DISEASES OF THE SPINE
0195-5616/92 $0.00 + .20
SPINAL TRAUMA Pathophysiology and ManageIllent of TrauIllatic Spinal Injuries Andy Shores, DVM, MS, PhD
A thorough knowledge of the recent advances in the pathophysiology and pharmacologic management of spinal injuries can augment the small animal clinician's treatment regimens for this frequently encountered malady. Key to the effective management of these injuries is developing an understanding of concussive versus compressive injuries, the secondary injury theory of acute spinal trauma, the threecompartment (column) theory as it pertains to vertebral stability, the generation and effects of oxygen free radicals and eicosanoids, and the effective dosage regimens and intervals recommended for posttraumatic corticosteroid therapy. Each of these topics and current information on spinal fixation techniques, radiographic assessment of the traumatized spine, and guidelines for determining the need for surgical or conservative management are discussed in this article. CAUSES OF SPINAL TRAUMA
Categories of internal and external sources of trauma apply. Internal trauma usually relates to intervertebral disc extrusion, pathologic fractures, or congenital vertebral anomalies or instability. External factors include automobile encounters, projectiles (gunshot injuries), falls from heights, injuries caused by other animals (including humans), and blunt trauma from objects (e.g., garage doors, falling objects).26 From the Department of Small Animal Clinical Sciences, Veterinary Teaching Hospital, Michigan State University College of Veterinary Medicine, East Lansing, Michigan
VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 22 • NUMBER 4 • JDLY 1992
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CLASSIFICATIONS OF SPINAL INJURY Spinal Cord Injury: Compression Versus Concussion
Regardless of etiology, perhaps the most important consideration outside the extent of injury is whether the insult is mainly compressive or concussive. Thus the first consideration as to the mode of therapeutic options applicable is made. Purely concussive injuries do not warrant surgical therapy. Compressive injuries always produce some concussion; however, it is the compression of the spinal cord that warrants consideration of surgical therapy. Instabilities can cause compression, but are also a source of recurrent concussive injury. External or internal stabilization is usually warranted when vertebral instability is the most prevalent factor in spinal trauma. 26 An illustration in consideration of the compression versus concussion concept in spinal trauma is the frequent occurrence of intervertebral disc (IVD) extrusion in chondrodystrophic dogs (Fig. 1). With tearing of the annulus, the nucleus pulposus extrudes into the spinal canal, compressing the spinal cord. The amount of compression is determined by the mass of the degenerative nucleus extruded into the canal, the ratio of vertebral canal diameters to spinal cord diameter (much greater in the cervical region than in the thoracic or upper lumbar region), and the relative amount of dehydration present in the degenerative disc. The process of chondroid degeneration involves loss of hyaluronic acid, which functions to imbibe water molecules. Progressively more degenerated nuclei are therefore more dehydrated and take on more water when extruded into the spinal canal, thereby constituting a large compressive mass. 25 The second factor, concussion, is determined by the force (velocity x mass) of the extruded nucleus as it impacts the spinal cord. One cannot equate the severity of injury with the compression because a large amount of extruded nucleus that gradually compresses the spinal cord may result in substantially less neurologic dysfunction than a small mass of nucleus, which virtually explodes into the spinal canal at a high velocity. 20 The aforementioned principles can be applied to other forms of spinal trauma. These include cervical versus thoracolumbar IVD extrusions (greater vertebral canal to spinal cord diameter in the cervical region results in less compression with an equal amount of nucleus extruded), vertebral fracture/luxations (minimal compression/massive concussion or vice versa), and IVD extrusions in nonchondrodystrophic breeds (fibroid degeneration of the IVD, extrusion ~ primarily compressive injury/minimally concussive; traumatic extrusion of normal, gelantinous IVD ~ primarily concussive injury/minimally compressive). These factors (concussion and compression) and their effects, which are the basic, underlying causes of spinal trauma, largely determine the immediate degree of compromise in spinal cord function. 26 Secondary effects, which may be substantial, are discussed in the pathophysiology section of this article.
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A
B Figure 1. Intervertebral disk extrusion as a form of spinal trauma in the chondrodystrophic dog. A, Large compressive extrusion of the nucleus pulposus; concussive effects may be minor if this material extrudes slowly. B, Small amount of nuclear material is in the spinal canal; concussive effects may be very damaging if this material impacts the cord at a high velocity.
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Vertebral Injury: Fracture Etiopathogenesis
Most spinal fractures and luxations occur at the junction of mobile and immobile segments of the spine (lumbosacral, thoracolumbar, cervicothoracic, and atlantoaxial or atlanto-occipital junctions). 20, 33 The forces responsible for vertebral fractures or luxations are bending (extension, flexion), torsion (rotation), and compression (axial loading).3,33 Most classification schemes for spinal fractures are based on either forces that created the fracture (extension, flexion), stability of the vertebral segments, or both. This classification is based on the forces responsible for vertebral fracture and displacement. Flexion injuries of the spine are more common than extension injuries and usually produce the more severe neurologic dysfunction. Pure hyperflexion produces vertebral body displacement with possible extrusion of the nucleus pulposus into the spinal canal (Fig. 2). Hyperflexion combined with rotational forces produces instability. 3, 33 Extension injuries to the spine usually result from forces applied to the dorsum of the spine. 33 Hyperextension results in collapse of the articular facets and tearing of the ventral annulus with expulsion of the nucleus pulposus ventrally (Fig. 3). Stability of the vertebrae is maintained by bony and ligamentous support. Conservative management is usually adequate .26, 33 Compression fractures result from axial loading plus flexion of the spine and have been classified as wedge compression fractures and burst fractures.3,33 Wedge compression fractures occur when the cancellous and cortical bone of the vertebral body are crushed by severe flexion forces when axial loading is applied to the head or pelvic area (Fig. 4). The most common sites for these fractures are the cervicothoracic, thoracolumbar, and lumbosacral areas. Instability may be minimal. 33
Flexion fracture
Figure 2. Hyperflexion of the spine.
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Extension fracture
Figure 3. Hyperextension of the spine.
Wedge compression fracture
Flexion + Axial loading
~
Figure 4. The forces applied to the spine result in a wedge compression fracture of the vertebral body.
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Burst fractures result from flexion and axial forces causing comminution of the vertebral bodies with fractures through one or both end plates. The nucleus pulposus may extrude in any direction, and bone fragments are driven outward or upward into the spinal canal. Stability of the fracture depends on the structures involved and the status of ligamentous support. When bone fragments compress and possibly lacerate the spinal cord, dorsal decompression is inadequate in treating these injuries. 3 Anterior approaches are used in human surgery, and hemilaminectomies are indicated in veterinary surgery.3, 23, 26 Without computed tomography, a full appreciation of the spinal compression caused by bone fragments in the spinal canal is difficult. 3 Combinations of flexion and rotational forces commonly result in displacement of vertebrae and are classified as subluxations, luxations, or fracture/luxations. Subluxation is minor vertebral displacement,33 and stability depends on the structures damaged. Carefully performed stress radiographs or fluoroscopy is used to evaluate spinal instability.26 A luxation is displacement of the intervertebral space when flexion is the primary force of injury and occurs simultaneously with rotational forces (Fig. 5). When the predominant force is rotational and is accompanied by simultaneous flexion, a fracture/luxation occurs33 (Fig. 6). Fracture luxations are frequently seen in the lumbosacral vertebral junction.
Flexion (primary force)
+ Rotation
,--- _ _ _I Luxation Figure 5. Application of flexion as the primary force, with simultaneous rotation (torsion), results in vertebral luxation.
Rotation (primary force)
+ Flexion
Fracture/Luxation Figure 6. Application of rotation (torsion) as the primary force, with simultaneous flexion, results in vertebral fracture and luxation.
Figure 7. A transverse fracture involving the transverse process, lamina, and pedicle. Note that the fracture does not involve the vertebral body, and displacement is minimal. 865
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Transverse fractures can result from any force that causes avulsion of a vertebral process. The fracture can involve the spinous process, transverse process, pedicles, or laminae (Fig. 7). Stability is often good. 3 Surgical intervention is unwarranted unless additional fractures are involved or the fractured pedicle or lamina invades the spinal canal, causing compression. PATHOPHYSIOLOGY OF SPINAL TRAUMA
Initial or primary (mechanical) injuries rarely cause physical transection of the spinal cord, although complete functional loss (physiologic transection) may occur. 31 Systemic, focal, cellular, and subcellular events occurring after the primary injury, collectively resulting in various biochemical and pathologic changes, can cause additional functional deterioration and compromise structural integrity of the spinal cord. These sequential, posttraumatic events have been described as the concept of secondary injury and are characterized by several pathophysiologic mechanism theories. 6, 31 Primary Spinal Cord Injury
Primary spinal cord injury, as previously discussed, may result from concussion or a combination of compression and concussion. Consequences range from minor damage, causing minimal dysfunction or structural changes, to laceration, crushing, or distraction (stretching) of the neuropil, resulting in permanent dysfunction. 26 Again, the concussion at the time of injury is largely responsible for the initial degree of neurologic dysfunction. Further deterioration is a result of the secondary injury factors. Secondary Spinal Cord Injury
Vascular, biochemical, and electrolyte mechanisms have been postulated as causes of secondary injury following primary, acute spinal cord injury.6, 31 Each of these mechanisms produces changes that alter spinal cord function, and most have been shown to result in permanent functional deterioration in experimental models. Figure 8 outlines the pathologic events associated with each of the proposed secondary injury mechanisms. Allen was the first to describe the gross and microscopic changes associated with acute spinal cord injury and also hypothesized the existence of a biochemical factor associated with the development of secondary changes. 31 Petechial to ecchymotic hemorrhages occur in the gray matter within minutes following acute spinal cord injury. Edema of the white matter accompanies the gray matter changes, and both
Physical damage Concussion Compression
Vascular disruption -->
-->. --> -->
Hemorrhage Microcirculation Thrombosis Vasospasm
Primary spinal cord damage
Neurogenic shock Autoregulatory loss Systemic hypotension • Microcirculation
eX)
0"1
~
Biochemical events • Catecholomines , Excitotoxins • Endogenous opioids 'Arachidonic acid release Lipooxygenase • Free oxygen radicals Cyclooxygenase • Vasoconstriction (thromboxane A-2a) • ATP Production Figure 8. Mediators of secondary spinal cord injury.
Electrolyte changes 'Ca++ influx 'K+ efflux , Na+ permeability
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white and gray matter changes may rapidly progress over the 4- to 6hour posttraumatic period. 1, 6, 13, 31 Complete hemorrhagic necrosis of the most severely injured segment may be evident grossly and microscopically within the first 24 to 48 hours. 6, 31 One theory suggests that gray matter may be more vulnerable to damage because of supernormal metabolic demands and decreased spinal cord blood flow in response to the injury, creating a substantial negative balance in the available energy metabolites. 6, 13, 22 Vascular Mechanisms of Secondary Injury
Systemic and focal vascular changes result from acute spinal cord trauma. These include mechanical damage to the spinal cord microvasculature and second injury effects on these and larger vessels. 31 After a brief rise in mean arterial blood pressure following acute spinal cord trauma, a persistent decline in mean arterial pressure and cardiac output occurs in the presence of neurogenic shock. 13 This phenomenon has recently been further substantiated by evidence that dobutamine, at levels that are both inotropic and chronotropic, is useful in the reversal of neurogenic pulmonary edema. 18 Acute central nervous system injury has been shown to produce myocardial ischemia in dogs. 17 The effect of these changes on the spinal cord is manifested by reduced spinal cord blood flow (SCBF).31 Secondary injury due to vascular mechanisms is a result of numerous factors, including loss of autoregulation, hemorrhage, effects from damage to microcirculatory vessels, and vasospasm/thrombosis. Each of these factors decreases SCBF.31 Reduced SCBF in the face of a postulated increased metabolic demand may facilitate the release of certain autodestructive factors, which further serve to feed the secondary injury.6 Biochemical Changes Associated with Secondary Injury
Numerous biochemical changes take place in the presence of reduced SCBF and hypoxia of the injured segment. These changes have previously been associated with the increased concentrations of catecholamines following acute spinal injury.1, 6, 31, 35 These include histamine, norepinephrine, and dopamine. Strong evidence that these neurotransmitters create an environment that propagates vasoconstriction, hypoxia, and necrosis is lacking. Evidence is mounting, however, that another neurotransmitter, serotonin, is involved in the autodestructive processes following acute spinal cord trauma. 6, 11, 35 Excitotoxic amino acids (glutamate, aspartate) have also been described as potent necrotizing substances capable of inducing neuronal degeneration and as potential mediators of the second injury phenom-
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ena. 6,31 Glutamate receptor activation may facilitate intracellular calcium ion influx, promoting vasospasm and ischemia. 31 Lipid peroxidation and vasoconstriction are end results of the arachidonic acid cascade following its interaction with cyclo-oxygenases and lipo-oxygenases. 6, 31 The products derived from these biochemical aberrations include the potent vasoconstrictor thromboxane-A2-a and the oxygen-free radicals that accumulate after lipid peroxidation (0 2 - , H 2 0 2 , OH-)6, 31 and destroy the cell membrane components rich in phospholipid-bound polyunsaturates. 31 The physiologic homeostasis that exists between the oxygen free radicals and the free radical scavengers (vitamin E, ascorbate, glutathione peroxidases) is disrupted with spinal cord injury and the overabundance of the radicals. 31 Hence further tissue damage, reduced SCBF, and the perpetuation of toxic biochemical product accumulation lead to cell death and permanent spinal cord damage. Reversal of this trend is a primary goal in the management of acute, severe spinal cord injury. Electrolyte Aberrations
The most frequently mentioned electrolyte change in association with central nervous system damage is the intracellular influx of calcium ions (Ca++). The role of excitotoxins has been mentioned in association with this change, with glutamate receptor activation facilitating the influx of Ca++. This Ca ++ shift creates microcirculatory vasospasm, alters mitochondrial function and therefore cellular respiration, and facilitates the production of vasoconstructive prostaglandins and leukotrienes.6, 12, 31 Other electrolyte changes that have been associated with central nervous system injury are increased extracellular potassium and increased sodium permeability of the cell wall. 6These changes may occur in conjunction with or in response to the elevated intracellular Ca++ levels, and all promote ischemic changes. Additional Secondary Injury Factors
Although numerous factors have been studied in the pathogenesis of acute central nervous system injury,1° the exact mechanism is speculative. Other factors that likely playa role in the destruction of tissue with the second injury mechanism include endogenous opioids l l (Le., dynorphins), an increased metabolic rate of oxygen consumption leading to decreased adenosine triphosphate availability, and edema associated with decreased venous return, vascular stasis, and physical obstruction of venous outflow (thrombosis, compression). The probable result of all factors contributing to the secondary injury is reduced SCBF and the resultant hypoxic changes. 4, 31
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INITIAL TREATMENT OF SPINAL TRAUMA
Therapy involving both medical and surgical management may be required. Determining the most appropriate therapy is a stepwise process that correlates with the diagnostic evaluations. The initial diagnostic step is the examination. The history, signalment, and physical and neurologic examinations assist the clinician in determining the presence or absence of life-threatening injuries, which require immediate therapy. After these are addressed and based on the history and localization of the injury, the need for immediate corticosteroid therapy can be determined. An unstable vertebral column warrants the application of a brace to prevent further damage to the spinal cord as the animal is manipulated during additional diagnostic procedures. 26 Experimental evidence suggests that corticosteroids, at prescribed doses, are effective in the management of acute spinal cord injuries during the first 8 hours following trauma. 5, 16 The widespread and consistent use of such a regimen has not been clinically tested in veterinary medicine. In view of the lack of experimental evidence that any other therapy improves the outcome in the treatment of acute spinal cord injury, however, the author has adopted this therapy for clinical use. Acute, severe spinal cord injuries of less than 8 hours' duration are initially treated with sodium prednisolone succinate or methyl prednisolone using the following regimen 26 : Time Zero (Initial Dose): 20 to 30 mg/kg intravenously (IV) T 3 hours: 10 to 15 mg/kg IV T 6 hours: 10 to 15 mg/kg IV T 9 hours through T 33 hours 2 mg/kg/h IV* At the end of this regimen, corticosteroids are discontinued. In practice, concerns about effects of this regimen on the gastrointestinal system and the acid-base balance should be addressed. Cimetidine (4 to 8 mg/kg orally or IV, every 6 to 8 hours) is administered, and arterial blood gases are analyzed as necessary. Gastrointestinal protectants (e.g., bismuth compounds, kaolin-pectin) may also be used. 26 Experimental and clinical trial studies have documented the efficacy of the 21-aminosteroid compound U74006F in the treatment of acute spinal cord trauma. 14 The effective dose is equivalent to that recommended for methylprednisolone and as shown in the schedule as given here. This new compound does not have glucocorticoid activity, is a superior oxygen radical scavenger, and has approximately 100 times the anti-inflammatory capabilities of methylprednisolone. Undoubtedly the clinical use of this drug in the treatment of acute spinal cord trauma will become standard. *May be administered as bolus at intervals of 2 hours or as a continuous infusion.
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DIAGNOSIS
Further evaluation of the animal occurs after emergency considerations and life-threatening conditions are stabilized. Figure 9 illustrates the diagnostic and therapeutic protocol for spinal cord injuries. Physical and Neurologic Examinations
The diagnostic protocol for trauma victims always begins with an assessment for life-threatening injuries or conditions, such as hemorrhagic shock and pneumothorax. After initial assessments are completed and necessary measures are undertaken to stabilize the patient, further assessment includes evaluation of all systems. The neurologic examination in the recumbent animal with possible spinal fracture or instability is restricted to the evaluation of the mental status, posture, cranial nerves, static muscle tone, segmental reflexes, and nociception. Localization of the spinal injury can be determined with these assessments. 26 All generalized trauma victims (i.e., those involved in a vehicular accident) should be assessed for thoracic, abdominal, and pelvic injuries. A standard minimal database should be established within each hospital and constructed to provide maximal information on the overall health status of the patient. In most institutions and practices, this consists of a complete blood count, chemistry profile, urinalysis, and electrocardiogram. 26 Radiography
The patient, if recumbent and vertebral instability is even a remote possibility, is transported on a stretcher or stiff board for the initial radiographic assessment. Lateral and across the table ventrodorsal views are obtained to avoid unnecessary patient manipulation. Additional radiographic studies (myelography, computed tomography reT], magnetic resonance imaging [MRI]) may be necessary and require anesthesia; however, the initial assessment serves to determine the presence or absence of a fracture or potentially unstable vertebral column. 26 When initial radiographic studies reveal a disruption of the vertebral column, the benefits of additional studies after anesthesia must be weighed against the potential risk for further spinal cord trauma during positioning of an anesthetized animal. Without the protection afforded the vertebral column by the muscle tone present in the awake animal, untoward movements in the positioning process could further compromise spinal cord function. A complete spinal radiographic series (cervical through lumbosacral regions) is optimal to rule out multiple fractures.
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Initial assessment
Collect minimum data base*
Life-threatening injuries
Localize spinal injury
Initiate corticosteroid therapy+
Diagnostic imaging
Stable spine§
Review minimum data base
General anesthesia
Radiography/Myelography
Surgical therapy
Conservative therapy
Figure 9. Algorithm for management of acute spinal cord trauma. *CBC, serum chemistries, UIA, ECG; tsee text for specific dose regimen; +history of trauma as evidenced on examination, etc.; §no known history of trauma, suspicion of intervertebral disc extrusion or other condition not associated with instability; IIprevent untoward movement by securing animal to spinal board or apply spinal brace or splints.
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Myelography
Myelography is indicated when plain film radiography does not adequately define the issue of compression versus concussion. Cervical or lumbosacral sites may be used to administer the contrast media. 26 The current use of nonionic, water-soluble, iodinated agents has reduced complications associated with myelography; however, postmyelographic generalized motor seizures can occur and could have devastating consequences in an animal with an unstable spine. If myelography is used in the diagnostic assessment, the clinician should be prepared to perform any necessary surgical procedures during the same anesthetic episode. Advanced Imaging
When available, advanced imaging techniques (CT and MRI) may enhance the clinician's three-dimensional perspective of the fracture and better define the position of the spinal cord with respect to the fracture segments (Fig. 10). It is the responsibility of the clinician to be
Figure 10. A, Myelogram demonstrating a vertebral luxation at T7-T8 (arrow) with a reduced flow of the contrast media. B, Axial plane computed tomography (CT) scan demonstrates fracture fragments but no evidence of compression of the spinal cord (surrounded by radiodense contrast media). C, Three-dimensional reconstruction of the CT scan, ventral view, demonstrates slight lateral displacement of the T7 vertebra.
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prudent in determining the necessity of advanced diagnostic imaging by considering the additional time and manipulation required for image acquisition. THERAPEUTIC MANAGEMENT OF SPINAL TRAUMA
Through the aforementioned diagnostic techniques, the presence or absence of spinal cord compression and vertebral fracture or instability can be determined. The need for decompression and for stabilization is then determined from the diagnostic information. Guidelines for conservative (nonsurgical) and surgical management of spinal fractures and luxations 24, 26 cannot be universally applied; however, an adaptation of a principle used in human medicine has standardized radiographic assessment for some. Although the success or failure of an animal to regain acceptable function following spinal trauma (ability to urinate and defecate voluntarily, ambulatory, free of pain) can be considered as evidence for or against the use of either modality (surgery versus conservative management), the rapidity and completeness of return to function should also be considered. Three-Compartment Theory of Radiographic Assessment of Spinal Fractures
A method used for the classification of spinal fractures in humans3 has been adapted for use in small animals. 26 Figure 11 shows a canine vertebrae divided into three compartments, defined by anatomic structures. The dorsal compartment contains the articular facets, laminae, pedicles, spinous processes, and supporting ligamentous structures (Le., ligamentum flava). The middle compartment contains the dorsal longitudinal ligament, the dorsal annulus, and the dorsal vertebral body (floor of the spinal canal). The ventral compartment contains the remainder of the vertebral body, the lateral and ventral aspects of the annulus, the nucleus pulposus, and the ventral longitudinal ligament. Radiographs are evaluated to assess which of the three compartments are damaged. When two or three of the compartments are damaged or displaced, the fracture is considered unstable. Instability and compression are the key indications for surgical intervention. If only one compartment is involved, stability is likely present and conservative management can be pursued when the absence of compression can be documented through myelography or advanced imaging (CT or MRI). Figure 11 can be applied to the evaluation of animals with spinal injuries to determine indications for surgery. The author has used this classification scheme in evaluating spinal fractures during the last 3 years and found it quite reliable. The reader is cautioned, however, because radiographic signs are mere static representations of the spinal column. Other factors to be considered
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Dorsal Middle Ventral
Dorsal ~
Middl
Figure 11. Illustration of the three compartment theory of radiographic evaluation of spinal fractures. The dorsal compartment contains the articular facets, laminae, pedicles, spinous processes, and supporting ligamentous structures (Le., ligamentum flava). The middle compartment contains the dorsal longitudinal ligament, the dorsal annulus, and the dorsal vertebral body (floor of the spinal canal). The ventral compartment contains the remainder of the vertebral body, the lateral and ventral aspects of the annulus, the nucleus pulposus, and the ventral longitudinal ligament. Radiographs are evaluated to assess which of the three compartments are damaged. When two or three of the compartments are damaged or displaced, the fracture is considered unstable.
include the concept of acute versus chronic instability, the neurologic status of the animal, and the presence or absence of spinal cord compression. 26 Acute instability implies the fracture is capable of further displacement or movement immediately after trauma. Acute instability is a consequence of fracture luxations and loss of all ligamentous support (usually involvement of the dorsal and middle compartments). Chronic instability is used to describe fractures that are not immediately displaced but will lead to progressive deformity and deteriorating neurologic status in weeks to months as a result of further angulation of the spine during the healing phase. In addition, chronic instability can also be
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applied to spinal injuries resulting in minimal luxation that does not stabilize and causes some compression and concussion of the spinal cord each time the animal moves. The latter form of instability may only be fully assessed using myelography combined with application of stress views or fluoroscopy. 20, 26
Conservative Management of Spinal Fractures and Luxations
Indications for conservative management are minor to no displacement of the vertebral column, minimal to no instability of the involved segments, and the absence of compression of the spinal cord. Evidence of minor compression and minimal to no neurologic dysfunction would be an indication for conservative management. Methods employed in conservative management include confinement (preferably in a hospital) and a brace or splint. Various types of braces or casts can be made from readily available bandage and casting materials, but custom-made canvas braces, reinforced -with metal rods and attached to the animal with Velcro straps (CO-I and CO-II Spinal Braces, Canine Orthopedics, Colorado Springs, CO) seem superior to J'lhome-made" types in most instances. Proper nursing care is equally important for a successful outcome. Serial monitoring of neurologic function and assessment of radiographic signs are necessary to ensure continued improvement and to rule out any changes in the fracture that may warrant reconsideration for surgical intervention. Urinary continence and confidence in the stability of the fracture are indications for discharge of the animal to the care of the owners. Strict confinement for at least 2, and usually 4, weeks is necessary in most animals treated conservatively. In young animals, continued monitoring is needed to detect any spinal deformities that may develop from continued growth of vertebrae adjoining the fracture site. When treated conservatively, animals should be braced and serial radiographs made during the 6 to 8 weeks following injury because vertebral instability with collapse of the fracture can occur as bone is reabsorbed during the initial stages of bone healing. This is particularly evident in young dogs when additional forces are applied to the fracture site as adjoining vertebrae continue to grow and may add compressive forces (axial loading) to the fracture site. 26
Conservative Management of Concussive Spinal Cord Injuries
In the absen.ce of evidence for spinal cord compression or instability of the spinal column and after the initial corticosteroid therapy to combat the effects of free oxygen radical damage, edema, and the development of additional secondary injury factors, general nursing
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care and physical therapy are the principle factors in management. The following are key components in providing the necessary care: 1. Thick, soft padding-change as necessary when soiled with urine or feces. 2. Range of motion-joints of all neurologically impaired limbs, 5 minutes for each limb, 3 or 4 times a day. 3. Express bladder 4 times a day when necessary; monitor for urinary tract infection-treat as appropriate: bethanechol (5 to 15 mg orally 3 times a day) for detrusor atony, bethanechol plus diazepam (2 to 10 mg orally 3 times a day) for reflex dyssynergia in males. 4. Adequate nutrition-when necessary to provide appropriate caloric intake, consider nasogastric tube (cats), pharyngostomy tube, or percutaneous enterogastric tube. 5. Hydrotherapy (whirlpool)-swimming exercises with support stimulate circulation to limbs, active movement, and skin care, 10 to 20 minutes once or twice daily. 6. Outside walks-on grass, with support, to encourage active limb movements and urinary and bowel elimination.
Generally, the animal can continue convalescence at home once control of the urinary bladder is established and the owners can comply with any special needs and concerns in the home environment. Surgical Management of Spinal Fractures and Luxations
A thorough knowledge of the forces that create spinal fractures and luxations and of the structure of the intact vertebral column is paramount in reconstructing an unstable spine. In addition, indications for spinal stabilization, spinal cord decompression, and surgical methods applicable to a given fracture or luxation must be recognized. When the veterinarian is not familiar with these factors, referral is necessary, and recommended methods for transport are followed. 26 Concussion, compression, and distraction constitute the forces responsible for acute spinal cord damage. Concussion is a dynamic force occurring at the time of injury and can be a recurrent factor if the vertebral column is unstable and the animal is improperly transported, restrained, or manipulated, before stabilization. Compression occurs from an extruded JVD or fracture fragments within the spinal canal, from subluxations, luxations, or foreign objects such as bullet fragments. Flexion, extension, and rotation are the principle forces responsible for vertebral fractures and luxations. The effects of these forces have already been summarized. Surgical management of acute spinal cord trauma is indicated for decompression and immobilization of an unstable vertebral column. Many factors must be considered in recommending the appropriate treatment of an acute spinal cord injury, including location of the injury, the type of fracture or compression,
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instability of the vertebrae, neurologic status, and severity of coexisting injuries. 26, 33 The principles of surgical management of spinal fractures include a thorough understanding of the biomechanics of the spinal segment and fracture type involved in the injury, adequate decompression when compression exists, anatomic realignment of the vertebral canal, and rigid internal fixation appropriate for the fracture type and sufficiently strong to allow early postoperative mobilization of the animal. These principles must be met without producing further injury to the spinal cord. 26 The ideal method of spinal fixation should incorporate the following qualities: 1. Can be used in any segment of the vertebral column. 2. Can be combined with either dorsal laminectomy or hemilaminectomy. 3. Fixation device stabilizes at least two of the three compartments. 4. Fixation method immobilizes only three or four vertebrae. 5. Fixation device is independent of the fractured vertebra. 6. The fixation should be sufficiently strong to allow early postoperative mobilization of the animal and not require additional external support. 26 Durotomy, piatomy, and myelotomy have each been advocated in instances of acute, severe spinal cord trauma;7 however, the efficacy of any of these procedures has not been demonstrated in clinical veterinary surgery. Hoerlein 16 reported decreased return to function in cats subjected to experimental spinal cord trauma and treated by decompression and a dorsal midline myelotomy. Myelotomy is designed to provide internal decompression of the spinal cord but is likely only effective during the first several minutes or few hours following injury. Special microsurgical equipment, including an operating microscope, is needed to perform this procedure properly.26 Cervical Fractures and Luxations
Most cervical fractures are transverse and can be managed with conservative therapy. Exceptions include atlantoaxial subluxations, fractures of the cranial vertebral body of the atlas, bilateral dorsal facet luxations (locked facets), and some atlanto-occipital fracure/luxations. Fixation methods are generally applied ventrally. Atlantoaxial subluxations are managed with K-wire or lag screw fixation and fusion of the atlantoaxial joints. An odontectomy can be performed from a ventral approach if necessary. Dorsal fixation methods 5 and conservative techniques32 have also been described. Cervical vertebral body fractures can be stabilized ventrally using small orthopedic plates or Steinmann pins and polymethylmethacrylate. 26 Cervical Spine Locking Plates (Synthes Spine, Paoli, PA) are
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Locking Screw
\
Expansion Head Screw -
Figure 12. The cervical locking screw plate, applicable to ventral fixation of cervical vertebral fractures. The locking screw locks the expansion head screw to the plate, preventing the screws from backing out of the vertebra when only the ventral cortex of the vertebral body is engaged by the screw.
recent additions to fixation devices used in the cervical spine but have been used limitedly in veterinary spinal surgery (Fig. 12). The chief advantage of this device is that the locking screws do not back out even though only one cortex is penetrated. Acute injuries to the cervical spine can produce autonomic nervous system aberrations, including hypotension, bradycardia, arrhythmias, and respiratory depression. 13 These aberrations can also be initiated or exacerbated during surgical manipulation of the cervical spine during the surgical procedure. Thoracic and Upper Lumbar Fractures and Luxations
Most spinal fixation techniques developed in veterinary surgery have addressed this region of the spine. Surgical techniques for fixation of the thoracic and upper lumbar spine include dorsal spinal plates l plastic, metal), vertebral body plates, 15, 20 combined dorsal spinal plates and vertebral body plates (Fig. 13),34 modified segmental fixation,21 .pins and polymethylmethacrylate (PPMMA) fixation (Fig. 14),2 U-pins I5 , spinal staples,15 and the Luque segmental fixation technique. 19, 30 Subluxations, luxations, and some fractures involving the dorsal compartment can be stabilized with dorsal techniques. Included are (Text continued on page 884)
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~ B Figure 13. A, Fracture luxation at T12-T13. B, Repair using a plastic dorsal spinal plate and a vertebral body plate. Ribs are disarticulated to allow placement of the vertebral body plate, then repositioned using orthopedic wire.
00 00 ~
00 00 N
A
Figure 14. A. Fractured L2 vertebrae. B. Repair using four Steinmann pins inserted into adjacent cranial and caudal vertebrae and surrounded by polymethylmethacrylate.
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dorsal spinal plates, modified segmental fixation, PPMMA, spinal staples, and V-pins. Dorsal spinal plates require intact spinous processes. 1S The modified segmental fixation technique requires intact articular facets. 21 The PPMMA technique requires placement of four vertebral body Steinmann pins and curing the exothermic synthetic polymer over the pins and vertebrae. 2 Spinal staples and V-pins require intact spinous processes and are limited to animals under 15 kg body weight. IS All of these techniques can be combined with a unilateral or bilateral hemilaminectomy. Dorsal laminectomies can be combined with techniques not requiring intact spinous processes. In the upper thoracic spine, dorsal fixation techniques are difficult to apply because of the size and shape of the spinous processes. 30 Pin placement for PPMMA fixation and closure of muscle over the pins and polymer are difficult in the upper thoracic spine. Accurate drilling and placement of wires through articular facets in the upper thoracic spine are difficult for the modified segmental technique. Further development of segmentaF7 and pedicular techniques9 should prove applicable to all areas of the thoracic and lumbar spine and can be combined with dorsal laminectomy or hemilaminectomy.26 Vertebral body plates are most easily applicable to the lower thoracic and upper lumbar spines. Restrictions in the middle to upper thoracic spine are the rib attachments and lateral exposure of the vertebrae. In the lower lumbar spine, location of the spinal nerves associated with the femoral and sciatic nerves precludes placement of the vertebral body plates. IS Evaluation of the strength and rigidity of several thoracolumbar fixation techniques revealed that combined dorsal spinal plate/vertebral body plate fixation was superior to other techniques of fixation. 34 Fixation of two compartments appears superior to fixation of only one. Caudal Lumbar and Lumbosacral Fractures
Fractures and luxations in the more caudal vertebral segments are seen frequently and are amenable to several types of fixation. At the lumbosacral junction, the cranial segment of the fracture is unstable and displaced dorsal to the stable segment with pelvic attachments. A dorsal approach to the lumbosacral spine is performed, and reduction with fixation using a single pin through the wings of the ilium and over the dorsal lamina of the cranial segment may be sufficient. 30 Migration of the pin before fracture healing is a common complication and has prompted development of newer techniques, including plastic dorsal spinal plates combined with transilial pins, 8 the modified segmental fixation technique,21 transilial bolts, and a combined dorsal spinal plate/Kirschner-Ehmer fixation technique 29 (Fig. 15). Using the concept of multiple compartment fixation, the combined dorsal spinal plate/Kirschner-Ehmer fixation was reported stronger than the modified segmental fixation in a biomechanical evaluation. 28 All of the aforemen-
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Figure 15. A, Lumbosacral fracture/luxation. B, Fracture repair incorporating multiple vertebral compartments by using a dorsal spinal plate and external fixator device. The pins exit the skin on each side and are secured using external connecting rods and clamps (not shown).
tioned techniques for lumbosacral fixation can be combined with dorsal laminectomy. Other lower lumbar fractures are repaired with dorsal spinal plates, the modified segmental fixation, PPMMA fixation, or combined dorsal spinal plate/Kirschner-Ehmer technique. Although the dorsal spinal plate/Kirschner-Ehmer fixation is considered superior in strength and rigidity,28 other techniques can be successfully employed. SUMMARY
Spinal trauma can originate from internal or external sources. Injuries to the spinal cord can be classified as either concussive or compressive and concussive. The pathophysiologic events surrounding 3pinal cord injury include the primary injury (compression, concussion)
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and numerous secondary injury mechanisms (vascular, biochemical, electrolyte), which are mediated by excessive oxygen free radicles, neurotransmitter and electrolyte alterations in cell membrane permeability, excitotoxic amino acids, and various other biochemical factors that collectively result in reduced SCBF, ischemia, and eventual necrosis of the gray and white matter. Management of acute spinal cord injuries includes the use of a high-dose corticosteroid regimen within the initial 8 hours after trauma. Sodium prednisolone and methylprednisolone, at recommended doses, act as oxygen radical scavengers and are antiinflammatory. Additional considerations are the stability of the vertebral column, other conditions associated with trauma (Le., pneumothorax), and the presence or absence of spinal cord compression, which may warrant surgical therapy. Vertebral fractures or luxations can occur in any area of the spine but most commonly occur at the junction of mobile and immobile segments. Dorsal and dorsolateral surgical approaches are applicable to the lumbosacral and thoracolumbar spine and dorsal and ventral approaches to the cervical spine. Indications for surgical intervention include spinal cord compression and vertebral instability. Instability can be determined from the type of fracture, how many of the three compartments of the vertebrae are disrupted, and on occasion, by carefully positioned stress studies of fluoroscopy. Decompression (dorsal laminectomy, hemilaminectomy, or ventral cervical slot) is employed when compression of the spinal cord exists. The hemilaminectomy (unilateral or bilateral) causes less instability than dorsal laminectomy and therefore should be used when practical. 34 The preferred approach for atlantoaxial subluxation is ventral, and the cross pinning, vertebral fusion technique is used for stabilization. Fracture luxations of C-2 are repaired with small plates on the ventral vertebral body. The thoracic and upper lumbar spine is stabilized with dorsal fixation techniques or combined dorsal spinal plate/vertebral body plate fixation. Several methods of fixation can be used with lower lumbar or lumbosacral fractures, including the modified segmental technique and the combined dorsal spinal plate/Kirschner-Ehmer technique. References 1. Allen AR: Remarks on the histopathological changes in the spinal cord due to impact. An experimental study. J Nerv Ment Dis 41:141, 1914 2. Blass CE, Seim HB: Spinal fixation for dogs using Steinmann pins and methylmethacrylate. Vet Surg 13:203, 1984 3. Bradford OS: Techniques of surgery. In Bradford OS, Lonstein JE, Moe JH, et al: (eds): Moe's Textbook of Scoliosis and Other Spinal Deformities, ed 2. Philadelphia, WB Saunders, 1987, p 135 4. Braughler JM, Hall ED: Correlation of methylprednisolone levels in cat spinal cord with its effects on (Na+ + K+)-ATPase, lipid peroxidation, and alpha motor neuron function. J Neurosurg 56:838, 1982 5. Braughler JM, Hall ED, Means ED, et al: Evaluation of intensive CNS injury dosing
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6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32.
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regimen of methylprednisolone sodium succinate dosing regimen in experimental spinal cord injury. J Neurosurg 67:102, 1987 Braund KG, Shores A, Brawner WR: The etiology, pathology, and pathophysiology of acute spinal cord trauma. Vet Med 85:684, 1990 Colter S, Rucker NC: Acute injury to the central nervous system. Vet Clin North Am Small Anim Pract 18:545, 1988 Dulisch ML, Nichols JB: A surgical technique for management of lower lumbar fractures: Case report. Vet Surg 10:90, 1981 Esses SI, Bednar DA: The spinal pedicle screw: Techniques and systems. Orthop Rev 18:676, 1989 Faden AI, Jacobs TP: Effect of TRH analogs on neurologic recovery after experimental spinal cord trauma. Neurology 35:1331, 1985 Faden AI, Jacobs TP, Holaday JW: Comparison study of early and late naloxone treatment in experimental spinal injury. Neurology 32:677, 1982 Guha A, Piper I, Tator CH: Effect of a calcium channel blocker on posttraumatic spinal cord blood flow. J Neurosurg 66:423, 1987 Guha A, Tator CH: Acute cardiovascular effects of experimental spinal cord injury. J Trauma 28:481, 1988 Hall ED: Effects of the 21-aminosteroid U74006F on posttraumatic spinal cord ischemia in cats. J Neurosurg 68:462, 1987 Hoerlein BF: Spinal fractures, luxations, and fusions. In Hoerlein BF, ed: Canine Neurology, ed 3. Philadelphia, WB Saunders, 1978, p 561 Hoerlein BF, Redding RW, Hoff EJ, et al: Evaluation of naloxone, crocetin, thyrotropin releasing hormone, methylprednisolone, partial myelotomy, and hemilaminectomy in the treatment of acute spinal cord trauma. J Am Anim Hosp Assoc 21:67, 1985. King J: Clinical exposures: Neurogenic cardiomyopathy and reflux esophagitis. Vet Med 86:799, 1991 Knudsen F, Jensen HP, Peterson PL: Neurogenic pulmonary edema: Treatment with dobutamine. Neurosurgery 29:269, 1991 Luque ER, Cassis N, Ramirez-Wiella G: Segmental spinal instrumentation in the treatment of fractures of the thoracolumbar spine. Spine 7:312, 1982 Matthiesen DT: Thoracolumbar spinal fractures/luxations: Surgical management. Comp Cont Ed Pract Vet 5:867, 1983 McAnulty JF, Lenehan TM, Maletz LM: Modified segmental spinal instrumentation in repair of spinal fractures and luxations in dogs. Vet Surg 15:143, 1986 Osterholm JL: The pathophysiological response to spinal cord injury. The current status of related research. J Neurosurg 40:5, 1974 Piermattei DL, Greeley RG: Approaches to the Bones of the Dog and Cat. Philadelphia, WB Saunders, 1979 Selcer RR, Bubb WJ, Walker TL: Management of vertebral column fractures in dogs and cats: 21 cases (1977-1985). J Am Vet Med Assoc 198:1965, 1991 Shores A: Intervertebral disk disease. In Newton CD, Nunnamaker OM, eds: Textbook of Small Animal Orthopaedics. Philadelphia, JB Lippincott, 1985, p 739 Shores A, Braund KG, Brawner WR: Management of acute spinal cord trauma. Vet Med 85:724, 1990 Shores A, Haut R, Bonner J: An in vitro study of plastic spinal plates and Luque segmental fixation of the canine thoracic spine. Prog Vet Neurol 2:279, 1991 Shores A, Nichols C, Koelling HA, et al: Combined Kirschner-Ehmer apparatus and dorsal spinal plate fixation of caudal lumbar fractures in dogs: Biomechanical properties. Am J Vet Res 49:1979, 1988 Shores A, Nichols C, Rochat M, et al: Combined Kirschner-Ehmer device and dorsal spinal plate fixation technique for caudal lumbar vertebral fractures in dogs. J Am Vet Med Assoc 195:335, 1989 Slocum B, Rudy RL: Fractures of the seventh lumbar vertebra in the dog. J Am Anim Hosp Assoc 11:167, 1975 Tator CH, Fehlings MG: Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. J Neurosurg 75:15, 1991 van Ee RT, Peckman R, van Ee RM: Failure of the atlantoaxial tension band in two dogs. J Am Anim Hosp Assoc 25:707, 1989
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33. Walker TL, Tomlinson J, Sorjonen DC, et al: Diseases of the spinal column. In Slatter DH, ed: Textbook of Small Animal Surgery. Philadelphia, WB Saunders, 1985, p 1367 34. Walter MC, Smith GK, Newton CD: Canine lumbar spinal internal fixation techniques: A comparative biomechanical study. Vet Surg 15:191, 1986 35. Zivin JA: Biochemical and histochemical studies of biogenic amines in spinal cord trauma. Neurology 26:99, 1976
Address reprint requests to Andy Shores, DVM, MS, PhD Department of Small Animal Clinical Sciences Veterinary Teaching Hospital Michigan State University College of Veterinary Medicine East Lansing, MI 48824
0195-5616/92 $0.00 + .20
SPINAL TRAUMA Pathophysiology and ManageIllent of TrauIllatic Spinal Injuries Andy Shores, DVM, MS, PhD
A thorough knowledge of the recent advances in the pathophysiology and pharmacologic management of spinal injuries can augment the small animal clinician's treatment regimens for this frequently encountered malady. Key to the effective management of these injuries is developing an understanding of concussive versus compressive injuries, the secondary injury theory of acute spinal trauma, the threecompartment (column) theory as it pertains to vertebral stability, the generation and effects of oxygen free radicals and eicosanoids, and the effective dosage regimens and intervals recommended for posttraumatic corticosteroid therapy. Each of these topics and current information on spinal fixation techniques, radiographic assessment of the traumatized spine, and guidelines for determining the need for surgical or conservative management are discussed in this article. CAUSES OF SPINAL TRAUMA
Categories of internal and external sources of trauma apply. Internal trauma usually relates to intervertebral disc extrusion, pathologic fractures, or congenital vertebral anomalies or instability. External factors include automobile encounters, projectiles (gunshot injuries), falls from heights, injuries caused by other animals (including humans), and blunt trauma from objects (e.g., garage doors, falling objects).26 From the Department of Small Animal Clinical Sciences, Veterinary Teaching Hospital, Michigan State University College of Veterinary Medicine, East Lansing, Michigan
VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 22 • NUMBER 4 • JDLY 1992
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CLASSIFICATIONS OF SPINAL INJURY Spinal Cord Injury: Compression Versus Concussion
Regardless of etiology, perhaps the most important consideration outside the extent of injury is whether the insult is mainly compressive or concussive. Thus the first consideration as to the mode of therapeutic options applicable is made. Purely concussive injuries do not warrant surgical therapy. Compressive injuries always produce some concussion; however, it is the compression of the spinal cord that warrants consideration of surgical therapy. Instabilities can cause compression, but are also a source of recurrent concussive injury. External or internal stabilization is usually warranted when vertebral instability is the most prevalent factor in spinal trauma. 26 An illustration in consideration of the compression versus concussion concept in spinal trauma is the frequent occurrence of intervertebral disc (IVD) extrusion in chondrodystrophic dogs (Fig. 1). With tearing of the annulus, the nucleus pulposus extrudes into the spinal canal, compressing the spinal cord. The amount of compression is determined by the mass of the degenerative nucleus extruded into the canal, the ratio of vertebral canal diameters to spinal cord diameter (much greater in the cervical region than in the thoracic or upper lumbar region), and the relative amount of dehydration present in the degenerative disc. The process of chondroid degeneration involves loss of hyaluronic acid, which functions to imbibe water molecules. Progressively more degenerated nuclei are therefore more dehydrated and take on more water when extruded into the spinal canal, thereby constituting a large compressive mass. 25 The second factor, concussion, is determined by the force (velocity x mass) of the extruded nucleus as it impacts the spinal cord. One cannot equate the severity of injury with the compression because a large amount of extruded nucleus that gradually compresses the spinal cord may result in substantially less neurologic dysfunction than a small mass of nucleus, which virtually explodes into the spinal canal at a high velocity. 20 The aforementioned principles can be applied to other forms of spinal trauma. These include cervical versus thoracolumbar IVD extrusions (greater vertebral canal to spinal cord diameter in the cervical region results in less compression with an equal amount of nucleus extruded), vertebral fracture/luxations (minimal compression/massive concussion or vice versa), and IVD extrusions in nonchondrodystrophic breeds (fibroid degeneration of the IVD, extrusion ~ primarily compressive injury/minimally concussive; traumatic extrusion of normal, gelantinous IVD ~ primarily concussive injury/minimally compressive). These factors (concussion and compression) and their effects, which are the basic, underlying causes of spinal trauma, largely determine the immediate degree of compromise in spinal cord function. 26 Secondary effects, which may be substantial, are discussed in the pathophysiology section of this article.
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A
B Figure 1. Intervertebral disk extrusion as a form of spinal trauma in the chondrodystrophic dog. A, Large compressive extrusion of the nucleus pulposus; concussive effects may be minor if this material extrudes slowly. B, Small amount of nuclear material is in the spinal canal; concussive effects may be very damaging if this material impacts the cord at a high velocity.
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Vertebral Injury: Fracture Etiopathogenesis
Most spinal fractures and luxations occur at the junction of mobile and immobile segments of the spine (lumbosacral, thoracolumbar, cervicothoracic, and atlantoaxial or atlanto-occipital junctions). 20, 33 The forces responsible for vertebral fractures or luxations are bending (extension, flexion), torsion (rotation), and compression (axial loading).3,33 Most classification schemes for spinal fractures are based on either forces that created the fracture (extension, flexion), stability of the vertebral segments, or both. This classification is based on the forces responsible for vertebral fracture and displacement. Flexion injuries of the spine are more common than extension injuries and usually produce the more severe neurologic dysfunction. Pure hyperflexion produces vertebral body displacement with possible extrusion of the nucleus pulposus into the spinal canal (Fig. 2). Hyperflexion combined with rotational forces produces instability. 3, 33 Extension injuries to the spine usually result from forces applied to the dorsum of the spine. 33 Hyperextension results in collapse of the articular facets and tearing of the ventral annulus with expulsion of the nucleus pulposus ventrally (Fig. 3). Stability of the vertebrae is maintained by bony and ligamentous support. Conservative management is usually adequate .26, 33 Compression fractures result from axial loading plus flexion of the spine and have been classified as wedge compression fractures and burst fractures.3,33 Wedge compression fractures occur when the cancellous and cortical bone of the vertebral body are crushed by severe flexion forces when axial loading is applied to the head or pelvic area (Fig. 4). The most common sites for these fractures are the cervicothoracic, thoracolumbar, and lumbosacral areas. Instability may be minimal. 33
Flexion fracture
Figure 2. Hyperflexion of the spine.
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Extension fracture
Figure 3. Hyperextension of the spine.
Wedge compression fracture
Flexion + Axial loading
~
Figure 4. The forces applied to the spine result in a wedge compression fracture of the vertebral body.
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Burst fractures result from flexion and axial forces causing comminution of the vertebral bodies with fractures through one or both end plates. The nucleus pulposus may extrude in any direction, and bone fragments are driven outward or upward into the spinal canal. Stability of the fracture depends on the structures involved and the status of ligamentous support. When bone fragments compress and possibly lacerate the spinal cord, dorsal decompression is inadequate in treating these injuries. 3 Anterior approaches are used in human surgery, and hemilaminectomies are indicated in veterinary surgery.3, 23, 26 Without computed tomography, a full appreciation of the spinal compression caused by bone fragments in the spinal canal is difficult. 3 Combinations of flexion and rotational forces commonly result in displacement of vertebrae and are classified as subluxations, luxations, or fracture/luxations. Subluxation is minor vertebral displacement,33 and stability depends on the structures damaged. Carefully performed stress radiographs or fluoroscopy is used to evaluate spinal instability.26 A luxation is displacement of the intervertebral space when flexion is the primary force of injury and occurs simultaneously with rotational forces (Fig. 5). When the predominant force is rotational and is accompanied by simultaneous flexion, a fracture/luxation occurs33 (Fig. 6). Fracture luxations are frequently seen in the lumbosacral vertebral junction.
Flexion (primary force)
+ Rotation
,--- _ _ _I Luxation Figure 5. Application of flexion as the primary force, with simultaneous rotation (torsion), results in vertebral luxation.
Rotation (primary force)
+ Flexion
Fracture/Luxation Figure 6. Application of rotation (torsion) as the primary force, with simultaneous flexion, results in vertebral fracture and luxation.
Figure 7. A transverse fracture involving the transverse process, lamina, and pedicle. Note that the fracture does not involve the vertebral body, and displacement is minimal. 865
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Transverse fractures can result from any force that causes avulsion of a vertebral process. The fracture can involve the spinous process, transverse process, pedicles, or laminae (Fig. 7). Stability is often good. 3 Surgical intervention is unwarranted unless additional fractures are involved or the fractured pedicle or lamina invades the spinal canal, causing compression. PATHOPHYSIOLOGY OF SPINAL TRAUMA
Initial or primary (mechanical) injuries rarely cause physical transection of the spinal cord, although complete functional loss (physiologic transection) may occur. 31 Systemic, focal, cellular, and subcellular events occurring after the primary injury, collectively resulting in various biochemical and pathologic changes, can cause additional functional deterioration and compromise structural integrity of the spinal cord. These sequential, posttraumatic events have been described as the concept of secondary injury and are characterized by several pathophysiologic mechanism theories. 6, 31 Primary Spinal Cord Injury
Primary spinal cord injury, as previously discussed, may result from concussion or a combination of compression and concussion. Consequences range from minor damage, causing minimal dysfunction or structural changes, to laceration, crushing, or distraction (stretching) of the neuropil, resulting in permanent dysfunction. 26 Again, the concussion at the time of injury is largely responsible for the initial degree of neurologic dysfunction. Further deterioration is a result of the secondary injury factors. Secondary Spinal Cord Injury
Vascular, biochemical, and electrolyte mechanisms have been postulated as causes of secondary injury following primary, acute spinal cord injury.6, 31 Each of these mechanisms produces changes that alter spinal cord function, and most have been shown to result in permanent functional deterioration in experimental models. Figure 8 outlines the pathologic events associated with each of the proposed secondary injury mechanisms. Allen was the first to describe the gross and microscopic changes associated with acute spinal cord injury and also hypothesized the existence of a biochemical factor associated with the development of secondary changes. 31 Petechial to ecchymotic hemorrhages occur in the gray matter within minutes following acute spinal cord injury. Edema of the white matter accompanies the gray matter changes, and both
Physical damage Concussion Compression
Vascular disruption -->
-->. --> -->
Hemorrhage Microcirculation Thrombosis Vasospasm
Primary spinal cord damage
Neurogenic shock Autoregulatory loss Systemic hypotension • Microcirculation
eX)
0"1
~
Biochemical events • Catecholomines , Excitotoxins • Endogenous opioids 'Arachidonic acid release Lipooxygenase • Free oxygen radicals Cyclooxygenase • Vasoconstriction (thromboxane A-2a) • ATP Production Figure 8. Mediators of secondary spinal cord injury.
Electrolyte changes 'Ca++ influx 'K+ efflux , Na+ permeability
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white and gray matter changes may rapidly progress over the 4- to 6hour posttraumatic period. 1, 6, 13, 31 Complete hemorrhagic necrosis of the most severely injured segment may be evident grossly and microscopically within the first 24 to 48 hours. 6, 31 One theory suggests that gray matter may be more vulnerable to damage because of supernormal metabolic demands and decreased spinal cord blood flow in response to the injury, creating a substantial negative balance in the available energy metabolites. 6, 13, 22 Vascular Mechanisms of Secondary Injury
Systemic and focal vascular changes result from acute spinal cord trauma. These include mechanical damage to the spinal cord microvasculature and second injury effects on these and larger vessels. 31 After a brief rise in mean arterial blood pressure following acute spinal cord trauma, a persistent decline in mean arterial pressure and cardiac output occurs in the presence of neurogenic shock. 13 This phenomenon has recently been further substantiated by evidence that dobutamine, at levels that are both inotropic and chronotropic, is useful in the reversal of neurogenic pulmonary edema. 18 Acute central nervous system injury has been shown to produce myocardial ischemia in dogs. 17 The effect of these changes on the spinal cord is manifested by reduced spinal cord blood flow (SCBF).31 Secondary injury due to vascular mechanisms is a result of numerous factors, including loss of autoregulation, hemorrhage, effects from damage to microcirculatory vessels, and vasospasm/thrombosis. Each of these factors decreases SCBF.31 Reduced SCBF in the face of a postulated increased metabolic demand may facilitate the release of certain autodestructive factors, which further serve to feed the secondary injury.6 Biochemical Changes Associated with Secondary Injury
Numerous biochemical changes take place in the presence of reduced SCBF and hypoxia of the injured segment. These changes have previously been associated with the increased concentrations of catecholamines following acute spinal injury.1, 6, 31, 35 These include histamine, norepinephrine, and dopamine. Strong evidence that these neurotransmitters create an environment that propagates vasoconstriction, hypoxia, and necrosis is lacking. Evidence is mounting, however, that another neurotransmitter, serotonin, is involved in the autodestructive processes following acute spinal cord trauma. 6, 11, 35 Excitotoxic amino acids (glutamate, aspartate) have also been described as potent necrotizing substances capable of inducing neuronal degeneration and as potential mediators of the second injury phenom-
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ena. 6,31 Glutamate receptor activation may facilitate intracellular calcium ion influx, promoting vasospasm and ischemia. 31 Lipid peroxidation and vasoconstriction are end results of the arachidonic acid cascade following its interaction with cyclo-oxygenases and lipo-oxygenases. 6, 31 The products derived from these biochemical aberrations include the potent vasoconstrictor thromboxane-A2-a and the oxygen-free radicals that accumulate after lipid peroxidation (0 2 - , H 2 0 2 , OH-)6, 31 and destroy the cell membrane components rich in phospholipid-bound polyunsaturates. 31 The physiologic homeostasis that exists between the oxygen free radicals and the free radical scavengers (vitamin E, ascorbate, glutathione peroxidases) is disrupted with spinal cord injury and the overabundance of the radicals. 31 Hence further tissue damage, reduced SCBF, and the perpetuation of toxic biochemical product accumulation lead to cell death and permanent spinal cord damage. Reversal of this trend is a primary goal in the management of acute, severe spinal cord injury. Electrolyte Aberrations
The most frequently mentioned electrolyte change in association with central nervous system damage is the intracellular influx of calcium ions (Ca++). The role of excitotoxins has been mentioned in association with this change, with glutamate receptor activation facilitating the influx of Ca++. This Ca ++ shift creates microcirculatory vasospasm, alters mitochondrial function and therefore cellular respiration, and facilitates the production of vasoconstructive prostaglandins and leukotrienes.6, 12, 31 Other electrolyte changes that have been associated with central nervous system injury are increased extracellular potassium and increased sodium permeability of the cell wall. 6These changes may occur in conjunction with or in response to the elevated intracellular Ca++ levels, and all promote ischemic changes. Additional Secondary Injury Factors
Although numerous factors have been studied in the pathogenesis of acute central nervous system injury,1° the exact mechanism is speculative. Other factors that likely playa role in the destruction of tissue with the second injury mechanism include endogenous opioids l l (Le., dynorphins), an increased metabolic rate of oxygen consumption leading to decreased adenosine triphosphate availability, and edema associated with decreased venous return, vascular stasis, and physical obstruction of venous outflow (thrombosis, compression). The probable result of all factors contributing to the secondary injury is reduced SCBF and the resultant hypoxic changes. 4, 31
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INITIAL TREATMENT OF SPINAL TRAUMA
Therapy involving both medical and surgical management may be required. Determining the most appropriate therapy is a stepwise process that correlates with the diagnostic evaluations. The initial diagnostic step is the examination. The history, signalment, and physical and neurologic examinations assist the clinician in determining the presence or absence of life-threatening injuries, which require immediate therapy. After these are addressed and based on the history and localization of the injury, the need for immediate corticosteroid therapy can be determined. An unstable vertebral column warrants the application of a brace to prevent further damage to the spinal cord as the animal is manipulated during additional diagnostic procedures. 26 Experimental evidence suggests that corticosteroids, at prescribed doses, are effective in the management of acute spinal cord injuries during the first 8 hours following trauma. 5, 16 The widespread and consistent use of such a regimen has not been clinically tested in veterinary medicine. In view of the lack of experimental evidence that any other therapy improves the outcome in the treatment of acute spinal cord injury, however, the author has adopted this therapy for clinical use. Acute, severe spinal cord injuries of less than 8 hours' duration are initially treated with sodium prednisolone succinate or methyl prednisolone using the following regimen 26 : Time Zero (Initial Dose): 20 to 30 mg/kg intravenously (IV) T 3 hours: 10 to 15 mg/kg IV T 6 hours: 10 to 15 mg/kg IV T 9 hours through T 33 hours 2 mg/kg/h IV* At the end of this regimen, corticosteroids are discontinued. In practice, concerns about effects of this regimen on the gastrointestinal system and the acid-base balance should be addressed. Cimetidine (4 to 8 mg/kg orally or IV, every 6 to 8 hours) is administered, and arterial blood gases are analyzed as necessary. Gastrointestinal protectants (e.g., bismuth compounds, kaolin-pectin) may also be used. 26 Experimental and clinical trial studies have documented the efficacy of the 21-aminosteroid compound U74006F in the treatment of acute spinal cord trauma. 14 The effective dose is equivalent to that recommended for methylprednisolone and as shown in the schedule as given here. This new compound does not have glucocorticoid activity, is a superior oxygen radical scavenger, and has approximately 100 times the anti-inflammatory capabilities of methylprednisolone. Undoubtedly the clinical use of this drug in the treatment of acute spinal cord trauma will become standard. *May be administered as bolus at intervals of 2 hours or as a continuous infusion.
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DIAGNOSIS
Further evaluation of the animal occurs after emergency considerations and life-threatening conditions are stabilized. Figure 9 illustrates the diagnostic and therapeutic protocol for spinal cord injuries. Physical and Neurologic Examinations
The diagnostic protocol for trauma victims always begins with an assessment for life-threatening injuries or conditions, such as hemorrhagic shock and pneumothorax. After initial assessments are completed and necessary measures are undertaken to stabilize the patient, further assessment includes evaluation of all systems. The neurologic examination in the recumbent animal with possible spinal fracture or instability is restricted to the evaluation of the mental status, posture, cranial nerves, static muscle tone, segmental reflexes, and nociception. Localization of the spinal injury can be determined with these assessments. 26 All generalized trauma victims (i.e., those involved in a vehicular accident) should be assessed for thoracic, abdominal, and pelvic injuries. A standard minimal database should be established within each hospital and constructed to provide maximal information on the overall health status of the patient. In most institutions and practices, this consists of a complete blood count, chemistry profile, urinalysis, and electrocardiogram. 26 Radiography
The patient, if recumbent and vertebral instability is even a remote possibility, is transported on a stretcher or stiff board for the initial radiographic assessment. Lateral and across the table ventrodorsal views are obtained to avoid unnecessary patient manipulation. Additional radiographic studies (myelography, computed tomography reT], magnetic resonance imaging [MRI]) may be necessary and require anesthesia; however, the initial assessment serves to determine the presence or absence of a fracture or potentially unstable vertebral column. 26 When initial radiographic studies reveal a disruption of the vertebral column, the benefits of additional studies after anesthesia must be weighed against the potential risk for further spinal cord trauma during positioning of an anesthetized animal. Without the protection afforded the vertebral column by the muscle tone present in the awake animal, untoward movements in the positioning process could further compromise spinal cord function. A complete spinal radiographic series (cervical through lumbosacral regions) is optimal to rule out multiple fractures.
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Initial assessment
Collect minimum data base*
Life-threatening injuries
Localize spinal injury
Initiate corticosteroid therapy+
Diagnostic imaging
Stable spine§
Review minimum data base
General anesthesia
Radiography/Myelography
Surgical therapy
Conservative therapy
Figure 9. Algorithm for management of acute spinal cord trauma. *CBC, serum chemistries, UIA, ECG; tsee text for specific dose regimen; +history of trauma as evidenced on examination, etc.; §no known history of trauma, suspicion of intervertebral disc extrusion or other condition not associated with instability; IIprevent untoward movement by securing animal to spinal board or apply spinal brace or splints.
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Myelography
Myelography is indicated when plain film radiography does not adequately define the issue of compression versus concussion. Cervical or lumbosacral sites may be used to administer the contrast media. 26 The current use of nonionic, water-soluble, iodinated agents has reduced complications associated with myelography; however, postmyelographic generalized motor seizures can occur and could have devastating consequences in an animal with an unstable spine. If myelography is used in the diagnostic assessment, the clinician should be prepared to perform any necessary surgical procedures during the same anesthetic episode. Advanced Imaging
When available, advanced imaging techniques (CT and MRI) may enhance the clinician's three-dimensional perspective of the fracture and better define the position of the spinal cord with respect to the fracture segments (Fig. 10). It is the responsibility of the clinician to be
Figure 10. A, Myelogram demonstrating a vertebral luxation at T7-T8 (arrow) with a reduced flow of the contrast media. B, Axial plane computed tomography (CT) scan demonstrates fracture fragments but no evidence of compression of the spinal cord (surrounded by radiodense contrast media). C, Three-dimensional reconstruction of the CT scan, ventral view, demonstrates slight lateral displacement of the T7 vertebra.
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prudent in determining the necessity of advanced diagnostic imaging by considering the additional time and manipulation required for image acquisition. THERAPEUTIC MANAGEMENT OF SPINAL TRAUMA
Through the aforementioned diagnostic techniques, the presence or absence of spinal cord compression and vertebral fracture or instability can be determined. The need for decompression and for stabilization is then determined from the diagnostic information. Guidelines for conservative (nonsurgical) and surgical management of spinal fractures and luxations 24, 26 cannot be universally applied; however, an adaptation of a principle used in human medicine has standardized radiographic assessment for some. Although the success or failure of an animal to regain acceptable function following spinal trauma (ability to urinate and defecate voluntarily, ambulatory, free of pain) can be considered as evidence for or against the use of either modality (surgery versus conservative management), the rapidity and completeness of return to function should also be considered. Three-Compartment Theory of Radiographic Assessment of Spinal Fractures
A method used for the classification of spinal fractures in humans3 has been adapted for use in small animals. 26 Figure 11 shows a canine vertebrae divided into three compartments, defined by anatomic structures. The dorsal compartment contains the articular facets, laminae, pedicles, spinous processes, and supporting ligamentous structures (Le., ligamentum flava). The middle compartment contains the dorsal longitudinal ligament, the dorsal annulus, and the dorsal vertebral body (floor of the spinal canal). The ventral compartment contains the remainder of the vertebral body, the lateral and ventral aspects of the annulus, the nucleus pulposus, and the ventral longitudinal ligament. Radiographs are evaluated to assess which of the three compartments are damaged. When two or three of the compartments are damaged or displaced, the fracture is considered unstable. Instability and compression are the key indications for surgical intervention. If only one compartment is involved, stability is likely present and conservative management can be pursued when the absence of compression can be documented through myelography or advanced imaging (CT or MRI). Figure 11 can be applied to the evaluation of animals with spinal injuries to determine indications for surgery. The author has used this classification scheme in evaluating spinal fractures during the last 3 years and found it quite reliable. The reader is cautioned, however, because radiographic signs are mere static representations of the spinal column. Other factors to be considered
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Dorsal Middle Ventral
Dorsal ~
Middl
Figure 11. Illustration of the three compartment theory of radiographic evaluation of spinal fractures. The dorsal compartment contains the articular facets, laminae, pedicles, spinous processes, and supporting ligamentous structures (Le., ligamentum flava). The middle compartment contains the dorsal longitudinal ligament, the dorsal annulus, and the dorsal vertebral body (floor of the spinal canal). The ventral compartment contains the remainder of the vertebral body, the lateral and ventral aspects of the annulus, the nucleus pulposus, and the ventral longitudinal ligament. Radiographs are evaluated to assess which of the three compartments are damaged. When two or three of the compartments are damaged or displaced, the fracture is considered unstable.
include the concept of acute versus chronic instability, the neurologic status of the animal, and the presence or absence of spinal cord compression. 26 Acute instability implies the fracture is capable of further displacement or movement immediately after trauma. Acute instability is a consequence of fracture luxations and loss of all ligamentous support (usually involvement of the dorsal and middle compartments). Chronic instability is used to describe fractures that are not immediately displaced but will lead to progressive deformity and deteriorating neurologic status in weeks to months as a result of further angulation of the spine during the healing phase. In addition, chronic instability can also be
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applied to spinal injuries resulting in minimal luxation that does not stabilize and causes some compression and concussion of the spinal cord each time the animal moves. The latter form of instability may only be fully assessed using myelography combined with application of stress views or fluoroscopy. 20, 26
Conservative Management of Spinal Fractures and Luxations
Indications for conservative management are minor to no displacement of the vertebral column, minimal to no instability of the involved segments, and the absence of compression of the spinal cord. Evidence of minor compression and minimal to no neurologic dysfunction would be an indication for conservative management. Methods employed in conservative management include confinement (preferably in a hospital) and a brace or splint. Various types of braces or casts can be made from readily available bandage and casting materials, but custom-made canvas braces, reinforced -with metal rods and attached to the animal with Velcro straps (CO-I and CO-II Spinal Braces, Canine Orthopedics, Colorado Springs, CO) seem superior to J'lhome-made" types in most instances. Proper nursing care is equally important for a successful outcome. Serial monitoring of neurologic function and assessment of radiographic signs are necessary to ensure continued improvement and to rule out any changes in the fracture that may warrant reconsideration for surgical intervention. Urinary continence and confidence in the stability of the fracture are indications for discharge of the animal to the care of the owners. Strict confinement for at least 2, and usually 4, weeks is necessary in most animals treated conservatively. In young animals, continued monitoring is needed to detect any spinal deformities that may develop from continued growth of vertebrae adjoining the fracture site. When treated conservatively, animals should be braced and serial radiographs made during the 6 to 8 weeks following injury because vertebral instability with collapse of the fracture can occur as bone is reabsorbed during the initial stages of bone healing. This is particularly evident in young dogs when additional forces are applied to the fracture site as adjoining vertebrae continue to grow and may add compressive forces (axial loading) to the fracture site. 26
Conservative Management of Concussive Spinal Cord Injuries
In the absen.ce of evidence for spinal cord compression or instability of the spinal column and after the initial corticosteroid therapy to combat the effects of free oxygen radical damage, edema, and the development of additional secondary injury factors, general nursing
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care and physical therapy are the principle factors in management. The following are key components in providing the necessary care: 1. Thick, soft padding-change as necessary when soiled with urine or feces. 2. Range of motion-joints of all neurologically impaired limbs, 5 minutes for each limb, 3 or 4 times a day. 3. Express bladder 4 times a day when necessary; monitor for urinary tract infection-treat as appropriate: bethanechol (5 to 15 mg orally 3 times a day) for detrusor atony, bethanechol plus diazepam (2 to 10 mg orally 3 times a day) for reflex dyssynergia in males. 4. Adequate nutrition-when necessary to provide appropriate caloric intake, consider nasogastric tube (cats), pharyngostomy tube, or percutaneous enterogastric tube. 5. Hydrotherapy (whirlpool)-swimming exercises with support stimulate circulation to limbs, active movement, and skin care, 10 to 20 minutes once or twice daily. 6. Outside walks-on grass, with support, to encourage active limb movements and urinary and bowel elimination.
Generally, the animal can continue convalescence at home once control of the urinary bladder is established and the owners can comply with any special needs and concerns in the home environment. Surgical Management of Spinal Fractures and Luxations
A thorough knowledge of the forces that create spinal fractures and luxations and of the structure of the intact vertebral column is paramount in reconstructing an unstable spine. In addition, indications for spinal stabilization, spinal cord decompression, and surgical methods applicable to a given fracture or luxation must be recognized. When the veterinarian is not familiar with these factors, referral is necessary, and recommended methods for transport are followed. 26 Concussion, compression, and distraction constitute the forces responsible for acute spinal cord damage. Concussion is a dynamic force occurring at the time of injury and can be a recurrent factor if the vertebral column is unstable and the animal is improperly transported, restrained, or manipulated, before stabilization. Compression occurs from an extruded JVD or fracture fragments within the spinal canal, from subluxations, luxations, or foreign objects such as bullet fragments. Flexion, extension, and rotation are the principle forces responsible for vertebral fractures and luxations. The effects of these forces have already been summarized. Surgical management of acute spinal cord trauma is indicated for decompression and immobilization of an unstable vertebral column. Many factors must be considered in recommending the appropriate treatment of an acute spinal cord injury, including location of the injury, the type of fracture or compression,
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instability of the vertebrae, neurologic status, and severity of coexisting injuries. 26, 33 The principles of surgical management of spinal fractures include a thorough understanding of the biomechanics of the spinal segment and fracture type involved in the injury, adequate decompression when compression exists, anatomic realignment of the vertebral canal, and rigid internal fixation appropriate for the fracture type and sufficiently strong to allow early postoperative mobilization of the animal. These principles must be met without producing further injury to the spinal cord. 26 The ideal method of spinal fixation should incorporate the following qualities: 1. Can be used in any segment of the vertebral column. 2. Can be combined with either dorsal laminectomy or hemilaminectomy. 3. Fixation device stabilizes at least two of the three compartments. 4. Fixation method immobilizes only three or four vertebrae. 5. Fixation device is independent of the fractured vertebra. 6. The fixation should be sufficiently strong to allow early postoperative mobilization of the animal and not require additional external support. 26 Durotomy, piatomy, and myelotomy have each been advocated in instances of acute, severe spinal cord trauma;7 however, the efficacy of any of these procedures has not been demonstrated in clinical veterinary surgery. Hoerlein 16 reported decreased return to function in cats subjected to experimental spinal cord trauma and treated by decompression and a dorsal midline myelotomy. Myelotomy is designed to provide internal decompression of the spinal cord but is likely only effective during the first several minutes or few hours following injury. Special microsurgical equipment, including an operating microscope, is needed to perform this procedure properly.26 Cervical Fractures and Luxations
Most cervical fractures are transverse and can be managed with conservative therapy. Exceptions include atlantoaxial subluxations, fractures of the cranial vertebral body of the atlas, bilateral dorsal facet luxations (locked facets), and some atlanto-occipital fracure/luxations. Fixation methods are generally applied ventrally. Atlantoaxial subluxations are managed with K-wire or lag screw fixation and fusion of the atlantoaxial joints. An odontectomy can be performed from a ventral approach if necessary. Dorsal fixation methods 5 and conservative techniques32 have also been described. Cervical vertebral body fractures can be stabilized ventrally using small orthopedic plates or Steinmann pins and polymethylmethacrylate. 26 Cervical Spine Locking Plates (Synthes Spine, Paoli, PA) are
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Locking Screw
\
Expansion Head Screw -
Figure 12. The cervical locking screw plate, applicable to ventral fixation of cervical vertebral fractures. The locking screw locks the expansion head screw to the plate, preventing the screws from backing out of the vertebra when only the ventral cortex of the vertebral body is engaged by the screw.
recent additions to fixation devices used in the cervical spine but have been used limitedly in veterinary spinal surgery (Fig. 12). The chief advantage of this device is that the locking screws do not back out even though only one cortex is penetrated. Acute injuries to the cervical spine can produce autonomic nervous system aberrations, including hypotension, bradycardia, arrhythmias, and respiratory depression. 13 These aberrations can also be initiated or exacerbated during surgical manipulation of the cervical spine during the surgical procedure. Thoracic and Upper Lumbar Fractures and Luxations
Most spinal fixation techniques developed in veterinary surgery have addressed this region of the spine. Surgical techniques for fixation of the thoracic and upper lumbar spine include dorsal spinal plates l plastic, metal), vertebral body plates, 15, 20 combined dorsal spinal plates and vertebral body plates (Fig. 13),34 modified segmental fixation,21 .pins and polymethylmethacrylate (PPMMA) fixation (Fig. 14),2 U-pins I5 , spinal staples,15 and the Luque segmental fixation technique. 19, 30 Subluxations, luxations, and some fractures involving the dorsal compartment can be stabilized with dorsal techniques. Included are (Text continued on page 884)
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~ B Figure 13. A, Fracture luxation at T12-T13. B, Repair using a plastic dorsal spinal plate and a vertebral body plate. Ribs are disarticulated to allow placement of the vertebral body plate, then repositioned using orthopedic wire.
00 00 ~
00 00 N
A
Figure 14. A. Fractured L2 vertebrae. B. Repair using four Steinmann pins inserted into adjacent cranial and caudal vertebrae and surrounded by polymethylmethacrylate.
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dorsal spinal plates, modified segmental fixation, PPMMA, spinal staples, and V-pins. Dorsal spinal plates require intact spinous processes. 1S The modified segmental fixation technique requires intact articular facets. 21 The PPMMA technique requires placement of four vertebral body Steinmann pins and curing the exothermic synthetic polymer over the pins and vertebrae. 2 Spinal staples and V-pins require intact spinous processes and are limited to animals under 15 kg body weight. IS All of these techniques can be combined with a unilateral or bilateral hemilaminectomy. Dorsal laminectomies can be combined with techniques not requiring intact spinous processes. In the upper thoracic spine, dorsal fixation techniques are difficult to apply because of the size and shape of the spinous processes. 30 Pin placement for PPMMA fixation and closure of muscle over the pins and polymer are difficult in the upper thoracic spine. Accurate drilling and placement of wires through articular facets in the upper thoracic spine are difficult for the modified segmental technique. Further development of segmentaF7 and pedicular techniques9 should prove applicable to all areas of the thoracic and lumbar spine and can be combined with dorsal laminectomy or hemilaminectomy.26 Vertebral body plates are most easily applicable to the lower thoracic and upper lumbar spines. Restrictions in the middle to upper thoracic spine are the rib attachments and lateral exposure of the vertebrae. In the lower lumbar spine, location of the spinal nerves associated with the femoral and sciatic nerves precludes placement of the vertebral body plates. IS Evaluation of the strength and rigidity of several thoracolumbar fixation techniques revealed that combined dorsal spinal plate/vertebral body plate fixation was superior to other techniques of fixation. 34 Fixation of two compartments appears superior to fixation of only one. Caudal Lumbar and Lumbosacral Fractures
Fractures and luxations in the more caudal vertebral segments are seen frequently and are amenable to several types of fixation. At the lumbosacral junction, the cranial segment of the fracture is unstable and displaced dorsal to the stable segment with pelvic attachments. A dorsal approach to the lumbosacral spine is performed, and reduction with fixation using a single pin through the wings of the ilium and over the dorsal lamina of the cranial segment may be sufficient. 30 Migration of the pin before fracture healing is a common complication and has prompted development of newer techniques, including plastic dorsal spinal plates combined with transilial pins, 8 the modified segmental fixation technique,21 transilial bolts, and a combined dorsal spinal plate/Kirschner-Ehmer fixation technique 29 (Fig. 15). Using the concept of multiple compartment fixation, the combined dorsal spinal plate/Kirschner-Ehmer fixation was reported stronger than the modified segmental fixation in a biomechanical evaluation. 28 All of the aforemen-
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Figure 15. A, Lumbosacral fracture/luxation. B, Fracture repair incorporating multiple vertebral compartments by using a dorsal spinal plate and external fixator device. The pins exit the skin on each side and are secured using external connecting rods and clamps (not shown).
tioned techniques for lumbosacral fixation can be combined with dorsal laminectomy. Other lower lumbar fractures are repaired with dorsal spinal plates, the modified segmental fixation, PPMMA fixation, or combined dorsal spinal plate/Kirschner-Ehmer technique. Although the dorsal spinal plate/Kirschner-Ehmer fixation is considered superior in strength and rigidity,28 other techniques can be successfully employed. SUMMARY
Spinal trauma can originate from internal or external sources. Injuries to the spinal cord can be classified as either concussive or compressive and concussive. The pathophysiologic events surrounding 3pinal cord injury include the primary injury (compression, concussion)
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and numerous secondary injury mechanisms (vascular, biochemical, electrolyte), which are mediated by excessive oxygen free radicles, neurotransmitter and electrolyte alterations in cell membrane permeability, excitotoxic amino acids, and various other biochemical factors that collectively result in reduced SCBF, ischemia, and eventual necrosis of the gray and white matter. Management of acute spinal cord injuries includes the use of a high-dose corticosteroid regimen within the initial 8 hours after trauma. Sodium prednisolone and methylprednisolone, at recommended doses, act as oxygen radical scavengers and are antiinflammatory. Additional considerations are the stability of the vertebral column, other conditions associated with trauma (Le., pneumothorax), and the presence or absence of spinal cord compression, which may warrant surgical therapy. Vertebral fractures or luxations can occur in any area of the spine but most commonly occur at the junction of mobile and immobile segments. Dorsal and dorsolateral surgical approaches are applicable to the lumbosacral and thoracolumbar spine and dorsal and ventral approaches to the cervical spine. Indications for surgical intervention include spinal cord compression and vertebral instability. Instability can be determined from the type of fracture, how many of the three compartments of the vertebrae are disrupted, and on occasion, by carefully positioned stress studies of fluoroscopy. Decompression (dorsal laminectomy, hemilaminectomy, or ventral cervical slot) is employed when compression of the spinal cord exists. The hemilaminectomy (unilateral or bilateral) causes less instability than dorsal laminectomy and therefore should be used when practical. 34 The preferred approach for atlantoaxial subluxation is ventral, and the cross pinning, vertebral fusion technique is used for stabilization. Fracture luxations of C-2 are repaired with small plates on the ventral vertebral body. The thoracic and upper lumbar spine is stabilized with dorsal fixation techniques or combined dorsal spinal plate/vertebral body plate fixation. Several methods of fixation can be used with lower lumbar or lumbosacral fractures, including the modified segmental technique and the combined dorsal spinal plate/Kirschner-Ehmer technique. References 1. Allen AR: Remarks on the histopathological changes in the spinal cord due to impact. An experimental study. J Nerv Ment Dis 41:141, 1914 2. Blass CE, Seim HB: Spinal fixation for dogs using Steinmann pins and methylmethacrylate. Vet Surg 13:203, 1984 3. Bradford OS: Techniques of surgery. In Bradford OS, Lonstein JE, Moe JH, et al: (eds): Moe's Textbook of Scoliosis and Other Spinal Deformities, ed 2. Philadelphia, WB Saunders, 1987, p 135 4. Braughler JM, Hall ED: Correlation of methylprednisolone levels in cat spinal cord with its effects on (Na+ + K+)-ATPase, lipid peroxidation, and alpha motor neuron function. J Neurosurg 56:838, 1982 5. Braughler JM, Hall ED, Means ED, et al: Evaluation of intensive CNS injury dosing
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6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32.
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regimen of methylprednisolone sodium succinate dosing regimen in experimental spinal cord injury. J Neurosurg 67:102, 1987 Braund KG, Shores A, Brawner WR: The etiology, pathology, and pathophysiology of acute spinal cord trauma. Vet Med 85:684, 1990 Colter S, Rucker NC: Acute injury to the central nervous system. Vet Clin North Am Small Anim Pract 18:545, 1988 Dulisch ML, Nichols JB: A surgical technique for management of lower lumbar fractures: Case report. Vet Surg 10:90, 1981 Esses SI, Bednar DA: The spinal pedicle screw: Techniques and systems. Orthop Rev 18:676, 1989 Faden AI, Jacobs TP: Effect of TRH analogs on neurologic recovery after experimental spinal cord trauma. Neurology 35:1331, 1985 Faden AI, Jacobs TP, Holaday JW: Comparison study of early and late naloxone treatment in experimental spinal injury. Neurology 32:677, 1982 Guha A, Piper I, Tator CH: Effect of a calcium channel blocker on posttraumatic spinal cord blood flow. J Neurosurg 66:423, 1987 Guha A, Tator CH: Acute cardiovascular effects of experimental spinal cord injury. J Trauma 28:481, 1988 Hall ED: Effects of the 21-aminosteroid U74006F on posttraumatic spinal cord ischemia in cats. J Neurosurg 68:462, 1987 Hoerlein BF: Spinal fractures, luxations, and fusions. In Hoerlein BF, ed: Canine Neurology, ed 3. Philadelphia, WB Saunders, 1978, p 561 Hoerlein BF, Redding RW, Hoff EJ, et al: Evaluation of naloxone, crocetin, thyrotropin releasing hormone, methylprednisolone, partial myelotomy, and hemilaminectomy in the treatment of acute spinal cord trauma. J Am Anim Hosp Assoc 21:67, 1985. King J: Clinical exposures: Neurogenic cardiomyopathy and reflux esophagitis. Vet Med 86:799, 1991 Knudsen F, Jensen HP, Peterson PL: Neurogenic pulmonary edema: Treatment with dobutamine. Neurosurgery 29:269, 1991 Luque ER, Cassis N, Ramirez-Wiella G: Segmental spinal instrumentation in the treatment of fractures of the thoracolumbar spine. Spine 7:312, 1982 Matthiesen DT: Thoracolumbar spinal fractures/luxations: Surgical management. Comp Cont Ed Pract Vet 5:867, 1983 McAnulty JF, Lenehan TM, Maletz LM: Modified segmental spinal instrumentation in repair of spinal fractures and luxations in dogs. Vet Surg 15:143, 1986 Osterholm JL: The pathophysiological response to spinal cord injury. The current status of related research. J Neurosurg 40:5, 1974 Piermattei DL, Greeley RG: Approaches to the Bones of the Dog and Cat. Philadelphia, WB Saunders, 1979 Selcer RR, Bubb WJ, Walker TL: Management of vertebral column fractures in dogs and cats: 21 cases (1977-1985). J Am Vet Med Assoc 198:1965, 1991 Shores A: Intervertebral disk disease. In Newton CD, Nunnamaker OM, eds: Textbook of Small Animal Orthopaedics. Philadelphia, JB Lippincott, 1985, p 739 Shores A, Braund KG, Brawner WR: Management of acute spinal cord trauma. Vet Med 85:724, 1990 Shores A, Haut R, Bonner J: An in vitro study of plastic spinal plates and Luque segmental fixation of the canine thoracic spine. Prog Vet Neurol 2:279, 1991 Shores A, Nichols C, Koelling HA, et al: Combined Kirschner-Ehmer apparatus and dorsal spinal plate fixation of caudal lumbar fractures in dogs: Biomechanical properties. Am J Vet Res 49:1979, 1988 Shores A, Nichols C, Rochat M, et al: Combined Kirschner-Ehmer device and dorsal spinal plate fixation technique for caudal lumbar vertebral fractures in dogs. J Am Vet Med Assoc 195:335, 1989 Slocum B, Rudy RL: Fractures of the seventh lumbar vertebra in the dog. J Am Anim Hosp Assoc 11:167, 1975 Tator CH, Fehlings MG: Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. J Neurosurg 75:15, 1991 van Ee RT, Peckman R, van Ee RM: Failure of the atlantoaxial tension band in two dogs. J Am Anim Hosp Assoc 25:707, 1989
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33. Walker TL, Tomlinson J, Sorjonen DC, et al: Diseases of the spinal column. In Slatter DH, ed: Textbook of Small Animal Surgery. Philadelphia, WB Saunders, 1985, p 1367 34. Walter MC, Smith GK, Newton CD: Canine lumbar spinal internal fixation techniques: A comparative biomechanical study. Vet Surg 15:191, 1986 35. Zivin JA: Biochemical and histochemical studies of biogenic amines in spinal cord trauma. Neurology 26:99, 1976
Address reprint requests to Andy Shores, DVM, MS, PhD Department of Small Animal Clinical Sciences Veterinary Teaching Hospital Michigan State University College of Veterinary Medicine East Lansing, MI 48824
