ch25

S E C T I O N IIc c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c

Spine

SECTION EDITORz z z z z z z z z z z z z z z z z z z z z z z z z z z

Alan M. Levine, M.D.

#6818 @ l 1/ id/CLS b k /GRP d /JOB b /DIV h25 10/17/02 18 P 1/25 P 683 COLOR T#6818 @ l 1/ id/CLS b k /GRP d /JOB b /DIV h25 10/17/02 18 P 1/25 P 683 BLACK T

#6818 @ l 1/ id/CLS b k /GRP d /JOB b /DIV h25 10/17/02 18 P 2/25 P 684 COLOR BLANK T#6818 @ l 1/ id/CLS b k /GRP d /JOB b /DIV h25 10/17/02 18 P 2/25 P 684 BLACK BLANK T

C H A P T E Rz z z z z z z z z z z z z z z z z z z z z z z z z z z25

Initial Evaluation and EmergencyTreatment of the Spine-Injured PatientInitial Evaluation and EmergencyTreatment of the Spine-Injured Patient

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Munish C. Gupta, M.D.Daniel R. Benson, M.D.Timothy L. Keenan, M.D.

BASIC CONSIDERATIONSz z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

Incidence, Etiology, and Demographics

Injury to the spinal column can be devastating. Somedegree of neurologic deficit occurs in 10% to 25% ofpatients at all levels of injury,10, 89 in 40% at cervical spinelevels,10, 12, 89 and in 15% to 20% at thoracolumbarlevels.10, 27 Even with the development of specializedspinal injury centers, the cost to society per patientremains staggering.28 The ultimate solution rests inprevention of the original injury, but in the meantime,those managing a patient with a spine injury can minimizethe risk of further damage by using accepted techniques ofinitial transportation and treatment. A thorough under-standing of the demographics, anatomy, and pathophysi-ology of spinal cord injury, use of logical algorithms forinitial evaluation and treatment, and knowledge of thepotential complications seen with specific patient popula-tions are critical for optimal patient management.

The magnitude of the problem and the difficulties withpast studies on the incidence rates of spinal injuriesprompted the U.S. Centers for Disease Control andPrevention to establish spinal cord injury surveillancesystems.23 The most recent estimates of incidence aregenerally unchanged from the previous estimates36, 112 ofapproximately 4.0 to 5.3 per 100,000 population.114 Thisincidence corresponds to 12,000 new spinal cord injuriesevery year for which treatment is sought and an additional4800 patients who sustain spinal cord injuries but diebefore arrival at the hospital.112

The causes of spinal column and spinal cord injury areillustrated in Figure 25–1.10, 12, 13, 27, 89, 112 The mostsignificant cause of spinal column injury is motor vehicleaccidents (45%), followed by falls (20%), sports-relatedaccidents (15%), acts of violence (15%), and miscella-neous causes (5%). At the extremes of age, the role of fallsincreases from 9% in the 0- to 15-year-old group to 60%in those older than 75 years.112 The male-to-female ratio is

4:1. When a neurologic deficit is associated with spinalcolumn injury, the overall survival rate for all levels ofinjury is 86% at 10 years.111 The survival rate drops off forpatients injured after age 29 to about 50% at 10 years. Inpatients older than 55 years, in nonwhites, and inquadriplegics, the leading cause of death is pneumonia.Accidents and suicides are most common in those youngerthan 55 years of age, in nonwhites, and in paraplegics.111

Although improvements in prevention and treatmenthave been slow in developing, they are clearly representedin the national statistics. The National Spinal Cord InjuryData Base reported fewer complete injuries and a higherpercentage of incomplete spinal cord injuries in 1985 thanin 1973,112 an improvement that can be attributed tobetter initial management. These changes evolved fromsevere deficiencies in the emergency medical services,which were described in a classic report released by theNational Academy of Sciences National Research CouncilCommittee on Shock and the Committee on Trauma in1966.22, 49 Progress in prevention was seen in a 14-yearreport from the National Football Head and Neck InjuryRegistry,115 which noted a decrease in the number offootball-related cases of permanent quadriplegia andcervical fractures between 1976 (34 and 110 cases,respectively) and 1984 (5 and 42 cases, respectively). Thisdecrease was attributed to tackling rules instituted in 1975in which deliberate ‘‘spearing’’ and the use of the top of thehelmet as the initial point of contact were banned.

The establishment of spinal cord injury centers and theimprovement in prehospital management of patients withspinal cord injuries have been of significant benefit in theoverall outcome of such patients. The concept of a spinalcord injury center as a separate unit began at the Ministryof Pensions Hospital, Stoke Mandeville, England, underthe supervision of Sir Ludwig Guttman in 1943. Foundingof this unit was followed by the establishment in 1945 ofa unit in Toronto, Canada, and later by the creation of eightunits in Veterans Affairs hospitals in the United States.When compared with the outcomes in other centers, such

685


specialized facilities in the United States are credited witha shorter length of hospitalization, a lower rate ofcomplications (e.g., urinary tract infection, pulmonarycomplications, decubitus ulcers), and therefore an overalllower cost of patient care. In addition, these centers havegreatly lowered the percentage of complete versus incom-plete injuries, with a decrease of 65% to 46% in onestudy113 and 20% to 9% in another.79

Anatomy and Pathophysiology

Understanding the conclusions drawn from the initialphysical examination of a spine-injured patient requires abasic knowledge of the osseous and neurologic structuresof the spinal column. Details of osseous structures andfracture patterns are presented in Chapters 28 through 31.Knowledge of fracture patterns allows the examiningphysician to assess the relative stability of the injury, therisk of an associated neurologic deficit, and the indicationsfor treatment.

SPINAL CORD ANATOMY

The spinal cord fills about 35% of the canal at the level ofthe atlas and then about 50% in the cervical andthoracolumbar segments. The remainder of the canal isfilled with cerebrospinal fluid, epidural fat, and duramater. The cord has a variable diameter, with swellings inthe cervical and lumbar regions for the exiting nerve rootsof the plexuses. The myelomere, or segment of cord fromwhich a nerve root arises, lies one level above thesame-numbered vertebral body in the cervical and highthoracic levels. For example, the T7 myelomere lies at thelevel of the T6 vertebral body. The lumbar and sacralmyelomeres are concentrated between the T11 and L1vertebral bodies. The end of the spinal cord (i.e., the conusmedullaris) is most commonly located at the level of theL1–L2 intervertebral disc. The conus medullaris consists ofthe myelomeres of the five sacral nerve roots.

The spatial relationships of the gray and white matterstructures remain consistent throughout the length ofthe cord, but their proportions change according to thelevel. Because the white matter carries the long tract fibersfrom the sacral, lumbar, thoracic, and cervical levels, itconstitutes more of the cervical than the sacral cross-sectional area. The gray matter, with its concentration oflower motor neurons, is predominant in the cervical andlumbar swellings, where the axons exit to the upperand lower extremities. Accurate examination of a patientwith a spinal cord injury depends on understanding thereflex arc and the organization of motor and sensoryelements.

Figure 25–2 presents a cross-sectional view of thespinal cord in the cervical region. The upper motorneuron, which originates in the cerebral cortex, crosses tothe opposite side in the midbrain and then descends in thelateral corticospinal tract to synapse with its respectivelower motor neuron in the anterior horn of the graymatter. The sacral fibers of the corticospinal tract are themost peripheral and the cervical fibers the most central(see Fig. 25–2). The lower motor neurons in the graymatter are organized with the extensor neurons anterior tothe flexor neurons. Upper motor neurons not crossing inthe midbrain descend in the smaller ventral corticospinaltract. The ascending sensory input originates in an axonfrom a cell body located in the dorsal root ganglion withinthe vertebral foramen. Sensory input enters the posteriorhorn of the gray matter and travels beyond, depending onthe type of sensation. Pain and temperature sensationscross immediately to the opposite level of the cord andascend in the lateral spinothalamic tract. Touch sensationalso crosses immediately and ascends diffusely but iscarried primarily in the ventral spinothalamic tract.Proprioceptive position and vibratory sensation fibersascend in the posterior column (funiculus cuneatus,funiculus gracilis) and cross higher in the brain stem. Theposterior column is structured with the sacral elementsmore peripheral and posterior relative to the lumbar,thoracic, and cervical levels. The reflex arc (Fig. 25–3; e.g.,bulbocavernosus) is a simple sensory motor pathway thatcan function without using ascending or descending whitematter long tract axons. If the level of the reflex arc is bothphysiologically and anatomically intact, the reflex canfunction despite disruption of the spinal cord at a higherlevel.

Below the level of the conus medullaris (L1–L2interspace), the spinal canal is filled with the cauda equina,with the motor and sensory roots yet to exit theirrespective intervertebral foramina distally. These roots areless likely to be injured because they have more roomwithin the canal and are not tethered to the same degree asis the spinal cord. Furthermore, the motor nerve root is thelower motor neuron axon (peripheral nerve), which isknown to be more resilient to trauma than central nervoustissue.

PATHOPHYSIOLOGY OF SPINAL CORDINJURY

The pathophysiology of spinal cord injury can be dividedinto two parts—primary and secondary. Primary injury

Falls20%

Sports15%

Acts ofviolence

15%Other5%

MVA45%

FIGURE 25–1. Causes of spinal column and spinal cord injury. Abbrevia-tion: MVA, motor vehicle accidents.

686 SECTION II • Spine


occurs at the moment of impact to the spine. When theenergy transmitted to the spinal column musculature,ligaments, and osseous structures exceeds the flexibility ofthe spinal column, the spinal column and cord become

injured. Primary injury to the spinal cord can develop intwo ways—direct injury by means of excessive flexion,extension, or rotation of the spinal cord and indirect injuryby impaction of displaced bone or disc material. Injury

FIGURE 25–3. The bulbocavernosus, a re-flex arc that is a simple sensorimotorpathway, can function without usingascending or descending white matter longtract axons.

S S

S

L

L

T

T

C

C

FlexorsExtensors

POSTERIOR

ANTERIOR

Fasciculus gracilis

Fasciculus cuneatus

Lateral corticospinaltract

Lateral spinothalamictract

Anteriorspinothalamictract

Anteriorcorticospinaltract

FIGURE 25–2. Transverse view of the spinal cord in thecervical region. Note that the sacral structures (S) aremost peripheral in the posterior columns and thelateral corticospinal tracts. The extensors are also morelateral than the flexors in the gray matter. Abbrevia-tions: C, cervical structures; L, lumbar structures;T, thoracic structures.

687CHAPTER 25 • Initial Evaluation and Emergency Treatment of the Spine-Injured Patient


secondary to contusion and compression is most commonand causes physiologic interruption rather than physicaltransection of the spinal cord.

Secondary injury to the spinal cord occurs after theinitial direct injury to neural tissue. The complicated eventsthat take place on a chemical, cellular, and tissue level arenot completely understood, however (Fig. 25–4). Thecascade is interrelated and eventually leads to cavitation,largely because of cell death (Fig. 25–5). Cell death canoccur as a result of necrosis or apoptosis. Necrosis isbrought on by cellular swelling and mitochondrial andmembrane damage. Apoptosis is programmed cell deaththat occurs normally but is evident to a greater extentin spinal cord injury. Chromatin aggregation and intactcellular organelles can be seen by electron micros-copy, which can differentiate between apoptosis andnecrosis.72

The three best known factors leading to cell death areexocytosis, inflammatory mediators, and free radicals, butother factors can also be involved. Release of excitotoxinsfrom damaged or hyperactive cells can liberate increasedamounts of neurotransmitters, such as glutamate andaspartate. These excessive neurotransmitters can bringabout an increase in Ca2+ entry into cells and cause animbalance in the homeostasis of mitochondrial function

and swelling, which eventually leads to cell death. Freeradicals such as O2

−, OH−, and nitric oxide have beenfound to take part in cell injury through lipid, protein, andnucleic acid damage.

Inflammatory mediators such as prostaglandins andcytotoxins are produced by inflammatory cells that enterthe area of spinal cord damage through a break in theblood-brain barrier. Cytokines such as tumor necrosisfactor-α can lead to damage to oligodendrocytes. Arachi-donic acids break down to prostaglandins, and eicosanoidscan lead to an increase in free radicals, vascular perme-ability, change in blood flow, and cell swelling.

The anatomic and morphologic changes in the spinalcord after injury have been well defined.3, 30, 31 Within 30minutes of injury, multiple petechial hemorrhages are seenwithin the central cord gray matter. Direct disruption ofthe myelin sheath and axoplasm is also seen. Over thecourse of 1 hour, these changes extend progressively tothe posterior of the cord. Several hours after injury, thehemorrhages tend to coalesce and progressive longitudinalnecrosis is seen. Histologic and ultrastructural changescharacteristic of edema are seen within 6 hours and aremost severe 2 to 3 days after trauma. At 1 week after injury,cystic degeneration of the previously necrotic areas of thecord develops.

Clinically, progressive neurologic deterioration after theinitial spinal cord injury is uncommon.106 It is difficult todefine a point in the anatomic injury cascade at whichsecondary injury factors become important, but the recentsuccess of some pharmacologic agents directed at theagents of secondary injury implies that intervention ispossible to some degree.

The initial mechanical injury disrupts neuronal activityin several ways. Microvascular endothelial damage andthrombus formation decrease local blood flow dramaticallyin the central gray matter without reperfusion. This effectis in contrast to the reperfusion that is frequently seen inthe peripheral white matter at about 15 minutes afterinjury and that is probably induced by vasospasm. Primaryinjury also leads to altered systemic vascular tone andhypotension, thus worsening this probably reversiblewhite matter hypoperfusion.

Relative cord ischemia can play a major role in thesecondary metabolic derangements of nervous tissue. Adecrease in membrane-bound sodium potassium adeno-sine triphosphatase (N+,K+-ATPase) causes severe alter-ations in the product of high-energy phosphorylationand the subsequent lactic acidosis. Abnormalities inelectrolyte concentration are believed to be associatedwith abnormal axonal conduction. Membrane damageand direct damage to intracellular organelles cause se-vere derangements in calcium homeostasis. Large intra-cellular shifts of calcium (Ca2+) induce further mito-chondrial dysfunction with decreased energy productionand eventual cell death. Uncontrolled influx of Ca2+

leads to the activation of phospholipases A2 and C,thereby resulting in accelerated breakdown of cellularmembranes and the production of arachidonic acid andfree radicals.59 Many recent advances in the treatment ofacute spinal cord injuries have attacked this secondaryinjury cascade at various levels, with varying degrees ofsuccess.

Apoptoticcells

Normal spinalcord

Compression injury

Acute stage - Primary changes(minutes after injury)-Central hemorrhage

Early secondary changes- Multiloculated cavitation of cord with apoptosis at the edges of the cavities

Wallerian degenerationand cell death of ascendingtracts above lesion

Wallerian degeneration and cell deathof descending tracts below lesion

Late secondary changes- Central cavitation- Cell death of oligodendrocytes in white matter

Hemorrhage

Cavityformation

FIGURE 25–4. An illustrated sequence of the progression from acuteprimary to late secondary injury. (From Lu, J.; Ashwell, K.W.; Waite, P.Advances in secondary spinal cord injury: Role of apoptosis. Spine25(14):1859–1866, 2000.)



SPINAL CORD REGENERATION

The promotion of regeneration of spinal cord axons afterinjury so that the cord again becomes functional is amonumental challenge that has been approached in manyways. The use of neurotrophic factors such as nervegrowth factor, brain-derived neurotrophic factor, neu-rotrophic factor 3, and ciliary neurotrophic factor has beenshown to be helpful in vitro in regenerating axons.Delivery of these factors by cells programmed to secretethem has helped in long-term release directly inside thecentral nervous system (CNS) so that they do not also haveto cross the blood-brain barrier. Growth-inhibiting factorshave been identified that may inhibit axonal regenerationin the CNS. Antibodies to these factors increase theregeneration of axons.97 Electrical stimulation has alsobeen shown to effect axonal growth, but the exact mech-anism is not clear.

Peripheral nerve and Schwann cell transplants haveshown the ability to lead to regeneration of motorpathways.24, 51 Fetal spinal cord tissue has been success-fully transplanted in neonates. Considerable functionalrecovery along with growth and regeneration of the cellshas been observed.21, 116 Similar success has not occurredwith transplantation in adults. Transplantation of olfactoryglial cells, which appear to continue to divide inadulthood, has been reported to regenerate corticospinaltracts in an adult rat.70

Classification of Neurologic Injury

An initial responsibility of the examining physician inevaluating a patient with a spinal cord injury is todetermine the extent of neurologic deficit. A patient withan incomplete neurologic deficit has a good prognosis for

at least some functional motor recovery, whereas func-tional motor recovery is seen in only 3% of those withcomplete injuries in the first 24 hours after injury andnever after 24 to 48 hours.12, 108 According to theStandards for Neurological Classification published by theAmerican Spinal Injury Association (ASIA), a completeinjury is one in which no ‘‘motor and/or sensory functionexists more than three segments below the neurologicallevel of injury.’’5 Likewise, an incomplete injury is one inwhich some neurologic function exists more than threesegments below the level of injury. Critical to thisdetermination is the definition of level of injury. The ASIAdefines it as the most caudal segment that tests intact formotor and sensory functions on both sides of the body. Amuscle is considered intact if it has at least antigravitypower (grade 3 out of 5) and if the next most cephaliclevel is graded 4 or 5.5 These definitions can makedetermination of completeness of an injury somewhatdifficult. At least one study has found the simplepresence or absence of sacral nerve root function to be amore stable and reliable indicator of the completeness ofan injury.118

The concept of sacral sparing in an incomplete spinalcord injury is important because it represents at leastpartial structural continuity of the white matter long tracts(i.e., corticospinal and spinothalamic tracts). Sacral spar-ing is demonstrated by perianal sensation, rectal motorfunction, and great toe flexor activity (Fig. 25–6).Electrical detection of sacral sparing by dermatomalsomatosensory potentials has been reported but is not incommon use.99 Comparison of the normal anatomy inFigure 25–2 with that of the injury depicted in Figure25–7A reveals how preservation of only the sacral whitematter is possible. Sacral sparing is defined as continuedfunction of the sacral lower motor neurons in the conus

Spinal cord injury

BBB breakdown andcell membrane injury

Release of excitotoxinsfrom damaged andhyperactive cells

Microglialactivations

activity ofantioxidants

Free radical releasefrom cell metabolism and

tissue breakdown NOS activation

Damageto cellular

macromolecules

Phospholipase,endonuclease,protein kinase

activation

Cell death

Cytochrome CreleaseSurvival

promoters(Bcl-2,Bcl-xL)

Activation ofapoptosispromoters(Bax, Bad)

Mitochondrialdamage

Caspaseand calpainactivation

Na in cells( Ca in cells)

Edema, tissue ischemiaand anoxia

Proinflammatorycytokines

Repairmechanisms

ion pumping

cell energysupply extracellular

glutamate

Ca in cells( Na in cells)

FIGURE 25–5. Pathways involved incell death after spinal cord injury.(From Lu, J.; Ashwell, K.W.; Waite, P.Advances in secondary spinal cordinjury: Role of apoptosis. Spine25[14]:1859–1866, 2000.)



medullaris and their connections through the spinal cordto the cerebral cortex. The presence of sacral sparingtherefore indicates an incomplete cord injury and thepotential for more function after the resolution of spinalshock. At the time of physical examination in theemergency room, sacral sparing may be the only sign thata lesion is incomplete; documentation of its presence orabsence is essential. Waters and coauthors118 found thatthe presence of external anal sphincter or toe flexor musclepower or the presence of perineal sensation accuratelypredicted the completeness of injury in 97% of 445consecutive patients. In addition, for prognostic purposes,no patients with initial sacral sparing were found to havehad complete injuries.

After a severe spinal cord injury, a state of completespinal areflexia can develop and last for a varying lengthof time. This state, conventionally termed spinal shock, isclassically evaluated by testing the bulbocavernosus reflex,a spinal reflex mediated by the S3–S4 region of the conusmedullaris (see Fig. 25–3). This reflex is frequently absentfor the first 4 to 6 hours after injury but usually returnswithin 24 hours. If no evidence of spinal cord function isnoted below the level of the injury, including sacralsparing, and the bulbocavernosus reflex has not returned,no determination can be made regarding the complete-ness of the lesion. After 24 hours, 99% of patients emergefrom spinal shock, as heralded by the return of sacralreflexes.107 If no sacral function exists at this point, theinjury is termed complete, and 99% of patients withcomplete injuries will have no functional recovery.107 One

exception to this dictum is an injury to the distal end ofthe spinal cord itself. A direct injury to the conusmedullaris can disrupt the bulbocavernosus reflex arc andthus make its absence an unreliable indicator of spinalshock.

CLASSIFICATION SYSTEMS

After a determination of its completeness, an injury canbe further classified according to the severity of theremaining paralysis. Classification systems are usefulbecause they allow patient outcomes to be comparedwithin and between clinical studies. The most commonlyused classification system is that of Frankel andcolleagues,39 which divides spinal cord injuries into fivegroups (Table 25–1). The ASIA has put forth the MotorIndex Score, which uses a standard six-grade scale tomeasure the manual muscle strength of 10 key muscles orfunctions in the upper and lower extremities (Fig. 25–8).All the individual muscle groups, both right and left, aremeasured, with a possible maximal score of 100. Thedisadvantage of the Frankel score is that an infinitecontinuum of injury severity is divided into five discretegroups. However, because recovery and repair of injuredneural tissue must occur through the injury site for aninjury to move to a higher grade, improvement by oneFrankel grade, especially improvement by two grades, isfunctionally quite significant. On the other hand, theASIA Motor Index Score represents injuries along acontinuum, but an improvement does not necessarily

S3S4S5

S4S3

S5

FIGURE 25–6. Sacral sparing may in-clude perianal sensation, rectal tone,and great toe flexion.



represent recovery in the injured spinal segment. Instead,the improved score may represent recovery in the mostcaudal level of function in a complete injury or ageneralized recovery of motor strength in previously weakbut functioning muscles.

INCOMPLETE SPINAL CORD INJURYSYNDROMES

If an incomplete spinal cord injury is diagnosed by theprotocols discussed, it can usually be described by one ofseveral syndromes (Table 25–2). As a general rule, thegreater the function distal to the injury, the faster therecovery and the better the prognosis.73

Central Cord Syndrome. Central cord syndrome, themost common pattern of injury, represents central graymatter destruction with preservation of only the peripheralspinal cord structures, the sacral spinothalamic andcorticospinal tracts (see Fig. 25–7A). The patient usuallypresents as a quadriplegic with perianal sensation and hasan early return of bowel and bladder control. Any return ofmotor function usually begins with the sacral elements (toeflexors, then the extensors), followed by the lumbarelements of the ankle, knee, and hip. Upper extremityfunctional return is generally minimal and is limited by the

TABLE 25–1z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

Frankel Classification of Neurologic Deficit

Type Characteristics

A Absent motor and sensory functionB Sensation present, motor function absentC Sensation present, motor function active but not useful

(grades 2/5 to 3/5)D Sensation present, motor function active and useful

(grade 4/5)E Normal motor and sensory function

z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

CTL

S

TC

LS

Dorsal columns

Lateralcorticospinaltract

Lateralspinothalamictract

Central cord syndromeA

CTL

S

TC

LS

Dorsal columns



Anterior cord syndromeB

CTL

S

TC

LS

Dorsal columns



Posterior cord syndromeC

CTL

S

TC

LS

Dorsal columns



Brown-Sequard syndromeD ´

FIGURE 25–7. A, This illustration of a central cord syndrome can be compared with Figure 25–2 to appreciate the spinal cord abnormality. An incompletespinal injury can affect the more central but not the peripheral fibers, thereby preserving the sacral white fibers. Abbreviations: C, cervical structures;L, lumbar structures; S, sacral structures; T, thoracic structures. B, Anterior cord syndrome. The dorsal columns are spared, so that the patient retainssome deep pressure sensation and proprioception over the sacral area and lower extremities. C, Posterior cord syndrome, a very rare traumatic lesionwith clinical features similar to those of tabes dorsalis. D, Brown-Sequard syndrome, also known as hemisection syndrome. Patients have motor paralysison the ipsilateral side distal to the lesion and sensory hypesthesia on the contralateral side distal to the level of the lesion.



degree of central gray matter destruction. The chance ofsome functional motor recovery has been reported to beabout 75%.109

Anterior Cord Syndrome. A patient with anteriorcord syndrome has complete motor and sensory loss, withthe exception of retained trunk and lower extremity deeppressure sensation and proprioception.98 This syndromecarries the worst prognosis for return of function, and onlya 10% chance of functional motor recovery has beenreported (see Fig. 25–7B).108

Posterior Cord Syndrome. Posterior cord syndromeis a rare syndrome consisting of loss of the sensations of

deep pressure and deep pain and proprioception, withotherwise normal cord function. The patient ambulateswith a foot-slapping gait similar to that of someoneafflicted with tabes dorsalis (see Fig. 25–7C).

Brown-Sequard Syndrome. Brown-Sequard syn-drome is anatomically a unilateral cord injury, such as amissile injury (see Fig. 25–7D). It is clinically character-ized by a motor deficit ipsilateral to the spinal cord injuryin combination with contralateral pain and temperaturehypesthesia. Almost all these patients show partial recov-ery, and most regain bowel and bladder function and theability to ambulate.109

TABLE 25–2z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

Incomplete Cord Syndromes

Syndrome Frequency Description Functional Recovery (%)

Central Most common Usually quadriplegic, with sacral sparing; upper extremitiesaffected more than lower

75

Anterior Common Complete motor deficit; trunk and lower extremity deep pressureand proprioception preserved

10

Posterior Rare Loss of deep pressure, deep pain, and proprioceptionBrown-Sequard Uncommon Ipsilateral motor deficit; contralateral pain and temperature deficit >90Root Common Motor and sensory deficit in dermatomal distribution 30–100

z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

FIGURE 25–8. The worksheet for the American Spinal Injury Association (ASIA) motor index score. The motor strengths for the 10 muscles on the leftside of the worksheet are graded on a scale of 0 to 5. All scores are added, for a total maximal score of 100. (Copyright, American Spinal Injury Association,from International Standards for Neurological and Functional Classification, Revised 1996.)



Root Injury. The spinal nerve root can be injured alongwith the spinal cord at that level, or an isolated neurologicdeficit of the nerve root can occur. The prognosis for motorrecovery is favorable, with approximately 75% of patientswith complete spinal cord injuries showing no root deficitat the level of injury or experiencing return of function.108

Those with higher cervical injuries have a 30% chance ofrecovery of one nerve root level, those with midcervicalinjuries have a 60% chance, and almost all patients withlow cervical fractures have recovery of at least one nerveroot level.109

MANAGEMENTz z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

Accident Scene Management

The initial evaluation of any trauma patient begins at thescene of the accident with the time-honored ABCs ofresuscitation, such as the advanced trauma life support(ATLS) method described by the American College ofSurgeons.1 The ABC (airway, breathing, and circulation)method can be described more accurately as A (airway),B (breathing), and C (circulation and cervical spine). Allpatients with potential spine injuries arriving at theemergency department should be on a backboard with thecervical spine immobilized. A spinal column injury shouldbe suspected in all polytrauma patients, especially thosewho are unconscious or intoxicated and those who havehead and neck injuries. Suspicion of a spine injury mustbegin at the accident scene so that an organized extricationand transport plan can be developed to minimize furtherinjury to neural tissue.

Regardless of the position in which found, the pa-tient should be placed in a neutral spine position withrespect to the long axis of the body. This position isachieved by carefully placing one hand behind the neckand the other under the jaw and applying only gentlestabilizing traction.49 An emergency two-piece cervicalcollar is then applied before extrication from the acci-dent scene. Any patient wearing a helmet at the time ofinjury should arrive at the emergency room with it stillin place unless a face shield that cannot be removedseparately from the helmet is obstructing ventilation, aloose-fitting helmet is preventing adequate cervical spineimmobilization, or the paramedic has been trained inhelmet removal.4 A scoop-style stretcher is now recom-mended for transfer; previously recommended maneu-vers such as the four-man lift and the logroll have beenshown to cause an excessive amount of motion at tho-racolumbar fracture sites.77 The victim on a scoopstretcher is then placed immediately onto a rigid full-length backboard and secured with sandbags on eitherside of the head and neck and the forehead taped to thebackboard.86 The method of transportation and ini-tial destination are determined by a multitude of fac-tors, including but not limited to the medical stabilityof the patient, distance to emergency centers, weatherconditions, and the availability of resources. Vale andcolleagues117 have shown that keeping the mean blood

pressure above 85 mm Hg results in a better neurologicoutcome.

Resuscitation

Patients with spinal injuries are frequently the victims ofmajor trauma and as such are at high risk for multi-ple injuries. Experience with such patients has docu-mented a clear relationship between head and facialtrauma and cervical spine injuries and between specificintrathoracic and abdominal injuries and thoracolumbarfractures. The evaluation and management of hypoten-sion in these multiply injured patients have been thesubject of much discussion. Although hemorrhage andhypovolemia are significant causes of hypotension, onemust be aware of the syndrome of neurogenic shock inpatients with cervical and high thoracic spinal cordinjuries. Neurogenic shock is defined as vascular hypoten-sion plus bradycardia occurring as a result of spinal injury.In the first few minutes after spinal cord injury, a systemicpressor response occurs through activation of the adrenalmedulla. This state of hypertension, widened pulsepressure, and tachycardia subsequently gives way to a dropin pressure and pulse. Neurogenic shock is attributed tothe traumatic disruption of sympathetic outflow (T1–L2)and to unopposed vagal tone, with resultant hypotensionand bradycardia.50, 85

Hypotension with associated tachycardia is not causedby neurogenic shock, so another cause must be sought. Areview of 228 patients with cervical spine injury revealedthat 40 (69%) of 58 patients with systolic blood pressurelower than 100 mm Hg had neurogenic shock.103 Theremaining 18 patients had hypotension caused by otherassociated major injuries. Another study demonstratedthat victims of blunt trauma with associated cervical spinalcord injury rarely sustain significant intra-abdominalinjuries (2.6%).2 Nonetheless, hemodynamic instabilitystrongly suggested occult intra-abdominal injuries. Thedegree of hypotension and bradycardia and the incidenceof cardiac arrest are directly related to the Frankel grade.For example, in a study of 45 patients with acute cervicalspinal cord injury, 87% of Frankel A patients had a dailyaverage pulse rate lower than 55 beats per minute, 21%had a cardiac arrest, and 39% required the administrationof atropine or a vasopressor. Among the Frankel B patients,62% had average pulses lower than 55 beats per minute,and none had cardiac arrest or needed vasopressors.85

A more recent study demonstrated that spinal cordinjury secondary to penetrating trauma is distinctlydifferent from that caused by blunt trauma with respect tothe origin of hypotension.119 Penetrating injuries rarelyresult in neurogenic shock. Of 75 patients with apenetrating spinal cord injury, only 5 (7%) showed classicsigns of neurogenic shock, and of the patients in whomhypotension developed, only 22% were found to have aneurogenic origin of their shock. As in all patients withmajor trauma, hypotension should be assumed to becaused by an injury involving major blood loss, especiallyin those with penetrating trauma.119

No matter what the cause of the hypotension, support



of blood pressure is critical in the early hours after spinalcord injury. As described previously, localized spinal cordischemia is an important cause of late neurologic disability.As the injured spinal cord loses its ability to autoregulatelocal blood flow, it is critically dependent on systemicarterial pressure.32 Hypotension needs to be aggressivelytreated by blood and volume replacement and, if indi-cated, by emergency surgery for life-threatening hemor-rhage and appropriate management of neurogenic shock.The initial treatment of neurogenic shock is volumereplacement, followed by vasopressors if hypotensionwithout tachycardia persists despite volume expansion.The patient’s legs should be elevated to counteract venouspooling in the extremities. Fatal pulmonary edema canresult from overinfusion of a hypotensive patient with aspinal cord injury.50 Endotracheal suctioning is a cause ofsevere bradycardia and can induce cardiac arrest, which isattributed to vagal stimulation. Repeated doses of atropinemay be necessary to maintain the heart rate, andvasopressors may be necessary to maintain blood pressure.Use of a gentle sympathomimetic agent (e.g., phenyleph-rine) may also be helpful.

Assessment

After the patient arrives at the emergency department,rapid assessment of life-threatening conditions and emer-gency treatment are begun in a logical, sequential manneras dictated by the ATLS protocols.1 The primary surveyincludes assessment of airway, breathing, circulation,disability (neurologic status), and exposure (undress thepatient) (ABCDE). As resuscitation (described earlier) isinitiated, a secondary survey is begun that includesevaluation of spinal column and spinal cord function. Theevaluation usually starts with a physical examination, witha more detailed history elicited later. The only part of theinitial assessment that absolutely pertains to the spine isthe emergency need for a lateral cervical spine radiograph(from the occiput to the superior end-plate of T1) toestablish the safest means of maintaining an airway. Apatient suspected of having a spine injury should, beforeintubation, have the airway maintained with a jaw thrustmaneuver rather than a head tilt method.

An unconscious or intoxicated patient is difficult toassess in terms of pain and motor sensory function. Carefulobservation of spontaneous extremity motion may be theonly information that can be obtained about spinal cordfunction, and a detailed examination may have to bedelayed until the patient can cooperate. An unconsciouspatient’s response to noxious stimuli and the patient’sreflexes and rectal tone can provide some information onthe status of the cord. Similarly, spontaneous respirationswith elevation and separation of the costal margins oninspiration indicate normal thoracic innervation andintercostal function. Unconscious patients should be rolledonto their side with the cervical spine immobilized whileon a full-length backboard, and the entire length of thespine should be inspected for deformity, abrasions, andecchymosis. The spine should be palpated for a step-off orinterspinous widening.

The locations of lacerations and abrasions on the skull

are critical for determination of cervical injuries. Occipitallacerations suggest flexion injuries, whereas frontal orsuperior injuries suggest extension or axial compression,respectively. The presence of a single spinal injury does notpreclude inspection of the rest of the spine.

Any associated head and neck trauma should increasethe suspicion of cervical spine injury, and any thoracic orabdominal trauma (e.g., shoulder or lap seat belt mark-ings) should raise suspicion of a thoracolumbar spineinjury. Clear patterns of associated injuries should berecognized. For example, in addition to the relationshipbetween head trauma and cervical spine injury, thepresence of multiple fractured ribs and chest trauma cansuggest thoracic spine injury. Massive pelvic injuries arefrequently associated with flexion-distraction injuries ofthe lumbar spine. Finally, falls from heights resulting incalcaneal or tibial plafond fractures are frequently associ-ated with injuries to the lumbar spine.

A responsive patient who is hemodynamically stablecan be examined in greater detail. Inspection and palpa-tion of the entire spine should be performed as describedfor an unconscious patient. The patient should be asked toreport the location of any pain and to move the upper andlower extremities to help localize any gross neurologicdeficit. If possible, the patient should be questioned aboutthe mechanism of injury, any transient neurologic symp-toms or signs, and any preexisting neurologic signs orsymptoms. The upper (Fig. 25–9) and lower (Fig. 25–10)extremities are examined for motor function by nerve rootlevel. The motor examination includes a digital rectalexamination for voluntary or reflex (bulbocavernosus) analsphincter contraction.

The sensory examination includes testing of the derma-tomal pattern of the proprioceptive and pain temperaturepathways, as described previously (Fig. 25–11). The sharpdull sensation of a pin tip is considered to reflect a painpathway (lateral spinothalamic tract), and this sensationshould also be tested in the perianal region. The presenceof pinprick sensation around the anus or perineal regionmay be the only evidence of an incomplete lesion.Proprioception (posterior columns) can be tested easily byhaving the patient report the position of the toes as up,down, or neutral as the examiner moves them. Tempera-ture sensation (lateral spinothalamic tract) is difficult toestablish in the often loud and busy emergency roomsetting, and testing for this function is usually deferreduntil a later time. The areas of sensory deficit should beaccurately recorded, dated, and timed on the medicalrecord progress note or a spinal injury flow sheet. It is alsorecommended that the sensory level be marked, dated,and timed in ink on the patient’s skin at the affected level.The practice of marking the sensory level on the skin canavoid much uncertainty when a number of examiners areinvolved.

Figure 25–12 reviews the locations of the upper andlower extremity stretch reflexes and their nerve roots oforigin. If spinal shock is present, all reflexes may be absentfor up to 24 hours, only to be replaced by hyperreflexia,muscle spasticity, and clonus. If a spine injury patient witha neurologic deficit has a concomitant head injury, it isimportant to distinguish between the cranial upper motorneuron lesion and a spinal cord lower motor neuron injury.



C5

C6

C7

C7

C8T1

FIGURE 25–9. An examination of the upperextremities must include, at a minimum, themuscle groups that are designated by theirrespective nerve root innervation. These areC5, elbow flexion; C6, wrist extension; C7,finger extension; C8, finger flexion; and T1,finger abduction. The strength (0 to 5)should be listed on the time-oriented flowsheet.

S1

L5

L3-L4

L1-L2

L5-S1

FIGURE 25–10. An examination of thelower extremities needs to include atleast these muscle groups, designatedby their respective nerve root inner-vation: L1–L2, hip abductors; L3–L4,knee extension; L5–S1, knee flexion;L5, great toe extension; and S1, greattoe flexion.


The presence of extremity stretch reflexes in a patientwithout spontaneous motion of the extremities or aresponse to noxious stimuli implies an upper motorneuron lesion. The absence of these reflexes in the samesetting implies lower motor neuron injury of the spinalcord.

The plantar reflex in the lower extremity is elicited by

stroking the plantar aspect of the foot firmly with a pointedobject and watching the direction of motion of the toes. Anormal plantar reflex is plantar flexion of the toes. Anabnormal plantar reflex (Babinski’s sign), in which thegreat toe extends and the toes splay out, represents anupper motor neuron lesion. Similar information can beobtained by running a finger firmly down the tibial crest;

FIGURE 25–11. Sensory dermatome chart. Note that C4 includes the upper chest just superior to T2.



abnormal great toe extension with splaying of the toes(Oppenheim’s sign) constitutes evidence of an uppermotor neuron lesion.

Other significant reflexes include the cremasteric, theanal wink, and the bulbocavernosus reflexes. The cremas-teric reflex (T12–L1) is elicited by stroking the proximalaspect of the inner part of the thigh with a pointedinstrument and observing the scrotal sac. A normal reflexinvolves contraction of the cremasteric muscle and anupward motion of the scrotal sac, whereas an abnormalreflex involves no motion of the sac. The anal wink (S2, S3,S4) is elicited by stroking the skin around the analsphincter and watching it contract normally; an abnormalreflex involves no contraction. The bulbocavernosus (S3,S4) reflex (see Fig. 25–3) is obtained by squeezing theglans penis (in a male) or applying pressure to the clitoris(in a female) and feeling the anal sphincter contract arounda gloved finger. This response can usually be elicited moreeasily by gently pulling the Foley catheter balloon againstthe bladder wall and feeling the anal sphincter contract.The bulbocavernosus reflex examination in a catheterizedfemale can be misleading; the Foley balloon can be pulledup against the bladder wall and thus be felt by a fingertipthat is past the anal sphincter, with this response beingmisinterpreted as contraction of the anal sphincter.

Not uncommonly, a more detailed history is delayeduntil the patient is hemodynamically stable and the overallneurologic status can be determined. In addition to aroutine review of systems, the patient should be specifi-cally questioned regarding previous spine injury, previousneurologic deficit, and details of the mechanism of injury.If the patient cannot respond, an attempt should be madeto interview family members in person or by telephone.

At some time during the physical examination, theinitial lateral cervical spine radiograph should be availablefor review. It should first be examined to ensure that theinterval from the occiput to the superior end-plate of T1can be seen clearly. If the radiographic appearance isnormal, the remainder of the cervical spine series isobtained. Interpretation of the film is discussed in Chapter26. Under no circumstances should spine precautions beremoved until the cervical spine and any suspicious areas

of the thoracolumbar spine have been cleared radiograph-ically. In the assessment of a polytraumatized patient, theassociation between thoracolumbar fractures and otherhigh-energy internal injuries (i.e., aortic and hollow viscusinjuries) must be kept in mind. Because these patients’thoracolumbar spines cannot be cleared of injury onclinical grounds, anteroposterior and lateral thoracic andlumbar spine films should be obtained on a routine basis.In addition, the 10% incidence of noncontiguous fracturesmust be kept in mind in a patient with multiple injuries.61

For example, the presence of a thoracolumbar burstfracture requires review of a complete plain radiographicseries of the cervical, thoracic, and lumbar spine in anypatient who is unable to fully cooperate or accuratelyreport pain during the physical examination.

Special Studies

After the initial cross-table lateral cervical spine radio-graph, a complete cervical spine series should be obtained.Several studies have reported that a technically adequateradiographic series consisting of a cross-table lateral view,an anteroposterior view, and an open-mouth odontoidview is almost 100% sensitive for detecting cervicalinjuries.29 In the trauma situation, it can be difficult to seethe atlantoaxial articulation and the cervicothoracic junc-tion, so additional studies may be needed. A limitedcomputed tomographic scan through the C7 to T1 levelscan rule out significant cervicothoracic junction injuries;however, most studies have shown such imaging to havevery low yield. In addition, computed tomography may berequired to clear the C1–C2 levels if plain radiographs areequivocal.94 In an awake, conversant patient, the physicalexamination can be used to guide further imaging studies.Numerous studies have demonstrated the occurrence ofconcomitant spinal fractures.61 Therefore, if a cervicalfracture is identified, especially in a patient with a spinalcord lesion, radiographs of the entire thoracic and lumbarspine are indicated.

Magnetic resonance imaging (MRI) has found anincreasing role in the evaluation of patients with spine

C5

C6

C7

S1

L4

FIGURE 25–12. Stretch reflexes andnerve roots of origin.



injuries. In a patient who has a clinical spinal cord injuryand minimal or no bony or ligamentous injury on otherimaging studies, MRI is useful for the identification of softtissue (ligamentous or disc) injuries, as well as abnormal-ities of the spinal cord itself. Findings on MRI have beenshown to have some prognostic significance with respectto the severity of spinal cord injury and neurologicrecovery.55, 83 In children, the syndrome of spinal cordinjury without radiographic abnormality (SCIWORA) hasbeen described,8, 56 and more recently, the use of MRI tobetter define these injuries has proved useful.48 MRI hasfound an important role in the evaluation of intervertebraldiscs in cervical dislocations35, 91 (see later discussion andligamentous description66).

Transportation of a cervical spine injury patient in skulltraction can be done safely with the patient in a hospitalbed, on a gurney, or in a Stryker frame, as long as a tractionpulley unit is used. The use of a Stryker frame has beenassociated with loss of reduction after turning and withworsening of neurologic deficits, especially in those withlumbar spine injuries.102 Traction can be compromisedwhile the patient lies on the radiographic table and therope hangs over the table edge without the use of a pulley.Disturbance of the magnetic field of MRI by the ferrouselements of traction equipment presents a problem, butsolutions are being sought. A traction system has beendescribed in which nonferrous zinc pulleys are bolted toan aluminum ladder with water traction bags attached tothe halo ring by nylon traction rope.76 A patient with ahigh cervical spine injury and dependence on a ventilatorwho needs MRI studies must be ventilated by hand or witha nonferrous ventilator.80 A patient with a thoracolumbarspine injury is easier to manage because plastic construc-tion backboards can now be used during conventionalradiographic and MRI studies. Experimental in-boardtraction sets can allow transport of cervical cord injurypatients without the danger of free weights.

Intervention

Once a spine-injured patient is resuscitated adequately, themainstay of treatment is prevention of further injury to analready compromised cord and protection of uninjuredcord tissue. Realignment and immobilization of the spinalcolumn remain critical to this end. Other life-threateningissues in a multiply injured trauma patient may takeprecedence over time-consuming interventions related tothe spine. Perhaps the most rapidly evolving interventionstoward limiting the degree of neurologic injury have beenpharmacologic.

PHARMACOLOGIC INTERVENTION

The most studied and clinically accepted pharmacologicintervention for a patient with a spinal cord injury hasbeen high-dose intravenous methylprednisolone (MPS).The efficacy of glucocorticoids has been studied since themid-1960s. In animal studies, high doses of MPS givenintravenously after spinal cord injury lessened the degreeof post-traumatic lipid peroxidation and ischemia, pre-vented neuronal degradation, and allowed improved

neurologic recovery.52 The initial National Acute SpinalCord Injury Study (NASCIS I) attempted to work out anappropriate dosage for MPS but failed to show a differencein outcome between patients who received a 100-mg bolusper day for 10 days and those who received 1000 mg/dayfor 10 days. In fact, the high-dose regimen was associatedwith an increased risk of complications.16

A second multicenter randomized trial compared MPS,naloxone, and placebo. The results of the NASCIS II study,completed in 1990, showed that patients who were treatedwith MPS within 8 hours had improved neurologicrecovery at 1 year, regardless of whether their injury wascomplete or incomplete.18, 19 Naloxone treatment was nobetter than the control. When MPS was given at a pointlonger than 8 hours after injury, patients recovered lessfunction than did placebo controls. A predictable trendtoward increased complications was seen in the steroidgroup, including a twofold higher incidence of woundinfection (7.1%); these differences, however, were notstatistically significant. Critics of this study question thesignificance of the improvement in treated patientsbecause the neurologic grading system used did not reporta true level of patient function.34 Nonetheless, this studyhas made acute treatment with MPS a standard of care forpatients with a spinal cord injury. The NASCIS II trialestablished a dosing schedule of an initial intravenousbolus of 30 mg/kg, followed by a continuous infusion of5.4 mg/kg/hr for 23 hours. Many centers are nowadministering a 2-g bolus of MPS in the ambulance or atthe accident scene in keeping with the intuition that theearlier the steroid is administered after injury, the betterthe outcome.

The third multicenter randomized trial, NASCIS III, iscompleted.20 One treatment arm in this study is thestandard MPS bolus and 23-hour infusion; a second armextends the infusion another 24 hours. The third treatmentarm consists of the initial MPS bolus followed by a10-mg/kg/day dose of tirilazad mesylate for 48 hours.Tirilazad mesylate is a 21-aminosteroid compound, agroup of MPS analogues that lack the hydroxyl functionnecessary for glucocorticoid receptor binding. Theoreti-cally, these drugs possess no glucocorticoid activity but arepotent inhibitors of lipid peroxidation. The negativesystemic side effects seen with prolonged use of high-doseMPS should be significantly reduced.15 The study showedthat the high-dose steroid regimen was effective only whengiven within 8 hours after injury. If the steroid bolusrecommendation is administration of the bolus within 1 to3 hours, the drip should be continued for 24 hours. If thebolus is given between 3 and 8 hours after injury, the dripshould continue for 48 hours rather than 24 hours. Thisdifference may increase the risk of complications but at thesame time should make the neurologic outcome better.Reanalysis of the data from NASCIS II and III has notdemonstrated a statistically solid beneficial effect. Addi-tionally, no other pharmacologic agent has been shown tobe effective in modulating secondary damage. The resultsof these studies have inspired some heated debate in theliterature.82, 101

Gangliosides are complex acidic glycolipids present inhigh concentration in the membranes of CNS cells.Experimental evidence has shown that these compounds



augment regeneration and sprouting of neurons in vitroand restore neural function after injury in vivo.45 Aprospective, randomized, placebo-controlled trial of GM1ganglioside in patients with spinal cord injury showed thatGM1 enhanced motor recovery when compared withplacebo controls.45 However, only 16 patients receivedGM1 once a day for 18 to 32 days, with the first dose givenwithin 72 hours. All patients received initial treatmentwith steroids at a dose much less than the current standarddose. Analysis of the results showed that improved motorscores in both the Frankel and ASIA grading systems wereattributable to restoration of power in initially paralyzedmuscles rather than improvement in strength in previouslyweak muscles. The authors postulated that GM1 allows forenhanced recovery of effectiveness in initiating the motorresponse of the circumferential white matter. Current trialsexploring combination therapy with GM1 and MPS areunder way. The combination of the early antioxidanteffects of high-dose bolus MPS and the late neuronalrecovery effects of GM1 may produce greater than additivebenefits.44

Opiate receptor blockade has been an attractive targetfor pharmacologic manipulation of the injury process.Theoretically, release of endogenous opiates can causesystemic hypotension and a decrease in spinal cord bloodflow. Naloxone and thyrotropin-releasing hormone (TRH)have been studied extensively in animal models and haveshown variable success in improving neurologic recov-ery.22, 54, 78, 106 The results of the NASCIS do not supportthe use of naloxone in humans because it performed nobetter than controls. Clinical trials of a more stableanalogue of TRH (longer half-life) are under way.

Various other agents have shown variable promise inthe laboratory but remain unproved in clinical trials. Theantioxidant effects of vitamin E have been shown to beuseful, but the need to give the drug before injury limits itsapplication.6 Calcium channel blockers have been used inan attempt to minimize the calcium-modulated elementsof the secondary injury cascade, but published reportshave been variable and clinical use is controversial.100 Anendothelial receptor antagonist has been shown to preventand delay the degeneration of axons after spinal cordinjury in rats. Osmotic diuretics used to reduce edema inhead trauma (mannitol, low-molecular-weight dextran)failed to provide evidence of clinical effectiveness withregard to spinal cord injury.59, 87 Table 25–3 summarizesthe most frequently studied drugs used for the treatment ofspinal cord injury in humans.

PHYSICAL INTERVENTION

After administration of the standard high-dose steroidNASCIS protocol, an assessment of the overall alignmentof the spinal column (and therefore the cord) should bemade. Any malalignment or dislocation causing the neuralelements to be under a severe degree of tension should benoted. Although treatment of the spinal injury cannot alterthe initial trauma, experimental evidence has shown thatimmediate immobilization protects the spinal cord.33 Inaddition, it has been demonstrated experimentally thatcontinued compression causes additive detrimental effectsthat result in ischemia and electrophysiologic changes in

the injured spinal cord.47 A highly unstable situation mayallow an already severely injured cord to undergo repeatedinjury with the slightest movement. Examination of thedorsal skin may reveal an impending breakdown over akyphotic deformity, in which case urgent reduction isimperative. If the neurologic injury can be determined tobe a complete injury (i.e., the bulbocavernosus reflex isintact), realignment may proceed at a less urgent pace. Anexception may be in the cervical spine, where urgentreduction may improve the rate of ‘‘root-sparing’’ recovery.In an incomplete lesion, reduction and stabilization shouldbe performed as quickly as possible to minimize continuedneurologic injury. In the cervical spine, such managementfrequently involves the application of skull traction. In thethoracolumbar spine, traction is less successful, so ifpositioning does not restore anatomic alignment, emer-gency surgical reduction is required.

The role of pretraction MRI became a focus of debateafter Eismont and colleagues,35 among others,74, 93 re-ported neurologic deterioration in patients with cervicaldislocations after they underwent traction and reduction.The high incidence of disc herniations with facet disloca-tions91 prompted these authors to advocate that an MRIstudy be obtained before closed reduction of the cervicalspine is attempted. Several large studies have refuted thiscontention by showing no worsening of neurologic levelswith closed traction and reduction in awake, cooperativepatients.25, 65, 105 Nonetheless, expediency is of the utmostimportance in the reduction of patients with incompleteinjuries. If it can be obtained quickly without putting anunstable patient at risk during transportation, pretractionMRI is reasonable. In many centers, such studies aredifficult to obtain within several hours. MRI is required ifthe patient is otherwise uncooperative, fails closed reduc-tion, or requires reduction under anesthesia for anyreason. If MRI demonstrates disc herniation, anteriordiscectomy plus fusion is performed before other surgeryis attempted. If operative reduction of a thoracolumbardislocation is planned, MRI should be obtained andoperative plans modified based on the results.

After adequate alignment and stabilization, furtherdiagnostic studies, such as computed tomography (or MRI,if not obtained previously), can be performed on a lessurgent basis. Frequent neurologic examinations, preferably

TABLE 25–3z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

Pharmacologic Agents for Spinal Cord Injury

Agent Mechanism of Action

Methylprednisolone(MPS)

Membrane stabilization by decreasein lipid peroxidation, prevention ofinflammatory cascade

Tirilazad mesylate Same as MPS, lacks glucocorticoidactivity

GM1 ganglioside Augmentation of neuron regenerationNaloxone Blocks effects of endogenous opiates

that cause local and systemichypotension and spinal cordischemia

Thyrotropin-releasinghormone

Same as naloxone

z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z



by the same physician, should be documented andrecorded, especially when the patient is returned afterdiagnostic tests. If worsening of a neurologic deficit isdocumented, emergency surgical decompression is indi-cated. In a patient with a stable or improving spinal cordinjury, the timing of surgical stabilization, if needed, iscontroversial. In the case of a polytrauma victim, earlystabilization, whether in a halo vest or by surgery, has beenshown to improve overall outcome and shorten thehospital stay.37

An overview of a suggested algorithmic approach to aspine-injured patient is shown in Figure 25–13. Althoughsuch an algorithm tends to oversimplify a complicated

decision-making process, adherence to a dedicated proto-col provides a basic framework from which to managethese often multiply injured, complicated patients.

In patients with isolated injuries, as well as those withcomplicated multiple injuries, a simple, reliable method ofcervical and thoracolumbar immobilization is necessary tosafely perform a complete evaluation. The most effectivemethod of initial cervical immobilization is the use ofbilateral sandbags and taping of the patient across theforehead to a spine board, along with the use of aPhiladelphia collar (which serves to limit extension).86 Inthe cervical spine, a soft collar, extrication collar, hardcollar, or Philadelphia collar alone is probably not

YES

Alignmentadequate

?

YES

YES

ExtricationSpinal stabilization

Transportation

ATLS protocolsResuscitation

Neurologyintact

?

NO YESMPS protocol30 mg/kg IV

5.4 mg/kg/hr x 23 hrs

Plain radiographsentire spine

Severemalalignment

dislocation?

EmergentClosed

realignmenttraction

R/O disc herniation

Severemalalignment

dislocation?

Plain radiographs

Furtherdiagnostic studies

as neededCT scan, MRI

Furtherdiagnostic studies

as neededCT scan, MRI

YES

YES

NONO

NO

Emergent

MRIR/O disc herniation

Neurologyincomplete

?

YESUrgent

Complete injury

YES

"Elective"

Surgicalreduction/decompression

stabilization

OR

NO

NO

"Elective"

Definitive closedtreatment

OR

Spine-Injury Patient

Worseningneurologic

deficit

±MRI

FIGURE 25–13. An algorithmic ap-proach to the spine injury patient.Abbreviations: ATLS, advanced traumalife support; CT, computed tomogra-phy; MPS, methylprednisolone; MRI,magnetic resonance imaging; R/O,rule out.



sufficient for immobilization.60, 86 A poster brace (e.g.,four-poster brace) or cervicothoracic brace (SOMI brace) isnot practical in the emergency setting. A standard longspine board is adequate for immobilization and turning ofthe thoracolumbar spine.77 Immobilization gear is re-moved only after radiographs have been interpreted asnormal.

An unstable or malaligned cervical spine requires eithermore stable immobilization or axial traction to achievereduction. Specific indications for skull traction arediscussed in Chapters 27 to 29. The concept of skulltraction was introduced by Crutchfield in 1933,26 but theCrutchfield skull tongs for traction have been replaced bythe Gardner-Wells40 and halo immobilization devices.Gardner-Wells tongs are a simple, effective means ofapplying axial traction for reduction, but they do notsignificantly limit voluntary rotation, flexion, or extension

in an uncooperative patient. Gardner-Wells tongs can beapplied with minimal skin preparation and withoutassistance. The halo ring allows axial traction for reductionand provides rather stable immobilization with theapplication of a vest, but in a busy polytrauma setting, itsapplication requires an assistant, and it takes longer toapply than Gardner-Wells tongs.

Gardner-Wells TongsThe halo should be applied for initial stabilization ofcervical spine injuries only if prolonged halo vest or castimmobilization is planned. If short-term traction followedby surgical stabilization and nonhalo external immobiliza-tion is planned, the use of Gardner-Wells tongs ispreferred. Gardner-Wells tongs are easily applied by oneperson and without anterior pin sites.

Gardner-Wells tongs (Fig. 25–14) are fast and easy toapply, with no assistance required. Directions for use aregenerally located on the tongs (Fig. 25–15). The pinsshould be positioned below the temporal ridges at a point2 cm above the external auditory canal and above thetemporalis muscle (Fig. 25–16). After shaving, the skin isinfiltrated with local anesthetic after the application of anantiseptic. The screws must be tightened symmetrically.The tongs are secure when the metal pressure pinprotrudes 1 mm (Fig. 25–17). Protrusion of the pressureindicator pin by 1 mm has been demonstrated in cadaversto provide a pull-off strength of 137 ± 34 lb.64 Pressureindicator pin protrusion of as little as 0.25 mm cansupport up to 60 lb.64 It is recommended that the pin betightened to 1 mm on the next day, but not againthereafter.

Traction should be initiated at 10 lb and increased by 5-to 10-lb increments. Reduction should be performed inawake patients with administration of intravenous mida-

FIGURE 25–14. MRI-compatible graphite Gardner-Wells tongs.

FIGURE 25–15. Directions for use of theGardner-Wells tongs are usually at-tached to the traction hook.



zolam if needed. Fluoroscopy or serial radiographs andserial neurologic examinations should be performed toavoid injury. In patients with neurologic symptoms orsigns or 1-cm distraction of a disc space, closed reductionshould be stopped and further images taken.

Gardner-Wells tongs have been reported to undergo pinand spring wear with repeated use. The pins and the tongsshould be inspected and replaced if necessary or theindicator given a lower pin pressure to prevent pull-out.67

Blumberg and associates11 have reported that the MRI-compatible titanium alloy Gardner-Well tongs are morepredisposed to plastic deformation and slippage thanstainless steel Gardner-Wells tongs. They warned againstusing MRI-compatible tongs for reduction, especially withweights greater than 50 lb. Tongs may be switched afterreduction to a lower weight if MRI is needed. A halo ringcompatible with MRI would be another option if MRI isneeded.

Halo Ring ApplicationA halo ring can be applied in the emergency departmentwhen definitive treatment is anticipated to be in a halo orin cases in which distraction should not be appliedthrough Gardner-Wells tongs. Placing a halo vest under-neath the patient during transfer to the bed can help attachthe ring to the vest while the patient is in traction afterreduction. Open halo rings offer the advantage overprevious whole rings of being able to put the ring onwithout putting the patient’s head on a head holder off thestretcher. The correct ring size is selected according tohead circumference. The ring is placed around the head,the pin holes in the ring are used to identify theposterolateral pin sites, and the hair is shaved in theseareas. The ring can be held in place temporarily with threeplastic pod attachments. The skin is prepared, and localanesthetic is infiltrated through the ring holes.

Placement of the halo pins too high on the convexity ofthe skull can result in slippage of the ring, especially withtraction. Placement of the anterior pin, as determined byskull osteology41 and by supraorbital nerve anatomy, isbest at a point in the middle to lateral third of the forehead,

just above the eyebrow (Fig. 25–18). Although notsupported by osteologic studies, placement of the anteriorpin more laterally and just into the hairline for cosmeticreasons has been reported to give good clinical results.46

This more lateral pin placement has been used by one ofthe authors (Benson), with similarly good clinical results.If the more lateral position is to be used, care must betaken to palpate and avoid penetration of the temporalmuscle and temporal artery on each side. The posterior pinis placed in the posterolateral position on the halo ring,with care taken to avoid skin contact with the ring becausepressure ulceration can result.

All pins are first secured to finger tightness. As the pinsare tightened, the patient should be encouraged to keepboth eyes tightly closed to avoid stretching the skin, whichlimits the patient’s ability to close the eyes. Once the pinsare finger tight, the ring is inspected carefully to ensure asymmetric fit. The pins are then tightened sequentially ina diagonally opposite manner (i.e., right front with left rearand left front with right rear) to 2 inch-lb, then 4 inch-lb,and finally 8 inch-lb in an adult or 4 to 6 inch-lb in a childyounger than 5 years. The pins should be retightenedwithin 24 hours (and thereafter) only if they are loose andresistant to tightening. A loose pin without resistance totightening should be moved to another position on theskull. Traction can then be applied with the traction barattachment. If a vest is to be applied, the size should beequal to the chest diameter measured in inches at the levelof the xiphoid process. MRI-compatible halo vests withgraphite rings are used routinely, as shown in Figure25–19.

Fleming and co-workers38 devised instrumented halovest orthoses with gauges that can measure pin force andshowed an 83% decrease in compressive force duringapproximately a 3-month typical halo vest wear period. Allpatients had some symptoms caused by the degradation inpin force, which signified some loosening. The high stresson the bone may cause resorption and is thus one of thepostulated causes of loosening. This potential complica-tion highlights the importance of clinical vigilance duringtreatment of patients with halo vests. Attention to detailsuch as pin site care is essential, as well as alertness to

FIGURE 25–16. Correct position for the Gardner-Wells tongs is 1 to 2 cmabove the external auditory canal and below the temporal ridge.

FIGURE 25–17. Pressure indication pins of the Gardner-Wells tongsshould protrude 1.0 mm.



symptoms of loosening or other complications duringtreatment.

Reports of complications with use of the halo ring andvest42, 46 have indicated significant rates of pin loosening(36%), pin site infection (20%), pressure sores under thevest or cast (11%), nerve injury (2%), dural penetration(1%), cosmetically disfiguring scars (9%), and severe pindiscomfort (18%). Skull osteomyelitis and subdural ab-scess have also been described. A lower rate of pinloosening and infection has been reported with an initialtorque of 8 inch-lb rather than 6 inch-lb in adults.14 Aprospective randomized study has, however, shown that 6-or 8-lb torque does not lead to any significant difference inpin loosening.92

The use of a halo ring in children requires specialconsideration43, 63, 81 because of a higher complicationrate in this population.9 The calvaria develops in threesignificant phases by age: (1) 1 to 2 years, wheninterdigitation of the cranial sutures ends; (2) 2 to 5 years,a period of rapid growth in diameter; and (3) 5 to 12 years,when skull growth ceases.43 Overall, the calvaria is thinnerin a child 12 years or younger than in an adult, and themiddle layer of cancellous bone may well be absent.Computed tomographic studies have demonstrated thatthe standard adult anterolateral and posterolateral pinpositions correspond to the thickest bone in a child, andthey are recommended as the site of halo pin place-ment.41, 43 In children younger than 3 years, a multiple-

FIGURE 25–18. The anterior pin shouldbe placed above the eyebrow in themedial to lateral third, avoiding thesupraorbital nerve.

FIGURE 25–19. MRI-compatible halo vests.



pin, low-torque technique is recommended.81 In this agegroup, custom fabrication of the halo ring and vest may berequired. Ten to 12 standard halo pins can be used. Thepins are inserted to a torque tightness of 2 inch-lbcircumferentially around the temporal and frontal sinusregions. Halo placement in children younger than 2 yearsis complicated because of incomplete cranial sutureinterdigitation and open fontanels.81

SPECIAL CONSIDERATIONSz z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

Pediatric Patients

The spine is thought to behave biomechanically as an adultspine by about the age of 8 to 10 years.8, 56, 57 Until then,spinal column injury is uncommon, usually involves softtissues, and therefore is not seen on plain radiographs inthe emergency room. In patients younger than 10 years,the most common injury occurs in the occiput to C3region.57, 110 The entire spectrum of neurologic involve-ment is associated with these injuries, including cranialnerve lesions and vertebral basilar signs such as vomitingand vertigo. SCIWORA is most common in childrenyounger than 10 years. Flexion, extension, and distractioncervical spine views and MRI scans can be helpful inidentifying the level, but they should be used with extremecare to avoid further injury. After the age of 10 years, thepattern of injury is similar to that of adults, except forflexion-distraction injuries in the lumbar spine. As a resultof seat belt injuries, pediatric patients can have a lumbarfracture with a more proximal thoracic level of paraplegia.

Initial immobilization of a pediatric patient requires anunderstanding of the supine kyphosis anterior translation(SKAT) phenomenon.56 A young child lying supine on astandard backboard can have the head forced into kyphosisbecause of the normally disproportionate relationship ofthe larger head and smaller trunk in a child. Cases of forcedkyphosis causing anterior translation of an unstable pediat-ric spine have been reported.56 In normal development of achild, head diameter grows at a logarithmic rate, with 50%of adult size achieved by the age of 18 months, and chestdiameter grows at an arithmetic rate, with 50% of adult sizeachieved by the age of 8 years. The problem can be avoidedby elevating the thorax of a child on a spine board with afolded sheet to bring the shoulders to the level of theexternal auditory meatus or by the use of a pediatricbackboard with a cutout to compensate for the prominentocciput of a young child.

Elderly Patients

Spinal trauma and spinal cord injury have traditionallybeen thought of as conditions of youth, but as many as20% of all spinal cord injuries occur in patients older than65 years.17 Some particular characteristics and injurypatterns are specific to elderly patients. For example,elderly patients with spinal cord injuries are more likely tobe female. Whereas spinal injury is commonly associatedwith high-energy trauma in young adults, simple falls arethe most common mechanism in patients older than 65

years.71, 95, 104 Cervical spine injury predominates in theelderly population and accounts for 80% or more oftraumatic spinal injuries. Injury to the C1–C2 complex issignificantly more common in elderly people and accountsfor a higher percentage of the total number of spinalinjuries, with odontoid fractures being the single mostcommon spinal column injury in these patients.96, 104

Elderly patients are more likely to have an incompleteinjury.95, 104 The frequent incidence of spondylosis in thispopulation predisposes this patient group to central cordsyndromes. Most importantly, the overall mortality rate forthe initial hospitalization period has been reported to be60 times higher in patients older than 65 years than inthose younger than 40 years.104 The causes of death aremore commonly related to the stress of the treatment(immobilization, recumbency) than to the injury itself.

Treatment of this patient population is problematic. Theoverall priority in treatment should be early mobilizationof the patient to avoid respiratory and other complications.Although previous reports have suggested that halo vestsare poorly tolerated by the elderly population,84 thesepatients are frequently poor operative candidates. A highindex of suspicion must be maintained when evaluating anelderly patient with neck pain, even after relatively trivialtrauma.

Multiply Injured Patients

Several important issues should be raised regardingmultiply injured patients with spinal trauma. Delay indiagnosis of a spine injury is a significant problem that canaffect a trauma patient’s care. The rate of delay in diagnosisin spinal trauma is 23% to 33% in the cervical spine12, 88

and about 5% in the thoracolumbar spine. As many as22% of all delays in diagnosis in one series occurred afterarrival at a tertiary referral center.88 The main cause is alow level of suspicion, as represented by the following: (1)failure to obtain a radiograph, (2) missing the fracture onradiography, or less commonly, (3) failure of the patient toseek medical attention. A secondary neurologic deficitdeveloped in 10% of patients with a delayed diagnosis ascompared with 1.5% of those in whom spinal injury wasdiagnosed on initial evaluation,88 but no progression of analready recognized deficit was observed. Other factorsassociated with a delay in diagnosis include intoxication,polytrauma, decreased level of consciousness, and non-contiguous spine fractures. Knowledge of the relationshipsbetween specific injury patterns and spinal injuries shoulddecrease the incidence of serious missed spinal injuries.Patients with severe head injuries, as evidenced by adecreased level of consciousness or complex scalp lacera-tions, have a high incidence of cervical spine injuries,which may be difficult to diagnose clinically.12, 58 Theincidence of noncontiguous spine fractures is about 4% to5% of all spine fractures10, 61, 62 but is higher in the uppercervical spine.68 Therefore, diagnosis of a spinal fractureshould in itself be an indication for aggressive investigationto rule out other, noncontiguous spinal injuries.

Conversely, the presence of a spinal fracture shouldheighten the awareness of the possibility of a serious,occult visceral injury. Thoracic fractures resulting in



paraplegia have a high incidence of associated multiple ribfractures and pulmonary contusions. Translational shearinjuries at these levels have significant associations withaortic injuries.69 A delay in the diagnosis of a visceralinjury can occur in up to 50% of patients with spinalinjuries.90 The relationship between the use of lap-styleseat belts and Chance-type flexion-distraction injuries ofthe thoracolumbar spine is now well appreciated.7 Almosttwo thirds of patients with flexion-distraction injuries fromlap belts have an associated injury to a hollow viscus.Overall, approximately 50% to 60% of spine-injuredpatients have an associated nonspinal injury ranging froma simple closed extremity fracture to a life-threateningthoracic or abdominal injury.10, 62

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