7. SIGNIFICANCE
• Unstable if middle column + either Anterior or
Posterior column is damaged
• Rupture of interspinous ligament is :
- associated with avulsion of spinous process
- Unstable spine
- Further flexion increases neurological injury
7
8. LEVEL OF SPINAL INJURY
• Neurological level is at the most lowest segment
with normal motor & sensory function
• Difficult to determine :
- As most muscle efferents receive fibers from more
than one level
- Closed cord lesions may extend over several cms.
- Dermatomes have imprecise boundaries.
8
9.
10. MECHANISM OF INJURY
1
• Impact with persisting compression
• Impact with no persistent compression
• Distraction
• Laceration/Transection
11. PATHOPHYSIOLOGY
• Primary Neurological damage
External compression- Direct trauma, hematoma
In 4hrs - Infarction of white matter occurs
In 8hrs - Infarction of grey matter and irreversible
paralysis
• Secondary damage
Hypoxia
Hypo-perfusion
Neurogenic shock
Spinal shock 11
12. CLINICAL FEATURES
• Pain
• Respiratory distress
• Sensitivity to stimuli
• Loss of reflex
• Autonomic disturbances
• Paralysis
12
13. PATIENT ASSESSMENT
Any of the following patients should be treated as having a SCI until proven
otherwise:
1. all victims of significant trauma
2. trauma patients with loss of consciousness
3. minor trauma victims with complaints referable to the spine (neck or back pain
or tenderness) or spinal cord (numbness or tingling in an extremity, weakness)
4. associated findings suggestive of SCI include
A. abdominal breathing
B. priapism (autonomic dysfunction)
13
14. RADIOGRAPH IN SPINAL
INJURY
• Lateral C spine views in diagnostic in 80%
• Complete set of C spine xray are 90% diagnostic
• CT of the C-spine is 98% diagnostic
• 22.50 logrolled view for better views of the facets
• 450 view shows the intervertebral foramen &
facets
14
15. 15
SCIWORA
• Incidence- 3% - 5%
• Higher in pediatric age group (35%)
• No radiological incidence of fracture/dislocation
• MRI findings:
» Intervertebral disc rupture
» Epidural hematoma
» Cord contusion
» Hematomylia
17. PREHOSPITAL TRANSFER
• Modified left lateral position at scene
• Scoop stretcher slotted together around the patient
• Repeated assessment enroute
• Head down if they vomit
• Remove objects from clothes to avoid pressure sores
17
18. 1.Spinal pain or tenderness, including any neck pain with a history of trauma
2. Significant multiple system trauma
3.Severe head or facial trauma
4.Numbness or weakness in any extremity after trauma
5.Loss of consciousness caused by trauma
6.If mental status is altered
7. Any significant distracting injury
SPINAL IMMOBILISTION
19. CARE IN ED
• Careful manual handling especially if unconscious
• Jaw thrust is safer
• Intubation if respiratory distress or RR>35
• Ryles tube if abdominal distention causes respiratory distress
• Catheterize to avoid over stretching of detrusor
• IV fluids – paralytic ileus in first 48hrs.
• Passive movements to rule out fractures
19
20. PRIMARY SURVEY
STEP 1. Airway:
A. Assess the airway while protecting the cervical spine.
B. Establish a definitive airway as needed.
STEP 2. Breathing: Assess and provide adequate oxygenation and
ventilatory support as needed.
21. STEP 3. Circulation:
A. Differentiate hypovolemic shock from
neurogenic shock
B. Replace fluids for hypovolemia.
C. IV Fluid resuscitation
D. DRE
21
22. STEP 4. Disability—Brief Neurologic Examination:
A. Determine level of consciousness and assess
pupils.
B. Determine Glasgow Coma Scale (GCS) score.
C. Recognize paralysis/paresis.
22
23. SECONDARY SURVEY
Step 1.Obtain AMPLE history.
A. History and mechanism of injury
B. Medical history
C. Identify and record drugs given prior to the patient’s arrival and during
the assessment and management phases
Step 2 Reassess level of consciousness and pupils.
Step 3.Reassess GCS score.
Step 4.Assess the spine
23
26. NEUROGENIC SHOCK
• Lesions above D6
• Minutes – hours (fall of catecholamines may take 24 hrs)
• Disruption of sympathetic outflow from D1 - L2
• Unopposed vagal tone
• Peripheral vasodilatation
• Hypotension, Bradycardia & Hypothermia
• BUT consider hemorrhagic shock if – injury below D6,
other major injuries, hypotension with spinal fracture
alone without neurological injury.
27
27. SPINAL SHOCK
• Transient physiological reflex depression of cord
function – ‘concussion of spinal cord’
• Loss of motor and sensory and reflexes below the
lesion
• Loss anal tone, reflexes, autonomic control within 24-
72hr
• Flaccid paralysis bladder & bowel and sustained
Priapism
• Lasts till reflex neural arcs below the level recovers.
28
28. 29
PHASES OF SPINAL SHOCK
Phases Physical findings Underlying mechanism
Phase-1
0-1 day
Areflexia Loss of descending facilitation
Phase-2
1-3 days
Initial reflex return Denervation supersensitivity
Phase-3
1-4 weeks
Hyper reflexia Axon supported synapse
growth
Phase-
1-12 months
Hyper reflexia, spasticity Soma supported synapse
growth
29. 30
RADIOLOGICAL ASSESSMENT
Awake asymptomatic- discontinuance of cervical
immobilization without cervical spinal imaging.
Awake symptomatic-continue cervical immobilization , CT
imaging
Awake symptomatic - normal CT normal X ray
Obtunded- CT imaging, if CT unavailable 3 series Xray
34. NORMAL CERVICAL SPINE
• Peg & lateral mass distance <2mm and symmetrical
• Peg & arch of atlas distance <2mm in adults < 4mm in kids
• Above C4 the width is <half of the VB width below C4 its
equal to one VB width
• Pseudosubluxation of C2 on C3 is normal in young kids& it
disappears on extension
• C1 and C2 interspinous space <10mm wide
• Distance between occiput and atlas <3.5mm
• Anterior compression of VB >40% suggest burst fracture 35
35. ABNORMAL CERVICAL SPINE
• Unilateral facet dislocation < half of the vertebral body
shifted on the lateral view
• Bilateral facet dislocation > half shifted forwards
• Wide interspinous gap is unstable (crush fracture or
subluxation) suggestive of rupture of the posterior
cervical ligament rupture and haematoma formation.
• Severe flexion injury – fractures the anteroinferior
margin of the vertebral body
• Severe extension injury – fractures the anterosuperior
margin of the VB. 36
36. PRINCIPLES OF DEFINITIVE
TREATMENT
The objectives of treatment are:
• To preserve neurological function;
• To minimize a perceived threat of neurological compression;
• To stabilize the spine;
• To rehabilitate the patient
37
37. ANTERIOR CORD SYNDROME
• Flexion rotational force to spine
• Due to compression fracture of vertebral body or
anterior dislocation
• Anterior spinal artery compression
• Loss of power, reduced pain and temperature below
the lesion.
38
38. POSTERIOR CORD SYNDROME
• Hyperextension injuries
• Posterior vertebral body fracture
• Loss of proprioception and vibration sense
• ataxia
39
39. CENTRAL CORD SYNDROME
• Older age with cervical spondylosis
• Hyperextension with minor trauma
• Cord is compressed by osteophytes from vertebral body
against thick ligamentum flavum.
• Damages the central cervical tract
• UMN lesion to legs (spastic)
• LMN to arms (flaccid paralysis)
40
40. BROWN SEQUARD SYNDROME
• Hemisection of the cord
• Stab injury and lateral mass fractures
• Uninjured side has good power but absent pinprick
and temperature.
• Spinothalamic tracts cross to opposite side of the
cord three segments below.
41
41. 42
CERVICAL SPINE FRACTURE
1. hyperextension fracture-dislocations
• Posterior fracture-dislocation of the dens
• Traumatic spondylolisthesis of the axis (hangman's
fracture
• hyperextension sprain (momentary dislocation) with
fracture
• Hyperextension fracture-dislocation with fractured
articular pillar
• Hyperextension fracture-dislocation with comminution of
the vertebral arch
42. 43
2. HyperfIexion fracture-dislocations
• Anterior fracture-dislocation of the dens
• HyperfIexion sprain: rare. Occurs when posterior ligaments are
disrupted but locking of articular facets does not occur
• Locked articular facets with fracture
• "Teardrop" fracture-dislocation
46. 47
ATLANTO AXIAL
DISLOCATION
Clinical findings
• Patients are usually young.
• Neurologic deficit is rare.
• Neck pain, headache, torticollis (~ 20° lateral tilt to one
side, 20° rotation to the other, and slight (~ 10°) flexion,
• Reduced range of motion, dislocation can increase with
head rotation towards the subluxed joint with potential
injury to the high cervical cord.
50. 51
. ATLAS (C1) FRACTURE
Sudden severe load on the top of the
head may cause a ‘bursting’ force
which fractures the ring of the atlas
(Jefferson’s fracture).
Classification
Type I: fractures involving a single
arch (31-45% of C1 fractures)
Type II: burst fracture (37-51%)
Type III: lateral mass fractures of
the atlas (13-37%)
52. 53
Landells Atlas Fractures Classification
Type-1 Isolated anterior or posterior arch fracture. A "plough fracture is an isolated
anterior arch fracture caused by a force driving the odontoid through the anterior arch.
Stable. Treat with hard collar.
Type-2 Jefferson burst fracture with bilateral fractures of anterior and posterior arch
resulting from axial load. Stability determined by integrity of transverse ligament. If
intact, hard collar. If disrupted, halo vest (for bony avulsion) or C1-2 fusion (for
intrasubstance tear).
Type-3 Unilateral lateral mass fx. Stability determined by integrity of transverse
ligament. If stable, treat with hard collar. If unstable, halo vest.
Dickman Transverse Ligament Injuries Classification
Type-1 Intrasubstance tear. Treat with C1-2 fusion.
Type-2 Bony avulsion at tubercle on C1 lateral mass. Treat with halo vest (successful in
75%)
54. 55
Levine and Edwards Classification
Tpe-1 Axial compression and
hyperextension
• < 3mm horizontal
displacement C2/3
• No angulation
• C2/3 disc remains
intact
• stable fx pattern
• Rigid collar x 4-6 weeks
Type-2 Hyperextension and
axial load followed by
rebound flexion
• > 3mm of horizontal
displacement
• Significant angulation
• Vertical fracture line
• C2/3 disc and PLL are
disrupted
• unstable fracture pattern
• If < 5mm displacement,
reduction with traction then
halo immobilization x 6-12
weeks
• If > 5mm displacement,
surgery or prolonged traction
• Usually heal despite
displacement (autofuse C2 on
C3
Type-2A Flexion-distraction • No horizontal
displacement
• Horizontal fracture line
• Significant angulation
• Avoid Traction in Type IIA.
• Reduction with gentle axial
load + hyperextension, then
compression halo
immobilization for 6-12
weeks.
Type-3 Flexion-distraction
followed by
hyperextension
• Type I fracture with
associated bilateral C2-3
facet dislocation
• Rare injury pattern
• Surgical reduction of
facet dislocation
followed by stabilization
required.
60. 61
CLASSIFICATION
Anderson and D'Alonzo Classification
Type -I Oblique avulsion fracture of tip of odontoid. Due to
avulsion of alar ligament. Although rare, atlanto-occipital
instability should be ruled out with flexion and extension
films.
Type -II Fracture through waist (high nonunion rate due to
interruption of blood supply).
Type -III Fracture extends into cancellous body of C2 and
involves a variable portion of the C1-C2 joint.
62. 63
TREATMENT
Type I fractures Isolated fractures
of the odontoid tip are
uncommon.
• They need no more than
immobilization in a rigid collar
until discomfort subsides.
63. 64
Type II fractures- often unstable and prone to non-
union, especially if displaced more than 5 mm.
Undisplayed fractures- held by fitting a halo vest or
in elderly patients a rigid collar.
Displaced fractures- traction and can then be held
by operative posterior C1/2 fusion, a drawback is
that neck rotation will be restricted
71. WHIPLASH INJURY
• Sudden hyperextension and flexion
• Increasing neck pain for the first 24hours
• Associated headache, pain radiating to both shoulders and
paraesthesia in hands
• Reduced lateral flexion
• Anterior longitudinal ligaments are torn causes dysphagia
• Forward flexion against resistance is painful
• 90% are asymptomatic after 2years
• 10% still have pain
• Some still claim money hence the need for proper
documentations.
72
75. 76
TAKE HOME MESSAGE
• Over half of spinal cord injury occurs in
cervical spine region
• Cervical spine immobilization(hard
collar+spinal board)
• Neurogenic shock is triad of hypotension,
bradycardia & peripheral vasodilatation
Notes de l'éditeur
The cervical spine is the most vulnerable to injury, because of its mobility and exposure. The cervical canal is wide in the upper cervical region, or from the foramen magnum to the lower part of C2.
Below the level of C3 the diameter of the spinal canal is much smaller relative to the diameter of the spinal cord, and vertebral column injuries are much more likely to cause spinal cord injuries.
Stability of this joint complex is primarily due to ligaments, with little contribution from bony articulations and joint capsules
ligaments that connect the atlas to the occiput:anterior atlanto-occipital membrane: cephalad extension of the anterior longitudinal ligament. Extends from anterior margin of foramen magnum to anterior arch of C1 posterior atlantooccipital membrane: connects the posterior margin of the FM to posterior arch of Cl the ascending band of the cruciate ligament
axis (viz. the odontoid) to the occiput: 1 tectorial membrane 2. alar ("check") Iigaments
axis to the atlas: transverse (atlantoaxial) ligament:B.atlanto-alar portion of the alar ligaments .descending band of the cruciate ligament
A stable injury is one in which the vertebral components will not be displaced by normal movements; • In a stable injury, if the neural elements are undamaged there is little risk of them becoming damaged. • An unstable injury is one in which there is a significant risk of displacement and consequent damage – or further damage – to the neural tissues.
Anterior column - Anterior longitudinal ligament+ Anterior annular ligament and anterior half of VB.
Middle column – Posterior long. Lig. + Posterior annular ligament +Posterior half of VB.
Posterior Column – Lig flavum + superior & Interspinous lig + inter transverse capsular lig + neural arch + pedicle & spinous process.
all patients with radiographic evidence of injury and all those with neurologic deficits should be considered to have an unstable spinal injury.
Clinical instability:Acute: by bony and ligamentous injury
Chronic: progressive deformity leading to neurological deterioration
Predisposing factor: ankylosing spondylosis, DDD, canal stenosis,RA, osteomylitis, malignancy
Classification
Incomplete Injury: some motor and sensory function below the lesion, sphincter contraction and toe flexion +
Complete Injury: Total motor and sensory loss below the lesion after spinal shock 24-48hrs.
Bulbocavernosus reflex + but no sacral sensation
Pitfalls: ▪ The sensory examination may be confounded by pain. ▪ Patients sometimes observe the examination itself, which may alter the findings. ▪ Altered level of consciousness limits the ability to perform a definitive neurologic examination.
Fracture dislocation and disc herniation
*Hyperextension injury
**hyperflexion
*** penetrating injury with Fracture dislocation
aim: immobilisation and resusitation
(including drugs, alcohol, trauma) ,no history is available, or the patient is found in a setting of possible trauma (eg, lying at the bottom of stairs or in the street); or the patient experienced near drowning with a history or probability of diving
a cervical collar, supports on either side of the head, and either long or short backboards with associated straps to attach and immobilize the entire patient’s body to the board.
Immobilization of the entire spinal column is necessary in these patients until a spinal cord injury (or multiple injuries) has been excluded or until appropriate treatment has been initiated.
A combination of a rigid cervical collar and supportive blocks on a backboard with straps is effective in limiting motion of the cervical spine and is recommended.
Definitive airway if respiratory compromise, if injury above CV5 level patient may require intubation
15ml/min o2
If spinal cord injury is present, fluid resuscitation should be guided by monitoring central venous pressure (CVP). (Some patients may need inotropic support.)
When performing a rectal examination before inserting the urinary catheter,assess for rectal sphincter tone and sensation.
ADJUNCT TO PRIMARY SURVEY: X-ray chest,pelvis, c-spine
FAST Abdomen, NGT, foleys catheter
ask mechanism of injury, ask if he feels sensation of touch, ask to move limbs or extremities
assess spine(log roll) for deformity, crepitus, tenderness,contusion or penetrating wound
assess pain paralysis paresthesia with level
test sensation DTR, Motor function
imaging-CT/MRI
Document the level of injury
Rule out other injuries
- Renal injurie- Chest and Sternal injuries - Wide Mediatinum due to fracture haematoma.
- Retroperitoneal injuries
Neurogenic shock results from impairment of the descending sympathetic pathways in the cervical or upper thoracic spinal cord. This condition results in the loss of vasomotor tone and in sympathetic innervation to the heart. Neurogenic shock is rare in spinal cord injury below the level of T6; if shock is present in these patients, an alternative source should be strongly suspected. Loss of vasomotor tone causes vasodilation of visceral and lower-extremity blood vessels, pooling of blood, and, consequently, hypotension. Loss of sympathetic innervation to the heart may cause the development of bradycardia or at least a failure of tachycardia in response to hypovolemia. In this condition, the blood pressure may not be restored by fluid infusion alone, and massive fluid resuscitation may result in fluid overload and pulmonary edema. The blood pressure may often be restored by the judicious use of vasopressors after moderate volume replacement. Atropine may be used to counteract hemodynamically significant bradycardia.
Spinal shock refers to the flaccidity (loss of muscle tone) and loss of reflexes seen after spinal cord injury. The “shock” to the injured cord may make it appear completely nonfunctional, although the cord may not necessarily be destroyed, duration is variable.
1-DTRs such as the AJ and the KJ are initially absent,muscles are flaccid and paralyzed.cutaneous (polysynaptic) reflexes such as the BC, CM begin to recover. bsence of all reflexes is uncommonly observed during the initial 24 h
*without neck pain/tenderness, normal neurological examination, is without an injury detracting from an accurate evaluation, complete functional range of motion examination radiographic evaluation of the cervical spine is not recommendedIf high-quality
**CT imaging is not available, a 3-view cervical spine series 3 view cervical spine Xray
*** 1. Continue cervical immobilization until asymptomatic, 2.Discontinue cervical immobilization following normal and adequate dynamic flexion/ extension radiographs, 3. Discontinue cervical immobilization following a normal magnetic resonance imaging (MRI) obtained within 48 hours of injury or,
STEP1. Assess adequacy and alignment
A. Identify the presence of all 7 cervical vertebrae and the superior aspect of T1.
B. Identify the:• Anterior vertebral line • Anterior spinal line• Posterior spinal line• Spinous processes
STEP2. Assess the bone-A. Examine all vertebrae for preservation of height and integrity of the bony cortex. B. Examine facets.C Examine spinous processes.
STEP3. Assess the cartilage, including examining the cartilaginous disk spaces for narrowing or widening
STEP4: assess Dens A.Examine the outline of the dens. B.Examine the predental space (3 mm). C.Examine the clivus; it should point to the dens. Assess the extra-axial soft tissues. A.Examine the extraaxial space and soft tissues space•7 mm at C3 •3 cm at C7 B.Examine the distances between the spinous processes.
Top of T1 visible Three smooth arcs maintained Vertebral bodies of uniform
height Odontoid intact and closely approximated to C1
An adequate film should include the entire odontoid and the lateral borders of C1-C2.
• Occipital condyles should line up with the lateral masses and superior articular facet of C1. • The distance from the dens to the lateral masses of C1 should be equal bilaterally.
• The tips of lateral mass of C1 should line up with the lateral margins of the superior articular facet of C2. • The odontoid should have uninterrupted cortical margins blending with the body of C2.
The height of the cervical vertebral bodies should be approximately equal
The height of each joint space should be roughly equal at all levels
Spinous process should be in midline and in good alignment
hi
administration of methylprednisolone (MP) for the treatment of acute spinal cord injury (SCI) is not recommended. Clinicians con- sidering MP therapy should bear in mind that the drug is not Food and Drug Administra- tion (FDA) approved for this application. There is no Class I or Class II medical evidence supporting the clinical benefit of MP in the treatment of acute SCI. Scattered reports of Class III evidence claim inconsistent effects likely related to random chance or selection bias. However, Class I, II, and III evidence exists that high-dose steroids are associated with harmful side effects including death.
Anterior cord syndrome is characterized by para- plegia and a dissociated sensory loss with a loss of pain and temperature sensation. Dorsal column func- tion (position, vibration, and deep pressure sense) is preserved. Usually, anterior cord syndrome is due to infarction of the cord in the territory supplied by the anterior spinal artery. This syndrome has the poorest prognosis of the incomplete injuries.
Central cord syndrome is characterized by a disproportionately greater loss of motor strength in theupper extremities than in the lower extremities, with varying degrees of sensory loss. Usually this syndrome occurs after a hyperextension injury in a patient with preexisting cervical canal stenosis (often due to degen- erative osteoarthritic changes), and the history is com- monly that of a forward fall that resulted in a facial impact. Central cord syndrome is thought to be due to vascular compromise of the cord in the distribution of the anterior spinal artery. This artery supplies the central portions of the cord. Because the motor fibers to the cervical segments are topographically arranged toward the center of the cord, the arms and hands are the most severely affected.
Central cord syndrome may occur with or without cervical spine fracture or dislocation. Recovery usually follows a characteristic pattern, with the lower extremi- ties recovering strength first, bladder function next, and the proximal upper extremities and hands last. The prognosis for recovery in central cord injuries is some- what better than with other incomplete injuries.
Brown-Séquard syndrome results from hemisec- tion of the cord, usually as a result of a penetrating trauma. Although this syndrome is rarely seen, varia- tions on the classic picture are not uncommon. In its pure form, the syndrome consists of ipsilateral motor loss (corticospinal tract) and loss of position sense (dor- sal column), associated with contralateral loss of pain and temperature sensation beginning one to two levels below the level of injury (spinothalamic tract). Even when the syndrome is caused by a direct penetrating injury to the cord, some recovery is usually seen.
Type I anterior dislocation of occiput relative to the atlas
Type II longitudinal dislocation (distraction) Type III posterior dislocation of occiput
CUNICAL PRESENTATION
1. may be neurologically intact, therefore must be ruled-out in any major trauma 2. bulbar-cervical dissociation3.may have lower cranial nerve deficits (as well as VI palsies) ± cervical cord injury 4worsening neurologic deficit with the application of cervical traction: check lateral C-spine films immediately after applying traction
One useful finding is a Power’s ratio >1 (BC/OA, where BC is the distance from the basion [B] to the posterior arch [C] of C1, and OA is the distance from the anterior arch of C1 [A] to the opisthion [O, the posterior margin of the foramen magnum]). Wackenheim’s line, drawn along the clivus, does not intersect the dens on a normal lateral cervical spine radiograph. If an atlanto-occipital injury is suspected, spinal immobilization should be preserved.
A. basion-axial interval (BAl) = distance from basion to rostral extension of posterior axial line (PAL) (the posterior cortical margin of the body of the axis). Better for anterior or posterior~ AOD
B. basion-dental interval (BDI) =distance from basion to the closest point on the tip of the dens (not used in children < 13 years because of variable age of ossification & fusion of the tip of the odontoid). Better for distracted AOD
Treatment: Do not apply cervical traction in an attempt to reduce AOD because of risk of neurologic deterioration Controversial whether operative fusion vs. prolonged immobilization (4-12 months) with halo brace is required. However, posterior occipito-cervical fusion is usually recommended
Rotational deformity at the atlanto-axial junction is Usually seen in children. May occur spontaneously, with rheumatoid arthritis·',with congenital dens anomalies, following major or minor trauma (including neck manipulation or even with neck rotation while yawning') , or with an infection of the head or neck in cluding upper respiratory tract.known as Grisel's syndrome": inflammation may cause mechanical and chemical injury to the facet capsules and/or transverse ligament (TL)).
flexion-extension xrays
atlanto-dens interval-distance between odontoid process and the posterior border of the anterior arch of the atlas,> 3.5mm considered unstable
space-available-cord (SAC) = posterior atlanto-dens interval (PADI) distance from posterior surface of dens to anterior surface of posterior arch of atlas: in adults < 14 mm associated with increased risk of neurologic injury and is an indication for surgery
open mouth odontoid
sum of lateral mass displacement measurement
lateral mass are connect by ring of C1, and therefore can only be displaced relative to each other if
there is a bony fracture (disruption of the ring)the transverse ligament is ruptured transverse ligaments binds them together adult parameters if > 8.1 mm, then a transverse ligament rupture is assured and the injury pattern is considered unstable
sum of lateral mass displacement measurement
lateral mass are connect by ring of C1, and therefore can only be displaced relative to each other if
there is a bony fracture (disruption of the ring)
the transverse ligament is ruptured
transverse ligaments binds them together
adult parameters if > 8.1 mm, then a transverse ligament rupture is assured and the injury pattern is considered unstable
Treatment Treatment of Grisel's syndrome: appropriate antibiotics for causative pathogen with
traction and then immobilization for the subluxation.
Traction: The subluxation may be reduced with gentle traction (in children start with 7-8 Ibs and gradually increase up to 151bs over several days, in adults start with 15 Ibs and gradually increase up to 20). If the subluxation is present> 1 month, traction is less successful. Active left-right neck rotation is encouraged in traction.
If reducible, immobilization in traction or halo is maintained X 3 months" (range: 6 12 weeks).
Subluxation that cannot be reduced or that recurs following immobilization should be treated by surgical arthrodesis after 2-3 weeks of traction to obtain maximal reduc tion. The usual fusion is C1 to C2 (see page 623) unless other fractures or conditions are present". Fusion may be performed even if the rotation between C1 & C2 is not complete ly reduced
Computed tomography (CT) imaging to determine the CCI (condyle-C1 interval) in pediatric patients with potential atlanto-occipital dislocation (AOD) is recommended.
Treatment with internal fixation and fusion using one of a variety of methods is recommended.
Traction is not recommended in the management of patients with AOD, and is associated with a 10% risk of neurological deterioration
Named for Sir Geoffrey Jefferson. Classically described as a four-point (burst) fracture of the Cl ring, but also taken to include the more common three or two-point fractures the latter through the Cl arches (thinnest portion). Usually from axial load (a "blow-out" fracture). 41% chance of an associated C2 fracture.~ ,
usually no neurologic deficit if isolated (due to large canal diameter at this level, plus tendency for fragments to be forced outwards).
EVALUATION
Complete C-spine series and thin section high-resolution CT from Cl through C3 to delineate details ofCl fracture and to assess for associated C2 injury. MRI is an option to assess the integrity of the transverse ligament.
Assessing integrity of transverse ligament
1. may be inferred indirectly from
A. abnormal overhang of lateral masses on open-mouth odontoid viewB.atlantodental interval (AD!) > 3 mm is also a marker for TL disruption 2. MRI may be able to image the ligament directly
Radiographs
lateral radiographs
atlantodens interval (ADI)
< 3 mm = normal in adult (< 5mm normal in child)
3-5 mm = injury to transverse ligament with intact alar and apical ligaments
> 5 mm = injury to transverse, alar ligament, and tectorial membrane
open-mouth odontoid
open-mouth odontoid view important to identify atlas fractures
sum of lateral mass displacement
if sum of lateral mass displacement is > 7 mm (8.1mm with radiographic magnification) then a transverse ligament rupture is assured and the injury pattern is considered unstable q q
CT
study of choice to delineate fracture pattern and identify associated injuries in the cervical spine
MRI
more sensitive at detecting injury to transverse ligament
Nonoperative
hard collar vs. halo immobilization for 6-12 weeks
indications
stable Type I fx (intact transverse ligament)
stable Jefferson fx (Type II) (intact transverse ligament)
stable Type III (intact transverse ligament)
technique
controversy exists around optimal form of immobilization
Operative
posterior C1-C2 fusion vs. occipito cervical fusion
indications
unstable Type II (controversial)
unstable Type III (controversial)
technique
may consider preoperative traction to reduce displaced lateral masses
bilateral fracture through the pars interarticularis of C2 with traumatic subluxation of C2 on C3, most often from hyperextension + axial loading usually stable with no neurologic deficit most do well with non-halo immobilization x 8-14 weeks (exceptions: severe/un- stable fractures or those that do not remain in alignment in brace) AKA traumatic spondylolisthesis of the axis. most patients are neurologically intact, those few with deficits are usually minor (paresthesias, monoparesis ) and many recover within one month , Almost all conscious patients will have cervical pain usually in the upper posterior cervical region, and occipital neuralgia is not uncommonI " . There is a high incidence of associated head injury and there will be other associated C-spine injuries (e.g. Cl fracture
Evaluation
Plain lateral C-spine x-rays show the fracture in 95% of cases. CT may be needed in the remainder. Most fractures pass through the pars or the transverse foramen''', 7% go through the body of C2. Instability can usually be identified as marked anterior displacement of C2 on C3 (guideline'l4 : unstable if displacement exceeds 50% of the AP diameter of C3 vertebral body), excessive angulation of C2 on C3, or by excessive motion on flexion-extension films
hangman's fractures may initially be managed with external immobilization in most cases (halo or collar) surgical stabilization should be considered in cases of:
A. severe angulation of C2 on C3 (Effendi II, Francis II & IV) B. disruption of the C2-3 disc space (Effendi III, Francis V) C. or inability to establish or maintain alignment with external immobilization
SURGICAL TREATMENT Few patients have indications for surgical treatment ofHF, and include those with:
1. inability to reduce the fracture (includes most Effendi Type III & some Type II)
2. failure of external immobilization to prevent movement at fracture site
3. traumatic C2-3 disc herniation with compromise of the spinal cordl23
4. established non-union: evidenced by movement on flexion-extension film '14 , see Flexion-extension cervical spine x-rays,(all failures of nonoperative treatment had displacement> 4 mm")
Hangman's fractures likely to need surgery'" are those with:
1. Effendi Type II or III
A. anterior displacement of C2 VB > 50% of the AP diameter of the C3 VB
B. or if angulation produces widening of either the anterior or posterior bor- ders of the C2-3 disc space> the height of the normal C3-4 disc below
Initial management of nondisplaced type I, type II, and type III odontoid fractures with external cervical immobilization is recommended, recognizing that a decreased rate of union (healing) has been reported with type II odontoid fractures compared with type I or type III odontoid fractures.
• Surgical stabilization and fusion of type II and type III odontoid fractures with dens displacement > 5 mm, comminution of the odontoid fracture, and/or inability to achieve or maintain fracture alignment with external immobilization are recommended. • If surgical stabilization is elected, either anterior or posterior techniques are recommended.
Odontoid fractures are uncommon.They usually Occur as flexion injuries in young adults after high velocity injuries.
• However, they also occur in elderly, osteoporotic people as a result of low-energy trauma in which the neck is forced into hyperextension, e.g. a fall onto the face or forehead
may be anterior (hyperflexion) or posterior (hyperextension)
anterior displacement is associated with transverse ligament failure and atlanto-axial instability, posterior displacement
caused by direct impact from the anterior arch of atlas during hyperextension
biomechanics-a fracture through the base of the odontoid process severely compromises the stability of the upper cervical spine.
Symptoms neck pain worse with motion
dysphagia may be present when associated with a large retropharyngeal hematoma
Physical exam myelopathy very rare due to large cross section area of spinal canal at this level
very rare due to large crs section area of spinal canal at this level
Type I – An avulsion fracture of the tip of the odontoid process due to traction by the
alar ligaments. The fracture is stable (above the transverse ligament) and unites without difficulty.
Type II – A fracture at the junction of the odontoid process and the body of the axis.
• This is the most common (and potentially the most dangerous) type.
The fracture is unstable and prone to non union
a vascular watershed exists between the apex and the base of the odontoid
apex is supplied by branches of internal carotid artery
base is supplied from branches of vertebral artery
the limited blood supply in this watershed area is thought to affect healing of type II odontoid fractures.
Type III – A fracture through the body of the axis.
• The fracture is stable and almost always unites with immobilization. • Clinical features
• The history is usually that of a severe neck strain followed by pain and stiffness due to muscle spasm.
dysphagia may be present when associated with a large retropharyngeal hematoma
• The diagnosis is confirmed by high quality x-ray examination;
• it is important to rule out an associated occipito- cervical injury. I
• myelopathy very rare due to large cross section area of spinal canal at this level
Radiographs-AP, lateral, open-mouth odontoid view of cervical spine
instability defined as atlanto-dens-interval (ADI) > 10mm < 13mm space available for cord (SAC)
findings-fx pattern best seen on open-mouth odontoid
CT-study of choice for fracture delineation and to assess stability of fracture pattern
CT angiogram-required to determine location of vertebral artery prior to posterior instrumentation procedures
MRI indicated if neurologic symptoms MRI has the advantage that it may reveal rupture of the transverse ligament; this can cause instability in the absence of a fracture.
Anterior screw fixation is suitable for Type II fractures,provided the fracture is not comminuted, that the transverse ligament is not ruptured, that the fracture is fully reduced and the bone solid enough to hold a screw; in that case neck rotation is retained.
If full operative facilities are not available, immobilization can be applied by using a halo- vest with repeated x-ray monitoring to check for stability.
Fractured odontoid – treatment (a) A severely displaced Type II odontoid fracture. (b) The fracture was reduced by skull traction and held by fixing the spinous process of C1 to that of C2 with wires. (c) An undisplaced Type II fracture, which was suitable for (d) anterior screw fixation.
Type III fractures If undisplaced, these are treated in a halo-vest for 8–12 weeks
If displaced, attempts should be made at reducing the fracture by halo traction, which will allow positioning in either flexion or extension, depending on whether the displacement is forward or backward; the neck is then immobilized in a halo-vest for 8–12 weeks.
Sudden flexion of the mid-cervical spine can result in damage to the posterior ligament complex (the interspinous ligament, facet capsule and supraspinous ligament). The upper vertebra tilts forward on the one below, opening up the interspinous space posteriorly
(a) The film taken in extension shows no displacement of the vertebral bodies, but there is an unduly large gap between the spinous processes of C4 and 5. (b) With the neck slightly flexed the subluxation is obvious. NB: flexion–extension views are potentially dangerous and should be used only in specific situations under direct supervision of an experienced surgeon.
If it is certain that the injury is stable, a semi- rigid collar for 6 weeks is adequate;
• if the injury is unstable then posterior fixation and fusion is advisable
The middle and posterior elements remain intact and the injury is stable.
All that is needed is a comfortable collar for 6– 12 weeks.
A note of warning: The x-ray should be carefully examined to exclude damage to the middle column and posterior displacement of the vertebral body fragment, i.e. features of a burst fracture (see below)which is potentially dangerous. If there is the least doubt, an axial CT or MRI should be obtained
With combined axial compression and flexion,an antero-inferior fragment of the vertebral body is sheared off, producing the eponymous ‘tear-drop’ on the lateral x-ray
Flexion tear drop It typically occurs from severe flexion and compression forces, most commonly at C5-6 (e.g. diving head first, motor vehicle collision deceleration).
there is a risk of posterior displacement of the vertebral body fragment and spinal cord injury.
• CT or MRI should be performed to look for retropulsion of bone fragments into the spinal canal. If there is no neurological deficit, the patient can be treated surgically or by confinement to bed and traction for 2–4 weeks, followed by a further period of immobilization in a halo-vest for 6–8 weeks. (The halo-vest is unsuitable for initial treatment because it does not provide axial traction).
If there is any deterioration of neurological status while the fracture is believed to be unstable, and the MRI shows that there is a threat of cord compression,then urgent anterior decompression is considered anterior corpectomy, bone grafting and plate fixation, and sometimes also posterior stabilization.
occurs due to forced extension of the neck with resulting avulsion of the anteroinferior corner of the vertebral body. Extension teardrop fractures are stable in flexion, and unstable in extension as the anterior longitudinal ligament is disrupted.
They occur due to forced extension of the neck (i.e. is a hyperextension injury) with resulting avulsion of the anteroinferior corner of the vertebral body.In older patients the C2 vertebral body is commonly affected due to degenerative ankylosis of lower levels. Associated cervical spine fractures are common.
anterior-inferior corner fracture avulsion fracture from the attachment of the anterior longitudinal ligament to the inferior corner of the vertebral body, usually a thin fracture fragment
the fragment is triangular in a shape reminiscent of a teardrop vertical height of fragment is equal to or greater than width anterior disc space widening
Sudden hyperextension and flexion
Increasing neck pain for the first 24hours
Associated headache, pain radiating to both shoulders and paraesthesia in hands
Reduced lateral flexion
Anterior longitudinal ligaments are torn causes dysphagia
Forward flexion against resistance is painful
90% are asymptomatic after 2years
10% still have pain
Some still claim money hence the need for proper documentations.
Often the victim is unaware of any abnormality immediately after the collision.
Pain and stiffness of the neck usually appear within the next 12–48 hours, or occasionally only several days later.
Pain sometimes radiates to the shoulders or interscapular area and may be accompanied by other, more ill-defined, symptoms such as headache, dizziness, blurring of vision, paraesthesia in the arms, temporomandibular discomfort and tinnitus.
Neck muscles are tender and movements often restricted; the occasional patient may present with a ‘skew neck’. Other physical signs – including neurological defects – are uncommon.
X-ray examination may show straightening out of the normal cervical lordosis, a sign of muscle spasm; in other respects the appearances are usually normal.
• In some cases, however, there are features of longstanding intervertebral disc degeneration or degenerative changes in the uncovertebral joints; it may be that these patients suffer more, and for longer spells,than others.
• Collars are more likely to hinder than help recovery.
• Simple pain-relieving measures, including analgesic medication, may be needed during the first few weeks.
• However, the emphasis should be on graded exercises,
• beginning with isometric muscle contractions and postural adjustments, then going on gradually to active movements and lastly movements against resistance.
• The range of movement in each direction is slowly increased without subjecting the patient to unnecessary pain.
