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!!!