vectors of compression, distraction, rotation, or shear. With vertebral hyperextension, compressive force is applied to the dorsal column and distractive force to the ventral column, whereas the reciprocal forces apply to hyperflexion injuries.
In all cases, the likelihood of associated spinal cord compression is higher in animals with abnormally narrow vertebral canals. Disk prolapse and fibrocartilaginous embolization of the spinal cord are rare in large animals and, when they occur, are usually associated with degenerative changes rather than with acute trauma, as may occur in dogs.4-6 Young animals are subject to fractures involving epiphyseal or growth plates (i.e., Salter- Harris fractures). Vertebral infections may be seeded along these cartilaginous plates hematogenously or by direct traumatic implantation, and osteomyelitis may progress to the point of pathologic vertebral fracture. Poorly balanced nutrition or undernutrition decreases bone density and increases susceptibility to vertebral fractures.Horses
In racehorses, cranial or vertebral fractures have accounted for 2.5% to 3% of deaths at flat races and 16% to 23% of deaths at chase and hurdle starts.7 In a 3-year study of fatal fractures/dislocations in the spine of 125 horses at racing events in Britain, 23% involved the cervical vertebrae, whereas the remainder involved the thoracolumbar vertebrae.8 Necropsies of 60 horses with vertebral trauma in Australia showed that 33 injuries involved cervical vertebrae; 10, thoracic; 10, lumbar; and 2, sacral.9 In general, cervical vertebrae are more prone to fractures during accidents at jumping events (e.g., crosscountry, showjumping, foxhunting, steeplechasing, and hurdling). The occipitoatlantoaxial region is most often involved in the following situations: (1) broad forehead impact, as in collisions with the ground, other horses, or fixed objects; (2) rearing and flipping over backward; or (3) when major distraction forces are applied to the head, as occurs in tied horses jerking backward on a halter. The atlantal ring or body of the axis may be fractured, the dens may fracture transversely anywhere along its length (including at the synchondrosis in young horses), or the dens may subluxate or dislocate from its usual position in the fovea dentis of the atlas.
Fracture of a single articular process is the most common fracture from C3 to C7. In young horses (especially those younger than 2 years), a characteristic and spectacular hyperextension fracture results in severe extension angulation of the intervertebral joint.10,11 On the more cranial of the affected vertebrae, the dorsal lamina and caudal articular processes are fractured and lifted dorsally. It is thought that this “deroofing” lesion provides natural decompression of the spinal cord while the surprisingly sturdy dorsal half of the intervertebral disk provides residual stability of the ventral column of the cervical spine.In the thoracolumbar spine, T1 to T3, T10 to TI6, and T18 to L6 appear to be relatively susceptible. Lumbar vertebral fractures reported in 38 Quarter Horse and 29 Thoroughbred racehorses primarily involved L5 and L6 and were the third most common musculoskeletal cause of death in Quarter Horses during the 22 years of data collection.12 All cases had abnormalities on the ventral aspect of the vertebral bodies, which suggests that preexisting pathologic conditions at the L5-L6 junction probably predispose horses to catastrophic fracture. Foals and young horses at pasture are prone to collide with fixed objects or other horses, get kicked by adult horses, or pitch forward headfirst into the ground, all while running at high speed. Such accidents often occur at night. Typical hyperflexion and hyperextension injuries of the cervical spine result from these falls, and cranial thoracic and midback fractures result from striking solid objects or being kicked. Horses may suffer contiguous or noncontiguous injuries of multiple vertebrae after high-speed impacts. Any horse that falls backward or struggles violently against a caudal barrier (e.g., in a trailer) may sustain sacrococcygeal fractures with damage to the cauda equina. There are reports that avulsion of the cauda equina can be caused by lifting or dragging a recumbent horse by its tail.
It is worth noting that horses may have serious spinal injuries while alone in a stall, without observed or external evidence of an accident, so trauma should always be considered in cases of acute onset of spinal cord signs, regardless of the environment.Livestock
The common sites of spinal fractures in calves are C2 to C4, T10 to T13, and L3 to L6 vertebrae. Vertebral fractures (particularly compression fractures) are especially common in 3- to 6-month-old ruminants as a result of nutritional problems including vitamin D, calcium, and copper deficiency or low calcium-to-phosphorus ratio.13 Nutrition-related fractures usually involve several animals and may also involve the ribs and long bones. Traumatic cervical vertebral fractures of cattle and small ruminants may be caused by injuries sustained in falls, roadway accidents, butting of other animals, collisions with moving farm machinery, predation, or accidents in tie-stalls, stanchions, or squeeze chutes.13-15 Spinal injury is especially likely to occur if the head is restrained in the chute or stanchion when the animal falls. Fractures or dislocations of the lumbar or sacrococcygeal spine frequently occur in cattle that slip in wet cemented areas and in performance-age bucking bulls.14,16 Many of these fractures occur in cows in estrus during mounting by herdmates. Spontaneous fractures of vertebrae weakened by congenital defects (e.g., hemivertebrae) or osteomyelitis also are common problems in calves.17 Traumatic dislocations, subluxations, or fractures of the atlantooccipital and atlantoaxial joints of pygmy goats may occur when the horns are held during restraint. Thoracolumbar fractures, particularly with epiphyseal separation of the middle to caudal thoracic vertebrae, may occur in calves transiting the birth canal during correction of dystocia.18-20
These fractures are mainly related to excessive traction and rotational force.21 Luxation of a sacroiliac joint in the dam may occur with the use of extreme force during manual extraction of a calf.
Mature Holstein bulls and rams may have a fused thoracolumbar spine and stenotic vertebral canal because of ankylosing spondylitis. This condition results in progressive pelvic limb paresis and ataxia.22 These animals are at risk for traumatic lumbar vertebral fracture, spinal cord injury, and recumbency if they are required to mount for semen collection or breeding.23 As described for horses, vigorous traction on the tail (e.g., when trying to assist a downer cow to stand) has the potential to cause stretching or avulsion of the cauda nerve roots and signs of cauda equina syndrome.■ Pathophysiology The primary phase of spinal cord injury is the direct effect of the mechanical events of the original trauma.24 The primary phase is irreversible, but additional rounds of primary injury can be prevented or minimized by surgery and external stabilization of the spine. The principal mechanical forces that are involved in acute traumatic injury are concussion, compression, shear, laceration, distraction, and contusion of the spinal cord. The secondary phase of spinal cord damage comprises the injurious molecular and biochemical events that are set in motion by the primary injury and occur in the first few hours after initial injury. The goal of medical therapy is to limit the damage that occurs from secondary injury. The most important events during this phase of injury are vascular damage with hemorrhage and microthrombosis, loss of autoregulation of blood flow, excessive release of the excitotoxic neurotransmitters aspartate and glutamate, increased neuronal intracellular calcium concentration, cellular damage from reactive oxygen species, and acute neutrophilic inflammation.
■ ClinicalSigns The most common sign of vertebral trauma in all large animal species is localized pain and limited mobility of the affected part. The atlantoaxial vertebral canal of horses is subject to fractures, subluxations, and dislocations, many of which do not cause signs of neurologic dysfunction, presumably because of the large cross-sectional area of the vertebral canal at this level of the spine.25 Two quite rare disorders result from spinal cord trauma and confound the rules of neuroanatomic localization: spinal shock and Schiff-Sherrington syndrome.
Spinal shock refers to loss of muscle tone and segmental spinal reflexes caudal to a focal severe transverse spinal cord injury, usually between T3 and L3.26 Although seldom described in the veterinary literature, it does occur in large animals, but, in contrast to the situation in humans, areflexia usually lasts less than 30 minutes, after which there is progressive recovery of segmental reflexes; persistence of signs is referable to a focal spinal cord lesion. With such a lesion, the thoracic limbs may be hypertonic, which reflects release from the inhibitory effect of tracts originating in the lumbar segments. This combination of paraplegia and thoracic limb stiffness is known as Schiff- Sherrington syndrome}'1 At least in small animals, signs regress by approximately 10 days. Spinal shock and Schiff-Sherrington syndrome may occur together or separately.■ Diagnosis and Treatment The first priority is the safety of attending personnel, which means that large patients that are thrashing and disoriented may need to be heavily sedated or anesthetized to allow for initial assessment, IV catheter placement, and treatment of any life-threatening conditions. Small ruminants theoretically can be taped to a backboard to immobilize them in lateral recumbency during initial procedures. Handlers must be careful not to exacerbate cervical vertebral trauma when restraining injured animals via lead rope and halter.
An indwelling IV catheter should be inserted and secured, and IV fluids and initial treatment should be provided as needed. Volume support and maintenance of normal arterial pressure and hematocrit are essential in all forms of CNS injury.28 Any animal with spinal injury and neurologic signs should be provided with full doses of analgesics. NSAIDs (e.g., flunixin meglumine, 1.1 mg/kg IV or PO bid) have the dual advantages of analgesic effect and inhibition of potentially injurious cyclooxygenase activity.24 Additional analgesia can be achieved if necessary by doses of butorphanol, morphine, or lidocaine or ketamine constant-rate infusions. The use of methylprednisone sodium succinate in this setting in human medicine remains highly controversial, although slight long-term benefits have been reported for a regimen of 30 mg/kg, followed by 5.4 mg/kg/h for 23 hours.29,30 Patients are at an increased risk for pneumonia, sepsis, and hyperglycemia. The use of methylprednisolone is becoming less popular because the risks of complications outweigh the potential benefits31; high-dose methylprednisolone sodium succinate is not recommended in large animals with acute spinal cord injury. As is the case for brain injuries, antiinflammatory doses of dexamethasone (0.05 to 0.1 mg/kg IV or IM once daily) should be administered routinely.
As soon as possible, a careful neurologic examination should be performed to localize the lesion. It is important that this examination be complete even if the site of injury seems obvious because multiple discontinuous spinal cord segments or the brain, or both, may be injured in a single traumatic incident.32
When technically possible, it is prudent to radiograph the entire vertebral column. In large animals under field conditions, views are generally restricted to laterolateral projections of the cervical vertebrae. Radiographs show the amount of spinal displacement at the time they are taken, however, not the amount of displacement that occurred at the time of injury. The two-column model can be used to assess spinal instability.1 Myelography is usually not necessary if it is determined that the spinal injury can be treated conservatively or if there is a substantially displaced fracture or luxation that is an obvious candidate for surgery. Myelography should be performed in animals with marked neurologic deficits and normal or equivocal radiographs. Additional information can be obtained from oblique and ventrodorsal radiographic views, C-arm fluoroscopy, CT, MRI, and osseous-phase nuclear scintigraphy. Techniques that necessitate general anesthesia in a large animal with spinal instability generally should be avoided unless there is an immediate surgical option.10
After these initial evaluations, the clinician has sufficient information to make recommendations for euthanasia, conservative treatment, or surgical management. Obviously, humane considerations, economic issues, and the intended use of the patient are driving considerations in this situation. In all cases, if quadriplegia and loss of deep pain are present, or in view of radiographic evidence of likely spinal cord transection, early euthanasia is appropriate. Otherwise, with the issues of handler safety and humane treatment kept paramount, it is reasonable to wait 12 to 24 hours to allow time for recovery of function before delivering a hopeless prognosis and euthanasia recommendation. Once the decision has been made to continue treatment, most large animals are still managed conservatively; surgery is an option in selected cases.
CONSERVATIVE MANAGEMENT. For large animals with vertebral column injury, 1 to 2 months of each of the following is recommended: full-time stall confinement; stall confinement with daily hand-led walking; turnout into a small paddock or round pen during the day with stall confinement at night. Pain control and sedation should be provided as needed. In horses that have difficulty getting to their feet, frequent use of an abdominal sling is essential. Such horses must be able to support their own weight once they are in the standing position. In cattle, a flotation tank can be used for the same purpose.
SURGERY. In the absence of evidence-based guidelines for surgical intervention in large animals, it is worth considering the potential adverse consequences of not performing surgery. Although conservative management has often been successful, the following negative outcomes have been observed in horses with spinal injuries managed conservatively: (1) sudden recumbency days to weeks after dens fracture, subluxation, or dislocation2,33; (2) limb ataxia and weakness after callus formation and joint remodeling around a fractured articular process11; (3) progressive torticollis, head tilt, or both after articular process and vertebral body fractures in the midcervical region; (4) limb ataxia and weakness after fibrous proliferation at the site of previous atlantoaxial subluxation; (5) abnormal head position and stiffness of the upper neck after upper cervical injury; and (6) a domino effect wherein there is progressive stenosis of the vertebral canal at the intervertebral joint or joints immediately caudal or cranial to a traumatized intervertebral joint that has healed in a marked flexed or extended angle.11,20
In view of these developments, reasonable indications for surgical intervention in horses are (1) prevention of neck stiffness or deformity; (2) prevention of callus formation or joint remodeling that may impinge on the spinal cord; (3) decompression, stabilization, or both of the atlantoaxial joint after dens fracture, subluxation, or dislocation25,33,34 and (4) decompression or reduction and stabilization of vertebral fractures/subluxations in response to deteriorating neurologic signs. Techniques have been described for each of these surgical procedures (generally with successful outcomes) in the cervical spine of horses.10,35-37 Canine surgical techniques can be adapted for use in the lumbosacral spine of valuable small ruminants, calves, and foals. In particular, the use of polymethylmethacrylate and Steinmann pins and plating of the dorsal spinous processes have wide potential application to thoracolumbar injuries in animals weighing less than 70 kg.38 Surgical decompression of the cauda equina by dorsal laminectomy of the sacrum has been described. In adult horses, the tuber sacrale of the pelvis interfere with the approach to the first and possibly the second sacral vertebrae, but the caudal part of the sacrum can be decompressed.39 In foals and heifers, sacral fractures may be reduced and stabilized with plates and screws.40
■ Prognosis For horses with spinal trauma without neurologic dysfunction that are treated conservatively, there is a fair to good likelihood that neurologic signs will not develop; however, there is also a fair chance that the neck will remain stiff, become deviated or rotated, or both. The prognosis for horses with spinal cord trauma associated with luxations or fractures of the vertebral body, arch, or articular processes must remain guarded to poor for return to use. Healing of such fractures frequently results in some degree of vertebral malalignment, sometimes with lordosis, kyphosis, scoliosis, or torticollis. Even after apparent healing and resolution of neurologic signs, delayed callus formation and degenerative changes in adjacent articulations can result in delayed spinal cord compression. When the injured spine is appropriately stabilized, improvement may continue for up to a year. In a small quadruped, it is estimated that even 10% survival of axons across a lesion site in the spinal cord may be compatible with walking. The limbs behind a permanent spinal cord lesion will be ataxic and weak to lateral pressure but spastic and stiff during walking and able to resist dorsal pressure.