Exogenous Spinal Trauma_Clinical Assessment and Initial Management

8/14/2019 Exogenous Spinal Trauma_Clinical Assessment and Initial Management

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20TH ANNIVERSARY Vol. 21, No. 12 December 1999

Refereed Peer Review

FOCAL POINT

KEY FACTS

5Accurate clinical assessment andimmobilization of animals with

spinal trauma are important for

successful patient management.

Exogenous SpinalTrauma: Clinical

Assessment and

Initial ManagementWashington State University

Rodney S. Bagley, DVM Anthony J. Cambridge, BVMSMichael L. Harrington, DVM, MS Rebecca L. Connors, LVTGena M. Silver, DVM, MS Michael P. Moore, DVM, MS

ABSTRACT: Spinal trauma is a common cause of spinal cord dysfunction in dogs and cats.

When the spine is subjected to exogenous injury, the resultant impact often causes vertebral

fracture or luxation. Because each spinal injury is unique, treatment guidelines must be indi-

vidualized. This article reviews clinical assessment and management of spinal trauma.

Spinal trauma, a common cause of spinal cord dysfunction in dogs andcats,18 can occur from exogenous or endogenous spinal injury. Interverte-bral disk extrusion remains the most common endogenous cause, whereas

automobile-related injury is the most common exogenous cause. Falls, traumafrom falling objects, and projectile damage are also common. External impactsoften result in vertebral fracture, subluxation, or luxation. This articles focuseson the clinical management and treatment of small animals with exogenousspinal injuries that result in vertebral fracture or luxation.

PATHOPHYSIOLOGYThe pathophysiologic changes that occur in the spinal cord after external impacthave been reviewed.17 Briefly, there are two major injuries: the primary mechani-cal injury and the resultant pathophysiologic sequelae or secondary injury. Theprimary injury usually includes shearing and disruption of axonal processes, nervecell bodies, and supporting structures (e.g., glial cells, vascular elements), resultingin physiologic or morphologic disruption of nervous impulses. Any change in thevertebral canal diameter may cause spinal cord displacement, compression, and in-creased intraspinal pressure. Nervous impulses in this area may be disrupted be-cause of increasing pressure applied to the axons and nerves or from ischemiacaused by alteration in spinal cord blood flow or hemorrhage. These increasedpressures set in motion numerous pathophysiologic consequences, including is-

CE

V

s Animals that are suspected of

having an unstable vertebral

segment should be rigidly

immobilized as quickly as

possible.

s Clinical assessment should

be done cautiously to avoid

iatrogenic damage to the spinalcord.

s When a nervous system injury is

suspected, a complete neurologic

assessment is mandatory to

determine the location and

severity of nervous tissue

damage.

s Because vertebral fractures

and subluxations can be subtle

and visually difficult to assess,good-quality, well-positioned

radiographs are essential.

s Methylprednisolone sodium

succinate should be administered

as soon as possible after an

animal has sustained spinal

injury.


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chemia, further hemorrhage,and edema.17

Because gray matter nor-mally receives proportional-ly higher blood flow than

does white matter, ischemic-related damage often occursto gray matter first. Centralhemorrhagic necrosis is thepathologic consequence. Allthese events lead to a self-perpetuating process ofdamage to the spinal cordthat often is equally, if notmore, detrimental than theinitial mechanical injury;this is referred to as the sec-

ond injury theory.

17

Putativemediators of this self-per-petuating process includeexcitatory neurotransmit-ters, endorphins, catechola-mines, lipid peroxidation,and free radicals released af-ter the initial insult.

Based on this informa-tion, two therapeutic con-siderations become para-mount when treating a

spinal injury with fractureor luxation. One is to pre-vent further mechanicaldamage to the spinal cordby stabilizing the vertebral column.4 The second con-sideration is to stop or hinder the development of sec-ondary pathophysiologic events that perpetuate themagnitude of spinal damage. Much of current medicaltherapeutic efforts have been directed at counterbalanc-ing or neutralizing the effects of these by-products oftrauma.

CLINICAL ASSESSMENTImmobilizationOwners often witness traumatic spinal injuries; how-

ever, some animals are found acutely dysfunctionalwithout a known traumatic history. When owners con-tact the veterinary office for advice on transporting aninjured animal, they should be advised to be cautiousbecause traumatized animals may become uncharacteris-tically aggressive. Animals with spinal injuries should beplaced on a rigid, movable surface. If a board or otherrigid device is not available, the animal can be transport-ed in a blanket or slinglike apparatus. Recruiting addi-

tional persons to help trans-port the animal can mini-mize the chance of addition-al injury.

After the animal arrives

at the veterinary clinic, itshould be rigidly immobi-lized to decrease the risk offurther mechanical damageto the spinal cord.4 It is im-portant to quickly obtain acomplete history of the in-

jury; significant informationincludes whether the owner

witnessed the accident, howlong ago it occurred, and

what movement the animal

was capable of immediatelyafter the trauma. For exam-ple, was the dog able to walk?Has it been able to urinate onits own?

During the initial evalua-tion, the animal should re-main in the same position asthat on admission (usuallylateral or sternal recumben-cy). Excessive manipulationshould be avoided. If the

history strongly suggests spi-nal trauma or if the animalis struggling to move, itshould be immediately re-

strained and immobilized by being firmly taped to arigid backboard or similar structure (Figure 1). A spinaltrauma board (8 to 10 inches wide by 4 to 5 feet longby 1 to 2 inches deep) works well; but any rigid, mov-able surface can be used. Before securing the animal,the board should be weighed so that an accurate weightof the animal can be recorded later. If thoracolumbarvertebral trauma is suspected, the animal can be se-

cured to the board by placing tape over the scapularand femoral trochanter regions. If a cervical injury issuspected, the head should also be secured.

Physical, Neurologic, and MusculoskeletalBecause spinal injury frequently occurs in concert with

multiorgan trauma, other life-threatening injuries shouldbe identified as quickly as possible. A standardized,stereotypical physical examination should be conducted9;critical care physical diagnosis checklists may be useful.Specific assessments include respiratory and heart rates,heart rhythm, degree of peripheral perfusion (capillary re-

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Figure 1A

Figure 1B

Figure 1 (A) A dog with spinal trauma that has been immo-bilized using a backboard. (B) The head can also be taped if acervical lesion is suspected.


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fill time, coolness of limbs),ability to move voluntarily,and level of consciousness.The level of consciousnesssignificantly influences subse-

quent neurologic evaluation(e.g., if the animal is poorlyresponsive because of inade-quate perfusion to the brain,assessment of deep pain sen-sation will be difficult).

When a nervous system in-jury is suspected, a completeneurologic assessment is man-datory to determine the lo-cation and severity of ner-vous tissue damage. However, if the animal has an

unstable vertebral fracture, the normal manipulationsand standard neurologic examination may not be possi-ble. The examination and diagnostic sequence as wellas mobilization method therefore need to be modifiedto accommodate possible unstable vertebral fracture.

If the animal is mentally alert but unable to move,immediate concerns should be directed toward the neu-rologic and musculoskeletal systems. Observing the an-imals posture can be helpful in determining whether aneurologic abnormality exists. For example, Schiff-Sherrington posture is characterized by thoracic limbextension and an inability to move the pelvic limbs

normally (Figure 2).

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Spinal reflexes in the pelviclimbs are usually normal. This results from a lesion inthe thoracolumbar spinal segments that interrupts theascending inhibitory impulses originating from bordercells in the lumbar gray matter and terminating on cellsresponsible for extension of the thoracic limbs. Thethoracic limbs are otherwise neurologically normal. Al-though Schiff-Sherrington posture usually occurs in an-imals with severe spinal cord injuries, this posture alonedoes not indicate that the spinal lesion is irreversible.The presence or absence of deep pain sensation in thepelvic limbs is a more important prognostic indicator.

Voluntary movement indicates that some nervous im-pulses are traversing the injured spinal area. It is impera-tive, however, to differentiate voluntary from reflexmovements. Reflex movements occur when animals aretouched or physically stimulated, whereas voluntarymovements are made without external stimulation. Talk-ing to the animal or calling its name may result in at-tempts to move its limbs or wag its tail. Such stimulationshould be attempted only while the animal remains re-strained. Until definitively proven otherwise, voluntarymovement should be assumed to be absent.

The animal should be in lateral recumbency when

the cranial nerves, spinal re-flexes, and cutaneous truncireflexes are assessed and thespine is palpated for hyper-esthesia. Finding an area of

focal spinal hyperesthesia isan important clue that spinalinjury may have occurred.

Deep Pain SensationThe initial assessment

should conclude with analy-sis of deep pain sensation.The presence or absence ofdeep pain sensation has ma-

jor ramifications for theprognosis. Using a hemostat, a painful stimulus should

be applied to affected digits; testing for skin sensationonly will not confirm retention of deep pain sensation.Deep pain sensation is intact if the animal reacts by vo-calizing or turning toward the stimulus, often attempt-ing to bite the examiner. However, simply pulling thefoot away from the stimulus does not indicate con-scious recognition of deep pain. Misinterpretation ofthis withdrawal reflex may lead to a falsely optimisticprognosis.

To evaluate the animals opposite (down) side, a sec-ond backboard can be placed on the upside of the ani-mal and the animal flipped over and secured to the sec-

ond backboard. The same techniques should befollowed as those already described.After spinal trauma has been established, the severi-

ty of injury needs to be determined before developinga management strategy and discussing a realistic prog-nosis with the owner. The severity of a spinal cord in-

jury is usually graded according to clinical findings(Table I). Animals with less severe trauma (painfulonly; mildly paretic) are more often managed withoutsurgical intervention.13Animals with more severe neu-rologic impairment (nonambulatory paretic or para-lyzed) are usually considered for surgical stabilization.

It is important to recognize, however, that scientificdata supporting many current treatment recommen-dations are lacking. Individual clinical experience withthe various treatments is often the overriding factor indecision making. Anecdotal experiences, however, aredifficult to prove without case-controlled studies. Un-fortunately, individual assessments based on clinicalexperience and owner wishes remain the guidingforces behind management decisions in animals withspinal trauma.

Animals lacking deep pain sensation are less likely toreturn to normal function.4 If animals with interverte-

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Figure 2A dog exhibiting the Schiff-Sherrington posture af-ter being hit by a car. Note the thoracic limb extension.


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bral disk disease have de-compressive surgery within48 hours of losing deep painsensation, they have approxi-mately a 50% or greater

chance of walking eventual-ly.14 In contrast, we have foundthat animals that lose deeppain sensation after sufferingspinal trauma have consider-ably less than a 50% chanceof recovery. If deep pain sen-sation has been lost for 48hours or longer, there is vir-tually no chance of func-tional recovery. Further-more, if deep pain sensation

is absent in an animal with100% or greater displace-ment of the vertebral canal,the prognosis for walking ishopeless (Figure 3).

DIAGNOSTIC TESTINGIf a vertebral injury is sus-

pected, survey radiographs ofthe affected area should betaken before continuing theexamination. Vertebral frac-

tures and subluxations can besubtle and visually difficult toassess. Thus good-quality,

well-positioned radiographsare essential.11,12 Initial radio-graphic assessment of obvi-ous displacements of the ver-tebrae can be done while theanimal is awake and immo-bilized. Sedation may be nec-essary in some animals; how-ever, it may influence the

results of further neurologicexamination. Animals shouldbe sedated only after deter-mining the extent and severi-ty of the trauma.

Survey radiographs pro-vide a static record of the po-sition of the vertebrae. In-formation regarding howextensive the displacementof vertebrae was at the timeof injury and before radiog-

raphy, however, may not beappreciated from a single im-age. Because of the strongparaspinal musculature, ver-tebrae can be displaced acute-

ly at the time of injury andsubsequently pulled back to amore normal position. Thispossibility should be consid-ered in patients with verte-bral trauma when clinicalsigns appear worse than thatsuggested by radiography.Disturbances to adjacent softtissue (e.g., paraspinal muscledisruption, hematoma) mayprovide radiographic clues to

the location of injury. Thedegree of displacement of thevertebral canal on radiographsis less important in determin-ing prognosis than is the de-gree of neurologic impair-ment.

CORTICOSTEROIDTHERAPY

Corticosteroid therapy isan important adjunctive ther-

apy for humans and animalswith spinal trauma.1524 Ideal-ly, corticosteroids are admin-istered as soon as possibleafter a spinal injury, eitherbefore or during radiographicevaluation. A multicenterstudy in humans also sug-gested that methylpred-nisolone sodium succinate(MSS) administered up to 8hours after spinal trauma was

beneficial.16

Experimentalstudies in small animals havesuggested that after spinaltrauma, the time frame in

which MSS is helpful may beless (possibly as little as 1hour).1524 This informationsuggests that recommenda-tions in human trials regard-ing the benefit of MSS maybe too long, thus emphasiz-ing the need to administer


S U R V E Y R A D I O G R A P H Y s D E G R E E O F D I S P L A C E M E N T s D R U G T H E R A P Y

TABLE I

Grading Scale for AssessingTreatment of Spinal Injuriesa

Grade Condition

8 Normal7 Pain only

6 Paresis (walking)

5 Paresis (not walking)

4 Paraplegia (urination and deep pain sensationintact)

3 Paraplegia (urination absent and deep painsensation intact)

2 Paraplegia (deep pain sensation absent 48 hr)

aFrom least to most severely injured.

Figure 3A

Figure 3B

Figure 3(A) Survey radiograph of a dog that lacks deep painsensation in the pelvic limbs. There is greater than 100% dis-placement of the vertebral canal L3-4. (B) Sagittal T2-weight-ed magnetic resonance image of the same area. The spinalcord has been severed at this location.


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MSS to small animals as quicklyas possible. Other corticoster-oids (e.g., dexamethasone)25 havenot been proven effective treat-ment of experimental spinal

trauma and have been associatedwith significant complications inclinically affected animals withspinal disease.2628

In studies in humans, a 30-mg/kg intravenous (IV) bolusof MSS was administered ini-tially, followed by 5.4-mg/kg/hour IV for the next 23 hoursas a constant-rate infusion in anattempt to keep high levels ofthe drug in the injured cord for

a longer period. This regimen,however, is labor intensive andrequires 24-hour monitoring ofthe animal. An alternative butexperimentally unproved proto-col is MSS as an initial bolus(time 0) at a dose of 30 mg/kgIV, with additional doses of 15mg/kg IV at 2 and 6 hours afterthe initial dose.

If MSS is administered tooquickly to an awakened ani-

mal, vomiting often occurs. IfMSS is given too rapidly to ananimal under general anesthe-sia, hypotension often is noted.In addition, a primary compli-cation of MSS administrationto dogs with spinal injury isgastrointestinal ulceration.2630

Acute death has also been not-ed experimentally with bolusinjections of MSS; however, this is very rare in clinicalpractice.31 Regardless, we advise administering IV MSS

over a period of approximately 5 to 10 minutes.

NONSURGICAL TREATMENTTreatment of spinal trauma can be separated into sur-

gical and nonsurgical categories, although combinedmodalities may be appropriate. Whether to use eitheror both of these treatments depends on numerous fac-tors, including anecdotal experiences of the examinerand such nonmedical factors as owner finances.

In general, major indications for surgery are reductionof spinal instability and alleviation of spinal cord com-pression. In some instances, however, cage confinement

for 4 to 6 weeks may be a satis-factory or equally beneficialtreatment for animals withspinal trauma.32,33 External sup-port bandages or casts have also

been successful as nonsurgicaltreatment of animals.34 Thegoals of external support shouldbe immobilization of the verte-bral segments above and belowthe damaged area. This supportshould be as rigid as possible toensure that minimal, and ideal-ly no, motion of the vertebralcolumn occurs around the af-fected area.

First, a soft bandage should

be extended above or below thethoracic limbs for thoracolum-bar and cervical fractures, re-spectively. Cast padding cov-ered by cling gauze and elastic

wrap works well as the initialbandage. A plaster or fiberglasscast can then be molded to theshape of the spine and used forrigid support; however, we pre-fer using aluminum rods bentin a rectangular shape and con-

toured to the curvature of thespine (Figure 4). The ends ofthe rectangular configurationcan then be bent outward andused as handles that will assistduring manipulation, physicaltherapy, and walking. Additionalhandles can be fashioned withthe bandage to serve the samepurpose (Figure 5). The casting

material or aluminum rods should be secured to the softwrap with bandage material (e.g., white porous tape).

In animals with a cranial cervical fracture, the ban-dage should be extended upward and over the animalshead to the level of the eyes (Figure 5). Holes can becut in the bandage to allow the ears to protrude nor-mally. If external support is applied after surgery, thebandage material immediately overlying the incisioncan be cut open to allow visual inspection of the inci-sion. With lower lumbar and lumbosacral fractures, es-pecially in male dogs, the penis or vulva should not bebandaged. To prevent males from urinating on the ban-dage, a plastic shield cut from a used IV fluid bag or

waterproof pads can be ventrally secured to the ban-


M E T H Y L P R E D N I S O L O N E S O D I U M S U C C I N A T E s E X T E R N A L S U P P O R T s B A N D A G I N G

Figure 4A

Figure 4B

Figure 4(A) A dog with an L-1 fracture that has hadan external spinal splint applied. The handles are helpful

when moving the dog. (B) A male dog with a T13-L1luxation that has had an external spinal splint applied. A

waterproof pad has also been applied to the ventral as-pect of the bandage to minimize the possibility of urinesoaking the bandage.


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dage, a plastic shield cut from a used IV fluid bag or waterproof pads can be ventrally secured to the ban-dage (Figure 4). If more protection against moisturedamage is needed, a trash bag or suitable barrier can beplaced over the bandage with the ends tucked into it.

After completing the bandaging, the animal shouldbe closely monitored for complications. For example,the layers of bandaging may cause an increase in the an-imals body temperature, especially if the ambient envi-ronment is warm. Thus the animals body temperature

should be monitored often. In addition, if the bandageis too tight around the thorax or cervical area, mechani-cal respiratory problems may develop.

External supports and bandaging should remain inplace for 4 to 6 weeks or until healing is complete. Thebandaging should be changed as needed, especially ifthe skin becomes irritated. Loose-fitting bandaging alsoshould be replaced.

Follow-up evaluations should be scheduled as nec-essary but ideally at 3 and 6 weeks after injury. How-ever, more frequent visits may be required if externalsupport bandaging needs to be changed. Radiograph-

ic reassessments of fracture healing can determine when cage confinement or external support can beterminated. Gradual return to exercise should be ini-tiated when healing is complete. During weeks 1 to 2of returning to exercise, short (10 to 15 minutes)leash-controlled walks should be initiated one tothree times a day on surfaces with good footing. Ifleash walks are tolerated, the duration and number of

walks during the day can be increased over the next 2to 4 weeks. If the animal tolerates this exercise, itshould be allowed free activity in enclosed activity ar-eas (e.g., a fenced backyard).

REFERENCES1. Shores A: Spinal trauma. Vet Clin North Am22:859887,

1992.2. Janssens LAA: Mechanical and pathophysiological aspects of

acute spinal cord trauma. J Small Anim Pract32:572578,1991.

3. Braund KG, Shores A, Brawner WR: The etiology, patholo-gy and pathophysiology of acute spinal trauma. Vet Med85:684689, 1990.

4. Rucker NC: Management of spinal cord trauma. Prog VetNeurol1:397412, 1990.

5. Berg RJ, Rucker NC: Pathophysiology and medical manage-ment of acute spinal cord injury. Compend Contin Educ PractVet7:646653, 1985.

6. Brown SA, Hall ED: Role of oxygen-derived free radicals inthe pathogenesis of shock and trauma, with focus on centralnervous system injuries.JAVMA200:18491859, 1992.

7. Turner WD: Fractures and fracture-luxations of the lumbarspine: A retrospective study in the dog.JAAHA23:460464,1987.

8. Quencer RM, Bunge RP: The injured spinal cord: Imaging,histopathologic, clinical correlates, and basic science ap-proaches to enhancing neural function after spinal injury.Spine21:20642066, 1996.

9. Connors RL, Bagley RS, Silver GM, Moore MP: Exogenousspinal trauma in dogs and cats: Recognition and manage-ment. Vet Tech18:301311, 1997.

10. deLahunta A: Veterinary Neuroanatomy and Clinical Neurol-ogy, ed 2. Philadelphia, WB Saunders Co, 1983.

11. Feeney DA, Oliver JE: Blunt spinal trauma in the dog andcat: Insight into radiographic lesions. JAAHA 16:885890,1980.

12. Brawner Jr WR, Braund KG, Shores A: Radiographic evalu-ation of dogs and cats with acute spinal cord trauma. Vet

Med85:703723, 1990.13. Selcer RR, Bubb WJ, Walker TL: Management of vertebral

column fractures in dogs and cats: 211 cases (19771985).JAVMA198:19651968, 1991.

14. Anderson SM, Lippincott CL, Gill PJ: Hemilaminectomy indogs without deep pain perception. Calif Vet45:2428,1991.

15. Hoerlein BF, Redding RW, Hoff EJ, McGuire JA: Evalua-tion of naloxone, crocetin, thyrotropin releasing hormone,methylprednisolone, partial myelotomy, and hemilaminecto-my in the treatment of acute spinal cord trauma. JAAHA21:6777, 1985.

16. Bracken MB, Shepard MJ, Collins WF, et al: A randomizedcontrolled study of methylprednisolone or naloxone in thetreatment of acute spinal-cord injury. N Engl J Med 322:14051411, 1990.

17. Bracken MB, Shepard M, Collins Jr WF, et al: Methylpred-nisolone or naloxone treatment after acute spinal cord in-

jury: 1-year follow-up data.J Neurosurg76:2331, 1992.18. Bracken MB, Holford TR: Effects of timing of methylpred-

nisolone or naloxone administration on recovery of segmen-tal and long-tract neurological function in NASCIS 2. JNeurosurg79:500507, 1993.

19. Meintjes E, Hosgood G, Daniloff J: Pharmaceutic treatmentof acute spinal cord trauma. Compend Contin Educ Pract Vet18:625635, 1996.

20. Means ED, Anderson DK, Waters TR, Kalaf L: Effect of


B A N D A G I N G C O M P L I C A T I O N S s F O L L O W - U P E V A L U A T I O N S s R E T U R N T O E X E R C I S E

Figure 5A dog with a C-2 fracture was wrapped in a sup-port bandage with handles.


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methylprednisolone in compression trauma to the felinespinal cord.J Neurosurg55:200208, 1981.

21. Hall ED, Braughler JM: Effects of intravenous methylpred-nisolone on spinal cord lipid peroxidation and (Na+ + K+)-

ATPase activity.J Neurosurg57:247253, 1982.22. Braughler JM, Hall ED: Lactate and pyruvate metabolism in

injured cat spinal cord before and after a single large intra-venous dose of methylprednisolone. J Neurosurg59:256261, 1983.

23. Braughler JM, Hall ED: Uptake and elimination of methyl-prednisolone from contused cat spinal cord following intra-venous injection of the sodium succinate ester. J Neurosurg58:538542, 1983.

24. Hall ED: The neuroprotective pharmacology of methylpred-nisolone.J Neurosurg76:1322, 1992.

25. Hoerlein BF, Redding RW, Hoff EJ, McGuire JA: Evalua-tion of dexamethasone, DMSO, mannitol and solcoseryl inacute spinal cord trauma.JAAHA19:216, 1983.

26. Moore RW, Withrow SJ: Gastrointestinal hemorrhage andpancreatitis associated with intervertebral disk disease in the

dog.JAVMA180:14431447, 1982.27. Toombs JP, Caywood DD, Lipowitz AJ, Stevens JB: Col-

onic perforation following neurosurgical procedures and cor-ticosteroid therapy in four dogs.JAVMA177:6872, 1980.

28. Hoerlein BF, Spano JS: Non-neurological complications fol-lowing decompressive spinal cord surgery.Arch Am Coll VetSurg4:1116, 1975.

29. Siemering GB: High dose methylprednisolone sodium succi-nate: An adjunct to surgery for canine intervertebral discherniation. Vet Surg21:406, 1992.

30. Galandiuk S, Raque G, Appel S, Polk HC Jr: The two-edged sword of large-dose steroids for spinal cord trauma.

Ann Surg218:419427, 1993.31. McDougal BA, Whittier FC, Cross DE: Sudden death after

bolus steroid therapy for acute rejection. TransplantationProc8:493495, 1976.

32. Selcer RR, Bubb WJ, Walker TL: Management of vertebralcolumn fractures in dogs and cats: 211 cases (19771985).JAVMA198:19651968, 1991.

33. Carberry CA, Flanders JA, Dietz AE, et al: Nonsurgicalmanagement of thoracic and lumbar spinal fractures andfracture/luxations in the dog and cat: A review of 17 cases.

JAAHA25:4354, 1989.34. Patterson RH, Smith GK: Backsplinting for treatment of

thoracic and lumbar fracture/luxation in the dog: Principlesof application and case series. VCOT5:179187, 1992.

About the AuthorsDrs. Bagley, Harrington, Silver, Cambridge, and Moore

and Ms. Connors are associated with the Department of

Clinical Sciences, Washington State University, College

of Veterinary Medicine, Pullman, Washington. Drs. Bagley

(Neurology and Internal Medicine), Harrington (Neurolo-

gy), and Moore are Diplomates of the American College

of Veterinary Internal Medicine. Dr. Silver is a resident in

neurology and neurosurgery. Dr. Cambridge is a resident

in surgery. Ms. Connors is a neurology veterinary techni-

cian.


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Exogenous Spinal Trauma_Clinical Assessment and Initial Management