spinal trauma by dr. shikher shrestha, fcps, neurosurgery , ninas, nepal
TRANSCRIPT
Spinal Trauma Series… an overview
Shikher ShresthaNINAS
INJURIES TO THE CERVICAL SPINE
Cervical spine – the most mobile portion and hence the most common site of spinal injuries
N.B. ~ 10,000 patients die each year due to spinal injuries
Common mechanisms of injury
Motor vehicle accidents
Falls – 18-30% in young age group (<8yrs) vs 11% in >8yrs
Sports – 20-28% in older age group
Common in 15-30 years
Non accidental trauma and penetrating injuries – less frequent cause
Epidemiology
M:F::3-4:1
Injury patterns:
Fractures – the most common
Ligamentous disruption and dislocations
Upper cervical spine (C1-C4): Lower cervical spine (C5-C7):: 2:1
Subluxation injuries without Fracture + SCIWORA – YOUNGER AGE !!!
Associated Neurological Injury
~ 15% will have concomitant neurological injury on average
More higher occurrence with cervical spine injury (2-100%) – overall 40-60%
Incidence still an underestimate: many patients die before reaching medical attention
Eg. Atlanto-Occipital Dislocations – 25% die due to respiratory arrest before evaluation
Factors influencing extent of neurological injury
Level of injury
Mechanism of injury
Force involved
Patient’s age
Patient’s medical status –Eg. Down’s and Ankylosing spondylitis – rigid spine with more likely neurological involvement
Clinical Assessment tool – ASIA gradingAmerican Spinal Cord Injury Association Grading
General Principles
High index of suspicion in all trauma patients
Immobilization until clinical evaluation
Immobilization from trauma scene and maintained during triage, resuscitation, primary and secondary survey
N.B> Primary survey (ABC) in improperly mobilized patients can exacerbate existing cervical spine injury in up to 10% cases
2002
American Association of Neurological Surgeons (AANS)
&Congress of Neurological Surgeons (CNS)
Joint section on disorders of Spine and Peripheral Nerves
Evidence based guidelines for the management of acute cervical spine and spinal cord injuries
Imaging..
Cross-table lateral radiograph
Swimmer’s view added to visualize cervicothoracic junction and the top of T1 vertebra
Combination : 85% sensitivity and 97% negative predictive value
Open-mouth odontoid view – assessment of C1/2 vertebrae and odontoid
Pillar (oblique) view can also be utilized to demonstrate odontoid
AP view (don’t ignore!!) – can identify rotatory component; unilateral facet dislocations
AP+Lat+OM view > sensitivity and negative predictive value – 92% and 97%
Imaging ..
CT Scan:
particularly useful in occipitocervical and cervicothoracic junctions
suspicious areas on plain xrays – further evaluated with fine cuts
coronal and sagittal reconstruction – further delineates
Difficult to determine level on SCIWORA patients
Clinical exam for localization and MRI vital in such cases
Imaging..
~10% patients with C-spine Fracture – non contiguous vertebral column fracture
Complete radiographic assessment of entire spinal column warranted
3D CT can be useful in complex fracture – operative planning
Does every patient in trauma setting require xray C-spine or CT ??AANS/CNS Guideline Neurosurgery 2002
1. normal neurological exam and GCS of 152. Not intoxicated3. No neck pain or midline tenderness4. No significant distracting injury such as long
bone fracture or visceral injury
NEXUS criteria 2000 NEJM (the National Emergency X-Radiograph Utilization study)
Canadian C-spine rules 2001 JAMA
Imaging..
MRI
identifies disc herniations and ligamentous injuries
longitudinal assessment of spine and cord with views in axial, sagittal and coronal planes
only modality to detect abnormality in SCIWORA
although extremely sensitive for ligamentous injury, cannot alone diagnose “unstable” injury
Imaging..
Dynamic Xrays/ flexion-extension lateral cervical views
determines presence of subluxation injuries or abnormal ligamentous laxity
done under fluoroscopy in obtunded or unconscious patient
Fluoroscopy indicated in high risk injuries:high speed MVAfall > 3 metersmajor associated injuriesvehicle crashes involving death at the scene
QUIZ .. Which view???
X ray interpretation guide
AABBCDS
A dequacy A lignmentB one abnormalityB ase of skullC artilageD isc spaceS oft tissue
Adequacy
Must visualize entire C spine
Should show upper border of T1
Caudal traction on arms help
Get swimmer’s view or CT if not adequate – shoot from the axilla and xray plate above the shoulder
Alignment
A step off > 3.5 mm is significant anywhere
Alignment
Anterior subluxation of one vertebra on another indicates facet dislocation
<50% of width of a vertebral body Unilateral facet dislocation
>50% bilateral facet dislocation
Bones
Disc
Disc spaces should be uniform
Assess spaces between the spinous processes
Soft tissue
Nasopharyngeal space (C1)10 mm (adult)
Retropharyngeal space (C2-C4)5-7 mm
Retrotracheal space (C5-C7)14 mm (children)22 mm (adults)
AP C spine films
Spinous processes should line up
Disc space should be uniform
Vertebral body height should be uniform
OM view
Adequacyall the dens and
lateral borders of C1 and C2
Alignmentlateral masses of C1
and C2
BoneInspect dens for
lucent fracture lines
SPECIFIC FRACTURE SUBTYPESAND
THEIR MANAGEMENT
Atlanto-Occipital Dislocation
High incidence of neurologicalmorbidity and mortality
Mechanism and force requiredto disrupt are often fatal
20-30% of all cervical spine injury related deaths – AOD
20% of AOD survivors – favorable outcome if therapy and immobilization instituted promptly
Highly unstable injury and can be missed on any imaging modality if normal alignment is temporarily restored
CT scan: diagnostic imaging of choice
Basion-dens interval (BDI) – 10 mm as the cutoff
Occipital condyle-C1 interval (CCI) >4 mm is abnormal
MRI showing OAD – “increased CCI”
Classification of AOD
NORMAL TYPE I (ANT) TYPE II (VERTICAL)TYPE III (POST)
Management
Use of rigid collars, which further distracts the OA joint discouraged
Sandbags on either side of the head and taping : for immobilization
Halo fixation after confirmation of diagnosis
Further treatment strategies depends on the grade of injury
Management
Grade I injury:
normal BDI and CCIhigh posterior ligamentous and occipitoatlantal signalmild to no change at the occipitoatlantal joint
Rx: non operative with Halo or collar
Grade II injury:
minimum of one abnormal finding on CT based criteriagrossly abnormal MRI finding of OA joints, tectorial
membrane, or alar or cruciate ligamentRx: surgical stabilization with ORIF
Occipital Condyle Fracture
Frequently missed on plain radiographs
Diagnosed in CT scan
incidence: 4-19%
Mean age: 32.4 yrs
M:F::2:1
Commonly occur as isolated injury
Presence of retropharyngeal hematoma on lateral Xray may be the only clue towards craniovertebral insult
Anderson and Montesano Classification
I: axial load and communitedII: extension of skull baseIII: avulsion of condylar fragment by alar ligament
Management
I and II: stable
External immobilization in collar
III: unstable
Rigid external immobilization in collar or haloEven ORIF at times
Atlas Fractures
Position and Shape (ring) makes it vulnerable to various fracture patterns
3-13% of all cervical spinal injuries
40-44% associated with fractures of C2
Neurological injury rare due to wide spinal canal
Jefferson’s Classification (Gehweiler modification)
I: involves posterior arch only
II: involves anterior arch only
III: posterior arch fractured bilaterally and associated uni or bilateral anterior arch fracture
IV: involves the lateral mass
V: transverse anterior arch fracture
Classical Jefferson’s Fracture: Type III; atlas burst fracture because lateral mass displaced laterally;
most common pattern; caused by axial loading
Jefferson’s Fracture .. illustration
Congenital anomaly may be mistaken for fracture
See the area of edema within the bone to differentiate
Integrity of transverse atlantal ligament (TAL) – key factor in determining the stability of atlas fractures
This is addressed by Dickman and associates
Rule of Spence..
Assesses the extent of lateral mass displacement of C1 over C2
Combined sum of the displacement of both lateral masses of C1 on C2 measured on OM view or coronal CT
Sum > or = 6.9 mm TAL incompetent and fracture considered unstable
Dickman demonstrated 61%TAL rupture being missed with this classical rule
Hence, new classification scheme
Dickman Classification of TAL rupture
I: Disruption at the midportion of the TAL or at the insertion of the medial tubercle
II: purely bony avulsions (can be treated by immobilization alone)
Treatment of Atlas Fracture
Axis Fracture
18% of all cervical spine traumatic injuries
Odontoid process fracture are the most common C2 fracture – 60%
Neurological deficit 8.5% and Mortality 2.4%
Anderson and D’Alonzo Classfication
Type I – the rarest formType II – the commonest
Anderson and D’Alonzo Classification
Rx of Types I and III – Rigid External Immobilization
Type III -97% fusion rate with halo vest
Type II – more difficult to treat; 40% non union with external immobilization alone
Type II fracture with < 5mm dens displacement – good candidates for halo stabilization
Rate of failure if > 5mm is around 86%
Compared to young, older patients >50 yrs: 21 x greater non union rate
Surgical Options:
Anterior Odontoid Screw Fixation
Posterior Atlantoaxial fusion
Odontoid Screw Fixation
Hangman’s Fracture / Traumatic spondylolisthesis
Bilateral fractures of the pars interarticularis
4% of all cervical spine fractures
20% of all axis fracture injuries
Low rate of neurological injury
EFFENDI CLASSIFICATION
I: non displaced fracturesII: anterior fragment displacedIII: anterior fragment in flexed position with
C2-C3 facet dislocation
Treatment of Hangman’s Fracture
Types I and II
External immobilization with halo vest and rigid collar
Type III
ORIF – C1-C3 posterior fusion
• Levine and Edwards further modified the Effendi classification to include the degree of angulation
Fractures involving body, pedicle, lateral mass, laminae and spinous process – 20%
C3-T1 Injuries
C3 in isolation- <1% of all cervical injuries
More vulnerable areas above and below: C1/2 complex and C5/6
75% of all c spine fractures – between C4 and T1
Most common level of fracture is C5
Most common level of subluxation is C5/6 interspace
Most common type of injury in subaxial cervical spine: V.Body Fracture
Subluxations
Facet dislocations
Laminar
PedicularSpinous process
In order of decreasing frequency, the occurrence of injuries:
Pattern of injury
Injury associated with high incidence of neurological involvement Subluxation with vertebral body fracture
Unilateral facet dislocation: root injuriesBilateral facet dislocation: complete spinal cord injury
Allen Classification of Mechanism of injury
Distraction/flexion: facet dislocationCompression/Flexion/Vertical
compression/Extension/Subluxation
Management principles
Early reduction and realignment
Early Operative decompression for nonreducible compression for incomplete spinal cord injury
Undisplaced vertebral body fracture and isolated posterior element fractures heal with external immobilization alone
Successfully reduced facet dislocation heals with non operative immobilization if there is associated facet fracture rather than ligamentous injury only
Serial and dynamic imaging for follow up of conservative arm
ORIF required if cannot be reduced nonoperatively
ORIF if non healing with external immobilization
ORIF if pure ligamentous injury
Goals: spinal cord and roots decompressionstabilizationfusion
Indications for surgical therapy
1. Non reducible spinal cord compression2. Ligamentous injury with facet instability3. Kyphosis > or = 15 degrees4. Vertebral body compression > or = 40%5. Subluxation > or = 20%
Whiplash Injury
Cervical spine – most mobile segment of spine
Vulnerable to high and low energy forces
“Any traumatic injury to the soft tissues of the cervical spine resulting from hyperextension, hyperflexion or rotation of the neck without associated fracture, dislocation, or intervertebral disc herniation”
Common with rare end collision
Acute or Insiduous, delayed presentation; mainly in the form of cognitive defects, chronic headaches or even lower back pain
Quebec Task Force Clinical Grading of Whiplash
Type I
neck pain, stiffness, or tenderness with no clinical signs of cervical spine injury
Type II
features of type I + signs of decreased range of motion (ROM) with point tenderness
Type III
features of I+II+ neurological signs (decreased or absent DTRs, muscle weakness, and sensory deficits)
Managment
Multimodal because
Many patients demonstrate signs of depression or deficits in their ability to work
Cord Injury
Management goals
prevent secondary insult to the cordprevent disability and deformityreduction of deficit and painrehabilitation
Management targeted to Incomplete injury
Management steps..
Time frame for intervention is CRITICAL
Admitted to ICU – maintenance of SPINAL CORD PERFUSION
Avoidance of hypotension and hypoxia
MAP maintained at 85 to 90 mm Hg or higher for the first week after injury
Any drop in pressure – corrected with pressors (dopamine)
Signs of complete injury with neurogenic shock – poor prognosis as to recovery of neurological function
Management Steps contd..
High dose steroid if at all, should be given within 8 hrs of injury
DVT preventive strategies should be followed meticulously(stockings, compression devices and anticoagulation)
Initial attempts at closed reduction followed by institution of rigid external immobilization(80% success rate; 1% permanent neurological damage and 2-4% chance of transient neurological change)
Obtaining prereduction MRI does not increase the safety of the procedure and may delay therapy
Recent Metaanalysis:
Early surgical intervention within 8 to 24 hrs of an acute SCI
Evidence also available on safety of early surgery (<72 hrs) after hemodynamic optimization
Urgent reduction of bilateral locked facets in a patient with incomplete tetraplegia
A small subset with SCIWORA with delayed presentation – properly immobilized and evaluated with CT, MRI and dynamic xrays
Poor prognostic indicators:
complete neurological injury
age < 4 yrs
Normal MRI scan in such circumstances, predict excellent prognosis
SCIWORA – 5 subgroups based on MRI
Complete transection
Major hemorrhage
Minor hemorrhage
Edema only
Normal
Management
Rigid immobilization in collar 12 wks then
Restriction of activities that exacerbates injury 12 wks
Follow up dynamic x rays
Many investigators have described delayed SCIWORA and recurrent cord injury in patients with SCIWORA
Thoraco Lumbar Spine Fractures..
Problem statement:
15-20% of traumatic fractures occur in thoracolumbar junction (T11-L2)
9-16% in thoracic spine T1-T10
Paraplegia secondary to thoracic fractures have a first year mortality of 7%
Biomechanics:
Long, rigid kyphotic thoracic spine with abrupt switch to shorter, mobile and lordotic lumbar spine
Transition zone susceptible to trauma
Leading cause: MVA followed by falls and sports related injuries
Additional organ systems injured in up to 50% patients
Load bearing supports: annulus fibrosus of disc, spinal ligamentous structures
Intact rib cage: increases the load resisting capacity by magnitude of 4
Thorax:
rib cage and facet articulations limit rotation
costovertebral articulation limit flexion
Injury mainly due to flexion and axial loading
Kyphosis of thorax axial forces transmitted to ventral portion of body Vertebral compression fracture
Associated injuries..
High incidence of concurrent injury (>80%)kinetic energy dissipated through soft tissue and
viscous elements
Petitjean et al - 65% incidence of head injuries associated with 12% SHI
Tearing and rupture of aorta hemodynamic compromise
Hemothorax – 1/3rd
Pulmonary injuries – 85%; typically contusions
Perforation of esophagus and tracheal injuries
Associated injuries..
Thoracolumbar region more vulnerable to concurrent injury (no rib cage)
Intestinal perforations
Mesenteric Avulsions
Solid organ injuries
blunt abdominal aortic dissections – distraction-rotational injuries
Most common mechanism of abdominal injuries – distraction/seatbelt injuries
Axial load injuries (jump/fall) – calcaneal fracture
Miller et al - 48% incidence of concurrent abdominal injuries with transverse process fractures
Radiographic Evaluation
5-15% multisystem trauma patients have occult fractures missed on initial evaluation
20-50% of superior thoracic fractures not diagnosed by admission plain radiographs
Initial radiographic assessment: AP and lateral films
Assess:Vertebral body height/ Pedicle fracture/
Increased interpedicular distance/ transverse process- rib fractures/ malalignment of bodies
Radiographic evaluation
Lateral Film
Loss of body height
Disruption of rostral or caudal end plate
Dorsal cortical wall fracture with retropulsed bone
Fracture of spinous processes
Widening of interspinous distance
Subluxation and angulation of bodies
AP plane
Cobb angle – apical and end vertebrae identified
Radiographic evaluation
Plain radiographs
CT scan
MRI
Classification
Based on Anatomical Structures
eg. Denis three column system
Based on proposed mechanism of injury
eg. Ferguson and Allen
Holdsworth Classification based on mechanism of injury
FlexionFlexion and rotationExtensionCompression
Holdsworth underscored instability if the posterior ligamentous complex are disrupted.
This include: intervertebral disc/ spinous ligaments/ facet capsule and ligamentum flavum
Denis 3 columns
Ventral columnALLanterior annulus fibrosisanterior half of the vertebral bodies
Middle columnPLLdorsal annulus fibrosisdorsal half of the vetebral bodies
Posterior column – analogous to Holdsworth dorsal ligamentous complex
Instability according to Denis 3 column
3 categories as defined by Denis
Mechanical instability – Dorsal ligamentous complex injury developing into late kyphotic deformity
Neurological instability
Both
20% patients with severe burst managed nonoperatively developed subsequent neurological deficit
Requires decompression and internal stabilization
Thoracolumbar Injury Severity Score (TLISS)2005Vaccaro et.al – GOOD “K” VALUE >90% AGREEMENT
Aid in medical decision making
Diagnostic and prognostic information
Stable injury TLISS <4 – treated nonoperatively
Unstable injury TLISS >4 – treated operatively
Operative principlesDeformity correctionNeurological decompressionSpinal stabilizationActive patient mobilization
TLISS
Management
One column injuries (compression fractures and posterior element fractures) – stable – nonoperative unless excessive kyphosis raising concern of pain and deformity in future
2 column (burst fractures)
neurologically intact
nonoperative – bedrest; early mobilization in TLSO (thoracolumbosacral orthotic) brace
continued close monitoring for increased kyphosis and neurological change
neurologic worsening 0-20% - low potential for chronic or glacial instability leading to pain and neurological deficit
Burst fractures – non operative treatment if
Less than 50% vertebral body collapse
less than 30 degrees of kyphotic deformity
No more than 3 cm of offset from the standard sagittal vertical angle on lateral scoliosis film
IF decline in neurological status - operative intervention
IF severe, have neurological deficit and canal compromise - operate
Harrington rods – first spinal implants widely used for vertebral fractures
disadvantage: loss of normal spinal curve
Pedicle screw fixation
allows instrumentation of vertebrae with fractured or absent laminae
purchase through all three columns
Increased rigidity necessitates fewer segments of fixation – leading to preservation of more motion segments
Timing of surgery
immediate decompression and stabilization within 72 hrs
Laminectomy and transpedicular decompression
Dorsal decompression via multilevel laminectomy alone is INEFFECTIVE and should NOT be performed loss of dorsal tension band progressive kyphosis and dorsal migration of cord
MIS – posterior percutaneous pedicle screws
SPINAL CORD INJURY
PathophysiologyBlunt or
penetrating injury
Force transmitted
to spinal column
Disruption of bony or
ligamentous structures
Damage to spinal cord or exiting nerve root
Types of injury
Primary injury
Secondary injury
Primary Injury
Primary injury refers to the destructive forces that directly damage the neural structure
Shear force tearing an axon or direct compressive force occluding the blood vessels, resulting in ischemia
Initiates cascade of cellular mechanism
Leads to secondary injury
Secondary Injury
Secondary injury may persists from hours to weeks to years
Thorough understanding of the cascade exploration of role of potential therapeutics “Translational Research”
Hypotension and hypoxia are amongst the important physiological and preventable parameters for secondary insult
Secondary Injury
Mechanisms leading to hypoperfusion to damaged area:
Global hypotensionDisruption of microvasculatureLoss of normal autoregulatory mechanismsIncreased interstitial pressure
Cytotoxic cell swelling blockade of action potential
Ionic dysregulation leads to cell deathN-methyl-D-aspartic acid receptor antagonist – potentialtarget for translational research
Calpain activation,
mitochondrial dysfunction & free radical production
Calcium dysregulation
& ionic disruption
Ca and Na influx
Activation of glutamate receptors
Failure of Na/K ATPase
leading to cell death
Extracellular glutamate
level rise more
Free radical mediated secondary injurypotential for translational research
Free radical Hydrogen peroxide,
hydroxyl, nitric oxide, superoxide and peroxynitrite
Lipid peroxidation
Cell lysis, organelle
dysfunction, calcium
dysregulation
Axonal dysruption and cell death
Remains elevated for a week and
returns to preinjury baseline
in 4-5 wks
Disruption of BBB leading to secondary injury
Inflammatory mediators affecting vascular permeabilityTNF a, IL b, matrix metalloproteinases, histamine, reactive
oxygen species
Permeability change stays for 2 wks
Previously very selective transmembrane proteins in BBB fails
Cells vulnerable to external milieu
Cell death
To add to the ever existing complexity…
2 types of inflammatory mediators
Non cellularTNF a, Interferons, Interleukins
CellularResident microglia, Peripheral inflammatory cells
2 Roles:Responsible for ongoing destruction
Clears cellular debris and Optimizes the environment for regenerative growth (Experimental TNF a deficient mice
have higher numbers of apoptotic cells, increased lesion size and worse function)
Cell death via Apoptotic pathway- selectively destroys oligodendrocytes than neurons
Microglia activation
after 2 to 48 hrs of SCI
Microglia expresses Fas
ligandFas ligand receptors
largely expressed on oligodendrocy
tesCommunicatio
n occurs via p75
neurotrophin receptors
Activation of caspase cascade
Proteolysis, cleavage and
cell death
To sum up once again..
Secondary injury causes:
Hypoxia/ ischemia
Ionic dysregulation
Excitotoxicity
Free radical and lipid peroxidation
Disruption of BBB
Inflammatory response
Apoptosis/ necrosis
Translational Research..
Identification of number of possible targets for prevention of secondary injury after indepth understanding of secondary mechanism
Agents currently under investigation
Broad categories of neuroprotective agents (minocycline, riluzole)
Myelin-associated inhibitors of neural regeneration (ATI 335 & Cethrin)
Cellular transplantation strategies (activated autologous macrophages, bone marrow stromal cells, human embryonic stem cells)
Neuroprotective agents
Minocycline
Tetracycline derivative
Neuroprotective properties in a diversity of animal models, including those that aim to study stroke, Parkinson’s dz., Huntington dz., ALS, MS
Mechanism of action:
inhibition of cytochrome c release decreased microglia activation inhibits apoptotic cell destruction
Riluzole
Benzothiazole anticonvulsant
Primarily used in patients with ALS – prolong lives of persons by 2-3 mo
Mechanism of action
blocks voltage sensitive sodium channels, whose overactivity in trauma has been associated with neural tissue destruction
blocks presynaptic calcium dependent glutamate release
Given for 10 days (translational research); same dose as in ALS
Non pharmacological neuroprotection: hypothermia
Cooling slows metabolism and enzymatic processes
Easy and faster cooling tried with femoral sheath catheter
Preliminary data based on
cooling temperaturetime to target temperatureduration of coolingany adverse event ……..
to be noted
Regenerative strategies..
The notion that the central nervous system cannot regenerate axons after injury was convincingly disproved in the 1980s
Innate mechanisms that stunt the growth – Myelin associated proteins (MAP) lack of regenerative capacity
Many inhibitors to MAP – focus of clinical trials ATI335 and Cethrin
Nogo-A monoclonal antibody (ATI335)
Antibody against myelin associated protein
Promotes axonal growth and functional recovery in primate model
Clinical trials underway in Europe and Canada
Cethrin..
Myelin inhibitors of axonal growth signal through Rho cascade
Rho (Guanosine triphosphatase) when activated binds to Rho kinase (ROCK) key regulator of axonal growth cone dynamics and cellular apoptosis
Disruption of this cascade facilitates axon growth
Clostridium botulinum and C3 transferase – specific inhibitors of Rho used in initial studies
Cethrin (recombinant protein + fibrin glue) – applied directly to dura promising result in phase I trial and now Phase II trial being done
Cellular transplantation strategies..
Concept:
optimizing the spinal cord for natural recovery
introduces the cell types with the goal of integrating these cells within the spinal circuits allowing neurological recovery
3 different cell types are in focus though many types studied
Activated Autologous Macrophages
Macrophages play a vital role in regeneration of peripheral nervous function – concept recognized for 2 decades
Macrophages recruited at the injury site clears myelin debris optimizes environment for regeneration
Autologous macrophages activated with peripheral myelin injected in damaged area of cord shortly after injury
Promising result in small no. of individuals
Cons – financial circumstances
Bone marrow stromal cells
They are relatively accessible multipotent stem cells
Potential to differentiate and integrate into existing spinal circuits to result in neural recovery
Researchers report significant neurological recovery after direct injection in the damaged area
Researchers in Prague, Czech Republic – significant improvement in ASIA grade and Electrophysiology
Improvement noted if injected within 3-4 weeks of injury
Human Embryonic Stem Cells
More promising strategy in cell replacement
Cells first cultured in vitroissue – purity/ viral contamination via delivery
vectors and acquisition of membrane polysaccharides may react with host immune system
Goal:
achieve differentiation of stem cells into oligodendrocyte aid in remyelination of spared by demyelinated axons
Clinical Management
ATLS protocol strictly adhered
Immediate life threatening condition addressed
Rigorous management of hypotension
Stabilization and proceeded to neurological examination (motor, sensory, relfexes and anal tone) and documented in standard ASIA forms
Imaging of spinal column (CT and MRI)
Two measurements are useful in quantifying the degree of injury – maximal spinal canal compromise and maximal cord compression
Calculation of compromise and restoration after decompressive surgery
Spinal Shock
Depressed spinal reflexes caudal to injury site following SCI
Important concept to understand because the initial neurological examination may not be an accurate reflection
Cause: Reflex pathways receive continuous input from the brain if this tonic input disrupted normal reflex pattern disrupted (vary from areflexia to hyperreflexia depending on time since injury)
Recommendation: re examination 72 hours post injury when the spinal shock will be over
Neurogenic Shock
Potentially life threatening condition
Disruption of sympathetic nervous system with preserved parasympathetic activity
Typically in patients of severe SCI at the level of T6 or higher
Three areas of cardiovascular system affected: coronary blood flow, cardiac contractility and heart rate
Bradycardia and cardiac arrhythmia in the setting of profound hypotension
Neurogenic shock contd..
Must distinguish from hypovolemic shock, which might be practically very difficult when 2 coexist frequently in the setting of trauma (theoretically – tachycardia with hypovolemia)
Consortium of Spinal Cord Medicine Recommendationto rule out other causes of shock before assuming
the diagnosis
TreatmentRestoration of intravascular volume vasopressors
(dopamine) if shock persistsBP Target – MAP of 85 mm Hg
Spinal Cord Syndromes..
There is a predictable pattern of neurological deficit when a select region of the spinal cord is damaged
Transverse Spinal Cord lesion
disrupt all motor and sensory pathways at and below the lesion
sensory level corresponds to the level of the lesion
Spinal Cord Syndromes..
Hemisection of spinal cord (Brown-Sequard Syndrome)
all motor and sensory pathways at the level of the lesion
ipsilateral upper motor neuron weakness
ipsilateral loss of vibration and position sense
contralateral loss of pain and temperature below the level of the lesion
may also be ipsilateral loss of pain and temperature at the level of the lesion for one or two spinal segments if the lesion has damaged posterior horn cells before the fibers have crossed the other side
Spinal Cord Syndromes..
Central Cord Syndrome
causes – traumatic contusion, post traumatic syringomyelia or medullary spinal tumor
affect pathways on immediate vicinity to the central portion
bilateral regions of suspended sensory loss to pain and temperature
if the lesions are larger – anterior horn cells, corticospinal tract, posterior columns affected
Spinal Cord Syndromes..
Posterior Cord Syndrome
bilateral loss of vibration and position sense below the level of the lesion
large lesion – UMN below lesion (lateral corticospinal tract)
causes – trauma, Vitamin B12 deficiency and tertiary syphilis
Spinal Cord Syndromes..
Anterior cord syndrome
loss of pain and temperature sensation below the level of the lesion
LMN at the level of the lesion (anterior horn cell damage)
UMN below the level of the lesion (lateral corticospinal tract)
urinary incontinence common because of the ventral location of the descending pathways controlling sphincter
Patterns in various spinal cord lesions…
EVIDENCE BASED MEDICINEIN
THE MANAGEMENT OF SPINAL CORD INJURIES
Evidence of Early Closed Reduction of Bilateral Locked FacetsInferior articular facet from one vertebral body is dislocated anteriorly with respect to the superior facets of the adjacent vertebra
Requisite:
Awake and alert patient who is able to participate in repeated neurological examination
DO NO HARM
Aim: to relieve spinal cord compression by restoring normal bony alignment
Class II and III evidence..
Gardner-Wells tongs or a halo crown – rigid fixation device to the skull and apply traction force
Increasing weight added over time while monitoring neurological status and lateral radiographs
Post reduction MRI to rule out disc herniation
Results: neurological deterioration to no neurological deterioration to neurological improvement
Several authors reported – improvement or transient neurological decline with improvement after removal of added weight
Evidence of Methylprednisolone Therapy
Controversial role in mitigating the deletrious effects of secondary injury
The National Acute Spinal Cord Injury Study (NASCIS) trial
NASCIS I, NASCIS II and NASCIS III
Multicenter trial
NASCIS I
Compared low and high dose methylprednisolone
No placebo arm
Randomized pts. Into 2 cohorts – Grp 1 – 100 mg loading dose followed by 25 mg 6hrly for 10 daysGrp 2 – 1000 mg loading dose followed by 250 mg 6hrly for 10 days
No differences in neurological outcome between 2 groups at 1 year after injury
NASCIS II
30mg/kg bolus methylprednisolone over 1 hour followed by 5.4 mg/kg/hr over the following 23 hrs
Compared with placebo group and naloxone administration group
Result from overall group – no significant differences in neurological outcome at 6 months
Subgroup analysis – improved motor and sensory outcomes in patients receiving methylprednisolone within 8 hours of injury
NASCIS III
Compared 30mg/kg bolus followed by 5.4mg/kg/hr for either 23 hours or 47 hours
Patients treated with methylprednisolone for 48 hrs had better neurological outcomes if started within 3 to 8 hours of injury
Increased risk of sepsis and pneumonia in 48 hrs group (Bracken’s review said safe though)
Interpretation
Results not overwhelmingly in favor of methylprednisolone
Considerable debate
Michael G. Fehlings –
acute nonpenetrating SCI – receives as per NASCIS II if started less than 3 hours of injury and as per NASCIS III if 3-8 hrs of injury
if >8hrs and penetrating SCI – NO steroids
take into account of patients comorbidity like DM and complete thoracic SCI
Blood glucose levels must be monitored and aggressively managed with insulin infusion in case of hyperglycemia
Evidence of Early Surgical Decompression
Indication for surgeryspinal instability – little controversy in this setting
aims to relieve compression that would othewise trigger ongoing series of deletrious cascades
Most important issue – timing of surgery
Early surgery performed within 24 hours – improved neurological outcome in series of animal study
Preliminary result of STASCIS (Surgical Treatment of Acute Spinal Cord Injuries) Trial – decompression within 24 hrs – improves outcome in patients with isolated SCI
Very early decompression, within 12 hours of injury, should be strongly considered for patients suffering
incomplete cervical SCI or those who are deteriorating neurologically
Based on both animal studies and RECENT CLINICAL INVESTIGATIONS
Thank you!!!