SPINAL TRAUMA
From the 7th Annual Chicago Trauma Symposium
| CERVICAL INJURIES: NEUROLOGIC CONCERNS George K. Bovis, MD, Staff Neurosurgeon, Lutheran General
Hospital, and Assistant Medical Director, Alexian Brothers Gamma Knife Center, Chicago
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| Background: 20% to 30% of spinal fractures occur in cervical spine; 20% of spinal fractures result in cervical spinal cord
injury (SCI); 50% of SCIs originate from cervical spine fractures; patients with injuries to C4 and above require ventilation;
costs $500,000 for first year, $100,000 per year thereafter; injuries at C5 and below cost $400,000 for first year,
$40,000 per year thereafter; life expectancy for 25-yr-old male with SCI 15 yr if ventilation-dependent, 30 yr if ventilation-independent;
lifetime cost $2.1 million
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| Clinical assessment of acute cervical SCI: perform and document detailed neurologic examination daily; any change deserves
complete investigation; most commonly used impairment scores are American Spinal Injury Association (ASIA) and
International Medical Society of Paraplegia (IMSOP); ASIA score describes motor and sensory examination, neurologic
level, completeness or incompleteness of injury, and zone of partial preservation; ranges from 0 (total paralysis) to 5 (normal
strength); identify most caudal motor level with score >3
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| Syndromes associated with cervical SCI
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 | Bells cruciate paralysis: injury at cervicomedullary junction; uncommon; consists of upper extremity paralysis and preservation
of lower extremity strength; resembles central cervical cord syndrome; damage occurs at midline
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 | Central cervical cord syndrome: relatively common; seen mostly in older adults; consists of upper extremity paralysis and
preservation of lower extremity strength; cervical spondylosis often preexisting; produces hyperextension injury with
inbuckling of hypertrophied ligamentum flavum and compression of medial arm fibers in corticospinal tract
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 | Brown-Séquard syndrome: produced by physiologic spinal cord hemisection, leading to ipsilateral paralysis and loss of
proprioception and vibration and contralateral loss of pain and temperature sensation; prognosis good, unless caused
by penetrating injury
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 | Anterior spinal cord syndrome: motor paralysis with pain and temperature loss and preservation of proprioception; usually
results from hyperextension injuries, axial loading injuries, central disc herniation, or teardrop fracture; has worst
prognosis of all cervical spinal cord syndromes (usually associated with injury to anterior spinal artery)
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 | Spinal shock: loss of all neurologic function below level of SCI; presents as flaccid paralysis and arreflexia, ultimately
leading to spasticity; diagnose from absence of bulbocavernous reflex
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| Pharmacologic therapy: goals are to minimize secondary SCI and improve neurologic function
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 | Methylprednisolone (MPI): reduces white matter edema, inflammation, and destructive effects of lipid peroxidation on cell
membranes; improves spinal cord blood flow and sodium-adenosine triphosphatase (ATPase) activity; according to
1984 National Acute Spinal Cord Injury Study (NASCIS) I, neurologic outcomes similar whether patients received 100
mg or 1000 mg MPI, but higher dose associated with greater risk for wound infections; in NASCIS II (1990 and 1993),
MPI administered within 8 hr of injury associated with better neurologic scores, compared to patients receiving naloxone,
placebo, or MPI >8 hr after injury; in NASCIS III (1997), 48-hr infusion of MPI associated with better outcomes
than 24-hr infusion of MPI or 48-hr infusion of tirilazad; however, also associated with higher rates of sepsis and pneumonia;
recovery similar in all groups if treatment began within 3 hr of SCI; conclusionsif MPI administered within 3
hr of SCI, continue for 24 hr; if administered 3 to 8 hr post-SCI, continue for 48 hr, anticipating higher rate of sepsis and
pneumonia; study had many shortcomings; led to 2002 publication of guideline stating MPI is option that should be undertaken
only with the knowledge that the evidence suggesting harmful side effects is more consistent than any suggestion
of clinical benefit; evidence insufficient to support its use as standard or its inclusion in guideline, although
medicolegal concerns persist (doctor may be held responsible for sequelae if drug not administered)
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| Indications for surgery: decompression of neurologic elements (only for incomplete injuries); stabilization of spine; deformity
correction
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| Injuries to vertebral artery: incidence 10%; patients often asymptomatic; usually associated with complete SCIs; may
cause stroke or cerebrovascular ischemia; indications for diagnostic work-up include injuries covered previously and
strokes or transient ischemic attacks (TIA) in posterior circulation; work-up should include angiography; no standards or
guidelines for treatment; options include observation, anticoagulation (14% complication rate), and stenting (5% complication
rate); if patient asymptomatic, observation recommended; consider anticoagulation if patient has had TIA
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| OCCIPITOCERVICAL AND C1-C2 LIGAMENT INJURIES Frank M. Phillips, MD, Professor of Orthopaedic Surgery,
Rush University Medical Center, Chicago
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| Craniocervical anatomy: bony restraintsconvex occipital condyles articulate with concave lateral masses of atlas
(flatter and less restrictive in children); posterior arch of axis at base of skull in extension; ligamentous restraints
paired alar ligaments, tectorial membrane, and apical ligaments main source of stability at occipitocervical junction
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| Vascular anatomy: locate vertebral artery during posterior approach, especially in occipitocervical region; artery closest to
midline at posterior ring of C1
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| Craniocervical motion: occipitocervical junction permits 21o of extension, 3o of flexion, 7o of rotation, and 5o of lateral
bending
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| Patient evaluation: suspect occipitocervical injury with any high-speed trauma; do not move patient until injury ruled out;
computed tomography (CT) key; magnetic resonance imaging (MRI) may detect soft tissue injuries, especially of transverse
ligament
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| Atlanto-occipital dislocations: rare; usually fatal, but survival increasing as treatment improves
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 | Type I: anterior displacement of occiput (most common)
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 | Type II: longitudinal distraction
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 | Type III: posterior displacement (rare)
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 | Management: traction contraindicated in type II; 5 lb of traction may be used for realignment with types I or III; avoid
heavier weights; other fractures may signal occipitocervical dislocation
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 | Complication of injuries: Wallenberg syndrome
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| Occipital condyle fractures: rare; often result from high-impact injuries; patient may arrive at hospital unconscious; CT
with coronal reconstruction usually needed for accurate diagnosis; evaluate stability
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 | Type I: undisplaced fracture of occipital condyle; usually results from impaction with axial loading; bilateral or unilateral
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 | Type II: linear component of skull-base fracture; often unilateral and related to direct blow; condyle may or may not be
displaced
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 | Type III: condyle avulsion near alar ligament attachment (greatest threat to stability); usually results from rotation or lateral
bending
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 | Treatment: stable types (I and II)rigid brace for 6 wk; unstable types (IIb [base-of-skull fracture with displaced
condyle] or III [if not displaced])put patient in halo for 8 wk; if type III injury involves displacement, occiput-to-
cervical spine fusion indicated, usually to C2
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| Transverse ligament ruptures: usually related to severe flexion injuries; also seen with C1 burst or odontoid fractures;
possibly associated with vertebral artery injury (signs include syncope, vertigo, and blurred vision); diagnosis based on
atlas-dens index (ADI; up to 3 mm in adults, 5 mm in children, measuring from back of ring of C1 to front of dens);
ADI of 5 to 7 mm suggests isolated transverse ligament rupture; ADI >7 mm suggests more extensive damage; injury
not immediately apparent if patient has muscle spasms or rigid neck; early flexion and extension views may be informative
after spasms resolve
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 | Type I: midsubstance ligamentous ruptures; less likely to heal than type II
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 | Type II: bony avulsions from ligament attachment to C1
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 | Clinical presentation: survival relatively rare; often associated with head trauma; flexion may exacerbate neurologic
symptoms; cardiac or respiratory symptoms may be present; check for vertebral artery injury
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 | Treatment: halo immobilization associated with 75% union rate, but patient must be neurologically intact, with ADI <5
mm; C1-C2 fusion indicated if neurologic findings or transverse ligamentous rupture present
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| Advances in occipitocervical fixation techniques: insert 10-mm screws around external occipital protruberance, with 8-
mm screws going laterally; 8-mm screws also provide rough guide going distally toward midline; C1 lateral mass screws
becoming popular for C1 fixation; drawbacks include possibility of hitting vertebral or internal carotid arteries
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| FUSION-RELATED SEGMENT DEGENERATION: DISC REPLACEMENT VS FUSION Jack E. Zigler, MD, Co-
Director, Fellowship Training Program, Texas Back Institute, Plano, and Clinical Associate Professor, Orthopaedic Surgery,
University of Texas-Southwestern School of Medicine, Dallas
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| Indications for lumbar spine fusion: posttraumatic multicolumn instability; some degenerative conditions
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| Benefits of fusion: eliminates source of pain and stabilizes spine; drawbacks include loss of motion at surgical site, questions
about sagittal balance, choice of bone, problems with autograft or allograft, donor site approach, possible muscle
or nerve injury, and time needed for fusion and rehabilitation
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 | Success rates: 93% to 96% fusion, depending on cage used; patients report high levels of satisfaction and work resumption;
however, patients do not do as well as their x-rays suggest they should
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 | Reasons for disparity between x-rays and clinical outcomes: fusion diseasesurgery-related injury to spinal muscles;
transition syndromeadjacent-level breakdown that occurs after even minimally invasive surgery, because those areas
must compensate for altered spinal mechanics; arthroplasty possible solution
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| Outcomes with ProDisc: prospective randomized 19-center Food and Drug Administration (FDA) study started in 2001;
patients had single-level or bilevel disease; for every 2 patients receiving disc, 1 underwent 360o -fusion; inclusion criteria
included disabling disc disease in 1 to 2 adjacent L3 to S1 segments and >40% impairment; 225 patients enrolled
(38 fusion, 78 ProDisc, and rest continued-access, nonrandomized ProDisc recipients)
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 | Average length of stay: ProDisc patients2 days; fusion patients3.3 days
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 | Pain: decreased immediately postoperatively in both groups, with continued improvement over 36 mo, but disc patients
experienced significantly greater improvement by 24 mo
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 | Would undergo surgery again: at 2 yr, <5% of disc patients said no; at 3 yr, all patients said yes; double-level patients do
as well as single-level patients
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 | Complications: one unusual coagulopathy and deep venous thrombosis requiring anticoagulation; one technical error; 2
cases of postoperative leg pain requiring negative decompression; few superficial infections; no deaths, paralysis, or
implant migration, and no need for posterior fusion for persistent pain
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| PEDIATRIC SPINAL CORD INJURY John Lubicky, MD, Professor, Orthopaedic Surgery, and Adjunct Professor, Pediatrics,
Rush Medical College, Chicago
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| SCI classification: completeloss of all function below level of lesion; incompletepreservation of some function below
lesion; Brown-Séquard has best prognosis of incomplete injuries; any functional recovery usually complete within 6
to 12 mo of injury
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| Types of paralysis: upper motor neuronspastic; associated mostly with cervical and thoracic lesions and conus lesions
in which thoracolumbar junction surrounding cauda equina not injured; lower motor neuronflaccid; usually associated
with root and cauda equina injuries
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| Peculiarities of pediatric SCI and spinal trauma: imaging studies difficult to interpret if vertebrae not yet completely ossified;
vertebral growth plates may separate; normal variant of C2-C3 may be diagnosed as subluxation (pseudosubluxation);
childs ligaments and disc bonds may be lax, permitting large deflection of spine not necessarily visible on
imaging; account for toddlers relatively large head; if immobilization necessary for cervical injury, elevate body to minimize
neck flexion; children injure upper cervical spine more frequently than lower due to bowling ball on neck (opposite
true for adults); drugs no more effective for children than for adults; however, childs prognosis often better
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 | Spinal deformity: results from skeletal immaturity plus paralysis; risk inversely related to skeletal maturity at time of injury;
surgery may affect growth, depending on number of vertebrae fused; if deformity seems excessive as child grows,
consider possible unrecognized spinal parenchymal injury (eg, syrinx)
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 | Severity: do not assess until spinal shock resolves
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| Neurologic outcomes: complete lesionsrecovery unlikely; incomplete lesionslikelihood of recovery depends on
type of lesion and efficacy of interventions
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 | Decompression: directremoval of retropulsed bone and other tissue that compresses cord; orthopaedic
realignment of spine to relieve pressure
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 | Stabilization: externalcasts, orthoses; internalfixation, fusion; permanent; restores anatomic alignment, prevents
further damage from continued instability, and permits early rehabilitation
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 | Special considerations with surgical stabilization: anatomy of injured area; preexisting deformities
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| Paralytic spinal deformity: risk factors include complete SCI above T12 and skeletal immaturity
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Educational Objectives
| The goal of this program is to review the diagnosis and management of spinal trauma in children and adults. After hearing
and assimilating this program, the clinician will be better able to:
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 | 1. Describe the syndromes associated with cervical spinal cord injuries.
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 | 2. Discuss the controversy surrounding the use of methylprednisolone in the treatment of cervical spine injuries.
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 | 3. Name the major types of occipitocervical and transverse ligament injuries.
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 | 4. Explain why patients who undergo lumbar fusion may not do as well as their postsurgical x-rays suggest they
should.
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 | 5. List some of the characteristics of pediatric spinal trauma not seen in adult patients.
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Discussed on This Program
Methylprednisolone [Medrol]
Naloxone HCl [Narcan]
Tirilazad mesylate (investigational) [Freedox]
Suggested Reading
Pharmacological therapy after acute cervical spinal cord injury. Neurosurgery 50 (3 Suppl):S63, 2002; Bracken MB: Methylprednisolone
and acute spinal cord injury: an updated of the randomized evidence. Spine 26 (24 Suppl):S47, 2001;
Bracken MB: Steroids for acute spinal cord injury. Cochrane Database Syst Rev (3):CD001046, 2002; Chappell ET:
Pharmacological therapy after acute cervical spinal cord injury. Neurosurgery 51:855, 2002; Fehlings MG, Perrin RG:
The role and timing of early decompression for cervical spinal cord injury: update with a review of recent clinical evidence.
Injury 36 Suppl 2:B13, 2005; Koestner AJ, Hoak SJ: Spinal cord injury without radiographic abnormality (SCIWORA) in
children. J Trauma Nurs 8(4):101, 2001; Meyer PG et al: Combined high cervical spine and brain stem injuries: a complex
and devastating injury in children. J Pediatr Surg 40 (10):1637, 2005; Papadpoulos CA et al: Surgical decompression
for cervical spondylotic myelopathy: correlation between operative outcomes and MRI of the spinal cord. Orthopedics
27: 1087, 2004; Vialle LR, Vialle E: Pediatric spine injuries. Injury 36 Suppl 2:B104, 2005; Vogel LC et al: Unique issues
in pediatric spinal cord injury. Orthop Nurs 23:300, 2004.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. The following has been disclosed:
Dr. Zigler is a consultant for Synthes Spine. Dr. Lubicky is a lecturer for Dupuy Spine.
This program was recorded at the 7th Annual Chicago Trauma Symposium, held August 11-14, 2005, in Chicago. The
Audio-Digest Foundation thanks the speakers and the sponsor for their cooperation in the production of this program.
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