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Spinal Injuries

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Page 1: Spinal Injuries
Page 2: Spinal Injuries

11,500 cases per year in US

1994: 207,000 SCI patients

2.6% of all admitted trauma

Summa 1999, Burnley 1993, Lasfargues 1995

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#1 : Male teenagers and young adults

Relative increase in 60-70 y/o MVA (44.5%) Falls (18.1%) Violence (16.6%)

Summa 1999

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Cervical 50-64% Thoracic 17-19% Lumbar (cauda equine)

20-24%

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C1-C2 Facet Joints› Horizontal plane› Facilitates axial rotation

Tectorial Membrane› Continuation of PLL› Major occip- cervical

stabilizer› Secondary restraint for

extension of occiput on atlas

Alar Ligaments

Netter’s Anatomy

Page 6: Spinal Injuries

Lateral mass: Consists of ipsilateral

sup/inf. facets Upward inclination of ~

400

Facet joint complex resists anterior translation and rotation

Vertebral artery Traverses foramen in TP Does not traverse C7

Netter’s Anatomy

Page 7: Spinal Injuries

Ribs and sternum limit thoracic spine movement; increase stability

Spinal cord takes up the majority of the canal space

Facet joints in coronal plane

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Lordotic sagittal alignment (20-600)

Significant (F/E) motion at each level

Biplanar facet joints

L2 -L5: Cauda Equina

Netter’s Anatomy

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FG Fasc. Gracilis (Sensory, lower part of cord, Proprioceptive, Deep pain, Vibration, Ipsilateral)

FC Fasc. Cuneatus (Sensory, Upper part of cord, Proprioceptive, Deep pain, Vibration Ipsilateral)

PH Posterior Horn (Sensory cell bodies)

AH Anterior Horn (Motor Cell Bodies)

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LCS Lateral Corticospinal Tract (Crossed Pyramidal Upper Motor Neurons to ipsi AH)

ACST Anterior Corticospinal Tract (Direct Pyramidal go to contra AH)

PSCT ASCT Spinocerebellar Tracts

LST Lateral Spinothalamic Tract (Sensory, Pain and Temp: cell bodies in contra PH)

AST Anterior Spinothalamic Tract. (Sensory, Touch: cell bodies in contra PH)

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Exits through intervertebral foramen C1 exits between skull and atlas C2 to C7 exit above corresponding vertebrae C8 exits below C7, above T1 Below T1; all nerves exit below corresponding

numbered vertebral pedicle

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Spinal nerves that have exited from the cord

L1-L5: Nerve cell bodies lie in the cord behind T11-T12

S1-S5: Nerve cell bodies line within the region of the conus medullaris

Cauda equina nerves are more like peripheral nerves withstand trauma better than CNS

Damage to this region causes LMN signs

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Primary mechanical insult Rapid compression due to bone

displacement from burst or dislocation Distraction *** Shear *** Penetration

Primary injury leads to cascade of secondary injury mechanisms

*** Portends poor prognosis !!!

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Vascular changes› Diminished blood

flow› Hemorrhage› Vasospasm › Thrombosis

Electrolyte shifts Free radical

production Inflammatory

cascade

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Final pathway is neuron death by:

Cell necrosis with structural dissolution

Apoptosis: chemical trigger initiates process that removes non-functioning neurons but also kills normal neurons in zone of injury

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Aggressive field resuscitation› Maintain systemic BP› Maintain optimal oxygenation

Steroids› NASCIS-2 8 hour window› NASCIS-3 < 3 hrs---24 hrs; 3-8 hrs---48 hrs.

30mg/kg bolus then 5.4mg/kg/hr Surgical decompression? Timing ?

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Complete Cervical tetraplegia Thoracic and lumbar paraplegia

Incomplete syndromes Anterior cord Central cord Brown-Sequard Posterior cord Conus medullaris

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Definition No motor or sensory function more than three

segments below the neurological level of injury

There is absence of sacral sparing

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Absent limb function

Ventilator dependence

C4 level may be vent independent

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C5 deltoids, biceps

C6 biceps, wrist extension

C7 wrist extension, triceps

C8 functional grasp

T1 intrinsic hand fct

4

5

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Better respiratory and trunk control with injury at more caudal levels

Thoracolumbar most commonL1

T12

12

L1

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L2 hip flexion L3/4 knee

extension L4 foot

dorsiflexion L5 EHL S1

gastrocsoleus

L2

L2

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Indicates some continuity of long tract fibers

Sacral structures are most peripheral in both posterior columns and lateral corticospinal tracts

Continued function of sacral LMNs in conusSkeletal Trauma

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Perianal sensation (S4-S5) dermatome

Voluntary external anal contraction

Great toe flexor activity

Skeletal Trauma

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Affects the anterior 2/3 of cord Preserves the posterior column:

proprioception, vibratory sensation May be due to persistent retropulsed

bone or disc material/ mechanical insult Vascular component

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Loss of all motor and sensory below injured level

Deep pressure sensation only

Poor prognosis for motor recovery

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Older patients with preexisting spondylosis

MOI: Hyperextension injury: fall, whiplash Spinal cord pinched by osteophytes

anteriorly and the underlying hypertrophic ligamentum flavum posteriorly; leads to significant injury to the “central portion” of the cord

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Best prognosis among common patterns

Upper extremity > lower extremity involvement

Distal > proximal Earliest and greatest

recovery in legs followed by bladder

Hand dexterity often slow to return, full recovery variable

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Results from functional hemisection of cord, projectile or penetrating wound

Loss of ipsilateral motor Loss of contralateral

pain, temperature, and light touch sensation

75% regain independent ambulation

80% recover bowel and bladder function

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Rare Loss of

proprioception Maintain

ambulation but rely on visual input

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Direct injury to conus region (L1-L2) Presents as mixed lesion of cord and

nerve root damage Bowel, bladder, and sexual dysfunction Injury to CM can disrupt the

bulbocavernosus reflex arc Therefore, the absence of a bulbocavernosus

reflex unreliable indicator of spinal shock in this clinical setting

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Modified From: Lockhart RD; Hamilton GF; Fyfe FW. Anatomy of the Human Body. JB Lippincott Company

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Lower motor neuron lesion (not cord)

Sacral segments more affected than lumbar

Saddle anesthesia with incontinence

Lumbar sparing

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Common mechanism for central cord injury in elderly—hyperextension with a spondylolytic neck

MRI findings impressive SCI protocol followed by observation until

recovery plateaus Treatment : same as central cord syndrome.

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Be aware of the clinical triad of

neurological injury and

concomitant lamina fracture with

burst pattern (Cammisa, 1989)---trapped roots

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Decompression rarely of benefit except forINTRA-CANAL BULLET AT THE T12 TO L5 LEVELS with incomplete injury

(better motor recovery than non-operative)

Fractures usually stable, despite “3-column” injury

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More favorable prognosis than cord injuries

In c-spine injuries: frequently see complete cord injury with varying levels of root injury Good chance of recovery of one level Recovery dependent on level of injury

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ATLS guidelines: A-B-C’s Examine for head, neck, or back

trauma –need to logroll Paradoxical diaphragmatic breathing Priapism Neurogenic shock: hypotension and

bradycardia Loss of sympathetic tone

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Log roll !!!!! Palpate

Tenderness Gap/ Step-off Crepitus

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Motor: 0-5 Sensory Rectal exam: sacral sparing? DTRs: LMN function Spinal reflexes: UMN function

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Biceps C5 Brachioradialis C6 Triceps C7 Quadriceps L4 Gastroc-soleus S1

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Perianal/perineal sensation Rectal tone Big toe flexion Implies partial structural continuity of

white matter long tracts May be only evidence of incomplete

injuryhigher chance of recovery Essential to check and document

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Bulbocavernosus reflex: Pull glans or press

clitoris anal contraction (int. sphincter) around gloved finger

Absence is indicator of spinal shock

Skeletal Trauma

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Scapulohumeral reflex (C3) Tap on spine of scapula =>abd and

elev arm Hoffman’s Inverted Radial Reflex Tap BR =>finger flexion (C6 root) Superficial abdomenal Cremaster Crossed adductor response Tap Medial Fem Condyle =>add contra

leg

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Temporary loss of all or most spinal reflex activity below level of injury

Lasts around 24 hours (max 48 hrs) Ends when bulbocavernosus reflex and/or

anal wink returns An injury cannot be considered complete

until resolution of spinal shock

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Neurologic level of injury (NLI)› Most caudal level

with bilateral normal motor and sensory function

Complete/Inc› Importance of

sacral levels Zone of partial

preservation

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A Complete:

B Incomplete:C Incomplete:

D Incomplete:

E Normal:

No motor or sensory below lesion

Sensory only below lesion to S4-5Preserved motor below lesion, key

muscle strength < 3Preserved motor below lesion, key

muscle strength > 3

Normal motor and sensory below lesion -ASIA

1992

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X-rays CT MRI MRA

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Lateral C-spine in trauma room› Must include down to C7-T1› Swimmer’s view or pull-down if necessary› Single most important radiographic

examination C-spine series

› AP, Open mouth (dens) T-L-S spine films as indicated (one

spine fracture mandates full spine radiographic evaluation) › T-L junction: 50% of injuries occur at T11-L1

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Lordosis Unreliable sign of

injury Prevertebral soft

tissues Unreliable No agreed upon

measure 6 mm at C3 22 mm at C6

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Anterior spinal line› Anterior aspect of vertebral

body along ALL

Posterior spinal line› Posterior aspect of

vertebral body along PLL

Spinolaminar line› Joins the anterior margins

of the junction of the lamina and spinous processes

Spinous process line› Joins tips of spinous

processes

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– Lateral masses of C1 Lateral masses of C1 should align over should align over facet joints of C2facet joints of C2

– combined lateral combined lateral mass displacement mass displacement over 7 mm suggests over 7 mm suggests transverse ligament transverse ligament tear (Spence’s Rule)tear (Spence’s Rule)

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Injury suspected on plain films Better visualize fracture (specificity and

sensitivity) Unable to adequately assess on plain

films Sagittal and/or coronal reconstructions

can be helpful (particularly at Oc.-cervical and C-T jcts.)

Fracture or soft tissue injury in the plane of the CT can be missed

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Invaluable for assessing cord and soft tissues

R/O associated disc herniation ( facet dislocations)

Hemorrhage vs edema in soft tissues ???? Ligamentous tears and facet capsule

disruptions visualized with fat suppression May allow prognostic assessment of final

motor function› Intrasubstance hematoma

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T1 T2 GRE

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Roaf, 1960 – pure axial load or pure flexion leads to little posterior ligamentous injury

Nagel, 1981 – 20 degrees of kyphosis or 10 degrees lateral angulation implies incompetence of PLL and posterior elements, thus inferring instability

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Panjabi, 1981 – it takes sectioning of PLL and posterior annulus to destabilize a motion segment with the addition of facet capsule and interspinous ligament disruption

James et al, ’94 – middle column offers little additional resistance to kyphosis with increasing axial load

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The Issues Often difficult to diagnose Missed or delayed diagnosis can lead to

catastrophic neurologic disability No agreed upon protocol in the intoxicated,

multiply-injured, or head-injured patient

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The Problems Unnecessary imaging?

Should every patient with blunt trauma gets x-rays?

Overzealous consultation When and who should ‘clear the c-spine’ ??

The Hard Collar Dilemma: Prolonged hard collar use leads to decubiti as

well as neck pain

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Hoffman, Mower, et al., NEJM 2000 Multicenter study 34,069 patients with blunt trauma AP/Lat/Open Mouth on all patients 810 with positive x-rays Only 8 with false-negative x-rays

Only 2 clinically significant

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Harris, Kronlage, et al. Spine 2000 Polytrauma, intoxicated, CHI patients IRB Protocol: Includes intra-op flex/ext with

fluoro after all films read as normal Goal: Identify ligamentous injuries 3/ 153 (+) --- all required surgical stabilization

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Criteria for clinical clearance› No posterior midline

tenderness› Full pain-free active ROM› No focal neurologic deficit› Normal level of alertness› No evidence of intoxication› No ‘distracting injury’

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If x-rays negative, but patient c/o neck pain, active flexion/extension x-rays when able. Rarely helpful in acute setting

If neurologic deficit attributable to neck injury, immediate MRI

Controversy over the polytrauma or intoxicated patient remains EAST practice guidelines: trauma series and

thin cut axial CT through C1-2 CT of cervical –thoracic junction if poor

visualization on plain and swimmer’s

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15-30% incid. uni-/bilat

Neuro intact: MRI prior to reduction attempt

Neuro injured: Reduction prior to MRI

Neuro unknown: MRI first

Attempt reduction without MRI ONLY if able to accurately monitor neurologic exam throughout process

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Experimental evidence Clinical evidence

Non-operative Operative

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Numerous studies Classic: Tarlov 1954 Delamarter 1995 Dimar 1999 Experimental models: Balloons, clips, cables,

spacers Beagles, rabbits, rats

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Severity of SCI dependent on: Force of compression Duration of compression Displacement, canal narrowing

Surgical decompression does attenuate the deleterious effects of acute SCI Persistent compression is a potentially

reversible form of secondary injury

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Most studies uncontrolled and retrospective analyses

Spontaneous recovery unpredictable, but generally occurs

Timing to reduction is important Most dramatic benefit in bilateral jumped

facets

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Surgical benefit must be weighed against limited non-operative benefit

Numerous studies, almost exclusively retrospective

Timing: early, late, and later

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The only prospective randomized trial 62 patients with cervical SCI

34 “Early” (< 72 hrs) surgery 28 Late (> 5 days) surgery

ASIA assessment No difference in neurological outcome

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Most studies retrospective with historical controls

No clear consensus on timing No statistical evidence that surgical

decompression influences neurologic outcome

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Tator et al 1999 Retrospective, multicenter (36) Examined use and timing of surgery in

acute SCI 9 month period 1994 to 1995 All within 24 hours of injury 16 to 75 years old Non-penetrating trauma

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585 patients Complete SCI in 57.8% Traction 47% Surgery 65.4%

< 24 hrs: 23.5% 25-48hrs: 15.8% 48-96hrs: 19% > 5 days: 41.7%

Page 77: Spinal Injuries

C-spine vs. T-L spine Partial vs. complete

› Spinal shock Definition of early surgery Role of steroids Type of decompression

› traction vs. anterior vs. posterior

High energy vs. low energy

Associated injuries

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There is strong experimental evidence in animals to indicate:

Decompressive surgery of the spinal cord improves recovery after SCI

Earlier surgery yields more improvement

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There is strong experimental evidence that suggests early decompression (<6-8 hrs) leads to a higher likelihood of neurological recovery.

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Extrapolating animal data to clinical practice may be a leap, but this data comprises the majority of current scientific evidence.

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The sole prospective randomized study concluded that there is no difference between early (<72 hrs) and late (> 5 days) surgical decompression with respect to neurological recovery.

Vaccaro, et al. Spine 1997

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